Seizures clinical presentation

Differentiate and classify seizure types when provided a description of the clinical presentation of the seizure and electroencephalogram. 

The clinical presentation of seizures will vary from patient to patient depending on the portion of brain involved in the seizure. Events will tend to be stereotypical for an individual patient. 

Coenzyme Q10 (CoQlO) deficiency. This mitochondrial encephalomyopathy has three main clinical presentations. A predominantly myopathic form is characterized by the triad of exercise intolerance, recurrent myoglobinuria, and CNS involvement. A more frequent ataxic form is dominated by ataxia and cerebellar atrophy, variously associated with weakness, developmental delay, seizures, pyramidal signs, and peripheral neuropathy, often simulating spinocerebellar atrophy. A third presentation with fatal infantile encephalomyopathy and renal involvement, has been described in two families. The biochemical defect (or defects) presumably involve different steps in the biosynthesis of CoQlO, but are still unknown, as are the molecular defects. Diagnosis, however, is important because all patients - and especially those with the myopathic and infantile forms - benefit from CoQlO supplementation [13,14]. 

The only clinical use for ethosuximide (Zarontin) is in the treatment of absence epilepsy. If absence attacks are the only seizure disorder present, ethosuximide alone is effective. If other types of epilepsy are present, ethosuximide can be readily combined with other agents. 

PEM is one of the most frequent cancer-associated syndromes. This complex disorder usually affects several areas of the CNS. Cerebellar and brain stem disorders, as well as limbic encephalitis, are the most common clinical presentations of PEM [31, 32], Focal involvement of the sensorimotor cortex has been described in a few cases [33], and PEM may manifest as epileptic seizures or epilepsia partialis continua [33, 34], or as extrapyramidal symptoms [35], Two-thirds of the patients are affected in both the CNS and the peripheral nervous system. The predominant feature in more than half of these is SN [32, 36], hence the commonly used term is PEM/SN. Autonomic dysfunction is common in PEM/SN patients [36], often presenting as gastrointestinal dysmotility [37]. 

In a retrospective analysis of all cases of hyponatremia associated with ecstasy (SEDA-25, 37) at the London Centre of the National Poisons Information Service from December 1993 to March 1996,17 patients were identified with a serum sodium concentration under 130 (range 107-128 mmol/1) (96). In 10, ecstasy was identified analytically, and six of them had SIADH. The clinical presentation was very consistent, with initial vomiting and delirium, and 11 had seizures. There was complete recovery in 14, but two died of cerebral edema 5 hours after ingestion. 

Compared with adults, mortality in children after acute chloroquine poisoning is extremely high. Although the clinical presentation is mostly similar to that in adults (apnea, seizures, cardiac dysrhythmias), a single 300 mg chloroquine tablet was enough to kill a 12-month-old female infant (SEDA-16, 302). 

Seizures are present in 30% of patients with star fruit intoxication [17], and most patients have convulsive [6, 8,10,11,13,14,17,18,19] or non-convulsive [16] status epilepticus. The mortality rate of patients with seizures occurring after star fruit intoxication (severe intoxication) is significantly higher than of patients without seizures [13, 17]. Phenytoin, midazolam, diazepam and phenobarbital seem to have little or no effect on the control of persistent seizures provoked by star fruit toxicity. However, significant clinical improvement of seizure was demonstrated in one patient after the use of profofol [20]. 

Intensive supportive care is rarely required. Measures that may be required based on the clinical presentation include endotracheal intubation and assisted ventilation if coma is present, intravenous fluid resuscitation if hypotension is present, pharmacological control of seizures, cooling if hyperthermia is present. 

The clinical manifestations of hyponatremia are nonspecific weakness and apathy occur in mild cases, and central nervous system changes (lethargy, coma, and seizures) are present in more severe cases. No signs or symptoms are specific for SIADH. History, physical examination, and routine laboratory test results often suggest that hyponatremia is dilutional or depietional. 

III. Clinical presentation. Tricyclic antidepressant poisoning may produce any of three major toxic syndromes anticholinergic effects, cardiovascular effects, and seizures. Depending on the dose and the drug, patients may experience some or... 

III. Clinical presentation. Shortly after acute ingestion, nausea and vomiting occur, followed by paresthesias of the tongue, lips, and face confusion tremor obtundation coma seizures and respiratory depression. Because chlorinated hydrocarbons are highly lipid soluble, the duration of toxicity may be prolonged. 

III. Clinical presentation. Abmpt onset of profound toxic effects shortly after exposure is the hallmark of cyanide poisoning. Symptoms include headache, nausea, dyspnea, and confusion. Syncope, seizures, coma, agonal respirations, and cardiovascular collapse ensue rapidly after heavy exposure. 

II. Toxic dose. Inhalation or ingestion of as little as 1 mg of fluoroacetate is sufficient to cause serious toxicity. Death is likely after ingestion of mote than 5 mg/kg. Clinical presentation. After a delay of minutes to several hours (in one report coma was delayed 36 hours), manifestations of diffuse cellular poisoning become apparent nausea, vomiting, diarrhea, metabolic acidosis, renal failure, agitation, confusion, seizures, coma, respiratory arrest, pulmonary edema, and ventricular arrhythmias may occur. One case series reported a high incidence of hypocalcemia and hypokalemia. 

IV. Diagnosis is usuaiiy made by history and clinical presentation. INH toxicity should be considered in any patient with acute-onset seizures, especially if unresponsive to routine anticonvulsant medications and if accompanied by profound... 

III. Clinical presentation. The time course of intoxication by these dmgs is usually brief, with resoiution within 4-6 hours (unless sustained-release preparations are involved). The major toxic effect of these drugs is hypertension, which may lead to headache, confusion, seizures, and intracranial hemorrhage. 

The clinical presentation of patients with endocrine pancreatic tumors will vary according to the type of hormone released. Hyperinsulinism manifested with diarrhea, abdominal pain, and low levels of glucose will be found in the majority of patients. Nesidioblastosis is a primitive pancreatic B cells hyperplasia. Approximately 5% of patients with hyperinsulinism may have this type of tumor. Hunger, jitteriness, lethargy, apnea, and seizures are common manifestations in newborns with nesidioblastosis, while older children may show diaphoresis, confusion, or unusual behavior. Zollinger-Elli-son syndrome will present with intractable peptic ulcers. Patients with vipomas will have watery diarrhea, hypokalemia, and achlorhydria, while multiple endocrine neoplasias have been reported with multiple endocrine neoplasia type 1 (MEN 1). 

Most frequent clinical presentations of brain AVMs are hemorrhage, seizure, chronic headache and focal deficits not related to hemorrhage (e.g. steal phenomenon)... 

Laudanosine or Af-methyltetrahydropapaverine is a recognized metabolite of atracurium and cisatracurium. Laudanosine decreases the seizure threshold, and thus, it can induce seizures if present at sufficient threshold concentrations however, such concentrations are unlikely to be produced consequent to chemodegradable metabolism of clinically admiiustered doses of cisatracurium or atracurium. Laudanosine also occurs naturally in minute amounts (0.1 %) in opium, from which it was first isolated in 1871. Partial dehydrogenation of laudanosine will lead to papaverine, the alkaloid found in the opium poppy plant (Papaver somniferum). Laudanosine is a benzyltetrahydroisoquinoline alkaloid. It has been shown to interact with GABA receptors, opioid receptors, and ificotinic acetylcholine receptors, but not benzodiazepinergic or muscarinic receptors which are also involved in epilepsy and other types of seizures. 

Clinical presentation may be that of a typical organic acidemia with life-threatening ketoacidosis early in life, or the onset may be more indolent with symptoms linked to the skin, hair or the nervous system. Some patients have presented as acrodermatitis enteropathica. Others have had immunodeficiency. In some seizures have been the only clinical manifestation. Later onset patients have had spastic diplegia or atrophy of the optic or auditory nerves. 

This complex consists of four subunits, all of which are encoded on nuclear DNA, synthesized on cytosolic ribosomes, and transported into mitochondria. The succinate dehydrogenase (SDH) component of the complex oxidizes succinate to fumarate with transfer of electrons via its prosthetic group, FAD, to ubiquinone. It is unique in that it participates both in the respiratory chain and in the tricarboxylic acid (TC A) cycle. Defects of complex II are rare and only about 10 cases have been reported to date. Clinical syndromes include myopathy, but the major presenting features are often encephalopathy, with seizures and psychomotor retardation. Succinate oxidation is severely impaired (Figure 11). 

The patient may present with or without clinically noticeable seizure activity. 

The neuronal ceroid lipofuscinoses (CLN), also referred to as Batten s disease, are a group of disorders characterized by the accumulation of autofluorescent lipopigments. Clinical hallmarks include blindness, seizures, cognitive and motor decline and early death. Age of onset varies from infancy to adulthood. Eight genetic forms have been identified [4]. Two involve lysosomal acid hydrolases. CLN1 codes for palmitoyl protein thioesterase 1. Clinically it presents most often in infancy and leads to loss of active movement and visual contact by 3 years of age. It is most common in Finland, where its incidence is 1 20,000. CLN2 codes for a lysosomal pepstatin-insensitive acid protease. 

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