Gait Abnormalities & Ataxia

Ataxia

Can co-occur with vertigo. Patients with gait ataxia alone, or ataxia out of proportion to vertigo, should be evaluated for a central neurological cause:

• Cerebellar disease
• Normal pressure hydrocephalus
• Cerebrovascular disease
• Peripheral neuropathy

Exception: aminoglycoside toxicity causes bilateral vestibular failure with gait ataxia plus motion-induced oscillopsia (oscillating vision) rather than vertigo.

Structured gait assessment

Gait assessment starts as the patient stands to leave the waiting room — useful for spotting deformities and identifying which phase of the gait cycle is affected.

History: pain, subjective gait complaints, higher-level mobility function (jumping, running); number of falls in the preceding 12 months (>3/year in an older adult is unacceptable and warrants investigation).

Before examining gait: check orthotics/prosthetics/footwear for pathognomonic wear patterns.

Examination sequence:

1. Sit-to-stand and stand-to-sit transfers.
2. Leg length discrepancy (true and apparent).
3. Static (sitting vs standing) vs dynamic balance.
4. Full neurological and joint exam of upper/lower limbs.
5. Supervised heel walking, toe walking, tandem gait, and Romberg’s test (a proprioception test — impaired in sensory ataxia, e.g. peripheral neuropathy; perform cautiously in patients whose gait is already very unsteady, given the fall risk).
6. Systematic visual observation (head to foot; anterior, posterior and lateral views).

Gait cycle phases: stance (heel strike → foot flat → mid-stance → toe-off) — assess balance, posture, base of support; swing (acceleration → mid-swing → deceleration) — assess cadence, stride length, foot clearance. Normal cadence 90–120 steps/min, step length 37–38cm.

Feature	Decreased by	Increased by
Cadence	Advancing age, fatigue, pain, poor vision; obstacles, poor lighting, slippery surfaces	—
Step length	Advancing age, fatigue, pain, poor vision, Parkinsonian gait, frontal gait disorder, marche à petit pas, normal pressure hydrocephalus; obstacles, poor lighting, slippery surfaces	—
Step height	Hip/knee flexor weakness, contractures, pain, proximal myopathy, advancing age, fatigue, Parkinsonism, frontal gait disorder, marche à petit pas, normal pressure hydrocephalus	Common peroneal nerve palsy, Charcot-Marie-Tooth disease, diabetic neuropathy, gastro-soleus spasticity, ankle contractures/pain

Spastic hemiplegic gait — pyramidal weakness/hypertonicity in one lower/upper limb, typically from a contralateral UMN lesion (e.g. stroke). Dynamic spasticity during walking often exceeds resting (static) spasticity — patients with underlying weakness may rely on this “spastic splint” to weight bear, so over-treating spasticity in the presence of weakness can paradoxically worsen mobility and falls risk. Check footwear for toe-box wear; address osteoporosis screening, falls prevention and balance exercises.

Spastic diplegic/“scissoring” gait — typical of spastic cerebral palsy (1–4 limbs affected), or paraparesis from an incomplete spinal cord lesion above the conus medullaris — disproportionate hip adductor spasticity distinguishes it from hemiplegic patterns. Falls are common — see Falls in Older People for assessment and prevention.

Functional gait disorder

Functional neurological disorder (FND) — motor, sensory or cognitive symptoms from disordered neural network function rather than identifiable structural disease — can present as a gait disorder. FND is a positive diagnosis (based on specific physical examination findings), not a diagnosis of exclusion, and is entirely distinct from factitious disorder/malingering (where symptoms are produced volitionally rather than unconsciously).

Findings supporting a functional gait disorder (variability/inconsistency between voluntary and automatic states is the unifying theme):

• Tandem gait: pronounced side-to-side “windmilling” arm movements without actually losing balance.
• Walking backwards: significant improvement in the gait abnormality (though some genuine disorders, e.g. task-specific dystonia, can also be direction-specific).
• Shoulder tap test: retropulsion without an applied posterior force (true retropulsion with an applied force suggests Parkinson’s disease).
• Give-way weakness (initial resistance then sudden loss of strength, with intermittent normal-power bursts) and a positive Hoover’s sign (hip extensor weakness resolves with contralateral hip flexion against resistance).
• Common patterns: monoplegic/dragging gait (whole leg drags from the hip, forefoot staying on the floor — inconsistent with true pyramidal weakness, which causes circumduction); inconsistent/variable limping without pain.

Functional overlay — functional neurological symptoms occur in up to 12% of patients with another neurological disorder (e.g. functional seizures superimposed on epilepsy). A genuine structural/neurological process and a functional gait disorder are not mutually exclusive — continue appropriate work-up for other diagnoses even when functional features are present, and acknowledge both the functional component and any diagnostic uncertainty to the patient.

Management: starts with an accurate, non-judgemental explanation of the diagnosis (patient resources: neurosymptoms.org, FND Australia). The GP has a central long-term management role; physiotherapy is often key, with psychotherapy for psychological/psychiatric comorbidity. Manage functional overlay alongside the coexisting neurological disorder, not instead of it.