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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrophysiological investigations were carried out on 20 healthy controls and 130 patients with peripheral facial nerve paralysis. The aetiology was as follows: idiopathic (Bell's palsy) in 60 cases, viral in 29, traumatic in 18, postoperative in 4, in connexion with chronic otitis media in 6, diabetes mellitus in 4, positive rheumatological tests in 3, disturbed lipid metabolism in 2, the Melkersson-Rosenthal syndrome in 1, as a complication of pregnancy in 2, and in association with a tumour in 1 case. The compound action potential (CAP) of the orbicularis oris muscle was determinedi n 370 occasions in a right/left comparision, the record of the muscle response was intergrated over the time of action (IAR) on 32 occasions and trison of 255 occasions. The normal values are given in the first place and their dependence of the age of the subject. Then, the prognostic sifnficance of the above-mentioned parameters is investigated in cases of peripheral facial nerve paralysis. It is apparent that the determination of the CAP in a right/left comparison is a valuable prognostic guide as early as the 4th day, insofar as a decrease in this parameter of under 50% can be interpreted as a favourable sign and satisfactory reversal of the paralysis can be expected within 6-8 weeks. By contrast, a decrease of over 70% in the CAP is a bad prognostic sign, indicative of presumably only a poor trend to reversal of the paralysis. An intermediate depression of the CAP in the range of 50-70% signifies an expected moderate recovery within 6-8 weeks ahe case of CAP determination at the time of maximum amplitude depression (as opposed to the 4th day), then a decrease of less than 70% is taken to be indicative of satisfactory functional recovery within 6-8 weeks; a decrease of 95-100% signifies a bad prognosis, whilst a decrease amounting to between 70 and 95% carries an uncertain prognosis. The maximum decrease in amplitude was registered on the 8th day on average; the range lay between the 4th and the 14th day. An exception to these figures was the delayed response of the CAP in the case of 6 patients, 5 of whom showed a maximum decrease during the 3rd week and the last patient as late as the 4th week following the onset of facial nerve paresis. Similar reliance can be placed on the prognostic value of the IAR. however, the decrease in the IAR is smaller than that of the CAP measured on the same potential in a right/left comparison, so that a decrease in the IAR of over 60% can already herald a poor recovery. Repeated determination of the latency in cases of facial nerve paralysis showed that the mean latency value for the entire group of patients was slightly prolonged at the end of the 1st week, but the latency values obtained in any one particular patient are of no prognostic significance. A comparison between CAP and latency values obtained with the opposite (i.e...
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PMID:[Prognostic assessment in peripheral facial nerve paralysis with particular reference to electroneurography (author's transl)]. 18 19

The literature concerning postcardiotomy delirium contains confusing definitions and contradictory results. In a critical review of the subject, we conclude that cardiac status, the severity of physical illness, the complexity of the surgical procedure, and preoperative organic brain disease are the determining factors in postcardiotomy delirium. Preoperative anxiety, denial, and depression also have some correlation. Age, sex, time on bypass, and preoperative psychological profile seem to have no influence on outcome. No psychological etiology for delirium has been proven consistently. The therapeutic influence of preoperative interviews in preventing postoperative psychiatric complications remains equivocal as do theories implicating sensory deprivation in the intensive care unit. Long-term follow-up studies suggest that psychological problems impair functional recovery from heart surgery. The suggested treatment of patients with delirium includes chemotherapy, psychotherapy, and environmental support. Finally we suggest that investigation of biochemical abnormalities in delirium may prove to be a model for clarifying the role of neurotransmitters in functional psychiatric illnesses.
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PMID:Postcardiotomy delirium: a critical review. 37 Apr 60

In an isolated dog heart preparation the influence of normothermic ischemic arrest and recovery of the ventricular function during the period of post-ischemic reperfusion were investigated. If ischemic arrest has caused a depression of ventricular function, the functional recovery of the myocardium cannot be improved significantly by a prolonged reperfusion of the empty beating heart.
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PMID:[The influence of postischemic reperfusion on the recovery of ischemic lesions of the left ventricle (author's transl)]. 71 51

Adult rhesus monkeys were subjected to complete cerebral ischemia for one hour and subsequent recirculation for up to 24 h. Animals with signs of functional recovery (e.g. spontaneous EEG activity) exhibited a partial replenishment of cellular energy sources (ATP, phosphocreatine) and a progressive normalization of cerebral lactate levels. Glucose and pyruvate concentrations showed a transient increase over control values during the early stages of postischemic recirculation. Monkeys without functional recovery lacked a significant resynthesis of energy-rich compounds; adenine nucleotides continued to decrease and lactate concentrations were higher than in animals subjected to ischemia without recirculation. Cerebral polysome profiles remained unaltered during the ischemic period but in all animals a marked disaggregation of polyribosomes with a concomitant increase in ribosomal subunits occurred after the onset of recirculation. In monkeys with indications of functional recovery these changes were reversible but a normal polysome profile was only observed after 24 h of recirculation. The results obtained indicate a postischemic depression of protein synthesis due to an inhibition of peptide chain initiation. After recirculation of the brain for 3-6 h there was evidence for an induction of enzymes involved in polyamine synthesis (ornithine decarboxylase and S-adenosylmethionine decarboxylase). No changes in the activity of these enzymes were observed at the end of the ischemic period, indicating that during complete cerebral ischemia not only the synthesis but also the catabolism of proteins is inhibited.
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PMID:Resuscitation of the monkey brain after one hour complete ischemia. III. Indications of metabolic recovery. 115 69

1. Anoxic injury in CNS white matter was studied using the in vitro rat optic nerve preparation. Optic nerves were subjected to 60 min of anoxia, and functional recovery was assessed using the area under the compound action potential (CAP). In normal cerebrospinal fluid, CAP area recovered to 33.5 +/- 9.3% (SD) of control. 2. Lidocaine and procaine (0.1 or 1.0 mM), applied beginning 1 h before anoxia, significantly improved postanoxic recovery of CAP area. However, both agents also depressed the preanoxic CAP. Procaine generally allowed greater recovery with less depression compared with lidocaine. 3. The quaternary derivatives QX-314 (0.1-1.0 mM) and QX-222 (0.3-3.0 mM) resulted in more complete recovery of the CAP area from anoxia, with less depression of preanoxic excitability, compared with the tertiary compounds. At 0.3 mM, QX-314 reduced the preanoxic CAP very little (to 94.4 +/- 14% of control CAP area), yet allowed the postanoxic CAP area to recover to 99.6 +/- 19%. 4. We conclude that quaternary local anesthetics are more effective at protecting CNS white matter tracts from anoxia than tertiary compounds and that these agents can result in markedly improved recovery even at concentrations that do not block conduction. Moreover, given the relative specificity of QX-314 for noninactivating Na+ channels, we hypothesize that this channel subtype plays an important role in mediating anoxic injury in central myelinated axons.
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PMID:Tertiary and quaternary local anesthetics protect CNS white matter from anoxic injury at concentrations that do not block excitability. 131 81

It was examined whether lactate influences postischaemic hemodynamic recovery as a function of the duration of ischaemia and whether changes in high-energy phosphate metabolism under ischaemic and reperfused conditions could be held responsible for impairment of cardiac function. To this end, isolated working rat hearts were perfused with either glucose (11 mM), glucose (11 mM) plus lactate (5 mM) or glucose (11 mM) plus pyruvate (5 mM). The extent of ischaemic injury was varied by changing the intervals of ischaemia, i.e. 15, 30 and 45 min. Perfusion by lactate evoked marked depression of functional recovery after 30 min of ischaemia. Perfusion by pyruvate resulted in marked decline of cardiac function after 45 min of ischaemia, while in glucose perfused hearts hemodynamic performance was still recovered to some extent after 45 min of ischaemia. Hence, lactate accelerates postischaemic hemodynamic impairment compared to glucose and pyruvate. The marked decline in functional recovery of the lactate perfused hearts cannot be ascribed to the extent of degradation of high-energy phosphates during ischaemia as compared to glucose and pyruvate perfused hearts. Glycolytic ATP formation (evaluated by the rate of lactate production) can neither be responsible for loss of cardiac function in the lactate perfused hearts. Moreover, failure of reenergization during reperfusion, the amount of nucleosides and oxypurines lost or the level of high-energy phosphates at the end of reperfusion cannot explain lactate-induced impairment. Alternatively, the accumulation of endogenous lactate may have contributed to ischaemic damage in the lactate perfused hearts after 30 min of ischaemia as it was higher in the lactate than in the glucose or pyruvate perfused hearts. It cannot be excluded that possible beneficial effects of the elevated glycolytic ATP formation during 15 to 30 min of ischaemia in the lactate perfused hearts are counterbalanced by the detrimental effects of lactate accumulation.
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PMID:The nucleotide metabolism in lactate perfused hearts under ischaemic and reperfused conditions. 148 52

The characterization of unique responses of immature hearts to ischemic injury is important in devising better methods of myocardial protection for neonatal cardiac operations. Two end-points used to assess the vulnerability of immature myocardium to ischemic injury, namely, the time between onset of ischemia to the beginning of contracture and the functional recovery after reperfusion, had yielded results that appeared to be contradictory. In this study both the immature and adult rabbit hearts were used to study these two end-points in the same model, to assess their relationships and physiologic implications. Our data confirmed that, although immature hearts have greater capacity than adult hearts for functional recovery after identical periods of ischemic insult, their times to ischemic contracture are not prolonged, as could have been expected. A negative correlation between the rise in resting myocardial tension (i.e., contracture) and the recovery of ventricular function after reperfusion was noted both in the neonatal and in the adult hearts. However, reperfusion undertaken after "the onset of contracture" showed that the ventricle could still regain a measure of its function, which indicates that the "irreversibility" in global ventricular function is a gradual and progressive phenomenon. Biochemical studies of sarcoplasmic reticular calcium-adenosinetriphosphatase activity indicated that the immature myocardium has a significantly lower activity of this enzyme. Further depression of this enzyme activity after ischemia is seen in the immature hearts and may in part explain the earlier onset of contracture reported. A unifying concept to explain these unique responses of neonatal hearts to ischemia is proposed, based on the immaturities of certain key enzymes. The implications of these findings in the development of better protective techniques are also discussed.
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PMID:Unique responses of immature hearts to ischemia. Functional recovery versus initiation of contracture. 153 57

During 10 mins of reperfusion after 25 mins global ischemia, subtoxic doses of ouabain (50, 100 microM) were used and followed by 20 mins reperfusion with standard buffer. At these doses ouabain had no harmful effects with 29% and 45% increase in developed pressure in aerobic hearts. Intracellular Na+ (Nai), 45Ca2+ uptake and recovery of ventricular function were measured. Nai increased from 15 to 64 mumol/g dw with no increase in 45Ca2+ uptake during ischemia. Upon reperfusion with standard buffer, additional gain in Nai at 2 mins (73 mumol/g dw) was followed by a rapid decline (at 10 mins: 48 mumol/g dw). 45Ca2+ uptake increased from 0.8 to 7.5 mumol/g dw after 30 mins reperfusion with decreased recovery of function (45%) and increased LVEDP (29 mmHg). Reperfusion with ouabain accelerated initial rise in Nai (2 mins: 79 and 83 mumol/g dw) and decline of Nai was retarded (10 mins: 65 and 83 mumol/g dw). Consequently, 45Ca2+ uptake and depression of function were augmented (Ca: 10.0, 11.5 mumol/g dw; function: 27%, 18%; LVEDP: 47, 48 mmHg) even when hearts were switched back to standard buffer. Combination of high K+ (20mM) reversed the effect of ouabain. The results suggested increased susceptibility to ouabain was caused by inhibited outward Na+ transport resulting in enhanced Ca2+ influx through Na+/Ca2+ exchange.
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PMID:[Enhancement of susceptibility to ouabain in ischemic rat heart]. 170 9

Twenty millimolar and 2 mM uridine triphosphate and 2 mM uridine were injected intra-arterially into rat leg muscles during a 20 min period of intense exercise and during the recovery phase (20 min). Administration of 20 mM uridine triphosphate during exercise, provoked a complete depression of muscle contractility. On the contrary, supply of 2 mM uridine triphosphate or 20 mM uridine induced a reduction in the decrease of muscular developed tension during the exercise period of time and favoured functional recovery. This positive effect of pyrimidine compounds on muscular functional parameters did not seem to be correlated with metabolic effects. Indeed, 2 mM uridine supply did not modify the evolution of intramuscular glycogen and lactate concentrations and made worsened the adenine nucleotide degradation induced by exercise.
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PMID:Functional and metabolic effects of uridine and UTP on the skeletal muscle of the rat submitted to exercise. 171 6

This study examined the strategies used by 101 older women, aged 65 to 94, to cope with their hip fractures. During an interview, the women described their health, income, ability to perform tasks of daily living, cognitive functioning, locus of control, levels of depression, informal network, and use of coping strategies. Results indicate that the women used a variety of different coping strategies, with "seeking social support" being the most frequent. A strong belief in external control was the only resource predictive of the coping strategies employed. The use of several emotional-focused strategies was associated with poorer functional recovery.
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PMID:Coping strategies of older women with hip fractures: resources and outcomes. 173 Aug 54


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