Current Opinions in Neurological Science What James Parkinson Really Thought was Behind Parkinson’s Disease

In May, 2017, a Norwegian study done by Berstad and Berstad threw its support behind revitalizing of the hypothesis that with regard to Parkinson’s disease (PD), the preponderance of convincing evidence points to a chronic infectious cause – not viral and most likely of the family Actinomycetales of which tuberculosis and the mycobacteria are premier members. The Berstads concluded that in accordance with such thoughts and despite the diagnostic challenges ahead, that further studies in human brain tissue from PD patients to detect such an underlying infectious cause were warranted. Such thoughts are really nothing new, and have been in circulation since James Parkinson mentioned this same infectious cause in An Essay on the Shaking Palsy in which he was the first to describe “ paralysis agitans ”, a condition that would later be renamed Parkinson’s disease by Jean-Martin Charcot. Here we review further evidence in support for this particular infectious cause of Parkinson’s. The positive function of MPTP seemed to be as method to induce Parkinsonism in test animals, then given various anti-Parkinson’s agents. Thoughts that environmental toxins might be responsible for Parkinsonism, centuries old, are still very much with us and led to the use of Deprenyl and tocopherol as a treatment for Parkinson’s disease (DATATOP) study [10]. Here, patients either received combination Deprenyl and tocopherol (vitamin E) or a placebo tablet with nothing in it. Researchers reasoned that the combined use of a monoamine oxidase (MAO) inhibitor, which is what Deprenyl (also called Eldepryl) is, and a free-scavenger like vitamin E might prevent some unknown toxin similar to MPTP from destroying dopamine-producing cells. But the patients receiving the MAO inhibitor (Deprenyl) and the vitamin did so much better that the study had to be called to an early halt. For a while, it seemed that the combination was not only increasing serum dopamine and reducing symptoms, but might even be halting Parkinson’s progression altogether. A study by Otaki, at Ichikawa and Oizumi [15] at the Kirume University in Japan showed similar marked improvement in a 79-year-old man placed on anti-tuberculous treatment after his upper right lung collapsed from the disease. Fuente-Aguado and Bordon [13], working out of the Infectious Disease Unit of Hospital Xeral in Bigo, Spain, treated a case of parkinsonism associated with tuberculous meningoencephalitis with TB medications. Seven days after starting tuberculous therapy, signs of Parkinsonism disappeared entirely, accompanied by overall improvement in the patient’s clinical picture. Fuente-Aguado and Bordon’s conclusion: The extinction of Parkinsonism after tuberculosis therapy supported tuberculosis as a cause of Parkinsonism. Solanki and Kothari [17] reported two cases of full-blown Parkinsonism developing in a 30-year-old Indian housewife and a 32-year-old male laborer, both of whom were being treated for CNS tuberculosis and both of whom lost their Parkinson’s with continued anti-tubercular medicines. Concurrently, Kurasawa, Ikeda, and Inoue [14], puzzled by a lung mass in a 71-year-old Parkinsonian man’s chest, thought it to be malignant. But when it proved mycobacterial instead and the patient was put on two first-line drugs for tuberculosis, the patient lost his Parkinson’s –and two years later remained without it.