Publications by authors named "Mia Zhang"

5 Publications

  • Page 1 of 1

Superior oblique myokymia treated with levobunolol.

J AAPOS 2018 02 20;22(1):67-69.e2. Epub 2017 Dec 20.

Department of Ophthalmology, Boston Children's Hospital; Department of Ophthalmology, Harvard Medical School. Electronic address:

Superior oblique myokymia (SOM) is an uncommon condition of unclear etiology that results in episodes of oscillopsia and diplopia. There is no established treatment protocol for SOM. We present 2 cases of SOM successfully managed with topical levobunolol 0.5%; both patients responded to a short course of medication administration and required minimal ongoing therapy. Case 1 was a 69-year-old woman with left SOM who had previously undergone a left Harada-Ito procedure. Her SOM improved immediately on administration of levobunolol and was maintained at follow-up 1 year later. Case 2 was a 49-year-old man with right SOM that affected his ability to work. After 2 days of topical levobunolol 0.5% nightly in the right eye, SOM episodes ceased; he continues to use drops intermittently for occasional recurrences.
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http://dx.doi.org/10.1016/j.jaapos.2017.08.010DOI Listing
February 2018

Superior oblique myokymia.

Surv Ophthalmol 2018 Jul - Aug;63(4):507-517. Epub 2017 Oct 19.

Department of Ophthalmology, Boston Children's Hospital, Boston, Massachusetts, USA; Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, USA. Electronic address:

Superior oblique myokymia (SOM) is a rare condition of unclear etiology. We discuss the history, etiology, clinical features, differential diagnoses, management, and prognosis of SOM. We conducted a meta-analysis of all 116 cases published since SOM was first described in 1906. The age at examination was 17-72 years (mean: 42 years.) There was a right-sided preponderance in 61% of cases (P < 0.02) that was statistically significant in females (63%, P < 0.04) but not in males (59%, P = 0.18). The pathophysiology of SOM may be neurovascular compression and/or ephaptic transmission. Although various pharmacological and surgical approaches to SOM treatment have been proposed, the rarity of the condition has made it impossible to conduct clinical trials evaluating the safety and efficacy of these approaches. Recently, topical beta blockers have managed SOM symptoms in a number of cases, including the first case treated with levobunolol. Systemic medications, strabismus surgery, and neurosurgery have been used to control symptoms, with strabismus surgery carrying a moderate risk of postoperative diplopia in downgaze. Although there is no established treatment for SOM, we encourage clinicians to attempt topical levobunolol therapy before considering systemic therapy or surgery.
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http://dx.doi.org/10.1016/j.survophthal.2017.10.005DOI Listing
September 2018

Pathophysiologic relationship between Alzheimer's disease, cerebrovascular disease, and cardiovascular risk: A review and synthesis.

Alzheimers Dement (Amst) 2017 9;7:69-87. Epub 2017 Feb 9.

Lifespan Clinical Research Center, Rhode Island Hospital, Providence, RI, USA; Department of Neurology, Warren Alpert Medical School of Brown University, Providence, RI, USA; Department of Psychiatry and Human Behavior, Warren Alpert Medical School of Brown University, Providence, RI, USA.

As the population ages due to demographic trends and gains in life expectancy, the incidence and prevalence of dementia increases, and the need to understand the etiology and pathogenesis of dementia becomes ever more urgent. Alzheimer's disease (AD), the most common form of dementia, is a complex disease, the mechanisms of which are poorly understood. The more we learn about AD, the more questions are raised about our current conceptual models of disease. In the absence of a cure or the means by which to slow disease progress, it may be prudent to apply our current knowledge of the intersection between AD, cardiovascular disease, and cerebrovascular disease to foster efforts to delay or slow the onset of AD. This review discusses our current understanding of the epidemiology, genetics, and pathophysiology of AD, the intersection between AD and vascular causes of dementia, and proposes future directions for research and prevention.
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http://dx.doi.org/10.1016/j.dadm.2017.01.005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5328683PMC
February 2017

MRI findings of optic pathway involvement in Miller Fisher syndrome in 3 pediatric patients and a review of the literature.

J Clin Neurosci 2017 May 10;39:63-67. Epub 2017 Feb 10.

Department of Pediatrics (Neurology) and of Neurology, Yale School of Medicine, New Haven, CT, United States. Electronic address:

Background: Miller Fisher syndrome (MFS) is a rare demyelinating condition which may have involvement of cranial nerves. There are a few case reports of optic pathway involvement in children. We describe 3 patients with optic pathway enhancement in pediatric patients with MFS.

Case Series: We retrospectively reviewed brain imaging findings in 17 pediatric patients with of Guillain-Barré syndrome (GBS) meeting Brighton criteria who had brain MRIs performed during their acute illness. Cranial nerve enhancement was seen in 6/17 patients and optic nerve/chiasm enhancement was seen in 3 patients.

Conclusion: Cranial nerve enhancement and optic pathway in particular, can be seen in patients with MFS. Imaging findings do not always correlate with clinical manifestations of cranial nerve involvement.
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http://dx.doi.org/10.1016/j.jocn.2016.12.049DOI Listing
May 2017

An encyclopedia of mouse DNA elements (Mouse ENCODE).

Genome Biol 2012 Aug 13;13(8):418. Epub 2012 Aug 13.

To complement the human Encyclopedia of DNA Elements (ENCODE) project and to enable a broad range of mouse genomics efforts, the Mouse ENCODE Consortium is applying the same experimental pipelines developed for human ENCODE to annotate the mouse genome.
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http://dx.doi.org/10.1186/gb-2012-13-8-418DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491367PMC
August 2012
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