POST TRAUMATIC PSYCHIATRIC SYNDROMES

Association between traumatic brain injury and variety of Neuropsychiatric Syndromes has been reported in medical literature for many years. In 1904 Adoph Meyer, who termed it as Traumatic Insanities Suggested some unique associations to specific lesion locations. Studies of war related head injury too identified high incidence of psychiatric complications following brain injury.

The famous case of frontal lobe injury was that of Phiness Gage, who suffered a penetrating frontal lobe injury after an explosion that shot an iron bar through the skull. He became a childish, capricious, inconsiderate and profane person with poor judgment after that. Victims of traumatic brain injury go through a variety of psychiatric symptomatology and syndromes. This paper aims at providing an overview of the Post traumatic psychiatric problems.

CLASSIFICATION OF SOME BEHAVIOURAL SYNDROMES OCCURRING AFTER TRAUMATIC BRAIN INJURY (DSM IV)

Delirium due to Traumatic brain Injury, Amnestic disorder due to Traumatic brain injury Transient Chronic Dementia due to Traumatic brain Injury, Personality change due to Traumatic brain Injury 

The early phase of recovery from traumatic brain injury is characterized by disorientation, confusion and impaired memory function. Apathetic withdrawal, agitation or severe delirium may be observed. Posttraumatic Amnesia occurs during the period when the patient is disoriented and has impaired memory.

Deficits in memory are observed in declarative memory affecting both retrograde and anterograde processes. Procedural memory, in contrast, is relatively spared.

Duration of posttraumatic amnesia has been widely used as a measure of severity of brain injury. It is also a good predictor of the degree of disability, vocational outcome and the severity of personality change following the injury.

In addition to the confessional syndrome, the patient may also exhibit associated perceptual disturbances like hallucinations and illusions, delusional thoughts, psychomotor agitation of retardation, emotional liability, and other neurovegetative symptoms like tachycardia, hypertension, and sleep-wake cycle disruption. The patient may be excited and may show violent aggressive outbursts.

Multiple conditions can contribute to the development of acute behavioural syndromes in traumatic brain injury. These include structural brain damage, cerebral oedema, secondary brain hypoxia, seizures, electrolyte imbalance, infections and substance or alcohol withdrawal. Old age, coexistent medical conditions and polypharmacy are risk factors.

Cognitive disturbances are one of the most important long-term sequels of severe traumatic brain injury.

Approximately one third of severely brain injured patients exhibit fluent, confluent or global aphasia syndromes. Brain Injured patients may show high order language alterations and may present with defective narrative discourse, a lack of semantic coherence, aprosody and impaired pregmatics of communication. The resultant impoverishment, disorganization and reduced communication proficiency may have to be differentiated from the incoherent speech of a psychotic.

Dementia due to head injury is characterized by prominent memory and executive dysfunction in a clear sensorium with relatively preserved visuospatial, praxic, and primary linguistic functions. These patients may be  severely dull and withdrawn and may exhibit marked decline in intellect and self care. Associated neurological deficits are also common. A chronic subdural haematoma in the elderly may present as a progressive dementia.

Traumatic Brain Injury patients may experience significant personality changes attributable to the pathophysiological changes triggered by the brain trauma. Some investigators group these changes to two distinct syndromes. The pseudodepressed personality syndrome is characterized by apathy and blunted emotional responses. The pseudopsychopathic personality syndrome is characterized by disinhibition, egocentricity and sexual inappropriateness. The DSM IV subtypes are labile, disinhibited, aggressive, apathetic, paranoid, combined and unspecified.

There are some interesting neuroanatomical correlations that are often discussed. Disinhibition, antisocial conduct, and hyper sexuality have been linked to orbitofrontal lesions; and aggression and poor impulse control to anterior temporal lesions.

Mood disorders are a frequent squeal of traumatic brain injury and it may play an important role in determining the long-term outcome. There are some empirical evidences suggesting an association between depression and specific lesion location.

It has been found to be more common in patients with right than left hemispheric lesions and among patients with frontal and parietal lesions. These association are relevant in depressions in the immediate trauma period, Delayed onset depressions are however related to a previous history of psychiatric disorder and with poor social support systems.

The emergence of an expansive, irritable mood with other symptoms of Mania has been reported in patients with traumatic brain injury. The onset of the symptoms is within one year of injury and the association with a family history of Bipolar disorder is not significant. A frequent coexistence of posttraumatic epilepsy especially of the partial complex type suggests an organic basis.

Other psychotic disorders characterized by paranoid ideation, poor impulse control, aggression, disinhibited behaviour and hyper sexuality have been also observed.

The Glasgow outcome scale has indicated five levels of outcome. It consist of death, persistent vegetative state, severe disability (Conscious, but dependent on others for daily living), moderate disability (disabled, but living independently), and good recovery (mild neuropsychiatric disability, yet able to lead a near normal life). It may be added that the psychosocial complexities of life after a traumatic brain injury are beyond these compartments. The journey of a victim of traumatic brain injury from coma through the acute syndromes of delirium and amnesia to the  chronic neuropsychological deficits is agonizing to patients and their caregivers.

The long-term outcome of patients with brain injury is primary related to the severity of the injury, the type and location of the  intracranial lesion, and the efficacy of the immediate medical and surgical treatments received. Outcome is also influenced by concurrent factors that include age, socioeconomic status, educational level, previous psychiatric disorder, history of alcohol or drug abuse and the premorbid social function level. Finally the quality and extent of rehabilitation services and availability of social and vocational support also play a significant role in the outcome.

The policy is starting low and go-slow, as the patients with brain injury are more susceptible for side effects of psychiatric medication. Agitation and violent behaviour may occur during the early phase of recovery. Calming down the patients is absolutely essential. Low doses of high potency antipsychotic like Haloperidol is the choice in excitements, hallucinatory phenomena and psychotic ideation in delirious states. For immediate effect it is ideal to give an intervenouse injection. The patient may need oral medication for variable period. Newer antipsychotic like Resperidone may also be used. Both these medications have a relatively lesser risk in lowering the seizure threshold. the dose of this medication needs to be reviewed and tapered as the patient stabilizes. Other medications that are found to be useful in agitation and aggression are Lorazapam, Carbamazapine, and Amantidine and Clonidine. Over sedation, poor coordination, cognitive disturbances and paradoxical rage are certain limiting factors in the usage of Benzodiazapines.

The is some evidence of clinical efficacy of dopamine agonists like Bromocryptine in patients with poor motivation and frontal lobe lesions. Psychostimulants like Methyl Phenedate also have been tried with variable results in the apathetic group.

Mild anticholinergic activity, low sedative activity and minimal lowering of seizure threshold are the most important factors to be considered while choosing an antidepressant in a brain-injured patient. SSRI (Fluoxetine, Sertraline, Citaloparm, Paroxetine) are ideal choices. Trazadone may be considered in patients who has severe sleep problem. The time-tested tricyclics can also be used with caution.

A part from Haloperidol that is used for quicker control of excitment, Carbamazepine, Sodium Vaproate, or Topiramate are also used as mood stabilizers in the management of secondary mania. Lithium is not preferred inview of the reported cognitive impairment it causes in brain-injured patients.

The victim of a traumatic brain injury needs to be retrained in self-care habits, interpersonal skills, problem solving skills and in stress reduction techniques. The goal is to increase the patient's repertoire of social and independent living skills, generalizing its use from rehabilitation environment to more demanding conditions of community living.

The total care in head injury should take into consideration the bitter experiences of physical disabilities and emotional handicaps thrust upon the victim. Saving a life is important. Adding life to it to all possible levels is equally important.