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)

Aspiration is the leading cause of anaerobic lung infections. Risk factors for these infections include a depressed level of consciousness, a history of seizure, general anesthesia, central nervous system or neuromuscular disease, cerebrovascular accident, impaired swallowing and use of a tracheal or nasogastric tube. Clinical presentation includes fever, weight loss, malaise and cough productive of foul-smelling sputum. Diagnosis is based on radiographic findings, clinical features and a characteristic morphology of mixed flora on Gram stain of uncontaminated pulmonary specimens. The diagnosis is confirmed by isolation of organisms, usually polymicrobial, on culture. Treatment includes proper drainage, debridement of necrotic tissue and an antibiotic regimen (often initially empiric) with an agent active against anaerobic and aerobic organisms.
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PMID:Anaerobic lung infections. 820 19

A 78-year-old woman was admitted to our hospital because of disorientation and fever on January 21, 1992. Two days before admission she experienced vomiting, anorexia and general malaise. Laboratory examinations on admission disclosed a hemoglobin level of 11.1 g/dl and a platelet count of 8,000/microliters. The peripheral blood smear revealed anisocytosis with numerous schistocytes and poikilocytes. Polychromatophilic and nucleated red blood cells were also seen, and the reticulocyte count was 38/1000. Her serum lactate dehydrogenase (LDH) value was 2,977 WU and the total serum bilirubin level was 3.5 mg/dl with 2.7 mg/dl indirect reacting fraction. Serum creatinine was 4.7 mg/dl. Her consciousness became semicomatose after a systemic seizure which lasted approximately 15 seconds and her hemoglobin level decreased to 8.5 g/dl on hospital day 2. Therefore, we diagnosed her as having thrombotic thrombocytopenic purpura (TTP) because of the presence of all 5 features, that is, thrombocytopenia, microangiopathic hemolytic anemia, fluctuating neurologic abnormalities, renal dysfunction and fever. A plasmapheresis with fresh frozen plasma (FFP) replacement was begun on that day. She was also treated with anti-platelet agents, 80 mg/day aspirin, and 300 mg/day dipyridamole. Moreover, packed red blood cells (PRC) were infused. While also receiving diphenylhydantoin and phenobarbital to prevent convulsions, status epilepticus developed on day 3. Because of inhibited spontaneous respiration which was an adverse effect derived from diazepam and sodium thiamylal administered intravenously to treat the status epilepticus, an artificial respiration was initiated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An elderly case of thrombotic thrombocytopenic purpura]. 848 87

Hyponatremia is rarely reported as a delayed complication of transsphenoidal resection of pituitary adenoma. Usually attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), hyponatremia causes nonspecific symptoms, often after hospital discharge. To clarify the frequency, presentation, and outcome of this poorly understood complication, we reviewed our database of 2297 patients who underwent transsphenoidal pituitary surgery between February 1971 and June 1993. Of 53 patients (2.3%) treated for symptomatic hyponatremia, 11 were excluded (2 received arginine vasopressin within 24 hours, 1 had untreated hypothyroidism, 4 had untreated adrenal insufficiency, and 4 had incomplete records). The remaining 42 patients (1.8%), 11 men and 31 women aged 21 to 79 years, presented 4 to 13 days (mean, 8 d) postoperatively with nausea and vomiting (20 patients), headache (18 patients), malaise (12 patients), dizziness (4 patients), anorexia (2 patients), and seizures (1 patient). Hyponatremia was unrelated to sex, age, adenoma type, tumor size, or glucocorticoid tapering. Although the clinical picture in our patients is consistent with SIADH, this was not supported by the antidiuretic hormone levels, which were normal or low-normal in the two patients in whom they were measured, suggesting the possibility that low serum sodium may not reflect SIADH. In all patients, hyponatremia resolved within 6 days (mean, 2 d); treatment consisted of salt replacement and mild fluid restriction in 37 patients and fluid restriction only in 4 (treatment unknown in 1). Delayed hyponatremia after transsphenoidal resection of pituitary adenoma is not as rare as previously thought, nor is it necessarily associated with SIADH or with hypoadrenalism during glucocorticoid tapering.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Delayed onset of hyponatremia after transsphenoidal surgery for pituitary adenomas. 855 92

The muscarinic antagonist scopolamine blocks conditioned taste aversion (CTA) when microinjected bilaterally into the rat insular cortex shortly before the exposure of the rat to a novel taste (the conditioned stimulus, CS) in CTA training. Scopolamine has no effect when microinjected shortly after the exposure to the novel taste or shortly before the application of the malaise-inducing agent (unconditioned stimulus, UCS). Scopolamine does not affect sensory, motor and retrieval mechanisms required for performing the CTA task, and does not block CTA when injected into another cortical area. The effect of scopolamine is independent of the taste used as CS. Furthermore, microinjection of scopolamine into the insular cortex shortly before the pre-exposure to a new taste in a latent inhibition paradigm, impairs the attenuation of CTA by that pre-exposure. Other muscarinic antagonists, pirenzepine and AF DX-116, have an effect similar to that of scopolamine. Comparison of the dose-dependency curves of the muscarinic antagonists suggests a predominant role in CTA for M2 subtype receptors. Carbachol, a muscarinic agonist, also impairs the encoding of taste in the insular cortex, but the results are confounded by the ability of that ligand to induce seizures. Our findings suggest that cholinergic neuromodulation participates in processing the CS in the gustatory cortex in CTA, either by encoding novelty at the cellular level, or by instructing the neural circuits to store the novel taste representation.
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PMID:Transient impairment of cholinergic function in the rat insular cortex disrupts the encoding of taste in conditioned taste aversion. 888 17

We retrospectively evaluated the clinical findings of 10 cases of tuberculous meningitis who had been admitted to our department from 1987 to 1994. Four patients were male and six were female. All of them were Japanese, and their age ranged from 17 to 74 years old. Regarding the patient's delay, nine patients visited a doctor in 1 to 20 days after the onset of headache, and one patient visited a doctor in 14 days after the onset of general malaise. It is suggested that the patient's delay could not be longer than 3 weeks because of progressively worsening symptoms of tuberculous meningitis such as severe headache and fever. The time interval between the first contact of the patient to a doctor and the commencement of antituberculous therapy (doctor's delay), ranged from 14 to 66 days. When the diagnosis of meningitis was obtained based on the findings of the cerebrospinal fluid (CSF), focal neurological signs including psychological symptoms, cranial nerve palsies and seizure were noted besides meningeal signs or the disturbance of consciousness in 4 patients. The CSF revealed an increase in cell counts with mononuclear cell dominance in 9 patients, but the findings typical for tuberculous meningitis such as increase in total protein content and a decrease in glucose concentration were obtained in only 5 patients. Mycobacterium tuberculosis had not been detected in all cases when the antituberculous chemotherapy was started. Later, it was found to be positive in the CSF sample from only three patients by culture or polymerase chain reaction (PCR) method. When the antituberculous therapy was completed, meningitis was cured without remaining any symptom or sign in all patients. All patients had no active pulmonary tuberculosis when the meningitis was diagnosed, and only one of them had sequels of lung tuberculosis. Four patients had the past history of tuberculosis, and 1 had the familial history of pulmonary tuberculosis. At the first contact to a doctor, seven patients were diagnosed as having common cold or headache related with fever because of the lack of typical signs of meningitis. Similarly three other patients were initially diagnosed as having meningitis due to viral infection or unknown etiology. In summary, it was difficult to obtain the solid diagnosis of tuberculous meningitis at the initial stage of this disease, since the symptoms and signs at its onset often similar to those of common cold or non-specific headache. Therefore, when we see the patients with subacute onset of headache and fever followed by the meningeal signs, tuberculous meningitis should always be included in the list of diseases requiring differential diagnosis. In addition, when tuberculous meningitis is suspected, the antituberculous therapy should be started without any delay.
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PMID:-Clinical features of 10 cases of tuberculous meningitis--with special reference to patient's delay and doctor's delay. 890 Dec 25

DRUG-RESISTANCE: Partial epilepsies are more often drug-resistant than generalized epilepsies, excepting severe syndromes which often begin in childhood. There is no need to try all anti-epileptic drugs before concluding as to the drug-resistant nature of the seizures. Refractory epilepsy can be diagnosed if well-conducted therapy (two alternative single-drug regimens with classical anti-seizure drugs and 1 or 2 trials with a two-drug regimen using new-generation compounds) is unsuccessful. MECHANISMS OF DRUG-RESISTANCE: The clinician should revisit the entire clinical history in patients with apparently refractory epilepsy, evaluating the treatments and the specific manifestations of the seizures. Conducted in a specialized center, this reassessment can recognize false cases of drug resistance such as non-epilepsy-related malaise or syncopes, inadequate regimens, or psychogenic "pseudo-seizures" which can be observed in patients with authentic epilepsy. Video-coupled EEG and ambulatory EEG may offer very useful information. SEVERAL EFFECTIVE THERAPEUTIC OPTIONS: Prognosis depends on effective and early control of seizures. This implies entertaining surgical excision of the epileptogenic focus early in the disease course. With several promising anti-epilepsy drugs, either recently marketed or under development, therapeutic indications in epilepsy should progress to more evidence-based prescriptions adapted to the type of epilepsy and the underlying cause.
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PMID:[Refractory epilepsy]. 989 95

Although the anticonvulsant hypersensitivity syndrome was first described in 1950, confusion still abounds regarding the syndrome. The triad of fever, rash and internal organ involvement occurring 1 to 8 weeks after exposure to an anticonvulsant heralds this rare (1 in 1,000 to 10,000 exposures) but serious reaction. Aromatic anticonvulsants [phenytoin, phenobarbital (phenobarbitone) and carbamazepine] are the most frequently involved drugs; however, there have also been several cases of anticonvulsant hypersensitivity syndrome associated with lamotrigine. Fever, in conjunction with malaise and pharyngitis, is often the first sign. This is followed by a rash which can range from a simple exanthem to toxic epidermal necrolysis. Internal organ involvement usually involves the liver, although other organs such as the kidney, CNS or lungs may be involved. Hypothyroidism may be a complication in these patients approximately 2 months after occurrence of symptoms. The aromatic anticonvulsants are metabolised to hydroxylated aromatic compounds, such as arene oxides. If detoxification of this toxic metabolite is insufficient, the toxic metabolite may bind to cellular macromolecules causing cell necrosis or a secondary immunological response. Cross-reactivity among the aromatic anticonvulsants may be as high as 75%. In addition, there is a familial tendency to hypersensitivity to anticonvulsants. Discontinuation of the anticonvulsant is essential in patients who develop symptoms compatible with anticonvulsant hypersensitivity syndrome. A minimum battery of laboratory tests, such as liver transaminases, complete blood count and urinalysis and serum creatinine, should be performed. Corticosteroids are usually administered if symptoms are severe. Patients with anticonvulsant hypersensitivity syndrome should avoid all aromatic anticonvulsants; benzodiazepines, valproic acid (sodium valproate) or one of the newer anticonvulsants can be used for seizure control. However, valproic acid should be used very cautiously in the presence of hepatitis. There is no evidence that lamotrigine cross-reacts with aromatic anticonvulsants. In addition, family counselling is a vital component of patient management.
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PMID:Anticonvulsant hypersensitivity syndrome: incidence, prevention and management. 1061 72

Despite limited understanding of therapeutic aetiopathogenesis of ulcerative colitis and Crohn's disease, there is a strong evidence base for the efficacy of pharmacological and biological therapies. It is equally important to recognise toxicity of the medical armamentarium for inflammatory bowel disease (IBD). Sulfasalazine consists of sulfapyridine linked to 5-aminosalicylic acid (5-ASA) via an azo bond. Common adverse effects related to sulfapyridine 'intolerance' include headache, nausea, anorexia, and malaise. Other allergic or toxic adverse effects include fever, rash, haemolytic anaemia, hepatitis, pancreatitis, paradoxical worsening of colitis, and reversible sperm abnormalities. The newer 5-ASA agents were developed to deliver the active ingredient of sulfasalazine while minimising adverse effects. Adverse effects are infrequent but may include nausea, dyspepsia and headache. Olsalazine may cause a secretory diarrhoea. Uncommon hypersensitivity reactions, including worsening of colitis, pancreatitis, pericarditis and nephritis, have also been reported. Corticosteroids are commonly prescribed for treatment of moderate to severe IBD. Despite short term efficacy, corticosteroids have numerous adverse effects that preclude their long term use. Adverse effects include acne, fluid retention, fat redistribution, hypertension, hyperglycaemia, psycho-neurological disturbances, cataracts, adrenal suppression, growth failure in children, and osteonecrosis. Newer corticosteroid preparations offer potential for targeted therapy and less corticosteroid-related adverse effects. Azathioprine and mercaptopurine are associated with pancreatitis in 3 to 15% of patients that resolves upon drug cessation. Bone marrow suppression is dose related and may be delayed. The adverse effects of methotrexate include nausea, leucopenia and, rarely, hypersensitivity pneumonia or hepatic fibrosis. Common adverse effects of cyclosporin include nephrotoxicity, hypertension, headache, gingival hyperplasia, hyperkalaemia, paresthesias, and tremors. These adverse effects usually abate with dose reduction or cessation of therapy. Seizures and opportunistic infections have also been reported. Antibacterials are commonly employed as primary therapy for Crohn's disease. Common adverse effects of metronidazole include nausea and a metallic taste. Peripheral neuropathy can occur with prolonged administration. Ciprofloxacin and other antibacterials may be beneficial in those intolerant to metronidazole. Newer immunosuppressive agents previously reserved for transplant recipients are under investigation for IBD. Tacrolimus has an adverse effect profile similar to cyclosporin, and may cause renal insufficiency. Mycophenolate mofetil, a purine synthesis inhibitor, has primarily gastrointestinal adverse effects. Biological agents targeting specific sites in the immunoinflammatory cascade are now available to treat IBD. Infliximab, a chimeric antibody targeting tumour necrosis factor-or has been well tolerated in clinical trials and early postmarketing experience. Additional trials are needed to assess long term adverse effects.
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PMID:Comparative tolerability of treatments for inflammatory bowel disease. 1108 48

A 55-year-old man presented with fever, malaise, dysarthria, and intermittent twitching of his right hand. He progressed rapidly to aphasia, intractable myoclonic seizures, and unresponsiveness. Magnetic resonance imaging (MRI) of the head demonstrated multiple nonenhancing areas of signal abnormality involving the cortex of both cerebral hemispheres. Extensive evaluation revealed no infectious cause for his symptoms. Muscle acetylcholine receptor binding and modulating antibodies, striational antibodies, and a neuronal autoantibody specific for collapsin response-mediator protein were detected. An invasive thymoma was discovered and resected. Brain biopsy revealed microglial activation, gliosis, and scant perivascular lymphocytic inflammation. His condition worsened despite treatment with anticonvulsants, intravenous corticosteroids, and antimicrobials. Plasma exchange was performed. The myoclonus stopped; he regained consciousness and gradually improved to the point that he could talk and ambulate with assistance. An MRI revealed regression of the lesions with residual cortical atrophy. This case demonstrates that paraneoplastic encephalitis may occur with thymoma and may extend to cortical regions outside the limbic system.
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PMID:Fulminant autoimmune cortical encephalitis associated with thymoma treated with plasma exchange. 1112 43

We report a case of fatal intoxication with 2% viscous lidocaine. A 18 month old infant was admitted after malaise and cardiorespiratory arrest at home. He was resuscitated, then seizures appeared before arrival at the hospital. Treatment was symptomatic, including cardiorespiratory resuscitation and administration of anticonvulsants. Identification of lidocaine and its metabolite monoethylglycinexylidide (MEGX) MEGX was performed after organic extraction by High Performance Liquid Chromatography (HPLC) with Diode Array Detection (DAD); the serum concentrations, determined by Fluorescence Polarisation Immuno Assay (FPIA), were: 1.1 micrograms/ml for lidocaine and 0.94 microgram/ml for MEGX (H + 7) and 0.30 microgram/ml for the lidocaine (Day + 1). Neurotoxic manifestations appear at lower concentrations than cardiotoxic symptoms which are correlated with plasma levels of lidocaine. The toxic symptoms begin with headache, hallucinations, seizure, coma, respiratory arrest and circulatory collapse. The toxic symptoms can persist even after the decrease of lidocaine concentration under therapeutic levels. There is no antidote and acute lidocaine toxicity is managed with supportive therapy (diazepam for seizures, intubation, chronotropic agents). Considering the gravity of these poisonings which remain rare, the 2% viscous lidocaine prescription is forbidden for children under 6 years old.
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PMID:[Fatal intoxication after accidental ingestion of viscous 2% lidocaine in a young child]. 1197 45


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