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PubMed1986

Behavioral impairments related to cognitive dysfunction in the autoimmune New Zealand black mouse.

The possibility that autoimmunological disorders involving neuronal constituents as autoantigens can result in measurable behavioral impairments prompted the behavioral analysis of the New Zealand black (NZB) mouse strain, known to have high levels of brain-reactive antibodies. Sensorimotor competence and performance in tasks requiring learning and memory were assessed in 7-10-month-old NZB and contrasted with those of CFW mice. The NZB mice showed pronounced deficits in performance of passive and active shock avoidance responses. These deficits could not be accounted for by the slight sensorimotor disadvantage of NZB mice relative to CFW mice. No difference between the two mouse strains was seen in passive avoidance behavior at 1.5 months of age. It is concluded that NZB mice display a behavioral deficit related to cognitive dysfunction and that autoimmune mechanisms may be involved in the etiology of this deficit. Such behavioral disturbances produced by an autoimmune mechanism may have relevance for the neurological declines observed in aging, since the incidence of autoimmune disorders increases markedly in old age.

Animals↗
PubMed1999

SPECT with 99mTc-HMPAO in subjects with HIV infection: cognitive dysfunction correlates with high uptake.

We prospectively studied a cohort of 25 HIV-1 infected individuals with no clinical signs of encephalopathy with 99mTc-HMPAO-SPECT. The findings were correlated with magnetic resonance imaging (MRI), neuropsychological testing and clinical staging aiming at the early diagnosis of HIV encephalopathy by single photon emission computed tomography (SPECT). A total of 25 matched seronegative controls were subject to neuropsychological testing only. A total of 24 patients and controls were monitored for 6-46 months (mean and median 26 months). No patients developed AIDS dementia complex during the study; 3 patients developed minimal symptoms (MSK classification stage 0.5). There was a significant decline in 99mTc-HMPAO uptake over time and neuropsychological abnormalities progressed. Unexpectedly, there was a correlation of high cortical and subcortical 99mTc-HMPAO uptake and low performance in cognitive dysfunction tests, indicating a possible inflammatory reaction in the brain with increased blood flow due to HIV infection. We conclude that, in non-demented HIV-infected individuals, both the 99mTc-HMPAO uptake and functional level slowly decrease over time, but the regional cerebral blood flow decrease could be masked by a direct HIV-induced inflammatory reaction in the brain, which gives a 99mTc-HMPAO hyperfixation.

AIDS Dementia Complex↗
PubMed2005

Pre-Injury magnesium treatment prevents traumatic brain injury-induced hippocampal ERK activation, neuronal loss, and cognitive dysfunction in the radial-arm maze test.

We studied the effect of pre-injury magnesium (Mg(2+)) treatment on hippocampal extracellular signal- regulated kinase (ERK) activation induced by lateral fluid-percussion (FP) brain injury, and on working and reference memory in the radial-arm maze test in rats subjected to such traumatic brain injury (TBI) (n = 56) or to sham injury (n = 12). In the ipsilateral hippocampus, an increase in the phospho-ERK level was detected at 10 min after injury in rats subjected to FP brain injury of moderate severity (1.9-2.0 atm) as compared to sham-injured controls (p < 0.01), and was maintained for at least 120 min after injury (p < 0.05). In the contralateral hippocampus, the phospho-ERK level was transiently increased at 10 min after injury but fell to nearly its basal level by 30 min. When MgCl(2) solution (150 micromol) was infused intravenously from 20 min to 5 min before injury (n = 4-5), brain injury-induced ERK activation was significantly inhibited in the ipsilateral hippocampus at 60 min but not at 10 min after injury. Mg(2+) treatment also significantly prevented injury- induced neuronal loss in the ipsilateral hippocampus (p < 0.05 vs. vehicle-treated, brain-injured controls). At 2 weeks after injury, Mg2+ treatment was found to have significantly prevented injury-induced impairments in working (p < 0.0001 vs. vehicle-treated, brain-injured controls) and reference memory (p < 0.05) in the radial-arm maze test. The present study demonstrates that pretreatment with Mg(2+) prevents post-traumatic hippocampal ERK activation and neuronal loss, and cognitive dysfunction in the radial-arm maze test.

Animals↗
PubMed2005

Reversal of neuromotor and cognitive dysfunction in an enriched environment combined with multimodal early onset stimulation after traumatic brain injury in rats.

This study was designed to investigate the additional benefits of a multimodal early onset stimulation (MEOS) paradigm when combined with enriched environment (EE) versus EE only and standard housing (SH) on the recovery after experimental traumatic brain injury (TBI). Male Sprague- Dawley rats were subjected to moderate lateral fluid percussion (LFP) brain injury (n = 40) or sham operation (n = 6). Thereafter, the injured and sham/EE + MEOS and EE only groups were placed into a complex EE consisting of tunnel-connected wide-bodied cages with various beddings, inclining platforms, and toys. Along with group living and environmental complexity, injured and sham/EE + MEOS animals were additionally exposed to a standardized paradigm of multimodal stimulation including auditory, visual, olfactory, and motor stimuli. In contrast, injured and sham/SH groups were housed individually without stimulation. A standardized composite neuroscore (NS) test was used to assess acute post-traumatic neuromotor deficits (24 h after injury) and recovery on days 7 and 15; recovery of cognitive function was assessed on days 11-15 using the Barnes maze. Neuromotor impairment was comparable in all injured animals at 24 h post-injury, but braininjured EE + MEOS rats performed significantly better than both brain-injured SH and EE groups when tested on post-injury days 7 and 15 (p = 0.004). Similarly, latencies to locate the hidden box under the Barnes maze platform were significantly shortened in EE + MEOS animals at day 15 (p = 0.003). These results indicate that the reversal of neuromotor and cognitive dysfunction after TBI can be substantially enhanced when MEOS is added to EE.

Acoustic Stimulation↗
PubMedDate not supplied

Classic conditioning and dysfunctional cognitions in patients with panic disorder and agoraphobia treated with an implantable cardioverter/defibrillator.

OBJECTIVE: A model for the development of anxiety disorders (panic disorder with or without agoraphobia) is needed. Patients with an implantable cardioverter/defibrillator (ICD) are exposed to repeated electric shocks. If the theory of anxiety development by aversive classic conditioning processes is valid, these repeated shocks should lead to an increased risk of anxiety disorders. To study this hypothesis, we retrospectively studied 72 patients after implantation of an automatic ICD. METHODS: Patients were assessed with the semistructured Diagnostic Interview of Psychiatric Disease 1 to 6 years after implantation of an automatic ICD. Panic disorder and/or agoraphobia was diagnosed in patients who fulfilled all DSM-III-R criteria for those conditions. RESULTS: Anxiety disorder developed in 15.9% of patients after ICD implantation. This was significantly related to the frequency of repeated defibrillation (shocks) to stop malignant ventricular arrhythmias. Dysfunctional cognitions are an additional vulnerability factor. CONCLUSIONS: The data support both the conditioning hypothesis and the cognitive model of anxiety development. These findings suggest that ICD patients are an appropriate risk population for a prospective study of the development of anxiety disorders.

Aged↗
PubMed2001

Treatment of cognitive dysfunction associated with Alzheimer's disease with cholinergic precursors. Ineffective treatments or inappropriate approaches?

The observations of the loss of cholinergic function in neocortex and hippocampus in Alzheimer's disease (AD) developed the hypothesis that replacement of cholinergic function may be of therapeutic benefit to AD patients. The different approaches proposed or tested included intervention with acetylcholine (ACh) precursors, stimulation of ACh release, use of muscarinic or nicotinic receptor agonists and acetylcholinesterase (AChE) or cholinesterase (ChE) inhibition. Inhibition of endogenous ACh degradation through ChE inhibitors and precursor loading were treatments more largely investigated in clinical trials. Of the numerous compounds in development for the treatment of AD, AChE and ChE inhibitors are the most clinically advanced, although clinical trials conducted to date did not always confirm a significant benefit of these drugs on all symptom domains of AD. The first attempts in the treatment of AD with cholinergic precursors did not confirm a clinical utility of this class of compounds in well controlled clinical trials. However, cholinergic precursors most largely used such as choline and phosphatidylcholine (lecithin) were probably not suitable for enhancing brain levels of ACh. Other phospholipids involved in choline biosynthetic pathways such as CDP-choline, choline alphoscerate and phosphatidylserine clearly enhanced ACh availability or release and provided a modest improvement of cognitive dysfunction in AD, these effects being more pronounced with choline alphoscerate. Although some positive results cannot be generalized due to the small numbers of patients studied, they probably would justify reconsideration of the most promising molecules in larger carefully controlled trials.

Age of Onset↗
PubMed2004

Low and high circulating cortisol levels predict mortality and cognitive dysfunction early after stroke.

OBJECTIVE: Elevated cortisol levels are associated with confusion and poor outcome after stroke. Dehydroepiandrosterone sulphate (DS), the most abundant adrenal androgen may act as an anti-glucocorticoid. An altered regulation of these steroids may affect numerous brain functions, including neuronal survival. The purpose of this study was to investigate serum cortisol and DS levels and the cortisol/DS ratio early after stroke and relate our findings to the presence of disorientation and mortality. DESIGN: Patients with acute ischaemic stroke (n = 88, 56 men and 32 women) admitted to a stroke unit were investigated with repeated clinical assessments and scores for degree of confusion, extent of paresis and level of functioning. Serum cortisol (C) and DS were measured on day 1 and/or day 4. Data for 28-day and 1-year mortality are presented. A control group of 65 age-matched healthy individuals was used. Multivariate analyses of mortality rates in the different tertiles or sixtiles of serum cortisol were performed with logistic regression, adjusting for age, sex, diabetes and level of consciousness. RESULTS: There was no difference in serum cortisol levels on day 1 for stroke patients when compared with control group values. Initial cortisol levels were significantly higher in the patients with acute disorientation versus orientated patients (P < 0.05). Cortisol levels on day 1 were an independent predictor of 28-day mortality, and patients with low cortisol levels (<270 nmol L(-1)) and increased levels (>550 nmol L(-1)) both had an increased 1-year mortality. DS levels on day 1 were significantly elevated in stroke patients. CONCLUSION: Hypercortisolism is associated with cognitive dysfunction early after ischaemic stroke. High and low circulating cortisol levels are associated with increased mortality after stroke. DS levels were not associated with clinical outcome.

Aged↗
PubMed2001

Cognitive dysfunction in patients with amyotrophic lateral sclerosis is associated with spherical or crescent-shaped ubiquitinated intraneuronal inclusions in the parahippocampal gyrus and amygdala, but not in the neostriatum.

Skeins or skein-like inclusions, one of the two types of ubiquitinated intraneuronal inclusions in amyotrophic lateral sclerosis (ALS), in the neostriatum are not specific to the disease, but it has not yet been determined whether the other, spherical or crescent-shaped inclusions (SCI) are pathognomonic. To clarify this and also to investigate whether the distribution of SCI in particular brain regions is associated with clinical parameters, we examined the occurrence of SCI in the brains of 24 patients with ALS and 94 controls. SCI in the neostriatum were specifically detected in 54% of the ALS cases, but not in any of the controls. No apparent phenotypic denominator, such as disease duration or the occurrence of dementia, correlated to the distribution of SCI in the neostriatum in ALS cases. On the other hand, the occurrence of SCI in both the second and third layers of the parahippocampal gyrus and amygdala was significantly correlated to the presence of dementia in ALS cases. SCI were distributed in association with each other among the parahippocampal gyrus, dentate gyrus of the hippocampus and amygdala, but not between the spinal anterior horn and any non-motor-associated brain regions. These findings suggest that these particular brain regions might be significantly involved in the neurodegenerative process associated with ALS. The relationship of SCI to either ALS pathogenesis or cognitive dysfunction depends on the brain regions in which they are distributed, and this indicates that the neurodegenerative processes in ALS proceed differentially in particular motor-associated and nonmotor-associated brain regions.

Aged↗
PubMedDate not supplied

Measurement of interthalamic adhesion thickness as a criteria for brain atrophy in dogs with and without cognitive dysfunction (dementia).

The criteria for brain atrophy in dogs have not yet been established, because of wide variation in the morphology of the ventricles and sulci of the brain depending on the breed and size. In this study, we examined the thickness of the interthalamic adhesion in a transverse magnetic resonance image to investigate normal, to examine the correlation with age, body weight, and breed, and to assess whether measurement would be a useful indicator of brain atrophy. The animals used in this study were of various breeds and weight, and had no identifiable intracranial lesion. They were divided into two groups: a normal group (0.6-15-year-old, n = 66) and a demented aging group (12-18-year-old, n = 12). The interthalamic adhesion thickness in both T1- and T2-weighted transverse images were measured in all dogs. The interthalamic adhesion thickness in the normal and demented groups was 6.79 +/- 0.70 and 3.82 +/- 0.79 mm, respectively. The interthalamic adhesion thickness in the demented group was significantly smaller. In an analysis of the correlation of interthalamic adhesion thickness with age and weight in normal dogs, significant negative and positive correlation was recognized, respectively. However, the strength of these correlations was low. These results suggest that interthalamic adhesion thickness may be a good parameter for evaluating brain atrophy in dogs with cognitive dysfunction.

Animals↗
PubMed1998

Tinnitus Cognitions Questionnaire: Development and Psychometric Properties of a Measure of Dysfunctional Cognitions Associated with Tinnitus.

The development of the Tinnitus Cognitions Questionnaire (TCQ), a scale designed to assess positive and negative cognitions associated with tinnitus, is described. Psychometric analyses of the TCQ are examined, with a total of 189 subjects from three separate samples. The results indicate good test-retest reliability (r = 0.88) and internal consistency (Cronbach's alpha = 0.91). Factor analysis revealed two factors that were interpreted as positive cognitions and negative cognitions. TCQ negative items and positive items were found to be unrelated (r = 0.09). Correlations between the TCQ and other self-report indices of depression, automatic negative thoughts, and tinnitus-specific symptomatology are reported. The TCQ may provide a useful index of the cognitive responses of tinnitus sufferers and may be employed as a measure of change in outcome research on psychological management of tinnitus.

Journal Article↗
PubMedDate not supplied

Clozapine-induced cognitive dysfunction in mice.

The atypical antipsychotic clozapine was examined for its ability to interrupt cognitive functions in mice on passive avoidance paradigm and elevated plus maze. The posttraining intraperitoneal injection of clozapine (0.1-7.5 mg/kg) induced dysfunction in acquisition as well as retrieval, which was reversed by physostigmine (0.05 mg/kg). Clozapine showed dose-related effects on scopolamine-induced cognitive dysfunction, with higher doses having no significant effect and lower doses reversing the dysfunction. These results are explained on the basis of clozapine's effects on central cholinergic receptors.

Animals↗
PubMed2004

[The cognitive dysfunction in Parkinson's disease].

Parkinson's disease (PD) is a slowly progressive disorder which begins with motor symptoms. Several cognitive deficits can be observed in nondemented patients with PD during their history. The core symptom in the cognitive deficits in PD is the executive dysfunction. Neuropsychological tests such as Wisconsin Card Sorting Test, Trail Making Test are used to measure the degree of this dysfunction. Executive dysfunction is thought related to abnormalities in the dorsolateral prefrontal circuit which largely passes through the caudate nucleus. The dysfunction emerges as the pathology spreads to the nigrocaudate project corresponding to Hoehn & Yahr stage II-III. Effective therapy for cognitive dysfunction in PD remains elusive, however donepezil, Attention Process Training, Music therapy and Transcranial magnetic stimulation have been reported to have partial efficacy.

Cognition Disorders↗
PubMedDate not supplied

Dietary enrichment counteracts age-associated cognitive dysfunction in canines.

Advanced age is accompanied by cognitive decline indicative of central nervous system dysfunction. One possibly critical causal factor is oxidative stress. Accordingly, we studied the effects of dietary antioxidants and age in a canine model of aging that parallels the key features of cognitive decline and neuropathology in humans. Old and young animals were placed on either a standard control food, or a food enriched with a broad spectrum of antioxidants and mitochondrial enzymatic cofactors. After 6 months of treatment, the animals were tested on four increasingly difficult oddity discrimination learning problems. The old animals learned more slowly than the young, making significantly more errors. However, this age-associated decline was reduced in the animals fed the enriched food, particularly on the more difficult tasks. These results indicate that maintenance on foods fortified with complex mixtures of antioxidants can partially counteract the deleterious effects of aging on cognition.

Aging↗
PubMed1999

Cognitive dysfunction in schizophrenia: a new set of tools for the assessment of cognition and drug effects.

Cognitive impairment in schizophrenia must be seen as a disturbance of cortico-sub-cortical connectivity with a neurotransmitter imbalance in a circuitry system, which connects thalamic input with prefrontal processing and supplementary motor cortex and basal ganglia output. The concept of maze-solving behaviour as a continuous cognitive task evoking a conflict between prefrontal cortex and basal ganglia activity is explained and introduced to distinguish between the effects of D2 blocking agents and substances with a predominant 5HT2A receptor affinity, such as clozapine and risperidone. Complex mazes show a cognitive deficit in untreated schizophrenic patients that are impaired by conventional and improved by atypical antipsychotic substances. Processing speed improves most on clozapine, while parallel processing is best supported by the non-sedative atypical substance risperidone. Maze paradigms are presented.

Antipsychotic Agents↗
PubMed2005

Use of a maze to detect cognitive dysfunction in a porcine model of hypothermic circulatory arrest.

BACKGROUND: Hypothermic circulatory arrest (HCA) can result in cognitive impairment not reflected by histopathology or gross neurologic observation. We tested the sensitivity of two multi-room maze tasks in detecting cerebral dysfunction after HCA in pigs. METHODS: Twenty-seven pigs were studied, divided between two tasks. 13 underwent 90 minutes HCA at 20 degrees C and were trained from postoperative day (POD) 7; 14 were unoperated controls. The maze includes a holding area, 8 rooms, and a center hallway. One piece of apple is placed in each baited room on each of 10 days of learning evaluation. After a pig enters a room, doors to all other rooms close, and the pig must return to the holding area. In task 1, 6 of 8 rooms were baited, and each day's session ended when each baited room had been entered, or after 20 trials. In task 2, initially only the right- or left-sided rooms were baited. Pigs were evaluated each day until they entered 4 baited rooms, or for 15 trials; the process was then repeated, baiting the other side. RESULTS: Intraoperative physiology and postoperative recovery showed no differences between task 1 or 2 pigs. Task 1 did not distinguish between control and HCA groups (p = 0.5), but task 2 revealed significantly (p = 0.04) better learning in controls. CONCLUSIONS: The significantly poorer performance of pigs after HCA suggests that the reversal of baited rooms in task 2 provides the sensitivity to detect cognitive dysfunction. The maze is a promising tool to investigate in pigs the mild cerebral damage often seen after HCA.

Animals↗
PubMed1988

The incidence of cognitive dysfunction in an encopretic population in children.

Cognitive testing was conducted in a clinical population of encopretic patients. Testing included the Weschler Intelligence Scale for Children-Revised (WISC-R), the Wide Range Achievement Test (WRAT) and the Bender Visual-Motor Gestalt Test (BVMGT). Although Full Scale, Verbal and Performance Intelligence Quotients on the WISC-R were not statistically different from general population means, subtests in Arithmetic (p less than 0.001), Digit Span (p less than 0.001) and Coding (p less than 0.05) were. There was also a high incidence of Verbal/Performance discrepancies and statistically significant differences on the WRAT in Spelling (p less than 0.01) and Arithmetic (p less than 0.01). Visual-motor integration was delayed two or more years in 43% of the patients on the BVMGT. These findings are consistent with the diagnosis of specific learning disabilities. An increased frequency of learning disabilities in an encopretic population may represent a subset of patients with a distinct syndrome in this disorder. These findings may point to the central nervous system (CNS) as the common point of pathology for the encopresis and learning disabilities, or reflect a common insult to both the CNS and gastrointestinal tract. Since histories in these patients did not reveal significant pregnancy or neonatal risk factors, this association could be related to genetic or environmental issues. Health professionals should be alert to the possibility of an increased incidence of learning disabilities in their encopretic patients. Further controlled studies are needed to determine if this finding is present in other settings, and if so, to determine the etiology.

Adolescent↗
PubMed2005

A new test battery to assess aphasic disturbances and associated cognitive dysfunctions -- German normative data on the aphasia check list.

Aphasia, defined as an acquired impairment of linguistic abilities, can be accompanied by a diversity of neuropsychological dysfunction. Accordingly, the necessity to include cognitive testing in the diagnosis of aphasia is increasingly recognized. Here we present the Aphasia Check List (ACL), a new test battery for the assessment of aphasic and associated cognitive disorders. The language part of the battery provides a differentiated profile of important linguistic abilities. In addition, the ACL includes nonverbal screening tests for three neuropsychological domains: memory, attention, and reasoning. Dysfunctions in these domains have been observed in aphasic patients and can have an impact on language function. The ACL is applicable to patients with language disturbances of different etiologies, different stages of disease, and to patients with mild to severe aphasia. As the entire test duration is only about 30 minutes, the ACL is also economically valuable. It thus presents an adequate starting point in aphasia diagnosis for a wide range of patients. Here we describe the construction of the ACL, and the normative study of its original German version with 154 aphasic patients and 106 healthy comparison subjects. The ACL cognition part revealed additional neuropsychological dysfunction in the aphasia group. We present the patterns of these dysfunctions and their correlations with language deficits.

Adult↗