Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep disorders occur in 74-98% of patients with idiopathic Parkinson's disease (PD), adversely affecting their quality of life. Sleep disruption takes the form of sleep fragmentation with frequent and prolonged awakenings and daytime sleepiness. Nocturia, difficulty in turning over in bed, painful leg cramps, vivid dreams/nightmares, back pain, limb/facial dystonia and leg jerks are the main causes of nocturnal awakening in PD patients. Sleep disturbance gradually worsens with disease progression, suggesting that it is related to the severity of the disease. Sleep disturbances may be generally considered as part of the normal aging process, being more common in the elderly. However, no significant associations between sleep disturbances and either age or disease duration was found in a survey of 100 PD patients. Disturbed sleep maintenance in PD patients was more severe than in age-matched controls, and nocturnal awakening was frequently caused by nocturia, pain, stiffness and difficulty in turning over in bed. Sleep disturbance is also a complication of chronic levodopa therapy. Recent data suggest that controlled-release levodopa is less likely to cause nocturnal symptoms than standard levodopa, particularly in mild-to-moderate disease. Depression, which is common in PD patients, contributes to sleep disturbance but has a lesser influence than the disease process itself. Hypnotic and sedative agents, as well as anti-depressants if required, are useful in ameliorating sleep disturbances in PD patients; intranasal desmopressin appears to be effective in reducing nocturia.
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PMID:Sleep disorder related to Parkinson's disease. 911 82

Chronic low back pain is the second most common illness reported by patients in the United States and accounts for substantial morbidity and health-care resource utilization. Many back and spine stressors can contribute to tissue injury, resulting in acute or chronic pain. In response to injury, biochemical processes that cause inflammation and nerve sensitization increase pain levels and contribute to a cycle of reactivity that further heightens patients' sensitivity to pain stimuli. Treatment of back pain depends on its severity, duration, and underlying cause. Traditional therapeutic options include exercise, oral anti-inflammatory or analgesic medication, antidepressants, physical therapy and, in severe cases, surgery. Unfortunately, dissatisfaction with treatment of back pain is common. Oral medications may not completely alleviate symptoms, and opioid analgesics must be used with caution because of their addictive properties. Surgery does not always produce relief and, in some cases, may even exacerbate the problem. Botulinum toxin, which has already been shown to alleviate pain associated with cervical dystonia and other conditions characterized by muscle spasticity, is now being studied for the treatment of back pain. Preliminary evaluations have shown that this treatment is safe and has the advantage of providing local relief directly to the site of injury or pain, without causing systemic side effects. Initial data from small trials also suggest that botulinum toxin is effective, alleviating back pain in selected patients. On the basis of these promising results, additional study in larger trials is warranted.
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PMID:A focused review of the use of botulinum toxins for low back pain. 1256 63

The efficacy of botulinum toxin (BTX) without systemic effects has led to the rapid development of applications in neuromuscular disorders, hyperactivity of sudomotor cholinergic-mediated glandular function, and pain syndromes. The successful use of BTX in conditions with muscle overactivity, such as dystonia and spasticity, has been established and new areas in the field of movement disorders such as tics, tremor, myoclonic jerks, and stuttering has been explored with satisfactory results. Strategies to temporarily inactivate muscle function after orthopaedic or neurosurgery have also been developed. BTX treatment of hyperhidrosis was followed by its application in other hypersecretory conditions (hyperlacrimation and nasal hypersecretion) and in excessive drooling. Studies are in progress, aimed at optimising the technique and protocol of administration. Other applications for BTX have been proposed in gastroenterological and urogenital practice; it appears to be effective in replacing standard surgical procedures. Trials of BTX in painful conditions are ongoing mainly on refractory tension headache, migraine, and backache as well as dystonia-complex regional pain syndrome and myofascial pain with promising results. Recently, the fastest growing use for BTX toxin has been in the cosmetic applications. Clearly, the indications for the use of BTX are expanding, but further clinical trials will be needed in many different areas.
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PMID:New therapeutic indications for botulinum toxins. 1502 69

Anaphylactic drug reactions are rare and often serious events. The Botulinum toxin A, marketed as BOTOX, was recently approved by the Food and Drug Administration for cervical dystonia and glabellar wrinkles, after its approved use and success with blepharospasm, strabismus, and disorders of the 7th cranial nerve. It has been well received due to its efficacy in improving facial lines. This case report documents the first death associated with a Botox-lidocaine mixture given to a woman for chronic neck and back pain. Based on the medical records, autopsy, and laboratory findings, the cause of death was determined to be anaphylaxis to the Botox-lidocaine mixture. The history, indications, off-label uses and possible future applications of Botox are reviewed as well as the uses and complications of lidocaine. Although the anaphylaxis cannot be definitively proven to be due to Botox alone, this case warns of an adverse reaction related to Botox, a drug that is rapidly expanding in range of use as well as increased usage.
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PMID:Fatal case of BOTOX-related anaphylaxis? 1583 Oct 14

Back pain is a frequent complaint seen in neurological practice. In evaluating back pain, neurologists are asked to evaluate patients for radiculopathy, determine whether they may benefit from surgery, and help guide management. Although disc herniation is the most common etiology of compressive radiculopathy, there are many other causes, including genetic disorders. This article is a discussion of genetic disorders that cause or contribute to radiculopathies. These genetic disorders include neurofibromatosis, Paget's disease of bone, and ankylosing spondylitis. Numerous genetic disorders can also lead to deformities of the spine, including spinal muscular atrophy, Friedreich's ataxia, Charcot-Marie-Tooth disease, familial dysautonomia, idiopathic torsional dystonia, Marfan's syndrome, and Ehlers-Danlos syndrome. However, the extent of radiculopathy caused by spine deformities is essentially absent from the literature. Finally, recent investigation into the heritability of disc degeneration and lumbar disc herniation suggests a significant genetic component in the etiology of lumbar disc disease.
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PMID:Genetic disorders producing compressive radiculopathy. 1704 53

The objective of our study was to describe the clinical features of camptocormia, an involuntary, marked flexion of the thoracolumbar spine in idiopathic Parkinson's disease (PD) and to understand its etiology. In a prospective, cross-sectional study, we examined 15 patients with PD and camptocormia using laboratory parameters, EMG, muscle magnetic resonance imaging, and biopsy of the paravertebral muscles. The clinical data were compared with a matched control group of PD patients without camptocormia, and the biopsies were compared with muscles from age-matched autopsies. Almost all the patients (median age, 68.0 years; 7 women) with camptocormia suffered from advanced PD. Camptocormia occurred at a median of 9.0 years after the PD diagnosis. Compared with our clinical control group, back pain was more frequent and less dopa-sensitive in the patients with camptocormia who suffered more often from additional diseases of the back. On EMG, we found mainly a myopathic pattern. The MRI of the paravertebral muscles showed localized changes ranging from edema with contrast enhancement, which are considered to be early signs, to atrophy and/or fatty degeneration, interpreted as late degenerative changes. Early signs were seen mainly during the first year and degenerative changes after 1.5 years. Biopsies revealed consistently myopathic changes and in some cases fatty degeneration. Clinical or electromyographic features favoring dystonia were absent. Camptocormia is a major disabling, non-fluctuating and levodopa-resistant complication of advanced PD. The cause of camptocormia in idiopathic PD is a focal myopathy. Our findings suggest that the myopathy has a progressive course, which finally leads to degeneration of the paravertebral muscles.
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PMID:Camptocormia in idiopathic Parkinson's disease: a focal myopathy of the paravertebral muscles. 2010 72

Evidence is emerging for the use of botulinum neurotoxin type-A (BoNT-A) for niche indications including pain independent of spasticity. Pain indications such as chronic nociceptive back pain, piriformis syndrome, chronic myofascial pain, pelvic pain, complex regional pain syndrome, facial pain and neuropathic pain are outlined in this paper. Of these, class I evidence is available for the treatment of chronic nociceptive low back pain, piriformis syndrome, myofascial pain, facial pain, neuropathic pain and plantar fasciitis. Peri-operative use of BoNT-A is emerging, with indications including planning for surgery and facilitating surgery, as well as healing and improving analgesia post-operatively. Evidence is limited, although there are some reports that clinicians are successfully using BoNT-A peri-operatively. There is class I evidence showing pre-operative use of BoNT-A has a beneficial effect on outcomes following adductor-release surgery. The use of BoNT for treatment of tremor, other than neck tremor in the setting of cervical dystonia, including evidence for upper limb tremor, cranial tremor and non-dystonic neck tremor is reviewed. The evidence is variable at this stage, and further study is required to develop definitive recommendations for the clinical utility of BoNT-A for these indications.
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PMID:Botulinum toxin assessment, intervention and aftercare for paediatric and adult niche indications including pain: international consensus statement. 2063 83

The main causes of the development a nd subsequent chronization of circulatory insufficiency in the vertebro-basiliar system is the deficient blood flow in vertebral arteries (VA) resulting from extravasal effects of degenerative and dystrophic changes (DDC) in the cervical segment of the spinal column. The rehabilitative treatment of the patients presenting with these disorders including either radon or iodine-bromine baths in combination with low-frequency pulsed currents (LFPC) applied to the cervico-nuchal region was shown to produce a fairly good therapeutic effect. The proposed physiobalneological combination (radon baths + LFPC) proved more efficacious than treatment with iodine-bromine baths + LFPC for the patients with exacerbation of cervical dorsopathy. The latter combination gave better results when applied to the patients with circulatory insufficiency in the vertebro-basiliar system having the history of vegetovascular dystonia, craniocervical injury, and cervical dorsalgia.
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PMID:[Potential of combined physiobalneotherapy for the treatment of circulatory insufficiency in the vertebro-basiliar system]. 2198 20

Subthalamic nucleus deep brain stimulation (STN-DBS) is effective for medically refractory Parkinson's disease. We retrospectively analyzed complications in 180 consecutive patients who underwent bilateral STN-DBS. Surgery-related complications were symptomatic intracerebral hemorrhage in 2, chronic subdural hematoma in 1, and transient deterioration of medication-induced psychosis in 2 patients. Device-related complications involved device infection in 5, skin erosion in 5, and implantable pulse generator malfunction in 2 patients. All of these patients required surgical repair. Surgery and device-related complications could be reduced with increased surgical experience and the introduction of new surgical equipment and technology. Treatment or stimulation-related complications were intractable dyskinesia/dystonia in 11, problematic dysarthria in 7, apraxia of eyelid opening (ALO) in 11, back pain in 10, and restless leg syndrome in 6 patients. Neuropsychiatric complications were transient mood changes in some, impulse control disorder in 2, severe depression related to excessive reduction of dopaminergic medications in 2, rapid progression of dementia in 1, and suicide attempts in 2 patients. Most complications were mild and transient. Dysarthria and ALO were the most frequent permanent sequelae after STN-DBS. Treatment-related adverse events may be caused not only by the effect of stimulation effect but also excessive reduction of dopaminergic medication, or progression of the disease. In conclusion, STN-DBS seems to be a relatively safe procedure. Although serious complications with permanent sequelae are rare, significant incidences of adverse effects occur. Physicians engaged in this treatment should have a comprehensive understanding of the probable complications and how to avoid them.
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PMID:Complications of subthalamic nucleus stimulation in Parkinson's disease. 2212 76

Botulinum neurotoxin A (BoNT/A) is a toxin produced by the naturally-occurring Clostridium botulinum that causes botulism. The potential of BoNT/A as a useful medical intervention was discovered by scientists developing a vaccine to protect against botulism. They found that, when injected into a muscle, BoNT/A causes a flaccid paralysis. Following this discovery, BoNT/A has been used for many years in the treatment of conditions of pathological muscle hyperactivity, like dystonias and spasticities. In parallel, the toxin has become a "glamour" drug due to its power to ward off facial wrinkles, particularly frontal, due to the activity of the mimic muscles. After the discovery that the drug also appeared to have a preventive effect on headache, scientists spent many efforts to study the potentially-therapeutic action of BoNT/A against pain. BoNT/A is effective at reducing pain in a number of disease states, including cervical dystonia, neuropathic pain, lower back pain, spasticity, myofascial pain and bladder pain. In 2010, regulatory approval for the treatment of chronic migraine with BoNT/A was given, notwithstanding the fact that the mechanism of action is still not completely elucidated. In the present review, we summarize experimental evidence that may help to clarify the mechanisms of action of BoNT/A in relation to the alleviation of headache pain, with particular emphasis on preclinical studies, both in animals and humans. Moreover, we summarize the latest clinical trials that show evidence on headache conditions that may obtain benefits from therapy with BoNT/A.
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PMID:Botulinum Toxin Type a as a Therapeutic Agent against Headache and Related Disorders. 2640 77


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