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)

Twenty-six patients with the syndrome of inappropriate secretion of antidiuretic hormone were reviewed. The underlying diseases were bronchogenic carcinoma (12 cases); myxoedema (five cases); diseases of the nervous system (five cases); bronchopneumonia, carcinoma of the oesophagus, acute intermittent porphria and chlorpropamide therapy (each one case). Serum sodium levels ranged between 104 and 125 mEq per litre. Eighteen patients presented neurological manifestations, which in 14 were considered to be due to hyponatraemia. Neurological signs included disorders of consciousness (stage I and II coma), extrapyramidal signs, asterixis and epileptic seizures. An hyponatraemic coma was the first manifestation of the syndrome in five cases. In all cases where the EEG was recorded it showed non-specific signs of metabolic coma. The fundi never showed signs of intracranial hypertension. Blood urea and creatinine levels were invariably low in the euthyroid patients; these values were normal or elevated in patients with myxoedema and hyponatraemia. Hypokalaemia was frequent, and hypocalcaemia constant. In eleven cases an excess of water intake revealed the clinical syndrome: six patients were excessive beer drinkers and five had received extensive intravenous infusions. In one case the deleterious effect of diuretics was evident, and in another, the syndrome became evident during radiotherapy of an oesophageal tumour. Treatment of the syndrome was successful in all cases. A review of the literature concerning the various pathogenic mechanisms corresponding to the different underlying diseases is presented. The concept of aberrant hormonal production by a tumour is illustrated by an electron microscopic study.
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PMID:Clinical, biological and pathogenic features of the syndrome of inappropriate secretion of antidiuretic hormone. A review of 26 cases with marked hyponatraemia. 100 53

The case of a child is described who at the age of 2 years showed the first evidence of a developing neurological disease. Within a couple of years, profound mental retardation and severe motor deficit with spastic tetraplegia became established. No seizures and no pigmentation of the retina were observed. The condition remained practically unchanged for some 8 years and the patient died at 12 years of age of terminal bronchopneumonia. At autopsy there was conspicuous diffuse atrophy of the brain. The cerebral cortex was particularly involved. Most of the cortical neurons were destroyed and neuroglia showed abundant proliferation. The few remaining neurons contained inclusion material which was identified as lipofuscin. Noticeable cedifferences from the various types of amaurotic idiocies are noted and similarities to a case of lipidosis recently reported from Finland are suggested.
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PMID:An unusual type of infantile lipofuscinosis. 113 10

One-hundred and thirty-one patients with chronic subdural haematoma were treated by burr holes and closed system drainage. Four patients died, and in 19 patients postoperative complications were noted: intracranial hypotension in eight, cerebral oedema in four, haematoma recurrence in three, bronchopneumonia in three, and intracerebral haematoma in one. The high risk groups were those in grade III and IV on admission, and the elderly. Follow-up revealed that more than 80% of patients recovered completely, 10% still had neurological or mental deficits and 7% suffered epileptic seizures.
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PMID:Chronic subdural haematoma treated by burr holes and closed system drainage: personal experience in 131 patients. 176 27

Due to the increased indications of using carbamazepine, a higher number of intoxications is to be expected. A case report is given of a 42-year-old patient who took about 250 tablets (50 g) carbamazepine (Finlepsin) in a suicide attempt. The maximum serum level of carbamazepine was 118.74 mumol/l. After a gastric lavage and the use of activated charcoal the detoxication was carried out by forced diuresis and one-time haemodialysis. The unconscious patient was ventilated for 8 days after intubation. Two hours after admission three generalised seizures occurred. A long-term hypotension and electrolyte shifts were balanced and a bronchoscopy and lavage were necessary. Bronchopneumonia occurred as a complication. The patient became conscious on the 5th day of treatment, the extubation was accomplished on the 12th day and on the 15th day she was transferred to the psychiatric clinic for further treatment of the basic disease. Since a specific antidote does not exist, general intensive therapeutic measure after carbamazepine intoxication are discussed. After gastric lavage to eliminate the poison, the patient should receive hourly doses of activated charcoal plus vigorous cathartic-like solutions of mannitol and sorbitol and forced diuresis. In case of complicated coma haemoperfusion is recommended.
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PMID:[Carbamazepine poisoning]. 188 28

To understand the febrile children in clinic practice, 3793 cases had been collected from our emergency unit from December 1984 to December 1985. Of them, 2841 (74.9%) were febrile with a male to female ratio of 3:2. Concerning age distribution, 22% were younger than 6 months, 21.5% between 7 months and 1 year, 17.6% 1-2 years and 38.9% older than 2 years. Cases happened most in February, followed by July. In these febrile children, the axillary temperature was 37.1-37.9 C in 778 cases (27.4%), 38-38.9 C in 1118 cases (39.3%), 39-39.9 C in 846 cases (29.8%), 40-40.9 C in 91 cases (3.2%), and 41-41.9 C in 8 cases (0.3). Convulsion associated with fever were noted in 112 cases (3.9%). Of them, axillary temperature was 37.1-37.9 C in 30 cases (3.9%), 38-38.9 C in 29 cases (2.6%), 39-39.9 C in 42 cases (4.9%), 40-40.9 C in 6 cases (6.6%), and 41-41.9 C in 5 cases (62.5%). Clinical diagnosis included acute pharyngitis (1125 cases, 39.6%), acute bronchitis (515, 18.1%), acute bronchiolitis (232, 8.2%), acute gastroenteritis (235, 8.3%), bronchopneumonia (159, 5.6%), acute tonsillitis (135, 4.7%), sepsis (88, 3.1%), and others (352, 12.4%). In conclusion, most emergency called children had fever. The underlying disease to induce fever is most frequently the respiratory tract infection. The possibility of convulsion increase with the rising of body temperature.
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PMID:[The clinical analysis of febrile children]. 280 90

A 46 years old male alcoholic was admitted with an assumed alcohol withdrawal syndrome accompanied by tonic-clonic seizures. Parenteral nutrition with fructose, sorbitol, xylitol, dextran, hydroxyethylstarch, electrolytes, vitamins and amino acids was undertaken. He died 20 d later due to renal insufficiency and bronchopneumonia. Calcium-oxalate-monohydrate (whewellite) was found in the central nervous system, the kidneys, the testes, the epididymis, the cardiac muscle cells and the lungs. The presence of urate crystals was suspected. The pathogenesis of secondary oxalosis is discussed.
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PMID:[Cerebrorenal oxalate formation--a metabolic abnormality following parenteral infusions of carbohydrate exchange substances]. 312 59

We describe 2 brothers with a malformation syndrome consisting of agenesis of the corpus callosum, cutaneous hypopigmentation, bilateral cataract, cleft lip and palate, and combined immunodeficiency. The clinical history of both patients was characterized by severe psychomotor retardation, seizures, recurrent severe respiratory infections, and chronic mucocutaneous candidiasis. The children died of bronchopneumonia at age 2 and 3 years, respectively. Immunological investigations showed, in one sib studied, skin anergy to recall antigens, profound depletion of T4+ lymphocytes, and serum IgG2 deficiency. Necropsy showed agenesis of the corpus callosum, hypoplasia of the cerebellar vermis, and profound hypoplasia of the thymus and of the peripheral lymphoid tissue. The distinctive features of these sibs appear to define a previously undescribed hereditary MCA/MR syndrome. The clinical and pathological findings seem to indicate, as a pathogenetic mechanism, a defect involving the embryonic organization of the central nervous system and of the immune system.
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PMID:Agenesis of the corpus callosum, combined immunodeficiency, bilateral cataract, and hypopigmentation in two brothers. 334 62

A retrospective analysis of 10 adult patients with community-acquired Staphylococcus aureus meningitis was performed in order to elucidate the characteristics and treatment of this lethal disease. In all patients, a focus of infection outside the central nervous system was apparent at presentation. A poor prognosis was associated with severe underlying disease, greater degree of hyponatremia at presentation, development of seizures, failure of nuchal rigidity to develop, persistent or recurrent bacteremia, and the presence of concurrent S. aureus bronchopneumonia. Degree of deterioration in mental status and cerebrospinal fluid pleocytosis, protein levels, and glucose levels did not appear to have any prognostic significance. Therapy with rifampin and a semisynthetic penicillin effected a cure in all six patients treated with this regimen. In contrast, three of four patients treated with other antibiotic combinations died. On the basis of this experience, it is concluded that further trials with rifampin in combination with another anti-staphylococcal antibiotic for the treatment of S. aureus meningitis are warranted.
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PMID:Meningitis due to Staphylococcus aureus. 401 71

Infections caused by Actinomyces organisms have been demonstrated to occur in association with IUD use. Uterine actinomycosis infection is usually superficial, but it is potentially invasive. It may prove fatal. When Actinomyces is detected in a vaginal Papanicolaou smear, establishment of the correct diagnosis followed by IUD removal and appropriate antibiotic therapy are recommended. A case history is presented of a 28 year old woman who had been using an IUD and who had systemic Actinomyces infection and a brain abscess develop several years after removal of her uterus and fallopian tubes. The woman was referred to the Johns Hopkins Hospital in Baltimore in 1977 for evaluation of headaches and grand mal seizures. 4 years earlier, in 1973, she had been seen at another hospital with a recent weight loss of 18 kg. She was found to have a tubo-ovarian abscess, for which she underwent a hysterectomy, bilateral salpingectomy, and unilateral oophorectomy. At the time of surgery, an IUD was in place. A histopathological diagnosis of botryomycosis tubo-ovarian abscess was made on submitted tissues. She received no antibiotic therapy. In 1975, pulmonary infiltrates developed that were attributed to bronchopneumonia. She was treated with a short course of tetracycline hydrochloride. Later that year she was thought to have sarcoidosis and was treated for 1 year with several doses of prednisone. Clinically, her condition remained stable until March 1977, when a pyogenic subcostal abscess was drained. In July 1977, she had headache, dizziness, generalized seizures, and an incomplete right homonymous hemianopsia develop. A craniotomy for excision and drainage of an abscess was performed. The presence of Actinomyces israelii in brain tissue was confirmed by direct immunoflourescence using specific antiserum. It was confirmed that Actinomyces had been present at the time of her 1st surgical procedure. She was treated with high doses of intravenous penicillin G potassium for the first 4 weeks, followed by lower doses of oral penicillin V potassium for an additional 15 months. She recovered completely, except for a persistent right homonymous hemianopsia. The case illustrates that systemic dissemination and potentially life threatening complications of uterine actinomycosis can occur if the infection is unrecognized and/or inadequately treated.
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PMID:Systemic Actinomyces infection. A potential complication of intrauterine contraceptive devices. 712 Jun 9

A female newborn, the second child of healthy non consanguineous parents, exhibited muscular hypotonia, areflexia, apathy, seizures, hepatomegaly and failure to thrive since birth. The peculiar skull shape was lacking. In the urine pipecolic acid and trihydroxycoprostanoic acid were excreted. At the age of seven weeks she died of bronchopneumonia. Lightmicroscopy revealed malformations and deficiency of myelinisation in the brain, renal cysts and fatty metamorphosis in the enlarged liver, which showed only minimal siderosis. Ultrastructurally no peroxisomes could be found in liver and kidney. No peroxisomes were detected by histochemical demonstration of catalase in frozen liver tissue which was taken immediately after death and stored for three months. Absence of peroxisomes is pathognomonic for the cerebro-hepato-renal syndrome of Zellweger and occurs in the liver irrespective of duration and degree of liver damage. It is best demonstrated by enzymehistochemical electron microscopy. With this method peroxisomes can be visualized even 30 h post mortem. In deep frozen normal liver tissue the activity of catalase remains very stable and enables the identification of peroxisomes even after a 12 months period of storage. In the cerebro-hepato-renal syndrome of Zellweger, frozen liver tissue should be stored for biochemical and diagnostic enzymehistochemical studies.
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PMID:[Morphology and diagnosis of Zellweger syndrome. A contribution to combined cytochemical-finestructural identification of peroxisomes in autopsy material and frozen liver tissue with case report]. 734 41


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