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Hyperintensity of cerebral white matter on MRI

MedGen UID:
811125
Concept ID:
C2938912
Pathologic Function
Synonym: White matter hyperintensities
 
HPO: HP:0030890

Definition

A brighter than expected signal on magnetic resonance imaging emanating from the cerebral white matter. [from HPO]

Conditions with this feature

Sulfite oxidase deficiency
MedGen UID:
78695
Concept ID:
C0268624
Disease or Syndrome
The spectrum of isolated sulfite oxidase deficiency ranges from classic early-onset (severe) disease to late-onset (mild) disease. Classic ISOD is characterized in the first few hours to days of life by intractable seizures, feeding difficulties, and rapidly progressive encephalopathy manifest as abnormal tone (especially opisthotonus, spastic quadriplegia, and pyramidal signs) followed by progressive microcephaly and profound intellectual disability. Lens subluxation or dislocation, another characteristic finding, may be evident after the newborn period. Children usually die during the first few months of life. Late-onset ISOD manifests between ages six and 18 months and is characterized by ectopia lentis (variably present), developmental delay/regression, movement disorder characterized by dystonia and choreoathetosis, ataxia, and (rarely) acute hemiplegia as a result of metabolic stroke. The clinical course may be progressive or episodic. In the episodic form encephalopathy, dystonia, choreoathetosis, and/or ataxia are intermittent.
Hereditary spastic paraplegia 5A
MedGen UID:
376521
Concept ID:
C1849115
Disease or Syndrome
Spastic paraplegia-5A (SPG5A) is an autosomal recessive neurologic disorder with a wide phenotypic spectrum. Some patients have pure spastic paraplegia affecting only gait, whereas others may have a complicated phenotype with additional manifestations, including optic atrophy or cerebellar ataxia (summary by Arnoldi et al., 2012). The hereditary spastic paraplegias (SPG) are a group of clinically and genetically diverse disorders characterized by progressive, usually severe, lower extremity spasticity; see reviews of Fink et al. (1996) and Fink (1997). Inheritance is most often autosomal dominant (see 182600), but X-linked (see 303350) and autosomal recessive forms also occur. Genetic Heterogeneity of Autosomal Recessive Spastic Paraplegia Autosomal recessive forms of SPG include SPG7 (607259), caused by mutation in the paraplegin gene (602783) on chromosome 16q24; SPG9B (616586), caused by mutation in the ALDH18A1 gene (138250) on 10q24; SPG11 (604360), caused by mutation in the spatacsin gene (610844) on 15q21; SPG15 (270700), caused by mutation in the ZFYVE26 gene (612012) on 14q24; SPG18 (611225), caused by mutation in the ERLIN2 gene (611605) on 8p11; SPG20 (275900), caused by mutation in the spartin gene (607111) on 13q12; SPG21 (248900), caused by mutation in the maspardin gene (608181) on 15q21; SPG26 (609195), caused by mutation in the B4GALNT1 gene (601873) on 12q13; SPG28 (609340), caused by mutation in the DDHD1 gene (614603) on 14q22; SPG30 (610357), caused by mutation in the KIF1A gene (601255) on 2q37; SPG35 (612319), caused by mutation in the FA2H gene (611026) on 16q23; SPG39 (612020), caused by mutation in the PNPLA6 gene (603197) on 19p13.3; SPG43 (615043), caused by mutation in the C19ORF12 gene (614297) on 19q12; SPG44 (613206), caused by mutation in the GJC2 gene (608803) on 1q42; SPG45 (613162), caused by mutation in the NT5C2 gene (600417) on 10q24; SPG46 (614409), caused by mutation in the GBA2 gene (609471) on 9p13; SPG48 (613647), caused by mutation in the KIAA0415 gene (613653) on 7p22.1; SPG50 (612936), caused by mutation in the AP4M1 gene (602296) on 7q22; SPG51 (613744), caused by mutation in the AP4E1 gene (607244) on 15q21; SPG52 (614067), caused by mutation in the AP4S1 gene (607243) on 14q12; SPG53 (614898), caused by mutation in the VPS37A gene (609927) on 8p22; SPG54 (615033), caused by mutation in the DDHD2 gene (615003) on 8p11; SPG55 (615035), caused by mutation in the MTRFR gene on 12q24; SPG56 (615030), caused by mutation in the CYP2U1 gene (610670) on 4q25; SPG57 (615658), caused by mutation in the TFG gene (602498) on 3q12; SPG61 (615685), caused by mutation in the ARL6IP1 gene (607669) on 1p12; SPG62 (615681), caused by mutation in the ERLIN1 gene on 10q24; SPG63 (615686), caused by mutation in the AMPD2 gene (102771) on 1p13; SPG64 (615683), caused by mutation in the ENTPD1 gene (601752) on 10q24; SPG72 (615625), caused by mutation in the REEP2 gene (609347) on 5q31; SPG74 (616451), caused by mutation in the IBA57 gene (615316) on 1q42; SPG75 (616680), caused by mutation in the MAG gene (159460) on 19q13; SPG76 (616907), caused by mutation in the CAPN1 gene (114220) on 11q13; SPG77 (617046), caused by mutation in the FARS2 gene (611592) on 6p25; SPG78 (617225), caused by mutation in the ATP13A2 gene (610513) on 1p36; SPG79 (615491), caused by mutation in the UCHL1 gene (191342) on 4p13; SPG81 (618768), caused by mutation in the SELENOI gene (607915) on 2p23; SPG82 (618770), caused by mutation in the PCYT2 gene (602679) on 17q25; SPG83 (619027), caused by mutation in the HPDL gene (618994) on 1p34; SPG84 (619621), caused by mutation in the PI4KA gene (600286) on 22q11; SPG85 (619686), caused by mutation in the RNF170 gene (614649) on 8p11; SPG86 (619735), caused by mutation in the ABHD16A gene (142620) on 6p21; SPG87 (619966), caused by mutation in the TMEM63C gene (619953) on 14q24; SPG89 (620379), caused by mutation in the AMFR gene (603243) on 16q13; and SPG90B (620417), caused by mutation in the SPTSSA gene (613540) on 14q13. Additional autosomal recessive forms of SPG have been mapped to chromosomes 3q (SPG14; 605229), 13q14 (SPG24; 607584), 6q (SPG25; 608220), and 10q22 (SPG27; 609041). A disorder that was formerly designated SPG49 has been reclassified as hereditary sensory and autonomic neuropathy-9 with developmental delay (HSAN9; 615031).
Krabbe disease due to saposin A deficiency
MedGen UID:
392873
Concept ID:
C2673266
Disease or Syndrome
Hereditary spastic paraplegia 48
MedGen UID:
462251
Concept ID:
C3150901
Disease or Syndrome
Spastic paraplegia-48 (SPG48) is an autosomal recessive neurologic disorder characterized by spasticity of the lower limbs resulting in gait difficulties. Most patients have onset in mid- or late-adulthood, although childhood onset has been reported in 1 patient. Additional features may include parkinsonism, urinary incontinence, neuropathy, and mild cognitive impairment (summary by Hirst et al., 2015). For a discussion of genetic heterogeneity of autosomal recessive SPG, see SPG5A (270800).
Specific language impairment 5
MedGen UID:
815813
Concept ID:
C3809483
Disease or Syndrome
Specific language impairment-5 (SLI5) is characterized by a delay in early speech acquisition and is usually associated with cerebral white matter abnormalities on brain MRI. Some individuals may show disorders in communication, consistent with autism spectrum disorder, or global developmental delay, although others ultimately show normal cognitive function. Penetrance is incomplete and expressivity is variable. This type of disorder is observed most commonly among individuals of East Asian descent (summary by Wiszniewski et al., 2013). For a phenotypic description and a discussion of genetic heterogeneity of specific language impairment, see SLI1 (602081).
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.
Congenital myasthenic syndrome 21
MedGen UID:
934621
Concept ID:
C4310654
Disease or Syndrome
Any congenital myasthenic syndrome in which the cause of the disease is a mutation in the SLC18A3 gene.
Hypermanganesemia with dystonia 2
MedGen UID:
934732
Concept ID:
C4310765
Disease or Syndrome
SLC39A14 deficiency is characterized by evidence between ages six months and three years of delay or loss of motor developmental milestones (e.g., delayed walking, gait disturbance). Early in the disease course, children show axial hypotonia followed by dystonia, spasticity, dysarthria, bulbar dysfunction, and signs of parkinsonism including bradykinesia, hypomimia, and tremor. By the end of the first decade they develop severe, generalized, pharmaco-resistant dystonia, limb contractures, and scoliosis, and lose independent ambulation. Cognitive impairment appears to be less prominent than motor disability. Some affected children have succumbed in their first decade due to secondary complications such as respiratory infections.
Childhood-onset motor and cognitive regression syndrome with extrapyramidal movement disorder
MedGen UID:
1626007
Concept ID:
C4540086
Disease or Syndrome
Childhood-onset neurodegeneration with brain atrophy (CONDBA) is a severe progressive neurodegenerative disorder characterized by loss of motor and cognitive skills between ages 2 and 7 years. Affected individuals may have normal development or mild developmental delay, but all eventually lose all motor skills, resulting in inability to walk, absence of language, and profound intellectual disability. Brain imaging shows progressive cerebral and cerebellar atrophy (summary by Edvardson et al., 2017).
Intellectual disability, autosomal dominant 53
MedGen UID:
1623344
Concept ID:
C4540481
Mental or Behavioral Dysfunction
Rubinstein-Taybi syndrome due to CREBBP mutations
MedGen UID:
1639327
Concept ID:
C4551859
Disease or Syndrome
Rubinstein-Taybi syndrome (RSTS) is characterized by distinctive facial features, broad and often angulated thumbs and halluces, short stature, and moderate-to-severe intellectual disability. The characteristic craniofacial features are downslanted palpebral fissures, low-hanging columella, high palate, grimacing smile, and talon cusps. Prenatal growth is often normal, then height, weight, and head circumference percentiles rapidly drop in the first few months of life. Short stature is typical in adulthood. Obesity may develop in childhood or adolescence. Average IQ ranges between 35 and 50; however, developmental outcome varies considerably. Some individuals with EP300-RSTS have normal intellect. Additional features include ocular abnormalities, hearing loss, respiratory difficulties, congenital heart defects, renal abnormalities, cryptorchidism, feeding problems, recurrent infections, and severe constipation.
Brain abnormalities, neurodegeneration, and dysosteosclerosis
MedGen UID:
1678789
Concept ID:
C5193117
Disease or Syndrome
Brain abnormalities, neurodegeneration, and dysosteosclerosis (BANDDOS) is an autosomal recessive disorder characterized by brain abnormalities, progressive neurologic deterioration, and sclerotic bone dysplasia similar to dysosteosclerosis (DOS). The age at onset is highly variable: some patients may present in infancy with hydrocephalus, global developmental delay, and hypotonia, whereas others may have onset of symptoms in the late teens or early twenties after normal development. Neurologic features include loss of previous motor and language skills, cognitive impairment, spasticity, and focal seizures. Brain imaging shows periventricular white matter abnormalities and calcifications, large cisterna magna or Dandy-Walker malformation, and sometimes agenesis of the corpus callosum (summary by Guo et al., 2019).
Microangiopathy and leukoencephalopathy, pontine, autosomal dominant
MedGen UID:
1684781
Concept ID:
C5231411
Disease or Syndrome
Autosomal dominant pontine microangiopathy and leukoencephalopathy (PADMAL) is a form of cerebral small vessel disease (CSVD) resulting in the onset of recurrent ischemic strokes in the thirties or forties. Affected individuals develop progressive, but variable, cognitive and motor impairment, consistent with progressive multi-infarct dementia. Brain imaging shows lacunar infarcts, often with a pontine predilection, as well as diffuse leukoencephalopathy affecting various brain regions. Although there are overlapping clinical features, the disorder is genetically and pathologically distinct from CADASIL (125310) (summary by Verdura et al., 2016).
Combined oxidative phosphorylation deficiency 48
MedGen UID:
1732052
Concept ID:
C5436602
Disease or Syndrome
Mitochondrial complex 2 deficiency, nuclear type 4
MedGen UID:
1782861
Concept ID:
C5543176
Disease or Syndrome
Mitochondrial complex II deficiency nuclear type 4 (MC2DN4) is a severe autosomal recessive disorder characterized by early-onset progressive neurodegeneration with leukoencephalopathy. Acute episodes of neurodegeneration are often triggered by catabolic stress such as infection or fasting.
Marbach-Rustad progeroid syndrome
MedGen UID:
1784907
Concept ID:
C5543388
Disease or Syndrome
Marbach-Rustad progeroid syndrome (MARUPS) is characterized by progeroid appearance with little subcutaneous fat and triangular facies, growth retardation with short stature, hypoplastic mandible crowded with unerupted supernumerary teeth, and cerebellar intention tremor. Psychomotor development is normal. Although features are reminiscent of Hutchinson-Gilford progeria syndrome (HGPS; 176670), MARUPS is less severe, with a relatively good prognosis. Two patients have been reported (Marbach et al., 2019).
Gastrointestinal defects and immunodeficiency syndrome 2
MedGen UID:
1811526
Concept ID:
C5676901
Disease or Syndrome
PI4KA-related disorder is a clinically variable disorder characterized primarily by neurologic dysfunction (limb spasticity, developmental delay, intellectual disability, seizures, ataxia, nystagmus), gastrointestinal manifestations (multiple intestinal atresia, inflammatory bowel disease), and combined immunodeficiency (leukopenia, variable immunoglobulin defects). Age of onset is typically antenatal or in early childhood; individuals can present with any combination of these features. Rare individuals present with later-onset hereditary spastic paraplegia. Brain MRI findings can include hypomyelinating leukodystrophy, cerebellar hypoplasia/atrophy, thin or dysplastic corpus callosum, and/or perisylvian polymicrogyria.
Chromosome Xq13 duplication syndrome
MedGen UID:
1809227
Concept ID:
C5677057
Disease or Syndrome
Neurodevelopmental disorder with microcephaly and speech delay, with or without brain abnormalities
MedGen UID:
1841049
Concept ID:
C5830413
Disease or Syndrome
Neurodevelopmental disorder with microcephaly and speech delay, with or without brain abnormalities (NEDMSBA) is an autosomal recessive disorder characterized by global developmental delay, hypotonia, delayed or absent walking, impaired intellectual development, and poor or absent speech, apparent from early infancy. Affected individuals have postnatal progressive microcephaly and may show poor overall growth and dysmorphic facial features. Additional more variable features include cortical visual impairment, seizures, hypotonia, spasticity, and sensorineural deafness. Brain imaging is abnormal in most patients, showing myelination defects, cortical atrophy, or thin corpus callosum. There is phenotypic variability, even within families (Bogershausen et al., 2022; Lin et al., 2022).

Professional guidelines

PubMed

Lebrun-Frénay C, Okuda DT, Siva A, Landes-Chateau C, Azevedo CJ, Mondot L, Carra-Dallière C, Zephir H, Louapre C, Durand-Dubief F, Le Page E, Bensa C, Ruet A, Ciron J, Laplaud DA, Casez O, Mathey G, de Seze J, Zeydan B, Makhani N, Tutuncu M, Levraut M, Cohen M, Thouvenot E, Pelletier D, Kantarci OH
Brain 2023 Aug 1;146(8):3431-3443. doi: 10.1093/brain/awad073. PMID: 36864688
Charidimou A, Boulouis G, Frosch MP, Baron JC, Pasi M, Albucher JF, Banerjee G, Barbato C, Bonneville F, Brandner S, Calviere L, Caparros F, Casolla B, Cordonnier C, Delisle MB, Deramecourt V, Dichgans M, Gokcal E, Herms J, Hernandez-Guillamon M, Jäger HR, Jaunmuktane Z, Linn J, Martinez-Ramirez S, Martínez-Sáez E, Mawrin C, Montaner J, Moulin S, Olivot JM, Piazza F, Puy L, Raposo N, Rodrigues MA, Roeber S, Romero JR, Samarasekera N, Schneider JA, Schreiber S, Schreiber F, Schwall C, Smith C, Szalardy L, Varlet P, Viguier A, Wardlaw JM, Warren A, Wollenweber FA, Zedde M, van Buchem MA, Gurol ME, Viswanathan A, Al-Shahi Salman R, Smith EE, Werring DJ, Greenberg SM
Lancet Neurol 2022 Aug;21(8):714-725. doi: 10.1016/S1474-4422(22)00208-3. PMID: 35841910Free PMC Article
Auriel E, Charidimou A, Gurol ME, Ni J, Van Etten ES, Martinez-Ramirez S, Boulouis G, Piazza F, DiFrancesco JC, Frosch MP, Pontes-Neto OV, Shoamanesh A, Reijmer Y, Vashkevich A, Ayres AM, Schwab KM, Viswanathan A, Greenberg SM
JAMA Neurol 2016 Feb;73(2):197-202. doi: 10.1001/jamaneurol.2015.4078. PMID: 26720093

Recent clinical studies

Etiology

Terracciano A, Cenatus B, Zhu X, Karakose S, Stephan Y, Marcolini S, De Deyn PP, Luchetti M, Sutin AR
J Psychiatr Res 2023 Sep;165:174-179. Epub 2023 Jul 21 doi: 10.1016/j.jpsychires.2023.07.026. PMID: 37506413Free PMC Article
Zhang W, Cheng Z, Fu F, Zhan Z
Neuroimage Clin 2023;37:103312. Epub 2023 Jan 3 doi: 10.1016/j.nicl.2023.103312. PMID: 36610309Free PMC Article
Yang Y, Knol MJ, Wang R, Mishra A, Liu D, Luciano M, Teumer A, Armstrong N, Bis JC, Jhun MA, Li S, Adams HHH, Aziz NA, Bastin ME, Bourgey M, Brody JA, Frenzel S, Gottesman RF, Hosten N, Hou L, Kardia SLR, Lohner V, Marquis P, Maniega SM, Satizabal CL, Sorond FA, Valdés Hernández MC, van Duijn CM, Vernooij MW, Wittfeld K, Yang Q, Zhao W, Boerwinkle E, Levy D, Deary IJ, Jiang J, Mather KA, Mosley TH, Psaty BM, Sachdev PS, Smith JA, Sotoodehnia N, DeCarli CS, Breteler MMB, Ikram MA, Grabe HJ, Wardlaw J, Longstreth WT, Launer LJ, Seshadri S, Debette S, Fornage M
Brain 2023 Feb 13;146(2):492-506. doi: 10.1093/brain/awac290. PMID: 35943854Free PMC Article
Dewenter A, Jacob MA, Cai M, Gesierich B, Hager P, Kopczak A, Biel D, Ewers M, Tuladhar AM, de Leeuw FE, Dichgans M, Franzmeier N, Duering M; SVDs@target Consortium and Alzheimer’s Disease Neuroimaging Initiative (ADNI)
Brain 2023 Feb 13;146(2):678-689. doi: 10.1093/brain/awac265. PMID: 35859352Free PMC Article
Chojdak-Łukasiewicz J, Dziadkowiak E, Zimny A, Paradowski B
Adv Clin Exp Med 2021 Mar;30(3):349-356. doi: 10.17219/acem/131216. PMID: 33768739

Diagnosis

Terracciano A, Cenatus B, Zhu X, Karakose S, Stephan Y, Marcolini S, De Deyn PP, Luchetti M, Sutin AR
J Psychiatr Res 2023 Sep;165:174-179. Epub 2023 Jul 21 doi: 10.1016/j.jpsychires.2023.07.026. PMID: 37506413Free PMC Article
Balestrieri A, Lucatelli P, Suri HS, Montisci R, Suri JS, Wintermark M, Serra A, Cheng X, Jinliang C, Sanfilippo R, Saba L
J Stroke Cerebrovasc Dis 2021 Aug;30(8):105905. Epub 2021 Jun 6 doi: 10.1016/j.jstrokecerebrovasdis.2021.105905. PMID: 34107418
Chojdak-Łukasiewicz J, Dziadkowiak E, Zimny A, Paradowski B
Adv Clin Exp Med 2021 Mar;30(3):349-356. doi: 10.17219/acem/131216. PMID: 33768739
Hilal S, Biesbroek JM, Vrooman H, Chong E, Kuijf HJ, Venketasubramanian N, Cheng CY, Wong TY, Biessels GJ, Chen C
Am J Geriatr Psychiatry 2021 Feb;29(2):156-165. Epub 2020 Jun 17 doi: 10.1016/j.jagp.2020.06.009. PMID: 32651052
Tubi MA, Feingold FW, Kothapalli D, Hare ET, King KS, Thompson PM, Braskie MN; Alzheimer’s Disease Neuroimaging Initiative
Neuroimage 2020 Feb 1;206:116327. Epub 2019 Nov 1 doi: 10.1016/j.neuroimage.2019.116327. PMID: 31682983Free PMC Article

Therapy

Markus HS, de Leeuw FE
Int J Stroke 2023 Jan;18(1):4-14. doi: 10.1177/17474930221144911. PMID: 36575578Free PMC Article
Yang Y, Knol MJ, Wang R, Mishra A, Liu D, Luciano M, Teumer A, Armstrong N, Bis JC, Jhun MA, Li S, Adams HHH, Aziz NA, Bastin ME, Bourgey M, Brody JA, Frenzel S, Gottesman RF, Hosten N, Hou L, Kardia SLR, Lohner V, Marquis P, Maniega SM, Satizabal CL, Sorond FA, Valdés Hernández MC, van Duijn CM, Vernooij MW, Wittfeld K, Yang Q, Zhao W, Boerwinkle E, Levy D, Deary IJ, Jiang J, Mather KA, Mosley TH, Psaty BM, Sachdev PS, Smith JA, Sotoodehnia N, DeCarli CS, Breteler MMB, Ikram MA, Grabe HJ, Wardlaw J, Longstreth WT, Launer LJ, Seshadri S, Debette S, Fornage M
Brain 2023 Feb 13;146(2):492-506. doi: 10.1093/brain/awac290. PMID: 35943854Free PMC Article
Grasso EA, Cacciatore M, Gentile C, Breda L, Giacomelli R, Verrotti A
Clin Exp Rheumatol 2021 May-Jun;39(3):651-659. Epub 2020 Sep 4 doi: 10.55563/clinexprheumatol/43pqih. PMID: 32896270
Li Q, Yang Y, Reis C, Tao T, Li W, Li X, Zhang JH
Cell Transplant 2018 Dec;27(12):1711-1722. Epub 2018 Sep 25 doi: 10.1177/0963689718795148. PMID: 30251566Free PMC Article
Clark D, Kebede W, Eggenberger E
Neurol Clin 2010 Aug;28(3):573-80. doi: 10.1016/j.ncl.2010.03.001. PMID: 20637989

Prognosis

Phuah CL, Chen Y, Strain JF, Yechoor N, Laurido-Soto OJ, Ances BM, Lee JM; Alzheimer's Disease Neuroimaging Initiative
Neurology 2022 Dec 5;99(23):e2535-e2547. doi: 10.1212/WNL.0000000000201186. PMID: 36123127Free PMC Article
Lahna D, Schwartz DL, Woltjer R, Black SE, Roese N, Dodge H, Boespflug EL, Keith J, Gao F, Ramirez J, Silbert LC
Ann Neurol 2022 Dec;92(6):992-1000. Epub 2022 Sep 6 doi: 10.1002/ana.26487. PMID: 36054513Free PMC Article
Jiménez-Balado J, Corlier F, Habeck C, Stern Y, Eich T
Sci Rep 2022 Feb 4;12(1):1955. doi: 10.1038/s41598-022-06019-8. PMID: 35121804Free PMC Article
Balestrieri A, Lucatelli P, Suri HS, Montisci R, Suri JS, Wintermark M, Serra A, Cheng X, Jinliang C, Sanfilippo R, Saba L
J Stroke Cerebrovasc Dis 2021 Aug;30(8):105905. Epub 2021 Jun 6 doi: 10.1016/j.jstrokecerebrovasdis.2021.105905. PMID: 34107418
Tamura Y, Araki A
Geriatr Gerontol Int 2015 Dec;15 Suppl 1:34-42. doi: 10.1111/ggi.12666. PMID: 26671155

Clinical prediction guides

de Havenon A, Smith EE, Sharma R, Falcone GJ, Bangad A, Prabhakaran S, Sheth KN
J Am Heart Assoc 2023 Jul 4;12(13):e029374. Epub 2023 Jun 22 doi: 10.1161/JAHA.123.029374. PMID: 37345754Free PMC Article
Sun Y, Guo Y, Li HQ, Tan L, Feng JF, Cheng W, Yu JT
J Neurochem 2023 Jul;166(2):414-423. Epub 2023 May 24 doi: 10.1111/jnc.15845. PMID: 37222503
Zhang W, Cheng Z, Fu F, Zhan Z
Neuroimage Clin 2023;37:103312. Epub 2023 Jan 3 doi: 10.1016/j.nicl.2023.103312. PMID: 36610309Free PMC Article
Jochems ACC, Arteaga C, Chappell F, Ritakari T, Hooley M, Doubal F, Muñoz Maniega S, Wardlaw JM
Neurology 2022 Nov 29;99(22):e2454-e2463. Epub 2022 Sep 19 doi: 10.1212/WNL.0000000000201205. PMID: 36123130Free PMC Article
Lahna D, Schwartz DL, Woltjer R, Black SE, Roese N, Dodge H, Boespflug EL, Keith J, Gao F, Ramirez J, Silbert LC
Ann Neurol 2022 Dec;92(6):992-1000. Epub 2022 Sep 6 doi: 10.1002/ana.26487. PMID: 36054513Free PMC Article

Recent systematic reviews

Zhang W, Cheng Z, Fu F, Zhan Z
Neuroimage Clin 2023;37:103312. Epub 2023 Jan 3 doi: 10.1016/j.nicl.2023.103312. PMID: 36610309Free PMC Article
Theodorou A, Palaiodimou L, Malhotra K, Zompola C, Katsanos AH, Shoamanesh A, Boviatsis E, Dardiotis E, Spilioti M, Sacco S, Werring DJ, Cordonnier C, Alexandrov AV, Paraskevas GP, Tsivgoulis G
Stroke 2023 Jan;54(1):178-188. Epub 2022 Dec 1 doi: 10.1161/STROKEAHA.122.040671. PMID: 36453271
Debette S, Schilling S, Duperron MG, Larsson SC, Markus HS
JAMA Neurol 2019 Jan 1;76(1):81-94. doi: 10.1001/jamaneurol.2018.3122. PMID: 30422209Free PMC Article
Roseborough A, Ramirez J, Black SE, Edwards JD
Alzheimers Dement 2017 Oct;13(10):1154-1167. Epub 2017 Mar 16 doi: 10.1016/j.jalz.2017.01.026. PMID: 28322203
Debette S, Markus HS
BMJ 2010 Jul 26;341:c3666. doi: 10.1136/bmj.c3666. PMID: 20660506Free PMC Article

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