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Migraine Headaches
Published in Alexander R. Toftness, Incredible Consequences of Brain Injury, 2023
Today's prevailing theories about what causes migraines are much more complex. Researchers have traced the causes to neurological dysfunction in the brain stem and other brain regions, although the precise neuronal mechanisms remain unknown (Goadsby et al., 2017). Importantly, the brain stem dysfunction seems to contribute to cortical spreading depression, which is when neurons get excited and then inhibited in a wave pattern, which is what causes the aura symptoms (Tfelt-Hansen, 2009). Depending on where in the brain the cortical spreading depression is happening, the symptoms vary from person to person, leading to those various visual, sensory, and aphasic categories of auras that I elaborated on earlier. It may be a small consolation to those suffering through the pain of a migraine, but it's a cool fact that we can somewhat tell which of your neurons are “doing the wave” based on your aura symptoms.
Regenerative Medicine in Pain Management
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Sharon McQuillan, Rafael Gonzalez
The exact pathophysiology of migraine is not exactly known. There seems to be a hereditary component, as high as 50%. Most research points to the activation and sensitization of neurons in the trigeminal nerve as the trigger to migraine headaches. There are two possible theories as to how the nerve is aggravated—cortical spreading depression (CSD) and neurogenic inflammation. Cortical spreading depression is a wave of neural excitation activity followed by the depolarization of neurons. This may explain the aura some patients experience before the migraine episode. Neurogenic inflammation theory proposes that inflammatory neuropeptides lead to vasodilation and mast cell degranulation, followed by a release of various inflammatory compounds.87
Therapeutic Gases for Neurological Disorders
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
R. Rachana, Tanya Gupta, Saumya Yadav, Manisha Singh
When NO level reduces, the brain becomes more vulnerable to cortical spreading depression. However, optimum levels of NO take actions for the restoration of impaired cerebrovascular reactivity that occurs after CSD. Therefore, while NO signaling has a key responsibility for the blood flow changes occurring after SAH, its reduction has a significant function in early brain injury, microthrombus formation, and cortical spreading depression. To prevent secondary neuronal injury, targeting this pathway may be beneficial and thus may partially restore physiological blood flow (Garry et al., 2014).
Central vestibular dysfunction: don’t forget vestibular rehabilitation
Published in Expert Review of Neurotherapeutics, 2022
Sulin Zhang, Dan Liu, E. Tian, Jun Wang, Zhaoqi Guo, Weijia Kong
Pathogenesis of VM is still poorly understood and researchers fail to agree regarding whether its origin is predominantly central or peripheral. The factors involved in the pathogenesis of VM do not work separately but are intricately interwoven [81,82]. Abnormal sensory modulation or integration within the thalamo-cortical network could result in dizziness and spatial disorientation, which may lead to a ‘higher level’ dysfunction of the multisensory integration function of spatial orientation. Activities such as ballet dancing and yoga can enhance spatial perception and physical coordination [64]. Cortical spreading depression hypothesis assumes that, during aura migraine, various factors stimulate the cerebral cortex and then the inhibitory cortical electrical activity spreads from the stimulation site to the surrounding regions. Vestibular connections can be divided into downward-projecting vestibulospinal tracts and upward projections [i.e. to the ocular motor nuclei that organize the VOR] [83]. When it diffuses to the vestibular cortex (the parietal lobe and insular lobe), the activity is inhibited, and the inhibitory effect on the brainstem vestibular nucleus is weakened, thereby affecting the processing of vestibular signals and causing vestibular symptoms, or leading to transient vestibulo-ocular dysfunction or vestibular hypersensitivity associated with migraine [84].
Neonatal treatment with ovarian hormones and suckling among distinct litter sizes: Differential effects on recognition memory and spreading depression at adulthood
Published in Nutritional Neuroscience, 2019
Noranege Epifânio Accioly, Rubem Carlos Araújo Guedes
It is now well established that some of the neuronal actions of ovarian hormones involve brain excitability.3 This issue can be experimentally addressed by analyzing the electrophysiological phenomenon known as cortical spreading depression (CSD10–12). CSD is a reversible wave of self-propagating depolarization of the cerebral cortex in response to electrical, chemical, or mechanical stimulation of one point of the cortical surface. The cerebral cortex response consists of a reduction of its spontaneous and evoked electrical activity that spreads concentrically from the stimulated point. CSD presents characteristic ionic, metabolic and hemodynamic changes that return to the pre-CSD levels after a few minutes.13,14 Compelling clinical and experimental evidence has linked CSD to excitability disorders of the human brain and their diseases such as migraine with aura and brain vascular disorders,15 and epilepsy.16 In the human neocortex during the aura phase of migraine attacks, CSD-like waves have been detected.17
Meta-analysis of randomized trials on percutaneous patent foramen ovale closure for prevention of migraine
Published in Acta Cardiologica, 2019
Ayman Elbadawi, Kirolos Barssoum, Ahmed S. Abuzaid, Ahmed Rezq, Nishit Biniwale, Erfan Alotaki, Ahmed H. Mohamed, Sowjanya Vuyyala, Gbolahan O Ogunbayo, Marwan Saad
Multiple pathophysiological mechanisms have been proposed to explain the relationship between PFO and migraines; hence, rationalise the potential benefit of PFO closure in migraine prophylaxis. Among these mechanisms, cortical spreading depression is considered a key effector the pathogenesis of migraine with aura. Cortical spreading depression is believed to be caused by micro-emboli, which could be mediated via an RLS through a PFO allowing micro-emboli to pass from the venous system [21]. In addition, fibrin and platelet micro-emboli are also suggested to occur secondary to the left atrial blood stasis associating a PFO [22]. Another mechanism proposed that PFO allows vasoactive amines to bypass the lung and escape directly to the systemic circulation [23]. Serotonin for instance, which is normally destroyed in the lung capillaries by mono-amine oxidase, can either cause platelet activation in the brain micro-circulation and thus promotes the formation of micro-thrombi or directly irritate the trigeminal nerve and trigger a migraine [23].