Convulsive affections

Coleus aromaticus Benth. C. amboinicus Lour. Labiatae Ind, Sri, cultivated leaves epileptic convulsive affections - 37. 64... 

Tay-Sachs disease was first described in a child of Ashkenazi Jewish descent by Warren Tay (1881) and Bernard Sachs (1887), and since these initial descriptions, numerous cases have been reported. Motor weakness is one of the earliest signs and may be manifested between the third and sixth postnatal month. This weakness becomes progressively more obvious, and hyperacusis may also be present. After about one year, progressive mental retardation becomes apparent, the status of the patient declines, with the onset of blindness, deafness, and convulsions. Affected children commonly die between age three and four. 

Hydraziae is toxic and readily absorbed by oral, dermal, or inhalation routes of exposure. Contact with hydraziae irritates the skin, eyes, and respiratory tract. Liquid splashed iato the eyes may cause permanent damage to the cornea. At high doses it can cause convulsions, but even low doses may result ia ceatral aervous system depressioa. Death from acute exposure results from coavulsioas, respiratory arrest, and cardiovascular coUapse. Repeated exposure may affect the lungs, Hver, and kidneys. Of the hydraziae derivatives studied, 1,1-dimethylhydrazine (UDMH) appears to be the least hepatotoxic monomethyl-hydrazine (MMH) seems to be more toxic to the kidneys. Evidence is limited as to the effect of hydraziae oa reproductioa and/or development however, animal studies demonstrate that only doses that produce toxicity ia pregaant rats result ia embryotoxicity (164). 

Mode of Action. DDT and its analogues specifically affect the peripheral sense organs of insects and produce violent trains of afferent impulses that result in hyperactivity, convulsions, and paralysis. Death results from metaboHc exhaustion and the production of an endogenous neurotoxin. The very high lipophilic nature of these compounds faciUtates absorption through the insect cuticle and penetration to the nerve tissue. The specific site of action is thought to be the sodium channels of the axon, through inhibition of Ca " ATPase. 

Mode of Motion. The cyclodienes, like lindane and toxaphene, affect the nerve axon produciag hyperactivity, convulsions, prostration, and death. The biochemical lesion is the competitive inhibition of the y-aminobutyric acid (GABA) neurotransmitter binding site of the nerve axon. Spray workers with lengthy exposure to dieldrin have suffered from prolonged and repeated central nervous system disturbances produciag epileptiform coavulsioas. Similar disturbances occurred ia workers heavily exposed to chlordecoae. 

Health Hazards Information - Recommended Personal Protective Equipment Eye protection Symptoms Following Exposure Vapors from very hot material may irritate eyes and produce headache, drowsiness, and convulsions General Treatment for Exposure Remove fresh air. Wash affected skin areas with water. Flush eyes with water Toxicity by Inhalation (ThresholdLimit Value) 5 mg/m Short-Term Exposure limits Not pertinent Toxicity by Ingestion Grade 1 LDjq 5 to 15 g/kg Late Toxicity Birth defects in rats polyneuritis in humans Vapor (Gas) Irritant Characteristics Not pertinent liquid or Solid Irritant Characteristics No appreciable hazard. Practically harmless to the skin Odor Threshold Data not available. 

Morphine. This alkaloid exerts both a depressing and a stimulating action on the central nervous system, the depression affecting the brain especially the sensation of pain and the respiration the cerebral motoi functions are less affected. The stimulant action in the cord is best seen in the cold-blooded animals, when it may develop into tonic convulsions. In higher animals, but rarely in man, there may be some indication of this stimulant action. In cats it may also involve the motor areas, and they... 

Peters s results for corycavine and corycavamine indicate that these two alkaloids produce narcosis in frogs followed by paralysis of the spinal cord, and in mammals increased secretion of tears and saliva and epileptiform convulsions without increase of reflex irritability they also adversely affect the heart. ... 

The effects of protein deficiency on endosulfan toxicity were studied in Wistar rats (Boyd and Dobos 1969 Boyd et al. 1970). Rats fed a diet totally deficient in protein for 28 days prior to administration of a single oral dose of endosulfan had an LDjq of 5.1 mg/kg of endosulfan. Rats fed a low-protein diet (3.5% protein) for 28 days had an LDjq of 24 mg/kg of endosulfan. Rats fed standard laboratory chow (26% protein) had an LDjq of 102-121 mg/kg. The immediate cause of death in all animals was respiratory failure following tonic-clonic convulsions. This study demonstrated that, while a protein-deficient diet does not affect the nature of the toxic reaction, it may affect the sensitivity of rats to the lethal effects of endosulfan. 

Acute exposure to large amounts of endosulfan results in frank effects manifested as hyperactivity, muscle tremors, ataxia, and convulsions. Possible mechanisms of toxicity include (a) alteration of neurotransmitter levels in brain areas by affecting synthesis, degradation, and/or rates of release and reuptake, and/or (b) interference with the binding of those neurotransmitter to their receptors. 

Epileptic seizures affect 0.5% of the population, are more common in the young and, except for partial seizures, often decrease with age. Convulsions associated with metabolic disturbances are not considered to be epileptic. 

There is ample precedent for a modulatory role of K channels in behavior. The K channel blocker, 4-AP, selectively blocks component T (Bartschat and Blaustein 1985a). prolongs nerve action potentials, and enhances neurotransmitter release (Llinas et al. 1975). In man, intoxication with this agent may lead to dissociative behavior, agitation, confusion, convulsions, and coma (Spyker et al. 1980). However, the behavioral aberrations induced by 4-AP differ qualitatively from those induced by PCP. This implies that block of various types of presynaptic K channels may modify behavior and mental activity however, the precise nature of the behavioral manifestations is likely to depend upon the specific type of K channel that is affected. 

Sociocultural, illness, and biological factors affect individual attitudes towards psychotropic medications. Health beliefs or explanatory models, particularly causal attributions regarding the illness and the treatment options afforded within such models, exert a profound influence on patients attitudes and behavior regarding medications (Smith, Lin Mendoza, 1993). Such effects can be subtle and can occur during the course of treatment even if there has been initial successful negotiation about the nature of the illness and treatment. In psychiatric illness little research has been leveled at the personal meaning that patients bring to treatment practices such as electro-convulsive therapy (ECT), oral medications, and depot injections, or to the transition between different administrative routes and types of medications. 

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