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)

We prospectively studied 19 children with severe hypertension to evaluate the spectrum of radiological changes, severity and reversibility of this entity. All of them were subjected to clinical and biochemical evaluation, followed by magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA). Headache was seen in 17 children, 13 had confusion and drowsiness, 12 had nausea and vomiting, 10 patients had visual disturbances, seizure and dyspnoea. Only two had focal neurological deficit (one with right facial palsy and another with right lateral rectus palsy). Of these 19 children, 15 patients had hypertensive retinopathy and four had normal fundi. The positive MRI findings in 17/19 patients were: bilateral leukoencephalopathic changes in occipitoparietal region (9/17), diffuse white/grey matter lesion (3/17) patients, brain stem hyperintensity (2/17) and haemorrhagic lesions (3/17). On MRA, 12/19 patients had attenuation of cerebral arteries of different degree. On follow up, MRI findings resolved in all except three patients. All patients had normal MRA on follow up, except one with persistent minimal attenuation of middle cerebral artery and another had spasm in anterior, middle and posterior cerebral arteries. The intracranial abnormalities in these patients with severe hypertension were reversible in many of the cases after control of blood pressure was achieved. We therefore conclude that severe hypertension may lead to leuoencephalopathy, which had a wide radiological spectrum. A better understanding of this complex syndrome may obviate unnecessary investigations and allow management of associated problems in prompt and appropriate ways.
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PMID:Spectrum of radiological changes in hypertensive children with reversible posterior leucoencephalopathy. 1739 98

Schistosomiasis is a parasitic disease caused by blood flukes of the genus Schistosoma. Currently more than 200 million people worldwide are affected. Neuroschistosomiasis constitutes a severe presentation of the disease. Neurological symptoms result from the inflammatory response of the host to egg deposition in the brain and spinal cord. Neurological complications of cerebral schistosomiasis include delirium, loss of consciousness, seizures, dysphasia, visual field impairment, focal motor deficits and ataxia. Cerebral and cerebellar tumour-like neuroschistosomiasis can present with increased intracranial pressure, headache, nausea and vomiting, and seizures. Myelopathy (acute transverse myelitis and subacute myeloradiculopathy) is the most common neurological complication of Schistosoma mansoni infection. Schistosomal myelopathy tends to occur early after infection and is more likely to be symptomatic than cerebral schistosomiasis. The conus medullaris and cauda equina are the most common sites of involvement. Severe schistosomal myelopathy can provoke a complete flaccid paraplegia with areflexia, sphincter dysfunction and sensory disturbances. Schistosomicidal drugs, steroids and surgery are the currently available treatments for neuroschistosomiasis. Rehabilitation and multidisciplinary team care are needed in severely disabled patients.
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PMID:Neurological complications of Schistosoma infection. 1790 71

Leptomeningeal carcinomatosis occurs in approximately 5% of patients with cancer. The most common cancers involving the leptomeninges are breast, lung cancer and melanoma. However, gastric adenocarcinoma has been rarely reported with leptomeningeal carcinomatosis. The presenting manifestations are usually headache, visual disturbances and seizures. We report a case of leptomeningeal metastasis that presented as a gastric cancer. A 49-year-old woman was admitted to our hospital with the symptoms of headache and melena for 10 days. The endoscopy showed a thickening of the folds of the stomach compatible with the diagnosis of a Borrman type IV gastric cancer. The biopsy revealed a signet ring cell carcinoma. The MRI of brain showed no abnormal findings; however, the patient complained of an intractable persistent headache, nausea and vomiting on admission day 6. The cytology examination of the cerebrospinal fluid supported the diagnosis of metastatic signet ring cell carcinoma.
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PMID:A case of gastric adenocarcinoma presenting as meningeal carcinomatosis. 1830 94

The article describes the case history of posterior leukoencephalopathy syndrome - a brain disorder that predominantly affects the cerebral white matter. Edematous lesions involve the posterior parietal and occipital lobes, and may spread to basal ganglia, brain stem and cerebellum. This rapidly evolving neurological condition is clinically characterized by headache, nausea and vomiting, seizures, visual disturbances and altered sensorial functions, and occasionally focal neurological deficit. Posterior leukoencephalopathy syndrome is often associated with an abrupt increase in blood pressure and is usually seen in patients with eclampsia, renal disease and hypertensive encephalopathy. It is also seen in the patients treated with cytotoxic and immunosuppressive drugs such as cyclosporine A, tacrolimus /FK-506, cisplatin, cytarabine, IVIg, erytrophoietin, and interferon alpha. The study demonstrated that lesions of posterior leukoencephalopathy syndrome are best visualized with magnetic resonance [MR] imaging. T2 weighted MR Images, at the height of symptoms, characteristically show diffuse hyper intensity selectively involving the parieto - occipital white matter. Occasionally the lesions also involve the grey matter. Computed tomography can also be used satisfactorily to detect hypodense lesions of posterior leukoencephalopathy. Early recognition of this condition is of paramount importance because prompt control of blood pressure, withdrawal of immunosuppressive agents will cause reversal of the syndrome. Delay in the diagnosis and treatment can result in permanent damage to affected brain tissues. The clinical data and radiological findings depicted in the study add to the investigation of the disorder.
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PMID:[Clinical report of posterior leukoencephalopathy syndrome]. 1832 87

We conducted a single institution phase II trial to evaluate the tolerability and effectiveness of therapy with arsenic trioxide (ATO) and ascorbic acid (AA) with temozolomide (TMZ) in patients with advanced melanoma. Planned enrollment was for 40 patients. Eligible patients were required to have metastatic melanoma with or without brain metastases, an ECOG performance status of 0-2, and adequate organ function. The primary endpoints were overall response rate and degree of grade 4 toxicity. ATO was administered as a loading dose at 0.25 mg/kg/day for 5 days during week 0, and then twice weekly at 0.35 mg/kg during an 8-week cycle. Each infusion of ATO was followed by an infusion of 1000 mg of AA. TMZ was given at the standard dose of 200 mg/m for 5 days during weeks 1 and 5 of each cycle. Eleven patients were enrolled with 10 evaluable for response, five with central nervous system disease. No responses were seen among the first 10 patients and on the basis of a predetermined stopping rule, the trial was terminated. Common grade 1 and 2 side effects included nausea and vomiting (10), fatigue (six), edema (six), rash (six), and elevated AST or ALT (six). Grade 3 and 4 side effects included nausea and vomiting (three), elevated AST or ALT (two), seizure (one), and renal failure (one). This is the first trial combining ATO with chemotherapy in a solid tumor. ATO and AA were administered in the outpatient setting with TMZ in 11 patients with an acceptable side effect profile. No responses were seen in the first 10 evaluable patients leading to early closure of the study. Further studies using ATO and AA with TMZ with this dosing schedule in advanced melanoma are not warranted.
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PMID:Phase II trial of arsenic trioxide and ascorbic acid with temozolomide in patients with metastatic melanoma with or without central nervous system metastases. 1833 52

Opioids have been used for analgesia in nearly all civilizations. In paediatrics their use has become widely accepted for combating severe pain, especially postoperative pain and tumour pain. Receptors in the central nervous system are the best known sites of action of opioids, but the existence of peripheral receptors is also probable. The action depends on whether the opioid is more agonist or antagonist and on the peculiarities of physiology in childhood: in the small child a hyperdynamic blood circulation makes resorption faster, and in newborn and premature infants distribution and excretion are influenced by the different composition of the body and the immaturity of liver and kidney. The best known opioid is morphine, and it is the reference substance with which all other opioids are compared. Fentanyl has been used even for the smallest ventilated prematures in recent times, as it is easy to manage and has an early onset of action. Its depressant action on the respiratory centre is an advantage when attempts of spontaneous breathing make mechanical ventilation difficult. Obstinate constipation is the disadvantage of both morphine and fentanyl, and an exacerbation of hyperbilirubinaemia has been seen with fentanyl. Nalbuphine causes a lower degree of respiratory depression. The newer opioids alfentanil and sufentanil have already been used for the relief of paediatric postoperative pain and during mechanical ventilation, but no special advantages of their use are reported. Meperidine has been favoured especially for postoperative pain, although it appears to have no advantages over morphine. Its active metabolite normeperidine may accumulate and cause seizures; meperidine should not be used in prematures or in children with renal dysfunction. There are few publications on the use of piritramide in paediatric pain. Tramadol is widely used for emergencies, as it has the least sedative action; but it has disadvantages in causing nausea and vomiting. Codeine is widely used for its antitussive action. While the necessity of good analgesia for even the smallest infant cannot be overstated, the opioid used must be carefully selected with reference to the age of the child and the pain to be controlled.
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PMID:[Analgesia with opioids in the paediatric patient.]. 1841 33

To avoid the neurological deficits after neurosurgical procedures, awake craniotomy applying intraoperative awake functional brain mapping has been employed. Anesthesia for awake craniotomy requires particular attention to airway management, control of seizures and measures for decreasing the anxiety of the patients. We investigated the current status of anesthetic management for awake craniotomy in Japan to establish a standard procedure for safe anesthesia. A questionnaire was sent to 80 universities with departments of anesthesia in Japan and 34 (43%) responded. In 19 institutes, awake craniotomies are being practiced. The first experience of awake craniotomy was in 1996 in Japan and since then most of the institutes have experienced only three or fewer cases. Airway management, control of nausea and vomiting, stable awakening during functional mapping and control of seizures were pointed out as problems during awake craniotomy. Based on the present results, our experience and the information from previous investigations, standard anesthetic management for awake craniotomy in our country will be documented.
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PMID:[Present state of anesthetic management for awake craniotomy in Japan]. 1841 13

Ictal vomiting is a rare manifestation most often associated with right temporal lobe epilepsy. The implication of the anterior insula in the occurrence of this symptom has been suggested based on the role of this region in swallowing and on the observation that electrical insular stimulation can elicit nausea and vomiting. We report the first case, to our knowledge, of a patient presenting with ictal vomiting who underwent bilateral intracranial exploration including insular depth electrodes. The seizure onset zone was localized in the left temporomesial structures, but the occurrence of ictal vomiting correlated in time with a discharge affecting exclusively the anterior part of both insular lobes. It is concluded that the occurrence of ictal vomiting reflects a propagation of the discharge to the insular cortex. Observation of this symptom at the very onset of the seizures in a patient with temporal lobe epilepsy is highly suggestive of an insular seizure onset zone.
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PMID:The role of the anterior insular cortex in ictal vomiting: a stereotactic electroencephalography study. 1862 92

A 15-year-old man presenting with cortical blindness as the initial symptom of mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) is reported. He showed fluctuating consciousness and severe occipital headache with nausea and vomiting. T2 and diffusion-weighted magnetic resonance imaging showed high signal intensity in the occipital lobes. Electroencephalography showed diffuse sharp waves with focal epileptic discharges over the posterior region. The nature of stroke-like episodes and seizure mechanisms is unexplained in MELAS. Consequently, the possible mechanisms of the cortical blindness in this case are discussed.
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PMID:Acute blindness. 1895 27

Lacosamide is an antiepileptic drug approved in the USA and Europe as adjunctive therapy for partial-onset seizures. Studies suggest that lacosamide selectively enhances slow inactivation of voltage-gated sodium channels and possibly interacts with collapsin response mediator protein-2. The efficacy of lacosamide has been shown in animal models of epilepsy and Phase II/III clinical trials. Pharmacokinetic studies show that it is renally excreted, minimally bound to plasma proteins and has no known clinically relevant drug-drug interactions. Clinical trials show that lacosamide is well tolerated; the most common adverse events were dizziness, nausea and vomiting. In a Phase II/III pooled analysis, lacosamide 200 and 400 mg/day significantly reduced partial-onset seizure frequency and improved the 50% responder rate compared with placebo.
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PMID:Lacosamide: pharmacology, mechanisms of action and pooled efficacy and safety data in partial-onset seizures. 1910 66


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