Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0599766 (functional recovery)
13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Delirium is a global impairment of upper brain functions caused by an organic substrate. It is frequently observed in the postoperative period, particularly in elderly people. Vascular and orthopedic surgery and long-duration surgery are associated with a higher incidence of postoperative delirium. When it occurs, postoperative delirium makes patient management much more difficult, increases costs, and, above all, causes severe discomfort to the patient. Delirium is also associated with higher postoperative mortality and morbidity, and with delayed functional recovery, but it is still unclear whether worse prognosis is directly caused by delirium or results from the neurological damage of which delirium is simply a symptom. Drug therapy should be part of a complex approach to prevent and treat this complication. Neuroleptics like haloperidol and droperidol, and benzodiazepines are usually employed in order to control symptoms like agitation, restlessness, and altered perceptions. Atypical neuroleptics, like risperidone, have not yet been studied in postoperative delirium, although some case reports in which they were successfully used have been published. Physiostigmine is effective in delirium caused by anticholinergic syndrome; vitamins may be useful in alcoholics; melatonin use has been suggested in order to prevent and treat delirium by normalizing sleep-wake cycle alterations. Environmental interventions are often costless and may be very useful to prevent and treat postoperative delirium in patients at risk.
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PMID:Postoperative delirium. 1630 59

The DSM-IV criteria for mania require: a distinct period that represents a break from pre-morbid functioning, a duration of at least one week, elevated or irritable mood, at least three to four classical manic signs and symptoms and the absence of any physical factors. Although not specifically mentioned in the ICD-10 or the DSM-IV definitions, delusional, hallucinatory, even first-rank, psychotic experiences can occur in mania. Acute mania can be subdivided into classical pure mania, mania with mood-congruent or mood-incongruent psychosis, mixed state and rapid-cycling mania. One quarter to two thirds of all manic episodes are associated with delusions, while 13% to 40% are associated with hallucinations. Mixed episode is a complex syndrome which is difficult to diagnose, has the most prolonged duration of bipolar episodes and more frequent psychotic profile than pure mania with high suicidality and poor response to drugs. Mixed state mania has been well known since Kreapelin and listed in classification systems with criteria that include both a manic and a major depressive episode nearly every day for at least a one-week period. On the other hand, mixed-like episodes that are clearly caused by somatic antidepressant treatment (e.g., medication, electro-convulsive therapy or light therapy) should not contribute toward a diagnosis of Bipolar I Disorder. Although, theoretically, mania is supposed to be resolved within 1-3 months even without treatment, psychiatric hospitalization is very common in especially severe cases due to functional impairment. Current treatments for mania aim to control the agitation, impulsivity, aggression and psychotic symptoms and to help patients regain their pre-morbid functionality. However, the clinical management of mania is challenging as most patients show syndromal remission but incomplete functional recovery after the first episode of mania.
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PMID:Treatment of acute mania. 1636 86

This prospective analysis aimed to study the influence of psychopathological dimensions on the global functioning of persons suffering from psychotic disorders, taking into account the role of a broad range of potential confounders. A large international cohort (n=1888) with ICD-10 non-affective psychosis was evaluated both at baseline during a hospital admission and three months after discharge. Trained interviewers administered a global functioning scale (GAF) and a psychopathological scale (BPRS) at baseline and follow-up). Baseline BPRS psychopathological dimensions were extracted using Principal Component Analysis. Results of multiple linear regression analyses demonstrated that affective symptoms (depressive or manic) prospectively predict a better global functioning, whilst agitation/cognitive symptoms determined poorer global functioning. Other predictors showing an independent effect on better global functioning were medication compliance, country of residence, female gender, married or coupled status, younger age and having a diagnosis of schizoaffective disorder rather than schizophrenia or other ICD-10 psychosis. A predicting model for global functioning in patients with psychosis is provided, showing that assessment of affective and agitation/cognitive symptoms should be emphasised during admission as they can be more informative than positive/negative symptoms in prospectively planning follow-up care that is geared towards a better functional recovery.
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PMID:Acute psychopathology as a predictor of global functioning in patients with ICD-10 non-affective psychosis: a prospective study in 11 European countries. 2162 22

Traumatic brain injury (TBI)-induced agitation and aggression pose major obstacles to clinicians in the acute hospital and rehabilitation settings. Thus, management of these symptoms is crucial. Antipsychotic drugs (APDs) are a common treatment approach for alleviating these symptoms. However, previous preclinical TBI studies have indicated that daily and chronic administration of these drugs (e.g., haloperidol; HAL) can exacerbate cognitive and motor deficits. Quetiapine (QUE) is an atypical APD that differs from many typical APDs, such as HAL, in its relatively rapid dissociation from the D2 receptor. The goal of this study was to test the hypotheses that intermittent HAL and QUE would not hinder recovery of cognitive and motor function following TBI and that daily QUE would also not impair functional recovery, which would be in contrast to HAL. Seventy anesthetized male rats received either a controlled cortical impact or sham injury and were then randomly assigned to TBI and sham groups receiving HAL (0.5mg/kg) or QUE (10mg/kg) intraperitoneally once per day or once every other day and compared to each other and vehicle (VEH) controls. Motor function was assessed by beam balance/walk tests on post-operative days 1-5 and cognitive function was evaluated with a Morris water maze task on days 14-19. No differences were revealed among the sham groups in any task, and hence the data were pooled. No overall differences were detected among the TBI groups, regardless of treatment or administration paradigm [p>0.05], but all were impaired vs. SHAM controls [p<0.05]. The SHAM controls also performed significantly better in the cognitive test vs. all TBI groups [p<0.05]. Moreover, the TBI+continuous HAL group performed worse than the TBI+continuous VEH, TBI+continuous QUE, and TBI+intermittent QUE groups [p<0.05], which did not differ from one another. Overall, the data suggest that QUE does not exacerbate TBI-induced cognitive and motor deficits, which supports the hypothesis. QUE may prove useful as an alternative APD treatment for management of agitation and aggression after clinical TBI. HAL may also be safe, but only if used sparingly.
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PMID:Intermittent treatment with haloperidol or quetiapine does not disrupt motor and cognitive recovery after experimental brain trauma. 2766 99

Antipsychotic drugs, such as haloperidol (HAL), are prescribed in the clinic to manage traumatic brain injury (TBI)-induced agitation. While preclinical studies have consistently shown that once-daily administration of HAL hinders functional recovery after TBI in male rats, its effects in females are unknown. Hence, the objective of this study was to directly compare neurobehavioral and histological outcomes in both sexes to determine whether the reported deleterious effects of HAL extend to females. Anesthetized adult female and male rats received either a controlled cortical impact (CCI) or sham injury and then were randomly assigned to a dosing regimen of HAL (0.5mg/kg, i.p.) or vehicle (VEH; 1mL/kg, i.p.) that was initiated 24h after injury and continued once daily for 19 consecutive days. Motor function was tested using established beam-balance/walk protocols on post-operative days 1-5 and acquisition of spatial learning was assessed with a well-validated Morris water maze task on days 14-19. Cortical lesion volume was quantified at 21days. No statistical differences were revealed between the HAL and VEH-treated sham groups and thus they were pooled for each sex. HAL only impaired motor recovery in males (p<0.05), but significantly diminished spatial learning in both sexes (p<0.05). Females, regardless of treatment, exhibited smaller cortical lesions vs VEH-treated males (p<0.05). Taken together, the data show that daily HAL does not prohibit motor recovery in females, but does negatively impact cognition. These task-dependent differential effects of HAL in female vs male rats may have clinical significance as they can direct therapy.
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PMID:Comparable impediment of cognitive function in female and male rats subsequent to daily administration of haloperidol after traumatic brain injury. 2869 31

Traumatic brain injury (TBI) and its potential long-term consequences are of major concern for public health. Neurorehabilitation of affected individuals has some specific characteristics in contrast to neurorehabilitation of patients with acquired brain lesions of other aetiology. This review will deal with the clinical consequences of the distinct lesions of TBI. In severe TBI, clinical course often follows a typical initial sequence of coma; followed by disturbed consciousness; later, post-traumatic agitation and amnesia; and finally, recovery of function occurs. In the different phases of neurorehabilitation, physicians should be aware of typical medical complications such as paroxysmal sympathetic hyperactivity, posttraumatic hydrocephalus, and posttraumatic neuroendocrine dysfunctions. Furthermore, we address questions on timing and on existing evidence for different rehabilitation programmes and for holistic neuropsychological rehabilitation approaches.
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PMID:Neurorehabilitation of Traumatic Brain Injury (TBI): A Clinical Review. 3088

This comprehensive review discusses clinical studies of patients following brain injuries (traumatic, acquired, or stroke), who have been treated with amantadine or memantine. Both amantadine and memantine are commonly used in the acute rehabilitation setting following brain injuries, despite their lack of FDA-approval for neuro-recovery. Given the broad utilization of such agents, there is a need to review the evidence supporting this common off-label prescribing. The purpose of this review is to describe the mechanisms of action for memantine and amantadine, as well as to complete a comprehensive review of the clinical uses of these agents. We included 119 original, clinical research articles from NCBI Medline, published before 2019. We focused on the domains of neuroplasticity, functional recovery, motor recovery, arousal, fatigue, insomnia, behavior, agitation, and cognition. Most of the existing research supporting the use of amantadine and memantine in recovery from brain injuries was done in very small populations, limiting the significance of conclusions. While most studies are positive; small effect sizes are usually reported, or populations are subject to bias. Furthermore, evidence is so limited that this review includes research regarding both acute and chronic acquired brain injury populations. Fortunately, reported short-term side effects generally are modest, and stop soon after amantadine/memantine is discontinued. However, responses are inconsistent, and the phenotype of responders remains elusive.
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PMID:Amantadine and memantine: a comprehensive review for acquired brain injury. 3207 7