blepharospasm/dopamín

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Decreased dopamine D receptor binding in essential blepharospasm.

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OBJECTIVE The purpose of this study was to investigate whether dopamine D(2) receptor binding was altered in the striatum of essential blepharospasm patients. METHODS Striatal dopamine D(2) receptor binding was measured with positron emission tomography and [(11)C]raclopride. We studied eight

A polymorphism in the dopamine receptor DRD5 is associated with blepharospasm.

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Abnormalities in dopamine neurotransmission are thought to underlie the generation of dystonic movements. The authors performed a case-control allelic association study in patients with the focal dystonia blepharospasm, using polymorphisms in the dopamine receptor and transporter genes. Allele 2 of

Fluoxetine for blepharospasm: interaction of serotonin and dopamine.

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Tardive Blepharospasm and Meige Syndrome during Treatment with Quetiapine and Olanzapine.

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Meige syndrome, which has been presented in tardive syndromes, is a form of blepharospasm accompanied by oromandibular dystonia with manifestations over the face, jaw, and neck. A blepharospasm can be induced by antihistamines, dopaminomimetic or sympathomimetic drugs, or long-term exposure to

Cannabinoid agonists in the treatment of blepharospasm--a case report study.

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The benign essential blepharospasm is a subliminal form of primary torsion dystonia with still uncertain aetiology. It is characterized by involuntary convulsive muscle contractions of the M. orbicularis occuli, accompanied by unbearable pain of the cornea, eye bulb and the muscle itself. It has

Animal model explains the origins of the cranial dystonia benign essential blepharospasm.

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The current study demonstrates that combining two mild alterations to the rat trigeminal reflex blink system reproduces the symptoms of benign essential blepharospasm, a cranial dystonia characterized by uncontrollable spasms of blinking. The first modification, a small striatal dopamine depletion,

Remission of tardive dystonia (blepharospasm) after electroconvulsive therapy in a patient with treatment-refractory schizophrenia.

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Tardive dystonia is a movement disorder dominated by involuntary muscle contractions that may be tonic, spasmodic, patterned or repetitive, associated with the use of dopamine-receptor blocking agents. Most of the patients with tardive dystonia present initially with blepharospasm. Treatment of

Blepharospasm--successful treatment with baclofen and sodium valproate. A case report.

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In a patient with idiopathic blepharospasm treatment with the gamma-aminobutyric acid (GABA)-mimetic combination of baclofen and sodium valproate resulted in complete and sustained remission of symptoms and signs. It is suggested that blepharospasm results from a relative deficiency of GABA-ergic

Ipsilateral blepharospasm and contralateral hemidystonia and parkinsonism in a patient with a unilateral rostral brainstem-thalamic lesion: structural and functional abnormalities studied with CT, MRI, and PET scanning.

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A patient developed progressive right hemidystonia in childhood. Subsequently, left-sided blepharospasm, slurred and stuttering speech, and right-sided rigidity and bradykinesia, responsive to dopamine agonists, appeared. Investigation with computed tomography and magnetic resonance imaging (MRI) at

Memory-contingent saccades and the substantia nigra postulate for essential blepharospasm.

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Essential blepharospasm and cranial dystonia are related focal dystonias of unknown aetiology. Blepharospasm induced by acute dopamine depletion in parkinsonism restricts saccade initiation possibly via the substantia nigra pars reticulata (SNpr). If essential blepharospasm and cranial dystonia

Bell's palsy-induced blepharospasm relieved by passive eyelid closure and responsive to apomorphine.

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OBJECTIVE We describe the case of a woman with Bell's Palsy-induced blepharospasm (BPIB) of the right eye that appeared simultaneously with a complete left facial nerve palsy. The involuntary spasm was relieved by passive lowering of the upper eyelid on the paretic side. METHODS The recovery curve

The control of blepharospasm by essential fatty acids.

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Dopamine depletion induced by administration of Ro4-1284 produces a condition of rapid and repeated eye blinking in rats. This condition mimics the human disorder, blepharospasm, which often accompanies parkinsonism and other dopamine deficiency disorders. When given a 3-week course of a compound

Assessing the role of DRD5 and DYT1 in two different case-control series with primary blepharospasm.

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Primary blepharospasm is a common adult-onset focal dystonia. Polymorphisms of the genes encoding TorsinA (DYT1) and the D5 dopamine receptor (DRD5) have previously been associated with lifetime risk for focal dystonia. We describe here experiments testing common variability within these two genes

Pharmacology of blepharospasm-oromandibular dystonia syndrome.

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Blepharospasm and oromandibular dystonia are clinically similar to other hyperkinetic movement disorders. Dopaminergic antagonist (neuroleptic) and purported cholinergic agonist (deanol) treatment improved symptoms, whereas dopaminergic agonist (carbidopa/levodopa) and cholinergic antagonist

Saccade responses to dopamine in human MPTP-induced parkinsonism.

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Depletion of dopamine content in the substantia nigra resulting from 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) toxicity produces parkinsonism. Management of 3 patients with MPTP-induced parkinsonism required drug holidays during which there was a state of dopamine depletion followed by

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