Neurological Physiotherapy
What is tested
Localising the lesion (central versus peripheral), scoring impairment, and choosing task-specific, dose-appropriate training for stroke, spinal cord injury, Parkinson's disease, multiple sclerosis and vestibular disorders.
Core rules
- UMN vs LMN. UMN: hyperreflexia, spasticity, Babinski sign present, no fasciculation, disuse atrophy. LMN: hyporeflexia, flaccidity, fasciculation, marked atrophy.
- ASIA key muscles. C5 elbow flexors, C6 wrist extensors, C7 elbow extensors, C8 finger flexors, T1 finger abductors, L2 hip flexors, L3 knee extensors, L4 ankle dorsiflexors, L5 long toe extensors, S1 plantarflexors.
- Stroke. Most are middle cerebral artery territory; thrombolysis window is up to 4.5 hours. Use high-repetition task practice, constraint-induced movement therapy for a suitable distal upper limb, and treadmill or circuit training for gait.
- Parkinson's disease. External cueing (auditory, visual), large-amplitude training, and a strategy for freezing - weight shift and stepping to a rhythm.
- Multiple sclerosis. Fatigue and heat sensitivity (Uhthoff phenomenon); pace sessions and avoid overheating.
- Guillain–Barré syndrome. Ascending areflexic weakness; monitor vital capacity and bulbar function, because decline is a medical emergency.
- BPPV. Dix–Hallpike identifies posterior canal involvement; Epley repositioning is the treatment, not general balance training alone.
Worked example
A patient has foot drop with ankle dorsiflexion 3/5, reduced pinprick over the L5 dermatome, and a preserved ankle jerk. Reasoning: an L5 radiculopathy produces an LMN pattern with dermatomal sensory loss and a preserved S1 reflex. A stroke produces an UMN pattern with hyperreflexia, often with hip or upper limb involvement and no dermatomal loss.
Traps
Missing respiratory decline in Guillain–Barré; assuming all stroke patients have sensory loss; giving resisted exercise too early in ataxia; not testing functional tasks, since carry-over matters more than isolated strength.