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Objective: The aim of this observational study was to evaluate the effects of duloxetine in the treatment of seasonal affective disorder (SAD)., Patients and Methods: 26 SAD patients were treated with open-label duloxetine 60-120 mg per day over 8 weeks. Ratings included the Structured Interview Guide for the Hamilton Depression Rating Scale (SAD version; SIGH-SAD) and the Clinical Global Impression (CGI). To estimate treatment effects on social functioning in SAD we employed the Social Adaptation Self Evaluation Scale (SASS), the Sheehan Disability Scale (SDS), and assessments of days lost due to illness and days with reduction in productivity., Results: Duloxetine led to a significant improvement (p<0.001) of SIGH-SAD, CGI severity, SASS, and SDS scores. Days lost due to illness and days with reduction in productivity were significantly diminished during treatment (p<0.001). Treatment with duloxetine over 8 weeks yielded a response rate (SIGH-SAD<50% of baseline value) of 80.8% and a remission rate (SIGH-SAD<8) of 76.9% in the intention to treat sample. The drop-out rate due to side effects was 15.4%., Conclusions: Our preliminary results indicate that duloxetine might be effective and able to ameliorate the negative social consequences of SAD.

Cognitive event-related potentials were recorded from 17 EEG leads in an auditory two-tone paradigm in 43 patients aged 51-79 years with the diagnosis of age-associated memory impairment (AAMI), in age-and sex-matched normal controls and in a control group 10 years older than the AAMI patients. In addition to P300 latencies, amplitudes and topographies, three-dimensional current density distribution utilizing low-resolution brain electromagnetic tomography (LORETA) was computed. P300 latency was delayed and P300 amplitude was reduced in both AAMI and older subjects. Topographically this amplitude reduction was most pronounced frontally. LORETA revealed medial (frontal and parietal) and lateral (dorso- and ventrolateral prefrontal, middle/superior temporal, posterior superior temporal/inferior parietal) sources. Significant reductions in LORETA source strength in normal aging and in AAMI were found mainly medially frontally, right dorsolaterally prefrontally and right inferiorly parietally. Since these anatomically highly interconnected brain regions in the right hemisphere are part of a network associated with sustained attention, the results speak for a decline in attentional resource capacity in AAMI patients and elderly subjects.

Middle latency and late components of event-related brain potential (ERPs) are closely related to perceptual and cognitive information processing, respectively. In a double-blind, placebo-controlled study, the acute effects of lorazepam (2 mg), haloperidol (3 mg), methylphenidate (20 mg) and citalopram (20 mg) on ERP latencies, amplitudes, topographies and tomographies were investigated in 20 healthy subjects of 23-34 years of age. After automatic artifact minimization and rejection, standard N1 and P2 and target N2 and P300 components were determined. The tranquilizer lorazepam prolonged P300 latency, which indicates an impairment of stimulus evaluation time. Low-resolution brain electromagnetic tomography (LORETA) revealed decreases in N1 and P300 source strength in those brain regions with relevant generators of these components, which reflects impairments of attentional and cognitive processing resources. The neuroleptic haloperidol decreased N1 and P300 source strength predominantly in those brain regions not involved in the generation of these components, suggesting a shift of resources. The psychostimulant methylphenidate increased P300 source strength in brain regions with major P3b generators, indicating increases in energetic resources associated with stimulus encoding. The antidepressant citalopram increased N1 and P3b source strength in multiple brain regions specifically in the left prefrontal cortex, a brain region in which reduced blood flow and metabolism was found in depressed patients.

Noninvasive electrophysiological neuroimaging applied to cognitive components of event-related potentials (ERPs) may differentiate between structural and energetic processes related to information processing. The structural level, revealed by the location of the local maxima of the current source density distribution, describes the time-dependent network of activated brain areas. The magnitude of the source strength, a measure of the energetic component, describes the allocation of processing resources. ERPs were recorded in an odd-ball paradigm and low-resolution brain electromagnetic tomography (LORETA) was applied for standard and target ERP components. In a group of 60 menopausal depressed patients of 45-60 years of age, reduced P300 source strength was observed bilaterally, temporally and medially prefrontally reaching to rostal parts of the anterior cingulate, compared with 29 age-matched controls. In a double-blind, placebo-controlled study, 2 mg of the antidepressant citalopram induced a significant increase of P300 source strength in the (left) prefrontal cortex and precuneus compared with placebo, reaching to the posterior cingulate. Similar increases were observed after 800 mg S-adenosyl-L-methionine (SAMe) administered intravenously in ten young healthy subjects aged 22-33, and they were even more pronounced in ten elderly healthy subjects aged 56-71. Thus, ERP-tomography identified changes in energetic sources in brain areas predominantly involved in depression and in antidepressant action.

The influence of a combined estrogen-progestin regimen (Climodien) on noopsyche, thymopsyche, personality and psychophysiological measures of menopausal syndrome patients was investigated in a double-blind, placebo-controlled, comparative, randomized 3-arm trial phase (Climodien 2/3 = estradiol valerate (CAS 979-32-8) 2 mg + the progestin dienogest (CAS 65928-58-7) 3 mg = regimen A, estradiol valerate 2 mg = regimen EV, and placebo = regimen P) followed by an open-label phase in which all patients received Climodien 2/2 (estradiol valerate 2 mg + dienogest 2 mg) = regimen A*. 49 women (16, 17, 16 valid patients per arm) aged between 46 and 67 years (mean 58, 58, 56 years, respectively) with the diagnoses of insomnia (G 47.0) related to postmenopausal syndrome (N 95.1) were included in the analysis of the double-blind phase. Both the double-blind and the open-label phase lasted 2 months. Noopsychic investigations demonstrated an improvement in associative verbal memory after 2 months of regimen A, which was significant as compared with both baseline and placebo. Regarding visual memory, regimen A* induced an improvement, which was significantly different from the decline in correct reproductions in the Benton Test observed under estradiol. Errors in the Benton Test decreased significantly after regimen A* as compared with regimen EV. These findings suggest that hormone replacement therapy with estradiol, and even more in combination with dienogest, improves verbal and visual memory, which is in line with the improvement in information processing speed and capacity objectified by event-related potentials (ERP). Thymopsychic investigations demonstrated a significant improvement in somatic complaints and trait anxiety after both regimen A and regimen EV as compared with baseline. State anxiety decreased significantly under regimen A* as compared with EV. The Freiburger Personality Inventory showed an improvement in aggressivity after regimen A* as compared with the preceding placebo as well as an improvement in striving after dominancy after both regimen A and regimen EV as compared with pre-treatment, but also after regimen A* as compared with regimen EV. Extraversion increased after 2 months of regimen A as compared to regimen P. Psychophysiological findings including pupillary and skin conductance variables were not significant.

The aim of the present study was to investigate the influence of the response criterion, the current well-being, and the speed of cognitive processing on fusion and flicker frequency measured by method of limits, in 65 healthy subjects, aged between 20 and 30 years. The findings demonstrated that the fusion and flicker frequency could not be measured exactly. Evaluation of the reliability of the obtained results was not possible, mainly because the necessary basic psychological variables could not be recorded using the method.

The P300 event-related potential (ERP) is considered to be closely related to cognitive processes. In normal aging, P300 scalp latencies increase, parietal P300 scalp amplitudes decrease and the scalp potential field shifts to a relatively more frontal distribution. Based on ERPs recorded in 172 normal healthy subjects aged between 20 and 88 years in an auditory oddball paradigm, the effects of age on the electrical activity in the brain corresponding to N1 and P300 components were estimated by means of low resolution electromagnetic tomography (LORETA). This distributed approach directly computes a unique 3-dimensional electrical source distribution by assuming that neighbouring neurons are simultaneously and synchronously active. N1 LORETA generators, located predominantly in both auditory cortices and also symmetrically in prefrontal areas, increased with advancing age for standards but remained stable for targets. P300 LORETA generators, located symmetrically in the prefrontal cortex, in the parieto-occipital junction and in the inferior parietal cortex (supramarginal gyrus) and medially in the superior parietal cortex, were differentially affected by age. While age did not affect parieto-occipital sources, superior parietal and right prefrontal sources decreased pronouncedly. Thus, in normal aging, P300 current density decreased in regions were a fronto-parietal network for sustained attention was localized.

In a double-blind, placebo-controlled study the effects of Actovegin on frontal and parietal electrical P300 sources revealed by low resolution electromagnetic tomography (LORETA) were studied in age-associated memory impairment (AAMI) patients. Actovegin is a protein-free metabolically active hemoderivative improving oxygen and glucose utilization. Each patient had, in randomized order, a treatment of 2 weeks with 250 ml 20% Actovegin and 250 ml placebo daily. Auditory ERPs were recorded before and 5 h after drug administration on day 1 (acute effect) and on day 15 (subacute and superimposed effect). Compared to age- and sex-matched normal controls, AAMI patients showed a trend towards P300 latency prolongation and a significantly reduced P300 global field power (GFP). Maximal LORETA source strength did not differ from controls. After Actovegin parietal P300 scalp amplitudes increased, while frontal and temporal amplitudes decreased as compared to placebo. This increase in hilliness, measured by the GFP, was significant. Moreover, the parietal P300 source strength increased after acute, subacute and superimposed infusion of Actovegin as compared to placebo. This may reflect improved availability of cognitive processing resources in the parietal cortex, an area that on the one hand plays an important role in fundamental aspects of attention and on the other hand has been found to be functionally impaired in dementia.

The P300 event-related potential (ERP) is considered to be closely related to cognitive processes. Previous reports regarding major generators contributing to the scalp-recorded P300 suggested widely distributed multiple sources. Based on ERPs recorded in 172 normal healthy subjects aged between 20 and 88 years in an auditory oddball paradigm, electrical activity in the brain corresponding to N1 and P300 components was localized by means of low resolution electromagnetic tomography (LORETA). The N1 LORETA generators, located in both auditory cortices, did not change over age. On the other hand, the P300 LORETA generators, located predominantly in the frontal neocortex and less pronounced in the posterior parietal cortex, decreased over age both in frontal and parietal source strength.

Event-related potentials (ERPs) were recorded at 17 leads in an auditory oddball paradigm in 172 normal healthy subjects aged between 20 and 88 years. With advancing age, N1 latency increased parietally (0.12 ms/year), P2 latency increased frontally (0.34 ms/ year) and N2 and P300 latencies increased all over the scalp (0.37 ms/year for N2; 0.92 ms/year for P300). P300 latency/age relationship was curvilinear with accelerated latency increase in elderlies (0.35 ms/year for subjects below 60 years; versus 2.03 ms/year for subjects above 60 years). With advancing age, standard tone ERP amplitudes were enhanced frontally (0.03 microV/year for N1; 0.07 microV/year for P2), N2 amplitudes were attenuated frontally (0.11 microV/year) and P300 amplitudes were attenuated parietally (0.15 microV/year). Multichannel analysis demonstrated that ERP latencies and amplitudes depended on electrode location. Standard tone ERP latencies changed their topographic distribution with age, whereas target tone ERP latencies did not. While N1 amplitude distribution was unaffected by age, P2, N2 and P300 topography changed significantly with age: P2 topography to a more frontal distribution and increased 'global field power'; N2 topography to a more parietal distribution: P300 topography to a more frontal and more equipotential distribution Thus, specific age effects on different ERP components were confirmed.

The topographic distributions of absolute delta and theta powers were used to classify demented patients and normals by means of z statistics, discriminant analysis and artificial neural networks (NN). The data were taken from two psychopharmacological studies in mildly to moderately demented patients (111 and 96 patients for studies I and II, respectively) and from 56 normal healthy controls. All patients were diagnosed according to DSM-III criteria and were free of medication for at least 2 weeks. The NN used was a strictly layered feed-forward network with complete connections. The z-transformed absolute power values in the combined delta and theta frequency range at 17 electrodes, recorded in a 3 min vigilance-controlled EEG with eyes closed, were used as input. After having trained the NN successfully by backpropagating of errors, the generalization test with independent data results in a classification performance of 90% determined by "relative operating characteristic" analysis. The NN out-performed z statistics and discriminant analysis. This high percentage of correct classifications may justify the development of further application of NNs based on topographic EEG data.

1. In a double-blind, placebo-controlled, cross-over study, acute pharmacokinetic, neurophysiological and psychotropic effects of suriclone, a new cyclopyrrolone derivative, were investigated and compared with alprazolam. 2. Fifteen normal young volunteers received randomized oral single doses of placebo, 0.1, 0.2 and 0.4 mg suriclone as well as 1 mg alprazolam as reference compound. Investigations were carried out before and 1, 2, 4, 6 and 8 h after drug administration. 3. Pharmacokinetic investigations by radioimmunoassay showed a dose-dependent fast rise of plasma concentrations with a peak at 1 h and a rapid decline thereafter. Both the Cmax and the AUC values exhibited a linear relationship to dose. 4. EEG brain mapping demonstrated significant CNS effects of both compounds, characteristic for tranquillizers (increase of beta, decrease of alpha and increase of delta activity; attenuation of total power and acceleration of the centroid, i.e. centre of gravity frequency). When compared with alprazolam, suriclone exerted less sedative effects. 5. Time-efficacy calculations showed the pharmacodynamic peak effect of suriclone from the 2nd to the 4th hour, and of alprazolam in the 1st hour. Dose-efficacy calculations showed that the most pronounced CNS changes occurred after 1 mg alprazolam, followed by 0.4, 0.2 and 0.1 mg suriclone. 6. Psychometric investigations demonstrated no significant effects after the two lower doses of suriclone, while 0.4 mg and 1 mg alprazolam induced a decrement both in noopsychic and thymopsychic variables seen after higher doses of anxiolytic sedatives. Psychophysiology (critical flicker fusion, pupillometry, and skin conductance measures) pulse rate, systolic and diastolic blood pressure remained unchanged. 7. Psychophysiology (critical flicker fusion, pupillometry and skin conductance measures) showed differential dose-dependent effects. Pulse rate, systolic and diastolic blood pressure remained unchanged. Anxiolytic-characteristic side-effects (tiredness, drowsiness, etc.) occurred predominantly after the highest doses 0.4 mg suriclone and 1 mg alprazolam.

In a single blind study the antiepileptic effects and safety of vigabatrin--a new anticonvulsant drug selectively inhibiting GABA-transaminase--was investigated in therapy resistant epilepsy, along with its central effects objectivated by mapping of EEG and event-related potentials (ERP). In addition to their current antiepileptic therapy, 10 patients with complex partial seizures (CP) (4 male, 6 female), aged between 22 and 57 years received placebo for 1 month, subsequently 2 g vigabatrin for 2 months and thereafter a titrated optimal dosage vigabatrin for another 2 months. Clinical investigations were carried out at the afore-mentioned periods, neurophysiological ones pre and post 2 months vigabatrin. After 2 months vigabatrin, 5 out of 10 patients had a 50% or greater decrease in CP frequency, after another 2 months 7 out of 10. The median number of CP per months decreased from 5.5 to 3.75 (p < 0.05) to 2.0 (p < 0.01), respectively. No clinically relevant side effects and laboratory changes were noted. EEG mapping showed decreased fast alpha and slow beta power and increased delta-theta frequency variability, reflecting most likely a decreased CP disposition. ERP mapping showed slightly increased N1 and P2 as well as reduced P300 amplitudes. Unchanged P300 latency indicated no delayed stimulus evaluation time after vigabatrin therapy.

The number and types of target variables quantified from the spectrally analyzed EEG used in topographic pharmaco-EEG studies are still being discussed. Drug-induced changes of target variables obtained in the alpha frequency band--four absolute and four relative powers as well as three frequency measures--were utilized to assess the effects of xantinolnicotinate in demented patients using a parallel group design and the effects of buspirone in a double-blind, placebo-controlled crossover design. We conclude that for the proper evaluation of the different drug effects on the alpha activity, all these target variables should be considered. Descriptive p values of multiple comparisons within the framework of descriptive data analyses are important tools in interpreting drug effects.

Mapping of the electroencephalogram (EEG) has been found to be a valuable method in clinical neuropsychopharmacology. It is evident that careful treatment of artifacts is of utmost importance for EEG data processing, as artifacts that contaminate the EEG data can lead to spurious results. The artifact-processing method described in this article splits signal analysis into a preprocessing step, yielding individual electro-oculographic (EOG) regression factors for EOG minimization, and into a processing step, yielding target variables. The combination of avoiding, minimizing, and identifying artifacts, as well as visual checking of face validity, will help remove artifactual effects from the EEG.

In a double-blind, placebo-controlled study, the acute central effects of amantadine infusions (200 mg for 1 h) were studied in 20 mildly demented patients (DSM-III-R) utilizing EEG mapping as well as psychometry and psychophysiology at the hours 0, 2, 4, 6 and 8. Multivariate analysis of the EEG demonstrated a significant CNS effect of 200 mg amantadine as compared with placebo mostly at the 4th and 6th hour. These effects were primarily over temporo-occipital, fronto-temporal and temporal regions. Univariate analysis showed a decrease of total power and of absolute power in all frequency bands. Furthermore, an increase of relative delta and beta activities, a decrease of theta and alpha activities, as well as an acceleration of the respective centroids of the alpha, beta and total activity were observed. The delta/theta centroid showed initially a slight increase and thereafter a clear decrease. The changes were similar to those seen after psychostimulants. Multivariate analysis of noopsychic variables showed an improvement in the 6th hour after amantadine and no changes after placebo, but inter-drug differences did not reach significance. Univariate analyses revealed differential results which included improvement in digit span and deterioration in the speed related test such as DSST and reaction time. In thymopsychic variables, de-activation was observed after amantadine as compared with placebo in the 2nd to the 6th hour with a maximum in the 4th hour. As patients felt themselves slightly over-activated before treatment, de-activation may be regarded as improvement of vigilance in the narrow sense of the word. There were no psychophysiological changes.

1. In a double-blind, placebo-controlled study the effects of venlafaxine--a novel nontricyclic compound inhibiting neuronal uptake of serotonin, noradrenaline and to a lesser extent dopamine--were investigated utilizing EEG brain mapping, psychometric and psychophysiological measures. 2. Sixteen healthy volunteers (eight males, eight females) aged 21-36 years received randomized and at weekly intervals single oral doses of placebo, 12.5 mg, 25 mg and 50 mg venlafaxine. EEG recordings, psychometric and psychophysiological tests, and evaluation of pulse, blood pressure and side-effects were carried out at 0, 2, 4, 6, and 8 h. 3. EEG brain mapping demonstrated that venlafaxine exerted a significant action on human brain function as compared with placebo at all three doses, characterized mostly by attenuation of absolute power, increase of relative delta/theta and beta, and decrease of alpha power, as well as by an acceleration of the total centroid fronto-temporally and by its slowing centrally and parietally. These findings are similar to antidepressants such as imipramine. Topographically, drug-induced alterations were most pronounced over both fronto-temporal and the right temporal to temporo-occipital regions. 4. Psychometric and psychophysiological investigations demonstrated significant dose-dependent psychotropic properties of the drug. Multivariate statistics exhibited an improvement of both the noopsyche (e.g. attention, concentration, attention variability, memory, fine motor activity, reaction time performance) and thymopsyche (e.g. drive, wakefulness)) but also significant psychophysiological activation (e.g. in c.f.f., pupillary and skin conductance measures). 5. Time-efficiency calculations showed significant central effects from the 2nd hour onwards, with increasing differences between placebo and treatment up to the 8th hour. Nausea was the most frequent complaint and appeared dose dependent.

In a double-blind placebo-controlled study, the effects of Actovegin on cognitive event-related potentials were studied in 18 age-associated memory impairment (AAMI) patients. Actovegin is a protein-free metabolically active hemoderivative improving oxygen and glucose utilization. Each patient was treated, in randomized order, for 2 weeks with 250 ml 20% Actovegin and 250 ml placebo daily with an interval of 3 weeks in between. Psychophysiological tests were carried out by means of the Viennese Psychophysiological Test System (VPTS) before as well as 5 h after the administration of one single infusion on day 1 (acute effect), before (subacute effect) as well as after one additional superimposed infusion on day 15 (superimposed effect). There was no effect on earlier stages of information processing measured by N1 and P2 component of nontarget ERP nor on ERP latencies. However, P300 amplitude increased after acute, subacute as well as superimposed infusion of Actovegin as compared to placebo, confirming the hypothesis that nootropic drugs may influence the P300 amplitude in the sense of an improved availability of cognitive processing resources. This increase of P300 amplitude (up to 4.8 microV), seen specifically in central and parietal regions, proved to be significant in a confirmatory test.

In a double-blind, placebo-controlled study the encephalotropic and psychotropic effects of Actovegin--a protein-free metabolically active hemoderivative improving oxygen and glucose utilization--were investigated in age-associated memory impairment (AAMI) patients, utilizing EEG brain mapping, psychometric and psychophysiological analyses. Each patient had a treatment of 2 weeks with 250 ml 20% Actovegin and 250 ml placebo daily with an interval of 3 weeks in between (the order of drugs sequence was randomized). Pharmacodynamic evaluations were carried out 0, 2, 4, 6 and 8 h after the administration of one single infusion on day 1 (acute effect), at 0 h on day 15 (subacute effect) as well as 2, 4, 6 and 8 h after one additional superimposed infusion on day 15 (superimposed effect). EEG brain mapping demonstrated that Actovegin exerted a significant action on the human brain function as compared with placebo characterized by a decrease of delta and theta, an increase of alpha-adjacent slow beta, a decrease of fast beta, an acceleration of the centroid of the delta/theta and alpha activity, a slowing of the beta centroid and an increase of the centroid of the total activity. Topographically the encephalotropic effects were mostly pronounced in the parietal, frontocentral and temporooccipital regions. These changes are indicative of an improvement of vigilance which was proven also by psychometric investigations at the behavioral level. Actovegin improved the noopsyche mostly in regard to attention, memory and rigidity/perseveration measures. In regard to the thymopsyche an improvement was noted in mood, affectivity, well-being and sedation. Psychophysiological evaluations demonstrated an increase in CFF, skin conductance, pupillary diameter and shortening of the latency and augmentation of the amplitude of the pupillary response. Time-efficacy calculations exhibited more effect after subacute than acute administration with the pharmacodynamic maximum in the 4th h after the superimposed dose. Evaluations of pulse, blood pressure and side effects demonstrated a very good tolerability of the drug. Our present neurophysiological, psychometric and psychophysiological findings confirm earlier results obtained in elderlies with similar methodology.

In a double-blind placebo-controlled study, the effects of tenilsetam, a novel antihypoxidotic/nootropic agent, on spontaneous and event-related activity of the central and autonomous nervous system were studied in 15 elderly subjects of both sexes aged 58-77 years by means of the Viennese Psychophysiological Test-System (VPTS). The VPTS includes a special selection and combination of experimental situations, physiological measurements, behavioral measurements and data analysis. At weekly intervals, the subjects received randomized single oral doses of placebo, 150 mg, 300 mg and 900 mg tenilsetam (TEN) and 5 mg co-dergocrine-mesylate (CDM) as reference drug. Psychophysiological testings were carried out before and 2 h after drug administration. Evaluation of the spontaneous EEG-activity demonstrated no significant drug effects as compared to placebo. In contrast, TEN showed a dose-dependent augmentation of the N1-P2 and N2-P300 amplitudes of the event-related potentials (ERPs) in specific experimental conditions. In reference to placebo, the increase of N2-P300 amplitude after the highest dosage of TEN, as well as after CDM, amounted to approximately 5 microV, which confirms the hypothesis that nootropic drugs may influence the P300 amplitude in the sense of an improved availability of cognitive processing resources. There was no effect on ERP latencies, on mean amplitudes of contingent negative variation and of post-imperative negative variation, on autonomous nervous system, on psychological measurements, nor on reaction time. However, specific improvements were observed in psychomotor measures, such as synchronization accuracy and rhythmicity. These findings highlight the importance of using EEG and ERP measures in different experimental situations in conjunction with behavioral, psychological and autonomous nervous system measures to study nootropic drug effects.

In order to find a psychophysiological paradigm for clinical application we have developed the Viennese Psychophysiological Test-System (VPTS), which includes a special selection and combination of experimental situations, physiological measurements, behavioral measurements and data analysis. This study presents detailed information concerning these four aspects. Experimental situations are related to the human model of information processing, where short changes of stimulus-reaction-correlated processes are selected: resting conditions (eyes open, eyes closed), habituation-orienting test, psychomotor-performance test, signal-detection test and reaction-time test. Physiological measures include central and peripheral activity of the cerebrospinal and autonomic nervous system: cortical activity (spontaneous electroencephalogram, auditory evoked potentials, late positive components, slow potentials), ocular activity (eye and eyelid movements), electrodermal activity (skin conductance), cardiac activity (heart rate measurement), respiratory activity (rate of respiration) and peripheral vascular activity (finger pulse volume). Behavioral measurements extend from micro behavior to complex diagnostic systems: psychomotor measurements, self-reported mood, arousal and visceral perception, psychological and psychiatric interviews. The application of this test system in 15 elderly subjects of both sexes aged 58-77 years gives information which exceeds the sum of the singular constructing elements of the VPTS.