Affective disorder and stress in multiple sclerosis.
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Publications and source records attributed to E Stip.
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Reports of frequency and interpretation of intellectual and mood disorders differ in multiple sclerosis (MS). Forty-one patients with MS defined according to MacAlpine's criteria were evaluated by psychometric tests (WAIS) and neuropsychologic examinations (study of language, gnosic and praxic activities, dynamic gestural organization, memory and learning) together with, in 24 of them, the AMDP psychopathologic rating scale. Intellectual disorders were noted in 65 p. 100 of patients. Although more frequent in severe and chronic forms they were nevertheless of early onset since more than a half of the patients with onset of disease less than 5 years ago were affected. Their semiology was fairly homogeneous, combining disturbances of dynamic gestural organization (decomposition or simplification) and memory and learning deficiencies without anomalies of instrumental functions or usual psychometric mental deterioration. Application of the AMDP scale failed to reveal any psychotic type of disorders. Mood disturbances were predominant, affecting 60 p. 100 of the subpopulation studied (24 cases) and combining, in an unexpected manner: dysphoria, euphoria and depression. Only euphoria appeared to be correlated with intellectual disorders. Frequency of both intellectual and mood disorders was similar to that reported in other series published. The relative homogeneity of semiology, seen by the correlation between the different disturbances (decomposition and simplification, plateau learning curve and euphoria) and the unusual grouping of these effects, is suggestive of their organic basis. In addition, signs and symptoms resemble the neuropsychological expression of frontal lobe lesions and certain lesions of central grey nuclei.(ABSTRACT TRUNCATED AT 250 WORDS)
While it has become commonplace to test the various components of memory in schizophrenia with paper-and-pencil or in-lab tasks, very little data exist on the subjective complaints of patients regarding their memory. Few instruments have been designed to collect systematically the complaints of patients with schizophrenia. We present a work in progress on the Subjective Scale to Investigate Cognition in Schizophrenia (SSTICS), a 21-item, Likert-type scale that is simple and easy to use. It allows a quantitative approach to the subjective and cognitive dimensions of schizophrenia. Stip constructed the scale based on a questionnaire covering several cognitive domains: memory (working memory, explicit long-term memory), attention (divided, distractibility, alertness, sustained), language, and praxia. We evaluated the psychometric properties of the SSTICS in a population of 114 French-speaking patients in Montreal. Patients were recruited in the community and assessed with the Structured Clinical Interview for DSM-III-R (SCID), the Positive and Negative Syndrome Scale (PANSS), and the Extrapyramidal Symptoms Rating Scale (ESRS). Cognition was measured using the Rey Auditory Verbal Learning Test (RAVLT) (long-term memory), Controlled Oral Word Association Test (verbal fluency), and Trails A and B. Preliminary analyses showed very good internal consistency for the global score (alpha=0.88), and alphas varying from 0.57 to 0.72 for the subscales. Stability over time was very good. The principal components analysis accounted for a multiple structure. Correlations between subjective scores and objective cognitive assessment were significant for several domains. Validation of the SSTICS needs to be completed through further exploration of the factorial structure and testing of the English version.
BACKGROUND: Despite immense importance of auditory verbal hallucinations (AVHs) in the phenomenology of schizophrenia, the neurocognitive and neurophysiological bases of AVHs remain obscure. On the neurocognitive level, it has been proposed that AVHs arise from the disordered monitoring manifested by patients' inability to recognize their inner speech as being their own. On the neurophysiological level, the AVHs have been attributed to the aberrant activity in the primary auditory cortex (Heschl's gyrus). Although interesting, these models cannot account for the very specific and restricted content of AVHs in individual patients. The specific content of AVHs persists across different psychotic episodes even after extended periods of remission. Furthermore, the AVHs are usually triggered by emotionally charged and stressful situations. DESIGN: We hypothesized that even during absence of AVHs, when patients are in remission, the verbal content remains present in the latent, pre-clinical form. In order to elucidate potential cerebral substrates of the dormant AVHs content, we employed functional magnetic resonance imaging (fMRI) in 6 schizophrenia patients in total remission of AVHs for at least 12 months, during listening to the words hallucinated by them in the past. Specifically, we created the list of previously hallucinated words for each patient and matched the words in terms of length, structure, emotional valence, semantic category and frequency of usage with the non-hallucinated words. Moreover, each patient was paired demographically with the control participant who was presented with the same words. We predicted that exposure to the hallucinated versus non-hallucinated words would result in increased activation in cerebral areas associated with cognitive and emotional content of previously experienced AVHs in patients, whereas the same comparison will not produce any significant changes in blood oxygen level-dependent (BOLD) signal in control participants. In addition, based on existing neuroimaging data obtained during experience of AVHs, we hypothesized that previously hallucinated words may elicit greater activation in the primary auditory cortex than the non-hallucinated words in patients. Each pair of participants was analyzed separately. RESULTS: The most consistent finding in patients, absent in all control participants, was significant activation in the orbitofrontal and medial prefrontal cortex (PFC) during listening to previously hallucinated versus non-hallucinated words. The orbitofrontal and medial PFC are both part of corticolimbic system and play an important role in cognitive control of emotion processing. DISCUSSION: Thus, present results imply that previously hallucinated words, even in remission, are associated with inappropriate emotional response on neurophysiological level in schizophrenia patients. The relative hyperactivation of orbitofrontal and medial PFC in patients may stem from and/or may contribute to anomalous neural plasticity and disordered connectivity in the corticolimbic circuitry. This in turn could lead to attribution of excessive emotional salience to normally neutral stimuli and over time via process of sensitization could result in hallucinations. Potential normalization of this dysfunction could reduce patients' susceptibility to experience AVHs in stressful situations. In addition to observed hyperactivations in the PFC, some schizophrenia patients exhibited anomalous BOLD signal in other regions of the corticolimbic system such as anterior cingulate gyrus and parahippocampal gyrus. These additional anomalies could be related to greater affective sensitivity to the hallucinated versus non-hallucinated words in some patients. CONCLUSION: Finally, in contrast to our initial hypothesis we did not observe any significant differences between processing of the hallucinated versus non-hallucinated words in the primary auditory cortex. In retrospect, this result is not surprising because patients did not experience internally generated AVHs while in the scanner, but instead were exposed exclusively to externally generated stimuli.
BACKGROUND: In this review, we conclude that cognitive impairments are as important as positive and negative symptoms in the clinical assessment and management of patients with schizophrenia. This is not a comprehensive review, considering that the new Measurement And Treatment Research to Improve Cognition in Schizophrenia (MATRICS) model will soon provide valuable data. It is however a product of the collective efforts of a French Canadian clinical research team that proposes a synthesis of data of pragmatic interest to clinicians. Medication with improved safety and cognition profile, gene-rally lead to better outcomes by facilitating compliance with drug regimens and rehabilitation programs. In addition, measures of attention and executive function (EF) appear to improve with novel antipsychotics when compared to traditional neuroleptics. Nevertheless, evaluating cognitive performance is not a routine procedure outside the domain of research. For example, procedural learning (PL) -- an important measure of cognitive function -- refers to cognitive and motor learning processes in which execution strategies cannot be explicitly described (ie learning by doing). These actions or procedures are then progressively learned through trial and error until automation of optimal performance is established. Procedural learning is rarely assessed in clinical practice. Inconsistent findings regarding the effects of neuroleptic drugs on PL have been reported. LITERATURE FINDINGS: Trials using acute administration of chlorpromazine in normal subjects induced PL deficits, suggesting the direct effect of neuroleptics, presumably via a D(2) dopamine blockade in the striatum. In a recent study by our group, schizophrenia patients, divided into three groups according to their pharmacological treatment (haloperidol, clozapine and risperidone) were compared to normal controls on two PL tasks; a visuomotor learning task (mirror drawing) and a problem solving learning task (Tower of Toronto). No deficits were detected in patients receiving clozapine, while haloperidol was associated with deleterious effects in both tasks. Risperidone, however, produced different effects depending on the task performed. Another 6-month double-blind Canadian study confirmed the beneficial effect of olanzapine on PL compared to haloperidol and risperidone. The differential effects of drugs on the striatal D(2) receptors, -irrespective of their classification as conventional or atypical neuroleptics and the specific process implicated in each of these PL tasks may explain these results. Tracer studies using radioactive benzamides (IBZM) specific to striatal D receptors determined a relationship between striatal D(2) receptor occupancy and PL performance such as the mirror drawing task. Using this method, data obtained in Montreal on schizophrenia patients receiving olanzapine and haloperidol have shown that the coefficient of determination in a visuomotor PL task varied inversely with D2 receptor saturation. DISCUSSION: This review probes the effect of impaired cognitive functions on schizophrenia patients' quality of life. Cognitive deficits found in schizophrenia affect planning, along with the aptitude to initiate and -regulate a goal-directed behaviour. These impairments have been repeatedly, yet inconclusively, attributed to frontal lobe dysfunction. Morphological findings obtained from neuroimaging studies remain inconsistent, some noting no differences between patients and controls while others observing reduced prefrontal volumes in schizophrenia patients. Conversely, functional neuroimaging (fMRI) demonstrated reduced frontal blood flow relative to global cerebral perfusion in schizophrenia patients. Overall, neuroimaging literature provides reliable evidence of frontal impairments in schizophrenia, although the average magnitude of difference between patients and controls is insufficient to defend a frontal lobe dysfunction hypo-thesis, as far as brain volume, resting cerebral metabolism or blood flow are concerned. The only measurement clearly distinguishing between patients and controls is fMRI of the frontal lobe while performing an experimentally controlled task. Here, schizophrenia patients fail to activate their frontal cortex when required. Sensitive to frontal lobe dysfunction are Neuropsychological tests of executive function. STUDY DESIGN: A study conducted in Montreal assessed the relation between EF impairments and difficulties in planning daily activities in schizophrenia patients scoring more than 3 on at least 4 items of the PANSS negative subscale. Performances on EF, memory and script generation were measured and compared to controls. Script production task required that subjects recite 10-20 actions that would normally be carried out for during daily life activity (going to a restaurant, buying groceries, etc.). Patients' performances were significantly lower with higher perserveration and sequencing impairments. Routine activities such as the ability to cook a meal were similarly investigated. Patients were videotaped in a kitchen while preparing a specific meal. RESULTS: Optimal sequence of micro- and macro-steps necessary to prepare the meal in a minimal time were measured. Sequencing errors, repetitions and omissions were significantly higher compared to controls. In addition, temporal organization was positively correlated with negative symptoms and low EF performance on neuro-psychological tasks. Thus concluding that EF impairment interferes with basic routine activities in schizophrenia patients, notably those with negative symptoms. Last but not least, we assessed the progress of patients' subjective complaints with regards to their cognitive functions using tests such as the SSTICS, specifically developed to address subjective cognitive complaints and insight. CONCLUSION: This review concludes that from now on cognitive deficit should be recognized as a major element in social and professional integration of schizophrenia patients, and should become a standardized assessment approach in clinical practice.
Recent studies suggest the occurrence of a neurological dysfunction in Obsessive-Compulsive Disorder (OCD). The purpose of the present study was to verify the clinical value of a neurological evaluation in patients with the disease. We submitted 15 patients with OCD (five of whom were under clomipramine) and 15 controls in a detailed neurological examination, including assessment of the neurological soft-signs. Eleven patients (73.3 percent) and four controls (26.7 percent) presented abnormalities on examination. The main findings among the patients were: palmomental reflex (six cases); mirror movements (five cases); agraphestesia and dysdiadochokinesia (three cases). Three out of the four patients who had a normal examination were on clomipramine. Palmomental reflex was the main finding among the controls. These results, although preliminary, stress the interest and usefulness of performing a detailed neurological examination in OCD.
GOALS: The aim of this study was to examine selective attention in patients with chronic and refractory schizophrenia who had been exposed for six months to atypical neuroleptic medications: risperidone or clozapine. METHOD: 17 patients satisfying DSM III-R criteria for schizophrenia were assessed according to BPRS and PANSS and abnormal involuntary movements to ESRS. Selective attention tasks were performed before treatment with risperidone or clozapine and at two times during the treatment (6 weeks, T1, and 24 weeks, T2). Patients' performance data were compared to data from a group of general population at T1. Selective attention refers to the ability to discriminate relevant information from irrelevant one. This was measured by a visual search task. Subjects had to search for a target specified by a conjunction of features (color and shape). The target was a black X, while the distracters were white X's, black O's and white O's. The stimuli were displayed on a Macintosh SE computer. A two-button response box was used for response production and the experiment was run in a dimly lit room. A white-fixation stimulus was shown at the center of the display screen between trials. The number of stimuli displayed on a single trial was 1, 4, 7 or 10. The median RTs and error rates of subjects were computed for each factor (target presence and number of stimuli). RESULTS: A Group X Number of items X Presence of target ANOVA applied on median correct RTs revealed a significant Group X Presence interaction [F(1,176) = 60.433, p < .0001]. Performances improved with the time (F2, p < .01). Correlations were found between positive score on PANSS and performance on selective attention (r39 = -.391). CONCLUSION: Atypical neuroleptic do not have a deleterious effect on selective attention but a favorable effect on the schizophrenic patients' performance.
In recent years, the presence of attention deficits has been recognized as a key feature of schizophrenia. Past studies reveal that selective attention, or the ability to select relevant information while ignoring simultaneously irrelevant information, is disturbed in schizophrenic patients. According to Treisman feature-integration theory of selective attention, visual search for conjunctive targets (e.g., shape and color) requires controlled processes, that necessitate attention and operate in a serial manner. Reaction times (RTs) are therefore function of the number of stimuli in the display. When subjects are asked to detect the presence or absence of a target in an array of a variable number of stimuli, different performance patterns are expected for positive (present target) and negative trials (absent target). For positive trials, a self-terminating search is triggered, that is, the search is ended when the target is encountered. For negative trials, an exhaustive search strategy is displayed, where each stimulus is examined before the search can end; the RT slope pattern is thus double that of the positive trials. To assess the integrity of these processes, thirteen drug naive schizophrenic patients were compared to twenty normal control subjects. Neuroleptic naive patients were chosen as subjects to avoid the potential influence of medication and chronicity-related factors on performance. The subjects had to specify as fast as possible the presence or absence of the target in an array of a variable number of stimuli presented in a circular display, and comprising or not the target. Results showed that the patients can use self-terminating search strategies as well as normal control subjects. However, their ability to trigger exhaustive search strategies is impaired. Not only were patients slower than controls, but their pattern of RT results was different. These results argue in favor of an early impairment in selective attention capacities in schizophrenia, which appears before the introduction of neuroleptics. The attention performance was also shown to present some association to clinical symptoms.
Deficits in procedural learning remain a controversial issue in schizophrenia. This may be related to the nature of the neuroleptic treatment of schizophrenic patients as conventional neuroleptics may be more deleterious than new atypical neuroleptics. However, there is no comparative study on the effect of specific neuroleptics on procedural learning. In this study, three groups of patients treated with different neuroleptics were compared to normal controls on two procedural learning tasks. In a visuo-motor task, patients and controls showed similar learning rates, although schizophrenic patients showed generally lower performances than normal controls. However, patients treated with a conventional neuroleptic, but not those treated with the atypical neuroleptics, showed many fluctuations during the initial learning phase. In a problem-solving task, all groups were comparable in performance and learning fluctuations, but learning rates were lower in patients treated with the neuroleptic showing the higher incidence of extrapyramidal symptoms. This suggests that procedural learning abilities may be significantly affected by neuroleptics in schizophrenia, although the effect may differ between tasks and the specific neuroleptics. Fluctuations in the initial learning phase of the visuo-motor task probably results from a frontal dysfunction while reduced learning rates, such as those observed in the problem solving task, may be attributed to a striatal dysfunction. This is concordant with the differential pharmacological actions of the conventional and atypical neuroleptics in these two cerebral areas.
Two case studies were conducted of patients suffering from paranoid schizophrenia with glossomanic schizophasia. Their dictation-taking performance was assessed via a comprehensive standardized neuropsychological test battery following a protocol specifically designed for the purpose (Lecours, 1996.). The patients' performance was compared with normative data from the general population. The results show that the patients committed graphemic paragraphias, that is, they replaced target graphemes with others representative of the corresponding phoneme (ph and f for/f/, in French) or with graphemes representative of a similar phoneme (v for/f/). These errors suggest that components of a cognitive model of writing are dysfunctional.
The study compared controlled and automatic processing in 17 people diagnosed with chronic tic disorder (CTD), 20 with habit disorder (HT), and 30 screened controls. Using a countermanding paradigm, time to initiate a response (GO-time) was compared with time taken to inhibit a response (STOP-time) under automated and controlled response conditions. The signals were 2 sets of traffic-light-like computer displays with ready, go, and stop lights. The automated response was a repetitive series of taps and the controlled response was a morse code pattern of taps. There were no group differences in GO time under any conditions. The control group but not the HD or CTD groups showed a significant practice effect over time. The CTD group was significantly slower to STOP the automated than the controlled response. The results suggest that the CTD group had specifically, greater difficulty inhibiting automated than controlled actions.
Cognitive deficits in schizophrenia have been observed with neuropsychological tests of executive function, traditionally considered sensitive to frontal lobe damage. These impairments affect planning abilities, as well as the aptitude to initiate and regulate a goal-directed behaviour. On the other hand, negative symptoms of schizophrenia are widely suspected to reflect a frontal lobe dysfunction. Based on a review of a hundred papers, the present article analyses the anatomical and neuropsychological evidence of disturbed frontal lobe functioning in patients with negative schizophrenic symptoms. The phenomenological similarity of some schizophrenic symptoms to the clinical features of patients with prefrontal injury inspired the hypothesis of damaged frontal lobe in the former disorder. The morphological findings of neuroimaging studies brought inconsistent conclusions, with some researchers noting no differences between patients and control subjects while others observing reduced prefrontal volumes in schizophrenia. The functional neuroimaging demonstrated a reduced frontal blood flow relative to the general cerebral perfusion in patients with schizophrenia. Even though the overall neuroimaging literature provides reliable evidence of frontal impairment in schizophrenia, the average magnitude of the difference between patients and healthy controls is insufficient to defend the hypothesis of frontal lobe dysfunction, as far as brain volume, resting metabolism or blood flow are concerned. The only measure, which clearly distinguishes between the patients' and controls' distributions, is the functional neuroimaging of the frontal lobe while subjects are performing an experimentally controlled task. Schizophrenic patients fail to activate their frontal cortex when the task requires it. Analysing executive abilities in relation to symptom expression leads to recognising the fact that frontal dysfunction is a characteristic of only a sub-syndrome of schizophrenia. The factor analysis of the clinical features consistently reveals three syndromes in schizophrenia, termed disorganisation, positive and negative syndromes. The substantial body of evidence that patients exhibit more than one syndrome indicates these are dimensions within a single illness rather than discrete diseases. Liddle labelled the negative syndrome as "psychomotor poverty" and associated it with malfunction of the neuronal projections from dorsal prefrontal cortex to thalamus via striatum, connections involved in the initiation of mental activity. His hypothesis was supported by the work of other, independent research groups. The patients with negative symptoms, in contrast with the nonnegative symptom group, tend to demonstrate reduced neuronal activation of the frontal cortex during executive task realisation. The nonnegative patients are indistinguishable from the healthy control subjects in this region. Neuropsychological studies reveal that severity of psychomotor poverty is associated with slowing of mental processing and deficits in tasks that require planning abilities. These frontal functions are identified with the selection, the initiation and monitoring of a wide variety of behavioural processes. It was hypothesised that executive dysfunction will appear through different patterns across symptom subtypes, but few studies sought to validate this assumption. Finally, researchers make little effort to develop theoretical conceptualisations of the aetiology of negative schizophrenic symptoms, despite the growing body of evidence on its resemblance to the dorsolateral frontal lobe syndrome. Frith proposes that defects in the initiation of spontaneous action underlie these clinical phenomena, but his definition is not specific enough to be confronted to existing literature, neither has been empirically tested. Disturbed executive functioning has detrimental impact on the quality of daily living in patients with schizophrenia. Indirect observation of the latter accounts for defective long-term adaptation, which has been correlated to severity of negative symptoms and, although not consistently, to executive deficit as assessed by neuropsychological testing. Unfortunately, this area of research lacks ecologically valid studies. Measuring executive dysfunction as it occurs in the natural setting of the patient and validating dissocialbility of frontal deficits with respect to the schizophrenic symptomatology could lead to greater individualization of treatment plans and therefore to more efficient therapy outcome.
Executive dysfunction has been extensively described in schizophrenia and has been found to correlate with the negative symptoms of the disease. However, executive dysfunction is usually assessed by cognitive tests, and these are not necessarily good predictors of an individual's daily functioning. This study aimed to discover whether executive dysfunction in schizophrenia can be measured by analyzing a daily routine such as cooking a meal. Behavior was scored on the basis of the optimal sequence of macrostructures (order of dishes) and microsteps (order of actions) that must be performed to prepare the meal in a minimum of time and with the smallest delay between the completion of the first and last dishes. The results showed that patients with schizophrenia make macrostructure but not micro-step sequencing errors. The number of repetitions and omissions and the delay between the completion of the first and last dish were all greater in patients than in control subjects. In patients with schizophrenia, but not in normal controls, these behavioral malfunctions were significantly correlated with both negative symptoms and performance on the executive tasks. Poor performance on the memory tests was not correlated with the behavioral malfunction. Therefore, daily functioning in schizophrenia may be specifically influenced by executive dysfunction in schizophrenia, and this can be quantitatively assessed with a behavioral scale of action sequences.
Despite the fact that most researchers acknowledge the high prevalence of comorbid substance abuse among schizophrenic patients, there is no common agreement regarding the etiology of this serious public health problem. At the center of this debate though, Khantzian's self-medication hypothesis has captured most of the attention. In the present literature review, the authors evaluate this hypothesis in the light of our current knowledge. Formulated in a clinical context, in reaction to the psychoanalytic interpretation of addiction as a pleasure seeking pathology, Khantzian's hypothesis holds that schizophrenic patients use psychoactive substances to relieve their symptoms. Properly understood, this conjecture presupposes that, with the relief of certain target symptoms, substance use would no more be a necessity. But in reality, the use of psychoactive substances usually leads to a general deterioration of the patients' condition. Pharmacodependent schizophrenic patients relapse more often, they are more frequently hospitalized, they show more violent behaviors, and they are more frequently homeless. In particular, the positive symptoms of these patients are generally exacerbated by the psychoactive drugs--with the possible exception of opiates. This observation is in lign with the fact that psychostimulants (cocaine, amphetamines), anesthesic dissociatives (PCP, ketamine) as well as hallucinogens (cannabis, LSD) are all known to exert psychotomimetic effects. As for negative symptoms, the reality is more complex. Preliminary results certainly suggest that stimulants (minor or major) relieve these symptoms, but in the case of the other psychoactive substances, empirical evidence remains fragmentary. Still, the properties of psychoactive substances invite to pay close attention, among the negative symptoms, to the cognitive deficits, the social inaptitudes and the hedonic deficits of these patients. Unsatisfied with the self-medication hypothesis, an increasing number of researchers hypothesize that schizophrenic patients abuse drugs in hope to relieve the negative affects (stress, depression) that commonly accompany their symptomatology. Interestingly, increasing data link these negative manifestations and substance abuse among schizophrenic patients. But these same data do not elucidate whether these manifestations are primary or secondary to drug abuse. For the moment, these findings must be replicated. Furthermore, it remains to be clarified what negative affect is involved here. Is it stress, anxiety or, as commonly thought, depression? Other paths aim in the direction of personality traits and dissociation. The first path is suggested by recent studies demonstrating that pharmacodependent schizophrenic patients differ from non-abusing schizophrenics in that their personality is characterized by traits such as sensation seeking and impulsivity. As for the second path, it is suggested by a recurrent observation in addictive medicine practice, that is: alcohol, cannabis, ketamine, LSD, opiates, PCP, all these substances can induce dissociative states (depersonalization, derealization, etc.). Surprisingly, most of the hypotheses advanced so far have been formulated without reference to neuroscience. However, from a biological perspective, substance abuse among schizophrenic patients appears paradoxical: while the positive symptoms of schizophrenia might involve an hyperactivity of the reward system, the drugs of abuse all seem to increase dopamine release in that same system. That very paradox further casts some doubt on the self-medication hypothesis. And it opens an alternative: schizophrenic patients might be biologically vulnerable to the rewarding effects of drugs abuse. On the therapeutic level finally, the authors argue that polypharmacy medications such as clozapine and quetiapine, known to act on the reward system preferentially to the extrapyramidal system and known to dissociate fastly from the dopamine-D2 receptor, could simplify clinical intervention.
According to the Resource Allocation Model, it is logical to think that emotional mood states modulate the allocation of capacity, most cognitive tasks require some allocation of capacity, and in many instances there is a positive correlation between effort and memory. In cognitive science, the experimental paradigm of lexical decision task is used to investigate visual words recognition and lexical access. According to the Resource Allocation Model, we postulated that depressed patients take more time to recognize items from an affective loaded list. In order to compare their behavior in lexical decision task in this study, depressed patients and healthy controls were studied. We hoped to find an interaction between the mood state of subjects and the categories (affective or neutral) of words. This kind of interaction is expected to figure among the cognitive markers of depression. Two groups of right-handed adults served as subjects in our experiment. The subjects were living in the north west region of Quebec. The first group consisted of 11 depressed patients (mean age: 40.2; SD: 6.8). All of them met the DSM III criteria for major depressive disorder and the RDC. Patients were rated using the 24-item Hamilton Depression Rating Scale (HDRS). All depressed patients were without medications. The control group was composed with 24 subjects (mean age: 32.7; SD: 7.9). We built a depressive word-list (Mood-list) and a neutral word-list (Neutral-list) and used a computer for the lexical-decision task. We noted a significant interaction [F(1.33) = 10,035, p < 0.001] between the subjects group (depression vs control) and the words category (Moodlist vs Neutral-list).(ABSTRACT TRUNCATED AT 250 WORDS)
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