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)

Clinical observations show a close relationship between neuralgia of the superior laryngeal nerve and disorders of the larynx. Neuralgia, and more minor symptoms are usually caused by hyper- and hypotonic phonatory disorders. An unphysiological compensation for glottic insufficiency causes irritation of the sensory telodendrons of the superior laryngeal nerve. As incomplete adduction of the vocal cords can often be found in patients with an autonomic laryngeal dystonia, a syndrome related to anxiety, these disturbances are often misinterpreted as "globus hystericus". However, this diagnosis does not take into account the cause and should therefore no longer be used.
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PMID:[Neuralgia of the superior laryngeal nerve caused by phonatory malfunctions]. 377 Dec 97

Adriamycin, an anthracycline antineoplastic agent, can swiftly be transported to the sensory or somatic motor neurons by way of axoplasmic transport when injected into the subepineurium of the trigeminal nerve or sciatic nerve in experimental animals, and is consequently able to induce degeneration of the neurons without any systemic side effects. Intraneural injection of this agent was carried out for the treatment of a total of 22 patients presenting with intractable neural dysfunction (12 with neuralgia, including 7 with post-herpetic neuralgia and 10 with facial dystonia). The nerve which innervated the affected site was exposed under local anesthesia and approximately 10-60 microliters of 1-20% adriamycin was injected into the subepineurium. Results of the treatment after average follow-up periods of 21.5 months were as follows: Out of 12 patients with neuralgia, good results were obtained in 2 cases (16.7%), fair results in 6 cases (50.0%) (overall effective rate 67.7%). There were no changes in symptoms in 4 cases (33.3%). Out of 10 patients with facial dystonia, good results were obtained in 2 cases (20.0%), fair in 2 cases (20.0%) (overall effective rate 40.0%), and no changes in symptoms in 6 cases (60.0%). No major complications were encountered during these procedures and, once symptoms had disappeared after the treatment, no recurrence of symptoms was experienced. This method clearly differs from other various kinds of simple peripheral neurotomy, since transection of the peripheral nerve does not cause any, destructive changes in the sensory ganglion or motor nucleus and, hence, symptoms may recur.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of intractable postherpetic neuralgia and blepharospasm: intraneural injection of adriamycin]. 787 32

This article concludes the series on cranial nerves, with review of the final four (IX-XII). To summarize briefly, the most important and common syndrome caused by a disorder of the glossopharyngeal nerve (craniel nerve IX) is glossopharyngeal neuralgia. Also, swallowing function occasionally is compromised in a rare but disabling form of tardive dyskinesia called tardive dystonia, because the upper motor portion of the glossopharyngel nerve projects to the basal ganglia and can be affected by lesions in the basal ganglia. Vagus nerve funtion (craniel nerve X) can be compromised in schizophrenia, bulimia, obesity, and major depression. A cervical lesion to the nerve roots of the spinal accessory nerve (craniel nerve XI) can cause a cervical dystonia, which sometimes is misdiagnosed as a dyskinesia related to neuroleptic use. Finally, unilateral hypoglossal (craniel nerve XII) nerve palsy is one of the most common mononeuropathies caused by brain metastases. Supranuclear lesions of cranial nerve XII are involved in pseudobulbar palsy and ALS, and lower motor neuron lesions of cranial nerve XII can also be present in bulbar palsy and in ALS patients who also have lower motor neuron involvement. This article reviews these and other syndromes related to cranial nerves IX through XII that might be seen by psychiatry.
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PMID:Cranial Nerves IX, X, XI, and XII. 2053 57

Despite the common belief that multiple sclerosis (MS) is a painless disease, several studies contradict this. There are a significant number of MS patients who actually suffer from painful conditions such as central and peripheral neuropathy, migraines, trigeminal neuralgia, painful tonic spasms, complex regional pain syndrome, glossopharyngeal neuralgia, and transverse myelitis. In addition, MS relapses are usually painful with many patients complaining of paroxysmal dystonia and neuropathic pain during these episodes. Additionally, treatments for MS such as use of beta-interferons may be associated with headache and pain at the injection site. The pathophysiology of pain in MS is poorly understood, but may be related to the development of demyelinating lesions involving certain neuroanatomic pathways such as the spinothalamic tract. Management of pain in MS patients is a therapeutic challenge for clinicians. Currently, various pharmacological agents such as antiepielptics, non-steroidal anti-inflammatory agents, and even corticosteroids are used to suppress various painful conditions associated with MS. Non-pharmacological procedures such as massage therapy have also been used in the treatment of MS patients. The authors present a review of recent findings in pathophysiology and management of pain in MS patients.
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PMID:Multiple sclerosis and pain. 2290 89

We report on a case of a 65-year-old (CD) woman who sustained an atraumatic neck fracture. A combination of Parkinson's disease with motor fluctuations, chronic cervical dystonia and osteoporosis provided the basis for this interesting diagnosis. Mrs CD had progressed to complex phase idiopathic Parkinson's disease within 13 years of diagnosis. During this time she remained independent, only using a wheelchair when her motor fluctuations were bad. In 2011, she developed a sudden onset of neck spasm and occipital neuralgia, initially attributed to severe spasmodic cervical dystonia. Despite a titration regime of analgesics and weaning off of her Parkinson's disease medications, the pain persisted. An X-ray of her cervical spine showed degenerative discopathies from C4 to C7. Mrs CD underwent a trial of Botox injections to no avail and she was admitted acutely under the spinal team after an MRI of her spine showed abnormal oedema of the odontoid peg. Subsequent CT diagnosed a type II fracture of the odontoid peg on the background of severe osteoporotic bone (spinal T score -3.4 on subsequent DEXA scan) and she underwent a successful occipital cervical fusion of C1-C6. What makes this case interesting is the fact that this lady's profound powerful neck movements on a background of osteoporosis led to fracture of her neck. Post-operatively, she admitted to non-adherence to her bisphosphonates, prioritising levodopa in the morning with food rather than taking her alendronate on an empty stomach. She is now pain free and receives annual zolendronate infusions.
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PMID:An osteoporotic fracture mimicking cervical dystonia in idiopathic Parkinson's disease. 2367 34

Pain is a natural protective mechanism and has a warning function signaling imminent or actual tissue damage. Neuropathic pain (NP) results from a dysfunction and derangement in the transmission and signal processing along the nervous system and it is a recognized disease in itself. The prevalence of NP is estimated to be between 6.9% and 10% in the general population. This condition can complicate the recovery from stroke, multiple sclerosis, spinal cord lesions, and several neuropathies promoting persistent disability and poor quality of life. Subjects suffering from NP describe it as burning, itching, lancing, and numbness, but hyperalgesia and allodynia represent the most bothersome symptoms. The management of NP is a clinical challenge and several non-pharmacological and pharmacological interventions have been proposed with variable benefits. Botulinum toxin (BTX) as an adjunct to other interventions can be a useful therapeutic tool for the treatment of disabled people. Although BTX-A is predominantly used to reduce spasticity in a neuro-rehabilitation setting, it has been used in several painful conditions including disorders characterized by NP. The underlying pharmacological mechanisms that operate in reducing pain are still unclear and include blocking nociceptor transduction, the reduction of neurogenic inflammation by inhibiting neural substances and neurotransmitters, and the prevention of peripheral and central sensitization. Some neurological disorders requiring rehabilitative intervention can show neuropathic pain resistant to common analgesic treatment. This paper addresses the effect of BTX-A in treating NP that complicates frequent disorders of the central and peripheral nervous system such as spinal cord injury, post-stroke shoulder pain, and painful diabetic neuropathy, which are commonly managed in a rehabilitation setting. Furthermore, BTX-A has an effect in relief pain that may characterize less common neurological disorders including post-traumatic neuralgia, phantom limb, and complex regional pain syndrome with focal dystonia. The use of BTX-A could represent a novel therapeutic strategy in caring for neuropathic pain whenever common pharmacological tools have been ineffective. However, large and well-designed clinical trials are needed to recommend BTX-A use in the relief of neuropathic pain.
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PMID:Botulinum Toxin Type A for the Treatment of Neuropathic Pain in Neuro-Rehabilitation. 2613 56

Botulinum neurotoxin (BoNT), derived from Clostridium botulinum, has been used therapeutically for focal dystonia, spasticity, and chronic migraine. Its spectrum as a potential treatment for neuropathic pain has grown. Recent opinions on the mechanism behind the antinociceptive effects of BoNT suggest that it inhibits the release of peripheral neurotransmitters and inflammatory mediators from sensory nerves. There is some evidence showing the axonal transport of BoNT, but it remains controversial. The aim of this review is to summarize the experimental and clinical evidence of the antinociceptive effects, mechanisms, and therapeutic applications of BoNT for neuropathic pain conditions, including postherpetic neuralgia, complex regional pain syndrome, and trigeminal neuralgia. The PubMed and OvidSP databases were searched from 1966 to May 2015. We assessed levels of evidence according to the American Academy of Neurology guidelines. Recent studies have suggested that BoNT injection is an effective treatment for postherpetic neuralgia and is likely efficient for trigeminal neuralgia and post-traumatic neuralgia. BoNT could also be effective as a treatment for diabetic neuropathy. It has not been proven to be an effective treatment for occipital neuralgia or complex regional pain syndrome.
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PMID:Botulinum Toxin for Neuropathic Pain: A Review of the Literature. 2628 42

Hashimoto encephalopathy (HE) is characterized by heterogeneous neurological symptoms. HE is diagnosed based on three criteria-the presence of antithyroid antibodies, neurological symptoms from the cerebrum and/or cerebellum, and a positive response to immunotherapy. We clinically analyzed 18 patients (3 men, 15 women; age range, 38-81years) diagnosed with HE in our hospital from May 2013 to January 2016. Eleven patients showed sensory abnormalities such as strong pain, deep muscle pain, dysesthesia, paresthesia, or neuralgia. Surprisingly, the majority of the pain was distributed in a manner that was not explainable anatomically. Seventeen patients showed motor disturbances, such as weakness, paresis of extremities, or dexterity movement disorder, and eight patients showed give-way weakness, which is disruption of continuous muscle contraction. Other symptoms indicative of brain-related anomalies such as tremor, dystonia, involuntary movements, cerebellar ataxia, parkinsonism, memory loss, and chronic fatigue were also seen. In most patients, such motor, sensory, or higher brain functions were markedly improved with immunosuppressive therapies such as prednisolone, azathioprine, or immunoadsorption therapy. Although give-way weakness and anatomically unexplainable pain are typically considered as being psychogenic in origin, the presence of these symptoms is indicative of HE. HE exhibits diffuse involvement of the entire brain and thus, these symptoms are explainable. We propose that physicians should not diagnose somatoform disorders without first excluding autoimmune encephalopathy.
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PMID:[Clinical Features and Treatment of Hashimoto Encephalopathy]. 2766 88

Botulinum toxin (BoNT) has been used as a treatment for excessive muscle stiffness, spasticity, and dystonia. BoNT for approximately 40 years, and has recently been used to treat various types of neuropathic pain. The mechanism by which BoNT acts on neuropathic pain involves inhibiting the release of inflammatory mediators and peripheral neurotransmitters from sensory nerves. Recent journals have demonstrated that BoNT is effective for neuropathic pain, such as postherpetic neuralgia, trigeminal neuralgia, and peripheral neuralgia. The purpose of this review is to summarize the experimental and clinical evidence of the mechanism by which BoNT acts on various types of neuropathic pain and describe why BoNT can be applied as treatment. The PubMed database was searched from 1988 to May 2017. Recent studies have demonstrated that BoNT injections are effective treatments for post-herpetic neuralgia, diabetic neuropathy, trigeminal neuralgia, and intractable neuropathic pain, such as poststroke pain and spinal cord injury.
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PMID:Botulinum Toxin for the Treatment of Neuropathic Pain. 2883 75