Central nervous system adverse effects

Ingestion. Most toxicity results from excess medicinal use. Adverse neuromuscular, central nervous system, cardiovascular, gastrointestinal, and renal effects. 

The coimnittee concludes that the evidence is sufficient to infer causal relationships between BLLs under 40 pg/dL and adverse effects on nervous system function (see Table 4-1). Effects on both the central and peripheral nervous systems have been observed, including effects on cognitive fmction, peripheral nerve function, visual and auditory function, posture and balance, and autonomic nervous system function. 

Common/serious adverse events central nervous system mediated sedation, dizziness and fatigue are common. Xerostomia is a common side effect that can be prohibitive in some patients. Patients should also be monitored for hypothermia, bradycardia and hypotension. 

Side Effects and Toxicity. Adverse effects to the tricycHc antidepressants, primarily the result of the actions of these compounds on either the autonomic, cardiovascular, or central nervous systems, are summarized in Table 3. The most serious side effects of the tricycHcs concern the cardiovascular system. Arrhythmias, which are dose-dependent and rarely occur at therapeutic plasma levels, can be life-threatening. In order to prevent adverse effects, as weU as to be certain that the patient has taken enough dmg to be effective, the steady-state semm levels of tricycHc antidepressant dmgs are monitored as a matter of good practice. A comprehensive review of stmcture—activity relationships among the tricycHc antidepressants is available (42). 

The Class I agents have many similar side effects and toxicities. The anticholinergic side effects include dry mouth, constipation, and urinary hesitancy and retention. Common gastrointestinal (GI) side effects include nausea, vomiting, diarrhea, and anorexia. Cardiovascular adverse effects are hypotension, tachycardia, arrhythmias, and myocardial depression, especially in patients with congestive heart failure. Common central nervous system (CNS) side effects are headache, dizziness, mental confusion, hallucinations, CNS stimulation, paraesthesias, and convulsions. 

Overexposure to tetrachloroethylene by inhalation affects the central nervous system and the Hver. Dizziness, headache, confusion, nausea, and eye and mucous tissue irritation occur during prolonged exposure to vapor concentrations of 200 ppm (15). These effects are intensified and include incoordination and dmnkenness at concentrations in excess of 600 ppm. At concentrations in excess of 1000 ppm the anesthetic and respiratory depression effects can cause unconsciousness and death. A single, brief exposure to concentrations above 6000 ppm can be immediately dangerous to life. Reversible changes to the Hver have been reported foUowing prolonged exposures to concentrations in excess of 200 ppm (16—22). Alcohol consumed before or after exposure may increase adverse effects. 

The site of action for Memantine is the central nervous system (CNS) and it has CNS affinity. Amantadine and Rimantadine can penetrate to the CNS and cause some adverse effects. 

In patients taking NSAIDs, monitor for increases in blood pressure, weight gain, edema, skin rash, and central nervous system adverse effects such as headaches and drowsiness. 

Short-term adverse effects from corticosteroids include fluid retention, hyperglycemia, central nervous system stimulation, weight gain, and increased risk of infection. Patients with diabetes should have blood glucose levels monitored carefully during the corticosteroid course. 

Use of diethylpropion for a period longer than 3 months is associated with an increased risk for development of pulmonary hypertension. When used as directed, reported common central nervous system adverse effects included overstimulation, restlessness, dizziness, insomnia, euphoria, dysphoria, tremor, headache, jitteriness, anxiety, nervousness, depression, drowsiness, malaise, mydriasis, and blurred vision. In addition, diethylpropion can decrease seizure threshold, subsequently increasing a patient s risk for an epileptic event. Other organ systems also can adversely be affected, resulting in tachycardia, elevated blood pressure, palpitations, dry mouth, abdominal discomfort, constipation,... 

The precise mechanism of dimethylhydrazine toxicity is uncertain. In addition to the contact irritant effects, the acute effects of dimethylhydrazine exposure may involve the central nervous system as exemplified by tremors and convulsions (Shaffer and Wands 1973) and behavioral changes at sublethal doses (Streman et al. 1969). Back and Thomas (1963) noted that the deaths probably involve respiratory arrest and cardiovascular collapse. The central nervous system as a target is consistent with the delayed latency in response reported for dimethylhydrazine (Back and Thomas 1963). There is some evidence that 1,1-dimethylhydrazine may act as an inhibitor of glutamic acid decarboxylase, thereby adversely affecting the aminobutyric acid shunt, and could explain the latency of central-nervous-system effects (Back and Thomas 1963). Furthermore, vitamin B6 analogues that act as coenzymes in the aminobutyric acid shunt have been shown to be effective antagonists to 1,1-dimethylhydrazine toxicity (reviewed in Back and Thomas 1963). 

The only common side effect associated with IFN-y is the characteristic flu-like symptoms. However, in rare instances and at high doses, adverse clinical reactions have been noted. These have included heart failure, central nervous system complications (confusion disorientation, Parkinsonian-like symptoms), metabolic complications (e.g. hyperglycaemia), and various other symptoms. 

It is clear that both the form of molybdenum administered and the route of exposure affect molybdenum metabolism and survival (Table 30.4). By comparison, adverse effects (some deaths) were noted at 250 mg Mo/kg body weight (BW) (in guinea pigs), at 50 mg/kg BW in domestic cats (central nervous system impairment), at 10 mg/L drinking water in mice (survival), at 10 to 15 mg total daily intake in humans (high incidence of gout-like disease), and at to 3 mg/m3 air in humans for 5 years (respiratory difficulties), or 6 to 19 mg/m3 in humans for 4 years (Table 30.4). 

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