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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

11 cases of cerebral venous thrombosis in adults are reported. Main clinical signs are: intracranial hypertension (headache, nausea, papilledema in 7 cases, loss of consciousness in 6 cases, neurological deficit in 6 cases, seizure in 4 cases. 1 patient is dead, who did not receive heparin treatment. Delay before diagnosis is between 2 and 20 days, and is shortened when arteriography or MRI are available and prescribed. At least one (or several) CT examination was performed in 10 patients. Direct signs of thrombosis are uneasily detected without contrast injection, seen here in 4 cases. Empty delta sign is observed in 7 patients, lately in 4 cases, and once only afterwards. Cerebral infarction is visualized in 7 cases over 10. Its features frequently seem evocative for cerebral venous thrombosis: triangularin 4 cases or nodular shape in 3 cases with hemorragic infarct in 7 cases, with bilateral topography in 6 cases, in frontal or central areas in 7 cases. 6 patients had a MRI examination. All cerebral infarctions appeared haemorragical, even at early stages. During subacute period, venous thrombosis is constantly and easily detected by the mean of methemoglobin high signal intensity on T1 weighted images. The prediagnosis delay is short, without necessity of arteriography. MRI should take the place of CT and arteriography in investigation of a clinically suspected cerebral venous thrombosis.
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PMID:[Thrombosis of the cerebral veins. X-ray computed tomography and MRI imaging. 11 cases]. 160 50

A 42-year-old black man, a physician, presented with a three week history of intermittent right arm and leg numbness and weakness, lasting about five minutes. This was not associated with headache, visual changes, seizures, aphasia or loss of consciousness. There was no history of head trauma, migraines, or previous attacks. Positive findings on physical examination were confined to a blood pressure of 182/80; evidence of hypertensive retinopathy; normal carotid pulses without bruits; and a Grade II/VI systolic ejection murmur with normal sinus rhythm. Initial hematocrit was 25.7%; white blood cell count 14,000 cu/mm with a normal differential; platelet count 532,000 cu/mm. An electrocardiogram showed left ventricular hypertrophy. Duplex scan demonstrated normal carotid bifurcations bilaterally, and arteriogram revealed no carotid or intracranial pathology. Hemoglobin electrophoresis revealed sickle cell disease of the SS type. He was treated with transfusion therapy and has remained asymptomatic at 40 months. Approximately 20% of children with the SS type sickle cell disease will have cerebrovascular symptoms caused by small intracranial artery occlusion due to sludging of the abnormal hemoglobin. This unusual cause of transient ischemic attacks can occur in older patients of African-American ancestry and must be recognized to enable early and effective therapy with exchange transfusion.
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PMID:An unusual cause of transient ischemic attacks: case report. 187

Hyperacute intracerebral hematomas were successfully created in five cats by injecting a prepared blood sample in which the oxygen (O2) saturation ranged from 0-80%. T1- and T2-weighted spin-echo sequences and T2-weighted gradient refocused scans were obtained 2.5-10 hr after injection on a 1.5-T imaging system. Detailed histology or electron microscopy was performed on each brain to confirm the presence of intact red blood cells in a retracted clot matrix. Areas of the hematoma were hypointense relative to brain in all five cats on the gradient refocused scans. The hematoma was isointense relative to brain on the T1- and T2-weighted spin-echo scans in all cats except one, which suffered a seizure/respiratory arrest and died during the scanning procedure. Portions of the hematoma in this animal had a hypointense T2-weighted signal and a hyperintense T1-weighted signal, which corresponded to the predicted MR properties of intracellular methemoglobin. We hypothesize that acute (less than 10 hr old) hematomas that contain virtually 100% intracellular deoxyhemoglobin may not appear hypointense relative to brain on T2-weighted scan sequences at 1.5 T unless surrounding tissue hypoxia and/or anoxia promote additional changes, one of which may be the formation of intracellular methemoglobin.
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PMID:MR imaging of hyperacute intracranial hemorrhage in the cat. 250 98

Hemorrhage within the central nervous system (CNS) may be associated with subsequent development of seizure states or paralysis. Prior investigations indicate that hemoglobin, released from extravasated erythrocytes, may be toxic to the CNS by promoting peroxidation of lipids and inhibition of Na,K-ATPase. These deleterious effects are blocked both in vitro and in vivo by the Fe3+ chelator, desferrioxamine, indicating the involvement of free iron derived from hemoglobin. We now report that the Fe2+ chelator, ferene, also inhibits methemoglobin- and ferric iron-mediated CNS lipid oxidation, reflecting the reduction of Fe3+ by some component of the CNS. This reduction is apparent in the accumulation of the highly chromophoric ferene: Fe2+ chelate after the addition of Fe3+ salts to supernatants of murine brain homogenates. Because large amounts of ascorbic acid occur in mammalian CNS, we suspected that this reducing substance might be responsible. Indeed, the peroxidative effects of hemoglobin and iron on murine brain are blocked by washing of CNS membranes or by preincubation of crude homogenates with ascorbate oxidase. Furthermore, the addition of ascorbate to washed CNS membranes fully restores hemoglobin/iron-driven peroxidation. We conclude that posthemorrhagic CNS dysfunction may stem from damaging redox reactions between hemoglobin iron, ascorbic acid, and oxidizable components of the nervous system.
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PMID:Hemoglobin-mediated oxidant damage to the central nervous system requires endogenous ascorbate. 284 56

This communication reports a case of acute toxic methemoglobinemia associated with hypoxia and general motor seizures following dental anesthesia using nitrous oxide and prilocaine hydrochloride. The dosage of prilocaine hydrochloride used was 5.6% of the recognized toxic dosage associated with clinical methemoglobinemia. The patient had no demonstrable congenital tendency toward methemoglobinemia, suggesting this case may represent a previously unreported and potentially fatal reaction to prilocaine hydrochloride. The etiology of the methemoglobin production, the diagnosis of the syndrome, and the emergency treatment are discussed.
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PMID:Acute toxic methemoglobinemia following dental analgesia. 722 78

The patient first noticed general muscle stiffness at the age of 36. Two years later, she suffered from a tonic-clonic seizure which brought her to a hospital for the first time. Choreoathetoid movement, ataxia and cognitive deficit were apparent. At the age of 44, tonic-clonic seizures became more frequent and she was admitted to our hospital as being status epilepticus. After the cessation of clinical seizures, she became appllic. Gradual increase of atrophic changes in cerebrum, cerebellum and brain stem were observed by MRI and CT. Hematological study showed that she had abnormal hemoglobin, Hb Takamatsu. Four of her five children were clinically examined; all of them showed abnormal EEG findings; three being mentally retarded and had clinical generalized convulsive seizures; two had hemoglobinopathy (Hb Takamatsu). The patient died from sepsis at the age of 50 and the autopsy was carried out. The brain weighed 930 gram. Histological findings confirmed the diagnosis of dentato-rubro-pallido-luysian atrophy; neuronal loss accompanied by gliosis in dentate nuclei, red nuclei, lateral part of globus pallidus, and subthalamic nuclei. The coincidence of the hereditary traits of two independent diseases, DRPLA and familial hemoglobinopathy (Hb Takamatsu) suggests closeness of their genetic loci.
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PMID:[A familial case of DRPLA diagnosed by an autopsy associated with hemoglobinopathy (Hb Takamatsu)]. 825 33

Individuals with methemoglobin exceeding 1.5 g/dl have clinically obvious central cyanosis. Hereditary methemoglobinemia is due either to autosomal dominant M hemoglobins or to autosomal recessive enzymopenic methemoglobinemia. Four types of enzymopenic methemoglobinemia have been described. In addition to methemoglobinemia, individuals with type II, which is the generalized cytochrome b5 reductase deficiency, have severe and progressive neurological disabilities. Here we report a 3-year-old Thai boy with type II hereditary enzymopenic methemoglobinemia. He was born to a second-cousin couple. His central cyanosis was first observed around 10 months of age. His neurological abnormalities were seizures beginning at 1 year of age, microcephaly, and inability to hold his head up. His cardiovascular and pulmonary evaluations were unremarkable. Methemoglobin level by spectral absorption pattern was 18 per cent. A qualitative enzymatic assay confirmed the deficiency of the cytochrome b5 reductase enzyme. With this definite diagnosis, a prenatal diagnosis for the next child of this couple will be possible.
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PMID:A Thai boy with hereditary enzymopenic methemoglobinemia type II. 1121 70

General anaesthesia and peripheral neuronal blockade are techniques which were introduced into clinical practice at the same time. Although general anaesthesia was accepted significantly faster due to effective new drugs and apparent ease of handling, neuronal blockade has recently gained great importance. The reasons are in particular newer aids such as industrially produced catheter sets, nerve stimulators and ultrasound guidance which have facilitated that these economical techniques can be used not only for intraoperative anaesthesia but also for perioperative analgesia without any major risks for the patients. In parallel to epidural anaesthesia a change of paradigms has recently taken place using catheter instead of single-shot techniques. This allows the loading dose of the local anaesthetics to be installed in a safe way, to reload the dose when intraoperatively required and to extend the analgesia perioperatively by this technique using lower concentrations of the same drugs or drug combinations. A great number of short, middle or long acting local anaesthetics are available to choose the right drug for any particular case. Short and middle acting drugs are characterised by a faster onset compared to long acting drugs, but toxic plasma levels are seen during long time application causing seizures or drowsiness or by using prilocaine methemoglobin. Therefore long acting local anaesthetics such as bupivacaine, ropivacaine or levobupivacaine are the first choice drugs for long time application via peripheral nerve catheters for perioperative anaesthesia and analgesia. By using low concentrations of these potent drugs even for a longer period of time, no toxic plasma levels are seen with the exception of artificial intravasal injections. Additives such as opioids and alpha 2-sympathomimetics are also used. While the use of opioids is controversial, alpha 2-sympathomimetics are able to accelerate the onset and to extend the duration of regional anaesthesia and analgesia.
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PMID:[Peripheral nerve block. An overview of new developments in an old technique]. 1141 66

Resorcinol is a pharmaceutical agent used topically in dermatological treatments for acne, eczema, psoriasis and related skin conditions. Although there are a few studies that indicate chronic toxic effects of resorcinol on humans after topical application, information on the effects of resorcinol in acute poisoning after oral ingestion is limited. Thus, we wish to report the clinical and laboratory findings of a patient who was admitted to our emergency department (ED) after inadvertent oral ingestion of resorcinol and later died, as well as the patient's autopsy findings. The major clinical and laboratory findings were unconsciousness, respiratory failure that required mechanical ventilation, generalized tonic-clonic seizures, leukocytosis and severe metabolic acidosis. In the blood sample taken at the autopsy, a high level of methemoglobin was found. In the serum, resorcinol was revealed by gas chromatography-mass spectrometry. It can be concluded that the basic approach to patients with resorcinol poisoning should include initial stabilization of the patient by supporting the airway, respiration and circulation, and treating complications such as seizures or metabolic acidosis in the ED, as soon as possible after oral ingestion.
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PMID:A case report of fatal oral ingestion of resorcinol. 1719 97

Cyanide causes intracellular hypoxia by reversibly binding to mitochondrial cytochrome oxidase a(3). Signs and symptoms of cyanide poisoning usually occur less than 1 minute after inhalation and within a few minutes after ingestion. Early manifestations include anxiety, headache, giddiness, inability to focus the eyes, and mydriasis. As hypoxia progresses, progressively lower levels of consciousness, seizures, and coma can occur. Skin may look normal or slightly ashen, and arterial oxygen saturation may be normal. Early respiratory signs include transient rapid and deep respirations. As poisoning progresses, hemodynamic status may become unstable. The key treatment is early administration of 1 of the 2 antidotes currently available in the United States: the well-known cyanide antidote kit and hydroxocobalamin. Hydroxocobalamin detoxifies cyanide by binding with it to form the renally excreted, non-toxic cyanocobalamin. Because it binds with cyanide without forming methemoglobin, hydroxocobalamin can be used to treat patients without compromising the oxygen-carrying capacity of hemoglobin.
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PMID:A review of acute cyanide poisoning with a treatment update. 2128 66


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