Abstract
The central notion of somatoform disorders (SFDs) are the presence of physical symptoms that are ‘medically unexplained’ or ‘disproportionate’ to the severity of an underlying medical disorder, thereby giving rise to the belief that psychological therapy rather than pharmacotherapy be considered as first line management [1]. However, pharmaceutical agents such as Tricyclic antidepressants (TCAs), Selective Serotonin Reuptake Inhibitors (SSRIs) and recently substituted benzamides have been used selectively for the treatment of a variety of SFDs [2]. We report three patients with various presentations of SFDs where the use of low dose amisulpride, another substituted benzamide, proved beneficial.
The first patient was a 45 year old businessman, referred to us with unremitting and changing nature of predominantly gastro-intestinal complaints including belching, feeling of bloating, nausea, vomiting and an irregular defecation pattern. He had been seen by several physicians including gastroenterologists; had been investigated thoroughly and had not responded to both SSRIs and TCAs. Diagnosed as somatization disorder, psychotherapy was offered but he refused citing time concerns. He showed poor response to an initial trial of duloxetine, was offered amisulpride on an empirical basis and he improved significantly with a dosage of 100 mg.
The second was a 36 year old married woman, referred to us with complaints of persistent pain and tingling sensation in the neck region for the past one year. She denied any personal and occupational stressors. Adequately investigated with MRI and other biochemical and haematological investigations which revealed no abnormalities, she was diagnosed as having somatoform pain disorder which did not respond to an adequate trial of escitalopram and amitriptyline. Amisulpride was offered following the success of the earlier patient and she reported up to 80% improvement with a dosage of 100 mg.
The third was a 24 year old single teacher, with several occupational stressors, who was referred to us due to persistent upper GI symptoms in spite of extensive investigations having ruled out any organic pathology. She received a diagnosis of undifferentiated somatoform disorder which had not responded to trials of several antidepressants of different classes and intense psychotherapy over a period of 6 months. Failing a trial of paroxetine, she was then tried on amisulpride and reported 75% improvement in symptoms at 100 mg.
Current assumptions about SFDs are that central nervous system processes modulate signals from the periphery and this central modulation of peripheral input underlies the conscious experience of physical symptoms [3]. In all the three cases, brain regions such as the right anterior insula, anterior cingulate, orbitofrontal cortex and surrounding areas are perhaps involved, which ‘perceive’ sensations from peripheral sense organs to give a heightened subjective awareness of the condition of the body [4]. A relative hypo-dopaminergic state in the prefrontal and frontal regions is also proposed [5]. The use of amisulpride is beneficial since at low doses it preferentially blocks presynaptic dopamine autoreceptors that control dopamine synthesis and release [5]. Low dose use leads to increased dopaminergic transmission in several cortical areas such as the striatum, prefrontal and frontal lobes thereby helping to correct the hypodopaminergic state. In addition, it also increases frontal blood flow leading to improved frontal cognitive functions [6]. Furthermore, recent studies point to a 5-HT7 receptor antagonist activity in addition to its effects on dopaminergic receptors as a possible substrate for amisulpride action [7]. Amisulpride activity at these receptors positively affects sleep quality and cognition [7] thus possibly contributing to its efficacy in these patients.