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Organophosphorus insecticide (OPI) poisoning is a major health problem in India. These are irreversible inhibitors of acetyl cholinesterase which produce a well-established triphasic effect. The first phase which is a cholinergic phase due to increased action of acetylcholine at muscarinic, nicotinic and central nervous system synapses produces symptoms like Miosis, Blurred Vision, Nausea, Vomiting, Diarrhea, Salivation, Lacrimation, Bradycardia, Abdominal Pain (Muscarinic), Fasciculations, Paralysis, Pallor, Muscle Weakness, Hypertension, Tachycardia, Mydriasis (Nicotinic), Confusion, Toxic Psychosis, Seizure, Fatigue, Respiratory Depression, Dysarthria, Unconsciousness, Ataxia, Anxiety (Central Effects). The second phase is intermediate syndrome which sets in 2-4 days after initial exposure, the signs and symptoms comprise of muscle fasciculations and neuromuscular paralysis involving the respiratory, bulbar and limb muscles. The third phase is Organophosphorus Induced Delayed Polyneuropathy (OPIDN), which is often noted after 7-21 days of exposure, initial symptoms include paraesthesias, pain in calves, foot drop etc. In addition, extrapyramidal manifestations are also described after acute organophosphorus poisoning such as Dystonia, Rest Tremors, Cog Wheel Rigidity And Choreathetosis. Cypermethrin is a synthetic pyrethroid used as an insecticide. Studies suggested that long term exposure to cypermethrin induces nigrostriatal dopaminergic neurodegeneration in adult rats. Acute ingestion of cypermethrin will cause nausea, vomiting, stomach pain, convulsions, coma and death in humans. The etiology of parkinsonism is multi factorial with genetic, environmental and toxic determinants, development of typical parkinsonism after brief exposure to organophosphorus compounds is a rare phenomena and there are only few reports in literature. We report a 40 year old female who presented with cholinergic crisis following acute ingestion of Profofenos and Cypermethrin mixed compound, developed parkinsonism on day 5 of admission and recovered completely after 2 days of treatment with Amantidine. [ABSTRACT FROM AUTHOR]

Abstract: Traumatic brain injury (TBI) is a devastating neurological injury with broad manifestations. Unfortunately, its diagnosis and efficacious treatments remain elusive. Different post injury symptoms are exhibited at different time frames, indicative of a time-related progression of the pathology. Therefore, particular treatments must be tailored to the post injury time frame. This overview is focused on the secondary chronic phase following TBI and the value of sympathomimetic therapy during this phase. The various direct- and indirect-acting drugs are reviewed, and the treatment protocol employed by the author is described. [Copyright &y& Elsevier]

Hepatitis C is usually treated with interferon or a combination of interferon and ribavirin, but these agents have numerous side effects, and interferon must be given by injection three time a week. An alternative oral medication would be a welcome advance for treating hepatitis C. Amantadine has been reported to have the potential to produce viral suppression in patients with hepatitis C. To gain further knowledge about the effects of amantadine on hepatitis C, we treated 24 patients for 3-12 months (average = 5.5 months; median = 4.5 months) with 100 mg amantadine twice daily. Twelve patients had stage 3 or 4 fibrosis on biopsy. Eleven patients had a fall in viral titer, but complete viral suppression was not seen in any patient. Three patients had no viral titer obtained after treatment, but their elevated transaminase levels did not change with treatment. Of the 15 patients with a decrease in enzyme levels, only two patients had normalization. Six patients had side effects during the treatment, but in only one was amantadine stopped solely because of side effects. Based on these results and a literature review, we do not believe amantadine is an effective single agent for the treatment of chronic hepatitis C. [ABSTRACT FROM AUTHOR]