Neurotoxins have existed on the earth from times immemorial. Old neurotoxic disorders were due to ingestion/ exposure of heavy metals and food like lathyrus sativus over a long period of time. The 20th Century with rapid industrialsation and expanding chemical and drug industry has spawned several new, hitherto unknown disorders. Old disorders continue to exist e.g. fluorosis, arsenicosis, lathyrism, manganism and lead neuropathy, along with new diseases like Minamata disease, subacute myelo optic neuropathy (SMON), MPTP-Parkinsonian syndorme, triorthcresyl phosphate (TOCP) neuroparalytic disease, pesticide induced seizures, tremor and neuropathy, solvent encephalopthy, antipileptic drug foetal syndrome and excitotoxin induced behavioural disorders. Studies on pesticides Organochlorine and organophosphates, synthetic pyrethrins, solvents, heavy metals and substances abuse in the Indian context confirm the neurotoxic nature of many synthetic substances. Future problems envisaged are of concern to clinical neurologists as many of these neurotoxic disorders mimic syndromes of well known neurological disease. The new millenium poses a challenge to the clinician as newer compounds in industry, food, drugs and chemical war agents are being developed. Molecular genetics has advanced rapidly with release of the human genome map. Animal cloning and genetically modified plant products have entered the food chain. How safe are these new inventions for the central nervous system is a big question? India cannot afford disasters like Union Carbide's Bhopal gas leak nor be a silent spectator to manipulative biotechnology. Unless it is proven beyond all doubt to be a safe innovation, Chemicals have to be cautiously introduced in our environment. To Study, ascertain and confirm safety or neurotoxicity is an exciting challenge for the neuroscientists of the 21st century.

Alzheimer's disease is characterized by degeneration of various structures in the brain, with development of amyloid plaques and neurofibrillary tangles. Deficiencies of acetylcholine and other neurotransmitters also occur. Pharmacological treatment of the disease generally seeks to correct the histopathology, the biochemical derangements or their defects. The incidence of the disease is increasing worldwide. About 35% of people develop Alzheimer’s disease by age 75, and the percentage rises with age. By age 85, almost half of all people get the ailment. Reliable estimates of prevalence of Alzheimer's disease in Indian subcontinent are not available as yet, however anecdotal data suggest a pattern consistent with worldwide trends. Physicians should be able to competently diagnose evaluate and initiate treatment in most patients with Alzheimer's dementia. Hence, it is imperative that neurologists familiarize themselves with the pharmacological treatments of this challenging illness. The authors attempt to given an overview of the various current pharmacologic treatments available for the disease. Contemporary treatment of the memory disturbance in Alzheimer's disease is to boost declining cholinergic function, which is characteristic of this disease. Therefore, the mainstay of current treatment is to use acetylcholinesterase inhibitors. The authors discuss the available acetylcholinesterase inhibitors and how they can be distinguished from each other on the basis of secondary pharmacologic properties. The article also discusses use of some other non-conventional and investigational drugs used for the treatment of Alzheimer's disease.

This is a study of B12 and folate deficiency in a hospital population. We studied the incidence of their deficiency by evaluating blood levels in every tenth hospital admission. Among the 450 patients chosen, 417 had normal levels of both, 2 had deficiency of folate alone (folate < 3ng.ml), 3 had B12 deficiency alone (B12<200pg/ml)and 11 had deficiency of both (total 3.5%). In addition 12 had borderline b12 level(200-300pg/ml), 2 had borderline folate level (3-4ng/ml)(0.44%)and 3 had borderline levels for both (0.66%) . Thus 33% had definite or borderline deficiency. This deficiency was more common in the elderly and in patients on vegetarian diet (5.7% definite deficiency, 8.8% borderline levels) compared to those on a non-vegetarian diet. During the 2 1/2 years of the study a total of 99 definite deficiency and 69 borderline deficiency were seen. In the definite deficiency group, 22.3% had neuropathy, 6.1% had evidence of myelopathy, 18.2% had neuropsychiatric changes (memory defect, dementia, behavioural abnormalities, depression) and 4.1% had cerebellar signs. The neurologic findings in the borderline group were almost similar (neuropathy 29%, myelopathy 8.6% and neuropsychiatric changes 18.4%). High mean corpuscular volume (MCV> 95) was seen in 69% of those with both B12 and folate deficiency, 43.4% with B12 deficiency and 61.15 with folate deficiency. Hypersegmented polymorphs were seen in 21.7% with B12 deficiency, 27.5% with folate both B12 and folate deficiency had either megaloblastosis or dimorphic picture. It is to be noted that B12 and folate deficiency in this population was more frequent than we previously considered and reliance on haematologic parameters will miss half to one third of all cases. As expected B12 deficiency is more frequent in vegetarians than non-vegetarians.

The complications of infective endorcarditis are well known. However the pattern of underlying heart disease, organisms, types of complications and outcome are likely to vary depending on the study population, local epidemiology and associated medical variables. In India the patterns of medical practice is changing with technical and medical advancement. These change are likely to influence the pattern of infective endorcarditis and its neurological complications. To study the profile of neurological complications out come, 22 consecutive patients with infective endorcarditis were studied. There were 13 males and nine female. Three patients had late prosthetic valve endorcarditis and rest had native valve endorcarditis. Two patients with native valve developed endorcarditis after balloon dilatation of mitral valve. All prosthetic valve patients survived while both patients with post dilatation endorcarditis expired. Staphylococcus aureus was the most frequent organism. Bland infarction was the commonest neurologic complication in this series. Two third patients with staphylococcus endorcarditis survived. Or results suggest that in patients with neurologic complications due to infective endorcarditis staphylococcus is the most frequent organism, bland infraction is the commonest radiological finding and mortality is high.

Giant axonal neuropathy is a rate disorder with an autosomal recessive inheritance. It should be differentiated from toxic neuropathies, and hereditary degenerative disorders of nervous system like Friedreich's ataxia and HMSN. Thick curly hair, though may not be present always is a useful clinical clue to identify cases. Prognosis is generally poor though course of the illness is variable. We report here a clinically and hisopathologically characteristic familial case of giant axonal neuropathy, which occurred in a 17-year-old boy, and his 21-year-old sister.

An unusual case of primary angiitis of central nervous system (PACNS) presenting with headache, seizures and focal deficits is presented. Despite multiple lesions noted on brain MRI, definitive diagnosis required a brain biopsy. A high index of clinical suspicious and the utility of brain biopsy for diagnosis are emphasized.