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Transient ischemic attack(TIA)

MedGen UID:
853
Concept ID:
C0007787
Disease or Syndrome
Synonyms: TIA; Transient ischemic attack (disease)
SNOMED CT: Temporary cerebral vascular dysfunction (266257000); Transient cerebral ischemia (266257000); Transient ischemic attack (266257000); TIA - transient ischemic attack (266257000)
 
HPO: HP:0002326
Monarch Initiative: MONDO:0005264

Definition

A brief attack (from a few minutes to an hour) of cerebral dysfunction of vascular origin, with no persistent neurological deficit. [from NCI]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • Transient ischemic attack

Conditions with this feature

Fabry disease
MedGen UID:
8083
Concept ID:
C0002986
Disease or Syndrome
Fabry disease is the most common of the lysosomal storage disorders and results from deficient activity of the enzyme alpha-galactosidase A (a-Gal A), leading to progressive lysosomal deposition of globotriaosylceramide and its derivatives in cells throughout the body. The classic form, occurring in males with less than 1% a-Gal A enzyme activity, usually has its onset in childhood or adolescence with periodic crises of severe pain in the extremities (acroparesthesia), the appearance of vascular cutaneous lesions (angiokeratomas), sweating abnormalities (anhidrosis, hypohidrosis, and rarely hyperhidrosis), characteristic corneal and lenticular opacities, and proteinuria. Gradual deterioration of renal function to end-stage renal disease (ESRD) usually occurs in men in the third to fifth decade. In middle age, most males successfully treated for ESRD develop cardiac and/or cerebrovascular disease, a major cause of morbidity and mortality. Heterozygous females typically have milder symptoms at a later age of onset than males. Rarely, females may be relatively asymptomatic throughout a normal life span or may have symptoms as severe as those observed in males with the classic phenotype. In contrast, late-onset forms occur in males with greater than 1% a-Gal A activity. Clinical manifestations include cardiac disease, which usually presents in the sixth to eighth decade with left ventricular hypertrophy, cardiomyopathy, arrhythmia, and proteinuria; renal failure, associated with ESRD but without the skin lesions or pain; or cerebrovascular disease presenting as stroke or transient ischemic attack.
Schimke immuno-osseous dysplasia
MedGen UID:
164078
Concept ID:
C0877024
Congenital Abnormality
Schimke immunoosseous dysplasia (SIOD) is characterized by spondyloepiphyseal dysplasia (SED) resulting in short stature, nephropathy, and T-cell deficiency. Radiographic manifestations of SED include ovoid and mildly flattened vertebral bodies, small ilia with shallow dysplastic acetabular fossae, and small deformed capital femoral epiphyses. Nearly all affected individuals have progressive steroid-resistant nephropathy, usually developing within five years of the diagnosis of growth failure and terminating with end-stage renal disease. The majority of tested individuals have T-cell deficiency and an associated risk for opportunistic infection, a common cause of death. SIOD involves a spectrum that ranges from an infantile or severe early-onset form with a greater risk of death during childhood to a juvenile or milder later-onset form with likely survival into adulthood if renal disease is appropriately treated.
Upshaw-Schulman syndrome
MedGen UID:
224783
Concept ID:
C1268935
Disease or Syndrome
Hereditary thrombotic thrombocytopenic purpura (TTP), also known as Upshaw-Schulman syndrome (USS), is a rare autosomal recessive thrombotic microangiopathy (TMA). Clinically, acute phases of TTP are defined by microangiopathic mechanical hemolytic anemia, severe thrombocytopenia, and visceral ischemia. Hereditary TTP makes up 5% of TTP cases and is caused mostly by biallelic mutation in the ADAMTS13 gene, or in very rare cases, by monoallelic ADAMTS13 mutation associated with a cluster of single-nucleotide polymorphisms (SNPs); most cases of all TTP (95%) are acquired via an autoimmune mechanism (see 188030). Hereditary TTP is more frequent among child-onset TTP compared with adult-onset TTP, and its clinical presentation is significantly different as a function of its age of onset. Child-onset TTP usually starts in the neonatal period with hematological features and severe jaundice. In contrast, almost all cases of adult-onset hereditary TTP are unmasked during the first pregnancy of a woman whose disease was silent during childhood (summary by Joly et al., 2018).
Telangiectasia, hereditary hemorrhagic, type 2
MedGen UID:
324960
Concept ID:
C1838163
Disease or Syndrome
Hereditary hemorrhagic telangiectasia (HHT) is characterized by the presence of multiple arteriovenous malformations (AVMs) that lack intervening capillaries and result in direct connections between arteries and veins. The most common clinical manifestation is spontaneous and recurrent nosebleeds (epistaxis) beginning on average at age 12 years. Telangiectases (small AVMs) are characteristically found on the lips, tongue, buccal and gastrointestinal (GI) mucosa, face, and fingers. The appearance of telangiectases is generally later than epistaxis but may be during childhood. Large AVMs occur most often in the lungs, liver, or brain; complications from bleeding or shunting may be sudden and catastrophic. A minority of individuals with HHT have GI bleeding, which is rarely seen before age 50 years.
Toriello-Lacassie-Droste syndrome
MedGen UID:
333068
Concept ID:
C1838329
Disease or Syndrome
Oculoectodermal syndrome (OES) is characterized by the association of epibulbar dermoids and aplasia cutis congenita. Affected individuals exhibit congenital scalp lesions which are atrophic, nonscarring, hairless regions that are often multiple and asymmetric in distribution, and may have associated hamartomas. Ectodermal changes include linear hyperpigmentation that may follow the lines of Blaschko and, rarely, epidermal nevus-like lesions. Epibulbar dermoids may be uni- or bilateral. Additional ocular anomalies such as skin tags of the upper eyelid and rarely optic nerve or retinal changes or microphthalmia can be present. Phenotypic expression is highly variable, and various other abnormalities have occasionally been reported, including growth failure, lymphedema, and cardiovascular defects, as well as neurodevelopmental symptoms such as developmental delay, epilepsy, learning difficulties, and behavioral abnormalities. Benign tumor-like lesions such as nonossifying fibromas of the long bones and giant cell granulomas of the jaws have repeatedly been observed and appear to be age-dependent, becoming a common manifestation in individuals aged 5 years or older (summary by Boppudi et al., 2016).
CARASIL syndrome
MedGen UID:
325051
Concept ID:
C1838577
Disease or Syndrome
HTRA1 disorder is a phenotypic spectrum in which some individuals have few to no symptoms and others manifest with the more severe CARASIL (cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy) phenotype. Those who have a heterozygous HTRA1 pathogenic variant may have mild neurologic findings (sometimes identified only on neuroimaging) or mild-to-moderate neurologic signs and symptoms of CARASIL. In this chapter, the term "classic CARASIL" refers to the more severe phenotype associated with biallelic pathogenic variants, and "HTRA1 cerebral small vessel disease" (HTRA1-CSVD) refers to the milder phenotype associated with a heterozygous HTRA1 pathogenic variant. Classic CARASIL is characterized by early-onset changes in the deep white matter of the brain observed on MRI, and associated neurologic findings. The most frequent initial symptom is gait disturbance from spasticity beginning between ages 20 and 40 years. Forty-four percent of affected individuals have stroke-like episodes before age 40 years. Mood changes (apathy and irritability), pseudobulbar palsy, and cognitive dysfunction begin between ages 20 and 50 years. The disease progresses slowly following the onset of neurologic symptoms. Scalp alopecia and acute mid- to lower-back pain (lumbago) before age 30 years are characteristic. The most frequent initial symptom in individuals with HTRA1-CSVD is slowly progressive gait disturbance after age 40 years, which may be followed by the development of mood changes and cognitive dysfunction. A majority of affected individuals have a stroke-like episode after age 40 years. Spondylosis and alopecia are seen in a minority of individuals with HTRA1-CSVD.
Moyamoya disease 2
MedGen UID:
339584
Concept ID:
C1846689
Disease or Syndrome
Moyamoya disease is a progressive cerebral angiopathy characterized by bilateral internal carotid artery stenosis and abnormal collateral vessels. The abnormal vessels resemble a 'puff of smoke' (moyamoya) on cerebral angiogram. Affected individuals can develop transient ischemic attacks and/or cerebral infarction, and rupture of the collateral vessels can cause intracranial hemorrhage (summary by Kamada et al., 2011). For a general phenotypic description and a discussion of genetic heterogeneity of moyamoya disease, see MYMY1 (252350).
Hereditary hemorrhagic telangiectasia type 4
MedGen UID:
341824
Concept ID:
C1857688
Disease or Syndrome
Hereditary hemorrhagic telangiectasia (HHT) is characterized by the presence of multiple arteriovenous malformations (AVMs) that lack intervening capillaries and result in direct connections between arteries and veins. The most common clinical manifestation is spontaneous and recurrent nosebleeds (epistaxis) beginning on average at age 12 years. Telangiectases (small AVMs) are characteristically found on the lips, tongue, buccal and gastrointestinal (GI) mucosa, face, and fingers. The appearance of telangiectases is generally later than epistaxis but may be during childhood. Large AVMs occur most often in the lungs, liver, or brain; complications from bleeding or shunting may be sudden and catastrophic. A minority of individuals with HHT have GI bleeding, which is rarely seen before age 50 years.
Hypertrophic cardiomyopathy 4
MedGen UID:
350526
Concept ID:
C1861862
Disease or Syndrome
Nonfamilial hypertrophic cardiomyopathy tends to be milder. This form typically begins later in life than familial hypertrophic cardiomyopathy, and affected individuals have a lower risk of serious cardiac events and sudden death than people with the familial form.\n\nWhile most people with familial hypertrophic cardiomyopathy are symptom-free or have only mild symptoms, this condition can have serious consequences. It can cause abnormal heart rhythms (arrhythmias) that may be life threatening. People with familial hypertrophic cardiomyopathy have an increased risk of sudden death, even if they have no other symptoms of the condition. A small number of affected individuals develop potentially fatal heart failure, which may require heart transplantation.\n\nThe symptoms of familial hypertrophic cardiomyopathy are variable, even within the same family. Many affected individuals have no symptoms. Other people with familial hypertrophic cardiomyopathy may experience chest pain; shortness of breath, especially with physical exertion; a sensation of fluttering or pounding in the chest (palpitations); lightheadedness; dizziness; and fainting.\n\nIn familial hypertrophic cardiomyopathy, cardiac thickening usually occurs in the interventricular septum, which is the muscular wall that separates the lower left chamber of the heart (the left ventricle) from the lower right chamber (the right ventricle). In some people, thickening of the interventricular septum impedes the flow of oxygen-rich blood from the heart, which may lead to an abnormal heart sound during a heartbeat (heart murmur) and other signs and symptoms of the condition. Other affected individuals do not have physical obstruction of blood flow, but the pumping of blood is less efficient, which can also lead to symptoms of the condition. Familial hypertrophic cardiomyopathy often begins in adolescence or young adulthood, although it can develop at any time throughout life.\n\nHypertrophic cardiomyopathy is a heart condition characterized by thickening (hypertrophy) of the heart (cardiac) muscle. When multiple members of a family have the condition, it is known as familial hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy also occurs in people with no family history; these cases are considered nonfamilial hypertrophic cardiomyopathy. 
Cerebral arteriopathy, autosomal dominant, with subcortical infarcts and leukoencephalopathy, type 2
MedGen UID:
895965
Concept ID:
C4225211
Disease or Syndrome
HTRA1 disorder is a phenotypic spectrum in which some individuals have few to no symptoms and others manifest with the more severe CARASIL (cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy) phenotype. Those who have a heterozygous HTRA1 pathogenic variant may have mild neurologic findings (sometimes identified only on neuroimaging) or mild-to-moderate neurologic signs and symptoms of CARASIL. In this chapter, the term "classic CARASIL" refers to the more severe phenotype associated with biallelic pathogenic variants, and "HTRA1 cerebral small vessel disease" (HTRA1-CSVD) refers to the milder phenotype associated with a heterozygous HTRA1 pathogenic variant. Classic CARASIL is characterized by early-onset changes in the deep white matter of the brain observed on MRI, and associated neurologic findings. The most frequent initial symptom is gait disturbance from spasticity beginning between ages 20 and 40 years. Forty-four percent of affected individuals have stroke-like episodes before age 40 years. Mood changes (apathy and irritability), pseudobulbar palsy, and cognitive dysfunction begin between ages 20 and 50 years. The disease progresses slowly following the onset of neurologic symptoms. Scalp alopecia and acute mid- to lower-back pain (lumbago) before age 30 years are characteristic. The most frequent initial symptom in individuals with HTRA1-CSVD is slowly progressive gait disturbance after age 40 years, which may be followed by the development of mood changes and cognitive dysfunction. A majority of affected individuals have a stroke-like episode after age 40 years. Spondylosis and alopecia are seen in a minority of individuals with HTRA1-CSVD.
Telangiectasia, hereditary hemorrhagic, type 1
MedGen UID:
1643786
Concept ID:
C4551861
Disease or Syndrome
Hereditary hemorrhagic telangiectasia (HHT) is characterized by the presence of multiple arteriovenous malformations (AVMs) that lack intervening capillaries and result in direct connections between arteries and veins. The most common clinical manifestation is spontaneous and recurrent nosebleeds (epistaxis) beginning on average at age 12 years. Telangiectases (small AVMs) are characteristically found on the lips, tongue, buccal and gastrointestinal (GI) mucosa, face, and fingers. The appearance of telangiectases is generally later than epistaxis but may be during childhood. Large AVMs occur most often in the lungs, liver, or brain; complications from bleeding or shunting may be sudden and catastrophic. A minority of individuals with HHT have GI bleeding, which is rarely seen before age 50 years.
Loeys-Dietz syndrome 6
MedGen UID:
1794251
Concept ID:
C5562041
Disease or Syndrome
Loeys-Dietz syndrome (LDS) is characterized by vascular findings (cerebral, thoracic, and abdominal arterial aneurysms and/or dissections), skeletal manifestations (pectus excavatum or pectus carinatum, scoliosis, joint laxity, arachnodactyly, talipes equinovarus, cervical spine malformation and/or instability), craniofacial features (widely spaced eyes, strabismus, bifid uvula / cleft palate, and craniosynostosis that can involve any sutures), and cutaneous findings (velvety and translucent skin, easy bruising, and dystrophic scars). Individuals with LDS are predisposed to widespread and aggressive arterial aneurysms and pregnancy-related complications including uterine rupture and death. Individuals with LDS can show a strong predisposition for allergic/inflammatory disease including asthma, eczema, and reactions to food or environmental allergens. There is also an increased incidence of gastrointestinal inflammation including eosinophilic esophagitis and gastritis or inflammatory bowel disease. Wide variation in the distribution and severity of clinical features can be seen in individuals with LDS, even among affected individuals within a family who have the same pathogenic variant.

Professional guidelines

PubMed

Lauder L, Mahfoud F, Azizi M, Bhatt DL, Ewen S, Kario K, Parati G, Rossignol P, Schlaich MP, Teo KK, Townsend RR, Tsioufis C, Weber MA, Weber T, Böhm M
Eur Heart J 2023 Jun 20;44(23):2066-2077. doi: 10.1093/eurheartj/ehac395. PMID: 36342266
Mendelson SJ, Prabhakaran S
JAMA 2021 Mar 16;325(11):1088-1098. doi: 10.1001/jama.2020.26867. PMID: 33724327
Caprio FZ, Sorond FA
Med Clin North Am 2019 Mar;103(2):295-308. Epub 2018 Nov 28 doi: 10.1016/j.mcna.2018.10.001. PMID: 30704682

Curated

UK NICE Guideline NG128, Stroke and transient ischaemic attack in over 16s: diagnosis and initial management, 2019

Recent clinical studies

Etiology

Amin HP, Madsen TE, Bravata DM, Wira CR, Johnston SC, Ashcraft S, Burrus TM, Panagos PD, Wintermark M, Esenwa C; American Heart Association Emergency Neurovascular Care Committee of the Stroke Council and Council on Peripheral Vascular Disease
Stroke 2023 Mar;54(3):e109-e121. Epub 2023 Jan 19 doi: 10.1161/STR.0000000000000418. PMID: 36655570
Perry JJ, Yadav K, Syed S, Shamy M
CMAJ 2022 Oct 11;194(39):E1344-E1349. doi: 10.1503/cmaj.220344. PMID: 36220167Free PMC Article
Coutts SB
Continuum (Minneap Minn) 2017 Feb;23(1, Cerebrovascular Disease):82-92. doi: 10.1212/CON.0000000000000424. PMID: 28157745Free PMC Article
Kernan WN, Ovbiagele B, Black HR, Bravata DM, Chimowitz MI, Ezekowitz MD, Fang MC, Fisher M, Furie KL, Heck DV, Johnston SC, Kasner SE, Kittner SJ, Mitchell PH, Rich MW, Richardson D, Schwamm LH, Wilson JA; American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, Council on Clinical Cardiology, and Council on Peripheral Vascular Disease
Stroke 2014 Jul;45(7):2160-236. Epub 2014 May 1 doi: 10.1161/STR.0000000000000024. PMID: 24788967
Easton JD, Saver JL, Albers GW, Alberts MJ, Chaturvedi S, Feldmann E, Hatsukami TS, Higashida RT, Johnston SC, Kidwell CS, Lutsep HL, Miller E, Sacco RL; American Heart Association; American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; Interdisciplinary Council on Peripheral Vascular Disease
Stroke 2009 Jun;40(6):2276-93. Epub 2009 May 7 doi: 10.1161/STROKEAHA.108.192218. PMID: 19423857

Diagnosis

Banyas P, Jadhav A
Prim Care 2024 Jun;51(2):283-297. Epub 2024 Apr 1 doi: 10.1016/j.pop.2024.02.004. PMID: 38692775
Amin HP, Madsen TE, Bravata DM, Wira CR, Johnston SC, Ashcraft S, Burrus TM, Panagos PD, Wintermark M, Esenwa C; American Heart Association Emergency Neurovascular Care Committee of the Stroke Council and Council on Peripheral Vascular Disease
Stroke 2023 Mar;54(3):e109-e121. Epub 2023 Jan 19 doi: 10.1161/STR.0000000000000418. PMID: 36655570
Perry JJ, Yadav K, Syed S, Shamy M
CMAJ 2022 Oct 11;194(39):E1344-E1349. doi: 10.1503/cmaj.220344. PMID: 36220167Free PMC Article
Patrick L, Halabi C
Neurol Clin 2022 Feb;40(1):33-43. doi: 10.1016/j.ncl.2021.08.003. PMID: 34798973
Coutts SB
Continuum (Minneap Minn) 2017 Feb;23(1, Cerebrovascular Disease):82-92. doi: 10.1212/CON.0000000000000424. PMID: 28157745Free PMC Article

Therapy

Lun R, Dhaliwal S, Zitikyte G, Roy DC, Hutton B, Dowlatshahi D
JAMA Neurol 2022 Feb 1;79(2):141-148. doi: 10.1001/jamaneurol.2021.4514. PMID: 34870698Free PMC Article
Pan Y, Elm JJ, Li H, Easton JD, Wang Y, Farrant M, Meng X, Kim AS, Zhao X, Meurer WJ, Liu L, Dietrich D, Wang Y, Johnston SC
JAMA Neurol 2019 Dec 1;76(12):1466-1473. doi: 10.1001/jamaneurol.2019.2531. PMID: 31424481Free PMC Article
Mojadidi MK, Zaman MO, Elgendy IY, Mahmoud AN, Patel NK, Agarwal N, Tobis JM, Meier B
J Am Coll Cardiol 2018 Mar 6;71(9):1035-1043. doi: 10.1016/j.jacc.2017.12.059. PMID: 29495983
Boehme AK, Esenwa C, Elkind MS
Circ Res 2017 Feb 3;120(3):472-495. doi: 10.1161/CIRCRESAHA.116.308398. PMID: 28154098Free PMC Article
McEvoy RD, Antic NA, Heeley E, Luo Y, Ou Q, Zhang X, Mediano O, Chen R, Drager LF, Liu Z, Chen G, Du B, McArdle N, Mukherjee S, Tripathi M, Billot L, Li Q, Lorenzi-Filho G, Barbe F, Redline S, Wang J, Arima H, Neal B, White DP, Grunstein RR, Zhong N, Anderson CS; SAVE Investigators and Coordinators
N Engl J Med 2016 Sep 8;375(10):919-31. Epub 2016 Aug 28 doi: 10.1056/NEJMoa1606599. PMID: 27571048

Prognosis

Feigin VL, Brainin M, Norrving B, Martins S, Sacco RL, Hacke W, Fisher M, Pandian J, Lindsay P
Int J Stroke 2022 Jan;17(1):18-29. doi: 10.1177/17474930211065917. PMID: 34986727
Iorga ER, Costin D
Rom J Ophthalmol 2020 Oct-Dec;64(4):323-332. doi: 10.22336/rjo.2020.54. PMID: 33367170Free PMC Article
Saw J, Humphries K, Aymong E, Sedlak T, Prakash R, Starovoytov A, Mancini GBJ
J Am Coll Cardiol 2017 Aug 29;70(9):1148-1158. doi: 10.1016/j.jacc.2017.06.053. PMID: 28838364
Portegies ML, Koudstaal PJ, Ikram MA
Handb Clin Neurol 2016;138:239-61. doi: 10.1016/B978-0-12-802973-2.00014-8. PMID: 27637962
Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ
Chest 2010 Feb;137(2):263-72. Epub 2009 Sep 17 doi: 10.1378/chest.09-1584. PMID: 19762550

Clinical prediction guides

van Dam-Nolen DHK, Truijman MTB, van der Kolk AG, Liem MI, Schreuder FHBM, Boersma E, Daemen MJAP, Mess WH, van Oostenbrugge RJ, van der Steen AFW, Bos D, Koudstaal PJ, Nederkoorn PJ, Hendrikse J, van der Lugt A, Kooi ME; PARISK Study Group
JACC Cardiovasc Imaging 2022 Oct;15(10):1715-1726. Epub 2022 Jun 15 doi: 10.1016/j.jcmg.2022.04.003. PMID: 36202450
Poorthuis MHF, Herings RAR, Dansey K, Damen JAA, Greving JP, Schermerhorn ML, de Borst GJ
Stroke 2022 Jan;53(1):87-99. Epub 2021 Oct 12 doi: 10.1161/STROKEAHA.120.032527. PMID: 34634926Free PMC Article
Ramanathan RS, Wisco D, Vela-Duarte D, Zafar A, Taqui A, Winners S, Buletko AB, Hustey F, Reimer A, Russman A, Uchino K, Hussain MS
J Stroke Cerebrovasc Dis 2021 Jul;30(7):105801. Epub 2021 Apr 18 doi: 10.1016/j.jstrokecerebrovasdis.2021.105801. PMID: 33878546
Andrade SE, Harrold LR, Tjia J, Cutrona SL, Saczynski JS, Dodd KS, Goldberg RJ, Gurwitz JH
Pharmacoepidemiol Drug Saf 2012 Jan;21 Suppl 1(Suppl 1):100-28. doi: 10.1002/pds.2312. PMID: 22262598Free PMC Article
Giles MF, Rothwell PM
Expert Rev Neurother 2006 Mar;6(3):381-95. doi: 10.1586/14737175.6.3.381. PMID: 16533142

Recent systematic reviews

Lun R, Dhaliwal S, Zitikyte G, Roy DC, Hutton B, Dowlatshahi D
JAMA Neurol 2022 Feb 1;79(2):141-148. doi: 10.1001/jamaneurol.2021.4514. PMID: 34870698Free PMC Article
Kolmos M, Christoffersen L, Kruuse C
J Stroke Cerebrovasc Dis 2021 Aug;30(8):105935. Epub 2021 Jun 18 doi: 10.1016/j.jstrokecerebrovasdis.2021.105935. PMID: 34153594
Ali A, Tabassum D, Baig SS, Moyle B, Redgrave J, Nichols S, McGregor G, Evans K, Totton N, Cooper C, Majid A
Stroke 2021 Jul;52(7):2445-2455. Epub 2021 May 27 doi: 10.1161/STROKEAHA.120.032979. PMID: 34039033
Rerkasem A, Orrapin S, Howard DP, Rerkasem K
Cochrane Database Syst Rev 2020 Sep 12;9(9):CD001081. doi: 10.1002/14651858.CD001081.pub4. PMID: 32918282Free PMC Article
Tramacere I, Boncoraglio GB, Banzi R, Del Giovane C, Kwag KH, Squizzato A, Moja L
BMC Med 2019 Mar 26;17(1):67. doi: 10.1186/s12916-019-1298-5. PMID: 30914063Free PMC Article

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    • NICE, 2019
      UK NICE Guideline NG128, Stroke and transient ischaemic attack in over 16s: diagnosis and initial management, 2019

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