Social adjustment after closed head injury: a further follow-up seven years after injury.

Oddy, Michael; Coughlan, Tara; Tyerman, Andy; Jenkins, David G.

doi:10.1136/jnnp.48.6.564

Cited by 435 publications

(185 citation statements)

References 13 publications

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“…TBI causes serious neurological pathologies culminating in cognitive impairment (2). To date, treatment has typically targeted physical manifestations of the injury, e.g., alleviating increased intracranial pressure, without addressing the underlying mechanisms contributing to injury-associated impairments.…”

mentioning

confidence: 99%

Dietary branched chain amino acids ameliorate injury-induced cognitive impairment

Cole¹,

Mitala²,

Kundu³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

132

139

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Neurological dysfunction caused by traumatic brain injury results in profound changes in net synaptic efficacy, leading to impaired cognition. Because excitability is directly controlled by the balance of excitatory and inhibitory activity, underlying mechanisms causing these changes were investigated using lateral fluid percussion brain injury in mice. Although injury-induced shifts in net synaptic efficacy were not accompanied by changes in hippocampal glutamate and GABA levels, significant reductions were seen in the concentration of branched chain amino acids (BCAAs), which are key precursors to de novo glutamate synthesis. Dietary consumption of BCAAs restored hippocampal BCAA concentrations to normal, reversed injury-induced shifts in net synaptic efficacy, and led to reinstatement of cognitive performance after concussive brain injury. All brain-injured mice that consumed BCAAs demonstrated cognitive improvement with a simultaneous restoration in net synaptic efficacy. Posttraumatic changes in the expression of cytosolic branched chain aminotransferase, branched chain ketoacid dehydrogenase, glutamate dehydrogenase, and glutamic acid decarboxylase support a perturbation of BCAA and neurotransmitter metabolism. Ex vivo application of BCAAs to hippocampal slices from injured animals restored posttraumatic regional shifts in net synaptic efficacy as measured by field excitatory postsynaptic potentials. These results suggest that dietary BCAA intervention could promote cognitive improvement by restoring hippocampal function after a traumatic brain injury.

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mentioning

confidence: 99%

Dietary branched chain amino acids ameliorate injury-induced cognitive impairment

Cole¹,

Mitala²,

Kundu³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

132

139

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“…The literature suggests that lack of awareness of illness is not simply a function of global cognitive deficits, but perhaps is more related to frontal-executive dysfunction (60,61). In individuals with TBI, this dimension is frequently the focus of family/caregiver concern, yet is often not recognized by the individuals themselves (8,(62)(63)(64)(65)(66). Even when the individual admits to some difficulties, he or she is often unable to predict the implications of these deficits in current or future social situations.…”

Section: Changes In Personalitymentioning

confidence: 99%

Neurobehavioral sequelae of traumatic brain injury: evaluation and management

2008

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Traumatic brain injury (TBI) is a universal public health problem. A recent review of epidemiological studies in Europe suggests an incidence of 235 hospitalized cases (including fatalities) per 100,000 population (1). In the US, the incidence is estimated at 150 per 100,000 population (2). Less data is available from other regions of the world, but TBI is acknowledged as a significant problem worldwide. Of note is that the incidence rates are calculated from hospitalized cases only, and do not include injured individuals who do not seek or have access to care. Thus, the actual incidence of injury is probably 3 to 4 fold larger than the quoted numbers. Most studies suggest that the incidence rates for TBI are greatest in the second and third decades of life, with a secondary increase in the elderly stemming from falls (2,3). Males are more likely to suffer a TBI than females (2,3).In developed countries, there has been a reduction in the mortality rates associated with TBI over the last several decades, generally attributed to improved systems of trauma care and improved motor vehicle safety design. Many individuals with mild traumatic brain injury and virtually all individuals who survive moderate and severe TBI are left with significant long-term neurobehavioral sequelae (4-6). Thus, the reduction in TBI-associated mortality rates (7) has led to a significant increase in the number of individuals with long-term neurobehavioral disorders related to TBI (8,9).Brain trauma can be caused in a number of ways, including mechanisms which penetrate the substance of the brain (e.g., projectiles) and those that do not. This paper focuses on non-penetrating injuries. Despite different contexts and instruments, the physics and biomechanics underlying damage to the brain from non-penetrating injuries have some common features. This results in certain brain regions being at greater risk for damage than others and allows for some general statements to be made about typical profiles of brain injury associated with trauma. The assessment and treatment of the neurobehavioral sequelae of TBI follow logically from an understanding of this injury profile. RELATIONSHIP OF PROFILE OF INJURY TO NEUROBEHAVIORAL SEQUELAEThere are two broad categories of forces that result in brain injury: contact (or impact) and inertial (acceleration or deceleration). Contact injuries result from the brain coming into contact with an object (which might include the skull, or some external object). Contact mechanisms often result in damage to scalp, skull, and brain surface (e.g., contusions, lacerations, hematomas) (10). Frequent sites of such injury are the anterior temporal poles, lateral and inferior temporal cortices, frontal poles, and orbital frontal cortices.Inertial injury results from rapid acceleration or deceleration of the brain that produces shear, tensile, and compression forces. These forces have maximum impact on axons and blood vessels, resulting in axonal injury, tissue tears, and intracerebral hematomas. These mechanisms also produc...

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“…Even those deemed to have made a good recovery often have residual psychological or emotional deficits which prevent them from returning to pre-injury levels of functioning [6][7][8]. However, several researchers suggest that good long-term adjustment after brain injury is achievable, even after severe TBI [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Predictors of positive growth after traumatic brain injury: A longitudinal study

Hawley

Joseph

2008

Brain Injury

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Research design:Longitudinal study. Method and Procedure:Long-term follow-up of a group of TBI survivors recruited between 1991-1995. In 2004, 240 of the 563 original participants were invited to take part in a follow-up study. At follow-up, survivors completed the Positive Changes in Outlook Questionnaire (CiOP) along with a structured interview/questionnaire which permitted a Glasgow Outcome Scale (GOSE) score to be assigned. Results:165 TBI survivors completed both questionnaire and CiOP.103(62%) participants had suffered severe TBI, 24(15%) moderate and 38(23%) mild. Mean length of follow-up was 11.5 years post-injury (range 9-25 years). On the GOSE at follow-up, 43(26%) had severe disability; 72(44%) moderate disability;and 50(30%) good recovery. Scores on the CiOP indicated positive psychological growth in over half of the sample, as evidenced by agreement with items such as "I don't take life for granted anymore" and "I value my relationships much more now".CiOP total scores did not correlate with any injury or early outcome variables.However, at long-term follow-up there was a negative correlation between positive growth and anxiety and depression.4 Conclusion:Survivors of mild, moderate and severe TBI showed evidence of long-term positive changes in outlook.

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Social adjustment after closed head injury: a further follow-up seven years after injury.

Cited by 435 publications

References 13 publications

Dietary branched chain amino acids ameliorate injury-induced cognitive impairment

Dietary branched chain amino acids ameliorate injury-induced cognitive impairment

Neurobehavioral sequelae of traumatic brain injury: evaluation and management

Predictors of positive growth after traumatic brain injury: A longitudinal study

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