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.

The illustrated cycle follows one highlighted limb through:

The support bar beneath the figure alternates double support → single support → double support during stance; once the highlighted limb leaves the ground, the opposite limb provides single support while it swings forward.

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 and a visually guided, stamping gait; a high step also appears when concomitant neuropathy causes foot drop

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:

The original neural-control diagram adds two useful ideas: the spinal central pattern generator (CPG) produces automatic stepping and is continuously modified by proprioceptive/skin afferents, while cortical–basal ganglia–thalamic loops support voluntary movement and limbic–brainstem circuits influence emotionally driven motor behaviour. The cerebellum compares ongoing movement through spinocerebellar feedback and adjusts the descending brainstem/spinal output.

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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• The normal footprint track is narrow and regular. The cerebellar track widens, varies from step to step and deviates laterally: the important visual message is variability plus poor line control, not merely “walking slowly.”
• Tandem gait deliberately removes the compensatory wide base. A mildly affected patient may manage ordinary walking but repeatedly step off a heel-to-toe line.
• The demonstration images also show an examiner positioned close enough to guard against a fall. Do not test tandem gait or eye closure unsupported in a patient who is already unstable.

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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Localisation caution: Miller Fisher syndrome can cause profound ataxia, but this is usually a peripheral sensory/proprioceptive ataxia accompanying ophthalmoplegia and areflexia, not a primary cerebellar lesion.

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]

Reading the pathology images: The normal midbrain section has a dark neuromelanin-pigmented substantia nigra; the PD specimen shows visible pallor from loss of pigmented nigral neurons. The adjacent microscopy image represents an intraneuronal Lewy body. These are pathological teaching images—not routine tests used to make the clinical diagnosis during life.

Why does this cause parkinsonism? The lecture's basal-ganglia circuit simplifies movement control into two pathways:

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

Dopamine from SNpc normally excites D1 direct-pathway neurons and inhibits D2 indirect-pathway neurons—both effects facilitate movement. When nigrostriatal dopamine is lost:

• Direct pathway becomes underactive → less Go signal
• Indirect pathway becomes overactive → more Stop signal
• Net result: increased inhibitory basal-ganglia output to the thalamus/brainstem → reduced scaling and initiation of movement ^[1][12]

The senior-note source estimates 60–80% dopaminergic-neuron loss before motor symptoms emerge. ^[12]

Treat that percentage as a teaching estimate rather than a diagnostic threshold. PD can have a long prodromal phase in which constipation, hyposmia or REM sleep behaviour disorder precedes motor parkinsonism, but none of these symptoms alone diagnoses PD.

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
• Fixed/flexed upper limbs: elbows and wrists held relatively fixed; back rigidity reduces normal trunk rotation
• Slight hip and knee flexion with hand or leg tremor visible during walking
• 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"

Reading the posture and footprint panels: The posture illustration combines axial flexion, flexed elbows/wrists, reduced arm swing and short shuffling steps. The footprint comparison shows a relatively narrow base with shortened step length and more closely spaced contacts, unlike the wide, irregular track of cerebellar ataxia. The patient photograph also reminds you to look for asymmetry at rest and during gait rather than relying on a single still pose.

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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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Tremor is an involuntary, rhythmic, oscillatory movement produced by alternating contraction of reciprocal antagonist muscles.

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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Reading the dyskinesia visual: Levodopa-induced dyskinesia is not a rhythmic tremor. The still image captures irregular flowing/choreiform limb and trunk displacement. Ask whether it occurs at peak “on,” while the dose is wearing off, or during an “off” period; that timing determines specialist medication adjustment.

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]

The first sentence remains useful, but the 2025 MDS consensus sharpens the visual phenotype: dystonic movements/postures are typically patterned and repetitive, may be tremulous or jerky, are often initiated or worsened by voluntary action and may show overflow into adjacent muscles ^[25].

Lecture-era etiology summary: 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]

That “primary versus secondary” split is now too coarse, and adult-onset isolated focal dystonia is common. Current classification uses two axes: clinical characteristics (age at onset, family history, body distribution, temporal pattern, phenomenology, isolated versus combined features) and etiology (genetic, acquired, neuroanatomical and mechanistic information) ^[25].

• Cervical dystonia: sustained patterned head turn/tilt, often with shoulder elevation; describe the direction rather than simply writing “abnormal neck.”
• Generalized dystonia: simultaneous abnormal posturing across trunk and multiple limbs, illustrated by the marked lower-limb crossing/twisting posture.
• Walking-induced dystonia: the resting photograph may look subtle; observe gait for reproducible foot inversion/plantar flexion, leg posturing or task-specific worsening. Patterned repetition distinguishes dystonia from random chorea.

Treatment of dystonia:

• Focal/segmental: Botulinum toxin is commonly first-line for cervical dystonia and blepharospasm, with muscle selection and dosing by an experienced clinician.
• Generalized/combined: Treat the cause where possible; oral options and adverse effects are individualized rather than applying one default drug list.
• Selected severe refractory disease: GPi deep-brain stimulation may be considered by a specialist multidisciplinary team.
• Acute drug-induced dystonia: Urgent locally recommended anticholinergic treatment; laryngeal involvement, stridor or respiratory compromise is an airway emergency ^[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]

Asterixis is a form of negative myoclonus—brief lapses of sustained posture that can occur in toxic-metabolic encephalopathy. Negative myoclonus is the broader category; it is not synonymous with asterixis in every patient.

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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