NEUROMEDICINE

UMN lesion LMN lesion

Afferent
Localization Above anterior horn Tract between anterior horn of
Along descending motor tracts spinal cord & relevant muscle tissue Pupillary Reflex Optic N.
(Brain, brainstem, cerebellum, spinal cord) (Light) Reflex (CN#2)
Tone Hypertonia Hypotonia Accommodation reflex Optic N.
(spasticity / Rigidity) (CN#2)
Reflexes Hyperreflexia Hyporeflexia Corneal reflex Trigeminal V
Plantar reflex Positive Negative (Ophthalmic divis
(Babinski) (Extensor, Upgoing) (Downgoing) Jaw jerk Trigeminal V
Positive weakness Gag reflex Glossopharyn
(CN#9)
Weakness Central paresis Peripheral paresis
Quadriplegia, hemiplegia, etc.
Spastic paresis Flaccid paresis Definition
Muscle Atrophy Negative Positive Proprioception body awareness
(wasting) sense.
Fasciculations Absent Present (Tounge) Stereognosis Identify shape & form
Hoffman sign Positive Negative of object.
(middle finger flicked) (Reflex thumb flexion) Graphesthesia recognize symbols
Abdominal reflexes Absent Present traced on skin.
Common etiologies Stroke Peripheral neuropathy

Reflexes Coardination tests:

Reflexes
Knee jerk L3/L4 Finger to nose test Heel-shin tes
Biceps C5/C6
Ankle S1 Disrupted tests → Most commonly from les
Brachioradialis C5/C6
Triceps C7/C8 Optic nerve tests:
- Confrontation test: For visal field
Reflexes Grade - Conversion test: For accomadatio
0 +1 +2 +3 +4 Acuity Pupillary re
Absent Hypo Normal Hyperreflexia Hyperreflexia
Without myoclonus With myoclonus
Cranial nerve lesions /palsy:
CN#3 Ptosis
(occulomotor) Blown pubil
Muscle strength/ Power Grade
Down & out gaze
0 No muscle contraction
CN#4 Hypertropia (Can’t see
1 Flicker/trace of contraction but no movement Rotated outside
(Trochlear)
2 Active Movement when gravity eliminated. Contralateral head tiltin
3 Active Movement against gravity but not against resistance. MC presenting SX → Dip
4 Active Movement against resistance but weaker than normal. CN#6 Can’t adduct eye.
5 Normal power (Abducens)
Aphasia Broca’s Aphasia Wernicke’s aphasia CN#5 Jaw deviate toward side
Other names Motor Expressive Non-fluent. Sensory Receptive Comprehensive CN#10 Uvual deviate Contralate
Telegraph like aphasia (Agrammatism)
CN#12 Tounge deviate toward s
Localization Inferior frontal gyrus Superior temporal gyrus
(Hypoglossal) (Lick your wounds).
Fluency Non-Fluent Fluent
Comprehension Intact comprehension Impaired comprehension
Repetition Impaired repetition
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Stroke:  Notes:
1) Ischemic stroke (Most common) (85%) 2) Hemorrhagic stroke  MRI can also differentiate btw hemorrhagic & Ischemic stroke (But need time).
Thrombo c Embolic Hypoperfusion Lacunar stroke sudden onset & progressive  Most accurate imaging test  Diffusion weighted MRI. (Earliest to detect changes).
Atherosclerosis Sudden & Rapid Water-shed areas Small vessel
Risk factors presentation (ACA-MCA) Lipohyalinosis
(HTN/DM)
Previous TIA
(MCA-PCA) Non – cortical  Most important risk factor for stroke  HTN.
 Carotid Bruit  carotid artery stenosis
 Stroke mechanism in A-FIB  Cardioembolic
 The target of TPA is to protect the penumbra (Not the core).
Suspicion of stroke:  HTN with Ischemic stroke
o First step  Immediate CT without contrast With thrombolysis Goal < 185/110 mmHg
 To exclude hemorrhage. No thrombolysis Goal < 220/120 (Permissive HTN).
 Ischemic changes (stroke changes) happens After 6 hours (Normal before).
 If no hemorrhage = Ischemic stroke
1st question to ask  If sudden neurologic decline occurs during rtPA infusion
 Duration.
o If ischemic stroke  evaluate for time window  Bleeding.
- Time window = time of onset of symptoms / (“last known normal”) Management  Discontinue tpa
- If time window < 4.5 hours & no contraindications  Initiate tPA  Repeat Non-contrast CT scan
- If time window (> 4.5 - < 6 hours)  mechanical thrombectomy. - (Most important investigation)

Absolute contraindica ons. / exclusion criteria before tPA.

 Write in exam
TIA: Temporary focal loss of neurologic function caused by ischemia
A) Previous hemorrhage on CT  Symptoms Last < 24 hours, Negative MRI.
TIA definition now is based
B) Ischemic stroke < 3 months.
on tissue (Imaging) not time.
C) Severe head trauma < 3 months
D) Acute hemorrhage on CT.  ABCD2 Score for TIA: (‫) ﻓﻛك ﺧﻠﯾك ﻋﺎﻟﻘدﯾم‬
 estimates risk of stroke within 2 days after TIA. -
 tPA /rtPA drugs (Plase)
o If hemorrhagic. Alteplase, Tenecteplase  Amaurosis fugax:
 Reduce BP, reverse anti-coagulants, surgery. Only given IV.
- Retinal artery (Type of TIA).
 Contraindicated thrombolysis tPA.
Type ischemic Hemorrhagic
CT Dark/ hypodense Bright / hyperdense
Timing Changes detected after 6 hours Visible from the start
Secondary preven on of stroke
(preferred to write) Others: Inves ga ons (Not preferred to write)
1) Anticoagulants (Warfarin) A) ECG Atrial fibrillation (Arrythmia)
- Used for A-Fib (arrythmia)
2) Antiplatelet (Aspirin) B) Carotid doppler Carotid artery stenosis
3) Control DM Opera ons:
- Carotid endarterectomy for Carotid artery stenosis
4) Control BP (Antihypertensive drugs See the table (other Opera on)
5) Statin (Control Dyslipidemia)
6) Life style modification
Weight loss Smoking cessation  Aspirin
7) DVT prophylaxis (In DVT related stroke) - No Thrombolysis Give aspirin direct
- Thrombolysis given Wait 24 hours before aspirin

- Thrombolysis not given  give aspirin direct.

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Dominant hemisphere Non-dominant hemisphere
(Left usually) (Right usually) Cortical strokes Stroke Syndrome / Clinical features.
◾ Contralateral weakness & sensory loss ( Lower limbs > upper limbs)  UMN lesions.
◾ Urinary incontinence
ACA-MCA watershed infarc on Man in a barrel
◾ Primitive reflexes (Grasp reflex), Behavioral abnormalites. (Due to hypoperfusion) (proximal limb weakness)
ACA ◾ Ipsilateral / contralateral ideomotor apraxia (inability to preform skilled movements/ gestures) Medial medullary syndrome.
◾ Transcortical motor aphasia ◾ Motor neglect ASA (Anterio spinal artery)  Ipsilateral hypoglossal dysfunction
 Difficulty initiating speech.  Underuse of one side, not explained by defects of  At level of medulla - Tounge flaccid paralysis
 Intact repetition and comprehension strength, reflexes or sensibility. - Deviates toward lesion.
🔘 Contralateral weakness & sensory loss (lower face & upper limbs > lower limbs).  Contralateral hemiparesis
🔘 UMN facial palsy (Lower facial droop, spared forehead). Others: (Low-yeild)
🔘 Gaze Preference (Gaze deviates toward side of lesion). (MC  Left in dominant). Loss of all sensory & motor.
🔘 Contralateral homonymous hemianopia without macular sparing
MCA Aphasia Hemineglect (hemispatial neglect)
ASA at spinal cord ◾ Bilateral paralysis/sensory loss below lesion
Except Dorsal column (intact)
(MC)  Agnosia of contralateral side of world (Left side) ◻ Preserved proprioception & vibration.
 Test by Drawing a clock. Superior cerebellar artery Ipsilateral ataxia (Gait & limbs)
 Right parietal lobe.
Agraphesthesia.
Asterognosis.
Contralateral homonymous hemianopia with macular sparing (Occipital lobe)
Lacunar stroke:
Mid brain involvement  Weber syndrome  Subcortical strokes (no cortical signs)
PCA 🔹 Ipsilateral 3rd nerve palsy (Mydriasis/ophthalmoplegia) 🔹 Contralateral hemiparesis
 Occur in small vessels.
Alexia without Agraphia syndrome Prosopagnosia  Pathophysiology: Lipohyalinosis.
Can’t read but can write - Inability to recognize familiar faces.
(affected Splenium of corpus callosum) - (Face blindness).  Associated with Hypertension.
 MC artery affected  Len culostriate artery. (Cause pure motor stroke).
Brain-stem stroke: (Shared clinical presentation) Subtype Symptoms Localization
1) Ipsilateral Cranial nerve lesion 2) Contralateral hemiparesis (Not all cases) Pure Motor Paralysis/weakness of face, arm, leg on one side. Posterior limb of internal
- (Half of body) (UL=LL) (MC) (Dense paralysis) capsule
Pure Sensory Complete sensory loss on one side of body. Thalamus (VPL)
Basilar artery stroke Locked in syndrome (in bilateral pon ne infarc on) Ataxic Weakness/ataxia Base pons - Internal
(Pons) - Quadriplegia & Anarthria Hemiparesis capsule
(Ventral pon ne) - Only thing: blink & vertical eye movement Dysarthria- Dysarthria and clumsiness (weakness) of the Base pons - Internal
Clumsy Hand hand capsule
(Ataxic hand)
Cerebellar artery AICA PICA Hemiballismus Wild, flailing (Wave/swing), flinging movement Subthalamic nucleus (STN)
Syndrome Lateral pontine Lateral medullary
(Wallenberg)
 NIH score:
Dis nguishing • Facial nucleus: Nucleus ambigus (CN 9, 10)
Vertebral artery stroke - ➔ Score: 0-42
can also cause
features Ipsilateral LMN facial palsy - Dysphagia
Wallenberg syndrome. - ➔ ⬆ score: ⬆ severity.
Ipsilateral full half face - Hoarseness of voice
- ↓ Gag reflex
 Aspect score:
Shared features (Low – yield info) - ➔ Based on affected MCA territories.
• Vestibular nuclei: Nystagmus, vertigo, N/V
• Sympathetic tract: ipsilateral Horner’s syndrome - ➔ Score = 10 – affected areas.
• Spinal V nucleus: ipsilateral face pain/temp loss
• Spinothalamic tract: Contralateral pain/temp loss - ➔ ⬇ score: ⬆ severity.
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Multiple sclerosis: Autoimmune inflammation & demyelination of CNS (Demyelinating disorder).
Female > male (2:1)
Epidemiology females = 20 - 35 years
Males = 35 - 45 years
Unknown
T lymphocytes & B lymphocytes, innate immune system.
Etiology - (Attack oligodendrocytes)
More than 200 genetic variants have been discovered
Not Mendelian inheritance pattern
Subtypes:
Relapsing remitting Relapse (Attach) with partial or complete recovery.
(MC type) No progression between attacks.
Secondary progressive Progressive disease after Relapsing remitting course.
Primary progressive Progressive from the start.
No Attacks (Relapses) no enhancing lesions on MRI
Progressive relapsing Progression from onset with clear scattered relapses.
(least common)
1) MRI Corpus callosum thinning or scalloping, Atrophy in chronic
disease, Enhancement with active lesions.
Investigations 2) CSF analysis Oligoclonal band (Best)
(Lumbar puncture) IgG index > 0.7
(Electrophoresis) Elevated myelin basic protein
3) Visual evoked potential
Treatment
◻ Only in active disease (Active = Relapse or new MRI activity)
◻ Progressive disease = Don’t benefit from drugs
Abortive Diz modifying therapy High disease activity. Symptomatic TX
(relapse prevention) (Maintenance) (Multiple enhancing lesions)
IV steroids Beta – Interferon injections (1ST line) MAB (natalizumab) Spasticity  Baclofen
------------------------------
Syndrome typical of MS
(IV fingolimod (Oral) (2nd line)
methylprednisolone) Fatigue  Amantadine Par al transverse myeli s ◻ Sensory level loss ◻ Weakness(paresis) ◻ below lesion lvl.
Glatiramer
Most common  Unilateral.
Red swollen painful eye followed by disc pallor.
MS famous loca ons Op c neuri s Decreased visual acuity, central scotoma, red desaturation.
Periventricular Juxta- cortical Infratentorial spinal
(Most common) cortical Diplopia /blurred vision
- RAPD (relevant afferent pupillary defect) Marcus Gunn public
 examined by flashlight swinging movement test.
Primary progressive MS
Direct pathway Indirect pathway
McDonald > 1 year of disability & 2 or more of: Mild constric on of both eyes More constric on of both eyes
A) > 1 (T2)-hyperintense lesions disseminated in brain (Famous locations) (Apparent dila on)
criteria B) > 2 (T2)-hyperintense lesions in spinal cord. 1) INO (Intranuclear ophthalmoplegia)
C) Oligoclonal bands. Brainstem syndrome Lesion in MLF (medial longitudinal fasciculus) At pons.
MRI of PPMS 1) Less enhanced Affected eye Normal eye
2) Less plaques Can’t move medially. Nystagmus during abduction
(Cant adduct)
Normal convergence
2) Area postrema syndrome Intractable vomiting
Cerebellar syndrome Ataxia Nystagmus vertigo Dysmetria
Intention tremor Rubral tremor Dysdiadochokinesia
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 Associated with MS:
Lhermi e sign An electrical sensa on that runs down the back when
bending the neck.
Uhthoff worsening of symptoms due to exposure to higher than
phenomenon. usual temperatures

 Painful condi ons associated with MS:

1) Optic neuritis. 2) Trigeminal neuralgia.

Favorable Prognosis Non- Favorable prognosis:

Early age of onset Later age of onset
Female Male
Acute onset of symptoms Chronic onset of symptoms
Excellent recovery from attacks Poor recovery from attacks
Long inter-exacerbation period Frequent exacerbations
Minimal dysfunction at 5 yrs= min. dysf. At 15
presen ng Optic neuritis cerebellar / motor Involvement.
episode Sensory symptoms Spinal cord lesions
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Epilepsy: Absence seizures = Generalized (non-motor) seizure
 Brief unresponsiveness state.
Seizure clinical manifesta on of abnormal, excessive, & hypersynchronous electrical
 Staring into space or daydreaming.
discharge
Lip smacking Perioral/eyelid twitching
Awareness Area involvement Childhood Eye fluttering Head nodding
Aware
simple
Impaired awareness
Complex
Partial (focal) Generalized
Focal to bilateral tonic clonic.
Absence 
Amnestic during seizures.
No convulsions & No postictal phase
(Focal  Generalized). epilepsy  Normal development. Multiple Per day
 ECG: 3HZ spikes & waves. (high number)
 Treatment: (Ethosuximide)
Seizure Children Generalized seizure.
Classifica on Juvenile
Myoclonus Tonic- clonic
/Terms epilepsy myoclonic
 Post-ictal confusion
epilepsy  Age group: 12 – 18 years.
Aura Automatism
Lennox-  Very bad refractory seizure
Gastaut  Associated with intellectual disability
syndrome  ECG: Generalized slow <2.5 HZ spikes & waves
Treatment:
1) AED (An epilep c drugs).  1st line.
Epilepsy Disease characterized by recurrent unprovoked seizures
1) A least two unprovoked (or reflex) seizures occurring >24 h apart
Focal Generalized
Epilepsy 2) One unprovoked (or reflex) seizure & a probability of further seizures similar to the general  Carbamazepine (1st line) Males, others. Young female
Criteria recurrence risk (at least 60%) after two unprovoked seizures, occurring over the next 10 years.  Phenytoin Valproic acid Lamotrigine
3) Diagnosis of an epilepsy syndrome
Levetiracetam
Post- ictal Time between end of seizure & return to baseline
Confusion, lack of alertness Drug resistant epilepsy: resistant to 2 or more drugs for > 1 year (In 30% of ptns)
state
Post ictal weakness/paralysis  Todd’s paralysis (progressive) 2) Surgery: Surgical resection of epileptogenic focus
Most common form of epilepsy 3) Other methods
E ology: Vagus nerve stimulation Responsive Neurostimulation (RNS),
Deep Brain Stimulation (DBS).
o Temporal lobe (Hippocampal) sclerosis (Found in histology).
Temporal o (Structural cause).
Ketogenic diet (Low carbs)
Palliative surgeries: Corpus Callosotomy; Subpial transections
lobe Focal seizure with impaired awareness (complex partial seizure)
epilepsy  Déjà vu, Rising Epigastric sensation.  Epilepsy inves ga ons: Epilepsy Drugs: (AED)
 Aura (Olfactory, gustatory, auditory hallucinations). 1) EEG 2) MRI Not stopped immediately  Taper dose
 Automatism
 Purposeless, stereotyped, repetitive behavior
 Oral automatism (lip-smacking) Status epilep cus:
Other lobes  Frontal lobe Seizure: Defini on A) Seizure that lasts ≥ 5 minutes or
B) Multiple seizures without complete return to baseline. (>2)
 Motor jerk movement, bicycle like.  Happen with Generalized tonic-clonic seizures
Notes
 brief recurrent with quick regain of  Emergent Life-threatening condition (Hypoxia)
consciousness Management ABC IV lorazepam : (IV phenytoin)
Not working
 occipital lobe Seizure: (*Airway*) (IV Benzodiazepines)
Still unresolved seizures  Anesthesia & intubation.
 elementary visual hallicunations
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Epilepsy DDX:
Seizure Generalized Focal 1) Syncope 2) TIA
MRI Generalized Focal lesion 3) Movement Disorder
abnormality
Aura ✔ Seizure Provoking factors:
Dura on shorter longer 1) Infection 2) Hypoglycemia

Pseudoseizure - Complete return to normal state (No post-ictal confusion)

(Psychogenic
non-epileptic seizure)
- Normal EEG
Associated with:
 Child abuse
 psychiatric disorders (Depression)
Most specific test  24-hour video monitoring.

Resolved epilepsy:
1) Individuals with age-dependent epilepsy syndrome & now past the applicable age.
2) Seizure-free for the last 10 years, with no seizure drugs for the last 5 years.

AED Drug S/E

Carbamazepine Hyponatremia. (SIADH) Hair loss Neutropenia Ataxia
Phenytoin Thrombophlebitis. Gingival hypertrophy Ataxia
Valproate Weight gain tremor Pancreatitis Thrombocytopenia.
Most teratogenic Hepatotoxic.
Topiramate Weight loss Metabolic acidosis kidney stone.
Leve racetam Somnolence, Fatigue, allergy.
Least effect on hepatic enzyme

 Carbamazepine is 1st line drug for Trigeminal neuralgia.

 Topiramate  Treatment for tremor.
 Lamotrigine is a sodium channel blocker.

 SUDEP (sudden unexpected death in epilepsy):

 With or without evidence of Seizures
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Giant cell arteri s (Temporal Arteri s)
INTRO  Systemic inflammatory vasculitis
 Affect the superficial temporal artery
Epidemiology  Old persons (>60 years, increases with age)
 More in females.
 Associated with PMR (Polymyalgia rheumatica).
 Temporal Headache.
Clinical  Tender temporal artery.
features  Fever, Jaw claudica on.
 Unilateral visual blurring or vision loss.
Inves ga ons ESR and CRP (elevated)
Superficial temporal artery biopsy (STAB): (Gold standard)
Treatment High-dose corticosteroids.

Pseudotumor cerebri syndrome (Idiopathic intracranial hypertension)

INTRO  Unknown etiology
 Chronically elevated intracranial pressure (ICP).
Epidemiology Obese Female childbearing age. (Young age)
Clinical Symptoms related to increased ICP and papilledema.
features Headache (MC) Mild-Moderate Diffuse bilateral may be progressive
Visual Transient visual loss blindness.
manifesta ons Diplopia papilledema
CN6 palsy (MC) *abducens* CN4 palsy (2nd MC )
Inves ga ons Lumbar puncture High opening pressure
MRI Exclude structural cause
MRV Exclude Cerebral venous thrombosis (CVT)
Treatment
Lifestyle modifica on Medical Surgical
weight loss Acetazolamide - Optic nerve sheath fenestration
- Shunt

Red flags associated with secondary headache (SNOOP):

1) Systemic signs and symptoms: (Fever, meningismus, vomiting, immunocompromised, anticoagulation)
2) Neurological symptoms: (AMS, weakness, seizures)
3) Onset is abrupt and severe.
4) Older age.
5) Progressive.
6) Papilledema.
7) Postural / Precipitated by Valsalva.
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o Peripheral Nerve Disorder:  Polyneuropathy Classifica on
1) Mononeuropathy: individual nerve. 1) Sensory or motor involvement or both.
A) Mononeuritis simplex (trauma, entrapment) Saturday night palsy, Carpal tunnel syndrome 2) Site of disease: • Myelin sheath: demyelinating neuropathy
B) Mononeuritis multiplex (Multifocal) systemic disorders such as DM, etc. • Nerve fiber: axonal neuropathy
2) Polyneuropathy: multiple peripheral nerves
3) Radiculopathy: Nerve root involvement.
 Polyneuropathy - causes
Infec on Leprosy Diphtheria Lyme disease HIV -
Mononeuropathies Inflammatory Guillain -Barre CIDP (Chronic inflammatory Vasculitis – Sarcoidosis
syndrome demyelinating polyneuropathy) lupus
 Carpal Tunnel Syndrome Nutri onal Thiamine deficiency B12 deficiency Niacin deficiency
E ology Compression of median nerve at wrist as it passes through carpal tunnel. Inherited CMT (Charcot – Marie tooth)
Clinical  Pain in the hand or arm (especially at night) Metabolic Diabetes mellitus Uremia Amyloid
Features:  Wasting and weakness thenar eminence muscles. Toxic Alcohol lead Arsenic
 pollicis brevis (Opponens, Abductor, Flexor) & lateral 2 lumbricals.
Drugs Isoniazid vincristine metronidazole phenytoin
 Sensory loss in hand (median nerve distribution).
Physical 1) Tinel’s test 2) Phalen’s test
exam tests (By tapping/percussing)  Paresthesia (Wrists flexion 90° at each other)
 Polyneuropathy - Clinical features
Inves ga ons A) NCS (nerve conduction study) B) EMG (Electromyography)
Sensory • Distal numbness.
Treatment Splinting Local corticosteroids injection Surgical decompression
• Pain or Paresthesia.
(Transverse ligament)
Motor • Distal weakness.
• muscle Wasting.
 Ulnar Neuropathy Longstanding neuropathy: Hand and foot deformity, ulcers.
E ology  Areas of entrapment: Cubital tunnel (elbow), Guyon’s canal(wrist).
 Under pressure damage at elbow
Clinical  Pain and/or tingling paresthesia Guillain-Barré Syndrome
Features:  Radiating from elbow down forearm to ulnar border of the hand. Intro Acute inflammatory demyelinating polyneuropathy
 Wasting & weakness of intrinsic muscles of the hand. (Hypothenar group). Attack Shawn cells  Peripheral myelin.
 Sensory loss in the hand in the distribution of the ulnar nerve Associated with Preceding event. (2/3 of cases).
 Claw hand deformity in chronic lesions
E ology
- Infection (Campylobacter jujuni) (Bloody diarrhea), VZV.
Treatment • Mild lesions: Cushioning medial epicondyle. - Surgery, trauma, Vaccine.
• Severe: Surgical decompression or ulnar nerve transposition. 1) Preceding event (1-3 weeks before).
Course 2) Progressive (Active diz) phase (up to 4 weeks). 3% recurrence
3) plateau (Months).
4) Regress (After years).
 Radial Palsy
Clinical o Motor > sensory.
 Saturday night palsy
o Progressive, Ascending, Symmetrical limb weakness
 Acute wrist drop. features o Legs  Arms  Cranial nerve  Respiratory muscle (Life threatening)
 sensory loss in radial nerve distribution o Very rapid course.
o Severe cases  Autonomic instability & respiratory involvement.
 Brachial Plexus Lesions Physical A) Flaccid paralysis.
Erb's paralysis Upper plexus injury (c5-c6) waiter tip deformity, winged scapula B) Hypo/areflexia
exam C) Minor sensory deficits
Klumpke's paralysis Lower plexus injury (C8-T1) Full claw hand.
D) CN palsies: CN#5, bulbar dysfunction.
Inves ga ons Lumbar puncture Cyto-Albumin Dissociation. (Don’t rule out diagnosis)
 Meralgia Paresthe ca NCS / EMG Demyelinating neuropathy
 Compression of lateral cutaneous nerve of the thigh
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GBS  IV – IG Notes:
treatment  Plasmapheresis  DM polyneuropathy  stocking-gloves pattern.
 Contraindicated  Steroids.
 Carpal tunnel systemic causes  DM, RA.
GBS Miller fisher vairant 1) Ophthalmoplegia
Variants 2) Ataxia  Palpable Enlarged Nerves  Hereditary Demyelinating Neuropathy
3) Areflexia  Respiratory failure (GBS, Myasthenic crisis)  do PFT (Forced vital capacity).
DDX Polymyositis Botulism Myasthenia gravis
(asymmetrical) (Descending) GBS (Acute demyelina ng polyneuropathy Chronic demyelina ng polyneuropathy
Don’t give steroids Can give steroids
- Onion bulb on nerve biobsy
Myasthenia Gravis Cyto-albumin dissocia on (high protein with normal cell count):
E ology Autoimmune Disorder
An bodies against acetylcholine receptors at neuromuscular junc on.
Associated thymus pathology (Thymoma).
Clinical Fa gable weakness:
features  worsens with muscle use (Movement) & improves with rest.
 Best at morning.
Fatigable ptosis
Ophthalmoplegia, Diplopia
Bulbar symptoms (Dysphagia, Dysarthria)
Myasthenic - Acute, life-threatening exacerbation of myasthenic symptoms,
crisis - Respiratory failure
Tests Tensilon test Ice pack test.
Inves ga ons Serum ACH receptor an body analysis
An -MUSK (muscle specific tyrosine kinase)
RNS (rapid nerve stimulation test) (Decremental response)
EMG (most sensitive test).
Treatment Cholinesterase inhibitors (Neos gmine, pyridos gmine)
Cor costeroids

Inflammatory myopathy
Polymyosi s Inflammatory myopathy
Dermatomyosi s Inflammatory myopathy & distinctive skin findings
Clinical  Proximal symmetrical muscle weakness.
 Skin Gottron papules (on hand extensors)
Features (Dermatomyosi s) heliotrope rash (Upper eyelids)
Associated with Arthralgia and Raynaud’s phenomenon
Inves ga ons Crea n kinase elevated
EMG
Muscle biobsy
Treatment A) Cor costeroids B) immunosuppressant drugs
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Neurocognitive Domains affected in dementia Frontotemporal dementia (Pick’s disease)

memory & Speech Behavioral domain Visuospatial Executive Variant → Behavioral variant of frontotem
Learning (Language) (Personality changes) disorientation function. Clinical features  Early behavioral &
 Compulsive beha
 Hyperorality (Bing
Alzheimer's disease Investigations: Brain MRI/CT scan
Epidemiology Most common cause of dementia in elderly (>65 years)
Risk factors 1) Age (Most important) > 65 years.
2) Family history. Lewy body Dementia
3) Low socio-economic status.  Parkinsonism & Dementia <
4) APOE4 gene alleles.
 Symmetrical rigidity (Not alw
➢ Cortex Degeneration/atrophy especially parietal & hippocampus
➢ Narrowing of gyri & widening of sulcus  Main Affected cognitive Dom
➢ Ex-vacou ventriculomegaly.
Etiology ➢ Main affected domain is memory. (Not only)
Aβ (Amyloid beta) protein Extracellular in gray matter
accumulation
Neurofibrillary tangles Hyperphosphorylated Tau proteins
Intracellular, Inside the neurons.
MRI Hippocampal atrophy
Investigations Cortical atrophy
Ex-vacou ventriculomegaly.
Clinical test ➢ Mini mental status exam (30 points) (MMSE)
- Normal >27
Histo- Amyloid plaques Neurofibrillary Granulovacuolar Neuron &
Pathology tangles degeneration synapses loss

Treatment Cholinesterase inhibitors (Donepezil, Rivastigmine Galantamine)

(1ST line)
(NMDA) antagonists (Memantine)
Notes ➢ Most common Variant → Amnestic variant early-onset AD:

Hypothyroidism
B12 deficiency
Reversible causes of Normal pressure hydrocephalus
dementia - Triad of : (Wet, wobble & wacky)
urinary gait apraxia Cognitive
incontinence dysfunction
Depression
Chronic SDH

Dementia Blood tests:

1) TSH 2) Vitamin B12