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Neurogenic pulmonary edema (NPE) can result from various central nervous system disorders such as brain malignancies, traumatic brain injuries, infections, and seizures. Although the pathogenesis is not completely understood, NPE creates an increase in pulmonary interstitial and alveolar fluid. It
Neurogenic pulmonary edema (NPE) is a clinical entity that can occur following central nervous system disorders. However, NPE occurs quite rarely in early childhood, and there has only been one report about pediatric NPE associated with febrile seizures. Two cases are reported here. One case
Intraparenchymal schwannomas of the brain are very rare, accounting for < 1% of intracranial schwannomas. We present a case of an 11-year-old boy with a left frontotemporal lobe schwannoma presented with seizure and neurogenic pulmonary edema. To our knowledge, this is the first case of
Acute pulmonary edema is one of the frequent causes of dyspnea encountered in everyday practice. It is broadly attributed to be either cardiogenic or noncardiogenic. It is usually treated with diuretics in addition to other medications depending on the underlying pathology. Here, we report a case of
Hyperbaric oxygen therapy (HBOT) for carbon monoxide (CO) poisoning is widely performed to prevent delayed neuropsychiatric syndrome. Although HBOT can generally be performed with safety, the appropriate management of HBOT still remains unestablished. A 31-year-old man was transferred to our
Data on the frequency and clinical relevance of neurogenic pulmonary edema (NPE) following epileptic seizures are limited. The aim of the present study was to analyze computed tomography (CT) examinations in patients with previous seizures.Incidence of NPE A case of neurogenic pulmonary edema following a grand mal epileptic seizure is presented. This condition is rather rare and the exact pathophysiology remains unknown, but it is believed that the event may be related to transitional increase of intracranial pressure during seizure attack. Pulmonary
Neurogenic pulmonary oedema (NPE) is avery rare complication of epileptic seizures, which could potentially increase mortality.The case of a66-year-old male patient with NPE caused by repeated epileptic seizures is reported. Rapid resolution of pulmonary We report a case of neurogenic pulmonary edema associated with epileptic seizure. A 36-year-old woman had had several episodes of fainting and postictal respiratory failure, and since July 1998 had been admitted to a nearby hospital three times. On October 12, 1999, she was again admitted to a
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
Cerebral partial pressure of O2 (PO2), relative changes in the ratio of reduced/oxidized cytochrome aa3, blood flow, and the arteriovenous difference in O2 content were measured during seizures with and without pulmonary edema. Seizures were induced with bicuculline (0.2-1.2 mg/kg iv) in rats
OBJECTIVE
Postictal pulmonary edema (PPE) is almost invariably present in human and animal cases of sudden unexpected death in epilepsy (SUDEP) coming to autopsy. PPE may be a contributing factor in SUDEP. The incidence of postictal PPE is unknown. We retrospectively investigated PPE following
We report a case of severe intoxication with extended-release verapamil. In addition to cardiovascular toxicities with hypotension, atrioventricular block and bradycardia, the patient suffered from grand-mal seizure and pulmonary edema 13 and 48 hours respectively, after ingestion of 4.8 g of
To examine whether pulmonary dysfunction leads to episodes of cerebral hypoxia during recurrent seizures, measurements were made of arterial blood pressure, blood-gases, cerebral pO2, and relative changes in cytochrome a,a3 redox levels in anesthetized, paralyzed rats. Seizures were induced serially
We report a seizure-related death in a patient with juvenile myoclonic epilepsy 3 months following a previous generalised tonic-clonic seizure complicated by pulmonary oedema. Seizure-related pulmonary oedema is rare but may indicate an increased susceptibility to epilepsy related death. We consider