Psychiatry and Clinical Neurosciences 2015; 69: 122–127
Letters to the Editor 125
(SGB) characterized by numerous belches/min. In SGB, air is either sucked or pushed into the upper esophagus by decreased intrathoracic pressure or contraction of pharyngeal muscles during closure of the glottis. The subsequent air expulsion results in a burping sound.1 Important differential diagnoses are persistent hiccups (singultus), aerophagia, dyskinesia as well as tics. We report the case of a 55-year-old man who presented with a 2-year history of therapy-refractory SGB with up to 25 belches/ min. He denied premonitory sensations and was unable to voluntarily suppress belching. Numerous medications, including gabapentin 2400 mg/day, tetrabenazine 150 mg/day, trihexyphenidyl hydrochloride 15 mg/day, tiapride hydrochloride 600 mg/day, valproate 1800 mg/day, carbamazepine 1200 mg/day and baclofen 30 mg/day, had not resulted in meaningful improvement. He had been on 40 mg pantoprazole for reflux esophagitis and recurrent gastric ulcers for at least 10 years without a marked effect on his belching. Esophageal impedance manometry demonstrated excessive SGB, but yielded no evidence for hiccups or respiratory dyskinesia. Cranial magnetic resonance imaging and thoracoabdominal computed tomography were without note. Gastroscopy demonstrated moderate erosive esophagitis. There is little evidence to guide the management of SGB. Biofeedback and behavioral therapy may be beneficial. However, these procedures are complex and few therapists have experience in this specific area.2 Here, combined treatment of 10 mg baclofen t.i.d. and 100 mg pregabalin t.i.d. resulted in sustained reduction of the rate of belching to less than 10% of the pretreatment value. The patient reported initial mild sedation, which resolved during the second week of treatment. We speculate that the combination of baclofen and pregabalin exerts synergistic effects by reducing both increased mechanosensitivity and chemosensitivity of the esophagogastric junction associated with SGB. Blondeau and co-workers showed a correlation between increased lower esophageal sphincter pressure under baclofen therapy and a reduction in belching events.2 Experimentally, baclofen inhibits mechanosensitivity of vagal afferents peripherally. However, baclofen does not affect chemosensitivity.3 Recently, a small placebo-controlled study showed that pregabalin attenuates the development of hypersensitivity in the proximal esophagus after distal esophageal acidification.4 In conclusion, clinicians should be aware of the disease entity of SGB. Further studies will have to establish an evidence-based approach to the management of these patients.
oesophageal hypersensitivity in healthy volunteers – a placebocontrolled study. Aliment Pharmacol. Ther. 2012; 35: 319–326.
REFERENCES 1. Bredenoord AJ, Weusten BL, Timmer R, Smout AJ. Psychological factors affect the frequency of belching in patients with aerophagia. Am. J. Gastroenterol. 2006; 101: 2777–2781. 2. Blondeau K, Boecxstaens V, Rommel N et al. Baclofen improves symptoms and reduces postprandial flow events in patients with rumination and supragastric belching. Clin. Gastroenterol. Hepatol. 2012; 10: 379–384. 3. Partosoedarso ER, Young RL, Blackshaw LA. GABA(B) receptors on vagal afferent pathways: Peripheral and central inhibition. Am. J. Physiol. Gastrointest. Liver Physiol. 2001; 280: G658–G668. 4. Chua YC, Ng KS, Sharma A et al. Randomised clinical trial: Pregabalin attenuates the development of acid-induced
Hagen Kunte, MD,1 Golo Kronenberg, MD,1 Katharina Fink, MD,3 Lutz Harms, MD2 and Rainer Hellweg, MD1 1 Departments of Psychiatry and Psychotherapy and 2Neurology, Charité-Universitätsmedizin Berlin, Berlin, Germany, and 3 Department of Neurology, Karolinska University Hospital, Stockholm, Sweden Email: [email protected] Received 14 March 2014; revised 13 June 2014; accepted 14 July 2014.
Psychosomatic consideration to the burning mouth syndrome doi:10.1111/pcn.12229
B
URNING MOUTH SYNDROME (BMS) represents a clinical condition of burning pain over the tongue and/or lips without abnormalities in the oral cavity examination. BMS can involve the whole oral cavity with the distress being described as ‘discomfort’, ‘tender’, ‘annoying’ or ‘burning pain’ accompanied with dryness, oral paresthesia and altered taste. Variety in the affected region and sensation make the terms diverse in the published work, including: glossodynia, glossopyrosis, and oral dysesthesia.1 Here, we report one case to highlight clinical wisdom. A 62-year-old woman visited the psychiatric clinic for insomnia. She was robust until 6 months ago, when she suffered from burning mouth pain. She had visited different professionals, including the dentist, the neurologist, the oral pathologist, and the ear–nose–throat doctors. All the examinations, including oral pathology, were normal but the pain persisted. She was then recommended to visit a psychiatrist. In the mental status examination, dysthymic mood, decreased interest and poor appetite were noted. Further interview presented her severe anxiety about salivary gland tumor – a hypochondriacal idea. Considering the symptoms, low-dose antipsychotics (quetiapine 12.5 mg/day) and antidepressants (duloxetine 30 mg/day) were prescribed. Three months later, her depression and sleep improved. Also, the hypochondriacal ideation and the anxiety were relieved partially. Although the burning mouth sensation did not disappear, her quality of life enhanced remarkably. With no conclusively identified cause, BMS predominantly affects women with increasing prevalence with age and following menopause.2 Besides the oral discomfort, psychiatric comorbidity is another focus worth noticing. Studies had reported BMS to have anxiety, depression and increased tendency for somatization as well as several other psychiatric features when measured by the Symptom Checklist-90 questionnaire.3 Evidence suggested that BMS is often chronic, with only 50% of patients spontaneously remitting within 6–7 years.4 Thus, BMS may exacerbate one’s long-term quality of life, making the treatment important. A recent Cochrane review had categorized the management into six types: antidepressants, cognitive behavioral therapy,
© 2014 The Authors Psychiatry and Clinical Neurosciences © 2014 Japanese Society of Psychiatry and Neurology
126 Letters to the Editor
Psychiatry and Clinical Neurosciences 2015; 69: 122–127
analgesics, hormone therapy, anticonvulsants and α-lipoic acid.5 Considering the high incidence of psychiatric features, it seemed that the psychiatric interventions for BMS were underestimated with only few randomized control trials focusing on treating BMS with psychotropic agents. In our opinion, BMS may include the disturbance of both the physiological and psychological systems. Anxiety, depression, pain disorder, hypochondriasis as well as delusional disorder should be considered for BMS. Thus, when clinicians see BMS patients, besides arranging a detailed physical examination, the psychological aspects should also be considered and psychiatric consultation may be needed. In this way, there will be a more comprehensive consideration for BMS.
easily and quickly evaluate overall function using a single continuous value with anchor points, and they are widely used in both clinical and research settings.1 These scales, however, are subject to variability and can be influenced by the rater’s level of education and experience and training with the scale, as well as the quality and quantity of the patient’s clinical information. Thus, the modified GAF (mGAF-original) scale was developed to improve the reliability and validity of the original GAF scale.2 We obtained the author’s permission to translate the mGAF-original scale into Japanese and to make new scales using the items and anchor points in it. Subsequently, we developed the Japanese version of the mGAF-original scale as well as the psychological symptom (mGAF-S) and social functioning (mGAF-F) subscales by splitting the items and anchor points of the mGAF-original scale. We used the lower value of the mGAF-S and mGAF-F scores for the mGAF score in accordance with instructions of the original GAF evaluation.1 We tested inter-rater reliability and concurrent validity for the new subscales. Developed scales, and detailed methods and results are shown in Supporting information. To test inter-rater reliability, five professionals administered the original and modified GAF scales to five patients with schizophrenia. To test concurrent validity, 10 professionals administered the original and modified GAF scales, and the Positive and Negative Syndrome Scale (PANSS) to 31 patients with schizophrenia. Participants gave written informed consent. The intra-class correlation coefficients (ICC) of the mGAForiginal, mGAF-S, mGAF-F, and mGAF scales were 0.94, 0.8, 0.96, and 0.96, respectively. The mGAF-original score was significantly correlated with the GAF score (r = 0.91, P < 0.001), and the mGAF score was significantly correlated with the GAF and mGAF-original scores (mGAF and GAF: r = 0.89, P < 0.001; mGAF and mGAF-original: r = 0.97, P < 0.001). The mGAF-S score was significantly correlated with the PANSS positive (r = −0.54, P = 0.002), negative (r = −0.50, P = 0.004), general psychopathology (r = −0.59, P < 0.001), and total scores (r = −0.61, P < 0.001). The mGAF-F score significantly correlated with the SOFAS score (r = 0.88, P < 0.001). Our study showed excellent inter-rater reliability and concurrent validity of the Japanese versions of the mGAForiginal, mGAF-S, mGAF-F, and mGAF scales. These modified versions of the GAF scale may be easier and more appropriate when separately evaluating current psychological symptoms and social functioning than the original GAF and SOFAS scales. The Japanese version of the mGAF-original, mGAF-S, mGAF-F, and mGAF scales are available within research settings for Japanese participants, and readers can contact the corresponding author (http://npsy.umin.jp/indicator.html) if they would like to use them.
There are no potential conflicts of interest and no financial support, including drug stores, for any authors. There is also no grant support for this report. At the same time, we have no special circumstances, vested interests, or sources of funding to disclose.
REFERENCES 1. Bergdahl J, Anneroth G. Burning mouth syndrome: Literature review and model for research and management. J. Oral Pathol. Med. 1993; 22: 433–438. 2. Basker RM, Sturdee DW, Davenport JC. Patients with burning mouths. A clinical investigation of causative factors, including the climacteric and diabetes. Br. Dent. J. 1978; 145: 9–16. 3. Eli I, Baht R, Littner MM, Kleinhauz M. Detection of psychopathologic trends in glossodynia patients. Psychosom. Med. 1994; 56: 389–394. 4. Grushka M, Sessle BJ. Burning mouth syndrome. Dent. Clin. North Am. 1991; 35: 171–184. 5. Zakrzewska JM, Forssell H, Glenny AM. Interventions for the treatment of burning mouth syndrome. Cochrane Database Syst. Rev. 2005; (1): CD002779.
Liang-Yu Chen, MD2 and Hsin-Chien Lee, MD, MPH3 1 Department of Psychiatry, Shuang-Ho Hospital, Taipei Medical University, New Taipei City, 2Center for Geriatrics and Gerontology, Taipei Veterans General Hospital, and 3Department of Psychiatry, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan Email: [email protected] Received 18 April 2014; revised 25 June 2014; accepted 25 July 2014. Yao-Tung Lee,
MD,1
Psychological symptom and social functioning subscales of the modified Global Assessment of Functioning scale: Reliability and validity of the Japanese version doi:10.1111/pcn.12250
T
HE GLOBAL ASSESSMENT of Functioning (GAF) scale and the Social and Occupational Functioning Scale (SOFAS)
REFERENCES 1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4rd edn. Text Revised. American Psychiatric Association, Washington, DC, 1994. 2. Hall RC. Global assessment of functioning. A modified scale. Psychosomatics 1995; 36: 267–275.
© 2014 The Authors Psychiatry and Clinical Neurosciences © 2014 Japanese Society of Psychiatry and Neurology
Letters to the Editor 125
(SGB) characterized by numerous belches/min. In SGB, air is either sucked or pushed into the upper esophagus by decreased intrathoracic pressure or contraction of pharyngeal muscles during closure of the glottis. The subsequent air expulsion results in a burping sound.1 Important differential diagnoses are persistent hiccups (singultus), aerophagia, dyskinesia as well as tics. We report the case of a 55-year-old man who presented with a 2-year history of therapy-refractory SGB with up to 25 belches/ min. He denied premonitory sensations and was unable to voluntarily suppress belching. Numerous medications, including gabapentin 2400 mg/day, tetrabenazine 150 mg/day, trihexyphenidyl hydrochloride 15 mg/day, tiapride hydrochloride 600 mg/day, valproate 1800 mg/day, carbamazepine 1200 mg/day and baclofen 30 mg/day, had not resulted in meaningful improvement. He had been on 40 mg pantoprazole for reflux esophagitis and recurrent gastric ulcers for at least 10 years without a marked effect on his belching. Esophageal impedance manometry demonstrated excessive SGB, but yielded no evidence for hiccups or respiratory dyskinesia. Cranial magnetic resonance imaging and thoracoabdominal computed tomography were without note. Gastroscopy demonstrated moderate erosive esophagitis. There is little evidence to guide the management of SGB. Biofeedback and behavioral therapy may be beneficial. However, these procedures are complex and few therapists have experience in this specific area.2 Here, combined treatment of 10 mg baclofen t.i.d. and 100 mg pregabalin t.i.d. resulted in sustained reduction of the rate of belching to less than 10% of the pretreatment value. The patient reported initial mild sedation, which resolved during the second week of treatment. We speculate that the combination of baclofen and pregabalin exerts synergistic effects by reducing both increased mechanosensitivity and chemosensitivity of the esophagogastric junction associated with SGB. Blondeau and co-workers showed a correlation between increased lower esophageal sphincter pressure under baclofen therapy and a reduction in belching events.2 Experimentally, baclofen inhibits mechanosensitivity of vagal afferents peripherally. However, baclofen does not affect chemosensitivity.3 Recently, a small placebo-controlled study showed that pregabalin attenuates the development of hypersensitivity in the proximal esophagus after distal esophageal acidification.4 In conclusion, clinicians should be aware of the disease entity of SGB. Further studies will have to establish an evidence-based approach to the management of these patients.
oesophageal hypersensitivity in healthy volunteers – a placebocontrolled study. Aliment Pharmacol. Ther. 2012; 35: 319–326.
REFERENCES 1. Bredenoord AJ, Weusten BL, Timmer R, Smout AJ. Psychological factors affect the frequency of belching in patients with aerophagia. Am. J. Gastroenterol. 2006; 101: 2777–2781. 2. Blondeau K, Boecxstaens V, Rommel N et al. Baclofen improves symptoms and reduces postprandial flow events in patients with rumination and supragastric belching. Clin. Gastroenterol. Hepatol. 2012; 10: 379–384. 3. Partosoedarso ER, Young RL, Blackshaw LA. GABA(B) receptors on vagal afferent pathways: Peripheral and central inhibition. Am. J. Physiol. Gastrointest. Liver Physiol. 2001; 280: G658–G668. 4. Chua YC, Ng KS, Sharma A et al. Randomised clinical trial: Pregabalin attenuates the development of acid-induced
Hagen Kunte, MD,1 Golo Kronenberg, MD,1 Katharina Fink, MD,3 Lutz Harms, MD2 and Rainer Hellweg, MD1 1 Departments of Psychiatry and Psychotherapy and 2Neurology, Charité-Universitätsmedizin Berlin, Berlin, Germany, and 3 Department of Neurology, Karolinska University Hospital, Stockholm, Sweden Email: [email protected] Received 14 March 2014; revised 13 June 2014; accepted 14 July 2014.
Psychosomatic consideration to the burning mouth syndrome doi:10.1111/pcn.12229
B
URNING MOUTH SYNDROME (BMS) represents a clinical condition of burning pain over the tongue and/or lips without abnormalities in the oral cavity examination. BMS can involve the whole oral cavity with the distress being described as ‘discomfort’, ‘tender’, ‘annoying’ or ‘burning pain’ accompanied with dryness, oral paresthesia and altered taste. Variety in the affected region and sensation make the terms diverse in the published work, including: glossodynia, glossopyrosis, and oral dysesthesia.1 Here, we report one case to highlight clinical wisdom. A 62-year-old woman visited the psychiatric clinic for insomnia. She was robust until 6 months ago, when she suffered from burning mouth pain. She had visited different professionals, including the dentist, the neurologist, the oral pathologist, and the ear–nose–throat doctors. All the examinations, including oral pathology, were normal but the pain persisted. She was then recommended to visit a psychiatrist. In the mental status examination, dysthymic mood, decreased interest and poor appetite were noted. Further interview presented her severe anxiety about salivary gland tumor – a hypochondriacal idea. Considering the symptoms, low-dose antipsychotics (quetiapine 12.5 mg/day) and antidepressants (duloxetine 30 mg/day) were prescribed. Three months later, her depression and sleep improved. Also, the hypochondriacal ideation and the anxiety were relieved partially. Although the burning mouth sensation did not disappear, her quality of life enhanced remarkably. With no conclusively identified cause, BMS predominantly affects women with increasing prevalence with age and following menopause.2 Besides the oral discomfort, psychiatric comorbidity is another focus worth noticing. Studies had reported BMS to have anxiety, depression and increased tendency for somatization as well as several other psychiatric features when measured by the Symptom Checklist-90 questionnaire.3 Evidence suggested that BMS is often chronic, with only 50% of patients spontaneously remitting within 6–7 years.4 Thus, BMS may exacerbate one’s long-term quality of life, making the treatment important. A recent Cochrane review had categorized the management into six types: antidepressants, cognitive behavioral therapy,
© 2014 The Authors Psychiatry and Clinical Neurosciences © 2014 Japanese Society of Psychiatry and Neurology
126 Letters to the Editor
Psychiatry and Clinical Neurosciences 2015; 69: 122–127
analgesics, hormone therapy, anticonvulsants and α-lipoic acid.5 Considering the high incidence of psychiatric features, it seemed that the psychiatric interventions for BMS were underestimated with only few randomized control trials focusing on treating BMS with psychotropic agents. In our opinion, BMS may include the disturbance of both the physiological and psychological systems. Anxiety, depression, pain disorder, hypochondriasis as well as delusional disorder should be considered for BMS. Thus, when clinicians see BMS patients, besides arranging a detailed physical examination, the psychological aspects should also be considered and psychiatric consultation may be needed. In this way, there will be a more comprehensive consideration for BMS.
easily and quickly evaluate overall function using a single continuous value with anchor points, and they are widely used in both clinical and research settings.1 These scales, however, are subject to variability and can be influenced by the rater’s level of education and experience and training with the scale, as well as the quality and quantity of the patient’s clinical information. Thus, the modified GAF (mGAF-original) scale was developed to improve the reliability and validity of the original GAF scale.2 We obtained the author’s permission to translate the mGAF-original scale into Japanese and to make new scales using the items and anchor points in it. Subsequently, we developed the Japanese version of the mGAF-original scale as well as the psychological symptom (mGAF-S) and social functioning (mGAF-F) subscales by splitting the items and anchor points of the mGAF-original scale. We used the lower value of the mGAF-S and mGAF-F scores for the mGAF score in accordance with instructions of the original GAF evaluation.1 We tested inter-rater reliability and concurrent validity for the new subscales. Developed scales, and detailed methods and results are shown in Supporting information. To test inter-rater reliability, five professionals administered the original and modified GAF scales to five patients with schizophrenia. To test concurrent validity, 10 professionals administered the original and modified GAF scales, and the Positive and Negative Syndrome Scale (PANSS) to 31 patients with schizophrenia. Participants gave written informed consent. The intra-class correlation coefficients (ICC) of the mGAForiginal, mGAF-S, mGAF-F, and mGAF scales were 0.94, 0.8, 0.96, and 0.96, respectively. The mGAF-original score was significantly correlated with the GAF score (r = 0.91, P < 0.001), and the mGAF score was significantly correlated with the GAF and mGAF-original scores (mGAF and GAF: r = 0.89, P < 0.001; mGAF and mGAF-original: r = 0.97, P < 0.001). The mGAF-S score was significantly correlated with the PANSS positive (r = −0.54, P = 0.002), negative (r = −0.50, P = 0.004), general psychopathology (r = −0.59, P < 0.001), and total scores (r = −0.61, P < 0.001). The mGAF-F score significantly correlated with the SOFAS score (r = 0.88, P < 0.001). Our study showed excellent inter-rater reliability and concurrent validity of the Japanese versions of the mGAForiginal, mGAF-S, mGAF-F, and mGAF scales. These modified versions of the GAF scale may be easier and more appropriate when separately evaluating current psychological symptoms and social functioning than the original GAF and SOFAS scales. The Japanese version of the mGAF-original, mGAF-S, mGAF-F, and mGAF scales are available within research settings for Japanese participants, and readers can contact the corresponding author (http://npsy.umin.jp/indicator.html) if they would like to use them.
There are no potential conflicts of interest and no financial support, including drug stores, for any authors. There is also no grant support for this report. At the same time, we have no special circumstances, vested interests, or sources of funding to disclose.
REFERENCES 1. Bergdahl J, Anneroth G. Burning mouth syndrome: Literature review and model for research and management. J. Oral Pathol. Med. 1993; 22: 433–438. 2. Basker RM, Sturdee DW, Davenport JC. Patients with burning mouths. A clinical investigation of causative factors, including the climacteric and diabetes. Br. Dent. J. 1978; 145: 9–16. 3. Eli I, Baht R, Littner MM, Kleinhauz M. Detection of psychopathologic trends in glossodynia patients. Psychosom. Med. 1994; 56: 389–394. 4. Grushka M, Sessle BJ. Burning mouth syndrome. Dent. Clin. North Am. 1991; 35: 171–184. 5. Zakrzewska JM, Forssell H, Glenny AM. Interventions for the treatment of burning mouth syndrome. Cochrane Database Syst. Rev. 2005; (1): CD002779.
Liang-Yu Chen, MD2 and Hsin-Chien Lee, MD, MPH3 1 Department of Psychiatry, Shuang-Ho Hospital, Taipei Medical University, New Taipei City, 2Center for Geriatrics and Gerontology, Taipei Veterans General Hospital, and 3Department of Psychiatry, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan Email: [email protected] Received 18 April 2014; revised 25 June 2014; accepted 25 July 2014. Yao-Tung Lee,
MD,1
Psychological symptom and social functioning subscales of the modified Global Assessment of Functioning scale: Reliability and validity of the Japanese version doi:10.1111/pcn.12250
T
HE GLOBAL ASSESSMENT of Functioning (GAF) scale and the Social and Occupational Functioning Scale (SOFAS)
REFERENCES 1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4rd edn. Text Revised. American Psychiatric Association, Washington, DC, 1994. 2. Hall RC. Global assessment of functioning. A modified scale. Psychosomatics 1995; 36: 267–275.
© 2014 The Authors Psychiatry and Clinical Neurosciences © 2014 Japanese Society of Psychiatry and Neurology
