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CLINICAL NEUROLOGY - Previous Year Question Analysis

PDF 1: 2011-2025 (4th Year BPT, 20-Mark Questions - "Elaborate on")

PDF 2: 2020-2025 (3rd Year BPT New Reg, 15-Mark Questions - "Elaborate on")

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PART A: REPEATED 20-MARK QUESTIONS (PDF 1 - 4th Year)

Frequency Count of All 20-Mark Questions

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TOP REPEATED 20-MARK QUESTIONS (Most Important - Study These First!)

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PART B: REPEATED 15-MARK QUESTIONS (PDF 2 - 3rd Year New Regulation)

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PART C: COMPREHENSIVE ANSWERS TO ALL REPEATED 20-MARK AND 15-MARK QUESTIONS

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1. MYASTHENIA GRAVIS (20 Marks) - Asked 6 Times: MOST IMPORTANT

Definition

Neuromuscular Junction (NMJ) - Normal Anatomy

• The NMJ is the synapse between a motor nerve terminal and a skeletal muscle fiber.
• The nerve terminal releases acetylcholine (ACh) into the synaptic cleft.
• ACh binds to nicotinic receptors on the motor end plate, causing muscle contraction.
• In MG, anti-AChR antibodies block and destroy these receptors.

Etiology/Pathogenesis

• Autoimmune: 85% have anti-AChR IgG antibodies
• 5-8% have anti-MuSK (muscle-specific kinase) antibodies
• Antibodies cause:
  • Receptor blockade
  • Complement-mediated destruction of the post-synaptic membrane
  • Accelerated receptor degradation
• Thymus gland role: 75% have thymic abnormality - 65% thymic hyperplasia, 10% thymoma
• Thymoma may be present in 10-15% (often older males)

Clinical Features

• Ocular (50% at onset): Ptosis (drooping eyelid) - asymmetric, variable; Diplopia (double vision)
• Bulbar: Dysphagia (difficulty swallowing), dysarthria (nasal voice), dysphonia, difficulty chewing
• Limb: Proximal muscle weakness - difficulty climbing stairs, raising arms
• Respiratory: Diaphragm and intercostal muscle weakness - may cause myasthenic crisis

Osserman Classification

• Class I: Ocular only
• Class IIA: Mild generalized, slow progression, no crisis
• Class IIB: Moderate generalized, severe bulbar involvement
• Class III: Acute fulminating, rapid progression, respiratory involvement
• Class IV: Late severe (same as III but slow onset)
• Class V: Muscle atrophy

Investigations

1. Tensilon (Edrophonium) test: IV edrophonium (short-acting anticholinesterase) - transient dramatic improvement confirms MG
2. Serum anti-AChR antibodies: Positive in 85% (diagnostic)
3. Anti-MuSK antibodies: If AChR negative
4. Repetitive nerve stimulation (RNS): Decremental response >10% at 3Hz
5. Single fiber EMG (SFEMG): Most sensitive - increased jitter
6. CT/MRI Chest: Screen for thymoma
7. Chest X-ray
8. Pulmonary Function Tests: Monitor respiratory involvement

Myasthenic Crisis

• Acute respiratory failure due to severe muscle weakness
• Triggered by infection, surgery, medications, stopping treatment
• Emergency: requires ICU, mechanical ventilation, plasmapheresis or IVIG

Cholinergic Crisis (vs Myasthenic Crisis)

• Over-treatment with anticholinesterase
• Features: SLUDGE (Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis), bradycardia, miosis
• Treatment: Atropine, stop anticholinesterase

Medical Management

1. Anticholinesterases: Pyridostigmine (Mestinon) - first line, symptomatic relief
2. Immunosuppression:
   • Prednisolone (corticosteroids) - long-term
   • Azathioprine - steroid-sparing
   • Mycophenolate mofetil
   • Cyclosporine
3. Thymectomy: Indicated in thymoma; also considered in generalized MG aged 15-60
4. Plasmapheresis: Crisis or pre-thymectomy
5. IVIG (Intravenous Immunoglobulin): Crisis management

Physiotherapy Management

• Energy conservation techniques
• Breathing exercises and respiratory physiotherapy
• Graded exercises avoiding fatigue
• ADL training
• Postural correction
• Assistive devices for ptosis (ptosis props)
• Patient and caregiver education

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2. DUCHENNE MUSCULAR DYSTROPHY (20 Marks) - Asked 4 Times

Definition

Etiology

• X-linked recessive - gene locus at Xp21
• Mutation/deletion in dystrophin gene
• Dystrophin protein is completely absent (vs Becker MD where it is reduced/abnormal)
• Female carriers - usually asymptomatic; rarely symptomatic ("manifesting carriers")
• Incidence: 1 in 3500 male births

Pathophysiology

• Dystrophin normally links actin cytoskeleton to extracellular matrix via DGC (Dystrophin-Glycoprotein Complex)
• Without dystrophin, repeated muscle contraction causes membrane fragility and fiber necrosis
• Muscle fibers replaced by fat and fibrous tissue
• Progressive weakness results

Clinical Features

• Waddling gait (Trendelenburg gait)
• Toe walking
• Frequent falls
• Difficulty climbing stairs
• Gower's Sign: Patient uses hands to "walk up" own legs when rising from floor - sign of proximal lower limb weakness
• Pseudohypertrophy of calves - muscle replaced by fat and fibrous tissue, calves appear large but weak

• Wheelchair bound by age 10-12 years
• Scoliosis develops after wheelchair confinement
• Contractures: hip flexors, knee flexors, ankle plantarflexors, elbow flexors

• Cardiac involvement: Dilated cardiomyopathy in nearly all by age 18 (ECG changes, arrhythmias)
• Respiratory: Progressive respiratory failure - main cause of death
• Intellectual impairment in ~30% (mild)

Investigations

1. Serum CK (Creatine Kinase): Massively elevated - 50-100x normal (most sensitive early marker)
2. EMG: Myopathic pattern - short duration, low amplitude polyphasic units
3. Muscle Biopsy:
   • Absence of dystrophin on immunohistochemistry (diagnostic)
   • Variation in fiber size, necrosis, regeneration, fat infiltration
4. Genetic testing: Deletion analysis (PCR) - confirms diagnosis
5. ECG: Tall R waves V1, deep Q waves in lateral leads
6. Echocardiogram: Dilated cardiomyopathy
7. Pulmonary Function Tests: Monitoring

Staging (Vignos Scale for DMD)

1. Walks/climbs stairs without assistance
2. Walks, climbs stairs with aid of railing
3. Walks, cannot climb stairs
4. Walks unassisted but cannot rise from chair
5. Walks with assistance (bracing/long leg orthosis)
6. Uses wheelchair
7. Wheelchair-bound, can still perform most ADL
8. Wheelchair-bound, needs assistance with some ADL
9. Wheelchair-bound, needs assistance for most ADL
10. Bedridden

Medical Management

• Corticosteroids: Prednisolone/Deflazacort - slow progression, improve strength (standard of care)
• Cardiac: ACE inhibitors, beta-blockers for cardiomyopathy
• Respiratory: NIV (BiPAP/CPAP) when FVC <50%
• Gene therapy (newer): Exon skipping (Eteplirsen), Ataluren (stop codon read-through)

Physiotherapy Management

• Goals: Maintain functional mobility, prevent contractures, delay wheelchair confinement
• Stretching: Daily passive stretching of hip flexors, hamstrings, Achilles tendon, ITB
• Strengthening: Gentle submaximal exercises (avoid eccentric overload and fatigue)
• Orthoses: AFO (Ankle-Foot Orthosis), KAFOs (Knee-Ankle-Foot Orthosis)
• Hydrotherapy/Aquatic therapy: Excellent - buoyancy reduces load
• Spinal support: Scoliosis bracing, spinal surgery if >20 degrees
• Respiratory physiotherapy: Breathing exercises, assisted cough, secretion clearance
• Wheelchair prescription: Powered wheelchair when walking ceases
• Family education: Handling, positioning, prevention of pressure sores

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3. EPILEPSY (20 Marks) - Asked 4 Times

Definition

• A seizure is a transient occurrence of signs/symptoms due to abnormal excessive neuronal activity.
• Epilepsy = recurrent unprovoked seizures (or one seizure with high recurrence risk)

Classification (ILAE 2017)

1. Focal (Partial) seizures - begin in one hemisphere
   • Focal aware (simple partial)
   • Focal impaired awareness (complex partial)
   • Focal to bilateral tonic-clonic
2. Generalized seizures - involve both hemispheres from onset
   • Tonic-clonic (Grand mal)
   • Absence (Petit mal)
   • Myoclonic
   • Tonic
   • Atonic (drop attacks)
   • Clonic
3. Unknown onset

Etiology

• Structural: Stroke, tumor, trauma, dysplasia, hippocampal sclerosis
• Genetic: Channelopathies (SCN1A mutations in Dravet), chromosome disorders
• Infectious: Meningitis, encephalitis, neurocysticercosis, TB
• Metabolic: Hypoglycemia, hyponatremia, hypocalcemia, uremia
• Immune: Autoimmune encephalitis
• Unknown

Pathophysiology

• Normal: Balance between excitatory (glutamate) and inhibitory (GABA) neurotransmission
• Epilepsy: Failure of inhibition or excessive excitation
• Neurons show paroxysmal depolarization shift (PDS) - large sustained depolarization with burst of action potentials
• Spread of excitation from focus to adjacent areas creates clinical manifestations
• Kindling phenomenon: Repeated sub-threshold stimulation lowers seizure threshold

Clinical Features

1. Prodrome: mood changes hours before
2. Aura: Focal onset - sensory, motor, autonomic, psychic
3. Tonic phase: Sudden loss of consciousness, rigid extension (10-30 sec) - may bite tongue, emit epileptic cry
4. Clonic phase: Rhythmic jerking movements (30-60 sec)
5. Postictal phase: Confusion, headache, lethargy, Todd's palsy (transient focal weakness)

• Sudden brief (5-30 sec) stare, blank expression
• No aura, no postictal phase
• 3 Hz spike-and-wave on EEG
• Common in children 4-14 years

• Aura, then impaired consciousness
• Automatisms (lip smacking, chewing, picking at clothes)
• Typically temporal lobe origin

Status Epilepticus

• Continuous seizure >5 minutes or two seizures without recovery
• Medical emergency
• Management: Diazepam/Lorazepam IV → Phenytoin/Valproate IV → Phenobarbital → General anesthesia

Investigations

1. EEG: Interictal epileptiform discharges, seizure pattern; 3Hz spike-wave in absence
2. MRI Brain: Structural causes - hippocampal sclerosis, tumors, malformations
3. CT Brain: Acute setting
4. Blood tests: CBC, electrolytes, glucose, calcium, liver/kidney function
5. Metabolic screen in children
6. Lumbar puncture if infection suspected

Medical Management (Anti-Epileptic Drugs - AEDs)

• Start with monotherapy, low dose, titrate up
• Drug-resistant epilepsy (failure of 2 adequate AEDs)

Surgical Management

• Temporal lobectomy (most common)
• Lesionectomy
• Corpus callosotomy (drop attacks)
• Vagus nerve stimulation (VNS)
• Ketogenic diet

Physiotherapy Management

• Education on seizure first aid
• Safety precautions (padding, helmets if frequent falls)
• Avoid triggers (sleep deprivation, photosensitivity)
• Regular exercise (does not increase seizure frequency)
• Driving restrictions counseling
• ADL training and vocational rehabilitation

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4. SPASTICITY / TONE (20 Marks) - Asked 3 Times

Definition of Tone

Spasticity - Definition

• Lance's definition (1980): "A motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex."

Rigidity - Definition

Differences: Spasticity vs Rigidity

Causes of Spasticity

• Stroke (most common in adults)
• Spinal Cord Injury
• Cerebral Palsy (most common in children)
• Multiple Sclerosis
• Traumatic Brain Injury
• Tumors of brain/spinal cord

Assessment of Spasticity

1. Modified Ashworth Scale (MAS): Most widely used clinical scale
   • Grade 0: No increase in tone
   • Grade 1: Slight increase - catch and release or minimal resistance at end range
   • Grade 1+: Slight increase - catch followed by minimal resistance through <50% ROM
   • Grade 2: Marked increase throughout most of ROM but part easily moved
   • Grade 3: Considerable increase - passive movement difficult
   • Grade 4: Rigid in flexion or extension
2. Tardieu Scale: Measures angle of catch at slow (R1) and fast (R2) velocities; more sensitive
3. Pendulum test: For lower limb spasticity (Wartenberg pendulum test)
4. Clinical examination: Clonus, deep tendon reflexes, Babinski sign
5. Functional measures: MAS, FIM, Barthel Index

Investigations

• MRI Brain/Spinal Cord: Identify underlying cause
• EMG/NCS: Distinguish from contracture
• Kinematics/Gait analysis (in specialized centers)

Management of Spasticity

• Stretching: Daily passive and active-assisted stretching
• Positioning: Antispastic patterns (reflex inhibitory postures)
• Splinting/Serial casting: Maintains range, reduces contracture
• Ice/Cold therapy: Temporary reduction
• Heat therapy
• Electrical stimulation: TENS, FES (Functional Electrical Stimulation)
• Bobath techniques (NDT)
• Inhibitory casting
• Task-specific training

• Baclofen (oral): GABA-B agonist at spinal cord - first line
• Tizanidine: Alpha-2 agonist - antispasticity + sedating
• Diazepam: GABA-A agonist - less preferred (sedation)
• Dantrolene: Acts peripherally on ryanodine receptor (blocks Ca2+ release)
• Intrathecal Baclofen (ITB) pump: Severe spasticity, SCI/CP
• Botulinum toxin type A (Botox): Focal spasticity - blocks ACh release at NMJ; effects last 3-6 months

• Selective Dorsal Rhizotomy (SDR): For CP
• Tendon lengthening/transfer
• Neurotomy
• Phenol/Alcohol nerve blocks

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5. MULTIPLE SCLEROSIS (20 Marks) - Asked 3 Times

Definition

Epidemiology

• Most common disabling neurological disease in young adults
• Female:Male = 2:1
• Peak onset: 20-40 years
• More prevalent farther from equator ("latitude gradient")

Etiology

• Genetic: HLA-DR2 (DRB1*1501) allele; 30% concordance in identical twins
• Environmental: Vitamin D deficiency, EBV infection, smoking
• Autoimmune: T-cell mediated attack on myelin

Pathology

• Plaques: Focal areas of demyelination with relative axonal preservation (early); later axonal loss
• Periventricular white matter most common
• Also: optic nerves, brainstem, cerebellum, spinal cord
• Inflammatory infiltrate (T cells, macrophages)
• Remyelination (shadow plaques) in relapsing MS
• Progressive axonal loss in chronic/progressive MS

Pathophysiology

1. Peripheral T-cells activated by molecular mimicry (EBV, other triggers)
2. T-cells cross blood-brain barrier
3. Attack myelin sheaths
4. Demyelination → conduction slowing/block → neurological deficits
5. Remyelination → partial recovery
6. Repeated attacks → cumulative axonal loss → permanent disability

Clinical Features

1. Optic Neuritis: Painful loss of vision in one eye; afferent pupillary defect (Marcus Gunn pupil); color desaturation; most common first presentation
2. Internuclear Ophthalmoplegia (INO): Failure of adduction of the ipsilateral eye with nystagmus in the abducting eye - due to MLF lesion; BILATERAL INO is almost pathognomonic of MS
3. Sensory symptoms: Numbness, tingling, Lhermitte's sign (electric shock sensation down spine on neck flexion)
4. Motor: Spastic weakness, UMN signs
5. Cerebellar: Ataxia, dysmetria, intention tremor, scanning speech
6. Bladder: Urgency, frequency, incontinence (neurogenic bladder)
7. Fatigue: Most common and disabling symptom
8. Uhthoff's phenomenon: Worsening of symptoms with heat/fever

Clinical Subtypes

• Relapsing-Remitting MS (RRMS): 85% at onset; attacks followed by partial/complete recovery
• Secondary Progressive MS (SPMS): RRMS that becomes progressive
• Primary Progressive MS (PPMS): Progressive from onset without relapses (10-15%)
• Progressive-Relapsing MS (PRMS): Progressive from onset with superimposed relapses

Investigations

1. MRI Brain + Spine: Gold standard
   • T2/FLAIR: Hyperintense plaques (periventricular "Dawson's fingers", juxtacortical, infratentorial)
   • T1 Gadolinium: Active plaques (enhancing)
   • Dissemination in space (DIS) and time (DIT) - McDonald criteria
2. Visual Evoked Potentials (VEPs): Prolonged P100 latency
3. CSF analysis: Oligoclonal bands (IgG) in >95%, elevated IgG index, mild pleocytosis
4. McDonald Criteria 2017: For diagnosis

Medical Management

• IV Methylprednisolone 1g/day x 3-5 days (shortens duration; does not affect long-term disability)

• First-line: Interferon-beta 1a/1b, Glatiramer acetate
• Highly effective: Natalizumab (anti-VLA-4), Ocrelizumab (anti-CD20), Alemtuzumab, Cladribine
• Oral: Dimethyl fumarate, Fingolimod, Teriflunomide
• PPMS: Ocrelizumab (first approved DMT for PPMS)

• Spasticity: Baclofen, Tizanidine, Botox
• Fatigue: Amantadine, Modafinil
• Bladder: Anticholinergics, intermittent catheterization
• Pain/Paresthesia: Gabapentin, Amitriptyline
• Depression: SSRI

Physiotherapy Management

• During relapse: Rest, energy conservation, position to prevent complications
• Post-relapse: Graded exercise programme
• Spasticity management
• Balance and coordination training
• Fatigue management (Pacing, energy conservation)
• Gait retraining with/without orthoses
• Aerobic exercise (has neuroprotective effects)
• Cooling techniques (Uhthoff phenomenon)
• Respiratory physiotherapy
• ADL and vocational training
• Assistive devices and wheelchair prescription

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6. CEREBRAL PALSY (20 Marks) - Asked 3 Times

Definition

Etiology

• Congenital brain malformations
• Periventricular leukomalacia (PVL) in premature infants
• Intrauterine infections (TORCH: Toxoplasma, Rubella, CMV, Herpes)
• Maternal toxemia, diabetes, Rh incompatibility
• Stroke in utero

• Birth asphyxia / HIE (Hypoxic Ischemic Encephalopathy) - most common overall cause
• Premature birth (<32 weeks)
• Low birth weight
• Difficult delivery (forceps, prolonged labor)

• Meningitis/Encephalitis
• Head injury
• Near-drowning
• Kernicterus (bilirubin encephalopathy)

Pathophysiology

• Brain injury during development (before, during, or after birth up to age 2 years)
• Results in permanent structural brain lesion
• Lesion does NOT progress but clinical picture may change as child grows
• PVL (Periventricular Leukomalacia) - most common in premature - affects corticospinal tracts (legs > arms)

Classification

1. Spastic CP (75-85%): Increased muscle tone, UMN signs (hyperreflexia, clonus, Babinski)
   • Spastic Diplegia: Both legs (premature infants, PVL)
   • Spastic Hemiplegia: One side
   • Spastic Quadriplegia/Tetraplegia: All four limbs (most severe)
2. Dyskinetic/Athetoid CP (10-15%): Involuntary writhing (athetosis), chorea; due to basal ganglia damage (often kernicterus)
3. Ataxic CP (5%): Poor balance, coordination, intention tremor; cerebellar damage
4. Mixed CP

Clinical Features

• Delayed motor milestones
• Abnormal muscle tone (spasticity most common)
• Primitive reflexes persist (ATNR, STNR, Moro)
• Abnormal postural reactions
• Abnormal movement patterns

• UL: Shoulder adduction/internal rotation, elbow flexion, wrist flexion/pronation, thumb-in-palm
• LL: Hip flexion/adduction/internal rotation, knee flexion, ankle plantarflexion (equinus), scissoring gait

• Intellectual disability (60%)
• Epilepsy (30-50%)
• Visual problems (strabismus, CVI)
• Hearing loss
• Speech disorders
• Learning disabilities
• Behavioral problems
• Feeding difficulties

Investigations

• MRI Brain: Identifies type and extent of lesion
• EEG: If seizures suspected
• Developmental assessment
• Metabolic/Genetic screen: To exclude progressive conditions
• Ophthalmological assessment
• Audiological assessment

Management

• NDT/Bobath approach - facilitate normal movement
• Stretching and strengthening
• Balance training
• Gait training with/without orthoses
• AFO (Ankle-Foot Orthosis) for equinus/foot drop
• KAFO for more proximal weakness
• Serial casting
• Hydrotherapy
• Functional training and ADL

• Upper limb function
• ADL training
• Splinting (resting/functional)

• Oral Baclofen, Tizanidine for spasticity
• Botulinum toxin (Botox): Focal spasticity (gastrocnemius, hip adductors)
• Intrathecal Baclofen: Severe generalized spasticity
• Antiepileptics if seizures

• Selective Dorsal Rhizotomy (SDR)
• Orthopaedic surgery: Tendon lengthening (Achilles), muscle release (adductor release), derotation osteotomies

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7. SPINAL CORD INJURY (20 Marks) - Asked 3 Times

Definition

Causes/Etiology

• Road traffic accidents (RTA) - most common
• Falls from height
• Sports injuries (diving into shallow water - cervical)
• Gunshot wounds
• Industrial accidents

• Cervical spondylosis/disc prolapse
• Spinal tumors
• Transverse myelitis
• Spinal abscess
• Vascular (anterior spinal artery syndrome)
• Tuberculosis of spine

Classification

• ASIA A: Complete - no motor/sensory function below injury
• ASIA B: Incomplete - sensory only preserved below injury
• ASIA C: Incomplete - motor preserved below, >50% key muscles <grade 3
• ASIA D: Incomplete - motor preserved below, >50% key muscles ≥ grade 3
• ASIA E: Normal

1. Central Cord Syndrome: UL > LL weakness, bladder dysfunction; most common; hyperextension in elderly with cervical spondylosis
2. Brown-Sequard Syndrome: Hemisection; ipsilateral motor + proprioception loss; contralateral pain/temperature loss
3. Anterior Cord Syndrome: Motor + pain/temperature loss (anterior 2/3); proprioception preserved (posterior columns intact); worst prognosis
4. Posterior Cord Syndrome: Proprioception loss; rare
5. Conus Medullaris Syndrome: Mixed UMN + LMN features; bowel/bladder/sexual dysfunction
6. Cauda Equina Syndrome: LMN; flaccid bladder/bowel, saddle anesthesia, lower limb LMN weakness

Clinical Features at D10 (T10) Level

• Trunk muscles below T10 paralyzed (lower abdominals)
• Lower limbs: Complete paraplegia (UMN pattern: spasticity, hyperreflexia, Babinski)
• Upper limbs: Normal
• Respiratory: Normal (intercostals up to T10, diaphragm C3-5)
• Beevor's sign: Positive (umbilicus moves upward - T9-10 lesion)

• Loss of all sensation below umbilicus (T10 dermatome)

• Neurogenic bladder (UMN bladder: reflex bladder with small capacity)
• Neurogenic bowel
• Sexual dysfunction
• Autonomic dysreflexia (lesions above T6)
• Orthostatic hypotension

Secondary Complications

1. Pressure ulcers/Decubitus ulcers
2. Urinary tract infections (UTI)
3. Respiratory complications (pneumonia, atelectasis)
4. Deep vein thrombosis (DVT) and pulmonary embolism
5. Heterotopic ossification
6. Spasticity
7. Autonomic dysreflexia
8. Contractures and deformities
9. Osteoporosis
10. Depression and psychological problems
11. Chronic pain

Physiotherapy Management - Acute Phase

• Prevention of complications
• Chest physiotherapy (secretion clearance, breathing exercises)
• Passive ROM to prevent contractures
• Positioning and turning (2-hourly)
• Splinting
• Patient/family education

Physiotherapy Management - Rehabilitation Phase

• Wheelchair skills training
• Transfers: bed ↔ wheelchair, wheelchair ↔ toilet
• Pressure relief techniques
• Mat exercises: Rolling, sitting, push-ups
• Standing in tilt table
• Ambulation training with KAFO + crutches (household ambulators)
• Bladder training: Intermittent catheterization
• Bowel programme
• ADL independence training

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8. PARKINSON'S DISEASE (20 Marks) - Asked 2 Times in PDF1, 2 Times in PDF2

Definition

Etiology

• Idiopathic (most common): >80%
• Genetic forms: LRRK2, PARK2 (Parkin), PINK1, SNCA mutations
• Environmental: Pesticide (MPTP, paraquat), heavy metals
• Age (risk factor)

Pathology

• Loss of dopaminergic neurons in substantia nigra pars compacta
• Lewy bodies: Eosinophilic intracytoplasmic inclusions containing alpha-synuclein - pathological hallmark
• Normal dopamine:acetylcholine balance disrupted → excess cholinergic activity

Pathophysiology

• Dopamine normally inhibits the indirect pathway and facilitates the direct pathway in basal ganglia
• Dopamine loss → hyperactivation of indirect pathway → excessive inhibition of thalamus → reduced thalamocortical activation → paucity and slowness of movement (bradykinesia, rigidity)

Clinical Features

1. Tremor: Resting tremor; pill-rolling; 4-6 Hz; disappears with action and sleep; worsens with stress
2. Rigidity: Leadpipe + cogwheel (tremor superimposed); present throughout range; Froment's maneuver
3. Akinesia/Bradykinesia: Slowness/poverty of movement; micrographia (small writing); hypomimia (masked face); hypophonia (soft voice)
4. Postural instability: Late sign; retropulsion; falls; festinant gait, freezing

• Autonomic: Constipation (often first symptom), orthostatic hypotension, urinary dysfunction, excessive sweating
• Cognitive: Parkinson's Dementia
• Psychiatric: Depression (most common), anxiety, psychosis (drug-induced)
• Sleep: REM sleep behavior disorder (RBD) - often precedes motor symptoms by years
• Sensory: Anosmia (early), pain

Hoehn & Yahr Classification

• Stage 1: Unilateral involvement only
• Stage 2: Bilateral, no balance impairment
• Stage 3: Mild-moderate bilateral, some postural instability, independent
• Stage 4: Severe disability, still able to walk/stand unassisted
• Stage 5: Wheelchair bound or bedridden, requires full assistance

Investigations

• Primarily clinical diagnosis
• MRI Brain: Normal (to exclude other causes)
• DAT scan (DaTscan/SPECT): Reduced dopamine transporter uptake in striatum - confirms dopaminergic deficit
• PET scan: Reduced F-DOPA uptake
• Levodopa challenge test: Marked improvement supports diagnosis

Medical Management

1. Levodopa + Carbidopa (Sinemet): Most effective; carbidopa prevents peripheral conversion; long-term: wearing-off, dyskinesias, on-off fluctuations
2. Dopamine agonists: Pramipexole, Ropinirole, Rotigotine (patch) - used especially in younger patients to delay levodopa
3. MAO-B inhibitors: Selegiline, Rasagiline - mild symptomatic + possible neuroprotection
4. COMT inhibitors: Entacapone, Tolcapone - extend levodopa effect
5. Amantadine: For dyskinesias

• Deep Brain Stimulation (DBS): STN (subthalamic nucleus) or GPi (globus pallidus interna); for advanced PD with motor fluctuations
• Pallidotomy: Older procedure for dyskinesias

Physiotherapy Management

• Gait training: Large step strategy, auditory cueing (metronome), visual cues (laser pointer on floor)
• LSVT BIG: High-amplitude movement training (like LSVT LOUD for speech)
• Balance training: Reduce fall risk
• Stretching: Prevent rigidity-related contractures
• Facial exercises: Hypomimia
• Breathing exercises: Maintain chest expansion
• Bed mobility: Rolling, getting up technique
• Nordic walking/Treadmill training
• Tai Chi (evidence-based for balance)
• Caregiver training
• Assistive devices: Walking frame, raised toilet seat

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9. HYDROCEPHALUS (20 Marks) - Asked 2 Times in PDF1

Definition

Normal CSF Circulation

• Produced by choroid plexus in lateral ventricles (500 mL/day)
• Flows: Lateral ventricles → Foramen of Monro → Third ventricle → Aqueduct of Sylvius → Fourth ventricle → Foramina of Magendie/Luschka → Subarachnoid space → Absorbed by arachnoid villi into dural sinuses

Classification

1. Non-communicating (Obstructive): CSF pathway blocked within ventricular system
   • Aqueductal stenosis (most common congenital)
   • Posterior fossa tumors
   • Dandy-Walker syndrome
   • Arnold-Chiari malformation
2. Communicating: Obstruction outside ventricles (at arachnoid villi or subarachnoid space)
   • Post-meningitis (arachnoid adhesions)
   • Post-subarachnoid hemorrhage
   • Normal Pressure Hydrocephalus (NPH)

• Normal Pressure Hydrocephalus (NPH): Triad of Hakim Adams - Wet (incontinence) + Wobbly (gait ataxia) + Wacky (dementia); responds to CSF drainage
• Ex-vacuo hydrocephalus: Ventricular enlargement due to brain atrophy (not true hydrocephalus)

Clinical Features

• Enlarging head circumference (>97th percentile)
• Bulging anterior fontanelle
• Sunset sign (downward deviation of eyes)
• Dilated scalp veins
• High-pitched cry
• Poor feeding
• Macewen's "cracked pot" sign on skull percussion

• Headache (worse in morning, with straining/coughing - increased ICP)
• Nausea and vomiting (projectile)
• Papilledema (blurred vision, visual loss)
• Diplopia (VI nerve palsy)
• Altered consciousness
• Gait ataxia
• Incontinence

Investigations

1. CT Brain: Ventricular enlargement; identifies cause
2. MRI Brain: More detailed; shows aqueductal flow void; better for posterior fossa
3. Head circumference measurement (infants)
4. Cranial Ultrasound: Neonates and infants (open fontanelle)
5. CSF analysis: After shunting or lumbar puncture

Management

1. VP Shunt (Ventriculo-Peritoneal): Most common; catheter from lateral ventricle to peritoneum
2. VA Shunt (Ventriculo-Atrial): To right atrium
3. Endoscopic Third Ventriculostomy (ETV): For aqueductal stenosis - fenestration of third ventricle floor; avoids shunt (preferred in older children/adults)
4. Temporary: External Ventricular Drain (EVD) for acute hydrocephalus

• Acetazolamide (reduces CSF production)
• Furosemide

• Post-shunt rehabilitation
• Head control exercises (infants)
• Developmental facilitation
• Gait training
• Balance exercises
• Monitoring for shunt malfunction symptoms

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10. TRAUMATIC BRAIN INJURY (20 Marks) - Asked 2 Times

Definition

Classification

• Mild TBI: GCS 13-15 (concussion)
• Moderate TBI: GCS 9-12
• Severe TBI: GCS 3-8

1. Primary Injury: At time of impact
   • Scalp laceration, skull fracture
   • Contusion, laceration
   • Diffuse axonal injury (DAI)
   • Extradural hematoma (EDH): Arterial - middle meningeal artery; lenticular/biconvex on CT
   • Subdural hematoma (SDH): Bridging veins; crescent on CT
   • Intracerebral hematoma
   • Subarachnoid hemorrhage (SAH)
2. Secondary Injury: Hours/days later
   • Cerebral edema
   • Raised ICP
   • Hypoxia, hypotension, hypoglycemia
   • Hydrocephalus
   • Infection

Clinical Features

• Lucid interval after initial LOC
• Then rapid deterioration
• Signs of raised ICP
• Ipsilateral pupil dilation (III nerve compression)
• Contralateral hemiparesis
• Emergency neurosurgery (evacuation)

• Acute: High-impact; rapid deterioration
• Chronic: Elderly, minor trauma; gradual headache, confusion, fluctuating consciousness
• Crescent-shaped hyperdensity (acute) on CT

• Racoon eyes (periorbital ecchymosis - anterior fossa)
• Battle's sign (mastoid ecchymosis - posterior fossa)
• CSF rhinorrhea (CSF from nose)
• CSF otorrhea (CSF from ear)
• Hemotympanum

• High-speed deceleration injury
• Immediate deep coma with no lucid interval
• Poor prognosis
• CT: Multiple petechial hemorrhages at grey-white interface

Investigations

1. CT Brain (non-contrast): First-line imaging - identifies hematomas, fractures
2. MRI Brain: Better for DAI, contusions, brainstem
3. Skull X-ray: Limited use
4. ABCs assessment, GCS monitoring
5. ICP monitoring in severe TBI

Stages/Management

• ABCDE approach (Airway, Breathing, Circulation, Disability, Exposure)
• Secure airway (intubation if GCS <8)
• Maintain O2 sat >95%, normotension
• Prevent secondary brain injury
• Surgical: Evacuate EDH/SDH/contusion if indicated
• ICP management: Head elevation 30°, osmotherapy (mannitol/hypertonic saline), mild hyperventilation, decompressive craniectomy

• Monitor for complications
• Nutritional support
• DVT prophylaxis
• Treat seizures
• Tracheostomy if prolonged ventilation

Physiotherapy Rehabilitation

• ICU/Acute: Positioning, PROM, chest physiotherapy, sensory stimulation (coma patients)
• Subacute: Bed mobility, sitting balance, transfers
• Cognitive rehabilitation: Attention, memory, executive function
• Gait retraining
• Spasticity management
• ADL training
• Communication (with SLT)
• Return to work/education planning
• Caregiver training

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11. TUBERCULOUS MENINGITIS / TB CNS Infection (20 Marks) - Asked 2 Times

Definition

Etiology

• Caused by Mycobacterium tuberculosis
• Reaches CNS by hematogenous spread from primary focus (usually lungs)
• Risk factors: Immunosuppression (HIV/AIDS), malnutrition, overcrowding, DM, alcoholism
• More common in developing countries

Pathology

• Rich foci: Small cortical/meningeal granulomas rupture into CSF space
• Thick gelatinous exudate at base of brain (basal meningitis)
• Vasculitis of cerebral arteries → infarction
• Hydrocephalus (communicating) due to CSF flow obstruction
• Cranial nerve palsies
• Tuberculoma formation

Clinical Stages (British Medical Research Council/MRC)

• Stage 1: Alert, no focal neurological deficits, no hydrocephalus
• Stage 2: Confusion/lethargy OR focal neurological deficits
• Stage 3: Stupor/coma OR severe neurological deficits

Clinical Features

1. Constitutional: Fever (low-grade), weight loss, night sweats, anorexia
2. Meningeal: Headache (severe), neck stiffness, Kernig's sign (+), Brudzinski's sign (+), photophobia
3. Cranial Nerve Palsies: III, IV, VI (diplopia, ptosis), VII (facial palsy)
4. Raised ICP: Vomiting, papilledema, altered consciousness
5. Focal deficits: Stroke-like (vascular involvement)
6. Seizures
7. Hydrocephalus: Progressive symptoms

Sequelae of TB Meningitis

• Hydrocephalus (most common sequela)
• Intellectual disability (children)
• Epilepsy
• Hearing loss
• Visual impairment
• Cranial nerve palsies
• Motor deficits (hemiplegia, paraplegia)
• Spinal arachnoiditis
• Hypothalamic-pituitary dysfunction

CSF Analysis in TB Meningitis

Investigations

1. Lumbar Puncture + CSF analysis (as above)
2. CSF AFB culture (gold standard)
3. CSF PCR for MTB (rapid, sensitive)
4. CT/MRI Brain: Basal meningeal enhancement, hydrocephalus, infarcts, tuberculomas
5. Chest X-ray: Primary TB focus
6. Mantoux/TST, IGRA (Quantiferon)
7. HIV testing

Treatment

• Intensive phase (2 months): HRZE - Isoniazid + Rifampicin + Pyrazinamide + Ethambutol
• Continuation phase (7-10 months): HR - Isoniazid + Rifampicin

• Dexamethasone 0.4 mg/kg/day tapering over 6-8 weeks
• Reduces vasculitis, cerebral edema; improves survival

• Hydrocephalus: VP shunt or ETV
• Seizures: Antiepileptic drugs
• Raised ICP: Mannitol, dexamethasone

Physiotherapy Management

• Rehabilitation of neurological deficits (hemiplegia, cognitive impairment)
• Prevention of pressure sores, contractures
• Gait retraining
• Cognitive rehabilitation
• Communication therapy

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12. ENTRAPMENT NEUROPATHY (20 Marks) - Asked 2 Times

Definition

Important Entrapment Neuropathies

1. Carpal Tunnel Syndrome (CTS) - Median Nerve at Wrist

• Most common entrapment neuropathy
• Anatomy: Median nerve compressed under flexor retinaculum
• Causes: Pregnancy, hypothyroidism, DM, RA, obesity, repetitive use, acromegaly
• Symptoms: Burning, tingling in thumb, index, middle, radial half of ring finger; nocturnal pain (waking patient); wrist pain radiating to forearm
• Signs: Tinel's sign (+), Phalen's test (+), Thenar wasting (late), weakness of APB (abductor pollicis brevis)
• Diagnosis: NCS (nerve conduction studies) - prolonged distal latency
• Treatment: Wrist splint (neutral), steroid injection, surgical decompression

2. Cubital Tunnel Syndrome - Ulnar Nerve at Elbow

• Ulnar nerve compressed at medial epicondyle/cubital tunnel
• Symptoms: Tingling in little and ring fingers; medial forearm; weak grip
• Signs: Froment's sign (+), Wartenberg sign, Claw hand (4th, 5th fingers), hypothenar wasting
• Tinel's sign at cubital tunnel
• Treatment: Elbow padding, avoid elbow flexion; surgical decompression/transposition

3. Radial Nerve - Posterior Interosseous Nerve (PIN) Syndrome

• Radial nerve compressed at radial tunnel (lateral epicondyle) or within arcade of Frohse
• Symptoms: Wrist/finger drop; pain over lateral forearm
• Signs: Wrist drop (cannot extend wrist/fingers)

4. Thoracic Outlet Syndrome (TOS)

• Compression of brachial plexus, subclavian artery/vein at thoracic outlet
• Types: Neurogenic (most common), Vascular
• Causes: Cervical rib, anomalous scalene muscles, poor posture
• Symptoms: Arm pain/tingling (C8/T1 distribution - ulnar), weakness, Raynaud's
• Tests: Adson's test, Roos test, Wright's test
• Treatment: Physiotherapy (posture correction, scalene stretching), rib resection in vascular type

5. Lateral Femoral Cutaneous Nerve (Meralgia Paresthetica)

• Compressed under inguinal ligament (ASIS area)
• Causes: Obesity, tight belts, pregnancy
• Symptoms: Numbness/burning pain on lateral thigh - no motor deficit
• Treatment: Weight loss, loose clothing, steroid injection, surgical decompression

6. Tarsal Tunnel Syndrome - Tibial Nerve at Ankle

• Tibial nerve compressed under flexor retinaculum behind medial malleolus
• Symptoms: Burning pain, tingling on sole of foot and toes
• Tinel's sign behind medial malleolus

General Management of Entrapment Neuropathies

• Splinting/orthoses
• Activity modification
• Steroid injections
• Physiotherapy: Nerve mobilization/gliding exercises, strengthening
• TENS for pain

• Decompression (open or endoscopic)
• Indicated if conservative fails after 3-6 months or severe motor/sensory deficit

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13. GUILLAIN-BARRE SYNDROME (20 Marks PDF1 / 15 Marks PDF2)

Definition

Etiology/Triggers (Antecedent infection 2-4 weeks before)

• Campylobacter jejuni (most common - especially AMAN variant)
• EBV, CMV, HIV
• Influenza, Hepatitis A/E
• Mycoplasma pneumoniae
• Rarely: Vaccinations, surgery

Subtypes

1. AIDP (Acute Inflammatory Demyelinating Polyneuropathy): Most common in West; autoimmune demyelination
2. AMAN (Acute Motor Axonal Neuropathy): Common in Asia/China; ganglioside antibodies (GM1, GD1a)
3. AMSAN (Acute Motor-Sensory Axonal Neuropathy)
4. Miller-Fisher Syndrome (MFS): Triad of Ophthalmoplegia + Ataxia + Areflexia; anti-GQ1b antibodies

Pathophysiology

• Molecular mimicry: Antibodies against nerve antigens (gangliosides) due to cross-reactivity with infectious agents
• Autoimmune attack on myelin (AIDP) or axolemma (AMAN)
• Results in demyelination/axonal injury → conduction block

Clinical Features

• Typically begins 2-4 weeks after infection
• Ascending weakness: Starts in legs, moves upward
• Areflexia/Hyporeflexia: Hallmark
• Sensory symptoms: Paresthesia, pain (often before weakness); "glove-and-stocking" pattern
• Back pain: Common early
• Autonomic dysfunction: Arrhythmias (sinus tachycardia, bradycardia), BP fluctuations, urinary retention, ileus
• Respiratory involvement: 25-30% need mechanical ventilation
• Cranial nerve: Bilateral facial palsy (VII), dysphagia, dysarthria

Brighton Criteria / Diagnostic Criteria

• Progressive bilateral limb weakness
• Decreased/absent deep tendon reflexes
• CSF: Albuminocytological dissociation

CSF Analysis in GBS

Investigations

1. CSF analysis: Albuminocytological dissociation (high protein, normal cells)
2. NCS (Nerve Conduction Studies): Demyelinating pattern - prolonged latencies, slowed conduction, conduction block; absent H-reflex
3. EMG
4. Anti-ganglioside antibodies: Anti-GM1, Anti-GQ1b
5. Pulmonary Function Tests: FVC monitoring for respiratory involvement
6. ECG, cardiac monitoring

Management

• ICU if respiratory compromise, autonomic instability
• Mechanical ventilation if FVC <15-20 mL/kg or declining
• Monitoring: Respiratory function, autonomic status, swallowing

1. IV Immunoglobulin (IVIG): 0.4 g/kg/day x 5 days - equal efficacy to plasmapheresis; easier to administer
2. Plasmapheresis: 5 exchanges over 2 weeks; removes antibodies; most effective if within 2 weeks of onset

• NOTE: Corticosteroids are NOT effective and not recommended in GBS

• DVT prophylaxis
• Pain management (gabapentin, opioids)
• Nutritional support (NG tube if bulbar involved)
• Bladder care
• Psychological support

Physiotherapy Management

• Acute ICU: Positioning, passive ROM, chest physiotherapy, prevent contractures
• Recovery phase: Active assisted → active exercises
• Hydrotherapy: Excellent during recovery
• Respiratory physiotherapy
• Gait retraining
• Orthotics (AFO for foot drop)
• ADL training
• Energy conservation (post-GBS fatigue is common)
• Prognosis: 85% recover full ambulation; 5-10% die; 5-10% have residual disability

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14. BLADDER DYSFUNCTION (20 Marks PDF1 / 15 Marks PDF2)

Normal Bladder Physiology (Micturition Reflex)

• Storage: Sympathetic (T10-L2) → relaxes detrusor, contracts internal urethral sphincter → storage
• Voiding: Parasympathetic (S2-S4) → contracts detrusor (via muscarinic receptors) + relaxes sphincter → voiding
• Voluntary control: Pudendal nerve (S2-S4) → voluntary external sphincter control
• Pontine Micturition Center (PMC): Coordinates detrusor-sphincter synergy

Types of Neurogenic Bladder

• Lesion above PMC (cortex, subcortex) or above conus medullaris (SCI above T10)
• Features: Small capacity, high pressure, uninhibited contractions, detrusor hyperreflexia
• Urgency, frequency, urge incontinence
• Detrusor-sphincter dyssynergia (above pontine center)
• Treatment: Anticholinergics (Oxybutynin), intermittent catheterization, Botox into detrusor

• Lesion at or below conus medullaris (S2-S4) or cauda equina
• Features: Large, atonic, overflow incontinence, no reflex contractions
• Dribbling incontinence, retention with overflow
• Treatment: Credé maneuver, Valsalva, intermittent self-catheterization (ISC), alpha blockers

• Lesion in sensory pathways (posterior columns)
• Causes: DM (most common), tabes dorsalis
• Large, atonic bladder; patient unaware of fullness

• Lesion in anterior horn cells/motor efferents
• Retention with intact sensation

Causes

• Spinal Cord Injury
• Multiple Sclerosis
• Parkinson's Disease
• Stroke
• Diabetes mellitus
• Spina Bifida
• Cauda Equina syndrome
• Radical pelvic surgery (prostatectomy, hysterectomy)

Investigations

• Urodynamic studies: Gold standard - cystometry, uroflowmetry, pressure-flow study
• Cystoscopy
• Ultrasound: Bladder capacity, post-void residual volume
• Urinalysis + culture
• MRI Spine: For spinal causes

Management

• Bladder training schedule
• Fluid management
• Pelvic floor exercises

• Intermittent self-catheterization (ISC) - most preferred for neurogenic bladder
• Indwelling catheter (long-term complications: UTI, stones, urothelial cancer)
• Suprapubic catheter

• Overactive bladder: Anticholinergics (Oxybutynin, Tolterodine), Mirabegron (beta-3 agonist)
• Retention: Alpha blockers (Tamsulosin), Bethanechol

• Botulinum toxin injection into detrusor (for overactive bladder)
• Sacral neuromodulation
• Bladder augmentation (enterocystoplasty)
• Urinary diversion

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PART D: ANSWERS TO 15-MARK QUESTIONS (PDF 2 - 3rd Year New Regulation)

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1. EPILEPSY (15 Marks) - Asked in 2020 PDF2

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2. PARKINSON'S DISEASE (15 Marks) - Asked 2020(Oct), 2025(Feb) in PDF2

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3. CEREBRAL PALSY (15 Marks) - Asked 2025(Feb) in PDF2

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4. MYASTHENIA GRAVIS (15 Marks) - Asked 2022(Jun) in PDF2

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5. GBS (15 Marks) - Asked 2022(Oct) in PDF2

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6. STROKE (15 Marks) - Asked 2023(Apr) in PDF2

Definition

Types

• Thrombotic: In-situ clot on atherosclerotic plaque; gradual onset; common in sleep
• Embolic: Clot from heart (AF, valvular disease) or carotid artery; sudden onset; may have TIA
• Lacunar: Small vessel disease (hypertension, DM); small deep infarcts; pure motor/sensory stroke

• Intracerebral hemorrhage (ICH): Hypertension (#1 cause); basal ganglia most common site
• Subarachnoid hemorrhage (SAH): Berry aneurysm rupture (#1 cause); thunderclap headache

Risk Factors

• Hypertension (most important modifiable risk factor)
• Atrial fibrillation
• Diabetes mellitus
• Hyperlipidemia
• Smoking
• Obesity, physical inactivity
• Alcohol excess
• Previous TIA/stroke

Clinical Features

• Contralateral hemiplegia (face + arm > leg)
• Contralateral hemisensory loss
• Aphasia (if dominant hemisphere) - Broca (non-fluent), Wernicke (fluent)
• Homonymous hemianopia
• Hemineglect (non-dominant parietal)

• Contralateral leg > arm weakness

• Contralateral homonymous hemianopia
• Thalamic syndrome (thalamic pain, sensory loss)

• Locked-in syndrome, cranial nerve palsies, cerebellar signs, coma

• Ipsilateral: Facial pain/numbness, Horner's, cerebellar ataxia, dysphagia/dysarthria, hiccups
• Contralateral: Body pain/temperature loss

Investigations

1. CT Brain (non-contrast): URGENT - distinguishes ischemic from hemorrhagic (dark in ischemic early, bright in hemorrhagic)
2. MRI Brain (DWI): Most sensitive for acute ischemia
3. MRI/CT Angiography: Vessel imaging
4. ECG: Atrial fibrillation
5. Echocardiogram
6. Carotid Doppler
7. FBC, coagulation, lipid profile, glucose, HbA1c

Acute Management

• Thrombolysis: IV Alteplase (tPA) within 4.5 hours of symptom onset (if no contraindications)
• Thrombectomy: Mechanical clot removal within 6-24 hours for large vessel occlusion
• Aspirin 300mg within 48 hours (if thrombolysis not given)
• Blood sugar, temperature, BP control
• "Time is brain" - door-to-needle <60 minutes target

• Reverse anticoagulation
• BP lowering
• Surgery if large hematoma with mass effect

Secondary Prevention

• Antiplatelets (Aspirin + Clopidogrel or Ticagrelor)
• Anticoagulation for AF (Warfarin/NOACs)
• Statin therapy
• Antihypertensives
• Carotid endarterectomy (>70% stenosis, symptomatic)

Physiotherapy in Stroke

• Early mobilization (within 24-48h if stable) - reduces DVT, pneumonia, contractures
• Positioning in antispasticity patterns
• Passive ROM

• Task-oriented training (repetitive practice of functional tasks)
• Constraint-Induced Movement Therapy (CIMT) for upper limb
• Treadmill training / BWS (Body Weight Support) for gait
• Balance training
• Spasticity management
• ADL retraining
• Speech therapy
• Swallowing therapy
• Shoulder subluxation management (strapping, FES)
• CIMT - immobilize unaffected limb, intensively use affected limb

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7. MENINGITIS (15 Marks) - Asked 2023(Apr) in PDF2

Definition

Types

1. Bacterial (Pyogenic): Most severe; medical emergency
2. Viral (Aseptic): Most common overall; usually self-limiting
3. Tuberculous: Subacute; see above
4. Fungal: Cryptococcal (AIDS patients)
5. Parasitic

Common Organisms

Clinical Features

1. Fever
2. Neck stiffness (nuchal rigidity)
3. Headache (severe, constant)

• Photophobia, phonophobia
• Vomiting
• Altered consciousness
• Seizures
• Kernig's sign: Pain/resistance on knee extension with hip flexed 90°
• Brudzinski's sign: Involuntary hip/knee flexion on neck flexion

• Petechial/purpuric rash (non-blanching) → Waterhouse-Friderichsen syndrome (septicemia + adrenal failure)

CSF Analysis Comparison

Treatment

• Empirical antibiotics immediately: Ceftriaxone 2g IV 12-hourly (covers most organisms)
• Add Dexamethasone (reduces cerebral edema, mortality, hearing loss)
• Add Ampicillin if Listeria suspected (elderly, immunocompromised, neonates)
• Adjust when culture results available

Complications

• Hydrocephalus
• Cerebral infarction
• Hearing loss (most common complication of bacterial meningitis in children)
• Cranial nerve palsies
• Intellectual disability
• Epilepsy
• SIADH
• Waterhouse-Friderichsen syndrome

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8. HEAD INJURY (15 Marks) - Asked 2021(Sep) in PDF2

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9. RADIAL NERVE INJURY (15 Marks) - Asked 2021(Sep) in PDF2

Anatomy of Radial Nerve

• Arises from posterior cord of brachial plexus (C5-C8, T1)
• Winds around spiral groove of humerus (most vulnerable site)
• Divides at lateral epicondyle into:
  • Superficial radial nerve (sensory - dorsum of hand, lateral 3½ fingers)
  • Posterior Interosseous Nerve (PIN) (motor to finger/wrist extensors)

Levels of Injury and Features

• Cause: Crutch palsy ("Saturday night palsy" if sleeping on arm), fracture of humeral head
• Wrist drop + Finger/thumb drop
• Triceps weak (elbow extension affected)
• Sensory loss: Posterior arm, forearm, dorsum of lateral hand

• Cause: Fracture of mid-shaft humerus, "Saturday night palsy" (drunk sleeping with arm over chair), tourniquet palsy
• Wrist drop + Finger drop (weak wrist, finger, thumb extension)
• Triceps spared (triceps branch given off above spiral groove)
• Sensory loss: Dorsum of hand and lateral 3½ fingers

• Cause: Radial tunnel syndrome, arcade of Frohse compression
• Finger drop (can still extend wrist weakly - ECRB spared)
• No wrist drop, No sensory loss (PIN is pure motor)

Clinical Features of Radial Nerve Palsy (Mid-humerus level)

• Wrist drop (inability to extend wrist)
• Weak extension of MCPs (metacarpophalangeal joints)
• Weak thumb abduction/extension
• Weak supination (with extended elbow)
• Sensory loss: Dorsum of hand, lateral 3½ fingers (1st web space most reliable)
• Note: No claw hand (interossei and lumbricals are intact via median and ulnar)

Investigations

• NCS/EMG: Localize level, assess severity
• X-ray humerus: Fracture

Management

• Wrist extension splint (cock-up splint): Maintains function, prevents overstretching
• Physiotherapy: Passive ROM, electrical stimulation of denervated muscles
• Nerve recovery: 1 mm/day (Seddon's classification)

• Nerve repair (if cut - neuroraphy)
• Nerve grafting (gap >5 cm)
• Tendon transfers (if permanent palsy): ECU to EDC, BR to EPL

Prognosis

• Neuropraxia: Complete recovery weeks to months
• Axonotmesis: Recovery at 1 mm/day from injury site
• Neurotmesis: No recovery without surgery

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QUICK REVISION SUMMARY TABLE

20-Mark Questions - Most Likely to Appear (Based on Frequency)

15-Mark Questions - PDF 2 Priority

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Study Strategy: Focus maximum time on Myasthenia Gravis (asked 6 times!), followed by DMD, Epilepsy, Spasticity, MS, and CP. These topics alone cover ~70% of the 20-mark questions. For 15-mark questions (PDF 2), Epilepsy and Parkinson's are the most repeated.