Acupuncture in Tension-Type Headache

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Different responses to rivastigmine in subcortical vascular dementia and multi-infarct dementia.

Vascular dementia (VaD) is associated with a large amount of heterogeneity, as it groups together a broad category of patients in whom various manifestations of cognitive decline are attributed to cerebrovascular or cardiovascular disease. Thus, a study was designed to determine the effects of rivastigmine on cognitive function, global daily living performance, and behavioral disorders in VaD patients versus an active control (nimodipine), stratifying patients according to the type of VaD, subcortical vascular dementia (sVAD), and multi-infarct dementia (MID). The trial was a prospective study. This study shows that long-term treatment with rivastigmine, at dosages approved for therapeutic use in Alzheimer's disease, produces significant improvement in all behavioral symptoms in 2 forms of VaD, MID and sVaD, except delusions. It also suggests that rivastigmine may enable a reduction in concomitant neuroleptics and benzodiazepines in VaD, especially in MID. The results are discussed with an overview of the literature

Risk factors for vascular dementia: Hypotension as a key point

Physiologically, the cerebral autoregulation system allows maintenance of constant cerebral blood flow over a wide range of blood pressure. In old people, there is a progressive reshape of cerebral autoregulation from a sigmoid curve to a straight line. This implies that any abrupt change in blood pressure will result in a rapid and significant change in cerebral blood flow. Hypertension has often been observed to be a risk factor for vascular dementia (VaD) and sometimes for Alzheimer disease although not always. Indeed, high blood pressure may accelerate cerebral white matter lesions, but white matter lesions have been found to be facilitated by excessive fall in blood pressure, including orthostatic dysregulation and postprandial hypotension. Many recent studies observed among other data, that there was a correlation between systolic pressure reduction and cognitive decline in women, which was not accounted for by other factors. Baseline blood pressure level was not significantly related to cognitive decline with initial good cognition. Some researchers speculate that blood pressure reduction might be an early change of the dementing process. The most confounding factor is that low pressure by itself might be a predictor of death; nevertheless, the effect of low blood pressure on cognition is underestimated because of a survival bias. Another explanation is that clinically unrecognized vascular lesions in the brain or atherosclerosis are responsible for both cognitive decline and blood pressure reduction. We discuss the entire process, and try to define a possible mechanism that is able to explain the dynamic by which hypotension might be related to dementia

Effect of Transcranial Magnetic Stimulation (TMS) on Parietal and Premotor Cortex during Planning of Reaching Movements

The activation of the superior parietal lobule (SPL) and premotor cortex (PM) has been investigated using transcranial magnetic stimulation (TMS) during planning of reaching movements under visual guidance. A facilitory effect was found when TMS was delivered on the parietal cortex at about half of the time from sight of the target to hand movement, independently of target location in space. Furthermore, at the same stimulation time, a similar facilitory effect was found in PM, which is probably related to movement preparation. This data contributes to the understanding of cortical dynamics in the parieto-frontal network, and suggests that it is possible to interfere with the planning of reaching movements at different cortical points within a particular time window. Since similar effects may be produced at similar times on both the SPL and PM, parallel processing of visuomotor information is likely to take place in these regions

Treatment of Fatigue in Multiple Sclerosis Patients: A Neurocognitive Approach

The objective of the study was to treat fatigue in patients with multiple sclerosis (MS) by a neurocognitive rehabilitation program aimed at improving motor planning by using motor imagery (MI). Twenty patients with clinically definite MS complaining of fatigue were treated for five weeks with exercises of neurocognitive rehabilitation twice a week. Patients were evaluated by Fatigue Severity Scale (FSS), Modified Fatigue Impact Scale (MFIS), MSQoL54, Expanded Disability Status Scale (EDSS), and MS Functional Composite (MSFC). After treatment, a decrease in fatigue was detected with both FSS (P = 0.0001) and MFIS (P = 0.0001). MSFC (P = 0.035) and MSQoL54 (P = 0.002) scores improved compared to baseline. At six-month followup, the improvement was confirmed for fatigue (FSS, P = 0.0001; MFIS P = 0.01) and for the physical subscale of MSQoL54 (P = 0.049). No differences in disability scales were found. These results show that neurocognitive rehabilitation, based on MI, could be a strategy to treat fatigue in MS patients

Blood transcriptomics of drug-na\uefve sporadic Parkinson's disease patients

BACKGROUND: Parkinson's disease (PD) is a chronic progressive neurodegenerative disorder that is clinically defined in terms of motor symptoms. These are preceded by prodromal non-motor manifestations that prove the systemic nature of the disease. Identifying genes and pathways altered in living patients provide new information on the diagnosis and pathogenesis of sporadic PD. METHODS: Changes in gene expression in the blood of 40 sporadic PD patients and 20 healthy controls ("Discovery set") were analyzed by taking advantage of the Affymetrix platform. Patients were at the onset of motor symptoms and before initiating any pharmacological treatment. Data analysis was performed by applying Ranking-Principal Component Analysis, PUMA and Significance Analysis of Microarrays. Functional annotations were assigned using GO, DAVID, GSEA to unveil significant enriched biological processes in the differentially expressed genes. The expressions of selected genes were validated using RT-qPCR and samples from an independent cohort of 12 patients and controls ("Validation set"). RESULTS: Gene expression profiling of blood samples discriminates PD patients from healthy controls and identifies differentially expressed genes in blood. The majority of these are also present in dopaminergic neurons of the Substantia Nigra, the key site of neurodegeneration. Together with neuronal apoptosis, lymphocyte activation and mitochondrial dysfunction, already found in previous analysis of PD blood and post-mortem brains, we unveiled transcriptome changes enriched in biological terms related to epigenetic modifications including chromatin remodeling and methylation. Candidate transcripts as CBX5, TCF3, MAN1C1 and DOCK10 were validated by RT-qPCR. CONCLUSIONS: Our data support the use of blood transcriptomics to study neurodegenerative diseases. It identifies changes in crucial components of chromatin remodeling and methylation machineries as early events in sporadic PD suggesting epigenetics as target for therapeutic intervention

Alzheimer's disease: the glycosaminoglycan sink

No abstract available

The intercosto-brachial anastomosis in the treatment of cervical roots avulsions: clinical and neurophysiological considerations.

The authors present their surgical and clinical experience about the intercosto-brachial anastomosis for treating traumatic avulsions of the cervical roots. The most interesting aspect in the post-operative course of these patients is their ability to regain a voluntary elbow flexion independently from the respiratory activity. A dynamic SPECT examination in a small series of cases suggests that some mechanisms of functional reorganization within the brain should be involved

LA DEMENZA VASCOLARE: REALT\uc0 CLINICHE, PROSPETTIVE TERAPEUTICHE, IDENTIT\uc0 BIOLOGICHE.

Secondo la pi\uf9 comune classificazione NINDS\u2013AIREN, si parla di demenza vascolare probabile quando vi \ue8 l\u2019oggettivit\ue0 di un impairment cognitivo, che compromette le attivit\ue0 comuni del vivere sociale, con coesistenza di segni neurologici focali compatibili con una diagnosi di ischemia cerebrale, associata ad un\u2019evidenza neuroradiologica e quando sia rispettato il nesso di correlazione temporale tra insorgenza di demenza e cerebro\u2013vasculopatia. Sembra che il danno ipossico/ischemico/metabolico esteso alle porzioni encefaliche sottocorticali sottenda la caratteristica della demenza vascolare, che non \ue8 un unicum concettuale. Si riconoscono attualmente la demenza multi\u2013infartuale, quella sottocorticale, quella da singoli infarti strategici. Tuttavia, uno dei cardini del NINDS\u2013AIREN, delle alterazioni della sostanza bianca, unicamente presenti nella demenza vascolare, \ue8 stato smentito da recenti studi, in cui si \ue8 dimostrato un\u2019alterazione evidente della sostanza bianca anche nella malattia di Alzheimer, a tal punto da poter far ipotizzare un trait\u2013d\u2019union fra le due vie etio\u2013patogenetiche, sottintendenti la demenza vascolare e quella degenerativa. Recenti conclusioni hanno stabilito quali rischi di involuzione verso forme franche di Alzheimer, siano in realt\ue0 fattori di rischio vascolari: il repentino declino perfusionale cortico\u2013cerebrale, l\u2019ipertensione, l\u2019iperlipidemia e il rischio di bassa portata. Il sovrapporsi e la possibile concomitanza della demenza degenerativa e di quella vascolare sono due realt\ue0 non solo non impossibili, ma anzi altamente probabili