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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although biofeedback has been of value in treating spastic paresis and torticollis, its effectiveness in other movement disorders is less clear. Blepharospasm, which has no definitive treatment, often has a strong psychogenic component. The authors report the use of electromyographic and temperature biofeedback in a women with blepharospasm who had responded poorly to psychotherapy. Her improvement during biofeedback treatment further elucidated psychogenic factors contributing to the disorder. At 3-months follow-up it seemed that the patient's secondary gain from the blepharospasm diminished the maximum treatment response she could have had to biofeedback.
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PMID:Biofeedback in the treatment of blepharospasm: a case study. 729 20

The highly potent neurotoxins produced by Clostridium botulinum lead to botulism when ingested in appreciable amounts. However, botulinum toxin injections delivered intramuscularly in very small quantities can produce a therapeutically intended focal paresis while producing only negligible local or systemic side effects. Over the past several years, various neurological disorders, especially those involving increased muscle tone and/or abnormal movements, have been successfully treated with local botulinum A toxin injections. The success of this method has led to a general change in the management of blepharospasm, torticollis spasmodicus, hemifacial spasm, and other disorders. Treatment is usually effective for 4 to 12 weeks; if symptoms recur, the injections can be repeated over a period of several years, usually with the same success. Side effects depend on the site of the injections, and are rare at the optimal dosage and always reversible. For optimum therapeutic results, this treatment must be restricted to specialized centers.
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PMID:[Therapeutic use of botulinum A toxin in neurology]. 805 1

A patient with neurofibromatosis type I and breast carcinoma developed a bilateral but asymmetric blepharospasm and paresis of the left abducens muscle over a 2-week course. MRI disclosed a small lesion in the left dorsomedial lower pontine region. Electrodiagnostic investigations revealed bilateral R1 responses after stimulation of the left supraorbital nerve and enhancement of R1 and R2 recovery curves. We concluded that lesions in the lower pontine tegmentum may cause blepharospasm.
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PMID:Blepharospasm in association with a lower pontine lesion. 904 Jul 74

A review is given of the aetiology and possible treatment of acquired (non-congenital), blepharoptosis, which is a common but not specific sign of neurological disease. The diagnostic categories of upper eyelid drooping are scheduled as (a) pseudo-ptosis due to a local process or overactivity of eye closure, including blepharospasm, and (b) true ptosis due to a paresis of the eyelid levators (m. tarsalis superior or m. levator palpebrae) or to a disinsertion of the m. levator palpebrae (aponeurotic ptosis). A paresis of the m. tarsalis is due to a lesion in the central, intermediate or peripheral neuron of the sympathetic chain and constitutes one of the components of Horner's syndrome. A paresis of the m. levator palpebrae may be due to a failure in central innervation, in oculomotor (n.III) function, in neuromuscular transmission or to a lesion in the muscle itself.
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PMID:Acquired blepharoptosis. 868 70

We report a case of a unique eye sign following right hemispheric infarction. This patient was a 78 year old right-handed woman. There was a history of a left hemispheric stroke 1 year previously. On admission, she showed left hemianopia, dysarthria, mild left central facial paresis, bilateral sensory deficit and quadriparesis which were marked on the left side. Babinski sign was elicited on the left. She did not have anosognosia or visual neglect. She had mild orofacial apraxia, but ideomotor and ideational apraxia was absent. There was no motor impersistence. Magnetic resonance imaging of the brain revealed a recent infarction in the territory of the right middle cerebral artery and an old infarction in the left tempro-parietal lobe. The patient could not open her eyelids to verbal command or voluntarily until about two weeks later, when she became able to open her eyes but showed difficulty keeping her left eye closed. She was aware of this problem and could repeat the command and comprehend what was requested to her. On verbal command to close the eyes, her right eye would be closed continuously and excessively and the left eye would only blink. When requested to blink, however, she could blink correctly without excessive eye closure. Spontaneous, reflex and voluntary blinking were normal. Her eyes were closed normally during sleep. Blepharospasm was not seen. The patient showed a striking dissociation between a failure to close her eyes continuously and a preserved ability to blink voluntarily. We suggest that her ability to contract palpebral portion of her left orbicularis oculi muscle is preserved. Regarding the mechanism of the voluntary eye closure system, separate control mechanisms should exist on closing eyes continuously and blinking.
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PMID:[Dissociation of voluntary eye closure--to keep the eyes closed and to blink--following right hemisphere stroke]. 1087 26

Botulinum toxin has been used for therapeutic purposes in medicine for more than 20 years. Its effective use now covers more than 50 conditions in a wide variety of areas. Its medicinal use was initially based on its blockade of neuromuscular and neurosecretory transfers. Its use for conditions in the field of specific pain therapy is currently authorized in Germany for spastic torticollis, blepharospasm, hemifacial spasm, spastic equine gait in cases of idiopathic cerebral paresis, and spasticity of the arm following stroke. New publications suggest that it can usefully be employed for numerous other painful conditions. The modes of action known today are not confined to the blockade of cholinergic innervation.Indeed, there is also evidence that therapeutic effects are mediated through a normalization of muscle spindle activity, retrograde intake into the CNS with modulation of the central neuropeptide function, inhibition of sterile neurogenic inflammation, and normalization of endplate dysfunction. In view of the methodological peculiarities of studies in the field of pain therapy, such as injection techniques, injection sites, blind study techniques, dosage etc., the scientific evidence for its use in a wide variety of pain syndromes is still patchy in many areas. For this reason the use of botulinum toxin for these syndromes is only justified after full use has been made of standard therapeutic methods and evaluation in specialized centers. The possibility of considering botulinum toxin in specific pain therapy contexts is a new option for patients and doctors.However, its use calls for detailed knowledge of functional neuroanatomy and extensive practical experience and expertise.
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PMID:[Botulinum toxin in specific pain therapy]. 1269 98

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 (Botox) is an exotoxin produced from Clostridium botulinum. It works by blocking the release of acetylcholine from the cholinergic nerve end plates leading to inactivity of the muscles or glands innervated. Botox is best known for its beneficial role in facial aesthetics but recent literature has highlighted its usage in multiple non-cosmetic medical and surgical conditions. This article reviews the current evidence pertaining to Botox use in the head and neck. A literature review was conducted using The Cochrane Controlled Trials Register, Medline and EMBASE databases limited to English Language articles published from 1980 to 2012. The findings suggest that there is level 1 evidence supporting the efficacy of Botox in the treatment of spasmodic dysphonia, essential voice tremor, headache, cervical dystonia, masticatory myalgia, sialorrhoea, temporomandibular joint disorders, bruxism, blepharospasm, hemifacial spasm and rhinitis. For chronic neck pain there is level 1 evidence to show that Botox is ineffective. Level 2 evidence exists for vocal tics, trigeminal neuralgia, dysphagia and post-laryngectomy oesophageal speech. For stuttering, 'first bite syndrome', facial nerve paresis, Frey's syndrome, oromandibular dystonia and palatal/stapedial myoclonus the evidence is level 4. Thus, the literature highlights a therapeutic role for Botox in a wide range of non-cosmetic conditions pertaining to the head and neck (mainly level 1 evidence). With ongoing research, the spectrum of clinical applications and number of people receiving Botox will no doubt increase. Botox appears to justify its title as 'the poison that heals'.
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PMID:An evidence-based review of botulinum toxin (Botox) applications in non-cosmetic head and neck conditions. 2347 31

BotuLinum toxin A (Botox, Allegan) is a potent neurotoxin that blocks the release of acetylcholine at the neuromuscular junction of cholinergic nerves. Botulinum toxin was introduced to clinical medicine in 1980. Since then it has become a major therapeutic drug in many medical sub-specialties and its use for facial rejuvenation has become increasingly popular. Diplopia after botulinum toxin injection for facial rejuvenation is a rare and transient complication which is related to chemodenervation of adjacent muscle groups. We would like to report 3 cases of double vision related to extra-ocular muscle paresis after an injection of botulinum toxin for facial rejuvenation and blepharospasm. In all 3 cases recovery occurred, without any treatment, over 3 to 4 months (apparently from regeneration of inactivated proteins necessary for degranulation of acetylcholine vesicles). The clinicians engaged in botulinum toxin injections for facial rejuvenation or blepharospasm, should be aware of the possible complications, and inform the patients about the risk of developing double vision. The clinicians should take into account and ask about Botox when treating patients complaining of diplopia.
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PMID:[Diplopia following subcutaneous injections of botulinum toxin for cosmetic or medical use]. 2351 1

Laryngeal dystonia is a movement disorder of the muscles within the larynx, which most commonly manifests as spasmodic dysphonia (SD). Rarer reported manifestations include dystonic respiratory stridor and dyscoordinate breathing. Laryngeal dystonia has been treated successfully with botulinum neurotoxin (BTX) injections since 1984. We reviewed prospectively collected data in a consecutive series of 193 patients with laryngeal dystonia who were seen at St. Vincent's Hospital between 1991 and 2011. Patient data were analyzed in Excel, R, and Prism. Laryngeal dystonia manifested as SD (92.7%), stridor (11.9%), dystonic cough (6.2%), dyscoordinate breathing (4.1%), paroxysmal hiccups (1.6%), and paroxysmal sneezing (1.6%). There were more women (68.4%) than men (31.6%), and the average age at onset was 47 years. A positive family history of dystonia was present in 16.1% of patients. A higher incidence of extra-laryngeal dystonia (ie, torticollis and blepharospasm) and concurrent manifestations of laryngeal dystonia were present in patients with dystonic cough, dyscoordinate breathing, paroxysmal sneezing, and hiccups than in other patients (P = 0.003 and P < 0.0001, respectively). The average starting dose of BTX decreased from 2.3 to 0.5 units between 1991 and 2011. The median treatment rating was excellent across all subgroups. Patients with adductor SD, stridor, extra-laryngeal dystonia and male patients had relatively better treatment outcomes. Technical failures were rare (1.1%). Dysphonia secondary to vocal cord paresis followed 38.7% of treatments. Laryngeal dystonia manifests predominantly as SD, but other manifestations include stridor, dyscoordinate breathing, paroxysmal cough, hiccups, and sneezing. BTX injections are very effective across all subgroups. Severe adverse events are rare.
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PMID:The clinical spectrum of laryngeal dystonia includes dystonic cough: observations of a large series. 2475 88


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