• Astrocytes = control the environment and form the blood–brain barrier. • Microglial cells = blood-derived mononuclear macrophages. • Oligodendrocytes = produce myelin sheath in the CNS • Schwann cells = produce myelin sheath in the PNS. • Between the brain and the skull are 3 meninges = dura mater, arachnoid and pia mater. • The subarachnoid space is filled with CSF. • Sensory cell bodies are situated in the dorsal root ganglia. • The motor cell bodies are in the ant. horns of the spinal cord

The onset, duration and pattern of symptoms over time often provide diagnostic clues: for example, in assessing headache or vertigo.

• Headache with nausea, vomiting, photophobia +/- phonophobia = migraine • Headache with neck stiffness, fever and rash = meningitis

• Headache is the most common neurological symptom and may be either primary or secondary to other pathology.

• Recurrent headache, usually unilateral. • Evolves over 30min-2hrs, lasting up to 72hrs. • It is classified into classic (with aura) and common (without aura). • Ass. with nausea/vomiting, photophobia/phonophobia.

• Orbital/retro-orbital; always same side during cluster, may switch sides between clusters. • Abrupt onset, attacks last up to 2hrs. Recurrent attacks 1-4x within 24hrs, lasting weeks to months. • Awakes the patient from sleep • Autonomic features (conjunctival injection, tearing, nasal stuffiness, ptosis, miosis, agitation). • During the attack the patient keep pacing around the room in an agitated state, or even head banging.

• Abrupt onset, lasting very briefly (seconds or less). • Can be felt anywhere. • Can be felt anywhere. • Common in patients with migraine.

Ass. with neck stiffness, fever, rash, signs of raised intracranial pressure and false localizing signs, meningism.

Abrupt onset, maybe fatal at onset, ass. with nausea, vomiting, reduced consciousness, false localizing signs, 3rd nerve palsy

In patients >55yrs, presents with jaw pain on chewing, visual symptoms, and tender temporal arteries, elevated ESR and CRP

• Stimulation of PNS due to pain, emotion or illness or when forced to stand in warm environment leading to vasodilation and bradycardia. • Preceded by light-headedness, vision dimming, tinnitus, and nausea. • MCC of transient loss of consciousness; • Lasts 1-2 minutes. due to inadequate cerebral perfusion. • It causes pale or grey skin and maybe associated with myoclonic jerks. • Maybe due to: If kept flat, recovery is rapid.

• With no previous alarm, triggered with exercise. • Causes: HCM, severe AS or arrhythmia.

1- Drugs (l-dopa or anti-HTN drugs). 2- Autonomic diseases (DM). 3- In people >65 years. 4- Hypovolemia.

1- Tonic phase: Early loss of consciousness ass. with body stiffening. 2- Clonic Phase: Rhythmical jerking increasing in intensity and subsiding over 0.5–2min. 3- Postictal phase: Period of unresponsiveness, heavy breathing, appearing deeply a sleep and finally confusion as the patient re-orientates. Caused by paroxysmal electrical discharges, • Simple (consciousness is preserved) or complex (impaired conciousness). can be: • Characterized by whichever part of the brain is involved. example: 1- Frontal lobe seizures = focal motor seizure. 2- Temporal lobe seizures = autonomic and/or psychic symptoms, ass. 2- Temporal lobe seizures = autonomic and/or psychic symptoms, ass. with automatisms (lip smacking or swallowing).

• Common, often more frequent than epilepsy, sometimes occurring multiple times in a day, and may last considerably longer, with symptoms waxing and waning. • Other features include asynchronous movements, pelvic thrusts, side-to-side rather than flexion/extension movements and absence of postictal confusion.

• A is a focal neurological deficit of rapid onset that is due to a vascular cause, can be ischemic or hemorrhagic. • TIA is the same but symptoms resolve within 24hrs. • 80% of are ischemic. Hemorrhagic stroke is much more frequent in Asian populations. We do brain CT w/o contrast to differentiate b/w them. • Factors in the history or examination that increase the likelihood of hemorrhage rather than ischemia include use of anticoagulation, headache, vomiting, seizures and early reduced consciousness.

• Very rare; present with an abrupt onset, depending on the level of spinal cord affected. • The ant. spinal artery syndrome is most common and causes loss of motor function and pain/temp. sensation with relative sparing of joint position and vibration sensation below the level of the lesion (sparing dorsal column).

• Recurrent ‘dizzy spells’ in 30% of those >65YO. • Causes = postural hypotension, cerebrovascular disease, cardiac arrhythmia or hyperventilation induced by anxiety and panic.

• BPPV= Recurrent episodes of vertigo lasting a few seconds, increased when sleeping on the affected side or with movement. • Ménière’s disease = Vertigo lasting minutes or hours (ass. with hearing Vertigo is the illusion of movement loss, tinnitus, nausea and vomiting). indicating a problem in the vestibular apparatus or, less commonly, the brain. • Migrainous vertigo (with or without headache) • Stroke •

• Neurological Sx that are not due to disease are called ‘functional’ but other terms include psychogenic, hysterical, somatisation or conversion disorders. • Sx include: blindness, , weakness and collapsing attacks, with fatigue, lethargy, pain, anxiety, etc.

A history of previous visual loss in someone presenting with numbness suggests multiple sclerosis A history of previous visual loss in someone presenting with numbness suggests multiple sclerosis

• Phenytoin toxicity = • Excessive intake of simple analgesia = medication overuse headache • Cocaine = provoking convulsions

• Single-gene defects = in myotonic dystrophy or Huntington’s disease. • Polygenic influences = in multiple sclerosis or migraine. • Charcot–Marie–Tooth disease may be AD, AR or X-linked. • Mitochondria DNA abnormalities = diabetes, short stature, deafness, migraine or epilepsy. • Parkinson’s or motor neuron disease, may be either due to single-gene disorders or sporadic.

• Alcohol is the most common toxin and damages both the CNS (ataxia, seizures, dementia) and the PNS (neuropathy). Alcoholism may cause vitamin deficiency. • Vegetarians may be susceptible to vitamin B12 deficiency. Nitrous oxide inhalation causes subacute combined degeneration of the cord due to vit. B12 pathway dysfunction. • A travel history may give clues to the underlying diagnosis, such as Lyme disease (facial palsy), neurocysticercosis (brain lesions and epilepsy) or malaria (coma).

• Lead exposure = motor neuropathy. • Manganese exposure = Parkinsonism. Note: the ex. sequence for OSCE purposes was provided by the doctors; you can ignore the ex. attached figures here and consider it only for understanding of the OSCE steps maneuvers

• Facial expression & Speech • & Posture • Involuntary movements • General demeanor

Dependent on the integrity of RAS, which extends from the brainstem to the thalamus, and describes how awake a person is.

Depends on the cerebral cortex, thalamus and their connections describing how aware the person is,

• Meningism (inflammation of the meninges) can lead to increased resistance to passive flexion of the neck (neck stiffness) or the extended leg (Kernig’s sign). Patients may lie with flexed hips to ease their symptoms. • Meningism suggests infection (meningitis) or subarachnoid hemorrhage, but can occur with non-neurological infections (UTI or pneumonia).

Increased resistance to passive flexion of the neck

Flexion of the knees in response to neck flexion

Increased resistance to passive extension of the leg

Bilateral UMN lesion of CNs 9, 10, 11 and 12.

Slow, harsh speech with a contracted, spastic tongue, brisk jaw jerk, emotional lability and difficulty pronouncing consonants

Bilateral LMN lesion of CNs 9, 10, 11 and 12.

• Weakness of the tongue = difficulty with lingual sounds. Slurred speech caused by • Palatal weakness = nasal quality to the speech. articulation problems due to a motor deficit, causes include: Slow and slurred, similar to alcohol intoxication.

Fatiguing speech becoming increasing nasal, and may disappear altogether. Dysarthria, dysphonia, with a low-volume, monotonous voice, words running into each other (festination of speech), and marked stuttering / hesitation.

Usually results from either vocal cord pathology (laryngitis), or damage to the recurrent laryngeal nerve leading to a 'bovine' cough.

Results from damage to Broca’s area, characterised by reduced verbal output with non-fluent speech and errors of grammar and syntax, however, comprehension is intact.

Due to dysfunction in Wernicke’s area. There is poor comprehension, and although speech is fluent, it may be meaningless and contain paraphasias and neologisms. Abnormalities of speech production and/or understanding. May also involve other It is a combination of expressive and receptive difficulties language symptoms, e.g. writing and reading caused by involvement of both areas. unlike dysarthria and dysphonia. Types include: • Dominant parietal lobe lesions affecting the supramarginal gyrus may cause dyslexia (difficulty comprehending written language), dyscalculia (problems with simple addition and subtraction) and dysgraphia (impairment of writing). • Gerstmann’s syndrome is the combination of dysgraphia, dyscalculia, finger agnosia (inability to recognise the fingers) and inability to distinguish left from right. It localizes to the left parietal lobe (angular gyrus).

• The posterior part of the frontal lobe is the precentral gyrus, which controls voluntary movement. • The area anterior to the precentral gyrus is concerned with personality, social behavior, emotions, cognition, expressive language, frontal eye fields and cortical center for micturition.

• It contains the primary auditory cortex, Wernicke’s area and parts of the limbic system. • It also contains the lower fibers of the optic radiation and the area of auditory perception. • The limbic system is important in memory, emotion and smell appreciation.

• The postcentral gyrus is the most ant. part of the parietal lobe and is the destination of sensations. The upper fibers of the optic radiation pass through it. • The dominant hemisphere contains aspects of language function and the non-dominant lobe is concerned with spatial awareness.

Analyses of visual information.

• Unsteadiness on standing with the eyes open = cerebellar disorders. • Instability which only occurs, or is markedly worse, on eye closure (Romberg’s sign) = proprioceptive sensory loss in the feet ().

• Hemiplegic gait = unilateral UMN lesion in the corticospinal tract. • Scissor gait = bilateral UMN lesion, associated with spastic . • Ataxic gait = dysfunction of the cerebellum • (Foot drop) = compression / injury to the common peroneal nerve (LMN). • = slow shuffling steps. • Festinant gait = rapid, short-stepped, hurrying gait due to impairment of postural reflexes. • Waddling gait with bilateral Trendelenburg signs = LL proximal muscle weakness. • Waddling gait with bilateral Trendelenburg signs = LL proximal muscle weakness. • Bizarre gaits = often functional but some diseases, including Huntington’s disease, produce unusual and chaotic gaits.

• Muscle wasting = LMN lesion or disuse in longstanding UMN lesions. • A motor neuron lesion in childhood = a smaller limb/hemiatrophy or lead to limb deformity, (pes cavus). • Muscle disorders usually result in proximal wasting, except in myotonic dystrophy, in which it is distal, often with temporalis wasting. • People in certain occupations (sports players) = physiological muscle hypertrophy. • Pseudohypertrophy = in muscular dystrophy but the muscles are weak.

• Irregular twitches under the skin overlying resting muscles caused by individual motor units firing spontaneously, occurring in LMN diseases, usually in wasted muscles. It is seen, not felt. • Physiological is common, especially in the calves. • is rapid bursts of repetitive motor unit activity often occurring in an eyelid or first dorsal interosseus, and is rarely pathological.

• Sudden shock-like contractions of one or more muscles, may be focal or diffuse and occur singly or repetitively. • Healthy people commonly experience these when falling asleep (hypnic jerks). • They may also occur pathologically in association with epilepsy, diffuse brain damage and some neurodegenerative disorders (prion diseases). • Negative myoclonus () is seen most commonly in liver disease (liver flap).

• Oscillatory movement about a joint or a group of joints resulting from alternating contraction and relaxation of muscles. • Classified according to their frequency, amplitude, position, and body part affected as shown in the pictures attached.

• Dystonia = sustained muscle contractions, leading to twisting, repetitive movements and sometimes tremor. It may be focal (as in torticollis), segmental (affecting two or more adjacent body parts) or generalized. • Chorea = brief, random, purposeless movements which may affect various body parts, but commonly the arms. • = slower, writhing movement, more similar to dystonia than chorea. • Ballism = violent flinging movements sometimes affecting only one side of the body (). • Tics = repetitive, stereotyped movements which can be briefly suppressed by the patient.

• LMN lesions, usually ass. with muscle wasting, weakness and hyporeflexia. • Found in cerebellar disease or signal the early phases of cerebral or spinal shock.

• Velocity-dependent resistance to passive movement: it is detected with quick movements • In mild forms it is detected as a ‘catch’ at the beginning or end of passive movement. • In severe cases it limits the range of movement and may be ass. with contracture. • In the upper limbs it may be more obvious on attempted extension; in the legs it is more evident on flexion.

• Sustained resistance throughout the range of movement; detected when the limb is moved slowly. • In parkinsonism, this is classically described as ‘lead pipe rigidity’. • In the presence of a parkinsonian tremor there may be a regular interruption to the movement, giving it a jerky feel (cog wheeling).

• Rhythmic series of contractions evoked by sudden stretch of the muscle and tendon. • Unsustained (<6 beats) clonus may be physiological. When sustained, it indicates UMN damage,

• Refers to the inability of muscles to relax normally, found in a myotonic dystrophy. • Patients may notice difficulty in letting go of things with their hands, or a stiff gait. It is an early feature of UMN lesions and it has good sensitivity and specificity

• UMN lesions = weakness of a relatively large group of muscles. • LMN damage = of an individual and specific muscle. • Myopathies tend to cause proximal weakness and neuropathies often give rise to more distal patterns, while mononeuropathies or radiculopathies lead to discrete focal weakness (foot drop). • Very few diseases cause power to fluctuate; the fatigable weakness of myasthenia is an exception. • Functional weakness = wildly fluctuating or sudden ‘giveway’ weakness tested using Hoover’s sign.

A sign of UMN damage.

• Due to LMN lesions. • In healthy elderly people, the ankle jerks may be reduced or lost, and in the Holmes–Adie syndrome, myotonic pupils are associated with loss of some reflexes. • Isolated loss of a reflex suggests a mononeuropathy or radiculopathy

• Caused by combined spinal cord and root pathology localizing to a specific spinal level. • It is most common at the C5/6 level. When elicited, the biceps reflex is absent or reduced but finger flexion occurs. • It is most commonly seen in cervical spondylotic myeloradiculopathy.

In cerebellar disease, the reflexes may be pendular due to slow muscle contraction and relaxation, however, they are not sensitive or specific cerebellar signs.

Positive Hoffmann’s and finger jerks suggest . It can occur in healthy individuals, and are not useful signs in isolation.

• They are lost in UMN lesions but are also affected by LMN damage affecting T8–12. • They are usually absent in the obese, the elderly or after abdominal surgery.

It is rarely elicited and typically is lost in spinal cord or root lesions.

• Babinski sign = activation of the extensor hallucis longus tendon coincides with contraction of other leg flexor muscles. This is a sign of UMN lesion. • Fanning of the toes is normal and not pathological.

• Normal in neonates and young infants but disappear as the NS matures. • They have little localizing value and in isolation are of little significance, but in combination suggest diffuse or frontal cerebral damage. The glabellar tap is an unreliable sign of Parkinson’s disease • Their return after early childhood is often ass. with brain damage or degeneration: unilateral grasp and palmomental reflexes may occur with contralateral frontal lobe pathology.

• In disorders predominantly affecting midline cerebellar structures, may be the only finding. • In the most severe cases, the patient cannot sit unsupported. • Tandem gait (heel–toe walking) may be impaired in less severe cases. • Tandem gait (heel–toe walking) may be impaired in less severe cases.

• Weakness may produce false-positive finger-to-nose test, so demonstrate that power is normal first. • or past-pointing = tendency to fall short or overshoot the examiner’s finger. • Intention tremor = in more severe cases there may be a tremor of the finger as it approaches the target finger and the patient’s own nose. • = the movement may be slow, disjointed and clumsy

Dysdiadochokinesis = impairment of rapid alternating movements (slowness, disorganisation and irregularity of movement).

• The normal response is to return to the original position • Abnormalities occurs when the displaced outstretched arm may fly up past the original position.

• It is abnormal if the heel wavers away from the line of the shin. • Weakness may produce false-positive heel-to-shin test, so demonstrate that power is normal first.

Nystagmus is a vision condition in which the eyes make repetitive, uncontrolled movements. Both Dysarthria and nystagmus also occur with cerebellar disease.

In disorders predominantly affecting midline cerebellar structures (tumors of the vermis and alcoholic cerebellar damage) the tests described may be normal and truncal ataxia (ataxic gait) may be the only finding.

• It is difficulty or inability to perform a task, despite no impairment of the necessary individual functions. • It is a sign of higher cortical dysfunction, usually localising to the non-dominant frontal or parietal lobes.

Difficulty drawing a figure. It is a feature of parietal disturbance.

Ass. with spatial disorientation and neglect. Usually due to non-dominant hemisphere parietal lesions.

• Conveyed in large, myelinated fast-conducting fibres in the peripheral nerves and in the posterior columns of the spinal cord • The posterior column remains ipsilateral from the point of entry up to the medulla.

• Carried by small, slow-conducting fibres of the peripheral nerves and the spinothalamic tract of the spinal cord. • Most pain and temperature fibres cross to the contralateral spinothalamic tract within one or two segments of entry to the spinal cord.

All sensory fibres relay in the thalamus before sending information to the sensory cortex in the parietal lobe

• Diseases affecting peripheral nerves, generally result in peripheral neuropathies or polyneuropathies. • Peripheral neuropathies tend to affect the lower limbs first (length-dependent). Symptoms affecting the upper limbs first suggest a demyelinating rather than axonal neuropathy or a disease process in the spinal cord.

• Guillain–Barré syndrome = vibration and joint position sense may be disproportionately affected. • Patients may report staggering when they close their eyes during hair washing or in the dark (Romberg’s sign). • When joint position sense is affected in the arms, pseudoathetosis may be demonstrated by asking the patient • Patients may report staggering when they close their eyes during hair washing or in the dark (Romberg’s sign). • When joint position sense is affected in the arms, pseudoathetosis may be demonstrated by asking the patient to close their eyes and hold their hands outstretched; the fingers/arms will make involuntary, slow, wandering movements, mimicking athetosis.

Reduced pinprick and temperature sensation; there may also be autonomic involvement. The most common causes worldwide are DM and HIV infection.

• Traumatic and compressive spinal cord lesions cause loss or impairment of sensation in a dermatomal distribution below the level of the lesion. • A zone of hyperaesthesia may be found immediately above the level of sensory loss. • Anterior spinal artery syndrome = Results in loss of spinothalamic sensation and motor function, with sparing of dorsal column sensation. • A similar dissociated pattern of pain and temperature loss and sparing of dorsal column sensation occurs in syringomyelia. • Brown-Séquard syndrome = When one-half of the spinal cord is damaged. This is characterized by ipsilateral motor weakness and loss of vibration and joint position sense, with contralateral loss of pain and temperature.

• Thalamic lesions may cause a patchy sensory impairment on the opposite side with unpleasant, poorly localised pain, often of a burning quality. • Cortical parietal lobe lesions typically cause sensory inattention but may also affect joint position sense, two-point discrimination, stereognosis (tactile recognition) and localisation of point touch. • Lower brainstem lesions may cause ipsilateral numbness on one side of the face (V nerve nucleus) and contralateral body numbness (spinothalamic tract).

• Carpal tunnel syndrome is the most common entrapment neuropathy and occurs commonly during pregnancy. • It may be compressed as it passes between the flexor retinaculum and the carpal bones at the wrist, initially producing sensory symptoms.

Most often affected at the elbow by external compression, or by injury, as in elbow dislocation/fracture. Compression usually occurs as the nerve passes through the condylar groove behind the medial epicondyle or as it passes through the cubital tunnel.

May be compressed as it runs through the axilla, in the spiral groove of the humerus (Saturday night palsy), or may be injured in fractures of the humerus. It typically causes wrist drop.

It may be damaged in fibular head fractures, or compressed particularly in thin, immobile patients, or as a result of repetitive kneeling or squatting. This typically presents with foot drop.

This purely sensory nerve may be compressed as it passes under the inguinal ligament, producing paraesthesiae in the lateral thigh (meralgia paraesthetica). • Bipolar cells in the olfactory bulb form olfactory filaments with small receptors projecting through the cribriform plate high in the nasal cavity. • These cells synapse with second-order neurons, which project centrally via the olfactory tract to the medial temporal lobe and amygdala.

It is purely sensory conveying the sense of smell.

• Hyposmia-anosmia = (reduction or loss of the sense of smell) may result from URTI, sinus disease, damage to the olfactory filaments after head injury or infection, local compression (olfactory groove meningioma) or invasion by basal skull. • Disturbance of smell= very early in Parkinson’s and Alzheimer’s diseases. • Patients often note hypogeusia/ageusia (altered taste) with anosmia too. • Parosmia is the perception of pleasant odors as unpleasant; it may occur with head trauma or sinus infection or be an adverse effect of drugs. • Olfactory hallucinations may occur in Alzheimer’s disease and focal epilepsies.

• The cell bodies of the sensory fibers are in the trigeminal (Gasserian) ganglion, which lies in a cavity (Meckel’s cave) in the petrous temporal dura. • From the trigeminal ganglion, the V nerve passes to the pons. From here, pain and temperature pathways descend to the C2 segment of the spinal cord, so ipsilateral facial numbness may occur with cervical cord lesions. • It has three major branches: Ophthalmic (V1), Maxillary (V2) and Mandibular (V3).

• Sensation to the face, mouth and part of the dura. • Common sensation from the anterior 2/3 of the tongue. • Motor supply to the muscles of the jaw involved in mastication.

• Sensory symptoms present as facial numbness and pain. • Unilateral loss of sensation in one or more branches of the V nerve may result from direct injury in association with facial fractures (particularly V2), local invasion by cancer or Sjögren’s syndrome. • Lesions in the cavernous sinus = loss of the corneal reflex and V1 or V2 cutaneous sensory loss. • Trigeminal neuralgia = severe, lancinating pain, typically in the distribution of V2 or V3. • Reactivation of herpes varicella zoster virus = affect V1 or a thoracic dermatome. In herpes zoster ophthalmicus (affecting V1) there is a risk of sight-threatening complications. • Hutchinson’s sign = vesicles on the side or tip of the nose, may be present. • Significant weakness of the muscles of mastication is unusual but may occur in myasthenia gravis, with fatigable chewing. • Brisk jaw jerk = bilateral UMN V lesions above the level of pons.

• From its motor nucleus in the lower pons, fibers of the VII nerve pass back to loop around the VI nerve nucleus before emerging from the lateral pontomedullary junction in close association with the VIII nerve; together they enter the internal acoustic meatus. • At the lateral end of the meatus, the VII nerve continues in the facial canal within the temporal bone, exiting the skull via the stylomastoid foramen. • Passing through the parotid gland, it gives off its terminal branches. In its course in the facial canal it gives off branches to the stapedius muscle and its parasympathetic fibers, as well as being joined by the taste fibers of the chorda tympani. • Sends motor fibers to the muscles of facial expression (frontalis, orbicularis oculi, buccinators, orbicularis oris and platysma). • Send parasympathetic fibers to the lacrimal, submandibular and sublingual salivary glands. • Receives taste sensation from the anterior 2/3 of the tongue.

• Unilateral LMN VII nerve lesion (lesions distal to the stylomastoid foramen / damage of the facial nerve in the facial canal) = weakness of both upper and lower facial muscles. • Ramsay Hunt syndrome = herpes zoster infection of the geniculate (facial) ganglion. This produces a severe LMN facial palsy, ipsilateral loss of taste and buccal ulceration, and a painful vesicular eruption in the external auditory meatus. • Other causes of a LMN VII lesion = cerebellopontine angle tumors (including acoustic neuroma), trauma and parotid tumors.

• Unilateral VII nerve UMN lesions = weakness is marked in the lower facial muscles with relative sparing of the upper face. The nasolabial fold may be flattened, and the corner of the mouth drooped, but eye closure is usually preserved. • Hemifacial = synchronized twitching of the ipsilateral eye and mouth. • Bilateral facial palsies are less common, but occasionally occur, as in Guillain–Barré syndrome, sarcoidosis, or infection such as Lyme disease, HIV or leprosy. • Facial weakness, especially with respect to eye closure = in some congenital myopathies (facioscapulohumeral or myotonic dystrophies). • Parkinson’s disease = loss of spontaneous facial movements, including a slowed blink rate, and involuntary facial movements (levodopa-induced ) may complicate advanced disease.

• Both nerves arise as several roots from the lateral medulla and leave the skull together via the jugular foramen. • The IX nerve passes down and forwards to supply the stylopharyngeus muscle, the mucosa of the pharynx, the tonsils and the posterior one-third of the tongue, and sends parasympathetic fibers to the parotid gland. • The X nerve courses down in the carotid sheath into the thorax, giving off several branches, including pharyngeal and recurrent laryngeal branches, which provide motor supply to the pharyngeal, soft palate and laryngeal muscles. • The main nuclei of these nerves in the medulla are the nucleus ambiguous (motor), the dorsal motor vagal nucleus (parasympathetic) and the solitary nucleus

• Both contain sensory, motor and autonomic components • 9th nerve mainly carries sensation from the pharynx, tonsils, and taste from the post.1/3 of the tongue. It also supplies the carotid chemoreceptors. • 10th nerve carries important sensory information but also innervates upper pharyngeal and laryngeal muscles. In the thorax and abdomen, it receives sensory fibers from the lungs and carries parasym. fibers to the lungs, heart and abdominal viscera.

• Isolated unilateral IX nerve lesions are rare. Unilateral X nerve damage = ipsilateral reduced elevation of the soft palate, causing deviation of the uvula (away from the side of the lesion). • Unilateral lesions of IX and X are most caused by strokes, skull-base fractures or tumors. • Damage to the recurrent laryngeal branch of the X nerve due to lung cancer, thyroid surgery, mediastinal tumors and aortic arch aneurysms = dysphonia and a ‘bovine’ cough. • Bilateral X nerve lesions = dysphagia and dysarthria that may be due to lesions at the UMN level (pseudobulbar palsy) or LMN level (bulbar palsy). Less severe cases can result in nasal regurgitation of fluids and nasal air escape when the cheeks are puffed out. • Always consider myasthenia gravis in patients with symptoms of bulbar dysfunction, even if the examination seems normal. • The accessory nerve has two components; 1- A cranial part; closely related to the vagus 2- A spinal part (C1-5); which provides fibers to the upper trapezius (shoulder shrugging) and SCM muscles (head turning) • The spinal nuclei arise from the anterior horn cells of C1–5. Fibers emerge from the spinal cord, ascend through the foramen magnum and exit via the jugular foramen, passing posteriorly.

• Wasting of the upper fibers of trapezius = displacement (winging) of upper border of the scapula away from the spine, and the lower border is displaced towards it. • Wasting and weakness of the SCM = dystrophia myotonica. • Weakness of neck muscles (Head drop) = myasthenia, motor neuron disease, and some myopathies. • Dystonic head postures causing antecollis (neck flexed), retrocollis (neck extended) or torticollis (neck twisted to one side) are not associated with weakness.

• The nucleus lies in the dorsal medulla beneath the floor of the fourth ventricle. • The nerve emerges anteriorly and exits the skull in the hypoglossal canal, passing to the root of the tongue supplying its muscles.

• Unilateral LMN lesions = wasting of the tongue on the affected side and deviation to that side on protrusion. • Bilateral LMN lesion results in global wasting, and involuntary twitching (Fasciculation). • Bilateral UMN lesions = Spastic tongue and the patient has difficulty flicking the tongue from side to side. • Tremor of the resting or protruded tongue = in Parkinson’s disease, although jaw tremor is more common. • Other orolingual dyskinesias (involuntary movements of the mouth and tongue) are often drug-induced and include tardive dyskinesias due to neuroleptics.

Bulbar palsy refers to impairment of function of the cranial nerves IX, X, XI and XII, which occurs due to a lower motor neuron lesion either at nuclear or fascicular level in the medulla oblongata or from lesions of the lower cranial nerves outside the brainstem.

In contrast, pseudobulbar palsy describes impairment of function of cranial nerves IX-XII due to lesions of the corticobulbar tracts in the mid-pons. For dysfunction to occur, lesions must be bilateral as these cranial nerve nuclei receive bilateral innervation. • The eye is protected by the eyelid, which affords protection and maintains the tear film. • Upper lid elevation = levator palpebrae superioris (innervated by the 3rd CN), and Müller’s muscle, (innervated by the sympathetic ANS). • Eyelid closure = orbicularis oculi muscle (innervated by 7th CN). • The orbit also contains the 6 extraocular muscles. In addition, the orbit houses the lacrimal gland, blood vessels, autonomic nerve fibers and CN 2, 3, 4, and 6. The contents are cushioned by orbital fat, which is enclosed anteriorly by the orbital septum and the eyelids. • The conjunctiva is a thin mucous membrane lining the posterior aspects of the eyelids. It is reflected at the superior and inferior fornices on to the surface of the globe. It is coated in a tear film that protects and nourishes the ocular surface. • The cranial nerves originate in the midbrain and pons and then pass through the cavernous sinus.

The eyeball has 3 layers. From outside in: • Outer fibrous layer = this includes the sclera and the clear cornea. The cornea accounts for 2/3 of the refractive power of the eye, focusing incident light on to the retina. • Middle vascular layer (uveal tract) = ant. this consists of the ciliary body and the iris, and post. the choroid. • Inner neurosensory layer (retina) = converting light to neurological signals.

The 6 extraocular muscles (superior rectus, medial rectus, lateral rectus, inferior rectus muscles, inferior oblique, and superior oblique muscle) are responsible for eye movements. All are innervated by CN 3, except superior oblique by CN 4 and lateral rectus by CN 6.

The visual pathway consists of the retina, optic nerve, optic chiasm, optic tracts, lateral geniculate bodies, optic radiations and visual cortex. Deficits in the visual pathway lead to specific field defects as attached.

• Afferent pathway = involves the optic nerve, chiasm (where some fibers decussate) and the optic tract, bypassing the lateral geniculate nucleus, synapsing in the pretectal nucleus of the midbrain then terminate in the III nerve (Edinger–Westphal) nucleus and then pass along the inferior division of the oculomotor nerve to synapse in the ciliary ganglion. • Efferent pathway = involves the inferior division of the III nerve, passing through the ciliary ganglion in the orbit to the constrictor muscle of the iris via short ciliary nerves, resulting in constriction.

• The sympathetic pathway originates in the hypothalamus, passing down to the ciliospinal center of Budge at the level of T1. • Fibers then pass to, and synapse in, the superior cervical ganglion before joining the surface of the internal carotid artery and passing to the pupil along the nasociliary and the long ciliary nerves. • If the degree of anisocoria is greater in brighter lighting, then it is the larger (dilated) pupil that is abnormal. • If it is more pronounced in dim lighting, the smaller (constricted) pupil is the abnormal. • An equal degree of anisocoria in all levels of lighting indicates physiological anisocoria.

• It is an important clinical sign that occurs when disease of the retina or optic nerve reduces the response of the eye to a light stimulus. • In normal patients, this results in symmetrical constriction of both pupils. • In RAPD, light in the affected eye causes weaker constriction (apparent dilatation) compared to light shone in the normal eye.

• It results from dysfunction of sympathetic nerve supply to the eye, which originates in the hypothalamus and emerges in the root of the neck before innervating the pupil. Damage at any point in this pathway will result in Horner’s syndrome. • On examination, there is a constricted pupil (loss of sympathetic dilator tone) and a partial ptosis resulting from denervation of Müller’s muscle in the upper eyelid. There may also be anhydrosis (loss of sweating) on the affected side. • Thus, Horner syndrome is triad of anhydrosis, partial ptosis and miosis. • Diagnosis may be confirmed by cocaine eye drops, which will cause pupil dilatation in the unaffected pupil but no dilatation on the affected side. • Causes of Horner’s syndrome include demyelination, neck trauma/surgery, apical lung tumor (Pancoast tumour) and carotid artery dissection.

• This is a benign, mid-dilated pupil that responds poorly to both light and accommodation. With time, however, the affected pupil can become constricted. • It is thought to result from parasympathetic pathway dysfunction in the orbit. • It typically affects young women. • When associated with diminished Achilles tendon reflexes, it is referred to as Holmes–Adie syndrome.

• Bilateral small, irregular pupils that reacts to accommodation (constrict on a near object) but not light (do not constrict when exposed to bright light). • This is classically the result of neurosyphilis. There are other causes of light-near dissociation, however, including DM, severe optic nerve disease and midbrain lesions.

• Starts from retina > optic nerve > the optic chiasm > optic tract > optic radiation > occipital cortex. • The nasal fibers of the optic nerve are responsible for the temporal visual field and vice versa.

• It is purely sensory; responsible for transmitting visual sensory information from the retina to the brain • It is the afferent part of the pupillary reflex and is unable to regenerate.

• Before the Optic chiasm = The visual field loss is seen on the same (ipsilateral) side as the lesion. • After the optic chiasm = The visual loss is seen on the opposite (contralateral) side of the lesion; because the optic nerves have already crossed over at the optic chiasm.

• It has both motor and parasympathetic function. • It innervates the superior, medial, and inferior recti, the inferior oblique and levator palpebrae superioris muscles. • It innervates the superior, medial, and inferior recti, the inferior oblique and levator palpebrae superioris muscles. • Its course is related to posterior communicating artery and cavernous sinus • Function: 1- It Moves the globe upwards, downwards, and medially 2- It elevates the upper lid 3- Pupillary reflex (constrict pupil)

• Unilateral ptosis that is often complete • Large pupil • The eye is looking inferolaterally

• Supplies the superior oblique muscle • Function: downward movement of the globe when the eye is adducted (inferiomedially).

• Supplies the lateral rectus muscle and abducts the eye (lateral gaze). • Has along course around the brainstem before it pierces the dura to enter the cavernous sinus. • In direct relation to the internal carotid artery before it passes through the superior orbital fissure to the lateral rectus muscle.

People with normal hearing can repeat words whispered at 60 cm.

• Normally, the noise is heard in the middle, or equally in both ears. • In conductive hearing loss the sound is heard louder in the affected ear. • In unilateral sensorineural hearing loss, it is heard louder in the unaffected ear • If there is symmetrical hearing loss it will be heard in the middle

• Normally, air conduction (AC) is better than bone conduction (BC) is recorded as ‘Rinne-positive’. • In conductive hearing loss, BC is better than AC, 'Rinne-negative'. • In sensorineural hearing loss, Rinne’s test will be positive. • A false-negative Rinne’s test may occur if there is profound hearing loss on one side. This is due to sound being conducted through the bone of the skull to the other ‘good’ ear.