Confounding and the dementia of schizophrenia

Schizophrenia is often said to cause dementia, and previous studies have found cognitive impairment to be associated with schizophrenia. It is possible, however, that other causes of dementia and the study of patients not representative of all schizophrenics have contributed to these findings. The neuropsychological test scores of 26 schizophrenic outpatients were compared to those of 82 other patients with a history of psychosis. After other known causes of cognitive impairment were controlled for, the schizophrenics were not found to have cognitive impairment when compared to the other patients.     

Stability and course of neuropsychological deficits in schizophrenia

BACKGROUND: Neuropsychological deficits in schizophrenia appear to predate clinical symptoms of the disease and become more pronounced at illness onset, but controversy exists about whether and when further neuropsychological progression may occur. OBJECTIVE: To identify and characterize any subset of patients who evidenced progressive neuropsychological impairment, we compared the longitudinal stability of neuropsychological functioning in schizophrenic outpatients and normal comparison subjects. METHODS: One hundred forty-two schizophrenic outpatients and 206 normal comparison subjects were given annually scheduled comprehensive neuropsychological evaluations during an average of 3 years (range, 6 months to 10 years). Clinically and demographically defined subgroups were compared, and test-retest norms were used to identify individual patients who showed unusual worsening over time. RESULTS: The schizophrenic group was neuropsychologically more impaired than the normal comparison subjects but showed comparable test-retest reliability and comparable neuropsychological stability over both short (mean, 1.6 years) and long (mean, 5 years) follow-up periods. No significant differences in neuropsychological change were found between schizophrenic subgroups defined by current age, age at onset of illness, baseline level of neuropsychological impairment, improvement or worsening of clinical symptoms, and occurrence of incident tardive dyskinesia. Norms for change also failed to show neuropsychological progression in individuals with schizophrenia. CONCLUSIONS: Neuropsychological impairment in ambulatory persons with schizophrenia appears to remain stable, regardless of baseline characteristics and changes in clinical state. Our results may not be generalizable to the minority of institutionalized poor-outcome patients.     

Vitamin B12 deficiency in dementia and cognitive impairment: the effects of treatment on neuropsychological function

BACKGROUND: Vitamin B12 assay is part of the routine investigation of dementia, although few studies have investigated the effects of treatment on cognition. We examined the effects of B12 treatment on neuropsychological function and disease progression in patients presenting with dementia or cognitive impairment. METHODS: From 1432 patients who were assessed at the Bristol Memory Disorders Clinic, 125 patients with low serum B12 were identified. Sixty-six patients presenting with dementia, and 22 with cognitive impairment were seen for a second assessment after treatment. Changes in neuropsychological test scores were compared with those of patients with normal serum B12, matched by age and diagnosis. RESULTS: The majority of patients with low serum B12 had normal Hb and MCV values. We found no cases of reversible B12 deficiency dementia. The B12 treatment patients who presented with dementia showed no significant improvement, and no less deterioration, in their neuropsychological function than their matched group. However, a treatment effect was demonstrated among the patients presenting with cognitive impairment. These improved significantly compared to matched patients on the verbal fluency test (p<0.01). CONCLUSION: All patients with cognitive impairment should be investigated for B12 deficiency. Vitamin B12 treatment may improve frontal lobe and language function in patients with cognitive impairment, but rarely reverses dementia.     

Prevalence of cognitive impairment and dementia as defined by neuropsychological test performance

The Canadian Study of Health and Aging (CSHA) provided a population-based estimate of the prevalence of dementia of 8% for those aged 65 and older. Other studies have produced both higher and lower prevalence estimates. Factors that may contribute to these differences include: the use of or the reliance on neuropsychological testing, the consideration of functional impairment as a criterion for dementia and the inclusion of the category of cognitive impairment without dementia in the diagnostic classification. We examined the impact of these methodological factors by reanalyzing the CSHA database for those individuals who completed neuropsychological testing. If the diagnosis of dementia required only impaired neuropsychological test performance, there was an increased prevalence of dementia relative to the clinical consensus diagnosis, but including the requirement of functional impairment for dementia reduced this discrepancy. The findings illustrate the need for clear operationalization of diagnostic criteria for cognitive impairment and dementia in neuroepidemiological studies.     

Fronto-temporal function may distinguish bipolar disorder from schizophrenia

OBJECTIVES: There is evidence for differential neural alterations within the prefrontal cortex (PFC) in bipolar disorder I (BDI) and schizophrenia that may translate into different cognitive deficits. Our objective was to compare the cognitive profile of stable BDI and schizophrenic patients using neuropsychological tasks which utilize frontal systems but differ in terms of the exact neural circuits and cognitive processes involved. METHODS: We studied 43 patients with BDI, 54 with schizophrenia and 46 matched healthy participants. All participants completed (i) the Wisconsin Card Sorting Test (WCST) which is known to recruit the dorsal and ventral PFC, (ii) the verbal fluency task (VFT), which engages frontal-temporal regions, and (iii) the Stroop Colour Word Test (SWCT) which depends on the integrity of the cingulo-frontal network. A series of multivariate analyses examined differences between the cognitive profiles of BD and schizophrenic patients relative to that of healthy participants controlling for general intellectual ability and gender. RESULTS: Bipolar disorder I patients showed minimal verbal fluency impairment while schizophrenic patients demonstrated marked deficits on this task relative to the control and BDI groups. The two patient groups had comparable performance on the WCST. In the SWCT, schizophrenic patients showed impairment in both congruent and incongruent conditions while BD patients had deficits only in the latter. CONCLUSIONS: Absence of significant verbal fluency abnormalities and by inference dysfunction in the associated fronto-temporal circuitry may distinguish BDI from schizophrenia. Both disorders may show impairment in tasks involving cingulo-frontal networks with evidence of greater cingulate dysfunction in schizophrenia.     

Third-ventricle enlargement and neuropsychological deficit in schizophrenia.

Cerebral ventricular enlargement is present in a substantial subgroup of schizophrenic patients. Most, but not all studies examining neuropsychological performance and ventricular size in schizophrenics show more severe cognitive impairment in those patients with greatest ventricular enlargement. Inconsistencies in this literature have been attributed to different neuroimaging techniques, variation in patient characteristics across studies, and the variety of neuropsychological batteries used. In the present study, schizophrenic patients (n = 49 men, n = 23 women) and normal controls (n = 13 men, n = 18 women) underwent magnetic resonance (MR) imaging of the brain and extensive neuropsychological testing including measures of frontal and temporal lobe function. A complete coronal set of MR images was used to calculate volumetric estimates of lateral and third cerebral ventricles. Highly significant associations were found between cognitive deficits and third-ventricle volume, with measures of frontal functioning, attention, and concentration showing the most robust correlations. In contrast, neuropsychological performance was not highly associated with lateral ventricular size. These findings further support the pathophysiological relevance of ventricular enlargement in schizophrenia. More specifically, third, but not lateral, ventricular enlargement was associated with greater cognitive disturbance in this sample. Results are consistent with pathological involvement of periventricular diencephalic structures resulting in dysfunctional frontal and limbic processing in a subgroup of patients.     

Neuropsychological function in Alzheimer's disease. Pattern of impairment and rates of progression

Although patients with Alzheimer's disease (AD) generally have impairments in multiple areas of cognitive function, there are those patients who appear to have neuropsychological deficits more prominent in one domain than in other domains. We examined the neuropsychological status of 86 patients with probable AD and 92 elderly control subjects and identified the patterns of impairments in the patients with AD. Independent deficits of visuoconstructional and lexical/semantic abilities were identified in a subset of patients by a principal components analysis. Individual patients were identified who were predominantly impaired in one, but not the other, neuropsychological domain. There were no striking relationships between the demographic characteristics of the patients and their pattern of deficits at the initial evaluation. There were no significant differences in age at onset or rate of progression of dementia among patients with different patterns of cognitive dysfunction. A review of the results of this and other studies suggests that the language impairment in AD may be associated with two distinct neuropsychological abnormalities: a lexical/semantic impairment that is unrelated to onset or progression of symptoms, and a syntactic impairment that may be associated with earlier onset and more rapid progression of dementia.     

Cognitive dysfunction 24-31 years after isolated optic neuritis

OBJECTIVE: Cognitive dysfunction is common in multiple sclerosis (MS), but long-term data on cognition in patients with clinically isolated syndromes are sparse. METHODS: We determined cognitive functions in 22 patients 44-75 years old diagnosed with optic neuritis 24-31 years earlier but had no further clinical bouts and had not progressed clinically to MS. We used a neuropsychological test battery covering nine cognitive domains. Magnetic resonance imaging (MRI) of the brain had been performed earlier and was normal in six patients and showed two or more white matter abnormalities compatible with demyelinating lesions in 16 patients. RESULTS: On neuropsychological testing, one patient was within normal range on all tests, six subjects showed borderline results, and 15 patients (68%) showed significantly impaired performance in at least one cognitive domain. Seven patients showed significant impairment in two or more domains. Executive function, visuo-spatial ability, and information processing speed were the most frequently affected domains. There was no apparent correlation between MRI findings and cognitive function. CONCLUSIONS: We conclude that cognitive dysfunction is common in patients many years after clinically isolated optic neuritis. Cognitive dysfunction was found even in patients who had no apparent demyelinating lesions on follow-up MRI.     

Relationship between CT scan findings and neuropsychological performance in chronic schizophrenia

Studies relating CT abnormalities to impairments on neuropsychological tests in schizophrenic patients are critically reviewed. The overall conclusion is that there appears to be an association between CT abnormalities and neuropsychological deficits in at least some schizophrenic patient samples. It is proposed that there may be two classes of CT abnormalities in schizophrenia: "incidental" versus "essential" CT abnormalities and that neuropsychological impairment above the baseline levels found in most schizophrenic patients may be associated only with the former type. Only attempts to replicate these findings in different schizophrenic samples drawn from different settings can reveal whether this association between CT abnormalities and neuropsychological deficits is widely generalizable.     

Origine et renouveau du concept de démence dans la schizophrénie

An increasing amount of current literature on schizophrenia is devoted to the role dementia may play in its course. This renewed interest had the way paved by the very history of the dementia concept. Before Kraepelin coined the term of "dementia praecox" as the hallmark of a common terminal state for hebephrenia, catatonia and paranoid psychosis, dementia acquired, as soon as the end of the 18th-century its cognitive meaning. In France, Pinel yet spoke of an "abolition of thinking", but in the same time considered dementia as one of the four forms of mental alienation, alongside with mania, melancolia and idiotism. During the 19-th century dementia was defined as an acquired deficit of intelligence supported by a brain disease, but which could be due to a mental illness. Owing to progress in neuropathology, several diseases such as Alzheimer or Pick illnesses were identified as causes of dementia, so that the concept was annexed by neurologists and received less interest from psychiatrists, during the last century. That seemed to change, twenty years ago, when clinical discussions emerged around the issues raised by depressive (pseudo) dementia. In psychiatry, the broader conceptualization of schizophrenia introduced by Bleuler in 1911 has not been widely adopted, many authors having been continuing sharing the Kraepelinian view that, at least one form of the disease, was a chronic progressive illness leading to severe impairments in cognitive and social functioning. Historical variations in diagnostic criteria used for schizophrenia had an impact on the way psychiatrists assessed outcome of the disease, leading some of them to consider schizophrenia as a nosological category without natural boundaries and propose to abandon the concept. However the use of narrow criteria is currently prevailing. Advances in neurocognitive testing and changes in theoretical models allowed, at the end of the last century, to document that schizophrenia was characterized by a broadly based cognitive impairment. Deficits were found in various domains: global and selective verbal memory, non-verbal memory, bilateral and unilateral motor performance, visual and auditory attention, general intelligence, spatial ability, executive function, language and interhemispheric tactile-transfer test performance. The hypothesis according to which the vast majority of these cognitive deficits had a neurodevelopmental origin was recently challenged by findings from longitudinal neurocognitive and neuroimaging studies. Some studies, for example, show that if first episode patients have smaller left hippocampal volumes as compared with controls, there is also an association of smaller right hippocampal volumes with increased illness duration in chronic schizophrenia. Others have shown that neuropsychological evaluations before treatment permitted differentiation of primary deficits from changes secondary to medication or chronicity. Clinicians reported that in some cases of chronic schizophrenic patients, dementia could be a complication of the disease, sharing common neuropsychological features with frontotemporal dementia. The effect of age was discussed too, as seeming to play sometimes a part. Even if the cause of the degenerative process that appears to occur in the brains of some schizophrenic patients remains largely unknown, advances in neuropathological models of degeneration in the brain as well as in mechanisms and factors underlying its process, gave rise to hypotheses liable to explain how degenerative dementia could occur in schizophrenia. Excess products of membrane degeneration which was evidenced by magnetic resonance spectroscopy suggests increased apoptosis in some schizophrenic patients. Deficits in neurotrophic factors, free radical oxidation, excess glutamate activity have been implicated as well as abnormalities in dopamine and cortisol metabolism. Growing evidence that some newer antipsychotics seem capable to interfere with these processes, slowing down their progression and even stopping it, has contributed to the renewal of the concept, opening new avenues to preventive strategies in the treatment of schizophrenia.     

Adult-onset Hallervorden-Spatz syndrome presenting as cortical dementia

The authors examined behavioral and pathophysiologic substrates in a patient with adult-onset Hallervorden-Spatz syndrome who presented with insidious cognitive decline but no motor impairment. The authors combined longitudinal case history and serial neuropsychologic testing with functional neuroimaging (positron emission tomography), structural neuroimaging (magnetic resonance imaging), and brain tissue analyses. Serial assessments of a 29-year-old woman showed progressive dementia. Marked cognitive and behavioral deficits were seen on neuropsychologic testing, corresponding to striking cortical abnormalities on positron emission tomography, magnetic resonance imaging, and histopathologic studies. Typical motor manifestations of the disorder did not emerge until the patient was 34 years old, 5 years after the onset of cognitive symptoms. Hallervorden-Spatz syndrome should be considered in the differential diagnosis of progressive cortical dementia in a young adult, even in the absence of motor dysfunction.     

Cognitive impairment and in vivo metabolites in first-episode neuroleptic-naive and chronic medicated schizophrenic patients: a proton magnetic resonance spectroscopy study

Involvement of the prefrontal cortex in schizophrenia has been implicated by neuropsychological, as well as neuropathological and imaging studies. Reductions of N-acetylaspartate (NAA), an in vivo marker of neuronal integrity, have repeatedly been detected in the frontal lobes of patients with schizophrenia by proton magnetic resonance spectroscopy (1H-MRS). In chronic medicated patients, a positive correlation between NAA levels of the prefrontal cortex and cognitive functioning has been observed, but to date, there have been no studies in first-episode neuroleptic-naive patients. In this study, single-voxel 1H-MRS was used to investigate neuronal function of the dorsolateral prefrontal cortex in 15 first-episode and 20 chronic schizophrenic patients. Outcomes were compared to 20 age-matched healthy controls to assess the relationship between prefrontal metabolism and neuropsychological performance. Patients with chronic schizophrenia had significant reductions of NAA, glutamate/glutamine, and choline levels compared to first-episode patients and healthy controls. Furthermore, creatine and phosphocreatine were significantly reduced in both patient groups compared to healthy controls. In the neuropsychological tests, chronic schizophrenic patients performed significantly poorer in the Auditory Verbal Learning Task (AVLT) compared to first-episode patients. In both patient groups, NAA levels of the left frontal lobe significantly correlated with performances in verbal learning and memory. These results corroborate data from recent structural and spectroscopic imaging studies of the frontal lobes in schizophrenia, in which cortical gray matter reductions after onset of symptoms as well as reduced levels of NAA in chronic, but not in first-episode schizophrenic patients have been reported.     

Does frontal normality exist in schizophrenia? A saccadic eye movement study.

Many observations have supported the general idea of impaired frontal function in schizophrenia. In particular, neuropsychological studies have shown severe frontal deficits. However, other studies found normal cognitive function in a proportion of patients. Since saccadic tasks also provide an index of frontal function, we examined the presence of frontal deficits in patients by means of both neuropsychological and saccadic tasks, and compared the sensitivity of both approaches for frontal impairment. In addition, we examined the relationship between saccadic and neuropsychological measures. Twenty-four schizophrenic patients and twenty healthy controls completed an extensive neuropsychological battery and three saccadic tasks. Based on the neuropsychological battery alone, 42% of the patients showed frontal deficits, whereas combined use of neuropsychological and saccadic tasks resulted in 79% with frontal deficits. The antisaccade task appeared able to detect frontal deficits in patients who were without frontal impairment on the neuropsychological battery. Saccadic deficits were, however, not necessarily accompanied by deficits on frontal neuropsychological measures. This suggests that the saccadic and neuropsychological tasks used in the present study targeted different frontal functions. This view was supported by the lack of correlations between saccadic and frontal neuropsychological measures.     

Schizophrenic dementia. Clinical and computed axial tomography correlates

Twenty-seven chronic schizophrenic patients and nine other psychiatric patients closely matched in education were compared on the Halstead-Reitan Battery and the Wechsler Adult Intelligence Scale (WAIS). The schizophrenic patients as a group showed significantly poorer performance on the WAIS (full scale: X +/- SD, 92.9 +/- 2.9 vs. 110.8 +/- 2.1, p less than .002) and the Halstead-Reitan Battery (HRB; Average Impairment Range = 2.1 +/- .2 vs. 1.12 +/- .06, p less than .003). In addition the schizophrenic patients did significantly worse than did nonschizophrenic patients on all WAIS subtests and scored in the impaired range on most HRB subtests. Computed axial tomography scans revealed large ventricles on nine schizophrenic patients and cortical atrophy on three others. Among schizophrenics, the enlarged ventricle group consistently scored the worst. No relationship was seen between neuropsychological test performance and degree of ongoing psychopathology as measured by the Brief Psychiatric Rating Scale. These findings are consistent with previous reports of cognitive impairment in schizophrenia and are discussed in terms of regional localization. They provide additional evidence that the impairment is related to the disease process and that structural abnormalities are associated with the more severe condition.     

Community based measures for managing mild cognitive impairment and dementia: the Osaki-Tajiri Project]

A cross-sectional study of aged patients with mild cognitive impairment in a local community was undertaken to investigate the clinical features of the condition, in addition to a longitudinal study to research its progression to cognitive deficit. Impairment of the basic functions of attention and executive function was confirmed, as opposed to impairment in the cognitive domain itself. Magnetic resonance imaging (MRI) findings showed a pattern close to that of healthy persons in their 80s, rather than that of patients with cognitive deficit. The results of the longitudinal study showed more progression to cognitive deficit when the clinical dementia rating was 0.5 in domains other than memory. No effects of lifestyle, internal diseases or psychosocial intervention were confirmed. In progression to Alzheimer's disease, generally low cognitive function and general atrophy were involved, whereas frontal lobe function, atrophy of the frontal and temporal lobes, white matter changes and cerebral infarction were related to progression to vascular dementia. Excessive dependence on primary prevention should be avoided for aged patients with mild cognitive impairment; rather, secondary prevention, using clinical dementia rating, psychological testing and MRI are desirable.     

Community based measures for managing mild cognitive impairment: The Osaki–Tajiri Project

A cross‐sectional study of aged patients with mild cognitive impairment in a local community was undertaken to investigate the clinical features of the condition, in addition to a longitudinal study to research its progression to cognitive deficit. Impairment of the basic functions of attention and executive function was confirmed, as opposed to impairment in the cognitive domain itself. Magnetic resonance imaging (MRI) findings showed a pattern close to that of healthy persons in their 80s, rather than that of patients with cognitive deficit. The results of the longitudinal study showed more progression to cognitive deficit when the clinical dementia rating was 0.5 in domains other than memory. No effects of lifestyle, internal diseases or psychosocial intervention were confirmed. In progression to Alzheimer's disease, generally low cognitive function and general atrophy were involved, whereas frontal lobe function, atrophy of the frontal and temporal lobes, white matter changes and cerebral infarction were related to progression to vascular dementia. Excessive dependence on primary prevention should be avoided for aged patients with mild cognitive impairment; rather, secondary prevention, using clinical dementia rating, psychological testing and MRI are desirable.     

Glial fibrillary acidic protein-immunoreactive astrocytosis in elderly patients with schizophrenia and dementia

Clinical and neuropsychological studies of chronically institutionalized patients with schizophrenia indicate that severe cognitive impairment and functional disability in late life are very prevalent. The biological substrates for this dementia remain unknown. While subtle cytoarchitectural and morphometric abnormalities have been described in patients with schizophrenia and interpreted as reflecting aberrant neurodevelopment, post-maturational injury or neurodegeneration associated with gliosis remain as plausible explanations of at least some of the clinical manifestations of schizophrenia. We monitored astrocytosis and neurofibrillary tangle (NFT) formation in 21 elderly patients with schizophrenia (14 with concurrent dementia, 7 without), and in 12 normal and 5 Alzheimer's disease (AD) control cases. Astrocytes in ventromedial temporal, frontal, and calcarine cortices were immunohistochemically identified with monoclonal antibodies directed at glial fibrillary acidic protein (GFAP) and vimentin, and NFTs were labeled with an anti-tau antibody specific for paired helical filaments. There were no increases in GFAP- or vimentin-immunoreactive astrocyte counts, GFAP optical density, or NFT counts for the schizophrenic group as a whole compared to the non-neuropsychiatric group, while both groups differed from AD. When patients with schizophrenia were divided into demented and non-demented subtypes, those with dementia demonstrated significantly greater numbers of GFAP-positive astrocytes than those without dementia. These data may reflect an up-regulation of GFAP in normal astrocytes or the presence of reactive astrocytosis in a subgroup of schizophrenics. In the absence of any diagnostic neuropathological findings in this subgroup, the implications of these observations for the pathogenesis of schizophrenia remain to be determined. Received: 24 July 1995 / Revised, accepted: 15 September 1995     

A follow-up study of cognitive impairment due to inferior capsular genu infarction

Abulia, memory loss, other cognitive deficits, and behavioral changes consistent with dementia can follow an inferior capsular genu infarction, but only little is known about the time course of these disturbances. The present study describes the long-term outcome of cognitive defects in four patients with inferior capsular genu infarction who underwent a neuropsychological examination within 3 and 12 months of onset. Three patients had infarcts in the inferior genu of the left internal capsule and had similar symptoms in the acute phase: disorientation, memory loss, language impairment, and behavioral changes. The patient with right-side infarct showed memory impairment and behavioral changes. Three patients had deficits in one or more cognitive domains on the first assessment, but none was demented. By the second evaluation all subjects had improved. In two patients there were a moderate memory defect persisted and a language disturbance. Improvement in these disturbances during long-time follow-up demonstrates that there are alternative pathways that reestablish the functional connections damaged by the strategically located capsular genu infarct. Inferior capsular genu infarction is not a cause of persisting “strategic infarct dementia.” Received: 20 October 1998 Received in revised form: 30 December 1998 Accepted: 11 February 1999     

Evaluation of various methods of assessing symptoms of cognitive impairment and dementia.

BACKGROUND AND PURPOSE: The effect of different diagnostic criteria for detecting dementia in both epidemiological and stroke cohort studies has been shown, but comparison between different assessment methods has only seldom been done. We compared both assessment methods and diagnostic criteria for dementia in a large well-defined stroke cohort. SUBJECT AND METHODS: A group of 227 of 486 patients aged 55 to 85 years who 3 months after ischemic stroke completed a comprehensive neuropsychological test battery, structured clinical mental status examination of defined cognitive domains with expanded Mini-Mental State Examination. The criteria for dementia were those of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III, DSM-III-R) and the National Institute of Neurological Disorders and Stroke-Associated Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN). RESULTS: The main differences between clinical and neuropsychological examinations were seen in memory functions: clinically 24.7% and neuropsychologically 54.2% had impairment in short-term memory and 10.4% versus 5.3% in long-term memory. Accordingly, the prevalence of dementia varied greatly: It was clinically 14.1% by DSM-III, 9.7% by DSM-III-R and 8.4% by NINDS-AIREN criteria. The corresponding frequencies based on neuropsychological evaluation were 27.3%, 4.0% and 25.6%. Between these 3 diagnostic criteria the concordance varied in clinical testing between 59.4%-68.8% (kappa 0.72-0.79) and in neuropsychological testing between 14.5%-81.1% (kappa 0.20-0.86). The concordance between clinical and neuropsychological testing was 56.8% (kappa 0.42) by DSM-III, 31.6% (kappa 0.35) by DSM-III-R and 25.5% (kappa 0.24) by NINDS-AIREN. CONCLUSIONS: The frequency of poststroke dementia and cognitive decline varied sharply when different systems of diagnostic classification and methods were used. This may have serious influences on investigation and treatment of patients. We underline the importance of further debate and studies to refine the categories of cognitive impairment used in the setting of CVD.     

ORIGINAL ARTICLE: Inter-peak Latency of Auditory Event-related Potentials (P300) in Cases of Aged Schizophrenia and Alzheimer-type Dementia

Background : Both patients with schizophrenia and those with dementia show cognitive difficulties, and in many cases of schizophrenia the cognitive disturbance is progressive, as it is in dementia. Event-related potentials have revealed cognitive impairments in patients with schizophrenia and dementia, but most studies of event-related potentials in cases of psychiatric illness or dementia have focused on the single peak latency of the event-related potential components. In the present study, we investigated the cognitive function in elderly patients with schizophrenia and Alzheimer-type dementia (AID) using auditory event-related potentials (P300).
Methods : P300 was recorded using the tone discrimination task and peak latencies for N1, P2, N2 and P3 at the Pz electrode site were measured. In addition to analyzing peak latencies of P300, we also analyzed inter-peak latencies (IPL; N1-P2, P2-N2, and N2-P3). Twenty-two elderly residual-type schizophrenics and 36 patients with AID were compared with 39 age-matched healthy volunteers.
Results : The mean latencies of P3 and mean IPL of P2-N2 in elderly schizophrenic patients were longer than those of the controls. In ATD the mean latencies of N2 and P3 and the mean IPL of P2-N2 were longer than those of the controls. When the mean latencies of ATD patients were compared with those in patients with schizophrenia, P2, N2, and P3 latencies and N1-P2 and P2-N2 IPL were longer.
Conclusion : These findings suggest that a similar impairment of the cognitive process is found in elderly patients with schizophrenia and those with ATD and that the degree of the impairment of patients with ATD is more severe than that of elderly patients with schizophrenia.