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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperbaric oxygen (HBO) therapy has been used to treat patients with numerous disorders, including stroke. This treatment has been shown to decrease cerebral edema, normalize water content in the brain, decrease the severity of brain infarction, and maintain blood-brain barrier integrity. In addition, HBO therapy attenuates motor deficits, decreases the risks of sequelae, and prevents recurrent cerebral circulatory disorders, thereby leading to improved outcomes and survival. Hyperbaric oxygen also accelerates the regression of atherosclerotic lesions, promotes antioxidant defenses, and suppresses the proliferation of macrophages and foam cells in atherosclerotic lesions. Although no medical treatment is available for patients with cerebral palsy, in some studies, HBO therapy has improved the function of damaged cells, attenuated the effects of hypoxia on the neonatal brain, enhanced gross motor function and fine motor control, and alleviated spasticity. In the treatment of patients with migraine, HBO therapy has been shown to reduce intracranial pressure significantly and abort acute attacks of migraine, reduce migraine headache pain, and prevent cluster headache. In studies that investigated the effects of HBO therapy on the damaged brain, the treatment was found to inhibit neuronal death, arrest the progression of radiation-induced neurologic necrosis, improve blood flow in regions affected by chronic neurologic disease as well as aerobic metabolism in brain injury, and accelerate the resolution of clinical symptoms. Hyperbaric oxygen has also been reported to accelerate neurologic recovery after spinal cord injury by ameliorating mitochondrial dysfunction in the motor cortex and spinal cord, arresting the spread of hemorrhage, reversing hypoxia, and reducing edema. HBO has enhanced wound healing in patients with chronic osteomyelitis. The results of HBO therapy in the treatment of patients with stroke, atherosclerosis, cerebral palsy, intracranial pressure, headache, and brain and spinal cord injury are promising and warrant further investigation.
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PMID:Hyperbaric oxygen in the treatment of patients with cerebral stroke, brain trauma, and neurologic disease. 1651 Mar 83

The central nervous system (CNS) is, after the peripheral nervous system, the second most frequently affected organ in mitochondrial disorders (MCDs). CNS involvement in MCDs is clinically heterogeneous, manifesting as epilepsy, stroke-like episodes, migraine, ataxia, spasticity, extrapyramidal abnormalities, bulbar dysfunction, psychiatric abnormalities, neuropsychological deficits, or hypophysial abnormalities. CNS involvement is found in syndromic and non-syndromic MCDs. Syndromic MCDs with CNS involvement include mitochondrial encephalomyopathy, lactacidosis, stroke-like episodes syndrome, myoclonic epilepsy and ragged red fibers syndrome, mitochondrial neuro-gastrointestinal encephalomyopathy syndrome, neurogenic muscle weakness, ataxia, and retinitis pigmentosa syndrome, mitochondrial depletion syndrome, Kearns-Sayre syndrome, and Leigh syndrome, Leber's hereditary optic neuropathy, Friedreich's ataxia, and multiple systemic lipomatosis. As CNS involvement is often subclinical, the CNS including the spinal cord should be investigated even in the absence of overt clinical CNS manifestations. CNS investigations comprise the history, clinical neurological examination, neuropsychological tests, electroencephalogram, cerebral computed tomography scan, and magnetic resonance imaging. A spinal tap is indicated if there is episodic or permanent impaired consciousness or in case of cognitive decline. More sophisticated methods are required if the CNS is solely affected. Treatment of CNS manifestations in MCDs is symptomatic and focused on epilepsy, headache, lactacidosis, impaired consciousness, confusion, spasticity, extrapyramidal abnormalities, or depression. Valproate, carbamazepine, corticosteroids, acetyl salicylic acid, local and volatile anesthetics should be applied with caution. Avoiding certain drugs is often more beneficial than application of established, apparently indicated drugs.
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PMID:Central nervous system manifestations of mitochondrial disorders. 1694 41

Alpha(2) agonists have been in clinical use for decades, primarily in the treatment of hypertension. In recent years, alpha(2) agonists have found wider application, particularly in the fields of anesthesia and pain management. It has been noted that these agents can enhance analgesia provided by traditional analgesics, such as opiates, and may result in opiate-sparing effects. This has important implications for the management of acute postoperative pain and chronic pain states, including disorders involving spasticity or myofascial pain, neuropathic pain, and chronic daily headaches. The clinical utility of these agents is ever expanding, as they are gaining broader use in neuraxial analgesia, and new applications are continuously under investigation. The alpha(2) agonists that are currently employed in anesthesia and pain management include clonidine, tizanidine, and dexmedetomidine. Moxonidine and radolmidine, which are not currently in clinical use in humans, may offer favorable side-effect profiles when compared with traditional alpha(2) agonists, and may thereby allow for more widespread pain management applications.
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PMID:Alpha(2) receptors and agonists in pain management. 1701 39

Botulinum toxin injection is used to treat various pain conditions including muscle spasticity, dystonia, headache and myofascial pain. Results are conflicting regarding the use of Botulinum toxin for trigger point injection in terms of improvement in pain. The aim of this study was to carry out a systematic review to assess the evidence for efficacy of Botulinum toxin A (BTA) compared with placebo for myofascial trigger point injection. Electronic databases on Medline, Cochrane Library, Scopus, CINAHL were queried using key words such as "botulinum toxin", "myofascial pain", "trigger point", "chronic pain" and "musculoskeletal pain". Relevant published randomized controlled trials that described the use of BTA as injection therapy for trigger points were considered for inclusion. The five-item 0-16 point Oxford Pain Validity Scale (OPVS) was used as a selection criteria for suitable clinical trials. Trials were also assessed based on quality using the Oxford Rating Scale. Data extracted from qualified trials included outcome measures such as pain intensity and pain pressure threshold. All studies were ranked according to the OPVS and the authors' conclusions were compared. Five clinical trials met the inclusion criteria. One trial concluded that BTA was effective, and four concluded that it was not effective for reducing pain arising from trigger points. OPVS scores ranged from 8 to 14 with the negative studies corresponding with higher validity scores. The current evidence does not support the use of BTA injection in trigger points for myofascial pain. The data is limited and clinically heterogeneous.
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PMID:Botulinum toxin A for myofascial trigger point injection: a qualitative systematic review. 1707 Nov 19

This paper will review the lumbosacral spine (L1-S5). Procedures performed in the lumbosacral spine include electromyography, spinal stimulator implants, spinal infusion implants for spasticity or pain medications, sacroiliac spine injections, facet blocks, and steroid injections. Complications from these procedures include iatrogenic paraplegia or paraplegia due to transverse myelitis, intravascular penetration, dural puncture, increased pain at the injection site, increased radicular pain, increased spine pain, lightheadedness, nausea, nonspecific headache, and vomiting. Long-term complications include implant infection, implant or catheter dislodgment/kinking, and device failure. This paper provides anatomically accurate schematics of innervations of the lumbosacral spine (L1-S5) that can be used to interpret magnetic resonance images of the muscles and nerves. Cross-sectional schematics of the lumbosacral spine were drawn as they appear on imaging projections. The relevant nerves were color coded. The muscles and skin surfaces were labeled and assigned the color of the appropriate nerves. An organized comprehensive map of the motor innervation of the lumbosacral spine allows the physician to increase the accuracy and efficacy of interventional procedures. This anatomical map could also assist the electromyographer in correlating the clinical and electrophysiological findings on magnetic resonance images.
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PMID:Sectional neuroanatomy of the lumbosacral spine (L1-S5). 1789

Increasingly, botulinum type A toxin is used to influence pathologically increased muscle activity in conditions such as dystonia and spasticity. Studies have also assessed its efficacy in tension-type headache, where muscle tenderness may be increased. We undertook a prospective, multicentre, randomized, double-blind, placebo-controlled trial. Patients received injections of Dysport (total dose of 420 or 210 units) or saline placebo in 18 sites on the head and neck. Of 125 patients treated, 118 were included in the intention-to-treat dataset. No significant differences between each verum group and placebo were seen for the primary efficacy parameter - change in the number of headache-free days at 4-8 weeks after injection compared with 4 weeks before injection. The groups receiving 420 or 210 units of Dysport experienced 2.60 and 2.87 more headache-free days respectively, compared with 1.93 more headache-free days for the placebo group (P = 0.66 versus 420 units; P = 0.52 versus 210 units). Treatment with 420 units of Dysport was associated with significant improvements compared with placebo for two secondary efficacy parameters: mean change in headache duration from baseline to weeks 8-12 (P < 0.05) and improved global physician and patient assessment scores (P < 0.05). Further studies should address the possible value of multiple injections with extended observation periods, dose optimization, and whether duration of headache history and number of previous treatments are predictors of patient response.
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PMID:Pericranial injection of botulinum toxin type A (Dysport) for tension-type headache - a multicentre, double-blind, randomized, placebo-controlled study. 1829 Aug 42

While pain is a common problem in patients with multiple sclerosis (MS), it is not frequently mentioned by patients and a more direct approach is required in order to obtain information about pain from patients. Many patients with MS experience more than one pain syndrome; combinations of dysaesthesia, headaches and/or back or muscle and joint pain are frequent. For each pain syndrome a clear diagnosis and therapeutic concept needs to be established. Pain in MS can be classified into four diagnostically and therapeutically relevant categories: (i) neuropathic pain due to MS (pain directly related to MS); (ii) pain indirectly related to MS; (iii) MS treatment-related pain; and (iv) pain unrelated to MS. Painful paroxysmal symptoms such as trigeminal neuralgia (TN), or painful tonic spasms are treated with antiepileptics as first choice, e.g. carbamazepine, oxcarbazepine, lamotrigine, gabapentin, pregabalin, etc. Painful 'burning' dysaesthesias, the most frequent chronic pain syndrome, are treated with TCAs such as amitriptyline, or antiepileptics such as gabapentin, pregabalin, lamotrigine, etc. Combinations of drugs with different modes of action can be particularly useful for reducing adverse effects. While escalation therapy may require opioids, there are encouraging results from studies regarding cannabinoids, but their future role in the treatment of MS-related pain has still to be determined. Pain related to spasticity often improves with adequate physiotherapy. Drug treatment includes antispastic agents such as baclofen or tizanidine and in patients with phasic spasticity, gabapentin or levetiracetam are administered. In patients with severe spasticity, botulinum toxin injections or intrathecal baclofen merit consideration. While physiotherapy may ameliorate malposition-induced joint and muscle pain, additional drug treatment with paracetamol (acetaminophen) or NSAIDs may be useful. Moreover, painful pressure lesions should be avoided by using optimally adjusted aids. Treatment-related pain associated with MS can occur with subcutaneous injections of interferon-beta or glatiramer acetate, and may be reduced by optimizing the injection technique and by local cooling. Systemic (particularly 'flu-like') adverse effects of interferons, e.g. myalgias, can be reduced by administering paracetamol, ibuprofen or naproxen. A potential increase in the frequency of pre-existing headaches after starting treatment with interferons may require optimization of headache attack therapy or even prophylactic treatment. Pain unrelated to MS, such as back pain or headache, is common in patients with MS and may deteriorate as a result of the disease. In summary, a careful analysis of each pain syndrome will allow the design of the appropriate treatment plan using various medical and nonmedical options (multimodal therapy), and will thus help to improve the quality of life (QOL) of the patients.
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PMID:Current management of pain associated with multiple sclerosis. 1833 59

Botulinum neurotoxin (BoNT) is produced by Clostridium botulinum as a complex of proteins containing the neurotoxin itself and other nontoxic proteins. Activation of the neurotoxin occurs upon proteolytic cleavage into the heavy and light chains. This di-chain moiety is essential for neurotoxin and each chain is playing a unique role; the heavy chain mediates neurospecifics cell binding and entry, whereas the light chain, a protease, catalyzes the cleavage and inactivation of neuronal proteins that mediate neurotransmitter release. There are seven BoNT serotypes (A,B,CI,D,E,F, and G), all of which inhibit acetylcholine release, though their intracellular target proteins, the characteristics of their actions, and their potencies vary substantially. BoNT type A has been the most widely studied and applied serotype for therapeutic purposes. It has been a mainstay in the treatment of cervical dystonia, blepharospasm, and hemifacial spasm for years. BoNT has more recently emerged as an increasingly important therapeutic option in the clinical management of a broad array of conditions, including other focal dystonias, spasticity, cerebral palsy, equinovarus, gastrointestinal (GI) and urogenital disorders, hypersecretory disorders, facial lines due to hyperfunctional facial muscles and recently, musculoskeletal pain disorders and headache.
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PMID:[Mechanism of therapy effects by botulinum neurotoxin]. 1854 57

Mitochondrial disorders, in particular respiratory chain diseases (RCDs), present either as single organ problem or as multi-system disease. One of the most frequently affected organs in RCDs, in addition to the skeletal muscle, is the central nervous system (CNS). CNS manifestations of RCDs include epilepsy, stroke-like episodes, migraine-like headache, ataxia, spasticity, movement disorders, psychosis, demyelination, calcification, but also dementia. Cognitive impairment may be a feature of syndromic as well as non-syndromic RCDs. Syndromic RCDs associated with cognitive impairment include MELAS, KSS, Leigh syndrome, and many others. RCDs with cognitive decline not only result from mtDNA mutations but also from mutations in nuclear genes. At onset there is often no general intellectual deterioration in these patients but specific cognitive deficits, particularly in the visual construction, attention, abstraction, or flexibility. Diagnosis of cognitive impairment from RCDs is based on neuropsychological testing, imaging studies, including MRI, PET, SPECT, or MR-spectroscopy, CSF investigations, or electroencephalography. Therapeutic strategies for dementia in RCDs rely on symptomatic measures. Only single patients may profit from cholinesterase inhibitors or memantine, antioxidants, vitamins, or other substitutes. Overall, cognitive decline in RCDs (mitochondrial dementia) needs to be included in the differentials of dementia.
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PMID:Cognitive decline as a manifestation of mitochondrial disorders (mitochondrial dementia). 1857 95

The protein botulinum neurotoxin A (BoNT/A) is one of seven distinct neurotoxins produced by Clostridium botulinum. BoNT/A blocks cholinergic synapses with an extremely high specificity and potency. Appropriately purified and diluted, BoNT/A serves as a reliable and well tolerated drug that is applied by local injection.The efficacy of BoNT/A is evident in the symptomatic therapy of disorders in which muscular hyperactivity plays a prominent role, such as focal dystonias and hemifacial spasm; in these disorders, BoNT/A is considered first-line therapy. BoNT/A is also beneficial in the treatment of both adults and children with spasticity of various causes. The pain that frequently accompanies these conditions is effectively reduced by BoNT/A. A genuine analgesic effect for BoNT/A unrelated to skeletal muscle spasmolysis has been suggested on the basis of in vitro and in vivo (animal) data. However, studies in humans designed to detect such an effect were negative, as were controlled studies of BoNT/A in patients with primary headache disorders.BoNT/A also acts on cholinergic synapses of the autonomic nervous system, and injection of BoNT/A into salivary glands significantly decreases the production of saliva. This may be beneficial for patients with Parkinson's disease, in whom the excessive production of saliva may be problematic.Overall, BoNT/A has been confirmed as an efficacious, predictable and well tolerated drug in an ever-increasing number of neurological disorders.
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PMID:Use of botulinum toxin A in adult neurological disorders: efficacy, tolerability and safety. 1869 73


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