Innovations In Clinical Neuroscience

MAR-APR 2018

A peer-reviewed, evidence-based journal for clinicians in the field of neuroscience

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H O T T O P I C S I N N E U R O S C I E N C E 44 ICNS INNOVATIONS IN CLINICAL NEUROSCIENCE March-April 2018 • Volume 15 • Number 3–4 TBI-INDUCED DISORDERS While the chronology of TBI has been established at a cellular level, it is difficult to interpret how such changes translate to the neurobehavioral and cognitive sequelae commonly reported after a TBI. In particular, people with TBI experience high rates of psychiatric disorders, including depression, anxiety, mania, irritability, aggression, panic or obsessive-compulsive tendencies, and drug abuse. 7,8 Depression has the highest prevalence in TBI-associated psychiatric impairment, with studies showing rates of 17 to 70 percent. 9-10 This wide range can be explained by the varying diagnostic criteria and amount of time elapsed since TBI. It has been shown that depression rates are highest during the first year following TBI and then decline, 10–12 though they remain elevated when compared to age-matched TBI-free controls. 10,12 Antidepressants are necessary for the treatment of depression in 11 to 44 percent of patients who are post-TBI. 10,11 Up to 76 percent of patients with TBI also develop comorbid anxiety, and up to 54 percent suffer executive function impairments, such as aggression. 12 Preexisting depression, anxiety, and poor social functioning before a brain injury increase susceptibility for relapse or worsening of psychiatric symptoms after TBI. 7–12 However, rates of depression in patients with a TBI without a psychiatric history are still higher than in TBI-free matched controls. 11,12 Lower levels of education have also been linked to greater morbidity; 7–10 yet educational attainment does not always predict prognosis. 12 While premorbid variables might predict mood disorders after a TBI, the anatomic severity and location of the injury are also contributing factors. Certain white matter tracts have been associated with TBI-related depression. For example, affective illness in patients following TBI has been linked to a reduction in microstructure of temporal and frontal white matter tracts when compared to those with TBI who did not develop a mood disorder. 10,13 The manifestations of TBI in persons with mood disorders follow established functional neuroanatomical relationships: damage to the left dorsolateral prefrontal cortex and left basal ganglia are associated with higher rates of post-TBI major depression, while right-sided hemispheric lesions are more often associated with anxious depression. 8 TBI severity is not correlated with risk for post-TBI depression, 10–11 suggesting that even minimal damage to the brain can precipitate psychiatric symptoms. PHARMACOTHERAPY When considering the treatment of mood disorders in patients with TBI, psychotropic drugs might have different effects in this population compared to those without TBI. Individuals with a history of TBI often have a low seizure threshold, resulting in a greater ictal risk. 14 Risks of medication- induced convulsions must be weighed against the potential psychiatric benefits of pharmacotherapy. Evidence-based practice guidelines are lacking for treating patients with TBI-induced mood disorders. Sertraline and other selective serotonin reuptake inhibitors (SSRIs) appear to have the most documented evidence for improving mood and/or cognition. 7,8,15–18 In one study, 16 patients with post-TBI depression received an eight-week course of sertraline. The most common side effects were nausea, abdominal cramps, dizziness, and diarrhea; one subject dropped out as a result of side effects. In all participants, neurocognitive testing demonstrated significant improvement in sleep, emotional and social function, and ability to work. Other research substantiates these findings, 16 and sertraline has been documented to be effective in the treatment of depression in people with TBI. 8 Recent research has assessed whether early sertraline therapy after TBI can prevent depression and improve TBI-associated cognitive impairments. Results do not indicate cognitive benefits in cases of TBI without depression, but do indicate that sertraline reduces the risk of post-TBI mood symptoms. 15,17 Cognitive impairments secondary to depression are unrelated to those resulting from TBI. Other antidepressant drugs have been tested for the treatment of depression in TABLE 1. Clinical data on post TBI depression and ECT therapy in three patients TREATMENT CHARACTERISTICS MARTINO 31 RUEDRICH 32 CROW 33 Depression prior to TBI Yes Yes Yes Duration of depression 6.5 years (6 months before TBI, 6 years after TBI) 3 months 18 years TBI etiology Motor vehicle accident with closed head injury Gunshot wound to the head Gunshot wound to the head, 18 years prior Therapies Buproprion, fluoxetine, sertraline, citalopram, mirtazapine, imipramine, tranylcypromine, gabapentin, lamotrigine, olanzapine, lithium Imipramine Fluoxetine, amitriptyline, trazodone, lithium, haloperidol, despiramine, venlafaxine, levothyroxine, psychotherapy Location and number of ECT treatments 12 bifrontal 17 bitemporal, brief pulse stimulation 8 right unilateral Adverse events None None None Response HAM-D score of 25 down to 7 Required further pharmacotherapy BDI score of 20 down to 7 Duration of improvement At 4 weeks, no mood symptoms At 6 months, no relapse nor neurological deficits Not described TBI: traumatic brain injury; ECT: electroconvulsive therapy; HAM-D: Hamilton Rating Scale for Depression; BDI: Becks Depression Inventory

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