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

The diagnosis of blepharospasm is rarely considered in patients complaining of face pain or headache. This patient illustrates the importance of looking for blepharospasm in patients who present with headache or face pain, as her pain and blepharospasm were successfully treated with botulinum toxin type A injections.
Headache 1998 May
PMID:Headache and facial pain responsive to botulinum toxin: an unusual presentation of blepharospasm. 963 Jul 89

A 76-year-old man had shown sustained excruciating facial pain in the maxillary region for more than 30 years. Since he was suffering from blepharospasm, facial electromyography was performed and revealed a perioral dystonia. This possible cause of facial pain might have been overlooked had dystonia not been considered and electromyographical studies performed. Repeated intramuscular perioral injections of botulinum toxin brought about complete pain relief. This case shows that involuntary activity of facial muscles can cause a severe chronic pain syndrome. Possible mechanisms include irritation of ascending trigeminal fibers, muscle ischemia due to compression of blood -vessels, or release of pain-producing substances.
Cephalalgia 1998 Dec
PMID:Facial pain in a case of cranial dystonia: a case report. 995 Jun 30

Gangliogliomas of the lateral ventricle are unusual tumours of the central nervous system. We report a 25-year-old female who presented with a 4-week history of generalized headaches associated with left-sided blepharospasm. Clinical examination revealed bilateral papilloedema but no focal neurological deficits. Computed tomography and magnetic resonance imaging demonstrated a large lesion within the left lateral ventricle. Gross total surgical resection of the lesion was performed through a para-sagittal, trans-callosal approach. Histopathological analysis revealed the diagnosis of ganglioglioma. The post-operative course was uneventful, with complete resolution of both the headaches and blepharospasm. The presentation with an ipsilateral blepharospasm has never previously been reported in the setting of a lateral ventricular tumour.
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PMID:Ganglioglioma of the lateral ventricle presenting with blepharospasm - case report and review of the literature. 1138 9

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

The botulinum A toxin inhibits the release of acethylcoline from the vesicles of presynaptic neuronal end plates. Its effect is a transient pharmacological neurectomy. The toxin is used more and more widespreadingly. It selectively inhibits certain muscles or groups of muscles. Its use is of outstanding importance in the treatment of blepharospasm, a disease possibly causing transient functional blindness. This blindness develops randomly, with undetermined duration, therefore it may even threaten the life of the patient. There is no alternative treatment. In ophthalmology, the toxin is used in the therapy of strabismus and nystagmus, as well as replacing entropion operations. Most often its use is suggested in the treatment of focal dystonies, dysphonia, tremor palatinus, dysphagia, spasm of the oesophagus sphincter muscle, nasal hypersecretion, hemifacial spasm, headaches, focal hyperhydrosis, proctalgia fugax, diabetic gastroparesis and difficulties in urination. In the past few years, the toxin has been used for esthetic reasons as well. By relaxing the muscles causing wrinkles, non-permanent result may be reached with its use. The botulinum A toxin does not have general side effects. As local side effects, haematomas and unwanted, transient paresis of the neighboring muscles can be mentioned.
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PMID:[Applications of the botulinum A toxin]. 1278 36

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

The use of botulinum toxin A in cosmetic dermatology has increased in popularity due to the efficacy and relative safety of the treatment. Botulinum toxin A is one of eight exotoxins produced by Clostridium botulinum, a Gram-positive, spore-forming anaerobe. Flaccid paralysis results from the denervation of muscle fibers at the neuromuscular junction after botulinum toxin A administration. While treating blepharospasm, the Carruthers incidentally found that botulinum toxin A improved glabellar frown lines. Dynamic rhytides occur in areas of dynamic motion. These types of lines may be improved with botulinum toxin A. There are two types of botulinum toxin A commercially available (BOTOX and Dysport); only BOTOX is currently available in the US. The efficacy and tolerability of BOTOX was best demonstrated with a multicenter, double-blind, randomized, placebo-controlled study of the efficacy and safety of botulinum toxin type A in the treatment of glabellar lines in 264 patients. There was a significantly greater reduction in glabellar line severity with BOTOX. The effect was maintained for the duration of the study (120 days). There was low occurrence (5.4%) of mostly mild blepharoptosis in the BOTOX group. In another prospective study, it was found that about 1% of BOTOX patients reported severe headache. Botulinum toxin A can provide an alternative treatment of palmar and axillary hyperhidrosis when options such as topical agents (aluminum chloride) and iontophoresis have failed.
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PMID:Botulinum toxin A: its expanding role in dermatology and esthetics. 1292 79

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

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

Methoxyisopropanol and Methoxyisopropyl Acetate, commonly known as propylene glycol monomethyl ether (PGME) and propylene glycol monomethyl ether acetate (PGMEA), respectively, have fragrance, solvent, and viscosity-decreasing functions in cosmetics, although only Methoxyisopropanol is in current use at concentrations ranging from 4% to 35%. Methoxyisopropanol is easily absorbed into the bloodstream upon inhalation or ingestion. The acetate ester is readily metabolized to Methoxyisopropanol in the body, which is excreted unchanged in the expired breath or in the urine as free or conjugated Methoxyisopropanol, or as the primary metabolite propylene glycol. In acute oral toxicity studies, the LD(50) values of Methoxyisopropanol were 4.6 to 9.2 g/kg in rats, with similar low acute toxicity in other animal species. Inhalation exposures of rats, mice, and rabbits to 3000 ppm Methoxyisopropanol for 6 h per day for 9 days to 13 weeks produced increased relative liver weights, signs of central nervous system (CNS) depression, and in some cases, elevated serum alkaline phosphatase, alanine aminotransferase, or hepatocellular hypertrophy, but the kidneys were unaffected. The no observed adverse effect level (NOAEL) for 13-week inhalation exposures to Methoxyisopropanol was 1000 ppm in rats and rabbits. In a 90-day dermal exposure study using rabbits, 10 ml/kg undiluted Methoxyisopropanol produced narcosis and increased kidney weights and the NOAEL was 7.0 ml/kg. Chronic (2-year) daily inhalation exposures of rats and mice to 3000 ppm Methoxyisopropanol produced signs of liver toxicity (rats and mice) and some evidence of renal toxicity in rats. The only observation at 1000 ppm was dark foci of the liver in male rats. For female rats and male and female mice, the NOAEL of this chronic inhalation study was 1000 ppm Methoxyisopropanol. Methoxyisopropanol and Methoxyisopropyl Acetate were found to be nonirritating to slightly irritating and non-sensitizing in rabbit and guinea pig skin. Repeated applications of undiluted Methoxyisopropanol to the eyes of rabbits produced transient slight to moderate irritation. Pregnant rats exposed to 200 or 600 ppm Methoxyisopropanol by inhalation on gestation days 6 to 17 had no effects on maternal health or normal fetal development. Adult male rats exposed to these concentrations had no effects on the reproductive organs. Pregnant rats and rabbits exposed to 500 to 3000 ppm Methoxyisopropanol by inhalation during gestation had no significant embryotoxic or fetotoxic effects, althougth CNS depression and reduced body weight gain were observed in the 3000 ppm group. In a two-generation inhalation study using rats, continuous inhalation of 3000 ppm Methoxyisopropanol produced CNS depression, prolonged estrous cycles, reduced fertility indices, reduced pup weights and pup survival, and delayed sexual development, with a NOAEL for reproductive and developmental effects of 1000 ppm. In a continuous breeding protocol using mice, 2.0% Methoxyisopropanol in drinking water produced reduced growth, reduced relative epididymis weight, reduced relative prostate weight, and increased liver weight (females only) in offspring, with a NOAEL at a 1% concentration. Exposure of mice or rats to 300 ppm to 3000 ppm Methoxyisopropanol by inhalation produced no signs of carcinogenicity. Methoxyisopropanol was negative for mutagenicity or genetic toxicity in the bacterial reverse mutation assay (<or= 5000 microg/plate), the unscheduled DNA synthesis (UDS) assay (<or= 0.1 M), V79 Chinese hamster lung assay (>100 mM), and in the Siberian hamster embryo assay (concentrations not reported). In other assays, 100 mM Methoxyisopropanol increased sister chromatid exchanges in V79 cells. In human inhalation exposure studies of 1 to 7 h duration, 50 to 75 ppm Methoxyisopropanol vapor had an objectionable odor; 150 ppm was slightly irritating to the eyes and throat; 250 ppm produced eye irritation, lacrimation, blinking, rhinorrhea, and headache; 300 ppm was mildly irritating to the eyes, nose, and throat; 750 ppm was extremely irritating; and 2050 ppm produced extreme discomfort with severe lacrimation, blepharospasm, and painful breathing. None of the concentrations tested impaired motor coordination or performance on neurological tests. The irritating effects subsided within 15 min to 24 h of removal from the inhalation chamber. The National Institute of Occupational Safety and Health (NIOSH) recommended an 8-h time-weighted average for occupational exposure of 100 ppm. A margin of safety of 500 was determined, based on a calculated exposure from the normal use of nail polish remover products (100% absorption) and the NOAEL for reproductive toxicity. The absorption of Methoxyisopropanol through the nail is likely to be low, suggesting this margin of safety is conservative. Because Methoxyisopropanol is volatile, exposure by inhalation is possible, but the odor becomes objectionable at 50 to 75 ppm in air. The Cosmetic Ingredient Review (CIR) Expert Panel concluded that Methoxyisopropanol and Methoxyisopropyl Acetate are safe for use in nail care products in the practices of use and concentration as described in this safety assessment.
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PMID:Final report on the safety assessment of methoxyisopropanol and methoxyisopropyl acetate as used in cosmetics. 1883 Aug 62


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