Cases reported "Epilepsy, Tonic-Clonic"

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1/14. Neurogenic pulmonary oedema after generalized epileptic seizure.

    The diagnosis 'tonic clonic seizure' is frequently established by emergency physicians on scene. In patients with epilepsy mortality due to accidents, asphyxia, cardiac arrhythmias or postictal neurogenic pulmonary oedema (NPO) is twice as high as in the general population. We report a case of acute pulmonary oedema after a tonic clonic seizure. Following this event, the patient developed respiratory insufficiency and evidence of pulmonary oedema not associated with the classic aetiologies of congestive heart failure, aspiration or toxic exposure. The patient survived the incident after aggressive prehospital treatment, long-term intensive care and subsequent rehabilitation. A systematic case analysis and an introduction to the pathophysiology of NPO are presented. We recommend a positive approach to the management of NPO consisting primarily of interventions to stabilize vital functions, decrease intracranial pressure and normalize vegetative dysregulation. Emergency physicians need to consider the possibility of NPO in all cases of pulmonary oedema of unknown origin.
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2/14. Acute pancreatic damage associated with convulsive status epilepticus: a report of three cases.

    Three cases involving a previously unreported association of acute pancreatic damage following convulsive status epilepticus (SE) are presented. A review of literature failed to reveal a similar association between SE and acute pancreatic damage. As possible pathophysiological mechanisms of this so far unknown sequel of SE, increased intraduodenal pressure during SE leading to the reflux of the duodenal contents into the pancreatic duct, along with altered metabolism of oxygen-derived free radicals during a prolonged seizure with hypoxia and ischemia resulting in acinar cell injury are suggested. We believe that SE should be considered as an additional risk factor of acute pancreatitis and that pancreatic enzymes should be monitored in patients who have prolonged seizures.
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3/14. Delayed asystolic cardiac arrest after diltiazem overdose; resuscitation with high dose intravenous calcium.

    A 51 year old man took a mixed overdose including 1.8-3.6 g of diltiazem, paracetamol, aspirin, isosorbide nitrate, and alcohol. He initially presented to hospital after six hours with mild hypotension and was treated with activated charcoal and intravenous fluids. Eighteen hours after the overdose he had two generalised tonic-clonic seizures. The patient remained unresponsive with junctional bradycardia, unrecordable blood pressure, and then became asystolic. He was resuscitated with high dose (13.5 g) intravenous calcium and adrenaline (epinephrine). He required inotropic support and temporary pacing over the next 48 hours. This case suggests there is a role for aggressive high dose intravenous calcium therapy in severe diltiazem overdose, particularly with the onset of asystole. It should be considered early in cases of cardiac arrest after diltiazem overdose. The case also highlights the problems with delayed toxicity when whole bowel irrigation is not administered.
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4/14. Late postpartum eclampsia coincident with postdural puncture headache: a case report.

    Preeclampsia developed in this patient 4 days' postpartum. Visual changes, headache, and elevated blood pressures were present on arrival to the emergency department. Coincident with the preeclampsia was a postdural puncture headache complicating the diagnosis of late postpartum preeclampsia. pregnancy-induced hypertension laboratory values were normal, and relief of the postdural headache and visual disturbances was obtained after placement of an epidural blood patch. Blood pressures continued to increase, however, and late postpartum eclampsia developed. We conclude that symptoms of a postdural puncture headache can mimic those of postpartum preeclampsia. Early recognition and treatment of postpartum preeclampsia may decrease patient mortality and morbidity by preventing late postpartum eclampsia.
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5/14. Progressive neurological decline after partial spontaneous thrombosis of a Spetzler-Martin Grade 5 arteriovenous malformation in a patient with Leiden factor v mutation: management and outcome.

    The coexistence of a large intracranial arteriovenous malformation (AVM) and a hypercoagulation disorder is rare. The AVM puts the patient at risk for progressive neurological deficit, seizures, and, most importantly, intracranial hemorrhage The hypercoagulation disorder may result in an increased risk of stroke. The authors describe a 42-year-old man with a Spetzler-Martin Grade 5 AVM who experienced progressive neurological decline. He was subsequently discovered to have partial thrombosis of the AVM, deep cerebral and cortical venous thrombosis, and a hypercoagulation disorder. Hypercoagulation disorders causing neurological deficits are usually treated with anticoagulant medications; however, this approach was not thought to be safe in the presence of a large AVM. Therefore, the AVM nidus was surgically extirpated and a ventriculoperitoneal shunt was placed to treat the increased intracranial pressure caused by the cortical and deep cerebral venous thrombosis. Subsequently, lifelong oral anticoagulation was prescribed. The patient had a progressive neurological recovery and is now living independently at home. The occurrence of partial or complete spontaneous thrombosis of an AVM nidus should raise the possibility of an underlying hypercoagulation disorder.
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6/14. Alveolar soft-part sarcoma presenting with multiple intracranial metastases.

    A 28-year-old man presented with history of raised intracranial pressure and one episode of generalized tonic clonic seizures. Computed Tomogram revealed multiple contrast enhancing intracranial lesions. biopsy of one of the lesions was reported as metastatic alveolar soft part sarcoma. He was advised whole brain radiotherapy.
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7/14. Responsiveness to phenobarbital in an adult with Crigler-Najjar disease associated with neurological involvement and skin hyperextensibility.

    We present the case of a 23-yr-old man who had had since birth marked and sustained unconjugated non-hemolytic hyperbilirubinemia and who had had several attacks of grand mal seizures. Analysis of serum bilirubin by diazoreactive methods showed serum levels of unconjugated bilirubin as high as 445 mumol/L that were not affected by phenobarbital administration. However, analysis of serum bile pigments by high-pressure liquid chromatography demonstrated marked decrease of unconjugated bilirubin after phenobarbital treatment (from 432.4 mumol/L to 291.0 mumol/L) associated with slight increase of bilirubin monoconjugates and disconjugates (from 0.25 mumol/L to 0.42 mumol/L). Furthermore, in the past few years the patient had exhibited striking skin hyperextensibility and diaphragm eventration. This case confirms that alkaline methanolysis-high-pressure liquid chromatography is the most reliable method for assessment of serum fraction bilirubin levels; that clinical parameters such as neurological signs do not unequivocally discriminate between type I and II Crigler-Najjar disease and that response to phenobarbital treatment remains the main diagnostic tool.
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8/14. Cranial vault and gigantic intracranial hydatid cyst in a young woman.

    The case of a young woman (20 years) with a gigantic intracranial hydatid cyst (110 x 90 x 65 mm) is presented. The first manifestation was a grand mal seizure followed by symptoms of raised intracranial pressure. The origin of the cyst was in the diploe of the right cheek, frontal, temporal, and parietal bones. An osteoplastic craniotomy was performed, and more than 100 fertile daughter cysts were removed, together with the wall of the cyst. A modification in the standard operative procedure is proposed for gigantic cysts that emerge from the diploe of the cranial vault and extend intracranially. Therapy with dexamethasone and phenobarbital was instituted preoperatively and continued postoperatively. The 3-month follow-up showed no relapse.
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9/14. Encephalopathy in renovascular hypertension associated with the use of oral contraceptives.

    Two female patients aged 19 years and 27 years presented with hypertensive encephalopathy and were subsequently found to have renal artery stenosis due to fibromuscular dysplasia. Both patients had had normal blood pressures recorded within the previous 6 months whilst taking the oral contraceptive pill. Their neurological state returned to normal with hypertensive control and in one case the hypertension was cured by dilatation of the renal artery stenosis by balloon angioplasty.
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10/14. Case report: Recurrent postictal pulmonary edema.

    A 32-year-old man with a long history of grand mal seizures but otherwise good health had recurrent episodes of postictal pulmonary edema when he failed to take anticonvulsant medication regularly. This case illustrates most of the features observed in other reported cases of postictal pulmonary edema. Symptoms include dyspnea and cough with production of various quantities of mucoid fluid that may be copious and frankly hemorrhagic. blood pressure is normal, and temperature may be normal also but is frequently elevated to 100 or 101 F. No cardiac irregularities are heard on auscultation, and the ECG is often normal, but a wide range of abnormalities may be seen. Considerable arterial hypoxemia may occur, and leukocytosis (11,000 to 14,000 cells per cubic millimeter) is common. Rales and rhonchi are audible, and chest films often show bilateral upper and middle lobe infiltrates. The patient is usually clinically improved within 24 hours and the pulmonary edema completely cleared in three to five days.
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