NeurologyTier 1Disease (DEADMAN)

Gait disorders

Description

Gait requires intact motor, sensory (proprioceptive, visual, vestibular), cerebellar, basal ganglia and frontal integration
- A single named gait pattern localises the lesion before any investigation

Gait patterns

Gait	Appearance	Localisation	Discriminator
Spastic hemiparetic	Circumduction, arm flexed + adducted, leg extended, toe scuff	Contralateral UMN - MCA stroke, tumour, MS	Unilateral, pyramidal weakness pattern
Spastic paraparetic	Scissoring, stiff, narrow base	Cord	Sensory level, sphincters
High-stepping	Foot slap, exaggerated hip/knee flexion	Peroneal nerve, L5 root, peripheral neuropathy, distal myopathy	Unilateral = nerve/root; bilateral = neuropathy/MND
Waddling (Trendelenburg)	Pelvic drop, lumbar lordosis, Gower's	Proximal myopathy	inc CK, no sensory signs
Cerebellar ataxic	Wide-based, irregular, falls toward the lesion	Cerebellum	Romberg negative - unsteady eyes open and closed
Sensory ataxic	Wide-based, stamping, eyes on the floor	Dorsal columns / large-fibre neuropathy	Romberg positive
Parkinsonian	Stooped, shuffling, reduced arm swing, festination, freezing, en-bloc turning	Basal ganglia	Asymmetric, responds to levodopa
Apraxic (frontal / magnetic)	Feet "stuck to floor", wide base, normal power and coordination lying down	Frontal lobes, NPH, small vessel disease	Disproportionate to limb examination
Antalgic	Short stance phase on painful side	Joint/bone	Pain
Functional	Inconsistent, excessive effort, dramatic near-falls without injury, improves with distraction	-	Variability and incongruence

Gait abnormality in ~15% over 60, >60% over 80
~1/3 of community-dwelling over-65s fall each year; half of these repeatedly
Abnormal gait is an independent predictor of dementia, institutionalisation and death
Commonest single identifiable neurological causes in the elderly: stroke, parkinsonism, cervical myelopathy, peripheral neuropathy
Most elderly gait disorders are multifactorial - neurological + musculoskeletal + visual + drug

By level

Cortical/frontal - small vessel disease, NPH, tumour, frontal infarct
Basal ganglia - Parkinson disease, vascular parkinsonism, PSP (early falls, backwards), drug-induced (metoclopramide, prochlorperazine, antipsychotics)
Cerebellum - stroke, alcohol (vermis - stance and gait), MS, paraneoplastic, SCA, Friedreich, hypothyroidism, phenytoin
Cord - cervical spondylotic myelopathy, B12/copper deficiency (subacute combined degeneration), MS, cord compression, tabes
Root/plexus/nerve - L5 radiculopathy, peroneal palsy, CMT, diabetic and other polyneuropathy
Muscle - inflammatory myopathy, dystrophy, steroid/statin myopathy, osteomalacia, thyroid
Vestibular - bilateral vestibulopathy (aminoglycoside), unilateral loss
Non-neurological - OA hip/knee, spinal canal stenosis (neurogenic claudication - relieved by flexion, walking uphill easier), vascular claudication, deconditioning, visual impairment

Spastic hemiparetic gait - cause of the underlying stroke

Embolism - cardiac, aortic arch, proximal vessel
Atherosclerotic plaque (carotid bifurcation)
Carotid artery dissection - commonest cause of stroke under 40
Hypercoagulable state
Also consider: space-occupying lesion, trauma, demyelination, MND (no sensory signs, no cortical signs)

Drugs

Benzodiazepines, antipsychotics, anticholinergics, opioids, antihypertensives, alcohol, phenytoin, lithium

Watch them walk - the highest-yield test

Initiation, step length, base width, arm swing, turning (count steps - >3 steps = en-bloc turn), festination, freezing
Tandem gait, heel walk (L5/dorsiflexion), toe walk (S1), walk on the spot
Romberg - positive (falls with eyes closed) = proprioceptive, not cerebellar
Rise from chair without arms - proximal power
Timed Up and Go >=12-14 s -> increased falls risk
Pull test - retropulsion (parkinsonism, PSP)

Focal patterns worth dissecting

Unilateral high-stepping (foot drop)

Look for a scar/mass around the fibular head - common peroneal compression
Test dorsiflexion, eversion and inversion
- Weak eversion + intact inversion -> common peroneal
- Weak inversion -> L5 radiculopathy (tibialis posterior is tibial-innervated)
Hip abduction weakness (gluteus medius, L5) also points to root
Sensation: dorsum and lateral foot = superficial peroneal; first web space = deep peroneal
Reflexes: ankle jerk preserved in both peroneal palsy and L5 (lost in S1 and sciatic lesions)

Spastic hemiparesis

Confirm UMN: tone, hyperreflexia, upgoing plantar, pyramidal distribution of weakness
Look for cortical signs (dysphasia, neglect), hemianopia -> cortical rather than lacunar

Investigations

Guided by localisation, not routine
Bloods: FBE, UEC, CK, B12, copper, TSH, HbA1c, vitamin D, ESR, SPEP
MRI brain (stroke, NPH, tumour, white matter disease); MRI cervical spine in any spastic/myelopathic gait
NCS/EMG for foot drop, neuropathy, suspected MND
Lying/standing BP, ECG, medication review, vision and hearing
DAT scan only when parkinsonism vs tremor is genuinely unclear

A. Treat the cause

Stroke - secondary prevention + rehabilitation
Cervical myelopathy - surgical decompression; the aim is to stop progression, not to restore function
NPH - large-volume LP/tap test then VP shunt (gait responds best, cognition least)
Parkinson disease - levodopa; vascular parkinsonism and PSP respond poorly
B12/copper replacement, thyroid, alcohol cessation
Stop or reduce culprit drugs

B. Restore function

Physiotherapy - gait retraining, strength and balance training (the single most effective intervention for falls)
OT home assessment - lighting, rails, rugs, footwear
Aids matched to the deficit: single-point stick, 4-wheel frame, AFO for foot drop
Vestibular rehabilitation if vestibular
Vision and hearing correction

C. Reduce falls risk

D. Spasticity

Falls, fracture, fear of falling and activity restriction (self-reinforcing)
Cognitive impairment - gait slowing precedes dementia diagnosis by years; dual-task gait deterioration is an early marker
Cerebral small vessel disease - gait apraxia, urinary urgency, cognitive slowing
Depression and social isolation
Sarcopenia, frailty, malnutrition
Osteoarthritis, spinal canal stenosis
Polypharmacy
Peripheral vascular disease, diabetes (neuropathy + ulcers)

Trajectory follows the cause: stroke plateaus, degenerative disease progresses, NPH and B12 improve if treated early
Cervical spondylotic myelopathy progresses in stepwise fashion - late decompression does not reverse established deficit
Gait speed is a robust prognostic marker: <0.8 m/s predicts adverse outcomes; <0.6 m/s marks high risk

Complications

Sudden deterioration in a chronic gait disorder = look for a new event (infection, subdural, drug, fracture), not disease progression

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