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The incidence of treatment-emergent EPS and change in EPS ratings indicated that there are no significant differences between second-generation antipsychotics and perphenazine or between second-generation antipsychotics in people with schizophrenia.

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Single, severe traumatic brain injury (TBI) which elevates CNS amyloid, increases the risk of Alzheimer's disease (AD); while repetitive concussive and subconcussive events as observed in athletes and military personnel, may increase the risk of chronic traumatic encephalopathy (CTE). We describe two clinical cases, one with a history of multiple concussions during a career in the National Football League (NFL) and the second with frontotemporal dementia and a single, severe TBI. Both patients presented with cognitive decline and underwent [18F]-Florbetapir positron emission tomography (PET) imaging for amyloid plaques; the retired NFL player also underwent [18F]-T807 PET imaging, a new ligand binding to tau, the main constituent of neurofibrillary tangles (NFT). Case 1, the former NFL player, was 71 years old when he presented with memory impairment and a clinical profile highly similar to AD. [18F]-Florbetapir PET imaging was negative, essentially excluding AD as a diagnosis. CTE was suspected clinically, and [18F]-T807 PET imaging revealed striatal and nigral [18F]-T807 retention consistent with the presence of tauopathy. Case 2 was a 56-year-old man with personality changes and cognitive decline who had sustained a fall complicated by a subdural hematoma. At 1 year post injury, [18F]-Florbetapir PET imaging was negative for an AD pattern of amyloid accumulation in this subject. Focal [18F]-Florbetapir retention was noted at the site of impact. In case 1, amyloid imaging provided improved diagnostic accuracy where standard clinical and laboratory criteria were inadequate. In that same case, tau imaging with [18F]-T807 revealed a subcortical tauopathy that we interpret as a novel form of CTE with a distribution of tauopathy that mimics, to some extent, that of progressive supranuclear palsy (PSP), despite a clinical presentation of amnesia without any movement disorder complaints or signs. A key distinguishing feature is that our patient presented with hippocampal involvement, which is more frequently seen in CTE than in PSP. In case 2, focal [18F]-Florbetapir retention at the site of injury in an otherwise negative scan suggests focal amyloid aggregation. In each of these complex cases, a combination of [18F]-fluorodeoxyglucose, [18F]-Florbetapir and/or [18F]-T807 PET molecular imaging improved the accuracy of diagnosis and prevented inappropriate interventions.

The neurobehavioral sequelae of traumatic brain injury consist of a spectrum of somatic and neuropsychiatric symptoms. The neuropsychiatric symptoms are divided into cognitive and behavioral presentations. In the literature, these neurobehavioral sequelae have been called postconcussive symptoms, postconcussive syndrome, and postconcussive disorder; however, the authors of this review do not use this terminology because the symptoms are not restricted to patients with concussion but instead can be found in all traumatic brain injury patients of all injury severities. The development of neurobehavioral sequelae after traumatic brain injury is a multifactorial process. The patient evaluation requires a multidisciplinary approach in order to delineate physiologic dysfunction and place deficits in the context of the patient's preinjury and postinjury psychiatric status. Consequently, the evaluation of the posttraumatic brain injury patient with neurobehavioral sequelae requires a carefully structured history and physical examination with an emphasis on neurological and psychiatric function. Adjunctive evaluations must be tailored to the patient with neuroimaging, neurophysiological, and neuropsychiatric testing. Maximized outcomes may be achieved by the performance of a careful and detailed assessment that places complaints within the context of the individual.

The results of this systematic review identify the consistent and prevalent indicators of concussion and their associations, derived from the strongest evidence in the published literature. The product is an evidence-based foundation from which to develop diagnostic criteria and prognostic indicators.

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