A multicentre study on the clinical utility of post-traumatic amnesia duration in predicting global outcome after moderate-severe traumatic brain injury.

BACKGROUND: Past research shows that post-traumatic amnesia (PTA) duration is a particularly robust traumatic brain injury (TBI) outcome predictor, but low specificity limits its clinical utility. OBJECTIVES: The current study assessed the relationship between PTA duration and probability thresholds for Glasgow Outcome Scale (GOS) levels. METHODS: Data were prospectively collected in this multicentre observational study. The cohort was a consecutive sample of rehabilitation patients enrolled in the National Institute on Disability and Rehabilitation Research funded TBI Model Systems (n = 1332) that had documented finite PTA duration greater than 24 h, and 1-year and 2-year GOS. RESULTS: The cohort had proportionally more Good Recovery (44% vs 39%) and less Severe Disability (19% vs 23%) at year 2 than at year 1. Longer PTA resulted in an incremental decline in probability of Good Recovery and a corresponding increase in probability of Severe Disability. When PTA ended within 4 weeks, Severe Disability was unlikely (<15% chance) at year 1, and Good Recovery was the most likely GOS at year 2. When PTA lasted beyond 8 weeks, Good Recovery was highly unlikely (<10% chance) at year 1, and Severe Disability was equal to or more likely than Moderate Disability at year 2. CONCLUSIONS: Two PTA durations, 4 weeks and 8 weeks, emerged as particularly salient GOS probability thresholds that may aid prognostication after TBI.

Neuropsychological outcome and community re-integration following traumatic brain injury: the impact of frontal and non-frontal lesions.

PRIMARY OBJECTIVE: To examine the relationship between cortical lesion location and brain injury outcome. It was hypothesized that focal frontal lesions after traumatic brain injury (TBI) would result in decreased executive and memory functioning and poor community participation outcome. RESEARCH DESIGN: Three quasi-experimental, prospective studies employed a total of 643 patients with focal frontal, fronto-temporal, non-frontal or no lesions in CT scans. METHODS AND PROCEDURES: CT scan analysis, neuropsychological assessment, the Neurobehavioural Functioning Inventory (NFI), the Community Integration Questionnaire (CIQ). MAIN RESULTS: In study 1, frontal and fronto-temporal groups performed worse in executive functioning and better in constructional ability. Study 2 found no differences in neuropsychological and community re-integration measures at 1-year follow-up. Study 3 found comparable neuropsychological test score improvement across groups over 1 year. CONCLUSIONS: Results are consistent with previous findings and document the potential for test score improvement with rehabilitation and suggest that lesion location needs to be considered when individual rehabilitation plans are being implemented in the post-acute stage of TBI.

Practice parameter: immunotherapy for Guillain-Barré syndrome: report of the Quality Standards Subcommittee of the American Academy of Neurology.

OBJECTIVE: To provide an evidence-based statement to guide physicians in the management of Guillain-Barré syndrome (GBS). METHODS: Literature search and derivation of evidence-based statements concerning the use of immunotherapy were performed. RESULTS: Treatment with plasma exchange (PE) or IV immunoglobulin (IVIg) hastens recovery from GBS. Combining the two treatments is not beneficial. Steroid treatment given alone is not beneficial. RECOMMENDATIONS: 1) PE is recommended for nonambulant adult patients with GBS who seek treatment within 4 weeks of the onset of neuropathic symptoms. PE should also be considered for ambulant patients examined within 2 weeks of the onset of neuropathic symptoms; 2) IVIg is recommended for nonambulant adult patients with GBS within 2 or possibly 4 weeks of the onset of neuropathic symptoms. The effects of PE and IVIg are equivalent; 3) Corticosteroids are not recommended for the management of GBS; 4) Sequential treatment with PE followed by IVIg, or immunoabsorption followed by IVIg is not recommended for patients with GBS; and 5) PE and IVIg are treatment options for children with severe GBS.

Concept of spastic hypertonia.

This introductory article highlights the definition of spastic hypertonia, and briefly introduces the reader to the incidence and most frequent causes of spastic hypertonia. The article also discusses the functional losses caused by spastic hypertonia that will be reviewed more thoroughly in the following articles. Also discussed is the neural physiology and the locations of the structural lesions within the central nervous system that are involved in spastic hypertonia, with an emphasis on the different clinical presentations depending on the location of the lesion.

Spastic hypertonia. Appendix.

This appendix reviews the most commonly used clinical methods for assessing the clinical treatment of spastic hypertonia. The definitions and rating scales shown often are accepted by the Food and Drug Administration for pharmaceutical and investigational trials to obtain a clinical indication for use in spasticity clinic.

Current concepts: diffuse axonal injury-associated traumatic brain injury.

OBJECTIVES: To review the probable physical, physiologic mechanisms that result in the medical and neuropsychologic complications of diffuse axonal injury (DAI)-associated traumatic brain injury (TBI). DATA SOURCES: Various materials were accessed: MEDLINE, textbooks, scientific presentations, and current ongoing research that has been recently reported. STUDY SELECTION: Included were scientific studies involving TBI, particularly direct injury to the axons and glia of the central nervous system (CNS) in both in vitro and in vivo models. These studies include pathologic findings in humans as well as the medical complications and behavioral outcomes of DAI. Studies that addressed animal models of DAI as well as cellular and/or tissue models of neuronal injury were emphasized. The review also covered work on the physical properties of materials involved in the transmission of energy associated with prolonged acceleration-deceleration injuries. DATA EXTRACTION: Studies were selected with regard to those that addressed the mechanism of TBI associated with DAI and direct injury to the axon within the CNS. The material was generally the emphasis of the article and was extracted by multiple observers. Studies that correlate the above findings with the clinical picture of DAI were included. DATA SYNTHESIS: Concepts were developed by the authors based on the current scientific findings and theories of DAI. The synthesis of these concepts involves expertise in physical science, basic science concepts of cellular injury to the CNS, acute medical indicators of DAI, neuropsychologic indicators of DAI, and rehabilitation outcomes from TBI. CONCLUSIONS: The term DAI is a misnomer. It is not a diffuse injury to the whole brain, rather it is predominant in discrete regions of the brain following high-speed, long-duration deceleration injuries. DAI is a consistent feature of TBI from transportation-related injuries as well as some sports injuries. The pathology of DAI in humans is characterized histologically by widespread damage to the axons of the brainstem, parasagittal white matter of the cerebral cortex, corpus callosum, and the gray-white matter junctions of the cerebral cortex. Computed tomography and magnetic resonance imaging scans taken initially after injury are often normal. The deformation of the brain due to plastic flow of the neural structures associated with DAI explains the micropathologic findings, radiologic findings, and medical and neuropsychologic complications from this type of injury mechanism. There is evidence that the types of cellular injury in TBI (DAI, anoxic, contusion, hemorrhagic, perfusion-reperfusion) should be differentiated, as all may involve different receptors and biochemical pathways that impact recovery. These differing mechanisms of cellular injury involving specific biochemical pathways and locations of injury may, in part, explain the lack of success in drug trials to ameliorate TBI.

Prospective assessment of tizanidine for spasticity due to acquired brain injury.

OBJECTIVE: To determine if orally delivered tizanidine will control spastic hypertonia due to acquired brain injury. DESIGN: Randomized, double-blind, placebo-controlled, crossover design, with 2 8-week treatment arms separated by a 1-week washout period at baseline. Patients were randomly assigned to receive tizanidine or a matching placebo. SETTING: Tertiary care outpatient and inpatient rehabilitation center attached to a university hospital. PARTICIPANTS: Seventeen persons recruited in a consecutive manner, 9 of whom had suffered a stroke and 8 a traumatic brain injury, and had more than 6 months of intractable spastic hypertonia. INTERVENTION: Over a 6-week period, subjects were slowly titrated up to their maximum tolerated dose (up to 36 mg/d). Following a 1-week drug taper and 1-week period in which no study drug was administered, patients were then crossed over to the other study medication following an identical titration regime. MAIN OUTCOME MEASURES: Subjects were evaluated for dose and effect throughout the trial as well as for side effects. Data for Ashworth rigidity scores, spasm scores, deep tendon reflex scores, and motor strength were collected on the affected upper extremity (UE) and lower extremity (LE). Differences over time were assessed via descriptive statistics, Friedman's analysis, and Wilcoxon's signed-rank. Data are reported as the mean +/- 1 standard deviation. RESULTS: Following 4 weeks of treatment when subjects reached their maximal tolerated dosage, the average LE Ashworth score on the affected side decreased from 2.3 +/- 1.4 to 1.7 +/- 1.1 (p <.0001). The spasm score decreased from 1.0 +/- 0.9 to 0.5 +/- 0.8 (p =.0464), while the reflex score was not statistically significant decreasing from 2.2 +/- 1.0 to 2.0 +/- 1.1 (p =.0883). The average UE Ashworth score on the affected side decreased from 1.9 +/- 1.1 to 1.5 +/- 0.9 (p <.0001). There was no significant change in the UE spasm and reflex scores. While there were positive placebo effects on motor tone, the active drug was still significantly better than placebo for decreasing LE tone (p =.0006) and UE tone (p =.0007). With a reduction in motor tone, there was an increase in motor strength (p =.0089). The average dosage at 4 weeks was 25.2mg/d. CONCLUSION: Tizanidine is effective in decreasing the spastic hypertonia associated with acquired brain injury, which is dose-dependent. There are limitations on its use due to side effects related to drowsiness.

Intrathecal baclofen for spastic hypertonia from stroke.

BACKGROUND AND PURPOSE: We sought to determine whether continuous intrathecal delivery of baclofen can effectively decrease spastic hypertonia due to stroke. METHODS: Stroke patients with >6 months of intractable spasticity were screened via a randomized, double-blind, placebo-controlled crossover design of either intrathecal normal saline or 50 microgram baclofen. Those who dropped an average of 2 points in either their affected lower extremity side Ashworth or Penn spasm frequency scores were then offered computer-controlled pump implantation for continuous ITB and followed prospectively for up to 12 months. RESULTS: In 21 stroke patients 6 hours after the active drug bolus, the average (+/-SD) lower extremity Ashworth score on the affected extremities decreased from 3.3+/-1.2 to 1.4+/-0.7 (P<0.0001), spasm score from 1.2+/-1.2 to 0.1+/-0.3 (P=0.0224), and reflex score from 2.1+/-1.2 to 0.1+/-0.5 (P<0.0001). The average upper extremity Ashworth score on the affected extremities decreased from 2.8+/-1.1 to 1.8+/-0.8 (P<0.0001), spasm score from 0.7+/-1.0 to 0.2+/-0.4 (P=0.1544), and reflex score from 2.1+/-0.9 to 1.2+/-0.9 (P=0.0004). All active drug scores were statistically different from placebo scores at 6 hours (P<0.05). With up to 12 months of continuous infusion of ITB in 17 implanted patients, the average lower extremity Ashworth score on the affected extremities decreased from 3.7+/-1.0 to 1.8+/-1.1 (P<0.0001), the spasm score dropped from 1.2+/-1.3 to 0.6+/-1.0 (P=0.4282), and the reflex score decreased from 2.4+/-1.3 to 1.0+/-1.3 (P<0.0001). The average upper extremity Ashworth score in the affected extremities decreased from 3.2+/-1.1 to 1.8+/-0.9 (P<0.0001), the spasm score dropped from 0.7+/-1.0 to 0.3+/-0.8 (P=0.8685), and the reflex score decreased from 2.4+/-0.8 to 1.5+/-1.2 (P=0.3337). The average continuous ITB dose required to attain these effects was 268 microgram/d. CONCLUSIONS: Intrathecal infusion of baclofen is capable of maintaining a reduction in the spastic hypertonia resulting from stroke.

Intrathecal baclofen in tetraplegia of spinal origin: efficacy for upper extremity hypertonia.

STUDY DESIGN: Retrospective analysis. OBJECTIVES: To evaluate the efficacy of intrathecal baclofen (ITB) for upper extremity spastic hypertonia in tetraplegia of spinal origin. SETTING: University of Alabama at Birmingham hospital. METHODS: The medical records of 14 individuals with tetraplegia of spinal origin who underwent intrathecal baclofen pump placement were reviewed. The effects of intrathecal baclofen on spasm frequency, deep tendon reflexes, and tone (Ashworth scale) were assessed for the upper and lower extremities for a 1-year follow-up period. RESULTS: There were statistically significant declines in upper extremity spasm scores (1.8 points, P=0.012), reflex scores (1.4 points, P<0.0001) and Ashworth scores (0.6 points, P<0.0001) for the 1-year follow-up period. For the lower extremities, all decreases were significant (P<0.0001). There was also a statistically significant (P<0.0001) increase in intrathecal baclofen dosage requirements during the 1-year follow-up period to maintain the reductions in spasm frequency, reflexes and tone. CONCLUSIONS: Intrathecal baclofen is a safe and effective intervention for treating upper extremity hypertonia of spinal origin. In addition, the level of intrathecal catheter placement is felt to be of importance.

Sertraline to improve arousal and alertness in severe traumatic brain injury secondary to motor vehicle crashes.

OBJECTIVE: To establish whether or not the serotonin reuptake inhibitor (SSRI) sertraline can improve arousal and alertness of patients with traumatic brain injury (TBI) and associated diffuse axonal injury (DAI). Serotonin is a major inhibitory as well an excitatory neurotransmitter, and serotonergic neurons modulate the activity of brain regions responsible for motor control, arousal, attention, and emotional regulation. SETTING: Tertiary care inpatient rehabilitation centre directly attached to a university hospital level-one trauma centre. DESIGN: Prospective placebo-controlled randomized trial utilizing sertraline on admission to acute rehabilitation. DATA SET: Eleven subjects, post-high speed motor vehicle crash and post-severe TBI (GCS < or = 8) with presumed DAI randomized to receive either sertraline 100mg per day or placebo for 2 weeks. All subjects were within 2 weeks of acute injury. Outcome measures recorded were the Orientation Log (daily), Agitated Behaviour Scale (daily), and the Galveston Orientation and Amnesia Test (weekly). RESULTS: Both placebo and active medication groups demonstrated similar rates of improvement on all three scales. There was no difference in the rates of recovery for either study group (p > 0.05, ANOVA with repeated measures). The groups did not demonstrate a statistically significant negative effect on recovery either, although the size is too small for a statistically reliable beta-effect. CONCLUSION: This pilot study fails to establish whether the early use of sertraline may improve alertness, decrease agitation or improve cognitive recall of material. This may be due to the small size of the study group, the brief duration of treatment or by a skewed placebo group. Larger studies will be required to prove any efficacy. There were no complications with its use and sertraline did not demonstrate a detrimental effect on recovery. This indicates that sertraline may be safe to use in the treatment of psychiatric or behavioural complications attributable to TBI.

Continuously infused intrathecal baclofen over 12 months for spastic hypertonia in adolescents and adults with cerebral palsy.

OBJECTIVE: To determine if the continuous intrathecal delivery of baclofen will control spastic hypertonia caused by long-standing cerebral palsy (CP). DESIGN: Case series. SETTING: Tertiary care outpatient and inpatient rehabilitation center directly attached to a university hospital. PATIENTS: Thirteen CP patients (average age, 25yr; range, 13--43yr) with intractable spastic hypertonia and quadriparesis (one of whom had predominate diplegia) who had not responded to oral medications including baclofen. INTERVENTION: Patients were screened via a bolus injection of baclofen intrathecally. Those who dropped an average of 2 points on their lower extremity (LE) Ashworth scores were offered computer-controlled pump implantation for 12 months of continuous delivery of intrathecal baclofen (ITB). MAIN OUTCOME MEASURES: Ashworth rigidity scores, spasm scores, and deep tendon reflex scores were collected for both the upper extremities (UEs) and LEs. Differences over time were assessed via descriptive statistics and Wilcoxon's signed-rank test. RESULTS: After 1 year of continuous ITB treatment, the average LE Ashworth score +/- standard deviation decreased from 3.4 +/- 1.2 to 1.5 +/- 0.7 (p <.0001), spasm score from 1.4 +/- 1.6 to 0.6 +/- 1.2 (p =.1024), and reflex score from 2.5 +/- 1.2 to 0.7 +/- 1.1 (p <.0001). The average UE Ashworth score decreased from 3.0 +/- 1.2 to 1.7 +/- 1.0 (p <.0001), spasm score from 1.2 +/- 1.6 to 0.2 +/- 0.6 (p =.0135), and reflex score from 2.3 +/- 0.7 to 0.5 +/- 0.9 (p <.0001). The average ITB dose required to attain these effects at 1 year was 263 +/- 91microg continuously infused per day. CONCLUSION: Continuously infused ITB can reduce spastic hypertonia in the UEs and LEs associated with long-standing CP. This reduction in tone will allow more freedom of movement and the potential for improved function.

Outcome after traumatic brain injury: pathway analysis of contributions from premorbid, injury severity, and recovery variables.

OBJECTIVE: To examine the relationship of premorbid variables, injury severity, and cognitive and functional status to outcome 1 year after traumatic brain injury (TBI) and to assess the feasibility of multivariate path analysis as a way to discover those relationships. DESIGN: Prospective, longitudinal. SETTINGS: Level I trauma center, acute inpatient rehabilitation hospital. PATIENTS: One hundred seven subjects (87 men, 20 women; mean age, 33.91 +/- 14.2 yr) who had experienced severe TBI, typically from motor vehicle crashes. INTERVENTIONS: Acute medical and rehabilitation care. MAIN OUTCOME MEASURES: Disability Rating Scale, Community Integration Questionnaire, and return to employment. Evaluated in acute rehabilitation, and at 6 and 12 months' postinjury. RESULTS: Path analyses revealed that premorbid factors had significant relationships with injury severity, functional skills, cognitive status, and outcome; injury severity affected cognitive and functional skills; and cognitive status influenced outcome. No significant relationships were found between injury severity and emotional status, injury severity and outcome, emotional status and outcome, and functional skills and outcome. CONCLUSIONS: Multivariate analysis is important to understanding outcome after TBI. Injury severity, as measured in this study, is less important to 12-month outcome than the premorbid status of the person and the difficulties (particularly cognitive deficits) exhibited at follow-up 6 months after the trauma.

Cognitive and functional recovery at 6 and 12 months post-TBI.

Outcome studies examining recovery from traumatic brain injury (TBI) often fail to provide a clear understanding of the time course of cognitive, emotional, and behavioural recovery. The present study represents an effort to prospectively study individuals with TBI at fixed intervals, specifically 6 and 12 months post-injury with a window of +/- 1 month. Seventy-two individuals with new-onset TBI underwent neuropsychological evaluation and clinical interview at 6 and 12 months post-injury. Results revealed significant improvements in cognitive abilities, including memory, processing speed, language abilities, and constructional skills. There were significant gains in community integration and involvement in productive activities, but limitations in driving activities remained. Although individuals with mild-moderate TBI performed better than individuals with severe TBI, both groups demonstrated equivalent rates of recovery across domains. The results of this study provide important information regarding the time course of TBI recovery.

Midthoracic catheter tip placement for intrathecal baclofen administration in children with quadriparetic spasticity.

OBJECTIVE: In an effort to increase the effect of intrathecal baclofen on upper-extremity spasticity, the tip of the intrathecal catheter was placed at the T6-T7 level rather than at the traditional T11-T12 level in children with spastic quadriparesis. METHODS: Twelve children with spastic quadriparesis from varying causes had significant reductions in spasticity after a test dose of intrathecal baclofen and subsequently underwent placement of a programmable pump and intrathecal catheter tip placed at the T6-T7 level with fluoroscopic guidance. With the use of Ashworth scores for four muscle groups in both the upper and lower extremities, degrees of spasticity were determined by a physiatrist preoperatively and at 1, 3, 6, and 12 months postoperatively. Mean changes in upper- and lower-extremity Ashworth scores and baclofen dosages for the entire cohort were compared with published results in which the catheter tip had been placed at the T11-T12 level. RESULTS: Spasticity was significantly reduced in all muscle groups (P < 0.001). The lower-extremity reduction in spasticity of 1.6 points at 3 and 12 months was greater than published reductions of 1.1 points at 3 and 12 months. The upper-extremity reduction in spasticity was noticeably greater at 3 and 12 months (1.7 and 2.0 points, respectively) than published results at 3 and 12 months (0.4 and 0.6 points, respectively). At 3, 6, and 12 months, our mean baclofen dosage remained below the dosages administered at the T11-T12 level. There were no complications related either to the positioning of the catheter higher in the spinal canal or to the administration of baclofen at the T6-T7 level. CONCLUSION: Compared with published results, placement of the tip of the intrathecal catheter at the T6-T7 level was associated with greater relief of upper-extremity spasticity without loss of effect on the lower extremities. The mean dosages of baclofen in our study group were lower compared with mean dosages administered at the T11-T12 level. There was no morbidity related to the more rostral location of the catheter.

Antiepileptic drugs.

Antiepileptics are a very important class of medications, and the number of these drugs available for clinical use has increased dramatically in the last decade. The pharmacology and indications for use in a variety of physiatric patient groups are comprehensively and systematically reviewed.

Intrathecal drug therapy.

The direct application of drugs for non-hospitalized patients became a practical therapeutic modality with the advent of implantable drug delivery devices, or "pumps". This article describes the use of pumps for the intrathecal infusion of baclofen, morphine and clonidine.

Continuously infused intrathecal baclofen for spastic/dystonic hemiplegia: a preliminary report.

The objective of this study was to determine whether the continuous intrathecal delivery of baclofen will control spastic hypertonia associated with long-standing hemiplegia from acquired brain injury. Six hemiparetic patients (average age, 50 (range, 42-66) yr) with more than 6 mo of disabling lower limb spastic hypertonia on one side caused by either a unilateral traumatic brain injury or a stroke were recruited in a consecutive manner. The setting was a tertiary care outpatient and inpatient rehabilitation center directly attached to a university hospital. Patients were screened via a randomized, double-blind, placebo-controlled, crossover design to receive either an intrathecally administered bolus injection of normal saline or 50 microg of baclofen. Data for Ashworth rigidity scores, spasm scores, and deep tendon reflex scores were collected on the affected upper limb and lower limb side. Those who dropped an average of two points on their affected lower limb side Ashworth scores were then offered computer-controlled pump implantation for continuous intrathecal administration of baclofen. Differences over time were assessed via descriptive statistics and Wilcoxon's signed-rank test. After 3 mo of treatment, the average lower limb Ashworth score on the affected side decreased from 3.7 +/- 1.0 to 1.9 +/- 0.6 standard deviation (SD) (P < 0.0001), the reflex score from 1.8 +/- 1.3 to 0.5 +/- 0.8 SD (P = 0.0208), and the spasm score from 1.3 +/- 1.2 to 0.8 +/- 1.3 SD (P > 0.05). The average upper limb Ashworth score on the affected side decreased from 3.4 +/- 0.9 to 2.1 +/- 0.9 SD (P = 0.0002), the reflex score from 2.3 +/- 0.5 to 1.7 +/- 0.5 SD (P > 0.050, and the spasm score from 0.8 +/- 1.3 to 0 +/- 0 SD (P > 0.05). The average intrathecally administered dose of baclofen that was required to attain these effects was 205.3 microg, which was continuously infused for 24 h. Continuous intrathecal infusion of baclofen is capable of maintaining a reduction in the dystonia on the hemiparetic side without significantly affecting motor strength on the normal side.

Long-term continuously infused intrathecal baclofen for spastic-dystonic hypertonia in traumatic brain injury: 1-year experience.

OBJECTIVE: To determine if the long-term use of continuously infused intrathecal baclofen (ITB) over a 1-year period will control spastic-dystonic hypertonia in patients with traumatic brain injury (TBI). SETTING: Tertiary care outpatient and inpatient rehabilitation center directly attached to a university hospital. SUBJECTS: Persons with TBI and intractable spasticity and dystonia for more than 6 months' duration recruited in a consecutive manner. DESIGN: TBI patients were admitted to the study after screening via a bolus injection of either intrathecal normal saline or 50 microg of baclofen. Data for Ashworth rigidity scores, spasm scores, and deep tendon reflex scores were collected for both the upper extremities (UE) and lower extremities (LE). Patients whose LE Ashworth scores decreased an average of 2 points were then offered implantation of a computer-controlled pump for continuous ITB. Changes over time were assessed statistically via Friedman's analysis for ordinal data and ANOVA for linear data. Differences between set points in time were also assessed via Wilcoxon signed rank. DATA SET: Seventeen patients (average age 29+/-11 yrs) with spasticity and/or dystonia treated over 1 year via a computer-controllable intrathecal delivery system for the delivery of ITB. RESULTS: After 1 year of continuous ITB treatment the average LE Ashworth score decreased from 3.5+/-1.3 (SD) to 1.7+/-0.9 (p < .0001), spasm score from 1.8+/-1.3 to 0.2+/-0.5 (p< .0001), and reflex score from 2.5+/-1.1 to 0.1+/-0.3 (p < .0001). The average UE Ashworth score decreased from 2.9+/-1.5 to 1.6+/-1.0 (p < .0001), spasm score from 1.2+/-1.5 to 0.2+/-0.6 (p < 0.0001), and reflex score from 2.2+/-0.5 to 1.0+/-0.8 (p < .0001). The average ITB dose required to attain these effects at 1 year was 302 microg continuously infused per day. CONCLUSION: Continuous intrathecal infusion of baclofen is capable of maintaining a reduction in spasticity and dystonia in both the upper and lower extremities of TBI patients.

Neuroleptic malignant syndrome induced by haloperidol following traumatic brain injury.

The use of neuroleptics in the acute management of traumatic brain injury (TBI) is controversial and may be detrimental to recovery. The following case report describes a patient developing neuroleptic malignant syndrome (NMS) secondary to the use of haloperidol given to control the patient's agitation. The patient began to exhibit symptoms consistent with NMS (high fever, dystonia, diaphoresis, tachycardia, and decerebrate posturing) shortly after administration of the haloperidol. Upon transfer to a rehabilitation hospital, the symptoms persisted. When NMS is suspected, the first intervention is to remove the offending agent; thus, the administration of haloperidol was suspended, and the patient was placed on Amantadine and propranolol. Amantadine was used to increase the availability of dopamine to the mid-brain region, and the propranolol was used to control the fever, which was believed to be central in origin. The patient was able to complete his rehabilitation with no further incidence of fever or agitation. The patient met or exceeded all short-term physical therapy goals and was able to complete most of the neuropsychological tasks presented. The patient returned home 38 days after admission to the rehabilitation hospital and was able to perform most activities of daily living. At the 6-months follow-up visit, the patient was considering entrance into an adult vocational school.

Elevated liver enzymes after nontraumatic intracranial hemorrhages.

OBJECTIVE: To determine the prevalence and possible etiologies of liver enzyme abnormalities in patients with acquired brain injury and to assess the impact of these abnormalities on the rehabilitative process. SETTING: University tertiary care rehabilitation center. DESIGN: Retrospective study. SUBJECTS: Fifty-six consecutive patients admitted to a brain injury unit in a 30-month period who had an intracranial hemorrhage without associated head or abdominal trauma. MAIN OUTCOME MEASURES: Liver function tests, Functional Independence Measure (FIM) scores, exposure to hepatotoxic drugs, antiepileptic medication serum levels, history of alcohol use, medical history, length of stay, and medical costs. RESULTS: There was an increase (from acute hospital admission to inpatient rehabilitation admission) in gamma-glutamyltransferase (GGT) levels from 42 to 147U/L (p=.0012). There was an increase in alkaline phosphatase from 83 to 125U/L (p=.0079). There was a significant relationship between the GGT level on rehabilitation admission and exposure to hepatotoxic drugs, particularly phenytoin (n=55, p=.0007). Similar findings were noted between alkaline phosphatase and phenytoin (n=55, p=.0022) and systemic steroids (n=50, p=.0277). History of alcohol use was not predictive of changes in liver function tests (p > .05). Correlation analysis revealed no detrimental effect of the elevated serum liver enzyme levels on the Rasch-converted FIM cognitive or motor admission or discharge scores or change in the scores while on rehabilitation (p > .05). All radiologic testing and hepatitis profiles were negative, and 10 of the 16 patients with follow-up laboratory tests showed improvement in their serum liver enzyme levels. CONCLUSIONS: After nontraumatic brain injury there is a characteristic pattern of enzyme elevation that statistically relates to phenytoin exposure. No additional etiologic abnormalities were found on further workup, suggesting that further evaluation should be guided by the patient's clinical status, not laboratory value alone.