Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 83 year-old woman with dementia. She was apparently well until December of 1993 when she was 81-year-old. At that time, she was operated or her cataract. Her post operative course was uneventful, however, shortly after her operation, she had an onset of memory loss and abnormal behavior. She showed a fluctuating course in her mental disturbance. In 1995, her dementia worsened with nocturnal agitation. She was admitted to our service on June 12, 1995. She was alert and her blood pressure was 140/100 mmHg. She showed recent memory loss and disorientation to time. Motor wise, she was unable to stand unsupported. Her gait with support showed small steps and a wide base. She was bradykinetic and ataxic in her finger-to-nose and heel-to-knee test, however, no rigidity or tremor was noted. Her MRI showed T2-high signal lesions in both medial thalamic areas, in the right occipital lobe, and in the bilateral cerebral white matters as well as in the basal ganglia. She was discharged for out-patient follow up on July 3, 1995. Four days after the discharge, she showed declining responses to stimuli and she developed dyspnea on July 14, 1995. She was admitted again on the same day. Her body temperature was 38.5 degrees C and moist rales were heard in the left lung field. She appeared drowsy and no verbal response was obtained; no apparent motor palsy was noted. Blood count showed leukocytosis (14,300/ml). Blood gas analysis under 61 of oxygen inhalation through a mask was as follows: pH 7.460, PCO2 39.6 mmHg, PO2 67 mmHg, and HCO3-28.5 mEq/l. Two days after admission, she developed a convulsion in her left arm and she became unconscious. Her EEG showed periodically recurring lateralized epileptic discharges on the right fronto-central areas. Her subsequent course was complicated by status epilepticus and respiratory distress. She died on July 26, 1995. She was discussed in a neurological CPC. The chief discussant arrived at a conclusion that she suffered from multi-infarct dementia. Bilateral thalamic infarctions were considered to have played a significant role in her dementia. Post-mortem examination revealed subcortical leukoencephalopathy of Binswanger's type and cerebral infarctions in the thalamic and basal ganglia regions and in the right occipital lobe. In addition, she showed isolated angitis of the central nervous system involving mainly in the small arteries located in the superficial areas of the brain and the spinal cord. This patient was interesting in that despite relatively mild leukoaraiosis in MRI, post-mortem examination revealed profound pathologic changes in the subcortical white matters. In addition, she showed the isolated angitis of the CNS. The cause and the clinical correlates of her angitis were unclear.
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PMID:[A 83 year-old woman with dementia, gait disturbance, and convulsion]. 904 33

Although midazolam has been proposed for the treatment of a variety of conditions such as anxiety, dyspnoea, hiccups and status epilepticus, terminal agitation is the only condition where its use is based on a reasonably large number of published clinical studies. A causal approach is generally recommended. Whenever possible, the aetiological condition (pain, fever, constipation, etc.) should be corrected. Such general measures as ensuring a peaceful, familiar environment, and the use of a night light, fluid therapy to counteract dehydration, and antipyretics for fever are beneficial. When symptomatic treatment is needed, drugs with little anticholinergic effect are to be recommended. The use of benzodiazepines as single drug treatment may exacerbate the condition. Haloperidol or risperidone (which has fewer side effects) are recommended. If the agitation is marked, a common strategy is to add lorazepam. Chlormethiazole is an alternative. Subcutaneous midazolam should be reserved for refractory cases. Attention should be paid to dosage, reduced doses being given to the elderly, patients on opioid medication, and patients with impaired liver or renal function. Overdosage may induce deep sedation, and result in carbon dioxide retention and subsequently heart failure and pulmonary oedema which may be fatal.
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PMID:[Midazolam (Dormicum) in terminal anxiety and agitation. The last choice alternative in palliative care]. 1035 70

In a patient, admitted for cerebral stroke with right side hemiparesis, an acute episode of dyspnea has developed 6 hours after admission. Based on a finding of fine rales on auscultation and a chest radiogram showing congestion, a diagnosis of pulmonary edema was made. The electrocardiogram and cardiac enzymes were normal. Other routine precipitating factors were excluded, and the acute left heart failure was ascribed to the patient's stroke. Neurogenic pulmonary edema may be a result of a vast range of neurological lesions or conditions, including status epilepticus, head trauma, subdural and subarachnoid hemorrhage, brain tumors, meningitis, multiple sclerosis and ischemic stroke. This condition is probably mediated by the sympathetic system outflow, leading eventually to an increase of left atrial pressure, or to an increase in pulmonary vessel permeability. It is treated conventionally, with diuretics and after-load reduction.
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PMID:[Neurogenic pulmonary edema]. 1835 78

The vagus nerve stimulator has become a standard modality for intractable pediatric epilepsy. We reviewed our experience with major adverse events, after accidental puncture of a stimulator wire by an emergency room physician seeking intravenous access to treat status epilepticus. The Children's National Medical Center database was reviewed for patients undergoing vagus nerve stimulator placement between January 1988 and June 2006. Patient characteristics, duration of therapy, and treatment-limiting adverse events were noted. Of 62 patients implanted over 8 years, 22 (35%) had adverse events which led to a change in therapy. Adverse events included prominent drooling, coughing, throat discomfort, dysphagia, wound infection, difficulty breathing, vomiting, vocal-cord weakness, lead failure, and iatrogenic (piercing of wire; surgical clipping of wire during revision). Eight patients required nonroutine surgical intervention (13%). There were two unusual case presentations. In a 13-year-old boy with status epilepticus at an outlying emergency department, the stimulator line was pierced in search of intravenous access. In a 25-year-old housepainter, neck paresthesias upon right lateral neck turning were attributed to insufficient strain relief. Treatment-limiting adverse events occurred in approximately one-third of patients. Unanticipated adverse events included misidentification of the wire for intravenous access, clipping of the wire during surgical dissection, and cervical dysesthesias associated with head-turning.
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PMID:Misidentification of vagus nerve stimulator for intravenous access and other major adverse events. 1835 2

Takotsubo cardiomyopathy is characterized by chest pain, dyspnea, electrocardiographic changes resembling an acute coronary syndrome, and transient wall-motion abnormalities without identifiable coronary culprit lesion explaining the wall-motion abnormality. Takotsubo cardiomyopathy occurs frequently after emotional or physical stress. Seizures have been reported as triggers of takotsubo cardiomyopathy. It is unknown if seizure-associated takotsubo cardiomyopathy differs from takotsubo cardiomyopathy associated with other triggers. Seizure-associated takotsubo cardiomyopathy cases from the literature were compared with takotsubo cardiomyopathy series comprising 30 or more patients. Thirty-six seizure-associated takotsubo cardiomyopathy cases (6 male, mean-age 61.5 years) were found. Seizure-type were tonic-clonic (n = 13), generalized (n = 5), status epilepticus (n = 6), grand mal (n = 2), or not reported (n = 13). Twelve patients had a history of epilepsy, in 15 patients takotsubo cardiomyopathy-associated seizure was the first or the information was not given (n = 9). In 17 patients takotsubo cardiomyopathy occurred immediately after the seizure, in 9 patients 1-72 h postictally, and in 10 patients, the interval was not reported. In 20 patients neurologic disorders were reported and in 14 psychiatric disorders were reported. There were medical comorbidities in 17 patients, arterial hypertension (n = 11), hyponatremia (n = 2), and cancer (n = 2). Compared with 974 patients reported in takotsubo cardiomyopathy -series, patients with seizure-associated takotsubo cardiomyopathy were younger (61.5 vs. 68.5 years, p < 0.0001), more frequently males (17 vs. 9%, p = 0.004), had less frequent chest pain (6 vs.76%, p < 0.005), more frequent cardiogenic shock (25 vs. 8%, p = 0.003), and more frequent recurrency (14 vs. 3%, p = 0.004). Seizure-associated takotsubo cardiomyopathy manifests frequently as sudden hemodynamic deterioration, which could result in death in the absence of adequate help. Probably some cases of sudden unexpected death in epilepsy are attributable to takotsubo cardiomyopathy.
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PMID:Seizure-associated Takotsubo cardiomyopathy. 2177 30

An Afro-Caribbean woman presented with worsening breathlessness, weight loss, lethargy and fevers, developing a bilateral florid erythematous rash on her legs. She was recently diagnosed with rheumatoid arthritis and bilateral hilar lymphadenopathy was found on thoracic CT imaging. She was tachycardic and investigations revealed pancytopenia, eosinophilia, raised serum ACE, acute kidney injury and deranged liver function tests. Biopsy of the lymphadenopathy revealed mixed lymphoid cells and liver biopsy revealed extramedullary haematopoiesis, with hypercellular marrow found on bone marrow biopsy. Cardiac MRI was normal, excluding cardiac sarcoid. The patient developed status epilepticus and phenytoin was started. She subsequently developed skin desquamation, in keeping with toxic epidermal necrosis. Skin biopsies revealed atypical granulomas and multinucleated giant cells, which subsequently resolved on steroid treatment. This case highlights an overlap syndrome, with an unclear diagnosis between sarcoidosis, drug reaction or rash with eosinophilia and systemic symptoms and/or hypereosinophilic syndrome and Still's disease. Hence varied serological and clinical features can complicate the distinction between diagnoses.
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PMID:Is this still just sarcoidosis, or should we a-DRESS a different diagnosis? 2612 53

We report an atypical case of anti-N-methyl-D-aspartate receptor encephalitis (ANMDARE). A 27-year-old man diagnosed with ANMDARE received immunotherapy and had a good recovery. However, within one month, he developed severe status epilepticus and decreased level of conscience with new hyperpyrexia and dyspnea, and was admitted to the emergency intensive care unit. Acinetobacter baumanii were found in the sputum culture; and anti-NMDAR antibodies were positive (titer: 1/80) in the cerebrospinal fluid. Repeated immunotherapy was administered with antibacterial agents, and the patient recovered except for mild psychiatric sequelae. This is the first report of ANMDARE that aggravates after acinetobacter baumannii pneumonia. Awareness and knowledge of this disorder should be extended, especially in the emergency medicine community.
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PMID:Anti-N-methyl-D-aspartate receptor encephalitis that aggravates after acinetobacter baumannii pneumonia: A case report. 2902 36

Takotsubo cardiomyopathy (TC) is acute stress-induced cardiomyopathy with characteristic transient wall motion abnormalities. TC has a clinical presentation similar to an acute coronary syndrome, including chest pain or dyspnoea, ECG changes and elevated cardiac enzymes. TC often occurs after emotional stress. There are approximately 50 TC cases reported related to seizure activity, and our review revealed 15 articles which were associated with status epilepticus. This condition can be a serious complication of seizures. We report a case of TC after status epilepticus in a patient who had been seizure-free for 20 years.
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PMID:Takotsubo cardiomyopathy triggered by status epilepticus: case report and literature review. 3070 Apr 51