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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood pressure, which ist the product of cardiac output and peripheral vascular resistance is regulated by a complex feedback mechanism involving the sympathetic and parasympathetic systems and hormones. An acute disturbance of regulation may lead to a life-threatening increase in blood pressure. Diagnosis is based upon a careful measurement of blood pressure, which must be performed under internationally standardized conditions. Hypertensive crisis refers to a rapid blood pressure increase greater than 30 mmHg above the age-related 95th percentile. The main causes of hypertension in childhood are renal diseases, which may be aggravated by additional conditions either by the clinician himself (e.g. cyclosporin, steroids) or by the patient (lack of compliance). Crisis affects the brain (hypertensive encephalopathy), the heart (left ventricular insufficiency), the retina (visual disturbances) and the mucous membranes (epistaxis). Hypertensive encephalopathy is induced by a break-through of the autoregulation of brain flow, leading to hyperperfusion and, thus to cerebral oedema. The clinical manifestations are characterized by restlessness, severe and diffuse headache, vomiting, nystagmus, impaired vision, dizziness, paraesthesia, seizures and palsies, which may lead - if untreated - to coma and death. The course is usually prolonged and reversible by adequate treatment. The morphological consequences are purpura cerebri, fresh retinal haemorrhages and papillary oedema, apart from left ventricular dilatation and hypertrophy. The diagnostic procedure rests on the quick realization of essential anamnestic (blood pressure, renal disease, drugs), clinical (oedema, cardiac action, central nervous system, fundus) and laboratory parameters (serum creatinine, electrolytes, glucose, blood count, urine). Treatment should start before the manifestation of clinical signs (hypertensive emergency) with rapidly acting antihypertensive drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hypertensive crisis in childhood]. 305 87

An infant female had connatal Pelizaeus-Merzbacher disease with neonatal onset of developmental failure, seizures, nystagmus, visual impairment, abnormal movements, and spasticity. There was nearly complete absence of central myelin with preservation of peripheral myelin. The 17 reported patients with connatal Pelizaeus-Merzbacher disease are summarized. Evidence of autosomal recessive inheritance is provided by our patient, 3 previously described girls, and 1 family with both boys and girls affected equally. This possible form of inheritance is important to consider in genetic counseling.
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PMID:Connatal Pelizaeus-Merzbacher disease: an autosomal recessive form. 350 78

An acute limbic-cerebellar syndrome was seen in six industrial workers who inhaled trimethyltin (TMT). Clinical features included hearing loss, disorientation, confabulation, amnesia, aggressiveness, hyperphagia, disturbed sexual behavior, complex partial and tonic-clonic seizures, nystagmus, ataxia, and mild sensory neuropathy. Severity paralleled maximal urinary organotin levels. One patient died and two remained seriously disabled.
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PMID:Acute trimethyltin limbic-cerebellar syndrome. 358 45

Some pharmacological effects of a potent tremorgenic mycotoxin, fumitremorgin A (FTA), on the rabbit were studied. FTA (10-200 micrograms/kg, i.v.) caused clonic and tonic convulsion accompanied by nystagmus and miosis in conscious rabbits, after a latent period. Even in decorticated or decerebrated rabbits, FTA (100-200 micrograms/kg, i.v.) could induce violent motor effects similar to those observed in conscious rabbits. Under light anesthesia with urethane and chloralose, a higher dosage (more than 100 micrograms/kg) was needed to cause clonic and tonic convulsion. FTA facilitated phrenic nerve discharges as well as efferent discharges of the vagal nerve and the cervical sympathetic nerve. Hypertension induced by FTA was inhibited by phentolamine, while bradycardia and arrhythmia caused by this toxin was abolished by atropine or bilateral vagotomy. The electroencephalogram showed persistent strong arousal response after intravenous injection of FTA. A seizure pattern was never observed. It was suggested that the main site of action of FTA was in the brain stem.
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PMID:Pharmacological effects of the tremorgenic mycotoxin fumitremorgin A. 373 99

Xeroderma pigmentosum is an unusual neurocutaneous disorder. Recent studies have classified patients with xeroderma pigmentosum into 10 groups by somatic cell hybridization methods. In this report we describe 32 patients with Group A xeroderma pigmentosum, including 1 patient with an atypical case, who were assessed for neurological complications. Of these patients, 17 had microcephaly, 13 short stature, and 21 mental retardation. In patients over 7 years of age, sensorineural deafness and spinocerebellar signs such as nystagmus, dysarthria, tremor, and ataxia were frequently observed; no patients below 7 years of age had such neurological complications. Electroencephalographic studies revealed abnormal slow and low voltage background activity. Two patients had focal abnormal discharges, one of whom developed versive seizures. Cranial computed tomographic scans revealed abnormalities, including ventricular dilatation, cerebral atrophy, cerebellar and brainstem atrophy, and cranial bone thickening. A patient with an atypical case of Group A xeroderma pigmentosum had less skin and neurological involvement, and higher levels of postultraviolet colony-forming ability and host cell reactivation than did a typical Group A case. It is possible that these less severe cytological findings are responsible for the less severe skin lesions and neurological complications noted clinically.
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PMID:Neurological manifestations in xeroderma pigmentosum. 374 Aug 15

In this study of ibuprofen overdose, symptoms developed in 19% of patients (24 of 126)--in 7% of children (6 of 88) and in 47% of adults (18 of 38). Central nervous system depression, seizures, gastrointestinal disturbances, bradycardia, hypotension, apnea, abnormal renal functions, hematuria, nystagmus, and blurred vision were observed. No patients became symptomatic more than four hours after ingestion. There was no significant difference (P greater than .05) between symptomatic and asymptomatic adult groups in either total milligrams or milligram-per-kilogram amounts ingested by history. Pediatric patients who became symptomatic had a mean ingestion by history of 440 mg/kg; those who remained asymptomatic had a mean ingestion by history of 114 mg/kg (P less than .001). No patients ingesting less than 99 mg/kg by history developed any symptoms. Two children had seizures or apnea and one died. Ibuprofen occasionally may cause serious toxicity in overdose.
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PMID:Ibuprofen overdose: 126 cases. 377 88

As a general trend, the diagnosis in medical clinics often depends on laboratory test results. Neurotological diagnosis, however, requires detailed neurological examinations on a patient by a neurotologist. Therefore, there are differing diagnostic skills among physicians, and there is a kind of "man-made flavor" in neurotological diagnostic procedure. In the present study, current development in the knowledge on the clinical diagnostic significance of pathological eye movement during the last 2-3 years is summarized. Acquired pendular wondering eye-movement. Fixation jerks. Spontaneous and transitory eyeball burst or seizure. Vertical rebound nystagmus. Optokinetic vertical ocular dysmetria. Divergence nystagmus. Counterolling, pure rotatory positioning nystagmus. Inversion of optokinetic after-nystagmus (OKAN). Vertical congenital nystagmus and inversion of optokinetic nystagmus (OKN). Treatment of congenital nystagmus. Vertical spontaneous nystagmus to lower eyelid or so-called "downbeat nystagmus." Downbeat nystagmus seen in bilateral labyrinthine dysfunction. The significance of bilateral vestibular lesion, or symmetric lesion in other is emphasized in the present report for reader's reference and criticism. Our experience on the clinical significance of the abnormal eye movement was reported. It is our wish that accumulation of data on important cases along with the results of experimental studies directly connected with clinical medicine may contribute to the progress of our neurotology in the right direction as "neurology of the posterior fossa."
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PMID:Recent development of the study on clinical significance of abnormal eye movement. 383 96

Twenty-two patients with temporal epilepsy (TE) in the interparoxysmal period were subjected to otoneurological examination. In the majority of cases, there were vestibular disorders of the irritative nature and disturbances of otokinetic nystagmus. The data obtained, along with specification of the localization of the epileptic focus, confirm the involvement of the brain on different levels--cortical-subcortical-truncal--in TE patients with polymorphic seizures.
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PMID:[Study of vestibular disorders in epileptics by means of electronystagmography and functional visual and vestibular loads]. 387 96

We studied a patient with stereotyped focal seizures characterized by leftward conjugate eye- and head-turning followed by nystagmus. Eye deviation was associated with the appearance of seizure activity, recorded over the right temporo-occipital scalp, that did not spread frontally. The initial eye deviation consisted of a staircase of small saccades. The subsequent nystagmus showed rightward decreasing-velocity exponential slow phases and normal leftward quick phases. Saccadic eye movements due to seizures may occur via projections from posterior cortical areas as well as from the frontal eye fields.
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PMID:Epileptic gaze deviation and nystagmus. 392 61

A patient with absence of the septum pellucidum, optic hypoplasia, congenital nystagmus, hemiatrophy, and seizures fulfilled clinical and radiological criteria for diagnosis of both septo-optic dysplasia and the syndrome of absent septum pellucidum with porencephalies. The anatomical and clinical similarities between these two syndromes suggest a common embryological basis. Their simultaneous presence in this case further supports this explanation. Clinically mild forms of both septo-optic dysplasia and the syndrome of absent septum pellucidum with porencephalies are now detected with the aid of computed tomographic scanning in patients with unexplained hemiatrophy, congenital nystagmus, seizures, and short stature.
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PMID:Absence of the septum pellucidum. Overlapping clinical syndromes. 402 11


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