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MPT PG-Level Practical Exam Preparation

Neurological & Musculoskeletal Conditions - Complete Guide

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1. STROKE (CVA - Cerebrovascular Accident)

Description & Pathophysiology

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Classification & Types (Tertiary Level)

A. Ischemic Stroke (85% of all strokes)

1. Thrombotic Stroke

• Mechanism: In-situ thrombosis over atherosclerotic plaques in large or small vessels
• Large vessel (atherothrombotic): Affects ICA, MCA, basilar artery - gradual onset, often preceded by TIA, stepwise progression
• Small vessel (lacunar): Affects penetrating arteries (lenticulostriate, basilar perforators) - pure motor hemiplegia, pure sensory stroke, ataxic hemiparesis, clumsy hand-dysarthria syndrome, sensorimotor stroke
• Clinical pattern: Often develops during sleep or on awakening; fluctuating course

2. Embolic Stroke

• Cardiogenic (CE): AF, valvular disease, MI (mural thrombus), PFO, dilated cardiomyopathy - sudden onset, maximum deficit from start, cortical signs (aphasia, neglect, hemianopia)
• Artery-to-artery: Plaque rupture from carotid/vertebral arteries → distal embolism
• Cryptogenic: No identifiable source (30-40% of ischemic strokes)

3. Lacunar Infarcts

• Size < 1.5 cm; in basal ganglia, internal capsule, thalamus, pons, corona radiata
• Five classic syndromes: Pure motor hemiplegia (posterior limb IC), pure hemisensory (thalamus), ataxic hemiparesis, dysarthria-clumsy hand, sensorimotor stroke
• No cortical features; good prognosis; associated with hypertension/diabetes

4. Hemodynamic Stroke

• "Watershed" or "border zone" infarcts
• Occurs at junctions of major arterial territories (ACA-MCA, MCA-PCA)
• Due to severe systemic hypotension, cardiac arrest, carotid stenosis
• "Man in barrel" syndrome (cortical sensorimotor sparing with proximal arm weakness)

5. Cryptogenic Stroke

• Diagnosed by exclusion after negative workup
• Often due to ESUS (Embolic Stroke of Undetermined Source) - recent classification

B. Hemorrhagic Stroke (15%)

1. Intracerebral Hemorrhage (ICH)

• Primary ICH (80%): HTN-related, rupture of Charcot-Bouchard microaneurysms
• Common sites: Putamen (most common, 35%), thalamus (15%), pons (10%), cerebellar hemisphere (10%), subcortical white matter (lobar)
• Secondary ICH (20%): AVM, amyloid angiopathy (lobar bleeds in elderly), coagulopathy, tumor, drug-induced
• Clinical: Severe headache, vomiting, rapid deterioration, blood on CT as hyperdense lesion

2. Subarachnoid Hemorrhage (SAH)

• Cause: Ruptured aneurysm (85%), AVM, no cause found (15%)
• Hallmark: "Thunderclap headache" - worst headache of life, instantaneous onset
• Common aneurysm sites: ACOM (30%), PCOM (25%), MCA (20%), ICA
• Diagnosis: CT (90% sensitive within 24h) → LP if CT negative (xanthochromia)
• Grading: Hunt & Hess (clinical), Fisher Scale (CT blood volume → vasospasm risk), WFNS (GCS-based)
• Complications: Vasospasm (days 4-14, treated with nimodipine), rebleeding (24-48h), hydrocephalus, SIADH/cerebral salt wasting

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TOAST Classification (Trial of Org 10172 in Acute Stroke Treatment)

1. Large artery atherosclerosis
2. Cardioembolism
3. Small vessel occlusion (lacunar)
4. Stroke of other determined etiology
5. Stroke of undetermined etiology

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Diagnosis - Tertiary Assessment

Clinical Assessment

• NIHSS (NIH Stroke Scale): Score 0-42; mild <8, moderate 8-16, severe >16; guides thrombolysis candidacy
• FAST: Face drooping, Arm weakness, Speech difficulty, Time to call
• BE-FAST: Balance, Eyes (vision loss), + FAST
• Rapid assessment: Onset time (critical for thrombolysis), last known well time

Imaging

Biomarkers

• GFAP, UCH-L1: Blood-based biomarkers distinguishing ischemic from hemorrhagic (FDA-cleared)
• BNP/NT-proBNP: Cardioembolic source
• Lipid profile, HbA1c, coagulation: Risk stratification

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Acute Management

Ischemic Stroke

• Within 4.5 hours of onset (rtPA 0.9 mg/kg, max 90 mg; 10% bolus, rest over 60 min)
• Extended window: MRI-guided (DWI-FLAIR mismatch) up to 9 hours or wake-up stroke
• Tenecteplase (TNKase): 0.25 mg/kg single IV bolus - now preferred in many guidelines (simpler administration)

• Up to 24 hours with CT perfusion/MRI mismatch (DAWN/DEFUSE-3 trials)
• For LVO (ICA, M1/M2 MCA, basilar)
• Modified Rankin Scale (mRS) improvement primary endpoint

• Aspirin 300 mg within 48h (if no thrombolysis)
• Dual antiplatelet (Aspirin + Clopidogrel) for minor stroke (NIHSS ≤3) or high-risk TIA for 21 days

Hemorrhagic Stroke

• BP control (target <140/90 within 1h for ICH - INTERACT2/ATACH-2)
• Reversal of anticoagulation (Vitamin K, PCC, idarucizumab for dabigatran)
• Surgical evacuation: Cerebellar hemorrhage >3 cm with deterioration, hydrocephalus
• ICP management: HOB 30°, osmotherapy (mannitol/hypertonic saline), EVD

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Physiotherapy Assessment (MPT Focus)

Bedside Assessment

1. Consciousness: GCS, FOUR Score
2. Cognitive-Perceptual: MMSE/MoCA, Hemispatial neglect (Star Cancellation Test, Line Bisection), Anosognosia
3. Motor: Brunnstrom Stages (1-6), Modified Ashworth Scale (spasticity), Fugl-Meyer Assessment (FMA) - gold standard for motor recovery
4. Sensory: Pin-prick, light touch, proprioception, vibration
5. Balance: Berg Balance Scale (BBS), Postural Assessment Scale for Stroke (PASS), Trunk Control Test
6. Gait: FAC (Functional Ambulation Classification), 10MWT, 6MWT, Timed Up & Go (TUG)
7. Upper Limb Function: Action Research Arm Test (ARAT), Wolf Motor Function Test (WMFT), Box & Block Test
8. ADL: Barthel Index, FIM (Functional Independence Measure)
9. Dysphagia: GUSS, Burke Dysphagia Screening Test
10. Communication: Frenchay Aphasia Screening Test

Key Outcome Measures Summary

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Physiotherapy Management

Acute Phase (Days 1-7)

• Early mobilization: First sit-up within 24-48h (AVERT trial - avoid very early aggressive mobilization within 24h)
• Positioning: Anti-spasticity positioning, pressure care, joint protection
• Passive/active-assisted ROM, chest physiotherapy
• DVT prophylaxis: Ankle pumps, compression stockings

Subacute Phase (Week 1 - 3 months)

• Task-specific training: Most evidence-based approach - repetitive practice of meaningful tasks
• CIMT (Constraint-Induced Movement Therapy): Constraining unaffected arm, massed practice of affected arm ≥6h/day for 2 weeks - EXCITE trial
• Mirror Therapy: Illusion of affected limb movement - Level 1A evidence for upper limb
• Mental Practice/Motor Imagery: Supplementary to physical practice
• Bilateral Arm Training (BAT): Symmetric bimanual activities
• Bobath/NDT: Neurological physiotherapy approach (historical - less RCT evidence vs. task-specific)
• Proprioceptive Neuromuscular Facilitation (PNF)
• Balance retraining: Sitting balance → standing → dynamic balance
• Treadmill training: Body-weight supported treadmill training (BWSTT)
• Gait retraining

Spasticity Management

• Stretching, positioning, serial casting
• Botulinum toxin A (intramuscular) - UL/LL
• Intrathecal baclofen (severe generalized spasticity)
• Phenol nerve blocks

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Recent Advances in Stroke Rehabilitation

1. Robot-Assisted Therapy: Lokomat (gait), Armeo, InMotion robot - high-repetition task practice; systematic reviews show modest but consistent UL functional gains
2. Non-invasive Brain Stimulation (NIBS):
   • rTMS (Repetitive Transcranial Magnetic Stimulation): Inhibitory 1 Hz over contralesional cortex OR excitatory high-frequency over ipsilesional cortex
   • tDCS (Transcranial Direct Current Stimulation): Anodal over ipsilesional M1; portable, inexpensive
3. Virtual Reality (VR): Immersive gaming environments for UL rehabilitation - HoloLens, Nintendo Wii adaptations
4. Brain-Computer Interface (BCI): EEG-triggered FES/robotic assistance based on motor intention
5. Functional Electrical Stimulation (FES): NMES for wrist/finger extensors, foot drop correction (WalkAide, Bioness)
6. Telerehabilitation: Remote video-based therapy delivery - COVID era expansion with RCT evidence
7. High-Dose Motor Training: Task-specific, high-repetition (hundreds of repetitions per session)
8. Spinal Cord Stimulation: Epidural stimulation facilitating gait recovery (Pittsburgh team - 2023 Nature Medicine reports)
9. Stem Cell Therapy: Still experimental (NSCs, MSCs)
10. Pharmacological Augmentation: Fluoxetine (FLAME trial, FOCUS trial - negative for disability at 6 months), Amphetamine studies

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2. SPINAL CORD INJURY (SCI)

Description & Pathophysiology

• Primary injury: Mechanical impact - contusion, compression, laceration, distraction
• Secondary injury: Glutamate excitotoxicity, calcium influx, free radicals, inflammation, ischemia (minutes to weeks) - therapeutic window for neuroprotection

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Classification

ASIA Impairment Scale (AIS) - International Standards for Neurological Classification of SCI (ISNCSCI)

Syndromes (Incomplete SCI)

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Diagnosis

Clinical Assessment

• Dermatomes: C2-S5 complete mapping (28 key points bilaterally - ISNCSCI)
• Myotomes: 10 key muscle groups bilateral (C5-T1, L2-S1)
• Sacral Sparing: Anal sensation, voluntary anal contraction, deep anal pressure - determines completeness
• Reflexes: Bulbocavernosus reflex (BCR), anal wink, deep tendon reflexes

Imaging

• X-ray: Initial screening
• CT: Bony injury - standard of care in acute trauma
• MRI: Gold standard for cord, ligament, disc injury; essential for incomplete lesions

Spinal Shock vs. Neurogenic Shock

• Spinal Shock: Temporary complete loss of all reflex activity below injury (BCR absent) - lasts hours to weeks
• Neurogenic Shock: Hypotension + bradycardia from sympathetic disruption (T1-T4 injuries) - requires vasopressors

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Management

Acute (<8 hours)

• Immobilization: Cervical collar, log rolling, spinal board
• ABC management: Maintain MAP 85-90 mmHg for 7 days (spinal cord perfusion)
• Surgical: Decompression within 24 hours - STASCIS trial (improved outcomes with early surgery)
• Methylprednisolone: Controversial - NASCIS trials (now NOT recommended by most guidelines due to complications)

Physiotherapy Assessment (MPT Focus)

1. ASIA/ISNCSCI classification - complete neurological assessment
2. Respiratory function: VC, MIP, MEP, cough peak flow
3. Spasticity: Modified Ashworth Scale, Penn Spasm Frequency Scale
4. Pressure areas: Waterlow score, NPUAP staging
5. Pain: Neuropathic pain (NRS, LANSS)
6. Functional: Spinal Cord Independence Measure (SCIM III) - disease-specific; 0-100
7. Balance: SCI-specific scales
8. Wheelchair skills: Wheelchair Skills Test

Physiotherapy Management

• Ventilator weaning, glossopharyngeal breathing
• Manual/mechanical cough assist, respiratory muscle training
• Suction, postural drainage

• Activity-based therapy (ABT): Locomotor training - treadmill with body weight support (BWSTT)
• Standing program: Tilt table, standing frames (prevents osteoporosis, spasticity, orthostatic hypotension)
• FES (Functional Electrical Stimulation): Cycle ergometry (RT300), FES gait (Parastep)
• Strength training: Available musculature above/at level of injury
• Hand function: Tenodesis grip training, tendon transfer

• Positioning, stretching, inhibitory casts
• Baclofen (oral/intrathecal ITB pump)
• Botulinum toxin

• Life-threatening emergency in T6 and above injuries
• Triggers: Bladder distension (most common), bowel impaction, pressure sores
• Presentation: Severe headache, hypertension (>20 mmHg above baseline), bradycardia, sweating, flushing above level, piloerection below
• Management: Sit patient up, identify and remove trigger, nifedipine/nitroglycerine if BP persists

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Recent Advances in SCI

1. Epidural Electrical Stimulation (EES): Louisville team/EPFL - lumbosacral epidural stimulation enabling voluntary movement and standing/walking in motor complete patients (Capogrosso et al., Nature 2016; Gill et al., Nature Medicine 2018, Wagner et al., Nature 2018)
2. Targeted epidural stimulation + locomotor training: Spatiotemporal stimulation patterns (AIS A patients walking with assistive device)
3. BCI + FES combinations: Thought-controlled FES exoskeletons
4. Exoskeletons: ReWalk, Ekso, Indego, Lokomat - approved for rehabilitation use; emerging evidence for community use
5. Neuroprotection: Riluzole (glutamate antagonist) - ongoing trials; Magnesium, minocycline
6. Cell therapies: OECs (Olfactory Ensheathing Cells), Schwann cells, iPSC-derived neurons - Phase I/II trials
7. Anti-Nogo-A antibody: Promotes axonal regeneration
8. Intrathecal drug delivery: Chondroitinase ABC (degrades glial scar)
9. HAL (Hybrid Assistive Limb): Cybernic suit - bioelectrical signal-driven exoskeleton
10. High-Intensity Training (HIT): 60-80% maximum effort locomotor training showing greater gains than conventional lower-intensity BWSTT

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3. FACIAL PALSY

Description & Types

Classification by Lesion Level

• Lesion above the facial nucleus (cortex, internal capsule, corona radiata)
• Forehead SPARED (bilateral cortical representation of forehead)
• Lower face contralateral weakness only
• Causes: Stroke, tumor, MS

• Lesion at or below the facial nerve nucleus
• ENTIRE ipsilateral face affected (forehead + lower face)
• Bell's phenomenon: Eyeball rolls upward on attempted eye closure
• Epiphora, hyperacusis, loss of taste (anterior 2/3 tongue)

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Causes by Site of Lesion

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Bell's Palsy - Detailed Description

• Sudden onset (usually within 48-72h)
• Unilateral complete (or partial) facial weakness
• Post-auricular pain preceding palsy
• Hyperacusis (if nerve lesion proximal to stapedius branch)
• Reduced lacrimation (if proximal to geniculate ganglion)
• Loss of taste (anterior 2/3 tongue - chorda tympani)
• Epiphora (due to poor eyelid closure)
• May have numbness (V2/V3 territory) though CN V not involved

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Diagnosis of Facial Palsy

Clinical Tests

• Topognostic Tests (historical):
  • Schirmer's test: Lacrimation (geniculate ganglion)
  • Stapedius reflex: Stapedial reflex (above stapedius nerve)
  • Taste: Chorda tympani (above stylomastoid foramen)
  • Submandibular salivary flow
• EMG/NCS:
  • Electroneurography (ENoG/ENOG): Nerve excitability; >90% degeneration = poor prognosis
  • EMG: Fibrillations (axonal degeneration), reinnervation potentials (recovery sign)
  • Nerve Conduction Velocity: Evoked CMAP amplitude comparison

Imaging

• MRI with Gadolinium: Enhancement of geniculate ganglion, tympanic/mastoid segments; rules out mass lesion
• CT: Fracture, cholesteatoma, bony erosion

Blood Tests

• Fasting blood glucose (diabetes)
• Lyme serology (endemic areas)
• ACE levels (sarcoidosis)
• HIV testing

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Management of Facial Palsy

Medical (Bell's Palsy)

• Prednisolone 60mg/day × 10 days (taper last 5 days) - Grade 1A evidence; SULLIVAN trial
• Antivirals (Aciclovir/Valaciclovir): Adjunct to steroids; modest additional benefit (start within 72h)
• Eye care: Artificial tears hourly, eye patch at night, lubricating ointment - prevent exposure keratopathy

Physiotherapy Assessment

1. House-Brackmann Scale (Grade I-VI) - primary grading
2. Sunnybrook Facial Grading System (FGS): Most detailed; composite score (resting symmetry, voluntary movement, synkinesis)
3. Facial Disability Index (FDI): Physical + social function subscales
4. Yanagihara Grading System (Japanese - often used)
5. EMG assessment: Recruitment pattern, spontaneous activity
6. Psychological assessment: Depression, body image (HADS)

Physiotherapy Treatment

• Eye protection (critical)
• Gentle massage, warmth to face
• Passive range of motion
• Neuromuscular facilitation
• Patient education

• Mime Therapy / Facial Neuromuscular Retraining:
  • Mirror biofeedback
  • Specific isolated muscle exercises
  • EMG biofeedback (gold standard adjunct)
  • Inhibition of synkinesis
• Neuromuscular re-education:
  • Specific movement isolation
  • Mental practice of facial expressions
• Manual therapy: Soft tissue mobilization
• Electrical stimulation: Controversial; NMES, TENS (evidence mixed - may promote synkinesis if used pre-maturely)
• Taping: Kinesio taping for support, improving oral competence

• Mime therapy, EMG biofeedback
• Botulinum toxin to synkinetic muscles

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Recent Advances in Facial Palsy

1. EMG biofeedback integrated with VR for facial retraining
2. Gracilis free muscle transfer: For long-standing complete palsy - reinnervated by masseteric branch of CN V
3. Hypoglossal-facial anastomosis: CN XII to CN VII jump graft
4. Selective neurectomy: For synkinesis
5. Stellate ganglion block: Studied for Bell's palsy (limited evidence)
6. Point-of-care testing: HSV PCR from middle ear fluid to guide antiviral therapy

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4. PARKINSON'S DISEASE & PARKINSONISM

Definitions (Critical Distinction)

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Parkinsonism Classification

Primary Parkinsonism

Secondary (Symptomatic) Parkinsonism

• Most common cause of secondary Parkinsonism
• Drugs: Neuroleptics (haloperidol, chlorpromazine), metoclopramide, prochlorperazine, reserpine, tetrabenazine, calcium channel blockers (flunarizine, cinnarizine)
• Usually symmetric, no resting tremor, reverses on drug withdrawal (weeks-months)

• Lower body Parkinsonism (gait freezing, lower limb bradykinesia)
• Normal upper limbs, no tremor typically
• Stepwise progression, associated with vascular risk factors
• MRI: Bilateral white matter lesions (Binswanger disease)

• Hakim-Adams triad: Gait apraxia + urinary incontinence + dementia ("wet, wobbly, wacky")
• Gait: Magnetic gait (shuffling, feet appear glued to floor)
• CT/MRI: Ventriculomegaly without cortical atrophy (Evans ratio >0.3)
• Treatment: VP shunt (gait responds best)

• MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) - contaminant in synthetic heroin
• Carbon monoxide poisoning
• Manganese (welders, miners)

• After Von Economo encephalitis (1920s pandemic)

• Boxers, contact sport athletes

Parkinson-Plus Syndromes (Atypical Parkinsonism)

• Key feature: Vertical supranuclear gaze palsy (especially downward gaze - "cannot look down")
• Backward falls (retropulsion) early, within first year
• Axial rigidity > limb rigidity
• Collisiondifficulty (frontal signs), no tremor
• Poor levodopa response
• Pathology: Tau inclusions (tufted astrocytes)
• MRI: "Hummingbird sign" (midbrain atrophy) and "morning glory sign"

• MSA-P (Parkinsonian): Previously Striatonigral degeneration - prominent Parkinsonism, poor levodopa response
• MSA-C (Cerebellar): Previously OPCA - cerebellar ataxia dominant
• Autonomic failure (prominent): Orthostatic hypotension (fall >30/15 mmHg), bladder, sexual dysfunction
• MRI: "Hot cross bun sign" (pontine cruciform T2 hyperintensity), putaminal atrophy with hyperintense rim
• Pathology: Glial cytoplasmic inclusions (GCI) - alpha-synuclein in oligodendrocytes

• Parkinsonism + dementia (cognitive symptoms within 1 year of motor symptoms)
• Fluctuating cognition, visual hallucinations, REM sleep behavior disorder
• Neuroleptic hypersensitivity
• DAT-SPECT: Reduced dopamine transporter uptake
• Treatment: Rivastigmine (cholinesterase inhibitor)

• Asymmetric parkinsonism + cortical features
• "Alien hand syndrome" - involuntary purposive movements of one hand
• Apraxia, cortical sensory loss, myoclonus
• Tau pathology (astrocytic plaques)
• No levodopa response

• Young-onset (< 40 years)
• Kayser-Fleischer rings, liver disease, psychiatric symptoms
• Low ceruloplasmin, low serum copper, high urine copper
• Treatment: D-penicillamine, zinc

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Parkinson's Disease - Detailed

Epidemiology

• 2nd most common neurodegenerative disease (after Alzheimer's)
• Prevalence: 1-2/1000; 1% of those >60 years
• Mean onset: 60-65 years; <50 years = Young onset PD (YOPD)

Pathophysiology

• Loss of dopaminergic neurons in substantia nigra pars compacta (>70% loss before symptoms appear)
• Lewy bodies: Intracytoplasmic inclusions containing alpha-synuclein (abnormal folding → aggregation)
• Braak staging (1-6): Pathology begins in olfactory bulb/dorsal vagal nucleus (Stage 1) → ascending to SN (Stage 3-4) → neocortex (Stage 5-6)
• Basal ganglia circuit: Normal: SN → striatum (dopamine) maintains balance between direct pathway (D1, facilitates movement) and indirect pathway (D2, inhibits movement)
• In PD: Decreased dopamine → reduced direct pathway activity + increased indirect pathway activity → excessive STN → increased GPi inhibition → thalamus cannot facilitate cortical movement

Cardinal Features (TRAP Mnemonic)

• Tremor: Resting tremor (4-6 Hz), "pill-rolling," suppressed by movement, returns at rest
• Rigidity: Cogwheel (with superimposed tremor) or lead-pipe; throughout ROM; positive Froment's manuever
• Akinesia/Bradykinesia: Slowness of initiation and execution; key diagnostic criterion; hypomimia, hypophonia, micrographia
• Postural instability: Late feature; pull test - abnormal if >2 retropulsion steps; greatest fall risk

Non-Motor Features (often precede motor features)

• REM sleep behavior disorder (RBD): Acts out dreams; greatest prodromal marker
• Constipation: >10 years before diagnosis
• Hyposmia/Anosmia: Early
• Depression/Anxiety: 40-50%
• Orthostatic hypotension
• Dementia (PDD): Late feature; if within 1 year → DLB
• Pain: Common, underrecognized
• Excessive daytime somnolence

Diagnostic Criteria (MDS - UK Brain Bank Criteria)

Hoehn & Yahr Scale

UPDRS (Unified Parkinson's Disease Rating Scale) - MDS-UPDRS

• Part I: Non-motor experiences of daily living (0-52)
• Part II: Motor experiences of daily living (0-52)
• Part III: Motor examination (0-132) - used in clinic
• Part IV: Motor complications (0-24)

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Medical Management of PD

Levodopa (L-DOPA)

• Most effective symptomatic treatment; given with carbidopa/benserazide (dopa decarboxylase inhibitor)
• Gold standard for motor symptoms
• Complications (long-term):
  • Wearing off (end-of-dose deterioration)
  • On-Off fluctuations
  • Peak-dose dyskinesia (choreiform movements)
  • Diphasic dyskinesia
• Management of complications: Controlled-release preparations, amantadine (dyskinesia), deep brain stimulation

Dopamine Agonists (DA)

• Pramipexole, ropinirole, rotigotine (patch), cabergoline
• First-line in younger patients (delay dyskinesia)
• Side effects: Nausea, somnolence, impulse control disorders (gambling, hypersexuality)
• Apomorphine: Rescue therapy for severe off periods (subcutaneous injection or infusion)

MAO-B Inhibitors

• Selegiline, Rasagiline, Safinamide
• Rasagiline: Modest symptomatic + possible neuroprotective effect (ADAGIO trial - controversial)

COMT Inhibitors

• Entacapone, Tolcapone (hepatotoxic)
• Used with levodopa to reduce wearing off

Amantadine

• Anti-dyskinesia effect
• Mild dopaminergic + anticholinergic properties
• NMDA antagonist

Anticholinergics

• Trihexyphenidyl, benztropine
• Mainly for tremor in young patients
• Avoid in elderly (cognitive effects)

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Physiotherapy Assessment for PD

1. MDS-UPDRS Part III (motor exam in clinic)
2. Hoehn & Yahr Stage
3. Timed Up & Go (TUG): Fall risk; >13.5 sec = increased fall risk
4. Berg Balance Scale (BBS)
5. Functional Gait Assessment (FGA)
6. Freezing of Gait Questionnaire (FOG-Q)
7. 10 Meter Walk Test (10MWT): Speed
8. Mini-BESTest (Balance Evaluation Systems Test): Reactive postural control
9. PDQ-39 (Parkinson's Disease Questionnaire): QOL
10. 6MWT: Endurance
11. Spirometry: Respiratory function

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Physiotherapy Management of PD

Exercise Principles

• High intensity exercise appears neuroprotective (animal models + SPARX2 trial for humans)
• Forced-use cycling (Tandem cycling) - Drake et al.: resting tremor reduction

Specific Interventions

• LSVT BIG (Lee Silverman Voice Treatment): 16 sessions over 4 weeks, high amplitude movements, carryover to all movements - Level 1A evidence for gait, upper limb, balance
• Rhythmic Auditory Stimulation (RAS): External auditory cues (metronome) to overcome basal ganglia timing deficit; increases gait velocity, stride length, cadence - Thaut et al.
• Visual cues (stripes on floor): Overcome freezing of gait
• Treadmill training: Promotes consistent stride length

• Attentional strategies (counting, marching)
• Rhythmic auditory/visual cues
• Laser cane (provides visual cues)
• Step-over strategies

• Tai Chi (Level 1A - Li et al., NEJM 2012)
• Tango dancing
• Virtual reality balance training
• Perturbation-based training

• PNF patterns, active assisted exercises
• Yoga, Pilates

• LSVT LOUD (speech) companion to LSVT BIG
• Respiratory muscle training
• Incentive spirometry

• Multifactorial (medication review, home modification, exercise)
• HiBalance program

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Recent Advances in Parkinson's

1. Alpha-synuclein targeted therapies: Monoclonal antibodies (prasinezumab, cinpanemab) - Phase III trials ongoing; antibodies against aggregated alpha-synuclein
2. LRRK2 inhibitors: For LRRK2 mutation carriers (most common genetic PD) - Phase II trials
3. GBA1 (glucocerebrosidase) therapy: Ambroxol, venglustat for GBA1-PD
4. Deep Brain Stimulation (DBS):
   • STN-DBS and GPi-DBS: Established for motor fluctuations/dyskinesia
   • Adaptive DBS (aDBS): Closed-loop stimulation based on real-time LFP biomarkers (STN beta oscillations)
   • DBS in early PD: EARLYSTIM trial showed STN-DBS superior to medical therapy in early stages
5. Focused Ultrasound (FUS): MRI-guided thalamotomy for refractory tremor (FDA approved 2016) - non-invasive, unilateral; bilateral under study
6. Levodopa-Carbidopa Intestinal Gel (LCIG/Duopa): Continuous jejunal infusion via PEG-J for advanced fluctuations
7. Continuous subcutaneous apomorphine infusion
8. Foslevodopa-foscarbidopa (Produodopa): Subcutaneous infusion - newer alternative to LCIG
9. Neuroprotective trial: STEADY-PD III (isradipine - failed), PRO-PD (exercise), PAUSE-PD (trophic factors)
10. Biomarkers: Seed amplification assay (SAA) for alpha-synuclein - detects misfolded alpha-syn in CSF/skin with 90%+ sensitivity; potential for pre-diagnostic detection
11. GLP-1 agonists (Liraglutide, Semaglutide): Phase II RCTs showing possible neuroprotection/disease modification

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5. BRACHIAL PLEXUS INJURY (BPI)

Anatomy Review

• Roots → Trunks → Divisions → Cords → Branches (Terminal nerves)
• Trunks: Upper (C5,C6), Middle (C7), Lower (C8,T1)
• Cords: Lateral (C5,C6,C7), Posterior (C5-T1), Medial (C8,T1)
• Terminal branches: MC nerve, axillary, radial, ulnar, median

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Classification

By Anatomical Level

• Nerve root avulsed from spinal cord
• No Tinel's sign along plexus
• EMG shows normal SNAP (sensory nerve action potential) despite sensory loss (dorsal root ganglion intact)
• No spontaneous recovery; requires nerve transfer
• Signs: Horner's syndrome (C8/T1 avulsion - T1 sympathetics), scapular winging (serratus anterior - C5,6,7), paralysis of ipsilateral hemidiaphragm (phrenic nerve - C3,4,5 - C5 avulsion), neuropathic pain (burning, severe)

• Nerve outside spinal cord; potential for recovery or graft repair
• Abnormal SNAP (normal nerve conduction requires intact DRG)

By Pattern

Sunderland Classification of Nerve Injury

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Diagnosis of BPI

Clinical Assessment

• Muscle testing: Detailed MRC grading of all muscles
• Sensory mapping: Dermatome-by-dermatome
• Reflexes: Biceps (C5,6), brachioradialis (C6), triceps (C7)
• Horner's syndrome: Ptosis, miosis, anhidrosis - indicates lower trunk/C8-T1 preganglionic avulsion
• Spurling's Test: Cervical radiculopathy (not BPI)

Investigations

• EMG/NCS: Essential after 3-4 weeks (Wallerian degeneration)
  • SNAP: Preserved in preganglionic injury
  • EMG: Fibrillations, positive sharp waves = denervation
  • No motor evoked potentials = complete injury
• MRI brachial plexus: Gold standard for visualization; pseudomeningocele = avulsion injury
• CT myelogram: Pre-operative; avulsion confirmed by absent root sleeve filling
• Chest X-ray: Elevated hemidiaphragm (phrenic nerve involvement)

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Management of BPI

Conservative

• ROM exercises (prevent contracture)
• Strengthening available muscles
• Sensory re-education
• Orthoses: Shoulder sling, wrist cock-up splint, dynamic orthoses
• Pain management: Amitriptyline, gabapentin, carbamazepine (neuropathic pain)
• TENS, NMES

Surgical

1. Primary repair: Direct end-to-end neurorrhaphy (if no gap, clean injury)
2. Nerve grafting: Sural nerve (most common donor); cable grafts for large defects
3. Nerve transfer (neurotization): For preganglionic avulsions; uses expendable donor nerves
   • Intercostal nerves → musculocutaneous (elbow flexion priority)
   • Phrenic nerve → musculocutaneous
   • Spinal accessory (CN XI) → suprascapular nerve (shoulder abduction)
   • Contralateral C7 → median nerve (controversial)
   • Ulnar nerve fascicle → biceps motor branch (Oberlin transfer) - gold standard for elbow flexion

• Latissimus dorsi transfer, pectoralis transfer for shoulder

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Physiotherapy Management of BPI

Assessment Tools

1. Medical Research Council (MRC) Scale - muscle strength (0-5)
2. DASH (Disabilities of Arm, Shoulder, Hand) questionnaire
3. QuickDASH
4. PSFS (Patient-Specific Functional Scale)
5. BPI-specific outcome measures: BPI-QOL
6. Pain: NRS, NPSI (Neuropathic Pain Symptom Inventory)

Treatment

• Maintain full PROM all joints
• Strengthen available muscles
• Sensory stimulation
• Education on compensatory strategies

• Immobilization as directed (nerve graft - protect from tension)
• Progressive mobilization
• Biofeedback EMG (detect earliest reinnervation)
• Sensory re-education

• Sensory re-education (Dellon's approach): Moving touch → constant touch → object recognition; localization training
• Motor re-education: When reinnervation noted (EMG biofeedback, muscle belly palpation)
• Mirror therapy: For deafferented limb (phantom limb pain, cortical reorganization)
• Graded motor imagery (GMI)
• NMES/FES: For reinnervated muscles
• Hydrotherapy: ROM, strengthening with gravity eliminated
• Orthotic management: Dynamic flexion splints, elbow orthoses, myoelectric prosthesis for flail arm

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Recent Advances in BPI

1. Targeted muscle reinnervation (TMR): Residual nerves rerouted to create additional EMG control sites for myoelectric prosthetics
2. Regenerative Peripheral Nerve Interface (RPNI): Amplifies residual nerve signals
3. End-to-side neurorrhaphy: Donor nerve kept intact while providing collateral sprouting to recipient
4. Babysitter procedures: Prevent end-organ atrophy during long reinnervation time
5. Intraoperative neuromonitoring: Real-time EMG/SSEP during nerve exploration
6. 3D nerve mapping with ultrasound: High-resolution US for fascicular anatomy
7. Photobiomodulation (LLLT): Promotes nerve regeneration in animal models
8. Conduit materials: Collagen, polyglycolic acid tubes with growth factors/stem cells

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6. DUCHENNE (DMD) & BECKER (BMD) MUSCULAR DYSTROPHY

Description & Pathophysiology

• DMD: Out-of-frame deletion/duplication/nonsense mutation → truncated/absent dystrophin (<5% of normal)
• BMD: In-frame mutation → partially functional, shorter dystrophin (>10% of normal)
• Monaco's Reading Frame Hypothesis: Predicts phenotype from mutation type

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DMD - Clinical Features

• Childhood (3-7 years): Proximal weakness (Gowers' sign, waddling gait, toe walking, pseudohypertrophy of calves)
• Pre-ambulatory loss (8-12 years): Equinus contractures, scoliosis development
• Loss of ambulation: Average 9-12 years (without steroids); 12-14 years (with steroids)
• Post-ambulatory phase: Scoliosis progression, respiratory decline, upper limb weakness
• Late (>18 years): Ventilatory support needed, cardiomyopathy

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BMD - Clinical Features

• Later onset: First symptoms 5-15 years; ambulation maintained to >15 years (definition)
• Milder progression: Variable; some ambulatory into middle age
• Cardiomyopathy: Can be severe, disproportionate to skeletal muscle weakness
• Cramps, exercise intolerance: Early complaints

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Diagnosis

Laboratory

• CK (Creatine Kinase): Markedly elevated (10-200× normal in DMD); moderately in BMD (5-10×); elevated at birth, falls as muscle mass destroyed
• Liver function tests: AST/ALT elevated (from muscle)
• Cardiac biomarkers

Genetic Testing

• Multiplex MLPA or NGS (next-generation sequencing): First-line; detects deletions/duplications (65-70% of cases)
• Full gene sequencing: If MLPA negative - detects point mutations/small indels
• Genetic counseling essential

Muscle Biopsy (if genetic testing inconclusive)

• H&E: Variation in fiber size, necrosis/regeneration, fibrofatty replacement
• Dystrophin immunofluorescence/Western blot:
  • DMD: Absent staining
  • BMD: Reduced/patchy staining
• Dystrophin protein quantification: Western blot

EMG

• Myopathic pattern: Short duration, small amplitude, polyphasic MUAPs; early recruitment

Cardiac

• ECG, Echo: Baseline and annual
• Cardiac MRI: Most sensitive for cardiomyopathy detection

Pulmonary Function

• FVC (upright + supine), MIP, MEP, PCF (Peak Cough Flow)
• Spirometry annually

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Management

Medical

• Prednisolone/Prednisone: 0.75 mg/kg/day (deflazacort preferred)
• Deflazacort: 0.9 mg/kg/day - fewer weight gain side effects; delays ambulatory loss 2-3 years
• Initiated at 4-6 years (plateau phase of motor development, before decline)
• CINRG-DNHS: Long-term outcomes data

• ACE inhibitors (enalapril) + beta-blockers from early cardiomyopathy
• Eplerenone: EFFECT trial - cardiac protection

• Exon skipping: Antisense oligonucleotides (AONs) restore reading frame
  • Eteplirsen (Exondys 51): Exon 51 skip - FDA approved 2016 (accelerated approval); ~13% eligible
  • Golodirsen (Vyondys 53): Exon 53 skip - FDA 2019
  • Viltolarsen (Viltepso): Exon 53 skip - FDA 2020
  • Casimersen (Amondys 45): Exon 45 skip - FDA 2021
• Stop codon read-through:
  • Ataluren (Translarna): For nonsense mutations (EMA approved, not FDA); ~11% eligible
• Micro-dystrophin gene therapy:
  • Delandistrogene moxeparvovec (Elevidys, SRP-9001): AAV-delivered micro-dystrophin; FDA accelerated approval June 2023; Phase III EMBARK trial ongoing; for ambulatory patients 4-5 years (expanded 2024)
• Base editing / Prime editing: Preclinical - highly precise correction

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Physiotherapy Assessment for DMD/BMD

1. North Star Ambulatory Assessment (NSAA): 17 functional activities; gold standard for ambulatory DMD; 0-34
2. 6 Minute Walk Test (6MWT): Distance; >330m = ambulatory; loss of 30m/year = clinical worsening
3. Timed Function Tests (TFT): Time to stand from floor, time to climb 4 stairs, 10m walk/run
4. Brooke Upper Limb Scale: Grades 1-6 (for non-ambulatory)
5. Vignos Scale: Grades 1-10 (lower limb function)
6. Performance of Upper Limb (PUL 2.0): Upper limb function in non-ambulatory
7. MFM (Motor Function Measure): 32-item; D1 (standing), D2 (axial/proximal), D3 (distal)
8. Spirometry: FVC, MIP, MEP, PCF
9. Joint ROM: Contracture assessment (ankle, hip, iliotibial band)
10. Scoliosis: Cobb angle (Xray if clinical curve)
11. Quality of life: PedsQL NMD Module

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Physiotherapy Management

Ambulatory Phase

• Activity: Encourage moderate physical activity; avoid eccentric muscle contractions (downhill walking, negatives)
• Hydrotherapy: Excellent for low-impact exercise
• Stretching: Daily ankle, hip flexor, iliotibial band, hamstring stretching - CRITICAL to delay contractures
• Night splints (AFO): Ankle-foot orthoses at night to maintain dorsiflexion
• Gait aids: AFOs during day when foot drop appears
• Standing program: If standing balance maintained → delay contractures + bone density preservation
• Powered mobility: Introduce early (before forced cessation of walking)

Post-Ambulatory Phase

• Powered wheelchair: Postural support (trunk support, lateral supports)
• Scoliosis management:
  • Spinal bracing (soft TLSO) - controversial efficacy
  • Surgical spinal fusion when curve >20° (and FVC >30%)
• Upper limb: Powered arm support, dynamic orthoses (ArmeoSpring)
• ADL: Environmental modifications, assistive technology

Respiratory Management

• Preventive: Incentive spirometry, deep breathing exercises
• When FVC drops <50% or PCF <270 L/min:
  • Manually Assisted Cough (MAC), Mechanical In-Exsufflation (MI-E, CoughAssist)
  • NIV (BiPAP): Nocturnal initially → daytime as needed
• Tracheostomy: Terminal-stage decision (family counseling essential)

Cardiac Monitoring

• Regular cardiology follow-up (annual Echo, ECG)

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Recent Advances in DMD (Additional)

1. SKIP-NMD trial: Systemic exon 45 skipping (viltolarsen)
2. Gene editing (CRISPR-Cas9): Exon deletion restoring reading frame - mouse models; human Phase I initiated
3. Utrophin upregulation: Ezutromid (Phase II - failed), other compounds
4. CAR-T for muscular dystrophy: Satellite cell-targeting immunotherapy
5. Givinostat (HDAC inhibitor): EPIDYS Phase III - muscle fibrosis reduction; EU approval 2024
6. Vamorolone: Non-steroidal dissociative steroidal anti-inflammatory; FDA approved 2023; fewer steroid side effects
7. Tamoxifen, idebenone: Cardiac protection studies
8. Wearable exoskeletons for ADL support: INDEGO, EksoNR

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7. ADULT CEREBRAL PALSY

Description

• Prenatal (80%): Periventricular leukomalacia (PVL), cortical malformations, TORCH infections, genetic
• Perinatal (10%): HIE (Hypoxic-Ischemic Encephalopathy), prematurity
• Postnatal (10%): Meningitis, head injury, stroke (<2 years)

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Classification (SCPE)

By Motor Type

By Distribution (spastic CP)

• Hemiplegia: Unilateral; arm > leg (MCA infarct)
• Diplegia: Bilateral; legs > arms (PVL in preterm)
• Quadriplegia/Tetraplegia: All four limbs; severe; associated with intellectual disability

GMFCS (Gross Motor Function Classification System)

MACS (Manual Ability Classification System)

• Levels I-V for hand function

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Why "Adult CP" is Important

1. Aging with CP: Progressive musculoskeletal decline, pain, fatigue
2. Post-impairment syndrome: Overuse injuries from compensatory strategies (shoulder pain in ambulatory CP)
3. Progressive loss of function: GMFCS level change over decades
4. Transition from pediatric to adult services: Major gap in healthcare
5. Comorbidities: Epilepsy (30%), intellectual disability (50%), visual impairment, hearing loss, communication disorders

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Adult CP - Specific Challenges

Secondary Conditions in Adult CP

1. Pain: Most common complaint (50-75%); back, hip, knee pain; neuropathic pain
2. Fatigue: Energy cost of movement significantly elevated (O2 consumption 2-3× normal)
3. Degenerative joint disease: Premature OA (hip dysplasia, knee valgus)
4. Hip dislocation/sub-luxation: Spastic hip disease (GMFCS III-V)
5. Scoliosis: Progressive in non-ambulatory adults
6. Contractures: Progressive without continued stretching
7. Osteoporosis: Reduced bone density (limited weight bearing, anti-epileptics, low calcium/vitamin D)
8. Neurological decline: Accelerated aging of CNS in CP; increased stroke and dementia risk
9. Urological: Neurogenic bladder (urgency, incontinence)
10. Dysphagia: 40-50% of quadriplegic CP; aspiration risk
11. Mental health: Depression (25%), anxiety, social isolation

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Diagnosis / Assessment in Adults

Impairment Level

• Spasticity: Modified Ashworth Scale (MAS), Tardieu Scale (velocity-dependent - more specific for spasticity vs. contracture)
• ROM: Goniometry - hip, knee, ankle
• Muscle strength: MRC scale
• Selective motor control: Selective Control Assessment of Lower Extremity (SCALE)
• Pain: NRS, multidimensional pain inventory

Activity Level

• GMFCS: Classify functional level
• GMFM-66/88 (Gross Motor Function Measure): Standardized motor assessment (used in children primarily; reference in adults)
• 10MWT, 6MWT, TUG
• Edinburgh Visual Gait Analysis Inventory (EVGAI)
• Instrumented gait analysis (3D): Gold standard for surgical planning; identifies crouch gait, scissor gait, lever arm dysfunction

Participation Level

• Cerebral Palsy Quality of Life for Adults (CPQOL-Adult)
• LIFE-H (Assessment of Life Habits)
• Activity level questionnaire (ALQ)
• Communication Function Classification System (CFCS)

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Management of Adult CP

Spasticity Management

• Conservative: Stretching, positioning, serial casting, orthoses (AFO, KAFO)
• Oral medications: Baclofen, tizanidine, diazepam, dantrolene - significant side effects (sedation)
• Focal: Botulinum toxin A (BoNT-A) injections - evidence-based for spastic CP; every 3-6 months
• Intrathecal baclofen (ITB) pump: For severe generalized spasticity (GMFCS IV-V)
• Phenol nerve blocks: Musculocutaneous nerve (elbow), obturator nerve (scissor gait)

Orthopedic Surgery

• Hip: Soft tissue (adductor tenotomy, iliopsoas lengthening) vs. bony (Dega osteotomy, shelf augmentation)
• Knee: Hamstring lengthening for crouch gait; patellar tendon advancement
• Foot/Ankle: Achilles tendon lengthening, split tibialis anterior transfer (SPLATT), calcaneal osteotomy
• Single event multilevel surgery (SEMLS): All procedures done simultaneously in one anesthesia to minimize rehabilitation periods

Physiotherapy Management

• Lifelong therapy to prevent secondary decline
• Balance activity and rest (energy conservation strategies)
• Goal-directed therapy (GAS - Goal Attainment Scaling)

• Aquatic/hydrotherapy: Low-impact, excellent for tone management
• Strength training: Evidence for improving strength without increasing spasticity
• Aerobic exercise: Reduced energy cost of walking (O2 consumption), cardiovascular benefit
• Stretch: Regular daily stretching to maintain ROM (minimize contractures)

• Treadmill training with/without body weight support
• FES (foot drop correction)
• AFOs: Solid, dynamic, floor-reaction
• Gait training aids: Walker, crutches
• 3D gait analysis guided therapy

• Positioning, manual therapy for joint pain
• TENS, heat/cold
• Movement-based pain management (pacing)
• Psychology referral (pain catastrophizing)

• Energy conservation, activity pacing
• Powered mobility (even for ambulatory adults)
• Environmental adaptation

Augmentative and Alternative Communication (AAC)

• For adults with limited verbal communication

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Recent Advances in Adult CP

1. Constraint-Induced Movement Therapy (CIMT) adapted for adults with hemiplegia: good evidence for upper limb function
2. Botulinum toxin for dystonic CP: Evidence building for dyskinetic type
3. Selective dorsal rhizotomy (SDR): Traditionally pediatric; growing evidence in adult CP for selected patients (ambulatory, spastic diplegia)
4. Stem cell therapy: Clinical trials (cord blood CD34+) - mainly in children currently
5. Wearable exoskeletons: Stride Management Assist (SMA), ReWalk - improving gait quality in ambulatory CP
6. High-Intensity functional training: HABIT (Hand Arm Bimanual Intensive Training) - evidence for improving bimanual function
7. Brain stimulation: rTMS and tDCS to reduce spasticity and improve motor control
8. Digital health/mHealth: Wearable sensors for activity monitoring, telehealth follow-up
9. Sleep disturbance management: Growing recognition of pain and sleep relationship in adult CP

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Summary Table - Key Outcome Measures (Quick Reference)

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Summary Table - Key Recent Advances

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Exam Strategy Tips for MPT Practical

1. History (onset, duration, progression, prior treatment)
2. General Observation (posture, gait, assistive devices)
3. Vitals (HR, BP, SpO2 - especially in SCI/stroke/DMD)
4. Specific clinical tests (list the validated scales above)
5. Outcome measures (state the scale + what it measures + cutoff scores)

1. State the phase (acute/subacute/chronic)
2. Goal-setting (SMART goals)
3. Interventions (group by: range of motion, strengthening, balance/coordination, functional training, modalities)
4. Evidence basis (quote trials - AVERT, EXCITE, CIMT studies, LSVT BIG, DAWN trial, etc.)
5. Discharge planning and community reintegration

• Stroke: TOAST classification, NIHSS scoring, Fugl-Meyer stages, CIMT, rTMS/tDCS, thrombectomy window
• SCI: ASIA grading + sacral sparing, Autonomic Dysreflexia emergency, SCIM III, Epidural stimulation
• Facial Palsy: UMN vs. LMN distinction (forehead sparing), House-Brackmann, Sunnybrook, Mime therapy vs. NMES controversy
• Parkinsonism: PSP vs. MSA vs. DLB distinction, TRAP, Braak staging, LSVT BIG, Tai Chi evidence, adaptive DBS
• BPI: Erb vs. Klumpke, Sunderland classification, preganglionic signs (Horner's, SNAP preserved), Oberlin transfer
• DMD/BMD: Reading frame hypothesis, NSAA + 6MWT, CoughAssist, Elevidys FDA approval 2023
• Adult CP: GMFCS levels, Tardieu vs. MAS difference, secondary conditions, SEMLS surgery, energy cost of walking