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Introduction: On March 11, 2020, the World Health Organization sounded the COVID-19 pandemic alarm. While efforts in the first few months focused on reducing the mortality of infected patients, there is increasing data on the effects of long-term infection (Post-COVID-19 condition). Among the different symptoms described after acute infection, those derived from autonomic dysfunction are especially frequent and limiting. Objective: To conduct a narrative review synthesizing current evidence of the signs and symptoms of dysautonomia in patients diagnosed with COVID-19, together with a compilation of available treatment guidelines. Results: Autonomic dysfunction associated with SARS-CoV-2 infection occurs at different temporal stages. Some of the proposed pathophysiological mechanisms include direct tissue damage, immune dysregulation, hormonal disturbances, elevated cytokine levels, and persistent low-grade infection. Acute autonomic dysfunction has a direct impact on the mortality risk, given its repercussions on the respiratory, cardiovascular, and neurological systems. Iatrogenic autonomic dysfunction is a side effect caused by the drugs used and/or admission to the intensive care unit. Finally, late dysautonomia occurs in 2.5% of patients with Post-COVID-19 condition. While orthostatic hypotension and neurally-mediated syncope should be considered, postural orthostatic tachycardia syndrome (POTS) appears to be the most common autonomic phenotype among these patients. A review of diagnostic and treatment guidelines focused on each type of dysautonomic condition was done. Conclusion: Symptoms deriving from autonomic dysfunction involvement are common in those affected by COVID-19. These symptoms have a great impact on the quality of life both in the short and medium to long term. A better understanding of the pathophysiological mechanisms of Post-COVID manifestations that affect the autonomic nervous system, and targeted therapeutic management could help reduce the sequelae of COVID-19, especially if we act in the earliest phases of the disease.
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Introduction: The coronavirus disease 2019 (COVID-19) pandemic represents a unified lifestyle modification model, which was developed by the globally applied measures. The lockdowns designed the perfect study settings for observing the interaction between migraine and the adopted changes in lifestyle. An experiment in vivo took place unexpectedly to determine how the lockdown lifestyle modifications can influence migraine. Subsection 1: Overall lifestyle modifications during the pandemic: People stay home, and outdoor activities and public contacts are restricted. Sleep is disturbed. Media exposure and prolonged screen use are increased. Working conditions change. In-person consultations and therapies are canceled. The beneficial effects of short-term stress, together with the harmful effects of chronic stress, were observed during the pandemic. Subsection 2: Short-term effects: Substantial lifestyle changes happened, and knowing how vulnerable migraine patients are, one could hypothesize that this would have resulted in severe worsening of headache. Surprisingly, even though the impacts of changing social conditions were significant, some patients (including children) experienced a reduction in their migraine during the first lockdown. Subsection 3: Long-term effects: Unfortunately, headache frequency returned to the basal state during the second pandemic wave. The risk factors that could have led to this worsening are the long-term disruption of sleep and dietary habits, stress, anxiety, depression, non-compliance to treatment, and working during the pandemic. Discussion: Sudden short-term lifestyle changes taking migraine patients out of their usual routine may be beneficial for headache management. It is not necessary to have a natural disaster in place for a drastic lifestyle modification with 6-8-week duration, if we know that this will improve migraine.
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OBJECTIVE: In the present work, we conduct a narrative review of the most relevant literature on cutaneous allodynia (CA) in migraine. BACKGROUND: CA is regarded as the perception of pain in response to non-noxious skin stimulation. The number of research studies relating to CA and migraine has increased strikingly over the last few decades. Therefore, the clinician treating migraine patients must recognize this common symptom and have up-to-date knowledge of its importance from the pathophysiological, diagnostic, prognostic and therapeutic point of view. METHODS: We performed a comprehensive narrative review to analyze existing literature regarding CA in migraine, with a special focus on epidemiology, pathophysiology, assessment methods, risk for chronification, diagnosis and management. PubMed and the Cochrane databases were used for the literature search. RESULTS: The prevalence of CA in patients with migraine is approximately 60%. The mechanisms underlying CA in migraine are not completely clarified but include a sensitization phenomenon at different levels of the trigemino-talamo-cortical nociceptive pathway and dysfunction of brainstem and cortical areas that modulate thalamocortical inputs. The gold standard for the assessment of CA is quantitative sensory testing (QST), but the validated Allodynia 12-item questionnaire is preferred in clinical setting. The presence of CA is associated with an increased risk of migraine chronification and has therapeutic implications. CONCLUSIONS: CA is a marker of central sensitization in patients with migraine that has been associated with an increased risk of chronification and may influence therapeutic decisions.
