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)

A 35-year-old man ingested food contaminated with lindane, an insecticide containing almost pure gamma hexachlorocyclohexane. Grand mal seizures and severe acidemia developed rapidly. The seizures recurred for nearly 2 hours, then ceased. In addition, the patient had muscle weakness and pain, headaches, episodic hypertension, myoglobinuria, acute renal failure and anemia. Pancreatitis developed 13 days after the ingestion of lindane. A muscle biopsy on the 15th day of illness demonstrated widespread necrosis and regeneration of muscle fibres. The patient's condition improved and he was discharged 24 days after the onset of his illness. During the year following the poisoning the patient noted difficulty with recent memory, loss of libido and easy fatigability. One year after lindane ingestion the results of physical examination, including those for muscle power and bulk, were normal.
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PMID:Acute lindane poisoning with development of muscle necrosis. 7 42

A 27-year-old man had limb weakness, short stature, neurosensory hearing loss, seizures, mild peripheral neuropathy, neurogenic bladder, elevated cerebrospinal fluid (CSF) protein content, primary lactic acidemia, and basal ganglia calcification. Muscle biopsy revealed numerous ragged-red fibers. On electronmicroscopy there were mitochondrial alterations, including many intramitochondrial inclusions. The mother of the patient had Vogt-Koyanagi-Harada syndrome, a combination of rare disorders in the same family that has not been previously described.
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PMID:Lactic acidemia, mitochondrial myopathy, and basal ganglia calcification. 22 42

There is much individual variability in the clinical manifestations of hypocalcemia. The rapidly of the development of hypocalcemia will determine whether or not symptoms will be present. Signs and symptoms of hypocalcemia consisted of tetany (Chvostek's and Trousseau's signs), seizures, diminshed to absent deep tendon reflexes, papilledema, mental changes (weakness, fatigue, irritability, memory loss, confusion, delusion, hallucination), and skin changes. Etiologic factors for hypocalcemia in man include (1) decreased calcium absorption or increased loss from the gastrointestinal tract; (2) parathyroid hormone deficiency; (3) skeletal resistance to parathyroid hormone; (4) ineffective parathyroid hormone; (5) decreased production or increased degradation of 25-hydroxycholecalciferol or 1,25-dihydroxycholecalciferol; (6) increased complex formation with calcium; (7) increased skeletal uptake of calcium; (8) hypomagnesemic state; and (9) direct inhibition of bone resorption. Measurement of total and ionic calcium, magnesium, parathyroid hormone, vitamin D metabolites (25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol), and nephrogenous cyclic adenosine monophosphate are especially helpful in the laboratory evaluation of the hypocalcemic patient.
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PMID:Hypocalcemia. Differential diagnosis and mechanisms. 22 22

Dantrolene sodium or dantrolene1 is 1([5-(nitrophenyl)furfurylidend] amino) hydantoin sodium hydrate. It is indicated for use in chronic disorders characterised by skeletal muscle spasticity, such as spinal cord injury, stroke, cerebral palsy and multiple sclerosis. Dantrolene is believed to act directly on the contractile mechanism of skeletal muscle to decrease the force of contraction in the absence of any demonstrated effects on neural pathways, on the neuromuscular junction, or on the excitable properties of the muscle fibre membranes. Controlled trials have demonstrated that dantrolene is superior to placebo in adults or children with spasticity from various causes, as evidenced by clinical assessments of disability and daily activities, and by muscle and reflex responses to mechanical and electrical stimulation. It is somewhat less effective in patients with multiple sclerosis than in those with spasticity from other causes. There has been a general clinical impression in controlled trials that dantrolene caused less sedation than would have been expected from therapeutically comparable doses of diazepam. In 2 controlled trials, there was no significant difference between dantrolene and diazepam in terms of reductions in spasticity, clonus, and hyperreflexia, but side-effects such as drowsiness and inco-ordination occurred significantly more frequently on diazepam. Long-term studies have indicated continuing benefit for patients taking dantrolene, though the incidence of side-effects has often been high and there has been a suggestion of exacerbation of seizures in children with cerebral palsy. Dantrolene may be of value in the medical treatment of spasm of the external urethral sphincter due to neurological and non-neurological disease, and animal studies suggest a potential use in the management of malignant hyperpyrexia. Chemical evidence of liver dysfunction may occur in 0.7 to 1% of patients on long-term treatment with dantrolene, with symptomatic hepatitis in 0.35 to 0.5% and fatal hepatitis in 0.1 to 0.2%. The drug commonly causes transient drowsiness, dizziness, weakness, general malaise, fatigue and diarrhoea at the start of therapy. Muscle weakness may be the principal limiting side-effect in ambulant patients, particularly in those with multiple sclerosis, and therapy could be hazardous in patients with pre-existing bulbar or respiratory weakness. The dosage of dantrolene has been fixed in most controlled trials, though long-term studies have indicated the need for individualisation of dosage. The initial dose is usually 25mg once daily, increasing to 25mg two, three or four times daily, and then by increments of 25mg up to as high as 100mg two, three or four times daily. The lowest dose compatible with optimal response is recommended.
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PMID:Dantrolene sodium: a review of its pharmacological properties and therapeutic efficacy in spasticity. 31 89

A case of primary interhemispheric subdural abscess was reported, which was not accompanied by abscess formation in other places such as subdural spaces of the convexity or in the brain. A 13-year-old school boy was admitted with 8 days' history of fever, headache and progressive weakness of the left lower extremity. Prior to admission he developed 2 spells of jacksonian seizure initiating from the left leg. Right carotid angiography was performed on admission and separation of the pericallosal and callosomarginal arteries with small avascular area was shown indicating possible abscess formation in the interhemispheric fissure. There was no evidence of purulent infection in the laboratory findings including the CSF and EEG showed diffuse slow wave discharge, more in the right frontocentral leads. He was placed on the vigorous treatment with antibiotics and steroids, and one month later the left lower weakness as well as the EEG abnormality showed some improvement. However, the separation of the anterior cerebral arterial branches became more prominent and formed a lens shaped avascular area, although the pericallosal artery was in the midline. A diagnosis of interhemispheric subdural abscess was made and was confirmed by surgery. Patient showed progressive recovery of the left lower paralysis, and the abscess was totally collapsed in the repeated angiographic follow-up study. Angiographic characteristics of the interhemispheric subdural abscess were described and particular emphasis was placed on the peculiar neurological symptoms referring to the previous reports in the literature.
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PMID:[Primary interhemispheric subdural abscess--case report (author's transl)]. 41 51

The paper contains a clinico-morphological description of a case with late sequelae of treated tubercular meningitis. The patient at 7 years of age had tuberculous meningitis which was treated by suboccipital and endolumbar administration of streptomycin. Following 12 years, epileptical seizures ensued with an eventual gradual weakness in the extremities leading to profound spastic tetraparesis. During the last years of life contractures and stem symptoms developed. The morphological picture was characterized by posttuberculous fibrous leptomeningitis with an extensive internal hydrocephalus, universal sclerosis of the cerebral and spinal vessels, disseminated demyelinization in the spinal cord and brain, a distinct improverishment of the grey matter by ganglionic cells. The result of liquorohemodynamical disorders was a syringolike cavity in the spinal cord. Under the ependima of the laral ventricle calcified cholesteatomas were found, which are considered as complications of suboccipital punctures in administering streptomycin.
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PMID:[Late sequelae of tuberculous meningitis]. 42 59

We describe a patient with a left facial paralysis and hemotympanum following left parieto-occipital skull trauma. The initial admission diagnosis of intratemporal facial nerve injury secondary to temporal bone fracture was incorrect. Normal facial movements during involuntary activity (yawning, laughing at a joke) and focal seizure activity on the paralyzed side of the face, seen subsequently, indicated the site of lesion as supranuclear. The diagnosis of opercular syndrome was made. This syndrome can result when the contralateral frontal lobe is injured. Supranuclear weakness of muscles supplied by the hypoglossal or spinal accessory nerves is also present. Unlike other central paralyses, the facial paralysis in operculum syndrome may not demonstrate "forehead sparing" and consequently it may be mistaken for a peripheral paralysis. The neuroanatomic basis for the syndrome is discussed. Signs and symptoms are outlined to help the otolaryngologist avoid this diagnostic pitfall.
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PMID:The opercular syndrome--diagnostic trap in facial paralysis. 43 Dec 42

While a clinical history is frequently sufficient for a localizing diagnosis of temporal lobe epilepsy, lateralization of the epileptogenic abnormality often is impossible on clinical grounds alone. Since we have noted facial asymmetry in such patients, 50 individuals with temporal lobe epilepsy were studied. In patients with unilateral foci, we found contralateral lower facial weakness of mild to severe degree in 73 percent while 13 percent had ipsilateral weakness, and in 13 percent the face was symmetrical. The facial weakness usually was more striking on emotional movement. In the group of patients with bitemporal independent discharges, 61 percent had some asymmetry, often facial weakness on the side opposite the major focus. Of 25 control individuals, only one third had a facial asymmetry and this was slight. Facial asymmetry in temporal lobe epilepsy is a useful though not an absolute clinical lateralizing sign. It is a factor to be considered in addition to other clinical, radiologic, neuropsychologic, and electroencephalographic findings in the evaluation of patients with temporal lobe seizures.
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PMID:Facial asymmetry in patients with temporal lobe epilepsy. A clinical sign useful in the lateralization of temporal epileptogenic foci. 55 26

A 11-year-old boy of short stature had recurrent right temporal pounding headaches of 7 months' duration, and progressive visual loss for 3 days. There was a left hemianopia, alexia without agraphia, and diffuse muscle weakness. Investigation established the presence of a mitochondrial myopathy with pyruvate and lactic acidemia and increased serum content of sarcoplasmic enzymes. On treatment with prednisone, the patient's strength and reading skill improved, symptoms resolved, and muscle enzymes returned to normal. Three attempts to reduce steroids resulted in accentuation of symptoms, seizures, weakness, regression of reading skills, and elevation of serum enzymes. The alexia was also reversible.
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PMID:Reversible alexia, mitochondrial myopathy, and lactic acidemia. 57 70

Clinical observations suggest that overt rhabdomyolysis may occur if severe hypophosphatemia is superimposed upon a pre-existing subclinical myopathy. To examine this possibility, a subclinical muscle cell injury was induced in 23 dogs by feeding them a phosphorus- and calorie-deficient diet until they lost 30% of their original weight. To induce acute, severe hypophosphatemia in the animals after partial starvation, 17 of the dogs were given large quantities of the same phosphorus-deficient diet in conjunction with an oral carbohydrate supplement, which together provided 140 kcal/kg per day. After phosphorus and caloric deprivation, serum phosphorus and creatine phosphokinase (CPK) activity were normal. Total muscle phosphorus content fell from 28.0+/-1.3 to 26.1+/-2.5 mmol/dg fat-free dry solids. Sodium, chloride, and water contents rose. These changes resembled those observed in patients with subclinical alcoholic myopathy. When studied after 3 days of hyperalimentation, the animals not receiving phosphorus showed weakness, tremulousness, and in some cases, seizures. Serum phosphorus fell, the average lowest value was 0.8 mg/dl (P <0.001). CPK activity rose from 66+/-357 to 695+/-1,288 IU/liter (P <0.001). Muscle phosphorus content fell further to 21.1+/-7.7 mmol/dg fat-free dry solids (P <0.001). Muscle Na and Cl contents became higher (P <0.01). Sections of gracilis muscle showed frank rhabdomyolysis.6 of the 23 phosphorus- and calorie-deprived dogs were also given 140 kal/kg per day but in addition, each received 147 mmol of elemental phosphorus. These dogs consumed their diet avidly and displayed no symptoms. They did not become hypophosphatemic, their CPK remained normal, and derangements of cellular Na, Cl, and H(2)O were rapidly corrected. The gracilis muscle appeared normal histologically in these animals. These data suggest that a subclinical myopathy may set the stage for rhabdomyolysis if acute, severe hypophosphatemia is superimposed. Neither acute hypophosphatemia nor rhabdomyolysis occur if abundant phosphorus is provided during hyperalimentation.
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PMID:Hypophosphatemia and rhabdomyolysis. 74 77


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