Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a clinicopathological report of a recent fatal case of a 27-year-old woman whom we consider to have had encephalitis lethargica. Clinical features of note were a presentation with vertigo, persistent vomiting and sleep disturbance including marked daytime somnolence and vivid nightmares. On examination, she had impaired slow pursuit vertical eye movements, dysarthria, an expressionless face and slow tongue movements. She went on to develop gross supranuclear gaze palsy, neck rigidity, bradykinesia, blepharospasm, profound somnolence and anarthria but no tremor, weakness or impairment of cognition. She died after an illness lasting 12 months. On investigation, the cerebrospinal fluid was found to contain a very high level of IgG with oligoclonal bands but no cells. Post-mortem examination revealed an active encephalitis, mainly centered on the upper brainstem and diencephalon with extensive Purkinje cell loss and marked plasma cell infiltrates and morula cells. No virus was recovered.
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PMID:A contemporary case of encephalitis lethargica. 1122 Jun 91

Hemifacial spasm (HFS) is characterized by tonic and clonic contractions of the muscles innervated by the ipsilateral facial nerve. It is important to distinguish this from other causes of facial spasms, such as psychogenic facial spasm, facial tic, facial myokymia, blepharospasm, and tardive dyskinesia. Magnetic resonance imaging and angiography studies frequently demonstrate vascular compression of the root exit zone of the facial nerve. Importantly, an underlying space-occupying lesion needs to be excluded in patients with associated atypical features such as facial numbness and weakness. Botulinum toxin injection to the facial muscles is an effective treatment for HFS, with few disabling side-effects.
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PMID:Hemifacial spasm and involuntary facial movements. 1214 88

One-patient, randomized, double-blind, controlled trials (N-of-1 RCTs) have traditionally been used to assess the efficacy of treatment. At the Drug Safety Clinic, Toronto, this methodology is used to evaluate adverse effects related to medication use, specifically when the symptoms are vague and are in response to more than one medication. Two patients are described with histories of drug allergies to multiple medications; as well, guidelines for conducting N-of-1 trials are summarized. The first patient had a history of prolonged periorbital and generalized weakness lasting up to one week after exposure to a variety of drugs. Because of the ambiguous results of local anesthetic skin testing, an N-of-1 trial was performed using lidocaine without preservative. Two short-lived episodes of blepharospasm and lethargy were observed with placebo; no subjective or objective reaction occurred with active drug. The second patient had a history of prolonged weakness and drowsiness after exposure to many medications; she had been told that she was allergic to all drugs with a benzene ring. During the first N-of-1 trial, generalized weakness was observed with 10 mg of dimenhydrinate and all four placebo doses. During the second N-of-1 challenge using codeine, no unwarranted reactions occurred with either active or placebo drug. Traditional testing of these patients to disprove the clinical symptoms is often difficult because of the anxiety level associated with the patients' past experiences. N-of-1 trials provide a useful alternative for the management of patients with nonspecific symptomatology attributed to drug ingestion.
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PMID:Confirming false adverse reactions to drugs by performing individualized, randomized trials. 1242 52

Botulinum toxin type A, a neurotoxin, is effective for treating a variety of disorders of involuntary muscle contraction including cervical dystonia, blepharospasm, and hemifacial spasm. It inhibits neuromuscular signaling by blocking the release of acetylcholine at the neuromuscular junction. The biological effects of the toxin are transient, with normal neuronal signaling returning within approximately 3 to 6 months postinjection. Recent clinical findings suggest that botulinum toxin type A may inhibit pain associated with migraine and other types of headache. However, the mechanism by which this toxin inhibits pain is not fully understood and is under investigation. Research findings suggest that botulinum toxin type A inhibits the release of neurotransmitters from nociceptive nerve terminals and, in this way, may possess an analgesic effect. A number of retrospective open-label chart reviews and 3 double-blind, placebo-controlled trials have demonstrated that localized injections of botulinum toxin type A significantly reduce the frequency, severity, and disability associated with migraine headaches. Although the majority of patients in these studies experienced no botulinum toxin type A-mediated side effects, a small percentage of patients did report transient minor side effects including blepharoptosis, diplopia, and injection-site weakness. Currently, 4 randomized, placebo-controlled, clinical trials are being conducted to evaluate the efficacy, optimal dosing, and side-effect profile of botulinum toxin type A as a novel treatment for migraine and other types of headache. These studies may provide further evidence that botulinum toxin type A is an effective option for the preventive treatment of migraine.
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PMID:Botulinum neurotoxin for the treatment of migraine and other primary headache disorders: from bench to bedside. 1288 91

Dystonias are frequently observed in Parkinson's disease or other parkinsonian syndromes. They can occur during off-periods, either in the morning (early morning dystonia) or during daily off-periods, and during on-periods. Dystonia involves more frequently the upper and lower limbs, the neck or the face. Dystonia can be painful in particular off-period feet dystonia. The mechanisms underlying dystonia are not fully understood, basal ganglia activity and levodopa levels seems to play an important role. There are several medical options to try and improve those dystonias, adjustment of levodopa doses, adding a dopamine agonist drug, anticholinergics, lithium, baclofene or clonazepam. Those options are not always very effective. Botulinum toxin injections are an alternative treatment for focal dystonia. Muscles have to be selected by observation of the dystonia. Deep muscles in particular in the legs can be injected under EMG guidance. Botulinum toxin injections are particularly helpful and safe for lower limb dystonia. They can be used also for other forms of dystonia. Upper limb dystonia can be injected, allowing more comfort and easier hygiene but not necessarily better function, weakness is the main side effect. Cervical dystonia, blepharospam and oromandibular dystonia can be managed the same way as idiopathic dystonia. The dose might be lower since the muscles are usually not as hypertrophic. Side effects are as expected dysphagia and neck weakness in case of cervical dystonia, ptosis, inocclusion and diplopia in case of blepharospasm, jaw opening difficulty with oromandibular dystonia. Basal ganglia surgery can also help dystonia in a selected population of parkinsonian patients.
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PMID:[Parkinsonian dystonia]. 1461 83

Botulinum toxin A (BoNT/A), a neurotoxin, is effective for treating a variety of disorders of involuntary muscle contraction, including cervical dystonia, blepharospasm and hemifacial spasm. It inhibits neurouscular signaling by blocking the release of acetylcholine at the neuromuscular junction. The biological effects of the toxin are transient with normal neuronal signaling returning within approximately 3-6 months post injection. Recently, clinical findings suggest that BoNT/A may inhibit pain associated with migraine and other headache types. The mechanism by which this toxin inhibits pain is under investigation, recent findings suggest that it inhibits the release of neurotransmitters from nociceptive nerve terminals and in this way may exert an analgesic effect. A number of retrospective open-label chart reviews and three placebo-controlled double-blind trials have demonstrated that localized injections of BTX-A significantly reduce migraine frequency, severity, and migraine-associated disability. The majority of patients in these studies experienced no BoNT/A mediated side effects; however, a small percentage of patients did report transient minor side effects including blepharoptosis, dipolpia, and injection-site weakness. Currently there are several large-scale randomized, placebo-controlled clinical trials in progress evaluating the efficacy, optimal dosing and side effect profile of this toxin as a novel treatment for migraine and other headache types. These studies may provide further evidence that BoNT/A is an effective option for the preventive treatment of migraine.
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PMID:Botulinum neurotoxin for the treatment of migraine and other primary headache disorders. 1515 49

Spasticity results in a resistance to passive movement and decrease of passive mobility of the involved joints and is defined as a state of hypertonicity with exaggeration of tendon reflexes mediated by a loss of inhibitory control of upper motor neurons. In patients with severe stages of multiple sclerosis (MS) spasticity of the lower limbs often leeds to a spastic pattern with hip adduction resulting in decreased range-of-motion (ROM), increased pain, spasms, and functional disability (disturbed gait and sitting position) as well as difficulties with perineal hygiene. Local botulinum toxin type A (Btx-A) injections in spastic muscles offer a new treatment approach for managing spasticity and associated problems. Up to now Btx-A is approved for the treatment of blepharospasm and cervical dystonia and the treatment of equinous gait in children with cerebral palsy in Austria and Germany. Up to now only in Switzerland Botox is licensed for the treatment of focal spasticity. Btx-A is a neurotoxin derived from Clostridium botulinum. In most european countries Btx-A is available as Dysport (vial = 500 units) and Botox (vial = 100 units). In prospective studies a ratio of 1 unit Botox to 3-4 units Dysport was found. Following intramuscular injection Btx-A blocks the release of acetylcholine at the neuromuscular junctions, thereby inhibiting muscle contraction, and decreases spastic muscle tone and muscle spindles afferent information to the spinal cord. The spectrum of side effects includes local weakening of the injected and adjacent muscles as well as pain and haematoma at the injection site. At therapeutic doses side effects are local and transient. According to a double blind, placebo controlled, dose ranging study published by Hyman et al. (2000, Dysport in a dose of 500, 1000 and 1500 units reduced the degree of hip adductor spasticity associated with MS, and this benefit was evident despite concomitant use of oral antispasticity medication. According to the results of the study there was a clear trend towards greater efficacy and duration of effects with higher doses of Dysport. Taking efficacy and adverse events into account (incidence of muscle weakness was higher for the 1500 units group than for placebo) the optimal dose for hip adductor spasticity seems to be 1000 units Dysport divided between the adductor magnus, longus and brevis muscles and between both legs. To increase Btx-A effects following injection of hip adductors additional physiotherapy and casting or orthosis to increase passive hip-abduction is recommended. According to the literature anatomical localisation of the adductor muscles for injection and aspiration following insertion of the needle, to avoid injection of the toxin into a vessel, should be performed. A maximum dose of 1500 units Dysport (400 units Botox) per treatment session and 250 units Dysport (50 units Botox) per injection site is recommended. See table for dose-range of Dysport, and Botox in the treatment of adult patients with hip-adductor spasticity. For evaluation of treatment effects in hip adductor spasticity clinical examination with specific scales and measurements (see Appendix) at baseline, 4 and 12 weeks following BtxA injection is recommended:--Global rating of severity (0-4; patient's self assessment and physician's rating) --Global rating of response (-4 - +4; patient's self assessment and physician's rating)--Visual Analogue Scale (patient's self assessment of pain)--Active and passive ROM (manual goniometer)--Distance between the medial femur condyles in thigh extension (distance in cm)--Modified Ashworth scale (0-4)--Ten meter walking time (seconds)--Functional Ambulation Categories (0-5)--Score of perineal hygiene (0-5).
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PMID:[Botulinum toxin treatment of hip adductor spasticity in multiple sclerosis]. 1550 48

Botulinum toxin type-A (BoNT-A) prevents the release of acetylcholine at cholinergic junctions, thereby causing temporary muscle weakness lasting 3-4 months. It is now widely used to treat a broad range of clinical disorders characterized by muscle hyperactivity. BoNT-A has proved effective in the management of several neurological conditions and, in particular, in the management of movement disorders (e.g. blepharospasm, cervical dystonia, laryngeal dystonia, limb dystonia, hemifacial spasm, focal tics, tremor and other hyperkinetic disorders). As a treatment of spasticity, BoNT-A can improve mobility and dexterity as well as preventing the development of distressing and costly secondary complications. In cerebral palsy, BoNT-A is of value, being able to delay or even avoid surgery until motion patterns have become established.
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PMID:Clinical value of botulinum toxin in neurological indications. 1711 46

Spasticity is characterized by increased muscle resistance. It is usually associated with muscle weakness or poor motor control. This condition not only reduces activities of daily living (ADLs), but also interferes personal hygiere and causes caregiuer's difficulty. The use of botulinum neurotoxin (BoNT) intramuscular injections is a simple and effective therapy for spasticity. The use of BoNT to treat adult patients with spasticity was first reported in 1989, since then, using the neurotoxin to treat spasticity became popular in some European countries. Now in Japan, BoNT can be used to treat only torticollis, blepharospasm and hemifacial spasm because of the legal limitation on its use. However, clinical research on the use of BoNT in spasticity caused by stroke is presently underway, and an adaptation of the toxin may be available in the near future. This article reviews the characteristics of BoNT and the techniques for injecting this neurotoxin.
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PMID:[Use of botulinum neurotoxin for spasticity]. 1911 Jul 53

Botulinum toxin type A (BoNT/A) is a well-established treatment for conditions characterized by muscle and autonomic nerve terminal overactivity, such as cervical dystonia and blepharospasm, and hyperhidrosis, respectively. BoNT/A is not digested in the gastrointestinal tract as it forms a complex with several proteins that protect and stabilize the neurotoxin. However, the pure neurotoxin is solely responsible for the therapeutic effect, and the complexing proteins have been shown to exhibit immunostimulating activity. The complexing proteins are not required for the stabilization of the neurotoxin in a formulation; the complexing proteins immediately dissociate from the neurotoxin at a physiologic pH, so they do not influence the spread of the neurotoxin. Xeomin is the only botulinum toxin that is free from complexing proteins and is stable at room temperature for a period of 4 years. When injected directly into muscles, Xeomin inhibits local neuromuscular cholinergic transmission, causing focal weakness. It binds to motor nerve terminal pre-synaptic receptors, is internalized via receptor-mediated endocytosis and then selectively cleaves a protein called SNAP-25. This is one of several so-called 'SNARE' proteins involved in exocytosis. Cleavage of SNAP-25 inhibits the secretion of acetylcholine causing the paralysis of the muscle. The clinical effects begin 24-72 h after injection, peak at approximately 4-6 weeks and are sustained for several months.
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PMID:Xeomin: an innovative new botulinum toxin type A. 2000 41


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