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INTRODUCTION: The aim of this study was to assess the results and adverse effects of bromocriptine in patients with traumatic brain injury-vegetative state (TBI-VS) or traumatic brain injury-minimally conscious state (TBI-MCS). METHODS: We conducted a retrospective review of 10 patients, six with TBI-VS and four with TBI-MCS. All patients received bromocriptine at a starting dose of 2.5mg twice daily. Bromocriptine was titrated up to 7.5 or 12.5mg twice daily according to response and was maintained for at least 4 weeks. Various assessment scales were used in the following stages: before bromocriptine administration, at 4 weeks post bromocriptine prescription, and at hospital discharge. The assessment scales used were the Coma Recovery Scale-Revised (CRS-R), Disability Rating Scale, Glasgow Coma Scale, Barthel Scale, and Marshall Scale. RESULTS: Of the 10 patients, four with TBI-MCS and four with TBI-VS achieved a score of 23 points at discharge in the CRS-R, thus emerging from VS or MCS and regaining functional status. There were only two patients who emerged from VS but remained in MCS (8 to 11 and 5 to 10 points in CRS-R). CONCLUSIONS: Considering the poor prognosis for recovery in these patients, bromocriptine use has a positive risk-benefit ratio at a dosage of at least 7.5mg twice daily for 4 weeks.

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BACKGROUND: Amantadine hydrochloride is one of the most commonly prescribed medications for patients with prolonged disorders of consciousness after traumatic brain injury. Preliminary studies have suggested that amantadine may promote functional recovery. METHODS: We enrolled 184 patients who were in a vegetative or minimally conscious state 4 to 16 weeks after traumatic brain injury and who were receiving inpatient rehabilitation. Patients were randomly assigned to receive amantadine or placebo for 4 weeks and were followed for 2 weeks after the treatment was discontinued. The rate of functional recovery on the Disability Rating Scale (DRS; range, 0 to 29, with higher scores indicating greater disability) was compared over the 4 weeks of treatment (primary outcome) and during the 2-week washout period with the use of mixed-effects regression models. RESULTS: During the 4-week treatment period, recovery was significantly faster in the amantadine group than in the placebo group, as measured by the DRS score (difference in slope, 0.24 points per week; P=0.007), indicating a benefit with respect to the primary outcome measure. In a prespecified subgroup analysis, the treatment effect was similar for patients in a vegetative state and those in a minimally conscious state. The rate of improvement in the amantadine group slowed during the 2 weeks after treatment (weeks 5 and 6) and was significantly slower than the rate in the placebo group (difference in slope, 0.30 points per week; P=0.02). The overall improvement in DRS scores between baseline and week 6 (2 weeks after treatment was discontinued) was similar in the two groups. There were no significant differences in the incidence of serious adverse events. CONCLUSIONS: Amantadine accelerated the pace of functional recovery during active treatment in patients with post-traumatic disorders of consciousness. (Funded by the National Institute on Disability and Rehabilitation Research; ClinicalTrials.gov number, NCT00970944.).

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UNLABELLED: The aim of the study was the evaluation of clinical condition of the children treated by Gliatilin and Dexamin for posttraumatic abulic state. MATERIAL AND METHOD: The study included 12 children (8 boys, 4 girls) at the age range between 7-16 years (mean age 7.8 years). The evaluation of clinical condition was performed on admission to the Department, and then at 3rd, 6th and 12th month after head injury. The authors analyzed the kind of injury (posttraumatic changes in neuroimaging) and evolution of patients' clinical condition in the follow-up. RESULTS: The most commonly observed reasons of trauma were motor vehicle accidents. The kind of pathology found on the base of neuroimaging did not affect the results of treatment. The patients were treated by Gliatilin, Dexamin or both. In spite of this treatment all children were rehabilitated and their hearing, sight and speech organ were stimulated. Six months after injury only one patient still presented abulic state and six of our patients were in good general condition. None of our patients revealed abulic state after 12 months of head trauma. In two children the Dexamin treatment was given up for seizures. We did not observe any side effects of Gliatilin. CONCLUSIONS: The kind of trauma and posttraumatic intracranial pathology do not determine the prognosis. The evaluation of treatment should be performed after 6-12 months. Gliatilin and Dexamin treatment improves the clinical state of patients with posttraumatic abulic state.

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PRIMARY OBJECTIVE: To evaluate the association between amantadine and recovery of consciousness from prolonged traumatic coma. RESEARCH DESIGN: A retrospective cohort study. METHODS: Subjects included 123 adults with severe traumatic brain injury (TBI) admitted over a 10-year period who remained in coma despite becoming medically stable. EXPERIMENTAL INTERVENTIONS: Cases received 100-200 mg of amantadine twice daily. MAIN OUTCOMES AND RESULTS: 46.4% (13/28) of cases emerged from coma compared to 37.9% (36/95) of controls (p = 0.42). Somatosensory evoked potential (SSEP) was the only significant predictor of emergence from coma (p = 0.02), while SSEP, age and Glasgow Coma Score (GCS) significantly predicted time to emerge from coma (p < 0.05). CONCLUSIONS: Although the study and its design do not support the view that amantadine has an effect on recovery of consciousness; it remains safe, inexpensive and has few side effects. The lack of treatment alternatives and anecdotal support for its use may warrant further study. Prospective controlled trials would yield more definitive results.

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A young semi-comatose male patient was investigated using 99mTc hexamethyl-propylene amine oxime (99mTc HMPAO) brain single photon emission computed tomography (SPECT) before and after administration of the gamma-aminobutyric acid (GABA) agonist zolpidem. It was observed that 15 minutes after application of the drug the patient awoke from his semi-comatose condition and remained awake for the next 3-4 hours. When drug action subsided he returned to his semi-comatose state. Brain SPECT before drug application showed large hypo-active areas in certain parts of the brain. Brain SPECT after drug application showed a generalised cortical activation relative to the cerebellum and a marked and amplified activation of the areas that were hypo-active before drug application.

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