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PubMed2005

Inhibition of neprilysin by thiorphan (i.c.v.) causes an accumulation of amyloid beta and impairment of learning and memory.

An accumulation of amyloid beta peptide (Abeta) due to an imbalance between anabolism and catabolism triggers Alzheimer's disease (AD). Neprilysin is a rate-limiting peptidase, which participates in the catabolism of Abeta in brain. We investigated whether rats continuously infused with thiorphan, a specific inhibitor for neprilysin, into the cerebral ventricle cause cognitive dysfunction, with an accumulation of Abeta in the brain. Thiorphan-infused rats displayed significant cognitive dysfunction in the ability to discriminate in the object recognition test and spatial memory in the water maze test, but not in other hippocampus-dependent learning and memory tasks. Thiorphan infusion also elevated the Abeta40 level in the insoluble fraction of the cerebral cortex, but not that of the hippocampus. There was no significant difference in the nicotine-stimulated release of acetylcholine in the hippocampus between vehicle- and thiorphan-infused rats. These results indicate that continuous infusion of thiorphan into the cerebral ventricle causes cognitive dysfunction by raising the level of Abeta in the cerebral cortex, and suggest that a reduction of neprilysin activity contribute to the deposition of Abeta and development of AD.

Acetylcholine↗

PubMed2005

Fatigue, menopausal symptoms, and cognitive function in women after adjuvant chemotherapy for breast cancer: 1- and 2-year follow-up of a prospective controlled study.

PURPOSE: We previously evaluated fatigue, menopausal symptoms, and cognitive dysfunction in patients receiving adjuvant therapy for breast cancer and matched healthy women. Here we report assessment of these women 1 and 2 years later. PATIENTS AND METHODS: Patients without relapse and controls were evaluated by the Functional Assessment of Cancer Treatment-General Quality of Life questionnaire, with subscales for fatigue and endocrine symptoms, and by the High Sensitivity Cognitive Screen. RESULTS: There were 104, 91, and 83 patients and 102, 81, and 81 controls assessed at baseline and at 1 and 2 years, respectively. Median Functional Assessment of Cancer Treatment-Fatigue scores (range, 0 to 52) for patients improved from 31 (on chemotherapy) to 43 and 45 at 1 and 2 years, respectively, but were stable in controls (46 to 48). Median Functional Assessment of Cancer Treatment-Endocrine Symptoms scores (range, 0 to 72) for patients improved from 57 (on chemotherapy) to 59 and 61 at 1 and 2 years, respectively, and were stable in controls (64 to 65). Differences between patients and controls remained significant for these scales. The incidence of moderate-severe cognitive dysfunction by the High Sensitivity Cognitive Screen decreased in patients from 16% (on chemotherapy) to 4.4% and 3.8% and in controls from 5% to 3.6% and 0% at 1 and 2 years, respectively. There were minimal differences between estrogen receptor-positive patients who started hormonal therapy (mainly tamoxifen) after chemotherapy and estrogen receptor-negative patients who did not. Differences in quality of life between patients and controls were significant only at baseline. CONCLUSION: Fatigue, menopausal symptoms, and cognitive dysfunction are important adverse effects of chemotherapy that improve in most patients. Hormonal treatment has minimal impact on them.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1986

A psychobiologic analysis of cognitive failures. Structure and mechanisms.

Impairments in memory, learning, and related cognitive functions can vary in most psychiatric or neuropsychiatric disorders. Although many methods have been used to measure the presence and severity of cognitive symptoms, little progress has been made in defining and contrasting possible determinants of cognitive dysfunction. We propose a theoretical framework that describes impairments of higher mental functions in terms of both "extrinsic" noncognitive processes and "intrinsic" cognitive processes. The latter include effort (capacity) demanding processes; automatic processes; episodic (recent biographical) memory; and processes involved in accessing previously acquired knowledge. Noncognitive processes include sensitivity to reinforcement, activation, sensorimotor function, and mood. Each of these processes can be expressed at the time of information acquisition or retrieval from memory. Findings from clinical studies of patients suffering amnestic disorders, progressive dementias, and mood disorders illustrate the utility of such a model for understanding some of the determinants of cognitive dysfunction, for developing diagnostic tools, and for considering therapeutic strategies that may be useful in treating cognitive dysfunctions.

Alcohol Amnestic Disorder↗

PubMed1991

Patient predictors of response to psychotherapy and pharmacotherapy: findings in the NIMH Treatment of Depression Collaborative Research Program.

OBJECTIVE: The authors investigated patient characteristics predictive of treatment response in the National Institute of Mental Health (NIMH) Treatment of Depression Collaborative Research Program. METHOD: Two hundred thirty-nine outpatients with major depressive disorder according to the Research Diagnostic Criteria entered a 16-week multicenter clinical trial and were randomly assigned to interpersonal psychotherapy, cognitive-behavior therapy, imipramine with clinical management, or placebo with clinical management. Pretreatment sociodemographic features, diagnosis, course of illness, function, personality, and symptoms were studied to identify patient predictors of depression severity (measured with the Hamilton Rating Scale for Depression) and complete response (measured with the Hamilton scale and the Beck Depression Inventory). RESULTS: One hundred sixty-two patients completed the entire 16-week trial. Six patient characteristics, in addition to depression severity previously reported, predicted outcome across all treatments: social dysfunction, cognitive dysfunction, expectation of improvement, endogenous depression, double depression, and duration of current episode. Significant patient predictors of differential treatment outcome were identified. 1) Low social dysfunction predicted superior response to interpersonal psychotherapy. 2) Low cognitive dysfunction predicted superior response to cognitive-behavior therapy and to imipramine. 3) High work dysfunction predicted superior response to imipramine. 4) High depression severity and impairment of function predicted superior response to imipramine and to interpersonal psychotherapy. CONCLUSIONS: The results demonstrate the relevance of patient characteristics, including social, cognitive, and work function, for prediction of the outcome of major depressive disorder. They provide indirect evidence of treatment specificity by identifying characteristics responsive to different modalities, which may be of value in the selection of patients for alternative treatments.

Adult↗

PubMed2000

Adaptation of cognitive function to hypoglycemia in healthy men.

OBJECTIVE: Antecedent hypoglycemia reduces hypoglycemic counterregulation and symptoms, thereby provoking the hypoglycemia unawareness syndrome. The effects of antecedent hypoglycemia on hypoglycemia-induced cognitive dysfunction are less well established. RESEARCH DESIGN AND METHODS: To determine whether antecedent hypoglycemia also reduces hypoglycemic cognitive dysfunction, we performed stepwise hypoglycemic clamp experiments (4.1, 3.6, 3.1, and 2.6 mmol/l) during a 6-h period in 30 young healthy men. A total of 15 subjects additionally received a 2.5-h antecedent hypoglycemic clamp (3.1 mmol/l) on the preceding day (prior-hypo group), whereas the other 15 subjects did not (control group). Cognitive function was assessed by auditory-evoked brain potentials (AEBPs) and reaction time during a vigilance task and short-term memory recall. Tests were performed during the stepwise hypoglycemic clamp at baseline and at each hypoglycemic plateau. RESULTS: In both groups, performance on all measures of cognitive function deteriorated during stepwise hypoglycemia (all P < 0.01). However, after antecedent hypoglycemia, the hypoglycemia-induced decrease in the amplitude of the P3 of the AEBP was distinctly reduced compared with the control condition (P < 0.05). Also, short-term memory performance was less impaired in the prior-hypo group than in the control group (P < 0.005), and a minor hypoglycemic impairment of reaction time (P < 0.05) was evident in the prior-hypo group. CONCLUSIONS: Data provide evidence that a single episode of mild antecedent hypoglycemia (3.1 mmol/l) attenuates several aspects of cognitive dysfunction during subsequent hypoglycemia 18-24 h later.

Adaptation, Physiological↗

PubMed1994

Cognitive function in depression: its relationship to the presence and severity of intellectual decline.

Cognitive dysfunction is an integral feature of depression, in some cases of sufficient severity to warrant a diagnosis of dementia. There has been little systematic investigation of whether cognitive dysfunction is an inevitable consequence of depression, or is specific to a subgroup of depressed patients. Related to this is the distribution of cognitive dysfunction, whether there is a continuum of impairment or a distinct demented subgroup. Finally, there is the question of which aspects of cognitive function are most sensitive to the intellectual decline seen in depression. A study is described which addresses these issues. The distribution of global cognition was found to be normally distributed in the sample of 29 patients assessed. Based on this distribution and the scores of a control sample, the patients were classified as unimpaired, borderline or impaired. Two sets of independent comparisons were carried out. First, the unimpaired depressed patients were compared to matched non-depressed controls. Significant deficits were found on a range of neuropsychological measures covering aspects of language function, memory, both recall and recognition, attention and behavioural regulation. These same patients were also compared with two groups of matched depressed patients, with varying degrees of global cognitive impairment. In general, the cognitive measures showed a gradient of dysfunction across the three patients groups. Significant differences between the depressed groups were shown on measures of immediate recall, attention and behavioural regulation. The possible significance of attentional factors for the observed memory dysfunction is discussed.

Adult↗

PubMed2006

Neuropsychological dysfunction in the absence of structural evidence for cerebral ischemia after uncomplicated carotid endarterectomy.

OBJECTIVE: Neurocognitive dysfunction has been shown to occur in roughly 25% of patients undergoing carotid endarterectomy (CEA). Despite this, little is known about the mechanism of this injury. Recently, several groups have shown that new diffusion weighted imaging (DWI)-positive lesions are seen in 20% of patients undergoing CEA. We investigated to what degree neurocognitive dysfunction was associated with new DWI lesions. METHODS: Thirty-four consecutive patients undergoing CEA were subjected to pre- and postoperative cognitive evaluation with a battery of neuropsychological tests. Postoperative magnetic resonance imaging was performed in all patients within 24 hours of surgery. Lesions that showed high signal on DWI and restricted diffusion on apparent diffusion coefficient maps but no abnormal high signal on the fluid-attenuated inversion recovery images were considered hyperacute. RESULTS: Cognitive dysfunction was seen in eight (24%) patients. New hyperacute DWI lesions were seen in three (9%). Only one (13%) of the patients with cognitive dysfunction had a new DWI lesion. Two thirds of the new DWI lesions occurred in the absence of cognitive deterioration. Patients with cognitive dysfunction had significantly longer carotid cross-clamp times. CONCLUSION: Neurocognitive dysfunction after CEA does not seem to be associated with new DWI positive lesions.

Aged↗

PubMed2003

Cognitive function, fatigue, and menopausal symptoms in women receiving adjuvant chemotherapy for breast cancer.

PURPOSE: There is evidence that cognitive dysfunction, fatigue, and menopausal symptoms may occur in women receiving adjuvant chemotherapy for breast cancer. Here, we determine their incidence and severity, and interrelationships between them and quality of life. PATIENTS AND METHODS: In this study, 110 women receiving adjuvant chemotherapy each nominated a female relative, friend, or neighbor (matched by age) as a control; 100 eligible matched pairs were evaluated. Patients and controls completed the following assessments: the High-Sensitivity Cognitive Screen, and the Functional Assessment of Cancer Therapy-General (FACT-G) quality of life scale with subscales for fatigue (FACT-F) and endocrine symptoms (FACT-ES). They also performed tests of attention and reaction time. RESULTS: Patients and controls were well matched for age and level of education. There was a higher incidence of moderate or severe cognitive impairment in the patient group (16% v 4%; P =.008). Patients experienced much more fatigue than controls (median FACT-F scores, 31 v 46; P <.0001) and more menopausal symptoms (median FACT-ES scores, 58 v 64; P <.0001). Self-reported quality of life of the patients was poorer than for controls, especially in physical and functional domains (median FACT-G scores, 77 v 93; P <.0001). There was strong correlation between fatigue, menopausal symptoms, and quality of life (P <.0001 for each pair), but none were significantly associated with the presence of cognitive dysfunction. CONCLUSION: Adjuvant chemotherapy causes cognitive dysfunction, fatigue, and menopausal symptoms in women with breast cancer. Priority should be given to the study of strategies that might reduce these toxic effects.

Adult↗

PubMed2005

Intraneuronal Abeta causes the onset of early Alzheimer's disease-related cognitive deficits in transgenic mice.

Progressive memory loss and cognitive dysfunction are the hallmark clinical features of Alzheimer's disease (AD). Identifying the molecular triggers for the onset of AD-related cognitive decline presently requires the use of suitable animal models, such as the 3xTg-AD mice, which develop both amyloid and tangle pathology. Here, we characterize the onset of learning and memory deficits in this model. We report that 2-month-old, prepathologic mice are cognitively unimpaired. The earliest cognitive impairment manifests at 4 months as a deficit in long-term retention and correlates with the accumulation of intraneuronal Abeta in the hippocampus and amygdala. Plaque or tangle pathology is not apparent at this age, suggesting that they contribute to cognitive dysfunction at later time points. Clearance of the intraneuronal Abeta pathology by immunotherapy rescues the early cognitive deficits on a hippocampal-dependent task. Reemergence of the Abeta pathology again leads to cognitive deficits. This study strongly implicates intraneuronal Abeta in the onset of cognitive dysfunction.

Alzheimer Disease↗

PubMed1997

Preliminary report of a genetic basis for cognitive decline after cardiac operations. The Neurologic Outcome Research Group of the Duke Heart Center.

BACKGROUND: Changes in memory and cognition frequently follow cardiac operations. We hypothesized that patients with the apolipoprotein E-epsilon 4 allele are genetically predisposed to cognitive dysfunction after cardiac operations. METHODS: The apolipoprotein E-epsilon 4 allele was evaluated as a predictor variable for postoperative cognitive dysfunction in 65 patients undergoing cardiac bypass grafting at Duke University Medical Center. The primary outcome measure was performance on a cognitive battery administered preoperatively and at 6 weeks postoperatively. RESULTS: In a multivariable logistic regression analysis including apolipoprotein E-epsilon 4, preoperative score, age, and years of education, a significant association was found between apolipoprotein E-epsilon 4 and change in cognitive test score in measures of short-term memory at 6 weeks postoperatively. Patients with lower educational levels were more likely to show a decline in cognitive function associated with the apolipoprotein E-epsilon 4 allele. CONCLUSIONS: This study suggests that apolipoprotein E genotype is related to cognitive dysfunction after cardiopulmonary bypass. Cardiac surgical patients may be susceptible to deterioration after physiologic stress as a result of impaired genetically determined neuronal mechanisms of maintenance and repair.

Age Factors↗

PubMedDate not supplied

Cerebral amyloid angiopathy: major contributor or decorative response to Alzheimer's disease pathogenesis.

Amyloid deposition within cerebral vessels, or cerebral amyloid angiopathy (CAA), is common in advanced age and even more common in Alzheimer's disease. CAA may be complicated by lobar intracerebral hemorrhage, while rare kindreds of autosomal dominant CAA also show propensity for intracerebral hemorrhage, due to germline mutations in specific amyloidogenic precursor proteins and apparent compromise of structural integrity of the blood vessel wall due to marked amyloid deposition. The relationship between cerebral amyloid angiopathy and cognitive dysfunction, however, is less clear. While cognitive dysfunction in familial CAA is likely related to prodigious amyloid deposits and vascular luminal compromise (e.g., hereditary cerebral hemorrhage with angiopathy-Dutch type (HCHWA-D)), cerebral amyloid angiopathy with intracerebral hemorrhage often presents sporadically in cognitively intact elderly patients. Moreover, while about 80% of subjects with Alzheimer's disease have demonstrable amyloid beta within blood vessel walls at autopsy, the vast majority of these fail to suffer clinically relevant intracerebral hemorrhage during life. The remaining 20% manage to progress and die of their disease with virtual no amyloid within blood vessels. Thus, the role of amyloid beta deposits in cerebral vessels as regards cognitive function on the one hand, and tendency for hemorrhage on the other, remain to be resolved for sporadic late onset Alzheimer's disease and CAA. Recent studies on transgenic APP23 mice suggest a relationship between passive immunization and amyloid angiopathy-associated cerebral hemorrhage, although the mechanism of hemorrhage was unclear from the data presented. We suggest that amyloid accumulation represents a response to chronic stress, and that the neurodegenerative process occurs at the neuronal level, encompassing oxidative stress and aberrant cell cycle activation. As such, CAA represents tissue homeostasis, such that an abrupt perturbation of this balance (e.g., amyloid beta immunization) is deleterious.

Alzheimer Disease↗

PubMed2005

Nicotinic effects on cognitive function: behavioral characterization, pharmacological specification, and anatomic localization.

RATIONALE: Nicotine has been shown in a variety of studies in humans and experimental animals to improve cognitive function. Nicotinic treatments are being developed as therapeutic treatments for cognitive dysfunction. OBJECTIVES: Critical for the development of nicotinic therapeutics is an understanding of the neurobehavioral bases for nicotinic involvement in cognitive function. METHODS: Specific and diverse cognitive functions affected by nicotinic treatments are reviewed, including attention, learning, and memory. The neural substrates for these behavioral actions involve the identification of the critical pharmacologic receptor targets, in particular brain locations, and how those incipient targets integrate with broader neural systems involved with cognitive function. RESULTS: Nicotine and nicotinic agonists can improve working memory function, learning, and attention. Both alpha4beta2 and alpha7 nicotinic receptors appear to be critical for memory function. The hippocampus and the amygdala in particular have been found to be important for memory, with decreased nicotinic activity in these areas impairing memory. Nicotine and nicotinic analogs have shown promise for inducing cognitive improvement. Positive therapeutic effects have been seen in initial studies with a variety of cognitive dysfunctions, including Alzheimer's disease, age-associated memory impairment, schizophrenia, and attention deficit hyperactivity disorder. CONCLUSIONS: Discovery of the behavioral, pharmacological, and anatomic specificity of nicotinic effects on learning, memory, and attention not only aids the understanding of nicotinic involvement in the basis of cognitive function, but also helps in the development of novel nicotinic treatments for cognitive dysfunction. Nicotinic treatments directed at specific receptor subtypes and nicotinic cotreatments with drugs affecting interacting transmitter systems may provide cognitive benefits most relevant to different syndromes of cognitive impairment such as Alzheimer's disease, schizophrenia, and attention deficit hyperactivity disorder. Further research is necessary in order to determine the efficacy and safety of nicotinic treatments of these cognitive disorders.

Alzheimer Disease↗

PubMed2000

Stress in schizophrenia: an integrative view.

Stress and the development of a (schizophrenic) psychosis are inextricably related. The process by which stress actually affects psychosis is far less clear. The hypothalamic-pituitary-adrenal system, and in particular the release of corticosteroids, has been attributed an essential role. However, schizophrenia is a disorder in which many functions are distorted. Dysfunctions can be found in behavior, cognition, coping, physiology, pituitary-adrenal and immune functioning. In this short paper, these functions are discussed as to how they contribute to the way stress is appraised and processed. Schizophrenic patients are impaired in their biological response to stress by showing a blunted cortisol response to psychosocial stress. It is hypothesized that this reflects rather cognitive dysfunction, based on biological dysfunctions in those brain structures that are responsible for these processes, i.e. the prefrontal cortex and the limbic system. Considering the blunted cortisol response as a maladaptive stress response, its consequences are commented on with an emphasis on the immune system. Finally, the role of neuroleptics, and in particular the atypical ones, is discussed for their beneficial effect, beyond their fear-and anxiety-reducing properties, in restoring some of the cognitive dysfunctions schizophrenic patients display. By doing so, they may improve perception of the environment, enhance adjustment and thus a proper stress response. Integration of these processes in stress research described, may provide new vistas of the stress concept in schizophrenia.

Humans↗

PubMed2000

[Rehabilitation and outcome of the adult traumatic brain injury].

One-hundred and seventy traumatic brain injured persons were admitted to Kanagawa Rehabilitation Hospital for a rehabilitation program during a five-years period. The average age was 30.7 years and the male to female ratio was 5:1. The most common cause of injury was an traffic accident. They exhibited various physical and cognitive dysfunctions. Patients with severe physical and/or cognitive dysfunction had difficulty in community re-integration after finishing the hospital rehabilitation. At present, social resources for traumatic brain injury patients and family to fulfill their various needs are so few that they tend to be isolated from the community.

Accidents, Traffic↗

PubMed1996

Cognitive-motor dysfunction in Parkinson's disease.

Patients with Parkinson's disease (PD) present with a wide range of cognitive and motor dysfunctions. Attempts to fit these deficits into a neuroanatomical framework have tended to emphasise their separateness. This paper, however, takes a broader perspective based on the concept of action-purposeful goal-directed behaviour-which serves to integrate the various deficits into a common framework. Of the motor symptoms of PD, akinesia is chosen as representing a breakdown in a distributed system of action control. Three aspects of akinesia are considered-slowness to initiate movement, slowness to execute movement and poverty of spontaneous movement. All are seen as being surface manifestation of the system's attempts to cope with or adapt to the limitations imposed by the disease process, at a cognitive, motor and integrative level.

Adaptation, Physiological↗

PubMed2005

The effects of benzodiazepines on cognition.

Initially thought to be virtually free of negative effects, benzodiazepines are now known to carry risks of dependence, withdrawal, and negative side effects. Among the most controversial of these side effects are cognitive effects. Long-term treatment with benzodiazepines has been described as causing impairment in several cognitive domains, such as visuospatial ability, speed of processing, and verbal learning. Conversely, long-term benzodiazepine use has also been described as causing no chronic cognitive impairment, with any cognitive dysfunction in patients ascribed to sedation or inattention or considered temporary and associated with peak plasma levels. Complicating the issue are whether anxiety disorders themselves are associated with cognitive deficits and the extent to which patients are aware of their own cognitive problems. In an attempt to settle this debate, meta-analyses of peer-reviewed studies were conducted and found that cognitive dysfunction did in fact occur in patients treated long term with benzodiazepines, and although cognitive dysfunction improved after benzodiazepines were withdrawn, patients did not return to levels of functioning that matched benzodiazepine-free controls. Neuroimaging studies have found transient changes in the brain after benzodiazepine administration but no brain abnormalities in patients treated long term with benzodiazepines. Such findings suggest that patients should be advised of potential cognitive effects when treated long term with benzodiazepines, although they should also be informed that the impact of such effects may be insignificant in the daily functioning of most patients.

Activities of Daily Living↗

PubMed2000

The absence of impairment of cliff avoidance reaction induced by subchronic methamphetamine treatment in inbred strains of mice.

Cliff avoidance reaction (CAR), an index of behavioral teratology in rodents, can be impaired by motor, arousal, or cognitive dysfunction. We formerly reported subchronic administration of methamphetamine (MAP) induced the CAR impairment, which might reflect MAP-induced cognitive dysfunction, in three strains of rats. In this study, the effects of subchronic MAP treatment on the behavioral sensitization in stereotypy (stereotypy sensitization) and CAR were examined in two inbred strains of male mice; C57BL/6J(C57) and DBA/2J(DBA). The animals received 4 mg/kg/day MAP intraperitoneally for 28 days. There were apparent strain differences in the development of stereotypy sensitization induced by chronic MAP; DBA mice developed stereotypy sensitization quickly, but C57 did not. Unlike rats, neither strains of mice showed the CAR impairment. These results suggest that chronic MAP (4 mg/kg) administration did not introduce any cognitive dysfunction measured by CAR in the two inbred mice, DBA and C57. The discrepancy between rats and mice is still unclear. It might relate to the species-selective effect of MAP on the CAR impairment. Further studies should to be required.

Animals↗

PubMedDate not supplied

Cerebral MRI abnormalities and their association with neuropsychiatric manifestations in SLE: a population-based study.

OBJECTIVE: To evaluate the volumetric brain magnetic resonance imaging (MRI) findings in a population-based sample of systemic lupus erythematosus (SLE) patients and to detect a possible relationship between cerebral MRI abnormalities and specific neuropsychiatric (NP) manifestations. METHODS: The study population consisted of patients with SLE (n = 43) in Pirkanmaa Health Care District, Finland and of a sex- and age-stratified reference group from the general population (n = 43). In addition to a clinical neurological investigation, all subjects received a detailed neuropsychological assessment and an MRI study. Volumetric measures of cerebral atrophy as well as T1- and T2-weighted lesions were obtained. SLE activity was assessed by the European Consensus Lupus Activity Measure (ECLAM) index, and accumulated NP abnormalities were measured by the Systemic Lupus International Collaborating Clinics (SLICC) damage index. A cumulative lifetime dose of glucocorticoids was determined from the patientrecords. RESULTS: Compared with controls, SLE patients had increased volumes of both T1- and T2-weighted lesions (p = 0.019 and p<0.0001, respectively) and increased cerebral atrophy (p<0.001). All the measured MRI parameters were statistically significantly higher in NPSLE than in non-NPSLE patients. In SLE patients, cerebral atrophy was associated with cognitive dysfunction, epileptic seizures, and cerebrovascular disease; T1-weighted lesions were associated with epileptic seizures and T2-weighted lesions with cognitive dysfunction. All MRI parameters correlated significantly with the SLICC index but not with the ECLAM index. A positive correlation was found between a cumulative dose of glucocorticoids and cerebral atrophy in SLE patients. CONCLUSION: MRI abnormalities, including brain atrophy and T1- and T2-weighted lesions, are significantly more common in patients with SLE than in the general population and they are related to specific NP manifestations. Our findings also provide support for the organic aetiology of cognitive dysfunction in SLE.

Adult↗