GC091 Unsteady Gait Cerebellar Lesions; Movement Disorders; Parkinsonism

"Gait is a sensitive indicator of overall health status. Self-selected walking speed closely correlates with life expectancy in elderly persons." ^[1]

This is clinically important: gait speed is sometimes called the "sixth vital sign" in geriatrics. A declining gait speed predicts falls, hospitalisation, and mortality.

Gait is a complex interplay of many parts of the nervous, musculoskeletal, and cardiorespiratory systems. It is influenced by age, personality, mood, and sociocultural factors. ^[1]

The gait cycle describes one complete sequence of events from initial contact of one foot to the next initial contact of the same foot. It has two phases:

Within the stance phase there is a period of double support (both feet on ground) — this increases with age and with fear of falling, and is a key compensatory mechanism.

Walking speed (m/s), cadence (steps/min), step width (midpoint to midpoint of both heels), step length (point of foot contact to contralateral foot contact), stride length (linear distance covered by one gait cycle). ^[1]

Understanding these is important because different pathologies alter them predictably:

• Parkinsonism → reduced stride length, reduced speed, increased cadence (festination)
• Cerebellar ataxia → increased step width, irregular step length
• Sensory ataxia → increased step width, high-stepping (to slam foot down for proprioceptive feedback)

Causes of gait disorders: Neurological conditions, Orthopedic conditions, Medical conditions. Prevalence increases with age — 10% at age 60–69, 60% in community-dwelling people over 80 years. ^[1]

Afferent nerves carry sensory information regarding body position sense to a centrally-integrating system consisting of the frontal cortex, brainstem, basal ganglia and cerebellum; movement is then carried out by the motor system of pyramidal tract, neuromuscular junctions and muscles. ^[1]

This is the framework for localisation:

Common neurological causes: Sensory ataxia, Parkinsonism, Frontal gait disorder, Cerebellar ataxic gait disorder. ^[1]

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Cerebellum is important in the act of balancing and coordinating movement. Cerebellar ataxia: poor coordination of gait and balance, limb and eye movement. ^[1]

The cerebellum doesn't initiate movement — it fine-tunes it. It acts as a comparator: it receives a copy of the intended motor command (from cortex via pontine nuclei) and sensory feedback (from spinocerebellar tracts), then calculates the error and sends corrections back via the thalamus to the motor cortex. Without it, movements are clumsy, poorly timed, and inaccurate.

Control of balance is predominantly localised in the vermis of the cerebellum. Paravermal structures are important for the control of the timing and amplitude of targeted limb movements. Unilateral lesions of cerebellar hemispheres induce ipsilateral limb ataxia. Isolated lesions of the vermis or the paravermal structures may cause gait ataxia without affecting the limbs. ^[1]

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Gait ataxia is amongst the first cerebellar deficits in cerebellar disorders. It is a disabling symptom with a high risk of falls. "Drunken gait." ^[1]

The classic mnemonic is DANISH: Dysdiadochokinesia, Ataxia, Nystagmus, Intention tremor, Scanning dysarthria (or Slurred speech), Hypotonia (pendular knee jerk).

Key examination findings:

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Causes: Vascular, Toxic (e.g. alcohol, drugs such as anti-convulsants), Degenerative (e.g. hereditary cerebellar ataxias), Inflammatory (e.g. multiple sclerosis), Neoplastic. ^[1]

This is a high-yield list. Expand it with temporal course classification from senior notes:

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From the 2020 SAQ ^[2]: A 39-year-old woman with sudden dizziness, vertigo, unsteady wide-based gait falling to the right, right-sided incoordination with past-pointing and intention tremor. CT brain shows no haemorrhage.

• Most likely diagnosis: Right cerebellar infarction (ischaemic stroke)
• Confirmation: MRI brain with diffusion-weighted imaging (DWI)
• Underlying conditions: Cardioembolism (AF, PFO, valvular disease), vertebral artery dissection, hypercoagulable state (OCP use), vasculitis

"Shaking palsy: Involuntary tremulous motion with lessened muscular power, in parts not in action even when supported, with a propensity to bend the trunk forward and to pass from a walking to a running pace." Other features: Unilateral onset, slow progression, non-motor symptoms such as constipation, drooling of saliva, sleepiness, delirium. ^[1]

James Parkinson's 1817 description is remarkably accurate. Notice he described the rest tremor ("not in action even when supported"), the stooped posture ("propensity to bend the trunk forward"), and festination ("pass from a walking to a running pace").

Loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). ^[1] Lewy bodies: intracellular inclusion bodies with main constituent being misfolded α-synuclein. ^[1]

Why does this cause parkinsonism? The basal ganglia circuit has two pathways:

• Direct pathway (D1 receptors): Facilitates movement (Go signal)
• Indirect pathway (D2 receptors): Inhibits movement (Stop signal)

Dopamine from SNpc normally excites the direct pathway and inhibits the indirect pathway — net effect = movement facilitation. When dopaminergic neurons die:

• Direct pathway becomes underactive → less Go signal
• Indirect pathway becomes overactive → more Stop signal
• Net result: excessive inhibition of the thalamus → reduced cortical excitation → bradykinesia, rigidity, and difficulty initiating movement ^[1][12]

60–80% of dopaminergic neurons are lost before motor symptoms emerge. ^[12]

This explains why PD has a long prodromal phase of non-motor symptoms (constipation, anosmia, REM sleep behaviour disorder) before motor features appear — the brain has remarkable compensatory capacity until the loss crosses a critical threshold.

Motor symptoms: Rest tremor, Bradykinesia, Rigidity, Postural instability. ^[1]

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Non-motor symptoms such as constipation, drooling of saliva, sleepiness, delirium. ^[1]

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Parkinsonian gait (rigid-akinetic gait): stooped posture, reduced arm swing, hesitation in initiation and difficulty in turning, shuffling gait, festination (rapid small steps and forward leaning). ^[1][7][12]

Features to observe:

• Stooped posture: trunk flexed forward
• Reduced arm swing: often asymmetric (worse on more affected side)
• Short shuffling steps: reduced stride length
• Hesitation: difficulty starting to walk (start hesitation) and freezing (especially at doorways, narrow spaces)
• En-bloc turning: turns whole body rather than leading with head
• Festination: involuntary acceleration with progressively smaller steps — the patient is "chasing their centre of gravity"

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Other causes of parkinsonism: Atypical parkinsonism or parkinsonism-plus syndromes (MSA, PSP, CBD, LBD), Vascular parkinsonism, Drug-induced. ^[1]

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Treatment: Drugs (dopamine replacement), Surgery (deep brain stimulation), Rehabilitation (PT/OT/ST/dietitian). ^[1]

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Chorea: Random, flowing, non-suppressible involuntary movements of the distal muscles and face. May be incorporated into semi-purposeful acts that mask the involuntary movements. ^[1]

This "incorporation" is called parakinesia — the patient tries to disguise the chorea by blending it into a purposeful movement (e.g., involuntary arm movement becomes a hair-smoothing gesture).

Athetosis: Slow chorea. Non-rhythmic, slow, writhing movements in distal muscles of hands and feet. ^[1]

Hemiballismus: Unilateral, rapid, non-rhythmic, non-suppressible, wildly flinging movement of proximal arm and/or leg. Severe form of chorea. ^[1]

These three form a spectrum (ballism → chorea → athetosis) from most violent to most subtle. They all reflect basal ganglia pathology.

Medication side effects: Levodopa, Anti-psychotics. Autoimmune disorder e.g. SLE. Rheumatic fever. Huntington disease. Metabolic: hyperglycemia, hyperthyroidism. Stroke: Hemiballismus — contralateral subthalamic nucleus; Hemichorea — contralateral putamen or caudate. ^[1]

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Dystonia: Involuntary muscle contractions which may be sustained or intermittent. May result in abnormal postures, movements, or both. ^[1]

Classification: Etiology — primary (inherited, idiopathic) or secondary (CNS disorders or medications). Distribution — focal, segmental, generalized. ^[1]

Etiology: Primary dystonia — usually generalized, beginning in childhood, most often due to genetic mutations. CNS disorders — Wilson's disease, stroke, cerebral palsy, off symptom of PD. Drugs — anti-psychotics, anti-emetics. ^[1]

Treatment of dystonia:

• Focal: Botulinum toxin injection (first-line for cervical dystonia, blepharospasm)
• Generalized: Anticholinergics (trihexyphenidyl/Artane), tetrabenazine, clonazepam
• Refractory: DBS at globus pallidus internus (GPi)
• Drug-induced acute dystonia: Anticholinergics (benztropine, diphenhydramine) — EMERGENCY if laryngospasm ^[15]

Myoclonus: Brief, shock-like, involuntary jerks which result in movement of a joint (positive myoclonus) or with sudden loss of muscle tone (negative myoclonus). ^[1]

Negative myoclonus = asterixis ("flapping tremor" of hepatic/renal failure) — not actually a tremor at all, but a brief involuntary loss of muscle tone.

Physiologic: Hypnic jerks, Hiccup. Pathologic: Secondary to underlying disorders or medications. ^[1]

Causes: Degeneration of basal ganglia (PD, Huntington's), Dementia (CJD, Alzheimer's), Encephalopathies and epilepsies (mitochondrial disorders, myoclonic epilepsies), Toxic/metabolic causes (hypoxic brain injury, hypercapnia, hypoglycemia, liver failure, uremia). ^[1]

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Q1. A 65-year-old man presents with gradual onset of shuffling gait, rest tremor in his right hand, and difficulty buttoning his shirt. Examination shows cogwheel rigidity in the right arm and masked facies. What is the most likely diagnosis?

• Answer: Idiopathic Parkinson's disease. Key: asymmetric rest tremor + bradykinesia + rigidity = PD until proven otherwise.

Q2. A 70-year-old woman presents with unsteady gait that is equally bad with eyes open and closed. She has nystagmus and past-pointing on finger-nose test on the left. Where is the lesion?

• Answer: Left cerebellar hemisphere. Key: Romberg negative = cerebellar, not sensory. Ipsilateral signs.

Q3. A patient with unsteady gait has significant worsening of balance when eyes are closed vs open, no dysmetria. Where is the lesion? (from 2020 MCQ Q27)

• Answer: Dorsal columns in spinal cord. Key: Romberg positive + no dysmetria = sensory ataxia. ^[3]

Q4. A man with clumsiness, unsteady gait, and slurred speech but no stiffness. Where is the lesion? (from 2023 MCQ Q13)

• Answer: Cerebellum. Key: ataxia + dysarthria + no spasticity = cerebellum. ^[17]

Q5. A woman with sudden involuntary movements affecting the left side of her body without weakness or numbness. Where is the lesion? (from 2023 MCQ Q10)

• Answer: Basal ganglia (right side). Key: unilateral involuntary movements without weakness = contralateral basal ganglia lesion (likely hemichorea/hemiballismus). ^[17]

Q6. List five causes of cerebellar ataxia. (5 marks)

• Vascular (cerebellar stroke)
• Toxic (alcohol, anticonvulsants)
• Degenerative (hereditary cerebellar ataxias e.g. SCA, Friedreich's)
• Inflammatory/autoimmune (multiple sclerosis)
• Neoplastic (cerebellar tumour, paraneoplastic)

Q7. A 60-year-old man has bilateral symmetrical parkinsonism with postural hypotension (systolic drop > 30 mmHg). Name the most likely diagnosis and two investigations.

• Diagnosis: Multiple system atrophy (MSA-P)
• Investigations: MRI brain (hot cross bun sign / putaminal rim), autonomic function tests (tilt-table test)

Q8. Examine this patient's gait and describe your findings.

• Approach: Watch patient walk naturally → assess stride length, base width, arm swing, posture, turning → then tandem walk → then Romberg. Describe pattern (e.g., "wide-based ataxic gait with inability to tandem walk, consistent with cerebellar ataxia").