Of all known neurotransmitters, 5-HT is the one most frequently mentioned in the pathophysiology of migraine. This review focuses on the relationship between the efficacy of sumatriptan and other migraine agents and their effects on specific 5-HT receptors in rodent models. These agents are seen to have effects on vascular constriction and the release of vasoactive and inflammatory peptides from trigeminovascular sensory neurons. Specific subtypes of the 5-HT1 receptors appear to mediate these effects.

Effective cognitive-behavioral therapy (CBT) programs have been developed for aU of the anxiety disorders. Common elements of CBT for these disorders include exposure to feared objects, situations, activities, thoughts, memories, and sensations; cognitive restructuring of dysfunctional beliefs; and training in anxiety management skills, such as controlled breathing and relaxation. This article describes CBT procedures for anxiety disorders and summarizes the research documenting its efficacy. Next, the article discusses the factors that influence the efficacy of these treatment program. Finally, emotional-processing theory is discussed to explain the efficacy of CBT for anxiety and how this theory can assist in selecting optimal treatment brocedures.

In this article, we present data on the analysis of maze-solving behavior as a tool for the investigation of cognitive disturbance in schizophrenic patients. Solving maze tasks efficiently requires both an interaction between and an integration of perceptive and action-oriented processes. Starting from the hypothesis that these domains are preferentially disturbed in schizophrenia, we propose that the maze-solving behavior of schizophrenic patients permits insight into specific impairments in disease-related cognitive processing. We present the results of a maze task study comparing medication-free schizophrenic patients and matched healthy controls. This analysis forms the basis for an investigation of the influence of psychopharmacological treatment strategies on the observed behavior in the maze-solving paradigm. Finally, a third study concerned with improvement over time associated with medication is presented, and possible influences of extrapyramidal motor disturbances on schizophrenic patients' maze performance are discussed.

A growing family of medications is used for mood stabilization in bipolar disorder. These medications fall into two broad categories according to likely mechanisms of action. Within the categories, specific drugs may vary in their efficacy for different phases of the disorder. The first category, including lithium, anticonvulsants, and some novel treatments, appears to have mechanisms related to intracellular second messengers. These medications have more pronounced antimanic than antidepressant effects, except for lamotrigine, which has antidepressant effects without precipitating mania. The second group of mood stabilizers is the atypical antipsychotics, which act through dopamine and other monoamines. Olanzapine and in all likelihood other drugs in the class possess marked, acute antimanic properties and possible antidepressant properties, but require further study before they can be used as routine options in long-term care. It is clear that the advent of multiple mood stabilizer candidates has not yet led to a single ideal therapy for bipolar disorder, but rather to options that can be flexibly tailored to the lifetime needs of individual patients, in sequences or combinations, and perhaps in conjunction with other classes of psychotropics.

Over the past decade, new functional neuroimaging tools have enabled researchers to identify the specific brain regions involved in obsessive-compulsive disorder (OCD). More recently, researchers have perfected several new techniques for stimulating the brain. With some exceptions, these new brain stimulation techniques are regionally specific and less invasive than older methods. As a class, these “somatic interventions” build on prior neuroanatomic information about OCD. This article reviews the past and current status of these brain stimulation methodologies, which promise to revolutionize neuropsychiatric research and therapy over the next 10 to 20 years. As the brain circuits in OCD and the pharmacology within those circuits become better understood, these brain stimulation techniques hold particular promise in helping to understand and perhaps treat OCD.

Traumatic brain injury (TBI) is a complex phenomenon affecting multiple areas of the brain in multiple ways. Both right and left hemispheres are affected as well as supratentorial and infratentorial compartments. These multifocal injuries are caused by many factors including acute mechanical injury, focal intracranial hemorrhage, blunt and rotational forces, epidural and subdural hematoma, hypoxemia, hypotension, edema, axonal damage, neuronal death, gliosis and blood brain barrier disruption. Clinicians and patients benefit by precise information about the neuroanatomical areas that are affected macroscopically, microscopically and biochemically in an individual patient.

Standard imaging studies are frequently negative or grossly underestimate the severity of TBI and may exacerbate and prolong patient suffering with an imaging result of “no significant abnormality”. Specifically, sophisticated imaging tools have been developed which reveal significant damage to the brain structure including atrophy, MRI spectroscopy showing variations in neuronal metabolite N-acetyl-aspartate, elevations of membrane related Choline, and the glial metabolite myo-inositol is often observed to be increased post injury. In addition, susceptibility weighted imaging (SWI) has been shown to be more reliable for detecting microbleeds versus calcifications.

We have selected two TBI patients with diffuse traumatic brain injury.

The first patient is a 43-year-old male who suffered severe traumatic brain injury from a motorcycle accident in 2016. Following the accident, the patient was diagnosed with seizures, major depression, and intermittent explosive disorder. He has attempted suicide and has neurobehavioral disinhibition including severe anger, agitation and irritability. He denies psychiatric history prior to TBI and has negative family history. Following the TBI, he became physically aggressive and assaultive in public with minimal provocation. He denies symptoms of thought disorder and mania. He is negative for symptoms of  cognitive decline or encephalopathy.

The second patient is a 49-year-old male who suffered at least 3 concussive blasts in the Army and a parachute injury. Following the last accident, the patient was diagnosed with major depressive disorder, panic disorder, PTSD and generalized anxiety disorder. He denies any psychiatric history prior to TBI including negative family history of psychiatric illness. In addition, he now suffers from nervousness, irritability, anger, emotional lability and concurrent concentration issues, problems completing tasks and alterations in memory.

Both patients underwent 1.5T multiparametric MRI using standard T2, FLAIR, DWI and T1 sequences, and specialized sequences including susceptibility weighted (SWAN/SWI), 3D FLAIR, single voxel MRI spectroscopy (MRS), diffusion tensor imaging (DTI), arterial spin labeling perfusion (ASL) and volumetric MRI (NeuroQuant). Importantly, this exam can be performed in 30–45 minutes and requires no injections other than gadolinium in some patients. We will discuss the insights derived from the MRI which detail the injured areas, validate the severity of the brain damage, and provide insight into the psychological, motivational and physical disabilities that afflict these patients. It is our expectation that this kind of imaging study will grow in value as we link specific patterns of injury to specific symptoms and syndromes resulting in more targeted therapies in the future.

There are many new findings in the area of comorbid insomnia. Almost 50% of all cases of chronic insomnia are due to a mental disorder, with depressive illness explaining the majority of cases related to mental disorder (Slide 1). Other common causes of comorbid, or secondary, insomnia include chronic respiratory disease such as asthma and chronic obstructive pulmonary disease, chronic pain, degenerative neurological disease, and some medications such as glucocorticoids and serotonin reuptake inhibitors. A general principle of management of insomnia related to mental or medical disorders is that the principal disorder must be fully treated as part of the insomnia treatment plan. If there is an offending medication, it must be discontinued if possible.

Schizophrenia is a neurodevelopmental disorder associated with persistent symptomatology, severe functional disability, and residual morbidity characteristic of neurodegenerative brain diseases. The illness begins with genetic susceptibility and generally expresses itself after puberty through subtle changes that begin during the prodromal stage. Symptoms get progressively worse and tend to become more resistant to treatment with each relapse. Evidence for a neuroprotective effect of some forms of early treatment is beginning to emerge. While the underlying mechanisms remain uncertain, atypical antipsychotics may counteract some of the progressive deteriorative effects by enhancing synaptic plasticity and cellular resilience. However, identifying and treating patients in the earliest disease states presents methodological challenges as there is no consensus on the best methods of intervention and differences in at-risk children are not readily detectable or substantial enough to predict which ones will develop schizophrenia.

In this expert roundtable supplement, Jeffrey A. Lieberman, MD, reviews the historical context of progressive deterioration in schizophrenia. Next, Diana O. Perkins, MD, MPH, reviews some of the challenges to early identification of illness as well as the impact of early versus delayed treatment. Finally, L. Fredrik Jarskog, MD, focuses on the neurobiology of functional progression in schizophrenia as well as pharmacology and the potential for neuroprotection.

Parkinson's disease (PD) is one of the most common neurodegenerative diseases. The last 5 years have been marked by rapid developments in understanding the pathophysiology of PD as well as by the introduction of a number of new drugs for symptomatic treatment of the disease. On the other hand, the diagnosis of PD is still made purely on clinical grounds. Due to continuing advances in therapy, it is increasingly important to recognize PD in its earliest stages and to distinguish it from other causes of parkinsonism, for which prognosis and response to treatment differ. This article reviews the epidemiology of PD and then elaborates on the diagnosis and differential diagnosis.