Cases reported "Brain Injuries"

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1/135. Parkinson's syndrome after closed head injury: a single case report.

    A 36 year old man, who sustained a skull fracture in 1984, was unconscious for 24 hours, and developed signs of Parkinson's syndrome 6 weeks after the injury. When assessed in 1995, neuroimaging disclosed a cerebral infarction due to trauma involving the left caudate and lenticular nucleus. Parkinson's syndrome was predominantly right sided, slowly progressive, and unresponsive to levodopa therapy. reaction time tests showed slowness of movement initiation and execution with both hands, particularly the right. Recording of movement related cortical potentials suggested bilateral deficits in movement preparation. Neuropsychological assessment disclosed no evidence of major deficits on tests assessing executive function or working memory, with the exception of selective impairments on the Stroop and on a test of self ordered random number sequences. There was evidence of abulia. The results are discussed in relation to previous literature on basal ganglia lesions and the effects of damage to different points of the frontostriatal circuits.
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2/135. Traumatic aphasia in children: a case study.

    Traumatic aphasia in children has been recognized as a distinct clinical pathology, differing from adult aphasia in symptomatology and course of recovery. The upper limit for complete recovery has been identified as age 10. However, there is a paucity of literature documenting recovery of children with traumatic aphasia. It is apparent that definitive statements of the upper age limit for complete recovery from traumatic aphasia in children cannot be made at this time. This article reviews the literature concerning traumatic aphasia and presents case information of a 10-year-old traumatic aphasic girl seen at the North texas State University speech and hearing Center. The design, execution, and assessment of therapeutic interaction and the observed language abilities of the client are reported.
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keywords = state
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3/135. Assessment of command-following in minimally conscious brain injured patients.

    OBJECTIVE: To develop a method for establishing the presence of command-following in individuals with traumatic brain injury, based on the principles of single-subject experimental design. DESIGN: A series of single-subject experiments, individualized to the particular command-following question about a particular patient. SETTING: An inpatient rehabilitation hospital with a specialized program for vegetative and minimally conscious brain injured patients. patients: Eight individuals with serious brain injury of traumatic or nontraumatic origin, presenting in vegetative or minimally conscious states. INTERVENTIONS: The frequency of performance of the behavior in question was assessed in response to commands and in relation to appropriate control conditions. Data were analyzed with chi2 or Fisher's exact test, as well as measures derived from signal detection theory. MAIN OUTCOME MEASURES: The frequency of performance of a specific behavior in the presence of a command and in relevant contrasting conditions. RESULTS: This method identified whether a specific behavior was being performed in response to command and whether the reliability of this behavior was changing over time either spontaneously or in response to treatment. CONCLUSIONS: Quantitative assessment of command-following based on principles of single-subject experimental design can determine whether patients are capable of following commands and whether this ability changes over time or in response to treatment.
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4/135. rupture of several parasagittal bridging veins without subdural bleeding.

    This case reports on a fatal craniocerebral trauma involving numerous ruptured cerebral bridging veins that did not bleed subdurally, despite approximately 15 hours of survival. A 15-year-old girl was severely injured as the passenger of a car that crashed sideways into a tree. She-suffered a cerebral trauma of the "diffuse injury" type and was unconscious after the accident. Her computed tomographic scan at admission showed massive brain edema, axial herniation, and marked hypodensity of the bilateral carotid flow area. Despite intensive care measures, the clinical course was characterized by central decompensation with therapy-resistant cardiocirculatory insufficiency. The autopsy revealed ruptures of numerous parasagittal bridging veins. The injured vessels were not thrombosed, and yet there was absolutely no subdural bleeding. This unusual combination of findings is assumed to be caused by an isolated collapse of cerebral circulation occurring shortly after the accident and primarily attributed to a rapid increase of intracranial pressure.
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5/135. Inappropriate secretion of antidiuretic hormone after cerebral injury.

    A case has been presented in which a patient sustained a closed head injury with concomitant maxillofacial injuries; early signs of water intoxication and ISADH developed six days after injury. This disorder was corrected by restricting free water intake for six days until equilibration occurred. Successful reduction of the facial fractures was accomplished after stabilization of the patient's neurological condition and correction of her metabolic disorder. The ISADH and resulting hyponatremia have been documented in a variety of disease states including trauma to the central nervous system. Disruption or irritation to the hypothalamic-neurohypophyseal system has been proposed as the mechanism of dysfunction after cerebral injury. The results of the secretion of inappropriate amounts of ADH relative to renal function and homeostatis have been discussed. Clinical and laboratory diagnosis as well as the elective and emergency management of ISADH have been reviewed. The fact that the sequelae of this abnormal metabolic state may mimic or mask the neurological deterioration which may follow cerebral injury is significant. This may contribute to the difficulty in making a correct diagnosis and designing proper therapy. The problem is basically one of differentiating a correctable metabolic disorder from a lesion that can be fatal unless surgically removed.
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6/135. Subarachnoid haemorrhage following rupture of an ophthalmic artery aneurysm presenting as traumatic brain injury.

    head trauma may provoke subarachnoid haemorrhage. The question sometimes arises whether in patients with trauma and subarachnoid haemorrhage the latter is of traumatic or aneurysmal origin. We present a 49-year-old patient who fell from a truck, struck his head and was unconscious immediately. On the brain computed tomography (CT) scan subarachnoid haemorrhage was present, initially diagnosed as of traumatic origin. Four-vessel angiography revealed rupture of a left ophthalmic artery aneurysm. We review the literature and give recommendations for angiography in patients with trauma and subarachnoid haemorrhage.
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7/135. Heterotopic ossification in childhood and adolescence.

    Heterotopic ossification, or myositis ossificans, denotes true bone in an abnormal place. The pathogenic mechanism is still unclear. A total of 643 patients (mean age, 9.1 years) admitted for neuropediatric rehabilitation were analyzed retrospectively with respect to the existence of neurogenic heterotopic ossification. The purpose of this study was to obtain information about incidence, etiology, clinical aspect, and consequences for diagnosis and therapy of this condition in childhood and adolescence. Heterotopic ossification was diagnosed in 32 patients (mean age, 14.8 years) with average time of onset of 4 months after traumatic brain injury, near drowning, strangulation, cerebral hemorrhage, hydrocephalus, or spinal cord injury. The sex ratio was not significant. In contrast to what has been found in adult studies, serum alkaline phosphatase was not elevated during heterotopic ossification formation. A persistent vegetative state for longer than 30 days proved to be a significant risk factor for heterotopic ossification. The incidence of neurogenic heterotopic ossification in children seems to be lower than in adults. A genetic predisposition to heterotopic ossification is suspected but not proven. As a prophylactic regimen against heterotopic ossification we use salicylates for those patients in a coma or persistent vegetative state with warm and painful swelling of a joint and consider continuous intrathecal baclofen infusion and botulinum toxin injection for those patients with severe spasticity. We prefer to wait at least 1 year after trauma before excision of heterotopic ossification.
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8/135. The rehabilitation of attention in individuals with mild traumatic brain injury, using the APT-II programme.

    Traumatic brain injury (TBI) is a prevalent cause of cognitive impairments and dysfunctions and affects over 2 million individuals each year. Mild traumatic brain injury (MTBI) is generally defined by a brief loss of consciousness, and post-traumatic amnesia that lasts for less than 24 hours. One region of the brain that is likely affected in patients with MTBI is the pre-frontal cortex. This region mediates several functions, including those required for adequate attention. Three individuals, diagnosed with MTBI and difficulties with attention, volunteered to participate in the study. Individuals were presented with 10 weeks of cognitive retraining with the attention Process Training-II (APT-II) programme, followed by 6 or 7 weeks of educational and applicational programmes. Cognitive tests were administered both pre- and post-training to assess the effectiveness of the programme. Analysis of the results showed that the APT-II programme improved attention and performance speed in each of the three individuals. In addition, any rehabilitated cognitive skills remained stable in each individual in the absence of the rehabilitation programme for at least 6 weeks.
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ranking = 0.47336059732346
keywords = consciousness
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9/135. naltrexone: effects on motor function, speech, and activities of daily living in a patient with traumatic brain injury.

    Evidence from many studies has suggested that endogenous opioid peptides participate in a number of pathophysiological responses to brain injury. This provides the rationale for the use of opioid antagonists for the enhancement of neural recovery after brain injury. A case is presented of an 18-year-old male who had loss of consciousness for 1 month after a severe brain injury. Three months of intensive rehabilitative therapies did not change his functional status. A trial of naltrexone was given while his performance in mobility, speech and overall Functional Independence Measure (FIM) scores were monitored. Results indicate an accelerated improvement in functional status and statistically improved FIM score.
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ranking = 0.47336059732346
keywords = consciousness
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10/135. Stimulating consciousness and cognition following severe brain injury: a new potential clinical use for lamotrigine.

    No medications clearly enhance consciousness or cognition following severe brain injury. This series (n = 13) suggests that lamotrigine may stimulate improvement of patients with impairment equivalent to level I-III on the Rancho Los Amigos Cognitive Scale. After a serendiptious clinical result, severely brain injured patients who were taking an anticonvulsant had an opportunity to start lamotrigine. This cohort had been transferred to this rehabilitation unit 14-304 (mean 73.9) days and started lamotrigine 20-310 (mean 87.5) days after acute brain injury. Compared to this unit's experience with patients with similar severe brain injuries, more patients (n = 10) were discharged to the conmmunity and fewer to skilled nursing facilities (n = 3) than were expected. This preliminary and provocative case series corresponds to basic science results, and further investigation of lamotrigine is warranted.
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