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Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Myerson’s sign, listed as a primitive reflex only by DeJong and Walton, is most often described by recent authors as a finding in Parkinson’s disease (e.g., A&V, p. 876; Rowl, p. 530; Bann, p. 342; MP&S, p. 35–36, 41–42), associated with focal damage in the substantia nigra—an extrapyramidal brain-stem structure—rather than with diffuse cerebral or bilateral pyramidal damage.3 Presumably, this is why other authors do not include Myerson’s sign as a primitive reflex. DeJong, however, claims that Myerson’s sign is present not only in “extrapyramidal disease” but also in “pyramidal tract disease” and “diffuse cerebral disease” (1979, p. 486), which may account for his listing it as a primitive reflex. On the other hand, Walton does not describe any association of Myerson’s sign with diffuse cerebral or bilateral pyramidal damage, so he may simply be using the term “primitive reflexes” in a broader sense, not as limited by the site of underlying pathology.
Neuro-ophthalmology of movement disorders
Published in Expert Review of Ophthalmology, 2018
The most common sensory ocular complaints reported by two-thirds of PD patients are dry eyes, burning eye pain, tearing, and photophobia indicating ocular surface irritation and resembling the symptoms of ocular discomfort reported by the patients with blepharospasm [1]. Reduced blink rate, a common feature of PD, is another manifestation of hypokinesia associated with brain dopaminergic deficit and contributing to the characteristic ‘parkinsonian stare’ and ‘masked facies’ (hypomimia). Dry eyes can also complicate treatment with anticholinergic drugs sometimes used in the treatment of PD-related tremor. Reduced blink rate in patients with PD and other parkinsonian disorders often coexists with glabellar reflex, also known as ‘Myerson sign,’ presenting as non-suppression of blinking with repetitive tapping of the glabella [2]. Corneal sub-basal nerve density was found to be markedly reduced in 15 patients with PD as compared to healthy controls but its influence on blink rate remains unclear [3]. Another study found no difference in sub-basal nerve density between patients with PD, progressive supranuclear palsy (PSP), and healthy controls but reported decreased corneal sensitivity in PD and PSP patients that correlated with decreased blink rate [4]. In one study, 3.3% of patients with PD (and 7.4% of those with atypical parkinsonism) had blepharospasm with or without apraxia of eyelid opening (discussed later) [5]. Although blepharospasm can result from primary basal ganglia dysfunction, its pathophysiology in PD might be more complex and can include a component of peripherally induced blepharospasm secondary to ocular surface irritation [6].