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Describe the pathophysiological symptoms and mechanisms that are…
Describe the pathophysiological symptoms and mechanisms that are associated with the main theories of migraine
Para 1
• Migraine is Complex life-span neurological (disruption to nervous system) disorder with poorly understood causes. Unilateral (One hemisphere) or bilateral (Two hemispheres) in nature.
Multifactorial predisposition: Neurological, gastrointestinal and autonomic (autonomic nervous system: breathing, regulation and homeostasis) features.
Phases
• Prodrome phase: Occurs before migraine- issues with concentration, speaking and reading
• Aura: Quite quick: Variety of things, sparks, lights, blind spots, tingling, ear-ringing, temporary loss of vision, change of smells or taste, Severity of headache can vary i.e. mild headache or excruciating,
• Postdrome: Unable to concentrate, depressed, fatigue or feeling euphoria due to excess serotonin. Hangover symptoms come in: Reverse hangover is a migraine.
Headache; Sensitivity or fear or sound of light, hypersomnia, tired
Para 2- Pathophysiology theories
• Neurovascular headache as consequence of blood vessel dilation, Referred pain from dura matter (covers whole of brain) and blood vessels, Dysfunction of brain stem that modulates sensory input: Misunderstanding signals, pain pathway via Trigeminal nerve pathway, Dysfunction to CGRP
• CGRP - Calcitonin Gene-Related Peptide, CGRP Released during blood vessel dilation, CGRP is potent vasodilator and allows blood vessels to dilate and for blood to flow. , CGRP associated with pain pathways, Link to gut-brain axis (foods can cause dysfunction)- What’s going on in gut can feed up to brain. More CGRP means more migraines. Mallick-Searle & Moriaty 2020
• Gut-brain axis- - Healthy Gut-Normal gut microbiota, Healthy levels of Inflammatory cells and/or mediators, Normal brain function BUT INCREASED GUT PERMEABILITY Intestinal Dysbiosis, altered levels of lipopolysaccharides, Inflammatory cells and/or mediators, changes in brain function – e.g. vagus nerve (sends more signals to dilate blood vessels) alterations in brain function results in migraines
(Van Hemert et al 2014)
Para 3 Pathophysiology continued
• Cortical Spreading depression is process that contributes to migraines. Initial wave of neuronal depolarization (action potential starts, signal sent through nerves).
Synchronised depolarisation done at same time. CSD continues moving forward – 2-6 mm/min. Relates to aura stage and photophobia.
As moves forward, area in front of wavefront has inhibitory and slower activity. Area behind wave front = inhibited cortical activity and reduced blood flow , which can cause migraine-related features such as auras (Olsen et al 2009).
• The pathophysiology behind Auras =Over stimulation of trigeminal pathway via CGRP, Nociceptive/pain signalling increases CSD starts Change in cortical activity = photophobia, phonophobia and other features e.g. auras. Rattanawong et al., 2022.
Para 4 Treatment for Pathophysiology
• Topiramate/Gabapentin – epilepsy drugs: possibly disrupting CSD (Cortical spreading depression). Propranolol BetaBlockers (in this case, controlling vascular system and blood)
• Probiotics- involves the use of micro-organisms and bacteria to treat migraines, with a possible mechanism being to strengthen intestinal wall. (Van Hemert et al., 2014)
• Also CGRP antagonists try to inhibit stimuli of Trigeminal Nucleus to prevent the vasodilation process that leads to pain. (Pellesi et al 2020)
• Systematic literature review was conducted and involved 2 studies.
However, the review found contradicting findings, with the 1st paper not showing significant changes between probiotic and placebo group in terms of migraine frequency, but Martami et al saw a reduction in migraine frequency of 9.6 days per month for chronic migraine group and 2.6 days for episodic group. per month compared to placebo.
Due to contrasting findings, more research should be done to investigate effectiveness of probiotics as a treatment for migraines. (Naghibi et al., 2019)
Conclusion
There are numerous pathophysiological features associated with migraines and there are numerous treatments that aim to resolve issues within human pathophysiology in order to relieve people of migraines.
One limitation of focusing on pathophysiology is that other factors such as genetics and non-biological factors that may influence migraines such as environmental triggers and emotional changes are being ignored in favour of one route of explanation.
The focus on pathophysiology associated with migraines may reduce credibility o the explanation due to the ignorance of other triggers and factors that may cause migraine.