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

Sclerosis of the cornu Ammonis or Ammon's horn sclerosis (AHS) is an "often-described, yet hitherto enigmatic phenomena" as Spielmyer put it in 1927. It has been found in cases with ischemia, anoxia or hypoglycemia and in more than half of the epileptic brains examined at autopsy. Various theories about its pathogenesis have been propounded. Among them, the "Pathoklise" theory of the Vogts and the vascular theory of Spielmeyer and his associates were prevailing until recently. In 1953, two articles were published to contribute to the pathogenesis of ictal automatism (a type of complex partial or temporal lobe seizures). One is the incisural sclerosis theory by Penfield and his associates and the other is the Ammon's horn sclerosis theory by Sano and Malamud. The former authors described a diffuse sclerosis of the infero-mesial temporal structures without, however, specifically relating it to AHS. They considered it was the result of localized anoxia of that portion of the brain caused by incisural herniation occurring during parturition. Sano and Malamud maintained that AHS is a result of convulsions, a distinct scar adjacent to which epileptogenic foci may develop in the course of time to cause ictal automatism. The latter theory was corroborated by Sano, Falconer and others. Falconer expanded the theory to the assertion that not only ictal automatism but other types of intractable epilepsy may be due to "mesial temporal (Ammon's horn) sclerosis". The most recent development in the pathogenesis of AHS is the excitotoxicity theory. Namely, AHS is caused by excessive excitation of neurons, probably by putative excitatory neurotransmitters, especially, glutamate. For this theory, there is a significant body of evidence. The problem of AHS, an old research subject and a matter of long-lasting controversy, has now been updated and become one of the newest topics in the field of experimental neurobiology.
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PMID:Ammon's horn sclerosis: its pathogenesis and clinical significance. 198 30

Febrile convulsions affect about 1 child in 30. Most of these children have a good outcome with no sequelae and do not require prophylactic medication. Differential diagnosis should include meningitis, epilepsy, hypoglycemia, and encephalopathies and other central nervous system disorders. Children with a high risk for recurrence of seizures may benefit from continuous anticonvulsant prophylaxis.
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PMID:Febrile convulsions. How dangerous are they? 200

We developed a nursery Neurobiologic Risk Score (NBRS) based on potential mechanisms of brain cell injury in preterm infants and correlated it with developmental outcome at the corrected ages of 6, 15, and 24 months. The NBRS was determined at 2 weeks of age and at the time of discharge from intensive care in 58 preterm infants with birth weights less than or equal to 1500 gm. The NBRS correlated significantly with the Bayley Scales of Infant Development, Mental Development Index (MDI) (r = -0.61 to -0.40) and Psychomotor Development Index (PDI) (r = -0.59 to -0.46), and with abnormal neurologic examination findings (r = 0.59 to 0.73) at the three testing periods. Although 12 of the 13 items composing the NBRS individually correlated with one or more outcome variables, seven items (infection, blood pH, seizures, intraventricular hemorrhage, assisted ventilation, periventricular leukomalacia, and hypoglycemia) accounted for almost all of the explained variance. Logistic regression of individual items demonstrated intraventricular hemorrhage to be the most important item for predicting the MDI at 24 months; pH was the most influential item for predicting the PDI at every testing period. A shorter, revised NBRS that included only the seven significant items demonstrated as strong a correlation with developmental outcome as the original NBRS. A revised 2-week score of greater than or equal to 5 or a discharge score of greater than or equal to 6 demonstrated 100% specificity and had a 100% positive predictive value for an abnormal outcome at 24 months of age in this group of infants. We conclude that the NBRS identifies during the intensive care nursery stay those infants at highest risk for an abnormal outcome related to nursery events. In addition, analysis of NBRS items provides insight into the relative importance of individual factors for influencing mental, motor, and neurologic outcome.
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PMID:Nursery Neurobiologic Risk Score: important factor in predicting outcome in very low birth weight infants. 201 35

Complications that can lead to death during shigellosis include intestinal as well as systemic manifestations. The former include intestinal perforation, toxic megacolon, and dehydration, and the latter include sepsis, hyponatremia, hypoglycemia, seizures and encephalopathy, hemolyticuremic syndrome, pneumonia, and malnutrition. Data on the frequency of these complications come primarily from hospital-based studies, in which sepsis-either with Shigella or with other Enterobacteriaceae-and hypoglycemia are the most common causes of death. Management of these two complications requires broad-spectrum empiric antibiotic treatment of all severely ill, malnourished patients with shigellosis as well as frequent feedings to prevent hypoglycemia. Unfortunately, in developing countries, access to parenteral broad-spectrum antimicrobial agents is often limited, and frequent feedings are often precluded by the severe anorexia that is characteristic of shigellosis. Realistic approaches to the reduction of mortality from shigellosis must continue to focus on prevention and early antimicrobial therapy rather than on treatment of established complications.
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PMID:Potentially lethal complications of shigellosis. 204 57

We report a girl with the Rett syndrome who had acute encephalopathy probably induced by calcium hopantenate (HOPA). This 4-year-6-month-old girl had a history of moderate developmental delay and had received HOPA administration when first admitted at 2 years 6 months of age with hypoglycemia, hyperammonemia, lactic and pyruvic acidemia, and non-ketotic dicarboxylic aciduria. After this episode, she showed the rapid destructive stage of the Rett syndrome, i.e., severe psychomotor retardation with loss of speech, peculiar stereotypic hand movements, autistic behavior and seizures. Despite subsequent investigations, including analysis of urinary metabolites of organic and amino acids, measurement of serum carnitine and a muscle biopsy, we could not clarify the primary metabolic abnormalities in this girl.
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PMID:A case of the Rett syndrome with acute encephalopathy induced during calcium hopantenate treatment. 206 99

A total of 107 babies with hypoglycaemia were studied over a period of 15 months. Symptomatic hypoglycaemia was found in 43 while it was asymptomatic in the others. Asymptomatic hypoglycaemia occurred at a relatively earlier post-natal age (4.5 +/- 2.2 h), as compared to symptomatic hypoglycemia (18.5 +/- 5.4 h, P less than 0.001). The mean blood glucose in hypoglycaemic babies with seizures was found to be significantly lower (P less than 0.001) when compared to those with other features as well as asymptomatic ones. Hypoglycaemia lasted for a significantly longer duration in symptomatic babies as compared to those without symptoms (P less than 0.001). On neurodevelopment follow up the mental developmental index (MDI) and the psychomotor developmental index (PDI) of symptomatic babies with seizures were significantly lower (P less than 0.001) as compared to those with other features of hypoglycaemia as well as asymptomatic babies. The neurodevelopmental status of babies with symptoms other than seizures was also significantly poorer (P less than 0.001), when compared to asymptomatic hypoglycaemic babies. The duration of hypoglycaemia was directly related to the MDI (r = -0.74, y = 102.5 - 0.69x) and PDI (r = -0.81, y = 105.6 - 0.86x). This study indicates that there is a need to identify babies vulnerable to symptomatic hypoglycaemia more precisely.
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PMID:Neurodevelopmental outcome of asymptomatic & symptomatic babies with neonatal hypoglycaemia. 207 Nov 85

We report the clinical characteristics and course of 38 children with fulminant liver failure. A viral etiology was demonstrated in 19 patients out of 25 with serologic screening (virus A in 17 patients, B in 2 patients). One patient had toxic liver damage from ingestion of a caustic substance. Mean age was 4 years and 6 months. Jaundice was present in all but 2 patients at admission. Encephalopathy developed at a mean of 13 days and 17 children were admitted with stage 3 or 4 coma. Evidence of severe liver failure was present in every patient. A lower prothrombin time and higher bilirrubin concentration were shown by non survivors. Hypoglycemia developed in 37% of patients, seizures in 37%, gastrointestinal bleeding in 45%, respiratory failure in 32% and severe infection in 32%. Overall mortality rate was 42% raising to 83% in patients with stage 3 coma at admission. Thus, although the etiology of fulminant liver failure differs in children as compared to adults, mortality rate and complications are similar.
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PMID:[Fulminant hepatic failure in children]. 213 23

Four insulin-treated diabetic patients presented over a 2-year period in hypoglycaemic coma and died secondary to this. At autopsy, there were widespread neuropathological changes, in all four cases consistent with hypoglycaemic damage. Abnormalities were also found in areas regarded as generally being spared in hypoglycaemic brain injury, particularly the brain stem, thalamus, globus pallidus, and cerebellum, and these lesions may relate to seizure activity and cardio-respiratory depression secondary to the hypoglycaemia. Although more than one aetiological factor may be contributing, it is concluded that the neuropathological changes in diabetic patients dying in hypoglycaemic coma are extremely diverse.
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PMID:Fatal hypoglycaemia in insulin-treated diabetes mellitus: clinical features and neuropathological changes. 214 89

To better understand and treat painful conditions, one needs to identify the cause, discover the source, and develop knowledge of peripheral and central pain transmission; headaches are no exception. The development of appropriate animal models is important. Accordingly, we have reviewed the anatomy, neurochemistry, electrophysiology, and pharmacology of the trigeminovascular system in experimental animals and emphasized whenever possible the relevance of this final common pathway to migraine, cluster, and other headache syndromes in humans. For example, based on recent anatomic dissections, the pericarotid cavernous sinus plexus was suggested as an important focus to investigate cluster headache pathophysiology. This plexus is an anatomic point of convergence for the nerves giving rise to the signs of sympathetic and parasympathetic activity and sensory symptoms that develop in cluster patients. As in other nociceptive systems, trigeminovascular axons assume at least two important roles. One concerns the transmission of nociceptive information. Electrophysiologic evidence supports the trigeminal nucleus caudalis as an important site for the convergence of visceral (vessel) and somatic (forehead) inputs to mediate the referral of vascular pain to superficial tissues. A second important role concerns the initiation of local increases in blood flow and enhanced protein permeability (sterile inflammation) via the axonal release of vasoactive neuropeptides. Plasma extravasation develops within the dura mater following trigeminal stimulation. Extravasation can be blocked by the administration of ergot alkaloids or sumatriptan, a new serotonin-like agonist, and a prejunctional (neuronal) mechanism of action for these drugs (such as blockade of release) was suggested based on experimental evidence. Whether vasoconstriction also relates to the therapeutic efficacy remains to be determined. As in other organ systems, real or threatened tissue injury provides an important stimulus for depolarizing sensory fibers. The stimulus may come from external conditions such as reduced blood flow or hypoglycemia. The brain may also possess intrinsic neuronal mechanisms by which nociceptors may be synthesized (e.g., glutamate-induced neurotoxicity, seizures). Molecules of relevance include bradykinin, prostaglandins, leukotrienes, and potassium. Experimental evidence was presented demonstrating that the trigeminal nerve mediates hyperemia within cortical gray matter by axon-reflex like mechanisms. An important role for this nerve was established during the hyperemic period of recirculation after ischemia or during severe hypertension above the limits of autoregulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Basic mechanisms in vascular headache. 217 82

We review the English-language literature on antibiotic-associated adverse reactions in patients with renal insufficiency in order to highlight this important but often overlooked clinical problem. Because many adverse reactions to antibiotics are not dependent on renal function, we have attempted to review only those reactions that are believed to be associated with renal insufficiency or that have been reported in patients with impaired renal function. Adverse effects of antibiotics in this setting can be divided into six major categories: neurologic toxicity, coagulopathy, nephrotoxicity, hypoglycemia, hematologic toxicity, and aminoglycoside inactivation by penicillins. Neurologic toxicity can be further divided into central nervous system toxicity consisting primarily of encephalopathy and seizures, ototoxicity, peripheral neuropathy, and neuromuscular blockade/respiratory depression. We explore the factors in uremia that may contribute to the susceptibility of patients with renal insufficiency to the adverse effects of antibiotics. Moreover, we make general recommendations regarding the use of the discussed antibiotics in patients with compromised renal function.
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PMID:Adverse antibiotic effects associated with renal insufficiency. 192 3


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