What you need to know for the exam

Neurological Diagnosis1) Topographically localize a lesion to various levels of the nervous system based on signs and symptoms.a. Peripheral nervous system: muscle, NMJ, nerve, plexus, root, cell body. i. Motor loss is lower motor neuron type: flaccid weakness, atrophy, hypotonia, +/- hyporeflexia, +/- fibrillation (nerve) or fasciculations (cell bodycan be seen)ii. Muscle disease (myopathy): Polymyositis, muscular dystrophy1. Motor only, usually proximal, usually symmetric, may see atrophy and reflex loss if severeiii. NMJ disease: myasthenia gravis, botulism1. Motor only, proximal AND distal AND bulbar/eye, fatigable weakness, NORMAL reflexesiv. Peripheral nerve disease (neuropathy): single nerve lesion or polyneuropathy1. Single nerve lesion: carpal tunnel syndromea. Motor, sensory (all modalities) and reflex loss in distribution of SPECIFIC NERVE2. Polyneuropathy: diabetic polyneuropathya. Motor +/- sensory +/- autonomicb. Usually affects legs before hands, more prominent distally, symmetricc. Further characterized as axonal or demyelinatingd. STOCKING GLOVE PATTERNv. Plexus (plexopathy): Mixed nerve and root injury1. Lower motor neuron weakness, sensory loss, reflex loss2. Brachial (formed from rami of C5-T1): traumaa. Waiters tip positionb. May see Horners if C8 root involved3. Lumbosacral (formed from rami of T12-S4): neoplasma. May see bowel/bladder dysfunction if pudendal nerve involvedvi. Nerve root (radiculopathy): disc herniation, especially between levels C5-T1 and L4-S11. Segmental pain, sensory, motor (LMN), and reflex loss2. Pain and sensory loss referable to distribution of affected POSTERIOR spinal root (DERMATOME)3. Weakness and atrophy in distribution of affected ANTERIOR spinal root (MYOTOME)vii. Nerve cell body: Anterior horn disease (LMN disease): spinal muscular atrophy, polio1. Motor only2. Diffuse or single limb proximal and distal LMN weakness and reflex loss3. Involvement of paraspinal musclesviii. Nerve cell body: Dorsal root ganglion (sensory ganglionopathy): paraneoplastic, Sjogrens, idiopathic1. Sensory loss to all modalities (esp proprioception)2. Usually proximal and distal +/- face/trunk, often asymmetric3. Diffuse reflex loss early MSPb. Central Nervous System: spinal cordi. Spinal cord (myelopathy): spondylosis, MS, trauma1. UPPER MOTOR NEURON dysfunction BELOW level of lesion2. LOWER MOTOR NEURON weakness AT level of lesion (if grey matter involved)3. Sensory level or dissociated sensory loss4. neurogenic bladder: retention, hesitancy, incontinenceii. Brainstem: strokes, clots, various other lesions1. Cranial nerve deficits, impaired consciousness (if RAS involved), impaired respiration2. Crossed or bilateral motor or sensory deficitsa. Left facial and right body sensory loss with left lateral medullary lesionb. Quadriplegia with pontine lesioniii. Cerebellum: 1. Signs during movement or sustained posture: Incoordination/ataxia, nystagmus, tremor2. No weakness, sensory loss, reflex changeiv. Thalamus: 1. Dense hemisensory loss and/or pain, impaired consciousness, memory disturbance, hemiataxia, aphasia or neglect, 2. Dysfunction most commonly due to strokeblood supply is almost entirely from vertebrobasilar systemv. Basal Ganglia: Parkinsons disease, Huntingtons chorea1. Signs at rest: muscle rigidity (co-contraction of agonist and antagonist), Involuntary movements (chrorea- jerk, athetosis- writhing, dystonia- contorting, tremor, ridigity)2. Slow movement (bradykinesia)vi. Cerebral Cortexdiffuse encephalopy1. Hemipareiss/spasticity/hyperreflexiaUMN dysfunction2. Hemisensory deficits: pattern differs from thalamic. Integrative sensory disturbance or reduction in single modality3. Hemianopia, aphasia or neglect, dementia, seizuresvii. Subarachnoid space/meninges: not actually part of CNS but can impinge on it. Meninges are pain sensitive structures and cranial nerves run through them1. Headache, neck stiffness, CN deficits, altered level of consciousness2. Meningitis, subarachnoid hemorrhage

Given signs and symptoms, topographically localize a lesion to the various levels of the motor system.a. Corticospinal tracts: voluntary movement, reflex archi. Upper motor defect: contralateral long tract signs: 1. Hyperreflexia, spasticity, clasp-knife reaction, spreading of stretch reflexes (Hoffman sign, crossed adductor reflex), pain sensing reflexes hyperactive (Babinski sign, triple flexion response), clonus2. Often associated with sensory defectii. Lesions of reflex arc: decreased muscle tone and hyporeflexia1. Lower motor neuron/axon lesion: weakness/paralysis, fasciculation (fibrillation on EMG) and muscle atrophy2. Sensory neuron/axons: sensory deficit, sensory ataxia, but NO weakness or fasciculation3. Examples: motor/sensory neuropathy, nerve entrapment, dorsal root ganglion lesion, spinal root compression, spinal cord mass/stroke/tumor/inflammationb. Basal ganglia: wanted movements, suppress unwanted movements, initiate and maintain movementsi. D1: direct (promotes movement), D2: indirect (inhibits movement)ii. Substantia nigra lesion (Parkinsons) stops D1 but especially D2: bradykinesia, rigidity, tremor at rest, decrement on repetitive/alternating movements, often dystonia, NO weaknessiii. Subthalamic lesion (ballism and hemiballism) stops D2 but doesnt touch D1: contralateral violent chorea (dancing like movements)iv. Striatum lesion (Huntingtons) stops D2 early=chorea, stops both later=parkinsonism (bradykinesia and rigidity)c. Thalamus: integration of input from input form cerebellum and basal gangliai. Pure thalamic lesions usually result in sensory symptoms with occasional tremor. No weakness, spasticity or increased reflexesii. RARELY see pure thalamic lesionusually involves internal capsule= Corticospinal tract lesion (UMN)d. Spinal cord:i. Lower motor neuron symptoms at the level of the cord lesion1. Cauda equine lesion causes only lower motor neuron lesionii. Upper motor neuron symptoms below the cord lesioniii. Sensory deficits:1. Ipsilateral----Dorsal column/medial lemniscal system: light touch, vibration sensation and joint position sensation2. Contralateral----Lateral spinothalamic tract: crude touch, pain and temp sensationiv. Hemisection of thoracic cord (T4)= Brown-Sequard syndrome1. Ipsilateral weakness and light touch, vibration sensation and joint position sensation loss2. Contralateral crude touch, pain and temp sensation losse. Brainstem: cranial nerves, posture, alertnessi. Lower motor neuron symptoms of cranial nerves at level of lesionii. Upper motor neuron symptoms of cranial nerves below level of lesioniii. Postural control1. Vestibular nuclei/vestibulospinal tract: postural control with head movement2. Reticular nuclei/reticulospinal tract: somatosensory control of posture3. Superior colliculi/tectospinal tract: visual control of postureiv. Other things in brainstem: Corticospinal tract crosses in medulla, reticular formation (alertness), sensory tracts, cerebellar crossing connectionsv. Facial Nerve Nucleus: upper part of face controlled by bilateral projections from cortex, lower face is only controlled by contralateral projections1. Cortical lesions on one side: weakens contralateral lower face, spares contralateral upper face, weakens contralateral limbs2. Brainstem lesions on one side: weakens ipsilateral upper/lower face, weakens contralateral limbsf. Cerebellum: correction of overshoot (ataxia)i. Lateral cerebellum: ipsilateral limb ataxia/dysmetria, limb tremorii. Medial cerebellum: ataxic gait (wide), trunk ataxia (titubation)iii. Hypotonia, does not affect reflexes

Localizing Lesions in the Visual Pathways1) Given pupillary and eye movement findings, be able to localize a lesion to individual cranial nerves, frontal eye fields, MLF, or PPRF (including whether it is ipsilateral or contralateral).a. If eyes are generally conjugate (move together) = supranuclear lesion. Disconjugate= inter or subnuclear lesionb. Pupils nerve (or tract) lesioni. Marcus Gunn Pupil (Decreased input from optic nerve)1. Afferent papillary defect poor constriction of both eyes if light in involved eye2. NEVER see anisocoria (different size pupils)ii. Horner Syndrome ptosis, miosis, anhydrosisiii. If you have pupillary signs and they are still reactive to light, its microvascular disease (DM). Pupil blown= trauma, tumor, aneurysm, herniation1. Since the parasympathetic fibers are on the outside of the nerve so they are more likely to be affected by ischemia. Trauma= more likely to affect center of nervec. Cranial nerve 3medial rectus, superior rectus, inferior rectus, inferior obliquei. Ipsilateral eye would be looking outwards and down with ptosisii. Sympathetic chain messed up= ptosis, miosisiii. Nuclear lesion= bilateral findings with symmetric droopy lids (rare)iv. Fasicular lesion= ipsilateral CN3 deficits and midbrain findingsv. Peripheral= pupillary sparing, which indicates microvascular disease. Trauma= pupillary involvingd. Cranial nerve 4superior obliquei. Hypertropia worse in contralateral gazeii. Head tilts away from lesioniii. Usually peripheral. iv. Bilateral= trauma. Unilateral= congenital or microvascular diseasee. Cranial nerve 6lateral rectusi. Ipsilateral inability to look temporally. Other eye would be looking in and affected eye would be straight aheadii. Ipsilateral facial paresis if nucleus affected, contralateral hemiparesis if w/wo facial paresis and brainstem findings if fascicle affected. If it is peripheral= isolated CN 6 lesionf. Frontal eye fields: right frontal eye field is responsible for signal of left frontal saccadei. Lesion causes contralateral eye to lose ability to saccade (jump quickly to horizontal object)g. MLF-- How CN6 tells contralateral CN 3 to do something. i. Internuclear opthalmoplegia. Abduction is fine but adduct doesnt work. Eyes cant communicate so when you look in the same direction as the lesion, its fine (abduction), but when you look the opposite direction, affected eye cant follow the other eye.ii. You can still converge (go cross eyed) iii. Unilateral= vascular. Bilateral= tumor, hemorrhage, demyelinationh. One and a half syndrome: MLF + CN 6 lesioni. Loss of aDduction of ipsilateral eye and gaze paralysisii. Only motion your eyes are capable of is contralateral ADductioni. PPRF-- controls conjugate horizontal gazei. Unilateral: loss of horizontal saccades directed toward side of lesion, contralateral gaze deviation, gaze evoked lateral nystagmus on looking away from side of lesionii. Bilateral: horizontal gaze palsy and slowing of vertical saccades

2) Visual field deficits associated with lesions of the optic nerve, chiasm, tract, radiations, and striate cortex.a. Optical eye, retina, optic nervediffuse loss of vision of ipsilateral eye (unilateral, respects horizontal only if nerve fiber within the eye)b. Optic chiasmbitemporal heteronymous vision loss (lateral half of each eye)c. Optic tractBilateral homonymous loss of ipsilateral side of eyerespecting verticald. Striate cortexi. Temporal lobeRespect to vertical, superior halfii. Parietal lobeRespect to vertical, lower halfiii. Occipital lobeRespect to vertical, both halves with macular sparing. If you have a lesion respecting vertical and horizontal, must be in occipital lobe.

Localizing Lesions in the Somatosensory System/Pain and Analgesics1) Typical sensory patterns of lesions of the peripheral nerve, spinal cord, brainstem, thalamus, and cortex.a. Peripheral nerve: small fibers= sharp pain, large myelinated fibers= dull aching paini. Reflexes are decreased or absentii. Distal polyneuropathy: stocking glove pattern, longest fibers affected first. Variable combo of negative (numbness) and positive (pain/paresthesias) symptoms. DM, alcohol, toxins, HIViii. Mononeuropathy: single or multiple nerves. Anatomy key. Pressure, trauma, vasculitis. Carpal tunnel syndrome. Pain worse at night due to loss of distraction.iv. Plexopathy: brachial or lumbarv. Radiculopathy: dermatomal or segmental organization/radiation. Disc disease or shinglesb. Spinal cordi. Dorsal column-medial lemniscal system1. Uncrossed in cord, synapse and decussation at medullary level, projects to thalamus2. Test with vibration and proprioceptionii. Spinothalamic system1. Crossed in cord, anterolateral portion of cord. Projects to thalamus, reticular substance, tectum2. Sharp (pain) and temperatureiii. Seek sensory level to localize lesioniv. Look for associated findings like UMN, LMN, bladder dysfunctionv. Syringomyeliacentral cord lesion (tube in spinal cord, tube= syringe) cape distribution of pain/temp loss. Sometimes segmental atrophyvi. Brown Sequard syndrometrauma/demyelinating lesions. Hemisection= loss of all sensation at lesion, Impaired proprioception and vibration ipsilaterally, impaired pain and temp contralaterallyc. Thalamusi. Negative signs include all modalities. Full hemisensory deficit common.d. Cortexi. Positive symptoms may be generated by seizures. Cortical organization reflects the use of function. Plasticity exists for cortical organization (not global loss, more of an inability to process)ii. Test complicated sensory tasks (2 point discrimination, graphesthesia (what is in your hand?))iii. S1= postcentral gyrus. Somatotopic organization with contralateral inputiv. S2= bilateral input, function is less known

Neuromuscular Disease1) Characteristic pattern of weakness, sensory loss, and reflexes associated with disease of muscle, axon, myelin, neuromuscular junction, and motor neuron cell body.a. Muscle (myopathy): i. Constant proximal weakness= Difficulty standing, climbing stairs. Gowers maneuver= how kids get off the ground (have to turn over on stomach, use hands to push on legs to get up). ii. Legs more effected than armssymmetric. iii. Normal/increased muscle size early but can eventually atrophy. iv. Normal sensory exam and tendon reflexes. b. Axon: i. Constant distal weakness, muscle atrophy (more distally), legs more than armsii. Distal (stocking glove) sensory lossiii. Reduced distal reflexes.iv. Can be symmetric or asymmetricc. Myelin: i. Constant proximal and distal weaknessconstantii. Normal muscle size, mild distal sensory loss, diffusely reduced tendon reflexesd. NMJ: i. Proximal, distal, and bulbar weakness. Sometimes fatigue. ii. Normal sensory and tendon reflexes. iii. Rapid improvement with treatment, variable throughout the daye. Motor neuron cell body: i. Selective modality loss (either motor or sensory)ii. Proximal and distal, cranial, not length dependent. iii. Motor weakness with atrophy and fasciculationsiv. No improvement with treatment