[Pathological Demand Avoidance: Current State of Research and Critical Discussion]. / Pathological Demand Avoidance ­ aktueller Forschungsstand und kritische Diskussion.

Pathological Demand Avoidance: Current State of Research and Critical Discussion Abstract: Pathological demand avoidance (PDA) describes children who obsessively avoid any demand to a clinically relevant extent and is presently the subject of controversial discussion. Their behavior may be interpreted as an attempt to reduce anxiety by establishing security and predictability through rigid control of the environment as well as the demands and expectations of others. The symptoms are described in the context of autism spectrum disorder. This article reviews the current state of research and discusses the questionable validity of pathological demand avoidance as an independent diagnostic entity. It also addresses the impact of the behavior profile on development and treatment. This paper concludes that PDA is not a diagnostic entity nor a subtype of autism; rather, it is a behavior profile that can be associated with adverse illness progression and unfavorable outcomes. PDA is one feature in a complex model. We must consider not only the patient's characteristics but also those of the caregiver and their psychopathology. The reactions of the interaction partners as well as the treatment decisions play a key role play for the affected individuals. Substantial research is needed concerning the occurrence of the behavior profile PDA in diverse disorders, treatment options, and treatment responses.

Epileptic seizures, coma and EEG burst-suppression from suicidal bupropion intoxication.

Bupropion, an amphetamine-like dual mechanism drug, is approved and increasingly used for the treatment of major depression, and its use is associated with a dose-dependent risk of epileptic seizures. Suicide attempts are frequent in major depression and often an overdose of the drugs available is ingested. Therefore, it is important to be aware of the clinical course, including EEG and neurological symptoms, as well as treatment and prognosis of bupropion intoxication. We report on the clinical and EEG course of a women who ingested 27 g of bupropion in a suicide attempt. Myoclonic seizures were followed by generalized tonic-clonic seizures and coma associated with EEG burst-suppression and brief tonic seizures. Active carbon and neuro-intensive care treatment, including respiratory support, were given. Within three days, the patient returned to a stable clinical condition with a mildly encephalopathic EEG. In conclusion, bupropion intoxication requires acute intensive care treatment and usually has a good prognosis, however, misinterpretation of the clinical and EEG presentation may lead to errors in management.

GABAergic modulation of diffuse noxious inhibitory controls (DNIC): a test by use of lorazepam.

Diffuse noxious inhibitory controls (DNIC) are an important supra-spinal mechanism of pain inhibition. Neurotransmitters and modulators involved in DNIC are serotonin and endogenous opioids. The influence of substances binding to the GABA(A) receptor complex, which has been suggested to play an important role in descending pain inhibition on DNIC has not yet been investigated. The aim of the present study was to find out whether the inhibitory action of DNIC might also be mediated by GABAergic mechanisms. Therefore, DNIC modulation via GABAergic mechanisms was studied in a double blind, placebo-controlled crossover design by oral application of 0.02 mg/kg(body weight )lorazepam in 20 healthy subjects. DNIC inhibition was induced by heterotopically administered tonic heat. The inhibitory effect was assessed by use of a multiple staircase method, measuring electrocutaneous detection, and pain thresholds in parallel. Concurrent tonic heat stimuli, at both painful and non-painful levels, significantly increased the electrical pain threshold whereas the electrical detection threshold was not affected. This pain-specific inhibitory effect did not differ significantly between sessions with lorazepam and placebo. Accordingly, lorazepam did not modify the inhibitory action of DNIC although lorazepam generally increased heat pain threshold. The results of the present study provided no evidence for DNIC being mediated by activation of the GABA(A) receptor complex.

Encephalomyelitis disseminata: a rare, but challenging differential diagnosis of anorectic disorder.

The frequent occurrence of psychiatric syndromes in encephalomyelitis disseminata is known to obscure its diagnosis. We here report on the case of a 19-year-old female patient presenting symptoms of anorexia nervosa and subsequently diagnosed as suffering from encephalomyelitis disseminata. High dose corticoid treatment resulted in a nearly complete remission of the neurological symptoms as well as the normalization of her eating behaviour. Our case report underscores the importance of considering 'organic' aetiology in patients with symptoms of distinct eating disorders. The clinical course confirms recent findings, suggesting that acute inflammation in encephalomyelitis disseminata may induce behavioural symptoms, which precede the onset of neurological signs. To our knowledge, only one previous case has been reported to date.