Abstract
The aim of this study is to evaluate the effects of diabetes mellitus, hypertension and hypercholesterolemia on the clinical presentation and outcome of Bell’s palsy. The study (comorbidity) group consisted of 50 patients with Bell’s palsy associated with diabetes, hypertension, or hypercholesterolemia; the control group included 46 patients with Bell’s palsy, but without comorbid diseases. The House–Brackmann grading system (I to VI) was used in order to assess the initial and final facial functions. Both groups of patients were treated with steroids and the antiviral agent acyclovir. The mean severity of initial facial paralysis was more significant in diabetes, hypercholesterolemia, and hypertension, in comparison to the control group. Patients suffering from Bell’s palsy and concomitant comorbidities have a poorer prognosis (HB III-VI) compared to patients without comorbidities. Increased glycosylated hemoglobin A1c levels (>6.7%) were significantly correlated with unsatisfactory facial recovery. The pathogenetic mechanisms by which diabetes, hypercholesterolemia, and hypertension affect the vasa nervosum of facial nerve have been described.
Highlights
Bell’s palsy (BP) is the most common form of acute facial nerve paralysis, with an annual incidence of about 20–30 per 100,000, and a lifetime incidence of one in 60–70 people [1,2].The etiology of BP implicates infective, immune, and ischemic mechanisms; among them, the viral hypothesis remains the most plausible, implying reactivation of neurotropic herpes viruses 1 (HSV-1), 2 (HSV-2), and Varicella zoster virus (HZV) at the level of geniculate ganglion [3,4]
BP [7,8,9]; in this study, we focused on the effect of diabetes mellitus (DM), hypertension (HT), and hypercholesterolemia (HC) on the clinical presentation and outcome of BP
Before treatment of BP, the mean severity (HB grade) of initial facial paralysis was more significant in DM (p < 0.001), HC (p < 0.01), HT (p < 0.05), and in DM combined with HT (p < 0.05), HC (p < 0.01), and HT-HC (p < 0.01), compared to the control group (Table 3)
Summary
Bell’s palsy (BP) is the most common form of acute facial nerve paralysis, with an annual incidence of about 20–30 per 100,000, and a lifetime incidence of one in 60–70 people [1,2].The etiology of BP implicates infective, immune, and ischemic mechanisms; among them, the viral hypothesis remains the most plausible, implying reactivation of neurotropic herpes viruses 1 (HSV-1), 2 (HSV-2), and Varicella zoster virus (HZV) at the level of geniculate ganglion [3,4]. Bell’s palsy (BP) is the most common form of acute facial nerve paralysis, with an annual incidence of about 20–30 per 100,000, and a lifetime incidence of one in 60–70 people [1,2]. Common immune pathways have been advocated for BP and Guillain–Barré syndrome, a cell-mediated, autoimmune neuritis [5]. Microcirculatory disorders induced by atherosclerosis have been reported to increase the accumulation of lipids in the intima of vasa nervosum of facial nerve, resulting in vascular inflammation, luminal obstruction, and ischemia [1]. As the endoneurial pressure increases, damage by either direct mechanical injury or by reducing blood flow occurs from compression of the narrowest portion of the bony facial canal [6]
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