LESIONS

A Guide to Localisation in Neurology

Case 15 - Dizziness and clumsiness

What is the lesion?

The tempo is the most important thing here, but the demographics can also be considered as certain pathologies are more likely in this young woman. They’re not the basis for diagnosis, but they act like probability ‘multipliers’ when we make our formulation.

The tempo is somewhere between acute and subacute – evolving over a short number of weeks. It is too slow for a vascular lesion, and too fast for other cerebellar pathologies such as genetic or sporadic ataxias – which are not typically lateralised ether.

Inflammatory demyelination is a concern. The parts of the brain within the posterior fossa are white-matter rich given the many tracts passing through this area, connecting the brain, spine, cerebellum and cranial nerves. This is a frequent site of disease in demyelinating disorders, particularly multiple sclerosis (MS). Peripheral nervous system demylination is also worth considering; Miller-Fisher syndrome is a Guillain-Barre variant that affects the cerebellar system, though is not likely here – we would expect areflexia and ophthalmoplegia.

A space-occupying lesion (SOL) is also a concern, and many exist which can affect the posterior fossa. Some originating in the cerebellum, others the brainstem or ventricular space. Some are tumours but other causes include vascular abnormalities (e.g. cavernoma) and infections (e.g. abscess, although there are no features of this) – so it is not only neoplastic SOLs we need to concern ourselves with. We might expect some other features such as headache but not necessarily.

Toxic and metabolic disorders often affect the cerebellum.

Alcohol is the best-known, with acute voluntary intoxication being undertaken for recreational purposes by billions worldwide, as well as chronic toxicities in those who have longstanding issues with excessive usage. Alcohol is also a major cause of Wernicke’s encephalopathy, which prominently features ataxia as well as other features this patient doesn’t have. Alcohol-related ataxia is generally central and symmetrical with prominent gait and truncal balance issues as well as dysarthria - but not lateralised limb signs.

Many other drugs, including anti-seizure medications, can cause acute or chronic ataxia. Other toxic causes of ataxia include carbon monoxide toxicity.

A number of other metabolic disorders are associated with ataxia including certain vitamin deficiencies (particularly E). Coeliac disease has associations with ataxia.

In this case however there is no suggestion of toxic exposures, she isn’t on medications, she doesn’t drink in excess (and while surreptitious alcohol abuse is common, there are no signs of this e.g. dysarthria), there are no features of Wernicke’s (e.g. nystagmus, amnesia), and toxic-metabolic causes of ataxia don’t tend to display strictly lateralised signs.

Overall, demyelination is a concern. From a demographic perspective, as a young woman, it is particularly suspicious. However, a SOL is also possible here.