Narrowing of the palpebral fissure in diabetes

Abstract

In 204 adult, white diabetics the palpebral fissure was measured and related to the state of metabolic control of the diabetes. A control group was formed of 204 persons matched by age and sex. The average palpebral fissure in the control group was 9.9 mm: there was a slight, but not significant, difference between the age groups and the sexes. In diabetics who were not insulin dependent the average width of the palpebral fissure was found to be 9.4 mm; in severe chronic deregulation of the diabetes, however, an average palpebral fissure of 8.0 mm was found, a significant narrowing. In insulin-dependent diabetics the average width of the palpebral fissure was 8.3 mm. This significant narrowing also increased if there was severe chronic deregulation of the diabetes. The average palpebral fissure associated with proliferative retinopathy in insulin-dependent type 1 diabetics was 6.0 mm (nearly 4 X standard deviation). This ptosis in diabetes is very probably due to chronic tissue hypoxia, to which the levator palpebrae muscle is probably extra sensitive, and in which thickening of the basal membrane of the capillaries may be one of the most important factors.

Palpebral Fissure Response to Phenylephrine Indicates Autonomic Dysfunction in Patients With Type 1 Diabetes and Polyneuropathy

“…Although Müller's muscle is admittedly dependent on sympathetic stimulation, it can also be influenced by other factors such as gaze direction, flexion or extension of the neck, and orbicularis oculi tone. We found a small, although highly significant difference in PFH between the treated eye and the untreated eye (∆PFH), in accordance with the measures reported by Bastiaensen et al 6 in a cohort of patients with insulin-dependent diabetes. The ∆PFH response in healthy particpants 3 – 5 is up to 70% higher in comparison with our measures, indicating a loss of sympathetic reserve capacity caused by decreased adrenergic excitability and autonomic dysfunction .…”

“…DAN leads to sympathetic paresis characterized by miosis and ptosis. 6 , 8 Pupillary denervation hypersensitivity to phenylephrine has been shown in diabetes 10 , 11 ; however, to our knowledge, denervation hypersensitivity to phenylephrine has not been investigated in DAN. In the case of denervation hypersensitivity, an increased ∆PFH response would be expected.…”

“…On average, people with diabetes who depend on insulin had a PFH of 8.3 mm, whereas healthy controls had a PFH of 9.9. 6 This decrease is associated with disease duration (in insulin-dependent diabetes) and with the severity of diabetic retinopathy (DR). 6 Thus, PFH may reveal a proxy of the autonomic sympathetic function and potentially serve as a cheap, sensitive clinical indicator of the sympathetic drive.…”

Obesity as a Potential Risk Factor for Blepharoptosis: The Korea National Health and Nutrition Examination Survey 2008-2010

“…Bastiaensen assumed that the cause of acute blepharoptosis in patients with diabetes is mostly oculomotor nerve palsy [ 23 ]. In another report, Bastiaensen identified blepharoptosis comorbidity in a large number of patients with diabetes and presumed that this finding may have been related to chronic tissue hypoxia, to which the levator palpebrae muscle is extra-sensitive, and in which thickening of the basal membrane of the capillaries may be an important factor [ 24 ].…”

Sarcopenia as a potential risk factor for senile blepharoptosis: Nationwide Surveys (KNHANES 2008–2011)

“…Several studies have reported that blepharoptosis is related to systemic diseases, such as hypertension, diabetes, dyslipidemia, and obesity 16,17,22,[26][27][28][29] . In these reports, the causative mechanisms of these relationships were suggested to be end-organ damage related to metabolic syndrome.…”