Head injury

Obliteration of mesencephalic cisterns, midline shift, subdural and epidural hematomas, shearing injuries involving the brainstem and/or interpeduncular cistern, fractures of the sphenoid body and/or clivus, as well as perfusion defects larger than the intracerebral hematoma have been identified in the recent literature as findings indicative of poor outcome in patients with head injury.     

Head injury and dementia

PURPOSE OF REVIEW: The link between head injury and dementia/Alzheimer's disease is controversial. This review discusses some recent epidemiological, human autopsy and experimental studies on the relationship between traumatic head injury and dementia. RECENT FINDINGS: Recent epidemiological studies have shown that head injury is a risk factor for the development of dementia/Alzheimer's disease, whereas others have not. After experimental brain trauma the long-term accumulation of amyloid beta peptide suggests that neurodegeneration is influenced by apolipoprotein E epsilon 4, and after human brain injury both amyloid beta peptide deposition and tau pathology are seen, even in younger patients. Amyloid beta peptide levels in the cerebrospinal fluid and the overproduction of beta amyloid precursor protein in humans and animals after traumatic brain injury are increased. Repeated mild head trauma in both animals and humans accelerates amyloid beta peptide accumulation and cognitive impairment. Retrospective autopsy data support clinical studies suggesting that severe traumatic brain injury with long-lasting morphological residuals are a risk factor for the development of dementia/Alzheimer's disease. The influence of the apolipoprotein E genotype on the prognosis of traumatic brain injury is under discussion. SUMMARY: Although epidemiological studies and retrospective autopsy data provide evidence that a later cognitive decline may occur after severe traumatic brain injury, the relationship between dementia after head/brain trauma and apolipoprotein E status is still ambiguous. Both human postmortem and experimental studies showing apolipoprotein beta deposition and tau pathology after head injury support the link between traumatic brain injury and dementia, and further studies are warranted to clarify this relationship.     

Head injury during childhood

Abstract

A review of the literature on psychological recovery from head injury in childhood reveals a lack of well designed, long-term follow-up studies. Tentative conclusions concerning cognitive and behavioural changes after childhood head injury are drawn and the implications for rehabilitation discussed. Most children with mild or moderate injuries appear to make excellent recoveries with little evidence of long-term sequelae. However, a cautious interpretation of these findings is recommended as the design and measures used in many studies may limit the identification of some cognitive and personality changes. The possibility of psychological changes becoming apparent only at later stages of development is discussed.     

Head injury and marital aggression

Of 31 consecutive male patients referred for evaluation of marital violence, 19 (61.3%) had histories of severe head injury. Although the relationship between child abuse and head injury did not reach an acceptable level of significance, it did indicate a trend toward a positive relationship. Alcohol abuse, reported by 48.4% of the sample, was significantly associated with head injury. Confirmation of biological etiologies in marital aggression would have implications for prevention and treatment.     

Head injury in early adulthood and the lifetime risk of depression.

BACKGROUND: Depressive symptoms are common and can be debilitating in the months after head injury. Head injury can also have long-term cognitive effects, but little is known about the long-term risk of depression associated with head injury. We investigated the lifetime rates of depressive illness 50 years after closed head injury. METHODS: Participants were male World War II veterans who served during 1944-1945 and were hospitalized at that time for a head injury, pneumonia, or laceration, puncture, or incision wounds. We used military medical records to establish the presence and severity of closed head injuries. Veterans with (n = 520) and without (n = 1198) head injuries were interviewed in 1996-1997 for their lifetime history of depressive illness. Men with dementia were excluded. RESULTS: Veterans with head injury were more likely to report major depression in subsequent years and were more often currently depressed. Using logistic regression and controlling for age and education, the lifetime prevalence of major depression in the head injured group was 18.5% vs 13.4% in those with no head injury (odds ratio = 1.54, 95% confidence interval = 1.17-2.04). Current major depression was detected in 11.2% of the veterans with head injuries vs 8.5% of those without head injury (odds ratio = 1.63, 95% confidence interval = 1.07-2.50). This increase in depression could not be explained by a history of myocardial infarction, a history of cerebrovascular accident, or history of alcohol abuse. The lifetime risk of depression increased with severity of the head injury. CONCLUSION: The risk of depression remains elevated for decades following head injury and seems to be highest in those who have had a severe head injury.     

Head injury and spinal cord injury: differential effects on psychosocial functioning

Closed-head injury (CHI) and spinal cord injury (SCI) cause significant permanent alterations in life style, social-role functioning, and psychological status. While the cognitive effects of CHI are well known, there have been questions concerning the psychosocial sequelae from CHI, and whether they are unique to this disability group rather than representing general effects of a life-threatening medical emergency with permanent life-altering consequences. This issue was examined with samples of ambulatory moderate (n = 31) and severe (n = 17) CHI patients and wheelchair-dependent SCI (n = 24) patients. Results indicate that there were no significant differences between the groups on pre- and post injury demographic factors. However, while the moderate CHI and SCI groups were equivalent on many indicators of psychosocial outcome, the severe CHI group was more depressed, angry and hostile, and confused and bewildered. As well, wives of the severe CHI patients rated their husbands as more belligerent, negative, helpless, suspicious, withdrawn and retarded, and with more general psychopathology than did wives of moderate CHI or wives of SCI patients. Implications of these findings for preventative psychosocial rehabilitation are discussed.     

Head injury and Parkinson's disease risk in twins

OBJECTIVE: Head injury is an inconsistently reported risk factor for Parkinson's disease (PD). Many related variables might confound this association, such as differences in childhood and adolescent lifestyles or genetically determined risk-taking behaviors. Twin studies circumvent some of these problems, because twins are genetically and environmentally much more similar than typical cases and control subjects. METHODS: We conducted a case-control study in 93 twin pairs discordant for PD ascertained from the National Academy of Sciences/National Research Council World War II Veteran Twins Cohort. RESULTS: A prior head injury with amnesia or loss of consciousness was associated with an increased risk for PD (odds ratio, 3.8; 95% confidence interval, 1.3-11; p = 0.014). Truncating observations 10 years before PD onset enhanced the association. Though less precise, the association was somewhat stronger in monozygotic than in dizygotic pairs. Risk increased further with a subsequent head injury (p trend = 0.022) and with head injuries requiring hospitalization. Duration of unconsciousness was not associated. In a subanalysis of 18 pairs concordant for PD, the twin with younger onset PD was more likely to have sustained a head injury, although numbers were small. INTERPRETATION: Our results suggest that mild-to-moderate closed head injury may increase PD risk decades later.     

Head injury induces increased prostaglandin synthesis in rat brain

Head injury was induced in the left hemisphere of rats. The rats were killed at various time intervals after trauma (immediately, 15 min, 1 and 18 h, and 4 and 10 days), and the rates of synthesis and release of prostaglandin PGE2, 6-keto-PGF1 alpha, and thromboxane TXB2 from cortical slices of both hemispheres were studied. The rate of synthesis of PGE2 after 18 h was six and four times higher than control in the contused and contralateral hemispheres, respectively. By 10 days post-trauma, both hemispheres had normal rate of PGE2 release. TXB2 and 6-keto-PGF1 alpha synthetases were affected already 15 min after the injury, and a similarly elevated rate of synthesis was found in both hemispheres. The maximal effect was detected after 1 or 18 h with return to normal after 4 or 10 days for TXB2 and 6-keto-PGF1 alpha, respectively. Tissue specific gravity was determined for both hemispheres using linear gradient columns. The results of these determinations indicate that development of edema occurs in the contused hemisphere as early as 15 min post trauma; it reaches its maximal level at 18 h and returns to normal at 10 days. Arterial pressure was monitored, and a transient increase was found at 10 min post trauma. We suggest that the production of edema after brain injury may be related to the increased rate of PGE2 and PGI2 synthesis, which occurs at similar time intervals after injury.     

Head injury as a risk factor for Alzheimer's disease

A case-control study was performed in which the frequency of prior head injury was assessed in 78 patients with dementia of the Alzheimer type (DAT) and 124 control subjects matched for age, sex, and race. A history of head injury with loss of consciousness was reported in 25.6% of patients and 5.3% and 14.6% of hospital and neighborhood controls, respectively. Matched-pair analysis of patients and hospital controls yielded an odds ratio of 4.50, which was significant (p less than 0.01). The ranges of times of occurrence of head injuries were similar in patients and controls, spanning several decades. The findings suggest a possible etiologic role for head injury in DAT.