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AUTHOR: DR. SHAHUL AMEEN, M.D.

3. ETIOLOGICAL FACTORS IN ORGANIC MENTAL DISORDERS

3.1 TRAUMATIC BRAIN INJURY

Epidemiology

Traumatic Brain Injury (TBI) is defined as brain damage secondary to an externally inflicted trauma (Rao and Lyketsos, 2002). TBI is the leading cause of death and disability in persons under 45 years of age, with an overall mortality rate of 25 per 100,000. Motor vehicle accidents are the most common cause of head injury, accounting for more than 50%, followed by falls (21%), violence (12%), and injuries from sports or recreational activities (10%) (McAllister, 1992). Closed head injuries in which the dura remains intact and the brain is not penetrated, comprise more than 90% of TBI (Hammeke and Gennarelli, 2003). Risk factors for TBI include being male aged 15 – 24 years (Kraus et al., 1989), alcohol use and abuse (Dikmen et al., 1993), attention-deficit hyperactivity disorder (Weiss and Hechtman, 1993) or other psychiatric disorders (Jennett, 1972) or having a previous head injury (Annegers et al., 1980). The major risk factors for neuropsychiatric disturbances after TBI include preinjury history of psychiatric illness, preinjury poor social functioning, increasing age, arteriosclerosis, and alcoholism (Deb et al., 1999, Fedoroff et al., 1992, Lishman, 1988)

Classification of Head Injury

Head injury can be classified along several lines.

1. Open and closed head injury, depending on whether the dura remains intact or not.

2. Primary and secondary injury: Primary injury is caused by direct mechanical impact of trauma and this might be focal or diffuse. Focal injuries include contusion (most common), intracerebral haematoma, intracranial hemorrhage, or focal hypoxic-ischemic injury, while the diffuse injuries include diffuse axonal injury (most common), edema, hypoxic ischemic injury and diffuse vascular injury. Secondary injury is caused by indirect trauma related factors like hypoxia, anemia, metabolic abnormalities and fat embolism (Rao and Lyketsos, 2002).

3. Another important classification system depends on the severity of initial impairment, combining the initial Glasgow Coma Scale (GCS), the duration of loss of consciousness (LOC), and the duration of posttraumatic amnesia (PTA) (Kraus, 1999).

The Galveston Orientation and Amnesia Test (Levin et al., 1979) can be used to measure the extent of PTA.

Neuropsychiatric Sequelae of TBI

Cognitive Deficits

Cognitive deficits can be divided into four groups according to when they occur in relation to the phases of the TBI (Levin, 1987; Cripe, 1987). The first is the period of loss of consciousness or coma, which occurs soon after injury. The second phase is characterized by a mixture of cognitive and behavioral abnormalities, such as agitation, confusion, disorientation, and alteration in psychomotor activity. This period is associated with inability to recall events, sequence time, and learn new information. These two phases last from a few days to 1 month after the injury, and are a form of posttraumatic delirium (Kwentus, 1985). Third phase is a 6–12 month period of rapid recovery of cognitive function, followed by plateauing of recovery over 12–24 months subsequent to the injury. The fourth phase is characterized by permanent cognitive sequelae, and includes problems with speed of information-processing, impairments in attention and vigilance, deficits in short- and long-term memory, and problems with executive functions and mental inflexibility.

Treatment is multidisciplinary and includes pharmacotherapy, physical therapy, occupational therapy, recreation therapy, speech therapy, and vocational rehabilitation. Cognitive rehabilitation is also important, especially during the first six months after injury, and involves techniques to retrain the patient in specific domains by providing a series of mental stimuli, tests, and activities (Wilson, 1997). Dopaminergic agents (Karli et al., 1999) or psychostimulants may improve deficits of arousal, poor attention, concentration, and memory. Cholinergic agents such as those developed to treat dementia are also showing promise in treating these deficits (Taverni et al., 1998).

Psychosis

Davison and Bagley (1969) reported that 0.7%–9.8 % of patients with TBI develop schizophrenia-like psychosis. Most of these patients do not have a family history of schizophrenia. Both right (Levine and Finkelstein, 1982) and left hemispheres (Lishman, 1968) have been implicated in the genesis of psychotic symptoms. A rational approach based on the knowledge of injury must be applied when choosing treatment options. For instance, when there is a suggestion of left-temporal involvement, there may be benefit from the use of an anticonvulsant. Delusional-type symptoms that seem more related to cognitive and behavioral impairments from frontal lobe dysfunction can benefit from dopaminergics. Animal studies have shown impaired neuronal recovery with the use of typical antipsychotics like haloperidol (Feeney and Sutton, 1997). Risperidone (Schreiber et al., 1998) and Clozapine (Rommel et al., 1998) have been found useful in the treatment of post-TBI psychotic symptoms.

Mood Disorders

Adolf Meyer, in 1904, referred to mood disorders associated with TBI as "traumatic insanities”. Major depression occurs in approximately 25% of patients with TBI (Jorge et al., 1993). Feelings of loss, demoralization, and discouragement seen soon after injury are often followed by symptoms of persistent dysphoria. Fatigue, irritability, suicidal thoughts, anhedonia, disinterest, and insomnia are seen in a substantial number of patients 6–24 months or even longer after TBI (Hinkeldy and Corrigan, 1990). Psychological impairments in excess of the severity of injury and poor cooperation with rehabilitation are strong indicators of a persistent depressive disorder (Kraus, 1999). The mechanism of depression following head injury is probably due to disruption of biogenic amine-containing neurons as they pass through the basal ganglia or frontal-subcortical white matter (Starksein et al., 1987). The presence of left dorsolateral frontal and left basal ganglia lesions is associated with an increased probability of developing major depression (Fedoroff et al., 1992).

The treatment of depression secondary to TBI is very similar to the treatment of major depressive disorder. Agents such as serotonin-specific reuptake inhibitors (SSRIs) are safe and well tolerated (Bessette and Peterson, 1992). Drugs with anticholinergic effects in general should be avoided. Psychostimulants (Kraus, 1995) and dopaminergics can be helpful in these cases, as they have an antidepressant effect. Electroconvulsive therapy is a highly effective mode of treatment for TBI patients refractory to antidepressants (Ruedrich et al., 1983).

Mania after TBI is seen in about 9% of patients (Jorge et al., 1993). Positive family history of affective disorder and subcortical atrophy prior to TBI are added risk factors (Robinson et al., 1988). Mania is often seen in patients with right-hemispheric limbic structure lesions (Jorge et al., 1993). Treatment with anticonvulsants such as carbamazepine or valproate may be more effective than lithium, which is not specific to the neuropathology of TBI and may worsen cognitive impairment (Kraus, 1999).

Anxiety Disorders

All variants of anxiety disorders are seen in patients with TBI, and they are more often associated with right-hemispheric lesions (Jorge et al., 1993). Anecdotal evidence suggests that antidepressants such as SSRIs, opioid antagonists such as naltrexone (Tennant, 1987) and buspirone (Gualiteri, 1988) are effective in the treatment of anxiety disorders. Benzodiazepines (Preston et al., 1989) and antipsychotics (Feeney et al., 1982) should be avoided because they cause memory impairment, disinhibition, and delayed neuronal recovery. Behavioral therapy and psychotherapy are as important as pharmacotherapy in the treatment of anxiety disorders.

Apathy

Apathy refers to a syndrome of disinterest, disengagement, inertia, lack of motivation, and absence of emotional responsivity. The negative affect and cognitive deficits seen in patients with depression are not seen in patients with apathy. Apathy may be secondary to damage of the mesial frontal lobe (Duffy and Campbell, 1994). It often responds well to psychostimulants, dextroamphetamine, amantadine, or bromocriptine (Gualiteri, 1991).

Behavior Dyscontrol Disorder

This is complex syndrome characterized by disturbance in mood, behavior and cognition (Rao and Lyketsos, 2002). The disorder has been subdivided into two variants: (1) major variant, in which the symptoms are chronic, persistent and severe and (2) minor variant, in which the symptoms are acute and transient.

Other Symptoms

TBI patients may present with a variety of other symptoms, such as sleep disturbances or headaches. Careful evaluation of these patients should be done to ascertain if they are just isolated symptoms or if they are part of a syndrome. Treatment should be aimed at a specific disorder rather than vague symptoms.

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