CNS system Flashcards

Question

What is the pathophysiology of nystagmus The types, causes and features?

Answer 1

Disorders in which excessive amount of CSF accumulates within cerebral ventricles or subarachnoid spaces which are dilated

Answer 2

 Obstructive (non-communicating) hydrocephalus * Obstruction in CSF circulation leading to accumulation of CSF in cerebral ventricles  Communicating hydrocephalus * Impaired absorption of CSF leading to accumulation of CSF in cerebral ventricles

Answer 3

* Increased CSF production: choroid plexus papilloma * Decreased CSF absorption: bacterial meningitis (leads to arachnoid granulation adhesions) * Obstruction of CSF flow: aqueductal stenosis, tumor

Answer 4

Interruption of sympathetic nerve pathway to the eye and face  Partial ptosis: Paralysis of Muller’s (superior tarsal) muscle which is innervated by sympathetic pathway and levator palpebrae superioris being unaffected  Miotic reactive pupil: Anisocoria with abnormal small pupil in the dark and associated dilation lag  Enophthalmos: NOT a true enophthalmos and occurs as an illusion due to ptosis and updrawing of lower eyelid which together narrows the palpebral fissure  Anhidrosis: Loss of sympathetic fibers for facial sweating and vasodilation

Answer 5

Acute confusional state characterized by global cognitive dysfunction and inattention * Confusional state refers to state of altered consciousness with disorder attention along with diminished speed, clarity and coherence of thought

Answer 6

 Defined by unarousable unresponsiveness  Medical emergency characterized by absence of consciousness * **Consciousness requires arousal (awake) and awareness (have content)**  Timely identification and treatment of reversible cause can be life-saving  Caused by structural brain lesions, diffuse neuronal dysfunction or psychiatric illnesses

Answer 7

* Vigilant = Hyperalert * Normal = Alert * Lethargy = Drowsiness but easy to arouse * Stupor = Difficult to arouse * Coma = Unarousable

Answer 8

 Ascending reticular activating system (ARAS) * Network of neurons originating in the tegmentum of upper pons and midbrain * Neurons project to thalamus and hypothalamus and subsequently to cerebral cortex * Responsible to induce and maintain alertness o Injury to ARAS with upper brainstem or cerebral hemispheres by focal lesions can cause alteration in consciousness

Answer 9

Must look out for reversible causes and treat promptly

Answer 10

 ABG/ VBG  CXR  ECG  EEG  CT brain  CT angiography  MRI venography

Answer 11

 β-blockers * Propranolol * Metoprolol * Timolol  Anti-depressants * Amitriptyline (TCA) * Venlafaxine (SNRI)  Anti-convulsants * Topiramate * V alproate

Answer 12

 Peripheral factors * Peripheral activation or sensitization of myofascial nociceptors * Associates with pericranial muscle tenderness  Central factors * Sensitization of pain pathways in CNS due to prolonged nociceptive stimuli from pericranial myofascial tissues

Answer 13

ICHD-3 (international classification of headache disorders-3rd edition)

Answer 14

 Belongs to an idiopathic headache entity known as trigeminal autonomic cephalalgias (TACs)  Severe unilateral headache typically accompanied by autonomic symptoms  Theory 1: Hypothalamic activation with secondary activation of trigeminal-autonomic reflex through a trigeminal-hypothalamic pathway  Theory 2: Neurogenic inflammation of walls of cavernous sinus obliterates venous outflow * Leads to injury of traversing sympathetic fibers of the intracranial ICA and its branches

Answer 15

 Recurrent brief episodes of unilateral electric shock-like pains that is abrupt in onset and offset  Located in the distribution of one or more divisions of CN V

Answer 16

Chronic systemic vasculitis involving large and medium sized arteries: aorta and great vessels. Commonly affects the temporal and other cranial arteries originating from the aortic arch Strongly associated with polymyalgia rheumatica in 40-60% of patients. Characterized by pain and morning stiffness around shoulder and hip girdles, neck as well as in the torso. However GCA only found in 15% of patients with PMR. Medical emergency (amourosis fugax) du to cranial arteritis without early detection and treatment

Answer 17

 Most subarachnoid hemorrhage are caused by ruptured intracranial saccular (berry) aneurysm  Anatomical location of intracranial aneurysm * Anterior circulation (85%) o Bifurcation of MCA o Junction of ACA and anterior communicating artery o Junction of ICA and posterior communicating artery * Posterior circulation (15%) o Top of basilar artery o Junction of basilar artery and superior cerebellar artery o Junction of basilar artery and anterior inferior cerebellar artery o Junction of vertebral artery and posterior inferior cerebellar artery

Answer 18

 Saccular (berry) aneurysm: Thin-walled protrusion from intracranial arteries that composed of a very thin or absent tunica media and a severely fragmented or absent internal elastic lamina  Fusiform aneurysm: Enlargement or dilatation of entire circumference of the involved vessel that may in part be formed due to atherosclerosis  Mycotic aneurysm: Result from infected emboli due to infective endocarditis

Answer 19

 General features * Most intracranial aneurysms are incidental findings  Imaging modalities * CT angiography * MRI angiography * Cerebral angiography

Answer 20

* AVM: possible neurological sequelae (most dangerous) * Cavernous malformation (cavernous angioma): possible neurological sequlae * Developmental venous anomalies (venous angioma); more benign * Capillary telangiectasia: more ebenign

Answer 21

 Pale infarction which is swollen and slightly softened * Blood cannot reach the area distal to obstruction and thus pale in appearance  Hemorrhagic infarction * Reperfusion to ischemic part of the brain will lead to hemorrhagic appearance o Capillaries are damage during ischemia and can no longer stand the BP when blood flow is reestablished  Cracking and liquefactive necrosis  Resorption with replacement by fluid filled cavities

Answer 22

Lenticulostriate arteries (branch of MCA)

Answer 23

Always assess vitals and resuscitate if necessary Locate the lesion from high to low: cortical signs --> CN --> UL, LL (muscle tone, power, reflex, sensation, vibration and proprioception) cerebellar signs

Answer 24

DSA for smal aneurysm as cause of SAH and if non invasive studies are inconclusive (invasive intracranial vascular study)

Answer 25

o Focal parenchymal hypoattenuation o Hypoattenuation involving ≥ 1/3 MCA territory o Hyperattenuation of large vessels (e.g. MCA occlusion) (“Dense MCA sign” which does not respond well to IV tPA) o Cortical sulcal effacement o Loss of gray-white differentiation in basal ganglia o Loss of insular ribbon o Obscuration of lentiform nucleus o Obscuration of Sylvian fissure

Answer 26

* Airway: airway support and ventilatory support if decreased consiousness or who have bulbar dysfunction that causes airway compromise * Breathing: supplemental O2 therapy taht should be provided to maintain sO2 >94%. Not reommended in non hypoxic patients * Circulation: BP. Target BP <185/110mmHg. BP should be maintained at <180/105mmHg for at least 24 hours after fibrinolytic therapy Patients not eligable for fibrinolysis: BP should not be treated acutely (permissive hypertension) unless hypertension is extreme as defined by >220/120mmHg, careful lowering of BP by about 15% in the first 24 hours after stroke is recommended. BP carefully lowered as it may be necessary to maintain cerebral blood flow to ischemic brain regions. * Body temp: source of hypothermia should be identiied and treated. Antipyretic medication should be administered to lower temp in hyperthermic patients with stroke * Blood glucose level: hyperglycemia (associated with worse outcomes) --> target BG = 7.8-10mmol/L. Hypoglycemia with serum glucose <3.33mmol/L should be treated * Diet and nutrition: enteral diet should be started within 7 days of admission (avoid acalculous cholecystitis), swallowing assessment to screen for dysphagia before initiating any oral intake --> dysphagia increases chance of aspiration pneumonia. NG tube feeding reasonable for patients with dysphagia in early phase of stroke. PEG tubes for longer anticipated patients. * Positioning and splinting to avoid aspiration, contractures, pressure nerve palsy, shoulder subluxation and pressure sores * Avoid bladder overdistension and UTI with catheterization * Avoid constipation or fecal impaction by high fiber diet and stool softeners

Answer 27

Antiplatelets: recommended to initiate within 24-48 hours of onset of acute ischemic stroke. Dosage = 160-325mg once daily Should be delayed until 24 hours later if IV alteplase (tPA) is given since increase risk of symptomatic ICH and may not improve functional outcome Anticoagulants are recommended against being used Only indicated if cardiogenic embolism for secondary prevention of stroke in patients with AF, DVT or PE, cerebral venous thrombosis

Answer 28

Acute: + hemorrhagic transformation, cushings ulcer, coma

Answer 29

Open Craniotomy Decompressive Craniectomy with clot evacuation CT-guided stereotactic aspiration Endoscopic aspiration

Answer 30

 Nimodipine * CCB to prevent vasospasm * Administered to ALL patients with aneurysmal subarachnoid hemorrhage

Answer 31

1. Cerebral infarction/hemorrhage at subcortical regiion 2. Infarction (hypodense lesion), hemorrhage (hyperdense lesion) 3. HT, DM, smoking, HL, strong FH of strokes

Answer 32

 CVS system * Mixed mitral valve disease * Pulmonary hypertension * Atrial fibrillation  CNS system * Wernicke’s aphasia from a cardioembolic stroke o Posterior part of the left superior temporal gyrus o Supported by the history of reduced exercise tolerance, palpitation (AF), mixed mitral valve disease and sudden onset of fluent aphasia

Answer 33

 CVS system * Pan-systolic murmur at apex radiating to axilla suggest mitral regurgitation * Mid-diastolic murmur with postural accentuation suggest mitral stenosis * Irregular pulse with higher apical rate than pulse suggest atrial fibrillation * Parasternal heave and loud pulmonic component of S2 suggest pulmonary hypertension  CNS system * Fluent aphasia with normal neurological examination suggest stroke affecting Wernicke’s area

Answer 34

 Features suggesting predominant mitral stenosis * Small volume pulse * Undisplaced tapping cardiac apex * Long diastolic murmur * Pulmonary hypertension  Features suggesting predominant mitral regurgitation * Displaced cardiac apex * Palpable systolic thrill

Answer 35

 Posterior part of the left superior temporal gyrus  Lesion involving this area will lead to Wernicke’s (receptive) aphasia

Answer 36

Epidural can also be caused by traumatic injury to head via veins in the scalp

Answer 37

If penetrating trauma can be scalp vein

Answer 38

Primary malignant CNS tumours are the 2nd most common childhood malignancy after hematological malignancy * Most common pediatric solid organ tumour * Highest mortality from childhood cancer surpassing ALL * Highest morbidity from childhood cancer primarily neurological deficits

Answer 39

* Astrocytoma/ Other gliomas * Primitive neuroectodermal tumours (PNETs) including medulloblastoma * Germ cell tumours (GCTs) (Asians: Caucasians = 6:1) * Ependymoma

Answer 40

Primitive neuroectodermal tumors (PNETs)(embyronal tumors)

Answer 41

Biochemical tests **CSF analysis** by lumbar puncture **Tumor markers: AFP and B-hCG for GCTs.**CSF cytology may reveal neoplastic cells which metastasize through CSF pathways Radiological tests **CT brain**: used for emergency situation. Detectin of metastasis to skull base, clivus or regions near foramen mangum **MRI brain**: with and without contrast is neuroimaging standard. Superior to CT scan for evaluation of leptomeninges, subarachnoid space, posterior cranial fossa and defining vascualr distribution of the abnoramlity * **Perfusion MRI**: imaging of blood flow in brain tumors with gadolinium in dynamic contreast MRI * **Functional MRI**: preop planning for patients whose tumor is located near eloquent areas of the brain. PET scan: detects malignant tumors with high metabolic rates. Localize areas of maxium glucose utilization within the tumor which guides biopsy of tumor location with most aggressive biological behaviour **SPECT scan**: utilizes isotopes such as thallium-201 to detect abnormalities in BBB --> distinguish benign from malignant brain lesions, predict histological grade of brain tumors, select aeras for biopsy **Surgical exploration and biopsy**: histological confirmation obtained at time of surgical exploration for resection

Answer 42

 Bimodal distribution * Early peak in 2nd and 3rd decades (female predominance) * Late peak in 6th – 8th decades (male predominance)

Answer 43

Avoid drugs that unmask or exacerbate MG Antibiotics o Fluoroquinolones o Aminoglycosides CVS drugs o β-blockers o Procainamide o Quinidine Others o Penicillamine o Magnesium sulphate o Chloroquine o Hydroxychloroquine

Answer 44

 Mestinon dose should be stepped up for inadequate response  Systemic corticosteroids and steroid sparing drugs such as azathioprine are NOT started * Due to concern of potential long-term adverse effects including lymphoproliferative diseases and teratogenicity in a young woman of child-bearing age  Thymectomy * Significant improvement can occur in the absence of a thymoma  Plasmapheresis * Used in intractable cases * Benefit is temporary

Answer 45

 CN III palsy * Usually complete ptosis * Ophthalmoplegia * Dilated unreactive pupil  Horner’s syndrome * Partial ptosis * Miotic reactive pupil * Anhydrosis (Failure of sweat glands) * Enophthalmos (Posterior displacement of eyes)

Answer 46

Most common immune-mediated inflammatory demyelinating disease of CNS * Demyelination of the PNS by definition is NOT considered MS * Demonstrates lesion disseminated in time and space

Answer 47

* Voluntary gaze to the right is initiated in the left cerebral hemisphere * Left cerebral hemisphere innervates right paramedian pontine reticular formation (PPRF) which is the horizontal gaze centre in pons * Innervates CN VI (abducens nerve) and thus lateral rectus muscle of right eye to abduct the right eye * Innervate CN III (oculomotor nerve) and thus medial rectus muscle of left eye to adduct the left eye via medial longitudinal fasciculus (MLF)

Answer 48

 Acute immune-mediated progressive polyneuropathy characterized by a monophasic paralyzing illness provoked by a preceding infection  Recognized as a heterogeneous syndrome with variant forms of distinguishing clinical, pathophysiological and pathological features

Answer 49

 Preceding infections * Bacterial: Campylobacter jejuni/ Mycoplasma pneumoniae * Viral: CMV/ EBV/ VZV/ HIV/ Zika virus  Recent vaccination  Surgery  Bone marrow transplant

Answer 50

 Monophasic illness pattern * Progresses over a period of about 2 weeks * Clinical symptoms reach a plateau (nadir) in 4 weeks

Answer 51

Revised EI Escorial criteria

Answer 52

 Enteroviral infection that causes meningitis, prolonged or permanent flaccid paralysis or death  Eradicated from most of the world due to mass vaccination

Answer 53

 Virus replicates initially in the throat and intestine  Disseminated via blood or lymphatic system  Invades the central nervous system (CNS) * Travel by anterograde axonal flow along peripheral nerves to spinal cord * Viral replication then occurs in the motor neurons * Leads to death of motor neurons leading to flaccid paralysis

Answer 54

* Flu like syndromes * Aseptic meningitis * Paralytic poliomyelitis (0.1-1% of cases) Spinal poliomyelitis: starts with severe myalgia which is accompanied by muscle spasms, fasciculation and paresthesia. Followed by flaccid paralysis --> usually asymmetrical. Proximal muscle involvement >distal muscle involvement Bulbar poliomyelitis: result of paralysis of muscle groups innervated by the cranial nerves: CN9 and 10 most commonly involved nerve --> dysphagia and pooling of oral secretions. Involvement of resp center of medulla oblongata leads to resp muscle paralysis

Answer 55

Modified Hoehn and Yahr staging of Parkinsons disease

Answer 56

 Depigmentation, neuronal loss and gliosis in substantia nigra pars compacta in midbrain and locus ceruleus in pons  Presence of Lewy bodies * Pathological hallmark of PD but not specific to PD (e.g. Dementia with Lewy bodies) * Lewy bodies are round eosinophilic intracytoplasmic neuronal inclusions which is made up of α-synuclein and ubiquitin

Answer 57

 Seizure = Transient neurological symptoms due to abnormal excessive or synchronous neuronal activity which can be provoked or unprovoked  Convulsion = Generalized tonic-clonic seizure

Answer 58

* Defined as those occurring up to several weeks (up to 2 – 4 weeks) after the event * Provoked seizure that are NOT expected to recur in the absence of provocation * Transient factors that temporarily lower the seizure threshold

Answer 59

Medical emergency Can be convulsive (tonicclonic) or non convulsive: non convulsive SE refers to alteration of awareness ranging from confusion to coma without motor manifestation of seizure (diagnosed with EEG) Definition: continous seizure lasting for >5 mins, >2 epilepitc seizures without full recovery of consiousness between attacks

Answer 60

* Syndrome defined by a distinctive combination of clinical features, signs and symptoms and electrographic (EEG) patterns * Epilepsy syndrome classification provides genetic, therapeutic and prognostic values * Examples o Juvenile myoclonic epilepsy o Genetic epilepsy with febrile seizures plus (GEFS+)

Answer 61

* Syncope: prodrome (lightheadedness, nausea, visual blurring) * Seizure (aura, TLOC, convulsion, tongue biting, urinary incontinence, post ictal state (headache, confuson, fatigue, muscle sores...) * TIA (hemiparesis and hemisensory loss, aphasia in TIA develops abruptly and typically do not evolve) * Transient global amnesia * Psychogenic non epileptic seizure (PNES) * Migraine: (+ve symptoms: visual (bright lines), auditory (tinnitus, noises), somatosensory (pain), motor (jerking or repetitive rhythmic movements) * Narcolepsy: daytime sleepiness with cataplexy, hypnagogic hallucination and sleep paralysis * Movement disorders: tics/ asterixis/choreoathetosis) * Hyperventilation: Environmental trigger will be evident

Answer 62

 Abnormal excessive or synchronous activity in brain leading to epileptiform behavior * Enhance connectivity * Enhanced excitatory (e.g. glutamate) transmission * Failure of inhibitory (e.g. GABA) mechanism * Changes in intrinsic neuronal properties

Answer 63

Principle of AED treatment = Monotherapy at the lowest effective dose AED monotherapy is prefferred initial management approach in epilepsy care since most patients may be successfully managed with the first or second monotherapy utilized with similar efficacy and better patient tolerability compared to polytherapy Polytherapy may only minimally increase seizure control and can substantially increase AED toxicity, drug interactions, seizure aggravation, noncompliance and cost

Answer 64

 To check anti-convulsants levels  Identify or exclude metabolic causes of epileptic seizures  Identify or exclude metabolic encephalopathy  Identify metabolic consequences of generalized seizures * ↑ Muscle enzymes * Neutrophilia * Hyperprolactinemia

Answer 65

 Inappropriate starting of anti-convulsants after one suspected epileptic seizure  Known narcotic abuser with positive urine test for methadone which makes drug overdose as a possible explanation of loss of consciousness  Driving is forbidden especially for people working as drivers  Drug level has not been checked to ensure adequate dosing and compliance prior to add-on therapy

Answer 66

 Bacterial causes * Mycobacterium tuberculosis * Treponema pallidum  Fungal causes * Cryptococcus neoformans (Yeasts) * Coccidioides immitis (Dimorphic fungi) * Histoplasma capsulatum (Dimorphic fungi)

Answer 67

 Secondary to solid or hematological malignancy * Solid tumours include breast cancer, lung cancer, GI malignancy and melanoma * Hematological tumours include acute leukemia and large cells lymphomas Remarks: Diagnosis of malignant meningitis requires cytological identification of malignant cells within CSF usually accompanied by lymphocytic pleocytosis, high protein and low glucose

Answer 68

 Raised ICP in meningitis is primarily due to cerebral edema * Vasogenic cerebral edema results from increased permeability of BBB (tumor: poor demaraction between the grey and white matter) * Cytotoxic cerebral edema results from cytotoxic factors produced by bacteria and neutrophils (clear differentiation between grey and white matter)

Answer 69

* CBC with DC * Electrolyte profile: hypoNa in SIADH * Clotting profile * Blood culture * CSF analysis by lumbar puncture: TCC with differentials + glucose + protein + gram stain + culture with sensitivity testing + enterovirus and HSV PCR + opening pressure * CSF smear, culture with sensitivity testing, antigen detection and PCR Gram smear and AFB smear: gram +ve diplococci (pneumococcal infection), gram +ve rods and coccobacilli (L.monocytogenes), gram-ve diplococci suggest meningococal infection, gram-ve coccobacilli suggest H.influenzae infection Culture: bacterial culture with drug sensitivity testing, viral or fungal culture is indicated if clinical picture suggests viral/fungal meningitis PCR: most important for CNS viral infection * Blood and urine for viral culture and PCR * Throat, rectal swabs for viral culture and PCR * Serology: for virus with low seroprevalence rate (arboviruswuc has WNV): virus specific IgM antibodies. Virus with high seroprevalence rate (HSV, VZV, EBV, CMV): less useful for dx of CNS viral infections

Answer 70

 Tuberculous salpingitis  Reactivation of TB with development of TB meningitis  Fungal meningitis  Partially treated bacterial meningitis

Answer 71

 IV high dose penicillin G + 3rd generation cephalosporin  Antibiotic change * High dose ampicillin instead of penicillin G should be changed

Answer 72

 Hydrocephalus: Shunting  CN palsy: Corticosteroids  Brain abscesses: Surgical drainage  Tuberculoma: Corticosteroids, anti-inflammatory drugs  Spinal block: Corticosteroids

Answer 73

 Duration of treatment: 9 – 12 months  Regimen * Isoniazid with vitamin B6 (pyridoxine) * Rifampicin * Ethambutol * Pyrazinamide

Answer 74

 For anti-inflammatory effects in Medical Research Council Stage II or III disease  Indicated in * Lethargy * Prominent meningeal irritation * CN palsy * Convulsion * Paralysis * Stupor * Coma

Answer 75

 Isoniazid with vitamin B6 (pyridoxine)  Rifampicin  Ethambutol

Answer 76

 Contraindications * Space-occupying lesions (Markedly ↑ ICP) o Unequal pressures between supra- and infra-tentorial compartments * Coagulopathy o Epidural or subdural hematoma * Spinal block * Local suppuration * Local congenital lesion  Complications * Headache * Dry tap * Brain herniation * Subdural hematoma * Aneurysmal subarachnoid hemorrhage

Answer 77

 Inflammation of brain parenchyma  Viral infections of the CNS results in syndrome including aseptic meningitis or encephalitis  Abnormal cerebral function in encephalitis is the most distinguishing feature between meningitis in which cerebral function remains normal * Altered mental status * Personality and behavioral change * Sensory or motor deficits * Speech and movement disorders

Answer 78

 Common viral infections * VZV (chickenpox) * Mumps virus * Measles virus * Rubella virus  Vaccination * Smallpox * Rabies virus * Influenza virus

Answer 79

 Meningitis (bacterial/ viral/ TB/ fungal) * Complicated with cerebral edema or cerebral venous thrombosis  Brain tumours (primary/ metastatic)  Brain abscess  Syphilis  Toxic encephalopathy  Metabolic encephalopathy * Hypoglycemia * Electrolyte disturbance

Answer 80

 Acyclovir (IV) * 10 mg/kg Q8h * For 10 – 14 days

Answer 81

 Early stage of lesion (1 – 2 weeks) = Cerebritis * Acute inflammation with no tissue necrosis * Poorly demarcated with localized edema  Late stage of lesion (After 2 weeks) * Necrosis and liquefaction * Lesion is surrounded by a fibrous capsule

Answer 82

 Fever  Headache * Most common presenting complaint * Onset can be sudden or gradual * Localized to the side of abscess * Severe pain which is NOT relieved by aspirin  Nausea and vomiting * Associated with increased ICP  Neck stiffness  Alteration in mental status * From lethargy progressing into coma * Indicates cerebral edema and is a poor prognostic sign  Focal neurological deficits * Hemiparesis * Seizures

Answer 83

Etiology: CMT1 anfd CMT2 mutation (AD inheritance mostly): located on chromosome 17p CMT is a group of hereditary of polyneuropathies involving both motor and sensory function Classification Type 1: primary demyelinating neuropathy Type 2: proxmary axonal neuropathy Type 3: Dejerine-Scottas disease Type 4: autosomal recessive demyelinating neuorpathy Type 5: associated with spastic paraplegia Type 6: maniefsts with neuropathy and optic atrophy Type 7: manifests with neuorpathy and retinitis pigmentosa

Answer 84

Early onset, slowly progressive course. Severity of symptoms depends on subtype, but most ahve normal lifespan Signs UL: small hand muscle wasting, claw hands LL: distal leg muscle wasting (inverted champagne bottle sign * Pes cavus (hallmark of early onset neuropathy) or pes planus * Claw toes * Foot drop high steppage gait +/-ataxis gait * Romberg test +ve (sensory ataxia) Motor: LMN signs with length dependent pattern (LL >UL> distal> proximal) Sensory: gove and stock pattern fo sensory loss, affect DCML but intact ST tract Secondary OA (Charcot joint)

Answer 85

Nerve conduction study: decreased impulse conduction velocity in both sensory and motor nerves Sural nerve biopsy: hypertrophuic neuropathy (onion bulb appearance from repeated demyelination and remyelination in large nerve fibers

Answer 86

 UMN lesions * Result from degeneration of frontal motor neurons located in motor strip (Brodmann area 4) and their axons traversing corona radiata, internal capsule, cerebral peduncles, pontine base, medullary pyramid and lateral corticospinal tract  LMN lesions * Result from degeneration of lower motor neurons in brainstem and spinal cord producing muscle denervation