Ataxia Blood plasma

Patients with hyperthyroidism due to Graves disease had TAC of blood plasma decreased by 17% (K10). Patients with ataxia telangiectasia were found to have... 

Despite the apparent effectiveness of traditional methods of preparing cassava dishes in reducing the cyanide content, there is evidence to indicate that a tropical disease known as ataxic neuropathy may be associated with the consumption of cassava (31, 32, 33). One of the metabolic routes whereby cyanide is detoxified involves the formation of thiocyanate as shown in Figure 7. Elevated levels of thiocyanate in blood plasma have been observed in individuals who suffered from ataxia neuropathy and who had a history of high consumption of cassava. Rats fed boiled or fermented cassava also showed high levels of thiocyanate in plasma and developed clinical signs of ataxia neuropathy. The mechanism whereby cyanide or its metabolic product, thiocyanate, are involved in the pathogenesis of this disease remains to be elucidated. 

Featherless chickens treated with DEF under laboratory conditions developed delayed neurotoxicity. Three birds were pretreated with atropine sulfate (20 mg/kg s.c.) 30 minutes before they were injected with DEF (800 mg/kg s.c. technical grade, 94 purity, Mobay Chemical Co.). (A second injection of atropine sulfate was administered 2 hours after treatment with DEF.) Control hens received two injections of atropine sulfate as above. The birds were observed daily for changes in behavior, weighed and blood samples taken 2, 6, 13, and 20 days after treatment. Ataxia developed 12 days after treatment with DEF. CHE decreased to low levels as expected, in both scaleless (Figure 6) and normal birds (not shown), and, in this study, did not return to normal levels by 20 days. CK levels rose after treatment with DEF, but did not rise in the controls. Plasma CK activity also rose in birds treated with TOCP and parathion (11). 

The elderly appear to be at increased risk of blood dys-crasias and liver reactions (39). Age above 55 years was associated with a greater risk of toxicity after rapid switch-over to a carbamazepine dosage designed to jdeld a plasma concentration of 10 pg/ml (76). Moderately severe to severe adverse effects in the 11 patients in either subgroup included sedation, ataxia, and confusion. 

At lower serum concentrations, euphoria and disinhibition may be noted. Slurred speech, altered perception of the environmeuL im-pairedjudgment, ataxia, incoordination, nystagmus, andhyperreflexia may occur. As plasma levels increase or in different individuals, combative and destructive behavior may occur. With higher levels still, somnolence and respiratory depression may ensue. The typical effects of various blood alcohol concentrations (BACs) are shown in Table 65-2, although effects vary from individual to individual. 

The major factor affecting the usefulness of AG is its toxicity. Side-effects are experienced by about 40% of patients [98], and necessitate discontinuation of treatment in about 5%. The most common side-effects include drowsiness, ataxia, morbilliform rashes, nausea and vomiting, and are usually transient, declining within 2-6 weeks. Rarer side-effects include depression and blood dyscrasias such as agranulocytosis [93]. The frequency of side-effects is related to the plasma concentrations of the drug in one study 80% of patients with serum AG concentrations of 12 mg/1 or above complained of... 

HUMAN HEALTH RISKS EPA group B2 probable human carcinogen Acute Risks wheezing pupil constriction blurred vision headaches nausea cramps diarrhea sweating respiratory failure anorexia giddiness ataxia rhinorrhea skin irritation Chronic Risks decreased plasma and red blood cholinesterease levels. 

HUMAN HEALTH RISKS Oral human LD50 3 mg/kg Acute Risks headache weakness excessive salivation abdominal cramps vomiting difficulty breathing confusion ataxia wheezing cardiac irregularity sweating rhinorrhea cyanosis vision problems paralysis respiratory failure spasms coma death Chronic Risks depressed red blood cell cholinesterase activity liver effects headaches depressed plasma birth defects. 

Gastric upset from CBZ may be diminished by taking the drug after meals. Common toxicities include blurred vision, dizziness, drowsiness, and ataxia. Tremor, depression, hyponatremia, and cardiac disturbances are seen at high serum concentrations. Idiosyncratic rashes are common rarer severe idiosyncratic effects include aplastic anemia, agranulocytosis, thrombocytopenia, and jaundice. Therefore, patients receiving CBZ should have periodic blood count determinations and liver function tests. Both CBZ and oxcarbazepine can reduce plasma 25-hydroxy vitamin D levels (45). CBZ increases levels of phenytoin and decreases levels of... 

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