Cortical & Hippocampal Atrophy > Memory Loss, Aphasia, Apraxia

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NEUROLOGY Retts syndrome: Girls only. Normal until MAOI. Bromocriptine/ pergolide: Degenerative Diseases 2yo then rapid regression. X-linked. stimulates D2, vasoconstriction, fibrosis Alzheimers: cortical & hippocampal Stereotyped hand movements (wringing, (bromocriptine is used for prolactinoma, atrophy > memory loss, aphasia, apraxia. tapping), hyperventilation, szs. No Tx. pergolide isn’t). Selegiline/ Eldypryl: ↓ Ach (N.B. of Meynert), NE, dopamine, Binswangers dz: HTN and dementia MAOI, slows progression; deprenyl: & serotonin. Chr 21 (Downs) (±14,19). Transient global amnesia: not seizures, MAOBI. Apolipoprotein E4/E4 ↑ # of plaques, probably 2° to transient ischemia of Parkinsonism: 80% Parkinsons disease, early onset. mesial temporal lobe. 10% Parkinsons-Plus (MSA, PSP, CBGD, Path: Neurofibrillary tangles: τ protein. Movement Disorders diffuse lewy body dz), 10% secondary. Neuritic plaques: βamyloid protein. Both: Tremors: physiologic: 8-13Hz, awake (drugs: neuroleptics, reserpine, Ca-channel cytoplasmic, silver stained, paired helical and asleep. Pathologic 4-7Hz, awake blockers, lithium) filaments. Granulovacular degeneration: only. Parkinsons: rest. Intention: PSP: downgaze palsy, pseudobulbar, gait dark cytoplasmic granules w/clear halo in cerebellar. palsy, eyelid freezing, no tremor, neurons. No gliosis. Essential: action, some familial, improves symmetric. MR: atrophy of midbrain & Tx: donepezil, tacrine w/alcohol, propanalol. tectum. 70yos. No Tx. (acetylcholinesterase inhibitors, slow Dystonia: Twisting/writhing movements, Multiple system atrophy = Parkinsons- progression). Vitamin E & selegiline stopped by touching affected area. Plus, poor response to DA, lack Lewy (MAOI, delay NH placement, not Idiopathic or secondary. Tx: L-dopa, bodies. Dx: Glial (esp. oligodendroglial) cognitive decline). anticholinergics. Thalamotomy. cytoplasmic inclusion bodies. Includes: CJD: prion infects oligodendroglia. Focal: Torticollis, blepharospasm, writers Striatonigral degeneration: syncope, Spongiform encephalopathy. Path: loss of cramp. Tx: botox stridor. Putamen atrophy cerebellar granule & purkinje cells, Tardive dyskinesia: Stereotyped Olivopontocerebellar atrophy: AD, Chr 6, atrophy. Gliosis (none in Alzheimers). No orolingual movement or dystonia. Caused 15yo, LE ataxia, atrophy middle cerebral inflammation. CSF WNL (14-3-3 by phenothiazines ↓ dopamine. peduncle proteinase inhibitor protein specific). Prevent/Tx: Reserpine, anticholinergics Shy-Drager: autonomic probs, impotence, Dementia, myoclonus, spasticity, (trihexyphenydil/Artane, benadryl.) no lewy bodies(?); loss in putamen, SN, & cerebellar & visual/oculomotor problems. Phenothiazines (& Reglan) may also interomediolateral horn cells 100% fatal. Normal protein PrPc on Chr cause parkinsonism, acute dystonic Corticalbasal Degeneration (CBD): 20, converted from α helix to β pleated reaction. Parkinsonism, cortical signs (apraxia, sheet by prion. 10% familial (have mutant Hemiballismus: thalamoperforators, myoclonus) and alien limb. No Tx, PrP in neurons & lymphocytes). EEG 1-2 contralateral STN etiology unknown. Chorea gravidarium: resolves post- Hz spikes, triphasic waves. MRI: ↑T2 Palatal myoclonus: central tegmental pregnancy signal in BG. Dx: Bx. Tx: 1) autoclave at tract or Mollaret’s triangle (red nucleus Meige’s syndrome: facial dystonia 250°F (132°C) at 20PSI for 1hr, 2) bleach, >< inferior olive >< dentate nucleus), (blinking, tongue thrust, etc) idiopathic 3)NaOH x 1hr . Transmitted from cadaver persists during sleep (not phenothiazines) Women, 60yo, Tx: GH injections. Parkinsons: Etiology unknown. ↓ Botox. Huntingtons: chorea, demetia, family Hx. neurons in SNpc, DMN vagus & locus Restless Legs: in uremia, DM etc. Occurs Personality change 1st, increased blinking, ceruleus. Lewy bodies (eosinophilic at night. Tx: Klonopin, Neurontin, L-dopa. abnormal eye mvmt. Caudate/putamen intracytoplasmic inclusions w/ halo). Rest Neuroleptics, caffeine, Ca-channel atrophy > boxcar ventricles. AD, CAG tremor, bradykineasia, cogwheel rigidity (micrographia, ↓ blink, masked facies, blockers worsen. repeat in huntingtin, chr 4. ↑ dopamine, Wilsons disease: Parkinsonism/ bulbar NE, somatostatin (vs AlzDz); ↓ GABA, festinating gain, pain in 50%, GI problems, dysautonomia, weight loss, signs/ dystonia/ ataxia/ psych probs. Wing- Ach. L-dopa worsens. beating” tremor. ↓ ceruloplasmin, ↓ serum Westphal variant: <20yo, more asymmetric). 20% have dementia. Dx: copper; ↑ urine copper; AR, chr 13; liver aggressive, seizures, parkinsonism. clinical. biopsy best; Kayser-Fleischer rings; Subcortical dementia: No aphasia, Tx: Surgical: lesion contralateral VL or hepatolenticular degeneration; Liver apraxia, or amnesia (memory OK). Seen Gpi (best for tremor/ rigidity/ fibrosis, Renal tubular acidosis (metabolic w/Parkinsons & Huntingtons dyskinesias); Vim = tremor, unilateral acidosis). Decreased blink, arm swing (like Picks: frontal/ temporal, balloon only (dysarthria), STN = bradykinesia. parkinsons) Alzheimer II & Opalski cells (“Picks”) cells (neurons, tau+), neuron 80% improve. DBS can be done in GP. Hypodense BG; Tx: penicillamine loss in cerebral cortex, gliosis, cortical bilaterally. (w/B6 to prevent anemia), ↓ dietary copper spongiosis. Younger. Arithmetic Fetal mesencephalic transplantation into Hallervorden-Spatz: cysteine preserved. Rare familial form, Chr17. SN caused dyskinesias, some Tauopathies: tau is a MAP, Chr 17. improvement <60yo. Adrenal medullary dioxygenase deficency. ↑ cysteine, Picks, CBD, PSP, Alzheimers, transplant abandoned. chelates iron > free radicals. Iron in basal Ubiquitin: binds abnormal proteins for Medical: ganglia; no serum test; ↓ T2 “eye of the transfer to lysosomes. Stains in benztropin (Cogentin)/ Artane: tiger” pallidum & substantia nigra; No Tx Parkinsons (Lewy bodies), Huntingtons, anticholinergics. Amantadine: releases Tourettes: AD. <21yo. >1yr sxs. Normal Alzheimers, & others dopamine, loses effect. Sinemet: dopa + IQ. Dopamine reuptake defect (VTA to carbidopa, dopa decarboxylase inhibitor, αSynuclein: structural protein, forms anterior cingulate pathway). Tx: Haldol. 2nd tier. SE: N/V, orthostatis, arrythmias, Lewy bodies (Parkinsons) on-off periods, dyskinesias (Tx B6). CI: Hereditary ataxias: with actin), fiber necrosis, face spared, invovles cranial mm, no ↑ serum K, Tx: Friedrichs ataxia: Chr 9 (protein CHF, woman carriers ↑ CK. Tx: Na. Paramyotonia Congenita exercise & frataxin, GAA repeat), AR, <10yo, Prednisone (slows progression) cold worsens degeneration spinocerebellar Becker: X-linked, onset 12yo, no MR, Ca channel (Chr 1): Hypokalemic: tracts/cerebellum, post columns, dystrophin abnormal, no necrosis hypertrophy, Tx: daily KCl. corticospinal; spares MNs; ataxia, pes Becker & Duchenne: calf Polymyositis: painless, nontender. No cavus/scoliosis, arreflexia (due to pseudohypertrophy skin lesions. Dysphagia, dysphonia. Ocular neuropathy 2° to dorsal root ganglia dz), Facioscapularhumeral: Chr 4., AD, mm. not affected. ↑ CK. Adults. Muscle dysarthria, cardiomyopathy; 10% congenital absence of a muscle necrosis (T-cells) diabetes mellitus, optic atrophy/retinitis (pectoralis, brachialis, biceps), has Dermatomyositis: Butterfly (heliotrope) pigmentosa, no dementia. CSF normal; inflammatory cells (only 1); CK WNL, no periorbital rash & rash over knuckles MRI: normal cerebellum, small spinal necrosis, MR, CHF; hearing loss (Gottrons papules). Children & adults. cord; Tx: serotonin? Diff Dx: Vit E def. Emery-Dreifuss: early contractures elbow Moderate CK. B-cell perivascular Mental status normal. flexors & neck extensors & calf; X-linked, inflammation (humoral – immune Abetalipoproteinemia: peripheral benign complexes in walls of veins & arterioles), neuropathy, retinitis pigmentosa, ataxia, Myotonic: hand/muscle atrophy; myotonia perifasicular atrophy – no necrosis. dysarthria, acanthosis (abnormal RBCs), (preceeds weakness), frontal balding (men Antibodies/C3 increased. Both: Tx: ↓↓ cholesterol, triglycerides; & women), MR, cataracts, testicular steroids, females, 10% have cancer, spinocerebellar/post columns (resembles atrophy, cardiomyopathy. Chr 19, CTG UE/neck > LE, proximal. Friedrichs); children; Vit E slows repeats on “myotonin”, AD, congenital Inclusion Body myositis: chronic progression form always from mother (resolves), myopathy, >50yo. Quads/hand & feet Ataxia-Telangiectasia: Chr 14, AR, face/larynx etc. affected then distal flexors. CK mild. Bx: ubiquitin+ inclusion decreased IgA,G & E. Begins 2yo, ataxia, extremities, most common adult form; bodies, denervation. premature aging, gaze paresis, red eyes, EMG: dive-bomber (reptitive discarges Congenital myopathies: central-core OKN lost. ↑ AFP. Severe degeneration of w/minor stimulation) (related to malignant hyperthermia), cerebellar cortex, anterior horn, Myasthenia Gravis: Women < 40yo, nemaline demyelination in post coluns, Men >50yo w/thymoma. 10% have Issac’s syndrome: myokymia spinocerebellar, peripheral nerves. T-cell thymoma (60% of thymoma have MG), (w/myotonia, hyperhydrosis), K+ channel Leukemia/ lymphoma common. 66% thymic hyperplasia. 10% have no Abs > presynaptic hyperexcitability. 20- Hartnup’s Disease: AR, Defect in renal AchR-antibodies. Pupil response OK. 30s, M=F. Tx: Dilantin, Tegretol, IVIG, transport of neutral amino acids Tx: anticholinesterase (pyridostigmine) > pheresis. (tryptophan). Gait ataxia (triggered by Thymectomy (16-60yo best, 1/3 work Stiff-man syndrome: anti-GAD sunlight & sulfa), emotional lability, without thymoma due to hyperplasia) > antibodies (forms GABA). IDDM assoc. delusions, tremor, rash on face (like steroids > azathioprine > plasma Tx: BZDs. Vs tenanus: EMG silent-period pellagra). Tx: nicotinamide – like pellagra exchange. Cholinergic (worsens) vs preserved, disappears during sleep, no (not tryptophan) myasthenic (improves) crisis: give trismus. Spinocerebellar ataxia (SCAs): All AD, edrophonium. Aminoglycosides worsen. Thyrotoxic myopathy: proximal mm 14 types, Trinucleotide repeats. D-penicillamine can cause autoimmune weakness, diplopia, hypokalemia, males Muscle Disease myasthenia. Spinal/Nerve EMG: denervation/ reinnervation = Neonatal MG: due to mothers with Mg, Amyotrophic Lateral Sclerosis: Atrophy increased duration, polyphasic. Myopathy resolves over weeks. and hyperreflexia. Tongue fasiculations = decreased duration. Both = decreased Eaton-Lambert: 60% have small-cell (worse prognosis). Anterior horn, Betz amplitude lung CA (1/3 no tumor). Antibodies to cell, and corticospinal tract degeneration. Muscle Biopsy: presynaptic Ca channels & synaptotagmin No sensory loss, no pain. CSF normal. Denervation: cause atrophy, angular fibers at NMJ, prevents Ach release. Proximal EMG: denervation in multiple limbs & (reduced to nuclei only). ALS, SMA, trunk/ LE weakness, Ocular mm spared, CN. Bunina bodies (MNs). Poss. peripheral neuropathy Autonomic problems. EMG: Low Mechanism: glutamate excitotoxicity. 10% Muscular Dystrophies: sarcomlemma amplitude to single stimulus (MG familial - Chr 21, AD, mutation in breaks, large, eosinophilic fibers normal), Incremental response to >50/s superoxide dismutase (SOD1), free radical (myonecrosis)> phagocytosis > fat & stimuli. No fasiculations (seen in scavenger. Tx: Riluzole (↓ glutamate fibrous tissue. neuropathy). Tx: guanidine & 3,4- release). DDx (anterior horn): polio, ALS, Myotonic dystrophy: multiple central diaminopyridine (DAP – K channel CJD, Werdnig-Hoffmann nuclei & ring fibers blocker, ↑ APs, also used in MS, can Spinal Muscular Atrophies (SMAs) Polymyositis: perifasicular inflammation cause szs) (both ↑ Ach release), All on Chr5, AR. Resembles childhood Dermatomyositis: perivascular plasmapheresis, steroids. No response to ALS clinically – due to anterior horn cell inflammation > ischemia > perifasicular anticholinesterase meds. Muscle relaxants loss & CN motor neurons. atrophy lethal. Werdnig-Hoffman (SMAI): congenital - Muscular dystrophy Periodic Paralysis: All AD. limp infant, no MR, fasiculations only in Duchennes: X-linked (30% not familial), Na channel (Chr 17): Hyperkalemic: tongue, ocular mm. spared. Possibly due to males (famales w/Turners), onset 3-6yo, precip by fasting, exercise, no mutations in motor neuron trophic factors mild MR, CK higher, heart affected, hypertrophy, Tx: glucose. Normokalemic: SMN1 or NAIP. dystrophin absent (membranous, interacts not precip by fasting, hypertrophy, Kugelberg-Welander (SMAIII): older Onion Bulb: Dejerine-Sotas (AR, Lower trunk: abnormal ulnar sensory (little children, less lethal children, enlarged nontender ulnar, finger), EIP (extensor indicis proprius) and Also adult types. median, radial & peroneal n.), Roussy- APL abnormal Viral myelopathy: Polio & West Nile Levy (ataxia, tremor, pes cavus), Charcot- Medial cord: ulnar sensory abnormal; EIP attack anterior horn cells. Marie-Tooth (AD, can affect UE, steroids normal Guillain-Barre: motor/autonomic > no effect, no autonomic effects, peroneal Lateral cord: abnormal median sensory, sensory. Autoimmune against Schwann muscle atrophy, segmental abnormal biceps and FCR, normal APB cells (or axons). All ages. Symmetric. demyelination), Refsums Posterior cord (Klumpkes): wrist drop, IM Mortality 3%. Peaks 10-14d. 20-30% Have mutation in peripheral myelin shoulder injections preceeding Campylobacter infection proteins (PMP22 in CMT) Brachial Neuritis = Parsonage-Turner; (diarrhea), also CMV. May occur Demyelinating: diptheria, lead, GBS, DM, pain then proximal arm weakness (3-10d postoperatively. EKG: t-wave ∆s hexacholophene later, > sensory, distal); no WBC, ESR, common. CSF: Normal except high Sensory: amyloid,DM,ETOH fever. Can be AD. protein (peaks 4-6wks). Path: Autonomic: Fabrys, amyloid, porphyria, Rheumation arthritis: PIP (Bouchard) Perivascular & endoneurial inflammation, GBS, DM, vincristine, botulism only; Degenerative = PIP + DIP segmental/ perivenular demyelination, Motor: GBS, diptheria, porphyria, uremia, (Heberdens) particuluarly in roots & plexuses. lead Hyperhydrosis – T2/3 ganglionectomy Plasmapheresis, IVIG (not steroids). Drugs: isoniazid (sensory), nitrous oxide (leave T1 to prevent Horners) GM1 ganglioside in campylobacter wall > Cranial neuropathies: III: DM, syphillis; Scleroderma: entrapment neuropathy anti-GM1 Abs (GM2 in CMV) V: arsenic, sjorgen; VII: Bell’s, Ramsay- (CTS), anti-Scl-70 or 86. Tx d- Miller-Fisher variant: opthalmoplegia, Hunt, sarcoid, lyme, porphyria, PAN;VIII: penicillamine ataxia, hyporeflexia, descending. Anti- wegeners, refsums; IX: diptheria. General: Sjorgens: xerostomia, conjunctivitis GQ1b IgG. Good prognosis. GBS, amyloid. (Schirmers test). Anti-Ro (SS-A) & La Also Acute Motor & Motor-Sensory Porphyria: Acute intermittent: AD, (SS-B). Vasculitis, neuropathy Axonal Neuropathy variants. abdominal pain/ gastroparesis/ Demyelinating Disease Tick paralysis: Dermacentor tick toxin. constipation, hypertension/ tachycardia ADEM: postviral/postvaccination. ↑ESR. Resembles Guillain Barre - ascending (2° to autonomic neuropathy), psychosis, CSF ↑ pressure, WBCs, RBCs, protein. paralysis, but more rapid, CSF WNL. Tick neuropathy (axonal motor/ autonomic), Perivenular demyelination. Involves deep removal – rapid improvement. Skin is normal. Seizures, SIADH. grey matter (vs MS) Tx: Steroids. 25-50% CIDP: polyradiculopathy, proximal Porphrobilinogen deaminase deficiency:↑ mortality. weakness, sensory loss/paresthesias, CSF: porphobilinogen, δ-aminolevulinic acid. Multiple Sclerosis: CSF: IgG index >1.7 ↑ protein, no cells. Demyelinating. EMG: May be provoked by porphyrigenic drugs: (>15%), protein not >100, ↑ MBP, ↓ nerve conduction. Tx: steroids barbs, PTN, sulfa, estrogens. Tx: IV oligoclonal bands, mild pleocytosis. Tx: Transverse myelitis: all ages, MRI hematin. ACTH, steroids (↓ duration, not with optic normal in 50%, prognosis variable. All others have skin manifestations: neuritis), βinterferon (↓ relapse, no ↑ 40% idiopathic – rest MS, vasculitis, etc. Varigate, hereditary corproporphyria, infections). VERs usually abnormal. Path: Myelopathy: ALS: corticospinal + Porphyria cutanea tarda (all above hepatic Perivenular demyelination w/axonal anterior horn; Polio: anterior horn; HIV: porphyrias), also erythopoetic porphyria sparing; perivascular lymphocytes, vacuolar (similar to B12); HTLV-1; Diabetic neuropathy: Opthalmoplegia, macrophages, reactive astrocytes. No PNS Friedrich’s ataxia: posterior columns, acute mononeuropathy, mononeuritis involvement. Risk equal to habitat when spinocerebellar, corticospinal; B12: multiplex have vascular origin, distal <15yo. Northern = worse. Optic neuritis Posterior columns & corticospinal; Tabes sensorimotor polyneuropathy due to direct causes ↑ blind spot, no VF defect. Lesions dorsalis: posterior columns neurotoxicity abut dorsal surface in spine. Tropical spastic paraparesis: Japan/ Mononeuritis multiplex: painful, Marburg=fulminant, Devic=optic n. and tropics; corticospinal ± post columns; due asymmetric, LE > UE, painful, prox > spinal cord; Schilders=kids, fatal to HTLV-1; chronic distal, evolves minutes to days, resolves in Experimental allergic encephalomyelitis = Ischemic myelopathy: due to aortic weeks Occurs w/DM, PAN model, T-cells to MBP aneurysm/dissection. Back/groin pain + Amyloidosis: Familial or secondary. Other Demyelinating Dz: PML, SSPE, myelopathy + claudication (2° to Neuropathy (from Ig light chains in rubella, HIV, Binswangers, CO, ischemia), from A. of adamkewicz. Aortic endoneurium of blood vessels, axonal leukodystrophies, EtOH, cyclosporin, bypass may worsen. degeneration, small unmyelinated ampotericin, hexachlorophene, triethytin, Radiation myelopathy: Painless pain/temp & autonomic fiber loss). CTS. radiation, MTX, lead, mercury paresthesia, sensory before motor, early Angiopathy. Polypeptide amyloids β- Oligoclonal bands: MS, SSPE, syphillis, transient (3-6mo, paresthesias) or delayed pleated sheets. Herditary = prealbumin, NOT TB progressive (12-15mo, coagulation transthyretin. Toxic/Metabolic necrosis of white matter, hyalinized Brachial plexus lesions: Vitamins: Thiamine: rice eaters, vessels – resembles infarct). Tx: steroids. Upper trunk (Erbs): abnormal deltoids, alcoholics. Wernickes, beriberi (heart dz); Neuropathies: DM, leprosy, amyloid, biceps; waiters tip painful sensory neuropathy (distal LE polyarteritis nodosa, acute intermittent Middle trunk:abnormal median sensory dysesthesias/hyperpathia), orthostasis (2° porphyria, uremia, metachromatic (index & middle finger), hand motor to neuropathy), Strachan’s syndrome leukodystrophy, Fabrys, Krabbes normal (sensory ataxia, optic n. atrophy, deafness). Niacin: pellagra (rash, post column/CNS probs), due to tryptophan def, corn eaters. Lead: enephalopathy (resembles AIP), EtOH: withdrawl 72hr (vs benzos 7-10d). B12 (Cobalmin): subacute combined diffuse brain swelling (kids), MR, wrist Prevention: chlordiazepoxide. Superior degeneration, megaloblastic anemia, drop (painless motor neuropathy), black vermis (Purkinje cell, molecular layer) neuropathy, centrocecal scotoma. Folate: gingiva, RBC basophilic stippling atrophy. megaloblastic anemia, neuropathy, due to (anemia), ↑ urinary corproporphyrin and Fetal alchohol syndrome: impaired methotrexate (dihydrofolate reductase δ-aminolevulinic acid. Tx: BAL & EDTA. neuronal migration., MR, microcephaly inhibitor) Pyridoxine (B6): due to Manganese: miners, Parkinsons, affects Wernicke’s: gait ataxia, nystagmus (most isoniazid (INH). Neuropathy. Vitamin A: striatum, Tx: l-dopa common) opthalmoplegia (bilateral lateral increase causes pseudotumor. Vitamin E: Mercury: fish, hat dyes/felts, paper/pulp rectus 2nd), confusion. Also), hypothermia. spinocerebellar degeneration/ ataxia, plants. cerebellar signs/ataxia, tremor, Thiamine def. Ocular problems recover 1st. polyneuropathy. Kids, hepatic dz. mood change, visual loss, renal tubular Mamillary body, PAG, PVG lesions Chromium: diabetes. Zinc: dermatitis. necrosis. Path: calcarine cortex & (enhance on MR). ↑ serum pyruvate, TTP, Methionine metabolism: cerebellar granular layer. Inhibits protein ↓ transketolase Methionine > homocysteine. translation. Tx: penicillamine (not BAL) Korsakoff’s: short-term retrograde Homocysteine > methionine (methionine Thallium: cardiac, GI probs, alopecia, memory deficits (immediate memory/ synthetase - requires B12 & folate arthropathy, neuropathy attention OK). DM thalamus. Only 20% (methyl- THF)) or Aluminum: dialysis pts, osteomalacia, improve w/Thiamine. Homocysteine > cysteine (by encephalopathy Central pontine myelinolysis: correction cystethionine βsynthetase – requires B6). Copper: OCPs, Wilsons Dz of hyponatremia. never extends into B12 def (SCD): ↑ homocysteine & Carbon Monoxide: GPm necrosis; medulla, demyelination, affects oligos, methylmalonic acid (Methylmalonic-CoA parkinsonism 1-3wks after event (suicide, preserved neurons, no inflammation > Succinyl-CoA also requires B12 in fire) Marchiafava-Bignami: demyelination of amino acid metabolism). Iron: desferoxamine corpus callosum and ant comissure B6/ CβS def: Marfans, homocystinuria, Gold: BAL, penacillamine Cocaine: causes noncaseating granulomas hyperhomocysteinemia: ↑ homocysteine Organophosphates: insecticides, rat of basal areas/ meningitis & methionine. poison. anticholinesterases (sweating, Diffuse Brain Swelling: in kids: lead, Folate/ MTHFR def: ↑ homocysteine cramps, n/v, ↑ salivation – not dry tetracycline, vitamin A Folate: folate > DHF > THF (by MTHFR) mouth). Tx: atropine + pralidoxime (2- CRF: peripheral neuropathy most common > methyl-THF > accepts methyl group PAM) (legs, mixed). Tx: transplant (not dialysis) from homocysteine in above reaction > TOCP: triorthocresyl phosphate, causes Hepatic encephalopathy: Ammonia ↑ THF rapid UMN & LMN paralysis GABA synthesis. Asterixis. Alzheimer Cyanocobalmin (B12): metabolized to Ergot: rye grains/bread. Posterior type II astrocytes, hyperplasia of cyanide colums/dorsal roots, neuropathy, skin protoplasmic astrocytes in deep cortical Subactue combined Degeneration: ulcers. vasoconstrictor layers & deep nuclei. T1 hyperintense Post. Columns (first) then corticospinal – Tylenol: N-acetylcysteine BGs. Involves cortex, spares hippocampus, esp. cervicothoracic (may occur in Cyclosporin: encephalopathy; occipital GP, deep folia of cerebellar cortex. EEG: medulla). Demyelination & axonal lobe white matter changes resembling triphasic waves (can occur w/others) Tx: degeneration, spongiosis (not seen in hypertensive encephalopathy – cortical lactulose. Friedrichs ataxia), vacuoles in myelin. blindness. Demyelinating. Transplant pts Reye syndrome: Virus + ASA. Hepatitis, May have visual probs – centrocecal Isoniazid: anti-TB. Neuropathy due to encephalopathy, hypoglycemia, cerebral scotoma. CSF WNL. pyridoxine deficiency. Give with edema. Tx: supportive Vitamin B12 (cobalmin). Absorbed in pyridoxine. High-altitude sickness: cerebral hypoxia. ileum. Methionine synthetase requires Nitrous Oxide (N2O): abuse (dentists, Tx: steroids, diamox, O2. B12 >Elevated serum methylmalonic acid health care). Peripheral neuropathy, Infectious Disease and homocysteine (best indicator of megaloblastic anemia. Numbness, Meningitis: H flu=alcholics, diabetics, intracellular B12 levels. Microbiological paresthesias, ataxia, spasticity (resembles kids, CSF leaks. Type B. Causes subdural assay best method for Serum B12 but is B12) effusions. 3rd gen cephalosporin. Steroids less reliable). DNA synthesis failure. Methanol: moonshine, hemorrhagic decrease deafness. Prophylaxis for all Nitric oxide also inactivates methionine putamen/claustrum necrosis, contacts <18yo. synthetase. blindness/acute central scotoma Tx: EtOH S. pneumo= elderly, skull fx/ CSF leaks Pernicious anemia: lack intrinsic factor to Ciguatoxin: food poisioning, (recurrent), TBI, alcoholics, sickle-cell. transport B12 in ileum. Schilling test: B12 tropics/South. Fish (snapper, grouper). ↑ Vanc + 3rd gen ceph, PCN. then B12 + IF. B12 IM qD. Tx: IM B12 permeability sodium channels – N. Meningiditis=rash, rapid, meningeal qmonth - Oral B12 will not correct. excitability. N/V (6hrs) > paresthesias, fibrosis. Waterhouse-Friedrichsen (shock, Intrinsic SCD: Idiopathic, not B12, motor HA, ataxia. Temperature reversal. adrenals) Gram (-) diplococcus. PCN, then post columns. Resolves 1-2d. Cephalosporin. Rifampin prophylaxis for Toxicology Lathyrism: spastic paraparesis from eating all contacts. Vaccine for epidemics, Arsenic: insecticides. encephalopathy, only chick-peas (toxin causes glutamate military recruits neuropathy (axonal), abdominal pain, toxicity) Listeria: Gram+ Rod (intracellular). palm/soles pigment, Mees lines Paraquat: insecticide, kills dopaminergic Neonates, renal transplant, CRF, (fingernails). BAL. Detect in hair cells, causes parkinsonism. immunosuppressed, steroids. Glucose, G/S may be normal. Amp/Gent GNR: Ceph/gent. Coccidiomycosis: So. Cal. Large yeast – Transmitted by saliva (not from mice/rats, Neonatal meningitis: GNR > group B “sporangia”. Usu. Pulmonary. rabbits, reptiles). strep > listeria. Parasites SSPE: caused by measles @ 5-15yo from Tuberculous: ↓↓ glucose. INH/Rif/PZA x Cystercercosis: Taenia solium. Pork infection <2yo. EEG: 2-3/s spikes, burst 12mo ± steroids tapeworm – but obtained thru fecal suppression pattern (bursts of high-voltage Skull fx: closed = pneumococcus > H flu. contamination (vs taeniasis and trichinosis slow waves w/ low-voltage stretches). Open = GNR – from eating undercooked pork). Ingest Dementia, seizures, myoclonus, ataxia.↑ Malignant otitis/ petrositis: facial palsy, eggs > penetrate gut > oncospeheres > measle serum & CSF titers; ↑ CSF IgG & otorrhea, elderly DM. Pseudomonas. larvae encyst in CNS. Tx: Praziquantel. oligoclonal bands (resembles MS). Steroids: infant H. flu; severe TB; Echinococcus: Taenia echinoccocus. Eosinophlic Nuclear & cytoplasmic neurocystercercosis w/↑ ICP. Hydatid disease. Dog tapeworm/easting inclusions in glia & neurons. Grey & white Brain abscess: aerobic/microaerophillic infected sheep. Larvae in cysts = hydatid matter. Gross demyelination, atroophy. Strep. Sinus infxn most common cause. sand (Small cysts in larger cyst) PML: JC papovavirus. Demyelinating. Infants Tetralogy of Fallot #1 (also Schistosomiasis: fluke. Deposits ova in Oligodendroglia in periphery of lesion transposition great vessels). Also Batsons veins > spinal cord granulomas altered to large, dark, ground-glass nuclei pulmonary AVMs (Rendu Osler Weber) >myelitis. Puerto Rico. Praziquantel w/ owls eye inclusion. Giant astrocytes Neonates: Citrobacter, Bacteroides, Toxo: Obligate intracelluar protozoa. (Alzheimer type I). No enhancement. No Proteus. SBE usually causes strokes, Cats/congenital. Cysts contain tachyzoites inflmmation (vs MS-has macrophages). mycotic aneurysm – not abscess. visible on H&E. Seurm IgG almost Spares cortex. Dx: CSF PCR. Occurs Bacterial Encephalitis: always (+), CSF usually mornal. Tx: w/HIV, lymphoma/ leukemia, sarcoid. Bacterial: Legionella (CSF -), pyrimethamine/ sulfadiazine (w/ HIV: dementia complex #1 (subcortical Mycoplasma, Listeria (immunosuppresed, Leucovorin rescue) dementia, motor deficits). Glycoprotein CSF +), Brucella. Amoebic meningitis: Naegleria & others. 160 (precursor > Gp120 & Gp41) attaches . Freshwater ponds, basilar meningitis. to CD4 receptor (T-helpers) and Subdural empyema: Streptococcus Enter cribiform plate. Tx: metronidazole. galactoceramide (oligos, neurons) – Epidural abscess: Staph aureus Malaria: Plasmodium falciparum. disrupts Ca/long term potentiation > ↑ (pseudomonas in addicts) Encephalopathy. Infected RBCs > stroke. intracellular Ca > neurotoxicity. Vacuolar Tuberculosis: CSF: ground glass, low Cl, Trypanozones: T. Brucei = African myelopathy: posterior & lateral columns, protein very high. Basilar exudate, basilar sleeping sickness (Tsetse fly). T. low thoracic. Myelitis: CMV causes pial & cortical “popcorn” calcifications, gambiense = chronic meningitis. T cruzi = enhancement. Encephalitis: unique parenchymal granulomas (ring- Chagas dz (reduviid bug) multinucleated giant cells (syncytial enhancing). Caseating (cheesy - Viral meningitis/ encephalitis: macrophages). Both HIV (perivascular) & yellowish) necrosis, Langhan’s giant cells. Enterovirus #1. Encephalitis: Arbovirus = CMV (subpial/ ependymal) (& toxo) Noctural wakefulness. Potts dz : affects #1 epidemic, HSV = #1 sporadic. produce microglial nodules. disk space 1st. Herpes & rabies enter nerves, use fast Tx: zidovudine (AZT - myopathy), 3TC Fungal: Immunocompetent: Histo, retrograde transport to enter CNS. (neuropathy) (CMV = Ganciclovir) Blasto, Coccidio. Immunodeficient: Most cause microglial nodules & CMV: large eosinophilc nuclear inclusions Candidiasis, Aspergillosis, Cryptococcus, perivascular lymphocyte cuffing. (Cowdry A) with halos. Causes neonatal Mucor. Arboviruses: Arthropod: Eastern encephalitis (see TORCH), HIV Yeast: crypto, coccidio, histo, blasto (summer, rare, 75% mortality, children); encephalitis, myelitis. Hyphae: aspergillosis, mucor Western (summer, more common, infants, Sarcoid: favors CN7. Mononeuritis Both: candida (pseudohyphae) 5% mortality); Venezuelan (epidemics, multiplex, (& other neuropathies, Tx for all: Ampho B. mortality <1%, adults, south); St Louis myopathy). Serum ACE up. Steroids. Aspergillosis: Invades blood vessels > (adults); LaCrosse (common, kids, Neurologic in 5%. Noncaseating infarcts. Dichotomous (45° Y-shaped) mortality <1%) granulomas, basal/hypothalamus. Dx: Bx Branching septate hyphae (silver stain on Herpes encephalitis: Limbic lobe: of non CNS tissue. Steroids. Note sarcoid all fungus). Immunocompromised. Most Bitemporal, cingulate, subfrontal, insula. may resemble MS but MS does not cause common fungal abscess. SF RBCs, mononuclear cells. EEG: neuropathy. Mucormycosis: Nasal infxn, diabetics, temporal PLEDs, slow waves. Dx: PCR VonEconomo’s encephalitis: immunosuppression. Angioinvasive. on CSF or Bx & Cx. (HSV2 = neonates, (encephalitis lethargica). After influenza, Nonseptate right-angle branching hyphae. diffuse). Path: Cowdry type A develop parkinsonism Cryptococcus: India ink/ mucicarmine (intranuclear eosinophilic inclusion) in Syndenham’s chorea: after rheumatic (stains capsule red). Bird feces. Single neurons, astrocytes, & oligos, found early. fever (group A strep, carditis + arthritis). bud w/halo. Meningitis. Gelatinous Tx: acyclovir. No Tx necessary. May recur years later. perivascular “pseudocysts” in BG, path: Rabies: Travels peripheral nerves to Preadolescent females perivascular macrophages & yeast. CNS. Glycoprotein G on envelope Whipples dz: Tropheryma whippleii. (“Swiss-Cheese” brain) attaches to nicotinic Ach receptor or Jejunal Bx: PAS+ cells. Ataxia, Candida: Most common CNS fungus. NCAM. Path: Negri bodies (eosinophilic ophthalmoparesis, dementia (myoclonus, ICU/immunosuppressed, causes retinitis. cytoplasmic) in Purkinje cells of szs). Resembles Wernickes. Histoplasmosis: usu pulmonary, very cerebellum & pyramidal cells of Oculomasticatory myorhythmia (penudular small, inside macrophages, Mississippi hippocampus, limbic neurons. Tx: Ig. convergance of eyes with rhythymic valley “smiling”) pathognomonic. Tx: antibiotics Syphillis: Meningovascular = Huebners Tetanus: Exotoxin transmitted by Bielschowskys sign – CN4 injury, head arteritis. General paresis of the insane retrograde axonal transport, inhibits tilted to opposite side; eye up & in (chronic meningoencephalitis). Tabes Renshaw cells (↓ glycine vesicle release Gradenigos Syndrome: osteomyelitis of dorsalis (Thoracic, lumbar, post columns, by cleaving synaptobrevin – Zinc petrous apex. CN6 (&3) palsy & dorsal roots, bladder/bowel incontinence, dependent protease) – tetany. May be retroorbital pain, from otitis (cholesterol absent DTRs, argyll-robinson pupils, local, generalized, or cephalic. 50% granuloma can also occur at petrous apex) charcot joints). Congenital (Hutchinsons mortality. Incubation days to weeks. Horners: no response to 2% cocaine. triad: notched teeth, deafness, keratitis) Usually in soil. May also occur in neonate + hydroxyamphetamine: no effect = 3rd Nontreponeal tests: RPR, VDRL – false by contaminated umbilical cord, order (postganglionic), dilation = 1st or 2nd (+). Treponemal: MHA-TP, FTA-ABS, contaminated heroin. EMG: continuous order (epinephrine opposite). confirmation. If serum (+), check CSF. discharges of normal motor units, loss of Sympathetics: hypothalamus > Cat-scratch fever: Bartonella. normal “silent period” (due to renshaw interomediolateral column > T1 root > Sup Epitrochlear lymphadenopathy (due to cells) Tx: Antitoxin (Ig), PCN, cervical ganglion > ICA (pupil) & ECA scratch on arms). MRI: Pulvinar debridement. (sweat). ICA Dz (dissection) doesn’t hyperintensity. Meningitis or enchpalitis Diptheria: ascending paralysis, produce anhydrosis. (immunosuppressed). ophthalmoplegia, demyelinating Tunnel vision: retinitis pigmentosa, Neonatal/TORCH: CMV (#1): migration sensorimotor neuropathy at DRG & roots glaucoma, papilledema abnormalities, HCP, periventricular without inflammation. Exotoxin inhibits Retinitis pigmentosa: Degeneration of all calcifications, microcephaly, myelin synthesis. Antiserum. layers of retina. Tunnel vision, Nyctalopia. chorioretinitis (Tx gangcyclovir)/optic Black Widow: depletes Ach into NMJ Occurs w/ mitochondiral dz, Laurence- atrophy, MR, deafness; Toxo: <26wks, no Leprosy: Neuropathy – due to bacillus Moon-Biedl, Friedrichs ataxia, Cockaynes, migration probs, chorioretinitis, growth in peripheral axons & Schwann abetalipoproteinemia, Refsums, or alone hydrocephalus, scattered cerebral cells (lepromatous) or due to perineural (AR, Chr 3). calcifications (not periventricular); granulomas (tuberculoid) Nystagmus:, downbeat = Rubella: BG/cortical calcification, small Ophthalmology cervicomedullary, ocular bobbing = pons, brain, cataracts, deafness, cardiac probs, Adie pupil: degeneration of cilliary oscillopsia = vestibular, impaired aqueductal stenosis. HSV: 2-4wks ganglion (parasympathetics), large pupil – opticokinetic reflex = parietal or vestibular postpartum, diffuse encephalomalacia (not no response to light (responds to near, (elicit by rotating drum away from lesion), just temporal). same as argyll-robertson); very sensitive see-saw = parasellar; convergence & Lyme Dz: Borrelia burgdorferi. Tickborn to miotics due to denervation nystagmus retractorius = pineal/ tectal spirochaete. erythema chronicum migrans hypersensitivity (0.1% pilocarpine – (Parinauds), ocular dysmetria (overshoot) = slowly spreading ring of erythema, normal pupils don’t respond); young = vermis, spasmus mutans = infants only, aseptic meningitis. Radiculopathies women; may have absent DTRs, benign congenital (nystagmus on gaze then (sciatica), neuropathies, Dieterle stain. Argyll-Robertson: small pupils, react to fixation on object) CN7 commonly affected (weeks after accomodation, not light. no response to INO: Ipsilateral MLF: Impaired adduction rash). Dx: ELISA. Ceftriaxone > mydriatics. Lesion unknown (pretectal ipsilateral eye, nystagmus in contralateral Tetracycline, erythromycin. area?) eye. Bilateral MLF: impaired adduction Ramsay-Hunt: herpes infection of CN7; Marcus-Gunn pupil = afferent pupillary bilaterally. Pathognomonic for MS. Both vesicles on EAM defect (APD) have preserved convergence. Bell’s Palsy: +- hyperacuisis, taste Colliers sign: Bilateral lid retraction – 1-1/2: MLF + PPRF/CN6. Complete changes; peaks 2-5d; ?HSV; Tx: steroids Diencephalic syndrome (wasting, ↑ food opthalmoplegia isilaterally, only abduction x 1 wk intake, euphoric) contralateral. Convergence OK. Botulism: Rapid onset bulbar paralysis. Nyctalopia: night blindness, retinal Optic neuropathy: Ischemic: painless, Pupils unreactive (large, fixed, vs MG - degeneration (retinitis pigmentosa) or Vit abrupt, inferior altitudinal defect. reactive) (also ptosis, opthalmoplegia, A deficiency. HTN/diabetes – posterior ciliary a. diplopia, dysphagia, dysarthria). EMG: Macular damage: severe visual loss Exclude temporal arteritis. Optic disc (looks like Eaton-Lambert) decremental Scintillating scotomas: migraine aura papillitis > pallor. Embolic: Central retinal response at low frequency (2-5Hz), Hypertensive retinopathy: segmental a. Cloudy retina, grey narrow arterioles w/ incremental response at high-frequency narrowing of arterioles (copper wire) segmented columns of blood, cherry-red (20-50Hz). Canned vegtables containing Diabetes: Pupil sparing CN3 palsy, fovea. Toxic/nutritional: bilat central exotoxin (raw honey in infants – organism painful, abrupt, resolves w/in 6mo scotoma injested & produces exotoxin in gut). 3 (Most deadly complication of diabetes = Optic neuritis: painful, visual loss/APD types of exotoxin : A (used in botox heart disease) (complete blindness resolves to enlarged injections), B, & E. Symptoms appear 12- Diabetic retinopathy: microaneurysms, blind spot/ centrocecal scotoma), 75% 36hrs. CSF WNL. vascular proliferation develop MS, recovers. Steroids (IV then po Presynaptic ↓ Ach release due to ↓ vesicle Most common cause acute diplopia: – po alone worsens) release (Zinc-dependent protease, cleaves CN6 (>3>4). CN4 most common injury in Papilledema: no visual acuity loss, synaptobrevin, SNAP25 & syntaxin) facial trauma. CN4 most commonly enlarged blind spot, venous pulsations Descending. Tx: Antitoxin, guanidine. affected w/herpes zoster opthalmica (V1). absent in 15% of normals (not reliable), DDx: Guillain Barre (abnormal NCV, Pupil affected 1st by CN3 compression engorged capillaries from short ciliary sensory affected, CSF abnl), tick paralysis (peripheral fibers) arteries Drusen: hyaline in optic n., resembles Ear stuff CBZ & PB, not PTN. PTN ↑s coumadin papilledema Hearing loss: conductive = low-pitch, levels, PB & CMZ ↓ them. Cavernous sinus thrombosis: pain, neural = high-pitch CBZ ↓ all other AEDs except PB. PB ↓ proptosis, visual loss Weber = forehead, Rinne = mastoid all. PTN ↓ all. VPA ↑ all (displaces PTN Diptheria polyneuropathy: Menieres Dz: vertigo, low-pitched from plasma proteins) opthalmoplegia tinnitus, low-pitch deafness (high pitch Phenobarbital SE: Dupuytren’s Tolosa-Hunt: eye pain + opthalmoplegia late), fullness in ear, nystagmus. contractures. T1/2 = 96hrs. + V1 sensory loss. Pupil spared. Lesion in Endolymphatic duct ruptures into scala Dilantin: Atrophy of Purkinje and cavernous sinus/SOF (III, IV, V1, VI) media dumping K into perilymph. Hair granular layers of cerebellum. Thyroid: afffects inferior & medial rectii cell degeneration. Tx: salt restriction, Neuropathy, gingival hyperplasia, (upgaze affected more than lateral) diuretics hirsutism arrythmias/ hypotension IV; Optic nerve thickening: Graves dz, Vestibular neuronitis: Vertigo without interferes w/vitamin K – bleeding & ↑s orbital pseudotumor, optic neuritis, tinnitus, deafness. Viral, self-limited (also coumadin. T1/2 = 24hrs. papilledema, cav-mal, glioma, caused by ASA, EtOH, quinine, Tegretol: leukopenia/pancytopenia. ↑ by meningioma, lymphoma, met aminoglycosides. ASA also causes erythromycin. T1/2 = 12hrs. Orbital pseudotumor: enhancing mass, tinnitus.) Valproate/Depakote: GABA agonist. SE: enlarges muscles or optic n., resembles Benign positional vertigo: middle-age, thrombocytopenia, alopecia, pancreatitis, lymphoma elderly. Turning head to affected side neural tube defects. T1/2 = 8hrs. Schirmers test: measures tear production causes vertigo & rotatory nystagmus. Felbamate: aplastic anemia/ hepatotoxicity (Sjorgens) Calcified otolith in posterior semicircular (not used). Leber’s optic atrophy: centrocecal canal. Tx: exercises. Absence: 3/s spike-wave. Last 10-15sec, scotoma, young men, mitochondrial DNA Presbycusis: neuronal degeneration, (+) automatisms, no aura, no postictum. mutation high-pitch loss Partial-Complex: Last 90sec, Neonates: no red reflex = congenital Pulsatile Tinnitus: dural AVM, glomus automatisms, aura, postictum. cataracts; white reflex = retinoblastoma tympanicum, aberrant ICA Geschwind syndrome: hyperreligious, Heterochromia iridis: due to congenital Seizures philisophical – from ↑ hippocampal Horners, injuries to sympathetic n. to Seizure foci: high glycine, extracellular activity/ kindling (attach emotional pupil during birth. Causes different color K; low GABA, taurine. Decreased binding significance to all stimuli). eyes (blue/brown) & anisocoria. and removing Ach. Surrounding = high Mesial temporal sclerosis: neuronal loss Sympathetic innervation required to eyes GABA. Diencephalon inhibits – goes in Ca1,3,4 & dentate gyrus. (Spares Ca2, to change from blue to brown. May be from tonic to clonic. Caused by cortical subiculum – unlike hypoxia). ↓ AD. pyramidal cells (glu) somatostatin & neuropeptide Y neurons. Myopia corrected by concave lens; AEDs: Neonatal = phenobarb. Complex Axonal sprouting in dentate (mossy fibers). astigmatism by cylindrical lens; hyperopia partial = tegretol > dilantin. Absence = Seen in 65-70% of temporal lobe epilepsy. by convex lens. ethosuximide > depakote. Myoclonic & MRI 80-90% sensitivity. Possible related Coloboma: Gap in the eye due to failure atonic = depakote (ACTH in infants). to febrile seizures. of embryonic fusion of choroid fissure, Lennox-Gastaut = depakote. Lennox-Gastaut: 2-6yo. Partial complex, usually in iris. Preeclampsia = MgSO4. Absence status Drop attacks, GTC. Cognitive decline. 2/s Amblyopia: “Lazy eye”, can be do to = IV BZDs. Complex partial status same spike/wave. TS may develop. Tx: anything that causes unilateral ↓ vision – as GTC. Depakote. usually cross-eye. Patch good eye. Best 2- Pregnancy: Recommened to continue Rasmussens: Intractable focal epilepsy w/ 4yo, 7-9yo latest. during. Risk of anomlies ↑ from 2% to progressive hemiparesis, 3-15yo, 50% Ocular albinism: defect in tyrosinase 4% (equal w/all AEDS). PTN ↑ bleeding epilepsia partialis continua. Meningitis/ gene, ↓ melanin in retina > misrouting of – give vitamin K, depakote ↑ neural tube encepahlitis, perivascular cuffing, ?Abs to fibers to LGB results in disordered defects. glutamate receptors. Tx: steroids layering in LGB > lack of binocular vision Mechanisms: Na channel blockers: PTN, Infantile spasms: “salaam spasms”, & diplopia Tegretol, Lamotrigine, Neurontin, myoclonic head jerks. Tx: ACTH. Can Junctional scotoma: lesion at junction of topiramate (& other new drugs); Barbs & occur in Tuberous sclerosis, PKU, Sturge- optic n. & chiasm. Ipsilateral scotoma + benzos (& topiramate) ↑ GABA; Weber or Wests syndrome contralateral superior quadrantopsia Felbamate NMDA block; Topiramate Wests syndrome: infantile spasms, EEG: (Meyers Loop) AMPA block; Tigabine blocks GABA hypsarrythmia (large slow waves), MR. Meyers loop (optic chiasm) vs von reuptake; ethosuximide & zonisamide ↓ Several hundred szs per day. Begins 3- Willebrands knee (temporal): Both give Ca current. 8mo, disappears by 5yo, Can lead to pie-in-the-sky (superior quadrantopsia). Interactions: All ↑d by INH; PTN & CBZ Lennox-Gaustaut. Willebrands = homonymous. Meyers = ↑ by chloramphenicol (also PB), Hyperexplexia: startle, glycine receptor ipsilateral scotoma. cimetidine, diltiazem, demerol ( also PB), defect, Tx: clonazepam Retinal emboli: Cholesterol (Hollenhorst Omeprazole; CBZ & VPA ↑ by Benign juvenile myoclonic epilepsy: plaque) = ICA. Calcific = cardiac valves. erythromycin; ASA ↓s all; PTN ↓d by common cause of myoclonus in Platelet-fibrin = large vessel mural antacids, cipro, rifampin, warfarin?, & adolescents. Initally occur after waking. 4- thrombi. Fat = long bone fracture. others, ↑ by sulfa, uremia. Dialysis affects 6Hz spike-wave. Depakote. Does not resolve w/age. Benign childhood epilepsy w/ organ dysfunction, polydactyly AR, Chr into interhemispheric fissure, parallel centrotemporal spikes: nocturnal, focal 17, LIS1 gene lateral ventricles. May have MR. “Bat- face, drooling, resolves by 16yo. Norman-Roberts wing” deformity. Breatholding spells: after startle, for of Walker-Warburg: lissencephaly, Aicardi’s syndrome: agenesis, infantile syncope, can include myoclonus, resolves congenital myotonic dystrophy, spasms, MR, chorioretinitis by 6yo, no ↑ risk of epilepsy hydrocephalus, agyria, retinal dysplasia/ Joubert syndrome: AR, dysgenetic split Febrile szs: GTC, <15min, nonfocal, micropthalmia, ± encephalocoele. AR. vermis, MR, agenesis, polydactyly, single, 6mo-5yr. No ↑ risk later szs Type II. oculomotor probs, cystic kidneys. (others say ↑ to 1%). <1yo requires LP to X-linked lissencephaly – subcortical band Rhombencephalosynapsis: fused r/o meningitis. heterotopia: Doublecortin (DCX), a MAP cerebellum Myoclonic Szs: Lafora body Dz, Pachygria: cortex has 4 layers (not 6). Phakomatoses: All AD except Sturge- Unverrict-Lundborg (8-13yo, no 12-16wks. Weber dementia, cystatin B cysteine protease Heterotpoias: Nodular/ periventricular: NF1: Chr 17, 50% sporadic. mutation), ceroid lipofuscinosis, normal IQ, szs. Familial: X-linked (lethal Neurofibromin: tumor suppressor, inhibits sialidosis, MERRF. in males), Filamin-1. Subcortical Band: ras oncogene by ↑ Ras-GTPase (also ? Lafora disease: AR, Lafora bodies: MR, szs EGFR, p53) PAS+ basophilic intracytoplasmic Polymicrogyria: 4 layer cortex, MR, szs Skin: >6 café au lait, axillary freckling, polyglycosan inclusions in brain, skin, Cortical dysplasia: focal areas of Eye: Lisch nodules (iris), buphthalmos liver (Bx). Begins 11-18yo, myoclonic abnormal cortical cytoarchitecture (cow-eye, due to lid neurofibroma), retinal szs, dementia, die by 25yo; Labs WNL. Schizencephaly: familial: defect in phakomas Tx: Depakote, methsuximide EMX2 homeobox gene Spine Xray: enlarged foramen, scoliosis, Temporal lobectomy: most often causes Colpocephaly: Seen in agenesis of corpus vertebral scalloping, dural ectasia, lateral superior quadrantopsia callosum, periventricular leukomalacia. thoracic meningocoele. EEG: Activity comes from pyramidal Damage to white matter 2-6mos gestation. CNS lesions: cell synaptic potentials – synapses from Aperts: Syndactyly, cleft palate, ± frontal 1. meningoangiomatosis (collars of thalamic (downward deflection) and encephalocoele, severe MR, prognathism meningothelial cells around vessels) cortical (upward) axons on pyramidal (anterior open bite). Coronal only 2. sphenoid dysplasia (empty orbit) dendrites (not nonpyramidal cells or (turribrachycephaly); GI/GU/cardiac 3. moya-moya, aneurysms, ectasia action potentials) anomalies 4. white matter nonneoplastic GTC: high frequency, high amplitude Crouzons: Malformed ears, agenesis of “hamartomtous” lesions: dysplastic waves. Focal sz: low frequency (2-4Hz), the corpus callosum, malaligned upper glia, diminish w/age, ↑ T2, can rectangular wave. 40% have interictal teeth, variable sutures. Increased HCP, enhance – obtain serial MR activity (60% w/multiple EEG). Vertex Less severe MR (64% IQ >90) Both: AD, 5. BG lesions: ↑ T2, nonenhancing transients: normal, at skull vertex, may be hypertelorism, blindness, deafness, CNS tumors: optic gliomas, spinal confused with spike. Stage 2. Other exorbitism. astrocytoma, neurofibromas normal variants: Lamba(awake) & POSTS Carpenter syndrome: all sutures fused Other tumors: plexiform neuromas (asleep, both triangular), K-complex Holoprosencephaly: Alobar: Severe common in V1, visceral, endocrine tumors (arousal during stage 2 sleep), .14 & 6 facial abnormalities, monoventricle, no NF2: Chr 22, Protein: Merlin (aka rhythm (kids, drowsiness) septum, falx, fused thalami/ BG. Maternal Neurofibromin2, schwannomin). Links PET: foci ↓ interictal, ↑ during sz. diabetes, trisomy. Semilobar: partial falx membrane to actin cytoskeleton. Tumor Posttraumatic: open (bullet/ shrapnel) = & interhemispheric fissure. Lobar: no suppressor. (Also in regular schwannomas 50%, Closed = 5%. facial abnormalities, grey matter over & meningiomas) Developmental/Genetic corpus callosum, anterioinferior fusion of No lisch nodules or cerebrovascular Reflexes: Disappear: rooting 3mo; moro cortex, squared frontal horns, thalami/BG abnormalities (Café-au-lait, cutaneous or & grasp 6mo; Babinski 6-12mo (abnormal separated. Azygous ACA common. plexiform neurofibromas rare). >2yo). Parachute appears 9mos. Septum absent in all. Skin plaques (rough, raised, hairy areas), Achondroplasia: Chr 4, spinal stenosis, Septo-optic Dysplasia: Absent septum & juvenile cataracts, calcified choroid plexus, hydrocephalus optic nerve hypoplasia. 50% meningiomatosis Neural Tube Defects schizencephaly. 50% pituitary Tumors: Bilateral acoustic schawnnomas Anencephaly: most common congenital dysfunction, ectopic pituitary (or 1 w/family history), other CN malformation. Area cerebrovascula Arrhinencephaly:: no olfactory tracts, schwannomas, spinal ependymoma, contains vessels, nerve tissue. Decreased grey matter in place of corpus callosum. meningiomas (multiple, kids), maternal folate, zinc or copper. Kallmans syndrome: anosmia, astrocytomas, Neuronal Migration Disorders hypogonadism (GnRH neurons in Tuberous sclerosis: Bournvilles, , usu Mouse models: mutant reelin gene hypothalamus missing – derived from sporadic, Chr 9/11/16, variable penetrance; Lissencephaly: Chr 17 deletion assoc. olfactory placode like olfactory receptor Genes: TSC1 (chr9, hamartin), TSC2 Type I: 4 layer cortex w/ thin overlying neurons), MR. (chr16, tuberin). Tumor suppressors, white matter. Type II: no layers, Agenesis of corpus callosum: Partial = functions unknown glioneuronal heterotopias. splenium, rostrum. Probsts bundles (white Triad: adenoma sebaceum, 65% MR, Miller-Diecker: lissencphaly, pachygyria, matter periventricular bundles), 50% seizures (infantile spasms). Seen in <50%; microcephaly, abnormal facies, multiple associated abnormalities (chiari, Dandy- CNS lesions: Walker). High riding 3rd ventricle opens 1. Cortical tubers: <5% enhance, no Trisomy: Pataus (13) = hypotelorism, Mucopolysaccharidoses: transformation, thick gyri cleft lip, polydactyly, dextrocardia, All AR except Hunters, ↑ 2. Subependymal nodules: candle holoprosencephaly, microcephaly/ glycosaminoglycans gutterings, 1/3 enhance, calcify (can opthalmia, hypertonia, cataracts, severe Hurlers: α-L-iduronidase, ↑ dermatan & see on Xray), no transformation MR. Edwards (18) = hypertelorism, heparan sulfate, gargoyle face, MR, 3. Subependymal giant cell astrocytoma dolichocephaly, microgyria, cortical corneal opacity, thick meninges 4. Hamartomatous white matter lesions dysplasias, callosal agenesis, Chiari II, Scheies: milder, no MR 5. Aneurysms, stenoses syndactyly, VSD; Downs (21) = Hunters: X-linked, iduronate sulfatase, Skin: ash leaf spots, subungal fibromas, hypotelorism, brachycephaly, heart dz, skin pebbling, normal corneas, ↑ dermatan shagreen patch; Alzheimers, cataracts, small abnormal & heparan sulfate, no MR Tumors: cardiac rhabdomyomas, retinal brain, BG calcification, moyamoya, os Sanfillipos: heparan sulfate in urine, phakomas/angiomyolipoma, visceral odontoidium, spinal stenosis. Most cortical atrophy cysts, pancreatic & liver adenoma common cause of MR. Fragile X = most Morquios: skeletal deformities, (malignant > benign) tumors common hereditary MR, 1/3 female, large ligamentous laxity, ↑ keratan SO4 Sturge-Weber: nonhereditary, port wine ears, arched palate, hypotelorism, vermian Sly: odontoid hypoplasia stain in V1, focal seizures, hemiparesis, hypoplasia, large testes, hyperextensible, Morquios & Scheies & Maroteaux-Lamy: hemianesthesia, tramtrack calcification of prominent thumbs (carrier women: arched normal IQ cortex (not cortical vessels), large palate, hypotelorism). Trinucleotide Farber: ceramidase def., ↑ chondroitin enhancing choroid ipsilateral, repeats. SO4. Hoarse cry, arthropathy, skin leptomeningial angioma (enhances), Cri-du-chat: 5q deletion, severe MR, granulomas, MR hemispheric atrophy, glaucoma in kids microcephaly, hypertelorism Leukodystrophy: VonHipel-Lindau: Chr3, AD, variable Praeder-Willi: 15p deletion, obesity, AR except ALD & P-M. penetrance; hemangioblastoma (CNS + hypogonadism, mod MR Adrenoleukodystrophy: peroxisome def., retinal), renal cell, pheochromocytoma, Klinefelter: XXY, male hypogonadism, X-linked, male children, long chain fatty viceral tumors/cysts, erythrocytosis; 25% MR acid accumulation (peroxisomal defect), hemangioblastomas have VhL. No skin Turners: XO, no MR, CNS probs perivascular lymphocytes (others – no lesions. Lesch-Nyan: X-linked. HPRT deficency. inflammation), begins occipital, bronze Klippel-Trenaunay-Weber: spinal cord ↑ uric acid, gout, coreoathetosis, self- skin, ↓ cortisol (adrenal) hemangioma & enlarged limb mutilation. Tx allopurinol Alexanders: rosenthal fibers, sporadic, Rendu-Osler-Weber: AD, AVMs (lung, Lawrence-Moon-Biedl: GnRH deficency frontal, megalencephaly/ macrocephaly liver, brain) and skin telangetasias, (like Prader-Willi). Hypogonadism, (above 2 enhance). Etiology unknown. No epistaxis, aneurysms, pulmonary AVF retinitis pigmentosa, polydactyly, MR serum test – requires Bx. Wyburn-Mason: unilateral facial nevi w/ Sphingolipidoses: all AR except Fabrys. Canavans: spongiform, complete optic pathway/midbrain AVMs Cherry-red spot from greying of nerve demyelination, aspartoacylase, ↑ N- Cowden Disease: AD, germline PTEN axons which ↑s prominence of fovea (no acetylaspartic acid. Infants. Affects U- mutation. Cobble-stone fibromas of oral axons). Most have accumulation in fibers (subcortical arcuate fibers - all mucosa, multiple hamartomas: skin, neurons with distension & glassy others spare), Internal capsule spared, thyroid, breast, adnexal. Lhermitte-Duclos appearance. macrocephaly (also neuromas, neurofibromas, Hepatosplenomegaly in Niemann-Pick & Krabbes: galactocerebrosidase, psychosine meningiomas). Gauchers?, Sandhoffs. kills oligodendrocytes, globoid cells (large Li-Fraumeni: AD, p53 germline Fabrys: α-galactosidase (lysosomal), ↑ multinucleated, nuclei at periphery), BG mutations, various brain tumors (mostly ceramide trihexosides, pain episodes, X- density, ↑ startle, spasticity w/ ↓ DTRs, glioma), sarcomas, etc linked. Childhood strokes (brainstem), normocephalic. Neuropathy (endoneurial Turcot syndrome: AD, colon polyps/ CA neuropathy (autonomic, lipid in fibrosis). & medullos, GBM. APC germline epineurium & endoneurium – not Metachromatic leukodystrophy: AR, most mutation in some. Schwann cells) common, arylsulfatase A, ↑ sulfatides Basal cell nevus syndrome (Gorlin’s): Gauchers: glucocerebrosidase, Jews, AD. PTCH mutation (Chr9q): Patched, (urine). <2yo, juvenile, or adult. Dx: nerve nonneural. ↑ AFP. ↑ Glucocererbrosides. Bx (PAS+), MR, ataxia, myelopathy, Sonic-hedgehog receptor (Shh > binds Niemann-Pick: sphingomyelinase, Ptch > releases inhibition of Smoothened infants. Neuropathy: sulfatides in supranuclear vertical gaze paresis, Jews, peripheral nerve Bx (macrophages & > TGFβ, Gli, Wnts). Basal cell CA (esp normal HC, hepatosplenomegaly Schwann cells): eosinophilic, around eyes & nose, at puberty), jaw Sandhoff: Hexosaminidase A & B, non- metachromasia w/ cresyl violet, toluidine cysts, skeletal abnormalities (synostosis, Jews, hepatosplenomegaly blue, or pseudo isocyanin stains (affinity hypertelorism, frontal bossing, Tay-Sachs: Hexosaminidase A, rectal Bx, for iron, all blue). prognathism, Sprengels), calcified falx, Jews, macrocephaly (no visceromegaly), Pelizaeus-Merzbacher: Complete absence plantar/ palmar pits. Pitted teeth, cleft lip/ Zebra bodies on EM. Carriers: 50% ↓ of myelin. No dysmorphia, X-linked, palate, ocular defects, cataracts. Hex-A in blood (also DNA testing) proteolipid protein (myelin) deficiency, Hydrocephalus, seizures, MR, deafness. Both of above: ↑ GM2 gangliosides “tigroid” pattern (myelin spared around Medulloblastoma, meningiomas. accumulate, cherry-red macula (& vessels), 100% pendular nystagmus, Gardner’s syndrome: osteomas, colonic Niemann-Pick, Pseudo-Hurlers) become symptomatic as infants, may polyposis, soft-tissue tumors Pseudo-Hurlers: βgalactosidase, ↑ GM1 survive to adulthood, sudanophilic (sudan gangliosides, cherry-red spots stain) Cockaynes: AR, dysmorphic facies, (ketoacidosis), lactic acidosis. Bilateral X-linked: Fabrys, Hunters, ALD, microcephaly, premature aging, deafness, “Punched out” (hypointense) GP - ?2° to Pelezius-Merzbacher, Menkes, Lowes, photosensitivity, defective DNA repair, ischemia. Tx: Limit protein, some respond Lesch-Nyan. AD: Huntingtons striatocerebellar calcification, retinitis to B12. Adult: MLD, Krabbe, Sanfillipos, pigmentosa Lowes Syndrome: Oculocerebral Renal. Glycogen stroage Dz, Wilsons, Leigh, Canavans & Alexanders: macrocephaly X-linked. Defective AA transport. MR, Niemann-Pick, Gaucher, ceroid Cockaynes & P-M: 100% nystagmus Fanconi’s, rickets. Small CSF-like spheres lipofucinoses, MELAS/ MERRF Aminoacidurias also cause in white matter. Laurence-Moon-Biedl: AR. MR, retinitis leukodystrophy Glutaric acidemia: dilated sylvian fissures, pigmentosa, hypogonadism, spastic Zellweger syndrome: AR, migration abnormalities paraplegia, obesity, polydactyly, cataracts, polymicrogyria, hypomyelination, Mitochondrial: MELAS, MERFF, Leigh renal anomalies, peroxisomal defect, cerebrohepataorenal (AR, ↑ pyruvate & lactate, BG/ PVG/ Refsums: AR, phytanic acid, ichthyosis, PAG spongiform necrosis, ↑ T2), Kearns- Pain/Functional deafness Sayre (AD, ↑ pyruvate, retinitis Cluster headaches: increased intraocular DNA Repair defects: Cockaynes, Ataxia- pigmentosa), Lebers hereditary optic pressure & skin temp (vs migraine). Tx Telangiectasia, Xeroderma Pigmentosa atrophy, Menkes. 100% O2, ergotamine. (Methysergide (cerebral, cerebellar atroophy, ataxia, Maternal inheritance. Most cause causes retropleural/peritoneal fibrosis). MR), Fanconis anemia, Blooms encephalopathy & myopathy, ↑ lactate. CCBs, steroids, Lithium may be Lysosomal disorders: MLD, Krabbe, Ragged red fibers: abnormal mitochondria prophylactic. Niemann-Pick, Fabry, GM1 & 2 (on Gomori stain) Migraine: Classic = visual aura; common gangliosidoses (Tay-Sachs etc), Canavan, Trinucleotide repeats: found in Fragile = no aura; basilar = more severe all mucopolysaccaridoses, ceroid X, myotonic distrophy, huntingtons, (blindness, hemiplegia, coma). Tx: lipofuscinoses spinocerebellar atrophies, friedrich’s Abortive: Sumatriptan (CI: CAD) > Peroxisomal disorders: Zellweger, ALD ataxia. Cause anticipation (worse/ earlier Ergotamine (N/V), Midrin. Prophylactic: Glycogen Storage Diseases: in successive generations) verapamil (CCBs), amitriptyline (TCAs), All AR, glycogen accumulation, Neuronal ceroid lipofuscinosis: propanolol, Depakote prevent. myopathies. Accumulation of lipid pigments ceroid & Postcoital HAs may mimic SAH. Pompes (Type II): acid maltase, Chr 17, # lipofuscin. Kids (Batten’s) or adults. Narcolepsy: REM occurs at onset (stages forms: 2 childhood & 1 adult, accumulates Dementia (kids), szs, blindness, reversed). 70% have cataplexy in DRG, ant horn & throughout body; myoclonus. Kids die, adults variable (consciousness preserved); sleep paralysis, PAS+ vacuolar myopathy course. Cortical atrophy (grey matter dz, hypnagogic hallucinations (not McArdles (Type V): myophosphorylase, not white). somnambulism). Tx: Ritalin, TCAs. Total cramps during exercise, myoglobinuria, Channelopathies: number hours sleep per day is normal (+) ischemic exercise test (lactate doesn’t K+: ataxia-myokymia, long QT, benign Cataplexy: consciousness preserved rise), glycogen in muscle only familial neonatal convulsions (KCNQ2/3), Raynauds: mast cell dysfunction, Tauris: phosphofructokinase def. Excerise Issacs syndrome sympathectomy not helpful cramps (as above) + hemolytic anemia (↑ Ca+: Eaton-Lambert, Hypokalemic Dejerine-Roussy: from VPM/VPL retics). periodic paralysis (skeletal muscle thalamus Aminoacidurias dihydropyridine-sensitive Ca channel), Vascular AR except Lowes. Cause Malignant hyperthermia (mutation in Stroke: 12-24h = neuronal necrosis starts, leukoencephalopathy, demyelination. RYR1 gene for muscle SR ryanodine- 1-2d = PMN infiltrate; 5-7d = lipid-laden Phenylketonuria (PKU): AR, channel), familial hemiplegic migraine, macrophages (gitter cells), 10-20d = phenylalanine hydroxylase deficiency, ↑ episodic ataxia type 2 gemistocytic astrocytes; >3m fibrillary phenylalanine, phyenylpuruvic acid, ↓ Menke’s kinky hair: X-linked, defective astrocytes tyrosine; MR, seizures, musty odor; GI copper absorption, seizures, MR, Lacunar: lipohyalinosis (HTN) blond, blue-eyed. tortuous intracranial vessels Atherosclerosis: fatty streak > foam cells. Biopterin deficency: PKU Variant. ↑ Familial dysautonomia (Riley-Day): 2% tandem lesions phenylalanine, normal hepatic AR, Jewish children, small fiber Vasculitis: Wegeners: phenylalanine hydroxylase, Stiff-baby. neuropathy – loss pain/temp, autonomic Glomerulonephritis, lung/sinus Homocysteinuria: AR. cystathionine dysfxn (loss of tears on crying, corneal granulomas, neuropathies Antineutrophil βsynthetase deficiency. ↑ methionine, & ulceration, nonreactive pupils, cytoplasmic antibodies (ANCA). homocysteine > collagen formation temperature dysregulation, sweating, Necrotizing. Small arteries. Tx: disorder. 50% MR, osteoporosis, hypotension, dysphagia, vomiting, ileus, Cyclophosphamide.. Takayasu: pulseless cataracts, infarcts/ thromboses. poor feeding), hyporeflexia. No tongue disease (aorta), vision loss & loss of Arachnodactyly & lens ectopia (like papillae. No tx. peripheral pulses. Kawasaki: lymph nodes, Marfans, Marfans has no MR) Tx: Vit B6. Hirschprungs: defect of neural crest aneurysms; Buergers: tobacco; Behcet: Methylmalonic acidemia: AR. migration, Chr 10. Japan/Mediterranean, oral/genital ulcers, Mitochondrial. Methylmalonic-CoA > Orofacial Digital Syndrome: Only uveitis, colitis, rash, brainstem Succinyl-CoA by methylmalonyl-CoA females. Psudoclefts of mandible, tongue, encephalitis. Steroids. mutase (deficient – requires B12). palate. Hypertrophied buccal frenuli. Also: amphetamines, ergot, cocaine. Neonatal encephalopathy, seizures, stroke. Tongue hematomas. Alopecia. MR. Temporal arteritis: All > 60yo. ECA only ↑ ammonia, glycine, propionic acid (except ophthalmic). Giant cells. Skip lesions (need large segment for Bx). Incr Hypertensive encephalopathy/ emotional lability may occur due to ESR Tx: steroids Eclampsia: Occipital lobe hypodensity/ adjacent frontal fiber damage. Polyarteritis nodosa: Fibrinoid necrosis hemorrhage Bulbar palsy: LMN CN palsy (usu IX-XII) of epineurium vaso nervorum (vs amyloid Superficial Siderosis: Hypointense Top-of-the-Basilar: sudden onset AMS, – endoneurium) > mononeuropathy covering of brain on T2, due to repeated EOM/ pupil/ visual (homonymous multiplex, nephritis, skin purpura, hemorrhages w/ hemosiderin in meninges. hemianopsia) abnormalities, usu. Embolic. microaneurysms. Asymmetric. Males. Causes sensorineural hearing loss & Cranial nerves Immune complex deposition. ataxia. Cortical fibers synapse directly on V, VII, Cogan syndrome: Vasculitis limited to Misc NucAmb, XII (NOT on III,IV,VI,DMNX) CNS. Deafness, keratitis. Paraneoplastic syndromes: Corticobulbar fibers bilateral except to Amyloid angiopathy: lobar hemorrhage, Stiff-man (anti-GAD), Sensory neuropathy lower VII (contra) & XII. amyloid β protein (Congo red > green (anti-Hu = antineuronal nuclear, small I (Olfaction): SVA. 1° receptor cells (= birefringence under polarized light). cell), cerebellar degeneration (anti-yo = bipolar cells) in mucosa, axons form Occurs in vessels of leptomeninges & anti-Purkinje cell, lung > ovarian > olfactory nerve, through cribiform plate > superfical cortex (not deep structures), lymphoma), opsoclonus (anti-Ri, peds 2°: mitral & tufted cells (= glomeruli) in causes aneurysmal dilations, >70yo. neuroblastoma, adults breast), retinal bulb, (also has granule cells – no axons, Mineralizing angiopathy: calcified degeneration (anti-Ri also, adults, small inhibitory); > Olf. Tract > vessels, seen w/ XRT + MTX in kids cell), limbic encephalitis (small cell, 1. Lateral olfactory stria: to anterior Marfans: AD (30% sporadic). CHr 15, medial temporal lobes) olfactory nuc. (aka olfactory tubercle, fibrillin (microfibrils abnormal). tall/ thin, Depression: ↓ NE & 5-HT. SSRIs: ↑ > medial forebrain bundle and stria arachnodactyly, lens ectopia, pectus 5HT. TCAs & MAOIs ↑ 5HT & NE medullaris), amygdala, and pyriform excavatum, pes cavus (high arches), (TCAs block reuptake for both). cortex (=primary, area 34, > entorhinal scoliosis, blue sclera, MVP/ aortic Schizophrenia: ↑ dopamine. cortex (=secondary), DM thalamus, regurgitation, thromboses, ↑ risk of Antipsychotics block dopamine and/or prefrontal cortex (conscious aneurysms, strokes(?), homocystinuria, no serotonin. ↑ activity of Nacc & temporal perception, input from pyriform and MR. No Tx. structures (amygdala), ↓ prefrontal cortex DM thalamus)), or (Homocystinuria has above but also has activity. 2. Medial olfactory stria > septal area, MR, strokes, & is AR. Lenses subluxed Anxiety: ↑ 5HT, NE. Tx: Buspar. anterior commisure to contralateral upward in Marfans, downward in OCD: ↓ serotonin. Tx: SSRIs. areas homocystnuria) Enuresis: Tx: Impiramine Olfactory tubercle neurons project to Hyperhomocysteinemia: Occurs in 5% directly, not to olfactory tract/bulb of population. Does not have stigmamta ANATOMY In mucosa: sustenacular cells support, (MR etc) of homocysteinuria & levels are Brainstem syndromes: basal cells are receptor precursors – lower. Due to multiple enzymatic defects Wallenbergs (lateral medullary): CN5 olfactory neurons are only ones to (cystethionine β synthetase most (ipsilateral facial analgesia), 8 (vertigo), 9, continually regenerate. common), folate/ B6/ B12 def., or 10 (hoarse,etc), sympathetics (ipsilateral There are >2000 different receptor cells for systemic dz. Asymptomatic til 30-40s Horners), solitary nuc. (taste), odorants. Use G-proteins > cAMP or IP3. then CAD/ atherosclerosis/ thromboses cuneate/gracile nuc. (ipsilateral 2 specific glomeruli in bulb for each (endothelial damage due to ROS due to numbness), spinothalamic tract odorant. homocysteine oxidation in plasma). Tx: (contralateral pain/ temp loss – only 1 Accessory olfactory system: For detection folate (B6 or B12 in certain cases). contralateral); no weakness of pheromones, rudimentary in humans. Lupus/ SLE: Antinuclear Abs. Stroke: Vomeronasal organ > vomeronasal/ Webers: ventral midbrain; CN3 w/crossed th due to antiphospholipid Abs. Vasculitis: hemiplegia terminal n. (“13 cranial nerve, CN0”) > less common, immune complex Claude: dorsal midbrain; CN3 w/ataxia accessory olfactory bulb > Vomeronasal deposition, segmental dilation & Benedikts: CN3 w/ ataxia and hemiplegia nucleus in amygdala. Contain GnRH cells narrowing, aneurysms. Scattered ↑ T2. Parinauds: upgaze palsy, loss of – related to GnRH cells in hypothalamus, Fibromuscular Displasia: ICA accomodation (fixed pupils) – only 1, mediates sexual dimorphism narrowing, beaded. Carotid dissection/ large pupils w/ light/ near dissociation, CN0 has Schwann cells > schwannoma stenosis. convergence nystagmus, nystagmus II: CNS tract – has oligodendroglial, not Moyamoya: Rete mirable “puff of retractorius, lid retraction Schwann cells. SSA. (rods/cones) > smoke” due to proximal ACA/ MCA Millard-Gubler: base of pons, CN6 & 7 bipolar cells (1°) > ganglion cells (2°) > 3° stenosis, transosseous/ transdural and contralateral hemiplegia centers: collaterals. <10yo present w/deficits, 20- Medial medullary: contralat hemiparesis 1. LGB > visual cortex (conscious 30yo w/SAH. Associated w/Downs. (not face), contralat numbness, ipsi CN12 vision) or Steroids for recurrent TIAs. ASA. EC-IC Lateral pontine (SCA): ipsi ataxia, 2. Pretectal/EW nuclei (pupillary reflex, bypass or EDAS. contralat pain/temp, deafness, N/V see below) or Sickle Cell Disease: strokes, moyamoya, Locked-in: Bilateral basilar pons 3. Superior colliculi (> tectopontine (> aneurysms Pseudobulbar palsy: lesion of bilateral cerebellum) & tectospinal tracts; Hemolytic-Uremic syndrome: Bilateral UMN corticobulbar tracts above pursuit, head/neck mvmt) or BG hypodensity 2° infarcts brainstem (eg IC); unable to move eyes, 4. suprachiasmatic nucleus of mouth but can yawn & cry (reflexive). hypothalamus (circadian rhythms) Brisk jaw-jerk/reflexes. Also frontal signs, Retina: Part of CNS – has blood-retina IVCβ & IVA) > inferior temporal. Color, CNV to principal sensory (2°, touch, wide barrier & Muller glia. shape (faces, etc. visual agnosias, rang of pressure, large receptive fields) and Receptor cells: rods/cones. rhodopsin achromotopsias) spinal nuclei of V (2°, pain/temp). (rods) > transducin (G-protein) > PDE > Critical period exists where inputs from Mesencephalic nuc. (proprioception, cGMP to GMP > ↓ Na & Ca current both eyes need to form cortical pressure, contains 1° neurons (only (hyperpolarizing) > ↓ glutamate release to connections. In amblyopia in kids patch nucleus in CNS w/1° sensory neurons, bipolar cells (> “on-center” cells dominant eye intermittently. NMDA from neural crest, analogous to sensory stimulated, “off-center” cells inhibited, receptors mediate connection forming. ganglia). “on-center” bipolar cells stimulate its Superior colliculi: lesion gives loss of Tracts: ganglion cells and inhibit ganglion cells pursuit (tracking) eye movement Ventral trigeminothalamic = pain, crossed from “off-center” bipolar cells also); Rods Blindsight: nonconscious response to (from principal sensory & spinal). Dorsal = B/W, dim light. Cone = color, daylight. visual stiumli (ie threat) – from = touch, uncrossed (principal sensory Both Use glutamate. Conduct by electric noncortical projections, superior only). Both to VPM. conduction, not action potentials. colliculus VI: GSE. Lateral Rectus. Longest CN. Ganglion cells: Only cells in retina that III: Nerve lesion causes unilateral lateral gaze can initiate action potential. Types: W = GSE to extraocular mm: Superior rectus, paralysis. Nuclear lesion causes deviation small, slow, tonic & phasic to SC & inferior rectus, inferior oblique, medial away bilaterally (i.e. of both eyes), gaze pretectum, dark; X (or P) = medium rectus toward lesion is paralyzed (opposite of sized, tonic, to layers 3-6 LGB & Levator palpebrae (Mullers muscle = frontal eye fields) called “lateral gaze pretectum, color; parvocellular stream;Y sympathetic, less severe ptosis); paralysis” (or M) = rapid, phasic to layers 1&2 LGB Parasymathetics (GVE): EW to short PPRF – horizontal gaze center adjacent to & SC, B&W, magnocellular stream; ciliary nn. (sympathetic = long & short) to CN6 nucleus. Inputs from cortex (FEFs), Horiztontal cells Synapses from & to iris (constriction) and ciliary mm. cerebellum, SC, & vestibular nuc. Output depolarize rods/cones for lateral inhibition (accomodation). to cerebellum, vestibular nuc., pretectal Amacrine cells: Bipolar > Amacrine > Accomodation: Ganglion cells(2°) to LGB region, IN of Cajal & Nuc. of Darkshevich Ganglion cells to cortex to (directly and indirectly) EW to integrate horizontal & vertical eye Fovea (center of macula) contains only & CN3 (motor) nuclei (not to pretectal movement cones. Rod goes to amacrine cell before nuclei) to Ciliary muscles (meridional and Stimulation: rostral = vertical gaze; caudal ganglion cell. circular fibers) causes eyeball to narrow, = ipsilateral horizontal. LGB: ipsilateral 2,3,5. contra 1,4,6. lens to relax and become more spherical VII: Geniculate ganglion: sensory/ taste Layers 1&2 magnocellular, 3-6 for accomodation cell bodies only. Nervus intermedius parvocellular, 3&4 off-center, 5&6 on- Pupillary light reflex: no LGB. (1°) carries sensory & parasympathetic fibers. center (1&2 mixed). bipolar cells in retina to (2°) ganglion Parasympathetics (GVE): Input from Ganglion cells and LGB cells have “on- cells to (3°) pretectal nuclei to (4°) EW hypothalamus & solitary nuc. center, off-surround” concentric fields. nuclei (via posterior commisure) to (5°) 1. Superior salivatory nuc. (1°) > greater Cortex: Primary: Area 17 (layer IVCα = ciliary ganglion to short ciliary nerves to petrosal n. > pterygopalatine gang. (2°) > magnocellular input, layers IVCβ & IVA iris lacrimal gland = parvocellular input, layer IVB = cortical Sympathetics to pupil: 1° hypothalamus > 2. Superior salivatory nuc. (1°) >chorda input, has stripe of Genarri), Secondary: via hypothalamospinal tract > 2° C8-T3 tympani > submandibular gang. (2°) > Areas 18 (±19) (no stripe of Gennari). lateral horn (Ciliospinal center of Budge) submandibular, sublingual glands. No concentric fields, cells repond to lines, > 3° superior cervical gangion > around Lesion distal to geniculate ganglion has no borders. Simple cells = position & ICA > short & long ciliary n. > iris & decreased lacrimation, greater petrosal n. orientation of line, rectangular fields. Mullers muscle already off Complex cells = orientation. movement IV: GSE. Superior Oblique > eye down & Motor (SVE): Facial nucleus > staepedius (not position in field). Hypercomplex cells In; only crossed n.; Lesion: worst = (hyperacusis), stylohyoid, posterior belly = length, shapes. downgaze to opposite side. Bielschowskys of digastric (anterior from CN5), Ocular dominance columns in cortex sign – head tilted to opposite side; eye up facialmm. (part of motor nucleus supplying alternate eye dominance, have orientation & in. Difficulty walking down stairs. lower face receive crossed input only from & location specificity. Together strips V: V1 = ophthalmic > SOF > nasociliary cortex) form ocular dominance bands. Absent in & lacrimal nn. V2 = maxillary > inferior Taste (SVA): Anterior 2/3 tongue. Chorda 2 areas of area 17: those representing orbital fissure or rotundum. V3 = tympani > geniculate ganglion (1°) > blind spot of retina & monocular temporal mandibular, > ovale. rostral nucleus solitarius (2°) > central crescent. Orientation columns also exist. Motor (SVE): Motor nucleus of V > tegmental tract > VPM thalamus (± Hypercolumn: 2 adjacent columns w/same tensor palatini & tympani (hypoacusis), parabrachial nuc. of pons) > insular cortex field from each eye. mastication (temporalis, masseter, (perception) (parabrachial > amygdala/ Magnocellular stream: “where stream”. pterygoids, anterior belly of digastric, hypothalamus for emotional response) Y-cells > Layer 1/2 LGB > area 17 (layer mylohyoid). Weakness causes deviation Sweet (sucrose), bitter (alkaloids), & IVCα) > parietal cortex. Spatial, of jaw away. umami (glutamate) receptors are movement, orientation (visual neglect, Sensation (GSA): metabotropic, sour (H+) & salty (Na) are apraxia). Trigeminal (aka Semilunar, Gasserian) ionotropic. (Spicy-hot mediated by Parvocellular stream: “what stream” X- ganglion (1°) projects via spinal tract of trigeminal nerve) cells > Layer 3-6 LGB > area 17 (layers Receptors may respond to multiple tastes, horizontal, saccule vertical. Sensation Motor (SVE): nuc. Ambiguus > pharyneal but usually 1 preferentially. occurs in macula – contain otoliths & hair br. (all mm except stylopharyngeus (IX) Sensation: ear (GSA), soft palate (GVA) > cells. and tensor veli palatini (V)) > sup. spinal nuc of V Semicircular canals: angular movement. Laryngeal n. > internal (sensory) & Mobius syndrome: congenital absence of Ampulla (dilation at 1 end) contains external laryngeal (cricothyroid) both facial nuclei (± abducens nucleus) endolymph and crista ampullaris – Recurrent laryngeal=(off ganglion)all VIII: SSA sensory organ). Fluid remains still but hair laryngeal except cricothyroid BAER: I° cochlear n. > II° cochlear nuc > cells move. Taste (SVA): > solitary nuc. (via trapezoid body) > III° Superior olive Hair cells > Horizontal SC & anterior SC Aortic sinus (GVA) Inf ganglion > solitary > IV° lateral lemniscus/ nucleus > V° Inf. (aka superior) to superior ganglion, nuc. Colliculus > VI° MGB > VII° Cortex posterior SC to inferior ganglion (1°) > Aortic Bodies (SVA): > Inf Ganglion > Dorsal cochlear neurons bypass Sup olive Vestibular nerve > medial & superior Reticular Formation & lateral lemniscus nuc, to Inf Coll (III°) vestibular nuclei or floculonodular lobe Parasympathetic (GVE): dorsal motor nuc. Lesions above trapezoid body cause directly (2°) Sensory (GSA): ear > spinal tract 5. partial deafness (contra > ipsilateral) Vestibular nuclei: Lateral: (Dieter’s) from XI: SVE. C1-6, to trapezius, SCM Commisure of Probst: in between lateral utricle ( & anterior saccule?) to lateral XII: All tongue mm. except palatoglossus lemniscus nuclei. Also has Inferior vestibulospinal tr. – extensor tone/posture; (X). Exits preolivary sulcus. GSE (not Colliculi commissure. inhibited by anterior lobe of cerebellum; SVE – comes from somites not brachial Cochlea: Sound enters scala vestibuli, has no connections w/other nuclei; arches). UMN crossed from contralateral transmitted to scala media by Reissner’s Inferior: from posterior saccule to cortex (UMN causes deviation away) membrane. Hair cells in scala media cerebellum; integrates input from CN Nuclei: (organ of Corti) sit on basilar membrane, vestibular labyrinth & cerebellum; Nuc. Ambiguus: motor (9,10,11) touch tectorial membrane; sit in Medial: largest, crossed to all extraocular Solitary nuc: rostral = taste (7,9,10), caudal endolymph (high K, low Na). Vibrations nuclei & cerebellum, medial = carotid sinus/body (9) at apex have lower frequency. Scala vestibulospinal tract to neck mm.; Superior salivatory: parasympathetic (7); vestibuli & tympani contain perilymph, Superior: uncrossed to CN3,4; Interstital: Inferior salivatory: parasympathetics (9) communicates w/CSF. Cochlear nerve cells lie among fibers of vestibular root (both in reticular formation) (bodies in spiral ganglion) synapse on hair MLF: Ascending: from medial & superior Dorsal motor nuc = parasymathetic (10) cells. vestibular nuclei to CN 3,4,6 nuclei to Ganglia: Nodose = inferior vagal; Cochlear nuclei: fibers group into 3 control eye movement. Descending: Gasserian = CN5 acoustic striae: ventral, dorsal (from medial vestibulospinal tract & medial Reflexes: Pupil = 2 & 3. Dolls = 3 & 8 respective nuclei) & intermediate (from reticulospinal tract to cervical cord (VestNuc > PPRF > CN3/6). Jaw-jerk = 5 both). Dorsal = high frequency, ventral = motorneurons to influence head/trunk only; Corneal = 5 & 7. Pupillary = 2 & 3. low. Ventral to superior olive, dorsal movements relating to eye & vestibular Gag = 9 & 10. Cough = 10 only. direct to inferior colliculus. movement (from superior colliculus, Oculocardiac: V1 to X. Superior olive: Attenuates loud sounds. PPRF, IN of Cajal, & medial vestibular Eye movement Input is from contralateral cochlear n. via nucleus). Saccades = frontal eye fields (area 8) & Caloric nystagmus: COWS = fast phase, parietal eye fields > contralateral PPRF trapezoid body; Output is via st olivocochlear bundle back to contralateral deviation is reverse (parietal synapse in Superior Colliculus 1 > PPRF). Right PPRF = Right gaze. cochlea directly to hair cells to ↓ Postrotatory nystagmus: Slow phase in Smooth Pursuit = eye > LGB > area 17 > sensitvity to sounds and to tensor tympani direction of rotation, fast phase opposite temprorooccipital eye fields (>< FEFs) > (V3) and stapedius (7) IX: dorsolateral pontine nucleus (DLPN) > Medial Sup. Olive = time differences Motor (SVE): Nuc. Ambiguus > vermis/flocculus > med vestibular nuc > Lateral Sup Olive = intensity difference stylopharyngeus NPH/CN nuclei; Trapezoid body is only commissure Parasympathetic (GVE): Inf salivatory Lateral Gaze: PPRF, CNVI nuclei (post needed for sound localization nuc > tympanic n./plexus > lesser petrosal limb IC); Vertical Gaze: FEFs > ant limb Cortex: AI = area 41, A2 = area 42. Area n. > otic gang. (2°) > parotid IC > synapse in riMLF & interstitial nuc of 22 = auditory association area. Wernickes Sensation (GSA): middle ear (tympanic Cajal 1st > PPRF. = posterior area 22. Prosody = Right n.), pharynx > Superior Gangion (1°) > Lesion of one CN6 nuc. impairs both eyes opercular (posterior temporal =- Spinal Nuc of V from moving to that side comprehension of prosody) Carotid Sinus (GVA): Herrings n. > CN9 FEFs go to riMLF/PPRF, not to CN nuclei Vestibular system > Inferior Ganglion (1°) > nucleus directly. Utricle > superior vest ganglion > Lateral solitarius (2°) > DMN of X (↑ BP Stimulation: rostral PPRF = vertical; vestibuluar nucleus decreases HR, TPR, force, BP, CO) caudal PPRF = ipsilateral horizontal; Saccule Posterior part > inferior vest Carotid Bodies (SVA): Chemoreceptor Superior colliculus & FEFs = contralateral ganglion > inferior vestibular nucleus. (CO2) > Inf Ganglion > Reticular horizontal. Anterior part > Superior vestiblar Formation > Reticulospinal fibers > Lesion: cortex/ putamen = toward; ganglion > lateral vestibular nucleus. inspiration. thalamic = persistent down gaze; pons/ Detect linear movement: utricle in long Taste (SVA): nuc. Solitarius > VPM cerebellar = away, pontine = pinpoint; axis of body, functions when upright; thalamus > postcentral gyrus midbrain = towards saccule in dorsoventral plane, fuctions X: when supine. When head is erect: utricle Pons/cerebellum (ie contralateral contralateral VL (VA?/VPL) > motor sympathetic n. – release NE to stimulate paramedian br. of basilar, contralateral cortex. VL: head medial, feet lateral, melatonin. Also has corpa arenacea or SCA) eyes deviate away; FEFs extremeties ventral, back dorsal. brain sand (calcifications). (contralateral MCA) eyes devate towards Only interposed synapse in caudal red Hypothalamus: anterior/medial = Opticokinetic reflex: keeps eyes straight nucleus. parasymp.; Posterior/lateral = symp. when head is moving (eg. on a train). Some fibers descend to contralateral (ant/post = temp, lat/med = feeding) Direct opticokinetic path: Retina > nuc of reticular nuclei and inferior olive then Preoptic: GnRH (sexually dimorphic) optic tract & Nuc of accessory optic decussate back to ipsilateral cerebellar Suprachiasmatic: circadian rhythym system > cerebellum/vestibular nuc. cortex. Supraoptic: ADH, uniform large cells (no Indirect path: Same as pursuit path Spinocerebellar tracts: Dorsal = LE, ICP, distinct groups). Projects to pituitary only. (temporalocciptal cortex); lesion gives from dorsal nucleus of clarke (C8-L2); Paraventricular: oxytocin, distinct cell defect with target moving towards same Ventral = LE, contralateral, SCP, L1-S2 groups (magnocellular (oxytocin) & side cell bodies; Cuneocerebellar = UE, parvocellular). Projects to brain Nucleus prepositus hypoglossi: provides analogous to dorsal SCT. All go to stem/spinal cord. Also TRH, CRH. info to CN6 nucleus about current anterior lobe. Arcuate: GHRH, dopamine. head/eye position. Note: propioception from LE in dorsal Anterior: parasympathetic, heat loss Cerebral peduncle: lat>med: spinocerebellar, UE in posterior column Ventromedial: staiety center POTpontine > corticospinal/bulbar Ganglia: medial to lateral: Dorsal: stimulation > feeding, savage (UE>LE>CN) > frontopontine Fastigial: to reticular formation & behavior Cerebellum: vestibular nuclei Lateral: feeding center Stimulation elicits nothing. Interposed: (emboliform & globose) to Posterior: sympathetic, heat conservation, Lobes: flocculonodular = vestibular red nucleus to thalamus to motor cortex wakefulness (nystagmus, imbalance). Anterior = Dentate: to VL (VA/VPL) thalamus to Median eminence: where axons from spinocerebellar, tone (sl. hyperreflexia). motor cortex arcuate etc. release releasing hormones Posterior = pontine, coordination. Inferior Olive: inputs from red nucleus, into venous plexus Zones: vermis (truncal ataxia, scanning cortex, and spinal cord to contralateral Pituitary axis: Supraoptic & speech), intermediate (appendicular ICP to cerebellum (ant & post lobes) via paraventricular nuclei contain ataxia, hypotonia), lateral (tremor, olivocerebellar tract magnocelluar neurons > synapse directly decomposition, dyscoordination, delay of Red nucleus: inputs: 1) interposed on posterior lobe of pitutary. (Both have initiation). (Note no hypertonia. nucleus of cerebellum to VL thalamus, 2) input from subfornicial organ) Hypotonia from vermis or intermediate cortex. Output: rubrospinal tract, inferior Arcuate etc. contain parvocellular neurons, zones.). olive (> contralateral cerebellum). synapse on venous plexus in median Gait ataxia may be due to cerebellar or Stimulation elicits contralateral flexion eminence > anterior pituitary. posterior colums disease (Romberg only + Feedback circuits: Feeding: Neuropeptide Y ↑ feeding thru in latter) 1. Frontal lobe > Pontine nuclei > paraventricular nucleus. Neuropeptide Y Vermis & IZ have somatotopic Cerebellar cortex > Dentate nucleus containing neurons in the arcutae nuc. organization, not lateral zone. > VL thalamus > Motor cortex Inhibited by leptin from fat cells. VMH & Layers: Molecular = basket, stellate. (Area4) LH centers oversimplified. Purkinje. Granular = granule, Golgi II. 2. Red nucleus > Inferior olive > Input: MFB, fornix (hippocampus), stria Cells: Granule=glutamate, all other Cerebellar cortex (ant & post) > terminalis (amygdala), DLF (midbrain GABA. Parallel fibers to Purkinje Interposed nuclei > Red nucleus central grey), retinohypothalamic, nucleus dendrites (spiny). 3. Spinocerebellar tracts > Anterior solitarius. Generally from limbic system/ Climbing fibers: from inferior olive, lobe cerebellum > Fastigial Nucleus amygdala/ hippocampus – not neoortex. crossed, to Purkinje dendrites (smooth) > Reticular formation/Vestibular Output: MFB, stria terminalis, Dorsal Mossy fibers: all others. End in Nuclei > Vestibulospinal & Longitudinal Fasiculus (parallels MFB thru glomerulus (Both: glutamate) Reticulospinal tracts medial hypothalamus), mamillothalamic, Glomerulus: (granular layer) Mossy fibers Diencephalon: thalamus, hypothalamus, mammillotegmental, hypophyseal, & Golgi axons > Granule dendrites subthalamus, epithalamus (pineal, descending autonomic Peduncles: habenulum, stria medullaris) Tuberoinfundibular tract:: hormones Inferior: Restiform: All afferent.dorsal (metathalamus = geniculate bodies) from arcuate nucleus (tuberal region) spinocerebellar, cuneocerebellar, Habenulum: Input/Output: septal area/ released in capillary plexus in median olivocerebellar (contralateral, largest # of hypothalamus (via stria medullaris); eminence to portal veins to capillaries in fibers). Juxtarestiform: Afferent: fasiculus retroflexus (>< VTA >< raphe anterior pituitary vestibulocerebellar (> flocculonodular nuc) Supraopticohypophyseal tract: lobe). Efferent: Cerebellovestibular. Stria medullaris thalami: anterior Magnocellular neurons from supraoptic & Middle: All afferent. Pontocerebellar thalamus, preoptic, septal areas to paraventricular nuclei (histologically (crossed) habenular nucleus identical, both nuclei in supraoptic region) Superior: Afferent: ventral Pineal: composed of glia (5%) & to posterior pituitary spinocerebellar, Efferent = pinealocytes. Secretes serotonin Pituitary: Anterior: Cerebellothalamic. (>melatonin). Antigonadotropic. Pars distalis: hormone secretion. Cerebellothalamic tract: dentate > Overactive delays puberty, hypofunction Basophils, acidophils, chormophobes. decussates at inferior colliculus > precocious puberty. Innervated by Pars intermedia: basophils, Basal Ganglia = Subiculum, hippocampus, dentate gyrus chromophobes, & colloid cysts (remnants Control intensity & timing of movement All archicortex - 3 layers. of Rathke’s pouch). Produces MSH 1. Direct Loop: ↑ thalamocortical (Parahippocampal gyrus has 5 layers). (melanotropin), stimulates melanocytes to excitation. Cortex (glu) > Striatum Hippocampus proper = Ammon’s horn produce melanin (GABA) > GPi (GABA) > (Ammon = egyptian god with rams’ head) Pars tuberalis: around stalk. Squamous VA/VL/CM (glu) > cortex C-shaped: Parahippocampal gyrus cells, follicles of suboidal cells, (VL>motor, VA>premotor) (outside) > Subiculum (transition) > hypophyseal plexus veins 2. Indirect Loop: ↓ thalamocortical hippocampus (CA1>2>3) > Dentate gyrus Posterior: Pars nervosa & infundibulum. excitation: : Cortex (glu) > Striatum (hilus = CA4) (curves back over Has pituicytes (resemble astrocytes). Has (GABA) > GPe (GABA) > subiculum). Herrings bodies (storage of ADH & Subthalamus (glu) > GPi (GABA) > CA1=parvocellular (vulnerable to anoxia. oxytocin) & glomeruli thalamus > cortex = Sommer’s sector). CA3=magnocellular Superior hypophyseal a. to infundibulum, 3. Nigrostriatal loop: Facilitates direct Alveus: white matter b/t hippocampus & median eminence, pars tuberalis. Inferior loop by D1 receptors & inhibits temporal horn composed of efferent fibers; hypophyseal a. to pars nervosa. Anterior indirect loop by D2 receptors. Cortex most medial portion is Fimbria (> fornix) lobe has no direct supply. (glu) > Striatum (GABA) > SNpr > Cellular Layers of Hippocampus (in to Anterior lobe from ectoderm (Rathkes SNpc (dop) > Striatum > GP > out): Polymorphic layer (axons,output) > pouch), Posterior from neurectoderm Thalamus > Cortex. pyramidal cell layer(soma) > molecular (diencephalon) D1 receptors on striatonigral neurons, D2 layer (input, dendrites). Dentate gyrus: Thalamus receptors on striatopallidal neurons. pyramidal cell layer replaced by granule Sensory: VPL (body), VPM (face)(both to Dopamine does not directly excite/inhibit cell layer. 3/2/1), VPI (vestibular), LGB (to 17), striatal neurons, but changes K Input: MGB (from inf coll. To 41/42, tonotopic) conduction to raise/lower RMP. 1. Entorhinal cortex, Via Non-specific: to parietotemporal GP = diencephalon, Put/Caud (& GPe?)= A. Perforant pathway >dentate (mossy association areas: telencephalon. fiber) >CA3 (Schaffer’s collaterals) > Pulvinar: Auditory/vision relay. Projects Output CA1 >subiculum) or to sensory association corticies: occipital Striatum: B. Alvear pathway (straight to (18/19), parietal, & temporal (not frontal). 1. to GP: GABA & to GPe = enkephalin hippocampus), LP: Output to 5/7 (SIII) (spiny type I), to GPi = substance P 2. Fornix (septal nuclei, substantia Motor: VL (VLo: from GP to area 6/8, (spiny type II) (Aspiny neurons are innominata etc) VLc from cerebellar/red nuclei to area4); intrinsic Putamen only) 3. Cingulate cortex VA (from GP, to area6 & nonspecifically 2. to SNpr (GABA) Output: Fornix. Subiculum / pyramidal to cortex (esp prefrontal) for recruiting), GPe: to STN cells of hippocampus > alveus > fimbria > Centromedian: (from GP/area4, to GPi: fornix. Subiculum > postcommisural putamen. Stimulation at 6-12 Hz produces 1. Thalamus: Ansa lenticularis + (Main output, to MB, ant thalamus, activity (recruiting) of large areas of Lenticular fasiculus (Forel’s field H2) hypothalamus). Hippocampus > cortex) > Thalamic Fasiculus (Forel’s field precomissural (septal area > lateral All 3 receive input from GP via thalamic H1) > VA/VL/CM (Thalamic hypothalamus). fasiculus. fasiculus also contains fibers from Also direct output to entorhinal cortex & Limbic/Behavioral: cerebellar dentate nucleus) amygdala (small). Anterior /LD: from MB (mammillo- 2. Pallidotegmental: to VTA Hippocampal commisure: between thalamic tract) and hippocampus (fornix), Thalamostriate fibers: from CM/ fornices to cingulate. parafasicular nuc. to striatum Schaffer’s collaterals: branches of DM: to/from prefrontal lobe (also input Damage: GP = athetosis, ST = pyramidal axons which synapse on other from limbic structures), affected in hemiballismus, Striatum = chorea, SN = hippocampal cells (i.e. CA3 to CA1) Korsakoffs, controls affective rigidity, tremor Dentate: efferent fibers only to behavior/memory, smell (from olfactory Subthalamus: Subthalamic nuclei + Zona hippocampus (mossy fibers). areas) incerta (grey matter b/t thalamic & Indusium griseum: remnants of Intralaminar: CM: To putamen (see lenticular fasiculi). Use glutamate hippocampus over corpus callosum. above). Parafasicular nuc.: To caudate. Substantia Nigra: Neurons contain Fornix: main efferent from hippocampus. Both receive ARAS/spinothalamic input melanin granules. Fibers to putamen, Body (rostral to thalamus) > Columns & have diffuse cortical projections for caudate, sup colliculus, thalamus (not (posterior to anterior commissure). arousal. Rostral intralaminar nuclei: GP). Pars Reticulata: input. Pars Forniceal commissure: aka psalterium. Is thalamic pacemaker. compacta: output, dopamine (to spiny rostral to anterior commissure. Thalamic reticular nucleus: thin sheet on neurons in putamen). Papez circuit: Probably serves short-term lateral wall. No cortical projections, Hippocampus memory (MB, Ant. Thalamus) more than projects to other thalamic nuclei & Function: integrating short-term memory, emotion. Bidirectional. Subiculum > reticular formation. Receives all affarents assigns salience to stimuli for emotion fornix > MB > MT tract > Ant. Thalamus & efferents w/ collaterals. Mostly (modulates limbic system/ hypothalamus) > Cingulum > entorhinal cortex > GABAeric? & memory. No olfaction. subiculum Extremities ventral, back dorsal; head medial, caudal lateral Amygdala Septal area: Subcallosal and paraterminal 3=commisural), 4 = thalamocortical Function: Interface between cortex and gyrus & septal nuclei (NucAcc, Meynert). (input), 5=pyramidal (corticospinal), 6= hypothalamus/brain stem for emotional Relay for hippocampal afferents to corticothalamic (5&6=projection) response & emotional memory. hypothalamus. Input from fornix Homotypic cortex: has typical layers Stimulation : Fear & Rage (hippocampus), brainstem, hypothalamus (association areas). Idiotypic/ heterotypic Corticomedial group: olfaction, > (MFB), anygdala (diagonal band of cortex has altered layers (primary hypothalamus/pituitary (high Broca), medial olfactory stria. motor/sensory areas) concentration of enkephalins, Output: MFB to hypothalamus, stria Has columnar organiztion of 100-300 somatostatin, and dopamine) medullaris to habenulum, diagonal band neurons w/same function. Central nucleus: input/output to of Broca to amygdala, also hippocampus Parallel networks for language, attention, hypothalamus & autonomic brainstem (fornix), cortex, thalamus, MB. (not basal learning/memory, face/object recognition, Basolateral group = cortical, sensory ganglia) & comportment. input (temporal), uses glutamate Medial Forebrain Bundle: septal area to 2 heteromodal association areas: Input: Olfactory (lateral olfactory stria), hypothalamus to brainstem (reticular temporoparietal (sensory integration), and taste (Nucleus solitarius), and auditory formation & autonomic areas). prefrontal (integrates motivation with (temporal cortex). Sensory, prefrontal & Bidirectional. stimuli – punishment/reward). cingulate cortex. Sunstantia innominata = Nucleus Allocortex: 3 layers. Pyriform cortex Output: basalis of Meynert. Ach. Functions in (paleopallium, 3-5 layers), hippocampus 1. Stria terminalis (CM > hypothalamus, sleep/wake, memory, emotion. Input: and dentate gyrus (archipallium, 3 layers). septal area), amygdala, olfactory cortex. Output: Note entorhinal cortex = parahippocampus, 2. Ventral amygdalofugal tract (BL > diffuse cortex (activating). ↓ in pyriform cortex = uncus. hypothalamus, PAG) Alzheimers. Mesocortex. 3-6 layers. Paralimbic areas: 3. Diagonal Band of Broca (septal area) Mesocorticolimbic system: Midbrain cingulate/ subcallosal/ paraterminal gyri, 4. Direct: Cortical/ hippocampus/ DM Ventral Tegmental Area (VTA, aka parahippocampal gyrus, temporal pole, thalamus/ striatum/ brainstem. interpeduncular nucleus) to limbic system insula, & caudal orbitofrontal cortex. Only meager projections back from (NAcc, amygdala, hypothalamus, cortex); Band of Baillerger: in layer 4b. In area hippocampus, thalamus & hypothalamus. Uses Dopamine; Acts similar to SN in 17 is Stripe of Gennari (not in 18/19 – Kluver-Bucy: Bilateral damage. Docility, BG system. ↑ excitation of Nacc to ↑ extrastriate cortex). Hyperorality, hypersexulaity, visual stimulation of DM thalamus & limbic Temporal lobe: medial = PCA, agnosia (psychic blindness), hyperphagia, cortex to ↑ responsiveness to stimuli. Role superior/lateral = MCA. Superior gyrus = exploring in positive reinforcement/Addiction language, middle & inferior = visual Limbic system: amygdala, septal area, Nucleus accumbens: where putamen & discrimination. Deficits: Bilat middle & inf hypothalamus, anterior thalamus, anterior caudate meet anteriorly; functions = psychic blindness, Bilat heschls = cingulate & orbitofrontal cortex, ± w/septal nuclei. Recives VTA input. Role deafness, unilat = slight contra loss; hippocampus. Controls emotion (self & in addiction/ gratification. vestibular cortex (post to Heschl) = species preservation, learning, emotional Reticular system: Functions in pain, decreased OKN; time perception (either processing/ social behavior). autonomic control, posture, eye side); dom = auditory leaning, nondom = Output of limbic system to brainstem: movements, arousal, sleep/wake. visual learning DLF (hypothalamus), fasiculus retroflexus ARAS: ascending reticular activating Parietal lobe: dom = math/language, (habenulum), Mamillotegmental fasiculus, system. Pons & midbrain: locus ceruleus nondom = spatial; MFB (amygdala/ septal area/ (NE), pedunculopontine nucleus (Ach), Parietal lesions: Dominant: Gerstmanns hypothalamus). ventral tegmental area (Dop) and Raphe (finger agnosia, right-left confusion, General path: hypothalamus (endocrine) > nuclei (serotonin) to acalculia, agraphia), also alexia, anomia, Midbrain PAG > Autonomic & Motor CN 1. central tegmental tract to thalamus tactile agnosia, ideational & contsructional nuclei (intalaminar & reticular nuclei) and apraxia; Non-Dom: anosognosia (= All tracts bidirectional. 2. medial forebrain bundle to septal neglect, denial of illness), dressing apraxia, Limbic system has analogous loops to nuclei/basal nucleus of Meynert topographic memory loss, constructional basal ganglia: Raphe nucleus in low pons/medulla is apraxia, asomatognosia (hemineglect) 1. Direct path: Limbic/Prefrontal cortex inhibitory (serotonin) Angular Gyrus: visual processing of & intralaminar nuclei > NAcc Raphe nuclei & locus ceruleus also send words; damage causes alexia and agraphia (ventral striatum) > ventral pallidum descending fibers to spinal cord. To affect - inability to read/ write with intact speech > DM/Ant thalamus > cortex. ↑ pain transmission (see analgesia) comprehension, Gerstmann’s responsiveness (memory/ emotion Nucleus reticularis pontis oralis functions Occipital lobe: Bilateral: cortical /learning) to stimuli. in wakefulness & REM sleep. Excited by blindness; Anton’s syndrome (aka Anton- 2. Indirect Path: same as above but VP hisaminergic neurons in posterior Babinski, denial of blindness); Dominant: > STN > VP. Inhibitory hypothalamus; inhibited by GABAergic simultagnosia (identify parts of picture, not 3. Mesolimbic: Nacc > VTA > Nacc. neurons in anterior hypothalamus. whole thing); prosoprognosia. Right Excitatory. Analogous to SNpc. (both Parvocellular Area: BP manitenance, occiptotemporal: color agnosia, left = color use dopamine). respiration? anomia; Balint synd: psychic gaze LAMP = membrane glycoprotein marker Cortex: paralysis/peripheral inattention (bilateral for limbic system neurons Neocortex: 6 layers. layers 2-3 posterior parietooccipital) corticocortical (2&3=association, Primary motor (Area 4): lesion = Apraxia: Ideational = dominant parietal, collateral sulcus); Occipitotemporal: hypotonia, paresis (no fine movement); failure to carry out sequences of acts, inferior, lateral to collateral sulcus. Inferior BG lesion = hypertonia. Neurons although can do parts. Have pt act as frontal: lateral: pars orbitalis > triangularis innervate synergistic sets of muscles (not combing hair w/out comb. Ideomotor = > opercularis. Medial: gyrus rectus > individual mm.) Cortical columns Dominant Parietal (supramarginal gyrus/ subcallosal area > paraterminal gyrus. represent movements, not individual arcuate fasiculus). Can perform acts (contiguous w/ cingulate) Supramarginal: muscles. Chiefly functions is distal mm. spontaneously but not on command. Can end of Sylvian fissure. Angular: end of Premotor area (6): Planning/ timing. conceive mvmt but not perform until superior temoral fissure (more posterior) Lesion produces apraxia of complex, cued; test by using utensils, dressing, etc. Both separated from superior parietal learned movements, unable to produced Note actions conceived in dominant lobule by intraparietal sulcus. Cingulate: delayed response; has homonculus parietal cortex, travels arcuate fasiculus to b/t cingulate sulcus (superior) & sulcus of SMA (medial area 6): LE anterior, face L frontal & corpus callosum to R frontal corpus callosum posterior. Functions in coordinating for performance. Corticobulbar fibers: Project to sensory bilateral movements. Stimulation – gross Aphasia: conduction = impaired relay nuclei (gracilis, cuneatus, trigeminal, bilateral movement w/urge to move repetition (Wernickes (fluent paraphasic) solitary nuclei), reticular formation, & (premotor – discreete movement, requires with retained comprehension & awareness motor CN nuclei. higher stim, no perception of urge to of deficit), transcortical motor/sensory = Fibers to gracilus & cuneatus nuclei leave move). Movement on either side activates. normal repetition, echolalia (sensory = pyramids & transverse reticular formation Lesion –spasticity (vs area 4) and temporoparietaloccipital jxn, motor = or medial lemniscus. involuntary grasping, akinesia, poverty of frontal lobe). Brocas & Wernickes = Fibers to trigeminal & solitary nuclei are speech (all resolve in 6 weeks). Unilateral impaired repetition. Pure word deafness from frontoparietal cortex. lesions usually cause no permanent (can still read, echolalia) = area 22, Corticoreticular fibers from premotor, deficits. anterior (bilateral > left). motor & sensory cortex to medulla Both SMA & premotor send fibers Subcortical (Left BG) lesions may also (gigantocellular) & pons (oral pontine). directly to spinal cord, have homunculi, cause aphasia. Motor fibers from 1° motor area; bilateral and higher threshold than MI. Exner’s area: superior to Brocas. Causes except CN 7 (lower) & 12. (However Frontal Eye Fields (area 8): area 8 > agraphia without aphasia. lesion to fibers to 12 is asymptomatic or Superior colliculus, IN of Cajal, Alexia without agraphia: Left occipital mild) Darkschewitsch Nuc > PPRF > MLF > lobe (geniculocalcarine tract and corpus Pseudobulbar palsy requires bilateral CN3,4,6 nuc. Fibers don’t go to CN nuclei callosum). Usu has hemianopsia & color lesions. directly. For voluntary saccades. anomia. With agraphia = left angular Internal capsule: Anterior limb: Stimulation: bilateral deviation away gyrus (Gerstmans). Without hemianopsia frontopontine, anterior thalamic radiations. Lesion: cant target objects on command = rare, deep white matter, corpus callosum Genu: corticobulbar, corticoreticular. (eyes tonically to same side). (not geniculocalcarine) Posterior limb: Corticospinal, Parieto- Occipital Eye Fields: aka posterior Color anomia: left mesial occipital-temporal-pontine, superior parietal, temporooccipital (widely occipitotemporal lobe; Achromatopsia: thalamic radiations, corticofugal fibers dispersed). Subserve involuntary smooth right inferior occipitotemporal (color Sublenticular = auditory radiations, pursuit. Stimulation: eye deviation away blindness) Retrolenticular = visual radiations. (like FEFs but higher threshold, longer Prefrontal cortex: Orbitofrontal: social Skull Base latency). Lesion: eye deviation to same appropriateness (lesion – disinhibition), Floor of 4th ventricle: Rostral to stria side (like FEFs) but can target w/ saccades connects w/limbic system; Dorsolateral: medullares: median eminence > facial And have problems following objects motivation (lesion – apathy), connects to colliculus > sulcus limitans.> inferior Sensory Cortex: 3a = muscle spindles, 3b motor areas. cerebellar peduncle. Caudal (Rhomboid = skin (slow & rapid), 1=rapidly adapt Fasiculi: Uncinate: antertior temporal to fossa): hypoglossal trigone > vagal trigone. skin, 2 = pressure/joint. Input: 3b > 2 > 1. orbitofrontal; Arcuate: Superior & Middle Area postrema most caudal. Below 4th Damage causes topagnosia (decreased frontal gyri to temporal (Wernicke to ventricle: dorsal median sulcus > gracile localization), astereognosis (no pain/temp Broca); Cingulate: medial frontal & tuburcle > dorsal intermediate sulcus > loss). parietal to parahippocampal. tuberculum cinereum > dorsolateral sulcus. Each has separate homunculus. Corpus callosum: Does not have Ventral: pyramid > preolivary sulcus/ XII Vestibular & gustatory cortex lie in projections between areas 1,2,3 (S1),4 > olive > postolivary sulcus > IX, X, XI. operculum. (M1), or 17 (V1). 3rd ventricle: SII: on superior bank of lateral sulcus. Section: splenium = unable to read left Infundibular recess: ventral to mamillary Homunculus is inverted. Stimulation field; ant. 1/3 = nothing; all = left hand bodies. elicits bilateral sensations. Role in apraxia Circumventricular organs: pineal, identifying objects by touch & storing Tapetum: white matter lateral to temporal subforniceal (at foramen of Monroe; memories (old view – pain perception) horn/ atrium (medial to optic radiations) detects serum osmolarity, controls ADH & Somatosensory association (areas 5&7) Calcar avis: medial to temporal horn/ oxytocin release, projects to supraoptic Agnosias: cant identify object. Visual = atrium nucleus, angiotensin II receptors), bilateral occipitotemporal (ex Gyri: Precuneus: medal b/t paracentral subcommisural (below posterior Prosoprognosia - faces). Tactile = area 40 lobule (S1) and cuneus (separated by commissure, has BBB), organum (supramarginal). Auditory = area 22. parietooccipital sulcus); Lingual: posterior vasculosum of lamina terminalis (GnRH & to parahippocampal gyrus (medial to somatostatin release), median eminence of hypothalamus (contains plexus for Lateral cerebellomedullary: PICA, Nucleus dorsalis of Clarke: thoracic to pituitary releasing hormones), choroid plexus of 4th ventricle. C8, layer 7, proprioception, forms dorsal neurohypophysis, area postrema (emesis, Spinal Cord spinocerebellar tract paired, sensitive to apomorphine & Descending Tracts Dorsal spinocerebellar tract: Muscle digitalis, consists of astroblasts & some Lateral motor system = corticospinal + spindles & Golgi tendon organs of LE (1°) neurons) rubrospinal > synapse ND of Clarke (lamina 7, T1-L2) Medial motor system = vestibulospinal + @ level of entry (2°) > DSCT > Inferior Nasal septum: ethmoid (superior) & reticulospinal Cerebellar Peduncle > ipsilateral anterior vomer (inferior). Cartilage anterior Corticospinal tract: Lateral: 90%. Cross lobe cerebellum. Uncrossed. Detects Orbit: maxilla (inferior), lacrimal (medial at decussation. Anterior/Ventral: 10%, Individual muscles. At levels L3-S5 ascend anterior), ethmoid (medial posterior), remain ipsilateral, then cross at level of in fasciculus gracilis to L1/2 then synapse frontal (superior), sphenoid (posterior termination in SC, posture control. All in NDC (2°). st superior), palatine (posterior inferior), synapse on interneurons 1 (2°) in ventral Ventral: LE, synapses ventral horn (2°) > zygomatic (lateral) horn & use glutamate. When damaged crosses @ level of entry > VSCT > crosses Inferior orbital fissure: occ V2 rubrospinal takes over. Babinski from in pons to contralateral Superior cerebellar Anterior clinoids: Optic canal & ICA corticospinal (or cortical) damage. peduncle > ant lobe. L1-S2 cell bodies, medial, SOF lateral Note no direct connection to CN 3, 4, 6, Golgi tendons organs only, detects muscle ICA dural rings: Proximal = oculomotor DMN vagus. From: Betz cells 3%; Area 4 groups (whole limb); membrane b/t ICA & CN3, roof of = 30%, area 6 = 30%; area 1,2,3 = 40%. Cuneocerebellar (& Rostral – cats only): cavernous sinus. Distal = dura. 40% of fibers are poorly myelinated. UE, analogous to dorsal & ventral; enter @ Lillequist’s membrane: Between CN3 Rubrospinal tract: (Fibers from cortex C1-8 > ascend in fasiculus cuneatus > medially, divides interpeduncular cistern 4/6 & cerebellum >) red nucleus > crosses synapse in accessory cuneate nucleus in from chiasmatic cistern. Seen b/t ICA & in ventral tegmental decussation > medulla (2°) > ant lobe cerebellum. CN2. cervical/thoracic cord. Flexor tone. Dorsal Colums/Medial Lemniscus: Cavernous sinus: CN6 only 1 inside Vestibulospinal tracts: Lateral: from Touch/Pressure. DRG (1°) > Gracilus (LE) Tendinous ring: CN2, 3, 6, nasocillary, lateral vestibular nuc, to all levels SC, / Cuneate (UE) Fasiculus > Gacilus/ & ophthalmic a. inside (Outside: frontal extensor tone; Medial: from medial Cuneate Nuc. (2°) > decussation > medial and lacrimal nn. off V1, CN4, ophthalmic vestibular nuc., to cervical cord only, lemniscus > VPL thalamus (3°) > area v.) CNXI Nuc. (neck mm.), role in vestibular 3/2/1 & SII ( > motor cortex for feedback) Dura: supratentorial = V, infratentorial = modulation of head position via neck, runs Note transmits proprioception only from X and C1-3 (no VII) in MLF. Both remain ipsilateral. UE, not LE. Falciform ligament: between anterior Tectospinal: From superior colliculus, Lateral cervical system: (aka spinocervical clinoids, over optic n. reflex movements for sight; cross at thalamic tract). Light touch. Enter C8-L4 > Floor of 3rd ventricle: Ant to post: optic origin; to cervical levels only synapse in lamina 4 > ascend in SCTT > chiasm > infundibulum > tuber cinereum Reticulospinal tracts: Pontine reticular synapse in lateral cervical nucleus (C1-4) > > MBs nuc > medial reticulospinal tr ipsilateral > medial lemiscus > VPL > area 3/2/1 Lateral ventricle: Medial to lateral: extensors. Medullary reticular nuc > Rexed’s lamina: lamina I: fast pain. = fornix/ septal v. > velum/ choroid > lateral reticulospinal tr bilateral > flexors lamina II: Substantiosa gelatinosa. Slow thalamus/thalamostriate/anterior caudate v & autonomic info. pain, ascend/descend several segments in Transvelum interpositum approach: Ascending Tracts Lissauer’s tract (outside lamina I). Both between choroid & thalamus (lateral) Lateral spinothalamic: pain/temp; body have substance P & glutamate receptors Pterion: frontal, greater wing of in DRG (1°) > axons enter Lissauer’s tract for 1° nociceptive afferents. Layer 3& 4: sphenoid, parietal, squamous temporal > synapse in Lamina II on soma (2°) > Asterion, Bregma, opisthion nucleus proprius cross @ level of entry in ventral white (touch/pressure/proprioception); Layer 7: Houghtons lines commissure > (most fibers to reticular Petrous bone: Geniculate ganglion: zona intermedia (dorsal nucleus of Clark); formation = spinoreticular tract) > VPL/ Layer 9: motor neurons. posterolateral to ICA, posteromedial to VPI & intralaminar nuclei (3°) > sensory formen spinosum, anterior to superior Dorsal roots: Ganglionic neurons use cortex. glutamate, substance P, somatostatin, semicircular canal, medial to cochlea; (some spinoreticular fibers remain lateral to middle ear cavity. GSPN: runs CCK. Roots divide into medial (from ipsilateral) encapsulated sensory organs, Golgi,muscle over & parallel to ICA. Dorello’s canal: Paleospinothalamic tract: C fibers to layer contains CN6. spindles, thick myelin) and lateral (from 2 to reticular formation, intralaminar free nerve endings, thin myelin, pain/temp) Petrous ICA: drill away Glasscocks nuclei, PAG; burning pain. triangle posteriormedial to foramen ovale bundles. In the spinal cord these divide Neospinothalamic tract: Aδ fibers to layer into ascending & descending branches. (foramen spinosum to arcuate eminence to 1 to VPL, sharp pain GSPN) Ventral horn SC: flexors = dorsal, Visceral pain: Aδ & C fibers in extensors = ventral (same as tracts); trunk Cavum: septum pellucidum, vergae sympathetic nerves > lamina 7 > (posterior), velum interpositum (3rd vent) = medial, hand = lateral spinothalamic tract (parasymathetics carry Somatotopic organization: Cortex, BG, Cisterns: Ambient: SCA, CN4, basal v. nonpainful sensation) Rosenthal. Interpeduncular: CN3, basilar Red nucleus, reticular formation, Vermis Anterior spinothalamic = light touch; & intermediate zone of cerebellum a. Quadrigeminal: Vein of Galen. CPA: cross @ level of entry. To VPL. CN5,7,8, AICA. Prepontine: Basilar a. Anaglesia: PAG (midbrain) & PVG (hypothalamus) (both enkephalin) to nucleus raphe magnus in medulla extensors/ supinator, APL (injury from Cervical ligaments: posterior longitudinal (serotonin, NE) to dorsal horn of spinal crutches). If cut in forearm no motor loss, ligament becomes tectorial membrane cord (enkephalin) to inhibit nociceptive 1° only sensory. Facets: Cervical: inferior facet is medial. sensory neuron axons and projection Autonomous zone = 1st web space dorsum Thoracic: coronally oriented. Lumbar: neurons’ dendrites. PAG stimulation Axillary: (posterior) deltoid, teres minor superior facet is medial. elicits fear, diplopia, etc. PVG better (injured with anterior shoulder Neck: Recurrent laryngeal n.: left around tolerated. dislocation) aorta, right around subclavian a.; both off Brainstem sections: Thumb: Median = Abductor pollicis vagus, posterior to inferior thyroid a. Medulla: Inferior Olive, accessory brevis (perpendicular to palm), FPB Superior laryngeal n.: travels w/superior cuneate, dorsal nucleus X, nucleus (superfical), opponens, FPL; Ulnar = thyroid a. in 15%. Phrenic n.: anterior to ambiguus, solitary nucleus adductor policis, FPB (deep); Radial = anterior scalene, behind IJ. Subclavian a. Pons: Superior vestibular nucleus, abductor pollicis longus (parallel to palm). & v. run between anterior & middle Spine/Peripheral Nerves: Ad/Abduction is perpendicular to palm, scalene. Stellate Ganglion: inferior cervical Brachial Plexus: Roots (C5-T1) > Trunks flex/extension is in plane of palm. + upper thoracic ganglia (Upper/ middle/ lower) > Divisions (ant/ Interosseous muscles: palmar = adduct Bladder: parasympathetics: pelvic n. Post) > Cords (Lateral/ Medial/ Posterior) fingers; dorsal = abducts 1&4, flexes (S2,3,4) to detrusor mm. Voluntary: Arise from roots before plexus: Lumbricals: extends IP joints, flexes Pudendal (S2,3,4) to external sphincter. Dorsal scapular: C5. rhomboids, levator MCP joints Sympathetics: inferior splanchnic n. to scapulae (stabilize scapula). Carpal tunnel: contains FPL, FCR, inferior mesenteric ganglion to inferior Long thoracic: C5,6,7. serratus anterior Median N., FDS, FDP hypogastric nn. to internal sphincter (α), & (abduct scapula > winged scapula, cut Guyons canal: ulnar a. & n. bladder wall relaxation by inhibiting during axillary node dissection). Lumbar plexus parasympathetics in pelvic ganglion. Arise from upper trunk: Superior gluteal: gluteus medius, min. (T10,11,12). UMN = spastic, propantheline Suprascapular: supra (abduction) & (thru greater sciatic foramen, above or oxybutnin (Ditropan), imipramine infraspinatus (ext rot) pyriformis m.; inf. Gluteal & sciatic (TCA, anticholinergic); LMN = atonic, Arise from cords: below pyriformis) bethanecol, methacholine. Lateral & medial pectoral: pectoralis Inferior gluteal: gluteus maximus Melanocytes located in cervicomedullary major; (lateral & medial cords) Femoral: iliopsoas, quads pia. Made by tyrosinase. Musculocutaneous: (lateral) brachialis, Obturator: adductors, gracilis Vascular coracobrachialis, biceps (elbow flexion) Sciatic: hamstrings (biceps), part of Internal capsule: Ant limb = Heubner; Median: (lateral & medial cords). Travels adductor magnus, semitendinous, Genu = ICA perfs/ Heubner; Post limb = w/ brachial a. in arm. Goes thru 2 heads of semimenbranous. To: ant. choroidal; Ant & post = pronator teres in forearm. Gives off Tibial: gastroc, TP, FHL (all foot mm.) lenticulostriate a (from M1). No PCA anterior interosseous n. (FPL, index FDP, Common peroneal: to Striatum: Lenticulostriate a, Heubner, Ant pronator quadratus). Palmar cutaneous Superficial peronal: peroneus longus choroidal branch: arises 5cm proximal to wrist. & brevis Thalamus:: PCA: ant & post choroidals, Recurrent motor br. To thenar muscles Deep Peroneal: Tib ant, extensors thalamoperforators (basilar, PCOM, P1), arises distal end carpal tunnel. Biceps fermoris only has innervation from thalamogeniculate (MCA doesn’t supply) Muscles: Hand = LOAF: Lumbricals 1&2, peroneal component of sciatic n. > Substantia Nigra: PCA/Pcom opponens, APB, FPB (superficial); all differentiate sciatic from peroneal n. Cortex: ACA = hemiparesis (LE), mild other flexors/ pronators in forearm, injuries sensory; Achor = hemiplegia, palmaris longus. Ilioinguinal n.: at risk in appendectomies hemianesthesia, homonymous hemianopia. Autonomous zone = tip of index finger. (McBurneys incision) PCA = cortical blindness, Balints, Ulnar: (medial cord). Runs behind medial Ulnar n. vs C8 root injury: ulnar n. splits prosopagnosia epicondyle, thru Guyons canal. Dorsal 4th digit, C8 covers entire finger. C8: Ventricles: lateral = anterior and lateral cutaneous branch (sensation to dorsum of EMG ↓ ECU (radial), APB (median), posterior choroidals, 3rd = medial posterior digits 4 & 5) leaves in forearm. paraspinous mm, NCV normal. Plexus SSS drains to right transverse sinus Muscles: Adductor pollicis, FPB (deep), (Lower trunk/ medial cord): normal Aortic arch: R Innominate (> R CCA > R hand intrinsics; FCU, FDP3/4 paraspinal, abnormal sensory median VA > R thyrocervical trunk > subclavian) Autonomous zone = tip of little finger antebrachial cutaneous n. > L CCA > L subclavian (> VA). Subscapular: (posterior) teres major Radial n. vs C7 root: C7: FCR (median). L VA off aortic arch in 5%. (adducts humerus), subscapularis (med rot Posterior cord: deltoid. Rarely can have nonbifurcating CCA w/ humerus) Peroneal n. vs L4/5: L4/5: loss of foot ECA branches. Thoracodoral: (posterior) lattisimus dorsi invertors Aberrant ICA: runs behind tympanum > (adducts shoulder) Femoral n. vs L3: L3: loss adductors/ pulsatile tinnitus. Do not biopsy. Radial: (posterior). Around spiral groove quads Persistent stapedial a.: intratympanic, from of humerus. Divides below elbow into C1: has no dorsal ramus petrous ICA to MMA posterior interosseous (thru arcade of Odontoid: 2 primary ossification centers Intracranial ICA: Frohse, all muscles in forearm & hand) at base, 1 secondary at apex. Petrous: > vidian a. > caroticotympanic a > and superficial branch (sensory) Canal diameter: Cervical =18mm, middle ear Muscles: triceps, brachioradialis stenosis = 12mm; Lumbar = 20-22mm, Cavernous: meningohypophyseal a. C4/5 (musculocutaneous = brachialis), stenosis <15mm (tentorial of Bernasconi & Cassanari, inf. Hypophyseal, dorsal meningeal), Labyrinthine a.: off AICA in 85%, basilar Schiller-Duval bodies: seen in endodernal inferolateral trunk C4, McConnel’s in 15%. sinus tumors capsular. SCA: supplies deep nuclei Alzheimer type II cells: Hyperplasic Supraclinoid: Sup. Hypophyseal. Superior Sagittal Sinus: to Right protoplasmic astrocytes with large Intradural: ophthalmic > pcom > ant transverse sinus (inferior SS to Left) irregular clear nuclei, prominent choroidal. Trolard: to SSS. Labbe to transverse nucleolus, paired nuclei, no cytoplasm. Hypophyseal a.: inferior = post pituitary sinus Seen in hepatic encephalopathy and superior = anterior pituitary Deep veins: Anterior caudate + terminal Wilsons disease (alzheimer type I more Ophthalmic a.: 0.5% arise from middle vv. > Thalamostriate + septal (anterior) + common – also has Opalski cells) meningeal. May also arise from cavernous epithalamic + atrial/ choroidal vv. > Perivascular lymphocyte cuffing: genu (C3) Internal cerebral v. (at venous angle) + gangliogliomas, herpes encephalitis, AIDS Fetal P-comm: unilateral in 20%, Basal v Rosenthal > VOG. Basal ganglia calcification: Fahr disease bilateral in 8% Basal Vein of Rosenthal: ambient cistern (familial), hypo & hyperparathyroidism, Anterior Choroidal: Cisternal segment > Thalamostriate v. : injury results anoxic, MELAS, Cockayne, NF, TS, Plexal point (enters choroidal fissure) > insomnolence, hemiparesis, & mutism Downs, carbon monoxide, lead Plexal segment. Supplies: optic tract, post (not seizures). Basal ganglia necrosis: hypoxic, Toxic: limb IC, BG, substantia nigra?, thalamus, Posterior fossa Vv.: Ant-Post: Precentral methanol (putamen), carbon monoxide amygdala, hippocampus (mostly from cerebellar v., Superior vermian v., (both (GPm), cyanide, manganese. Leighs (↓ PCA), tail of caudate (not hypothalamus). to vein of Galen, both sacrificed in T1), Wilson, Alexanders, Canavans, MLD, Had been sacrificed as Tx for Parkinsons. infratentorial supracerebellar approach) Hallervorden-Spatz, metachromatic Anterior temporal lobe masses displace it Inferior vermian (to straight sinus) leukodystrophy, toxo, crypto, HUS, medially. Adamkiewicz: Left T11 (T4-T8 most hepatic encephalopathy (↑T1), TPN (↑ T1) Injury: Hemiplegia, hemihypesthesia, vulnerable to low flow) Cerebellar atrophy: EtOH, chronic homonymous hemianopsia (cognition Persistent fetal arteries: Persistent Dilantin, Friedrichs unimpaired) trigeminal: 0.1-0.5%, cavernous ICA to Kernicterus: unconjugated bilirubin, GP, ACA: A1 to ACOM> A2 to pericallosal/ basilar, ↑ AVMs, aneurysms; Persistent hiipocampus, STN callosomarginal jxn> A3 hypoglossal: cervical ICA to basilar thru Seen in Rh incompatibility (hydrops A1: medial lenticulostriate aa. (8-10 perfs hypoglossal canal, basilar may be fetalis), heridatary sperocytosis, hemolysis, to optic n, chiam, hypothalamus, etc). hypoplasic or absent below; Persistent Crigler-Najjar (glucuronyl transferase ACOM: perfs to chiasm otic: petrous ICA to basilar thru IAC; def.), Dubin-Johnson Heubner: (medial striate a.) from A2 > Proatlantal intersegmental: b/t arch C1 & Conjugated bilirubin doesn’t cross BBB A1. anterior limb IC, BG occiput, ECA or ICA to vert. Inclusions: MCA: M1 (to bifurcation)> M2 (insula, Cowdry type A: intranuclear, halo, large. to sylvian fissure edge) > M3 (cortical, PATHOLOGY HSV, CMV measles. opercular) Stains: Neuron: body = Nissl, processes = Cowdry B: small, no halo. polio Sylvian point:most posterior branch of silver (Golgi, Bodian, Bielschowski), Ground glass: intranuclear. JC (PML) MCA leaving sylvian fissure Luxol-fast blue = myelin. Gomori Intracytoplasmic: rabies (Negri), Picks, (Lateral) Lenticulostriate a.: from M1. trichrome = muscle.India ink, Lewy (parkinsons), Lafora, Hirano BG, IC. mucicarmine = cryptococcus. Fat = (Alzheimers), Bunina (ALS), Marinesco Anterior temporal a. from M1. Sudan, oil-red-O, Congo Red = β (aging) PCA: P1 (to PCOM)> P2 (in ambient amyloid, PAS = glycogen, carbohydrate Astrocytes: corpora amylacea (normal cistern) >P3 (quadrigeminal) > (fungi, parasites also), Gomori methamine aging, polyglucosan, often subpial, stain w/ parietooccipital, calcarine (GMS) = fungi, AFB = mycobacteria fungal stains); Rosethal fibers Thalamoperforators: from basilar tip, Hamartoma: disorganized cells in right Microglia: elongated nuclei, scant pcom, P1 location. Choristoma: Normal cells in cytoplasm. Medial post choroidals: from P1; midbrain wrong location Pituitary: Anterior = nests of epithelioid tectum, thalamus, 3rd ventricle Markers: AFP = endodermal sinus; cells separated by fibrovascular septae. Lateral post choroidal: from P2; thalamus, chromogranin = pituitary adenoma, Posterior = loose spindle cells, has lateral ventricle choroid paraganglioma; cytokeratin = cranio, pituicytes (astrocytes). Med & Lat thalamogeniculate a. : from chordoma, choroid plexus; desmin = Pencil bundles of Wilson: myelinated P2, post thalamus, crus cerebri teratoma; EMA, vimentin = meningioma; fibers in the caudate. P3: Post temporal a. (anast. W/MCA); BHCG = choriocarcinoma; S100 = Fibrinoid necrosis: (of vessels) in post- Internal occipital> Parietooccipital (to schwannoma, glioma, pnet, etc; PTAH = XRT, PAN, temporal arteritis. MCA), Calcarine (to ACA) ependymoma. CD20, (CD45, CD3) = Calcospherites: prolactinoma, oligo, Vertebral a: Left dominant in 50%, right lymphoma (B-cells). CD1a = Langerhans ganglioglioma, adult pilocytics 25%, neither 25%. 40% one hypoplastic. cells. Melanoma: cytokeratin, HMB45, Segmental demyelination: PNS: 1-25% terminates in PICA. Both off S100, (AE1/3-) diptheria, MLD, Charcot-Marie-Tooth subclavian a. Rosenthal fibers: pilocytic, alexanders Rosettes: PICA: vermis, medial cerebellum. Loops (large brain, cause unknown, sporadic) Pseudorosettes: around blood vessel, around tonsils Babes nodule: glial nodules, form in viral ependymoma AICA: anterolateral cerebellum. encephalitis True Rosettes: around fibrillary material, ependymoma Homer-Wright: fibrillary material, MRSpect: Tumor: ↑ Choline & cells bind to these (recognize RGQ medullos, neuroblastoma, pineocytoma, Choline:creatinine ratio, ↓ NAA. ↑ lactate seuence). Cell adhesion molecules PNETs in mitochondrial encephalopathies. (CAMs, ie N-CAM & Ng-CAM) bind cells Flexner-Wintersteiner: resembles cone Magnetoencephalography (MEG): to each other. photoreceptors, central lumen; measures neuron firing (function), G-proteins: α unit binds GDP, βγ units pinealblastoma, Retinoblastoma noninvasive, accuracy to 1mm. Uses anchor, inhibits activation by stabilizing Eosinophilic Granular Bodies: SQIUD to pick up very low voltages. Use binding of GDP and inhibiting GTP intracytoplasmic. Seen in pilocytics, PXA, for epilepsy to map seizure foci, sensory/ binding. Binding of ligand > GDP/GTP ganglioglioma visual/ auditory (> motor/ speech) areas. transfer > βγ units dissociates > protein Immunohistochemistry: Magnetic Source Imaging: MEG overlaid activates > automatic GTPase > GDP > βγ Neurons: synaptophysin (axons & on high-res MRI. reassociates. Activation of 1 G-protein periphery of cell body), NSE (not neuron Diffuse dural enhancement: meningitis, inhibits activation of other G-proteins in specific), NeuN (nucleus). EM: dense core carniomatosis, postop, sarcoid, the membrane. Pertussis & cholera ADP- granules. histiocytosis, intracranial hypotension, ribosylate, prevent GTP hydrolysis & Astrocytes: GFAP, S100 (nonspecific idiopathic hypertrophic pachymeningitis inactivate. glial) Second messengers: Phosphorylate/ Oligodendroglia: NONE. (Myelin Basic PHYSIOLOGY dephosphorylate or directly open/close Protein experimentally) Cell cycle: M & G1 susceptible to channels to alter activity. Ependyma: S100. (GFAP- except radiation. 1. Phospholipase C forms IP3 & DAG tanycytes - GFAP+). PTAH is a stain, not DNA syntyhesis: RNApol (3’-5’) primer from PIP. IP3: releases Ca from ER. Ca IHC marker. > DNApol (moves 3’-5’). Lagging strand binds calmodulin & protein kinase C. Choroid plexus: Transthyretin, S100. – Okazaki frags, 5’-3’. UV – thymidine DAG: activates PKC w/Ca. Used by α1 & Microglia: HAM56, KP1 dimers. Transcription: RNApol 5’-3’. muscarinic receptors Leptomeninges: EMA GTP energizes translation. Hydroxyurea 2. cAMP: Used by β-adrenergic, H2 & D1 Melanocytes: HMB45, S100 blocks ribonucleoside diphosphate receptors, ACTH & TSH. Closes K reductase & deoxynucleotide/DNA channels - ↑ excitability, activates PKA. RADIOLOGY synthesis rate limitng step. UV light 18 Adenyl cyclase forms; Phosphodiesterase PET: Positron Emission Tomography. F makes thymidine dimers. degrades. flouro-deoxyglucose (FDG) – measures Transcription: RNA polymerase binds to 15 3. cGMP: stimulated by NO. glucose metabolism (also H2 0 – blood promoter – adds nucleotides 5’ to 3’. 4. Arachadonic acid: DAG > AA by flow). Requires cyclotron (for Poly-A tail on 3’ end. Terminated by rho. phospholipase A2. Then forms radioisotopes. Positron = same mass of Amanita & rifampin (nonhuman) inhibit prostaglandins, etc. Used by histamine. electron but + charge.). Resolution 8mm. RNApol by binding to initiation sites. Steroid hormones: have cytosolic Findings: GBM/ high grade tumor ↑, Low Elongation inhibited by actinomycin D. receptors which binds to chromatin grade tumor ↓, radiation necrosis ↓, Reverse transcription: RNAdep-DNApol affecting mRNA transcription. hetertopia normal or ↑, cortical dysplasia makes DNA from RNA. Neurons: no anaerobic glycolysis. Require ↓, most seizure foci ↓ interictal, ↑ ictal, Translation: GTP energizes. Cytoplasmic O2 & glucose. Don’t require insulin. mesial temporal sclerosis ↓. ribosome 80S (60S+40S). Mitochondrial Glucose crosses BBB by facilitated SPECT: Single Proton Emission 70S (50S+30S). transport. Tomography. Measures blood flow. 99Tc cytosolic proteins: translated by free Dendrites have all organelles except Golgi; (technetium, HMPAO) or 133Xe used. ribosomes, little modification; axons & hillock lack RER (Nissl), Golgi, Resolution 10mm. Findings similar to secretory/organelle proteins: translated by ribosomes. Dendrites only have graded PET. ER, extensive modification (ex potentials, not APs. Myelogram: “Feathering” = extradural; neuropeptides cleaved in ER/Golgi); Nissl substance = Rough ER. meniscus = intradural, extramedullary. nuclear & mitochondial proteins targeted Psuedounipolar = sensory (dorsal root) Diffusion-weighted MRI (DWI): ↓ by posttranslational importation. ganglia; Bipolar = CN8 ganglia, CN I&II. diffusion (acute infarct) = bright, ↑ (cyst) Inhibited by mercury, dipitheria toxin, Multipolar = all others = dark, Can detect infarct instantly (after erythromycin. Golgi I: single long axon, projection. 14d stroke becomes isointense). Organelles: SER: steroids, lipoprotein Goligi II: short axon, cortical. Tumors: Tumor = dark, edema = bright. synthesis; RER: export protein translation, Intrinsic burst firing: due to low voltage Necrosis = bright, abscess = dark. Ribosomes: cellular proteins translation activated (LVA) Ca channels Apparent Diffusion Coefficient (ADC (N-linked glycosylation), Golgi complex: Cytoskeleton: Actin & spectrin link map): Ischemia: hours = bright, days = export protein modification (fatty acid cytoskeleton to plasma membrane. dark. attachment, O-linked sugars, sugar Microfilaments: actin. (βγ) Perfusion MRI: Contrast given during phosphorylation, sulfation of tyrosine), Neurofilaments: Neuron-specific high-speed MRI to evaluate perfusion. If mitochondria: matrix = Krebs cycle, intermediate filaments. Form perfusion defect is larger than diffusion membrane = electron transport chain neurofibrillary tangles (paired helical defect (mismatch) – represents penumbra. Extracellular matrix: composed of filaments assc w/tau MAP).Nonpolarized. Proton-density: high signal in glycosaminoglycans & proteoglycans, Microtubules: polymerize w/GTP. demyelination (MS plaque) collagen/elastin, and “adhesive” proteins: Polarized. Depolymerized by colchicine, fibronectin (fibroblasts), laminin stabilized by Taxol. Synthesis inhibited by (epithelium), tenascin (glia). Integrins on vincristine. MAPs: microtubule-associated proteins. Both to cardiac pacemaker cells & Neuropeptides made in soma, cleaved from Include tau, kinesins, dyneins. myocytes, & bladder prohormone, longer action. Small- Intermediate filaments: GFAPin Neuron labeling: Horseradiash molecule NTs (all others) made in cytosol astrocytes & Schwann cells peroxidase (retrograde), 2-DG of nerve terminals, actively transported Nerve transport: anterograde (- to +) autoradiography (metabolic, labeling new into vesicles (some enzymes in vesicles – slow = 1mm/d, enzymes/proteins; fast = AAs, anterograde), MRI, Gold (motor i.e. for NE). Amines & neuropeptides 100mm/d, organelles, kinesin; retrograde endings), Golgi staining, Axon stored in dense-core vesicles. = fast, dynein. Fast = vesicles. Slow = degeneration (Fink-Heimer) Receptors: ionotropic = ion channels; microtubules, neurofilaments. Fast: actin, Astrocytes: Absorb extracellular GABA, metabotropic = G-protein coupled. Ach, enzymes, organelles. Inhibited by K around neurons. Have K (only) GABA & glutamate use both, colchicine. All use microtubles (not channels & neurotransmitter receptors. neuropeptides & amines only use neurofilaments). Only fast is ATP Depolarize following ↑ extracellular K metabotropic (except 5-HT3). dependent. Retrograde transport of herpes, following APs in adjacent neurons Locations: Ach: Nucleus basalis of rabies, polio, tetanus & cholera toxins. (contribute to EEG). Do not conduct APs, Meynert (& Nuc diagonal band of broca, Dynamin: GTPase, involved w/Clatharin (-)RMP. Have gap junctions b/t each medial septum & lateral hypothalamus), in vesicle recycling. other. Neurons & astrocytes have no Pedunculopontine nucleus, striatal Toxins: Diabetes = turnaround transport, contact, separated by 20nm. Store interneurons, habenula, olivocochlear vincrisitine, vinblastine = microtubules, glycogen. Phagocytosis/ Gliosis. bundle, septohippocampal. NE: Locus dinitrophenol = oxidative Processes form outer & inner limitimg ceruleus (midbrain, to CTT, MFB, & phosphorylation. glial membranes at pia & ependyma. DLF), pontine & meullary reticular Kindling: repeated stimulation results in Fibrous: white matter, GFAP(+). formations. Serotonin: Raphe nuclei synaptic reorganization into positive Protoplasmic: grey matter, GFAP(-). (medulla), enteric. Dopamine: Substania feedbackk circuit.. Afterdischarge: cell Oligodendrocytes: Small body, no nigra, Ventral Tegmental Area (both circuits continue to fire after stimulus is filaments. Myelinates >1 axon, doesn’t midbrain), Tuberoinfubdibular area ended. Results in secondary generalization have basement membrane (vs schwann (hypothalamus), zona incerta, area of seizures. cell). Nodes of Ranvier every 0.5-2mm. postrema. Epi: medullary reticular Autonomic: Sympathetic fibers to skin Myelin: composed of proteolipid protein formation (dorsal tegmentum). synapse in paravertebral ganglia thru & myelin basic protein. Contains Glutamate: Cortical. GABA: BG rami, then to skin. Preganglionic = Schmidt-Lanterman clefts – gaps in sheath Non-neurotranmitter first messengers: myelinated (white rami – T1-L3); to transmit nutrients. Gases, work by diffusion. Incl. CO & NO. postganglionic = unmyelinated (grey rami, Obersteiner-Redlich area: CNS/PNS NO (nitric oxide): aka EDRF, synthesized all levels). Visceral symapthetic junction. in neurons from arginine via nNOS (type preganglionic fibers synapse directly on Ependymocytes: cuboidal, have I) (also in endothelium by eNOS (III) & adrenal medulla or thru . Splanchnic microvilli. Have cilia only in embryonic inflammatory cells by iNOS (II)), type I & nerves to prevertebral ganglia – coeliac, stages (blepharoplasts at base, stain III stimulated by Ca/NMDA; ↑s cGMP, aortorenal, & mesenteric. w/PTAH). Gap junctions, not tight inhibits platelet aggregation, vasodilation, Parasymathetic preganglionic fibers junctions. Tanycytes: line floor 3rd type II stimulated by cytokines, etc after synapse in ganglia in organ wall. ventricle over median eminence & injury & is proinfammatory > ↑ BBB Splanchnic n. also carry internal sensory circumventricular organs, have end feet permeability & vasodilation > edema; info. on capillaries of portal system (transport Acetylcholine: Synth in nerve terminal by Small intensely flourescent cells (SIF): from CSF to portal system) & tight choline acetyltransferase. 1 quantum interneurons of sympathetic ganglia, use junctions. Choroidal cells: secrete CSF, (vesicle) = 10K = 1 MEPP. Release dopamine have tight junctions, “plumper”, have blocked by botulism, tetanus, VIP: used w/Ach in parasympathetic meningothelial (arachnoidal) rests. aminoglycosides, Eaton-Lambert. terminals Microglia: Resting have small oval Inactivation: acetylcholinesterase (not GI plexuses: Auerbachs = intramuscular, nuclei, when activated (macrophages, reuptake – choline then reuptaked) movement. Meissners = submucosal, Gitter cells) are large & spherical Acetylcholinesterase inhibtors: secretion. Peripheral ganglia: Have neurons, neostigmine etc (reversible), Sympathetic: viscous salivary secretion, satellite cells (analogous to Schwann organophosphates (irreversible). bronchiole dilation, vasoconstriction cells) & fibrocytes. Nicotinic: α2βγδ. α = binding sites` (2). In (except coronary/ pulmonary & some Neurotransmitters: Definition: 1) in autonomic ganglia only have 2 subunits N- skeletal muscle (Ach) – dilation), ↓ GI presynaptic terminals. 2) release w/AP, 3) & C- terminals extracellular. 4 motility, ↑ sphicter tone, glycogenolysis/ exogenous NT has same effect, 4) transmembrane segments (most conserved, lipolysis in liver, renin in kidney, sweat concentration-response effect of drugs on M3-4 least conserved). 7 types – all (Ach), pilomotor, ejaculation, adrenal exogenous NT same as on endogenous inonotopic. All presynaptic, motor. medulla (80% epi, 20% NE) NT, 5) local mechanism for inactivation. Blocked by: Parasympathetic: watery salivary/ lacrimal 4 classes: Ach (from cholesteral, Depolarizing: hexamethonium/ secretion, lung mucous secretion, Monoamines (derived from amino acids; decamethonium & succinylcholine (↑ with vasodilation only in head & pelvis, GI catecholamines from tyrosine, ↓ temp, not reversed by motility/ secretion, ↓ sphincter tone, indolamines from tryptophan, histamine anticholinesterases) glycogen synthesis in liver, erection (uses from histadine), Neuropeptides, and Nondepolarizing: curare & α- NO – Viagra), none to skin Amino Acids (Glutamate, GABA). bungarotoxin, MG antibody Reversible: neostigmine, etc. Serotonin: Raphe nucleus. From packaged & modified in Golgi appparatus, Muscarinic: 5 types, all metabotropic. tryptophan (rate limiting enzyme usually cleaved from prohormone. Blocked by atropine, pertussis; acts thru tryptophan hydroxylase, cofactor Inactivated in synapse by peptidases. G-protein to open or close K, Ca or Cl tetrahydrobiopterin), to melatonin. Opioids: Include enkephalins (widespread, channel. Parasympathetic postsynaptic & Inactivation: Reuptake, MAO (forms 5- esp in midbrain, PAG, vagal nucleus sympathetic to sweat glands, in brain. Can HIAA). Neurons destroyed by 5,7-DHT; (antiemetic), locus ceruleus & amygdala be inhibitory (cardiac) or excitatory (GI). p-chlorophenylalanine depletes brain (euphoria), spinal cord; inhibitory), Oxytremorine: selective muscarinic levels. dynorphin (limbic/ hypothalamus), β- agonist. Receptors: 20+ (5HT1 to 7 & subtypes). endorphin (arcuate nuc. only). Precursors: Nicotinic: Fast EPSP (open Na & K); All metabotropic (↑ cAMP) except 5-HT3 POMC, proenkephalin, and prodynorphin. Muscarinic: Slow EPSP (Open Na & Ca, (cation channels). 5-HT3 presynaptic on All can produce enkephalins. Receptors are close K), Slow IPSP (open K, Cl). dopaminergic neurons –↑s dopamine metabotropic: µ (morphine, endorphin As membrane of motor neuron depolarize, release. Excitatory: 1D, 2, 3. Inhibitory: agonist, naloxone antagonist), δ EPSP ↓, IPSP ↑. 1B, 4. Both: 1A. (enkephalins, ↑K - hyperpolarization), κ Dopamine: (phenylalanine >) tyrosine > SSRIs: eg fluoxetine (Prozac) (dynorphin). (by tyrosine hydroxylase, rate-limiting, antidepressants. Gut-brain peptides: substance P (dorsal requires tetrahydropteridine, Atypical antipsychotics: combined horn of SC - primary nociceptive afferents phosphorylation ↓ activity, NE inhibits, serotinin (5HT2A)/ dopamine (weak D2) & widespread in CNS, excitatory), CCK, present only in nerve terminals) dopa > antagonists (fewer extrapyramidal Sxs). bradykinin, VIP, somatostatin, (dopa decarboxylase) dopamine > Include clozapine, risperidone, olanzipine neurotensin. (dopamine βhydroxylase, requires (Zyprexa), ziprasidone. Pituitary & Releasing Hormones: some ascorbic acid, in vesicles) NE > (PNMT, Nefazadone (Serzone): nonspecific 5HT2 project outside hypothalamus. transcription ↑ by steroids) Epi. blocker, antidepressant POMC: > ACTH (> αMSH & CLIP) & Primary inactivation of all is by reuptake Migraines: 5-HT1B & 5-HT1D on βlipotropin (> γlipotropin & βendorphin) (Uptake I: presynaptic, high-affinity, trigeminal n. to cerebral blood vessels. Histamine: found only in TCAs inhibit; Uptake II: glia, low- Triptans (eg sumatriptan – Imitrex) tuberomammillary nucleus of affinity. Both energy-dependent. Uptake 5HT1D antagonist. hypothalamus into vesicles by VMAT1,2 – inhibited by Ondonsetron: 5-HT3 antagonist Adrenergic: α1 = poststynaptic, α2 = reserpine) Also metabolized by MAO (antiemetic, ↓ dopamine). presynaptic; β1 = heart, β2 = bronchi; (intracellular- mitochondrial memberane, Buspirone (Buspar): antianxiety, 5HT1A β = ↑ cAMP; α = Ca/ IP3 & ↓cAMP A-form in neurons, B-form in astrocytes, partial agonist Neuropeptides in sympathetic ganglia X chromosome, forms HVA) & COMT Fenfluramine: serotonin-releasing agent, function as modulators (not transmitters) causes panic disorder experimentally. (intracellular, forms DOPAC). MAOI-A = Adrenergic Drugs: , Prazosin α1 agonist, antidepressants, MAOI-B = anti- LSD: blocks 5HT receptors. Clonidine central α2 agonist, parkinsons. Lower dose of dopamine w/ Melatonin: from serotonin Phenoxybenzamine (dibenzyine) MAOI. Glutamate: doesn’t cross BBB, noncompetitive α antagonist, Receptors: 5, all metabotropic. D2 synthesized from glucose in Krebs cycle (&D3,D4) = parkinsons, pre- & and from glutaminase in astrocytes. Phentolamine competetive α antagonist,; postsynaptic, inhibitory ↓ cAMP, blocked Involved in long-term potentiation/ Yohimbine: α2 antagonist; Isoproterenol: by antipsychotics/ phenothiazes; D1 memory. β agonist, Metoprolol: β1 antagonist., (&D5)= postsynaptic, excitatory, ↑cAMP. Receptors: 3 ionotropic (NMDA, AMPA, Sulpiride: D2 antagonist, Guanethidine: Apomorphine: nonspecific agonist. kainate), 8 metabotropic. blocks release of NE. GABA: Inhibitory. Chloride channel. NMDA: requires glycine coagonist, Hexamethonium: ganglionic Ach blocker Brain & spinal cord. Glutamate > GABA blocked by Mg (released by Action Potential: RMP: resting membrane by glutamic acid decarboxylase (GAD, depolarization), Ca (also Na & K) potential mostly from K. Axons –95, cofactor B6 – deficiency causes szs, Abs channel. Ligand & voltage gated. Blocked neurons –65. Na open > Na close in stiff-man syndrome). Inactivation by by 2-amino-5-phosponovaleric acid. (absolute refractory) > K open (relative reuptake (metabolized to succinic NMDA & AMPA receptors activated in refractory), Cl unchanged. aldehyde by GABA transaminase – seizures. Kainate (K-type): Na, K channel, Na & Ca channels excitatory; K & Cl Vigabatrin (anticonvulsant) inhibits) binds AMPA, excitotoxicity. channels inhibitory. Receptors: GABA-A: Ionotropic, rapid AMPA (Quisqualate, Q-type): binds Equilibrium potential: electrical force = chemical force, no net movement of ions Cl- influx. Postsynaptic. αβ subunits – AMPA & glutamate. Na, K. across membrane. both bind GABA & barbs, Benzos bind α Both: ligand only, no Ca, don’t require Na/K pump: 3 Na out, 2 K in. Uses 1 only (positive modulator, not direct glycine, blocked by quinozalinediones ATP. 2subunits (αβ). Inhibited by ouabain. agonist). Blocked by bicuculline, (NBQX); Hyperpolarizes membrane. Electrogenic. picrotoxin. Muscimol = agonist. GABA- L-AP4: metabotropic receptor in retina, Contributes to RMP. B: Metabotropic, ↓ cAMP (↓ Ca pre, ↑ K hyperpolarizing. Tetrodotoxin: blocks Na channels; TEA post). Pre & postsynaptic, bind baclofen. Riuzole blocks – stops excitotoxicity block K channels Glycine: inhibitory – spinal cord & brain (used in ALS) Membrane stabilizers: Hypercalcemia, stem only, Renshaw cells. Strychnine Aspartate: excitatory, climbing fibers hypokalemia, anesthetics, acidosis. blocks receptor (causes rigidity). Opens Neuropeptide transmitters: Made in Cl- Channels. soma on ribosomes from mRNA, Destabilizers: alkalosis (induces szs), length, regulate spasticity. Activity ↓ after Synthesized as precursors, activated in caffeine, strychnine lesions of spinocerebellum cascade. 12 members, 3 (also 1 & 9) Synapse: Ca entry causes release of Intrafusal fibers: nuclear bag = dynamic especially important in neurons. Cleave/ vesicles. Synaptic Delay 0.5sec. 20-50nm or static, 1° ending; nuclear chain = inactivate Rb & other cell-cycle proteins. (NMJ) wide. Ca channels in presynaptic dynamic, 1° and 2°. Bcl-2: inhibits apoptosis. bcl-x, NAIP active zone. Endoneurium = axon. Perineurium = (deficent in SMAs), & p35 also inhibit. Ca removed by: 1)active transport into fasicle. Epineurium = nerve. Bax & Bad promote. SER, mitochondria, & out of cell Nerve injury: Chromatolysis = PNS only, ↓ trophic support > ↓ MAPK, IP3 > 2)cytosolic binding proteins 3) diffusion cell body, increased protein synthesis, changes in mitochondria + Bax > (not reversal of flow thru Ca channels). Nissl substance disappears, nucleus at cytochrome C release from mitochondria > Release: Vesicles anchored to actin periphery, swelling; reversible. apaf-1 > Caspase 9 > caspase 1 > Caspase cytoskeleton by synapsin & rab3A – Wallerian degeneration = distal axon 3 released by phosphorylation by Calcium- (proximally to next node of Ranvier). Necrosis: exogenous insults - ischemia, dependant kinase (CAMKII). NT released Regenerates 1-2mm/d (80% original cell swelling/rupture by fusion pore or exocytosis. diameter, ↓ conduction velocity, Myelination: myelin same composition Fusion: SNAREs on vesicle remyelinated). Retraction bulbs form CNS & PNS; myelin genes turned on by (synaptobrevin) & plasma (syntaxin, Rab3 from proximal & distal ends of cut nerve. Schwann cells in PNS, astrocytes in CNS st removes Sec1 blocking protein 1 ) Mixed nerves have poorer recovery. Oil- NCV: Normal sensory = 50m/s (0.5- membranes fuse. Ca binds to Red-O shows fat macrophages in nerve, 120m/s). Axonal: ↓ amplitude. synaptotagmin which releases it from EM shows myelin degeneration. Demyalination: ↑ latency, ↓ velocity. SNARE complex, allowing binding & Neuroma: tangles of axons & collagen Sensory = SNAP, motor = MAP (normal stabilization by SNAPs & NSF. Tetanus Terminal degeneration: synapse 40-60m/s – slightly slower than SNAP). & botulinum toxins cleave these proteins. degeneration (immediate, before Conduction block = focal myelin problem, Vesicle recovery: synaptotagmin/AP2/ Wallerian). usu reversible (neuropraxia). AP3 causes formation of clatharin coat, Transneuronal degeneration: of upstream NCV Increases with increased Ca/calcineurin activates dynamin – or downstream neurons (ie optic n. > transmembrane resistance, decreased intitiates endocytosis LGN). internal resistance, decreased capacitance; Types: Axodendritic: excitatory, Axon regeneration doesn’t occur in CNS, myelin increases transmembrane resistance axosomatic: inhibitory, dendrodendritic: axon sprouts form for 2 wks then die. and decreases capacitance olfactory builb only, axoaxonic: Reasons: No endoneurial tubes, oligos H-reflex: submaximal stimulation, reflex inhibitory, ↓ NT release. don’t form distal tubes like schwann cells, arc (sensory>motor. Monosynaptic = Gray type I: excitatory, wide, assymetric astrocyte scar, inhibitory factors – Achilles). Can detect S1 radiculopathy (large postsynaptic density), round semaphorins, Nogo (from myelin), IN-1, (also affected by neuropathy – ie sciatic) in vesicles. Gray II: inhibitory, narrow, astrocyte-associated proteo glycans: 1-2d after onset. F-response: supramaximal symmetric, oval vesicles. Condrotin SO4 (instead of heaprin SO4), stimulation, antidromic In PNS (not CNS) is surrounded by basal tenasin (instead of laminin in immature (motor>motor).Used for median, ulnar, lamina. CNS). Does occur in olfactory n. (has peroneal, tibial n. M-response: direct Nerve types: IA = Aα,muscle spindle (1°, laminin, olfactory glia ensheath) motor response from stimulating mixed annulospiral); IB = Aα,golgi tendon; II = Neurotmesis: complete disruption of motor-sensory nerve. Aβ, Aγ,muscle spindle (2°, flower-spray); nerve Axonotmesis Perineurium and Renshaw cells: use glycine. Recurrent III = Aδ, temp/touch; IV = C, pain,itch epineurium intact. Wallerian degeneration negative feedback on αmotorneurons, Motor: Aα = skeletal; Aγ = muscle occurs. other Renshaw cells & IA inhibitory spindle; C = sympathetic Neuropraxia Lasts 6-8 weeks, motor > neurons (inhibit antagonist muscles in Sensory receptors: Meissners: touch, sensory; demyelination, conduction block stretch reflex) – releasing antagonist rapidly adapt, encapsulated, superficial, on NCV inhibition. Also receive input from low-frequency, fluttering; Merkel disc: Neuronal death: Excitotoxicity: descending tracts. pressure/touch, slow, superficial, finger glutamate/ NMDA > ↑ intracellular Ca. Reflexes: tips, Braille; Ruffini: pressure, slow adapt, Apoptosis: chromatin condensation, DNA Stretch (Knee-jerk): muscle spindles – IA encapsulated, deep; Pacinian: vibration, fragmentation, cell membrane blebbing, afferent (excitatory) > αMN, rapid adapt, encapsulated, deep, high- loss of nuclear membrane, fragmentation monosynaptic. Golgi tendon organs > IB frequency, humming. into phagocytosable apoptotic bodies (for inhibitory interneuron > αMN (inhibits Superficial in dermal papillae, small macrophages – attracted by BDCF, reflex). Tonic & phasic components. receptive fields; deep have large fields. recognize phosphatidylserine on bodies Flexor-withdrawl: disynaptic/polysynaptic Golgi tendon organ: tension. Increases membrane). Occurs w/ radiation, steroids (has excitatory interneuron). w/ active contraction and passive stretch; (lymphoma), cytotoxic T-lymphoctosis, Babinksi sign: abnormal plantar flexion group I sensory fibers, disynaptic growth factor withdrawl during reflex (polysynaptic), L5-S2. Muscle spindle: rate of velocity/change development, cell cycle control. DNA Muscle: I-band = actin (thin); H-zone = of muscle stretch; increases firing w/ cleaved into 180bp fragments by myosin (thick); A band = both. Z-line = stretch, decreases w/contraction; group I endonuclease, can be marked by insitu actin. Thin (actin) filaments have troponin, & II sensory fibers, monosynaptic reflex; reaction – TUNEL stain. tropomyosin attached. Gamma motor neurons innervate Caspases (cysteine proteases) uniqely Sarcoplamic reticulum releases Ca, binds intrafusal fibers to account for change in cleave on carboxy side of aspartate.. troponin, releases tropomyosin from actin, binds to myosin. Requires ATP for protein lower. Protein < 45. Prealbumin in after inspiration) =pons; Cluster = binding (cocks head – movement > ADP) CSF, not plasma (on electrophoresis) pons/medulla; Biot (ataxic, irregular) & release. Froin’s syndrome = loculated CSF in =medulla Type I: Red. lost in MD, Werdnig, ↑ lumbar cistern with very high protein Pituitary hormones: oxidative enzymes, ↓ glycolytic enzymes, Xanthochromia takes 1-2d to appear. Prolactin: milk production. ↑ by TSH, ↓ by more mitochondria & myoglobin, fire Cerebral Blood Flow: normal 50- dopamine. Cortisol ↑ prolactin receptors tonically, slower, less fatigueable ; Type 55ml/100g/min. 8-23 = penumbra, <8 = (permissive) Type II: White, lost in MG. infarction. Nerves (sympathetic) little Oxytocin: milk ejection, uterine Smooth muscle: no troponin, Ca binds effect. 1° controlled by local metabolism contraction in labor (direct stimulation of calmodulin to activate myosin kinase & (glutamate, NO, adenosine, etc), ↑ CO2 cervix, nipple; higher centers). phosphorolate myosin. Stimulated by (thru NO) & hypoxia. Autoregulated b/t LH: Leydig cell > testosterone production. local factors, not APs. Ca comes from CPP of 60-140. Primarily by large > ↓ GnRH & LH. extracellular, not SR.. arteries/ arterioles. FSH: spermatogenesis. Sertoi cells > Cardiac: gap junctions. AP last longer due Endothelial factors (NO, prostaglandins). inhibin > ↓ FSH. to slow CA channels, slower velocity. Ca NO also stimulated by Ach, substance P, In middle of menstrual cycle estrogen ↑ from SR & extracellular. ADH, oxytocin, trypsin, etc. FSH & LH. Cardiovascular: Parasymp.: heart only, K channels in vascular muscle open (by GH: Stimulates IGF-1 (aka somatomedin Sympathetic: heart & all vessels except NO/ cGMP, cAMP, AA, ↓O2, ↑ CO2) > C) which directly ↓ GH. Anti-insulin, ↑ capillaries. Vasomotor center in medullary hyperpolarize muscle cell > Ca channels glucose (directly & thru IGF-1). Highest reticular formation (C1). Baroreceptors: close > ↓ Ca > dilation. Closure of K 1st hour of sleep. carotid sinus > Herrings nerve (IX) > channels > contriction. TSH: inhibited by T3 & T4 (TRH isn’t). solitary tract > C1 inhibition. Aortic Vasospasm: may be due to ↑ endothelin Also ↓ by dopamine, cortisol. reprtors > vagus. Chemoreceptors: (blocked by endothelin A antagonists). ACTH: peak in am, nadir at night. Carotid & aortic bodies . same path as Hgb & thrombin induce endothelin. NO/ ADH: stimulated by hyperosmolarity above. cGMP also impaired. (osmoreceptors in carotid/ aortic bodies) EMG: Myopathy = ↓ Voltage, ↓ duration, BBB: Transport mediated by diffusion ↓BP (baroreceptors in carotid/ aortic no ↓ motor units or recruitment; (barbs), active transport (K, organic sinus); also by nausea, pain, skin warmth Denervation/Reinnervation = ↑ duration, acids), carrier mediated. Not vesicular etc. Inhibited by alcohol. Causes H20 polyphasic, early ↓ voltage, late ↑ transport. reabsorption in distal tubules of kidney voltage, fibrillation, ↓ motor units & Carrier-mediated: glucose/hexoses (not Releasing Hormones recruitment (begins 1-2wks; earlier in galactose), AAs (3 types Na-dep. TRH: from paraventricular, ↑ TSH, axonal than myelin dz); Myotonic transporters: basic, acidic & neutral), prolactin? discharges = slight movement of needle lactate, purines (adenosine, not CRH: paraventricular, ACTH causes repetitive discharges (dive bomber) pyrimidines), choline, vitamins. GnRH: preoptic, LH/ FSH. Pulsatile Myokymia: undulating contractions, Capillary endothelial tight junctions release every 90min. ↑ be NE, ↓ by usually facial, 2-10 Aps at 1s intervals (5- (Blood-CSF in choroid = cuboid epithelial dopamine, endorphins 60 Hz), usu due to brainstem dz tight junction). Ependyma has no barrier. GHRH: arcuate, GH Jolly test: evoked potential testing Serum Osmolarity: controlled by Dopamine: arcuate, ↓ prolactin subforniceal organ & organum muscles (APs) Somatostatin: periventricular area, ↓ GH vasculosum of lamina terminalis Fasiculations: 3-5 phases, 5-15ms, 200uv Menstrual cycle: 1st half risning estrogen Respiration: Dorsal respiratory group Visible, motor unit, indicate irritability (low progestoerone) ↑ FSH/LH by (dorsal medulla) = inspiration, main Fibrillations: 2-3phase, 1-5ms, >300uv, pulsatile GnRH release. Ovulation GnRH single fiber, invisible, takes 10-25 days. center. Ventral group = ventral medulla, surge (nonpulsatile) - ↑↑ LH > ovulation. Positive sharp waves. Denervation. nucleus retroambigualis, inspiration After ovulation: Corpus lutem ↑ estrogen, UMN injury: normal EMG, no (rostral) & expiration (caudal), not active fasiculations. LMN: fasiculations, EMG normally. Botcinger complex = retrofacial ↑ progesterone, and inhibin - ↓ FSH/LH w/fibrillation, atrophy nucleus. Inhibitory, expiration. Active in Sleep: Stage 2: spindles, K-complex, 3: SSEP: Erbs (N9) > N11 cervical > normal breathing. pre-Botcinger complex delta, 4: night terrors, somnambulism, N13/P13 medulla > N19/P22 = has intrinsic pacemaker for respiration. REM: dreams (REM & non-REM) thalamocortical. Variables: age, sex, limb Pneumotaxic center = pons, controls rate (nightmares), desynchronization of EEG. length, temp & pattern. Hering-Breuer inflation reflex Glucose metabolism ↑ in REM & ↓ in ICP waves (Lundberg): A=>50mmHg (mechanoreceptors): TV > 1.5l. Bronchi > non-REM compared to waking. for 5-20 min. B=shorter. vagus > inhibit dorsal group. Alpha: 8-12/s, occipital lobes, closed eyes. CSF: 0.33cc/min (450cc/d). 70% from Chemoreceptors: in ventral medulla, sense Beta : 12-25/s, frontal. Theta: 4-7/s, choroid. Active process – Na/K pump. increase in H+ (less with CO2, pH), temporal in elderly, children. Delta: 1-3/s, Decreased by NE, acetazolamide, excites resp center. Indirect: O2 via dleep, brain disease. furosemide, bumetanide; incr by CO2, carotid bodies, etc (glomus cells have O2 Active inhibition of ARAS (by raphe volatile anesthetics. Check B-transferrin sensitive K channels). CO2 required for nucleus, serotonin). Muramyl peptides for leak. breathing stimulation. accumulate during wakefulness. Compared to blood: Osm & Na same, Cl, Cheyne-Stokes (speed up/ slow down) Awake: ↑ NE/5HT ↓ Ach; REM ↑ Ach ↓ Mg higher, K, Ca, UA, Glu (45-80), =hemispheric, central hyperventilation 5HT/NE. Pedunculopontine nuc. has Ach =midbrain/pons, apneustic (3sec pause & NE Hypoxia/Ischemia: cortex layers 3, 5, 6; Apolipoprotein E4/E4: Cholesterol – M-phase at ependymyal surface and S- striatum, cerebellar Purkinje cells, CA1 transport protein. 4 alleles (E1-4). E4/E4 phase at marginal zone. SVZ occurs later, (pyramidal). Penumbra 8-23cc/100g genotype: worse prognosis in TBI, ↑ no variation during cell cycle. Occurs (normal 55). Neurons use glucose only plaques in Alzheimers) ventral-dorsal gradient in spinal cord, (no glycogen). Man-in-the barrel. Development/Embryology lateral to medial in thalamus. Projection Venous = white matter. Resistant = U- Primitive streak d13, notochord d17, neurons before interneurons. SVZ fibers, claustrum. neural tube d22, anterior neuropore d24 (> progenitors remain in adults. Decerebrate rigidity: transection below lamina terminalis, failure = anencephaly), Disorders: Phakomakoses, microcephaly, red nucleus but above vestibular nuclei (or posterior neuropore d26. megaencephaly, arachnoid cyst, AVMs between the colliculi), lose cortical and Gastrulation: Formation of 3 germ layers Neuronal migration: 2-5mo. Occurs 1st in rubrospinal stimulation of medullary in gastrula. midbrain/ pons. (astrotactin = receptor; Slit reticular nuc > extension. Spasiticity Induction: Sonic hedgehog (Shh) from proteins – diffusible factors) abolished by sectioning dorsal roots to cut Notochord (mesoderm, Spemann’s VZ > preplate (transient) > marginal zone off γ loop. Anterior cerebellar lobe organizer – follistatin, chordin, noggin) (becomes layer 1). Preplate split into damage removes Purkinje inhibition of induces neural plate/ neurectoderm. Cajal-Retzius neuron layer & Subplate. lateral vestibular nuc > ↑extensors (makes Also Hensen’s node secretes TGFβ to Axons form intermediate zone (>white it worse) induce neurectoderm. matter). Layers 6 > 5 > 4 > 3 > 2 form. Decorticate: above red nuclei. Regionalization: Foot plate produces Shh Reelin mutation reverses this. Spasticity has hyperreflexia, rigidity for ventral determination, FGF8 & BMP Neuronal differentiation: Isl-1 = spinal doesn’t dorsal. Homeobox genes – axial. cord motorneurons. Memory: Working: few seconds Primary neurulation: 3-4wks, Growth cones: composed of lamellipodia (telephone #). Long-term: Explicit/ anencephaly, myelomeningocoele, Chiari (feet) & filopodia (toes). Integrins bind to declarative = facts. Subdivided into: I/II, cranioraschisis, cephalocoele laminin & fibronectin in ECM and Episodic (autobiographical) and semantic Neural plate > neural groove > neural tube cadherins on target cells. Also cell (worldly knowledge). Implicit/ Disjunction: adhesion molecules (CAMs) – Nerve- nondeclarative/ procedural = motor skills. Secondary neurulation: 4-5wks, vertebrae, CAM (N-CAM) & Nerve-glial CAM (Ng- Explicit: Long term potentiation at dura, skull form. sacral, > occult CAM). Neurotrophins (NGF – sympathetic perforant pathway/dentate and CA3/1 dysraphism: diastematomyelia, & DRG, BDNF, CNTF, GDNF, CT-1, synapses. Theories: Synaptic(Long Term meningocoele, lipoma, dermal sinus, NT3) produced by target cells guide axons potentiation): Glutmate > NMDA/AMPA tethered cord, neurenteric cyst, caudal (bind to TrkA, B & C respectively, as well receptors > 1) Ca influx initiates regression syndrome as p75). Agrin: released by motor neurons, downstream changes (PKC required) to Ventral induction: 5-10wks, causes Ach receptor aggregation. modify synapse (↑ NMDA/AMPA holoprosencephaly, SOD, Dandy-Walker. Synaptogenesis: Coincides with wave of receptors etc) & 2) NO released, to Placodes: Olfactory: forms olfactory apoptosis – nonsynapsed neurons die due presynaptic terminal to ↑ glutamate receptor neurons/ nerve, induces olfactory to lack of NGF. release. Neurochemical: Any bulb. Otic: forms CN8, organ of Corti, Gliogenesis: from progenitors in VZ & neurotransmitter > G-protein > Ca release cristae ampullares, maculae of utricle & SVZ. Radial glial produced during from ER (ryanodine-sensitive Ca saccule, vestibular & spiral ganglion neurogenesis. ↑ EGFR expressions on Vesicles: Pros- to tel & di; Mes; Rhomb progenitors > gliogenesis. channels) > ↑ ryanodine receptors, ↓ th th postsynaptic K channels. to met (pons/ cerebellum) and myel. Myelination: PNS/SC=4 mo, brain = 5 Implicit: stored in motor systems. Flexures: cephalic & cervical. Pontine mo; caudal to cephalad, dorsal to ventral. Lesions: Bilateral DM thalamus, then forms b/t met & myel & persists. Corticospinal tracts finished at 2yo. hippocamus (role in consolidation, short- Telencephalon: cortex, striatum, nucleus Neural Crest: craniospinal ganglia (dorsal term > long-term). Also accumbens, claustrum, amygdala, root, sympathetic), APUD (enteric) perirhinal/perihippocampal cortex, septal hippocampus, olfactory bulbs. neurons, schwann cells (& satellite cells in nuclei & Meynert (Ach necessary). NOT Diencephalon: GP, optic cups ( > retina, ganglia), melanocytes, pigmented layers of fornices, mamillary body, amygdala. optic n.), posterior pituitary, thalamus, the retina, odontoblasts, leptomeninges, Hippocampal lesion causes anterograde (> hypothalamus, subthalamus, epithalamus cartilage of brachial arches, , adrenal retrograde) amnesia. Thalamic lesion (pineal/ habenulum). medulla, aorticopulmonary septum of causes only retrograde amnesia. Cerebellum: forms from rhombic lips. heart, thyroid parafollicular cells (C-cells, Aging: ↓ Ach, norepi, epi, dop, NOT Granule Neurons: VZ to external granular produce calcitonin) . serotonin. Gliosis in locus ceruleus & SN, layer to internal granular layer. Other cells Dura from mesoderm, pia/arachnoid from loss dendrites layers 3 & 5, neuronal VZ to cortex. neural crest (others say arachnoid from lipofuscin (cytoplasmic remnants of Stem cells: self-renewing (divide to mesoderm) lysosomes) granules, Marinesco bodies produce progenitor cell & another stem Corpus callosum forms anterior to (eosinophilic intranuclear) & iron (inf cell). Progenitors divide only to produce posterior except rostrum olive, thalamus, BG). Astrocytes: corpora downstream progenitors. Adults stem cells Adult neurogenesis: occurs only in amylacea (laminated basophilic bodies @ present in olfactory bulb, dentate gyrus of olfactory bulb, dentate gyrus of the foot processes, subpial). Memory & hippocampus, SVZ. Bone-marrow cells hippocampus, and SVZ. learning are not routinely impaired. can be induced to produce neurons. Notochord: forms nucleus propulsus ↓ diastolic fxn (not systolic), ↓ renal fxn Neuronal proliferation: Neurogenesis. 2- Toxins (Cr stable), WBC stable, ↓ FVC/FEV1. 4mo. In VZ cells migrate during cell cycle Curare, αBungarotoxin, muscle blockers, Lidocaine: doesn’t work in abscess/ acidic Pseudodiabetes: ↑ACTH > aminoglycosides, quinine, procainamide, environment. IV > seizures, arrythmias gluconeogenesis MG: blocks/ inactivates AchR (esp bupivicaine) Air embolism: precordial doppler (most Botulinum, Tetanus, Eaton-Lambert, sea Glycopyrrolate: anticholinergic, ↓ sensitive), ↓ EtCO2 (earliest), ↑ FEN2, ↓ snake toxin, tick paralysis: prevents Ach secretions, reverse MR. CO, ↑ PAP, ↑ pulmonary vascular vesicle release. Spinal (subarachnoid) vs Epidural: resistance, ventilation-perfusion mismatch Organophosphates: Achase blockers quicker onset, more hypotension, ↓ dose > Neurogenic pulmonary edema: from Cholera, Pertussis: ADP-ribosylates G- ↓ systemic toxicity, LP headache. Both caudal hypothalamus (also nucleus tractus proteins, prevents GTP hydrolysis. use local ± opioid. solitarius & reticularis gigantocellularis & Diptheria: inactivates tRNA transferase RSI: Preoxygenate > Sedative (Propofol, parvocellularis in medulla) w/systemic Cocaine: Blocks reuptake of dopamine, etomidate – less BP change, thiopental) > hypertension, may be blocked with NE Cricoid pressure/muscle relaxant (sux). sympathetic blockade. Amphetamines: block NE/dopamine Pseudocholinesterase deficency: of Oxygen: O2 mostly bound to Hgb; Hgb & reuptake, ↑ release. plasma cholinesterase, metabolizes Sux > SaO2 (percentage of hemoglobin bound to Dihydropyridone: Ca channel blocker proloned muscle relaxation. Inherited. O2, may be falsely↑ in anemia) important. TEA: block K channels Analgesics: Opioids: Morphine constricts Plasma O2 small role. O2 toxicity: >60% Tetrodotoxin: blocks Na channels sphincter of Oddi (Demerol doesn’t). for >48hrs. Cyanide: block Na/K pump Renal excretion (↓ in CRF), histamine O2 Curve: shifted right (decreased Strychnine: block glycine CL channels release. Demerol: normeperidine affinity) with H+, CO2, ↑ temp, 2,3-DPG; (Renshaw) accumulates > seizures. CI w/ MAOIs. left by banked blood, hypothermia. Picrotoxin, bicuculline: blocks GABA-A OD Tx: naloxone. Benzos: OD Tx: Shunt Fraction is 10%, (Cc-Ca)/(Cc-Cv). receptors flumenazil. ↑ Fi02 has no effect if >50%. (Shunt ↓ O2, Latrotoxin (black widow): ↑ Ach release Malignant hyperthermia: occurs w/ dead space ↑ CO2) Reserpine: dumps NE/dopamine from halothane + succinylcholine. ARDS: CXR bilateral infiltrates, PCWP < vesicles, prevents reuptake by VMAT 1,2. Rhabdomyolysis., acidosis. ↑ ETCO2 20 (noncardiac), PaO2:FiO2 < 200. Acute Produces long-lasting depletion Familial mutation in RYR1 gene for lung injury (ARDS Precursor) PaO2:FiO2 Atropine: muscarinic blocker. ↓ muscle SR ryanodine- Ca channel. Tx: <300. peristalsis, ↓ sweating, ↑ pulse, dry dantrolene, HCO3. AD. Neonatal RDS: Lecithin: sphyingomyelin mouth, blurred vision Trauma: Cricoidthyroidotomy b/t thyroid <1.5, ↓ surfactant, ground glass CXR & cricoid (<12yo do needle crico). Ventilator: TV: 10cc/kg. PEEP: ↓ work CRITICAL CARE Tension PTX: hypotension, ↓ BS, trachea of breathing, CPP; ↑ dead space, Anethesia: deviates away. Emergent (no CXR) compliance. Barotrauma. Extubate: PO2 nd ↑ metabolism (CMRO2): ketamine, N2O. needle thoracostomy midclavicular 2 >70, CO2 <50, NIF > -20, TV > 5cc/kg, th ↑ CBF: halothane > ketamine > enflurane intercostal space. Chest tube 4 intercostal MV > 10L/m. > isoflurane > N2O (not thiopental, space. Do not place CT w/ acute abdomen Keep plateau pressure < 35-40 to reduce fentanyl, etomidate). & hemothorax. PTX <3cm can observe. barotrauma. Ketamine: ↑ ICP, dissociative (PCP Pulses: radial = 80, femoral/carotid = 60. Assist-control: vent delivers TV when pt analog). Foley CI: pelvic fx in men, blood @ initiates (Pt says rate). Inhalational: all ↓ BP. Enflurane: urethral meatus, high-riding prostate, Brochospasm: Nebulized β-agonist (> seizures. Halothane: hepatitis, perineal injury (get retrograde racemic epi) st hypotension, ↓ CO, most ↑ ICP. urethrogram 1 ). Facial fx: place OGT N-acetylcysteine (Mucomyst) cross- Isoflurane best for CNS (not for (not NGT). Thoracic: Only 10% thoracic allergic w/sulfa. induction, irritating). Etomidate: adrenal aortograms (+) w/aortic injury. Pelvic fx: NT intubation CI in apnea, facial fxs, suppression when infused, seizures. do DPL above umbilicus. Can lose 3l. coagulopathy, ↑ ICP. Thiopental: cardiovascular depression. Agram for embolization – do not explore PFTs: Vital capacity = max. inspiration to Methohexital (Brevital): ultra-short acting unless major vessel injury DPL: >10cc max expiration. Tidal volume = normal barb, lasts 5-10 min. Seizures, myoclonus aspiration > lap. Neck zones: III = above inspiration to expiration. Functional N2O: CI in PTX, SBO (expands). angle of mandible, II = mandible to residual capacity = left after normal Diprivan: has 1kcal/ml as fat. Midazolam: cricoid (must be explored), I = below expiration. Residual volume = left after amnestic, premedication (not analgesic). cricoid. I & III = agram. Fluids: Give 3l max. expiration. COPD = ↓ VC, FEV1, ↑ crystalloid for 1 liter blood loss. Avoid Succinylcholine: depolarizing, ↑K. CI in MV; Restrictive = normal FEV1, ↓ VC, ↓ subclavian CVL. Hct may be normal hyperkalemia, hemiparesis/muscular RV. w/blood loss. Infants can lose blood in weakness, burns, eye trauma (↑ ICP & Tracheostomy: Tracheoinnominate head to cause shock. If only 1 vial of IOP). Duration 6 mins. Metabolized by fistula: finger pressure thru stoma or ↑ cuff blood send T&M. CHI: causes 50% of pseudocholinesterase (plasma). pressure. deaths. Nondepolarizing: Vercuronium/ CXR: Diaphragm can hide 500cc pleural Metabolic response to trauma: pancuroinium. Reverse with fluid. Mediastinum >8cm = aortic injury. hyperglycemia, ↑ lipolysis, ↑ Na anticholinesterase (neostigmine etc - Pleural edema: Kerley B lines. pretreat with atropine to prevent reabsorption, ↑ H2O reabsorption, Acid-Base: Most common problem in bradycardia). Mivacurium metabolized by metabolic alkalosis mild-mod injuries = resp or met acidosis. pseudocholinesterase. Metabolic alkalosis: caused by diuretics, FFP, ± Heparin (thrombotic) (cryo if Antiplatelet agents: Aspirin: COX hypokalemia, Cushings dz, primary fibrinogen low, platelets if low) inhibitor > ↓ TXA2 > ↓ GpIIb/IIIa aldosteronism, hypovolemia (tx NaCl). Platelets: Aggregation ↑ by thromboxane, /fibrinogen binding. Bleeding increased Metabolic acidosis: Addisons (nomal ADP, serotonin. 1 pack platelets raises by w/Tegretol, PB, cephalosporins, sulfa, AG). Salicylates: resp alk > met acid. 6K. Glycoprotein Ib – vWF bind to PCN, EtOH. Clopridrogel (Plavix): ADP Ketoacidosis: Tx: volume, insulin, not endothelium (absent in Bernard-Soulier); receptor blocker on plts. SE: TTP (less HCO3. Glycoproteins IIb-IIIa bind other platelets. than ticlid). Ticlopidine (Ticlid): ADP NG suction/emesis = hypokalemic (absent in Glanzmann’s Dz). receptor blocker; neutropenia, TTP. hypochloremic metabolic acidosis, Thrombocytopenia: 20K = spontaneous Dipyramidole (Persantine, Agrrenox): paradoxic alkalotic aciduria (H+ loss for bleeding. Prophylactic transfusion <10K. inhibits platelet phosphodiesterase. Na+ retention). Platelets “live” 7-10 days. (RBC life GPIIb/IIIa inhibitors: amaxicab (Reopro), For ↑ CO2 by 10, pH ↓ by 0.08. 120d) eptifibatide (Integrillin), tirofibran Coagulation: Intrinsic(PTT): 12>11>9> Heparin induced: causes thrombosis, not (Aggrastat). Extrinsic(PT): Thromboplastin>7 Both: hemorrhage. Occurs 4-15d after starting. Anemia: Fe-def: microcytic, hypochromic, 10/5>2(prothrombin)>1(fibrinogen)>fibri 10% of patients develop Abs. TTP: ↓ MCV, ↑ TIBC. Folate/B12 : macrocytic. n (req. 13) Nonimmune (angiopathic). Adults. Fever, Hereditary spherocytosis: splenectomy Vit K dependent: 2,7,9,10,C,S. Shortest delerium, anemia, ARF. Treat corrects anemia (not RBC defect), perform half-life = 7. w/antiplatelet agents and plasmapheresis >4yo, may relapse 12 activated by kallikrein. Fibrinogen (not platelets) Transfusion: binds platelets to each other, vWF binds ITP: immune. Steroids/ splenectomy. Use washed PRBCs: allergic rxn or IgA to endothelium by glycoprotein 1b. Children & adults. Others: H2-blockers, deficiency. γ irradiation prevents graft-vs- Plasmin causes fibrinolysis. tPA activates thiazides, folate/ B12. host disease. plasmin from plasminogen. EACA Impaired platelets: uremia, vWF dz, Does cause immunosuppression, inhibits plasminogen > plamin. bypass, ASA, PCN. Tx: DDAVP Causes hypothermia, immunosuppression, (Aprotonin ↓ fibrinolysis by inhibiting (releases vWF & VII), cryo. ↑K, ↓Ca, ↓Mg; doesn’t improve wound plasmin & kallikrein). Prostaglandins: Arachadonic acid > healing. Citrate binds Ca > hypocalcemia Brain thromboplastin causes coagulopathy thromboxane, prostacyclin, prostaglandins (infuse Ca after 10 units PRBCs). O- = in TBI. (PGEs), and leukotrienes by COX. universal donor. Don’t infuse w/ LR (Ca – von Willebrands Dz: vWF & VIII:C Thromboxane (TXA2): from coagulation). (complete VIII); AD; abnormal PTT & platelets,vasoconstrictor, promotes Autotransfusion: Cell-saver. Can cause BT (Tx: cryo or VIII). platelet aggregation, responsible for ASAs coagulopathy. CI: infection, enteric Hemophilia A = procoagulant portion of platelet effects. Prostacyclin (PGI2): from contamination, malignancy, sickle-cell VIII (Tx: cryo - not just VIII, more endothelium, vasodilator, inhibits platelet Infection: HIV risk: 1/300K to 1 million. common,), B (Christmas Dz) = IX (FFP). aggregation thru ↑ cAMP. PGE2: ↓ IL-1, HCV risk 1/30K. Also: CMV, EMV, Both ↑ PTT, X-linked recessive. ↓ platelet aggregation, ↓ tumor cell malaria, yersinia, trypanosoma cruzi Malnutrition and VII def. : abnormal PT. proliferation, vasodilates depending on (Chagas). XIII def.: normal. receptor, ASAs GI effects. PGE1 keeps HBV: Vaccine = anti-HBs Ab. Infection = Dysfibrogenemia: ↑ PT, PTT & BT PDA open (indomethacin closes). anti-Hbe & HBs Abs. Exposure: IG + Hypercoaguability: Antiphospholipid Abs NSAIDs ↓ PGEs – renal vasoconstriction. vaccine. HCV: lower transmission by (Lupus anticoagulant & anticardiolipin), Leukotrienes: ↑IL1. needle stick, no prophylaxis on exposure. Protein C (inhibits V & VIII, treat w/ FFP Other endothelium-derived factors: PRBCs have no clotting factors. – contains C & heparin) & Protein S Endothelin: produced by ECE. Febrile nonhemolytic: begins 1-6hrs. (promotes C) deficiency, antithrombin III Vasoconstricts thru vascular muscle antibodies to donor WBCs – don’t stop (bnds thrombin & X), Factor V Leyden. receptors (A & B) by ↑ Ca/ PKC or transfusion. Tylenol. Use leukocyte-poor Also nephrotic syndrome - ↓ protein C & dilates thru endothelial receptors by ↑ RBCs. Allergic (anaphylaxis): Abs to S. cAMP. May play role in vasospasm. plasma proteins, IgA deficency. No need to Heparin: ↑ ATIII. T1/2 = 90min. ↑ PTT, stop transfusion if no fever. Tx: Benadryl, can ↑ PT at high dose. In OR can check Epi, IVF, washed PBRCs. Acute ACT (activated clotting time, abnormal pulmonary injury: begins 1-2hr. Donor >120 secs). SE: thrombocytopenia (below, Abs to WBS > aggregation. Stop not with SubQ), osetoporosis (chronic). transfusion, resolves. Acute hemolytic Tx: protamine (anaphylxaxis w/IDDM). reaction: ABO incompatibility. Occurs Coumadin: Inhibits vitK factors. T1/2 = within minutes – fever, CP, LBP. Stop 40hrs. SE: teratogenic, dermatitis. Tx; transfusion for early fever, Lasix, HCO3 VitK, FFP. Metabolized by cytochrome p- (alkalinize urine). Check plasma & urine 450 in liver. Decreased by: barbs, tegretol, for Hgb, Coombs test. rifampin, cholestyramine, nafcillin, Cryoprecipitate: has fibrinogen, vWF, sulcrafate. Increased by most others. CI in factor VIII, ATIII. Tx: factor 7,8 pregnancy (crosses placenta). deficiency, uremia, hemophilia A (8), DIC: ↑ PT, PTT & BT. ↓ fibrogen best vonWillebrands, cardiac bypass; (contains correlation (↑ d-dimer). best treated with fibrinogen, factor8, vWF, fibronectin, antithrombin III) FFP=hemophilia B (9), liver dz, dose) > β1 > α1 (with ↑ dose). CVL: Staph epi. Change CVL if Cx coumadin. Dobutamine: β1. ↓ SVR. Epi α = β. >15CFU. Propofol – lipid content ↑ DVT/PE: more common left iliac v. Norepi: α, mild β1. Neosynephrine pure infection (change line qd) (aorta crosses). Homan’s sign. (only 33% α agonist. Isoproterenol: β1 & 2 (SBP no Pneumonia: ICU = GNR. symptomatic). CXR: westermarks (wedge ∆, ↓ DBP, ↓ PVR, relaxes smooth Pleural empyema: Staph aureus > Hflu hyperdensity due to ↓ vasculature). muscle). Tetanus prophylaxis: 0 or 1 immunizations S1Q3T3. U/S no compressibility most Digitalis: = give toxoid + Ig, 2 = toxoid only, 3 in sensitive. Tx: 100% O2, Heparin (10K Digoxin: inhibits Na-K ATPase, ↑ <5yrs = none. unit bolus > 1K/hr) > Coumadin x 3mos. intracellular Ca – inotrope. Quinidine, Antibiotics: Aminoglycosides/Gent: V/Q: high prob – treat. Intermediate/ Low amiodarone, verapamil, erythromycin, inhibit 30s ribosome; poor CSF – agram. atropine ↑ levels. Long PR, short QT. penetration, bactericidal, worsen Parameters: CVP <5, PCWP <12 (= Toxicity: visual changes, AV block, myasthenic crisis, nephrotoxic (ATN), LAP or LVEDP, preload, on vent best mesenteric ischemia – Tx w/ Dig Ab. vestibular probs, ototoxic. Gram (-)no measured at end expiration, not accurate strep. PCN: inhibits bacterial cell wall Dopamine vs dobutamine: affects β1 in ARDS, pulmonary HTN, valve dz), CO synthesis. NO staph (extended PCNS do), Frank-Starling curve: ↑ preload (EDV) > 4-8L/m; CI 2.5-3.5 L/m/M2. PVR = 100. GNR coverage. hemolytic anemia. MAP = DBP + 1/3 (SBP-DBP). Lactate, ↑ CO to a point then ↓. Aztreonam: GNR, no GPC, no cross-rxn SvO2 & pH assses O2 delivery. Antihypertensives: ACEI: CI in renal w/PCN. AmphoB: nephrotoxic (RTA). Swan-Ganz: RA mean 8; RV 15-30/0; PA artery stenosis. β-blockers: CI in asthma, Fluconazole/Diflucan: no nephrotoxicity. 15-30/8; PCWP 15 mean. w/ Ca-channel blockers. Vanc: Red man’s, ototoxic, nephrotoxic. Shock: PCWP, CO, SVR: cardiogenic MI: periop risk ↑ for 6mos post-MI. Tx: Metronidazole (Flagyl): disulfiram (↑↓↑), septic/anaphylactic (↓↑↓, use nitrates, ASA O2, Morphine, β-blocker, reaction w/alcohol, neuropathy. Norepi for septic, epi for anaphylactic), heparin (postop), tPA (BeMOAN); occur Ciprofloxacin: Gram (-), Pseudomonas. hypovolemic (↓↓↑, IVF ± dobutamine). postop day 2-5 (often silent). Aortic cannot give to children/pregnant women Spinal: hypotension & bradycardia. dissection: Tearing pain. Nipride or (interferes w/growth plate). Oxygen uptake >110, arterial lactate <4 labetalol for SBP <110. Cephalosporins: 8% cross-allergy w/PCN. % blood loss: 15-30% = tachycardia (not Arrythmias No enterococcus coverage. Cefoxitin: 2nd in spinal shock), ↓ pulse pressure (DBP ↑ Afib/Aflutter: Verapamil, Diltiazem. (also gen. Better GNR/Anaerobes/Bacteroides due to vasoconstriction), 20% = digoxin for flutter) If unstable cardiovert (better for surgical prophylaxis). . 100J. rd orthostatic hypotension, 30% = ↓ systolic Ceftriaxone: cholestasis. Ceftazidime: 3 Other SVT: Vagal maneuver, Adenosine, BP, oliguria, confusion >40% = anuria, gen. Psuedomonas, GPC (↓ GNR). Clinda: verapamil, diltiazem (procainamide). If lethargy. Dextrans ↑ coagulopathy, Inhibits 50s ribosome. Anaerobes. unstable cardiovert 100J. hetastarch does at > 1.5l. NO proven Quinolones: inhibit DNA gyrase. Vtach, Vfib: Pulseless: Epi; Other: advantage crystalloid vs colloid in shock. Imipenem: inhibits cell walls. Cilastatin ↓ Lidocaine > procainamide > bretylium. BCxs (-) in 50% sepsis. renal excretion. SE: seizures. VT most common in CAD, ↓K. Torsades EKG: hyperkalemia: peaked T, Staph: vanc, Strep: PCN, enterococcus: de pointes w/quinidine, procainamide. hypokalemia: u-wave, hypocalcemia & amp or vanc/gent, Clostridium: spore- Asystole: Epi, atropine quinidine:↑ QT; MI: subendocardial = ST forming GPR. HIV: Abs dectectable 6- Bradycardia: atropineif HR<60 & depression, transmural = ST elevation. 8wks > ELISA, Western symptomatic Pulmonary emboli: nonspecific ST change Probenecid: Inhibits organic acid Preop risk: MI w/in 6mos, age >70, S3 (Right side strain, tachycardia). transport by epithelial cells (choroid), gallop, JVD, >5 PVCs, aortic stenosis, Hypothermia: j-point elevation. keeps PCN elevated in brain (also 5- emergency. Spinal = general for CAD. Hyperthyroidism: afib. Pulsus paradoxus: HIAA) Quitting smoking 2wks before surgery ↓ ↓ of SBP of >10 on inspiration, cardiac Alkalize urine: ↑ exretion of phenobarb, risk in chronic smokers. Most important tamponade. TCAs, ASA (weak acids) (not tests: EKG > Hgb > ABG > Cr. Cardiac tamponade: Becks triad: amphetamines - basic) Periop infections: hypotension, muffled heart sounds, ↑ Chemotherapy: Vincristine: neuropathy, Wound: Postop day 5-7. Staph aureus microtubule inhibitor (mitosis). MTX: JVD. Also pulsus paradoxus,↓ QRS. CT st most common (fever in 1 24hrs = Strep, folate antagonist (dihydrofolate reductase, & tenion ptx both ↑ JVD & ↓ pulse clostridium). ↑ with steroids, age > 70, pressure, ptx doesn’t have pulsus FH2 > FH4, ↓ purines, glycine, malnutrition, remote infection, thymidylates), necrotizing paradoxus. Tx: subxiphoid uncontrolled DM (not controlled). pericardiocentesis @ left costal margin leukencephalopathy, myelosuppression; ↑ Necrotizing fasciitis = strep, debrediment, by PTN, sulfa, ASA. Leukovorin rescue: Cardiac Drugs: Nitroglycerine: Tdt. venodilator. causes methemoglobinemia folinic acid, normal cells take up, tumor Gas gangrene: Clostridum. Tx: PCN, doesn’t. Cisplatin: alkylating agent; (cyanosis w/normal ABG); CI include fasciotomy, debridement (+- hyperbaric increased ICP, glaucoma. Nipride: nephrotoxicity, ototoxicity, neuropathy, O2, no antitoxin (give tet-toxoid, Tet-Ig)) TTP. XRT sensitizer. Procarbazine: mood venodilation = arteriodilation. cyanide Rates: clean <1.5%, clean-contaminated (converted to thiocyanate in liver, changes, G6PD deficency problems; 3%, contaminated 5%, dirty 33%. Uremia BCNU (Carmustine): alkylating agent. excreted in urine, half life 4 days – causes ↑s. ARF, psychosis. Tx w/hydroxocobalmin). Myelosuppression (dose-limiting), C. diff: Occurs w/ all abx. Watery nephrotoxicity. Amrinone not α or β, Dopamine: D (renal diarrhea, cramps. Tx: oral Flagyl > vanc Above cross BBB except MTX, also Fluid status: best assessed by UOP (CVP MEN: All AD. I (Wermers) = pancreatic etoposide, 5-FU, hydroxyurea do. if CRF or CHF). LR = low K+ (OK for islet cell tumors, parathyroid adenomas, IL/interferon: parkinsonism. Tamoxifen: bolus), also lactate, Ca; may precipitate pituitary adenomas. IIA (Sipples) = pheo, retinopathy. 5-FU: cerebellar ataxia. panic attacks. 20-30% of NS remains parathyroid, thyroid (medullary CA). IIB = Tumor biology: N-myc = oncogene, intravascular after 3 hrs. Pheo, thyroid, mucosal neuromas/ neuroblastoma. Kidney: Renin/angiotensin: marfanoid habitus. Wound healing: 12h epithelial migration; juxtaglomerular apparatus produces renin Zollinger-Ellison: duodenal or pancreatic 5d wound contraction (myofibroblasts, > angiotensinogen to angiotensin I > ACE gastrinoma, duodenal ulcers, increased actin), collagen synthesis); 42d (6wk) max > angiotensin II > vasoconstriction, ↑ serum gastrin (increases w/IV secretin). amount collagen; 2y max tensile strength aldosterone. System stimulated by ↑K, ↓ Occurs in MENI. (80% in 30d). Na. Aldosterone: from adrenal cortex, Carcinoids: most common in appendix Also Inflammation (24hrs, PMNs & stimulated by AgII, ↓Na, carotid/aortic Hemachromatosis: ↑ Fe in blood. Genetic macrophages) > epithelialzation 48h > baroreceptors. ↑ Na reabsorption K & H (HFE) or 2°. ↑ serum Fe, ferritin. Tx: proliferative/ scar (fibroblasts secrete secretion from distal tubules. ADH: phlebotomy. Carried by transferrin – collagen 1-12d) > contraction stimulated by ↑osmolarity, ADH, minimal brain depsotion Collagen: Contain unique AAs carotid/aortic baroreceptors. ↑ H2O Nelsons disease: adrenalectomy causes hydroxyproline & hydroxylysine (require reabsorbption in distal tubules. rapid pituitary adenoma growth Vitamin C & Zinc for hydroxylation), also Hyperaldosteronism: hypokalemia, rd Loop of Henle: Reabsorption of Na ↑ proline. Glycine every 3 residue. passively follows active transport of Cl ↑DBP, metabolic alkalosis, polyuria, no Triple helix. edema st Distal renal tubules: Na in, K, H out. Type III appears 1 (24-48h) frame work; Renal disease: ATN: due to sepis, toxins, Acromegaly: = adults. Cretinism = kids I = 72hrs, fibroblasts, most common in drugs, etc. Epithelial (granular) casts. (hydrocephalus) skin, IV = basement membrane, II = Acute interstitial nephritis: immunologic, Hypothyroidism: Primary (Hasimoto’s): cartilage. due to PCN, NSAIDS, Lasix. Fever, rash, ↓ T4, ↑ TSH. Secondary/ pituitary: ↓ TSH, Collagenase: secreted by T-lymphocytes arthralgias. WBC casts, urine FT4. T4 coverted to T3 (more potent). (by IL-1) and migrating epithelial cells eosinophilia. Acute glomerular nephritis: Critically ill pts (sick euthyroid state) have Macrophages (> fibroblasts) secrete GFs, st RBC casts. Prerenal: Hyaline casts. ↓ T3 & T4, normal free T4 & TSH. steroids inhibit, most important cell in 1 Pyelonephritis: WBC casts. Replacement doesn’t benefit. 4 days. Nephrotoxic drugs: Aminoglycosides, Thyroid measurements: If TBG ↑ Growth factors: TGFβ - stimulates ampho B, PCN, NSAID, ACEI. (pregnancy, liver dz), total T4 ↑ but free collagen synthesis; bFGF & PDGF – ARF Renal: BUN/Cr <20, U.S.G. <1.020, T4 normal. T3RU ↑ in hyperthyroidism, ↓ make fibroblasts competent; IGF & EGF FeNa > 1, UNa > 40, Una < 350. Prerenal in hypothroidism. Free T4 index = cause fibroblast replication; is opposite. FeNa = (Una x Pcr/ Ucr x T3RU/norm x total T4. Should agree w/ Angiogenesis: bFGF begins angiogenic Pna) x 100 (U Need Pee). May be oliguric T3RU. cascade; VEGF stimulated by hypoxia, (<500cc/d) or nonoliguric. D/C Hyperthyroidism: ↓ TSH. chemotactic & mitogenic for endothelium Mg/antacids, ↓ digoxin, Nipride, Opthalmoplegia (IR & MR), proximal TGFα endothelial proliferation; TNFα procainamide. 10% > CRF. Dialyze for girdle weakness/ myopathy. Tx: PTU (anti- stimulates capillary tubule formation AEIOU (acidosis, electrolytes/K, thyroid, β-blockers) Iron def: only transient effect ↓ tensile inflammatoin/pericarditis, fluid overload, Hypocortisolism: Addisons. Hypotension, strength – unknown mechanism. Diabetes: uremic encephalopathy) hyponatremia, hyperkalemia,, affects all phases (collagen glycosylation, Tx: CVVHD (continuous > intermittent hyperpigmentation (in 1°, not 2° - low etc). XRT: prevents hypoxia-induced dialysis. Dopamine, Lasix no benefit.) ACTH/MSH). Dx: Cortrosyn test – if no ↑ angiogensis. Nicotine: ↑ platelet adhesion Urinary retention: Tx: bethanecol. in cortisol then 1°. Addison’s crisis: & vasoconstriction. Steroids: stabilizes RTA: I=nephrocalcinosis, urine pH >5.5; tachycardia/ hypotension refractory to lysosomal membranes (Vitamin A II= ↓ HCO3 reabsorption. Both: non- IVP/ pressors. Tx: hydrocortisone IV + destabilizes). anion gap acidosis, hypokalemia fludrocortisone PO (mineralocorticoid). Glycosaminoglycans: in skin = hyaluronic Myoglobinuria: Alkalinize urine (HCO3 Chronic steroid users at risk for up to 1 acid, chondroitin SO4, dermatan SO4, IV), mannitol, IVF. year after stopping steroids. heparin; not heparin SO4 or keratan SO4 Fanconi’s syndrome: Proximal renal Hypercortisolism: Cushings Dz > adrenal Anion gap: Na – (Cl + HCO3), 12 normal tubular defects. Lowes, Wilsons dz. Lose tumor > ectopic. Hyperglycemia, High with ↑ acids (ARF, ketones, ASA, glucose, Aas, PO4 etc in urine. Rickets hypertension, hypokalemia etc. Low-dose lactate, etc). Normal w/ ↓ HCO3 (Cl- Diuretics: Lasix: inhibits Na/K DST = 0.5mg QID x2d. High dose = 2mg increases; diarrhea, RTA). ↓ albumin reabsorption in ascending limb; ↓ Ca & QID (suppresion with Cushings, not causes ↓ AG. K. Lasts 6 hours. In ARF double dose (20- others). Metyrapone test: increased 17- Free H2O def=(Na-140) x kg x 0.6 40-80) until result. Thiazides: inhibits hydroxycorticosteroids (with Cushings, not Osmolarity = 2(Na+K) + Glu/18 + Na/CL transport in distal tubule. ↑ Ca. CI: with ectopic ACTH) BUN/2.8. Free H2O deficit = .6 x kg x diabetes, hyperuricemia, Steroid potency: cortisol = hydrocortisone (Na/140 – 1). hyperaldosteronism. Mannitol: Osmotic = 1; prednisone = prednisolone = 4; Body H2O: Intracellular 66%, interstitial/ diuresis in proximal tubule. SE: cardiac, methylprednisolone = 5 (less extracellular 20%, vascular/cavity 10%. renal, H/A, N/V. mineralocorticoids); dexamethasone = 30. Vol = 70ml/kg (females 60). Avg 5l. Steroid Side-effects: ulcers, Hypophosphatemia: weakness cells > viral Ag on MHC I or II > T-cell hypokalemia, hyperglycemia/DM, HTN, (respiratory) destruction. osteopenia, obestity, cataracts/glaucoma, Diabetes: #1 cause of death is MHC: Glycoproteins (ABO = glycolipids) myopathy, infections, avascular necrosis cardiovascular. Nonketotic hyperglycemic Class I: HLA-A,B,C. On all cells, for Tc of hip. (Vitamin A counters wound coma: Glu >900 (<600 in DKA), NIDDM. cells. Class II: HLA-DP,DQ,DR. On healing effects) ↓ fatty acid concentration than DKA. macrophages, B-cells, for Th cells. HLA- Parathyroid hyperplasia: Mortality >50%. A,B & DR important for transplantation. hypercalcemia, MENI & II. ↑ Ca, ↑ PO4, DKA: ↑K (watch for hypokalemia Glia express low MHC I. Neurons express ↑ AlkPhos, fractures w/correction). Tx: Insulin, NS, HCO3 for no MHC I or II. Stevens-Johnson syndrome: Dilantin shock, pH < 7.1. Cytokines: Inflammatory: IL-1. Anti- and Tegretol (also PCN, sulfa, barbs, SIADH: Causes: Oat cell, Dilantin, inflammatory: IL-4,10,13. Mycoplasma, HSV, strep) Tx: steroids. Tegretol, thiazides, COPD. Tx: Hemostasis: Surgicel = cellulose; Fibrin Dilantin hypersensitivity: S-J + Hepatitis, demeclocycline. glue = fibrinogen + thrombin fever, eosinophilia,lymphadenopathy. DI: Tx: DDAVP, pitressin, EtOH withdrawl: 12hrs hallucinations, Absence of epoxide hydroxylase > arene chlorpropamide. 12-24hrs seizures, 3-4d DTs. oxides Fat embolism: 12-48h later, always Statistics: Sensitivity = TP/TP+FN. Haldol: lowers seizure threshold, w/dyspnea, petechiae over shoulders/ Specificty = TN/TN+FP. Positive neuroleptic malignant syndrome – treat chest, tachycardia, tachypnea. ↑ serum Predictive Value = TP/TP+FP. NPV = w/dantrolene lipase in 50%. Look for fat in blood, TN/TN+FN. Prevalence = TP+FP/all. Droperidol: antiemetic, antipsychotic, urine. CNS dz does not occur without Study results: Type I error = false positive butyrephone, causes arrythmias (↑QT, lung disease unless PFO/ ASD. conclusion of hypothesis. Type II = false torsades de point) Nutrition: Req: Protein 1g/kg/d, Calories negative. P-value is chance of type I error Ethambutol: anti-TB. Causes optic 35/kg/d (25 in paraplegics). TBI ↑ 1.7x (<0.05, 5%). Power = chance of not having neuritis, color blindness BMR. (Burns ↑ 2-3x) Fat 9kcal/g, Pro 4, type II error. (>80%). Mann-Whitney test: Hypomagnesemia: Ca Carbonate, Carbs 4. Measure status w/prealbumin compare 2 groups where variable is not ethacrynic acid, amphotericin, (T1/2 = 2d – shorter than albumin, normally distributed (wide variation). T- aminoglycosides. Same Sxs as ↓ Ca transferrin; ↑ in CRF, steroids, ↓ in liver test: compare 2 groups with normally Hypocalcemia: seizures, psych, dz).Respiratory Quotient = VCO2/V02, distributed variable. Chi-square test: compare frequency values b/t 2 groups. dysrhythmias, tetany (Chvostek, <0.8 = fats 1° nutrient, >0.8 = carbs. Tube ANOVA: examines differences of >2 Trousseau); adjust for hypoalbuminemia. feeds: hepatic = branched chain Aas groups. Validity: test measures what it Ionized Ca best measure. Causes: (aromatic Aas cause encephalopathy); intends to. Reliability: gives consistent pancreatitis, ↓ Mg, CRF. EKG: Prolonged renal = essential AAs, pulmonary = ↓ results. QT. Tx: 10% Ca gluconate – must correct carbs, ↑ fats (25-50% of cals). TPN: most st 800-237-4558 - 247 hypomagnesemia 1 . (Calcium choride common complication = hepatic steatosis. 3X more ioized Ca than gluconate. IV (benign, resolves, ↑ LFTs). Glutamine infiltration causes necrosis.) important after injury/ stress. Essential Hypercalcemia: Sarcoid, fatty acids: linoleic (& linolenic?) acid, hyperparathyroidism. Sxs: hypotension, Deficency: alopecia, dermatitis from TPN, stones, AMS, ulcers, pancreatitis. Short ↓ arachadonic acid ↑ eicosatrienoic acid. QT. Tx: Volume, Lasix, calcitonin Zinc: impaired wound healing. Tube (mithramycin, etidronate). feeding diarrhea tx: check Cdiff 1st,change Hyperkalemia: weakness, arreflexia. formula, ↓ feeds, add fiber (psillium), Peaked Ts. Tx: CaGluconate (for cardiac), GI meds: Sucralfate: needs H+ to activate kayexalate, lasix, insulin/D5, HCO3, – do not use w/H2 blockers. Omeprazole dialysis (Prilosec) = K+/H+ - ATPase inhibitor. Hypokalemia: EKG: flat Ts, U-waves. Metoclopromide (Reglan) = dopamine (10meq/hr IV, 20/hr CVL max.) antagonist, worsens Parkinsons. Exacerbates digoxin toxicity. UrineK <30 Phenergan: dystonia (tx w/benadryl). = diarrhea. > 30 then if serum HCO3 < 24 Pancreatitis: Causes: hypercalcemia, = RTA. If >24 then If Ucl < 10 = emesis, (DIC, ARDS?) NG, >10 = diuretics, steroids. Causes ARDS: use PEEP, not diuretics, steroids tetany, ileus. Pseudohyponatremia = due Respiratory stimulants: Doxapram – to hyperglycemia, hyperlipidemia. Must stimulates central centers correct hypomagnesemia 1st. Vasovagal syncope: Tx anticholinergics Hyponatremia: caused by Addisons, (propantheline) hypothyroidism, renal failure, SIADH Immunology: (euvolemic). Correct at 2.5meq/hr or Humoral: Viral Ag > B cells > antibodies 20meq/d max to avoid CPM. + complement. Hypernatremia: correct at 1meq/hr. Cellular: T-cells, T-helper (CD4) & T- Hyperphosphatemia: treat w/aluminum suppressor/cytotoxic (CD8). Infected hydroxide.