Brissaud's lectures

Opening showing an extract of Brissaud's lectures on the causes of: la maladie de ParkinsonĖdouard Brissaud (1852-1909) was a favourite pupil of Charcot and in 1893 temporarily succeeded to his mentor's post.

In 1894 Brissaud's lectures on the causes of ‘la maladie de Parkinson’ examined the evidence for the belief that the disease was caused by severe psychological shock, particularly fear.

Brissaud held that this theory was incompatible with what was known about the condition’s clinical and neuropathological characteristics.

Although he conceded that trauma could be a contributory cause of the malady, he did not accept that this progressively deteriorating, lifelong disease could be caused by a lesion-less neurosis, understood solely as dysfunction.

Opening showing reference to a report by Paul Blocq and Georges MarinescoHe had observed that many patients showed both emotional detachment and exaggerated sadness or joy in response to trivial or banal stimuli.

These responses were similar to those of people who suffered from pseudo-bulbar palsy, the cause of which had been linked to ischaemia* in the brainstem, which convinced Brissaud that la maladie also had an organic cause.

Brissaud examined case reports which also reported on autopsies, and noted that several had described lesions in the region of the basal ganglia.

He was particularly impressed by a report of an 1893 presentation by Paul Blocq and Georges Marinesco, which found a tuberculous mass ‘circumscribed, enucleable with no signs of invasion of surrounding tissue’ in the lower part of the brain, on the side opposite to the patient’s symptoms. The lesion had ‘completely destroyed the niger locus’ (now known as the substantia nigra).

Brissaud concluded that, ‘a lesion of the niger locus may well be the anatomical substratum of Parkinson’s disease.’ He was the first to implicate damage to this area as a cause of ‘la maladie de Parkinson.’

*Ischaemia. Insufficient blood supply to an area of tissue or an organ, due to obstruction or functional constriction of one or more blood vessels, or as part of a more general circulatory failure. 

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