Psychotic anxiety has not been systematically included in standard psychopathologic and diagnostic literature, presumably because anxiety is implicitly perceived to be an emphatically comprehensible consequence of the cognitive symptoms of psychosis. This review gives an overview of neurophysiologic studies that indicate different pathogenic mechanisms for different types of psychosis. Convergent and complementary structural and functional imaging findings, biochemical and neuropsychological data allow conjecture as to neurophysiologic-psychopathologic links in cycloid psychosis. Intriguing results suggest that in cycloid psychosis, a generalized hyperasousal related to the tonus of the noradrenergic system may be the basic disturbance causing the delusionary and perceptual psychotic distortions. The findings are specific for cycloid psychoses, which are diagnosed as polymorphous psychosis in the International Classification of Diseases and Related Health Problems, 10th Edition. Furthermore, these findings are consistent with the author's hypothesis that the emotional derailment is the primary disturbance in cycloid psychosis (anxiety-elation). In contrast, cognitive disturbances are secondary and remit after the exceptional emotional state is rebalanced.

Although the precise etiological nature of autism—the most common development disorder—remains elusive, two main biological factors have been suggested. One is related to a possible neurochemical dysfunction at the level of the serotonergic system; the other underlines the presence of neuroanatomical abnormalities in different areas, in particular, in the cerebellum.

The authors propose a unifying hypothesis linking serotonin (5-hydroxytryptamine, or 5-HT) to the cerebellum on the basis of the observation of a specific 5-HT receptor subtype, 5-HT5A, in this area. The 5-HT5A receptors may be involved in the pathophysiology of autism, and perhaps, in autism-related disorders, since they are mainly expressed in Purkinje's cells. Future studies with specific drugs that interact with 5-HT5A receptors should permit the testing of this hypothesis through the evaluation of the receptors themselves in autopsied brain samples or in vivo by positron emission tomography. Theoretically, such compounds might prove effective in the treatment of autism.

Opioid use disorder (OUD) is a major public health problem in the United States. It has resulted in devastating consequences for people with this condition, including psychosocial and legal problems, in addition to contraction of infectious diseases such as HIV and hepatitis B and C. Furthermore, this disease can cause fatalities from drug overdoses and drug–drug interactions. OUD shatters families and destroys relationships. Effective treatment is crucial in order to curtail the consequences of this condition. The objective of this article is to provide a review of the pharmacotherapies currently being used to treat OUD.

Parkinson's disease was first described in 1817 by James Parkinson. Based on his observation of only six individuals, Parkinson accurately described the resting tremor and festinate gait, bradykinesia, and postural instability associated with the disease today. Parkinson's disease primarily affects people >50 years of age and causes progressive neurological degeneration, physical disability, and worsening quality of life.

Consequently, most currently available drugs aim to restore striatal dopamine signaling. This can be best reached by increasing the supply of dopamine with oral levodopa (L-dopa), but also by stimulating dopamine receptors directly using dopamine agonists, or by inhibiting the reuptake of endogenous dopamine. Unfortunately, mainly due to the short half-life of L-dopa and the erratic absorption of oral L-dopa (causing pulsatile dopaminergic stimulation) these treatment strategies become increasingly ineffective in the course of this disease, and motor complications may further reduce the quality of life in these patients.

Medical presentations can be designed as a data dump or as a story. One effective communication strategy is to organize a lecture as a three act play, starting with previews as the first act and ending with reviews as the third act. Previews facilitate learner achievement and may help learners view a medical instructor more positively. Reviews also help consolidate audience learning and ensure that messages have been clearly delivered and received. The main act is in the middle and is the content itself. Delivering this content in small multiples gives learners manageable packets of information and can help them to see the differences and similarities between conditions, deepening their understanding of what was presented.

Applying principles of adult learning can enhance the effectiveness of a medical presentation. A previous “Trends in Psychopharmacology” presented an overview of these principles and discussed targeting the learner rather than the content or the lecturer as the focus for a medical presentation. Here we cover the concept of presenting content to a learner as a story and show how to organize or “storyboard” it as a three act play.

Lectures can be arranged as a dull recitation of facts or as a story that makes the facts come alive. Generally speaking, a participant is less interested in hearing the facts that a lecturer has to present than in listening to a story the lecturer has to tell. Organizing content into a “three act play” can make a lecture memorable and its lessons practical. Classically, teachers have explained the three parts as: “Say what you are gonna say; say it; then say what you said.” More specifically, the previews are the first part, the presentation itself is the second part, and the reviews are the third part of this structure.

Alzheimer’s disease (AD) research is progressing rapidly and on multiple fronts. Advances are being made in early diagnosis, neuroimaging, and biomarkers; optimal care uses currently available medications and strategies; and new therapies are emerging. Early diagnosis is necessary for optimal patient management. Biomarkers are critical to early diagnosis, and biomarker development is dependent on better understanding of disease pathophysiology (Slide 1). The discussions in this supplement examine how progress in AD research can be translated into clinical care.

Primary care practitioners (PCPs) provide most of the care of patients with AD, and these clinicians are optimally poised to discover new cases emerging among elderly patients. Caregivers are most likely to voice concerns about declining memory in a family member to a PCP before seeking specialty evaluation. PCPs, however, have little time to devote to complex assessments and cannot have specialty-level expertise in all disorders. PCPs must have clinical tools that assist them in rapidly identifying potential problems and triaging them for further evaluation or specialty referral.

A case of pure mutism without pseudobulbar palsy and other neurological findings resulting from simultaneous bilateral lenticulostriate artery territory infarction is presented. A 45-year-old woman suffered a transient ischemic attack with nonfluent aphasia and right hemiparesis. Six months later, she developed pure mutism without oral apraxia, pseudobulbar signs, and motor deficits. Magnetic resonance imaging revealed bilateral infarction in the lentiform nucleus regions. In the available data, there is only one report of simultaneous bilateral lenticulostriate infarction.To date, in all reported cases of mutism of subcortical vascular origin there are also various degrees of pseudobulbar signs and motor deficits and the responsible lesions are mostly consecutive.The case presented here is the first to show pure vascular mutism without other neurological findings.

There are several options and approaches available to practicing psychiatrists for the pharmacologic management of acute psychotic episodes that present in emergency room settings. This article focuses on the first hours and days of such episodes, the goals of treatment, and comparison of the “old favorites,” such as combination haloperidol and lorazepam (in liquid, tablet or injectable formulations), with the newer second-generation antipsychotic agents, such as olanzapine, ziprasidone, risperidone, quetiapine, or aripiprazole, which are available in different formulations. The speed of titration to an effective target dose for these newer agents are addressed as well.

Psychopharmacology is rapidly becoming an adjuvant treatment to traditional rehabilitation strategies for patients with stroke or brain injury because it helps to facilitate recovery in a time-efficient manner. Norepinephrine, dopamine, acetylcholine, and serotonin appear to play important roles in recovery from stroke or brain injury. Animal models have shown that blockade of these neurotransmitters inhibits recovery, whereas recovery is promoted by drugs that promote norepinephrine, dopamine, acetylcholine, and serotonin activity. Preliminary evidence from human trials supports these finding. Further study is needed, but expanded use of pharmacologic agents for stroke and brain-injured patients appears imminent.

A 15-year-old Hispanic female was started on risperidone for new-onset psychosis. The patient responded well to the gradual dose increase but developed rapid weight gain secondary to polydipsia and polyphagia. She also begain complaining of nipple discharge and griping abdominal pain on the left lower quadrant by the third week of treatment. Her prolactin level escalated to three times normal with a weight gain of 12 pounds in 16 days. Risperidone was switched to another antipsychotic. Her prolactin level then dropped to a normal level within 7 days and she lost 7 pounds in the next 2 weeks. Her abdominal pain, galactorrhea, polydipsia, and polyphagia subsided within the first few days of the cessation of risperdione.

Animal models of obsessive-compulsive disorder may be derived naturally or generated experimentally. Either may be considered a full or partial model, depending on the extent of resemblance to human OCD. Although many models appear to be valid at first glance, complete models should demonstrate “compelling similarities” in all areas examined. Partial models may have only one or two OCD-like features; however, they still provide some opportunities for research. Criteria to consider when evaluating potential models are etiology, symptomatology, and use in indicating methods of therapy and prevention. Demonstration of common underlying physiological mechanisms, patterns of development and expression, and familial associations are some specific elements to consider when assessing the relevance of more complete models.

Cognitive aspects of OCD are difficult, if not impossible, to explore in animals at present and may be quite different from what is found in humans. It is hard to imagine that animals experience ego-dystonicity; however, dogs with acral lick dermatitis (ALD) that have been scolded by their owners will resort to licking themselves when out of sight, implying that they know it is wrong. Because of the difficulty in evaluating an animal's internal state, some adopt the position that there is no complete animal model of OCD and that animal models are at best partial models. However, children who exhibit compulsive behaviors frequently do not experience accompanying obsessions. Even the expression of OCD in children—for example, licking and walking in geometric designs—resembles what is seen in animals.

In the descriptions that follow, only directly comparable aspects of compulsive behavior in animals will be discussed. Naturally occurring models that appear to correspond most closely to full models may be useful in understanding the fundamental mechanisms underlying OCD and the OC spectrum, including genetics and neurobiology. Experimental models, which may be either full or partial models, could contribute similarly or provide limited but specific information in a targeted area of study, depending on the extent of their similarity to OCD.

Parkinson's disease is the most common basal ganglia disorder that is caused by the degeneration of dopaminergic neurons in the substantia nigra. This article reviews the normal physiology of the basal ganglia in the normal state, as well as the pathophysiology of Parkinson's disease (PD) and other movement disorders associated with the basal ganglia. Also discussed is the pathophysiological basis for the surgical treatment of PD.

A 60-year-old patient with a clinical diagnosis of schizophrenia underwent a magnetic resonance imaging (MRI) scan related to the evaluation of isolated seizures that emerged while medicated with clozapine. Unexpectedly, the MRI scan revealed evidence of asymmetric and enlarged cerebral ventricles that were interpreted as congenital in origin. The presence of both congenital lateral ventricular asymmetry and ventriculomegaly may interact to increase risk of schizophrenia. The history and clinical features, including cognitive testing, of the illustrative patient are presented.