A systematic review of 208 studies comprising functional magnetic resonance imaging and diffusion tensor imaging data in patients with 'autism spectrum disorder' (ASD) was conducted, in order to determine whether these data support the forthcoming DSM-5 proposal of a social communication and behavioral symptom dyad. Studies consistently reported abnormal function and structure of fronto-temporal and limbic networks with social and pragmatic language deficits, of temporo-parieto-occipital networks with syntactic-semantic language deficits, and of fronto-striato-cerebellar networks with repetitive behaviors and restricted interests in ASD patients. Therefore, this review partially supports the DSM-5 proposal for the ASD dyad.

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Sir: In the only 2 studies that estimate prevalence of mania secondary to traumatic brain injury (TBI), Jorge et al.1 diagnosed mania in 9% of 66 consecutive brain-injured patients and Van Reekum et al.2 found 22% of 18 TBI patients developed a bipolar spectrum disorder after mild or moderate TBI. Both of these estimates are higher than the known lifetime prevalence of bipolar I disorder, which is 0.4% to 1.6%.3 Several other differences suggest mania secondary to TBI is phenomenologically distinct from primary mania. First, 4% to 24% of first-degree relatives of those with bipolar I disorder also have bipolar I disorder, 3 but none of Jorge and colleagues' subjects had a first-degree relative with bipolar disorder.1 Also, the average age at onset of mania is 20 years, 3 but mania secondary to TBI has been reported in subjects aged as young as 10 years 4 to as old as 70 years. 5 Finally, brain injury-related bipolar disorder may result in more rapid cycling 6 or prolonged manic states 7 compared to primary mania. These phenomenological differences account for the controversy over considering these syndromes within the bipolar spectrum, as mood disorders secondary to general medical condition, versus neuropsychiatric sequelae of TBI. Regardless of how these disorders are characterized, medication management of psychiatric symptoms following TBI is commonplace.The pharmacologic management of mania secondary to TBI is complicated by animal studies suggesting some antiepileptics and antipsychotics interfere with cognitive or motor recovery. Rats exposed to diazepam after experimental brain injury had persistent sensorimotor asymmetry. 8 Brain-injured rats treated with phenobarbital had significantly delayed recovery in somatosensory deficits. 9 Phenytoin increases the severity of cortical hemiplegia in rats.10 Haloperidol impairs cognitive performance after traumatic brain injury in rats, 11 retards motor recovery, 12 and blocks the acceleration in motor recovery caused by amphetamine. 13 No controlled trials of treating mania secondary to TBI have been published, but there are case reports of successfully using chlorpromazine and carbamazepine, 14 In an open-label flexible-dose study, Kim and Bijlani 26 reported quetiapine was effective for treating irritability and aggression following TBI at doses from 25 to 300 mg/day. That study was only of the target symptoms of aggression and irritability, however, not the full syndrome of mania. We report the first 2 cases in the literature of mania secondary to TBI successfully treated with quetiapine. Case 1. Mr. A, a 27 year-old man with DSM-IV alcohol dependence since adolescence but no family or personal history of mood disorders, was involved in a motor vehicle accident while intoxicated in 2007. At the scene, he was spontaneously moving all extremities, but was combative; initial Glasgow Coma Scale 27 score was 8 (intubated). A head computed tomography scan at the receiving hospital revealed extensive subarachnoid hemorrhages in the interpeduncular, perimese...