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Emotional crying is hypothesized to serve intra- and interpersonal functions. Intrapersonal functions are assumed to facilitate the capacity to recover from emotional distress, thus promoting well-being. Interpersonal functions are postulated to have a major impact on social functioning. We hypothesized that non-criers would have lower well-being and poorer social functioning than criers.
Study participants included 475 people who reportedly lost the capacity to cry and 179 “normal” control criers. Applied measures assessed crying, well-being, empathy, attachment, social support, and connection with others. Prevalence estimates of not crying by gender were obtained from a panel survey of 2,000 Dutch households.
In the main survey, tearless cases had less connection with others, less empathy, and experienced less social support, but were equal in terms of well-being. They also reported being less moved by emotional stimuli and had a more avoidant and less anxious attachment style. In multivariate analyses, being male, having an avoidant attachment style, and lacking empathy were independent predictors of tearlessness. Some 46.1% felt that not being able to cry affected them negatively; however, despite these findings, only 2.9% had sought any kind of professional help. Loss of the capacity to cry occurred in 8.6% of the men and 6.5% of the women in the large panel survey.
Despite reduced empathy, less connection with others, and a more avoidant/less anxious attachment type, well-being is maintained in tearless people. Additional clinical and therapeutic investigations of tearlessness may lead to clarification of bidirectional associations between psychiatric disorders (e.g., alexithymia, posttraumatic stress disorder, psychopathy) and tearlessness.
Research into the neuropsychiatry of epilepsy has become a central focus of interest in the last five years. Comorbidity of epilepsy with behavioral problems is now recognized widely, and the neuroscientific basis for such comorbidity is an active area of investigation. With an expanded international team of authors, this fully revised new edition builds on the strengths of its predecessor, examining in detail the subtleties of behavioral changes in patients with seizure disorders and offering both a diagnostic and a management perspective. New chapters cover genetic disorders, the effects of epilepsy on social behavior as viewed through theory of mind, a discussion of the precuneus, the importance and nature of peri-ictal psychiatric symptoms, depression and the interictal dysphoric disorder, and the relationship between antiepileptic drugs and suicide. This new edition is a must for anyone involved in diagnosing or managing epilepsy.
This chapter presents a short history of postictal psychosis (PIP) studies and established clinical pictures of nuclear PIP. It discusses the interrelationship between PIP and interictal psychosis (IIP), results of neuro-imaging studies of PIP, premorbid predisposition (including family history) or risk factors, and PIP-related peri-ictal phenomena including discussion of PIP subtypes. Four different combinations of PIP and IIP have been recognized: progression of PIP to chronic psychosis; PIP changing into IIP without a break during an episode of psychosis; PIP and IIP episodes occurring in an alternating manner; and PIP episodes follow after remission of IIP episodes. As with SPECT studies, only a few depth-EEG studies during active PIP episodes are available, though the results suggest interesting subtypes. Psychopathological features of PIP are highly suggestive of association with bipolar disorder, which is supported by data from different perspectives.
This introduction presents an overview of the concepts discussed in this book The Neuropsychiatry of Epilepsy. In the intervening years, there has been a clear appreciation in biological psychiatry of the neurobiological bases of psychopathologies as major depressive disorder, obsessive-compulsive disorder and other anxiety-related conditions, and there has been further development of psychotropic and anticonvulsant drugs (AEDs). The second edition starts with epidemiology, which has become a prominent discipline in research attempting to disentangle the extent and variety of psychiatric comorbidities in epilepsy. The clinical presentations and the wide spectrum of peri-ictal disorders are then discussed. Depression in epilepsy may not be quite like depression in the absence of epilepsy, the neuroanatomy giving a special stamp on the phenomenology. The book concludes with a discussion on the brain mechanisms of consciousness as may be revealed through investigations of patients with seizure disorders.
In recent years a number of newer antidepressant drugs have been introduced into clinical practice. The new generation of antipsychotic drugs essentially fall into two categories; those that are clozapine related, which included olanzapine and quetiapine, and others such as risperidone. It is also known that many patients with epilepsy receive psychotropic drugs, sometimes but not always on account of psychiatric symptoms. Neuroleptics, such as phenothiazines, are metabolized by intestinal sulfoxidases, although CYP2D6 plays an important role in chlorpromazine and thioridazine metabolism. Antidepressants have been extensively evaluated in relation to the general problem of their proconvulsant activity. Historically, antipsychotic drugs have been considered proconvulsants possibly because of their D2-receptor blocking activity. As far as antidepressant drugs are concerned, fluoxetine and nefazodone interactions are probably the most relevant in epilepsy from a clinical point of view.
Functional brain imaging with technetium-99m d,l-hexamethyl propyleneamine oxime (HMPAO) Single Photon Emission Tomography (SPET) allows us to explore the cerebral pathophysiology of Gilles de la Tourette's Syndrome (GTS).
Fifty patients and 20 controls were examined. Patients were rated for tic severity and mood. Scans were analysed quantitatively using internal ratios to the occipital cortex.
Patients differed from controls on measures of relative blood flow to the left caudate, anterior cingulate cortex and the left dorsolateral prefrontal cortex. Severity of tics was related to hypoperfusion of the left caudate and cingulate and a left medial temporal region. Hypoperfusion in the left dorsolateral prefrontal region was related to mood.
The areas found to be hypoperfused in this study are consistent with known functions of fronto-striatal circuits. A wide range of perfusion patterns is seen, however, and no characteristic patterns for behavioural subgroups has been documented with this technique.