Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nervous system is particularly susceptible to the harmful effects of alcohol. These include Wernicke-Korsakoff syndrome, which is related to thiamine deficiency secondary to chronic alcohol abuse. Other neurotoxic effects of alcohol with cognitive impairments include delirium tremens, alcoholic seizures or "rum fits," and alcoholic neuropathies. It has become recognized in recent years that alcohol and its metabolites directly damage the nervous system even in the absence of nutritional deficiencies. Cerebral blood flow (CBF) measurements provide a noninvasive indirect monitor of cerebral metabolic activity. It has been shown conclusively that CBF measured by the 133Xe inhalation method is decreased in chronic alcoholism, correlating well with the amount of alcohol consumed. With abstinence, CBF returns toward normal levels provided the neurotoxic effects of chronic alcoholism are of recent onset. Clinical and pathological studies show significant loss of brain volume with ventricular dilatation after alcohol abuse even among young "social" drinkers. This toxic effect of alcohol is accompanied by varying degrees of cognitive impairments ranging from slight memory loss to frank dementia. Both the decrease in brain volume and the cognitive impairments, which occur with or without nutritional deficiency, are to a large extent reversible with abstinence and nutritional supplementation. Alcohol appears to accelerate age-related declines in CBF while nutritional deficiencies enhance the neurotoxic effects of alcohol. Measurements of local CBF (LCBF) and partition coefficients (L lambda) in deep cerebral structures, including the hypothalamus, thalamus, forebrain nuclei, and limbic system, can be achieved utilizing three-dimensional methods after inhalation of stable xenon as a contrast medium combined with serial computed tomographic imaging of the brain. Among chronic alcoholics, there are significant and diffuse reductions in cortical and subcortical gray matter CBF that are especially remarkable in hypothalamus and substantia innominata, which includes the nucleus basalis of Meynert, a major source of cholinergic input to neocortex and hippocampus. Reductions in LCBF are measurable in cognitively impaired patients with and without Wernicke-Korsakoff syndrome. Reductions of CBF include white matter and are more severe in patients with Wernicke-Korsakoff syndrome. Both types of encephalopathy improve with treatment, but recovery is usually more rapid and complete if nutritional deficiency is absent. Alcohol also appears to be a risk factor for stroke, possibly by depleting neuronal reserves and unfavorably influencing cardiovascular risks.
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PMID:Cerebral hemodynamic and metabolic effects of chronic alcoholism. 270 68

We report our experience with 90 neurologically impaired children treated with gastrostomy and Nissen fundoplication. Malnutrition was the main problem, followed by aspiration, recurrent pneumonia, and vomiting. The symptomatology was caused by swallowing incoordination and gastroesophageal reflux. The diagnosis of gastroesophageal reflux was confirmed by upper gastrointestinal series and pH probe. Nissen fundoplication was performed following a standard technique with preservation of the vagus nerves and its branches, repair of the diaphragmatic crura, reconstruction of the angle of His, and a 360 degree wrap. A gastrostomy and pyloroplasty or pyloric dilatation were part of the operative procedure. There were no deaths and few complications related to the surgical procedure. Marked nutritional improvement was seen in most cases with an average weight gain of 3.2 kg/patient 3 months following surgery. There was also improvement in milestones and seizure control. The majority of parents were very satisfied and would recommend the procedure to other parents with similar problems.
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PMID:Gastrostomy and Nissen fundoplication in neurologically impaired children. 280 49

Rats born to dams fed either a 6% (malnourished) or a 25% (control) casein diet during gestation and lactation and maintained on the diet of the dam after weaning were tested for electrographic and behavioral responses to electrically induced kindling of the CA1 field of the hippocampus beginning at 44 days of age. Animals in the 6% diet group had a significantly lower threshold to afterdischarge (AD), a significantly faster spread of AD activity to distal recording sites, significantly longer average duration of AD activity at all recording sites and a markedly altered behavioral progression toward seizure activity compared to control animals. These findings indicate that prenatal protein malnutrition results in hippocampal dysfunction as evidenced by both the electrographic and behavioral correlates of the kindling process. The data presented suggest that prenatal proteins malnutrition alters the response of hippocampal CA1 pyramids to electrical stimulation and that this alteration results in marked changes to both the electrographic and behavioral correlates of kindling.
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PMID:Effect of protein malnutrition on hippocampal kindling: electrographic and behavioral measures. 302 67

Seventy-five children with different nutritional status, who were receiving phenobarbitone for treatment of various seizure disorders, were monitored for their plasma steady state level, therapeutic efficacy and toxicity. A wide inter individual variation in the steady state level was observed. About 10 percent of them had subtherapeutic level, while nearly 30 percent of them had potentially toxic levels, the remaining were within therapeutic range of 10-25 micrograms/ml. Poor compliance was found to be an important contributing factor for the variations in the level. Steady state levels were significantly higher in children with grade II protein energy malnutrition (PEM) than normally nourished children. A good correlation existed between plasma drug level and therapeutic response in nearly 60 percent of the children. Clinical toxicity was observed in nearly two thirds of the children, sedation and behavioral problems being the most common. The importance of monitoring the drug level is discussed for the proper management of epileptic children.
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PMID:Monitoring of phenobarbitone in epileptic children. 310 16

An 8-year-old boy with vitamin D-deficiency rickets, increased serum creatine kinase (CK), and hypocalcemia is described. At 5 years of age, he was evaluated because of recurrent tonic seizures. He had growth retardation, microcephaly, quadriplegia, mental retardation, and epilepsy. Muscle strength was difficult to assess because of multiple joint contractures. Deep tendon reflexes were hyperactive. Laboratory data indicated rachitic changes on x-ray, hypocalcemia, low serum 25-hydroxyvitamin D3 (25-OH-D) and 1-alpha-25-dihydroxyvitamin D3 (1-alpha-25-[OH]2-D) levels, a normal response to the Ellsworth-Howard test, and markedly increased CK. Electromyography and nerve conduction velocities were normal. The patient responded to 1-alpha-OH-D treatment with increased serum calcium and normal CK activity; a significant correlation (p less than 0.01) was observed between calcium and log CK. The clinical course and laboratory findings supported the hypothesis that the increased CK was due to hypocalcemia, which in turn was due to the vitamin D deficiency in the severely handicapped child with malnutrition.
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PMID:Increased serum creatine kinase due to hypocalcemia in vitamin D deficiency. 350 46

A 3 year survey at the University of Nigeria Teaching Hospital was conducted to determine causes of childhood deafness in children seen for that condition. Of the many factors causing this handicap, measles, seizures, and meningitis were identified most frequently. Due to poor medical facilities and widespread malnutrition, communicable diseases in children produce high rates of morbidity and mortality. As a result, a high percentage of infants acquire disabilities, including profound deafness. Improvement of the health care delivery system, breastfeeding, and compulsory immunization of all babies against infectious diseases, as well as making specialist centers accessible to all are suggested as the most efficacious ways to arrest the high incidence of profound deafness in childhood in Nigeria and other developing countries.
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PMID:Profound childhood deafness in Nigeria: a three year survey. 358 6

Severely ill patients often do not eat or cannot retain ingested food. Malnutrition occurs frequently in hospitalized individuals and is known to be associated with substantial changes in the pharmacokinetics of certain drugs. On the other hand, little is known about the effect of acute starvation or malnutrition on the pharmacodynamics (concentration-effect relationship) of drugs. To explore the effects of acute starvation on the pharmacodynamics of drugs that depress or stimulate the central nervous system, adult male Sprague-Dawley rats were deprived of food (but not water) for 3 days, whereas control animals had free access to food and water. Slow i.v. infusion of phenobarbital to onset of loss of righting reflex showed that the starved animals required a larger body weight normalized dose and that they had higher phenobarbital concentrations in serum, serum water, brain and cerebrospinal fluid at the pharmacologic endpoint. Refeeding of the rats for 2 or 7 days did not normalize the decreased body weight and serum total protein concentration. The starvation-associated decrease in the sensitivity of the central nervous system to the hypnotic effect of phenobarbital was only reversed slightly by refeeding for 2 days and persisted even after 7 days of refeeding. Acute starvation had no apparent effect on the dose of i.v. infused ethanol required to cause loss of righting reflex and on ethanol concentrations in serum, brain and cerebrospinal fluid at that time. The infused dose and the concentrations of pentylenetetrazol in serum, brain and cerebrospinal fluid at onset of maximal seizures did not differ significantly between starved and control (fed) rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kinetics of drug action in disease states. XX. Effects of acute starvation on the pharmacodynamics of phenobarbital, ethanol and pentylenetetrazol in rats and effects of refeeding and diet composition. 361 21

Vitamin B-6 deficient rats exhibit changes in behavior, sensory function, and other nervous system abnormalities such as convulsive seizures and motor disturbances. Sensorimotor reactivity was evaluated quantitatively by measuring auditory and tactile startle responses in 12 week old female Long-Evans rats fed a diet devoid of added vitamin B-6 (DEF) or a control diet, either ad lib (AL-CON) or pair-fed to deficient rats (PF-CON). Deficiency was confirmed with a tryptophan-load test administered to a separate group of rats fed simultaneously according to the same protocol. At week 18, body weight and feed efficiency were different among groups (p less than 0.001), and were lowest in DEF. Amplitude of response to both acoustic and tactile stimuli was depressed in DEF compared to both control groups, which generally did not differ in response. This effect was seen most dramatically in responses to the acoustic stimulus (p = 0.034), and especially to the first presentation (p = 0.017). Latency to maximum response was not affected by diet. Possible mechanisms for this nervous system abnormality, not previously reported in vitamin B-6 deficiency, are discussed.
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PMID:Attenuation of acoustic and tactile startle responses of vitamin B-6 deficient rats. 362 44

Increased concentrations of the endogenous tryptophan metabolite 3-hydroxykynurenine (3-HK) were measured in the brains of vitamin B6 deficient neonatal rats. Mean concentrations of 3-HK in B6 deficient cerebellum, corpus striatum, frontal cortex, and pons/medulla ranged from 9.7 to 18.6 and 102 to 142 nmol/g of wet tissue at 14 and 18 days of age, respectively. 3-HK was not significantly increased in control neonatal or adult rat brain, vitamin B6 deficient rat brain at 7 days of age, or in brains from adult rats deprived of vitamin B6 for 58 days. The administration of daily intraperitoneal injections of vitamin B6 from the 14th to the 18th day of age decreased the concentration of 3-HK to control levels. 3-HK has been shown by other investigators to produce seizures when injected into the cerebral ventricles of adult rodents. Thus, our studies show the accumulation in brain of a putative endogenous convulsant as the result of a nutritional deficiency.
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PMID:Increased concentrations of 3-hydroxykynurenine in vitamin B6 deficient neonatal rat brain. 368 2

Central nervous system symptoms due to hyponatremia is highly dependent on its acuteness and cause. Severe acute hyponatremia (serum sodium less than 125 mEq/l) often causes confusion, lethargy, seizures or frank coma due to brain oedema. If therapy is delayed, hyponatremia carries a high mortality rate, and risk of irreversible brain damage. Hyponatremia should probably be corrected to 125-130 mEq/l at a rate of 1.5-2.0 mEq/l/h. Malnourished alcoholic patients with hyponatremia may represent a special case with possible dangers of central pontine myelinolysis if a very low serum sodium is corrected acutely to normonatremic or hypernatremic levels. Mortality in this subgroup is high whatever the therapy.
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PMID:Hyponatremia: cerebral symptoms and role in central pontine myelinolysis. 370 29


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