Parkinson's Disease With Visual Hallucinations Is Associated With Epileptiform Activity on EEG

Background: Visual hallucinations (VHs) in Parkinson's disease (PD) are the cardinal symptoms which declare the onset of PD psychosis (PDP). The anthropomorphic and zoomorphic VHs of PD resemble those of Charles Bonnet syndrome and temporal lobe epilepsy. In both of these disorders electroencephalography (EEG) abnormalities have been described. We therefore sought to examine whether VHs in PD were associated with similar EEG abnormalities.Methods: This retrospective observational study searched the medical records of 300 PD patients and filtered for those containing clinical 20-min scalp EEGs. Remaining records were separated into two groups: patients with reported VHs and those without. The prevalence of epileptiform discharges in the EEGs of both groups was identified.Results: Epileptiform discharges were present in 5 of 13 (38.5%) PD patients with VHs; all localized to the temporal lobe. No epileptiform discharges were observed in the EEGs of the 31 PD patients without VHs.Conclusion: The significantly high incidence of temporal lobe epileptiform discharges in PD patients with VHs as compared to those without VHs lends to the possibility of an association visual cortex epileptogenic focus. Accordingly, for treatment-refractory patients, antiepileptic drugs might be considered, as in the case of Charles Bonnet syndrome, temporal lobe epilepsy and migraine with visual aura. Future prospective studies involving larger samples and multi-center cohorts are required to validate these observational findings.

Prevalence and impact of visual aura in migraine and probable migraine: a population study

Visual aura (VA) presents in 98% of cases of migraine with aura. However, data on its prevalence and impact in individuals with migraine and probable migraine (PM) are limited. Data from the nation-wide, population-based Circannual Change in Headache and Sleep Study were collected. Participants with VA rating scale scores ≥ 3 were classified as having VA. Of 3,030 participants, 170 (5.6%) and 337 (11.1%) had migraine and PM, respectively; VA prevalence did not differ between these cohorts (29.4% [50/170] vs. 24.3% [82/337], p = 0.219). Participants with migraine with VA had a higher headache frequency per month (4.0 [2.0–10.0] vs. 2.0 [1.0–4.8], p = 0.014) and more severe cutaneous allodynia (12-item Allodynia Symptom Checklist score; 3.0 [1.0–8.0] vs. 2.0 [0.0–4.8], p = 0.046) than those without VA. Participants with PM with VA had a higher headache frequency per month (2.0 [2.0–8.0] vs. 2.0 [0.6–4.0], p = 0.001), greater disability (Migraine Disability Assessment score; 10.0 [5.0–26.3] vs. 5.0 [2.0–12.0], p < 0.001), and more severe cutaneous allodynia (12-item Allodynia Symptom Checklist score, 2.5 [0.0–6.0] vs. 0.0 [0.0–3.0], p < 0.001) than those without VA. VA prevalence was similar between migraine and PM. Some symptoms were more severe in the presence of VA.

Have You Seen A Kaleidoscope? A Case of Visual Migraine Aura

This is a case of migraine, presenting with the interesting visual aura of a ‘kaleidoscope’: waves with flickering movements made up of a variety of colors (red, blue, green, yellow), commencing laterally and spreading superiorly in the visual field of the left eye. This description is quite similar to a fortification spectrum, which usually expands and spreads in a C-shape fashion over one side of the visual field. Several different possible pathophysiological explanation are shared as well as the common differential diagnoses. In the work up of a patient with visual aura migraine, a comprehensive and detailed history is important, together with the appropriate investigations, in order not to miss any serious syndromes, including stroke syndromes and epilepsy.

Effect of Maternal Migraine during Gestation and Delivery Outcomes

Background: Migraine is defined as a condition accompanied with head ache, nausea, visual and sound sensitivity. Objective: To determine the effect of migraine on maternal and neonatal health. Study Design: Case control study Place and Duration of Study: Department of Obstetrics & Gynaecology, Sandeman Provincial Hospital, Quetta from 1st August 2018 to 31st August 2021. Methodology: One hundred pregnant women divided into migraine and non-migraine groups were enrolled. Both groups were assessed for their sociodemographic, clinical and biochemical status. Their information was documented. Results: Group I females were above 36 years of age and were in their first trimester. There were 56% women who did not presented visual aura. More irritability, pre-term labour and preeclampsia, risk of C section and hypertension was noticed in group I than Group II. Conclusion: Migraine is linked with higher risk of hypertension, preeclampsia, C section and low birth weight new born. Key words: Migraine, Pregnancy, Low birth weight

Parenchymal neuroinflammatory signaling and dural neurogenic inflammation in migraine

Background Pain is generally concomitant with an inflammatory reaction at the site where the nociceptive fibers are activated. Rodent studies suggest that a sterile meningeal inflammatory signaling cascade may play a role in migraine headache as well. Experimental studies also suggest that a parenchymal inflammatory signaling cascade may report the non-homeostatic conditions in brain to the meninges to induce headache. However, how these signaling mechanisms function in patients is unclear and debated. Our aim is to discuss the role of inflammatory signaling in migraine pathophysiology in light of recent developments. Body Rodent studies suggest that a sterile meningeal inflammatory reaction can be initiated by release of peptides from active trigeminocervical C-fibers and stimulation of resident macrophages and dendritic/mast cells. This inflammatory reaction might be needed for sustained stimulation and sensitization of meningeal nociceptors after initial activation along with ganglionic and central mechanisms. Most migraines likely have cerebral origin as suggested by prodromal neurologic symptoms. Based on rodent studies, a parenchymal inflammatory signaling cascade has been proposed as a potential mechanism linking cortical spreading depolarization (CSD) to meningeal nociception. A recent PET/MRI study using a sensitive inflammation marker showed the presence of meningeal inflammatory activity in migraine with aura patients over the occipital cortex generating the visual aura. These studies also suggest the presence of a parenchymal inflammatory activity, supporting the experimental findings. In rodents, parenchymal inflammatory signaling has also been shown to be activated by migraine triggers such as sleep deprivation without requiring a CSD because of the resultant transcriptional changes, predisposing to inadequate synaptic energy supply during intense excitatory transmission. Thus, it may be hypothesized that neuronal stress created by either CSD or synaptic activity-energy mismatch could both initiate a parenchymal inflammatory signaling cascade, propagating to the meninges, where it is converted to a lasting headache with or without aura. Conclusion Experimental studies in animals and emerging imaging findings from patients warrant further research to gain deeper insight to the complex role of inflammatory signaling in headache generation in migraine.

From “Transient Hemiopsia” to Migraine Aura

This paper outlines the historical development of the concept of the visual aura of migraine, from the first comprehensive published description by the physician Hubert Airy, in 1870. Airy’s description of the phenomenon he called “transient hemiopsia” became widely copied and highly influential as a consequence of the language and images that he used in his presentation. This paper outlines the subsequent development of theories of aura from the time of Airy’s publication to the first demonstration of spreading oligaemia by Lautitzen and Olesen in the 1980s.

Polygenic risk provides biological validity for the ICHD-3 criteria among Finnish migraine families

Background Migraine is diagnosed using the extensively field-tested International Classification of Headache Disorders (ICHD-3) consensus criteria derived by the International Headache Society. To evaluate the criteria in respect to a measurable biomarker, we studied the relationship between the main ICHD-3 criteria and the polygenic risk score, a measure of common variant burden in migraine. Methods We used linear mixed models to study the correlation of ICHD-3 diagnostic criteria, underlying symptoms, and main diagnoses with the polygenic risk score of migraine in a cohort of 8602 individuals from the Finnish Migraine Genome Project. Results Main diagnostic categories and all underlying diagnostic criteria formed a consistent continuum along the increasing polygenic burden. Polygenic risk was associated with the heterogeneous clinical picture starting from the non-migraine headache (mean 0.07; 95% CI 0.02–0.12; p = 0.008 compared to the non-headache group), to probable migraine (mean 0.13; 95% CI 0.08–0.18; p < 0.001), migraine headache (mean 0.17; 95% CI 0.14–0.21; p < 0.001) and migraine with typical visual aura (mean 0.29; 95% CI 0.26–0.33; p < 0.001), all the way to the hemiplegic aura (mean 0.37; 95% CI 0.31–0.43; p < 0.001). All individual ICHD-3 symptoms and the total number of reported symptoms, a surrogate of migraine complexity, demonstrated a clear inclination with an increasing polygenic risk. Conclusions The complex migraine phenotype progressively follows the polygenic burden from individuals with no headache to non-migrainous headache and up to patients with attacks manifesting all the features of the ICHD-3 headache and aura. Results provide further biological support for the ICHD-3 diagnostic criteria.