Pain perception and hypnosis: findings from recent functional neuroimaging studies.

Hypnosis modulates pain perception and tolerance by affecting cortical and subcortical activity in brain regions involved in these processes. By reviewing functional neuroimaging studies focusing on pain perception under hypnosis, the authors aimed to identify brain activation-deactivation patterns occurring in hypnosis-modulated pain conditions. Different changes in brain functionality occurred throughout all components of the pain network and other brain areas. The anterior cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis. Most studies also showed that the neural functions of the prefrontal, insular, and somatosensory cortices are consistently modified during hypnosis-modulated pain conditions. Functional neuroimaging studies support the clinical use of hypnosis in the management of pain conditions.

[Functional neuroimaging of the amygdala: the response to threatening and phobogenic stimuli]. / Neuroimaging funzionale dell'amigdala: la risposta a eventi minacciosi o fobigeni.

Recent functional neuroimaging studies show that the amygdala has a central role in threat evaluation, in response to conditioned and unconditioned stimuli, in fear learning and fear extinction. The amygdala is involved in the pathophysiology of phobias and anxiety. In this review we critically examine the main findings of functional neuroimaging studies reporting data on the amygdala. Findings suggest that the response of the amygdala to threatening stimuli is mainly modulated by the infralimbic and prefrontal cortices, which inhibit activation of the amygdala (top-down inhibition), and by the hippocampus, the function of which is related to stimulus learning. The activity of the amygdala is modulated by various factors, like stimulus type and origin, emotion triggered by stimulus perception, and attention. The neural network comprising the amygdala and the frontal cortex is involved not only in top-down inhibition, but also in the emotional perception of facial expressions. This network also includes the thalamic pulvinar, which is densely interconnected with the amygdala, directly or indirectly, and which is activated by emotional face recognition of scary fear. Both top-down inhibition mechanisms and emotional face recognition are altered in anxiety disorders, particularly in specific and social phobia, resulting in reduced amygdalar activity inhibition after anxiety - or fear - inducing stimulus perception. Future functional neuroimaging studies will be able to provide new insights of normal and altered neurophysiology of the amygdala.

Deep transcranial magnetic stimulation for treatment-resistant bipolar depression: a case report of acute and maintenance efficacy.

Deep Transcranial Magnetic Stimulation (dTMS) is currently being evaluated as a possible treatment for several neuropsychiatric disorders and has been demonstrated as a safe and effective procedure. This case presents a patient with bipolar depression that has been treated with 20 daily consecutive dTMS sessions and with one dTMS session every 2 weeks for the following 3 months. Depressive symptoms improved rapidly and response was maintained during the next 6 months; cognitive performances also improved. This report suggests that add-on dTMS may help overcoming drug-resistance in bipolar depression and protect from subsequent bipolar episodes of any polarity.

A case of resolution of an acute psychotic episode after high fever.

Fever (pyretotherapy) was used for psychosis during the turn of the 19th century, but pyretotherapy (ie, the treatment of a disorder by inducing fever) fell out of use after the introduction of convulsive methods. Here, we report on a case of schizoaffective disorder and review classical and recent literature on fever and psychosis. The patient developed auditory hallucinations, persecutory delusional ideas, and was terrified soon upon his arrival in a foreign country. After being treated for 12 days with olanzapine and haloperidol, he developed a fever due to urinary infection; his creatine phosphokinase levels were high, prompting the suspension of antipsychotics. Psychotic symptom resolution followed immediately fever abatement. Antipsychotics were reintroduced at lower dosages. He was discharged asymptomatic with a prescription of olanzapine 15 mg/day and haloperidol 3 mg/day. The time course of symptom resolution in this patient suggests that fever had a beneficial role in this case. The associations between body temperature changes and psychotic symptoms need to be further studied.