This page contains a Flash digital edition of a book.
Brain Trauma


Table 2: Checklist of Risk Factors for Major Depression Following Moderate to Severe Traumatic Brain Injury


Anxiety, panic Aggression – verbal, physical, chronic agitation, restlessness and frustration Substance use – alcohol and/or drugs Sleep difficulties – difficulty falling asleep, early awakening, reduced sleep time Low income – poverty level, 1–3 times above poverty level, financial problems Personal relationship problems – lack of intimate partner, no close friends, discord in close relationships Poor social skills – problem-solving, social withdrawal, lonely, uncomfortable around others Unemployment – unstable pre-injury work history, post-injury job loss Negative thinking/rumination – physical symptoms, losses, failures, low self-esteem, hopelessness


core features of MD and may precede or partially account for the markedly higher rates of somatic and cognitive symptoms reported by depressed versus non-depressed persons with TBI.12


Associated Disorders/Risk Factors for Major Depression


Research based primarily on univariate analyses of the TBI population and supported with evidence from the general population indicates that nine disorders and psychosocial features have consistently been associated with MD (see Table 2).


Anxiety commonly co-occurs with both early- and late-onset depression after TBI, with rates ranging from 41–77%.4,23,24


Persons


who are diagnosed with both depression and anxiety disorders following TBI have longer symptom duration (7.5 months) than patients with depression alone (1.5 months).23


Epidemiological


research in the general population indicates that anxiety disorders co-occur with depression in about 58% of cases and precede the depressive disorder in 85% of cases.25


Aggression also commonly co-occurs with depression at six, 12 and 60 months post-TBI.26–28


soon after injury were at a greater risk of developing post-TBI MD.29


Persons who reported irritability and anger In


the general population, impulse-control disorders were the second most commonly co-occurring disorder (17%) in persons with depression, and preceded the depressive disorder in 79% of cases.25


Alcohol abuse is associated with higher rates of depression in the first year post-injury.23,30–32


In the general population, substance use was


the third most commonly co-occurring disorder (9%) with depression. It preceded depression diagnoses in half (51%) of the cases.25


Sleep disorders are one of nine core symptoms of MD and trouble falling asleep was six times more likely to be reported by depressed than non-depressed persons with TBI.6


Objective laboratory studies have


confirmed night-time sleep disorders and excessive daytime sleepiness in 25–53% of those self-reporting sleep difficulties.33,34


Persons with TBI


who had objective findings of sleep maintenance insomnia evidenced moderate to severe Beck Depression Inventory scores.34


Despite this, no


In the general population, growing empirical literature suggests that insomnia is a precipitant of depression35–38


persistent insomnia were 40 times more likely to develop depression within one year compared with persons with no insomnia.35


26


association was found between excessive daytime sleepiness and mood.33


and that persons with Pathophysiology


Lesion location may be related to the development of depression following TBI. Pathophysiology in such patients is similar to the general population, involving the left dorsal lateral frontal cortex and left basal ganglia and, to a lesser extent, focal lesions in the right hemisphere and parieto-occipital region.4,23,51–55


Imaging studies have


shown that hypometabolism of the lateral and dorsal frontal cortex, especially the dorsal prefrontal cortex and cingulate gyrus, may be associated with depressive symptoms, along with increased activation in the ventral limbic and paralimbic structures, including the prelimbic cortex, amygdale and medial thalamus.10,51,56


However,


these patterns of anatomical dysfunction are not universally observed in persons with MD and variations between studies are likely attributable to heterogeneity in MD symptoms and the existence of subtypes of depression.10,56 Drevets,57


Davidson,56 Moldover10


For detailed reviews of this topic, see and Jorge.51


Pre-injury Psychiatric History


Pre-injury psychiatric history has not been consistently associated with MD after TBI. Three studies found a significant association between history of mood and/or anxiety disorders and the development of post-TBI MD,4,12,23 similar association.11,30


while two studies did not show a In contrast, a population-based study


that assessed the presence of TBI and affective disorders found that persons without a prior psychiatric illness had almost five-times higher rates of affective disorders at seven to 12 months post-TBI. Individuals with TBE were more than twice as likely as the general population to be depressed 13–18 months post-TBI.58


EUROPEAN NEUROLOGICAL REVIEW


Poor social skills and personal relationship problems, including perceived lack of social support and a close confiding relationship, have been associated with greater levels of early- and late-onset MD in persons with TBI.4,11,12,23,29,39–41 associated with MD after TBI.4,6,23


Current marital status has not been In contrast, divorced, separated or


widowed persons in the general population reported higher lifetime and 12-month rates of MD; persons who have never been married had the highest 12-month rate of MD.25


Unemployment and/or unstable work history is consistently associated with higher rates of depression after TBI.6,30,42,43


These


findings are consistent with research in the general population, which shows that unemployment and disability are significantly associated with increased lifetime prevalence rates of MD.25


has a linear association with depression after TBI.6,11,41


Lower income level Similarly,


persons in the general population whose income was below the poverty line were four times more likely to report a 12-month rate of depression. Persons who were one to three times above the poverty rate were twice as likely to be depressed.25


Negative thinking reflects a tendency to view one’s self as defective or inadequate, a pervasive and absolute evaluation of one’s own life experience as resulting in loss or failure and hopelessness regarding the future.44–47


Research has found that rumination, self-criticism, distress and guilt were part of a symptom cluster that most differentiated depressed from non-depressed persons after TBI.15 These findings are consistent with research in the general population indicating that rumination is prevalent in both the development and maintenance of depression. Rumination worsens depressive symptoms over time and is a risk factor for developing future major depressive disorders.44,48–50


Page 1  |  Page 2  |  Page 3  |  Page 4  |  Page 5  |  Page 6  |  Page 7  |  Page 8  |  Page 9  |  Page 10  |  Page 11  |  Page 12  |  Page 13  |  Page 14  |  Page 15  |  Page 16  |  Page 17  |  Page 18  |  Page 19  |  Page 20  |  Page 21  |  Page 22  |  Page 23  |  Page 24  |  Page 25  |  Page 26  |  Page 27  |  Page 28  |  Page 29  |  Page 30  |  Page 31  |  Page 32  |  Page 33  |  Page 34  |  Page 35  |  Page 36  |  Page 37  |  Page 38  |  Page 39  |  Page 40  |  Page 41  |  Page 42  |  Page 43  |  Page 44  |  Page 45  |  Page 46  |  Page 47  |  Page 48  |  Page 49  |  Page 50  |  Page 51  |  Page 52  |  Page 53  |  Page 54  |  Page 55  |  Page 56  |  Page 57  |  Page 58  |  Page 59  |  Page 60  |  Page 61  |  Page 62  |  Page 63  |  Page 64  |  Page 65  |  Page 66  |  Page 67  |  Page 68  |  Page 69  |  Page 70  |  Page 71  |  Page 72  |  Page 73  |  Page 74  |  Page 75  |  Page 76