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Background: Autonomic dysfunction and hypersensitivity to light are core features of the migraine attack, and there is growing evidence that alterations in these parameters also exist between attacks. Though sensory and autonomic responses likely interact, they have not been studied together in migraine patients. Methods: Interictal photophobia thresholds (PPT) were tested in 36 migraineurs (14 episodic, EM; 12 chronic, CM; 10 probable, PM) and 24 age-and sex-matched nonheadache controls using a rheostat-modulated halogen light and digital infrared pupillometry. Quantitative pupillary light reflex (PLR) in response to a brief pulse of light was also assessed in a subset of individuals; parameters included dark adapted baseline pupil size, as well as measures of parasympathetic (constriction latency, constriction velocity, amplitude constriction) and sympathetic (re-dilation velocity, percent recovery at 5 seconds) arms of the light reflex arc. Migraine diagnoses were made using a structured questionnaire based on the International Classification of Headache Disorders II; the questionnaire also included HIT-6, MIDAS, and PHQ-9. Clinical and pupillary parameters were compared between migraineurs and controls. Among migraineurs, correlations between physiological and clinical parameters were calculated. Results: PPT was lower in migraineurs than nonheadache controls; this difference was most significant in CM (CM>EM5PM>NH). Lower PPT also correlated with smaller dark-adapted pupil size and impaired sympathetically mediated re-dilation at 5 seconds. In addition, measures of sympathetic re-dilation were significantly reduced in migraineurs with HIT-6 over 50 and MIDAS greater than 6. When compared to non-headache controls, migraineurs also had reduced constriction velocity on PLR testing, a parasympathetically mediated function. Conclusion: This study provides evidence that lower photophobia thresholds between migraine attacks may be associated with interictal alterations in pupillary responses to light. Mechanisms underlying these pupillary function changes could link to centrally mediated adaptations to chronic light sensitivity. Significant differences with measures of headache impact and chronicity suggest these differences are clinically meaningful. Background: Deficient habituation of evoked cortical responses characterizes episodic migraine patients between attacks and is probably secondary to a thalamocortical dysrhythmia. Some preventive anti-migraine drugs such as beta-blockers are able to normalize habituation of cortical potentials, and this effect is correlated with their therapeutic response. In a recent study, noninvasive vagus nerve stimulation (nVNS) was effective for migraine attack treatment. In patients with refractory epilepsy, invasive VNS modulated thalamic and cortical activities. We therefore hypothesized that nVNS with gammaCore V R could modify the habituation of evoked responses in migraine patients between attacks. The objective of this study was to determine the effect of one session of ...
Background: Autonomic dysfunction and hypersensitivity to light are core features of the migraine attack, and there is growing evidence that alterations in these parameters also exist between attacks. Though sensory and autonomic responses likely interact, they have not been studied together in migraine patients. Methods: Interictal photophobia thresholds (PPT) were tested in 36 migraineurs (14 episodic, EM; 12 chronic, CM; 10 probable, PM) and 24 age-and sex-matched nonheadache controls using a rheostat-modulated halogen light and digital infrared pupillometry. Quantitative pupillary light reflex (PLR) in response to a brief pulse of light was also assessed in a subset of individuals; parameters included dark adapted baseline pupil size, as well as measures of parasympathetic (constriction latency, constriction velocity, amplitude constriction) and sympathetic (re-dilation velocity, percent recovery at 5 seconds) arms of the light reflex arc. Migraine diagnoses were made using a structured questionnaire based on the International Classification of Headache Disorders II; the questionnaire also included HIT-6, MIDAS, and PHQ-9. Clinical and pupillary parameters were compared between migraineurs and controls. Among migraineurs, correlations between physiological and clinical parameters were calculated. Results: PPT was lower in migraineurs than nonheadache controls; this difference was most significant in CM (CM>EM5PM>NH). Lower PPT also correlated with smaller dark-adapted pupil size and impaired sympathetically mediated re-dilation at 5 seconds. In addition, measures of sympathetic re-dilation were significantly reduced in migraineurs with HIT-6 over 50 and MIDAS greater than 6. When compared to non-headache controls, migraineurs also had reduced constriction velocity on PLR testing, a parasympathetically mediated function. Conclusion: This study provides evidence that lower photophobia thresholds between migraine attacks may be associated with interictal alterations in pupillary responses to light. Mechanisms underlying these pupillary function changes could link to centrally mediated adaptations to chronic light sensitivity. Significant differences with measures of headache impact and chronicity suggest these differences are clinically meaningful. Background: Deficient habituation of evoked cortical responses characterizes episodic migraine patients between attacks and is probably secondary to a thalamocortical dysrhythmia. Some preventive anti-migraine drugs such as beta-blockers are able to normalize habituation of cortical potentials, and this effect is correlated with their therapeutic response. In a recent study, noninvasive vagus nerve stimulation (nVNS) was effective for migraine attack treatment. In patients with refractory epilepsy, invasive VNS modulated thalamic and cortical activities. We therefore hypothesized that nVNS with gammaCore V R could modify the habituation of evoked responses in migraine patients between attacks. The objective of this study was to determine the effect of one session of ...
ImportancePostdural puncture headache (PDPH) can follow unintentional dural puncture during epidural techniques or intentional dural puncture during neuraxial procedures, such as a lumbar puncture or spinal anesthesia. Evidence-based guidance on the prevention, diagnosis, and management of this condition is, however, currently lacking.ObjectiveTo fill the practice guidelines void and provide comprehensive information and patient-centric recommendations for preventing, diagnosing, and managing PDPH.Evidence ReviewWith input from committee members and stakeholders of 6 participating professional societies, 10 review questions that were deemed important for the prevention, diagnosis, and management of PDPH were developed. A literature search for each question was performed in MEDLINE on March 2, 2022. Additional relevant clinical trials, systematic reviews, and research studies published through March 2022 were also considered for practice guideline development and shared with collaborator groups. Each group submitted a structured narrative review along with recommendations that were rated according to the US Preventive Services Task Force grading of evidence. Collaborators were asked to vote anonymously on each recommendation using 2 rounds of a modified Delphi approach.FindingsAfter 2 rounds of electronic voting by a 21-member multidisciplinary collaborator team, 47 recommendations were generated to provide guidance on the risk factors for and the prevention, diagnosis, and management of PDPH, along with ratings for the strength and certainty of evidence. A 90% to 100% consensus was obtained for almost all recommendations. Several recommendations were rated as having moderate to low certainty. Opportunities for future research were identified.Conclusions and RelevanceResults of this consensus statement suggest that current approaches to the treatment and management of PDPH are not uniform due to the paucity of evidence. The practice guidelines, however, provide a framework for individual clinicians to assess PDPH risk, confirm the diagnosis, and adopt a systematic approach to its management.
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