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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rhinocerebral mucormycosis is a rare and fatal deep fungus infection occurring in debilitated patients. Its reports have been recently increased because of the increase of such conditions as uncontrolled diabetics, leukemia, and cancer. A 60-year-old male suffering from continuous headache and fever was diagnosed as meningitis, and repeated culture of cerebrospinal fluid was negative. Antibiotic therapy was ineffective. CT scan revealed brain abscess in the right frontal lobe and bone defect over the right posterior ethmoidal sinuses. Both maxillary and ethmoidal sinuses were operated on 38 years ago. The patient was suspected to have rhinologic brain abscess. We intended to remove the source of infection in the right posterior ethmoidal sinuses beneath the base of the skull and to repair the defect of dura mater. The operation was tried on the 6th hospital day. There was a cyst in the posterior ethmoidal sinuses and an intact denuded dura mater over the cyst. The causative organism was not detected by smear test, bacteriological and fungal culture. He relapsed into lethargy, and died on the 21st hospital day due to the vast cerebral infarction. Autopsy revealed rhinocerebral mucormycosis. The literature on this disease was also reviewed and discussed.
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PMID:[Phinocerebral mucormycosis--report of a case]. 229 52

To determine whether treatment with hyperbaric oxygen (HBO) or dimethyl sulfoxide (DMSO) could mitigate the fatal effects of cerebral ischemia, we anesthetized 68 gerbils with ketamine, ligated the right carotid artery (CA), and placed a snare occluder around the left CA. After 48 hours, 30 gerbils that were neurologically normal or had suffered only mild deficits were subjected to left CA occlusion without anesthesia for periods of 2 to 60 minutes. The onset of circling, posturing, falling, and lethargy began immediately; seizures and coma ensued 4 to 5 minutes later and persisted until release of the left CA occluder. All gerbils recovered after 2-minute staged bilateral CA occlusions. The mortality rate was 33% after both 5- and 10-minute occlusions and 100% after 20- and 60-minute bilateral occlusions. Twelve gerbils were placed in an HBO chamber (100% oxygen at 1.5 atmospheres) for 15 minutes during 20-minute bilateral occlusion; only 2 died (16% mortality rate). Thus, HBO therapy conferred significant protection against death from untreated ischemia (P less than 0.001). Histological examination showed that the extent of patchy bilateral ischemic neuronal damage was much less in surviving gerbils that received HBO therapy than in those that died after 20-minute occlusions. Fourteen gerbils were treated with DMSO, 2.5 g/kg intraperitoneally, during 5- or 10-minute bilateral CA occlusion; 12 died (86% mortality rate). Thus, DMSO provided no protection against fatal cerebral infarction; in fact, the results in the 10-minute reperfusion group suggest that DMSO may have a deleterious effect.
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PMID:Effect of hyperbaric oxygen therapy or dimethyl sulfoxide on cerebral ischemia in unanesthetized gerbils. 371 99

Cerebral arterial infarction is a more common cause of neonatal seizures than has been previously appreciated. In 50 full-term newborns with seizures studied, 7 had cerebral infarction which was the second most common definable cause of seizures. We describe these 7 full-term infants with cerebrovascular accidents who presented with focal or generalized seizures. Obstetrical histories were normal in 5 of these patients. Their neurological examinations demonstrated lethargy and generalized hypotonia. Electroencephalograms demonstrated focal abnormalities in 4 infants. Computed tomographic scans in the first week of life showed infarctions in 6 newborns and in another at age 6 months. Neonatal stroke should be considered as a cause of seizures in a full-term newborn in spite of a normal obstetrical history and a nonfocal neurological examination.
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PMID:Seizures and cerebral infarction in the full-term newborn. 400 59

The case of a 26 year old woman who had been taking tranexamic acid to prevent uterine bleeding due to an IUD and who died from thrombosis of the left internal carotid artery is reported. The patient's father had died at age 54 of myocardial infarction. Otherwise the family history was entirely negative for thromboembolic disease. The patient was a mild smoker. She had been previously healthy and in particular, she was not affected with hypertension, diabetes, or dyslipidemia. She had carried to term 2 uncomplicated pregnancies. 40 days prior to hospital admission her gynecologist had inserted an IUD. The insertion of the IUD was followed by persistent uterine bleeding, and for this reason she began treatment with tranexamic acid (1.5 g/daily). Uterine bleeding persisted despite this treatment, and the IUD was removed. Because of persistence of a mild uterine bleeding, tranexamic acid was continued. 2 hours before admission the patient suddenly presented a left sided hemiparesis with disarthria and vomiting. On admission she was stuporous. The left side of her face drooped and the strength of the left arm and leg was markedly decreased. Both arm and leg reflexes were symmetrical. Her blood pressure was 110/70. An electroencephalogram on arrival confirmed a right sided cerebral lesion. Subsequently the patient's condition deteriorated rapidly. She developed a full left hemiplegia and became deeply comatose. A CAT scan performed 4 hours after admission showed no abnormalities. A CAT scan performed 3 days after admission showed a large cerebral infarction involving nearly the whole right cerebral hemisphere. The patient's condition remained essentially unchanged until she died 6 days after admission. Permission for autopsy was refused. Antifibrinolytic drugs competitively inhibit plasminogen activators and noncompetitively plasmin. Thromboembolic complications after the administration of antifibrinolytic drugs have long been recognized. The use of IUDs is often associated with troublesome uterine bleeding and particularly excessive menstrual bleeding. To avoid these complaints, antifibrinolytic drugs are increasingly used.
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PMID:Tranexamic acid, intrauterine contraceptive devices and fatal cerebral arterial thrombosis. Case report. 710 62

Hypernatremia resulting in neurologic symptoms ranging from lethargy to coma, and with underlying lesions of cerebral hemorrhage and thrombosis, has been reported in human beings. Herein we report two cases of cerebral infarction with venous thrombosis in cynomolgus monkeys. Both animals were severely hypernatremic because of water deprivation, with serum sodium levels of 185 and 193 meq/liter, respectively. At necropsy, there were bilateral multiple hemorrhagic and malacic areas visible on the surface of the cerebrum and extending into the parenchyma, primarily involving the occipital lobes. These lesions were interpreted microscopically as infarcts because, in addition to hemorrhage and necrosis, multiple thrombi were present in small and medium-sized veins of gray matter and meninges. The pathogenesis of hypernatremia-induced cerebral lesions is believed to involve cellular dehydration that caused shrinkage of the brain. Because the vasculature of the brain is tightly adherent to the skull, this shrinkage results in tearing of blood vessels, with consequent hemorrhage and thrombosis.
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PMID:Cerebral infarction in two cynomolgus macaques (Macaca fascicularis) with hypernatremia. 881 42

A 60-year-old diabetic male presented with transient ischemic attacks. Initial neurological examination and head CT were normal. Dysarthria, ataxia, delirium, and lethargy developed. A diagnosis of cryptococcal meningitis was made after lumbar puncture and treatment with intravenous amphotericin B and 5-fluorcytosine was begun. A repeat head CT showed an anterior cerebral artery territory infarct. His condition worsened and he died of associated complications three weeks after admission. The case is used to discuss the association between cryptococcal meningitis and diabetes, transient ischemic attacks, and vasculitis with cerebral infarction.
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PMID:Case of the month: July 1997--diabetic male with transient ischemic attacks. 945 81

Although hypercalcemia may cause drowsiness, lethargy, weakness, confusion and coma it rarely causes seizures or cerebral infarction. The patient presented had a clinical evolution from hallucinosis to a generalized tonic-clonic seizure, and subsequent cortical blindness with occipital cerebral ischemia as evidenced by SPECT and MRI scans. EEG revealed occipital PLEDs. With reversal of hypercalcemia, there was a return of vision, resolution of EEG epileptiform activity, although with some residual occipital infarction. This case, in concert with a literature review of hypercalcemia, reveals examples of occipital and watershed ischemia, blindness, seizures and hypertension, a pattern markedly similar to that of eclampsia. Furthermore, medications such as magnesium sulfate, believed to reverse cerebrovasospasm responsible for the eclamptic neurologic findings, may counter the effects of hypercalcemia at a cellular level, lending support to a calcium-mediated injury in eclampsia.
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PMID:Reversible hypercalcemic cerebral vasoconstriction with seizures and blindness: a paradigm for eclampsia? 966 11

We report continuous bilateral intracranial pressure (ICP) monitoring immediately after transtentorial herniation in a patient with massive cerebral infarction to: 1) determine presence and time course of compartmental ICP differences, and 2) to study effects of therapy on both hemispheres. A 55-year-old man admitted with watershed infarctions in the left anterior-middle-posterior cerebral arteries distribution. Initial investigations demonstrated highly narrowed left extracranial internal carotid artery. Eight days later he developed unexplained lethargy and anisocoria. Head computerized tomography (CT) showed massive left hemispheric infarction, edema, and midline shift. Bilateral subarachnoid bolts demonstrated equally elevated ICP in both hemispheres. Hyperventilation and osmotic therapy produced near-identical ICP reduction bilaterally with resolution of anisocoria. Later, plateau waves and autonomic instability developed. Shortly before loss of brainstem function, interhemispheric ICP gradients (left greater than right) of 30-40 mm Hg developed. Intracranial pressure did not equalize prior to brain death determination. Bilateral ICP monitoring did not reveal an interhemispheric ICP gradient soon after transtentorial herniation in massive MCA infarction. The presence of interhemispheric ICP gradients in massive stroke remains unproven and further clinical study is necessary.
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PMID:Interhemispheric intracranial pressure gradients in massive cerebral infarction. 1235 87

A 29-year-old man presented with lethargy, headache, high fever, and visual disturbance. Neurological examination showed mydriatic pupil, ptosis, diminished light reflex, and ophthalmoplegia on the left. Magnetic resonance (MR) imaging showed the typical findings of pituitary apoplexy, and cerebral angiography disclosed mild narrowing of the A1 segment of the left anterior cerebral artery (ACA). Transsphenoidal tumor resection was performed. Transient severe right hemiparesis occurred directly after the operation. Computed tomography demonstrated cerebral infarction in the territory of the left Heubner's and medial lenticulostriate arteries. Pituitary apoplexy followed by cerebral infarction is very rare. Vasospasm of the perforating arteries of the ACA probably caused the cerebral infarction. Subarachnoid blood or vasoactive agents released from the tumor were the most likely cause of the vasospasm. MR imaging findings of contrast enhancement around the vessels may indicate reactive processes around the vessels.
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PMID:Cerebral infarction following pituitary apoplexy--case report. 1560 Feb 83

The hyperdense vessel sign is a debated topic in terms of its sensitivity and specificity for acute cerebral ischemia. Bilateral, hyperdense middle cerebral artery signs are rare presentations of bilateral cerebral infarction. We describe a 17-year-old boy with a history of cerebral palsy and a repaired atrial septal defect, presenting with lethargy and respiratory failure. Noncontrast computed tomography of the brain revealed bilateral, hyperdense middle cerebral artery signs, and he subsequently demonstrated bilateral cerebral infarctions in the distributions of the middle cerebral arteries. Hyperdense artery signs must alert physicians to evaluate patients for stroke, with an especially high index of suspicion for pediatric patients with hyperdense vessels, who are less likely to present with atherosclerotic disease causing vascular calcifications; rather, hyperdense artery signs could be an early sign of large-vessel thrombosis and cerebral infarction.
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PMID:Bilateral, hyperdense middle cerebral arteries predict bihemispheric stroke. 1894 May 62


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