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Opinion statement Cognitive impairment is a common consequence of traumatic brain injury (TBI) and a substantial source of disability. Across all levels of TBI severity, attention, processing speed, episodic memory, and executive function are most commonly affected.The differential diagnosis for posttraumatic cognitive impairments is broad, and includes emotional, behavioral, and physical problems as well as substance use disorders, medical conditions, prescribed and self-administered medications, and symptom elaboration. Thorough neuropsychiatric assessment for such problems is a pre-requisite to treatments specifically targeting cognitive impairments.First-line treatments for posttraumatic cognitive impairments are non-pharmacologic, including education, realistic expectation setting, environmental and lifestyle modifications, and cognitive rehabilitation.Pharmacotherapies for posttraumatic cognitive impairments include uncompetitive N-methyl-D-aspartate receptor (NMDA) antagonists, medications that directly or indirectly augment cerebral catecholaminergic or acetylcholinergic function, or agents with combinations of these properties.In the immediate post-injury period, treatment with uncompetitive NMDA receptor antagonists reduces duration of unconsciousness. The mechanism for this effect may involve attenuation of neurotrauma-induced glutamate-mediated excitotoxicity and/or stabilization of glutamate signaling in the injured brain.During the sub-acute or late post-injury periods, medications that augment cerebral acetylcholinergic function may improve declarative memory. Among responders to this treatment, secondary benefits on attention, processing speed, and executive function impairments as well as neuropsychiatric disturbances may be observed. During these post-injury periods, medications that augment cerebral catecholaminergic function may improve hypoarousal, processing speed, attention, and/or executive function as well as comorbid depression or apathy.When medications are used, a “start-low, go-slow, but go” approach is encouraged, coupled with frequent reassessment of benefits and side effects as well as monitoring for drug-drug interactions. Titration to either beneficial effect or medication intolerance should be completed before discontinuing a treatment or augmenting partial responses with additional medications.

Pathological laughing and crying (PLC) is characterized by frequent, brief, intense paroxysms of uncontrollable crying and/or laughing due to a neurological disorder. When sufficiently frequent and severe, PLC may interfere with the performance of activities of daily living, interpersonal functioning, or both, and is a source of distress for affected patients and their families. PLC is also often misunderstood by patients and their families, and is under-recognized by the clinicians caring for patients with this disorder. However, this syndrome is easily recognized when understood properly and is highly responsive to treatment with a variety of pharmacological agents. This review aims to facilitate the diagnosis and treatment of patients with PLC, and begins by providing definitions of mood and affect that will help clinicians distinguish between mood disorders, such as major depression and mania, and disorders of affect, such as PLC. In addition, the various terms used to describe this syndrome are reviewed and a recommendation for the use of the term PLC is made. The core clinical features of PLC are also presented and the epidemiology of this syndrome is reviewed. A discussion of the pathophysiology of PLC, including the neuroanatomic and neurochemical bases, is provided. Finally, the evaluation and treatment of patients with PLC is described. Based on the pathophysiology of PLC and on a detailed review of published treatment studies, SSRIs are recommended as first-line pharmacotherapy for this disorder. When SSRIs are ineffective or poorly tolerated, other treatment options, including TCAs, noradrenergic reuptake inhibitors, novel antidepressants, dopaminergic agents and uncompetitive NMDA receptor antagonists may be useful second-line treatments.

This column is the third in a series describing a model for therapeutic risk management of the suicidal patient. In the preceding column, we described augmenting clinical suicide risk assessment with structured instruments. In this column, we describe how clinicians can use the totality of available clinical data to offer a two-dimensional risk stratification that qualifies risk in terms of both severity and temporality. By offering two separate designations that reflect severity for both acute and chronic risk, conceptualizing and communicating a patient's risk for suicide is accomplished in a more nuanced way, providing the level of detail necessary when working with high risk individuals, especially those struggling with chronic suicidal ideation. Formulations reflecting suicide risk need to be accurate and facilitate good clinical decision-making in order to optimally balance the principles of autonomy, non-maleficence, and beneficence. Stratifying risk in terms of both severity and temporality helps identify situations in which involuntary hospitalization is warranted, while also helping to minimize unnecessary admissions. Hence, two-dimensional risk stratification that addresses both acute and chronic risk for suicide is an essential component of therapeutic risk management of the suicidal patient.

While the practice of psychiatry involves many challenges, few scenarios are as clinically and emotionally demanding as managing the patient who is at high risk for suicide. Risk management is a reality of psychiatric practice, and this necessitates practicing and documenting thoughtful suicide risk assessment and management. Therapeutic risk management is based on clinical risk management that is patient-centered, supportive of the treatment process, and maintains the therapeutic alliance. In this article, the authors present a broad overview of a model for achieving therapeutic risk management of the suicidal patient that involves augmenting clinical risk assessment with structured instruments, stratifying risk in terms of both severity and temporality, and developing and documenting a safety plan. These elements are readily accessible to and deployable by mental health clinicians in most disciplines and treatment settings, and they collectively yield a suicide risk assessment and management process (and attendant documentation) that should withstand the scrutiny that often occurs in the wake of a patient suicide or suicide attempt.

This column is the fourth in a series describing a model for therapeutic risk management of the suicidal patient. Previous columns presented an overview of the therapeutic risk management model, provided recommendations for how to augment risk assessment using structured assessments, and discussed the importance of risk stratification in terms of both severity and temporality. This final column in the series discusses the safety planning intervention as a critical component of therapeutic risk management of suicide risk. We first present concerns related to the relatively common practice of using no-suicide contracts to manage risk. We then present the safety planning intervention as an alternative approach and provide recommendations for how to use this innovative strategy to therapeutically mitigate risk in the suicidal patient.

Recent scientific reports and popular press describing chronic traumatic encephalopathy (CTE) collectively link this condition to a broad array of neuropsychiatric symptoms, including extremely rare and multi-determined behaviors such as murder-suicide. These reports are difficult to reconcile with several decades of research on the science of traumatic brain injury (TBI) and its consequences, especially the natural history and prognosis of mild TBI. This article attempts to reconcile these sources by reviewing the state of the science on CTE, with particular attention to case definitions and neuropathological criteria for this diagnosis. The evidence for links between TBI, CTE, and catastrophic clinical events is explored, and the complexity of attributing rare frequency behavioral events to CTE is highlighted. The clinical and medicolegal implications of the best available evidence are discussed, concluding with a cautionary note against prematurely generalizing current findings on CTE to entire populations of persons with, or at risk for, concussion exposures.