Poster Abstracts

Poster 1

AN EVALUATION OF A STANDARDIZED ART THERAPY TREATMENT OF PATIENTS WITH A MOOD DISORDER AT THE CREATIVE EXPRESSION UNIT

Dr Roland Kaiser¹, Ms Ute Kruse², Mr Danny Rock³

1. University of Western Australia, Perth, Western Australia, Australia

2. Creative Expression Unit, Perth, Western Australia, Australia

3. Centre for Clinical Research in Neuropsychiatry, Perth, Western Australia, Australia

The aim of this study was to quantitatively evaluate psychosocial outcome and well-being of an art psychotherapy programme trialled at the Creative Expression Unit (CEU), a rehabilitation facility of Graylands Psychiatric Hospital in Perth (WA). Five patients diagnosed with a mood disorder were matched with controls on age, gender, and severity of depression. Patients from the treatment group received 15 individual art therapy sessions, whereas controls attended the CEU studio workshop. All patients were assessed using the Composite International Diagnostic Interview (CIDI). Multi-faceted, standardized instruments were selected to measure specific effects of art therapy; the Well-being questionnaire, which consists of the Sense of Coherence Scale (SOCS), the Social Adjustment Scale (SAS), and the Symptom Checklist (SCL-90-R), as well as the Hamilton Depression Scale. All scales were administered on 4 occasions (before the start of the treatment, after 7 sessions, at the end of the trial, and 6 months after the last session). The results indicate that patients in the treatment group as well as in the control group benefit from art therapy treatment.

Poster 2

SEROTONIN REGULATION OF THE HUMAN STRESS RESPONSE

Dr Sean Hood¹, Dr Dana Hince², Ms Hayley Robinson¹, Ms Melita Cirillo¹, Dr David Christmas¹, Dr Joey Kaye³

1. School of Psychiatry & Clinical Neurosciences (M521) Western Australia, Australia

2. Psychopharmacology Unit, University of Bristol, United Kingdom

3. Department of Endocrinology and Diabetes, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia

Background: Acute Tryptophan Depletion (ATD) is a technique that has been used to evaluate the effects on humans of acutely reducing serotonin neurotransmission. We have developed a model using a single breath of 35% CO2 that activates the hormonal axis and produces autonomic and behavioural arousal, thus modelling a stress response. This study combines ATD and single breath 35% CO2 inhalation to study stress responses in volunteers in a safe and reliable way.

Method: A randomised, double-blinded, placebo-controlled, crossover trial involving 14 healthy adult volunteers aged between 18 and 65 years. Subjects underwent double-blind tryptophan depletion over 2 days and were then crossed over one week later. During each study day, at the time of peak depletion, participants were single blinded to receive a single breath of 35% CO2 or Air. This was followed 40 minutes later by the other gas. Psychological outcomes were assessed with the Spielberger State Anxiety Inventory (SSAI), Visual Analogue Scales (VAS), Panic Inventory (PI), Panic and Agoraphobia Scale (PSI) and Beck Depression Inventory (BDI). Physiological outcome was measured by serial plasma cortisol, prolactin and tryptophan levels, pulse and blood pressure.

Results: No effect of tryptophan depletion plus 35% CO2 inhalation was seen on anxiety symptoms. Single breath CO2 robustly increased plasma cortisol levels in comparison to an Air inhalation; this was less certain for prolactin levels. ATD produced influenced the HPA axis, apparently independent of CO2 or Air inhalation stressors. ATD and 35% CO2 inhalation both induced a pressor response and bradycardia in these normal volunteers.

Conclusion: Both 35% CO2 and ATD activate the human stress response and have cardiovascular activity in normal volunteers.

Poster 3

ARIPIPRAZOLE FOR RELAPSE PREVENTION IN BIPOLAR DISORDER IN A 26-WEEK TRIAL

Dr Lee Anne Griffiths¹, Dr Raymond Sanchez², Dr Ronald Marcus³, Dr William Carson⁴, Dr Linda Rollin³, Dr Taro Iwamoto⁵, Dr Elyse Stock³

1. Bristol-Myers Squibb Company, Melbourne, Australia

2. Bristol-Myers Squibb Company, Paris, France

3. Bristol-Myers Squibb Company, Wallingford, CT, United States of America

4. Otsuka America Pharmaceutical Co., Princeton, NJ, United States of America

5. Otsuka Pharmaceutical Co., Ltd., Tokyo, Japan

Objective: To compare aripiprazole treatment with placebo in the maintenance of stability of patients with Bipolar I Disorder in a 26-week, double-blind relapse prevention study.

Method: Patients who had recently experienced a manic or mixed episode entered an initial stabilization phase, in which they received open-label treatment with aripiprazole 15–30 mg/day (starting dose = 30 mg/day), for 6–18 weeks. Patients meeting the stabilisation criteria (Y-MRS ≤10 and MADRS ≤13 for 4 consecutive visits or 6 weeks) were then randomised to double-blind treatment with aripiprazole or placebo for 26 weeks in the maintenance phase of the study. The primary endpoint was time to relapse of manic, mixed, or depressive symptoms, defined as discontinuation due to lack of efficacy (hospitalisation for manic or depressive symptoms, or requiring a dosing change in psychotropic medications other than study drug).

Results: 161 patients met stabilisation criteria and were randomised to aripiprazole or placebo. The time to relapse of symptoms was significantly longer with aripiprazole treatment than with placebo (P = 0.020). In addition, significantly fewer aripiprazole-treated patients experienced relapse (manic, mixed, or depressive symptoms) than those receiving placebo (25% vs 43%, P = 0.013). The only adverse events (≥10% incidence) more commonly reported with aripiprazole than with placebo were anxiety and nervousness.

Conclusion: Aripiprazole prolongs time to relapse of symptoms in stabilised patients with Bipolar I Disorder who previously experienced a mixed or manic episode.

Competing interests: LG, RS, RM, LR, ES are employed by Bristol-Myers Squibb Company; WC, TI are employed by Otsuka Pharmaceuticals Co.

Poster 4

BARRIERS TO THE DIAGNOSIS OF CATATONIA

Dr Joseph W Y Lee¹, Professor Brendan T Carroll², Professor Gabor S Ungvari³, Dr Arthur Thalassinos⁴, Ms Tressa D. Carroll⁵

1. Graylands Hospital & University of Western Australia, Perth, Western Australia, Australia

2. University of Cincinnati, Chillicothe VA Medical Center, Chillicothe, Ohio, United States of America

3. Chinese University of Hong Kong, Hong Kong, China

4. Mt. Carmel Healthcare, Columbus, Ohio, United States of America

5. The Neuroscience Alliance, West Jefferson, Ohio, United States of America

Background: Catatonia is a neuropsychiatric syndrome of diverse aetiology. Various studies showed that catatonia was diagnosed in about 10% of patients admitted to acute psychiatric facilities. However, it remains a common belief that catatonia has disappeared in modern psychiatric facilities. A recent study (Van der Heijden et al, 2005) found that under 2% of patients were diagnosed with catatonia although 18% had 2 or more catatonic signs, suggesting that catatonia is underrecognized.

Objective: This study intended to identify barriers to the diagnosis of catatonia in psychiatric practice, a concern for the Catatonia Consortium, a freestanding department of clinicians and researchers in the field of catatonia and related conditions.

Method: (a) We reviewed the clinical barriers to the diagnosis of catatonia identified in 3 books written on the subject. (b) A10-question test was developed to detect comprehension of catatonic signs among consortium members and clinicians from other settings. (c) We reviewed the terminology and criteria for catatonia used in DSM-IV-TR, the Bush-Francis Catatonia Rating Scale, and in one book (Fink & Taylor, 2003) written on the subject. (d) A field test on graduate interviewers was conducted using the criteria and terminology to examine the issue of a clinical interview versus a neurocognitive motor examination to detect catatonic signs.

Results: (a) 13 separate clinical barriers to the diagnosis of the catatonia were identified. (b) On the catatonia test, we found a lack of consensus among consortium members and low scores among clinicians from other settings. (c) We found 29 terms used in the diagnosis of catatonia. Clear and unambiguous descriptions of terms were as follows: DSM-IV-TR = 6 (20.7%), Bush-Francis Scale = 26 (89.7%), Fink & Taylor = 12 (41.4%). (d) The field test revealed that graduate level interviewers were unable to detect catatonic signs with a clinical interview alone in the absence of a limited physical examination.

Discussion: We found a range of clinical barriers to the diagnosis of catatonia including the lack of clearly defined terminology, inadequacy of the diagnostic and classification systems, and inadequacy of the clinical interview alone to detect catatonic signs. Our findings support the use of a motor rating scale with clearly defined terms to diagnose catatonia.

Poster 5

SELECTIVE MODIFICATION OF STIMULUS PARAMETERS IN A CLINICAL TRIAL OF RTMS IN DEPRESSION: INTRODUCTION OF A METHOD AND PRELIMINARY DATA

Dr Greg Price¹, Dr Joseph Lee¹, Dr Nathan Gibson², Dr Geoff Riley³

1. Centre for Clinical Research in Neuropsychiatry/ School of Psychiatry and Clinical Neurosciences, University of Western Australia, Perth, Western Australia, Australia

2. Graylands Hospital, Perth, Western Australia, Australia

3. Primary Care Mental Health Unit/ School of Psychiatry and Clinical Neurosciences, University of Western Australia, Perth, Western Australia, Australia

The clinical trials unit at CCRN recently initiated a protocol to investigate the clinical efficacy of repetitive Transcranial Magnetic Stimulation (rTMS) in depression. This study prospectively evaluates the antidepressant efficacy of rTMS in a double-blind head-to-head trial; similar to recent placebo controlled trials that showed a beneficial effect of rTMS over placebo. An improvement in the Montgomery-Asberg Depression Rating Scale of 15% for rTMS, compared with 1% for placebo, was found using the same parameters as our trial (Fitzgerald PB, et al. 2003: Transcranial magnetic stimulation in the treatment of depression: a double-blind, placebo-controlled trial. Archives of General Psychiatry 60:1002–8). A similar trial, only using 20Hz stimulation (George MS, et al. 2000: A controlled trial of daily left prefrontal cortex TMS for treating depression. Biological Psychiatry 48:962–70.), found a decrease of 36% in the Hamilton Rating Scale for Depression (HamD-21) for rTMS, compared with 21% for sham. Other researchers (Loo C, et al. 1999: Double-blind controlled investigation of transcranial magnetic stimulation for the treatment of resistant major depression. American Journal of Psychiatry 156:946–8) have not found such an effect, however, and exact clinical efficacy remains unclear (Couturier JL 2005: Efficacy of rapid-rate repetitive transcranial magnetic stimulation in the treatment of depression: a systematic review and meta-analysis. Journal of Psychiatry & Neuroscience 30:83–90).

The trial compares standard rTMS parameters (10Hz; 5 second train; 25second rest; 100%MT), with a modified stimulus delivery method that provides the same pulse parameters (number of pulses over the same average time) but in a different temporal arrangement. The stimuli are applied in response to selected patterns of background EEG on the basis that coincident afferent activity affects the response to a stimulus. Such an effect has previously been shown at a cellular level (Steriade M, 2001: Impact of network activities on neuronal properties in corticothalamic systems. Journal of Neurophysiology 86:1–39), at an ERP level for auditory stimuli (Rahn E, et al., 1993: Prestimulus EEG-activity strongly influences the auditory evoked vertex response: a new method for selective averaging. International Journal of Neuroscience 69:207–20) and TMS (Price GW, 2004: EEG-dependent ERP recording: using TMS to increase the incidence of a selected pre-stimulus pattern. Brain Research Brain Research Protocols. 12:144–51), and in the motor cortex (Thickbroom GW, et al., 2005: Repetitive paired-pulse TMS at I-wave periodicity markedly increases corticospinal excitability: A new technique for modulating synaptic plasticity. Clinical Neurophysiology (In Press)). The study thus extends the protocol to the clinical level, and compares its efficacy to the de facto standard protocol in rTMS treatment of depression.

The trial comprises daily sessions of rTMS for four weeks, at the same time of day, using a Magstim Super Rapid2 (1–100Hz) device. Along with HAMD-21, Beck and RBans ratings at baseline, two weeks and study end, we acquire EEG and NCT data (concept shifting task) on a sessional basis. We report pilot data from a scheduled 10 participants in each arm of the comparison groups and discuss the responses in terms of previous comparisons with placebo.

Poster 6

JIMI HENDRIX, DISTORTION AND FEEDBACK: MUSICAL AUDITORY HALLUCINOSIS

Dr Ramon Mocellin, Dr Dennis Velakoulis, Dr Mark Walterfang

Neuropsychiatry Unit, The Royal Melbourne Hospital, Melbourne, Victoria, Australia

Musical hallucinosis (MH) can be defined as the perception of music without the presence of an external musical stimulus in which the subject maintains insight (for example, interprets the perceived music as “a trick of the mind”). Although MH has been described in psychotic illness, epilepsy and a variety of brain lesions, it more is often seen in elderly patients with acquired deafness[1].

Three illustrative cases of MH are presented. Case One is of an 82 year old married woman residing in an isolated farmhouse who described choral singing voices. Initially she insisted her husband drive her around neigh boring properties to discover the source of the music, but soon realized that this was impossible. She was found to had moderately severe deafness and extensive white matter disease on MRI. She tolerated trial of an atypical antipsychotic and sodium valproate poorly and only listening to recorded music with headphones provided relief. Case Two is of a 62 year old man with severe ear canal hyperostosis and deafness who described hearing music he identified as the opening bars of the Jimi Hendrix classic Voodoo Child. After eliminating a number of possible sources he was able to link his experience to deafness. Surgical treatment of the hyperostosis resulted in the replacement of the MH with simple tinnitus.

Case Three is of a 78 year old man with a past history of cerebrovascular disease residing in a residential care facility. He described hearing pleasant and familiar music, particularly at night. He was found to have profound sensorineural deafness and features of Vascular dementia. These MH caused him no distress and no treatment apart from the fitting of amplifying hearing aids was undertaken. MH is similar to the entity of Charles Bonnet Syndrome, or the experience of complex visual hallucinations in the context of visual impairment. Some of the forms of MH are similar to the subtypes of complex visual hallucinations. Mechanisms underlying the generation of MH remain poorly understood. The most compelling neurobiological model is one of spontaneous activity arising in a de-afferented auditory system which is then involved in recognition of this stimulus by a cortical pattern recognition system[2].

Pharmacological treatments are invariably ineffective; most authors recommend audiological assessment and appropriate amplification. Prognosis is usually guarded with MH persisting and worsening as deafness progresses.