Background: Lifetime prevalence rates of cognitive dysfunction and depression in multiple sclerosis (MS) have typically been reported to be ∼50%. However, an inconsistent relationship between these two common features of MS has been reported in the literature. Because neurovegetative depression symptoms overlap with MS symptoms, it may be that literature inconsistencies can partly be explained by the fact that only those depression symptom clusters unambiguously reflective of depression are associated with cognitive dysfunction.

Objective: To explore the relationship between different depression symptom clusters and a battery of tests measuring cognitive domains commonly impaired in MS and was examined at two time points 3 years apart.

Methods: The Chicago Multiscale Depression Inventory was employed to measure mood, negative evaluative, and neurovegetative symptom clusters in 53 MS patients who were also administered a battery of neuropsychological tests.

Results: At time point 1, Mood and Evaluative Chicago Multiscale Depression Inventory scales were significantly associated with tasks of complex speeded attention, planning, and working memory. At time point 2, the Evaluative scale was still significantly associated with these domains, in addition to spatial memory; however, all of the significant correlations with the Mood scale dropped out.

Conclusion: These results show that negative evaluative depression symptoms are most consistently predictive of cognitive dysfunction in MS. It may be that negative evaluative depression symptoms use up available cognitive capacity, thus compromising performance on cognitive capacity demanding tasks in MS patients.

Postpartum psychiatric changes can range from maternity blues to psychosis. Causality is still undetermined, but explanations for these disturbances often focus on hormonal changes and dysregulation. Researchers have begun the process of delineating what neurobiological factors may be associated with depressive disorders in pregnancy and the postpartum. This article reviews the current literature on the roles of gonadal and pituitary hormones in the psychopathophysiology of postpartum mood disorders. Other biological factors, such as biogenic amines, neuroactive steroids, cholesterol, and fatty acids, are also discussed. The potential benefits of neuroimaging to aid in understanding neuropsychiatric changes that occur in the context of postpartum depression are also considered.

Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder characterized by chronic abdominal discomfort or pain in the absence of detectable organic disease. IBS is common and is associated with a significant impairment in health-related quality of life. Enhanced perception of visceral stimuli (“visceral hypersensitivity”) appears to be an important patho-physiological mechanism. Early IBS studies using functional brain imaging techniques suggest an alteration in central pain modulation circuits, rather than an increased sensitivity of peripheral visceral pain pathways. The frequent comorbidity with psychiatric disorders suggests the possibility of shared pathophysiological mechanisms and etiologic factors.

Anxiety disorders are common and often disabling. They fall into five main categories: panic disorder, social anxiety disorder, generalized anxiety disorder, obsessive-compulsive disorder and posttraumatic stress disorder, each of which have characteristic symptoms and cognitions. All anxiety disorders respond to drugs and psychological treatments. This review will focus on drug treatments. Recent research has emphasized the value of antidepressants especially the selective serotonin reuptake inhibitors, benzodiazepines, and related sedative-like compounds. The common co-existence of depression with all of the anxiety disorders means that the selective serotonin reuptake inhibitors are now generally considered to be the first-line treatments but the benzodiazepines have some utility especiaRy in promoting sleep and working acutely to reduce extreme distress.

The operational criteria for seasonal affective disorder (SAD) have undergone several changes since first proposed in 1984. SAD is currently included as a specifier of either bipolar or recurrent major depressive disorder in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. The International Classification of Diseases, Tenth Edition has provisional diagnostic criteria for SAD. The most characteristic quality of SAD is that the symptoms usually present during winter and remit in the spring. Furthermore, the symptoms tend to remit when the patients are exposed to daylight or bright light therapy. The cognitive and emotional symptoms are as in other types of depression but the vegetative symptoms are the reverse of classic depressive vegetative symptoms, namely increased sleep and increased appetite. SAD is a common condition, but the exact prevalence rates vary between different studies and countries and is consistently found to be more common in women and in youth. SAD probably possibly occurs in children although not as commonly as in young adults. Some studies have found that certain ethnic groups who live at high northern latitudes may have adapted to the long arctic winter.

This review discusses the clenching-grinding spectrum from the neuropsychiatric/neuroevolutionary perspective. In neuropsychiatry, signs of jaw clenching may be a useful objective marker for detecting or substantiating a self-report of current subjective emotional distress. Similarly, accelerated tooth wear may be an objective clinical sign for detecting, or substantiating, long-lasting anxiety. Clenching-grinding behaviors affect at least 8% of the population. We argue that during the early paleolithic environment of evolutionary adaptedness, jaw clenching was an adaptive trait because it rapidly strengthened the masseter and temporalis muscles, enabling a stronger, deeper and therefore more lethal bite in expectation of conflict (warfare) with conspecifics. Similarly, sharper incisors produced by teeth grinding may have served as weaponry during early human combat. We posit that alleles predisposing to fear-induced clenching-grinding were evolutionarily conserved in the human clade (lineage) since they remained adaptive for anatomically and mitochondrially modern humans (Homo sapiens) well into the mid-paleolithic. Clenching-grinding, sleep bruxism, myofacial pain, craniomaxillofacial musculoskeletal pain, temporomandibular disorders, oro-facial pain, and the fibromyalgia/chronic fatigue spectrum disorders are linked. A 2003 Cochrane meta-analysis concluded that dental procedures for the above spectrum disorders are not evidence based. There is a need for early detection of clenching-grinding in anxiety disorder clinics and for research into science-based interventions. Finally, research needs to examine the possible utility of incorporating physical signs into Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition posttraumatic stress disorder diagnostic criteria. One of the diagnostic criterion that may need to undergo a revision in Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition is Criterion D (persistent fear-circuitry activation not present before the trauma). Grinding-induced incisor wear, and clenching-induced palpable masseter tenderness may be examples of such objective physical signs of persistent fear-circuitry activation (posttraumatic stress disorder Criterion D).

A 48-year-old woman suffering from treatment-resistant psychogenic stiff neck and severe depression had been treated with a varied regimen of medications, including antidepressants, neuroleptics, and antiepileptics. These treatments did not result in improvement. Therefore, she was treated with a combination of sertraline and risperidone. Depressive symptoms decreased within a few weeks of treatment initiation. The psychogenic stiff neck, which had begun to improve within the first 2 weeks, had disappeared completely after 6 months of treatment with risperidone alone. This case report suggests that risperidone may be effective in some neurological motor disorders comorbid with mood disorders.

Recently, findings on a wide range of auditory abnormalities among individuals with autism have been reported. To date, functional distinctions among these varied findings are poorly established. Such distinctions should be of interest to clinicians and researchers alike given their potential therapeutic and experimental applications. This review suggests three general trends among these findings as a starting point for future analyses. First, studies of auditory perception of linguistic and social auditory stimuli among individuals with autism generally have found impaired perception versus normal controls. Such findings may correlate with impaired language and communication skills and social isolation observed among individuals with autism. Second, studies of auditory perception of pitch and music among individuals with autism generally have found enhanced perception versus normal controls. These findings may correlate with the restrictive and highly focused behaviors observed among individuals with autism. Third, findings on the auditory perception of non-linguistic, non-musical stimuli among autism patients resist any generalized conclusions. Ultimately, as some researchers have already suggested, the distinction between impaired global processing and enhanced local processing may prove useful in making sense of apparently discordant findings on auditory abnormalities among individuals with autism.

Atherosclerotic disease accounts for ~25% of ischemic strokes. Atherosclerotic stroke is caused mainly by embolic events from the carotid artery bifurcation or the aortic arch, although intracranial thrombosis can occur, more often in African Americans, Asians, and diabetes patients. Primary prevention of stroke is critical for patients with risk factors for atherosclerosis, including hypertension, diabetes, smoking and hypercholesterolemia. Stroke can be prevented in patients with established atherosclerotic disease by identification and management of patients with carotid artery stenosis by non-invasive testing. Particular attention must be paid to patients with transient symptoms of brain ischemia.

Rats treated chronically with the D2/D3, dopamine receptor agonist quinpirole show a pattern of behavior that meets a set of ethologically derived criteria of compulsive behavior in obsessive-compulsive disorder (OCD). Moreover, in both quinpirole-treated rats and OCD patients, the structure of compulsive rituals appear similar in being composed of relatively few motor acts that are organized in a flexible yet recurrent manner. In addition, the development of compulsive behavior in quinpirole-treated rats is attenuated by the OCD pharmacotherapeutic drug clomipramine. These similarities support the validity of quinpirole-treated rats as a psychostimulant-induced animal model of OCD. Considering that the induction of compulsive behavior in the rat model involves chronic hyperstimulation of dopamine receptors, this raises the possibility that dopaminergic mechanisms may play a role in OCD, at least in some subtypes of this disorder.

There is increasing evidence that supports the view that irritable bowel disorder (IBS) is a disorder of brain-gut function. Cognitive-behavioral therapy (CBT) has received increased attention in light of this recent shift in the conceptualization of IBS. This review has two main aims. The first is to provide a critical review of controlled trials on CBT for IBS. The second is to discuss ways of further developing CBT interventions that are more clinically relevant and meaningful to health care providers and individuals with a diagnosis of IBS. A theme from a CBT intervention will be presented to illustrate how CBT interventions can be incorporated within a larger social context. A review of CBT for IBS lends some limited support for improvement in some IBS symptoms and associated psychosocial distress. This conclusion needs to be expressed with some caution, however, in light of many methodological shortcomings including small sample sizes, inadequate control conditions and failure to identify primary versus secondary outcome measures. In addition, future studies will need to further develop more relevant CBT protocols that more fully integrate the patient's perspective and challenge social cognitions about this stigmatized disorder.

Psychotic major depression is a severe condition that frequently proves difficult-to-treat. The most effective traditional treatments (electroconvulsive therapy and combinations of antipsychotics with tricyclic antidepressants) are associated with significant side effects, and the use of tricyclic antidepressants alone is largely ineffective. Recent evidence has indicated that the selective serotonin reuptake inhibitors, either alone or in combination with antipsychotics, may provide a desirable alternative to traditional treatments. Among selective serotonin reuptake inhibitors, fluvoxamine has been the best studied and, somewhat surprisingly, has proven effective in several studies as a monotherapy without the need to combine with an antipsychotic. It is proposed that the apparent efficacy of fluvoxamine in psychotic major depression may be related to its unique property of high affinity for the σ1receptor, which is thought to play a role in psychosis and in the action of some antipsychotic drugs.

Blood disorders have been implicated in ~5% to 10% of ischemic stroke, with an increased frequency in younger patients. Most disorders are associated with an increased thrombotic tendency and, therefore, an increased risk of ischemic stroke. Less commonly, a bleeding diathesis may predispose a patient to intracranial hemorrhage. While many conditions predisposing to thrombosis have been associated with stroke, there are relatively few prospective, epidemiological studies addressing hypercoagulable states and arterial stroke compared with the number of studies on the genetic thrombophilias, which are predominantly associated with venous thrombosis. When ordering tests of coagulation in stroke patients, one should keep in mind whether the results will influence therapy and/or patient outcome. It is generally not advocated to screen all stroke patients for a “hypercoagulable workup”. Typically, patients to be screened for coagulation defects will have a prior history of one or more unexplained thromboembolic events. The yield for diagnosing a hypercoagulable state is typically greatest for young stroke patients or those with a family history of thrombosis and who have no other explanations for their stroke (cryptogenic stroke). The yield in typically low in unselected ischemic stroke patients and older patients. Treatment of a first stroke with a documented hypercoagulable state is typically long-term or indefinite duration warfarin, although there is a paucity of clinical trial data supporting this clinical approach.

Animal models are considered essential in research ensuing elucidation of human disease processes and subsequently, testing of potential therapeutic strategies. This is especially true for neurodegenerative disorders, in which the first steps in pathogenesis are often not accessible in human patients. Alzheimer's disease is vastly becoming a major medical and socioeconomic problem in our aging society. Valid animal models for this uniquely human condition should exhibit histopathological, biochemical, cognitive, and behavioral alterations observed in Alzheimer's disease patients. Major progress has been made since the understanding of the genetic basis of Alzheimer's disease and the development and improvement of transgenic mouse models. All present Alzheimer's disease models developed are partial but nevertheless essential in further unraveling the nature and spatial and temporal development of the complex molecular pathology underlying this condition. One of the more recent transgenic attempts to mode Alzheimer's disease is the APP23 transgenic mouse. This article describes the development and assessment of this human amyloid precursor protein overexpression model. We summarize histopathological and biochemical, cognitive and behavioral observations made in heterozygous APP23 mice, thereby emphasizing the model's contribution to clarification of neurodegenerative disease mechanisms. In addition, the first therapeutic interventions in the APP23 model are included.