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

Botulinum toxin is a dreaded biological toxin elaborated by Clostridium botulinum. The action of this toxin is to cause paralysis of both voluntary and involuntary muscles. The unique property of paralysing capability of muscles has been used for the benefit of human beings. Dr Allan Scot, an ophthalmologist, first used the toxin in a patient with squint in 1981 and since then the botulinum toxin is being used in various disorders characterised by muscle overactivity such as spasticity in both children and adult, dystonic conditions such as blepharospasm, cervical dystonia, spasmodic dysphonia, writer's cramp, etc, hemifacial spasm and headache. Its main action is at the terminal nerve endings of myoneural junction and it prevents release of acetylcholine from vesicles thus causing chemical denervation. Its action persists for 3 to 4 months on an average. Its side effects such as drooping, diplopia, dysphagia, depending on the sites of injection, are few and usually transient. Generalised anaphylaxis is almost unknown. Now botulinum toxin is being used in non-neurological conditions where muscles are under spasmodic state such as achalasia cardia, anal fissure, spasm of urethral sphincter, etc. Because of wider safety range and fewer complications, botulinum toxin has been an important therapeutic armamentarium in different branches of medicine and surgery.
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PMID:Botulinum toxin: a dreaded toxin for use in human being. 1245 15

A report of two female patients with persistent unilateral retroauricular pain and cranial synkinesis following Bell's palsy. Pain occurred during menses in the first patient and was exacerbated by menses in the second patient. Retroauricular pain often precedes or follows Bell's palsy. Pain normally disappears within 2 weeks from the onset of paralysis. Neurological examination, brain magnetic resonance imaging (MRI), computed tomography of the head and cranial electrophysiological testing were performed. The first patient had severe right retroauricular pain during her menses for several years following Bell's palsy. Her brain MRI showed non-specific T2 white matter hyperintensities. On her electromyogram she had facial synkinesis with tonic motor unit discharges on her right orbicularis oris and mentalis muscles during sustained eye closure. The second patient reported hearing a sound over her left ear when she blinked or protruded her jaw after Bell's palsy. She had ipsilateral retroauricular pain, exacerbated during menses. Her brain MRI was normal. Electromyogram showed facial synkinesis. Chronic retroauricular pain, occurring or exacerbated during menses, may be a rare complication of Bell's palsy. It can be associated with facial subclinical synkinetic dystonia and trigemino-facial synkinesis.
Cephalalgia 2003 Apr
PMID:Catamenial synkinetic retroauricular pain. 1266 89

In otorhinolaryngology, botulinum toxin is a suitable therapeutic option in the muscular and the autonomic nervous system concerning dysfunctions. Respecting some special aspects, it is an effective treatment for disorders of different etiology with very few side-effects. The positive therapeutic effect is temporarily limited, so that the patients need further treatment. Beside the classical indications like the facial hyperkinesias (i.e. blepharospasms, hemifacial spasm) the treatment of complex dystonias (oromandibular dystonia, laryngeal dystonia, cervical dystonia), gustatory sweating, hypersalivation and crocodile tears is successful. Botulinum toxin is an alternative treatment of tension type headache and migraine. A new indication of botulinum toxin application may lay in the treatment of nasal hypersecretion through the effect on the nasal glands.
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PMID:[Botulinum toxin in ENT medicine]. 1267 23

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.
Headache
PMID:Botulinum neurotoxin for the treatment of migraine and other primary headache disorders: from bench to bedside. 1288 91

A 3 year review of neurologic admissions into the adult medical wards at the UCH, Ibadan, Nigeria between January 1998 and December 2000 is presented. The study design involved the scrutiny of the records of all the neurological admissions, male and female to the medical ward. The identified cases were then classified and only cases confirmed as neurological were further analysed. Stroke, predominantly non-hemorrhagic accounted for 50.4% of cases for the period of study. Stroke is therefore the most common cause of adult neurologic admissions on medical wards of UCH. Central nervous system infections, comprising mainly of tetanus and meningitis accounted for 14.2% (111) and 12.4% (97) of case respectively. The myelopathies were the cause of neurologic admissions in 8.1% (63) of cases followed by seizure disorders. Headache was the reason for admission in 0.9% (7) of cases. Parkinsons disease, hypertensive encephalopathy, Guillian Barne syndrome, seasonal ataxic neuropathy, cavernous sinus thrombophlebitis, normal pressure hydrocephalus were rarely the cause of admission. Similarly, dystonia, and cerebral malaria recorded 0.13% (1) of cases each. A case is made for the establishment of regional stroke units in Nigeria.
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PMID:A 3-year review of neurologic admissions in University College Hospital Ibadan, Nigeria. 1452 26

Migraine is a chronic headache disorder manifesting in attacks lasting 4-72 hours. Characteristics of headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity, and association with nausea, photophobia and phonophobia. The migraine aura is a complex of neurological symptoms, which occurs just before or at the onset of migraine headache. Botulinum toxin A represents a completely new option for patients with chronic pain conditions. Numerous retrospective open-label chart reviews and 4 double-blind, placebo-controlled studies have demonstrated that botulinum toxin type A is significantly effective in migraine prophylaxis and reduces the frequency, severity, and disability associated with migraine headaches. Studies have generally reported a good and consistent efficacy. The differential therapeutic use of botulinum toxin appears to be worth attempting in migraine patients with the following characteristic features: (1) Muscular stress as migraine trigger, e. g., in craniocervical dystonia, pericranial painful muscular trigger points or tender points, oromandibular dysfunction, (2) concurrent chronic tension-type headache with the aggravating factors of muscular stress or oromandibular dysfunction, (3) chronic migraine with frequent migraine attacks on more than 15 days per month for longer than 3 months and if other therapeutic options have been either ineffective or have not been tolerated. The use of the agent does not cause CNS side effects. Migraine patients in particular, often suffer greatly, as a result of the adverse effects of the drugs used, from fatigue, dizziness, reduced concentration, loss of appetite, weight gain, hair loss and changes in libido. These side effects are not known in association with botulinum toxin A. To date, neither organic damage nor allergic complications have been reported. Thus, both the tolerability and the safety of this therapeutic measure are high. The mode of action by which botulinum toxin is effective in migraine prophylaxis is not fully understood and is under investigation. Currently, a number of other randomized, placebo-controlled, clinical trials are being conducted to evaluate the efficacy, optimal dosing, and side-effect profile of botulinum toxin type A in the prophylaxis of migraine and other headache entities.
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PMID:Botulinum toxin in migraine prophylaxis. 1499 36

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

Progressive multifocal leukoencephalopathy (PML) is caused by replication of JC virus in oligodendrocytes of immunocompromised patients. Common manifestations are focal motor and sensory deficits, gait abnormalities, speech and language disturbances, cognitive disorders, headache, and visual impairment. Although the occurrence of movement disorders is rare in PML, bradykinesia, rigidity, dystonia, myoclonic jerks and myoclonic ataxia have been described. Head tremor associated with PML has not been previously reported. We report two cases of PML in whom head tremor was present.
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PMID:Head tremor and progressive multifocal leukoencephalopathy in AIDS patients: report of two cases. 1583 82

This article is structured around a literature review that was carried out using Ovid and Medline with the key words "botulinum," "toxin," and "ENT." Botulinum toxin has been used safely in humans for more than 20 years. The effects are transient, such that treatments are required to be repeated at intervals. Its application to ENT provides a useful tool to treat dystonia, autonomic dysfunction, facial nerve paresis, and hyperfunctional lines. It may also be of benefit in laryngeal rebalancing and the treatment of headaches. Further research is being carried out and new indications for treatment with botulinum toxin may include sialorrhea and rhinorrhea.
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PMID:Botulinum toxin-physiology and applications in head and neck disorders. 1682 77

Most movement disorders, reflecting degenerative disorders, develop in a slowly progressive fashion. Some movement disorders, however, manifest with an acute onset. We wish to give an overview of the management and therapy of those acute-onset movement disorders.Drug-induced movement disorders are mainly caused by dopamine-receptor blockers (DRB) as used as antipsychotics (neuroleptics) and antiemetics. Acute dystonic reactions usually occur within the first four days of treatment. Typically, cranial pharyngeal and cervical muscles are affected. Anticholinergics produce a prompt relief. Akathisia is characterized by an often exceedingly bothersome feeling of restlessness and the inability to remain still. It is a common side effect of DRB and occurs within few days after their initiation. It subsides when DRB are ceased. Neuroleptic Malignant Syndrome is a rare, but life-threatening adverse reaction to DRB which may occur at any time during DRB application. It is characterised by hyperthermia, rigidity, reduced consciousness and autonomic failure. Therapeutically immediate DRB withdrawal is crucial. Additional dantrolene or bromocriptine application together with symptomatic treatment may be necessary. Paroxysmal dyskinesias are childhood onset disorders characterised by dystonic postures, chorea, athetosis and ballism occurring at irregular intervals. In Paroxysmal Kinesigenic Dyskinesia they are triggered by rapid movements, startle reactions or hyperventilation. They last up to 5 minutes, occur up to 100 times per day and are highly sensitive to anticonvulsants. In Paroxysmal Non-Kinesiogenic Dyskinesia they cannot be triggered, occur less frequently and last longer. Other paroxysmal dyskinesias include hypnogenic paroxysmal dyskinesias, paroxysmal exertional dyskinesia, infantile paroxysmal dystonias, Sandifer's syndrome and symptomatic paroxysmal dyskinesias. In Hereditary Episodic Ataxia Type 1 attacks of ataxia last for up to two minutes, may be accompanied by dysarthria and dystonia and usually respond to phenytoin. In Type 2 they can last for several hours, may be accompanied by vertigo, headache and malaise and usually respond to acetazolamide. Symptomatic episodic ataxias can occur in a number of metabolic disorders, but also in multiple sclerosis and Behcet's disease.
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PMID:Diagnosis and management of acute movement disorders. 1620 29


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