Diagnosis and Management of Facial Pain
John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie in Basic Sciences Endocrine Surgery Rhinology, 2018
Although previously believed to be a neurovascular disorder, the mechanism for migraine is now believed to be a disorder of the brain itself.10 Cortical spreading depression is a wave of intense depolarization that starts in the occipital lobe, propagates through the brain and is followed by a period of suppressed activity. Consequent activation of the trigemino-vascular system causes the release of neuropeptides (e.g. calcitonin gene-related peptide, substance P) from peripheral trigeminal nerve endings. It is these neuropeptides that are thought to play a role in causing and maintaining the headache. The pulsating quality of migraine is thought to be caused by a process of peripheral sensitization. The condition runs in families in approximately two-thirds of cases, is more common in women and sufferers may describe triggers, which can be encountered up to 24 hours prior to the onset of an attack.11-13 Some examples of triggers include stress, hunger, fatigue, hormonal changes, foodstuffs containing tyramine (aged cheeses, smoked fish, cured meats, some types of beer), monosodium glutamate, indoor air quality and lighting, although the evidence base for all of these is poor.
Migraine Headaches
Alexander R. Toftness in 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.
Migraine: Management and Treatment with Herbal Drugs
Vikas Kumar, Addepalli Veeranjaneyulu in Herbs for Diabetes and Neurological Disease Management, 2018
A second theory of migraine is the neurological theory of migraine. This theory suggests that migraine arises as a result of abnormal neuronal firing and neurotransmitter release in brain neurons. This theory focuses on an explanation for certain symptoms, such as premonitory symptoms occurring prior to an attack (prodrome), which are difficult to explain based on the vascular hypothesis. The fact that migraine headaches begin and develop slowly coupled to the fact that external factors, such as stress, and hunger can precipitate migraine attacks to pathologies arising in the neuronal system, thus supporting a neurological basis of migraine.29 Cortical spreading depression, an expanding depolarization of cortical neurons which is well characterized in many species but not in man is often suggested to underlie the aura or prodrome associated with initiation of migraine attack. During spreading depression, cortical function is disrupted subsequent to neuronal depolarization and increased extracellular potassium. These cortical changes are thought to be the cause of the transient sensory or motor impairments that frequently proceed the painful period of a migraine attack.
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
Lactation in large litters influences anxiety, memory, and spreading depression in adult male rats that were chronically subjected to a non-convulsive pilocarpine dose
Published in Nutritional Neuroscience, 2022
Regina de Deus Lira Benevides, Suênia Marcele Vitor de-Lima, Camila Lima Chagas, Clara Farah de Lima, Ricardo Abadie-Guedes, Rubem Carlos Araujo Guedes
Previously, we have investigated the behavioral and electrophysiological effects of a single pilocarpine administration at various non-convulsive doses (45 to 190 mg/kg) [13] and repeated pilocarpine administration at a very low dose (45 mg/kg/day) in young rats [14]. However, the effects of a chronic administration of sub-convulsive doses of pilocarpine on mature rats remain unclear. Using this repeated administration paradigm, we have demonstrated that pilocarpine, when administered early in life, can affect behavior and the propagation of the excitability-related phenomenon, known as cortical spreading depression (CSD), without provoking convulsion [14–16]. CSD is a reversible, depolarizing response that consists of a reduction in spontaneous electrical activity in the cerebral cortex, i.e. a transitory depression of the electrocorticogram waves (ECoG depression). Once CSD is elicited, it propagates over the entire cortex [17]. In addition to electrocorticogram (ECoG) depression, CSD is accompanied by a slow direct current (DC) potential change that is generated in the depressed cortical surface [18]. CSD is associated with neurological disorders that generate diseases such as epilepsy, migraine with aura, malignant ischemic stroke, subarachnoid hemorrhage, and traumatic brain injury [19,20], and can be modulated by a number of factors such as aging [21].
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].
Related Knowledge Centers
- Cerebral Cortex
- Depolarization
- Dravet Syndrome
- Electrophysiology
- Hypoxia
- Ischemia
- Aura
- Migraine
- Sudden Unexpected Death In Epilepsy
- Vasoconstriction