Central nervous system seizures

The electroconvulsive therapy performed in the past is a far cry from the process used today in the treatment of major depressive disorder. In ECT a generalized central-nervous-system seizure is induced by means of an electric current. The objective is to achieve the full seizure threshold until the full therapeutic gains can be established. The exact process by which ECT works is unknown however, the shock results in an increase in different neurotransmitter responses at the cell membrane. Four to twelve treatments are generally given until therapeutic results are noted (Sachs, 1996). 

B. The neuromuscular blockers produce complete muscle paralysis with no depression of central nervous system function (they are positively charged and water-soluble compounds that do not rapidly cross the brain-blood barrier). Thus, patients who are conscious will remain awake but unable to move and patients with status epilepticus may continue to have central nervous system seizure activity despite flaccid paralysis. Furthermore, they do not relieve pain or anxiety. 

The central nervous system is a major target of endosulfan-induced toxicity in both humans and animals (Blanco-Coronado et al. 1992 Boyd and Dobos 1969 Boyd et al. 1970 Garg et al. 1980 Kiran and Varma 1988 Terziev et al. 1974). Therefore, individuals with seizure disorders, such as epilepsy, may be particularly susceptible because exposure to endosulfan may reduce the threshold for tremors, seizures, and other forms of neurotoxicity, as demonstrated in studies in rats (Gilbert and Mack 1995 Gilbert 1992). 

Isolated seizures that are not epilepsy can be caused by stroke, central nervous system trauma, central nervous system infections, metabolic disturbances (e.g., hyponatremia and hypoglycemia), and hypoxia. If these underlying causes of seizures are not corrected, they may lead to the development of recurrent seizures I or epilepsy. Medications can also cause seizures. Some drugs that are commonly associated with seizures include tramadol, bupropion, theophylline, some antidepressants, some antipsy-chotics, amphetamines, cocaine, imipenem, lithium, excessive doses of penicillins or cephalosporins, and sympathomimetics or stimulants. 

Severe pain should be treated with an opioid such as morphine, hydromorphone, methadone, or fentanyl. Moderate pain can be treated effectively in most cases with a weak opioid such as codeine or hydrocodone, usually in combination with acetaminophen. Meperidine should be avoided owing to its relatively short analgesic effect and its toxic metabolite, normeperidine. Normeperidine may accumulate with repeated dosing and can lead to central nervous system side effects including seizures. 

Central nervous system meningoencephalitis, strokes, seizures, and focal paralysis... 

Central nervous system confusion, headache, lethargy, seizures, and coma... 

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,... 

Exposure to doses below the level that will produce seizures can result in long-lasting central nervous system sensitization such as an increased susceptibility to sound induced (audiogenic) seizures. 

Signs and Symptoms Symptoms in immunocompromised individuals may include fever, difficulty breathing (dyspnea), nonproductive cough, bloody sputum (hemoptysis), bloody nose (epistaxis), a vague feeling of bodily discomfort (malaise), pneumonia, weakness, chest pain, and anorexia. May progress to inflammation of the eyes (endophthalmitis), sensitivity to light (photophobia), and/or inflammation of the heart (endocarditis). May also cause abscesses in the heart, kidneys, liver, spleen, other soft tissue, or the bone. If the central nervous system becomes involved, can cause altered mental states and seizures. 

McCarty, J. H, Lacy-Hulber, A., Charest, A., Bronson, R. T., Crowley, D., Housman, D., Savill, J., Roes, J. and Hynes, R. O. Selective ablation of (alpha)V integrins in the central nervous system leads to cerebral hemorrhage, seizures, axonal degeneration and premature death. Development 132 165-176,2005. 

Zinc is important to the normal functioning of the central nervous system (CNS). At low concentrations, zinc protects mammalian brain neurons by blocking N-methyl-D-aspartate receptor-mediated toxicity. At high concentrations, zinc is a potent, rapidly acting neurotoxicant in the mammalian brain, as judged by zinc-induced neuronal injury of in vitro mature cortical cell cultures (Choi et al. 1988). Increased brain levels of zinc are associated with Pick s disease in certain strains of rodents with inherited epileptic seizures. Intravenous injection of zinc in rats with genetically inherited epilepsy produces seizures a similar response occurs with intracranial injection of zinc in rabbits with inherited audiogenic seizures (Choi et al. 1988). 

The most serious toxicological effect of endrin is central neurotoxicity (Klaasen et al. 1986). Organo-chlorines interfere with the normal flux of cations across the axon, disrupting central nervous system homeostasis (Finkel 1983 Klaasen et al. 1986). Endrin is one of the most toxic cyclodienes, and seizure activity may develop rapidly after exposure (Proctor et al. 1988). In most cases, recovery is rapid. However, headaches, dizziness, weakness, and anorexia may persist for 2-4 weeks. 

Neurologic effects Convulsive seizures and peripheral neuropathy, the latter characterized mainly by numbness or paresthesia of an extremity, have been reported in patients treated with nitroimidazole drugs including tinidazole and metronidazole. The appearance of abnormal neurologic signs demands the prompt discontinuation of tinidazole therapy. Administer tinidazole with caution to patients with central nervous system diseases. 

Exposed individuals with evidence of central nervous system depression or seizures should be evaluated for the presence of some other underlying disorder. Diazepam or phenobarbital may be administered to alleviate seizures. Supplemental oxygen can also be administered. If pulmonary edema occurs, conventional therapy should be considered. Additional information regarding the treatment of individuals exposed to cresols may be obtained from Bronstein and Currance (1988), Haddad and Winchester (1990), and Stutz and Janusz (1988). 

Baclofen is a GABA agonist at GABA B receptors and it has a presynaptic inhibitory function by reducing calcium influx. Its indication is increased extensor tone and clonus. Intrathecal administration may control severe spasticity pain. It is used for the treatment of spastic movement, especially in instances of spinal cord injury, spastic diplegia, multiple sclerosis and amyotrophic lateral sclerosis. Its central nervous system effects include drowsiness, somnolence and seizure activity in epileptic patients. 

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