Minor head trauma – induced sporadic hemiplegic migraine coma

Familial hemiplegic migraine is a severe, rare subtype of migraine. Gene mutations on chromosome 19 have been identified in the calcium channel, voltage-dependent, P/Q type, alpha-1A subunit gene (chromosome 19p13) for familial hemiplegic migraine. Recently a gene mutation (Serine-218-Leucine) for a dramatic syndrome associated with familial hemiplegic migraine, commonly named “migraine coma”, has implicated exon 5 of this gene. The occurrence of trivial head trauma, in such familial hemiplegic migraine patients, may also be complicated by severe, sometimes even fatal, cerebral edema and coma occurring after a lucid interval. Sporadic hemiplegic migraine shares a similar spectrum of clinical presentation and genetic heterogeneity. The case report presented in this article implicates the involvement of the Serine-218-Leucine mutation in the extremely rare disorder of minor head trauma–induced migraine coma. We conclude that the Serine-218-Leucine mutation in the calcium channel, voltage-dependent, P/Q type, alpha-1A subunit gene is involved in sporadic hemiplegic migraine, delayed cerebral edema and coma after minor head trauma.

Emergence of conscious awareness of underlying verbal and visual rules over time in moderate closed-head trauma patients

Please consult the paper edition of this thesis to read. It is available on the 5th Floor of the Library at Call Number: Z 9999.5 E38 L64 2008

Indices and Implications of Emotional Underarousal for Persons with a History of Head Trauma

We examined the role of altered emotional functioning across the spectrum of injury severity (mild head injury [MHI], moderate/severe traumatic brain injury [TBI]), its implications for social behaviours, and the effect of modifying arousal and its relation to cognitive performance. In the first study (N = 230), students with self-reported MHI endorsed engaging in socially unacceptable and erratic behaviours significantly more often than did those with no MHI. We did not find significant differences between the groups in the measure of emotional intelligence (EI); however, for students who reported a MHI, scores on the EI measure significantly predicted reports of socially unacceptable behaviours such that lower scores predicted poorer social functioning, accounting for approximately 20% of the variance. Also, the experience of postconcussive symptoms was found to be significantly greater for students with MHI relative to their peers. In the second study (N = 85), we further examined emotional underarousal in terms of physiological (i.e., electrodermal activation [EDA]) and self-reported responsivity to emotionally-evocative picture stimuli. Although the valence ratings of the stimuli did not differ between students with and without MHI as we had expected, we found evidence of reduced and/or indiscriminate emotional responding to the stimuli for those with MHI which mimics that observed in other studies for persons with moderate/severe TBI. We also found that emotional underarousal followed a gradient of injury severity despite reporting a pattern of experiencing more life stressors. In the third study (N = 81), we replicated our findings of emotional underarousal for those with head trauma and also uniquely explored neuroendocrine aspects (salivary cortisol; cortisol awakening response [CAR]) and autonomic indices (EDA) of emotional dysregulation in terms of stress responsivity across the spectrum of injury severity (MHI [n = 32], moderate/severe TBI [n = 9], and age and education matched controls [n = 40]). Although the manipulation was effective in modifying arousal state in terms of autonomic and self-reported indices, we did not support our hypothesis that increased arousal would be related to improved performance on cognitive measures for those with prior injury. To our knowledge, this is the only study to examine the CAR with this population. Repeated measure analysis revealed that, upon awakening, students with no reported head trauma illustrated the typical CAR increase 45 minutes after waking, whereas, students who had a history of either mild head trauma or moderate/severe TBI demonstrated a blunted CAR. Thus, across the three studies we have provided evidence of emotional underarousal, its potential implications for social interactions, and also have identified potentially useful indices of dysregulated stress responsivity regardless of injury severity.

Brainstem injury by penetrating head trauma with a knife

The authors describe a rare case about a traumatic lesion of brain and brain stem with a knife. In this case the patient had good clinical condition, diagnosed with TBI by infectious complications. We have highlighted the unusual diagnosis, proximity of vascular structures, the technique used in the treatment and the good outcome of the injury.

Rare retinal haemorrhages in translational accidental head trauma in children

PURPOSE: The characteristic findings in accidental head injury consist of linear skull fracture, epidural haematoma, localized subdural haematoma, or cortical contusion because of a linear or translational impact force. Retinal haemorrhages have been found, although uncommon, in accidental head trauma. METHODS: We performed a retrospective study of 24 consecutive cases of children with severe head injuries caused by falls. Inclusion criteria were skull fractures and/or intracranial haemorrhages documented by computerized tomography. All patients underwent a careful ophthalmic examination including dilated indirect fundoscopy within the first 48 h following admission. RESULTS: No retinal haemorrhages could be found in patients whose accidents were plausible and physical and imaging findings were compatible with reported histories. Excessive bilateral retinal haemorrhages were found in only three children with the typical signs of shaken baby syndrome. In eight children, trauma had led to orbital roof fractures. CONCLUSIONS: Retinal haemorrhages were not found in any of the patients with accidental trauma despite the severity of their head injuries. Hence, we add more evidence that there are strong differences between the ocular involvement in accidental translational trauma and those in victims of non-accidental trauma. Fall-related injuries carry a very low risk of retinal haemorrhages.

SEVERE HEAD TRAUMA, EMERGENCY TRANSPORT, AND PATIENT OUTCOME

Trauma and severe head injuries are important issues because they are prevalent, because they occur predominantly in the young, and because variations in clinical management may matter. Trauma is the leading cause of death for those under age 40. The focus of this head injury study is to determine if variations in time from the scene of accident to a trauma center hospital makes a difference in patient outcomes.^ A trauma registry is maintained in the Houston-Galveston area and includes all patients admitted to any one of three trauma center hospitals with mild or severe head injuries. A study cohort, derived from the Registry, includes 254 severe head injury cases, for 1980, with a Glasgow Coma Score of 8 or less.^ Multiple influences relate to patient outcomes from severe head injury. Two primary variables and four confounding variables are identified, including time to emergency room, time to intubation, patient age, severity of injury, type of injury and mode of transport to the emergency room. Regression analysis, analysis of variance, and chi-square analysis were the principal statistical methods utilized.^ Analysis indicates that within an urban setting, with a four-hour time span, variations in time to emergency room do not provide any strong influence or predictive value to patient outcome. However, data are suggestive that at longer time periods there is a negative influence on outcomes. Age is influential only when the older group (55-64) is included. Mode of transport (helicopter or ambulance) did not indicate any significant difference in outcome.^ In a multivariate regression model, outcomes are influenced primarily by severity of injury and age which explain 36% (R('2)) of variance. Inclusion of time to emergency room, time to intubation, transport mode and type injury add only 4% (R('2)) additional contribution to explaining variation in patient outcome.^ The research concludes that since the group most at risk to head trauma is the young adult male involved in automobile/motorcycle accidents, more may be gained by modifying driving habits and other preventive measures. Continuous clinical and evaluative research are required to provide updated clinical wisdom in patient management and trauma treatment protocols. A National Institute of Trauma may be required to develop a national public policy and evaluate the many medical, behavioral and social changes required to cope with the country's number 3 killer and the primary killer of young adults.^

N-Methyl-d-aspartate antagonists and apoptotic cell death triggered by head trauma in developing rat brain

Morbidity and mortality from head trauma is highest among children. No animal model mimicking traumatic brain injury in children has yet been established, and the mechanisms of neuronal degeneration after traumatic injury to the developing brain are not understood. In infant rats subjected to percussion head trauma, two types of brain damage could be characterized. The first type or primary damage evolved within 4 hr and occurred by an excitotoxic mechanism. The second type or secondary damage evolved within 6–24 hr and occurred by an apoptotic mechanism. Primary damage remained localized to the parietal cortex at the site of impact. Secondary damage affected distant sites such as the cingulate/retrosplenial cortex, subiculum, frontal cortex, thalamus and striatum. Secondary apoptotic damage was more severe than primary excitotoxic damage. Morphometric analysis demonstrated that the N-methyl-d-aspartate receptor antagonists 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonate and dizocilpine protected against primary excitotoxic damage but increased severity of secondary apoptotic damage. 2-Sulfo-α-phenyl-N-tert-butyl-nitrone, a free radical scavenger, did not affect primary excitotoxic damage but mitigated apoptotic damage. These observations demonstrate that apoptosis and not excitotoxicity determine neuropathologic outcome after traumatic injury to the developing brain. Whereas free radical scavengers may prove useful in therapy of head trauma in children, N-methyl-d-aspartate antagonists should be avoided because of their propensity to increase severity of apoptotic damage.

Increased mRNA levels for components of the lysosomal, Ca2+-activated, and ATP-ubiquitin-dependent proteolytic pathways in skeletal muscle from head trauma patients.

The cellular mechanisms responsible for enhanced muscle protein breakdown in hospitalized patients, which frequently results in lean body wasting, are unknown. To determine whether the lysosomal, Ca2+-activated, and ubiquitin-proteasome proteolytic pathways are activated, we measured mRNA levels for components of these processes in muscle biopsies from severe head trauma patients. These patients exhibited negative nitrogen balance and increased rates of whole-body protein breakdown (assessed by [13C]leucine infusion) and of myofibrillar protein breakdown (assessed by 3-methylhistidine urinary excretion). Increased muscle mRNA levels for cathepsin D, m-calpain, and critical components of the ubiquitin proteolytic pathway (i.e., ubiquitin, the 14-kDa ubiquitin-conjugating enzyme E2, and proteasome subunits) paralleled these metabolic adaptations. The data clearly support a role for multiple proteolytic processes in increased muscle proteolysis. The ubiquitin proteolytic pathway could be activated by altered glucocorticoid production and/or increased circulating levels of interleukin 1beta and interleukin 6 observed in head trauma patients and account for the breakdown of myofibrillar proteins, as was recently reported in animal studies.

Increasing Skin Pigmentation Following Severe Head Trauma: All That Glitters Is Not Gold!

We report the case of a 67-year-old man who was admitted to our Intensive Care Unit because of traumatic brain injury. During his prolonged hospitalization, gradual darkening of the skin all over his body was observed. An excess corticotropin (ACTH) production syndrome was considered. The patient’s hormone study showed high levels of ACTH (978 pg/ml) with normal cortisol levels. Extensive clinical and laboratory investigations revealed adenocarcinoma of the colon, which was likely the site of the ectopic ACTH production. This is a very rare manifestation of paraneoplastic syndrome during the course of colon adenocarcinoma. The most important feature of this case report is that this rare syndrome was accidentally discovered, in a patient hospitalized for unrelated reasons, by simple clinical investigation.

Is a black eye a useful sign of facial fractures in patients with minor head injuries? A retrospective analysis in a level I trauma centre over 10 years

Orbital blunt trauma is common, and the diagnosis of a fracture should be made by computed tomographic (CT) scan. However, this will expose patients to ionising radiation. Our objective was to identify clinical predictors of orbital fracture, in particular the presence of a black eye, to minimise unnecessary exposure to radiation. A 10-year retrospective study was made of the medical records of all patients with minor head trauma who presented with one or two black eyes to our emergency department between May 2000 and April 2010. Each of the patients had a CT scan, was over 16 years old, and had a Glasgow Coma Score (GCS) of 13-15. The primary outcome was whether the black eye was a valuable predictor of a fracture. Accompanying clinical signs were considered as a secondary outcome. A total of 1676 patients (mean (SD) age 51 (22) years) and minor head trauma with either one or two black eyes were included. In 1144 the CT scan showed a fracture of the maxillofacial skeleton, which gave an incidence of 68.3% in whom a black eye was the obvious symptom. Specificity for facial fractures was particularly high for other clinical signs, such as diminished skin sensation (specificity 96.4%), diplopia or occulomotility disorders (89.3%), fracture steps (99.8%), epistaxis (95.5%), subconjunctival haemorrhage (90.4%), and emphysema (99.6%). Sensitivity for the same signs ranged from 10.8% to 22.2%. The most striking fact was that 68.3% of all patients with a black eye had an underlying fracture. We therefore conclude that a CT scan should be recommended for every patient with minor head injury who presents with a black eye.

The social consequences of mild head injury and executive dysfunction /

Mild head injury (MHI) is a serious cause of neurological impairment as is evident by the substantial percentage (15%) of individuals who remain symptomatic at least 1-year following "mild" head trauma. However, there is a paucity of research investigating the social consequences following a MHI. The first objective of this study was to examine whether measures of executive functioning were predictive of specific forms of antisocial behaviour, such as reactive aggression, impulsive antisocial behaviour, behavioural disinhibition, and deficits in social awareness after controlling for the variance accounted for by sex differences. The second objective was to investigate whether a history of MHI was predictive of these same social consequences after controlling for both sex differences and executive functioning. Ninety university students participated in neuropsychological testing and filled out self-report questionnaires. Fifty-two percent of the sample self-reported experiencing a MHI. As expected, men were more reactively aggressive and antisocial than women. Furthermore, executive dysfunction predicted reactive aggression and impulsive antisocial behaviour after controlling for sex differences. Finally, as expected, MHI status predicted reactive aggression, impulsive antisocial behaviour, and behavioural disinhibition after controlling for sex and executive fimctioning. MHI status and executive functioning did not predict social awareness or sensitivity to reward or punishment. These results suggest that incurring a MHI has serious social consequences that mirror the neurobehavioural profile following severe cases of brain injury. Therefore, the social sequelae after MHI imply a continuum of behavioural deficits between MHI and more severe forms of brain injury.