Neurologic signs

Neurological signs nystagmus, miosis, blurred vision, tremor, slurred speech, dystonia, convulsion, amnesia, confusion, peripheral numbness... 

Neurologic signs did not occur over a 30-day period in male prisoner volunteers in California who ingested daily doses of methyl parathion ranging from 1.0 to 19 mg. There were no uniform changes in plasma or erythrocyte cholinesterase levels at any of these doses (Rider et al. 1969). By increasing concentrations of methyl parathion administered to the same experimental population and using the same protocol, a dose that inhibited cholinesterase values was established. These additional studies were published nearly 20 years ago in abstract form only therefore, they are not discussed in this section. 

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of these receptors results in muscle fasciculations even greater stimulation results in blockade and muscle paralysis (Lefkowitz et al. 1996 Tafliri and Roberts 1987). Hyperactivity of central nervous system receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not... 

Another condition involving ceruloplasmin is aceru-loplasminemia. in this genetic disorder, levels of ceruloplasmin are very low and consequently its ferroxidase activity is markedly deficient. This leads to failure of release of iron from cells, and iron accumulates in certain brain cells, hepatocytes, and pancreatic islet cells. Affected individuals show severe neurologic signs and have diabetes mellitus. Use of a chelating agent or administration of plasma or ceruloplasmin concentrate may be beneficial. 

Intracranial hemorrhage (spontaneous or following trauma), with headache, vomiting, change in mental status, and focal neurologic signs... 

Neurological Signs and Symptoms in Adults. The most severe neurological effect of lead in adults is lead encephalopathy, which is a general term to describe various diseases that affect brain function. Early symptoms that may develop within weeks of initial exposure include dullness, irritability, poor attention span, headache, muscular tremor, loss of memory, and hallucinations. The condition may then worsen, sometimes abruptly, to delirium, convulsions, paralysis, coma, and death (Kumar et al. 1987). Histopathological findings in fatal cases of lead encephalopathy in adults are similar to those in children (see discussion below). 

Several clinically distinct forms of Wilson s disease have been described. Thus, a relatively mild, late-onset form of the disease, has been described in Jewish patients from Eastern Europe. These patients usually present with the neurologic signs of the disease. In contrast, the more common early-onset (childhood) forms of the disease often present first with liver problems, followed by neurologic manifestations. 

A combination of neurological signs is usually a biomarker of organophosphate exposure. Neurological signs such as pupil miosis, muscular tremors, and increased salivation have been observed in humans accidentally exposed to disulfoton (Yashiki et al. 1990) and in animals given disulfoton (Schwab et al. 1981). 

Inhibition of erythrocyte acetylcholinesterase activity or serum cholinesterase activity with or without concomitant neurological signs is usually a good indicator of organophosphate exposure. In addition, T-lymphocyte acetylcholinesterase activity was found to be rapidly and greatly depressed in rats during a 14-day daily exposure to disulfoton, but rapidly recovered after exposure (Fitzgerald... 

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