Neuropsychiatric Consequences of Traumatic Brain Injury

Presenter Dr Ankur Chairperson Dr O P Gangil Co-Chairperson Dr DMS Rathore

 The neuropsychiatric consequences of traumatic brain injury (TBI) may be divided into disorders that are also seen in patients without brain injury and those that are unique to patients with brain damage.

 The disorders also seen in patients without brain injury cover the whole spectrum of psychiatric disorders, including substance abuse, mood, anxiety, psychotic, and personality disorders. Many of these disorders are included in the revised fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IVTR) as disorders due to a medical condition, in this case, traumatic brain injury

 The disorders that are unique to brain injury also cover a wide range of disorders, including pathological laughing or crying, apathy, anosognosia, aprosody, and neglect.

DSM-IV-TR Classification of Behavioral Syndromes Occurring after Traumatic Brain Injury

Delirium due to traumatic brain injury Amnestic disorder due to traumatic brain injury--Transient and chronic types Dementia due to traumatic brain injury Personality change due to traumatic brain injury --Labile, disinhibited, aggressive, apathetic, paranoid, combined, other, and unspecified types

 Mood disorder due to traumatic brain injuryWith depressive features ,With major depressive-like episode ,With manic features, With mixed features, Anxiety disorder due to traumatic brain injury -With generalized anxiety ,With panic attacks ,With obsessive-compulsive symptoms,Posttraumatic stress disorder, Psychotic disorder due to traumatic brain injuryWith delusions With hallucinations

ICD 10
In ICD 10 classifies these under personality and behavioural disorders due to brain diseaes ,damage and dysfunction. It includes . Organic personality disorder . Postencephalitic syndrome . Postconcussional syndrome . Other disorders

 Mental disorders due to brain damage and dysfunction and to physical disease Organic hallucinosis Organic catatonic disorders Organic delusional disorders Organic mood disorders Organic anxiety disorders Organic dissociative disorders Organic emotionally labile disorder

HISTORY
Adolf Meyer, identified a number of disorders that he refererred as insanities. He suggested that there may be some unique associations between these disorders and specific lesion locations. Studies of war-related head injuries identified the high prevalence of psychiatric complications after traumatic brain injury. Several of these studies emphasized the importance of frontal lesions in the pathogenesis of behavioral disturbances

 The most famous case of frontal lobe injury, however, was Phineas Gage, who suffered a penetrating frontal brain injury after an explosion that shot an iron bar through his skull. After the injury, he was described as childish, capricious, inconsiderate, and profane and as having poor judgment

MEASURING HEAD INJURY SEVERITY

First stage in assessing is to determine severity of head injury. 3 commonly used clinical; measures are Glasgow coma scale Duration of loss of consciousness Duration of post traumatic amnesia

Indicators of head injury severity1.Depth of unconsciousness as assesed by GCS 15 Normal level 3 Absent responses 2. Duration of loss of unconsciousness 3. Evidence of behavioural /cognitive change in immediate aftermath suggestive of delirium 4.Neurological signs and symptoms

 5.Abnormalities of skull fracture or other abnormalties in neuroimaging 6. Blood in CSF 7. Duration of PTA:Time b/w injury and return of normal day to day memories

 Less useful markers are 1. Duration of retrograde amnesia 2.Abnormalities on eeg 3. Markers of cell damage (eg s 100b) 4. Evidence of injury to head eg,laceration,bruising,bleeding,fracture of maxilla/zygoma

 The Glasgow Coma Score (GCS) is commonly used to grade severity of traumatic brain injury. Scale gives quantitative estimate of level of consciousness and neurological status based on patterns of eye opening, as well as best verbal and motor responses. GCS scores 13-15 - mild brain injury, 9 12 moderate brain injury, and 3 - 8 define severe brain injury

Loss of consciousness
Duration of loss of unconsciousness Most common consequence of head injury is impairment of consciousness, ranging from transient confusion to protracted coma. . Duration of LOC after a closed head injury is a good marker of injury severity. . In concussion injuries LOC is usually absent and if present rarely lasts more than 5 minutes. . In severe brain injuries LOC is usually longer in duration

Post Traumatic Amnesia

Posttraumatic amnesia occurs during the period when the patient ( emerging from coma) is disoriented and confused and has disrupted memory functioning. Deficits are observed in declarative memory (i.e., memory of recent events and times), affecting anterograde and retrograde processes. Procedural memory, in contrast, appears to be relatively spared. Duration of posttraumatic amnesia has been widely used as a measure of traumatic brain injury severity

 Duration of post traumatic amnesia This has close correlation with objective evidence of brain damage. It is a permanent index of severity and can be used if history is taken long after injury . End of PTA during post injury period Is determined by 3 consecutive days of perfect scores on simple memory tasks

 Head injury severity according to PTA (Russel and Smith) PTA>1 Hour slight concussion PTA 1-24 Hour moderate concussion PTA 1-7 DAYS Severe concussion PTA>7 Days very severe PTA 8-28 DAYS Very severe injury >28 days extremely severe injury

 Patients with PTA>2 weeks had higher rates of failure to return to working level.(zomeren and vanderburg)

Pathology and pathophysiolgy

Concussion and traumatic brain injury concussion is an immediate and transient alteration/loss of consciousness or other disturbance of neurological function ,when sudden mechanical forces are applied to head. Loc is common when in acceleration/deceleration injuries with a rotational component ,with rotation around a coronal axis as in side to side movement is more dangerous than in sagittal plane i.e up and down movement

 Here impact on temporoparietal area causes concussional injury commonly . Static crush closed head injuries where there are no acceleration deceleration are unlikely to cause LOC In open head injury dura is breached and laceration of brain tissue is present at site of impact but contrecoup is absent.

 Contusion is a mixture of hemorrhages and necrosis near surface of brain due to impact . Sites of predeliction are medial sides of orbital surface of frontal lobe and tips of temporal lobe

 Diffuse axonal injury Acceleration deceleration injuries produce swirling movements through out the brain resulting in shearing forces causing tearing and damage to nerve fibres through out the brain ,with resorption of myelin and retaractional ball formation.

 They produce ventriculomegaly with thinning of corpus callosum which presents clinically with prolonged LOC in absence of contusion,and delayed sequeale like slurring of speech and ataxia when there is damage to white matter tract . This term is now used to describe a clinical syndrome of diffuse injury where loss of consciousness is not explained by focal lesions.

 Vascular lesions 1. Include scattered punctate heomarrages along with small and large infarcts. 2. Bleeding may occur in subarachnoid space with blood in CSF forming SDH,may lead to hydrocephalaus if adhesions are formed in basal cisterns 3. bleeding in brain tisssue intracerebral hematoma

 Cerebral oedema - Develop in acute stages causing complications - Occurs in regions of infarcts ,contusions, lacerations and hematomas. - Cellular mechanisms play predominant role and not disruption of BBB - Severe cases of raised ICT may result in herniation and coning

 Cerebral Anoxia Occurs due to cerebral oedema, hypotension ,blood loss, disturbance in cerebral regulation In golden hour after injury maintainence of arterial oxygenation and blood pressure are crucial to management .

CLINICAL FEATURES
Acute Behavioral Consequences wide range of severity, from patients who die at the moment of trauma to those who do not require medical evaluation or assistance. Most patients admitted to hospital with head injury diagnosis have mild injury. Minority of these mildly affected patients develop acute complications (e.g., brain swelling, delayed hematoma, and intracranial infection) or prolonged postconcussional symptoms.

 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 also be observed in these patients

 Some important acute effects are 1-impairment of consciousness. 2-post traumatic delirium occurs during recovery phase .Duration required for recovery is directly proportional to severity of injury (alderso and novack 2002). Usually longer in those with cerebrovascular disorders and alcohol dependence . Confabulations delusions ,hallucinations may occur

 3. Post traumatic agitation-Usually with frontotemporal injury ,doubles later risk of emotional sequelae. Presents with hyperactive delirium like picture 4. Post traumatic amnesia-defined as amnesic gap from moment of injury to time of consumption of normal continous memory ,. May last from several minutes to weeks. End of PTA marks beginning of normal memory functions

 Retrograde amnesia-defined as time between moment of injury and last clear memory from before the injury which patient can recall. Long RA may be seen with severe head injury but prolonged RA following mild head injury are mostly psychogenic in origin

Chronic Behavioral Consequences

1.Cognitive Disorders Most important long-term sequelae Patients with mild or moderate head injuries may also show cognitive impairment after brain trauma. They complain of lack of concentration and memory deficits during the first weeks after traumatic brain injury. However, spontaneous recovery is the rule for the majority of these patients.

 Repetitive, mild head injury, such as that observed among certain athletes (e.g., soccer and football players). Result in repeated concussions and is associated with reduced cognitive performance. Also there is evidence indicating that repeated concussions among amateur soccer players is associated with deficits in memory and executive functions.

 Attentional deficits are among the most frequent neuropsychological symptoms observed in traumatic brain injury patients after resolution of posttraumatic amnesia Traumatic brain injury patients may present with restricted verbal or visuospatial attention span, altered vigilance patterns (i.e., sustained attention deficits), or slowed information processing.

 The most consistent findings, however, are associated with performance in the most demanding tasks (e.g., in divided attention paradigms, such as the Paced Auditory Serial Addition Task).

 Memory functions Distinctively impaired in traumatic brain injury patients. Memory deficits are the most frequent cognitive disturbances reported by patients and relatives in the chronic phase . Memory dysfunction is characterized by anterograde and retrograde deficits, faulty sequencing of events, and inefficient encoding and storage strategies

 Linguistic competence Frequently affected by traumatic brain injury. one-third of severely brain injured patients showed fluent , nonfluent , or global aphasic syndromes. Aphasia tends to resolve in the majority of cases during the first year after trauma. Anomia, however, constitutes the most prevalent longterm linguistic deficit after trauma.

 Traumatic brain injury patients also have highorder language alterations and present with a defective narrative discourse, a lack of semantic coherence, aprosody, and impaired pragmatics of communication. All of these result in impoverished and disorganized language and in a reduced proficiency in communication.

 Defect in control or executive functions has been consistent in patients surviving severe head injury. Executive functions include goal formation, planning, selection of adequate response patterns, and monitoring of ongoing behavior. Simple cognitive tests, such as the verbal and figural fluency tasks, document the lack of spontaneity and perseverative tendencies frequently observed in patients with traumatic brain damage .

 The executive dysfunction observed in traumatic brain injury patients is strongly associated with dysfunction of frontosubcortical pathways. When confronted with a demanding environment, the adaptive functioning of traumatic brain injury patients is also often impaired.

. Visuospatial and praxis abilities are usually preserved during the chronic phase. This is probably due to the relative sparing of posterior association cortices in traumatic brain injury. . Unawareness (anosognosia) or denial of deficits is a cognitive disorder ,seen in those who have experienced extensive frontal lobe damage. This constitutes a severe behavioral sequel that impedes realistic goal setting and interferes with the rehabilitation process

Dementia
Dementia due to head trauma is characterized by prominent memory and executive dysfunction with relatively preserved visuospatial, praxis, and primary linguistic functions. These patients may be severely apathetic and withdrawn and may demonstrate markedly slow information processing. Physical examination may reveal the presence of extrapyramidal signs.

Chronic subdural hematoma in the elderly may present as a progressive dementia Previous traumatic episodes constitute a risk factor for the development of Alzheimer's disease. Traumatic brain injury is associated with expression of amyloid precursor protein, oxidative stress, and an increased deposition of amyloid- peptides that might ultimately lead to the onset of dementia.

 Dementia pugilistica - Multiple traumatic brain injuries associated with boxing . The diagnosis of this severe complication is dependent on documenting progressive dementia that is associated with chronic and repeated brain trauma and that is unexplainable by an alternative pathophysiological process. Pathologically, dementia pugilistica shares many characteristics with Alzheimer's disease (i.e., neurofibrillary tangles, diffuse amyloid plaques, or tau immunoreactivity, or a combination of these).

Personality Changes
These patients have been described as irritable, childish, inconsiderate, capricious, anxious, or aggressive They lack foresight and misjudge the consequences of their actions. Disinhibition is a frequent and striking clinical feature that may lead to antisocial behavior. On the other hand, they may become apathetic, abulic, and withdrawn.

These changes have been grouped into two distinct syndromes: . Pseudodepressed personality syndrome, which is characterized by apathy and blunted affect . Pseudopsychopathic personality syndrome, which has disinhibition, egocentricity, and sexual inappropriateness as its outstanding features

Mood Disorders
DEPRESSIVE DISORDERS The reported frequency of depressive disorders after traumatic brain injury has varied from 6 to 77 percent differential diagnosis of post traumatic brain injury Major depression includes adjustment disorder with depressed mood, apathetic syndromes, and emotional lability.

 Major depressive episodes seen shortly after lesion may be due to lesion location while late onset depression is mostly due to psychosocial factors (Jorge et al 1993)or improved insight (sadder but wiser) . Phenomenologically apathy is more common in organic depression .Other Sx like fatigue frustration ,poor concentration,sleep disturbance are equal in depressed or non depressed. Feeling of hopelessness ,lack of confidence may be true indicators of depressive episodes.

 Suicide Increase in incidence found after head injury occurs in 1 %. Social stressors ,breakdown of relationships ,depression are contributing factors. Lesions in frontal and temporal areas of brain are associated with completed suicides (vaukhonen 1959).

 Pathological laughter and crying is characterized by the presence of sudden and uncontrollable affective outbursts (e.g., crying or laughing), which may be congruent or incongruent with the patient's mood. These emotional displays are excessive to the underlying mood and can occur spontaneously or may be triggered by minor stimuli. Pathological laughter and crying were associated with the presence of anxiety disorders and frontal lobe lesions involving the lateral and ventral aspects of the prefrontal region .

 Traumatic brain injury patients presenting with apathetic syndromes interfere with the rehabilitation process. Apathy is frequently associated with psychomotor retardation and emotional blunting. Apathy is frequently associated with medial prefrontal lobe damage

Secondary Mania
Secondary mania is associated with the presence of lesions in the ventral and anterior aspects of the temporal lobe. Mean occurance is 2.8 years following head injury(shukla etal 1987) The development of abnormal electrical activation patterns in limbic networks, functional changes in aminergic inhibitory systems, and the presence of aberrant regeneration patterns may all play a role in the genesis of these syndromes.

 Epilepsy is a predisposing factor. Irritable moods and aggression are commoner than euphoria . Excess of manic episodes over depressives are found . Finding that mania is more common with lesion of right hemisphere is not supported now .Mania is common in injury involving orbitofrontal and temporal cortex irrespective of laterality

 The differential diagnosis of mania after traumatic brain injury include substanceinduced mood disorder, psychotic syndrome associated with epilepsy, and personality change due to traumatic brain injury

Anxiety Disorders
Anxiety disorders after traumatic brain injury may manifest themselves in a variety of ways. Pathological worrying, anxious foreboding, and autonomic symptoms are commonly associated with anxious depressions The prevalence of obsessive-compulsive disorder (OCD) occurring after traumatic brain injury has been estimated to be 2 to 4 percent.

 There is controversy regarding whether PTSD can develop after traumatic brain injury. loss of consciousness and posttraumatic amnesia after traumatic brain injury prevent the development of PTSD in moderate and severe traumatic brain injury.

Psychotic Disorders
The majority of patients develop psychotic symptoms within the first 2 years after moderate or severe head injury. Positive symptoms (e.g., paranoid delusions and auditory hallucinations) are more prominent, Negative symptoms (e.g., alogia, avolition, and affective flattening) are relatively infrequent. Posttraumatic psychosis has been associated with seizure disorder in 33 to 58 percent of cases. Epileptic foci are often located in limbic or paralimbic cortical regions.

 Psychotic episodes may be temporally linked to seizures or may have a more prolonged interictal course. In the latter case, the clinical picture is characterized by the presence of partial or complex-partial seizures, or both, and by a schizoaffective syndrome

LABORATORY TESTS
SERUM MARKERS serum markers for traumatic brain injury include neuronal (e.g., neuron specific enolase, creatine kinase-BB isoenzyme) and glial (e.g., myelin basic protein, S-100B) proteins. serum S-100B is reported to have 90-percent sensitivity and 99-percent sensitivity for detecting intracranial pathology on head CT scans. In addition, serum S-100B levels greater than 2.0 g/L predicted unfavorable outcome among patients with moderate to severe brain injury even more accurately than traditional clinical measures, such as the GCS

 In mild head injury, early detection of serum S-100B levels greater than 0.2 g/L predicted long-term neuropsychological dysfunction, even in cases in which MRI was negative Newer markers used are Calpain derived N Terminal fragment of alpha spectrin and phosphorylated forms of neurofilament H. Plasma micro RNA s are being studied .

 HORMONES- Head trauma has been associated with neuroendocrine dysfunction, particularly with pituitary hormone deficiencies. Diabetes insipidus is easily recognized in the acute stage, but other pituitary hormone deficits may present insidiously, escaping detection for months or years. The potential importance of such deficiencies is increased by the emergence of the syndrome of growth hormone deficiency (GHD) in adults, which is characterized by decreases in strength, energy, and sense of well-being..

 loss of cholinergic neurons secondary to traumatic brain injury might disinhibit hypothalamic somatostatin secretion, resulting in suppression of growth hormone (GH) and TSH levels resulting in hypothyroidism and decreased cortisol and gonadotropin levels would lead to hypogonadism

Neuroimaging
CT is most efficient means of detecting surgically treatable hematomas and is the study of choice for evaluating patients with rapid changes in their neurological status MRI is more sensitive in detecting the more prevalent posttraumatic nonhemorrhagic lesions (e.g., cortical contusions and deep white matter lesions) and in identifying small subdural collections.

 Functional neuroimaging studies, for example, PET and SPECT, provide additional information with regard to the metabolic rates of cortical and subcortical structures and of the status of specific neurotransmitter systems. PET and SPECT have greater sensitivity than CT and MRI in detecting local abnormalities in chronic traumatic brain injury patients.

 Electrophysiological Studies Primary diagnostic procedure to localize a posttraumatic epileptic focus Video-EEG monitoring and 24-hour ambulatory recordings are useful in the differential diagnosis of patients presenting with unclear paroxysmal behavioral disturbances. Quantitative EEG (QEEG) is currently used as an adjunctive diagnostic technique in the evaluation of slow wave abnormalities associated with brain injuries and in diagnosis of posttraumatic temporal lobe epilepsy. Polysomnography permits the diagnosis of atypical sleep disturbances that may occur in traumatic brain injury patients. These include atypical night terrors, sleep apnea, nocturnal myoclonus, and restless leg syndrome.

 Visual, auditory, and somatosensory evoked potentials are useful to localize the level of injury to the CNS. Auditory evoked potentials are particularly effective in detecting brainstem pathology. There has also been increasing interest in more complex electrophysiological responses. A recent study evaluated P50 physiology and sensory gating mechanisms in traumatic brain injury patients. The P50 ratio might serve as a marker of hippocampal dysfunction in this population.

COURSE AND PROGNOSIS

The long-term outcome of traumatic brain injury patients is primarily related to severity of brain injury, type and location of intracranial lesion, patient age, and efficacy of acute medical and surgical treatment . Outcome is also influenced by concurrent factors that include socioeconomic status, educational level, previous psychiatric disorders (e.g., history of alcohol and drug abuse and personality disorders), and premorbid social functioning levels. Finally, the quality and extent of rehabilitation services and the availability of social and vocational support also play significant roles in traumatic brain injury outcome.

TREATMENT OF NEUROPSYCHIATRIC COMPLICATIONS

Involves different pharmacological and nonpharmacological strategies. Treatment of the neurobehavioral consequences of traumatic brain injury should begin early in the acute phase after injury. Patients with brain injury are are sensitive to psychotropic drugs .

 Common dictum is start low go slow Drug interactions should be carefully monitored Augmentation strategies should be employed if required. For antipsychotics atypical and typical both have been tried but atypical have favourable side effect profile .

 Antidepressants like ssri are preferred over older antidepressants. Lithium and valproate both have neuroprotective effects and can be used. Psychostimulants like methylphenidate may modestly improve arousal and speed of information processing ,reducing distractability,and may be beneficial as antidepressants.

 Donepezil and rivastigmine improve cognitive functions . ECT is not C/I and used if other methods fail. Emotional dysregulation may respond to SSRI.

BEHAVIOURAL MANAGEMENT
Deficits in self care habits,interepersonal skills,response to environmental stress is amenable to behavioural intervention. Psychotherapeutic strategies like family therapy ,peer support ,help enhance coping for patients and family members. Behavioral interventions like Differential reinforcement of other behaviours (DRO)may reduce problematic behaviour.

 Substance abuse can be treated by Systematic Motivated Counselling .

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