Repetitive transcranial magnetic stimulation (rTMS) is a relatively new technique for activating the cerebral cortex through the scalp and skull. By inducing electrical currents in the brain, rTMS is able to produce a variety of effects, including muscle twitching, changes in motor performance, disruption of cognitive and perceptual processes, and changes in mood. Although the technique is noninvasive and easily tolerated by patients and normal subjects, rTMS can produce epileptic seizures and, potentially, other undesirable effects on brain function. Further studies will be required to fully define the safe ranges of the stimulation parameters.

In spite of the fact that migraine seems to have been present throughout the history of man (Areteus of Cappadocia gave a detailed description of it in the first century AD) and has a high prevalence, its pathophysiology is poorly understood. This is probably due to the fact that it is an episodic and self-limiting, although discomforting, disorder.

It is only in the last few decades that migraine has undergone systematic investigation exploring possible genetic, hormonal, biochemical, and psychological factors. As a result, its nature is now becoming less enigmatic, and some comprehensive models on the underlying mechanisms are available.

We review the most intriguing hypotheses related to the pathophysiology of migraine, focusing especially on theories of serotonin dysfunction, which may also explain the high prevalence of psychiatric disorders detected in migraine patients.

As an individual with autism, I have learned that, unfortunately, some therapists and physicians are unaware of autistics' overly acute senses, specifically hyperacute hearing. For example, the birthday party fun of noise-makers for a normal child was torture for me. There are many first-person reports of people with autism who, like me, find certain loud sounds intolerable.

Some children and adults with autism also have visual sensitivity problems. I enjoyed visually stimulating things such as flags or automatic supermarket doors, but individuals with severe visual sensitivities cannot tolerate even fluorescent lights. In her book, Somebody Somewhere, autistic Donna Williams describes how the flicker from fluorescent lights causes her visual overload. A study conducted by Coleman et al indicates that fluorescent lights can increase repetitive behavior in children with autism.

Autistic sensory problems are highly variable. When I was a child, I liked to play with running water; however, another child with autism may not be able to tolerate the same sound. I was attracted to automatic supermarket doors and I liked to watch them move. Another autistic child or adult may scream and run away from these same automatic doors because sudden movement hurts his or her eyes. Maybe a small anomaly in my visual processing caused me to be attracted to the movement of the doors. A greater anomaly may cause another individual to avoid the same stimulus. Waterhouse et al found it puzzling that I was attracted to strong visual stimuli, yet high-pitched auditory stimuli hurt my ears.

A high prevalence of comorbidity has been reported between migraines and psychiatric disorders. It has been proposed that migraine headaches are mediated by stimulation of serotonin (5-HT) receptors. Past studies have demonstrated that migraine-like headaches have been produced following administration of the partial 5-HT agonist m-chlorophenylpiperazine (m-CPP; believed to primarily affect the 5-HT2C receptor) in patients with migraines or eating disorders, especially bulimia, as well as in normal controls. We review the association between 5-HT dysfunction, as determined by response to m-CPP challenge, and migraines, looking specifically at the relationship between migraines and obsessive-compulsive disorder and gender effects.

Progress in biological psychiatry is contingent upon progress in neurobiology and progress in research of proper characterization and assessment of abnormal behavior. Advances in neurobiology are rapid and steady; however, advances are few and far between in psychopathology. In many ways, developments over the past two decades run counter to what I believe to be diagnostic pre-requisites for fruitful biological research in psychiatry. I presume this to be a major reason why thus far biology has made no significant contributions to the diagnoses of mental disorders.

For progress to occur in biological psychiatry, the traditional diagnostic philosophies and attitudes must be reevaluated and alternative diagnostic approaches put into practice. This and the diagnostic method of functional psychopathology are reviewed in this article, with a focus on how the functional psychopathological approach could contribute to the advancement of the diagnostic process in psychiatry, and the opportunities it provides for biological psychiatric research.

In initial studies using animal models of depression, we primarily focused on the similarities of transcranial magnetic stimulation (TMS) to electroconvulsive therapy (ECT). However, our investigations show that TMS has its own, unique, potentially diagnostic and therapeutic effects, distinct from those of ECT. These effects need further exploration in animal and clinical studies.

In this article, we review attempts to account for the thought disorder present in some schizophrenic patients in terms of cognitive deficits in the domains of working memory, attention, language, and semantic memory. Although each psychological construct can account for some of the data described here, establishment of a primary cognitive impairment responsible for thought disorder is not forthcoming, perhaps due to its underlying multidimensional pathology. While the relationship of working memory, attention, and language processing to thought disorder is ambiguous, semantic memory is emerging as a promising construct, that may yield insight into cognitive mechanisms that underlie thought disorder and neuroleptic responsiveness.

Obsessive-compulsive (OC) symptoms and schizophrenia may present, as intertwined phenomena whose relationship remains poorly understood. The purpose of this paper is to provide a detailed phenomenological description of OC symptoms in schizophrenia.

Fifty long-term patients with chronic schizophrenia or schizoaffective disorder from a continuing day-treatment program were assessed using the Structured Clinical Interview for DSM-IV and the Yale-Brown Obsessive-Compulsive Scale symptom checklist. Forty-six percent (n=23) reported clinically significant OC symptoms. Twenty-six percent (n=13) met criteria for OCD, from which three subgroups emerged: (1) patients whose OCD was unrelated to their psychotic symptoms, (2) patients whose OCD was related to, but not restricted to, their psychotic symptoms, and (3) patients whose OC symptoms existed on a continuum with their psychosis. The last group tended to incorporate their OC symptoms into delusional beliefs during the active phase of illness and shift to OCD during full or partial remissions. Eight percent met all inclusion criteria for OCD, but their OC symptoms were better accounted for by their psychosis.

We conclude that these findings support previous clinical constructs that OCD and schizophrenia are not always dichotomous disorders, but may be interconnected.

Research evidence attests to the parallel similarities and the reciprocal nature of obsessive-compulsive disorder (OCD) and schizophrenia (SCZ) in such a manner that OCD and SCZ may progress into one another. We explore this evidence by presenting a theoretical and empirical phenomenological perspective to account for and elucidate the shared psychopathology of thought, perception, and motor impairment between these disorders. The purpose of this paper is to communicate that OCD and SCZ, while preserving their individuality, share related accounts of their phenomenology within a temporal and spatial frame of reference.

On the surface, epilepsy seems like an easy diagnosis to make—how could anyone miss a major event like a seizure? However, epilepsy can be deceiving. There are many types of seizures that are more subtle than the obvious tonic-clonic seizure, and many seizure types that look bizarre are misdiagnosed as nonepileptic. As a result, a large number of people with epilepsy experience lengthy delays before appropriate diagnosis and therapy provide relief. Conversely, there are many nonepileptic events that are easily mistaken for seizures, which lead to numerous misdiagnoses of epilepsy in nonepileptic patients. These patients are subjected to unnecessary treatment with toxic medications. In this article, I examine the range of diagnostic tests that can be used to establish a diagnosis of epilepsy, to help select the most appropriate form of therapy, to monitor and adjust therapy, to select appropriate surgical candidates, and to decide when therapy can be discontinued.

Nonepileptic seizures (NES) are clinical events that can resemble almost any seizure phenotype, but are behavioral and emotional manifestations of psychological distress, conflict, or trauma. Intractable NES is a disabling disorder that drastically affects patients' emotional well-being. Differential diagnosis, assessment, and treatment of NES is complex, with differentials scattered across an array of neurological and psychiatric disorders. This paper provides an overview of issues related to the diagnosis and treatment of NES. It highlights characteristics and risk factors of the disorder, issues in differential diagnosis, and treatment considerations.