Epileptic convulsive seizures

Similarly, convulsive seizures and a sustained epileptic state persisted after stomach contents were pumped and activated charcoal and anticonvulsive medication were administered in a 43-year-old man who ingested approximately 260 mg/kg endosulfan (Boereboom et al. 1998). At 4 days after exposure, the man was pronounced brain dead, and autopsy revealed cerebral hernia from massive cerebral edema. Eight additional accidental and/or intentional cases of acute poisoning with endosulfan resulting in adverse neurological effects have been reported in more recent studies, six by Blanco-Coronado et al. (1992), one by Lo et al. (1995), and one by Pradhan et al. (1997) two out of the eight resulted in death. Tonic-clonic convulsions were seen in the Blanco-Coronado et al. (1992) cases, whereas Lo et al. (1995) reported the development of muscle fasciculations and episodes of convulsions in their case. In the case reported by Pradhan et al. (1997), the patient had consumed about 75 mL of hquid endosulfan (35% w/v). In this case, in addition to tonic-clonic seizures and myoclonic jerks, the patient developed... 

Parenteral Adjunct in status epilepticus and severe recurrent convulsive seizures. Rectal For selected, refractory patients on stable regimens of anti-epileptic agents who require intermittent use of diazepam to control bouts of increased seizure activity. 

Sedation is uncommon and instead many patients will find that these drugs may impair sleep, which is why the dose is best taken in the morning. There is also little effect on psychomotor function. Occasional patients have a small reduction in heart rate but otherwise effects on the cardiovascular system are rare. Epileptic convulsions can occur but are rare and much less common than with tricyclic antidepressants. There is some evidence for potentiation of electroconvulsive therapy (ECT)-induced seizures. Sexual dysfunction is reported, principally delayed ejaculation and anorgasmia. 

Anticonvulsants or antiepileptics are agents that prevent epileptic seizures or modulate the convulsant episodes eflcited by seizure activity. Certain of these agents, eg, the BZs, are also hypnotics, anxiolytics, and sedatives, reinforcing the possibiUty of a common focus of action at the molecular level (1). 

Neuronal excitotoxicity AEA levels are elevated in the hippocampus of mice treated with kainic acid. 2-AG levels are elevated in rats treated with pilocarpine These are two animal models of epileptic seizures, where the endocannabinoids play an anti-convulsant and protective function Inhibitors of cellular re-uptake... 

All such animal procedures suffer from the obvious and basic problem that laboratory animals do not behave like humans and that humans cannot reliably interpret their reactions and behaviour. Thus we know that Parkinson s disease is caused by a degeneration of the dopaminergic nigrostriatal tract but its lesion in animals does not produce any condition which resembles human Parkinsonism, except in primates, even though there are functional tests (e.g. rotational movements) which readily establish that loss of dopamine function and also respond to its augmentation (Chapter 15). By contrast, there are many ways, e.g. electrical stimulation and the administration of certain chemicals, to induce convulsions in animals and a number of effective antiepileptic drugs have been introduced as a result of their ability to control such activity. Indeed there are some tests, as well as animals with varied spontaneous seizures, that are even predictive of particular forms of epilepsy. But then convulsions are a very basic form of activity common to most species and epileptic seizures that are characterised by behavioural rather than motor symptoms are more difficult to reproduce in animals. 

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. 

Convulsions Convulsions may increase in some epileptics receiving diethylpropion. Seizures Use sibutramine cautiously in patients with a history of seizures discontinue in any patient who develops seizures. 

You are called to the Emergency Department where a known epileptic is having recurrent grand mal seizures. A friend, who has come with him, says he knows he has not taken any of his anti-convulsant medication for at least a week, as he has been travelling and he had left the drugs behind. 

Epilepsy (or epilepsies, since markedly different clinical entities exist) is a common neurological abnormality affecting about 1% of the human population. Epilepsy is a chronic, usually life-long disorder characterized by recurrent seizures or convulsions and usually, episodes of unconsciousness and/or amnesia. Table 32.1 illustrates the major types of epileptic seizures. Patients often exhibit more than one type. In most instances, the cause of the seizure disorder is not known (idiopathic epilepsy), although trauma during birth is suspected of being one cause. 

Anti-epileptic. An agent that combats the convulsions or seizures of epilepsy. 

Epilepsy is an example of excessive neural signaling in the central nervous system. Relative cellular and extracellular space (ECS) volume has been demonstrated to play an important role in the propensity for epileptic seizures. For example, reducing ECS volume by exposure to hypotonic medium produces hyperexcitability and enhanced epileptiform activity, whereas hyperosmolar medium reduces excitability. The hypothesis that AQP4-dependent water transport in astrocytes might modulate intrinsic brain excitability was tested by seizure susceptibility in response to the GABAa antagonist convulsant pentylenetetrazol... 

Prostaglandin therapy can cause electroencephalo-graphic abnormalities (105). Convulsions, which occur occasionally, are a particular risk in epileptic patients (5,104,105). The combination of prostaglandins and oxytocin can be complicated by tonic-clonic seizures (106). 

Benzodiazepines are used to treat insomnia and for the acute treatment of epileptic seizures, convulsive disorders, and spastic disorders such as cerebral palsy,... 

By 1912, von Mering and Fischer developed and commercially introduced a new barbiturate compound for sleep and anxiety called phenobarbital or Luminal. However, this medication quickly found its place as treatment for a very different medical condition, epilepsy, which is a condition of periodic, unprovoked convulsions or seizures. The main goal of epilepsy treatment is to decrease the frequency of seizures. Alfred Hauptmann discovered the anti-epileptic properties of phenobarbital accidentally. A 1912 report by Hauptmann described epileptic patients who were given phenobarbital for sedation and incidentally had fewer seizures. Seizures are caused by an abnormal impulse in the brain, which spreads and sends inappropriate message to the body. These messages result in... 

An epileptic seizure is a transient symptom of abnormal, excessive or synchronous neuronal activity in the brain (normal brain activity is marked by unsynchronised firing of neurons). It can manifest as an alteration in mental state, tonic or clonic movements and convulsions. The medical syndrome of recurrent, unprovoked seizures is termed epilepsy, but seizures can occur in people who do not have epilepsy. 

Picrotoxin is described as irritating the respiratory center, exciting the vomiting center, rendering the pain center(s) more sensitive, and causing convulsions resembling epileptic seizures and death. The early findings were reviewed by Porter (2). It was Porter who found that the two components of the molecular compound... 

These two molecules illustrate how subtle changes in molecular structure can affect action. Amobarbital requires 30 min to take effect and sedation lasts for 5-6 h, while pentobarbital takes effect in 15 min and sedation lasts only 2-3 h. Phenobarbital (R=ethyl, R =phenyl), on the other hand, requires over an hour to take effect, but sedation lasts for 6-10 h. When the alkyl chains are made much longer the sedative properties decrease and the substances become anticonvulsants, which are used to treat epileptic seizures. If the alkyl group is too long or is substituted at one of the two nitrogens, convulsants are produced. 

Epileptic seizures in overdosed patients may indicate a degree of nervous system toxicity. Convulsions in poisoned patients are reported to be more hkely with mefenamic acid than with other compounds (1). Other nervous system reactions (such as headache) are less frequent than with the arylcarboxylic acid derivatives. Coma has also been described as a consequence of mefenamic acid overdosage (2). 

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