Examine this patient, who presented with a history of falling to one side. Demonstrate the cerebellar signs.



· History of falls, wide-based gait, clumsiness and difficulty with fine coordinated movements.

· Tremor.

· Waxing and waning of symptoms (multiple sclerosis).

· Stroke (brainstem vascular lesion).

· Drug toxicity: phenytoin, alcohol abuse, lead poisoning and solvent abuse.

· History of intracranial tumours (posterior fossa including cerebellopontine angle tumour).

· History of hypothyroidism (a reversible cause).

· Family history (Friedreich's ataxia and other hereditary ataxias).

· Birth defects (congenital malformations at the level of the foramen magnum).


· Ask the patient a few questions to assess his speech.

· Ask the patient to keep his arms outstretched; then give them a small push down-ward and look for rebound phenomenon.

· Examine for rapid alternating movements with the hand.

· Do the finger-nose test: look for past-pointing and intention tremor.

· Do the heel-shin test.

· Examine the gait, in particular tandem walking. If ataxia is not marked, the patient's gait may be tested with eyes closed; he

often progresses to the side of the lesion.

· Tell the examiner that you would like to examine the fundus for optic atrophy as demyelination is the commonest cause of

cerebe!lar signs.


This patient has a cerebeilar syndrome with optic atrophy (lesion) due to multiple sclerosis (aetiology) and is markedly ataxic

(functional status).


How may cerebellar signs manifest?

· Disorders of movement:

-Nystagmus: coarse horizontal nystagmus with lateral cerebellar lesions; its

direction is towards the side of the lesion.

-Scanning dysarthria: a halting, jerking dysarthria which is usually a feature of

bilateral lesions.

-Lack of finger-nose coordination (past-pointing): movement is imprecise in

force, direction and distance - dysmetria.

-Rebound phenomenon - inability to arrest strong contraction on sudden

removal of resistance. This is known as Holmes' rebound phenomenon.

- Intention tremor.

- Dysdiadochokinesia - impairment of rapid alternating movements (clumsy).

- Dyssynergia - movements involving more than one joint are broken into parts.

· Hypotonia.

· Absent reflexes or pendular reflexes.

· Lack of co-ordination of gait - patient tends to fall towards the side of the lesion.


1. The classical clinical triad of cerebellar disease is Ataxia, Atonia, Asthenia.

2. The cerebellum is not primarily a motor organ. It is developed phylogenetically from a primary vestibular area and is involved in

modulation of motor activity. It receives afferents from the vestibular nuclei, spinal cord and cerebral cortex via the pontine


What are the causes of cerebellar syndrome?

· Demyelination (multiple sclerosis).

· Brainstem vascular lesion.

· Phenytoin toxicity.

· Alcoholic cerebellar degeneration (there is atrophy of the anterior vermis of the cerebellum).

· Space-occupying lesion in the posterior fossa including cerebellopontine angle tumour.

· Hypothyroidism (a reversible cause).

· Paraneoplastic manifestation of bronchogenic carcinoma.

· Friedreich's ataxia and other hereditary ataxias.

· Congenital malformations at the level of the foramen magnum.


How are cerebellar signs localized?

· Gait ataxia (inability to do tandem walking): anterior lobe (palaeocerebellum).

· Truncal ataxia (drunken gait, titubation): fiocculonodular or posterior lobe (archicerebellum).

· Limb ataxia, especially upper limbs and hypotonia: lateral lobes (neocerebellum).

What is the difference between sensory ataxia and cerebellar ataxia?

If you were allowed to perform one investigation, which one would you choose in a patient with a suspected cerebellar


Magnetic resonance imaging (MRI).

Sir Gordon M. Holmes (1876-1965), consultant neurologist, National Hospital for Nervous Diseases, Queen Square, London, whose

observations on wartime gunshot wounds allowed him to study cerebellar disease (Lancet 1922; ii: 59, 111; Brain 1939; 62: 1-30).

He was the editor of the journal Brain.