Motion sickness--key to neurobiologic variation.

Individual variation in motion sickness susceptibility correlates with a wide variety of perceptual, cognitive, and personality variables suggesting that it may be a unique index of individual difference in fundamental mechanisms of the orientation process. Data from a large ongoing clinical study involving over 1,500 psychiatric inpatients indicate a clear-cut association between a number of the MMPI scales (including Social Isolation, Ego Strength and Schizophrenia) and motion sickness susceptibility. Marked difference across the motion sickness susceptibility spectrum in the condition on discharge of lithium and antidepressant treated patients was also found, when compared to other drug therapies, suggesting specific drug responses by the motion sick group.     

Torture: psychiatric sequelae and phenomenology.

Torture has been defined by the United Nations (declaration of December 9, 1975) as "every act by which a public functionary (or another person at his instigation) intentionally inflicts on another person serious pain or suffering, ...physical or mental, with the object of obtaining information or of punishing him...or of intimidating that person or others." In Chile, from the 1973 military coup d'Etat up to the 1988 plebiscite, torture was practiced in a systematic way, as a method of interrogation and as a means of intimidation of detainees and, indirectly, of the population at large. In the beginning, torture was applied in military station units and in police stations, in the facilities of sport fields and prisoners' camps; but above all, in clandestine detention centers and prisons belonging to the secret police (Amnesty International 1977, 1983; CODEPU 1984, 1985, 1986; Lira and Weinstein 1987; Mu?oz 1986; Rodríguez de Ruiz-Tagle 1978). In spite of the bloodshed of the 1973 coup d'Etat, the phenomenon of torture came as a total surprise for the detainees, who had very often voluntarily surrendered themselves to the new authorities, and who, given the civil traditions of the country, expected treatment in accordance with a society subject to the law. The military government regularly denied having undertaken the practice of torture. According to Lira and Weinstein (20), this denial of such an extreme experience or horror made it even more difficult to overcome the trauma and fostered the development of chronic psychiatric pathology.     

Normal sleep and circadian rhythms: neurobiologic mechanisms underlying sleep and wakefulness.

Sleep is a vital, highly organized process regulated by complex systems of neuronal networks and neurotransmitters. Sleep plays an important role in the regulation of central nervous system and body physiologic functions. Sleep architecture changes with age and is easily susceptible to external and internal disruption. Reduction or disruption of sleep can affect numerous functions varying from thermoregulation to learning and memory during the waking state.     

Delirium: phenomenologic and etiologic subtypes.

While all delirious patients have clouding of consciousness (alteration of attention) and cognitive dysfunction, the level of alertness of different patients may range from stuporous to hyperalert. We, therefore, developed an analog scale to rate the alertness of delirious patients, and a separate scale to rate the severity of their clouding of consciousness. Based on these scales, patients were categorized overall as relatively "activated" (relatively alert despite clouding of consciousness), or "somnolent" (relatively stuporous along with clouding of consciousness). Cognitive function was estimated using the Mini-Mental Status Exam. Separate ratings were made of hallucinations, delusions, illusions, and agitated behavior. Activated and somnolent patients had similar ages, overall severity of delirium, and Mini-Mental Status Exam scores. Activated patients, however, were more likely to have hallucinations, delusions, and illusions than somnolent patients, and were more likely to have agitated behavior. Patients with hepatic encephalopathy were more likely to have somnolent delirium, while patients with alcohol withdrawal appeared more likely to have activated delirium. These data indicate that phenomenologic subtypes of delirium can be defined on the basis of level of alertness. These subtypes are validated in part by their differing associations with symptoms unrelated to alertness. These subtypes may have different pathophysiology, and thus, potentially different treatments.     

Drug resistance in epilepsy: putative neurobiologic and clinical mechanisms

Drug-resistant epilepsy with uncontrolled severe seizures despite state-of-the-art medical treatment continues to be a major clinical problem for up to one in three patients with epilepsy. Although drug resistance may emerge or remit in the course of epilepsy or its treatment, in most patients, drug resistance seems to be continuous and to occur de novo. Unfortunately, current antiepileptic drugs (AEDs) do not seem to prevent or to reverse drug resistance in most patients, but add-on therapy with novel AEDs is able to exert a modest seizure reduction in as many as 50% of patients in short-term clinical trials, and a few become seizure free during the trial. It is not known why and how epilepsy becomes drug resistant, while other patients with seemingly identical seizure types can achieve seizure control with medication. Several putative mechanisms underlying drug resistance in epilepsy have been identified in recent years. Based on experimental and clinical studies, two major neurobiologic theories have been put forward: (a) removal of AEDs from the epileptogenic tissue through excessive expression of multidrug transporters, and (b) reduced drug-target sensitivity in epileptogenic brain tissue. On the clinical side, genetic and clinical features and structural brain lesions have been associated with drug resistance in epilepsy. In this article, we review the laboratory and clinical evidence to date supporting the drug-transport and the drug-target hypotheses and provide directions for future research, to define more clearly the role of these hypotheses in the clinical spectrum of drug-resistant epilepsy.     

Mood disorder and epilepsy: a neurobiologic perspective of their relationship

Mood disorders are the most frequent psychiatric comorbidity in epilepsy, and in particular in temporal lobe epilepsy For a long time, depressive disorders were considered to be the expression of a reactive process to the obstacles of a life with epilepsy. Data obtained in the last two decades, however, have demonstrated biochemical, neuropathological, and neurophysiologic changes mediating the development of mood disorders, which in fact can be tested in animal models. Furthermore, there is also evidence that mood disorders and epilepsy have a complex relationship which is bidirectional; that is, not only are patients with epilepsy at greater risk of developing depression, but patients with depression have a higher risk of developing epilepsy. Such a relationship can only be explained by the existence of common pathogenic mechanisms that are operant in both conditions. These include changes in neurotransmitters, such as serotonin, norepinephrine, glutamate, and y-aminobutyric acid. Such a bidirectional relationship also appears to have important clinical consequences. Indeed, patients with a history of mood disorders are twice as likely to develop pharmacoresistant epilepsy as those without such a history. These data are reviewed in this article.     

Dystonia: phenomenology

In 1984, dystonia was defined by an ad hoc committee of the Dystonia Medical Research Foundation as a syndrome of involuntary, sustained muscle contractions affecting one or more sites of the body, frequently causing twisting and repetitive movements, or abnormal postures. In 2011, dystonia remains a purely clinical diagnosis. Primary dystonia includes syndromes in which dystonia is the sole phenotypic manifestation with the exception that tremor can be present as well. Primary dystonias are typically mobile and may show task specificity. Fixed dystonias are often psychogenic or associated with complex regional pain syndrome. Fixed dystonia may also be the terminal consequence of long-standing, inadequately-treated, severe appendicular or cervical dystonia. The vast majority of primary dystonias have their onset in adults. Late-onset, primary, focal dystonia, particularly blepharospasm, may spread to affect other anatomical segments. Patients with focal dystonia may also exhibit spontaneous remissions that last for years. Although sensory tricks are commonly reported by patients with primary dystonia, they have also been described in subjects with secondary dystonia. Another important sensory aspect of dystonia is pain which is relatively common in cervical dystonia but also reported by many patients with masticatory dystonia, hand-forearm dystonia and blepharospasm. In conclusion, "dystonia" can be used to delimit a clinical sign or loosely define a neuropsychiatric sensorimotor syndrome.     

Paraphilias: phenomenology and classification

DSM-III incorrectly designates the majority of paraphilias as atypical. Only eight are named, and those because of their forensic history, rather than their pathology and therapeutic need. In this paper, thirty-odd paraphilias are subdivided into six categories on the basis of their phenomenological dynamics. The new concept of the developmental lovemap is introduced for the first time. A new treatment originated by the author in 1966 combines an androgen agonist with counseling therapy.     

Delirium: how its concept has developed.

The development of the concept of delirium spans nearly 2,500 years. Its core clinical features were recognized at least as early as the 16th century, while its management reflected a humane approach from the beginning of the modern era. In the 19th century delirium became linked with the concepts of disordered consciousness and confusion, but these two terms were also used in regard to certain functional mental disorders. The most important contribution in this century was the work of Engel, Romano, and associates, who postulated that the syndrome was due to reduction in brain metabolic rate, as reflected in slowing of the EEG background activity. These and other developments are discussed in this article. A list of proposed research priorities is included.     

Depression in epilepsy: phenomenology, diagnosis and management.

1) Depression is a common and important accompaniment of epilepsy. 2) Depression in epilepsy is phenomenologically different from the usual forms of depression and it is essential that treating physicians assess for these varied forms as well. 3) Depression in epilepsy may be managed more effectively if the relationship to the ictus is better understood. 4) Other factors such as stressful life events, related or unrelated to epilepsy, may contribute to the depressive symptoms. 5) Antiepileptic drugs, particularly GABAergic agents such as vigabatrin, tiagabine, topiramate and phenobarbitone are depressogenic in nature. 6) The newer antidepressants, SSRIs such as sertraline, citalopram and paroxetine do not lower seizure threshold and can be safely used to treat depression in epileptic individuals. Fluoxetine may be avoided because of its longer half-life.     

Akathisia: clinical phenomenology and relationship to tardive dyskinesia.

Akathisia and tardive dyskinesia (TD) are disorders of movement that are often associated with administration of antipsychotic medication. We surveyed 196 outpatients in a schizophrenia clinic, all receiving antipsychotic medication, for the presence of these disorders. Clinical global ratings of akathisia were reliable. Akathisia was found in 36% of patients, and TD in 23.5%. Akathisia was disproportionately common in patients receiving high-potency neuroleptics. The data affirmed recent revisions in the dose-equivalence formulas used with fluphenazine decanoate. Akathisia and TD did not seem to be interrelated. Because akathisia is common and often limits medication dose and contributes to noncompliance, psychiatrists must take this into account when prescribing antipsychotic medication.     

The phenomenology of depression.

The article attempts to identify the basic mechanism of depression as implied by various clinical formulation of depression. In this context, depression appears to result from a faulty system of thinking, developed during the individual's formative years. The depressed person perceives reality based on either absoluted social moral values or distorted evaluations of his limitations and expectations.     

Psychoanalysis--a phenomenology of language.

It is often said that there is an unbridgeable gap between phenomenology and psychoanalysis. But this is only half the truth. Starting from Merleau-Ponty's proposal of an objectivistic and an idealistic divergence of Freud's enterprise the paper tries to reconstruct two possible movements: the objectivistic divergence of Husserl's enterprise as a phenomenological shift towards psychoanalysis and the idealistic divergence of Freud's enterprise as a psychoanalytical shift towards phenomenology. It is shown that this approach is possible on the field of language and semiotics where psychic life, as the essence of our subjectivity, may be rendered as a uniform phenomenon of an articulation in the world of signs. This thesis is elucidated at the end of the paper by discussing first (to the phenomenological side) a certain interpretation of the use of Husserl's reduction as a method of investigation in psychiatry and second (to the psychoanalytic side) the importance of Lacan's difference between repression and foreclosure for a psychopathological understanding of psychosis.