What Do We Know About Neuropsychological Aspects Of Schizophrenia?

Application of a neuropsychological perspective to the study of schizophrenia has established a number of important facts about this disorder. Some of the key findings from the existing literature are that, while neurocognitive impairment is present in most, if not all, persons with schizophrenia, there is both substantial interpatient heterogeneity and remarkable within-patient stability of cognitive function over the long-term course of the illness. Such findings have contributed to the firm establishment of neurobiologic models of schizophrenia, and thereby help to reduce the social stigma that was sometimes associated with purely psychogenic models popular during parts of the 20th century. Neuropsychological studies in recent decades have established the primacy of cognitive functions over psychopathologic symptoms as determinants of functional capacity and independence in everyday functioning. Although the cognitive benefits of both conventional and even second generation antipsychotic medications appear marginal at best, recognition of the primacy of cognitive deficits as determinants of functional disability in schizophrenia has catalyzed recent efforts to develop targeted treatments for the cognitive deficits of this disorder. Despite these accomplishments, however, some issues remain to be resolved. Efforts to firmly establish the specific neurocognitive/neuropathologic systems responsible for schizophrenia remain elusive, as do efforts to definitively demonstrate the specific cognitive deficits underlying specific forms of functional impairment. Further progress may be fostered by recent initiatives to integrate neuropsychological studies with experimental neuroscience, perhaps leading to measures of deficits in cognitive processes more clearly associated with specific, identifiable brain systems

Examining the utility of a clustering method for analysing psychological test data

The belief that certain disorders will produce specific patterns of cognitive strengths and weaknesses on psychological testing is pervasive and entrenched in the area of clinical neuropsychology, both with respect to expectations regarding the behaviour of individuals and clinical groups. However, there is little support in the literature for such a belief. To the contrary, studies examining patterns of cognitive performance in different clinical samples without exception find more than one pattern of test scores. Lange (2000) in his comprehensive analysis of WAIS-R/WMS-R data for a large sample of mixed clinical cases found that three to five profiles described variations in test performances within clinical diagnoses. Lange went on to show that these profiles occurred with approximately equal frequency in all diagnostic groups. He additionally found four profiles in an exploratory analysis of WAIS-III/WMS-III data from a similar sample. The goals of the current dissertation were to: a) replicate Lange’s findings in a larger clinical sample; b) extend the scope of these findings to a wider array of psychological tests; and c) develop a method to classify individual cases in terms of their psychological test profile. The first study assessed 849 cases with a variety of neurological and psychiatric diagnoses using hierarchical cluster and K-Means analysis. Four WAIS-III/WMS-III profiles were identified that included approximately equal numbers of cases from the sample. Two of these profiles were uniquely related to two of Lange’s profiles, while the remaining two demonstrated relationships with more than one of Lange’s clusters. The second study expanded the neuropsychological test battery employed in the analysis to include the Trail Making Test, Boston Naming Test, Wisconsin Card Sorting Test, Controlled Oral Word Association Test, and Word Lists from the WMS-III reducing the number of clinical cases to 420. In order to compensate for the impact of the reduced number of cases and increased number of variables on potential cluster stability, the number of test score variables was reduced using factor analysis. In this manner the 22 variables were reduced to six factor scores, which were then analysed with hierarchical cluster and K-Means analysis yielding five cognitive profiles. The third study examined the potential clinical utility of the five cognitive profiles by developing a single case methodology for allocating individual cases to cognitive profiles. This was achieved using a combination of a multivariate outlier statistic, the Mahalanobis Distance, and equations derived from a discriminant function analysis. This combination resulted in classification accuracies exceeding 88% when predicting the profile membership based upon the K-Means analysis. The potential utility of this method was illustrated with three age-, education-, gender-, and diagnostically-matched cases that demonstrated different cognitive test profiles. The implications of the small number of cognitive profiles that characterise test performance in a diverse sample of neurological and psychiatric cases as well as the clinical utility of an accurate classification method at the individual case level was discussed. The role of such a classification system in the design of individualised rehabilitation programmes was also highlighted. This research raises the intriguing possibility of developing a typology based on human behaviour rather than a medical nosology. In effect, replacing the medical diagnosis so ill-suited to encompassing the complexities of human behaviour, with a more appropriate “psychological diagnosis” based on cognitive test performance

What Do We Know About Neuropsychological Aspects Of Schizophrenia?

Application of a neuropsychological perspective to the study of schizophrenia has established a number of important facts about this disorder. Some of the key findings from the existing literature are that, while neurocognitive impairment is present in most, if not all, persons with schizophrenia, there is both substantial interpatient heterogeneity and remarkable within-patient stability of cognitive function over the long-term course of the illness. Such findings have contributed to the firm establishment of neurobiologic models of schizophrenia, and thereby help to reduce the social stigma that was sometimes associated with purely psychogenic models popular during parts of the 20th century. Neuropsychological studies in recent decades have established the primacy of cognitive functions over psychopathologic symptoms as determinants of functional capacity and independence in everyday functioning. Although the cognitive benefits of both conventional and even second generation antipsychotic medications appear marginal at best, recognition of the primacy of cognitive deficits as determinants of functional disability in schizophrenia has catalyzed recent efforts to develop targeted treatments for the cognitive deficits of this disorder. Despite these accomplishments, however, some issues remain to be resolved. Efforts to firmly establish the specific neurocognitive/neuropathologic systems responsible for schizophrenia remain elusive, as do efforts to definitively demonstrate the specific cognitive deficits underlying specific forms of functional impairment. Further progress may be fostered by recent initiatives to integrate neuropsychological studies with experimental neuroscience, perhaps leading to measures of deficits in cognitive processes more clearly associated with specific, identifiable brain systems

Malingering base rates and detection methods in Australia

Neuropsychology malingering base rates have not been widely investigated in Australia. Estimates in North America vary with as many as 4 in 10 people evaluated for personal injury or compensation cases suspected of exaggerating symptoms. Data on Australian neuropsychology symptom exaggeration base rates were estimated using a modified and expanded version of a survey previously designed for this purpose (Mittenberg, Patton, Canyock, & Condit, 2002). Figures were based on an estimated 1818 annual cases involved in personal injury, (n = 542), disability (n = 109), criminal (n = 108), or medical (n = 1059) matters. Symptom exaggeration base rates associated with referral type and diagnoses were variable. Specifically, 17% of criminal, 13% of personal injury, 13% of disability or workers compensation, and 4% of medical or psychiatric cases were reported to involve symptom exaggeration or probable symptom exaggeration. The highest rates of symptom exaggeration included cases referred for mild head injury (23%), pain or somatoform disorders (15%), moderate to severe head injury (15%), and fibromyalgia or chronic fatigue (15%). Overall, Australian symptom exaggeration base rates reported in this study were lower compared with base rates previously reported in North America

Methods of Detecting Malingering and Estimated Symptom Exaggeration Base Rates in Australia

Neuropsychology malingering base rates have not been widely investigated in Australia. Estimates in North America vary with as many as 4 in 10 people evaluated for personal injury or compensation cases suspected of exaggerating symptoms. Data on Australian neuropsychology symptom exaggeration base rates were estimated using a modified and expanded version of a survey previously designed for this purpose (Mittenberg, Patton, Canyock, & Condit, 2002). Figures were based on an estimated 1818 annual cases involved in personal injury, (n = 542), disability (n = 109), criminal (n = 108), or medical (n = 1059) matters. Symptom exaggeration base rates associated with referral type and diagnoses were variable. Specifically, 17% of criminal, 13% of personal injury, 13% of disability or workers compensation, and 4% of medical or psychiatric cases were reported to involve symptom exaggeration or probable symptom exaggeration. The highest rates of symptom exaggeration included cases referred for mild head injury (23%), pain or somatoform disorders (15%), moderate to severe head injury (15%), and fibromyalgia or chronic fatigue (15%). Overall, Australian symptom exaggeration base rates reported in this study were lower compared with base rates previously reported in North America

Increased frequency of alpha-synuclein in the substantia nigra in human immunodeficiency virus infection.

The frequency of neurodegenerative markers among long surviving human immunodeficiency virus (HIV)-infected individuals is unknown, therefore, the present study investigated the frequency of alpha-synuclein, beta-amyloid, and HIV-associated brain pathology in the brains of older HIV-infected individuals. We examined the substantia nigra of 73 clinically well-characterized HIV-infected individuals aged 50 to 76 years from the National NeuroAIDS Tissue Consortium. We also examined the frontal and temporal cortical regions of a subset of 36 individuals. Neuritic alpha-synuclein expression was found in 16% (12/73) of the substantia nigra of the HIV+cases and none of the older control cases (0/18). beta-Amyloid deposits were prevalent and found in nearly all of the HIV+cases (35/36). Despite these increases of degenerative pathology, HIV-associated brain pathology was present in only 10% of cases. Among older HIV+adults, HIV-associated brain pathology does not appear elevated; however, the frequency of both alpha-synuclein and beta-amyloid is higher than that found in older healthy persons. The increased prevalence of alpha-synuclein and beta-amyloid in the brains of older HIV-infected individuals may predict an increased risk of developing neurodegenerative disease

A 1-week sleep and light intervention improves mood in premenstrual dysphoric disorder in association with shifting melatonin offset time earlier

To test the hypothesis that 1 week of combined sleep and light interventions (SALI), which phase-advance (shift earlier) melatonin circadian rhythms, improves mood significantly more than phase-delay (shift later) SALI. After a 2-month diagnostic evaluation for premenstrual dysphoric disorder (PMDD per DSM-5 criteria) in a university clinical research setting, 44 participants enrolled in baseline studies were randomized in the luteal phase at home to (A) a phase-advance intervention (PAI): 1 night of late-night wake therapy (LWT: sleep 9 pm-1 am) followed by 7 days of the morning (AM) bright white light (BWL), or (B) a phase-delay intervention (PDI): 1 night of early-night wake therapy (EWT: sleep 3-7 am) plus 7 days of the evening (PM) BWL. After a month of no intervention, participants underwent the alternate intervention. Outcome measures were mood, the melatonin metabolite, 6-sulfatoxymelatonin (6-SMT), and actigraphy (to assess protocol compliance). At baseline, atypical depression correlated positively with phase delay in 6-SMT offset time (r = .456, p = .038). PAI advanced 6-SMT offset from baseline more than PDI (p < .05), and improved raw mood scores more than PDI (p < .05). As hypothesized, percent improvement in mood correlated positively with a phase advance from baseline in 6-SMT offset time (p < .001). Treatment with 1 night of advanced/restricted sleep followed by 7 days of AM BWL (PAI) was more efficacious in reducing PMDD depression symptoms than a PDI; mood improvement occurred in association with phase advance in 6-SMT offset time. Combined SALIs offer safe, efficacious, rapid-acting, well-tolerated, non-pharmacological, non-hormonal, affordable, repeatable home interventions for PMDD. Clinical Trials.gov NCT # NCT01799733