PERSONLITY clinical syndrome; while medial and orbito-frontal

PERSONLITY CHANGETBI may lead several enduringchanges in the personality of an individual. DSM-5 classifies it under”Personality change due to another medical condition”. It is further classifiedinto following subtypes: labile, disinhibited, aggressive, apathetic, paranoid,combined, and unspecified (other) type. ICD-10 classifies it as organicpersonality disorder.

Commonly described changes are being irritable,aggressive, apathetic, childish or anxious. However, studies have shownvariable results. Koponen et al studied 60 TBI patients and found 23% to have apersonality disorder, in order of avoidant (15.0%), paranoid (8.3%) andschizoid (6.7%). In a previous study, the order was borderline, avoidant,paranoid, obsessive–compulsive and narcissistic disorder (Hibbard et al. 2000).

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Damage to the lateral surface of thefrontal cortex can lead to apathy and indifference with a pseudodepressiveclinical syndrome; while medial and orbito-frontal lesions present withantisocial, sexually inappropriatetactless, impulsive and irritable behavior,known as pseudopsychopathic syndrome. Damage to cortico-striatal-pallidal-thalamicpathways, enclosing the anterior cingulate cortex, can also lead to decreasedmotivation and apathy.  MOOD DISORDERS Disorders of mood occur frequentlyafter TBI. Both pathophysiology and symptom assessment here, is challenging.The pathophysiology is interplay of factors that were present prior totraumatic event (e.

g., genetic vulnerability and previous history ofpsychiatric illness); factors related to the trauma itself (e.g., type, extent,and location of brain injury); and factors following the injury (e.g., family,social support and rehabilitation). Symptoms sometimes become complicated toassess as they occur in the background of cognitive deficits and presentationlike apathy, emotional blunting or even jocularity become difficult to be classified.

 DEPRESSIONDepressive disorders are common inpatients with traumatic brain injury. The burden of disorder ranges from 6% to77%. This variability of symptoms is attributed to heterogeneity of assessmenttools in individual studies. However, broadly it is considered that depressionin the first year post TBI is 25-50%.

  DSM-5 classifies it under Mooddisorder due to another medical condition, with the following subtypes: (1)with major depressive-like episode, (2) with depressive features, and (3) withmixed features. History of TBI is associated with increasedlifetime prevalence of TBI, which ranges from 26-64% .Clinical presentation is somewhatdifferent when compared with controls. Anger, irritability and aggression arefrequently present than complaints of sadness. Fatigue, insomnia, blunt affectand executive dysfunction are also seen; however depressive ruminations,feelings of guilt and self-criticism are more suggestive of depression.Patients with history of TBI were four times more likely to attempt suicidewhen compared with controls. Social isolation, poor coping styles, poorpremorbid functioning and past history of psychiatric illness are risk factorsassociated with post TBI depression. Lesions in the left dorsolateralprefrontal cortex and left basal ganglia have been found to be linked withpost-TBI depression; with reduction in left prefrontal grey matter volume onMRI and lower bilateral hippocampal volume.

Polymorphismof various genes (5HTT-P, tryptophanhydroxylase, MAO, COMT, FKBP5) is studied with respect to symptomatology andeven treatment response APATHYApathy has been increasingly recognizedas a significant consequence of TBI having implications in the recoveryphase.  Apathy was operationalized as’reductions in goal-directed behaviors (e.g. lack of effort, initiative, andproductivity), reductions in goal-directed cognitions (e.

g. decreasedinterests, lack of plans and goals and lack of concern about one’s own healthor functional status), and reduced emotional concomitants of behaviors (e.g.flattened affect, emotional indifference, and restricted responses to importantlife events’. The frequency of apathy in TBI has been reported to range from20-72%. Apathy can be concurrent withdepression.

It can be differentiated in that apathy often does not appeardistressed by their symptoms, but it can impair patients’ ability toparticipate in rehabilitation process, and there is absence of the corepsychological symptoms of depression (related to sad mood and depressivecognition). Variable association of apathy has been found; however a fewstudies suggest link of apathy to severity of head injury as well as severityof disability. Knutson et al found that damage tospecific brain areas like the left frontal lobe, the supplementary motorregion, the anterior cingulate, and the insula, as well as the white matter inthe corona radiata and corpus callosum were significantly associated withsevere apathy.

A high resolution MRI (magnetic resonance imaging) and diffusion tensor imaging (DTI) study found positive correlation betweenmean diffusivity values and apathy scale scores in the thalami, but theassociation was significant only for female subjects.  BIPOLARAND RELATED DISORDERSAscompared to depression, bipolar and related disorders are less frequent in postTBI cases. The incidence of such disorders range from 1.7% to 9.0% and theestimated lifetime relative risk ranges from 1.

1 (in a sample of more than 5000community-dwelling individuals interviewed in the Epidemiologic Catchment Areastudy) to 5.0 (in a review of 5 studies comprising 354 clinical subjects.However, selection biases, variable assessment tools and lack of longitudinalstudies significantly influence the results.

 DSM-5 classifies the above as Bipolar andRelated disorders due to another medical condition (TBI) with (1) manic orhypomanic-like episode, (2) with manic features, and (3) with mixed features.The diagnosis often poses a challenge due to the presence of TBI-relateddisturbances in affect regulation (e.g. brief episodes of irritability,pathological laughing, disinhibited behaviors, alterations in sleep and appetitivebehaviors); symptoms present during immediate post injury phase includingagitation, distractibility, irritability and disinhibition; and post injurypersonality changes. PostTBI mania was found to have no relation with family history of bipolar, but didhave a relation with injury severity and posttraumatic epilepsy (predominantlycomplex partial type). However,studies have found that unaffected family members of persons with bipolardisorder have elevated frequency of TBI, which suggests that heritablecomponents of bipolar phenotype (like reduced harm avoidance, novelty seeking,and impaired decision making) possibly increase the risk of TBI.Individualstudies have suggested that subcortical region is largely affected in patientswith post-TBI bipolar disorder (right caudate and right thalamus), whereasright orbitofrontal and basotemporal corticices is implicated in patients withpredominant manic symptoms.


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