99mTc-HMPAO SPECT of the brain in mild to moderate traumatic brain injury patients: compared with CT--a prospective study

Single photon emission computed tomography (SPECT) with Technetium-99m hexamethyl propylenamine oxime (Tc-99m-HMPAO) was used in 20 patients with mild to moderate traumatic brain injury (TBI) to evaluate the effects of brain trauma on regional cerebral blood flow (rCBF). SPECT scan was compared with CT scan in 16 patients. SPECT showed intraparenchymal differences in rCBF more often than lesions diagnosed with CT scans (87.5% vs. 37.5%). In five of six patients with lesions in both modalities, the area of involvement was relatively larger on SPECT scans than on CT scans. Contrecoup changes were seen in five patients on SPECT alone, two patients with CT alone and one patient had contrecoup lesions on CT and SPECT. Of the eight patients (50%) with skull fractures, seven (43.7%) had rCBF findings on SPECT scan and five (31.3%) demonstrated decrease in rCBF in brain underlying the fracture. All these patients with fractures had normal brain on CT scans. Conversely, extra-axial lesions and fractures evident on CT did not visualize on SPECT, but SPECT demonstrated associated changes in rCBF. Although there is still lack of clinical and pathological correlation, SPECT appears to be a promising method for a more sensitive evaluation of axial lesions in patients with mild to moderate TBI.     

Post-concussive symptoms in children with mild traumatic brain injury.

To investigate postconcussive symptoms (PCS) following pediatric mild traumatic brain injury (mTBI), 8- to 15-year-old children with mTBI (n = 186) and a comparison group with uncomplicated orthopedic injuries (OI, n = 99) were recruited from two emergency departments. Parent and child ratings of PCS and symptom counts were obtained within 3 weeks after injury (baseline) and at 1, 3, and 12 months postinjury. The mTBI group also completed magnetic resonance imaging at baseline. Group differences were examined using growth modeling, controlling for age at injury, sex, socioeconomic status, and (for parent-based measures) preinjury symptom levels. Relative to the OI group, the mTBI group had higher ratings of somatic PCS and parent counts of PCS at the initial assessments, but higher parent ratings of cognitive PCS and child counts of PCS throughout follow-up. Higher levels of PCS in the mTBI group were associated with motor-vehicle-related trauma, loss of consciousness, neuroimaging abnormalities, and hospitalization. The findings validate both transient and persistent PCS in children with mTBI and document associations of symptoms with injury and noninjury factors. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Verbal fluency in individuals with mild traumatic brain injury.

Tests of verbal fluency that require either retrieval by semantic category or retrieval by initial letter were presented to 19 participants with mild traumatic brain injury (MTBI) and 24 control (NC) participants. Performance on these tasks was analyzed for total number of words produced, the presence of semantic clusters in the order of words produced, the presence of phonemic clusters in the order of words produced, and number of errors (i.e., perseverations, words out of category). Individuals with MTBI produced fewer words and made more errors than NCs, but their production contained an equal proportion of semantic and phonemic clusters. These data are discussed in relation to a previous study in patients with Parkinson's disease (PD). PD participants did not make more errors than age-matched NCs despite reduced production. Implications for memory and executive function deficits following MTBI are discussed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Assessment of executive function in patients with mild traumatic brain injury

BACKGROUND: The nature of functional deficit after mild traumatic brain injury (TBI) defined by Glasgow Coma Score of 13-15 is not fully described. This study explored the sensitivity of several neuropsychological tests to identify sequelae of mild traumatic brain injury (TBI). METHODS: Eleven adult patients with mild TBI admitted to a Level 1 trauma center were studied. The battery of tests included the Wechsler Intelligence Scale for Children -Revised: Mazes Subtest, Trails A and B, the Boston Naming Test, The Multilingual Aphasia Examination: Controlled Oral Word Association Test, and the Paced Auditory Serial Addition Task. RESULTS: Control subjects performed significantly better than patients with mild TBI on Trails A and B, the Controlled Oral Word Association Test, and Paced Auditory Serial Addition Task (subtests 2-4). No significant differences in performances between patients and controls was found for the Wechsler Intelligence Scale for Children -Revised: Mazes Subtest, Boston Naming Test, and Paced Auditory Serial Addition Task Subtest 1. CONCLUSION: The results suggest that tests of specific frontal lobe executive functions are valuable in diagnosing and monitoring recovery from mild TBI.     

The relationship between sexual abuse and mild traumatic brain injury

It remains unclear why some individuals with mild traumatic brain injury (MTBI) complain of cognitive deficits many months after the injury. Given neuropathological changes associated with prolonged stress, such as occurs with repeated sexual abuse (SA), it seems possible that individuals who experienced SA might be predisposed to greater deficits after MTBI. Four groups of subjects were administered measures of cognitive and emotional functioning. These groups were those with MTBI (n = 10), those with a history of SA (n = 10), those with both MTBI and SA (n = 10), and normal control (NC) subjects (n = 10). Compared to the NC subjects, those with MTBI demonstrated deficits in working memory, those with SA demonstrated deficits in executive functioning, and those with both MTBI and SA demonstrated the greatest number of deficits which were in working memory, executive functioning and memory. Tests of anxiety, depression and post-traumatic stress disorder, while demonstrating significant symptoms in all clinical groups, did not correlate with the neuropsychological tests that differentiated the groups.     

A randomized trial of two treatments for mild traumatic brain injury

The purpose of this study was to compare an education-oriented single session treatment (SS) for mild traumatic brain injury (MTBI) to a more extensive assessment, education, and treatment-as-needed intervention (TAN). Participants were 111 adults with MTBI who were recruited from consecutive admissions to two hospital emergency wards. They were randomly assigned to either the SS or TAN modality. The groups did not differ on any demographic, injury-related, or questionnaire variable when first seen within 3 weeks of injury. The groups generally improved a similar amount and did not differ from each other on any symptom-related, functional, or vocational variables 3-4 months after their baseline session. Patient satisfaction ratings with services provided were also similar for the two groups. Brief educational intervention given soon after MTBI appears to be adequate for most MTBI survivors.     

The neuronal cytoskeleton is at risk after mild and moderate brain injury

Recent studies have described alterations in cytoskeletal proteins such as microtubule-associated protein 2 (MAP-2) and neurofilament (NF) resulting from moderate and severe experimental brain injury; however, few have investigated the consequences of mild injury, which is associated clinically and experimentally with cognitive dysfunction and neuronal damage. To contrast cytoskeletal changes within 7 days following mild injury with those following moderate injury, we subjected anesthetized, adult rats to mild (1.1-1.3 atm) or moderate (2.3-2.5 atm) lateral fluid percussion brain injury or sham injury. Rats were sacrificed at 6 h (n=4 mild; n=4 moderate; n=2 sham), 24 h (n=4 mild; n=4 moderate; n=1 sham), or 7 days (n=5 mild; n=4 moderate; n=1 sham) following injury, and immunohistochemistry was performed for MAP-2 and NF. Both mild and moderate injury produced notable cytoskeletal changes in multiple brain regions; however, mild injury generally resulted in a lesser degree of MAP-2 and NF loss over a smaller spatial extent. When compared to moderately injured animals, animals subjected to mild injury showed substantially delayed MAP-2 and NF alterations within the cortex and hippocampal dentate gyrus and no evidence of MAP-2 loss in the hippocampal CA3 region. While mild and moderate injury resulted for the most part in similar patterns of axonal injury, tissue tears in the fimbria and loss of NF immunoreactivity in regions containing injured axons were only observed following moderate injury. Elucidating the effects of modulating injury severity may yield insight into the mechanisms involved in traumatic damage to the cytoskeleton and guide future treatment strategies.     

Recovery of time estimation following moderate to severe traumatic brain injury.

Objective: Accurate time estimation abilities are thought to play an important role in efficient performance of many daily activities. This study investigated the role of episodic memory in the recovery of time estimation abilities following moderate to severe traumatic brain injury (TBI). Method: Using a prospective verbal time estimation paradigm, TBI participants were tested in the early phase of recovery from TBI and then again approximately one year later. Verbal time estimations were made for filled intervals both within (i.e., 10 s, 25 s) and beyond (i.e., 45 s 60 s) the time frame of working memory. Results: At baseline, when compared to controls, the TBI group significantly underestimated time durations at the 25 s, 45 s and 60 s intervals, indicating that the TBI group perceived less time as having passed than actually had passed. At follow-up, despite the presence of continued episodic memory impairment and little recovery in episodic memory performance, the TBI group exhibited estimates of time passage that were similar to controls. Conclusion: The pattern of data was interpreted at suggesting that episodic memory performance did not play a noteworthy role in the recovery of temporal perception in TBI participants. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Motor performance following a mild traumatic brain injury in children: an exploratory study

Mild Traumatic Brain Injury (TBI) is a common occurrence in the paediatric population and, as the concept of motor performance has not been assessed specifically in this population, the purpose of this study was to determine if motor performance deficits are present and can be objectively identified in a sample of children having sustained a mild TBI (Glasgow Coma Scale score 13-15). Twenty-eight children aged between 5 and 15 years were recruited immediately post-trauma. Subjects were considered normal on standard neurological exam at the time of discharge. They were assessed 13-18 days post-trauma using the Bruininks-Oseretsky Test of Motor Proficiency, a norm referenced clinical standardized assessment tool. Compared to published norms, motor performance was significantly lower in domains of balance, response speed and running speed an agility (t-test p < 0.01), and significantly higher in domains of upper extremity coordination and visual motor control (t-test p < 0.01). Although excellent performance can be observed in domains requiring upper limb coordination, motor planning and execution of motor tasks, deficits in balance and response speed can be identified in a significant number of children even after mild TBI. More specific and sensitive evaluations are necessary to identify the exact nature of the problems and evaluate their functional impact on daily activities.     

Toward a neuropsychological model of functional disability after mild traumatic brain injury.

Discusses investigations into the nature, causes, predictors, and treatment of functional disability after minor traumatic brain injury (TBI). Distinctions among minor head injury, mild traumatic brain injury, postconcussion syndrome, and posttraumatic stress disorder (PTSD) are clarified, and methodological and information-processing issues in minor TBI are identified. Four stages of clinical research related to minor TBI are described: identification of functional scenarios (1983–1987), development of educational materials (1985–1986), ongoing research (1988–1992), and clinical applications (1992 and continuing). Finally, a neuropsychological model of functional disability after minor TBI is presented, with implications for assessment and treatment. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Neuropsychological impairments after spinal cord injury: A comparative study with mild traumatic brain injury.

Objective: To determine if individuals with mild traumatic brain injury (MTBI) perform differently on neuropsychological measures than individuals with spinal cord injury (SCI) having no loss of consciousness. Design and Participants: Data were collected prospectively on 33 matched pairs of individuals with SCI or MTBI. Independent t tests were performed to identify differences between the SCI and MTBI groups. Results: Although those with SCI generally outperformed individuals with MTBI, no meaningful between-groups differences were noted on 5 of the 10 neuropsychological tests administered. Greater than 40% of the SCI patients were identified as having impairments in processing speed, motor speed, and verbal learning. Conclusions: Treatment planning after SCI should include procedures to identify cognitive deficits that may complicate adjustment to disability and delay acquisition of new skills. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of auditory stimuli on intracranial pressure and cerebral perfusion pressure in traumatic brain injury

In the kidney, ischaemia-reperfusion results in both hypoxic and oxidant cellular injury which is most marked in the tubules of cortex and outer medulla. These contrasting conditions may have opposite effects on the expression of enzymes that reduce or repair oxidant damage. To investigate this, the activities of CuZn and Mn superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione S-transferase (GST) were measured after 4 h and 3, 6, and 10 days of reperfusion following sham surgery or 45- or 90-min left renal artery occlusion. The right kidney served as internal control. Sham surgery had no effect on Mn SOD or GPx, but caused small (p < 0.05) reductions in CuZn SOD and GST activities. Forty-five minutes of ischaemia had no net effect on Mn SOD, increased GPx activity (maximum at 6 days, p < 0.01), and reduced CuZn SOD (nadir 3 days, p < 0.02) and GST (nadir 6 days, p < 0.02) activities. Ninety minutes of ischaemia again had no net effect on Mn SOD, prevented the induction of GPx, and further suppressed the activities of CuZn SOD and GST. The activity of the non-anti-oxidant enzyme lactate dehydrogenase was equal in left and right kidneys after 45 min of ischaemia, but different (p < 0.01) 10 days following 90-min injury, due to a combination of reduced activity in the ischaemic kidney and an increase of activity in the internal control. The immediate effect of ischaemia-reperfusion injury on the kidney is to reduce the activity of intracellular anti-oxidant enzymes in proportion to the severity of the ischaemic insult. Recovery or net induction of enzyme activity paralleled tubular regeneration. Protection resulting in acquired resistance to a second ischaemic event is unlikely to be due to induction of anti-oxidant enzymes if it occurs within 6 days.     

Combined therapy affects outcomes differentially after mild traumatic brain injury and secondary forebrain ischemia in rats

Muscarinic and NMDA receptors contribute to post-traumatic hypersensitivity to secondary ischemia. However, the effect of these receptor antagonists on behavior and CA1 neuronal death after traumatic brain injury (TBI) with acute (1 h after TBI) forebrain ischemia has not been systematically assessed. We examined cognitive and motor dysfunction and the relationship of behavior deficits to neuronal death in this model using muscarinic and NMDA antagonists. Three behavioral groups (n=10/group) of Wistar rats were subjected to mild TBI and 6 min of forebrain ischemia imposed 1 h after TBI with 45 days survival. Motor and spatial memory performance were assessed using the rotarod task and Morris water maze. Seven additional groups (n=6/group) were evaluated only for CA1 death after 7 days survival following sham, individual or combined injury with and without drug treatments. Rats were given 0.3 mg/kg MK-801 (M) and 1.0 mg/kg scopolamine (S) alone or combined (M-S) before or 45 min after TBI. Rotarod performance was tested at days 1-5 and maze performance on days 11-15 and 40-44 after M-S treatment. The 7-day studies showed M-S treatment (p<0.01) reduced CA1 neuronal death better than either S or M alone. Behavioral groups had inadvertent post-ischemic hypothermia that decreased CA1 death and likely influenced behavioral morbidity. M-S given before TBI (p<0.01) decreased memory deficits on day 15, while M-S treatment given after TBI was ineffective. Unexpectedly, M-S treatment before or after TBI produced transient motor deficits (p<0. 01). Memory improvement occurred independent of CA1 death.     

Comparison of technetium-99m-ECD to Xenon-133 SPECT in normal controls and in patients with mild to moderate regional cerebral blood flow abnormalities

Technetium-99m-1,1-ethyl cysteinate dimer (ECD) has been proposed as a "chemical microsphere" for SPECT measurement of regional cerebral blood flow (rCBF). However, its distribution has not yet been compared in humans to an established rCBF measure. Therefore, we compared the uptake and distribution of ECD with rCBF measured by 133Xe SPECT in subjects with mild to moderate flow abnormalities and in normal volunteers. Blood and urine chemistries and vital signs were unchanged from pre-ECD values up to seven days postinjection. Profile plots demonstrated pattern agreement between rCBF ratios (133Xe) and ECD count density ratios. A significant correlation of rCBF ratios to ECD count density ratios was observed (r = 0.77), with a slope of 0.64 and intercept of 0.36. To explore whether or not the relationship between rCBF and ECD was dependent on absolute flow, ECD region of interest data were expressed in units of ml/min/100 g by equating global CBF (133Xe) and ECD global count density. A closer correlation (r = 0.88) was found for these data than for the count ratio data. The slope was closer to one (m = 0.83) and the intercept was closer to zero (b = 8.2). Also, a significant correlation was observed between ECD-derived rCBF and 133Xe rCBF in the lesion area (r = 0.92) for patients with well-demarcated rCBF lesions. The slope (0.80) suggested a slight underestimation of lesion flow by ECD. Finally, ECD clearance from cortical gray matter ROIs derived from high-resolution scans from 1 to 4 hr postinjection was slow (2.4%/hr). In summary, ECD is a safe and effective marker of regional cerebral perfusion. The distribution of ECD is linearly related to rCBF measured by 133Xe SPECT, although our data suggest a mild underestimation of flow at the high end of the normal range.     

The prospective course of postconcussion syndrome: The role of mild traumatic brain injury.

Objective: To investigate whether postconcussion syndrome (PCS) represents long-term sequelae associated with mild traumatic brain injury (mTBI). Methods: Prospective consecutive admissions to a Level 1 trauma hospital were assessed a mean 4.9 days and again 106.2 days post-injury. The final sample comprised 62 mTBI and 58 nonbrain injured trauma controls (TC). Change or lack of change in individual PCS-like symptoms and PCS was examined. Multilevel logistic regression was used to analyze whether mTBI predicts 3-month PCS (Time 2; T2); whether predictors of PCS (within 14 days of injury, Time 1; T1) predict 3-month PCS, and how change in these predictors from T1 to T2 were associated with change in PCS status. Variables included demographic, injury-related, financial incentives, neuropsychological, and psychiatric disorder. Results: MTBI did not predict PCS. PCS was comparable (T1: mTBI: 40.3%, TC: 50.0%; T2: mTBI: 46.8%, TC: 48.3%). At T2, 38.6% were new cases of PCS; between 30.8% and 86.2% reported either a new or more frequent symptom. A pre-injury depressive or anxiety disorder (OR = 2.99, 95% CI [1.38, 6.45]), and acute posttraumatic stress (OR = 1.05, 95% CI [1.00, 1.00]) were early markers of PCS, regardless of mTBI. An interaction between time and posttraumatic stress disorder (PTSD) suggested the relationship between the severity of PTSD symptoms and PCS strengthened over time (OR = 2.66, 95% CI [1.08, 6.55]). Pain was related to PCS. Females were more likely than males to have PCS. Conclusion: The data suggest the phenomenon of PCS in trauma patients does not show an association with mTBI. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Rehabilitation after traumatic brain injury in adults

PURPOSE: Traumatic brain injury (TBI) stands as a major public health problem and one of the most important challenges for neurological rehabilitation. This review discusses advances that have occurred in the past 10 years in rehabilitation after severe TBI in adults. METHOD: First, theoretical concepts, goals of rehabilitation and organization of resources are reviewed. Then specific questions that arise in the rehabilitation of severe TBI patients are considered. RESULTS: Three phases are distinguished in post-traumatic evolution. Acute rehabilitation takes place during coma and arousal states. Specific aims are to prevent orthopaedic and visceral complications, and to provide sensory stimulations with the hope of accelerating arousal. Secondly subacute (generally inpatient) rehabilitation is designed to facilitate and accelerate recovery of impairments, and to compensate for disabilities. Motility, cognition, behaviour, personality and affect should be simultaneously addressed in an holistic approach. Physical as well as psychological independence and self-awareness are the major goals to emphasize. A third, post-acute rehabilitation phase includes outpatient therapy for achieving physical, domestic and social independence, reduction of handicaps and re-entry into the community. CONCLUSIONS: Problems with returning home, obtaining financial independence, driving, returning to work, participating in social relationships and leisure activities, and the importance of psychosocial adjustment and self-acceptance, are outlined. Questions about economic aspects and rehabilitation in the future are addressed.     

Oxidative stress following traumatic brain injury in rats

BACKGROUND: Free radicals may be involved in the pathophysiology of traumatic brain injury (TBI) through oxidative damage of neurovascular structures. Endogenous antioxidants, such as ascorbate and alpha-tocopherol, may play a critical role in combating these oxidative reactions and their oxidized products can serve as an important index of oxidative stress. METHODS: We used electron spin resonance (ESR) spectroscopy and in vivo spin trapping (reaction of an organic compound with free radical species) to detect the possible generation of free radicals after TBI. Injury was inflicted by a weight drop technique over the head (5.7 kg-cm). Rats were intravenously infused with either 1 mL, 0.1 M of the spin trap, alpha-phenyl-N-tert-butyl nitrone (PBN), or an equivalent volume of saline immediately before TBI or sham-injury. Animals were divided into four groups: (1) Group I: PBN-infused sham-injured, (2) Group II: PBN-infused injured, (3) Group III: saline-infused sham-injured, and (4) Group IV: saline-infused injured. Additional groups of saline-infused uninjured, saline-infused, and PBN-infused injured animals were used for histopathology. Sixty minutes after TBI or sham-injury, rats were again anesthetized and decapitated. The brains were removed within 1 minute, homogenized, and extracted for lipids. The extracts were analyzed by ESR spectroscopy. Brain ascorbic acid (AA) concentration was determined spectrophotometrically, using the ascorbate oxidase assay. RESULTS: No PBN spin adduct signals (indicating trapped free radical species) were visible 60 minutes after TBI. All groups of rats showed an ascorbyl free radical signal. The ascorbyl signal intensity (AI) was, however, significantly higher in the injured rats, while the brain (AA) was significantly reduced. In addition, the ratio of AI/AA, which eliminates the effect of variable ascorbate concentrations in the brain, was also significantly higher in the injured animals. CONCLUSIONS: We conclude that 60 minutes following TBI there was a significantly increased level of oxidative stress in the brain. This may reflect formation of free radical species with subsequent interaction with ascorbate (antioxidant) during the 60 minute period. The lack of PBN spin adduct signals 1 hour after TBI may indicate that free radical generation is time dependent and might be detectable earlier or later than the 60 minute period.