In a systematic review entitled “Mental Health Outcomes in Guillain–Barre Syndrome and Chronic Inflammatory Demyelinating Polyneuropathy” published in this issue of the Canadian Journal of Neurological Sciences, ^{Reference Li, Wong and Fabiano1} Li et al. reported several studies that showed increased incidence of mental health disorders including anxiety, depression and reactive psychosis in patients with Gullain–Barre syndrome. Even though up to half of the patients with chronic inflammatory demyelinating polyneuropathy (CIDP) describe mental health symptoms, so far these issues have not been systematically explored.

This review is of great clinical relevance as it highlights the often overlooked and underappreciated cognitive comorbidities in conditions that are generally thought to only affect the peripheral nervous system (PNS). In a study by Yalachkov et al. (2020), they found that CIDP patients who had blood-brain barrier dysfunction were more likely to fail neuropsychological tests, ^{Reference Yalachkov, Uhlmann and Bergmann2} suggesting that neural inflammation in the PNS could potentially spread through the blood-brain barrier into the brain. In addition to mood symptoms, other cognitive dysfunctions have also been found. In a study by Lochmann et al. (2003) on 29 patients with CIDP, executive function including verbal fluency and digit span processing was significantly impaired. ^{Reference Lochmann, Wyrobnik and Kupper3}

In addition to inflammatory demyelinating polyneuropathies, the neurophysiological basis for cognitive dysfunction in other inflammatory diseases previously thought to be confined to the PNS is also becoming increasingly recognized. In a recent paper in the journal Nature, Eyting et al. (2025) evaluated the development of dementia in older individuals in Wales who received the herpes zoster vaccine for the prevention of shingles. ^{Reference Eyting, Xie and Michalik4} Of the 296,324 individuals studied, they showed that those who were vaccinated had a 20% relative risk reduction in developing dementia compared to age-matched controls. The underlying reasons for this are likely due to reduced risk of reactivation of the herpes zoster virus in the dorsal root ganglion as well as through immunomodulatory effects independent of the virus. In animal models, these processes have been shown to result in vasculopathy, amyloid deposition, tau protein aggregation and neuro-inflammation in the brain. ^{Reference Nagel and Bubak5}