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

The involvement of the nervous system in malaria is reviewed in this paper. Cerebral malaria, the acute encephalopathy which complicates exclusively the infection by Plasmodium falciparum commonly affects children and adolescents in hyperendemic areas. Plugging of cerebral capillaries and venules by clumped, parasitized red cells causing sludging in the capillary circulation is one hypothesis to explain its pathogenesis. The other is a humoral hypothesis which proposes nonspecific, immune-mediated, inflammatory responses with release of vasoactive substances capable of producing endothelial damage and alterations of permeability. Cerebral malaria has a mortality rate up to 50%, and also a considerable longterm morbidity, particularly in children. Hypoglycemia, largely in patients treated with quinine, may complicate the cerebral symptomatology. Other central nervous manifestations of malaria include intracranial hemorrhage, cerebral arterial occlusion, and transient extrapyramidal and neuropsychiatric manifestations. A self-limiting, isolated cerebellar ataxia, presumably caused by immunological mechanisms, in patients recovering from falciparum malaria has been recognized in Sri Lanka. Malaria is a common cause of febrile seizures in the tropics, and it also contributes to the development of epilepsy in later life. Several reports of spinal cord and peripheral nerve involvement are also available. A transient muscle paralysis resembling periodic paralysis during febrile episodes of malaria has been described in some patients. The pathogenesis of these neurological manifestations remains unexplored, but offers excellent perspectives for research at a clinical as well as experimental level.
 ...
PMID:Neurological manifestations of malaria. 130 75

A functional, insulin-secreting pancreatic (islet cell) carcinoma was diagnosed in a 17-year-old male Siamese cat. Diagnosis was made on the basis of clinical signs (i.e., seizures and stupor) that resolved temporarily after correction of hypoglycemia with feeding or intravenous administration of glucose, the finding of an inappropriately increased serum insulin concentration in the face of hypoglycemia, and prolonged resolution of hypoglycemia after surgical removal of the tumor. Primary islet cell tumor of the pancreas was confirmed by biopsy. The cat died 18 months later, and necropsy revealed metastases to regional lymph nodes and liver. Specimens of the tumor and metastatic lesions both stained positively for insulin.
 ...
PMID:Insulin-secreting pancreatic (islet cell) carcinoma in a cat. 132 Jan 19

A 58-year-old female was admitted and discovered to be a victim of thyrotoxicosis. She had experience periodic seizure attacks for 14 months. These seizures disappeared when function of the thyroid returned to normal. We performed many studies to search for the cause of the seizures. No epileptic focus could be detected from an EEG or a MRI of the brain. There was no abnormal laboratory data such as: hypoglycemia, hypoxemia, serum electrolyte imbalance, or an acid-base imbalance. No evidence of CNS infection was noted. She had good response to antithyroid treatment. We therefore suggest, that the seizure attacks may be related to thyrotoxicosis. In reviewing the literature, we found that only 13 cases of thyrotoxicosis with seizures have been reported since 1956 [1-9].
 ...
PMID:Thyrotoxicosis accompanied with periodic seizure attacks a case report and review of literature. 133 94

Management of accidental overdosage with oral hypoglycemic agents in toddlers may be difficult when the history of ingestion is overlooked. We report a 21-month-old girl who presented with lethargy and generalized seizures 12 hours after ingestion of an unknown number of glibenclamide pills. The blood glucose on admission was 0.5 mM/l. Symptoms resolved promptly after an intravenous bolus of glucose. Metabolic and infectious causes of hypoglycemia were ruled out. The parents denied drug ingestion initially, but further investigation revealed that she had ingested several glibenclamide pills used by her diabetic father 12 hours prior to admission. This case illustrates the problem involved in diagnosis and management of accidental drug overdosage in children when no such history is elicited and symptoms are delayed.
 ...
PMID:[Overdosage of glibenclamide presenting with lethargy and seizures in a child]. 142 74

Classification, management and prevention of seizures in children are summarized for clinicians in Papua New Guinea. Seizures are classified as febrile with or without underlying brain pathology, and afebrile, including neonatal fits, infantile spasms, myoclonic jerks, akinetic seizures, tonic clonic fits, petit mal, benign focal, and psychomotor seizures. In all cases the first step is to secure the airway, then do a fingerstick and treat hypoglycemia, and finally stop the fit if it is prolonged with paraldehyde, diazepam, phenobarbitone or phenytoin. A cause for the seizure should be sought: physical exam, especially tympanic membranes and throat, blood slide for malaria, lumbar puncture for signs of meningitis, blood culture, serum calcium, and other chemistries. Some empirical treatments to use for negative findings include: dextrose, calcium gluconate, magnesium SO4, pyridoxine, quinine and Fansidar. Hyperthermia in a febrile child can be reversed with cool sponging. The author recommends prescribing phenobarbitone to prevent subsequent simple febrile seizures if the child has 3 or more, then slowly withdrawing the drug if the child is seizure free for a year. Drug therapy for the various other types of seizures available in Papua New Guinea include sodium valproate by special order, and phenobarbitone, phenytoin, carbamazepine, nitrazepam, ethosuximide, and prednisolone. A table is provided to help select the drug for each seizure type, e.g. ethosuximide for petit mal, prednisolone for infantile spasms, and carbamazepine for various types of focal and psychomotor seizures.
 ...
PMID:Convulsions in children. 150 14

We treated a girl aged 3.5 years (15 kg) with ethanol intoxication, using peritoneal dialysis. The blood ethanol concentration was 6.4 g/l (640 mg/dl; 138.9 mmol/l). It was calculated that the child drank a total amount of 67.2 g of ethanol (4.5 g/kg). The spontaneous ethanol elimination rate before peritoneal dialysis was 0.27 g/l (5.86 mmol/l) per hour; during peritoneal dialysis we found an ethanol elimination rate of 0.32 g/l (6.94 mmol/l) per hour, which was lower than expected. In childhood the ethanol elimination rate with peritoneal dialysis is only slightly faster in comparison to the high spontaneous elimination rate. We conclude that treatment of severe ethanol intoxication should include mainly the maintenance of the vital functions and the meticulous control of blood sugar levels and acid-base disturbances, especially in children. Indications for dialysis are complications caused by ethanol and resistant to supportive therapy, such as seizures, metabolic disturbances, persistent hypoglycemia and the possibility of combined intoxication with other dialysable drugs.
 ...
PMID:The value of peritoneal dialysis in the treatment of severe ethanol intoxication in childhood revised. 151 Dec 8

A total of 2248 infants born at All India Institute of Medical Sciences Hospital, New Delhi were selectively screened for hypoglycemia over a period of 15 months. Hypoglycemia (blood glucose less than 30 mg/dl) was diagnosed in 107 cases (4.8%). Preterm babies had three times increased risk (12.8%) as compared to term babies (3.6%). Small-for-dates (SFDs) and large-for-dates (LFDs) infants were at increased risk of manifesting hypoglycemia (7 and 10 times, respectively) as compared to the appropriate-for-dates (AFDs) babies (2.7%). Approximately two-thirds of the hypoglycemic babies (67.3%) had one or more risk factors including birth asphyxia (24.2%), diabetic mothers (23.8%), respiratory distress (13.9%) and septicemia (11.6%). A total of 59.8% cases were asmyptomatic while the rest had one or more symptoms. The most common symptom observed was lethargy (81.4%), followed by jitteriness (67.4%), respiratory abnormalities (41.9%), hypotonia (39.5%) and seizures (30.2%). The amount of glucose (mg/kg/min) needed to maintain a stable blood sugar in various categories of hypoglycemic babies was observed to be in the following decreasing order of amount; symptomatic babies with seizures (Gp IV), IGDM's/IDM's and symptomatic babies with other features (Gp III), SFDs and LFDs (Gp II) and AFDs (Gp I). Such a categorization of hypoglycemic babies will help to treat them more precisely.
 ...
PMID:Neonatal hypoglycemia--clinical profile and glucose requirements. 159 96

Epileptogenic complications after supratentorial intracranial surgery are, strictly defined, the events which promote a further complication, i.e. seizures in any form, partial, simple or complex, or generalized. The most common epileptogenic complications are, therefore, electrolyte imbalance, hypoxia, hypoglycemia, hypocapnia, and intracerebral or extradural hematoma. However, also inadequate anticonvulsant prophylaxis and use of convulsant drugs can yield to the onset of post-operative seizures. Anesthetic drugs have been each time defined pro or anti-convulsant: however, data from the literature show that it is not possible to certainly define the role of general anesthetics in the genesis of post-operative seizures.
 ...
PMID:[Epileptogenic complications of neurosurgical interventions]. 162 Apr 64

Direct and indirect evidence suggests that Na+/K(+)-ATPase activity is reduced or insufficient to maintain ionic balances during and immediately after episodes of ischemia, hypoglycemia, epilepsy, and after administration of excitotoxins (glutamate agonists). Recent results show that inhibition of this enzyme results in neuronal death, and thus a hypothesis is proposed that a reduction and/or inhibition of this enzyme contributes to producing the central neuropathy found in the above disorders, and identifies potential mechanisms involved. While the extent of inhibition of Na+/K(+)-ATPase during ischemia, hypoglycemia and epilepsy may be insufficient to cause neuronal death by itself, unless the inhibition is severe and prolonged, there are a number of interactions which can lead to a potentiation of the neurotoxic actions of glutamate, a prime candidate for causing part of the damage following trauma. Presynaptically, inhibition of the Na+/K(+)-ATPase destroys the sodium gradient which drives the uptake of acidic amino acids and a number of other neurotransmitters. This results in both a block of reuptake and a stimulation of the release not only of glutamate but also of other neurotransmitters which modulate the neurotoxicity of glutamate. An exocytotic release of glutamate can also occur as inhibition of the enzyme causes depolarization of the membrane, but exocytosis is only possible when ATP levels are sufficiently high. Postsynaptically, the depolarization could alleviate the magnesium block of NMDA receptors, a major mechanism for glutamate-induced neurotoxicity, while massive depolarization results in seizure activity. With less severe inhibition, the retention of sodium results in osmotic swelling and possible cellular lysis. A build-up of intracellular calcium also occurs via voltage-gated calcium channels following depolarization and as a consequence of a failure of the sodium-calcium exchange system, maintained by the sodium gradient.
 ...
PMID:Inhibition of sodium-potassium-ATPase: a potentially ubiquitous mechanism contributing to central nervous system neuropathology. 166 97

Dopamine beta-hydroxylase (DBH) deficiency is a genetic disorder in which affected patients cannot synthesize norepinephrine, epinephrine, and octopamine in either the central nervous system or the peripheral autonomic neurons. Dopamine acts as a false neurotransmitter in their noradrenergic neurons. Neonates with DBH deficiency have had episodic hypothermia, hypoglycemia, and hypotension, but survivors sometimes cope relatively well until late childhood when overwhelming orthostatic hypotension profoundly limits their activities. The hypotension may be so severe that clonic seizures supervene. Most currently recognized patients are young or middle-aged adults. The diagnosis is established by the observation of severe orthostatic hypotension in a patient whose plasma norepinephrine/dopamine ratio is much less than one.
 ...
PMID:Dopamine beta-hydroxylase deficiency. A genetic disorder of cardiovascular regulation. 167 40


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>