Search

To study whether attention deficits differ between TBI (traumatic brain injury) patients with and without depressive symptoms.The study group (n = 61, mean age = 59 years) consisted of symptomatic TBI patients injured on average 30 years earlier. They were studied with a broad range of attention tasks including computerized methods. The patients were divided into those with depressive symptoms (n = 32) and those without (n = 29), according to the short form of the Beck depression scale with a cut-off score of 5. In addition, a diagnosis of major depression was applied according to the Schedules for Clinical Assessment in Neuropsychiatry (SCAN) (n = 6). The groups with depression or depressive symptoms were compared with the non-depressed TBI patients and with an age- and education-matched healthy control group (n = 31).Cognitive methods that require flexibility (Trail making B, Card sorting, Word fluency) and working memory (Subtraction test) were sensitive to discriminate TBI patients without depressive symptoms from the control subjects (p0.001). Only a few methods were able to discriminate the TBI patients with depressive symptoms from those without (p0.001 for Simple reaction time, p0.003 for Vigilance test). The depressed TBI patients (assessed by SCAN) did not differ from the non-depressed TBI patients in attention functions.The results suggest that problems in complex attention processing are more specific to TBI, while slowness in simple psychomotor speed and impaired sustained attention may be mostly related to depressive symptoms in patients with chronic TBI sequelae.

Objective: To examine the association between hippocampal volumes, general brain atrophy, and apolipoprotein E ( APOE ) polymorphism in patients with a remote traumatic brain injury (TBI). Methods: MRI-based volumetric analyses of the hippocampus and lateral ventricles were performed in 58 patients with TBI of varying severity on average 31.3 years after the trauma. The APOE genotype was determined using standard methods and correlated with the MRI volumetric measurements. Results: Hippocampal or lateral ventricle volumes did not differ significantly in those patients with the APOE -e4 allele ( APOE 4) vs those without this allele. Conclusions: The APOE -e4 allele was not associated with the development of hippocampal or ventricular atrophy after traumatic brain injury. If the APOE -e4 allele is associated with an unfavorable outcome after traumatic brain injury as proposed, this association may involve mechanisms other than those responsible for the development of brain atrophy.

The objective was to evaluate whether hormone therapy (HT) gives any benefit against the possible impairment of cognitive performance when challenged by acute sleep deprivation. Twenty postmenopausal women volunteered (age range 59-72 years, mean=64.4 years, SD=4.4): 10 HT users and 10 nonusers. Eleven young women served as a control group for the cognitive age effect (age range 20-26 years, mean age 23.1 years, SD=1.6). The subjects spent four consecutive nights at the sleep laboratory and were exposed to acute sleep deprivation of 40 h. Measures of attention (reaction speed and vigilance), alertness, and mood were administered every 2 h during the daytime and every hour during the sleep deprivation night. Postmenopausal women performed slower than young controls, whereas young controls made more errors. In HT users, the recovery night did not fully restore the performance in the simple and two-choice reaction time tasks, but in nonusers it did so. Sleep deprivation had a detrimental, yet reversible effect on vigilance in all groups. In all groups, sleepiness started to increase after 15 h of sleep deprivation and remained elevated in the morning after the recovery night. Prolonged wakefulness or HT had no effect on mood. In conclusion, sleep deprivation impaired cognitive performance in postmenopausal as well as young women. Postmenopausal women kept up their performance at the expense of reaction speed and young women at the expense of accuracy. One night was not enough for HT users to recover from sleep deprivation. Thus, HT gave no benefit in maintaining the attention and alertness during sleep deprivation.

Objective: To evaluate longitudinal cognitive changes in patients over three decades following traumatic brain injury (TBI). Method: Two hundred ten patients with substantial TBI of variable severity were initially assessed between 1966 and 1972 at Turku University Hospital (Finland). Of these, 61 patients could be studied using the same assessments in the follow-up examination, on average 30 years after the TBI. The results of the follow-up assessment were also compared with an age- and education-matched control group. During each examination, patients were assessed with five subtests of the Wechsler Adult Intelligence Scale, three tests for episodic memory, and the general cognitive decline was determined. Results: The general pattern of slight cognitive decline during a 30-year follow-up contrasted with improvement in semantic memory. Women maintained their cognitive level, but men showed a decline during the follow-up, especially in visuospatial ability and visual memory. Younger patients were likely to maintain or even improve their cognitive functioning. Conclusions: Most of the patients had mild cognitive decline during the follow-up, but this decline was influenced by gender and age at injury. Unlike the long-term course in the other domains of cognition, semantic memory showed good recovery potential after traumatic brain injury (TBI). The profile of long-term cognitive decline after TBI seems to be qualitatively different from the early signs of dementia of the Alzheimer type.

The aim of the study was to relate cognitive effects of a remote traumatic brain injury (TBI) to MRI findings and severity of injury.Sixty-one patients were assessed on average 30 years after a TBI of variable severity. A comprehensive cognitive test battery was used to evaluate memory, executive functions and cognitive overall impairment. Multiple regression analyses were used to examine the relationships between cognitive variables and MRI volumetric findings (the volumes of the hippocampus and the lateral ventricles) and local contusions on MRI. Also, the effect of injury severity on cognitive outcome was evaluated.Reductions in hippocampal volumes and lateral ventricular enlargement were significantly associated with impaired memory functions, memory complaints and executive functions. Of the MRI parameters used, the best predictor for cognitive outcome was the volume of the lateral ventricle. There was only a modest relationship between severity of injury and cognitive performance.The results show that long-term memory impairments after TBI are associated with MRI volumetric measures. This suggests that the degree of diffuse injury leading to atrophic changes is prognostically more important than the initial severity of TBI.

The nature of the visual perception deficits in Parkinson's disease (PD) has remained unclear. The present study explored whether there emerge deficits in the different stages of visual object recognition in early PD. Twenty-eight patients and 14 healthy controls were studied. A set of reaction time tasks were applied to measure the different stages of object recognition. The results indicate some selective problems in both basic perceptual and semantic visual processing at an early stage of cognitive deterioration in PD.

Objectives – The purpose of the present study was to divide visual object recognition into different stages and to reveal which of these stages are impaired in early Alzheimer's disease (AD). Methods – Performance in object detection, familiarity detection, semantic name and word categorization, and identification with naming were studied by using two-choice reaction-time tasks. Ten patients with newly diagnosed AD and 14 healthy subjects were studied. Results – Patients with early AD had impairments in several stages of the object recognition process. After controlling for the basic visuomotor slowness, they were as fast and as accurate as the controls in object detection, but had difficulties in all stages that required semantic processing. Conclusions – Semantic memory impairments contribute to the deficits in visual object recognition in early AD. Thus, the semantic memory deficit may be manifested in several ways in the difficulties that AD patients experience in everyday life.

Patients who had suffered traumatic brain injury were evaluated to determine the occurrence of psychiatric disorders during a 30-year follow-up.Sixty patients were assessed on average 30 years after traumatic brain injury. DSM-IV axis I disorders were diagnosed on a clinical basis with the aid of the Schedules for Clinical Assessment in Neuropsychiatry (version 2.1), and axis II disorders were diagnosed with the Structured Clinical Interview for DSM-III-R Personality Disorders. Cognitive impairment was measured with a neuropsychological test battery and the Mini-Mental State Examination.Of the 60 patients, 29 (48.3%) had had an axis I disorder that began after traumatic brain injury, and 37 (61.7%) had had an axis I disorder during their lifetimes. The most common novel disorders after traumatic brain injury were major depression (26.7%), alcohol abuse or dependence (11.7%), panic disorder (8.3%), specific phobia (8.3%), and psychotic disorders (6.7%). Fourteen patients (23.3%) had at least one personality disorder. The most prevalent individual disorders were avoidant (15.0%), paranoid (8.3%), and schizoid (6.7%) personality disorders. Nine patients (15.0%) had DSM-III-R organic personality syndrome.The results suggest that traumatic brain injury may cause decades-lasting vulnerability to psychiatric illness in some individuals. Traumatic brain injury seems to make patients particularly susceptible to depressive episodes, delusional disorder, and personality disturbances. The high rate of psychiatric disorders found in this study emphasizes the importance of psychiatric follow-up after traumatic brain injury.

We examined the relation between the dopaminergic function and the cognitive performance of patients with Parkinson's disease (PD). The subject sample consisted of ten patients in the early course of PD and with no previous antiparkinsonian medication. The dopaminergic function of the caudate nucleus and the putamen was studied with [(18)F]fluorodopa positron emission tomography, and the cognitive performance with a comprehensive battery of neuropsychological tests including tests sensitive to frontal lobe function. The decreased [(18)F]fluorodopa uptake in the right caudate nucleus was found to be related to slow processing time, measured as the difference between the incongruent and the congruent subtests of the Stroop Test (r=-0.85, P=0.002), a similar trend was seen in the left caudate (r=-0.60, P=0.07). Similar correlation was not detected in the putamen. The present findings provide evidence that the decreased dopaminergic function in the right caudate nucleus is related to the impaired performance in tests sensitive to frontal lobe function in patients at an early stage of PD and with no antiparkinsonian medication.

The aim of the present study was to determine whether a cognitive decline, related to multiple sclerosis (MS), also involves deficits in semantic memory. Semantic memory function was evaluated by studying the conscious understanding of conceptual meanings. A group of MS patients with cognitive decline was presented with four tasks concerning concepts, their attributes and relationships to other concepts. The tasks were designed to measure spontaneous, cued and recognition performance separately. The patients had difficulties in understanding conceptual meanings. Easing the retrieval demands of the tasks did not help them to improve their performance which was poorer than the control group's on every task used. The results indicate a retrieval deficit combined with an underlying storage deficit in the semantic memory of MS patients with cognitive decline.

The purpose of this study was to illustrate how cognitive functioning evolves over time in patients with multiple sclerosis. We followed the evolution of cognitive performances in two clinically and demographically similar multiple sclerosis groups, the 'cognitively preserved' (n = 20) and the 'cognitively mildly deteriorated' (n = 22), and in healthy controls (n = 34). We conducted the follow-up examination using the Mild Deterioration Battery, the Mini-Mental State Examination, and a set of additional neuropsychological measures after an interval of 3 years. The drop-out rate in our study was only 5%. The 'cognitively preserved' multiple sclerosis group showed substantial neuropsychological stability by performing as well as the controls both at baseline and at follow-up. By contrast, the initially 'cognitively mildly deteriorated' group demonstrated progressive cognitive decline on many neuropsychological tests. The intermediate-length screening battery, the Mild Deterioration Battery, was sensitive to this decline, whereas the briefer Mini-Mental State Examination was not. The progressive cognitive decline could not be predicted from other disease variables. The study demonstrated that intact cognitive functioning in multiple sclerosis may remain stable, whereas incipient cognitive decline seems to be widespread and progressive in nature. Thus, progressive cognitive deterioration should be considered as one of the characteristics of multiple sclerosis.

The present study focused on perceptual identification priming (implicit memory) in early stages of dementia by studying demographically and cognitively matched patients with Alzheimer's disease (AD) and Parkinson's disease (PD). The AD and PD groups performed normally on perceptual identification priming, whereas their explicit recognition memory was equally impaired compared to normal controls. These results imply that priming in perceptual identification relies on the perceptual memory system which can resist not only impairments of explicit memory but also widespread cognitive deterioration induced by the neurodegenerative processes in AD or PD.

SynopsisFour WAIS (Wechsler Adult Intelligence Scale) subtests, and tasks of memory and cognitive control were administered to a population sample of 143 men and 179 women. Subjects with a minor advantage in years of education out-performed those with only primary schooling. Gender-related effects were also remarkable. Whereas the general abilities were equal in the genders, women out-performed men on recall of word pairs and objects, on verbal cognitive control and on Digit Symbol. In contrast, men excelled on Trail Making A, and on Block Design. The findings emphasize the need for age norms by gender and education for cognitive tests.

To evaluate the underlying mechanisms of cognitive decline in multiple sclerosis, two clinically and demographically matched multiple sclerosis groups differing in cognitive status were assessed with attention related tasks. In addition to the attention tests recommended by the Cognitive Function Study Group of the American National Multiple Sclerosis Society, a test of sustained attention was used to evaluate the role of possible fatigue on cognitive performance. The cognitively mildly deteriorated group was slower than the cognitively preserved group and the controls on all tests of attention. The mildly deteriorated group did not, however, consistently differ from the other groups in the error scores of the attention tests. The preserved group exhibited slowness at the end of the visual vigilance test, but no deficits were found on the other attention related tests in this group. It is suggested that dissociable kinds of processing slowness are the origin of the deficits found on the attention tests in the two multiple sclerosis groups. Our preserved group exhibited signs of motor and fatigue related slowness, whereas the mildly deteriorated group also had extensive cognitive slowness. As sensitive indicators of cognitive slowness, attentional tests should be included in evaluation of the cognitive status of patients with multiple sclerosis.

The purpose of this study was to evaluate the kind of slowing of information processing associated with multiple sclerosis and how this possible slowness is related to cognitive deterioration. We selected 45 patients with definitive multiple sclerosis diagnosis and 35 control subjects. Twenty-two patients had mild cognitive deterioration and 23 patients had preserved cognitive capacities, otherwise the groups were matched. Using computerized tests, we investigated three separate stages of information processing: automatic and controlled processing, and motor programming. The results indicate that patients with mild cognitive deterioration are slower than patients with preserved capacities or controls in every stage of processing measured in this study. Additionally, the preserved patients showed signs of mild slowing in automatic visual processing. These results show that, in multiple sclerosis patients, widespread information processing slowness is associated with multiple sclerosis-related cognitive deterioration. This study emphasizes the importance of studying subgroups rather than cognitively heterogeneous patient samples and, furthermore, the need to divide information processing into different stages is indicated.

In this study, we criticize the notion of bradyphrenia and argue that "slowness of thought" in Parkinson"s disease (PD) must be analyzed as slowness of different information-processing stages and that unselected patients should not be used in experimental studies. We selected 32 patients with a long history of PD and 50 control subjects. Sixteen patients had mild cognitive deterioration (not dementia) and 16 patients had preserved cognitive capacities; otherwise the groups were matched. By using computerized tests, we investigated three separate stages: automatic and controlled processing and motor programming. The results indicate that patients with mild cognitive deterioration are slower than patients with preserved cognitive capacities or controls in automatic visual and in controlled processing but not in motor programming. We conclude that the slowing of controlled processing reflects the disruption of central neural networks, that a long history of PD does not necessitate cognitive slowing, and that PD is not a neuropsychologically serviceable category.

Significant traumatic brain injury (TBI) is nearly always associated with cognitive deficits, but in a highly variable manner. Apolipoprotein E (ApoE) plays a pivotal role in CNS response to injury. To examine the association of ApoE genotype with long-term outcome in TBI patients, we determined the ApoE genotype from 61 TBI patients who had been injured over three decades earlier. All patients had been studied neuropsychologically after their injuries. The long-term outcome was evaluated with repeated neuropsychological testing and by applying various measures of everyday functioning and quality of life. After three decades, TBI patients with the ApoE epsilon4 allele showed significantly poorer general cognitive level than those without this allele. This decline was wholly accounted for by a subgroup of these patients who had developed incident or clinical dementia, while the majority of the ApoE epsilon4 positive patients showed no decline at all. The other outcome measures describing vocational, physical, or subjective symptom outcome did not show significant relationships to the ApoE genotype. A portion of the TBI patients with the ApoE epsilon4 allele seem to be at risk of long-term cognitive decline.

We studied the association between psychiatric disorders and the presence and location of traumatic lesions on magnetic resonance imaging (MRI) in 58 patients, on average, 30 years after traumatic brain injury. Axis I psychiatric disorders that had begun after the injury were assessed with the Schedules for Clinical Assessment in Neuropsychiatry (version 2.1), and Axis II disorders with the Structured Clinical Interview for DSM-III-R Personality Disorders. A 1.5-Tesla MRI scanner was used. One-third of the subjects had traumatic lesions visible on MRI. Only three psychiatric disorders, that is, delusional disorder, dementia, and the disinhibited type of organic personality syndrome, were significantly more common in subjects with contusions. Concerning the location of contusions, organic personality syndrome and its disinhibited subtype were associated with frontal lesions, and major depression was, surprisingly, inversely associated with temporal lesions. These results, which should be interpreted with caution due to the limited size of the study group, suggest that the majority of psychiatric disorders after traumatic brain injury are not closely related to the specific location or even the presence of contusions detectable with post-acute MRI.

The predictive value of cognitive impairment together with demographic and health factors on long-term survival was evaluated. The population sample comprised 389 subjects, all 62 years old. Cognitive performances were measured using verbal, visuomotor and memory tests. Cognitive impairment was determined by comparing performances with norms derived from healthy controls. Ten years after testing, the probability of survival was 89% for the cognitively preserved subjects, 80% for those with mild impairment, and 71% for those with moderate impairment ( p = 0.009). Relative risk (RR) for shortened survival was 1.7 (95% CI 0.9–3.2) for the mildly, and 2.6 (95% CI 1.4–4.8) for the moderately impaired. Perceived health problems were, as expected, related to reduced survival ( p

Parkinson disease (PD) is commonly characterized by cognitive deterioration, but it is still unclear whether PD is associated with semantic impairments.To evaluate semantic knowledge of concepts in patients with idiopathic PD, addressing concrete and abstract concepts, conceptual attributes, and conceptual relations.Twelve patients with preserved cognitive status, 12 patients with mildly deteriorated cognitive status, and 12 control subjects were studied. The cognitive status of patients and controls was determined using detailed cognitive testing. Patients were participants in a university-based movement disorder program, and their PD diagnoses were clinically confirmed during long-term follow-up. The 2 patient groups were similar in age, level of education, disease duration, and parkinsonian disability. Patients were required to produce verbal descriptions of concrete and abstract concepts, to give ratings of the importance of concept attributes, and to assess and construct conceptual hierarchies. The description tasks included guiding questions, which were used if the spontaneous productions of the patients lacked any essentials expected in the answers.Patients with mild cognitive deterioration performed less well than the other groups in defining concrete and abstract concepts (P.001 for both). External guidance did not help them markedly improve their performance. They also had difficulties in tasks calling for knowledge of the importance of given attributes to the concepts and in tasks demanding evaluation of hierarchical semantic relations between concepts (P.001 for both).Semantic disruption is implied in idiopathic PD in association with incipient cognitive impairment.

To investigate the role of the brain dopaminergic system in cognitive impairment in patients with Parkinson disease (PD).We studied 28 patients with PD and 16 age-matched healthy control subjects using [18F] fluorodopa (fluorodopa F 18) positron emission tomography. Patients with PD showed a variable degree of cognitive impairment, which was assessed using the Mini-Mental State Examination and detailed neuropsychologic assessment, including tests sensitive for frontal lobe function.[18F] Fluorodopa uptake was reduced in the putamen (to 36% of the control mean; P.001), the caudate nucleus (to 61% of the control mean; P.001), and the frontal cortex (to 45% of the control mean; P.001) in patients with PD compared with controls. There was no significant association between the degree of overall cognitive impairment of patients and [18F] fluorodopa uptake values. The influx constant (Ki(occ)) in the caudate nucleus had a negative association with performance in the attention-demanding Stroop interference task, especially with the interference time. The Ki(occ) in the frontal cortex had a positive correlation with performance in the digit span (backwards), verbal fluency, and verbal immediate recall tests. Thus, the better the patient performed in tasks demanding immediate and working memory and executive strategies, the better the [18F] fluorodopa uptake in the frontal cortex. In the putamen, no significant correlation was seen between the Ki(occ) value and any of the cognitive tests. The severity of the motor symptoms of PD and [18F]fluorodopa uptake showed a negative correlation in the putamen (r = -0.38; P = .04), and in the caudate nucleus a similar trend was seen (r = -0.36; P = .06).Reduced [18F]fluorodopa uptake in PD in the caudate nucleus (and frontal cortex) is related to impairment in neuropsychologic tests measuring verbal fluency, working memory, and attentional functioning reflecting frontal lobe function. This indicates that dysfunction of the dopamine system has an impact on the cognitive impairment of patients with PD. However, our results do not exclude the possibility of more generalized cognitive impairment in PD, the pathophysiology of which is probably different and more generalized.

Patients suffering from Alzheimer's disease (AD) have severe difficulties in tasks requiring the use of semantic knowledge. The semantic deficits associated with AD have been extensively studied by using behavioral methods. Many of these studies indicate that AD patients have a general deficit in voluntary access to semantic representations but that the structure of the representations themselves might be preserved. However, several studies also provide evidence that to some extent semantic representations in AD may in fact be degraded. Recently, a few studies have utilized event-related brain potentials (ERPs) that are sensitive to semantic factors in order to investigate the electrophysiological correlates of the semantic impairment in AD. Interest has focused on the N400 component, which is known to reºect the on-line semantic processing of linguistic and pictorial stimuli. The results from studies of N400 changes in AD remain somewhat controversial: Some studies report normal or enlarged N400 components in AD, whereas others report diminished ones. One issue not reported in previous studies is whether word-elicited ERPs other than N400 remain normal in AD. In the present study our aim was to find out whether the ERP waveforms N1, P2, N400, and Late Positive Component (LPC) to semantically congruous and incongruous spoken words are abnormal in AD and whether such abnormalities specifically reºect deficiencies in semantic activation in AD. Auditory ERPs from 20 scalp sites to semantically congruous and incongruous final words in spoken sentences were recorded from 17 healthy elderly adults and 9 AD patients. The early ERP waveforms N1 and P2 were relatively normal for the AD patients, but the N400 and LPC effects (amplitude difference between congruous and incongruous conditions) were significantly reduced. We interpret the present results as showing that semantic-conceptual activation and other high-level integration processes are defective in AD. However, a word congruity effect earlier than N400 (phonological mismatch negativity), reflecting lexical selection processes, is at least to some extent preserved in AD.

Automatic and controlled influences of memory were examined in 12 patients with early Alzheimer's disease (AD) and 12 control subjects. The subjects studied a list of words and then received three-letter word stems in three different retrieval tasks. In an indirect memory task (word-stem completion priming), they were asked to produce the first word that came to mind in response to each stem. In an inclusion task, they were required to produce a studied word in response to each stem, and in an exclusion task they were asked to produce a new, unstudied word for each stem. The performance of the subjects with AD was equal in the inclusion and exclusion conditions, showing no evidence of controlled recollection for the studied words, while their automatic memory as well as priming were preserved. The results provide neuropsychological support for the distinction between controlled and automatic memory processes.

Patients with Parkinson's disease (PD) and healthy controls took a computerized test of tone duration discrimination (TDD) using pairs of tones of 0.4–1.6 sec duration, presented at intervals of 0.5–4 sec. In PD patients as well as controls, TDD was impaired by even slight degrees of cognitive deterioration. PD yielded impaired TDD in females, but not in males. This suggests that the dopamine-powered biological clock, which is vulnerable to PD, is more important for the processing of durations in the 1-sec range in women than in men.

The present study focuses on semantic deficits in Alzheimer's disease (AD). We distinguish three different levels of semantic knowledge: (1) lexical, (2) semantic-conceptual, (3) conscious understanding. We devised methods that tap levels (2) and (3). Our aim was to determine how much guidance AD patients need to consciously access a given semantic-conceptual field and how well they can understand the meanings of concepts and semantic relations. Four different tasks were used to tap different kinds of concepts, the relationships between concepts and their attributes, and the hierarchical structure among different concepts. The retrieval demands of the tasks were eased by presenting guiding questions. The results revealed that AD patients have deficient voluntary access to semantic-conceptual representations. The deficits persist even in passive recognition and forced-choice tasks. We conclude that AD patients have a generalized access deficit, although some aspects of the results are suggestive of storage deficit.

Although the mechanisms of cognitive impairment in multiple sclerosis (MS) have been extensively studied, evaluation of language functions has been given little attention. In the present study, we evaluated whether impairment of language functions is associated with cognitive decline in MS. We studied naming, reading, and writing performance of two carefully matched patient groups differing only with respect to cognitive status. In language tasks, the patients with incipient cognitive decline not only demonstrated performance slowness but also made more errors than the patients with preserved cognitive capacity and the healthy controls. The comprehensive naming error analysis revealed that the cognitively deteriorated patients produced error types not present in the other two study groups. Contrary to previous suggestions, the present study indicates that impaired language performances in MS are attributable to mild cognitive deterioration rather than to sensory or motor factors. Thus, assessment of language functions should be included in neuropsychological evaluations of MS patients.

(1968). Simulation of Cues Eliciting Aggressive Responses in Mice at Two Age Levels. The Journal of Genetic Psychology: Vol. 113, No. 1, pp. 53-63.