Migrainous infarction

Last updated

A migrainous infarction is a rare type of ischaemic stroke which occurs in correspondence with migraine aura symptoms. [1] Symptoms include headaches, visual disturbances, strange sensations and dysphasia, all of which gradually worsen causing neurological changes which ultimately increase the risk of an ischaemic stroke. [2] Typically, women under the age of 45 who experience migraine with aura (MA) are at the greatest risk for developing migrainous infarction, especially when combined with smoking and use of oral contraceptives. [3]

Contents

Symptoms and signs

Migraine with aura

Overall, 30% of the population with migraines will experience aura during their lifetime. [4] Aura can be broadly defined as gradually developing attacks which cause neurological deficits in vision, sensation and language. [5]

Visual disturbances

Visual disturbances are commonly associated with MA, with 97% of patients experiencing visual symptoms. [6] Only 14% of patients with MA experience visual disturbances for more than 60 minutes at a time, with the median duration of visual disturbance being 30 minutes. [6] Typically, visual disturbances in MA patients begin as a zig zag line in the middle of the ocular field which appears to be flickering. [7] Some patients describe symptoms of an expanding red circle in the centre of their visual field. [8] A scotoma often occurs when the visual disturbance moves to the periphery of the visual field. [7] Additionally, a scotoma can sometimes occur in the center of the visual field which will appear as a more distinct blindspot, although this is less common. [9]

Individuals with persistent MA may also report a visual disturbance called 'visual snow'. Generally, they will describe their visual field as consisting of many small flickering spots which may resemble snow. [10]

Sensory symptoms

Sensory symptoms are known to occur in 32% of patients with MA and only occur for longer than 60 minutes in 21% of these patients, with the median duration being 20 minutes. [6] Typically, the sensory aura will consist of strange sensations and pain which gradually move from the hand, through the arm, to the face and tongue areas. It is extremely rare for MA patients to experience sensory symptoms in their legs and feet. [7]

Dysphasic symptoms

Dysphasic symptoms appear in 11% of MA patients, occurring for over 60 minutes in only 17% of patients with a median time span of 20 minutes. [6] Dysphasia in patients with MA appears as a moderate language generation deficit, for example, the patient may be unable to state their home address. [5] Sometimes, the patient may also experience language comprehension deficits in which they may be unable to comprehend the instructions of complex tasks. [5]

Ischaemic stroke

Public knowledge of stroke symptoms is scarce, with only 17.2% of people being able to correctly identify an individual experiencing a stroke. [11] Cerebral ischaemia refers to a severely reduced flow of blood in the brain due to narrowing or blocking of arteries or blood vessels causing inflammation. [12] Ischaemic stroke is characterised by dizziness, sudden weakness and numbness, visual deficits, difficulty speaking and comprehending speech, and a severe headache. [13]

Embolism

Approximately 36.6% of ischaemic strokes are caused by an embolism. [14] Embolisms are an obstruction of a blood vessel in the brain, often due to a blood clot formed in the heart which travels through the blood vessels to the brain. [15] Usually, embolic strokes cause multiple ischaemic lesions which are found in 41.2% of migrainous infarction patients. [16] [1]

Thrombosis

In 21.4% of cases, ischaemic strokes are caused by thrombosis. [14] A thrombus is a blood clot which forms in a cerebral blood vessel, reducing the flow of blood through that vessel. [17] This occlusion of blood vessels causes localised cytotoxic edema which damages the energy-dependent pumps of the cellular membrane causing intracellular inflammation. [18]

Migrainous infarction

A history of MA is significant predictor of migrainous infarction, with 80% of migrainous infarction patients having experienced MA previously. However, migrainous infarction can also occur in those with migraine without aura, although this is less common with only 20% of migrainous infarction patients never having experienced aura. [19] Typically, in the month prior to the cerebral infarction, the patient will experience more severe MA symptoms. [20]

Pathophysiology

Platelet activation

Enhanced platelet activation during MA has been observed which directly increases the risk of developing thrombosis. [21] Additionally, platelet activation is enhanced in patients with MA, even during aura-free and headache-free periods. [22] Moreover, this effect is exemplified through administration of non-selective beta-adrenergic antagonists (e.g. propranolol) which are often prescribed to reduce migraine symptoms. [23]

Reduced regional cerebral blood flow

Contrary to the suggestion that MA initiates ischaemic infarction, one theory suggests that ischaemia may in fact cause MA. This theory is based on the finding that reduced regional Cerebral Blood Flow (rCBF) has shown to be present in patients with MA due to underlying ischaemia. [24] Therefore, it is possible that infarction occurs due to another unknown factor causing ischaemia and MA is merely a symptom associated with the process.[ citation needed ]

Vasoconstriction

Migraines have a direct negative impact on the control of vessels in the brain, causing cerebral vasoconstriction which ultimately narrows blood vessels in the brain leading to cerebral hypoxia and tissue ischaemia. [25] Vasoconstriction of blood vessels and arteries during migraine is thought to be caused by vasospasm. [26] Use of a Transcranial Doppler revealed that patients with MA show prolonged diffuse vasospasm even during asymptomatic periods, although the vasospasm tends to be more severe during an aura attack. [27]

Diagnosis

Classification

For a diagnosis of migrainous infarction, the patient must meet criteria set out by the International Headache Society (IHS). The criteria include: One or more persistent aura symptom lasting more than 60 minutes and a previous medical history of migraine attacks with aura. The clinician must be certain that the infarction cannot be better explained by another medical problem or disorder. A diagnosis is confirmed when neuroimaging of the patient's brain exhibits an ischaemic infarction in an area associated with the migraine. [20]

Overall, only 18% of patients with MA will experience any aura symptoms for longer than 60 minutes. [6]

Localisation

CT scans, Magnetic Resonance Imaging (MRI) and Magnetic Resonance Angiography (MRA) are all common techniques which allow the localisation of brain lesions after stroke. [28] Approximately 82% of migrainous infarction patients experience lesions in the posterior circulation, with 21% of patients also experiencing lesions in the cerebellum. [2]

Treatment

Clot-busting agents

Clot busting agents or thrombolytic therapy are a treatment option for migrainous infarction caused by enhanced platelet activation leading to thrombosis. [29]

Streptokinase

Streptokinase is a thrombolytic agent which aims to permit reperfusion, allowing the restoration of blood flow to the ischaemic areas. [30] Recent trials indicate that Streptokinase can improve function after a 6-month period, however, the risk of mortality due to intracerebral haemorrhage resulting from use of this thrombolytic agent is extremely high and therefore, treatment using streptokinase is not recommended. [30]

Alteplase

Alteplase is a recombinant tissue plasminogen activator which enhances the conversion of plasminogen into plasmin to aid in the degradation of blood clots. [31] Effectiveness depends highly on swift administration of the medication, notably, the treatment should be administered within 3 to 4.5 hours of onset of the ischaemic stroke for the most effective results. [32] In a similar manner to Streptokinase, Alteplase increases the risk of intracranial haemorrhage, however, mortality rate is not affected. [32]

Aspirin

Aspirin is a class anti-aggregation drug, often used to treat headaches in patients with MA. [22] Administration of aspirin in patients with MA has been shown to be effective in reducing platelet factor 4 (PF4) concentration. PF4 promotes blood coagulation which can cause ischaemia, therefore, aspirin's ability to reduce PF4 concentration in people with MA greatly reduces the risk of migrainous infarction. [22]

Related Research Articles

<span class="mw-page-title-main">Migraine</span> Disorder resulting in recurrent moderate-severe headaches

Migraine is a genetically influenced complex neurological disorder characterized by episodes of moderate-to-severe headache, most often unilateral and generally associated with nausea and light and sound sensitivity. Other characterizing symptoms may include vomiting, cognitive dysfunction, allodynia, and dizziness. Exacerbation of headache symptoms during physical activity is another distinguishing feature. Up to one-third of migraine sufferers experience aura, a premonitory period of sensory disturbance widely accepted to be caused by cortical spreading depression at the onset of a migraine attack. Although primarily considered to be a headache disorder, migraine is highly heterogenous in its clinical presentation and is better thought of as a spectrum disease rather than a distinct clinical entity. Disease burden can range from episodic discrete attacks to chronic disease.

A transient ischemic attack (TIA), commonly known as a mini-stroke, is a minor stroke whose noticeable symptoms usually end in less than an hour. A TIA causes the same symptoms associated with a stroke, such as weakness or numbness on one side of the body, sudden dimming or loss of vision, difficulty speaking or understanding language, slurred speech, or confusion.

<span class="mw-page-title-main">Headache</span> Pain in the head, neck, or face

Headache, also known as cephalalgia, is the symptom of pain in the face, head, or neck. It can occur as a migraine, tension-type headache, or cluster headache. There is an increased risk of depression in those with severe headaches.

<span class="mw-page-title-main">Micropsia</span> Medical condition

Micropsia is a condition affecting human visual perception in which objects are perceived to be smaller than they actually are. Micropsia can be caused by optical factors, by distortion of images in the eye, by changes in the brain, and from psychological factors. Dissociative phenomena are linked with micropsia, which may be the result of brain-lateralization disturbance.

<span class="mw-page-title-main">Cerebrovascular disease</span> Condition that affects the arteries that supply the brain

Cerebrovascular disease includes a variety of medical conditions that affect the blood vessels of the brain and the cerebral circulation. Arteries supplying oxygen and nutrients to the brain are often damaged or deformed in these disorders. The most common presentation of cerebrovascular disease is an ischemic stroke or mini-stroke and sometimes a hemorrhagic stroke. Hypertension is the most important contributing risk factor for stroke and cerebrovascular diseases as it can change the structure of blood vessels and result in atherosclerosis. Atherosclerosis narrows blood vessels in the brain, resulting in decreased cerebral perfusion. Other risk factors that contribute to stroke include smoking and diabetes. Narrowed cerebral arteries can lead to ischemic stroke, but continually elevated blood pressure can also cause tearing of vessels, leading to a hemorrhagic stroke.

<span class="mw-page-title-main">Stroke</span> Death of a region of brain cells due to poor blood flow

Stroke is a medical condition in which poor blood flow to the brain causes cell death. There are two main types of stroke:

<span class="mw-page-title-main">Amaurosis fugax</span> Medical condition

Amaurosis fugax is a painless temporary loss of vision in one or both eyes.

<span class="mw-page-title-main">Visual snow syndrome</span> Visual impairment

Visual snow syndrome (VSS) is an uncommon neurological condition in which the primary symptom is that affected individuals see persistent flickering white, black, transparent, or colored dots across the whole visual field.

<span class="mw-page-title-main">Aura (symptom)</span> Symptom of epilepsy and migraine

An aura is a perceptual disturbance experienced by some with epilepsy or migraine. An epileptic aura is actually a minor seizure.

<span class="mw-page-title-main">Cerebral infarction</span> Stroke resulting from lack of blood flow

Cerebral infarction, also known as an ischemic stroke, is the pathologic process that results in an area of necrotic tissue in the brain. In mid to high income countries, a stroke is the main reason for disability among people and the 2nd cause of death. It is caused by disrupted blood supply (ischemia) and restricted oxygen supply (hypoxia). This is most commonly due to a thrombotic occlusion, or an embolic occlusion of major vessels which leads to a cerebral infarct. In response to ischemia, the brain degenerates by the process of liquefactive necrosis.

<span class="mw-page-title-main">Photopsia</span> Presence of perceived flashes of light in ones field of vision

Photopsia is the presence of perceived flashes of light in the field of vision.

<span class="mw-page-title-main">Almotriptan</span> Chemical compound

Almotriptan is a triptan medication discovered and developed by Almirall for the treatment of heavy migraine headache.

<span class="mw-page-title-main">Carotid artery dissection</span> Human disease

Carotid artery dissection is a separation of the layers of the artery wall in the carotid arteries supplying oxygen-bearing blood to the head. It is the most common cause of stroke in younger adults. The term 'cervical artery dissection' should also be considered in the context of this article.

<span class="mw-page-title-main">Cortical spreading depression</span> Type of evoked potential

Cortical spreading depression (CSD) or spreading depolarization (SD) is a wave of electrophysiological hyperactivity followed by a wave of inhibition. Spreading depolarization describes a phenomenon characterized by the appearance of depolarization waves of the neurons and neuroglia that propagates across the cortex at a velocity of 1.5–9.5 mm/min.

<span class="mw-page-title-main">Cerebral venous sinus thrombosis</span> Presence of a blood clot in the dural venous sinuses or cerebral veins

Cerebral venous sinus thrombosis (CVST), cerebral venous and sinus thrombosis or cerebral venous thrombosis (CVT), is the presence of a blood clot in the dural venous sinuses, the cerebral veins, or both. Symptoms may include severe headache, visual symptoms, any of the symptoms of stroke such as weakness of the face and limbs on one side of the body, and seizures, which occur in around 40% of patients.

Persistent aura without infarction (PAWOI) is a rare and seemingly benign condition, first described in case reports in 1982 as "prolonged/persistent migraine aura status", and in 2000 as "migraine aura status", that is not yet fully understood. PAWOI is said to possibly be a factor involved in a variety of neurological symptoms, including visual snow, loss of vision, increased afterimages, tinnitus, and others. The pathogenesis of PAWOI is unknown. It is not clear which medical examinations are useful in diagnosing PAWOI. At present, PAWOI is usually diagnosed solely based on the patient's current and past symptoms. It is possible that an "overactive brain" or a chemical imbalance underlies the disorder. Various medications have been tried as treatment, notably acetazolamide, valproate, lamotrigine, topiramate, and furosemide.

<span class="mw-page-title-main">Retinal migraine</span> Medical condition of the eye

Retinal migraine is a retinal disease often accompanied by migraine headache and typically affects only one eye. It is caused by ischaemia or vascular spasm in or behind the affected eye.

<span class="mw-page-title-main">Illusory palinopsia</span> Subtype of palinopsia

Illusory palinopsia is a subtype of palinopsia, a visual disturbance defined as the persistence or recurrence of a visual image after the stimulus has been removed. Palinopsia is a broad term describing a heterogeneous group of symptoms, which is divided into hallucinatory palinopsia and illusory palinopsia. Illusory palinopsia is likely due to sustained awareness of a stimulus and is similar to a visual illusion: the distorted perception of a real external stimulus.

<span class="mw-page-title-main">Recurrent painful ophthalmoplegic neuropathy</span> Medical condition

Recurrent painful ophthalmoplegic neuropathy (RPON), previously known as ophthalmoplegic migraine (OM), is a rare neurological disorder that is characterized by repeated headache attacks and reversible ipsilateral paresis of one or more ocular cranial nerves (CN). Oculomotor nerve (CNIII) is by far the most common cranial nerve involves in RPON, while abducens nerve (CNVI) and trochlear nerve (CNIV) involvements are also reported. Globally, RPON was estimated to have an annual incidence rate of 0.7 per million as of 1990, no further epidemiological studies have been conducted. It occurs more often in children and females.

Spinal cord stroke is a rare type of stroke with compromised blood flow to any region of spinal cord owing to occlusion or bleeding, leading to irreversible neuronal death. It can be classified into two types, ischaemia and haemorrhage, in which the former accounts for 86% of all cases, a pattern similar to cerebral stroke. The disease is either arisen spontaneously from aortic illnesses or postoperatively. It deprives patients of motor function or sensory function, and sometimes both. Infarction usually occurs in regions perfused by anterior spinal artery, which spans the anterior two-thirds of spinal cord. Preventions of the disease include decreasing the risk factors and maintaining enough spinal cord perfusion pressure during and after the operation. The process of diagnosing the ischemic and hemorrhagic spinal cord stroke includes applying different MRI protocols and CT scan. Treatments for spinal cord stroke are mainly determined by the symptoms and the causes of the disease. For example, antiplatelet and corticosteroids might be used to reduce the risk of blood clots in ischaemic spinal stroke patients, while rapid surgical decompression is applied to minimize neurological injuries in haemorrhagic spinal stroke patients instead. Patients may spend years for rehabilitation after the spinal cord stroke.

References

  1. 1 2 Wolf, M. E.; Szabo, K.; Griebe, M.; Förster, A.; Gass, A.; Hennerici, M. G.; Kern, R. (2011-05-31). "Clinical and MRI characteristics of acute migrainous infarction". Neurology. 76 (22): 1911–1917. doi:10.1212/WNL.0b013e31821d74d5. ISSN   0028-3878. PMID   21624990. S2CID   12877187.
  2. 1 2 Laurell, K.; Artto, V.; Bendtsen, L.; Hagen, K.; Kallela, M.; Meyer, E. Laudon; Putaala, J.; Tronvik, E.; Zwart, J.-A.; Linde, M. (2011). "Migrainous infarction: a Nordic multicenter study". European Journal of Neurology. 18 (10): 1220–1226. doi:10.1111/j.1468-1331.2011.03364.x. ISSN   1468-1331. PMID   21414105. S2CID   39572704.
  3. ↑ Laurell, K.; Lundström, E. (2012-06-01). "Migrainous Infarction: Aspects on Risk Factors and Therapy". Current Pain and Headache Reports. 16 (3): 255–260. doi:10.1007/s11916-012-0262-2. ISSN   1534-3081. PMID   22527790. S2CID   39992424.
  4. ↑ Rasmussen, B. K.; Olesen, J. (1992-08-01). "Migraine With Aura and Migraine Without Aura: An Epidemiological Study". Cephalalgia. 12 (4): 221–228. doi:10.1046/j.1468-2982.1992.1204221.x. PMID   1525797. S2CID   24120063.
  5. 1 2 3 Nieuwkamp, D. J.; van der Schaaf, I. C.; Biessels, G. J. (2010-08-01). "Migraine aura presenting as dysphasia with global cognitive dysfunction and abnormalities on perfusion CT". Cephalalgia. 30 (8): 1007–1009. doi:10.1111/j.1468-2982.2009.02007.x (inactive 31 January 2024). PMID   20656713.{{cite journal}}: CS1 maint: DOI inactive as of January 2024 (link)
  6. 1 2 3 4 5 Viana, M.; Linde, M.; Sances, G.; Ghiotto, N.; Guaschino, E.; Allena, M.; Terrazzino, S.; Nappi, G.; Goadsby, P. J.; Tassorelli, C. (2016-04-01). "Migraine aura symptoms: Duration, succession and temporal relationship to headache". Cephalalgia. 36 (5): 413–421. doi:10.1177/0333102415593089. ISSN   0333-1024. PMID   26156076. S2CID   10701108.
  7. 1 2 3 Russell, M. B.; Olesen, J. (1996). "A nosographic analysis of the migraine aura in a general population". Brain. 119 (2): 355–361. doi: 10.1093/brain/119.2.355 . ISSN   0006-8950. PMID   8800932.
  8. ↑ Santos, E.; Sánchez-Porras, R.; Dohmen, C.; Hertle, D.; Unterberg, A. W.; Sakowitz, O. W. (2012-03-09). "Spreading depolarizations in a case of migraine-related stroke". Cephalalgia. 32 (5): 433–436. doi:10.1177/0333102412441414. PMID   22407661. S2CID   25190650.
  9. ↑ Schott, G. D. (2007-06-01). "Exploring the visual hallucinations of migraine aura: the tacit contribution of illustration". Brain. 130 (6): 1690–1703. doi: 10.1093/brain/awl348 . ISSN   0006-8950. PMID   17264093.
  10. ↑ Schankin, C. J.; Maniyar, F. H.; Sprenger, T.; Chou, D. E.; Eller, M.; Goadsby, P. J. (2014-06-01). "The Relation Between Migraine, Typical Migraine Aura and "Visual Snow"". Headache: The Journal of Head and Face Pain. 54 (6): 957–966. doi: 10.1111/head.12378 . ISSN   1526-4610. PMID   24816400. S2CID   4164884.
  11. ↑ Greenlund, K. J.; Neff, L. J.; Zheng, Z. J.; Keenan, N. L.; Giles, W. H.; Ayala, C. A.; Croft, J. B.; Mensah, G. A. (2003-11-01). "Low public recognition of major stroke symptoms". American Journal of Preventive Medicine. 25 (4): 315–319. doi:10.1016/S0749-3797(03)00206-X. ISSN   0749-3797. PMID   14580633.
  12. ↑ Iadecola, C.; Alexander, M. (2001-02-01). "Cerebral ischemia and inflammation". Current Opinion in Neurology. 14 (1): 89–94. doi:10.1097/00019052-200102000-00014. ISSN   1350-7540. PMID   11176223.
  13. ↑ Pancioli, A. M.; Broderick, J.; Kothari, R.; Brott, T.; Tuchfarber, A.; Miller, R.; Khoury, J.; Jauch, E. (1998-04-22). "Public Perception of Stroke Warning Signs and Knowledge of Potential Risk Factors". JAMA. 279 (16): 1288–1292. doi: 10.1001/jama.279.16.1288 . ISSN   0098-7484. PMID   9565010.
  14. 1 2 Montaner, J.; Perea-Gainza, M.; Delgado, P.; Ribó, M.; Chacón, P.; Rosell, A.; Quintana, M.; Palacios, M. E.; Molina, C. A.; Alvarez-Sabín, J. (2008-01-16). "Etiologic Diagnosis of Ischemic Stroke Subtypes With Plasma Biomarkers". Stroke. 39 (8): 2280–2287. doi: 10.1161/STROKEAHA.107.505354 . ISSN   0039-2499. PMID   18535284. S2CID   1690024.
  15. ↑ Wessels, T.; Röttger, C.; Jauss, M.; Kaps, M.; Traupe, H.; Stolz, E. (2005-04-01). "Identification of Embolic Stroke Patterns by Diffusion-Weighted MRI in Clinically Defined Lacunar Stroke Syndromes". Stroke. 36 (4): 757–761. doi: 10.1161/01.STR.0000158908.48022.d7 . PMID   15746460. S2CID   15123728.
  16. ↑ Jauss, M.; Wessels, T.; Trittmacher, S.; Allendörfer, J.; Kaps, M. (2006-08-01). "Embolic Lesion Pattern in Stroke Patients With Patent Foramen Ovale Compared With Patients Lacking an Embolic Source". Stroke. 37 (8): 2159–2161. doi: 10.1161/01.STR.0000231645.22128.ab . PMID   16825590. S2CID   6290227.
  17. ↑ Ameri, A.; Bousser, M. G. (1992-02-01). "Cerebral Venous Thrombosis". Neurologic Clinics. 10 (1): 87–111. doi:10.1016/S0733-8619(18)30235-4. ISSN   0733-8619. PMID   1557011.
  18. ↑ Stam, J. (2005-04-28). "Thrombosis of the Cerebral Veins and Sinuses". New England Journal of Medicine. 352 (17): 1791–1798. doi:10.1056/NEJMra042354. ISSN   0028-4793. PMID   15858188. S2CID   42126852.
  19. ↑ Rothrock, J.; North, J.; Madden, K.; Lyden, P.; Fleck, P.; Dittrich, H. (1993-12-01). "Migraine and migrainous stroke: Risk factors and prognosis". Neurology. 43 (12): 2473–6. doi:10.1212/WNL.43.12.2473. ISSN   0028-3878. PMID   8255442. S2CID   19346752.
  20. 1 2 Headache Classification Committee of the International Headache Society (IHS) (2018-01-25). "The International Classification of Headache Disorders, 3rd edition". Cephalalgia. 38 (1): 1–211. doi: 10.1177/0333102417738202 . ISSN   0333-1024. PMID   29368949. S2CID   45901670.
  21. ↑ Zeller, J. A.; Frahm, K.; Baron, R.; Stingele, R.; Deuschl, G. (2004-07-01). "Platelet–leukocyte interaction and platelet activation in migraine: a link to ischemic stroke?". Journal of Neurology, Neurosurgery & Psychiatry. 75 (7): 984–987. doi:10.1136/jnnp.2003.019638. ISSN   0022-3050. PMC   1739108 . PMID   15201354.
  22. 1 2 3 D'Andrea, G.; Toldo, M.; Cananzi, A.; Ferro-Milone, F. (1984-03-01). "Study of platelet activation in migraine: control by low doses of aspirin". Stroke. 15 (2): 271–275. doi: 10.1161/01.STR.15.2.271 . PMID   6230778. S2CID   18475833.
  23. ↑ Hedman, C.; Winther, K.; Knudsen, J. B. (1988). "Platelet function in classic migraine during attack-free periods". Acta Neurologica Scandinavica. 78 (4): 271–277. doi:10.1111/j.1600-0404.1988.tb03656.x. ISSN   1600-0404. PMID   2851913. S2CID   22505883.
  24. ↑ Olesen, J.; Friberg, L.; Olsen, T. S.; Andersen, A. R.; Lassen, N. A.; Hansen, P. E.; Karle, A. (1993-02-01). "Ischaemia-induced (symptomatic) migraine attacks may be more frequent than migraine-induced ischaemic insults". Brain. 116 (1): 187–202. doi:10.1093/brain/116.1.187. ISSN   0006-8950. PMID   8453456.
  25. ↑ Kreling, G. A. D.; de Almeida, N. R.; dos Santos, P. J. (2017-06-30). "Migrainous infarction: a rare and often overlooked diagnosis". Autopsy & Case Reports. 7 (2): 61–68. doi:10.4322/acr.2017.018. ISSN   2236-1960. PMC   5507571 . PMID   28740841.
  26. ↑ Lee, H.; Whitman, G. T.; Lim, J. G.; Yi, S. D.; Cho, Y. W.; Ying, S.; Baloh, R. W. (2003-01-01). "Hearing Symptoms in Migrainous Infarction". Archives of Neurology. 60 (1): 113–116. doi: 10.1001/archneur.60.1.113 . ISSN   0003-9942. PMID   12533097.
  27. ↑ Thie, A.; Spitzer, K.; Lachenmayer, L.; Kunze, K. (1988). "Prolonged Vasospasm in Migraine Detected by Noninvasive Transcranial Doppler Ultrasound". Headache: The Journal of Head and Face Pain. 28 (3): 183–186. doi:10.1111/j.1526-4610.1988.hed2803183.x. ISSN   1526-4610. PMID   3290157. S2CID   40373513.
  28. ↑ Marshall, N.; Maclaurin, W. A.; Koulouris, G. (2007). "MRA Captures Vasospasm in Fatal Migrainous Infarction". Headache: The Journal of Head and Face Pain. 47 (2): 280–283. doi:10.1111/j.1526-4610.2007.00695.x. ISSN   1526-4610. PMID   17300370. S2CID   30746415.
  29. ↑ Wehinger, C.; Stöllberger, C.; Länger, T.; Schneider, B.; Finsterer, J. (2001-10-01). "Evaluation of Risk Factors for Stroke/Embolism and of Complications Due to Anticoagulant Therapy in Atrial Fibrillation". Stroke. 32 (10): 2246–2252. doi: 10.1161/hs1001.097090 . PMID   11588308. S2CID   14703460.
  30. 1 2 Hommel, M. (1996-07-18). "Thrombolytic Therapy with Streptokinase in Acute Ischemic Stroke". New England Journal of Medicine. 335 (3): 145–150. doi: 10.1056/NEJM199607183350301 . ISSN   0028-4793. PMID   8657211.
  31. ↑ Hacke, W.; Kaste, M.; Fieschi, C.; von Kummer, R.; Davalos, A.; Meier, D.; Larrue, V.; Bluhmki, E.; Davis, S.; Donnan, G.; Schneider, D. (1998-10-17). "Randomised double-blind placebo-controlled trial of thrombolytic therapy with intravenous alteplase in acute ischaemic stroke (ECASS II)". The Lancet. 352 (9136): 1245–1251. doi:10.1016/S0140-6736(98)08020-9. ISSN   0140-6736. PMID   9788453. S2CID   53549605.
  32. 1 2 Hacke, W.; Kaste, M.; Bluhmki, E.; Brozman, M.; Dávalos, A.; Guidetti, D.; Larrue, V.; Lees, K. R.; Medeghri, Z.; Machnig, T.; Schneider, D. (2008-09-25). "Thrombolysis with Alteplase 3 to 4.5 Hours after Acute Ischemic Stroke". New England Journal of Medicine. 359 (13): 1317–1329. doi: 10.1056/NEJMoa0804656 . ISSN   0028-4793. PMID   18815396. S2CID   12016921.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.