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At least 415 records · Page 23Linked to original sources
PubMed2000

Carbohydrate-deficient glycoprotein syndrome type 1a: a variant phenotype with borderline cognitive dysfunction, cerebellar hypoplasia, and coagulation disturbances.

An 8-year-old boy is described with borderline cognitive impairment, cerebellar hypoplasia, a stroke-like episode, and venous thrombosis of the left leg after a period of immobilization. The pattern of multiple abnormalities in blood coagulation suggested carbohydrate-deficient glycoprotein syndrome type 1a. Isoelectric focusing of serum transferrin was abnormal. The activity of phosphomannomutase in leukocytes and fibroblasts was decreased. Mutation analysis of the PMM2 gene revealed the R141H/E151G genotype. These results confirm the presence of carbohydrate-deficient glycoprotein syndrome type 1a without severe psychomotor retardation.

Blood Coagulation Disorders↗
PubMedDate not supplied

Vestibular disease and cognitive dysfunction: no evidence for a causal connection.

OBJECTIVE: To evaluate the contribution of vestibular pathology to cognitive and affective complaints of patients with and without brain trauma. SETTING: An outpatient balance disorders clinic within a tertiary care neuroscience institute. PARTICIPANTS: 200 patients with dizziness--half with a recent history of brain trauma and half without. MAIN OUTCOME MEASURES: The Dizziness Handicap Inventory, the Beck Depression Inventory, and the Neurobehavioral Symptom Inventory were prospectively administered. Neurological examination and vestibular testing were performed to arrive at a diagnosis for the dizziness. Multiple regression analyses were carried out using vestibular diagnosis, psychiatric diagnosis, and trauma history as predictors of the inventory scores. RESULTS: Perceived disability was higher in dizzy patients with a history of brain trauma compared with dizzy patients without a history of trauma. A diagnosis of vestibular disease had no influence on perceived disability. Similarly, cognitive complaints were more common in dizzy patients with a history of brain trauma compared to dizzy patients without a history of trauma, but a diagnosis of vestibular disease had no influence on the frequency of cognitive complaints. CONCLUSIONS: In patients with postconcussive dizziness, cognitive complaints are likely due to neurologic injury or affective disturbance. In dizzy patients without brain trauma, cognitive complaints are likely due to concurrent affective disturbance.

Adult↗
PubMed2000

MRI correlates of cognitive dysfunction in multiple sclerosis patients.

Studies with conventional magnetic resonance imaging (MRI) support the hypothesis that cognitive impairment in multiple sclerosis (MS) patients is related with the lesion burden. Patterns of frontal lobe cognitive decline were also found to be related with the corresponding regional lesion load, although the total lesion load on T2-weighted MRI scans of the brain seems to be more relevant in determining frontal lobe deficits. Other non-conventional MRI techniques with a higher specificity to the heterogeneous substrates of MS pathology, such as the assessment of hypointense lesion load on T1-weighted scans and the histogram analysis of magnetisation transfer ratio (MTR) maps, have recently been applied to MS cognitive studies. Results from these studies suggest that three factors play a role in the pathogenesis of MS dementia: the burden of MS lesions, the severity of the pathological damage within individual lesions and that of the normal-appearing white matter.

Cognition Disorders↗
PubMed1991

[Disseminated sclerosis: organic basis for mental disorders and cognitive dysfunction].

The MRI-(magnetic resonance imaging) scanner has improved the knowledge of the organic basis of cognitive defects in multiple sclerosis. Recent studies demonstrated a correlation of MRI-verified single lesions, atrophy of the corpus callosum and cognitive defects; but failed to demonstrate the convincing correlation between psychic symptoms and MRI-verified lesions.

Atrophy↗
PubMed1975

Delayed hypoxic encephalopathy without cognitive dysfunction.

Three days after an episode of hypoxia, a 20-year-old man developed profound motor deficit in the absence of behavioral or cognitive disturbance. Previous reviews of delayed hypoxic encephalopathy have stressed behavioral and cognitive disturbances as the initial symptoms. This patient's pyramidal tract dysfunction in the absence of higher cortical dysfunction serves to illustrate that delayed hypoxic encephalopathy is predominantly a white matter rather than a gray matter disorder.

Adult↗
PubMed2006

Estrogen treatment effects on anticholinergic-induced cognitive dysfunction in normal postmenopausal women.

Estrogen has been shown to interact with the cholinergic system and influence cognition in animal models. This study investigated the interaction of estrogen and cholinergic system functioning and the effects of this interaction on cognitive task performance in healthy older women. Fifteen post-menopausal women were randomly and blindly placed on 1 mg of 17-beta estradiol or placebo for 3 months after which they participated in five anticholinergic challenge sessions, where they were administered one of two doses of the antimuscarinic drug scopolamine (SCOP) or the antinicotinic drug mecamylamine (MECA) or placebo. After the first challenge phase, they were crossed over to the other hormone treatment for another 3 months and repeated the challenges. Performance in multiple domains of cognition was assessed during anticholinergic drug challenge, including attention and verbal and nonverbal learning and memory. Results showed that estrogen pretreatment attenuated the anticholinergic drug-induced impairments on tests of attention and tasks with speed components. This study is the first to demonstrate the interaction of estrogen and the cholinergic system and the effects on cognitive performance in humans. The results suggest that estrogen status may affect cholinergic system tone and may be important for cholinergic system integrity.

Aged↗
PubMed1985

The value of Luria's Neuropsychological Investigation for the assessment of cognitive dysfunction in Alzheimer-type dementia.

Items from Luria's Neuropsychological Investigation (LNI) were used to assess cognitive functioning in three groups: patients with Alzheimer-type dementia (ATD), with alcoholic Korsakoff syndrome (KS) and control subjects of comparable age. The LNI was shown to be a sensitive assessment in that it distinguished differences within the ATD group and among the three groups. The validity and usefulness of the LNI in Alzheimer-type dementia are discussed.

Aged↗
PubMed2003

[A patient with Hashimoto's encephalopathy showing subacute global cognitive dysfunction].

We report a 66-year-old woman with Hashimoto's encephalopathy who showed rapidly developing cognitive deficits, inactivity, and gait disturbance without involuntary movements or convulsions. She had had right-sided hemiparesis and dysarthria caused by a lacunar infarction and had been admitted to our hospital for 2 weeks. Although the dysarthria and hemiparesis gradually improved, difficulty in walking, disorientation, and drowsiness developed 2 months after discharge. Upon readmission, the patient was alert but apathetic and sometimes sleepy. The right upper and lower limbs showed mild weakness, which was considered to be due to the previous infarction. Cerebrospinal fluid showed mild elevation of protein without pleocytosis. An electroencephalogram was normal, and a magnetic resonance imaging of the brain showed only the old lacunar infarction. Titers of antithyroglobulin antibodies and levels of thyroid stimulating hormone in serum were elevated. We made a diagnosis of Hashimoto's encephalopathy and treated the patient with high-dose corticosteroids. Within 1 week, her mental status improved and she was able to walk. Generalized seizure, myoclonus, and tremor, which are characteristic of Hashimoto's encephalopathy, never developed. The findings in this patient suggest that Hashimoto's encephalopathy, a treatable condition, should be included in the differential diagnosis of dementia.

Aged↗
PubMedDate not supplied

Cognitive dysfunction at baseline predicts symptomatic 1-year outcome in first-episode schizophrenics.

The present study addresses the consequences of cognitive disturbances on symptomatic outcome. Fifty-three first-episode schizophrenics were reassessed (n = 32) 1 year after admission. Simple regression analyses revealed that several self-perceived cognitive deficits at baseline as measured with the Frankfurt Complaint Questionnaire significantly predicted increased Brief Psychiatric Rating Scale global scores at follow-up (p = 0.05 to p = 0.005). A stepwise regression analysis proved memory dysfunction to be the strongest predictor of symptomatic worsening (p = 0.005). It is suggested that the exploration and treatment of neuropsychological deficits in schizophrenia is of great clinical importance with regard to its impact on both functional and symptomatic outcome in schizophrenia.

Acute Disease↗
PubMed2004

Cognitive dysfunctions in medicated and unmedicated patients with recent-onset schizophrenia.

Schizophrenia is associated with impairments in many cognitive domains on which the influence of antipsychotics, whether conventional or atypical, remains unclear. We conducted a study of recent-onset schizophrenic patients (DSM IV) that included unmedicated (n=19), and medicated (n=19) patients matched for age and IQ. Both groups of patients had comparably low extra-pyramidal symptoms (EPS). Cognitive tasks included attentional tasks (alertness and divided attention tests), a working memory task (a verbal n-back test) and the Wisconsin Card Sorting Test (WCST). After adjustment for the Total PANSS score, we found no significant difference between the two groups of patients in any of the cognitive tasks. When compared to a group of healthy controls (n=20) matched for IQ level, unmedicated patients performed significantly worse in all cognitive tasks, with significantly longer reaction times for alertness, divided attention and working memory. These results confirm the presence of cognitive impairments in attentional and executive functions in recent-onset patients whether or not they are medicated. There was no evidence that either conventional or atypical antipsychotics had an influence on patients when EPS were excluded. Altogether, our results further support the idea that cognitive deficits in schizophrenia are enduring features per se and cannot be considered as secondary to psychiatric symptoms or to the adverse effects of medication. In addition our results suggest that antipsychotics do not have a major effect on these impairments.

Adult↗
PubMed2002

Modulatory role of cyclooxygenase inhibitors in aging- and scopolamine or lipopolysaccharide-induced cognitive dysfunction in mice.

Inflammation processes may play a critical role in the pathogenesis of the degenerative changes and cognitive impairments associated with Alzheimer's disease (AD). Non-steroidal anti-inflammatory drugs are reported to be effective in reducing the risk of developing AD or cognitive impairments. Present experiments were performed to study the possible effect of various NSAIDs on cognitive performance of young, aged and scopolamine or lipopolysaccharide (LPS) treated mice (an animal model of AD) using one trial step through type of passive avoidance and in elevated plus maze task. Chronic administration of NSAIDs at the ED(50) doses (nimesulide, rofecoxib and naproxen for 15 days) significantly reversed the age or scopolamine-induced retention deficits in both test paradigms. However, in both the memory paradigms chronic administration of NSAIDs failed to modulate the retention performance of young mice. Acute administration of LPS (50 mcg/mouse, i.p.) significantly exhibited retention deficits after 24 h and seventh day of its administration in both test paradigms. Chronic administration (7 days) of rofecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor (1.92 mg/kg, p.o.) significantly reversed the LPS-induced retention deficits in both tests. The results of this study showed chronic treatment of NSAIDs reverses the cognitive deficits in age and scopolamine or LPS treated mice. These findings establish a link between the central nervous system expression of various pro-inflammatory cytokines and learning impairment in mice.

Aging↗
PubMed2003

Cognitive dysfunctions in parents of schizophrenic patients parallel the deficits found in patients.

Schizophrenia is characterized by a global cognitive impairment, with varying degrees of deficit in all ability domains. Since genetic factors are important in the etiology of schizophrenia we investigated whether parents of schizophrenic patients also show cognitive deficits, particularly on those cognitive ability domains that are most severely affected in patients. Both biological parents of 37 patients with schizophrenia (N=74 subjects) and 28 comparable healthy married control couples (N=56 subjects) were included. A comprehensive and standardized cognitive battery was used including tests measuring verbal memory, executive functioning, language, attention, and psychomotor functioning. Parents of patients differed from control couples on those cognitive constructs that are generally considered to be most impaired in schizophrenic patients, i.e. global verbal memory, bilateral motor skill, continuous performance, and word fluency. In addition, parents differed significantly from control couples on some other cognitive constructs on which patients show a smaller but also significant difference compared to healthy controls, i.e. unilateral motor skill and digit span. Results suggest that the cognitive constructs on which patients show relatively most severe impairment may prove suitable as endophenotypic markers in schizophrenia.

Cognition Disorders↗
PubMed2026

CNNM2 in schizophrenia: multilevel evidence of genetic susceptibility, magnesium homeostasis, neurodevelopment and cognitive dysfunction.

Schizophrenia (SCZ) is a common psychiatric disorder with a complex, genetically and environmentally influenced etiology, but the specific pathogenesis remains unclear. In recent years, the SCZ susceptibility gene CNNM2 (encoding cyclin M2) located at the 10q24.32-33 locus has received widespread attention. The well-validated SCZ risk interval 10q24.32-33 harbors two independent risk variants: rs11191580 in NT5C2 (significantly associated with CNNM2 mRNA and protein levels) and rs7914558 in CNNM2. Results from functional genomic analyses indicate that lower CNNM2 expression is significantly associated with SCZ. Imaging genetics studies have demonstrated that carriers of risk alleles of CNNM2 SNPs exhibit alterations in brain structure. Animal model studies have revealed that Cnnm2 downregulation in mice leads to impairments in sensorimotor gating and cognitive function. As an Mg2+ transporter, CNNM2 primarily maintains systemic Mg2+ homeostasis. According to clinical studies, a proportion of patients with SCZ exhibit reduced Mg2+ concentrations in plasma and cerebrospinal fluid. CNNM2 dysfunction may contribute to the pathology of SCZ by disrupting Mg2+ homeostasis, thereby affecting neurodevelopment and synaptic plasticity. A systematic consolidation of current evidence supporting the involvement of CNNM2 in SCZ pathogenesis provides a direction for further investigation of the pathological mechanisms underlying this disease, and for identification of novel targets for clinical intervention..

Schizophrenia↗