Observations on the Mechanism of Parkinsonian Blepharospasm and its Treatment with L-Dopa

Klawans, H.L.; Erlich, Michael

doi:10.1159/000113999

Cited by 15 publications

(4 citation statements)

References 3 publications

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“…In our series, an obvious cause was evident only in 14-3% of patients. These included Parkinson's disease and other forms of Parkinsonism, [9][10][11][12] neuroleptic-induced tardive dystonia'3 14 (other drugs including levodopa15 and nasal decongestants16 may also precipitate blepharospasm), and occasional focal structural lesions in basal ganglia,"7 18 diencephalon,19 or upper brainstem.2023 However, no consistent pathology has been found in the few cases of idiopathic blepharospasm that have come to necropsy. 2425 We have also examined the brains of three patients with blepharospasm and/or oromandibular dystonia; one was found to have a brainstem angioma, but no abnormality was discovered in the other three.…”

Section: Discussionmentioning

confidence: 99%

Blepharospasm: a review of 264 patients.

Grandas¹,

Elston²,

Quinn³

et al. 1988

Journal of Neurology, Neurosurgery & Psychiatry

320

172

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Accepted 5 January 1988 in the information, the patient was contacted or seen again in the clinic to obtain the missing data.The mean age of onset was 55 8 (SD 12 5) years (range 11-81). There were 170 females (644%) and 94 males (35-6%). The female/male ratio was 1-8:1. Antecedent eventsThere was a psychiatric illness before or at onset of blepharospasm in 47 cases (17-8%). Twenty nine patients (11%) were depressed; two had a bipolar manic-depressive illness; 10 (3 8%) suffered an anxiety state; four were schizophrenic; two had a single unspecified psychotic episode. Fourteen of these cases (5-3% of the total series) were exposed to neuroleptics before the onset of their blepharospasm, so may have been examples of tardive dystonia. Thus, only 33 patients (13-2%) with non-tardive blepharospasm had a prior history of psychiatric disorder.Thirty two cases (12-1 %) had experienced local ocular disease in the year before the onset of their blepharospasm. In addition, a larger number of patients (55-3%) complained of ocular symptoms prior to or at the onset of their blepharospasm (table 1). However, only 13 patients (4 9%) developed new eye problems later during the course of their blepharospasm. The commonest complaints were of irritation, watering or grittiness of the eyes. Pain occurred in only 2 cases. Family historyA history of movement disorders in other first or second degree family members was given by 52 cases (19 7%). Relatives, either affected or unaffected, were not examined in this study (indeed many of them were already deceased).

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Section: Discussionmentioning

confidence: 99%

Blepharospasm: a review of 264 patients.

Grandas¹,

Elston²,

Quinn³

et al. 1988

Journal of Neurology, Neurosurgery & Psychiatry

320

172

View full text Add to dashboard Cite

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“…A reduced activity of dopaminergic circuits in the pathogenesis of blepharospasm is suggested by the benefi cial effects of dopamine agonists in some subsets of blepharospasm patients [7], and by the observation of blepharospasm in dopamine deficiency states, such as Parkinson's disease [8,9] -where a hyperexcitable blink reflex recovery cycle is also present [10,11] -in posten cephalitic [12] and MPTP-induced parkinsonism [13]. Finally, a reduced dopamine turnover in the substantia nigra, striatum, and nucleus accumbens has been found on postmortem examination in a patient with Meige syn drome [14].…”

Section: Introductionmentioning

confidence: 99%

Different Effects of Levodopa and Apomorphine on Blink Reflex Recovery Cycle in Essential Blepharospasm

Napolitano

Bonuccelli²,

Rossi³

1997

Eur Neurol

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With the aim of assessing dopaminergic responsiveness in essential blepharospasm, we investigated the effects of oral levodopa and subcutaneous apomorphine on blink reflex recovery cycle in 7 blepharospasm patients. We found that in blepharospasm the excitability of the blink reflex recovery cycle was increased compared with control subjects. The oral administration of levodo-pa/carbidopa (500/50 mg) did not significantly modify the blink reflex recovery cycle. The 50 µg/kg dose of apomorphine decreased the amplitude of conditioned responses at 300 and 500 ms, whereas the 10 µg/kg dose was ineffective. We conclude that the excitability of the blink reflex recovery cycle in blepharospasm is partly under dopaminergic control. The partial normalization of the blink reflex recovery cycle excitability observed with 50 µg/kg apomorphine is consistent with the reported clinical efficacy of the drug in this condition.

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“…A major theory suggests that the main lesions are in the motor inhibitory cortical system above the facial nuclepo-13 or in the bulbar reticular formation.r' Spastic disorders have been associated with progressive supranuclear palsies, parkinsonism, and various postencephalitic states. 6,[15][16][17][18] A second, small group of patients who have essential blepharospasm have had previous eye surgery or trauma. This is especially true following cataract procedures with implantable lenses, postirradiation iritis states (postmaxillectomy patients) and posttraumatic forms of ophthalmitis.…”

Section: Discussionmentioning

confidence: 99%

Selective Facial Neurectomy for Spastic Disorders of the Facial Nerve

Spector¹

1985

Otolaryngol.--head neck surg.

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Selective facial neurectomy in combination with bilateral musculocutaneous resection, plication brow lift, upper lid blepharoplasty, and limited rhytidectomy was performed on 18 patients with essential blepharospasm, eight with hemifacial spasm, and two with CNS vascular compression malformations. Microscopy showed the nerve tissues to be normal. Initial results were excellent. At 3 months there was a slight, persistent spastic twitching of the affected muscles in five nerves (a 14% failure rate in correcting blepharospasm). After 13 months there were four additional failures resulting from nerve regrowth in three and from one patient not completing therapy. The overall blepharospasm failure rate was 26%. On repeat neurectomy those with nerve regrowth presented with a diffuse, fine meshwork of nerve fibers reinnervating the mimetic facial musculature. In six of seven patients operated on again, spasticity was eliminated. The initial surgical failure rate has been corrected by resecting the frontal branch and the superior division of the buccal branch of the facial nerve. Only repeat neurectomy can correct long-term failures resulting from facial nerve regrowth.

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Observations on the Mechanism of Parkinsonian Blepharospasm and its Treatment with L-Dopa

Cited by 15 publications

References 3 publications

Blepharospasm: a review of 264 patients.

Blepharospasm: a review of 264 patients.

Different Effects of Levodopa and Apomorphine on Blink Reflex Recovery Cycle in Essential Blepharospasm

Selective Facial Neurectomy for Spastic Disorders of the Facial Nerve

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