Neurosurgery
Unprotected copy By: Dr.JKR [email protected]
Dr.JKR NS Neurosurgery Stewart Lo, Matt Stacey and Sara Temple, chapter editors Kathryn Howe and Kim Tsoi, associate editors Mark Pahuta, EBM editor Dr. Abhaya Kulkarni and Dr. Taufik Valiante, staff editors
Basic Anatomy Review 2 Dermatomes/Myotomes 21 Differential Diagnoses of Common Presentions 4 Approach to LimblBack Pain 22 Extradural Lesion INTRACRANIAL PATHOLOGY Intradural Intramedullary Lesion
Intracranial Pressure (ICP) Dynamics ...4 Spinal Cord Syndromes 24 ICPNolume Relationship Brown-Sequard Syndrome ICP Measurement Anterior Cord Syndrome Cerebral Blood Flow (CBF) Central Cord Syndrome Elevated ICP Posterior Cord Syndrome
Herniation Syndromes 6 Root Compression 25 Subfalcine Cervical Disc Syndrome Central Tentorial Lumbar Disc Syndrome Lateral Tentorial Cauda Equina Syndrome Upward Lumbar Spinal Stenosis Tonsillar Neurogenic Claudication Treatment of Herniation Syndromes Peripheral Nerves 27 Hydrocephalus 7 Peripheral Nerve Injury Nerve Entrapment Benign Intracranial Hypertension 8 (Pseudotumour Cerebri) SPECIALTY TOPICS
Tumour 9 Neurotrauma 29 Metastatic Trauma Assessment Astrocytoma Head Injury Meningioma Brain Injury Vestibular Schwannoma ("Acoustic Neuroma") Late Complications of Head/Brain Injury Pituitary Adenoma Spine Injury Neurologically Determined Death Pus 12 Cerebral Abscess Pediatric Neurosurgery 33 Spinal Dysraphism Blood 13 Intraventricular Hemorrhage Extradural ("Epidural") Hematoma Hydrocephalus in Pediatrics Subdural Hematoma Dandy-Walker Malformation Chiari Malformations Cerebrovascular Disease 15 Craniosynostosis Subarachnoid Hemorrhage (SAH) Pediatric BrainTumours Intracerebral Hemorrhage (ICH) Intracranial Aneurysms Functional Neurosurgery 36 Carotid Stenosis Common Medications 36 Vascular Malformations 20 Arteriovenous Malformations (AVMs) Summary Key Questions 37 Cavernous Malformations References 38 EXTRACRANIAL PATHOLOGY
Toronto Notes 2008 Neurosurgery N51
Dr.JKR NS2 Neurosurgery Basic Anatomy Review Toronto Notes 2008
See Functional Neuroanatomy software Basic Anatomy Review
MRI Brain
Central sulcus Frontal lobe \ . Parietal lobe Cingulate gyrus ' Septum pellucldum
Corpus callosum Thalamus Hypothalamus
Occipital lobe
Midbrain Pons Fourth ventricle Cerebellum
Medulla
Dens of C2 Spinal cord
Body of C3 A. Sagittal section
Frontal lobe
Caudate nucleus
Lateral ventricle
Putamen Internal capsule
Insula
Thalamus
Parietal lobe
Occipital lobe
B. Axial section
Figure 1. MRI Neuroanatomy From Stewart Pet al. Functional Neuroanatomy (Version 2.1). Health Education Assets Library, 2005.
Dr.JKR Toronto Notes 2008 Basic Anatomy Review Neurosurgery NS3
Cervical Region ~ (1 c:J c:] (2 CJ C3 d (4 (5
(6 8 C7 fJB (8 T1
Lumbar Region
~~"""--L2
1\\\1~\"""':'~~-- L3
~",,==:=j----- L4
Figure 2. Relationship of Nerve Roots to Vertebral Level in the Cervical and Lumbar Spine Note: AP views depict left-sided C4-5 and L4-5 disc herniation, and correlating nerve root impingement
/ anterior communicating artery
/ . anterior cerebral artery
internal carotid artery
middle cerebral artery
posterior communicating artery
L~~i-\~::/-l--;-- posterior cerebral artery
L~~-'.--...!....+-...... l_ superior cerebellar artery
basilar artery
labyrinthine (internal auditory) artery
anterior inferior cerebellar artery
posterior inferior cerebellar artery
vertebral artery
Figure 3. Circle of Willis
Dr.JKR NS4 Neurosurgery Differential Diagnoses of Common Presentionsflntracranial Pressure Dynamics Toronto Notes 2008
Differential Diagnoses of Common Presentations Intracranial Mass Lesions • tumour • metastatic tumours • astrocytoma • meningioma • vestibular schwannoma (acoustic neuroma) • pituitary adenoma .....' • primary CNS lymphoma .)------,, • pus/inflammation • cerebral abscess Primary eNS lymphoma reported • cerebritis (i.e. HSV encephalitis) ill 6-20% of IHIV-infectedl patients. • tumefactive multiple sclerosis (MS) • blood • extradural (epidural) hematoma • subdural hematoma • ischemic stroke • hemorrhage: subarachnoid hemorrhage (SAH), intracerebral hemorrhage (rCH), intraventricular hemorrhage (rVH) • cyst Disorders of the Spine • extradural • degenerative: disc herniation, canal stenosis, spondylolisthesis/spondylolysis • infection/inflammation: osteomyelitis, discitis • ligamentous: ossification of posterior longitudinal ligament (OPLL) • trauma: mechanical compression/instability, hematoma (onset = minutes to hours) • tumours (55% of spinal tumours): lymphoma, metastases (lymphoma, lung, breast, prostate), neurofibroma • intradural extramedullary • vascular: dural arterio-venous fistula, subdural hematoma (anticoagulation) • tumours (40% of spinal tumours): meningioma, schwannoma, neurofibroma • intradural intramedullary: • tumours (5% of spinal tumours): astrocytomas and ependymomas most common; also hemangioblastomas and dermoid • syringomyelia (common causes: trauma, congenital, idiopathic) • infectious/inflammatory: TB, sarcoid, transverse myelitis • vascular (AVM, ischemia) Peripheral Nerve Lesions • neuropathies • traumatic ..... • entrapments '.\------,, • iatrogenic Monro-Kellie hypothesis • inflammatory • tumours Vbrain +Vblood +VCSF +Vles;on = Vskull =constant INTRACRANIAL PATHOLOGY ICP mmHg '~f~.): Intracranial Pressure (lCP) Dynamics :r-----J 20 '~-) ...,---- : ICPNolume Relationshi I I : 0 : : Volume .. : • adult skull is rigid with a constant intracranial volume When amass expands I • however, as a lesion expands, rcp does not rise initially due to: within the skull Eventually further small increments in • cerebrospinal fluid (CSF), blood, extracellular fluid (ECF) and intracellular fluid com~ensatory volume produce mechanisms initially larger and (rCF) displacpd out of the head mam:ain anormal larger increments in • brain tissue shifts into compartments under less pressure (herniation) intracranial pressure intracranial • once compensation is exhausted, rcp rises exponentially pressure • normal rcp <15 mmHg (8-18 cm H 20) for adult, 3-7 mmHg (4-9.5 em H 20) for Figure 4. ICP·Volume Curve child; varies with patient position Adaptej from Lindsay 'fm, Bone I: Neurology and • waveform comprised of respiratory and blood pressure pulsations Neurosurgery Illustrated. Copyright 2004 with • consider therapy for high rcp when rcp >20-25 rnmHg permission from Elsevier.
Dr.JKR Toronto Notes 2008 Intracranial Pressure Dynamics Neurosurgery NS5
ICP Measurement
• lumbar puncture (LP) (contraindicated with known/suspected intracranial mass lesion) • intraventricular catheter/ventriculostomy/external ventricular drain ("gold standard", permits therapeutic drainage of CSF to decrease rcp; if mass and pressure gradient present, drainage may increase gradient) • other: fibreoptic monitor (intraventricular, intraparenchymal, subdural), subarachnoid bolt (Richmond screw), and epidural monitor
Cerebral Blood Flow (CBF) ~------L CPP=MAP-ICP - • CBF depends on cerebral perfusion pressure (CPP) and cerebral vascular resistance • normal CPP >50 mmHg in adults • cerebral autoregulation maintains constant CBF by compensating for changes in CPP, unless: Autoregulation: CSF maintained despite • high rcp such that CPP <60 mmHg change in CPP • MAP>150 mmHg or MAP <50 mmHg • brain injury: Le. subarachnoid hemorrhage (SAH), severe trauma /~ Elevated ICP ~j <60 m~Hg i>150 mmHg Etiology of Raised ICP low BP or high ICP High BP • increased intracranial blood volume Cerebral perlusion pressure IMA~ICPI • hypoventilation --> increased pCO:Jdecreased paz .-+ vasodilatation • venous outflow obstruction (venous sinus thrombosis, superior vena cava (SVC) Figure 5. Cerebral Autoregulation syndrome) Curve • cranial dependency, Valsalva Adapted from Lindsay et al: Neurology and Neurosurgery Illustrated. Copyright 2004 with permission from Elsevier. • cerebral edema: vasogenic (vessel damage), cytotoxic (cell death), osmotic (acute hyponatremia, hepatic encephalopathy) • hydrocephalus • intracranial mass lesion (tumour, pus, blood, depressed skull fracture, foreign body) • tension pneumocephalus • status epilepticus • hypertensive encephalopathy (loss of autoregulation and cerebral edema)
..... CLINICAL FEATURES '.. )------,, Acute Raised ICP Cushing'sTriad of Acute Raised ICP • headache (H/A) Full triad seen in 1/3 of cases • nausea and vomiting (N/V) 1. hypertension 2. bradycardia (late finding) • decreased level of consciousness (LaC) if diastolic BP or midbrain compressed rcp = 3. abnormal respiratory pattern • drop in Glasgow Coma Scale (GCS) --+ best index to monitor progress and predict outcome of acute intracranial process (see Neurotrauma, NS29) • papilledema ± retinal hemorrhages (may take 24-48 hours to develop) • abnormal extra-ocular movements (EOM) • CN VI palsy often falsely localizing (causative mass may be remote from nerve) • upward gaze palsy (especially in children with obstructive hydrocephalus) • herniation syndromes (see next page) • focal signs/symptoms due to lesion Chronic Raised ICP • H/A • postural: worsened by coughing, straining, bending over (Valsalva) • morning/evening H/A --+ vasodilatation due to increased CO2 with recumbency • visual changes • due to papilledema • enlarged blind spot, if advanced .-+ episodic constrictions of visual fields ("grey-outs") • optic atrophy/blindness • differentiate from papillitis (usually unilateral with decreased visual acuity)
Dr.JKR NS6 Neurosurgery Herniation Syndromes Toronto Notes 2008
1. Subfalcine Herniation Syndromes 2. Central 3. Uncal 4. Upward Subfalcine (Cingulate) Herniation 5.Tonsillar • definition: cingulate gyrus herniates under falx • etiology: lateral supratentorial lesion • clinical features • usually asymptomatic, pathological/radiological observation warns of impending transtentorial herniation, risk of ACA compression Figure 6. Herniation Types Central Tentorial (Axial) Herniation • definition: displacement of diencephalon and midbrain through tentorial notch • etiology: supratentorial midline lesion, diffuse cerebral swelling, late uncal herniation • clinical features: • rostral to caudal deterioration (sequential failure of diencephalon --> medulla) • decreased LOC (midbrain compressed) • EOM/upward gaze impairment ("sunset eyes") • brainstem hemorrhage ("Duret's" secondary to shearing of basilar artery perforating vessels) • diabetes insipidus (traction on pituitary stalk and hypothalamus) --> end stage sign Lateral Tentorial (Uncal) Herniation • definition: uncus of temporal lobe herniates down through tentorial notch • etiology: lateral supratentoriallesiun (often rapidly expanding trawnatic hematoma) • clinical features: • ipsilateral non-reactive dilated pupil (earliest, most reliable sign), EOM paralysis (CN III compressed) • decreased LOC (midbrain compressed) contralateral hemiplegia, ± extensor (upgoing) plantar response ± "Kernohan's notch": contralateral cerebral peduncle compressed due to shift of brain -> ipsilateral hemiplegia (a false localizing sign) Upward Herniation • definition: cerebellar vermis herniates through tentorial incisura, compressing midbrain • etiology: large posterior fussa mass causing herniation of cerebellum rostrally, common after VP shunting • clinical features: • superior cerebellar artery (SCA) compression * cerebellar infarct • compression of cerebral aqueduct --> hydrocephalus Tonsillar Herniation (1IConing") • definition: cerebellar tonsils herniate through foramen magnum • etiology: infratentoriallesion or following central tentorial herniation • clinical features: • compression of cardiovascular and respiratory centers in medulla (rapidly fatal) may be precipitated by LP in presence of space occupying lesion (particularly in the posterior fossa) Treatment of Herniation Syndromes ------' • goals: keep Iep <20 mmHg, CPP >60-70 mmHg General Measures • elevate head of bed at 30-45° --> increases intracranial venous outflow • prevent hypotension with fluid and pressors pm • ventilate to normocarbia (pC0235-40 mmHg) --> prevents vasodilatation • oxygen pm to maintain p02 >60 mmHg -> prevents hypoxic brain injury • CT or Mill to identify etiology, assess for midline shift/herniation Specific Measures (proceed stepwise prn) • mannitol (20% IV solution 1-1.5 glkg, then 0.25 glkg q6h) • can give rapidly, acts in 30 minutes, must maintain sBP >90 mmHg • hyperventiTate to pCO:? 30-35 mmHg
Dr.JKR Toronto Notes 2008 Herniation Syndromes/Hydrocephalus Neurosurgery NS7
• sedation ("light" e.g. codeine --> "heavy" e.g. fentanyl/MgS04 ± paralysis with vecuronium --> reduces sympathetic tone, HTN induced by muscle contraction) • corticosteroids • decreases edema over subsequent days around brain tumour, abscess, blood • no proven value in head injury or stroke • surgeryd• ram. 3- 5 m 1CSF'VIa ventnc. Ies, assess eac h"SItuation m. d epen d ent1 y • remove mass lesion, insert external ventricular drain (if acute) or shunt • decompressive craniectomy is a last resort
Hydrocephalus ~[ o Definition • increased CSF volume Etiology • decreased CSF absorption (majority) • increased CSF production (rarely) - e.g. choroid plexus papilloma (0.4-1% of intracranial tumours) Epidemiology • estimated prevalence 1-1.5%; incidence of congenital hydrocephalus -] -2/1000 live births Classification 4 1. Obstructive (Non-Communicating) Hydrocephalus 5 • absorption blocked within ventricular system proximal to the arachnoid granulations 6 • acquired causes: 1. Choroid plexus • acquired aqueductal stenosis (adhesions following infection, hemorrhage) 2. Lateral ventricles intraventricular lesions (tumours - e.g. 3rd ventricle colloid cyst, hematoma) 3. Third ventricle 4. Cerebral aqueduct (of Sylvius) ~ • mass causing tentorial herniation, aqueduct/4th ventricle compression 5. Fourth ventricle :-:: others: neurosarcoidosis, abscess/granulomas, arachnoid cysts 6. Foramen Luschka and Magendie .~ • congenital causes: 7. Arachnoid granulations u:: • aqueductal stenosis, Dandy-Walker malformation, Chiari malformation (see 8. Subarachnoid space ~ Pediatric Neurosurgery, NS34) 9. Sagittal sinus @ • CT findings: • ventricular enlargement proximal to block Figure 7. The Flow of CSF
2. Non-Obstructive (Communicating) Hydrocephalus ..... ' , • CSF absorption blocked at extraventricular site = arachnoid granulations ~}------, • causes: • post-infectious (#1 cause) -... meningitis, cysticercosis CSF produced by choroid plexuses, • post-hemorrhagic (#2 cause) --> SAH, NH, traumatic flows to: --t ventricles'" foramina of • Choroid plexus papilloma (rare, causes l' CSF production) Luschka and Magendie ... subarachnoid • idiopathic normal pressure hydrocephalus space'" absorbed by arachnoid • CT findings: villi/granulations into venous sinuses. • all ventricles dilated 3. Normal Pressure Hydrocephalus (NPH) • gradual onset of classic triad developing over weeks or months • gait disturbance (ataxia and apraxia usually initial symptoms) • urinary incontinence • dementia Luschka =lateral, Magendie =medial • CSF pressure within clinically "normal" range, but symptoms abate with CSF shunting • idiopathic etiology 4. Hydrocephalus Ex Vacuo • enlargement of ventricles and sulci secondary to cerebral atrophy, not hydrocephalus ~, • usually a function of nonnal aging, also in Alzheimer's, Creutzfeldt-Jacob Disease NPH Progression "AID" = Clinical Features (see Pediatric Neurosurgery for infant/child, NS34) Ataxia/Apraxia of gait ... Incontinence
• Acute Hydrocephalus --t Dementia • signs and symptoms of acute raised ICP (see NS5) • impaired upward gaze ("sunset eyes") and/or CN VI palsy • Chronic Hy'droceEhalus • simIlar to NPH (see above) Investigations • CT'MRI . • ventricular enlargement, may see prominent temporal horns ..... ' , • periventricular hypodensity (transependymal migration of CSF forced into ~}------, extracellular space) CSF production =CSF reabsorption = • narrow/absent sulci • ultrasound (through anterior fontanelle in infants) - 500mllday in normal adults • ICP monitoring (e.g. LP) may be used to investigate NPH, test response to shunting Normal CSF volume -150 ml (lumbar tap test) (50% spinal, 50% intracranial'" 25 cc • radionuclide cistemography can test CSF flow and absorption rate (unreliable) intraventricular, 50 cc subarachnoid)
Dr.JKR NS8 Neurosurgery HydrocephaluslBenign Intracranial Hypertension Toronto Notes 2008
Treatment • surgical removal of obstruction (if possible) or excision of choroid plexus papilloma • shunts: • ventriculoperitoneal (VP) - most common ventriculo-atrial (VA) - not first choice because of l' infections, shunt emboli • ventriculopleural • lumbopentoneal - for communicating hydrocephalus and pseudotumour cerebri • third ventriculostomy (for obstructive hydrocephalus) via ventricUloscopy • LPs (for transient, IVH in premature infants, etc.) Shunt Complications • obstruction (most common cause of shunt malfunction) • etiology: obstruction by choroid plexus, buildup of proteinaceous accretions, blood, cells (inflammatory or tumour), infection, disconnection or damage • clinical features: acute hydrocephalus, increased ICP • investigations: "shunt series" (plain x-rays of entire shunt that only rule-out disconnection, break, tip migration), CT, radionuclide "shuntogram" • shunt tap and surgical exploration pm • infection (3-6%) • etiology: 5. epidermidis, 5. aureus, P. acnes, Gram-negative bacilli clinical features: fever, N/V, anorexia, irritability, meningitis, peritonitis, signs and symptoms of shunt obstruction, shunt nephritis (VA shunt) • investigations: CBC, blood culture, tap shunt for C&S (LP usually NOT recommended) • overshunting (10% over 6.5 years) • ± slit ventricle syndrome (collapse of ventricles leading to occlusion of shunt ports by ependymal lining) • ± subdural effusion, hematoma (collapsing brain tears bridging veins, especially in NPH patients) • ± secondary craniosynostosis (children) • ± low pressure headache • seizures (5.5% risk in 1st year, 1.1% after 3rd year) • inguinal hernia (17% incidence with VP shunt inserted in infancy), skin breakdown over hardware Benign Intracranial Hypertension (Pseudotumour Cerebri) Definition • raised intracranial pressure and papilledema without evidence of any mass lesion, hydrocephalus, infection or hypertensive encephalopathy (a diagnosis of exclusion) Etiology • unknown (majority), but associated with • lateral venous sinus thrombosis • habitus/diet: obesity, hyper/hypovitaminosis A endocrine: reproductive age, menstrual irregularities, Addison's/Cushing's disease, thyroid irregularities • hematological: iron aeficiency anemia, polycythemia vera drugs: steroid administration or withdrawal, tetracycline, nalidixic acid, etc. • risk factors overlap with those of venous sinus thrombosis and similar to those for gallstones Epidemiology • incidence -0.5/100,000/year • usually in 3rd and 4th decade (F>M) Clinical Features • symptoms and signs of raised ICP (H/A in >90%, pulsatile intracranial noise), but NO decreased LaC or diplopia • -J, visual acuity, papilledema, visual field defect, optic atrophy (key morbidity, preventable cause of often pennanent blindness) • usually self-limited, recurrence is common, chronic in some patients • risk of blindness is not reliably correlated to symptoms or clmical course Investigations • CT: nonnal • CSF studies: nonnal • MRI: must look for venous sinus thrombosis Treatment • rio conditions that cause intracranial hypertension • D/C offending medications, encourage weight loss, fluid/salt restriction • phannacotherapy: acetazolamide (decreases CSF production), thiazide diuretic or furosemide • if above fail ---> serial LPs, shunt • optic nerve sheath decompression (if progressive impainnent of visual acuity) • 2-year follow-up with imaging to rule out occult tumour, ophthalmology follow-up
Dr.JKR Toronto Notes 2008 Tumour Neurosurgery NS9
Tumour Definition • primary vs. metastatic, intra-axial (parenchymal) vs. extra-axial, supratentorial vs. infratentorial, adult vs. pediatric • benign: non-invasive, but can be devastating due to expansion of mass in fixed volume of skull • malignant: implies rapid growth, invasiveness, but rarely extracranial metastasis
Table 1. TumourTypes: Age, Location Age Supratentorial Infratentorial (posterior fossa) <15 years . astrocytoma lall grades) 150%1 . medulloblastoma 115-20%) • incidence: 2-51100.000Iyear - craniopharyngioma 15-10%) - cerebellar astrocytoma 115%1 • 60% infratentorial - others: pineal region tumours, choroid plexus - ependymoma 19%) tumours, ganglioglioma, DNET - brainstem astrocytoma
>15 years • high grade astrocytoma (e.g. glioblastoma - metastasis • 80% supratentorial multiforme (GBM) (12·15%) - acoustic neuroma Ischwannomal (5-10%) • metastasis 115-30%, includes infratentorial) - hemangioblastoma 12%) • meningioma 115-20%1 - meningioma - low grade astrocytoma 18%) - pituitary adenoma 15-8%) - oligodendroglioma 15%) - other: colloid cyst, eNS lymphoma, dermoid/epidermoid cysts Clinical Features OIl' • progressive neurological deficit (70%) - usually motor weakness, ± CN deficits, DDx for ring enhancing lesion sensory, cognitive, personality, endocrine deficits may localize lesion on CT with contrast: "MAGICAL DR" • HJA (50%) ± raised ICP (acute or chronic depending on growth rate), H/A 'Metastases classically worse in am but non-specific (likely hypoventilation during sleep 'Abscess causing vasodilatation -->1' ICP), also may worsen with bending forwardNalsalva 'Glioblastoma • NN (40%) (high grade astrocytomal • seizures (25%) Infarct • papilledema, obscured vision Contusion • symptoms suggestive of TIA (ictal, post-ictal, or ischemic 2° to "steal phenomenon") AIDS (toxoplasmosisl • rarely presents with hemorrhage Lymphoma • familial syndromes associated with CNS tumours: Demyelination Resolving hematoma • von Hippel-Lindau (hemangiomas) [' by far the 3 most common Ox's] • tuberous sclerosis (astrocytomas) • neurofibromatosis type 1 and 2 (astrocytomas, acoustic neuromas respectively) • Li-Fraumeni (astrocytomas) • Turcot syndrome (GBMs) • multiple endocrine neoplasia type 1 (pituitary adenoma) Investigations • CT, MRI, stereotactic biopsy (tissue diagnosis), metastatic work-up pm Treatment • conservative - serial Hx, Px, imaging for slow growinglbenign lesions • medical- corticosteroids to reduce cytotoxic cerebral edema, pharmacological (see Pituitary Adenoma, NSll) • surgical- total or partial excision (decompressive, palliative), shunt if hydrocephalus • radiotherapy - conventional fractionated radiotherapy (XRT), stereotactic radiosurgery M (Gamma KnifeT ) • chemotherapy - e.g. alkylating agents (temozolomide)
MetastaticTumours ..... '~)------, ,
• most common brain tumour seen clinically Primary Sources of Metastatic • 15-30% of cancer patients present with cerebral metastatic tumours Brain Tumours • usually spread hematogenously Lung 44% Breast 10% Location Kidney (RCC) 7% • 80% are hemispheric, often at grey-white matter junction or junction of GI 6% temporal-parietal-occipital lobes (likely emboli spreading to terminal MCA branches) Melanoma 3%
Dr.JKR NSIO Neurosurgery Tumour Toronto Notes 2008
Investigations • metastatic work-up (OCR, cr chest/abdo, abdominal D/S, bone scan, mammogram) • cr with contrast ~ round, well-circumscribed, often ring enhancing, ++ edema, often multiple • MRI more sensitive, especially for posterior fossa • consider biopsy in unusual cases
Treatment • medical • phenytoin for seizure prophylaxis if patient presents with seizure • dexamethasone to reduce edema (often Significant cause of symptoms), given with ranitidine • chemotherapy (small cell lung cancer) • radiation Figure 8. Multiple Brain Metastases • whole brain radiation therapy (WERT) can help reduce symptoms in inoperable cases (some tumours respond poorly e.g. melanoma), typically the sole treatment if multiple lesions • post-op WERT is commonly used • stereotactic radiosurgery • multiple lesions: 1. metastatic work-up negative --+ brain biopsy 2. metastatic work-up positive -. biOpsy affected sites other than the brain • surgical • single/solitary lesions ~ surgery + radiation • prognosis: median survival without treatment once symptomatic is -1 month, with optimal treatment 6-9 months but varies depending on primary
'jt ~ Astrocytom_a _ • most common primary intra-axial brain tumour
Table 2. Astrocytoma Grading System (one of many schemes) World Health Organization (WHO) Typical CTIMRI Findings Survival 1- pilocytic astrocytoma No mass effect, no enhancement >10 years, cure if gross total resection .. 1 II-low grade/diffuse Mass effect, no enhancement 5years
--- 2 III - anaplastic Complex enhancement 1.5-2 years
IV - glioblastoma multiforme Necrosis (ring enhancement) 9 months
Clinical Features • middle aged, recent onset of new/worsening H/A, N/V, seizure ± focal 1. heterogenous contrast enhancement deficits or symptoms of increased ICP 2. ill-defined borders (infiltrativel 3. perilumour edema 4. central necrosis Investigations 5. compression of ventricles, midline shift • CT with contrast ~ variable appearance depending on grade (see Table 2) • tissue biopsy ~ WHO grade correlates with prognosis, but 25% chance of sampling Figure 9. High Grade Astrocytoma on error due to tumour heterogeneity CT Treatment • low grade astrocytoma: • close follow-up, radiation, chemotherapy, surgery all valid options • surgery: not curative, trend towards better outcomes • radiotherapy alone or post-op prolongs survival (retrospective evidence) • chemotherapy - usually reserved for tumour progression • high grade astrocytomas (comprised of anaplastic astrocytoma and glioblastoma multiforme (GBM» • surgery: gross total removal with radiation to tumour bed ± WERT is the standard treatment unless: extensive dominant lobe GBM, Significant bilateral involvement, end of life near, extensive brainstern involvement • aim to prolong "quality" survival • chemotherapy: -20% response rate • multiple gliomas: WERT ± chemotherapy
Dr.JKR Toronto Notes 2008 Tumour Neurosurgery NSll
Meningioma • mostly benign (1 % malignant), slow-growing, extra-axial, circumscribed (non-infiltrative), arise from arachnoid membrane • often cause hyperostosis of adjacent bone, often calcified, classically see Psammoma bodies on histology Common Locations • parasagittal convexity or falx (70%), sphenoid wing, tuberculum sellae Clinical Features • middle aged, symptoms of increased rcp, focal deficits Investigations • CT with contrast: homogeneous, densely enhancing, along dural border ("dural tail"), well circumscribed (see Figure 10) • contrast enhanced MRI provides better detail 1. homogenous contrast enhancement • angiography: most are supplied by external carotid feeders (meningeal vessels) 2. dural attachment • also assesses venous sinus involvement, "tumour blush" commonly seen 3. distinct margins (prolonged contrast image) Figure 10. Meningioma on CT Treatment • conservative management for non-progressive, asymptomatic lesions • surgery is treatment of choice if symptomatic or progression on sequential imaging (curative if complete resection) • stereotactic radiosurgery (SRS) may be an option for lesions <3 em • endovascular embolization to facilitate surgery • SRS or XRT for recurrent atypical/malignant meningiomas
Prognosis • >90% 5-year survival, recurrence rate variable (often -10-20%) • depends on extent of resection (Simpson's classification)
Vestibular Schwannoma e'Acoustic Neuroma")
• progressive unilateral or asymmetrical sensorineural hearing loss = acoustic neuroma until proven otherwise (earliest symptom) • slow-growing (average of 1-10 mm/yr), benign posterior fossa tumour • arises from vestibular component of CN VITI at cerebello-pontine angle (CPA) • if bilateral = neurofibromatosis type II
Clinical Features • compression of structures in CPA, often CN VITI (hearing loss 98%, tinnitus, dysequilibriurn), then V, then VII • ataxia and raised rcp are late features
Investigations • MRI with gadolinium or T2 FIESTA sequence (>98% sensitive/specific), CT with contrast 2nd choice Figure 11. Vestibular Schwannoma • audiogram, brainstem auditory evoked potentials, caloric tests (tumour in cerebella-pontine angle\
Treatment • conservative: serial imaging • radiation: stereotactic radiosurgery is the treatment of choice • surgery if: 1. lesion >3 em; 2. brainstem compression; 3. edema; 4. hydrocephalus • several routes, curable if complete resection (almost always possible) • operative complications: CN VII, VITI dysfunction (only significant disability if bilateral), CSF leak
Pituitary Adenoma o • primarily from anterior pituitary, 3rd-4th decade, M=F • microadenoma <1 em in diameter; macroadenoma ~1 em in diameter • may be functional (secretory) or non-functional
Dr.JKR NSI2 Neurosurgery TumourlPus Toronto Notes 2008
Clinical Features • mass effects • H/A • bitemporal hemianopsia (compression of optic chiasm) (see Neurology, N26 for details of visual field deficit) • CN III, IV, Vv V'l' VI palsy (compression of cavernous sinus) • endocrine effects • hyperprolactinemia (prolactinoma) ---> infertility, amenorrhea, galactorrhea, decreased libido • ACTH production -. Cushing's disease, hyperpigmentation • GH production ---> acromegaly/gigantism • panhypopituitarism (hypothyroidism, hypoadrenalism, hypogonadism) • associated MEN I syndrome • diabetes insipidus • pituitary apoplexy • apoplexy (sudden l:'xpansion of mass due to hemorrhage or necrosis) • abrupt onset B/A, visual disturbances, ophthalmoplegia, and reduced mental status, and panhypopituitarism • CSF rhinorrhea and seizures (rare presenting signs of pituitary tumour) • signs and symptoms of SAH (rare) (see NSI5)
Investigations • formal visual fields, CN testing, endocrine tests (PRL level, TSH, 8 a.m. cortisol, fasting glucose, FSH/LH, IGF-I), electrolytes, urine electrolytes and osmolarity, imaging (Mill with and without contrast) Differential • parasellar tumours (e.g. craniopharyngioma, tuberculum sellae meningioma), carotid aneurysm
Treatment • medical ~, • rapid corticusteroid ..tdministration ± surgical decompression for apoplexy Go Look For The Adenoma Please • dopamine agonists (e.g. bromocriptine) for prolactinoma GH, LH, FSH,TSH, ACTH, Prolactin • serotonin antagonist (cyproheptadine), inhibition of cortisol production Acompressive adenoma in the pitu (ketoconazole) for Cushing's itary will impair hormone production in • somatostatin analogue (octreotide) ± bromocriptine for acromegaly this order (i.e. GH-secreting cells are • endocrine replacement therapy most sensitive to compression) • surgical • trans-sphenoidal. transethmoidal, transcranial approaches
Sources of Pus • subdural empyema --> pus in pre-existing space with no capsule barrier thus rapid expansion is commoll (from sinusitis, mastoiditis - rare, 20% mortality) • meningitis, encephalitis, toxoplasmosis (AIDS) • osteomyelitis of skull (Pott's puffy tumour), usually seen with sinusitis • granuloma (TB, sarcoid) • cerebral abscess (see below)
Cerebral Abscess Definition • pus in brain substance, surrounded by tissue reaction (capsule formation)
Etiology • modes of spread • hematogenous spread (most common) • adults: chest is #1 source --> lung abscess, bronchiectasis, empyema • children: congenital cyanotic heart disease (CCHO) with R to L shunt • immunosuppression (AIDS - toxoplasmosis) • contiguous spread (adjacent infection) • otitis media, mastoiditis, sinusitis, osteomyelitis, dental abscess • dural disruption • surgery, trauma (especially with continued CSF leak) • congenital defect (e.g. dermal sinus)
Dr.JKR Toronto Notes 2008 PuslBlood Neurosurgery NS13
• pathogens • Streptococcus (most common), often anaerobic or microaerophilic 3 • Staphylococcus (penetrating injury) • Gram negatives, anaerobes • immW1ocompromised: Toxoplasma, Nocardia, Candida albicans, Listeria monocytogmes, Mycobacterium and Aspergillus
Risk Factors • lW1g abnormalities (infection, AV fistulas (especially Osler-Weber-Rendu syndrome)) • CCHD • bacterial endocarditis • penetrating head trauma • AIDS
Clinical Features 1. surrounding edema • focal neurological signs and symptoms 2. central low density (pus) • mass effect, increased ICP and sequelae (cranial enlargement in children) 3. ring enhancement • hemiparesis and seizures in 50% • ± signs of systemic infection (mild fever, leukocytosis) Figure 12. Brain Abscess on CT Investigations • WBC/ESR may be normal, blood cultures rarely helpful and LP contraindicated • CT scan often 1st test in emergency department • ~fRl • imaging of choice • diffusion/apparent diffusion coefficient (ADC) used to differentiate abscess (black) from tumour (white)
Treatment • multiple aspiration ± excision and send for Gram stain, acid fast bacillus (AFB), C&S, fungal culture • excision preferable if location suitable • antibiotics • empirically: vancomycin + ceftriaxone + metronidazole or chloramphenicol or rifampin (6-8 weeks therapy) • revise antibiotics when C&S known • anti-convulsants (1-2 years) • follow up CT is critical (do weekly initially, more frequent if condition deteriorates)
Prognosis • mortality with appropriate therapy -10%, permanent deficits in -50% Blood
Extradural (6IEpidural") Hematoma
Etiology • temporal-parietal skull fracture ---+ ruptured middle meningeal artery Epidemiology • young adult, male> female Clinical Features • classically there is lucid interval between concussion and coma • signs and symptoms depend on severity but can include H/A, N/V, amnesia, altered LaC Investigations • CT without contrast ---+ high density biconvex mass against skull, "lenticular-shaped," usually with uniform density and sharp margins, usually limited by suture lines 1. compression of ventricles (midline shift) Treatment 2. blood • head elevation, mannitol pre-op, craniotomy to evacuate clot Figure 13. Extradural Hematoma on Prognosis CT • good with prompt management, as the brain is often not damaged
Dr.JKR NS14 Neurosurgery Blood Toronto Notes 2008
Subdural Hematoma ACUTE SUBDURAL HEMATOMA Etiology • rupture of vessels that bridge the subarachnoid space (e.g. cortical artery, large vein, or venous sinus) or cerebral laceration Risk Factors • anticoagulants, EtOH, cerebral atrophy Clinical Features CT dInIity IIld III..,....of blood • no lucid period, signs and symptoms can include altered LOC, pupillary irregularity, hemiparesis tiiiit CT .. IIIIi Investigations ·n ·12 AMI Hyper. Grey BlICk • CT - high density concave mass, "crescentic" usually less uniform, less dense and «72hl more diffuse than extradural hematoma SubIcuIe Iso. White White «4w) Treatment ClvIlIic Hypo. Blaci Blaci • craniotomy if causing mass effect, optimal if surgery <4 hrs from onset (>4wl Prognosis MR~ T1: 'George Washington Bridge' • poor overall since the brain is often injured MRH2: 'Oreo' cookie - BlackiWh~d1act compression of ventricles midline shift old blood\ .blood /
Figure 14. Subdural Hematoma on CT
CHRONIC SUBDURAL HEMATOMA
Etiology • acute subdural with neomembranes, neocapillaries, and liquefaction of clot • recurrent bleeding from the neocapillaries • leads to expansion of the hematoma, increased rcp, herniation, and death Risk Factors • older, alcoholic, patients with CSF shunts, anticoagulants
Clinical Features • often due to minor injuries or no history of injury • symptoms of raised rcp ± seizures, progressive dementia, gait problem • obtundation disproportionate to focal deficit; "the great imitator" of dementia, tumours
Investigations • CT --+ hypodense (liquefied clol), crescentic mass
Treatment • burr hole drainage as clot liquefies, craniotomy if recurrent
Prognosis • good overall as brain usually undamaged, but may require repeat drainage
Dr.JKR Toronto Notes 2008 Cerebrovascular Disease Neurosurgery NS15
Cerebrovascular Disease
Ischemic Cerebral Infarction (80%) • embolic (heart, carotid artery, aorta) or thrombosis of intracerebral arteries (see Carotid Stenosis section, NSI9, and Neurology. N59)
Intracranial Hemorrhage (20%) • subarachnoid hemorrhage (SAH), spontaneous intracerebral hemorrhage (ICH), intraventricular hemorrhage (IVH)
Subarachnoid Hemorrhage (SAH)-,:..----...--- o ..... ' , Definition ~}------, • bleeding into subarachnoid space (intracranial vessels between arachnoid and pia) Fisher Grade (SAH on CT scan) Graae finding Etiology 1 Normal scan • trauma (most common) • spontaneous <1 mm thick blood • aneurysms (75-80%) • idiopathic (14-22%) >1 mm thick blood • AVMs(5%) • coagulopathies (iatrogenic or primary), vasculitides, tumours (<5%) IVH or ICH ±SAH Epidemiology • -10-28/100,000 population/year , ~}------, • peak age 55-60, 20% of cases occur under age 45 Hunt and Hess Grade Risk Factors (clinical grading scale for SAHI • hypertension Grade Description • pregnancy/parturition in patients with pre-existing AVMs, eclampsia 1 No Sx or mild H/A and/or mild meningismus • oral contraceptive pill 2 Features of 1t CN palsy • substance abuse (cigarette smoking, cocaine, alcohol (debatable») 3 Confusion/lethargy, mild • conditions associated with high incidence of aneurysms (see Intracranial Aneurysms hemiparesis or aphasia section, NSI8) 4 GCS <15 but>8, moderate-severe hemiparesis, Clinical Features of Spontaneous SAH mild rigidity • sudden onset (seconds) severe headache: "worst headache of my life" Coma (GCS <9), decerebrate, (up to 97% sensitive, 12-25% specific) moribund appearance • history of exertion is common (straining, intercourse) Mortality of Grade 1·2 20%, t with grade • nausea/vomiting, photophobia • meningismus (neck pain/stiffness, positive Kernig's and Brudzinski's sign) .... , '~I------, • decreased LOC (can include raised ICP, ischemia, seizure) • focal deficits: cranial nerve palsy (e.g. III, IV), hemiparesis World Federation of Neurological • ocular hemorrhage in 20-40% (due to sudden raised ICP compressing central retinal vein); subhyaloid/pre-retinal hemorrhages Surgeons grading of SAH • reactive hypertension WFNS GCS Aphasia. • sentineVwarningleaks Grade Score Hemiparesis. • SAH-like symptoms lasting <1 day ("thunderclap H/A") or Hemiphagia • may have blood on CT or LP • -50% of patients with full blown SAH giw history suggestive of a warning leak O' within past 3 weeks 1 15 • differential diagnosis of severe HIA, onset within seconds: SAH; thunderclap H/A; 13-14 dissection/thrombosis of aneurysm; venous sinus thrombosis; benign exertional H/A 13-14 Investigations • non-contrast CT (see Figure 15) 7-'2 tor - • 98% sensitive within 12h, 93% within 24h; 100% specificity • may be negative if small bleed or presentation delayed several days 5 3-6 tor - • positive history for SAH with negative CT - MUST do LP (may be negative <12h) , Intact aneurysm • acute hydrocephalus, IVH, ICH, infarct or large aneurysm may be visible • CT may also suggest site of aneurysm that has bled
Dr.JKR NS16 Neurosurgery Cerebrovascular Disease Toronto Notes 2008
blood in blood in blood in interhemispheric basal cisterns suprasellar cistern fissure
,, blood on blood 'in surface of sylvian tentorium fissures
Figure 15. Diagnosis of SAH
• lumbar puncture (LP) - findings (highly sensitive):
• elevated opening pressure (>18 em H 20) • bloody initially, xanthochromic supernatant with centrifugation ("yellow") by -12h, lasting 2 weeks • spectrophotometry is most sensitive for xanthochromia • RBC count usually>100,000/mm3 without Significant drop from 1st to last tube as in traumatic tap • protein elevated due to blood breakdown products • cerebral angiography ("gold standard for aneurysms") • demonstrates source of SAH in 80-85% of cases • "angiogram negative SAH": repeat angiogram in 7-14 days, if negative-+ "perirnesencephalic SAH" • magnetic resonance angiography (MRA) and CT angiography • emerging technologies, sensitivity may be up to 95% for aneurysms
BP level of consciousness limb movements stiff neck fundi
conscious, alert, no neurological findings. I CT scan fundi normal I f [,- i~bar puncture I~ negative I ~i~-eJ
clear, colorless. no microscopicT---• blood C.;o;;;;-J CTNMRNangiography Figure 16. Approach to SAH
Treatment • admit to lCU or NICU • oxygen/ventilation pm • NPO, bed rest, elevate head of bed 300, minimal external stimulation, neurological vitals qlh • aim to maintain sBP = 120-150 (balance of vasospasm prophylaxis, risk of re-bleed, risk of hypotension since CBF autoregulation impaired by SAH) • IV NS with 20 mmol KCl/L at 125-150 cclh • phenytoin if seizure or temporal lobe clot • mild sedation pm • nimodipine for vasospasm neuroprotection --> 21 days; may d/c earlier if patient is clinically well and ready for discharge
Dr.JKR Toronto Notes 2008 Cerebrovascular Disease Neurosurgery NS17
• cardiac rhythm monitor • Foley pm, strict ins & outs • 4 vessel angiography, early surgery or coiling to prevent rebleed
Complications • vasospasm • definition: constriction of blood vessels in response to arterial blood clot outside vessels at the base of the brain • clinical features: confusion, -J., LOC, focal deficit (speech or motor) • onset: 4-14 days post SAH (if deterioration within first 3 days, MUST look "Triple H"Therapy for Vasospasm for other cause) • Hypertension • "radiographic" vasospasm in 30-70% of arteriograms performed 7 days • Hypervolemia following SAH (peak incidence) • Hemodilution • "symptomatic" vasospasm in 20-30% of SAH patients • detect clinically and/or with angiogram or transcranial Doppler (increased velocity of blood flow), CBC/electrolytes/CT urgently to rio other causes • risk factors: large amount of blood on CT (i.e. high Fisher grade), smoking, l' age, prior HTN risk of cerebral infarct and death (biggest cause of morbidity and mortality in patients who reach hospital) • treatment • "triple H" therapy (hypertension, hypervolemia, hemodilution) using fluids and pressors (examples: norepinenphrine, phenylephrine) • angioplasty for refractory cases • hydrocephalus (15-20%) - due to blood obstructing arachnoid granulations or subarachnoid space • can be acute or chronic - requiring intraventricular catheter or shunt respectively • neurogenic pulmonary edema • hyponatremia - (SIADH, cerebral salt wasting) • diabetes insipidus • cardiac - arrhythmia (>50% have ECG changes), MI, CHF
Prognosis • 10-15% mortality before reaching hospital, overall 50% mortality (majority within first 2-3 weeks) • 30% of survivors have moderate - severe disability • a major cause of mortality is rebleeding, for aneurysms: • risk of rebleed: 4% on first day, 15-20% within 2 weeks, 50% by 6 months • if no rebleed by 6 months risk decreases to same incidence of unruptured aneurysm (2%) • only prevention is early clipping or coiling • rebleed risk for "perimesencephalic SAH" is - same as for general population
Intracerebral Hemorrhage (lCH) --~-~----~--- Definition • hemorrhage within brain parenchyma, accounts for -10% 01' strokes • can dissect into ventricular system (NH) or through cortical surface (SAH)
Etiology • hypertension (usually at putamen, thalamus, pons and cerebellum) • hemorrhagic transformation (reperfusion post stroke, surgery, strenuous exercise, etc.) • vascular anomalies • aneurysm, AVMs and other vascular malformations (see Vascular Malformations, NS20) • venous sinus thrombosis • arteriopathies (cerebral amyloid angiopathy, lipohyalinosis, vasculitis) • tumours (1 %) - often malignant (e.g. GBM, lymphoma, metastases) • drugs (amphetamines, cocaine, EtOH, etc.) • coagulopathy (iatrogenic (coumadin, tPA), leukemia, TTP, aplastic anemia) • CNS infections (fungal, granulomas, herpes simplex encephalitis) • post trauma (immediate or delayed, frontal and temporal lobes most commonly injured via coup/contre-coup mechanism) • eclampsia • post-operative (carotid endarterectomy, craniotomy) • idiopathic
Dr.JKR NS18 Neurosurgery Cerebrovascular Disease Toronto Notes 2008
Epidemiology • 12-15 cases/lOO,OOO population/year Risk Factors • increasing age (mainly >55 years) • male gender • hypertension • Black/Asian> Caucasian • previous CVA of any type (23x risk) • both acute and chronic heavy EtOH use; cocaine, amphetamines • liver disease Clinical Features • rIA-like symptoms often precede ICH, can localize to site of impending hemorrhage • location: basal ganglia/internal capsule (50%), thalamus (15%), cerebral white matter (15%), cerebellum/brainstem (15%) • gradual onset of symptoms over minutes to hours, usually during activity • H/A, vomiting, decreased LOC are common • specific symptoms/deficits depend on location of ICH Investigations • high density blood on CT without contrast Treatment • medical: • decrease BP to pre-morbid level or by -20%; check PTT, INR, and correct coagulopathy (stop anticoagulation for 1-2 weeks) • control raised ICP • phenytoin for seizure prophylaxis • follow electrolytes (SIADH common) • angiogram to rio vascular lesion UNLESS >45 yrs, known HTN, and putamen/thalamic/posterior fossa ICH (yield - 0%) • surgical: • craniotomy with evacuation of clot under direct vision, resection of source of ICH (Le. AVM, tumour, cavernoma), ventriculostomy to treat hydrocephalus • indications: • symptoms appear related to raised ICP or mass effect • rapid deterioration (especially with signs of brainstem compression) • favourable location, e.g. cerebellar, non-dominant hemisphere • young patient (<50 y.o.) • if tumour, AVM, aneurysm, or cavernoma suspected (resection or clip to decrease risk of rebleed) • contraindications: • small bleed: minimal symptoms, GCS >10 (not necessary) • poor prognosis: massive hemorrhage (especially dominant lobe), low GCS/coma, lost brainstem function Intemltionll Sublndmoid Aneurysm Trill (lSAn of IlIUIUIagicII clipping VI. IlldOVIICU • medical reasons (e.g. very elderly, severe coagulopathy, difficult location III coifing in 2143 petienlI with ruplUred (e.g. basal ganglia, thalamus» intraCllllilllllturysms: IlindomiZld trill ILancet 2002; 360:1267-741 InllOduction: This randomized control trial aimed to Prognosis compare endovascular detachable coil treatment against craniotomy and dipping for ruptured • 30-day mortality rate is 44%, mostly due to cerebral herniation intracranial aneurysms in patients who were consid • rebleed rate is 2-6%, higher if HTN poorly controlled ered eligible for either modality of therapy. Mat!lods: 2143 patients were randomized to neuro surgical dipping In=10701 vs. treatment by endovas cular coilln=10731.The primary clinical outcome was ___---....I~ l~ assessment using the modified Rankin scale for a Intracranial Aneurysms score of 3-6 (dependellCf or death) at 1year. Results: Patients in this trial tended to be of good Epidemiology dillital grade prior to in!mention and amajority of aneurysms were in the anterior circulatory system. • prevalence -5% (20% are multiple) 190 out of 801123.7%1 patients who completed fol • female> male; age 35-65 years low up in the endovascular treatment were depend ent or dead at 1year compared with 243 of 793 130.6%1 in the neurosurgical treatment group Risk Factors (p:O,0019j.This showed arelative risk reduction of • autosomal dominant polycystic kidney disease (15%) 22.6% {95% CI8.9-34.21 and an absolute risk reduc tion of 6.9 (95 CI2.5-11.3) when comparing endovas • fibromuscular dysplasia (7-21%) cular to neurosurgical therapy, • AVMs Conclusion: In patients with aruptured intracranial aneurysm who are suitable for either endovascular • connective tissue diseases (Ehlers-Danlos, Marfan's) coiling or neurosurgical clipping, the outcome of • FHx dependellCf or death at one year favours the endovascular coiling therapy. Further neuropsycho • bacterial endocarditis logical assessment is being planned in subgroups to • Osler-Weber-Rendu syndrome allow for subtle outcomes to be detected. Further fol • atherosclerosis and H1N low up for dependency death is planned as well. • trauma
Dr.JKR Toronto Notes ZOOS Cerebrovascular Disease Neurosurgery NS19
Types • saccular (berry) • most common type • located at branch points of major cerebral arteries (Circle of Willis) • 85-95% in carotid system, 5-15% in vertebrobasilar circulation • fusifonn • atherosclerotic • more common in vertebrobasilar system, rarely rupture • mycotic • secondary to any infection of vessel wall, 20% multiple • 60% Streptococcus and Staphylococcus • 3-15% of patients with SBE
Clinical Presentation • rupture (90%), most often SAH, but 30% ICH, 20% IVH, 3% subdural bleed • sentinel hemorrhage ("thunderclap H/A") ---+ IMMINENT RISK • mass effect (giant aneurysms) • internal carotid or anterior communicating aneurysm may compress: • the pituitary stalk or hypothalamus causing hypopituitarism • the optic nerve or chiasm producing a visual field defect • basilar artery aneurysm may compress midbrain, pons (limb weakness), or CN III • posterior communicating artery aneurysm may produce CN III palsy • intracavernous aneurysms (CN III, IV, Vv V~ VI) • small infarcts due to distal embolization (amaurosis fugax etc.) IMMINENT RISK • seizures • headache (without hemorrhage) • incidental CT or angiography finding (asymptomatic)
Investigations • CT, magnetic resonance angiography (MRA), angiogram
Treatment • ruptured aneurysms: • overall trend towards better outcome with early surgery or coiling (48-96 hours afterSAH) • choice of surgery vs. coiling not yet well defined, morphology/location can aid decision • treatment options: surgical placement of clip across aneurysm neck, trapping (clipping of proximal and distal vessels), thrombosing using Gugliemi detachable coils (endovascular technique), wrapping as last resort Prevention of dbabling and fatal strokas by • unruptured aneurysms: succeuful carotid endarterectomy in patiants • 1% annual risk of rupture: risk dependent on size and location of aneurysm w~hout recent neurolGgical symptoms: ran· • no clear evidence on when to operate: need to weigh life expectancy domised controlled trial. - (lancet 2004; 363:1491·1502.) • risk of morbidity/mortality of SAH (20%/50%) vs. surgical risk (2%/5%) • generally treat unruptured aneurysms>10 mm Studr Asymptomatic Carotid Surgery TriaIIACST), a • consider treating when aneurysm 7-9 mm in middle-aged, yow1ger patients or randomized, controlled trial with follow·up at 5 years. patients with a family history of aneurysms Patients: 3120 asymptomatic patienls with signifi· • follow smaller aneurysms with serial angiography cant carotid artery stenosis were randomized equally between immediate carotid endarterectomy ICEAI and indefinite deferral of CEA and were followed for up to 5years Imean 3.4 yearsl. Carotid Stenosis Main Outeome: Any stroke lincluding fatal or dis• abling}. Results: The risk of stroke or death within 30 days of Definition CEA was 3.1% (95% CI2.3-4.1). Comparing all • narrowing of the internal carotid artery lumen due to atherosclerotic plaque patients randomized to immediate CEA vs. deferral, formation, usually near common carotid bifurcation into internal and external carotids the 5-year stroke risks were 3.8% vs. 11% Igain 7.2% [95% CI 5.0-9.41. p