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Results for “Cognitive Dysfunction”

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PubMed1994

Pursuit eye movements in chronic schizophrenics: relationship between increased saccades and negative symptoms.

Smooth pursuit eye movements of chronic schizophrenics (n = 16) and controls (n = 10) were recorded while subjects tracked a sinusoidally-moving target. Negative symptoms in schizophrenics were rated using the Schedule for the Assessment of Negative Symptoms. An increased frequency of smooth pursuit eye movement abnormalities was found in the schizophrenic group, including greater variability of gain and more frequent and larger saccades. Frequency of saccades was positively correlated with the Negative Symptoms scales for attentional impairment and alogia. The results confirm findings of eye movement dysfunction in schizophrenics and provide new evidence that the motor and cognitive dysfunctions of schizophrenia may be related.

Adult↗

PubMed2006

Treatment of cognitive impairment in multiple sclerosis.

Cognitive impairment in multiple sclerosis is an increasingly recognized entity. This article reviews the cognitive impairment of multiple sclerosis, its prevalence, its relationship to different types of multiple sclerosis, and its contribution to long-term functional prognosis. The discussion also focuses on the key elements of cognitive dysfunction in multiple sclerosis which distinguish it from other forms of cognitive impairment. Therapeutic interventions potentially effective for the cognitive impairment of multiple sclerosis are reviewed including the effects of disease modifying therapies and the use of physical and cognitive interventions.

Adjuvants, Immunologic↗

PubMed2004

Amyloid angiopathy-related vascular cognitive impairment.

We review accumulating evidence that cerebrovascular amyloid deposition (cerebral amyloid angiopathy [CAA]) is an independent risk factor for cognitive dysfunction. The two population-based autopsy studies that have analyzed cognitive status during life as a function of CAA have each suggested deleterious effects of CAA on cognition even after controlling for age and Alzheimer disease pathology. We also review data from patients with CAA-related intracerebral hemorrhage (the one form of CAA that can be noninvasively recognized) suggesting associations of CAA with radiographic white matter abnormalities and cognitive impairment. These data highlight the importance of elucidating the effects of vascular amyloid on cerebrovascular function and of developing therapeutic strategies for this potentially widespread form of microvascular cognitive impairment.

Cerebral Amyloid Angiopathy↗

PubMed2006

Somatropin therapy and cognitive function in adults with growth hormone deficiency : a critical review.

Both growth hormone (GH) and insulin-like growth factor (IGF)-I have receptors in the brain, in particular in areas that are involved in cognitive function. Therefore, it has been hypothesized that GH deficiency can lead to cognitive dysfunction, and that somatropin replacement therapy may have beneficial effects on cognitive function in GH-deficient patients. In this review, an overview is given regarding the possible effects of decreased activity of the GH/IGF-I axis and somatropin therapy in GH deficiency in relation to cognitive function. The available data regarding cognitive function in GH-deficient patients are limited, but suggest that this condition can lead to specific cognitive changes, in particular attentional deficits and altered processing speed. The underlying mechanisms and the effects of somatropin treatment on cognitive function in GH deficiency are still unclear. Similar studies to those performed in patients with GH deficiency have been performed regarding the cognitive changes in elderly patients with relatively low GH and/or IGF-I levels. Large controlled studies regarding the effects and safety of somatropin treatment in healthy elderly patients have not been performed.

Adult↗

PubMed1997

Neurocognitive and psychosocial correlates of ventroposterolateral pallidotomy surgery in Parkinson's disease.

The purpose of this study was to characterize the neuropsychological and psychosocial profile of patients with Parkinson's disease before and after they underwent unilateral left or right pallidotomy, to assess specific cognitive and personality changes caused by lesioning the globus pallidus, and to predict favorable surgical outcome based on these measures. Eighteen patients underwent comprehensive neuropsychological assessment before and after left-sided pallidotomy (10 patients) or right-sided pallidotomy (eight patients). The findings support the presence of frontosubcortical cognitive dysfunction in all patients at baseline and a specific pattern of cognitive impairment following surgery, with side of lesion being an important predictor of pattern and degree of decline. Specifically, patients who underwent left-sided pallidotomy experienced a mild decline on measures of verbal learning and memory, phonemic and semantic verbal fluency, and cognitive flexibility. Patients who underwent right-sided pallidotomy exhibited a similar decline in verbal learning and cognitive flexibility, as well as a decline in visuospatial construction abilities; however, this group also exhibited enhanced performance on a delayed facial memory measure. Lesioning the globus pallidus may interfere with larger cognitive circuits needed for processing executive information with disruption of the dominant hemisphere circuit, resulting in greater deficits in verbal information processing. The left-sided pallidotomy group also reported fewer symptoms of depression and anxiety following surgery. This enhanced mood functioning was not seen for the right-sided pallidotomy group. No relationships were noted between cognitive impairment or advanced age at baseline and surgicaloutcome. This study provides objective evidence for specific changes in neurocognitive and psychosocial functioning following left- and right-sided pallidotomy.

Journal Article↗

PubMedDate not supplied

Visual and auditory cognitive processing affected by epilepsy.

Neuropsychological studies on epileptic patients may be expected to reveal specific cognitive dysfunction even in patients with normal general intellectual ability. Difficulties in cognitive processing by visual-spatial and auditory-verbal modes are indicated by this investigation employing the Wisconsin Card Sorting Test and the Token Test, with epileptics of normal intelligence. Impairment in capacity for sustained, focused attention significantly affects performance of epileptic patients on these clinical measures, and others as well which require vigilance and attention and sensory-perceptual discrimination.

Adult↗

PubMedDate not supplied

Visual and auditory cognitive processing affected by epilepsy.

Neuropsychological studies of epileptic patients may be expected to reveal specific cognitive dysfunction even in patients with normal general intellectual ability. Difficulties in cognitive processing by visual-spatial and auditory-verbal modes are indicated by this investigation employing the Wisconsin Card Sorting Test and the Token Test, with epileptics of normal intelligence. Impairment in capacity for sustained, focused attention significantly affects performance of epileptic patients on these clinical measures, and others as well which require vigilance and attention and sensory-perceptual discrimination.

Adult↗

PubMed1989

Mental status assessment in the elderly.

Mental status testing is an essential element of evaluating elderly patients. A structured examination often helps identify the etiology of symptoms that are responsible for changes in patient behavior, that lead to family stress, but that are otherwise not indicative of cognitive dysfunction. A structured mental status examination is also helpful in distinguishing cognitive changes caused by dementia, delirium, and depression. This article examines the steps in mental status assessment and the commonly used assessment instruments. The experience of a family medicine ambulatory multidisciplinary evaluation service in mental status testing is discussed.

Aged↗

PubMed2005

Frontotemporal white matter changes in amyotrophic lateral sclerosis.

Cognitive dysfunction can occur in some patients with amyotrophic lateral sclerosis (ALS) who are not suffering from dementia. The most striking and consistent cognitive deficit has been found using tests of verbal fluency. ALS patients with verbal fluency deficits have shown functional imaging abnormalities predominantly in frontotemporal regions using positron emission tomography (PET). This study used automated volumetric voxel-based analysis of grey and white matter densities of structural magnetic resonance imaging (MRI) scans to explore the underlying pattern of structural cerebral change in nondemented ALS patients with verbal fluency deficits. Two groups of ALS patients, defined by the presence or absence of cognitive impairment on the basis of the Written Verbal Fluency Test (ALSi, cognitively impaired, n=11; ALSu, cognitively unimpaired n=12) were compared with healthy age matched controls (n=12). A comparison of the ALSi group with controls revealed significantly (p<0.002) reduced white matter volume in extensive motor and non-motor regions, including regions corresponding to frontotemporal association fibres. These patients demonstrated a corresponding cognitive profile of executive and memory dysfunction. Less extensive white matter reductions were revealed in the comparison of the ALSu and control groups in regions corresponding to frontal association fibres. White matter volumes were also found to correlate with performance on memory tests. There were no significant reductions in grey matter volume in the comparison of either patient group with controls. The structural white matter abnormalities in frontal and temporal regions revealed here may underlie the cognitive and functional imaging abnormalities previously reported in non-demented ALS patients. The results also suggest that extra-motor structural abnormalities may be present in ALS patients with no evidence of cognitive change. The findings support the hypothesis of a continuum of extra-motor cerebral and cognitive change in this disorder.

Adult↗

PubMedDate not supplied

Neurocognitive dysfunction in dually-diagnosed patients: a potential roadblock to motivating behavior change.

Substance abuse has been associated with cognitive dysfunction, such as problems with attention, reasoning, and memory. Certain psychiatric disorders also have been associated with cognitive difficulties, thus placing dually-diagnosed patients at high risk for cognitive impairment that could interfere with successful entry into or completion of therapy. Twenty-two dually-disordered inpatients were administered the Brief Readiness to Change Questionnaire to measure levels of motivation to change substance use, and a neuropsychological test battery that included the Wechsler Adult Intelligence Scale-Revised (WAIS-R), the Halstead Category Test (HCT), and the Wechsler Memory Scale-Revised (WMS-R). Higher general intellectual, executive, and memory functioning were significantly related to greater scores in readiness to change substance abuse in this sample. Cognitive ability may be an important variable to consider in the motivation and treatment of dually-diagnosed patients.

Adolescent↗

PubMed2001

The 5-HT(6) receptor antagonist SB-271046 selectively enhances excitatory neurotransmission in the rat frontal cortex and hippocampus.

Preclinical evidence has suggested a possible role for the 5-HT(6) receptor in the treatment of cognitive dysfunction. However, currently there is little neurochemical evidence suggesting the mechanism(s) which may be involved. Using the selective 5-HT(6) antagonist SB-271046 and in vivo microdialysis, we have evaluated the effects of this compound on the modulation of basal neurotransmitter release within multiple brain regions of the freely moving rat. SB-271046 produced no change in basal levels of dopamine (DA), norepinephrine (NE) or 5-HT in the striatum, frontal cortex, dorsal hippocampus or nucleus accumbens. Similarly, this compound had no effect on excitatory neurotransmission in the striatum or nucleus accumbens. Conversely, SB-271046 produced 3- and 2-fold increases in extracellular glutamate levels in both frontal cortex and dorsal hippocampus, respectively. These effects were completely attenuated by infusion of tetrodotoxin but unaffected by the muscarinic antagonist, atropine. Here we demonstrate for the first time the selective enhancement of excitatory neurotransmission by SB-271046 in those brain regions implicated in cognitive and memory function, and provide mechanistic evidence in support of a possible therapeutic role for 5-HT(6) receptor antagonists in the treatment of cognitive and memory dysfunction.

Animals↗

PubMed2002

Cognitive correlates of apathy in traumatic brain injury.

OBJECTIVE: To investigate the relation between apathy and cognitive deficits in patients with severe traumatic brain injury (TBI). BACKGROUND: Apathy defined as reduced goal-directed behavior due to lack of motivation constitutes a major neuropsychiatric symptom following TBI. According to definition, apathy should not be associated with global cognitive reduction, but rather with specific areas of cognitive dysfunction. METHODS: results from the Apathy Evaluation Scale (AES) and a comprehensive neuropsychologic assessment were collected in up to 53 patients with severe TBI. Neuropsychologic tests were organized in the following seven areas of cognitive function: acquisition and memory, attention span, executive function, psychomotor speed, verbal skills, nonverbal skills, and motor speed. RESULTS: Apathy score was significantly correlated with reduced performance on acquisition and memory, psychomotor speed, and executive functions. A principal component analysis showed that these specific areas of cognitive functions clustered together with the cognitive dimension of apathy, not with behavioral or emotional aspects of apathy. CONCLUSIONS: Apathy is associated with specific cognitive deficits related to frontal lobe dysfunction. The results are in accordance with the definition of apathy and confirm apathy-cognitive function relationships reported in other neurologic populations.

Adolescent↗

PubMed2003

Posterior ocular malformations in children: somatic, neuroradiological and cognitive aspects.

AIM: To investigate associated neurological, endocrinological and cognitive dysfunctions in children with visual impairment caused by optic nerve hypoplasia or optic nerve/fundus coloboma and/or microphthalmus. METHODS: Forty children born between 1990 and 1998 were assessed by neurological examination, re-evaluation of neuroradiological investigations, review of medical records and examination of cognitive levels. RESULTS: Neurological dysfunctions (epilepsy and/or motor impairment) were found in 13/28 children with optic nerve hypoplasia and in 3/12 children with coloboma/microphthalmus. The optic pathways were thin in 22/24, an abnormal posterior pituitary gland and/or thin infundibulum was found in 16/22 and absence of septum pellucidum in 14/27 children with optic nerve hypoplasia. Other types of cerebral abnormalities occurred in 9/26 children. Among children with coloboma/microphthalmus, the optic pathways were thin in 4/8 children but none had pituitary or cerebral midline abnormalities. Sixteen children with optic nerve hypoplasia were receiving hormone substitution but none of the children with coloboma/microphthalmus. Thirteen of the 16 children with optic nerve hypoplasia and with an abnormal pituitary region had endocrinological deficiencies. Mental retardation was found in 9/24 of the children with optic nerve hypoplasia and in 5/10 of the children with coloboma/microphthalmus. CONCLUSION: Endocrinological. neurological and neuroradiological defects seem more common in children with optic nerve hypoplasia than in children with coloboma. A pituitary region that appears abnormal in magnetic resonance imaging seems to predict endocrinological deficits in children with optic nerve hypoplasia.

Blindness↗

PubMed2005

Soluble Abeta oligomers ultrastructurally localize to cell processes and might be related to synaptic dysfunction in Alzheimer's disease brain.

Soluble Abeta oligomers have recently been considered to be responsible for cognitive dysfunction prior to senile plaque (SP) formation in Alzheimer's disease (AD) brain. To investigate the ultrastructural localization of soluble Abeta oligomers, we conducted the post-embedding immunoelectron microscopic (IEM) study using an antibody against a molecular mimic of oligomeric Abeta. We examined autopsied brains from AD patients and nondemented subjects. Oligomer-specific immunoreactions detected by IEM tended to be found with higher density (1) in AD than in nondemented brains and (2) at the axon and axon terminal in AD than in nondemented brains. These findings imply that soluble Abeta oligomers might be related to synaptic dysfunction in AD brain.

Aged↗

PubMed2003

Hippocampal synaptic dysfunction in a murine model of human immunodeficiency virus type 1 encephalitis.

Alterations in hippocampal physiology affect cognition in human immunodeficiency virus type 1 (HIV-1)-associated dementia (HAD). The mechanism for how this occurs is not well understood. To address this, we investigated how changes in synaptic transmission and plasticity are affected by viral infection and macrophage activation using a severe combined immunodeficiency mouse model of human HIV-1 encephalitis (HIVE). HIVE was induced in mice by stereotactic injection of HIV-1-infected human monocyte-derived macrophages (MDM) into the striatum. Animals were sacrificed after 3, 7 and 15 days. Hippocampal slices were prepared from HIV-1, MDM- and sham-injected animals. Electrically evoked field excitatory postsynaptic potentials were recorded in the CA1 region of the hippocampus. Neuronal physiology was assessed by input-output and by long-term potentiation (LTP) assays. We observed that a higher stimulation intensity (mA) was required to induce a 1-mV response in the HIVE mice (0.32+/-0.06) compared with shams (0.17+/-0.01) at day 7. The stimulation intensities at day 15 were 0.44+/-0.07 and 0.23+/-0.05 in the HIVE and shams, respectively. An impairment of synaptic function was detected through measuring synaptic responses induced by stimuli with different intensities. Paired-pulse facilitation (PPF) showed deficits in HIVE mice at days 3, 7, and 15. At day 3, PPF ratios were 1.13+/-0.02 and 1.24+/-0.04 in HIVE and sham. The induction and maintenance of LTP was also impaired in HIVE mice. The average magnitude of LTP was 131.23+/-15.26% of basal in HIVE as compared with sham animals of 232.63+/-24.18%. MDM-injected mice showed an intermediate response. Taken together, the results show a range of neuronal synaptic transmission and plasticity changes in HIVE mice that may reflect the mechanisms of cognitive dysfunction in human HAD.

Animals↗

PubMed2000

The cholinergic deficit in Alzheimer's disease: impact on cognition, behaviour and function.

Although the neurodegeneration occurring in Alzheimer's disease (AD) affects multiple neurotransmitters, the cholinergic system has received the greatest attention. Acetylcholine (ACh) is fundamental to mnemonic function, assisting in the septal hippocampal pathway and facilitating cortical activation. One of the earliest pathological events in AD is the degeneration of ACh-synthesizing neurons in the subcortical nuclei of the human basal forebrain. Indeed, the loss of cholinergic function in AD is correlated with the density of histopathological markers of AD, the severity of cognitive dysfunction and disease duration. However, the precise mechanism by which the cholinergic system influences cognition, and behaviour, is unknown. Recent preliminary data from functional imaging and ligand-binding studies implicate a dynamic interaction between the nicotinic-muscarinic cholinergic receptor systems. The relatively preserved thalamic nicotinic system, compared with the dysfunctional cortical muscarinic system, may facilitate thalamocortical metabolic excitation in the failing AD brain. Thus, it is hypothesized that thalamic influence within frontal-subcortical circuits is augmented in AD patients who demonstrate a marked improvement to cholinesterase inhibitor therapy. Understanding the cholinergic basis of the cognitive, functional and behavioural deficits in AD, and the differential treatment response to various agents, will ultimately improve patient care and neuropharmacological insights. This paper reviews the current understanding of the cholinergic influence in cognition, behaviour and, as a result, function in AD patients.

Journal Article↗

PubMed2000

Attenuation of neurodegeneration-relevant modifications of brain proteins by dietary soy.

Epidemiological studies show that postmenopausal women who undertake estrogen-replacement therapy have significantly lower risk for the onset of Alzheimer's disease (AD) than women who do not. Animal behavior studies have shown that ovariectomy results in the development of cognitive dysfunction that is prevented by estrogen-replacement, suggesting that normal mammalian cognitive function is impaired by estrogen reduction. Soy isoflavones in particular genistein have been demonstrated to have weak and selective estrogenic actions in various models of human chronic diseases. A hallmark of several human dementias including AD and fronto temporal dementia with Parkinsonism on chromosome 17 (FTDP-17) is the hyperphosphorylation of the microtubule-associated protein tau. Preliminary experiments are discussed here which show that isoflavones delivered in a soy protein matrix attenuated selected AD-relevant tau phosphorylations in a primate model of menopause. The rationale is discussed for the use of soy-based foods for protection against postmenopausal neurodegeneration.

Alzheimer Disease↗

PubMed1996

Measurement of cognitive function: relating rodent performance with human minds.

Rodents are the most commonly employed animals to model human cognitive dysfunction, but many of the behavioural paradigms employed for evaluation of rodent cognitive abilities measure functions rather different from those generally assessed in humans. This may be one reason for the failure of these models to allow valid predictions about drug effects in demented patients. One solution to this may be the use of a more comparative approach. Careful experimental designs indicate that comparative attentional as well as mnemonic processes can be assessed in rat and human subjects. This could be an essential step towards the successful development of drugs with therapeutic potential in cognitive disorders.

Animals↗