Poster · Headache & Migraine
Body Mass Index and Neurological Disease Severity: A Comparative Preliminary Analysis of Migraine and Peripheral Neuropathy Cohorts in Hawaiʻi
Jaelynn Yim1,3, Lindsay Oshiro1,3, Leigh Antoinette Medina3, Emma O’Keefe3, Katie Siarot3, Natalia Gonzalez, MD3, Barbara Pitts, PhD2, Enrique Carrazana, MD1, Kore Liow, MD1,2
- 1 John A. Burns School of Medicine, University of Hawaiʻi at Mānoa, Honolulu, HI
- 2 Memory Disorders Center, Hawaiʻi Pacific Neuroscience, Honolulu, HI
- 3 MS and Neuroimmunology Center, Hawaiʻi Pacific Neuroscience, Honolulu, HI
Background: Peripheral neuropathy and migraines are common neurological disorders that have each been associated with elevated body mass index (BMI). Obesity has been shown to increase migraine risk by approximately 27%, while metabolic dysfunction associated with higher BMI has also been implicated in the development and progression of peripheral neuropathy. Hawai’i provides a unique setting to study these relationships because of the large Asian, Native Hawaiian and other Pacific Islanders (NHOPIs), with NHOPI populations experiencing the highest obesity rates in the United States (48-50%). The objective of this study is to compare BMI between patients with migraine and peripheral neuropathy and determine whether elevated BMI is associated with greater disease severity in either condition.
Methods: This study conducted a retrospective chart review of patients seen at Hawai’i Pacific Neuroscience between January 2021 and June 2026. Adult patients diagnosed with migraine without aura (ICD-10 G43.009, G43.109, G43.709, G43.909) or peripheral neuropathy (ICD-10 G62.0, G62.1, G62.2, G62.9, E11.40, E11.42) with a documented body mass index (BMI) were identified through the eClinical works electronic health record (EHR) system. Patients diagnosed with both migraine and peripheral neuropathy, including those diagnosed with isolated mononeuropathies, were excluded from the study. The remaining sample size included 152 patients in the peripheral neuropathy cohort (N = 152) and 140 patients (N = 140) in the migraine cohort. Clinical data included demographic characteristics, BMI and disease-specific clinical variables were extracted. Migraine variables included headache frequency, pain severity (on a 1-10 scale), history of procedural interventions and status migrainosus. Peripheral neuropathy variables included neuropathy subtype, ankle reflexes (0 = Dead/Absent, 1 = Sluggish (1+), 2 = Normal (2+)), sensory loss (0 = Normal, 1 = Mild, 2 = Moderate, 3 = Severe) and electrodiagnostic (EMG/NCS) findings (0 = Normal, 1 = Mild/Pure Sensory 2 = Moderate/Sensorimotor, 3 = Severe/Absent). Correlation analyses were performed to evaluate statistical associations between BMI and headache severity in the migraine cohort and between BMI, ankle reflexes and sensory loss in the peripheral neuropathy cohort.
Results: The study examined the relationships between BMI and both migraine severity and peripheral neuropathy severity. While a positive correlation was observed between BMI and headache frequency, it was not statistically significant (r = 0.014, t = 0.17, p = 0.87). In contrast, Spearman rank correlations revealed significant associations between BMI and specific measures of peripheral neuropathy severity. Higher BMI was significantly correlated with both EMG/NCS results (rs = 0.18, t = 2.29, p = 0.02) and sensory loss (rs = 0.19, t = 2.32, p = 0.02). However, no significant correlation was found between BMI and ankle reflex (rs = -0.06, t = -0.83, p = 0.41).
Discussion: The primary objective of this study was to investigate the relationships between BMI, migraine severity, and peripheral neuropathy severity. Our findings revealed that while BMI demonstrated no significant association with migraine frequency, it exhibited a significant positive correlation with objective markers of peripheral neuropathy, specifically, EMG/NCS results and sensory loss. The absence of a statistically significant correlation between BMI and headache frequency (p = 0.87) stands in contrast to some existing literature that names obesity as a risk factor for migraine chronification. This finding may be attributed to our sample's size or the reliance on headache frequency alone rather than standardized migraine disability scores (MIDAS/HIT-6). However our findings suggest that in this cohort, metabolic status does not directly drive migraine recurrence. In contrast, the significant positive rank correlations between BMI and both EMG/NCS results (rs = 0.18) and sensory loss (rs = 0.19) support the growing body of evidence linking higher BMI to peripheral nerve impairment. Increased adiposity is known to promote chronic systemic inflammation, which can induce microvascular damage and axonal degeneration. Interestingly, BMI was not significantly correlated with ankle reflex changes (p = 0.41). This variation suggests that while a higher BMI may impair sensory pathways and electrical conduction, they may not impact deeper motor reflexes. This study highlights a significant association between elevated BMI and peripheral neuropathy severity, contrasted by no apparent relationship between BMI and migraine frequency. Specifically, higher BMI scores correlated with greater EMG/NCS abnormalities and sensory loss, but not ankle reflex. These findings suggest that an elevated BMI may drive peripheral nerve impairment and plays a negligible role in migraine recurrence. This study may highlight the importance of early sensory and electrophysiological screening in patients with higher BMIs to detect peripheral neuropathy before motor deficits occur. Future research is needed to determine whether weight management interventions can prevent progression or reverse these neuropathic changes.