Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neonatal necrotizing enterocolitis is the most common serious gastrointestinal disorder encountered in neonatal intensive care units. It is a major cause of morbidity and mortality in the newborn, particularly in premature infants. Consistent risk factors are birth weight and prematurity. Polycythemia and hyperviscosity altering blood flow and infectious agents are also implicated. Clinical findings include abdominal distention and diarrhea, and systemic symptoms such as apnea, acidosis, and lethargy. Pneumatosis intestinalis can be demonstrated radiographically. Mucosal ulcerations, hemorrhage, and thrombosis occur early, followed by inflammatory changes. Later still necrosis develops. Ischemia, infection, and enteral feedings are suspected to be involved in the pathophysiology. Eicosanoids, especially thromboxane, platelet-activating factor, and leukotrienes are likely mediators.
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PMID:Neonatal necrotizing enterocolitis. Inflammatory bowel disease of the newborn. 312 29

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

A persistent vegetative state (severe dementia) developed in a 30-year-old man following hypoglycemic coma. Despite the poor clinical outcome, sensory evoked response recovered between 6 and 34 months after the insult. The cerebral blood flow level at rest after 34 months was slightly above the normal range. This finding contrasts with the low cerebral blood flow regularly reported in patients who are comatose or stuporous following severe brain hypoxia-ischemia.
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PMID:Persistent vegetative state with high cerebral blood flow following profound hypoglycemia. 663 60

Unilateral brain ischemia was induced in the rat by injecting radioactive microspheres into the left internal carotid artery. The microspheres were mainly distributed in the left cerebral hemisphere which contained 8 to 10 times more microspheres than the contralateral hemisphere. Embolization caused dopamine (DA) and noradrenaline (NA) depletion only in the left hemisphere. NA levels were already reduced 2 hours after injury while DA was still unaltered after 6 hours. A 30--40% depletion was observed for the two amines after 24 hours. Catecholamine turnover was estimated by measuring the amine depletion after synthesis inhibition with alpha-methyl-p-tyrosine. During the first 2 hours following embolization, DA and NA depletions were slightly increased only in the left hemisphere, indicating an increase in catecholamine efflux. At times 24 hours, an important retardation in amine disappearance after synthesis inhibition was found for DA and NA in the left hemisphere and to a lesser extent for DA in the right hemisphere, suggesting a reduction of the physiological activity of catecholaminergic neurons. These biochemical alterations can be related to the post-stroke behavioural changes of the embolized animals which exhibited an initially increased motor activity followed by a lethargic state.
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PMID:Catecholamine levels and turnover during brain ischemia in the rat. 740 Aug 6

Most shunt-dependent hydrocephalic patients present with predictable symptoms of headache and mental status changes when their cerebrospinal fluid shunts malfunction. Their intracranial pressure (ICP) is usually high, and they usually respond to routine shunt revision. This report describes 12 shunted patients who were admitted with the full-blown hydrocephalic syndrome but with low to low-normal ICP. All 12 patients had been maintained previously on medium-pressure shunts. Their symptoms included headache, lethargy, obtundation, and cranial neuropathies. At peak symptoms, their ventricular sizes were large (ventricular/biparietal ratio of 0.35 to 0.45) in six and massive (ventricular/biparietal ratio > 0.45) in six and their ICPs ranged from 2.2 to 6.6 mm Hg, with a mean of 4.4 +/- 1.3 mm Hg (+/- standard deviation), i.e., below or well within the pressure range of their shunts. The pressure volume index of three patients at peak symptoms ranged from 39.2 to 48.5 ml, with a mean of 43.9 +/- 4.6 ml, which represents a 190% increase from the predicted normal value. Seven patients failed to improve with multiple shunt revisions, including the use of low-pressure valves. In 11 patients, symptoms and ventriculomegaly were not reversed except with prolonged external ventricular drainage at subzero pressures (mean external ventricular drainage nadir pressure of -5.7 +/- 3.6 mm Hg, for a mean period of 22.2 days). During external ventricular drainage treatment, symptoms correlated only with ventricular size and not with ICP. All 11 were subsequently treated successfully with a new medium- or low-pressure shunt. One patient was treated successfully with prolonged shunt pumping. We postulate that: 1) the development of this low-pressure hydrocephalic state is related to alteration of the viscoelastic modulus of the brain, secondary to expulsion of extracellular water from the brain parenchyma, and to structural changes in brain tissues due to prolonged overstretching; 2) certain patients are susceptible to developing low-pressure hydrocephalic state because of an innate low brain elasticity due to bioatrophic changes; 3) low-pressure hydrocephalic state symptoms are due not to pressure changes but to brain tissue distortion and cortical ischemia secondary to severe ventricular distortion and elevated radial compressive stresses within the brain; and 4) treatment must be directed toward allowing the entry of water into the brain parenchyma and the restoration of baseline brain viscoelasticity.
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PMID:Low-pressure hydrocephalic state and viscoelastic alterations in the brain. 780 7

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

A significant number of moribund and dead lobsters Homarus americanus were reported to New York state authorities by lobster fishers in Long Island Sound (LIS) during the summer of 2002. Morbid lobsters were characterised by an orange discolouration of the abdomen, lethargy, an excess of epibionts and poor post-capture survival. On necropsy, severe extensive multifocal or diffuse mineralised granulomatous inflammation of the gills and antennal glands was the most striking pathology. In the gills, granulomas often occluded the lumen of filaments, resulting in congestion, ischemia and coagulative necrosis of gill tissues. In the antennal glands, granulomas were concentrated along the border between the coelomosac and labyrinth. No significant pathogens were recovered from diseased individuals. In prechronic individuals, however, it was evident that granulomas were focused around calcium carbonate (aragonite) crystals. This disease may result from anomalously high sea-bottom temperatures in LIS (approximately 23 degrees C) during the summer of 2002 and associated disruptions of the calcium chemistry of lobsters in favour of deposition of minerals in soft tissues. The ultimate cause of death of affected lobsters is probably respiratory failure due to reduced effective surface area of the gills, exacerbated by hypermetabolic temperatures and an abundance of epibionts.
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PMID:Excretory calcinosis: a new fatal disease of wild American lobsters Homarus americanus. 1510 45

An 81-year-old woman with chronic dementia developed lethargy, confusion, binocular blindness, and episodic left-beating nystagmus. Diffusion magnetic resonance imaging (MRI) revealed high signal in the right occipital region suggesting recent ischemia. A concurrent electroencephalogram (EEG) showed a right occipital seizure focus that spread to the opposite occipital lobe. A single photon emission computed tomography (SPECT) performed during the seizure epoch showed bilateral occipital lobe hyperperfusion. This is the second report to document SPECT bi-occipital hyperperfusion in seizure-related cortical blindness.
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PMID:Bilateral occipital lobe hyperperfusion demonstrated by single photon emission computed tomography during seizure-related cortical blindness. 1520 34

We are presenting the case of a 63 year-old man with a dural arteriovenous malformation of the transverse sigmoid sinus who developed focal deficits followed by less localized symptoms such a disorientation, lethargy and eventually comatose status. Initial cerebral angiography showed retrograde filling of the cortical and deep cerebral venous system with marked delay in venous empting. Following embolization clinical symptoms completely cleared at the time that control angiography showed retrograde venous flow turning anterograde. Patient's symptoms recurred four months later when there was a relapse of retrograde cerebral venous drainage at the time he developed thrombosis of the superior longitudinal and right transverse sinuses. Sinus thrombosis and thrombosis of the central retinal artery were coincidental with hypercoagulability related to hyperhomocysteinemia. Since control angiography still showed persistence of the AV shunting radical excision of the involved dural sinuses was performed. The final outcome was excellent. The physiopathological mechanism responsible for neurological deficits in our patient most likely was ischemia of venous origin secondary to venous hypertension resulting from retrograde cerebral venous drainage. The clinical and angiographic presentation in few similar cases reported in the literature is reviewed.
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PMID:Unruptured dural arteriovenous malformation of the transverse-sigmoid sinus presenting with focal symptoms and coma. 1555 3

Patients with subarachnoid hemorrhage (SAH) are at risk for seizures and delayed cerebral ischemia, both of which can be detected with continuous EEG monitoring (cEEG). Ischemia can be detected with EEG at a reversible stage. CEEG may be most useful in patients with poor grade SAH, as the neurological exam is of limited utility in these stuporous or comatose patients. Seizures have been detected in 19% of SAH patients undergoing cEEG, with the vast majority (95%) of these seizures being nonconvulsive and without any detectable clinical correlate. Applying quantitative analysis to the cEEG (relative alpha variability, post-stimulation alpha/delta ratio) allows reliable detection of ischemia from vasospasm, with EEG changes often preceding changes in the clinical exam and other non-continuous monitoring techniques by up to two days. In patients at risk for developing vasospasm, cEEG monitoring, preferably with quantitative EEG analysis, should be started as early as possible and carried out for up to 14 days after the SAH. CEEG findings may lead to therapeutic (e.g., antiepileptic medication, hypertensive therapy, angioplasty) or additional diagnostic interventions such as angiography, CT or MRI.
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PMID:Continuous EEG monitoring in patients with subarachnoid hemorrhage. 1580 8


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