Psychiatric sequelae of traumatic brain injury
Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/0975-2870.114638
Almost half of the people suffering traumatic brain injury (TBI) may later be diagnosed with psychiatric disorders. The literature (PubMed, IndMed of past 30 years) on psychiatric disturbances associated with TBI is reviewed. The authors highlight the close link between head injury and psychiatry and provide an overview of the epidemiology, risk-factors, and mechanisms of psychiatric sequelae including, cognitive deficits, substance abuse, psychoses, mood disorders, suicide, anxiety disorders, dissociative disorders, post-concussion syndrome, and personality changes following head injury. The various psychiatric sequelae are briefly discussed. Keywords: Cognitive deficits, personality change, post-concussion syndrome, psychiatric sequelae, traumatic brain injury
Traumatic brain injury (TBI) is a major global health problem with an annual incidence of 10 million. [1] The most common cause of TBI is road traffic accidents. TBI remains the single largest cause of trauma morbidity and accounts for nearly one-third of all trauma deaths. [2] Despite the emphasis placed on physical deficits during the early stages of recovery from a severe TBI, it is cognitive and behavioral deficits that give rise to the major morbidity, which most impairs the capacity to return to work and maintain social activities. [3] Psychiatric disorders following TBI are important for a number of reasons. Firstly, TBI accounts for most cases of permanent disability after trauma. Given that trauma injuries occur most frequently in the young (<45 years), the cost, both to the individual and to society, is enormous. [4] Secondly, the psychiatric sequelae of TBI may frequently be overlooked, and as such, under treated. Nowhere is this more apparent than in people with mild TBI, who comprise over 85% of all TBIs, and who routinely do not receive adequate follow-up care. [5] In addition, TBI is associated with an increased risk of developing numerous psychiatric disorders and will need psychiatric interventions years after the injury. [6] An increased awareness of these sequelae with consequent early psychiatric intervention may result in improving function and limiting disability. For the present review a literature search (PubMed, IndMed) of past 30 years was made using the following search terms: Psychiatric effects, neuropsychiatric effects, TBI and head injury. Articles in English were identified and meta-analysis and studies with large samples were included, though for unusual disorders case reports only were available, which were also included in the review.
TBI is "an alteration in brain function, or other evidence of brain pathology, caused by an external force". [7] The alteration in brain function may manifest as loss or decreased level of consciousness, alteration in mental state, incomplete memory for the event, or neurological deficits. Examples of external forces include the head striking or being struck by an object, rapid acceleration or deceleration of the brain, penetration of the brain by a foreign object, and exposure to forces associated with blasts. The external force requirement separates TBI from other acquired brain injuries due to cerebrovascular, neoplastic, or neurodegenerative conditions. The term brain injury is preferred to head injury, since the latter term might be limited to damage to the face or scalp. [8]
Country-based incidence range from 108 332 new cases admitted to hospital per 100,000 population per year. The incidence of TBI is rising in because of increased transport-related injuries, and young men (who are over-represented in transport, work, and recreational injuries) are particularly affected. The ageing populations have given rise to a new cohort-elderly people-who sustain TBI from fairly low-impact falls. Furthermore, blast injury to the brain is common in civilians and military personnel who are exposed to improvised explosive devices and suicide terrorist attacks. [9] A meta-analysis of 15 general population studies including 25,134 adults revealed a 12% prevalence of TBI. Men had more than twice the odds of having had a TBI than did women, suggesting that male gender is a risk-factor for TBI. [10]
The major risk-factors include increasing age, arteriosclerosis, and alcoholism. [11],[12] A history of psychiatric disorder, premorbid personality, [13] pre-injury psychological resilience and mood status, [14] fewer years of formal education, marital discord, poor interpersonal relationships, problems at work, or financial instability are important contributors to the psychiatric disability. [3],[12]
Psychiatric symptoms found in 120 persons with severe TBI included apathy (42%), irritability (37%), dysphoria/depressed mood (29%), disinhibition (28%), eating disturbances (27%), and agitation (24%). [15] In 939 TBI patients the prevalence of any psychiatric illness in the 1 st year was 49% following moderate to severe TBI and 34% following mild TBI. Whereas moderate to severe TBI is associated with a higher initial risk, mild TBI is associated with persistent psychiatric illness. [16] The common psychiatric disorders after head injury [17] include major depression (44%), substance abuse (22%), posttraumatic stress disorder (PTSD) (14%), obsessive compulsive disorder (OCD) (6.5%), mania (4%) and psychosis (1%). A long-term follow-up of 254 individuals revealed a higher incidence of cognitive, behavioral and emotional changes at 5 years than at 2 years post-TBI. Thirty-two percent of those working at 2 years were unemployed at 5 years. [18] TBI clearly may cause decades long, and possibly permanent, vulnerability to psychiatric illness. [19] In chronic TBI, the incidence of psychosis is 20%, depression is 18-61%, mania is 1-22%, PTSD is 3-59% and post TBI aggression is 20-40%. [20] A 30-year retrospective follow-up study of 60 TBI patients showed that 48% had a DSM IV axis I disorder that began after head injury; 62% had an axis I disorder during their lifetimes. Common new disorders following TBI were major depression (27%), alcohol abuse or dependence (12%), panic disorder (8%), specific phobia (8%) and psychotic disorders (7%); 23% had at least one personality disorder. [21]
Cognitive Deficits These are common after TBI. Additionally, patients who report full recovery may continue to experience reduced mental efficiency under conditions of physical or psychological stress. These residual deficits are thought to reflect a basic disorder in information processing capacity, either in terms of speed of processing or in terms of the amount of information that can be handled simultaneously. [22] Disturbances of executive functioning include poor planning, organizing, sequencing, and set-shifting, with impaired judgment and impulse control. Attention Our ability to maintain a goal-directed focus without support from the environment requires the endogenous control of behavior. This ability is compromised following TBI leading to increased lapses of attention. [23] Memory Memory deficits are the most prevalent complaints. The degree of memory impairment is correlated with the length of post-traumtic amnesia PTA. Newly acquired knowledge is forgotten. Both recent and remote memory may be impaired, but immediate memory may be spared. [24] Perception Visual dysfunction affects about 50% of TBI patients. Visuo-perceptual disturbances such as impaired figure-ground perception and constructional abilities may be present in severe TBI. Focal visuo-perceptual and visuo-constructive disabilities are rare. [25] Language Anomia and word finding difficulties are present after TBI. Expressive aphasias are more common compared to receptive aphasias. Recovery from aphasia and related language disorder is greater than recovery from memory and other cognitive deficits when patients were tested after 1 year. [26] Intelligence Both performance and verbal intelligence quotient IQ are reduced in severe TBI, but not after mild TBI. Recovery of verbal IQ is faster. Performance IQ may be lower even after 3 years. The "punch drunk" syndrome may be seen in boxers 5-40 years after retirement. [27]
Many TBI patients are intoxicated at the time of injury. Presence of high alcohol levels in blood not only has a negative impact on length of unconsciousness, behavioral changes, and neurocognitive changes but can also affect mortality. In 158 TBI survivors alcohol dependence and abuse was identified in 24.1-10.8% respectively. [28] In a population based study involving 1600 individuals interviewed 1 year after TBI, revealed heavy alcohol use in 15.4%, moderate use in 14.3% and abstinence or infrequent use in 70.3% of cases. [29]
Substantial clinical, and neurobiological differences exist between the psychosis secondary to head injury (PSTHI) and the primary psychotic disorders. [30] PSTHI occurs in 4-8.9% of individuals who sustain TBI. The mean latencies between TBI and onset of psychosis are between four to 5 years, but can range from a few days to over 20 years. Despite the wide range of latencies, about half of patients with PSTHI demonstrate symptoms within the first year, and roughly 72% of patients have symptoms within the first 5 years. [31] Latencies of less than 1 year have been associated with diffuse injuries, paranoid symptoms and visual hallucinations. By contrast, patients with longer latencies before the onset of symptoms were found to have localized damage to the temporal lobe and presence of epilepsy. Academic or vocational deterioration and social withdrawal were each reported by roughly one third of the patients. [31],[32] The most common symptom of PSTHI is persecutory delusions seen in up to 80% of all patients. Auditory hallucinations are also common, present in 60-93% of patients. Visual hallucinations, negative symptoms and formal thought disorder are less common, occurring in 8-32%, 15-22.2%, and 4.4% of patients, respectively. [31],[32] Impairments in memory and executive functioning are consistent findings. Localization data consistently report abnormalities in the temporal areas, [31],[33] and less commonly, in the frontal lobes. [33],[34] There is no consistent finding for hemispheric laterality of lesions. About 0.7-9.8% of patients with TBI develop schizophrenia-like psychosis. [33] Most of these patients do not have a family history of schizophrenia. A recent meta-analysis of nine case-controlled population-based studies supports an increased risk of schizophrenia following TBI, with a larger effect in those with a genetic predisposition to psychosis. [35] Chronicity was associated with premorbid schizoid personality. [33] A higher percentage of schizophrenic psychosis (63%) versus delusional disorders (40%) demonstrated a chronic course. [34]
This is a frequent complication that exerts a deleterious effect on the recovery process. [36] Depression The prevalence of depression in TBI is approximately 30% across multiple time points up to and beyond a year; 27% met criteria for depression 3-6 months from injury; 32% at 6-12 months; and 33% beyond 12 months. [37] Depression is associated with executive dysfunction, negative affect, and prominent anxiety symptoms. Depression occurs more frequently with left dorsolateral frontal and left basal ganglia lesions. Feelings of loss, demoralization, and discouragement seen soon after injury are often followed by symptoms of persistent dysphoria. Suicide potential should always be evaluated. [38] Fatigue, irritability, disinterest, and insomnia are seen in a substantial number of patients 6-24 months or even longer after head injury. Psychological impairments in excess of the severity of injury and poor cooperation with rehabilitation are strong indicators of a depressive disorder. Mania after TBI is less common than depression but much more common than in the general population. It is seen in about 9% of patients. The confluence of either anterior subcortical atrophy and a focal lesion of a limbic or limbic-connected region of the right hemisphere, or genetic loading and a limbic-connected right hemisphere lesion may account for mania after TBI. [16] In post-traumatic mania irritable mood is more common than euphoric mood. Almost 50% of patients have abnormal electroencephalogram EEG.
TBI is associated with high rates of suicidal ideation, [39] suicide, [40] and completed suicide. [41] Suicide is considerably increased after TBI and accounted for 14% of all deaths in an 18-year follow-up of those with war brain injuries. Change of character, alcoholism and interpersonal difficulties are frequently present. An association with lesions in frontal and temporal lobes has been reported. [42] Individuals with TBI were 1.55 times more likely to have died by suicide than non-TBI counterparts. [43]
Anxiety disorders, including generalized anxiety disorder, panic disorder, phobic disorders, PTSD, and OCD are common after TBI and range in frequency from 11% to 70%. TBI patients often experience generalized "free-floating" anxiety associated with persistent worry, tension, and fearfulness. Right-hemispheric lesions are more often associated with anxiety disorder than left-sided lesions. PTSD Mayou et al. [44] found that PTSD is "not associated with a neurotic predisposition" but is "strongly associated with horrific memories of the accident." PTSD did not occur, in their sample, in subjects who lost consciousness during the head injury or who were amnesic for the event. Similarly, while 13% of 47 veterans who had suffered a moderate TBI and who were amnesic for the event developed avoidance and arousal criteria of PTSD, none developed the full syndrome, and none met the criteria of re-experiencing the event. [45] Women were predisposed to develop PTSD: 6 of 10 women, versus 2 of 14 men, developed PTSD following TBI. [46] PTSD occurred in 82% of mild - TBI patients who had experienced acute stress disorder earlier (1 month post-injury), but in only 11% of those who did not suffer acute stress disorder. [47] OCD OCD is seen less commonly with a prevalence of 1.6-15%. [48] It is associated with dysfunction in orbitofrontal cortex, frontal subcortical circuits and in executive functioning. [49],[50]
Dissociative (conversion) symptoms including fits, fugues, amnesia, Ganser states, paralysis, anesthesia, and disturbance of speech, sight or hearing are not uncommon. A neurasthenic reaction may incapacitate the patient for months or even years.
A concussion is a transient brief interruption of neurologic function after minor head trauma, with or without a LOC, usually as a result of acceleration-deceleration forces to the head. [51] Individuals sustaining concussion often report a constellation of physical, cognitive, and emotional/behavioral symptoms referred to as Post-Concussion Syndrome (PCS). The most commonly reported symptoms are headache and other pain, dizziness or light headedness, memory and concentration difficulty, amnesia, sleep disturbance, frustration, irritability, fatigue and weakness, visual disturbances, sensitivity to light, sensitivity to noise, tinnitus, periods of confusion or mental dullness, emotional and behavioral changes, loss of self-confidence, slow reactions, judgment problems, depression, and anxiety. [52] Patients are amnestic for the traumatic event, and the duration of amnesia suggests the severity of the sustained injury. In young children, acute symptoms of concussion often include restlessness, lethargy, confusion, or irritability. Onset of PCS is usually during the first month after TBI. Most patients recover within 3-6 months after injury. However, about 15% of patients will have symptoms lasting longer than 1 year. The underlying pathogenesis is thought to be diffuse axonal injury DAI from acceleration and deceleration forces. Abnormal audiologic examination has been reported in PCS patients complaining of dizziness, hearing disturbances and tinnitus. PET has demonstrated changes in cerebral glucose metabolism greater than would be expected by the lesions detected by computed tomography and magnetic resonance imaging scans. Single-photon emission computed tomography studies have shown focal abnormal regional cerebral blood flow.
Commonly reported changes include excessive tiredness, indifference, concentration and attention disorders, inflexibility, tendency towards perseveration, absence of ability to anticipate, behavioral disinhibition, irritability, a change in quality of relationship with more shallowness, and obsessive-compulsive symptoms. van Reekum [17] reported that avoidant, borderline, and narcissistic personality disorders were the most common. The numbers, however, are very low. [17] In 60 patients assessed 30 years after TBI 23.3% had at least one personality disorder. The most prevalent were avoidant (15.0%), organic (15.0%), paranoid (8.3%), and schizoid (6.7%) personality disorders. [21] Some localization of personality change due to frontal lobe injury has been reported. Damage to the dorsolateral prefrontal cortex and its circuitry impairs executive functions such as working memory, decision making, problem solving and mental flexibility. Damage to the orbitofrontal cortex and related nodal points impairs intuitive reflexive social behaviors and the capacity to self-monitor and self-correct in real time within a social context. Damage to anterior cingulate and related circuitry impairs motivated and reward-related behaviors. Damage to medial temporal regions impairs other aspects of memory and the smooth integration of emotional memory with current experience and real-time assessment of stimulus salience. The frontal-subcortical circuits responsible for these critical domains of higher intellectual function and empathic, motivated, nuanced human behavior are highly vulnerable to injury in the typical TBI. [53] Aggression This is one of the most common consequences of TBI with a prevalence of 16.4-33.7%. [54],[55] Aggression interferes with rehabilitation and is particularly difficult for family members to manage. It may occur alone or as a manifestation of another psychiatric disorder (delirium, mood disorder, or personality change secondary to TBI) or an exaggeration of previous personality. Post-TBI aggression was associated with new-onset major depression, poorer social functioning, and increased dependency in activities of daily living. [56] Apathy Ten percent of patients tend to have apathy without depression, and 60% have some degree of apathy and depression following TBI. [57] Affective Instability TBI patients may show exaggerated displays of emotional expression, out of proportion to both the precipitating stimulus and the pre-injury range of response to similar stimuli. The prevalence of affective instability varied from 10.9% to 3.7%. [54],[55]
Sexual dysfunction is a major ongoing problem in the TBI population, affecting 40-60% of individuals. [58] Limbic structures particularly amygdala, septal nuclei, hypothalamus, and various cortical areas which form part of the neuroanatomic and physiologic substrate of human sexual behavior may be damaged in TBI, resulting in impaired sexuality. Transient hypogonadism is common acutely following a TBI, yet it persists in 10-17% of long-term survivors. Beyond just the fertility and psychosocial issues presented by hypogonadism, muscle weakness and osteoporosis may have a significant impact on long-term function and health with consequences exacerbated by immobility of long durations following a TBI. [59]
Sleep disturbance are reported by 30-75% of individuals following TBI, and include insomnia, hypersomnolence, altered sleep-wake cycles, reduced sleep efficiency, increased sleep fragmentation and reduced evening melatonin production. [60] Disturbed sleep, as measured by polysomnogram, was reported in 45% of 71 individuals 3 years post TBI. [61] Sleep disturbances after TBI can exacerbate other symptoms such as pain, cognitive deficits, fatigue, or irritability, and thus can compromise the rehabilitation process and the ability to return to work.
The prevalence of fatigue after TBI ranges from 40% to 70%. [62],[63] Fatigue may be due to failure in the integration of the limbic input and the motor functions affecting the striatal-thalamic-frontal cortical system. [64]
Post-traumatic Headache (PTH) is common and at times persistent and disabling sequelae of TBI. Acute PTH is defined as beginning within 7 days of the trauma and resolving within 3 months. Chronic PTH is defined as beginning within 7 days of trauma (or after awakening there from) and persisting beyond three months. [65] Estimates of PTH vary from 30% to 90%. [66] Most cases of PTH clinically resemble tension type headache although many have migrainous features like nausea, unilaterality, pulsatility and photosensitivity. In 112 chronic PTH patients 37% had tension-type headache, 27% migraine like, while the rest did not fit into any category. [67]
Patients with TBI, whether mild, moderate, or severe, often experience enduring emotional and cognitive consequences. Evidence suggests that depression is the most common comorbidity, occurring not merely as a coincidence, but seemingly intrinsic to the neuropathologic process. However, there is no single factor-psychological, physiological, somatic, or demographic-that uniformly predicts psychiatric comorbidity. Of interest is that the frequency of minor depression/dysthymia is not significantly different among patients with head injury or general trauma. Furthermore, the emergence of psychiatric disorders appears to have no direct relationship to the severity of brain trauma.
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