Sympathetic Skin Reflex In Patients With Major Depression

The core clinical features of the depressive disorders are included in the diagnostic criteria for a major depressive episode and for dysthymia. Depression is associated with greater cardiac morbidity and mortality. One of the contributory factors for this may be altered cardiac autonomic activity in depression. Standardized tests of heart rate variability (HRV) allow a quantitative estimation of autonomic nervous system function. However, cardiac autonomic involvement in depression remains controversial because of methodological issues.Electrodermal activity(EDA) reflects sympathetic cholinergic sudomotor function which induces changes in skin resistance to electrical conduction. EDA, assessed by the Sympathetic Skin Response (SSR), has been proposed as an easily obtainable index of sudomotor function and as a sensitive index of bodily arousal related to emotion and attention. One study showed major depressive patients (MD) developed a significantly larger sympathetic skin response than controls, but others manisfestedthe latencies and amplitudes of the waves were significantly decrease in major depressive patients than in the controls. The latencies and amplitudes would be increased with antidepressed therapy. Sympathetic Skin Response, a sensitive measure of neurocardiac autonomic regulation was used conventional methods of measuring autonomic functions. Our study compared SSR between untreated patients with ICD-10 major depression and healthy controls. The study was undertaken to clarify whether a correlation exists between SSR and the severity of depressive symptoms or the effect of antidepressed therapy in patients with major depression.Materials and methods1.SubjectsPatients and controls gave their written informed consent. The sample comprised 50 patients, who in a structured interview fulfilled the ICD-10 criteria for a major depressive disorder. 50 healthy volunteers participated in the study. Age, sex-and height did not differ significantly between the two groups(P>0.05).2. Definition of clinical severity and response, remission of clinical improvementThe severity of depressive symptoms was assessed by the Hamilton Depression Rating Scale (HDRS) ;patients were divided into subgroups with moderate (HDRS≤24) or severe depressive symptoms (HDRS≥25). Clinical response was defined as greater than or equal to a 50% reduction in total HDRS-17 score (endpoint - baseline visit). Remission was defined as a HDRS-17 score of 7 or less at week 6. 3.ElectrophysiologySSR was determined and analyzed before treatment and the six weeksafter treatment, by conventional procedures with an EMG/EP machine (Keypoint, Danmark) with surface recording and stimulating electrodes. The unilateral median nerve was stimulated at the wrist with square electrical electrodes. Standard surface electrodes 10 mm in diameter were attached to the mid-palm (active electrode) and the nail of the index finger (reference electrode). SSR waveforms were classified into three types based on the amplitudes of the positive and negative components: the P type, the N type and the M type. 4. Data analysisThe SSR test results of MD patients were compared with age and gender matched normal controls using unpaired t-test. The waveform, latency, and amplitude of each SSR response were analyzed using a one-way ANOVA with Scheffe's F-test. Correlation between severity of depression or the effect of antidepressant and SSR parameters was analyzed using Pearson's correlation, set at 5% (p＜0.05). Correlations between variables and the latency or the amplitude was analyzed by multiple linear regression.Results1. Basic InformationSSR was obtainable in all normal subjects but could not be recorded from 5 of 50 patients whose HDRS exceeded 28. SSR waveform patterns were analyzed in these 45 patients. Among the 45 patients, 7, 21, and 17 had P, N, and M patterns, respectively. Twenty-one patients entered treatment with SSRI,15 of whom were treated successfully.2. SSR waveform in MD patientsThe MD patients had a longer latency and lower amplitude than the controls. There were no differences in age, coures and HDRS among the patients with the 3 different SSR patterns. The N pattern is the most amongthe 45 patients. The P pattern had a shorter latency and larger amplitude than the N pattern. While there was no significant difference in amplitude between the P and M patterns, the M pattern had a larger amplitude than the N pattern.3. Relation between decreased latency, amplitude and MDThe latency of SSR had a significant positive relation with HDRS (F=12.953, P=0.001) . There were no differences in age, coures and HDRS among the patients with the decreased latency and amplitude of SSR in MD patients (P>0.05). The moderate MD patients had a shorter latency than the severe. There was no difference in amplitude.4. Relation between increased latency, amplitude and antideppressant9 of these 21 patients to treat with fluoxetine were remitters. 6 patients were clinical responders. These 15 patients had a shorter latency and larger amplitude after treatment than the initiation,but there were still defferences in latency and amplitude than the controls.Conclusions1.SSR waveform in MD patientsThere were significant damage in sympathetic function of severe MD patients, whose.SSR could not be easily recorded and had a longer latency than the moderate. The N pattern is the most among the 45 patients, which showed MD patients had lower sympathetic excitability than the controls. 2. Relation between decreased latency, amplitude and MDThe severe MD patients had lower sympathetic excitability than the controls and the moderate. The latency of SSR had a significant positive relation with HDRS. Therefore, SSR is a sensitive measure of neurocardiac autonomic regulation ,which could be used to measur clinical severity in MD patients.3. Relation between increased latency, amplitude and antideppressantThe MD patients had a longer latency and lower amplitude than the controls. Which implies MD patients are disturbed in autonomic nerve function. They had a shorter latency and larger amplitude after treatment than the initiation, but there were significant defferences in latency and amplitude than the controls. This hypothesis implies that in MD patients at least a proportion of the pathology in ANS function is clearly independent of the existence of depressive symptoms. Following from this, we think disruptions of autonomic nerve regulation may represent a trait marker for MD.