Neurological injury in primary Sjogren’s syndrome

The incidence of neurological injury in primary Sjogren’s syndrome varies between 2.5 and 60%. The authors aimed to evaluate its prevalence and characteristics in patients with primary Sjogren’s syndrome in a sample of the Syrian population. PATIENTS AND METHODS: Forty-eight patients with primary Sjogren’s syndrome, attending outpatient clinics at Damascus Hospital between January 2020 and January 2022 in this cross-sectional study at the outpatient clinics, were interviewed and examined, and the necessary laboratory and radiological examinations were demanded. Information was collected on disease duration, onset time, and patterns of neurological symptoms. RESULTS: Forty-eight patients, including 42 females, aged 56.1±10.3 years were enroled. Central nervous system involvement was found in 34 patients. 85% of patients had generalized nerve manifestations, while local nerve manifestations were found in 77,5% of patients. The common neurological manifestation was headaches, then cognitive disorders, and the most common pattern of headache was migraine. Beck Depression Index showed a significant increase in the apathy evaluation scale. The study of cognitive changes showed a significant increase in the Mini-Mental State Examination (MMSE) index. Carotid Doppler showed the presence of injury in 42.4% of patients. The magnetic resonance imaging showed positive findings in 21 patients and positive evoked potentials in 52% of patients. DISCUSSION: Studies showing the prevalence of Sjogren’s neurological injury patterns are insufficient, but this was changed when the criteria for diagnosing Sjogren’s syndrome was modified, and the definition of neurological traits in the context of the syndrome was expanded. The presence of a high rate of headaches, cognitive changes, and fatigue confirms that generalized nervous system injuries are more common than local injuries. Migraine was the most common pattern of headache found in patients with the syndrome compared with other patterns such as tension headaches and headaches due to medications, especially analgesics. This was associated with the presence of anti-SSA antibodies and Raynaud’s phenomenon, which suggest that the headache mechanism may be due to vascular endothelial dysfunction or an immune-mediated inflammation injury of the neurovascular system. The changes that appeared on the MRI images suggested premotor cortex involvement rather than mesolimbic cortical impairment, and its presence was also associated with SSA antibody positivity, and it is caused by inflammation. CONCLUSION: Primary Sjogren’s syndrome should be considered as having any unspecified or specific neurological disorder.