Rehab Centers: The Effect of Dry Needling in the Treatment of Myofascial Pain Syndrome: A Randomized Double-Blinded Placebo-Controlled Trial.

The effect of dry needling in the treatment of myofascial pain syndrome: a randomized double-blinded placebo-controlled trial.

Filed under: Rehab Centers

Clin Rheumatol. 2012 Nov 9;
Tekin L, Akarsu S, Durmu? O, Cakar E, Dinçer U, K?ralp MZ

The objective of this study was to test the hypothesis that dry needling is more effective than sham dry needling in the treatment of myofascial pain syndrome (MPS). This was a prospective, double-blinded, randomized-controlled study conducted in an outpatient clinic. Thirty-nine subjects with established myofascial trigger points were randomized into two groups: study group (N?=?22) and placebo group (N?=?17). Dry needling was applied using acupuncture needles, and sham dry needling was applied in the placebo group. The treatment was composed of six sessions which were performed in 4 weeks; the first four sessions were performed twice a week (for 2 weeks) and the last two, once a week (for 2 weeks). The visual analog scale (VAS) and Short Form-36 (SF-36) were used. When compared with the initial values, VAS scores of the dry needling group following the first and sixth sessions were significantly lower (p?=?0.000 and p?HubMed – rehab

The Pharmacological Management of Post-Stroke Muscle Spasticity.

Filed under: Rehab Centers

Drugs Aging. 2012 Nov 9;
Bakheit AM

Muscle hypertonia following upper motor neurone lesions (referred to here as ‘spasticity’) is a common problem in patients with neurological disease, and its management is one of the major challenges in clinical practice. Understanding the pathogenesis and clinical course of spasticity is essential for the effective management of this condition. The hypertonia initially results from increased excitability of the alpha motor neurones due to an imbalance between the excitatory and inhibitory influences of the vestibulospinal and reticulospinal tracts. This is the ‘neural component’ of muscle hypertonia. However, usually within 3-4 weeks, changes in the structure and mechanical properties of the paralysed muscles and the effect of thixotropy also contribute to the hypertonia. The selection of the optimal treatment option is often influenced by whether the neural or the non-neural component is more pronounced. Muscle spasticity often interferes with motor function or causes distressing symptoms, such as painful muscle spasms. If untreated, spasticity may also lead to soft tissue shortening (fixed contractures). However, spasticity can also be beneficial to patients. For example, despite severe leg muscle weakness, most hemiplegic patients are able to walk because the spasticity of the extensor muscles braces the lower limb in a rigid pillar. Other reported benefits of spasticity include the maintenance of muscle bulk and bone mineral density and possibly a reduced risk of lower limb deep vein thrombosis. Several factors, such as skin pressure sores, faecal impaction, urinary tract infections and stones in the urinary bladder, can aggravate muscle spasticity. These factors should always be looked for as their adequate treatment is often sufficient to reduce muscle tone without the need for specific antispasticity medication. Therefore, a careful evaluation of the patient’s symptoms and their impact on function, and the setting of clear and realistic therapy goals are important prerequisites to treatment. The best treatment outcomes are usually achieved when pharmacological and non-pharmacological treatment modalities are used in tandem. Different drugs are available for the management of spasticity, including oral muscle relaxants, anticonvulsant drugs, intrathecal baclofen, cannabis extract, phenol and alcohol (for peripheral nerve blocks) and botulinum toxin injections. Similarly, there is a range of non-pharmacological methods of treatment, e.g. regular muscle stretching, the use of splints and orthoses, electrical stimulation, etc. Although these are not discussed here, this should not detract from the importance of combining them with antispasticity drugs in order to maximize the clinical benefit of treatment.
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Transcranial direct current stimulation (tDCS) and language.

Filed under: Rehab Centers

J Neurol Neurosurg Psychiatry. 2012 Nov 8;
Monti A, Ferrucci R, Fumagalli M, Mameli F, Cogiamanian F, Ardolino G, Priori A

Transcranial direct current stimulation (tDCS), a non-invasive neuromodulation technique inducing prolonged brain excitability changes and promoting cerebral plasticity, is a promising option for neurorehabilitation. Here, we review progress in research on tDCS and language functions and on the potential role of tDCS in the treatment of post-stroke aphasia. Currently available data suggest that tDCS over language-related brain areas can modulate linguistic abilities in healthy individuals and can improve language performance in patients with aphasia. Whether the results obtained in experimental conditions are functionally important for the quality of life of patients and their caregivers remains unclear. Despite the fact that important variables are yet to be determined, tDCS combined with rehabilitation techniques seems a promising therapeutic option for aphasia.
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The language profile of posterior cortical atrophy.

Filed under: Rehab Centers

J Neurol Neurosurg Psychiatry. 2012 Nov 8;
Crutch SJ, Lehmann M, Warren JD, Rohrer JD

BACKGROUND: Posterior cortical atrophy (PCA) is typically considered to be a visual syndrome, primarily characterised by progressive impairment of visuoperceptual and visuospatial skills. However, patients commonly describe early difficulties with word retrieval. This paper details the first systematic analysis of linguistic function in PCA. Characterising and quantifying the aphasia associated with PCA is important for clarifying diagnostic and selection criteria for clinical and research studies. METHODS: 15 patients with PCA, seven patients with logopenic/phonological aphasia (LPA) and 18 age matched healthy participants completed a detailed battery of linguistic tests evaluating auditory input processing, repetition and working memory, lexical and grammatical comprehension, single word retrieval and fluency, and spontaneous speech. RESULTS: Relative to healthy controls, PCA patients exhibited language impairments across all of the domains examined, but with anomia, reduced phonemic fluency and slowed speech rate the most prominent deficits. PCA performance most closely resembled that of LPA patients on tests of auditory input processing, repetition and digit span, but was relatively stronger on tasks of comprehension and spontaneous speech. CONCLUSIONS: The study demonstrates that in addition to the well reported degradation of vision, literacy and numeracy, PCA is characterised by progressive oral language dysfunction with prominent word retrieval difficulties. Overlap in the linguistic profiles of PCA and LPA, which are both most commonly caused by Alzheimer’s disease, further emphasises the notion of a phenotypic continuum between typical and atypical manifestations of the disease. Clarifying the boundaries between Alzheimer’s disease phenotypes has important implications for diagnosis, clinical trial recruitment and investigations into biological factors driving phenotypic heterogeneity in Alzheimer’s disease. Rehabilitation strategies to ameliorate the phonological deficit in PCA are required.
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