Chronic Manganese Toxicity in Indian Mines-An Historical Account of the Contributions of Dr. T.P. Niyogi.

The mining of manganese ore in India started in the year 1899, in Nagpur district of the Central Provinces. Almost six decades later, in 1957, Dr. T. P. Niyogi examined several young men involved in dry drilling of Manganese ore, who had symptoms of muscular pain, weakness, clumsy movements, asthenia, anorexia, insomnia, and gait difficulties. These patients were also emotionally disturbed and prone to falls and accidents. He concluded that these symptoms were due to chronic manganese toxicity with parkinsonian features and psychiatric manifestations which he published in 1958.[1] This lead to the formation of an Enquiry Committee by the Ministry of Labour and Employment, Government of India which instituted corrective measures in mining of manganese in India. Very few reports of chronic toxicity due to inhalation of manganese have been reported subsequently. This paper highlights the contributions of Dr. T.P. Niyogi who was the Civil Surgeon in Chhindwara, MP during that period.

Central nervous system tuberculosis.

The purpose of this article is to review the many facets of central nervous system tuberculosis (CNS-TB). The entities described are tuberculous meningitis (TBM) and its complications, spinal cord disorders, tuberculomas and co-infection with the human immune-deficiency virus (HIV). The latter has become a common problem worldwide becoming a more fulminant disease. The accuracy of the conventional and the modern molecular techniques for the diagnosis of TBM have a high specificity but a low to moderate sensitivity. Computerised tomographic scans and magnetic resonance imaging have many characteristic features which have vastly improved the diagnostic accuracy of CNS-TB. The recommended therapeutic regimens are an extrapolation of the regimen used for pulmonary TB, hence the optimal composition, dosage and duration of the therapy are not yet established. Multidrug resistant TB is emerging as a global threat and the delay in recognition of drug resistance combined with the lack of data on appropriate drug regimen adds to its high mortality.

The neurology of COVID-19 revisited: A proposal from the Environmental Neurology Specialty Group of the World Federation of Neurology to implement international neurological registries.

A comprehensive review of the neurological disorders reported during the current COVID-19 pandemic demonstrates that infection with SARS-CoV-2 affects the central nervous system (CNS), the peripheral nervous system (PNS) and the muscle. CNS manifestations include: headache and decreased responsiveness considered initial indicators of potential neurological involvement; anosmia, hyposmia, hypogeusia, and dysgeusia are frequent early symptoms of coronavirus infection. Respiratory failure, the lethal manifestation of COVID-19, responsible for 264,679 deaths worldwide, is probably neurogenic in origin and may result from the viral invasion of cranial nerve I, progressing into rhinencephalon and brainstem respiratory centers. Cerebrovascular disease, in particular large-vessel ischemic strokes, and less frequently cerebral venous thrombosis, intracerebral hemorrhage and subarachnoid hemorrhage, usually occur as part of a thrombotic state induced by viral attachment to ACE2 receptors in endothelium causing widespread endotheliitis, coagulopathy, arterial and venous thromboses. Acute hemorrhagic necrotizing encephalopathy is associated to the cytokine storm. A frontal hypoperfusion syndrome has been identified. There are isolated reports of seizures, encephalopathy, meningitis, encephalitis, and myelitis. The neurological diseases affecting the PNS and muscle in COVID-19 are less frequent and include Guillain-Barré syndrome; Miller Fisher syndrome; polyneuritis cranialis; and rare instances of viral myopathy with rhabdomyolysis. The main conclusion of this review is the pressing need to define the neurology of COVID-19, its frequency, manifestations, neuropathology and pathogenesis. On behalf of the World Federation of Neurology we invite national and regional neurological associations to create local databases to report cases with neurological manifestations observed during the on-going pandemic. International neuroepidemiological collaboration may help define the natural history of this worldwide problem.

Familial Creutzfeldt-Jakob Disease in an Indian Kindred.

It is now known that the inherited prion disease is caused by over 60 different mutations in the Prion protein (PRNP) gene. Four missense mutations at codons 102, 178, 200 and 210, account for over 95% of these cases. In this study we describe, a large Indian family with familial Creutzfeldt Jakob Disease (fCJD). One affected member presented with a presenile dementia, a protracted clinical course and characateristic MRI features. Genetic analysis revealed a D178N mutation in the 2 affected individuals and 7 unaffected members. The neuropathological examination of the brain of one of the affected member was conspicuous by spongiform degeneration, neuronal loss and gliosis. This is a detailed report of a genetically and neuropathologically proven fCJD from India.