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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighteen adult chacma baboons were fed Cannabis sativa, the plant material being incorporated into their food. They were divided into three equal groups. Group 1 animals were fed on 2% cannabis in food for 4 months, after which 2 animals remained on 2%, 2 were given 4% and 2 6% cannabis in food for the next 4 months. They became mildy apathetic. Five gained weight. Serum glucose, potassium and CO2 values decreased. Neuropathological examination of their brains did not show any significant abnormality. Group 2 animals were fed 10% cannabis for several weeks. They ate less and lost weight, and later became very apathetic. Right temporal biopsies were done in all and in 3 the tissue was analysed for glutamine, glutamate, tryptophan, ammonia and cyclic AMP. No significant change was found. Serum glucose and CO2 levels rose and potassium levels fell. Blood cholesterol values decreased in 3 of the 9 males. Group 3 animals were fed 6% cannabis for 2--4 months. Radio-immunoassay of sera and urine showed the presence of cannabinoids. They became apathetic, and 5 lost weight. Serum glucose and potassium levels (measured in the males) decreased. No neuropathological lesions were found in the brains, apart from an incidental leptomeningitis in 1 animal which died suddenly. The question of cannabis encephalopathy is discussed.
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PMID:Effects of the oral administration of Cannabis sativa (dagga) on chacma baboons (Papio ursinus). 11 92

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.
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PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

A retrospective study of the complications of treatment with the carbon dioxide (CO2) laser of 17 patients diagnosed to be suffering from recurrent laryngeal papillomatosis is presented. No immediate complications occurred except one case of laryngospasm and failure to intubate during anaesthesia leading to hypoxic encephalopathy. Three patients were completely free from disease and complications. Another patient was free from laryngeal lesions but developed a papilloma in the right tonsillar pillar. Five other patients showed one or more multiple sites of involvement in addition to the larynx. Laryngeal scarring developed in ten patients. Six patients (35.29 per cent) developed scarring as anterior glottic webs while in two scarring (11.7 per cent) occurred as posterior glottic webs. One developed scarring in the supraglottic region. The remaining one had scarring in both the glottic and supraglottic regions. One patient developed tracheal scarring necessitating laryngo-tracheal separation. Two patients were psychologically disturbed during treatment requiring psychiatric consultation and therapy.
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PMID:Complications of treatment of recurrent laryngeal papillomatosis with the carbon dioxide laser in children. 140 64

Continuous monitoring of the cerebral blood flow, oxyhemoglobin, deoxyhemoglobin, total hemoglobin, oxidized cytochrome a, a3, and tissue pH during prolonged CO2 or N2 loading in 2-week-old rabbits was performed by near-infrared spectroscopy, the thermocouple method, and a tissue pH meter. Near-infrared spectroscopy demonstrated decreases in oxyhemoglobin and oxidized cytochrome a, a3 and increases in deoxyhemoglobin and total hemoglobin in the early stage within 5 min, which gradually lessened with time on both 10% concentration of inspired O2 with CO2 and N2. CBF increased with venous retention in the early stage and then slowly decreased in parallel with blood pressure and oxidized cytochrome a, a3 on abolition of autoregulation. These changes were more remarkable during the 10% concentration of inspired O2 with CO2 than N2 which may be caused by marked acidosis and hypotension associated with hypercarbia. Oxidized cytochrome a, a3, however, demonstrated a gradual decrease in 10% concentration of inspired O2 with N2 rather than CO2; therefore, the continuous monitorings demonstrated hemodynamic and oxygenation changes despite the same extent of prolonged hypoxic loading. These changes in prolonged hypoxic conditions may occur in human intrapartum asphyxia which develops into postnatal hypoxic-ischemic encephalopathy.
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PMID:Monitoring of immature rabbit brain during hypoxia with near-infrared spectroscopy. 155 75

Propionic acidemia occasionally produces a toxic encephalopathy resembling Reye syndrome, indicating disruption of mitochondrial metabolism. Understanding the mitochondrial effect of propionate might clarify the pathophysiology. Liver mitochondria are inhibited by propionate (5 mM) while muscle mitochondria are not. Preincubation is required to inhibit liver mitochondria, suggesting that propionate is metabolized to propionyl CoA. Liver and skeletal muscle mitochondria incubated with [1-14C]propionate contain similar quantities of matrix isotope and release comparable [14C]CO2. However, only liver mitochondria accumulated significant propionyl CoA, which was largely (68%) synthesized from propionate. Carnitine reduced the level of liver matrix propionyl CoA. Inhibition of respiratory control ratios by propionate correlated with propionyl CoA levels. These results support the hypothesis that acyl CoA esters are toxic and that carnitine exerts its protective effect by converting acyl CoA esters to acylcarnitine esters.
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PMID:Propionate mitochondrial toxicity in liver and skeletal muscle: acyl CoA levels. 188 30

To elucidate the role of free radicals in the pathogenesis of neonatal hypoxic encephalopathy, we determined the content of thiobarbituric acid reactants (TBARs), as an index of lipid peroxidation related with a free radical reaction, in the brains of newborn mice during hypoxia and recovery from hypoxia. Hypoxic stress was induced by 100% nitrogen gas breathing (N2 group) or 100% carbon dioxide gas breathing (CO2 group). TBARs increased with 20 minutes of hypoxia and returned to the control level during the recovery period in both groups. The increase in TBARs in the CO2 group was greater than that in the N2 group. These results may suggest that free radical reaction occurs during the hypoxic period and that CO2 hypoxia is more effective on free radical production in the newborn brain than N2 hypoxia.
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PMID:Lipid peroxidation in neonatal mouse brain subjected to two different types of hypoxia. 190 42

A multidisciplinary workshop held from September 29 to October 1, 1989, at Airlie House, Warrenton, Virginia, considered the neurologic complications of whooping cough and pertussis vaccine. Pertussis mortality in the U.S. in 2-3/1000 cases. Seizures occur in 1.9% of cases, and encephalopathy in 0.3%. Reviewing all data, it appears likely that a combination of one or more bacterial toxins, asphyxia, CO2 retention and loss of cerebral vascular autoregulation is responsible for neurologic symptoms. The timing of the encephalopathy suggests that it results from increased lysis of bacteria, and release of endotoxin. The encephalopathy is not confined to the paroxysmal phase. In evaluating side-reactions to the vaccine, the following must be kept in mind: 1. Vaccines are not standardized between manufacturers. 2. For a given manufacturer, vaccines are not standard from one batch to the next. 3. Unless the vaccine is properly prepared and refrigerated, its potency and reactivity varies with shelf life. In fact, the whole question of vaccine detoxification has never been systematically investigated. Listed in order of increasing severity, observed adverse reactions include irritability, persistent, unusually high pitched crying, somnolence, seizures, a shock-like "hypotensive, hyporesponsive" state, and an encephalopathy. Since the neurologic picture is not specific for pertussis vaccination, its temporal relationship to the vaccination is the critical variable for determining causation. Although the majority of seizures following pertussis vaccination are associated with fever, it was the consensus of the neurologists attending the workshop, that these do not represent febrile convulsions, but are non-benign convulsions. The incidence of post-vaccine encephalopathy is difficult to ascertain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Workshop on neurologic complications of pertussis and pertussis vaccination. 198 Dec 51

The authors studied the effects of hypocapnic-hyperventilation on cerebral blood flow (CBF) (study 1) and on cerebral oxygenation (study 2) during mechanical ventilation in 8 patients, 4 with hepatic (HE) and 4 with septic encephalopathy (SE). In study 1, a positive linear relationship between CBF(y) and PaCO2 (x) was observed (y = 2.44x - 55.5, r = 0.6276, P less than 0.01, n = 18). In the study 2, hypocapnic-hyperventilation produced a reduction in CBF below the level required to meet the demand in 4 of 8 patients. A good linear relationship was observed between CBF/CMRO2 (CMRO2 = cerebral oxygen consumption, y) and jugular venous PO2 (PjVO2, x) (y = 0.99x - 15.53, r = 0.8962, P less than 0.01, n = 18). It is concluded that cerebrovascular reactivity to CO2 was preserved in these patients, therefore, intentional or inadvertant hyperventilation may produce cerebral ischemia. Moreover, JPVO2 may be useful in monitoring cerebral oxygenation in such patients.
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PMID:Cerebrovascular reactivity to CO2 in patients with hepatic or septic encephalopathy. 216 Jul 9

Plasma hyperviscosity is a striking abnormality in patients suffering from subcortical arteriosclerotic encephalopathy (SAE) and is thought to perpetuate the chronic ischaemic demyelinating process of the periventricular white matter. Ancrod, a defibrinating enzyme, was given to 10 patients with SAE in an attempt to reduce plasma fibrinogen, which would thus normalise hyperviscosity. This was paralleled by a significant improvement of the initially abnormal retinal arteriovenous passage time, as well as a significant augmentation of the CO2-induced cerebral vasomotor response. This did not lead, however, to any clinical improvement with respect to performance of neuropsychological tests, recurrences of strokes during a 6 month observation period or improvement of various audiological parameters. The findings indicate that hyperviscosity in patients with SAE is merely an epiphenomenon. A potentially reversible, chronic penumbral state of the brain tissue apparently does not exist in SAE.
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PMID:Effects of enzymatic blood defibrination in subcortical arteriosclerotic encephalopathy. 306 76

Gaseous metabolism and carboanhydrase activity of erythrocytes of the capillary and venous blood were studied in 115 persons, including 19 apparently normal subjects, 66 patients with ischemic stroke, and 30 with discirculatory encephalopathy. Patients with cerebral stroke presented gross disorders in the function of carboanhydrase and gaseous metabolism from the first day of the disease which was expressed in an increased oxygenation of the venous blood and hypocapnia, whose severity was correlated with the gravity of the disease course. The authors have established an important pathogenetic role in gaseous metabolism impairment of erythrocyte carboanhydrase, whose activity in the capillary bed in hypocapnia was drastically inhibited, compromising, therefore, the entry of carbon dioxide into erythrocytes, which deteriorated oxyhemoglobin dissociation. The authors consider the possibility of normalizing gaseous metabolism in stroke patients via eliminating CO2 deficit in tissues.
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PMID:[Erythrocyte carboanhydrase and gas metabolism in patients with ischemic stroke]. 312 92


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