Cerebral Dysfunction (cerebral + dysfunction)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Neuropsychiatric disturbances in SLE are associated with antibodies against NMDA receptors

EUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2005
R. Omdal
To determine whether neuropsychiatric manifestations in patients with systemic lupus erythematosus (SLE) are influenced by antibodies against the human N-methyl- d -aspartate (NMDA) receptor types NR2a or NR2b. A decapeptide was synthesized containing a sequence motif present in the extracellular ligand-binding domain of NMDA receptors NR2a and NR2b, bound by the monoclonal murine anti-DNA antibody R4A. In an ELISA with the murine monoclonal R4v as positive control, plasma samples of 57 patients with SLE were examined for the anti-peptide (anti-NR2) antibody after the patients had been subjected to comprehensive psychological and cognitive testing. Poor performance on the Visual Paired Associates test (immediate), the Grooved Pegboard test, as well as high scores on the Beck Depression Inventory, and scales D-2 (depression), Pd-4 (psychopathic deviate), Sc-8 (schizophrenia), and Ma-9 (hypomania) of the MMPI-2 were significantly associated with elevated levels of anti-NR2 antibodies. The findings in several domains indicate an association between anti-NR2 antibodies and depressed mood in addition to decreased short-time memory and learning. Antibodies to NMDA receptors thus may represent one of several mechanisms for cerebral dysfunction in patients with SLE. [source]

AIDS dementia complex and Hashimoto encephalopathy in a senescent woman

INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 12 2007
Robert Waltereit
Abstract AIDS dementia complex is one of the specific infectious dementias, which is rarely seen in senescent (>75 years of age) subjects. Hashimoto encephalopathy has been described as the cause of several neurological and psychiatric syndromes including dementia. The proposed pathophysiological mechanism is an autoimmune reaction to shared, thyroid gland and CNS epitopes with subsequent cerebral dysfunction. We report here the first case of a patient who fulfils both, the criteria for AIDS dementia complex and Hashimoto encephalopathy, yet being unresponsive to steroid therapy. Diagnostic and therapeutic implications are discussed. Copyright © 2007 John Wiley & Sons, Ltd. [source]

Increased glutamate/glutamine compounds in the brains of patients with fibromyalgia: A magnetic resonance spectroscopy study

ARTHRITIS & RHEUMATISM, Issue 6 2010
Manuel Valdés
Objective Fibromyalgia (FM) has been defined as a systemic disorder that is clinically characterized by pain, cognitive deficit, and the presence of associated psychopathology, all of which are suggestive of a primary brain dysfunction. This study was undertaken to identify the nature of this cerebral dysfunction by assessing the brain metabolite patterns in patients with FM through magnetic resonance spectroscopy (MRS) techniques. Methods A cohort of 28 female patients with FM and a control group of 24 healthy women of the same age were studied. MRS techniques were used to study brain metabolites in the amygdala, thalami, and prefrontal cortex of these women. Results In comparison with healthy controls, patients with FM showed higher levels of glutamate/glutamine (Glx) compounds (mean ± SD 11.9 ± 1.6 arbitrary units [AU] versus 13.4 ± 1.7 AU in controls and patients, respectively; t = 2.517, 35 df, corrected P = 0.03) and a higher Glx:creatine ratio (mean ± SD 2.1 ± 0.4 versus 2.4 ± 1.4, respectively; t = 2.373, 35 df, corrected P = 0.04) in the right amygdala. In FM patients with increased levels of pain intensity, greater fatigue, and more symptoms of depression, inositol levels in the right amygdala and right thalamus were significantly higher. Conclusion The distinctive metabolic features found in the right amygdala of patients with FM suggest the possible existence of a neural dysfunction in emotional processing. The results appear to extend previous findings regarding the dysfunction in pain processing observed in patients with FM. [source]

Motor impairment in liver cirrhosis without and with minimal hepatic encephalopathy

ACTA NEUROLOGICA SCANDINAVICA, Issue 1 2010
M. Butz
Butz M, Timmermann L, Braun M, Groiss SJ, Wojtecki L, Ostrowski S, Krause H, Pollok B, Gross J, Südmeyer M, Kircheis G, Häussinger D, Schnitzler A. Motor impairment in liver cirrhosis without and with minimal hepatic encephalopathy. Acta Neurol Scand: 2010: 122: 27,35. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Aim,,, Manifest hepatic encephalopathy (HE) goes along with motor symptoms such as ataxia, mini-asterixis, and asterixis. The relevance of motor impairments in cirrhotics without and with minimal HE (mHE) is still a matter of debate. Patients and methods,,, We tested three different groups of patients with liver cirrhosis: no signs of HE (HE 0), mHE, and manifest HE grade 1 according to the West Haven criteria (HE 1). All patients (n = 24) and 11 healthy control subjects were neuropsychometrically tested including critical flicker frequency (CFF), a reliable measure for HE. Motor abilities were assessed using Fahn Tremor Scale and International Ataxia Rating Scale. Fastest alternating index finger movements were analyzed for frequency and amplitude. Results,,, Statistical analyses showed an effect of HE grade on tremor and ataxia (P < 0.01). Additionally, both ratings yielded strong negative correlation with CFF (P < 0.01, R = ,0.5). Analysis of finger movements revealed an effect of HE grade on movement frequency (P < 0.03). Moreover, decreasing movement frequency and increasing movement amplitude parallel decreasing CFF (P < 0.01, R = 0.6). Conclusion,,, Our results indicate that ataxia, tremor, and slowing of finger movements are early markers for cerebral dysfunction in HE patients even prior to neuropsychometric alterations becoming detectable. [source]

Tau haplotype influences cerebral perfusion pattern in frontotemporal lobar degeneration and related disorders

ACTA NEUROLOGICA SCANDINAVICA, Issue 5 2008
B. Borroni
Objective,,, The modulating factors on phenotypic expression of frontotemporal lobar degeneration (FTLD) remain still unknown. The aim of this study was to determine whether tau genetic variability modulates the brain functional and the clinical phenotypic expression of FTLD. Materials and methods,,, Clinical and neurological evaluations, a standardized neuropsychological assessments as well as a brain single photon emission tomography perfusion imaging studies were performed in 48 FTLD patients. Cerebral perfusion patterns were analysed according to H1 or H2 tau haplotypes by statistical parametric mapping and principal component analysis. Results,,, Two different patterns of cerebral dysfunction characterized the haplotypes, as hypoperfusion of frontal medial and cingulated cortex in H2-carriers and a prevalent involvement of posterior parietal regions in H1-carriers. Further, a significant increase of cerebrospinal fluid total tau and phospho tau levels was found in H2-carriers. Conclusions,,, These findings support a role of tau haplotype in modulating disease phenotype by influencing the hypoperfusion pattern and cerebrospinal fluid tau levels in FTLD. [source]