psychopharmacotherapy of somatic symptoms disorders

Correspondence: Bettahalasoor Somashekar, Coventry and Warwickshire Partnership NHS trust, Psychiatry, Windmill Point, Windmill Road, Coventry, CV6 7AT, UK. Tel: � 44 2476245860. Fax: � 44 2476245801. E-mail: [email protected]

(Received 11 August 2012 ; accepted 9 September 2012 )

Psychopharmacotherapy of somatic symptoms disorders

BETTAHALASOOR SOMASHEKAR 1 , ASHOK JAINER 1 & BALAJI WUNTAKAL 2

1 Adult Mental Health Services, Coventry and Warwickshire Partnership NHS trust, Coventry, UK, and 2 Older Adults Mental Health Services, Solent NHS Trust, St James Hospital, Langstone Centre, Portsmouth, Hampshire, UK

Abstract Somatic symptoms are often common causes for medical consultation. The treatment of somatic symptoms disorders is complicated by lack of boundary, conceptual clarity, and overemphasis on psychosocial causation and effectiveness of psychological treatments. In clinical practice all classes of psychotropics are used to treat somatic symptoms disorder. Five principal groups of drugs such as tricyclic antidepressants (TCA), serotonin reuptake inhibitors (SSRI), serotonin and noradrenalin reuptake inhibitors (SNRI), atypical antipsychotics and herbal medication are systematically studied. The evidence indicates that all fi ve groups are effective in a wide range of disorders. All classes of antidepressants seem to be effective against somatoform and related disorders. SSRIs are more effective against hypochondriasis and body dysmorphic disorder (BDD), and SNRIs appear to be more effective than other antidepressants when pain is the pre-dominant symptom. Research leaves many unanswered questions regarding dosing, duration of treatment, sustainability of improvement in the long term and differential response to different class drugs. Further studies need to focus on treatments based on clinical features/psychopathology and collaborative research with other specialists in understanding the relation of somatic symptom disorders and functional somatic syndromes (FSS), and comparing psychotropics and non-psychotropics and combinations treatments.

Introduction

Somatic symptoms are common presenting com-plaints to doctors amounting up to one third of contacts within general medical practice. Somatic presentation is also common in other medical specialisms especially in psychiatry, neurology, rheu-matology, cardiology and gastroenterology. They consume signifi cant health resources, they are often subject to disproportionate investigations, and are a cause of disability similar to major psychiatric disor-ders. Overemphasis on psychosocial causation of symptoms further alienates these patients and does not provide adequate support to professionals in treating them. They are a source of distress and dis-satisfaction to patients, a challenge to professionals and are grossly neglected by psychiatry (Bass & Benjamin, 1993, Bass et al., 2001; Chaturvedi et al., 1988; Fink & Rosendal, 2008; Jeffery & Kroenke, 2008; Kroenke, 2003; Kroenke & Mangelsdorff, 1989; Noyes et al., 1995).

The treatment of somatic symptom disorder is multi-modal as none of the methods on their own provide a satisfactory outcome (Kroenke, 2007; Noyes et al., 1995). The article reviews pharmaco-logical aspects of treatment and provides suggestions for future research.

Conceptual issues

Somatic symptoms are commonly understood as physical complaints without demonstrable organic pathology and their severity or duration cannot be explained even when an organic pathology is present. Traditionally somatic symptoms have been presumed to be because of psychological and social causes.

Conceptually they can be grouped into two broad categories.

Somatic symptoms seen in general practice or 1. psychiatric clinics. They receive a diagnosis of somatization disorder, somatoform disorder or its subgroup, hypochondriasis, body dysmor-phic disorder (BDD) and conversion disorders according to current classifi catory systems (DSM-IV, APA, 1994; ICD-10, WHO, 1992). The terminology of these diagnostic categories will change in the forthcoming International Classifi cation of Diseases (ICD-11) and Diag-nostic and Statistical Manual of Mental Disor-ders (DSM-V). All the categories are likely to be subsumed under somatic symptoms disorder and this is the terminology used throughout this article.

International Review of Psychiatry, February 2013; 25(1): 107–115

ISSN 0954–0261 print/ISSN 1369–1627 online © 2013 Institute of PsychiatryDOI: 10.3109/09540261.2012.729758

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108 B. Somashekar et al.

Somatic symptoms seen in functional somatic 2. syndromes. There are about 13 functional somatic syndromes (most common are chronic fatigue syndrome, irritable bowel syndrome, and fi bromyalgia). They are commonly seen in non-psychiatric specialisms and are diagnosed by presence of constellation somatic symptoms. Although there is no defi nite evidence of organic cause, functional somatic syndromes receive legitimate diagnosis and are effectively treated with several interventions including pharmaco-logical and psychological treatments.

The above mentioned categorization is artifi cial as there is signifi cant overlap of somatic symptoms dis-orders and functional somatic syndromes. The same patient may receive several diagnoses depending on the theoretical orientation of doctors, for example irritable bowel syndrome may be diagnosed as gen-eralized anxiety disorder by a psychiatrist and soma-toform disorder as fi bromyalgia in a rheumatology clinic. Functional somatic syndromes cannot be assumed to be independent as it may not be possible to differentiate one from another due to overlap of symptoms (Wessely et al., 1999).

In addition there are patients with somatic symp-toms that neither fulfi ls diagnostic criteria for func-tional somatic syndrome nor a somatic symptoms disorder. Furthermore they are presumed to be due to psychological or understandable life circumstances and may not fi t into a category with a clear indication for drug treatment or psychotherapy. Patients who do not meet the threshold of diagnostic criteria nev-ertheless experience signifi cant, social, emotional and behaviour problems and merit intervention. Therefore the term somatic symptoms should include all functional problems rather than a sub-group who meet operational criteria for a diagnosis.

The focus of this article is on pharmacological intervention for fi rst category of somatic symptoms.

Review of evidence

General considerations

Pharmacological treatment for somatic symptoms disorder has not been subjected to rigorous scien-tifi c scrutiny. The reasons for paucity of quality studies include lack of conceptual clarity, overlap of somatoform disorders and functional somatic syn-drome, overemphasis on psychosocial causation and effectiveness of psychological therapies. There are problems related to feasibility of conducting drug trials due to their high prevalence in general practice rather than in psychiatric specialist clinics.

The evidence comes from systematic reviews, meta-analysis, randomized control trials, open trials

and case series. However, several trials on pharma-cotherapy do not satisfy the diagnostic and other methodological requirements. Only a small number of open label trials and placebo-controlled trials spe-cifi cally examined effi cacy of drugs in somatization and somatoform pain disorders, other somatoform disorders, body dysmorphic disorder and hypochon-driasis. In addition, use of a wide range of pharma-cological agents in clinical practice indicates lack of neurobiological boundaries and conceptual clarity.

A systematic review (Kroenke, 2007) critically evaluated the evidence of treatment for somatoform disorder and identifi ed the paucity of sound research involving pharmacological agents. The review found 31 randomized controlled clinical trials involving 3,922 patients on the treatment of somatoform disorders. The majority of studies examined non-pharmacological intervention and only fi ve studies examined the effi cacy of antidepressants. They include two trials on St John ’ s wort, one each on venlafaxine, opipramol and fl uoxetine.

Barriers to pharmacological treatment

There are a number of professional, patient and healthcare system barriers to pharmacological interventions, and the important factors include the following.

Overemphasis on psychosocial causation despite 1. absence of defi nite evidence. Presumed psycho-social causation can be easily contested and gen-erally rejected by patients. This results in making consultation a battle zone about who is correct as to the cause of the illness. Overemphasis on the benefi ts of psychological 2. treatment despite diffi culty in providing it to all patients. It is not available for general patients in most countries because of cost and limited avail-ability of trained professionals. In addition, drug treatment is seen as a competitor to psychologi-cal treatment rather than as another treatment modality. Lack of conceptual clarity and blurred boundary 3. with functional somatic syndromes. The current classifi catory systems, the ICD-10 and the DSM-IV are unhelpful to physicians in both diagnosis and management of patients presenting with somatic symptoms (Lowe et al., 2008). They at best pro-vide some guidelines and at worst overemphasize psychosocial causation for patient suffering. Clas-sifi catory systems may also pass a moral judgement on a theoretical foundation which is easily contest-able and diffi cult to test. The other ironic factor is that somatic presentations are not specialism-specifi c and present to various specialisms result-ing in poor attention from any specialism.

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Pharmacotherapy, somatic symptoms 109

Unreasonable fear of ‘ medicalization of patient ’ s 4. problems ’ among professionals. Pharmacological treatment is seen as a last desperate measure to help patients rather than as a treatment in its own right. It also appears that among professionals there is a limited inclination to treat, and patients are passed from one specialist to another – a phenomenon of ‘ patient shopping ’ something similar to ‘ doctor shopping ’ among patients. Professionals are overcautious to consider psy-5. chotropics, perhaps due to fear of side effects refl ecting lack of confi dence in the effectiveness of medication in patients with somatic symptom disorder. Patients are hypersensitive to side effects of medi-6. cation due to the nature of illness. They may misinterpret benign side effects of medications as a symptom of illness and symptoms of illness as side effect of medication. This results in inad-equate and inappropriate treatment; in the selec-tion of drug, the dosage used and the duration of treatment. Less importance is given by the healthcare sys-7. tem with consequent limited funding for research on pharmacological interventions.

Benefi ts and rationale of pharmacological treatments

Pharmacotherapy is effective irrespective of the cause in reducing the severity of symptoms and patients suffering. In fact drug treatment is the most common method of intervention in routine clinical practice for somatic symptom disorder despite advocacy for psychological treatment.

A high proportion of patients with somatic symp-tom disorder also have co-morbid anxiety and depressive disorders which are often under detected, inadequately treated, and could contribute to per-sistence of symptoms. Sometimes somatic presen-tation could be an underlying depressive or anxiety disorder itself. Medications are more acceptable to patients as they may feel relieved that there is something wrong and treatment is available.

Pharmacotherapy is cost effective and simple. It can be initiated by any doctor including general practitioners and others specialists familiar with these illnesses and does not always need a referral to a psychiatrist for assessment and to initiate treatment. This results in effective and appropriate use of secondary care resources. Doctors are at ease in prescribing medication rather than focus-ing on fi nding a social or psychological cause for somatic symptoms which is speculative rather than a proof.

Evidence shows that SSRI ’ s and SNRI ’ s act both peripherally and centrally in reducing the perception of pain and other heightened perceptions, a common

presenting symptom in somatic symptom disorder (Lynch, 2001; Sussman, 2003). The common side effects such as somnolence and increased appetite of some of the antidepressants can be a therapeutic advantage as many patients have poor sleep and appetite.

Five principal groups of drugs such as tricyclic antidepressants (TCA), serotonin reuptake inhibi-tors (SSRI), serotonin and noradrenalin reuptake inhibitors (SNRI), antipsychotics and herbal med-ication are the commonly used pharmacological therapies.

Antidepressants

Antidepressants are the most commonly used class of drugs for somatic symptoms disorder. There is merit in using antidepressants for a number of rea-sons: Antidepressants have analgesic property as pain is often a common cause for consultation irrespective of the cause. Somatic symptoms may be a presenta-tion of undiagnosed anxiety and depressive disorder. There is a high prevalence of somatic symptoms in several psychiatric illnesses, particularly depression, which respond to antidepressants. Antidepressants have benefi cial effect on associated symptoms such as anxiety, decreased sleep and appetite even when the criteria for syndromal psychiatric illness are not met. There is evidence that some patients with somatic symptoms have heightened perception to stimuli and antidepressants may have a benefi cial effect by acting through both central and peripheral mechanisms. (Fishbain et al., 1998; Lynch, 2001; Sussman, 2003).

Antidepressants in somatoform and related disorders

Several reviews indicate that medically unexplained symptoms and functional somatic syndromes respond to psychological interventions and antide-pressants. However, fewer studies have focused on somatoform disorders and its subgroups in their own right (Fallon, 2004; Kroenke, 2007; O ’ Malley et al., 1999; Sumathipala, 2007).

The studies have examined newer antidepressants such as SSRIs and SNRIs more often than other classes of antidepressants such as tricyclics, mir-tazapine or other antidepressants.

Open label trails have reported positive outcome with nefazodone and fl uvoxamine. Signifi cant improvement was noted in somatization disorder with nefazodone 300 mg twice a day (bd) (Menza et al., 2001). Although multiple measures were used to detect the outcome, the trial was short term (8 weeks) and with a small number (15 patients). Similarly Fluvoxamine 300 mg per day was found to be effective and well tolerated in an 8 weeks trial

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on 29 patients with somatoform disorders (Noyes et al., 1998).

In placebo-controlled studies, tricyclic opipramol (Volz et al., 2000) SNRI venlafaxine (Han et al., 2008) SSRI escitalopram (Muller et al., 2008) and fl uoxetine (Luo et al., 2009) were superior to placebo in patients with somatization disorder, undifferenti-ated somatoform disorder and multisomatoform dis-orders (patients with three or more somatic symptoms present for more than 2 years).

In a multicentre, randomized 6-week placebo-controlled clinical trial on 200 patients, opipramol 200 mg per day was found to be more effective than placebo as measured by somatic subscore of the Hamilton Anxiety Scale. Opipramol, a tricyclic anti-depressant available in Germany and some European countries and not available in many other countries, acts as a sigma receptor agonist. The duration of the trial was too short to rule out placebo effect.

A 12-week double-blind placebo-controlled trial with 51 patients reported superior effi cacy of 10 – 20 mg escitalopram in patients with multisoma-toform disorder (patients with three or more somatic symptoms present for more than 2 years) compared to placebo (Muller et al., 2008). Signifi cant improve-ment was seen as early as 6 weeks of treatment and patients tolerated it well. After 12 weeks of 10 – 20 mg escitalopram per day, the outcome as measured by Patient Health Questionnaire 15 (score PHQ-15) was signifi cantly lower than placebo. A number of secondary outcome measures indicated improve-ment in response rate and functioning.

Another 8-week double-blind randomized controlled trial of 80 patients who meet ICD-10 diagnostic criteria for persistent somatoform pain disorder reported signifi cantly lower pain measures in the fl uoxetine group compared to placebo (Luo et al., 2009).

A 12-week open label randomized parallel group trial found that venlafaxine and mirtazapine were effective and well tolerated in the treatment of undif-ferentiated somatoform disorder (Han et al., 2008). Out of 95 subjects 71 completed 12 weeks and the outcome was measured by the General Health Ques-tionnaire (GHQ), Patient Health Questionnaire (PHQ-15) and Beck Depression Inventory (BDI).

A meta-analysis of 11 randomized controlled trials examining psychogenic and somatoform pain among 832 patients reported that tricyclic antidepressants decreased pain intensity signifi cantly compared to placebo (Fishbain et al., 1998).

There is some evidence to suggest antidepres-sants with both serotonergic and noradrenergic activity are more effective than SSRIs in somato-form pain disorder and the analgesic effect of anti-depressants may be attributed to interaction with opioid systems and modulation of central inhibitory

pain pathways (Lynch, 2001; Schreiber et al., 2002; Sussman, 2003).

Although tricyclic antidepressants, especially amitriptyline, have been commonly used in clinical practice, it is not systematically evaluated specifi -cally in somatic symptoms disorders.

Antidepressants in hypochondriasis and body dysmorphic disorder (BDD)

Several studies have reported positive results with antidepressants in treatment of hypochondriasis (Fallon et al., 1993, 1996, 2008; Greeven et al., 2007; Magarinos et al., 2002; Pilowsky, 1968; Stone, 1993; Wesner & Noyes, 1991). Fluoxetine was found to be effective in hypochondriasis in a 12-week ran-domized placebo-controlled study (Fallon et al., 1993). Small sample size and high drop-out rate (only 16 of the 25 patients completed the study) limits its clinical utility. Similar fi ndings were reported in a placebo-controlled study with 20 patients, 8 of 12 patients on fl uoxetine responded well compared to 4 of 8 with placebo (Fallon et al., 1996). In another randomized double-blind placebo-controlled study on 45 patients, fl uoxetine showed a better response compared to placebo as measured by clinical global impression (CGI) at 12 weeks. The mean dose of fl uoxetine at 12 weeks was 51.4 � 23 mg. The response was maintained at week 24 among responders independent of severity of psychiatric comorbidity (Fallon, 2008).

A 16-week randomized placebo-controlled trial compared paroxetine, cognitive behaviour therapy (CBT), and placebo in 112 patients with hypochon-driasis. The study found both CBT and paroxetine performed better than placebo and there was no statistically signifi cant difference between the two interventions. The sample had high (about 75%) comorbid depression, anxiety and/or another soma-toform disorder (Greeven et al., 2007).

A 10-week open trial of imipramine in hypochon-driasis, reported improvement in 8 out of 10 patients who completed 4 weeks trial (Wesner & Noyes, 1991).

In a retrospective study on 66 patients with pri-mary hypochondriasis Pilowsky reported positive benefi ts with antidepressants and electro convul-sive therapy (ECT). The study also reported good outcome in patients with short duration of illness and absence of comorbid personality disorder (Pilowsky, 1968).

One review identifi ed several reports of cases with hypochondriasis successfully treated with imip-ramine, clomipramine, fl uoxetine and fl uvoxamine (Magarinos et al., 2002). Several studies have con-sistently shown superior effi cacy of serotonin reuptake inhibitors in patients with BDD, and a Cochrane

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review concluded that fl uoxetine and clomipramine are effective in the treatment of body dysmorphic disorder (Isper et al., 2009; Phillips, 2004; Phillips & Hollander, 2008).

Prospective open label studies have reported ben-efi cial effects of fl uvoxamine (Perugi et al., 1996; Phillips et al., 1998) and citalopram in patients with BDD (Phillips & Najar, 2003). Fluvoxamine at a mean dose of 238.3 � 85.8 mg per day was found to be safe and effective in delusional variant of BDD (delusional disorder somatic type) and the mean time to response was 6.1 � 3.7 weeks as measured by the Yale – Brown Obsessive Compulsive Scale modi-fi ed for BDD (BDD YBOCS). The response rate was 63.3% (19 out of 30 patients responded) (Phillips et al., 1998). In another study fl uvoxamine was effec-tive in 10 out of 12 patients who completed 12 weeks of treatment with fl uvoxamine (Perugi et al., 1996).

Similarly, citalopram was found to be safe and effective at a dose of 51.3 � 16.9 mg per day and the mean time for response was 4.6 � 2.6 weeks with similar measures. The response rate was slightly higher 73.3% (11 out of 15 patients responded) (Phillips & Najar, 2003). The study reported improvement in obsessive preoccupation with perceived body defect, repetitive behaviour and global improvement.

In a 12-week double-blind placebo-controlled study fl uoxetine was more effective than placebo as measured by BDD YBOCS and CGI in both delu-sional and non-delusional BDD. Improvement was noticed at week 8 and a response rate of 53% was attained at week 12 in the fl uoxetine group (n � 34) compared with 18% in the placebo group (n � 33) (Phillips et al., 2002). In another prospective double-blind cross-over trial (n � 29 randomized patients) clomipramine, a serotonin reuptake inhibitor was more effective than the selective noradrenaline reuptake inhibitor desipramine indicating deferential response to serotonin reuptake inhibitor than nora-drenalin reuptake inhibitors (Hollander et al., 1999). The study reported improvement in obsessive preoc-cupation with perceived body defect, repetitive behaviour and global improvement. The response was independent of comorbidity of obsessive – compulsive disorder (OCD), depression, or social phobia and insight. Clomipramine was more effec-tive even in patients with delusional intensity of dysmorphic misconception. Similarly, retrospective studies have reported that serotonin reuptake inhi-bitors are more effective than other medication (Phillips et al., 2001).

There is some evidence to suggest combination of pharmacotherapy with SSRI may be more effective than monotherapy in body dimorphic disorders (Phillips, 2008). In the UK, National Institute for Health and Clinical Excellence (NICE) guidelines emphasize CBT for patients with body dysmorphic

disorder irrespective of severity. It recommends aug-mentation of CBT with antidepressants, preferably SSRI for moderate severity and combination of CBT and SSRI for severe form (NICE, 2005).

Antipsychotics

Literature on the use of antipsychotics in treatment of somatic symptoms disorder is sparse. In a double-blind placebo-controlled cross-over study of 74 patients with somatoform disorders levosulpiride signifi cantly reduced the number of somatoform dis-order symptoms as measured by the Comprehensive International Schedule for Somatoform Disorder – Somatoform Disorder Schedule (CISSD-SDS) com-pared to placebo after 4 weeks of treatment (Altamura et al., 2003). There were no differences in side effects compared to placebo, and the authors concluded that Levosulpiride is a safe and effective drug at dose 50 mg bd for the treatment of somatoform disorders. The limitations of the study are small sample size and short duration as placebo response rate is usually high in short studies.

Although thinking processes rather than mood is the predominant abnormality in hypochondriasis and body dysmorphic disorder, surprisingly limited trials examined effectiveness of antipsychotics in these disorders.

Anticonvulsants

Anticonvulsants are predominantly used in pain con-ditions and limited literature suggests that they may be useful in somatoform disorders. An open label trial of topiramate reported signifi cant improvement in pain in patients with multisomatoform disorder (Garcia-Campayo & Sanz-Carillo, 2002).

Herbal medications

In placebo-controlled studies St John ’ s wort was superior to placebo in patients with somatization disorder, undifferentiated somatoform disorder and multisomatoform disorders (Muller et al., 2004; Volz et al., 2002).

In routine clinical practice, in addition to anti-depressants, antipsychotics, and anticonvulsants, several other agents such as beta-blockers, benzodi-azepines, non-steroidal anti-infl ammatory drugs, opiates and trace elements are used in the treatment of somatic symptoms disorder. To the best of our knowledge there are no studies which systematically evaluated the effectiveness of pharmacotherapy in conversion disorders.

In summary, the evidence indicates that all classes of antidepressants are superior to placebo in most subtypes of somatic symptoms disorders in the short

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term for up to 12 weeks. They improve outcome including symptoms and disability. There is limited evidence regarding deferential benefi ts with specifi c antidepressants. Antidepressants with dual action serotonin and noradrenaline seem more effective than other antidepressants if pain is the main symp-tom, and specifi c serotonin reuptake inhibitors seem to more effective in hypochondriasis and BDD. The dosages of antidepressants appear less than those used in depressive disorder in somatoform and related disorder, and higher than typically used in depression for hypochondriasis and BDD. The min-imum time for improvement is 6 weeks or more and limited evidence suggests that it is sustained for up to 24 weeks. Very limited evidence indicates that atypical antipsychotics may be effective in somato-form disorder and surprisingly no systematically con-ducted trails of antipsychotics on hypochondriasis and BDD.

The studies leave several unanswered questions regarding optimum dose, duration of treatment and long-term outcome. Further research with larger sample sizes and longer duration of treat-ment are required to validate this evidence and also to evaluate whether the improvement is sustained over a long term.

Practical issues

The following factors are important in planning pharmacological treatment for somatic symptom disorder.

Take a pragmatic approach rather than purist – 1. provide symptomatic treatment until a defi nite aetiology and intervention are identifi ed; it is nei-ther an inferior nor ineffective approach as long as the patient ’ s suffering is reduced. Prepare patients well before initiation of medica-2. tion by explaining the rationale, expected out-come and common side effects. Focus on care rather than cause or cure. 3. Aim at improving quality of life. 4. Focus on relief, coping and return to function. 5. Give adequate trail for at least 12 weeks before 6. declaring any drug as ineffective and explain patient to expect improvement over several weeks or months. Emphasize that different treatments are not 7. mutually exclusive and both may be required as they may act synergistically. Psychological treat-ments are not a substitute for pharmacological treatment as highlighted above, and different treatments are complementary not competitive. Start low in dosage and titrate gradually over 8. weeks rather than days as patients are usually sensitive to side effects because of the nature of

the illness. Compliance can be an issue if the medication is titrated upwards too quickly.

Take home messages

Somatic symptoms disorders are common presenta-tions across primary and secondary care, presenting to various specialists attracting varied diagnosis. Under-recognition and under-treatment are com-mon, often as a result of unclear nosological and conceptual clarity. Evidence for pharmacological treatment is overwhelming for antidepressant medi-cation, with the choice determined by specifi c symp-tom profi le and tolerability. Treatments should be symptomatic with emphasis on reliving suffering whilst simultaneously trying to fi nd causes, rather than overemphasizing psychosocial causation and undue focus on CBT.Future directions.

Studies have established an association of psycho-social factors with somatic symptoms disorder. How-ever, it is diffi cult to delineate whether they are causes or consequences, and pathogenicity of psychosocial factors is yet to be determined in somatic symptoms disorders. Terms such as multifactorial causation and cognitive behaviour therapy seem to have become the new answer to all problems faced by psychiatry in the last two decades. Overemphasis on psychosocial causation has done more harm to this group of patients and decreased the opportunity for further understanding and investigations into the pharmaco-logical treatments. In addition, overemphasis on CBT alone has undervalued the importance of other forms of psychological treatment.

Psychiatry can learn from other branches of medicine which legitimately diagnose functional somatic syndromes and all forms of treatment such as psychotropics, non-psychotropics and non-pharmacological interventions are used by these specialisms. Unfortunately this does not happen in psychiatry, and pharmacotherapy is underutilized or even discouraged.

Research seems to have tried all classes of psycho-tropics as a desperate measure to fi nd an effective treatment, resulting in lack of specifi city. The selection of a drug or a particular class of drugs in trials is not based on clear rationale, especially in somatoform and related disorders. It is neither based on the psychopa-thology nor symptom. In addition, measurement of response varied with trials, leaving doubts about which aspect of illness improves with which medications. Unfortunately this does not guide clinicians in select-ing the right drug for a given patient.

Future research requires fi lling these gaps to enhance utility of pharmacological trials in management of somatic symptoms disorder. This can be done by two ways, fi rstly by targeting pharmacological agents based on psychopathology,

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and secondly, collaborative research with non-psychiatric medical specialists.

The fi rst aspect can be approached by adopting illness paradigm and categorizing patients ’ presenta-tion into predominant illness beliefs and predomi-nant illness experience.

Patients with predominant illness beliefs, phenom-enologically have psychopathology ranging from excessive worry and preoccupation, obsessive ideas, overvalued ideas to delusions. Patients with excessive worry and preoccupation may benefi t from anxiolyt-ics and/or antidepressants and SSRIs can be a target for obsessive ideas. Antipsychotics can be targets for overvalued ideas or delusions seen in body dysmor-phic disorder and hypochondriacal disorder.

Similarly, patients with predominant illness experi-ence present with symptoms of autonomic arousal, pain, fatigue, for example. They can be targeted with pharmacological agents ranging from anxiolytics, antidepressants to antipsychotics, NSAIDS, opiates, beta blockers, for example.

This atheoretical approach focuses on the ‘ form ’ of psychopathology and may help in refi ning selec-tion of the appropriate drug for a specifi c constella-tion of symptoms and increase effi cacy of a drug.

The second area is a collaborative approach with other branches of medicine which deal with func-tional somatic syndromes. There is a considerable overlap of symptomatology between somatic symp-toms disorders particularly somatoform disorders and functional somatic syndromes. It may not be possible to differentiate them as separate disorders and perhaps we may be dealing with the same condi-tion, as some patients receive a different diagnosis based on their physician ’ s theoretical orientation. These issues raise an important question of which specialism should take care of somatic symptoms disorders. A paradigm shift is required in conceptu-alization and management of somatic symptoms disorders if it has to remain within the domain of psychiatry. There is urgent need to explore interventions beyond psychological interventions to retain responsibility for this group of patients. Further research comparing psychotropics and non-psychotropics (for example antidepressants and pain medication) and combination treatments such as psychotropics and non-psychotropics with drugs and psychological treatments will help more effective use of medication.

Future directions

Clarity is required with regard to ‘ nosology ’ of somatic symptoms disorders and their relation with functional somatic syndromes. Choice of medica-tions remains a ‘ clinical dilemma ’ being guided by symptom profi le, rather than neurobiological

causation. Longer duration of trials with larger sample sizes, comparing psychotropics and non psychotropics with psychological interventions are necessary to guide clinicians. Psychiatry can learn from other medical specialists about recognizing and treating these often distressing disorders with unknown cause.

Conclusion

Pharmacological treatment of somatic symptom dis-orders has not been subjected to rigorous scientifi c scrutiny due to lack of boundary, conceptual clarity and overlap with functional somatic syndromes. Evidence from systematically conducted placebo-controlled trials indicates that all groups of psycho-tropics are effective in the short term. All classes of antidepressants appear to be effective in somatoform and related group of disorders, and SSRIs are more effective against hypochondriasis and BDD than other antidepressants. SNRIs appear better than other antidepressants when pain is the predominant symptom. However, the evidence does not provide confi dence to clinicians due to lack of specifi city in selection of drugs and long term benefi ts. Further research is needed on dosage, sustainability of improvement in the long term and differential drug selection. It is also necessary to understand the relation between somatic symptoms disorder and functional somatic syndrome. Further research com-paring psychotropics versus non psychotropics and combinations treatment are needed.

Acknowledgements

We thank Dr Seshadri Dhadesugur, Mersey Deanery, for his valuable comments and Linda Cunningham, Coventry and Warwickshire Partner-ship NHS Trust, for her secretarial support in the preparation of this manuscript.

Declaration of interest: The authors report no confl icts of interest. The authors alone are respon-sible for the content and writing of the paper.

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psychopharmacotherapy of somatic symptoms disorders

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