Parkinson’s disease

In 1872, Jean-Martin Charcot identified general slowness of movement (‘bradykinesia’) as a prominent feature of paralysis agitans.¹ Bradykinesia is now known as one of the characteristic, or ‘cardinal’, features of PD.¹ Charcot also distinguished between the tremors caused by paralysis agitans and those associated with multiple sclerosis.² The description of paralysis agitans was refined accordingly, and the condition was subsequently known as ‘Parkinson’s disease’.^1,2

Physicians set about investigating the underlying causes of the disease.² Although Charcot considered PD to be a neurosis, or mental health disorder, others looked for non-psychiatric pathologies.² An autopsy was carried out on an individual who had suffered from PD, leading eventually to the identification of an abnormality in a part of the brain called the ‘substantia nigra’ as the most likely source of the disease.²

In his efforts to treat patients suffering from PD, Charcot tried several anti-cholinergic agents (which reduce the action of the neurotransmitter acetylcholine).² Through his observations, he discovered that one anti-cholinergic agent was at least partially effective at controlling symptoms.²

References:
1.Goetz CG. The history of Parkinson’s disease: early clinical descriptions and neurological therapies. Cold Spring Harb Perspect Med 2011; 1 (1): a008862.

2.Pfeiffer RF, Wszolek ZK, Ebadi M. Parkinson’s Disease, 2nd edition. Boca Raton: CRC Press, 2012.

3.Weatherall M. Parkinson’s eponym. Lancet Neurol 2024; 23 (2): 143.