The most credited etiology involves the mechanical detachment of otolithic fragments from the utricular macula and their migration into one of the semicircular canals. Being mechanical in origin, it is therefore not susceptible to pharmacotherapy, and its treatment of choice is constituted by physical therapy. Repositioning maneuvers can successfully free the affected semicircular canals from the displaced otoconia in almost the totality of patients, even if performance of this treatment in the older population could be challenging because of some orthopedic problems limiting the range of motion in the cervical spine. Also, a previous history of vertebrobasilar insufficiency, stroke, or cervical spine instability should suggest caution in performing extension of the cervical spine [43, 44].
Neurologic Interventions For Physical Therapy 3e Downloads Torrent
Download: https://shurll.com/2vF1IN
Currently, a strongly effective preventive treatment is not known. Considering MD as a heterogeneous category of diseases with the same phenotypic presentation but multiple pathogenetic mechanisms, prevention should ideally consider the specific etiology. Consequently, migraine-associated MD should be prevented by migraine-preventing therapies, and vascular MD should be prevented through primary prevention of cardiovascular risk factors and therapies in order to improve local blood perfusion and circulation. In cases of autoimmune labyrinthopathy (including Cogan syndrome and delayed endolymphatic hydrops), preventive therapy is constituted by steroids or immunosuppressive medications. Despite the fact that dietary interventions through low-sodium or hyper-hydrating meal plans are advised by practitioners, at the moment, no scientific evidence has been reported [62].
In this picture, vertigo attacks have subsided, but general postural instability remains as a consequence of the vestibular deficit produced by past crises. In such cases, pharmacotherapy does not help, while physical therapy and mobilization are encouraged in order to favor balance compensatory mechanisms.
In the treatment of VM, antidepressants should be started at a low dosage and increased until the minimum effective dosage for maintenance is found. Also, in the case of suspension, the dosage should be tapered slowly and gradually. Before evaluating the efficacy of antidepressants for VM, at least 3 months of therapy should have passed. The treatment is considered effective if the frequency of crises is reduced at least by 50%. When possible, it is advisable to check for triggering factors, such as physical exercise, variation in sleep patterns, stress, or certain foods (chocolate, cheese, alcohol). Often, VM patients also present motion sickness, and this should be considered when performing diagnostic exams, planning functional rehabilitation, or advising the patient about lifestyle modifications.
The current treatment for cSVD-associated dizziness involves preventive measures, such as control of vascular comorbidities and risk factors (especially by lowering blood pressure), together with lifestyle interventions, such as an encouragement to increase physical activity and aerobic exercises. Proposed new therapeutic approaches include endothelin antagonists, neurotrophins, peroxisome proliferator-activated receptor-γ agonists and prostacyclin mimics [121]. In patients with cSVD and dizziness, remarkable results have been reported using sulodexide [122]. Moreover, polyphenol supplementation seems to reduce oxidative stress load in patients with a pre-existing imbalance, and as a consequence, it improves dizziness symptoms [120]. However, a double-blind, placebo-controlled study is needed to confirm the preliminary results reported in the abovementioned studies. 2ff7e9595c
Comments