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)

A 74-year-old female who complained of severe attacks of pain in the throat and neck on the left side was first admitted to our hospital in 1971. Carbamazepine was effective at this time, and so she could be discharged. She was readmitted to the hospital in 1974 because of severe stabbing paroxysms of pain in the left throat, radiating into the auricular region as frequent as more than ten times a day. Paroxysms could not be alleviated by large doses of Carbamazepine, and side effects of the drug ensued. The pain could be easily elicited by talking, laughing, swallowing, pulling the left ear and pushing the left tragus. Block of the left 9th nerve with xylocaine produced complete relief of pain for 30 minutes to 1 hour; Plain skull X-rays and veretebral angiograms were normal. The patient was operated under general anesthesia in the sitting position. With the left suboccipital craniectomy, the left 9th nerve was cut without any change on ECG. Pulse rate, and blood pressure. Upon touching vagus nerve, the ventricular extrasystole and hypotension occurred. After the blood pressure restored to normal level and the extrasystole disappeared with administration of atropine and carnigen, the uppermost rootlet of the vagus nerve was cut. The blood pressure dropped abruptly again followed by the right bundle-branch block on ECG for approximately 20 minutes. Postoperatively, she was lethargic and had disorientation, delusion and disorientation. We attributed these symptoms to the hypoxia in operative procedure. The symptoms completely disappeared on the fifth postoperative day. The patient has been perfectly free from pain at the 15 month's follow-up without neurological or mental deficit except diminished gag reflex on the left side. We reported this our experienced case and discussed about the mechanism of the hypotension on sectioning a rootlet of the vagus nerve with literatures.
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PMID:[Glossopharyngeal neuralgia associated with the right-bundle branch block and hypotension on sectioning a rootlet of the vagus nerve--case report (author's transl)]. 55 84

During neurophysiologic studies in the rat [Crl:COBS CD(SD)BR], chloral hydrate was given intraperitoneally to produce anesthesia for brain electrode implantation. The incidental occurrence of adynamic ileus in six of these rats, 5-16 days after surgery, prompted further investigation. Pathological evaluations and transmission experiments using ingesta and viscera from affected rats failed to reveal an infectious agent. Subsequently chloral hydrate-induced adynamic ileus leading to morbidity or death was experimentally produced in 14 of 27 rats, 3--36 days after intraperitoneal administration of the anesthetic at a dose of 400 mg/kg body weight and concentrations of 125--275 mg/ml. The experimentally produced condition was characterized by lethargy, anorexia, abdominal distension, ruffled hair coat, inactivity, drowsy expression, constipation, and death. Gross pathologic findings included gaseous distension and atony of the cecum and segments of the small intestine. Small intestine contents varied from liquid to solid. The colon and rectum contained only a few dry hard fecal pellets. A few animals showed excess abdominal fluid. Microscopic findings were limited to focal chronic serositis and serosal fibrosis affecting the visceral peritoneum. On the basis of the experimental studies, it was concluded that the condition described was not an infectious disease but was an abnormal physiologic condition produced by the irritating or pharmacologic action of chloral hydrate given at high concentrations in the abdominal cavity.
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PMID:Adynamic ileus in the rat induced by chloral hydrate. 85 88

One hundred seventeen patients undergoing cardiac operations over a two-year period were studied. Electroencephalograms were recorded preoperatively, in the recovery room (up to 12 hours following operation), 24 hours later, and further as required. Operative and anesthesia data were correlated with EEG findings. All patients had normal EEGs preoperatively. This unusual occurrence may largely reflect the absence of congenital heart disease and the small number of valvular lesions in our patients. Prognosis was not significantly influenced by age. Bypass time appeared directly related to outcome by group but not individually. Hypotension prior to pumping occurred most often and mean blood loss was greatest in the patients who had abnormal EEGs in the recovery room with progressively worsening patterns until death. In the recovery room many patients were awake, while others were either drowsy, lethargic, or asleep. Some were comatose. The level of consciousness was not as prognostic as was the EEG. The pattern of EEGs in the first few postoperative days is more important than any single record by itself. All those who showed progressive deterioration in the first two or three days died shortly thereafter.
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PMID:Prognostic value of electroencephalography in cardiac surgery. 111 50

The interrelationships between cerebral edema, intracranial pressure (ICP), and cerebral blood flow (CBF) were studied in acute and chronic triethyl tin sulfate treated rats. Prior to pentobarbital anesthesia behavioral observations were made. ICP and regional CBF were measured under steady state conditions and brain water content was determined by vacuum drying of the right cerebral hemisphere. Control and chronic animals were neurologically normal. There were two distinct acute groups: (1) acute low pressure (ALP) animals - alert but tetraperetic, and (2) acute high pressure (AHP) animals - deeply stuporous, with minimal pain response and gross EEG slowing. ICP was significantly elevated only in AHP animals. Hemispheric CBF was significantly reduced in AHP and chronic animals. The interaction of increased pressure and edema (AHP) produced the greatest decrease in CBF, although deep white flows were significantly affected in all experimental groups. Chronic animals had significantly lower flow in four of seven regions compared to ALP animals despite no significant difference in ICP. Water content was significantly increased in all experimental groups with the greatest increase in the chronic animals. In the absence of any significant increase in ICP, cerebral edema appears to cause a significant reduction in cerebral blood flow and this reduction corresponds with the magnitude and location of the edema.
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PMID:Alterations in behavior, brain electrical activity, cerebral blood flow, and intracranial pressure produced by triethyl tin sulfate induced cerebral edema. 125 1

A study was carried out to compare the haemodynamic and respiratory effects, as well as the quality of recovery, of anaesthesia with ketamine, sodium gamma-hydroxybutyrate (GOH) and etomidate in children undergoing cardiac catheterization. Thirty children, mean age 48 +/- 35 months, ranked ASA 2 or 3 on account of congenital heart disease, were assigned to one of three groups (n = 10). They were given: in group E1, a 0.3 mg.kg-1 bolus of etomidate, followed by 0.1 mg.kg-1.min-1 for 10 minutes, and 0.026 mg.kg-1.min-1 thereafter; in group G2, a 50 mg.kg-1 bolus of GOH, and in group K3, a 4 mg.kg-1 bolus of ketamine followed by a continuous infusion of 0.083 mg.kg-1.min-1. The patients breathed spontaneously. Monitoring included heart rate, systolic, diastolic and mean blood pressure, pulse oximetry, and capnography. Femoral venous or arterial catheterization was performed after local anaesthesia (with no more than 2 mg.kg-1 of lidocaine). Measurements were performed before induction, and then 1, 10, 30 and 60 minutes afterwards. The quality of anaesthesia was assessed according to Steward's scale. The investigation lasted between 50 and 100 min in all three groups. There were no significant differences in haemodynamic and respiratory parameters during the investigation between the groups. Recovery was shorter and of better quality in group E1. On the opposite, 30 minutes after the end of the catheterization, all the patients in group K3 were stuporous, with 5 of them displaying involuntary movements. The patients of the other two groups reacted correctly to stimuli, but those in group G2 went back to sleep very rapidly. There were no complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anesthesia for heart catheterization in children. Comparison of 3 techniques]. 178 1

Methemoglobinemia is a condition in which more than 2% of the hemoglobin of the blood has been oxidized to the ferric form, a molecule which is incapable of binding oxygen or carbon dioxide. Clinically, the patient appears lethargic, cyanotic, and does not respond to oxygen. We describe a patient with esophageal carcinoma who developed severe methoglobinemia following application of benzocaine in spray for local anesthesia prior to intraluminal irradiation. Review of the literature is presented.
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PMID:Methemoglobinemia induced by topical anesthetic (benzocaine). 221 71

Alterations in the course of and histopathologic response to influenza viral infections by halothane, enflurane, and diethyl ether anesthesia were evaluated in ferrets. There were no significant differences in the incidence and duration of lethargy, pyrexia, rhinorrhea, or sneezing in infected animals given one of the three anesthetic agents under investigation, compared with those receiving no anesthesia. There were no differences in lung pathology in infected animals given one of the three anesthetic agents, or no anesthesia, though histopathologic changes in the nasal turbinates were significantly greater in ferrets given enflurane. This study suggests that general anesthesia administered to ferrets infected with influenza virus carries minimal morbidity, although enflurane anesthesia was found to produce greater histopathologic changes than the other agents.
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PMID:Alterations in the course of and histopathologic response to influenza virus infections produced by enflurane, halothane, and diethyl ether anesthesia in ferrets. 283 25

This study was undertaken to investigate the influence of the arterial baroreceptors on the response of renal sympathetic nerve activity (rSNA) during naloxone-precipitated morphine abstinence in rats. In chronically baroreceptor-denervated, morphine-dependent rats, rSNA, mean arterial pressure (MAP) and heart rate (HR) were studied before and after repeated i.v. bolus doses of naloxone (0.005-5 mg kg-1), during chloralose anaesthesia or in the conscious state. In the anaesthetized animals, naloxone doses of 0.05-5 mg kg-1 caused a pronounced inhibition of rSNA, reaching a level 61% below pre-naloxone activity. This was accompanied by increases in MAP and HR. In the conscious rats, the lower doses of naloxone elicited an initial state of increased somatomotor activity. This was paralleled by slight increases in rSNA and MAP. After 4-5 min, the behavioural excitation faded and was replaced by lethargy. The rats exhibited still signs of withdrawal in the form of piloerection, chromodacryorrhoea and defaecations. Concomitantly, rSNA returned towards the pre-naloxone level, while MAP showed a sustained increase. The higher naloxone doses exacerbated the hypertension without any further changes in rSNA or in behaviour. We conclude that the influence of the baroreceptors is of minor significance for the inhibition of rSNA during naloxone-precipitated abstinence in anaesthetized rats. In conscious, intact rats, however, the baroreceptors seem to contribute to rSNA inhibition since no significance decrease of rSNA occurred in baroreceptor-denervated rats in the present study. This is in contrast to our previous finding of a marked inhibition of rSNA in rats with intact baroreceptors.
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PMID:Renal sympathetic nerve activity during morphine abstinence in sino-aortic baroreceptor-denervated rats. 325 Feb 17

Measurement of regional cerebral blood flow (rCBF) using the i.v. 133Xe technique was carried out during resection of a right temporooccipital arteriovenous malformation (AVM) with ipsilateral middle and posterior cerebral arterial supply. Intraoperatively, a rCBF detector was in place over the right frontotemporal area, about 5 to 6 cm from the border of the AVM. Anesthesia was 0.75% isoflurane in oxygen and nitrous oxide. After dural exposure, the rCBF was 27 ml/100 g/min at a pCO2 of 29 mm Hg and a mean arterial pressure (MAP) of 90 mm Hg. The pCO2 was then elevated to 40 mm Hg, and the rCBF was increased to 55 ml/100 g/min at a MAP of 83 mm Hg. After AVM removal, the rCBF rose to 50 ml/100 g/min at a pCO2 of 27 mm Hg and a MAP of 75 mm Hg. The pCO2 was elevated to 33 mm Hg and the rCBF increased to 86 ml/100 g/min at a MAP of 97 mm Hg. During skin closure, the rCBF was 94 ml/100 g/min at a pCO2 of 26 mm Hg and a MAP of 97 mm Hg. The patient was neurologically normal postoperatively except for a mild, new visual field defect. After 2 to 3 days, the patient gradually developed lethargy, confusion, and nausea with relatively normal blood pressure. An angiogram revealed residual enlargement of the posterior cerebral artery feeding vessel. Computed tomography showed edema extending from the area of AVM resection as far as the frontal region, producing a significant midline shift anteriorly. Intraoperative rCBF monitoring revealed significant hyperperfusion after AVM resection, which was associated with signs and symptoms of the normal perfusion pressure breakthrough syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:133Xe blood flow monitoring during arteriovenous malformation resection: a case of intraoperative hyperperfusion with subsequent brain swelling. 337 91

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


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