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

Cranioplasty is indicated for patients with a skull bone defect. Patients may achieve subjective and objective improvements after cranioplasty. Some patients with severe brain swelling treated with decompressive craniectomy may develop hydrocephalus associated with severe brain bulging or even herniation via the skull bone defect. Consequently, these patients require a ventriculoperitoneal (V-P) shunt to relieve hydrocephalus. However, after shunting for hydrocephalus, they may develop severe sinking at the skull defect. Subsequently, when doing a cranioplasty for such a depressed defect, it may result in the dysfunction of the underlying brain, or even hematoma formation due to the large dead space. In this study, we advocate a temporary procedure to occlude the V-P shunt tube to allow the expansion of a depressed scalp flap to facilitate the subsequent cranioplasty. We report four patients with severe depression of the skull defect resulting from previous traumatic brain swelling followed by decompressive craniectomy and V-P shunting for communicating hydrocephalus. A simple subcutaneous clipping of the shunt tube was performed to allow the expansion of the depressed scalp to obliterate the dead space before the cranioplasty. All four patients obtained a satisfactory result without complications and achieved good functional recovery. A temporary occlusion of the shunt tube with an aneurysm clip before cranioplasty for patients with a severely depressed scalp flap is a simple and useful procedure. This procedure can safely and effectively eliminate the dead space between the skull plate and the dura to facilitate the cranioplasty, and thus prevent the potential complication of intracranial hematoma.
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PMID:Cranioplasty for patients with severe depressed skull bone defect after cerebrospinal fluid shunting. 1238 14

Traumatic brain injury (TBI) is one of the few known risk factors for Alzheimers disease (AD) and for depression. The mechanisms by which trauma causes delayed cognitive deficits are largely unknown. In recent studies, it was demonstrated that the complement system (an important component of the immune system and a mediator of inflammation) is activated both in human AD and following experimental TBI in rats. Amyloid proteins are also present in AD and following TBI, and are known to activate complement in vitro. Based on these and other previous studies, it was hypothesized that regulation of the complement system will attenuate the long-term consequences of TBI. Vaccinia virus complement control protein (VCP) is a protein encoded by vaccinia virus. It blocks both the classic and alternative pathways of complement activation in vitro, and by doings so prevents the generation of proinflammatory chemotactic factors. Based on in vitro studies VCP can block the complement activation by the amyloid beta peptide. Using a fluid percussion rat model that causes traumatic brain injury (TBI), it was found that VCP significantly enhances functional recovery as determined by the Morris Water Maze test. Taken togther these studies indicate that potentially VCP could block molecular signals such as the formation of amyloid beta or the activation of complement to inhibit formation of AD following TBI.
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PMID:Potential intervention by vaccinia virus complement control protein of the signals contributing to the progression of central nervous system injury to Alzheimer's disease. 1248 87

Concern about the effects of anesthesia on physiological measurements led us to develop methodology to assess left ventricular (LV) pressure in conscious mice. Polyethylene-50 tubing filled with heparinized saline was implanted in the LV cavity through its apex via an abdominal approach and exteriorized to the back of the animal. This surgery was done under anesthesia with either an intraperitoneal injection of ketamine (80 mg/kg) and xylazine (5 mg/kg) (K+X) in 11 mice or isoflurane (ISF; 1.5 vol%) by inhalation in 14 mice. Postoperatively, mice were trained daily to lie quietly head first in a plastic cone. LV pressure, the first derivative of LV pressure (dP/dt), and heart rate (HR) in the conscious state were compared between the two groups at 3 days and 1 wk after recovery from surgery using a 1.4-Fr Millar catheter inserted into the LV through the tubing, with the mice lying quietly in the plastic cone. Acutely during anesthesia, K+X decreased HR (from 698 to 298 beats/min), LV systolic pressure (from 107 to 65 mmHg), and maximal dP/dt (dP/dt(max)) (from 15,724 to 4,445 mmHg/s), all P < 0.01. Similar but less marked negative chronotropic and inotropic effects were seen with ISF. HR and dP/dt(max) were decreased significantly in K+X mice 3 days after surgery compared with those anesthetized with ISF (655 vs. 711 beats/min, P < 0.05; 14,448 vs. 18,048 mmHg/s, P < 0.001) but increased to the same level as in ISF mice 1 wk after surgery. In ISF mice, recovery of function occurred rapidly and there were no differences in LV variables between 3 days and 1 wk. LV pressure and dP/dt can be measured in conscious mice with a micromanometer catheter inserted through tubing implanted permanently in the LV apex. Anesthesia with either K+X or, to a lesser extent, ISF, depressed LV function acutely. This depression of function persisted for 3 days after surgery with K+X (but not ISF) and did not recover completely until 1 wk postanesthesia.
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PMID:New technique for measurement of left ventricular pressure in conscious mice. 1456 61

The dentate gyrus is believed to play a key role in the pathogenesis of temporal lobe epilepsy. In normal brain the dentate granule cells serve as a high-resistance gate or filter, inhibiting the propagation of seizures from the entorhinal cortex to the hippocampus. The filtering function of the dentate gyrus depends in part on the near absence of monosynaptic connections among granule cells. In humans with temporal lobe epilepsy and in animal models of temporal lobe epilepsy, dentate granule cells form an interconnected synaptic network associated with loss of hilar interneurons. This recurrent mossy fiber pathway mediates reverberating excitation that can reduce the threshold for granule cell synchronization. Factors that augment activity in this pathway include modest increases in [K+]o; loss of GABA inhibition; short-term, frequency-dependent facilitation (frequencies of 1-2 Hz); feedback activation of kainate autoreceptors; and release of zinc from recurrent mossy fiber boutons. Factors that diminish activity include short-term, frequency-dependent depression (frequencies < 1 Hz); feedback activation of type II metabotropic glutamate receptors; and the potential release of GABA, neuropeptide Y, adenosine, and dynorphin from recurrent mossy fiber boutons. The axon sprouting and reactive synaptogenesis that follow seizure-related brain damage can also create or strengthen recurrent excitation in other brain regions. These changes are expected to facilitate participation of these regions in seizures. Thus, reactive processes that are often considered important for recovery of function after most brain injuries probably contribute to neurological dysfunction in epilepsy.
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PMID:The recurrent mossy fiber pathway of the epileptic brain. 1458 19

The aim of this study was to identify the efficacy of in-patient stroke rehabilitation, to evaluate the relationship between clinical characteristics and functional outcome, and to determine factors predicting functional outcome at discharge in Turkish stroke patients with a team approach. Retrospective data were collected from 102 of 116 patients with first stroke who were admitted to our rehabilitation unit at Ankara University. Demographic data, length of hospital stay (LOHS), onset to admission interval (OAI), type, side and location of stroke lesion, and most common medical complications were recorded. Functional Independence Measure (FIM) and Brunnstrom's motor recovery stages (BMRS) were assessed on admission and at discharge. The mean age was 61.6 +/- 10.9 years and the mean LOHS was 69.7 +/- 28.2 days. The mean FIM total scores were 69.2 +/- 27.4 and 83.2 +/- 25.7 on admission, and at discharge, respectively. The mean FIM total score was significantly correlated to age, LOHS and motor recovery. The FIM total scores of patients with aphasia and depression were found to be lower than those of patients without aphasia and depression. In a stepwise multiple regression analysis, FIM total score on admission, age and OAI were found to be valid predictors of FIM total score at discharge. Functional Independence Measure total score on admission was the strongest variable. Our results suggest that knowledge of the poor prognostic factors effecting functional outcome on admission can provide information to clinicians in identifying severity of stroke. Admission FIM total score, can be used to predict the patients' functional recovery. Advanced age, aphasia and post-stroke depression contribute to lower FIM scores.
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PMID:Rehabilitation outcome of Turkish stroke patients: in a team approach setting. 1463 61

Patients who suffer severe brain damage may be left unaware of self and of the environment and in a permanent vegetative state (PVS). The difficulties in correctly ascertaining unawareness after brain injury have been emphasized by a number of authors. It is well recognized that toxic-metabolic and drug-induced cerebral depression occurs acutely after brain injury. However, less attention has been drawn to the effects of medication months after brain injury and the way in which medication may confound assessment of awareness and, thus, the reliable assessment of long-term prognosis. This paper describes two patients who sustained a severe and well-documented structural brain injury, one hypoxic and one traumatic. Both were unaware when first seen at 3 months post-injury, but both have made useful functional recovery. The paper discusses their progress and how the early prescription of large doses of anti-epileptic drugs, sedatives and anti-spastic agents in these circumstances may result in an initial misdiagnosis of the vegetative state.
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PMID:Misdiagnosing the vegetative state after severe brain injury: the influence of medication. 1466 Feb 32

Pharmacotherapy is the foundation of treatment for bipolar disorder, but research suggests that adjunctive psychosocial interventions that are manualized, reproducible, time-limited, empirically supported, and strategically target a number of critical domains, can efficiently provide additional benefits. Psychoeducation as an adjunct of pharmacotherapy may be beneficial, but questions remain about the utility of this treatment for patients who are already compliant with medication treatment. Family educational interventions have demonstrated encouraging results in relapse prevention, but follow-up data are limited and application to patients who have limited social networks may be problematic. Reports on interpersonal and social rhythm therapy in patients with bipolar disorder are scarce, and what is available shows no differential effect on time to remission or relapse, but a significant impact on subsyndromal symptoms. Follow-up data suggest that patients receiving cognitive behavior therapy have significantly fewer bipolar episodes, shorter episodes, fewer hospitalizations, and less subsyndromal mood symptoms. It is unclear, however, if cognitive behavior therapy is superior to other active psychosocial treatments and whether its mechanism in patients with bipolar disorder is through changing dysfunctional cognitions or simply enhancing early symptom detection. Psychotherapies should be considered early in the course of illness to improve medication compliance and to help patients identify prodromes of relapse in order to take steps for prevention. In addition, some strategies may have a beneficial effect on residual symptoms, particularly symptoms of depression, and thus help move patients toward a more comprehensive functional recovery.
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PMID:Targeted psychosocial interventions for bipolar disorder. 1470 17

Pathological processes in the vitreous will be reflected in the morphology and function of the retina, and these processes can originate from sources outside the vitreous. The purpose of vitreous surgery is to remove the qualitatively and/or morphologically diseased vitreous. Successful vitrectomy will be manifested by an improvement in the structure and/or function of the retina. We have evaluated the morphology of the vitreoretinal interface, and the function of the retina before and after vitreous surgery. Plasmin-assisted vitrectomy was used in some cases to remove the diseased vitreous more efficiently and less invasively. The effect of this procedure was assessed by examining the morphology and function of the retina. First, the relationship between the qualitative and structural abnormality of the vitreous in macular diseases was studied. In aphakic/pseudophakic eyes with cystoid macular edema, there was a depression of retinal function over the entire retina which may have been caused by chemical mediators released into the vitreous. These mediators may have been produced by inflammation in the anterior segment of the eye. In eyes with an idiopathic macular hole, optical coherence tomographic (OCT) images suggested that the progression of the macular hole might depend on a balance between foveal adhesion and the posterior vitreous. Second, the efficacy, surgical damage, and limitations of vitreous surgery were investigated. The recovery of macular function was assessed by focal macular electroretinograms (FMERGs) after vitrectomy for epiretinal membrane, choroidal neovascularization, and diabetic macular edema. The concurrent examination by optical coherence tomography (OCT) suggested that a decrease in retinal thickness contributed to the functional recovery. Macular functional recovery was delayed and limited after macular translocation, diabetic macular edema, and internal limiting membrane peeling. Third, we studied the effect of plasmin-assisted vitrectomy on the retina. The plasmin was used to remove the vitreous more completely and less invasively. In rabbits, ERG, OCT, and histological examinations demonstrated that the use of commercially-available plasmin at a concentration used on human patients resulted in temporary adverse effects on the retina. For human patients, we purified the plasmin from the patients' serum at the Nagoya University Hospital and the activity was about the same as in previous reports. The purified plasmin was approved by our hospital's institutional review board, and written informed consent was obtained from each patient. Patients with macular edema, idiopathic macular hole, and epiretinal membrane without posterior detachment underwent plasmin-assisted vitrectomy and were evaluated morphologically and electrophysiologically. The efficacy of the plasmin in separating the vitreo-retinal interface was demonstrated by an occasional spontaneous posterior vitreous detachment with or without core vitrectomy, and the presence of less vitreous cortex attached to the internal limiting membrane that was removed during vitrectomy. This was the first histological demonstration of the effectiveness of plasmin in the living eye. Full-field ERGs before and after surgery demonstrated clear evidence that no alteration of retinal functional had occurred, although we did detect a possible osmotic effect by an increase in OCT-determined retinal thickness by the high-molecular weight autologous plasmin. In future studies, the proper concentration and reaction time for each condition of the vitreous should be determined. In conclusion, the pathophysiology of the vitreous should reflect the retinal function. The recovery of the structure of the retina is important for the recovery of retinal function. This should always be the primary goal of surgeons who perform quality surgery.
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PMID:[Relationship between vitrectomy and the morphology and function of the retina]. 1473 33

The idea that damage to one part of the nervous system can have effects at a distance was popular during the 19th century. Constantin von Monakow, MD, accepted this idea and blended it with the newly formulated neuron doctrine early in the 20th century to account for ipsilateral paralyses and recovery of function. He called his theory of neural depression caused by loss of inputs to structures tied to the damaged area diaschisis. In this article, we examine the origins of diaschisis and the goals of Monakow. Credit is given to Monakow for drawing needed attention to the dynamics of the nervous system, remote lesion effects, and recovery of function, even though the fine details or specifics of his theory have had a mixed reception.
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PMID:The Monakow concept of diaschisis: origins and perspectives. 1496 81

This study investigated the differential effect of losartan, an AT1 receptor blocker, when administered in pre- and postischemic phases, on the biochemical, hemodynamic and oxidative stress associated with regional ischemic-reperfusion injury in cat. Losartan (5 microg/kg/min) or normal saline was administered intravenously in open chest barbiturate anesthetized cats, 15 min before and 10 min after the occlusion of the left anterior descending (LAD) coronary artery. The LAD was occluded for 15 min followed by 60 min reperfusion. In the saline treated group, there was significant depression of hemodynamic functions, i.e., mean arterial pressure (MAP), heart rate (HR), left ventricular end diastolic pressure (LVEDP) and left ventricular (LV) peak (+/-) dP/dt, along with depletion of adenosine triphosphate (ATP) of the affected myocardium. Oxidative stress during reperfusion injury was evidenced by significant increase in plasma thiobarbituric acid reactive substances (TBARS) accompanied by significant reduction in myocardial superoxide dismutase (SOD) activities. In both treatment groups, losartan caused recovery of all the hemodynamic parameters and repletion of ATP along with no significant change in plasma TBARS and myocardial SOD activity. There was no effect on catalase activity. Results from the study suggest that the effects of pre- and posttreatment of losartan are comparable in functional recovery of the heart from ischemic-reperfusion injury.
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PMID:Effect of pre- and posttreatment of losartan in feline model of myocardial ischemic-reperfusion injury. 1498 40


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