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Introduction
CLINICAL
DIFFERENTIALS
WORKUP
TREATMENT
MEDICATION
FOLLOW-UP
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AUTHOR AND EDITOR INFORMATION

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Author: Marta Ugarte, MBBS, PhD, DPhil, MRC(Ophth), Clinical Lecturer in Ophthalmology, University of Manchester, UK

Marta Ugarte is a member of the following medical societies: Association for Research in Vision and Ophthalmology, British Medical Association, International Society of Ocular Trauma, Royal College of Ophthalmologists, and Royal Society of Medicine

Editors: Ron W Pelton, MD, PhD, Private Practice, Colorado Springs, Colorado; Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles; Mark T Duffy, MD, PhD, Consulting Staff, Division of Oculoplastic, Orbito-facial, Lacrimal, and Reconstructive Surgery, Green Bay Eye Clinic, BayCare Clinic; Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri; Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Author and Editor Disclosure

Synonyms and related keywords: blepharocolysis, focal eyelid dystonia, involuntary levator palpebrae inhibition, pretarsal blepharospasm, atypical blepharospasm, freezing and akinesia of lid function, ALO, ILPI, orbicularis oculi, OO, levator palpebrae superioris, LPS, intermittent involuntary closure, frontalis suspension, botulinum toxin, BOTOX®


INTRODUCTION

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Background

Apraxia of lid opening (ALO) is a nonparalytic motor abnormality “characterized by difficulty initiating the act of lid elevation after lid closure.”1 Controversy surrounds the designation of this syndrome. ALO is not strictly an apraxia or “inability to perform a motor action to command despite both an adequate understanding of the action and the elementary ability to carry out.” 2 However, the designation ALO addresses the main feature of the condition (ie, the inability to open the eyes at will with preservation of the ability to open them and keep them open at other times);3 ALO may present in isolation or in association with blepharospasm,4, 5 and the challenge lies in differentiating these 2 entities.

Pathophysiology

Although the underlying mechanisms have not been clearly elucidated, apraxia of lid opening (ALO) may be due to an abnormality in the supranuclear control of voluntary eyelid elevation, which requires the activation of the levator palpebrae superioris (LPS) and the concurrent inhibition of orbicularis oculi (OO) activity.

Electromyographic studies of the LPS and OO have demonstrated that the following may cause ALO:

  • Involuntary levator palpebrae inhibition (ILPI),6 either intermittent7 or prolonged8
  • Pretarsal OO persistent contraction9, 6
  • ILPI (either intermittent or prolonged) and pretarsal OO persistent contraction10, 6

The LPS is innervated bilaterally from the central caudal subdivision of the oculomotor (III) nucleus, and the OO is innervated unilaterally from the facial (VII) nucleus. The cortex, extrapyramidal motor systems, and rostral midbrain structures may control LPS motoneuron activity (see Media file 1).11

Disturbances in burst, tonic, or pause neurons within any of the above-mentioned premotor structures may result in abnormal inhibitor inputs onto the LPS motoneurons. Some patients may experience an associated disruption in reciprocal activation of the LPS and OO.

Frequency

International

Apraxia of lid opening (ALO) has been reported in 7%,5 10%,4 and 55%12 of patients with blepharospasm. Benign essential blepharospasm has a prevalence of 12 per million in Japan,13 17 per million in Rochester, MN, in the United States,14 30 per million in Northern England,15 and 36 per million in the Epidemiologic Study of Dystonia in Europe.16 The wide variation in these figures may reflect sample bias.

Mortality/Morbidity

Apraxia of lid opening (ALO) does not directly cause mortality. Morbidity is mostly related to the underlying disease and to the visual impairment in individuals with severe eye closure.

Race

Racial differences have not been reported.

Sex

Apraxia of lid opening appears to be more common in women than in men. In 1998, Defazio et al described 10 new individuals with apraxia of lid opening (ALO) and reviewed 11 cases previously mentioned in the literature.17 A female-to-male preponderance of 2:1 was found.

Age

The peak age of onset is in the sixth and seventh decades of life.


CLINICAL

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History

Apraxia of lid opening (ALO) can present spontaneously in otherwise healthy individuals.6, 17  

In patients with Parkinson disease, progressive supranuclear palsy, and Shy-Drager syndrome, Lepore and Duvoisin reported in 1985 that extrapyramidal symptoms preceded the inability to open the eyelids by a mean of 9.7 years.10 

ALO is typically a chronic disorder, but spontaneous remission has been reported in patients within 1 month of strokes involving the nondominant hemisphere.18, 19, 20 

In instances of ALO that may be drug induced, the symptoms have been reported to remit within 2 weeks of withdrawal of the agent;21 however, in one individual, the symptoms persisted for 7 months.22

Physical

Clinical signs include the following (video of an illustrative case may be seen in Media file 2):23 

  • Individuals experience difficulty opening the lids at will subsequent to voluntary or involuntary closure. The inability may be due to involuntary levator palpebrae inhibition (ILPI) or persistent pretarsal orbicularis oculi (OO) motor activity, which, in some instances, may be detectable electromyographically but not clinically.
  • The inability to reopen the lids is not evident during spontaneous or reflex blinking. The premotor pathways that regulate and control the state of voluntary activity of the levator palpebrae superioris (LPS) and make it parallel with OO inhibition differ, at least in part, from the pathways of spontaneous and reflex blinking.
  • The patient has no difficulty in keeping the lids open once they have been opened. LPS tonic activity is normal while the lids are open.
  • Intermittent involuntary closure of the eyes may occur in some patients, both in the presence and absence of spasmodic contractions of the OO in blepharospasm. ILPI not accompanied by blepharospasm may cause the eyelid to drop and to be kept closed as long as inhibition of the LPS activity persists.
  • Attempted eye opening can result in forceful contraction of the frontalis muscle, backward thrusting of the head, and delay in lid closure.
  • Different tricks may be used to help open the eyes, such as manual lifting of the lids, opening of the mouth, light touch of the temporal region, and massaging of the lids. The physiology of these maneuvers is unknown.
  • Some patients have been reported to have associated supranuclear limitation of eye movements.10
  • The coordination of eyelid movement is preserved.

Causes

Apraxia of lid opening (ALO) has been attributed to a variety of CNS lesions in various parts of the brain, including the following:

  • Nondominant hemisphere19
  • Medial frontal lobe24, 25
  • Basal ganglia11
  • Rostral brainstem21, 22

ALO has been described in association with certain CNS diseases: 

  • Progressive supranuclear palsy (PSP; one of the most common causes of ALO)26
  • Parkinson disease (another common cause of ALO)10, 27, 5, 28, 29
  • Idiopathic dystonias29
  • Hydrocephalus30
  • Motor neuron disease31
  • Dystonia due to kernicterus6
  • Choreoathetosis6
  • Huntington chorea1
  • Shy-Drager syndrome10
  • Postencephalitic parkinsonism10
  • Neuroacanthocytosis32 

In addition, the use of the following medications has been reported to induce ALO:1, 10, 26, 33 

  • Lithium intoxication resulted in development of ALO. On withdrawal of lithium, symptoms remitted within 2 weeks.21 
  • Sulpiride may be associated with ALO; the condition lasted approximately 7 months after discontinuation of sulpiride.22 
  • An analog of meperidine (MPTP) has been attributed to the induction of parkinsonism associated with ALO.34 

A diagnosis of Wilson disease was made in one patient after he presented with a severe, intermittent inability to open his lids; the original diagnosis was ALO.35


DIFFERENTIALS

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Other Problems to Be Considered

Cerebral ptosis


WORKUP

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Imaging Studies

Neuroimaging studies using CT scanning or MRI may help reveal whether pathology, such as atrophy or infarct, is present in the cortex, basal ganglia, or rostral midbrain.  

Positron emission tomography (PET) may be used to assess brain function by mapping the glucose metabolism in neurons. PET studies of patients with ALO have demonstrated glucose hypometabolism in the basal ganglia,24 medial frontal lobe (unilaterally or bilaterally),24, 25 and primary visual cortex,25 suggesting abnormal neuronal activity.

Other Tests

Levator palpebrae superioris (LPS) and orbicularis oculi (OO) activity may be assessed using electromyelography (EMG) recordings from these muscles during lid movements.

Neuropsychological testing may reveal the presence or absence of frontal lobe pathology.


TREATMENT

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Medical Care

Botulinum toxin (Botox®) injections in the pretarsal portion of the orbicularis oculi (OO) may be beneficial in individuals with associated blepharospasm. Botox® may also benefit those whose apraxia of lid opening (ALO) is due to pretarsal OO motor activity persistence, but not those in whom ALO is due to involuntary levator palpebrae inhibition (ILPI).36  

Levodopa (benserazide 25 mg/L-dopa 100 mg; carbidopa 50 mg/levodopa 200 mg) has been reported to improve the symptoms of ALO in a patient with progressive supranuclear palsy in whom electromyelography (EMG) was used to confirm that the ALO resulted from involuntary levator palpebrae inhibition (ILPI).37 Levodopa has also reportedly been used to improve ALO symptoms in patients with Parkinson disease.38, 28  
 
The symptoms of ALO in isolated individuals have been reported to improve with the use of sodium valproate39 and the anticholinergic trihexyphenidyl.40

Surgical Care

Patients with apraxia of lid opening (ALO) may benefit from frontalis suspension.41 In this procedure, the contraction of the frontalis muscle elevates the eyelids.

Orbicularis oculi (OO) resection may be carried out in combination with frontalis suspension if essential blepharospasm is present.41

Levator palpebrae superioris (LPS) aponeurosis reinsertion may be necessary in some individuals. Disinsertion may result from manual traction on the lids or the repeated OO contraction.

Consultations

Consult a neurologist for an evaluation for underlying disease.


MEDICATION

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Drug Category: Neuromuscular blocker agents

Help produce symptomatic improvement of orbicularis spasm and autonomic symptoms.

Drug NameBotulinum toxin type A (BOTOX®)
DescriptionOne unit of botulinum toxin type A corresponds to the calculated median intraperitoneal lethal dose (LD50) in mice. Each vial contains 100 units (U) of clostridium botulinum type A neurotoxin complex, 0.5 mg of albumin human, and 0.9 mg of sodium chloride in a sterile, vacuum-dried form without a preservative. It blocks neuromuscular transmission by binding to receptor sites on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylcholine.
Adult DoseFor blepharospasm, reconstituted botulinum toxin type A is injected with initial dose of 1.25-2.5 U (0.05-0.1 mL at each site) into the medical and lateral pretarsal orbicularis oculi of the upper lid and into the lateral pretarsal orbicularis oculi of the lower lid; avoiding medial lower lid injections, and thereby reducing diffusion into the inferior oblique, may reduce the complication of diplopia
Pediatric DoseNot established
ContraindicationsInjection is contraindicated in the presence of infection at the proposed injection site(s) and in individuals with known hypersensitivity to any ingredient in the formation
InteractionsCoadministration with aminoglycosides or other agents interfering with neuromuscular transmission (eg, curare-like compounds) should be performed with caution as the effect of the toxin may be potentiated; excessive neuromuscular weakness may be exacerbated by administration of another botulinum toxin prior to the resolution of the effects of a previously administered botulinum toxin
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsCaution should be used when botulinum toxin type A treatment is used in the presence of inflammation at the proposed injection site(s) or when excessive weakness or atrophy is present in the target muscle(s); reduced blinking from botulinum toxin type A injection of the orbicularis muscles can lead to corneal exposure, persistent epithelial defect, and corneal ulceration, especially in patients with VII nerve disorders

Drug Category: Antiparkinson agents

These agents reduce morbidity associated with dopamine deficiency.

Drug NameLevodopa (Sinemet)
DescriptionBenserazide 25 mg/L-dopa 100 mg; carbidopa 50 mg/levodopa 200 mg. Levodopa, the metabolic precursor of dopamine, crosses the blood-brain barrier, and presumably is converted to dopamine in the brain to relieve the symptoms of neurological diseases that are related to depletion of dopamine. Carbidopa inhibits the decarboxylation of peripheral levodopa, making more levodopa available for transport to the brain.
Adult DoseInitiate with one tablet of Sinemet 25-100 three times a day; dosage may be increased by one tablet every day or every other day, as necessary, until a dosage of eight tablets of Sinemet 25-100 a day is reached
Pediatric DoseNot established
ContraindicationsNonselective monoamine oxidase (MAO) inhibitors are contraindicated for use with levodopa; contraindicated in patients with known hypersensitivity to any component of the drug and in patients with narrow-angle glaucoma; may activate a malignant melanoma and should not be used in patients with suspicious, undiagnosed skin lesions or a history of melanoma
InteractionsCaution should be exercised when coadministered with the following drugs; symptomatic postural hypotension may occur in a patient receiving antihypertension drugs; concomitant therapy with selegiline and carbidopa-levodopa may be associated with severe orthostatic hypotension; rare reports of adverse reactions, including hypertension and dyskinesia, resulting from the concomitant use of tricyclic antidepressants and Sinemet; dopamine D2 receptor antagonists (eg, phenothiazines, butyrophenones, risperidone) and isoniazid may reduce the therapeutic effects of levodopa; beneficial effects of levodopa in Parkinson disease have been reported to be reversed by phenytoin and papaverine
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsPeriodic evaluations of hepatic, hematopoietic, cardiovascular, and renal function are recommended during extended therapy; levodopa may be associated with somnolence and very rarely episodes of sudden onset of sleep; patients must be informed of this and advised to exercise caution while driving or operating machines.

Drug Category: Anticholinergic agents

These agents are thought to work centrally by suppressing conduction in the vestibular cerebellar pathways. They may have an inhibitory effect on the parasympathetic nervous system.

Drug NameTrihexyphenidyl
DescriptionCentrally-acting anticholinergic that tends to diminish muscle spasms.
Adult DoseInitially, administer 1-2 mg PO the first d and increase by 2 mg at intervals of 3-5/d, to a maximum of 6-10 mg/d PO
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; glaucoma, peptic ulcers, pyloric or duodenal obstruction, stenosing prostatic hypertrophy or bladder neck obstructions, achalasia, and toxic megacolon
InteractionsAmantadine and anticholinergic coadministration may increase anticholinergic adverse effects that disappear when dose is reduced; haloperidol and anticholinergic coadministration may result in worsening of schizophrenic symptoms, decreased haloperidol serum concentrations; pharmacologic/therapeutic actions of phenothiazines may be reduced by concurrent administration of anticholinergics
PregnancyC - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
PrecautionsDose adjustment may be required in geriatric patients; caution in patients with tachycardia, cardiac hypotension, prostatic hypertrophy, arrhythmias, hypertension, or tendency toward urinary retention, liver or kidney disorders, and obstructive disease of GI or GU tract; if dry mouth is severe and impairs swallowing or speaking, or if loss of appetite and weight occurs, reduce dosage or temporarily discontinue medication

Drug Category: Anticonvulsants

These agents are used to treat severe muscle spasms.

Drug NameValproic acid
DescriptionThe delayed-release or extended-release dosage forms are used for prophylaxis of migraine headaches. Although mechanism of action is not established, activity may be related to increased brain levels of gamma-aminobutyric acid (GABA), or enhanced GABA action.
Adult DoseDelayed-release: 250 mg PO bid initially; may titrate upward, not to exceed 1000 mg/d divided bid
Extended-release: 500 mg PO qd initially; may increase dose, not to exceed 1000 mg/d
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; hepatic disease/dysfunction; hyperammonemic encephalopathy and urea cycle disorders
InteractionsCoadministration with cimetidine, salicylates, felbamate, and erythromycin may increase toxicity; rifampin may significantly reduce valproate levels; in pediatric patients, protein binding and metabolism of valproate decrease when taken concomitantly with salicylates; coadministration with carbamazepine may result in variable changes of carbamazepine concentrations with possible loss of seizure control; valproate may increase diazepam and ethosuximide toxicity (monitor closely); valproate may increase phenobarbital and phenytoin levels while either one may decrease valproate levels; valproate may displace warfarin from protein binding sites (monitor coagulation tests); may increase zidovudine levels in HIV-seropositive patients
PregnancyD - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
PrecautionsThrombocytopenia and abnormal coagulation parameters have occurred; risk of thrombocytopenia increases significantly at total trough valproate plasma concentrations >110 mcg/mL in females and 135 mcg/mL in males; at periodic intervals and prior to surgery, determine platelet counts and bleeding time before initiating therapy; reduce dose or discontinue therapy if hemorrhage, bruising or a hemostasis/coagulation disorder occur; hyperammonemia may occur, resulting in hepatotoxicity; closely monitor patients for appearance of malaise, weakness, facial edema, anorexia, jaundice, and vomiting; may cause drowsiness


FOLLOW-UP

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Further Outpatient Care

Patients who benefit from BOTOX® injection should be observed every 2-3 months, because repeat injections may be required.

Prognosis

In patients with isolated apraxia of lid opening (ALO), the prognosis is excellent. In the presence of other underlying diseases, ALO may result in morbidity or mortality from the associated condition.


MISCELLANEOUS

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Medical/Legal Pitfalls

Failure to exclude significant underlying diseases or medications that may be associated with apraxia of lid opening (may result in serious morbidity and even mortality from the associated condition)


FURTHER READING

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Boghen D. Apraxia of lid opening: a review. Neurology. 1997;48(6):1491-4.

Esteban A, Traba A, Prieto J. Eyelid movements in health and disease. The supranuclear impairment of the palpebral motility. Neurophysiol Clin. 2004;34(1):3-15.

Schmidtke K, Buttner-Ennever JA. Nervous control of eyelid function.
A review of clinical, experimental and pathological data. Brain. 1992;115 Pt 1:227-47.


MULTIMEDIA

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Media file 1:  Diagram of the possible central pathways involved in the generation of inhibitory responses of the levator palpebrae superioris muscle. Caudal central nucleus (CCN), central caudal subdivision of the oculomotor (III) nucleus.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  Chart

Media file 2:  A man with apraxia of lid opening is unable to open his lids at will. Eye movements were full. Attempted eye opening resulted in frontalis muscle contraction, backward thrusting of the head, and pretarsal orbicularis oculi activity. Spontaneous reflex blinking was normal. The lids remained open following manual elevation.
Click to see larger pictureClick to see detailView Full Size Image
 
Media type:  Video


REFERENCES

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  1. Goldstein JE, Cogan DG. Apraxia of Lid Opening. Arch Ophthalmol. Feb 1965;73:155-9. [Medline].
  2. Geschwind N. The apraxias: neural mechanisms of disorders of learned movement. Am Sci. Mar-Apr 1975;63(2):188-95. [Medline].
  3. Boghen D. Apraxia of lid opening: a review. Neurology. Jun 1997;48(6):1491-4. [Medline].
  4. Jordan DR, Anderson RL, Digre KB. Apraxia of lid opening in blepharospasm. Ophthalmic Surg. May 1990;21(5):331-4. [Medline].
  5. Krack P, Marion MH. "Apraxia of lid opening," a focal eyelid dystonia: clinical study of 32 patients. Mov Disord. Nov 1994;9(6):610-5. [Medline].
  6. Aramideh M, Bour LJ, Koelman JH, Speelman JD, Ongerboer de Visser BW. Abnormal eye movements in blepharospasm and involuntary levator palpebrae inhibition. Clinical and pathophysiological considerations. Brain. Dec 1994;117 (Pt 6):1457-74. [Medline].
  7. Esteban A, Gimenez-Roldan S. Involuntary closure of eyelids in parkinsonism. Electrophysiological evidence for prolonged inhibition of the levator palpebrae muscles. J Neurol Sci. Jul 1988;85(3):333-45. [Medline].
  8. Esteban A, Giménez-Roldán S. [Nociceptive reflex of the orbicularis oculi. Study in normal subjects and in peripheral facial lesions]. Arch Neurobiol (Madr). Jul-Aug 1973;36(4):283-94. [Medline].
  9. Elston JS. A new variant of blepharospasm. J Neurol Neurosurg Psychiatry. May 1992;55(5):369-71. [Medline].
  10. Lepore FE, Duvoisin RC. "Apraxia" of eyelid opening: an involuntary levator inhibition. Neurology. Mar 1985;35(3):423-7. [Medline].
  11. Schmidtke K, Büttner-Ennever JA. Nervous control of eyelid function. A review of clinical, experimental and pathological data. Brain. Feb 1992;115 Pt 1:227-47. [Medline].
  12. Tolosa E, Martí MJ. Blepharospasm-oromandibular dystonia syndrome (Meige's syndrome): clinical aspects. Adv Neurol. 1988;49:73-84. [Medline].
  13. Nakashima K, Kusumi M, Inoue Y, Takahashi K. Prevalence of focal dystonias in the western area of Tottori Prefecture in Japan. Mov Disord. Jul 1995;10(4):440-3. [Medline].
  14. Nutt JG, Muenter MD, Melton LJ 3rd, Aronson A, Kurland LT. Epidemiology of dystonia in Rochester, Minnesota. Adv Neurol. 1988;50:361-5. [Medline].
  15. Duffey PO, Butler AG, Hawthorne MR, Barnes MP. The epidemiology of the primary dystonias in the north of England. Adv Neurol. 1998;78:121-5. [Medline].
  16. A prevalence study of primary dystonia in eight European countries. J Neurol. Oct 2000;247(10):787-92. [Medline].
  17. Defazio G, Livrea P, Lamberti P, De Salvia R, Laddomada G, Giorelli M, et al. Isolated so-called apraxia of eyelid opening: report of 10 cases and a review of the literature. Eur Neurol. 1998;39(4):204-10. [Medline].
  18. Nutt JG. Lid abnormalities secondary to cerebral hemisphere lesions. Ann Neurol. Feb 1977;1(2):149-51. [Medline].
  19. De Renzi E, Gentilini M, Bazolli C. Eyelid movement disorders and motor impersistence in acute hemisphere disease. Neurology. Mar 1986;36(3):414-8. [Medline].
  20. Lepore FE. So-called apraxias of lid movement. Adv Neurol. 1988;49:85-90. [Medline].
  21. Micheli F, Cersosimo G, Scorticati MC, Ledesma D, Molinos J. Blepharospasm and apraxia of eyelid opening in lithium intoxication. Clin Neuropharmacol. May-Jun 1999;22(3):176-9. [Medline].
  22. Tsuji S, Kikkawa S, Horiguchi J, Yamashita H, Kagaya A, Morinobu S, et al. Meige syndrome with apraxia of lid opening after the discontinuation of sulpiride treatment. Pharmacopsychiatry. Jul 2002;35(4):155-6. [Medline].
  23. Ugarte M, Teimory M. Apraxia of lid opening. Br J Ophthalmol. Jul 2007;91(7):854. [Medline].
  24. Smith D, Ishikawa T, Dhawan V, Winterkorn JS, Eidelberg D. Lid opening apraxia is associated with medial frontal hypometabolism. Mov Disord. May 1995;10(3):341-4. [Medline].
  25. Suzuki Y, Kiyosawa M, Ohno N, Mochizuki M, Inaba A, Mizusawa H, et al. Glucose hypometabolism in medial frontal cortex of patients with apraxia of lid opening. Graefes Arch Clin Exp Ophthalmol. Jul 2003;241(7):529-34. [Medline].
  26. Golbe LI, Davis PH, Lepore FE. Eyelid movement abnormalities in progressive supranuclear palsy. Mov Disord. 1989;4(4):297-302. [Medline].
  27. Brusa A, Meneghini S, Piccardo A, Stoehr R. Apraxia of lid opening. Ital J Neurol Sci. Dec 1981;2(4):367-70. [Medline].
  28. Lee KC, Finley R, Miller B. Apraxia of lid opening: dose-dependent response to carbidopa-levodopa. Pharmacotherapy. Mar 2004;24(3):401-3. [Medline].
  29. Esteban A, Giménez-Roldán S. Involuntary closure of eyelids in parkinsonism. Electrophysiological evidence for prolonged inhibition of the levator palpebrae muscles. J Neurol Sci. Jul 1988;85(3):333-45. [Medline].
  30. Roh JK, Kim BG, Kim DE, Ahn TB. Apraxia of lid opening associated with hydrocephalus. Eur Neurol. 2001;45(1):53-4. [Medline].
  31. Abe K, Fujimura H, Tatsumi C, Toyooka K, Yorifuji S, Yanagihara T. Eyelid "apraxia" in patients with motor neuron disease. J Neurol Neurosurg Psychiatry. Dec 1995;59(6):629-32. [Medline].
  32. Bonaventura I, Matias-Guiu J, Cervera C, Codina Puiggros A. Neuroacanthocytosis syndrome, apraxia of eyelid opening, and progressive supranuclear palsy. Neurology. Sep 1986;36(9):1276. [Medline].
  33. Friedman DI, Jankovic J, McCrary JA 3rd. Neuro-ophthalmic findings in progressive supranuclear palsy. J Clin Neuroophthalmol. Jun 1992;12(2):104-9. [Medline].
  34. Langston JW, Ballard P, Tetrud JW, Irwin I. Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis. Science. Feb 25 1983;219(4587):979-80. [Medline].
  35. Keane JR. Lid-opening apraxia in Wilson's disease. J Clin Neuroophthalmol. Mar 1988;8(1):31-3. [Medline].
  36. Forget R, Tozlovanu V, Iancu A, Boghen D. Botulinum toxin improves lid opening delays in blepharospasm-associated apraxia of lid opening. Neurology. Jun 25 2002;58(12):1843-6. [Medline].
  37. Yamada S, Matsuo K, Hirayama M, Sobue G. The effects of levodopa on apraxia of lid opening: A case report. Neurology. Mar 9 2004;62(5):830-1. [Medline].
  38. Dewey RB Jr, Maraganore DM. Isolated eyelid-opening apraxia: report of a new levodopa-responsive syndrome. Neurology. Sep 1994;44(9):1752-4. [Medline].
  39. Chand RP, Park DM. Atypical blepharospasm responsive to sodium valproate. Mov Disord. Jan 1994;9(1):116-7. [Medline].
  40. Klostermann W, Vieregge P, Kompf D. Apraxia of eyelid opening after bilateral stereotaxic subthalamotomy. J Neuroophthalmol. Jun 1997;17(2):122-3. [Medline].
  41. Kerty E, Eidal K. Apraxia of eyelid opening: clinical features and therapy. Eur J Ophthalmol. Mar-Apr 2006;16(2):204-8. [Medline].
  42. Aramideh M, Ongerboer de Visser BW, Koelman JH, Speelman JD. Motor persistence of orbicularis oculi muscle in eyelid-opening disorders. Neurology. May 1995;45(5):897-902. [Medline].
  43. Esteban A, Traba A, Prieto J. Eyelid movements in health and disease. The supranuclear impairment of the palpebral motility. Neurophysiol Clin. Feb 2004;34(1):3-15. [Medline].
  44. Tozlovanu V, Forget R, Iancu A, Boghen D. Prolonged orbicularis oculi activity: a major factor in apraxia of lid opening. Neurology. Sep 25 2001;57(6):1013-8. [Medline].

Apraxia of Lid Opening excerpt

Article Last Updated: Jun 10, 2008