U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

Cerebral hemorrhage

MedGen UID:
423648
Concept ID:
C2937358
Pathologic Function
Synonym: Intracerebral hemorrhage
SNOMED CT: Intracerebral hemorrhage (274100004); ICH - intracerebral hemorrhage (274100004); Cerebral hemorrhage (274100004)
 
HPO: HP:0001342
Monarch Initiative: MONDO:0013792

Definition

Hemorrhage into the parenchyma of the brain. [from HPO]

Conditions with this feature

Pheochromocytoma
MedGen UID:
18419
Concept ID:
C0031511
Neoplastic Process
Hereditary paraganglioma-pheochromocytoma (PGL/PCC) syndromes are characterized by paragangliomas (tumors that arise from neuroendocrine tissues distributed along the paravertebral axis from the base of the skull to the pelvis) and pheochromocytomas (paragangliomas that are confined to the adrenal medulla). Sympathetic paragangliomas cause catecholamine excess; parasympathetic paragangliomas are most often nonsecretory. Extra-adrenal parasympathetic paragangliomas are located predominantly in the skull base and neck (referred to as head and neck PGL [HNPGL]) and sometimes in the upper mediastinum; approximately 95% of such tumors are nonsecretory. In contrast, sympathetic extra-adrenal paragangliomas are generally confined to the lower mediastinum, abdomen, and pelvis, and are typically secretory. Pheochromocytomas, which arise from the adrenal medulla, typically lead to catecholamine excess. Symptoms of PGL/PCC result from either mass effects or catecholamine hypersecretion (e.g., sustained or paroxysmal elevations in blood pressure, headache, episodic profuse sweating, forceful palpitations, pallor, and apprehension or anxiety). The risk for developing metastatic disease is greater for extra-adrenal sympathetic paragangliomas than for pheochromocytomas.
Acquired polycythemia vera
MedGen UID:
45996
Concept ID:
C0032463
Neoplastic Process
Polycythemia vera (PV), the most common form of primary polycythemia, is caused by somatic mutation in a single hematopoietic stem cell leading to clonal hematopoiesis. PV is a myeloproliferative disorder characterized predominantly by erythroid hyperplasia, but also by myeloid leukocytosis, thrombocytosis, and splenomegaly. Familial cases of PV are very rare and usually manifest in elderly patients (Cario, 2005). PV is distinct from the familial erythrocytoses (see, e.g., ECYT1, 133100), which are caused by inherited mutations resulting in hypersensitivity of erythroid progenitors to hormonal influences or increased levels of circulating hormones, namely erythropoietin (EPO; 133170) (Prchal, 2005).
Sneddon syndrome
MedGen UID:
76449
Concept ID:
C0282492
Disease or Syndrome
Sneddon syndrome is a noninflammatory arteriopathy characterized by onset of livedo reticularis in the second decade and onset of cerebrovascular disease in early adulthood (summary by Bras et al., 2014). Livedo reticularis occurs also with polyarteritis nodosa, systemic lupus erythematosus, and central thrombocythemia, any one of which may be accompanied by cerebrovascular accidents (Bruyn et al., 1987).
Hereditary cerebral amyloid angiopathy, Icelandic type
MedGen UID:
279656
Concept ID:
C1527338
Disease or Syndrome
Cerebral amyloid angiopathy (CAA), defined by the deposition of congophilic material in the vessels of the cortex and leptomeninges, is a major cause of intracerebral hemorrhage in the elderly (Vinters, 1987, Greenberg, 1998). Palsdottir et al. (1988) referred to the disorder in Icelandic patients as hereditary cystatin C amyloid angiopathy (HCCAA).
Chuvash polycythemia
MedGen UID:
332974
Concept ID:
C1837915
Disease or Syndrome
Familial erythrocytosis-2 (ECYT2) is an autosomal recessive disorder characterized by increased red blood cell mass, increased serum levels of erythropoietin (EPO; 133170), and normal oxygen affinity. Patients with ECYT2 carry a high risk for peripheral thrombosis and cerebrovascular events (Cario, 2005). Familial erythrocytosis-2 has features of both primary and secondary erythrocytosis. In addition to increased circulating levels of EPO, consistent with a secondary, extrinsic process, erythroid progenitors may be hypersensitive to EPO, consistent with a primary, intrinsic process (Prchal, 2005). For a general phenotypic description and a discussion of genetic heterogeneity of familial erythrocytosis, see ECYT1 (133100).
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.
Heterotopia, periventricular, X-linked dominant
MedGen UID:
376309
Concept ID:
C1848213
Disease or Syndrome
FLNA deficiency is associated with a phenotypic spectrum that includes FLNA-related periventricular nodular heterotopia (Huttenlocher syndrome), congenital heart disease (patent ductus arteriosus, atrial and ventricular septal defects), valvular dystrophy, dilation and rupture of the thoracic aortic, pulmonary disease (pulmonary hypertension, alveolar hypoplasia, emphysema, asthma, chronic bronchitis), gastrointestinal dysmotility and obstruction, joint hypermobility, and macrothrombocytopenia.
Vitamin K-dependent clotting factors, combined deficiency of, type 1
MedGen UID:
376381
Concept ID:
C1848534
Disease or Syndrome
Deficiency of all vitamin K-dependent clotting factors leads to a bleeding tendency that is usually reversed by oral administration of vitamin K. Acquired forms of the disorder can be caused by intestinal malabsorption of vitamin K. Familial multiple coagulation factor deficiency is rare. Clinical symptoms of the disease include episodes of intracranial hemorrhage in the first weeks of life, sometimes leading to a fatal outcome. The pathomechanism is based on a reduced hepatic gamma-carboxylation of glutamic acid residues of all vitamin K-dependent blood coagulation factors, as well as the anticoagulant factors protein C (612283) and protein S (176880). Posttranslational gamma-carboxylation of proteins enables the calcium-dependent attachment of the proteins to the phospholipid bilayer of membranes, an essential prerequisite for blood coagulation. Vitamin K1 acts as a cofactor for the vitamin K-dependent carboxylase in liver microsomes, GGCX. Genetic Heterogeneity of Combined Deficiency of Vitamin K-Dependent Clotting Factors Combined deficiency of vitamin K-dependent clotting factors-2 (VKFCD2; 607473) is caused by mutation in the gene encoding vitamin K epoxide reductase (VKORC1; 608547) on chromosome 16p11.
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.
Cerebral cavernous malformation 3
MedGen UID:
355121
Concept ID:
C1864040
Disease or Syndrome
Cerebral cavernous malformations (CCMs) are vascular malformations in the brain and spinal cord comprising closely clustered, enlarged capillary channels (caverns) with a single layer of endothelium without mature vessel wall elements or normal intervening brain parenchyma. The diameter of CCMs ranges from a few millimeters to several centimeters. CCMs increase or decrease in size and increase in number over time. Hundreds of lesions may be identified, depending on the person's age and the quality and type of brain imaging used. Although CCMs have been reported in infants and children, the majority become evident between the second and fifth decades with findings such as seizures, focal neurologic deficits, nonspecific headaches, and cerebral hemorrhage. Up to 50% of individuals with FCCM remain symptom free throughout their lives. Cutaneous vascular lesions are found in 9% of those with familial cerebral cavernous malformations (FCCM; see Diagnosis/testing) and retinal vascular lesions in almost 5%.
Cerebral cavernous malformation 2
MedGen UID:
400438
Concept ID:
C1864041
Disease or Syndrome
Cerebral cavernous malformations (CCMs) are vascular malformations in the brain and spinal cord comprising closely clustered, enlarged capillary channels (caverns) with a single layer of endothelium without mature vessel wall elements or normal intervening brain parenchyma. The diameter of CCMs ranges from a few millimeters to several centimeters. CCMs increase or decrease in size and increase in number over time. Hundreds of lesions may be identified, depending on the person's age and the quality and type of brain imaging used. Although CCMs have been reported in infants and children, the majority become evident between the second and fifth decades with findings such as seizures, focal neurologic deficits, nonspecific headaches, and cerebral hemorrhage. Up to 50% of individuals with FCCM remain symptom free throughout their lives. Cutaneous vascular lesions are found in 9% of those with familial cerebral cavernous malformations (FCCM; see Diagnosis/testing) and retinal vascular lesions in almost 5%.
Pseudoxanthoma elasticum, forme fruste
MedGen UID:
357280
Concept ID:
C1867450
Disease or Syndrome
Pseudoxanthoma elasticum (PXE) is a systemic disorder that affects the elastic tissue of the skin, the eye, and vascular system. Individuals most commonly present with angioid streaks of the retina found on routine eye examination or associated with retinal hemorrhage and/or characteristic papules in the skin. The most frequent cause of morbidity and disability in PXE is reduced vision due to complications of subretinal neovascularizations and macular atrophy. Other manifestations include premature gastrointestinal angina and/or bleeding, intermittent claudication of arm and leg muscles, stroke, renovascular hypertension, and cardiovascular complications (angina/myocardial infarction). Most affected individuals live a normal life span.
Pheochromocytoma-islet cell tumor syndrome
MedGen UID:
401431
Concept ID:
C1868392
Neoplastic Process
Moyamoya angiopathy-short stature-facial dysmorphism-hypergonadotropic hypogonadism syndrome
MedGen UID:
463207
Concept ID:
C3151857
Disease or Syndrome
This multisystem disorder is characterized by moyamoya disease, short stature, hypergonadotropic hypogonadism, and facial dysmorphism. Other variable features include dilated cardiomyopathy, premature graying of the hair, and early-onset cataracts. Moyamoya disease is a progressive cerebrovascular disorder characterized by stenosis or occlusion of the internal carotid arteries and the main branches, leading to the development of small collateral vessels (moyamoya vessels) at the base of the brain. Affected individuals can develop acute neurologic events due to stroke-like episodes (summary by Miskinyte et al., 2011). For a general phenotypic description and a discussion of genetic heterogeneity of moyamoya disease, see MYMY1 (252350).
Thrombophilia due to protein S deficiency, autosomal recessive
MedGen UID:
482722
Concept ID:
C3281092
Disease or Syndrome
Autosomal recessive thrombophilia due to protein S deficiency is a very rare and severe hematologic disorder resulting in thrombosis and secondary hemorrhage usually beginning in early infancy. Some affected individuals develop neonatal purpura fulminans, multifocal thrombosis, or intracranial hemorrhage (Pung-amritt et al., 1999; Fischer et al., 2010), whereas others have recurrent thromboses later in childhood (Comp et al., 1984). See also autosomal dominant thrombophilia due to protein S deficiency (THPH5; 612336), a less severe disorder caused by heterozygous mutation in the PROS1 gene.
Seizures-scoliosis-macrocephaly syndrome
MedGen UID:
909039
Concept ID:
C4225248
Disease or Syndrome
Seizures, scoliosis, and macrocephaly/microcephaly syndrome (SSMS) is an autosomal recessive neurodevelopmental disorder characterized by global developmental delay apparent from early infancy, impaired intellectual development, behavioral problems, poor or absent speech, seizures, dysmorphic facial features with macro- or microcephaly, and skeletal abnormalities, including scoliosis and delayed bone age. Other features may include hypotonia, gastrointestinal problems, and exostoses (summary by Gentile et al., 2019).
Pseudo-TORCH syndrome 2
MedGen UID:
1373355
Concept ID:
C4479376
Disease or Syndrome
Pseudo-TORCH syndrome-2 (PTORCH2) is an autosomal recessive multisystem disorder characterized by antenatal onset of intracranial hemorrhage, calcification, brain malformations, liver dysfunction, and often thrombocytopenia. Affected individuals tend to have respiratory insufficiency and seizures, and die in infancy. The phenotype resembles the sequelae of intrauterine infection, but there is no evidence of an infectious agent. The disorder results from inappropriate activation of the interferon (IFN) immunologic pathway (summary by Meuwissen et al., 2016). For a discussion of genetic heterogeneity of PTORCH, see PTORCH1 (251290).
Primary familial polycythemia due to EPO receptor mutation
MedGen UID:
1641215
Concept ID:
C4551637
Disease or Syndrome
Primary familial and congenital polycythemia (PFCP) is characterized by isolated erythrocytosis in an individual with a normal-sized spleen and absence of disorders causing secondary erythrocytosis. Clinical manifestations relate to the erythrocytosis and can include plethora, the hyperviscosity syndrome (headache, dizziness, fatigue, lassitude, visual and auditory disturbances, paresthesia, myalgia), altered mental status caused by hypoperfusion and local hypoxia, and arterial and/or venous thromboembolic events. Although the majority of individuals with PFCP have only mild manifestations of hyperviscosity such as dizziness or headache, some affected individuals have had severe and even fatal complications including arterial hypertension, intracerebral hemorrhage, deep vein thrombosis, coronary disease, and myocardial infarction. To date 116 affected individuals from 24 families have been reported.
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.
Brain small vessel disease 1 with or without ocular anomalies
MedGen UID:
1647320
Concept ID:
C4551998
Disease or Syndrome
The spectrum of COL4A1-related disorders includes: small-vessel brain disease of varying severity including porencephaly, variably associated with eye defects (retinal arterial tortuosity, Axenfeld-Rieger anomaly, cataract) and systemic findings (kidney involvement, muscle cramps, cerebral aneurysms, Raynaud phenomenon, cardiac arrhythmia, and hemolytic anemia). On imaging studies, small-vessel brain disease is manifest as diffuse periventricular leukoencephalopathy, lacunar infarcts, microhemorrhage, dilated perivascular spaces, and deep intracerebral hemorrhages. Clinically, small-vessel brain disease manifests as infantile hemiparesis, seizures, single or recurrent hemorrhagic stroke, ischemic stroke, and isolated migraine with aura. Porencephaly (fluid-filled cavities in the brain detected by CT or MRI) is typically manifest as infantile hemiparesis, seizures, and intellectual disability; however, on occasion it can be an incidental finding. HANAC (hereditary angiopathy with nephropathy, aneurysms, and muscle cramps) syndrome usually associates asymptomatic small-vessel brain disease, cerebral large vessel involvement (i.e., aneurysms), and systemic findings involving the kidney, muscle, and small vessels of the eye. Two additional phenotypes include isolated retinal artery tortuosity and nonsyndromic autosomal dominant congenital cataract.
Pseudo-TORCH syndrome 3
MedGen UID:
1708513
Concept ID:
C5394391
Disease or Syndrome
Pseudo-TORCH syndrome-3 (PTORCH3) is an autosomal recessive disorder of immune dysregulation and neuroinflammation apparent from early infancy. Affected individuals have developmental delay with acute episodes of fever and multisystemic organ involvement, including coagulopathy, elevated liver enzymes, and proteinuria, often associated with thrombotic microangiopathy. Brain imaging shows progressive intracranial calcifications, white matter abnormalities, and sometimes cerebral or cerebellar atrophy. Laboratory studies show abnormal elevation of interferon (IFN)-stimulated gene (ISG) transcripts consistent with a type I interferonopathy. The phenotype resembles the sequelae of intrauterine infection, but there is usually no evidence of an infectious agent. The disorder results from defects in negative regulation of the interferon immunologic pathway. Death in early childhood is common (summary by Duncan et al., 2019 and Gruber et al., 2020). For a discussion of genetic heterogeneity of PTORCH, see PTORCH1 (251290).
Autoinflammatory disease, X-linked
MedGen UID:
1811268
Concept ID:
C5676885
Disease or Syndrome
X-linked systemic autoinflammatory disease (SAIDX) is characterized by the onset of systemic autoinflammation in the first months of life. Features include lymphadenopathy, hepatosplenomegaly, fever, panniculitis, and nodular skin rash. Additional manifestations may include inflammation of the optic nerve, intracranial hemorrhage, and lipodystrophy. Laboratory studies show hypogammaglobulinemia, increased or decreased white blood cell count, autoimmune cytopenias, elevated serum inflammatory markers, and a type I interferon signature (de Jesus et al., 2020 and Lee et al., 2022).
Cardiomyopathy, dilated, 2G
MedGen UID:
1801983
Concept ID:
C5676995
Disease or Syndrome
Dilated cardiomyopathy-2G (CMD2G) is characterized by early-onset severe dilated cardiomyopathy that progresses rapidly to heart failure in the neonatal period without evidence of intervening hypertrophy. Cardiac tissue exhibits markedly shortened thin filaments, disorganized myofibrils, and reduced contractile force generation, resulting in the severe ventricular dysfunction observed. There is no evidence of skeletal muscle hypertrophy (Ahrens-Nicklas et al., 2019). For a general phenotypic description and a discussion of genetic heterogeneity of dilated cardiomyopathy, see 115200.
Congenital myopathy 2c, severe infantile, autosomal dominant
MedGen UID:
1840969
Concept ID:
C5830333
Disease or Syndrome
Congenital myopathy-2C (CMYP2C) is an autosomal dominant disorder of the skeletal muscle characterized by severe congenital weakness usually resulting in death from respiratory failure in the first year or so of life. Patients present at birth with hypotonia, lack of antigravity movements, poor head control, and difficulties feeding or breathing, often requiring tube-feeding and mechanical ventilation. Decreased fetal movements may be observed in some cases. Of the patients with congenital myopathy caused by mutation in the ACTA1 gene, about 90% carry heterozygous mutations that are usually de novo and cause the severe infantile phenotype. Some patients with heterozygous mutations have a more typical and milder disease course with delayed motor development and proximal muscle weakness, but are able to achieve independent ambulation (CMYP2A; 161800). The severity of the disease most likely depends on the detrimental effect of the mutation, although there are probably additional modifying factors (Ryan et al., 2001; Laing et al., 2009; Sanoudou and Beggs, 2001; Agrawal et al., 2004; Nowak et al., 2013; Sewry et al., 2019; Laitila and Wallgren-Pettersson, 2021). For a discussion of genetic heterogeneity of congenital myopathy, see CMYP1A (117000).
Mitochondrial trifunctional protein deficiency 2
MedGen UID:
1841010
Concept ID:
C5830374
Disease or Syndrome
The mitochondrial trifunctional protein, composed of 4 alpha and 4 beta subunits, catalyzes 3 steps in mitochondrial beta-oxidation of fatty acids: long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD), long-chain enoyl-CoA hydratase, and long-chain thiolase activities. Trifunctional protein deficiency is characterized by decreased activity of all 3 enzymes. Clinically, classic trifunctional protein deficiency can be classified into 3 main clinical phenotypes: neonatal onset of a severe, lethal condition resulting in sudden unexplained infant death (SIDS; 272120), infantile onset of a hepatic Reye-like syndrome, and late-adolescent onset of primarily a skeletal myopathy (summary by Spiekerkoetter et al., 2003). Some patients with MTP deficiency show a protracted progressive course associated with myopathy, recurrent rhabdomyolysis, and sensorimotor axonal neuropathy. These patients tend to survive into adolescence and adulthood (den Boer et al., 2003). See mitochondrial trifunctional protein deficiency-1 (609015), caused by mutation in the HADHA gene (600890), the alpha subunit of mitochondrial trifunctional protein.
Neurodevelopmental disorder with intracranial hemorrhage, seizures, and spasticity
MedGen UID:
1841145
Concept ID:
C5830509
Disease or Syndrome
Neurodevelopmental disorder with intracranial hemorrhage, seizures, and spasticity (NEDIHSS) is an autosomal recessive disorder characterized by prenatal or neonatal onset of intracranial hemorrhage, usually with ventriculomegaly and calcifications, resulting in parenchymal brain damage. Some affected individuals have symptoms incompatible with life and die in utero. Those that survive show profound global developmental delay with almost no motor or cognitive skills, hypotonia, spasticity, and seizures. Other features may include facial dysmorphism, retinal vascular abnormalities, and poor overall growth. The pathogenesis of the disease likely results from dysfunction of vascular endothelial cells in the brain (Lecca et al., 2023).

Professional guidelines

PubMed

Overton E, Tobes D, Lee A
Best Pract Res Clin Anaesthesiol 2022 May;36(1):107-121. Epub 2022 Feb 10 doi: 10.1016/j.bpa.2022.02.003. PMID: 35659948
Greenberg SM, Ziai WC, Cordonnier C, Dowlatshahi D, Francis B, Goldstein JN, Hemphill JC 3rd, Johnson R, Keigher KM, Mack WJ, Mocco J, Newton EJ, Ruff IM, Sansing LH, Schulman S, Selim MH, Sheth KN, Sprigg N, Sunnerhagen KS; American Heart Association/American Stroke Association
Stroke 2022 Jul;53(7):e282-e361. Epub 2022 May 17 doi: 10.1161/STR.0000000000000407. PMID: 35579034
Magid-Bernstein J, Girard R, Polster S, Srinath A, Romanos S, Awad IA, Sansing LH
Circ Res 2022 Apr 15;130(8):1204-1229. Epub 2022 Apr 14 doi: 10.1161/CIRCRESAHA.121.319949. PMID: 35420918Free PMC Article

Recent clinical studies

Etiology

Khalil F, Badshah M, Sathyanarayanan SP, Amin N
S D Med 2023 Apr;76(4):170-173. PMID: 37566673
Sheth KN
N Engl J Med 2022 Oct 27;387(17):1589-1596. doi: 10.1056/NEJMra2201449. PMID: 36300975
Li L, Murthy SB
Stroke 2022 Jul;53(7):2131-2141. Epub 2022 Jun 8 doi: 10.1161/STROKEAHA.122.036884. PMID: 35674043Free PMC Article
Garg R, Biller J
F1000Res 2019;8 Epub 2019 Mar 18 doi: 10.12688/f1000research.16357.1. PMID: 30906532Free PMC Article
Thabet AM, Kottapally M, Hemphill JC 3rd
Handb Clin Neurol 2017;140:177-194. doi: 10.1016/B978-0-444-63600-3.00011-8. PMID: 28187799

Diagnosis

Nat Rev Dis Primers 2023 Mar 16;9(1):15. doi: 10.1038/s41572-023-00428-3. PMID: 36928647
Ziai WC, Carhuapoma JR
Continuum (Minneap Minn) 2018 Dec;24(6):1603-1622. doi: 10.1212/CON.0000000000000672. PMID: 30516598
Noorbakhsh-Sabet N, Pulakanti VC, Zand R
J Stroke Cerebrovasc Dis 2017 Oct;26(10):2043-2049. Epub 2017 Aug 18 doi: 10.1016/j.jstrokecerebrovasdis.2017.07.012. PMID: 28826581
Sansing LH
Semin Neurol 2016 Jun;36(3):223-4. Epub 2016 May 23 doi: 10.1055/s-0036-1583296. PMID: 27214696
Labovitz DL, Sacco RL
Curr Opin Neurol 2001 Feb;14(1):103-8. doi: 10.1097/00019052-200102000-00016. PMID: 11176225

Therapy

Qureshi AI, Huang W, Lobanova I, Barsan WG, Hanley DF, Hsu CY, Lin CL, Silbergleit R, Steiner T, Suarez JI, Toyoda K, Yamamoto H; for ATACH-II trial investigators
JAMA Neurol 2020 Nov 1;77(11):1355-1365. doi: 10.1001/jamaneurol.2020.3075. PMID: 32897310Free PMC Article
Hanley DF, Thompson RE, Rosenblum M, Yenokyan G, Lane K, McBee N, Mayo SW, Bistran-Hall AJ, Gandhi D, Mould WA, Ullman N, Ali H, Carhuapoma JR, Kase CS, Lees KR, Dawson J, Wilson A, Betz JF, Sugar EA, Hao Y, Avadhani R, Caron JL, Harrigan MR, Carlson AP, Bulters D, LeDoux D, Huang J, Cobb C, Gupta G, Kitagawa R, Chicoine MR, Patel H, Dodd R, Camarata PJ, Wolfe S, Stadnik A, Money PL, Mitchell P, Sarabia R, Harnof S, Barzo P, Unterberg A, Teitelbaum JS, Wang W, Anderson CS, Mendelow AD, Gregson B, Janis S, Vespa P, Ziai W, Zuccarello M, Awad IA; MISTIE III Investigators
Lancet 2019 Mar 9;393(10175):1021-1032. Epub 2019 Feb 7 doi: 10.1016/S0140-6736(19)30195-3. PMID: 30739747Free PMC Article
Newman CB, Preiss D, Tobert JA, Jacobson TA, Page RL 2nd, Goldstein LB, Chin C, Tannock LR, Miller M, Raghuveer G, Duell PB, Brinton EA, Pollak A, Braun LT, Welty FK; American Heart Association Clinical Lipidology, Lipoprotein, Metabolism and Thrombosis Committee, a Joint Committee of the Council on Atherosclerosis, Thrombosis and Vascular Biology and Council on Lifestyle and Cardiometabolic Health; Council on Cardiovascular Disease in the Young; Council on Clinical Cardiology; and Stroke Council
Arterioscler Thromb Vasc Biol 2019 Feb;39(2):e38-e81. doi: 10.1161/ATV.0000000000000073. PMID: 30580575
Sperling RA, Jack CR Jr, Black SE, Frosch MP, Greenberg SM, Hyman BT, Scheltens P, Carrillo MC, Thies W, Bednar MM, Black RS, Brashear HR, Grundman M, Siemers ER, Feldman HH, Schindler RJ
Alzheimers Dement 2011 Jul;7(4):367-85. doi: 10.1016/j.jalz.2011.05.2351. PMID: 21784348Free PMC Article
Lancet 1988 Aug 13;2(8607):349-60. PMID: 2899772

Prognosis

Chen T, Qian Y, Deng X
Cardiovasc Diabetol 2023 Jun 29;22(1):156. doi: 10.1186/s12933-023-01893-6. PMID: 37386419Free PMC Article
Peng J, Wang H, Rong X, He L, Xiangpen L, Shen Q, Peng Y
Alcohol Alcohol 2020 Feb 7;55(1):20-27. doi: 10.1093/alcalc/agz087. PMID: 31845978
Fallenius M, Skrifvars MB, Reinikainen M, Bendel S, Curtze S, Sibolt G, Martinez-Majander N, Raj R
Stroke 2019 Sep;50(9):2336-2343. Epub 2019 Jul 17 doi: 10.1161/STROKEAHA.118.024560. PMID: 31311464
Pinho J, Costa AS, Araújo JM, Amorim JM, Ferreira C
J Neurol Sci 2019 Mar 15;398:54-66. Epub 2019 Jan 14 doi: 10.1016/j.jns.2019.01.013. PMID: 30682522
van Asch CJ, Luitse MJ, Rinkel GJ, van der Tweel I, Algra A, Klijn CJ
Lancet Neurol 2010 Feb;9(2):167-76. Epub 2010 Jan 5 doi: 10.1016/S1474-4422(09)70340-0. PMID: 20056489

Clinical prediction guides

Wang P, Wu F, Wang Y, Du F, Yang X, Li J, Sheng J, Yu H, Jiang R
Medicine (Baltimore) 2022 Mar 4;101(9):e28912. doi: 10.1097/MD.0000000000028912. PMID: 35244045Free PMC Article
Gómez-González A, Lazcano U, Vivanco-Hidalgo RM, Prats-Sánchez L, Guisado-Alonso D, Delgado-Mederos R, Camps-Renom P, Martínez Domeño A, Cuadrado-Godia E, Giralt Steinhauer E, Jiménez-Conde J, Soriano-Tárraga C, Avellaneda-Gómez C, Rodríguez-Campello A, Martí-Fábregas J, Ois A, Roquer J
Cerebrovasc Dis 2021;50(4):435-442. Epub 2021 Apr 8 doi: 10.1159/000515169. PMID: 33831860
Heit JJ, Coelho H, Lima FO, Granja M, Aghaebrahim A, Hanel R, Kwok K, Haerian H, Cereda CW, Venkatasubramanian C, Dehkharghani S, Carbonera LA, Wiener J, Copeland K, Mont'Alverne F
AJNR Am J Neuroradiol 2021 Jan;42(2):273-278. Epub 2020 Dec 24 doi: 10.3174/ajnr.A6926. PMID: 33361378Free PMC Article
Sporns PB, Kemmling A, Minnerup J, Hanning U, Heindel W
Acta Neurochir (Wien) 2018 Aug;160(8):1663-1670. Epub 2018 Jun 26 doi: 10.1007/s00701-018-3605-x. PMID: 29943191
Lanfranconi S, Franco G, Borellini L, Denaro F, Basilico P, Parati E, Micieli G, Bersano A
Panminerva Med 2013 Mar;55(1):11-28. PMID: 23474661

Recent systematic reviews

Ebell MH, Barry HC, Baduni K, Grasso G
Ann Fam Med 2024 Jan-Feb;22(1):50-62. doi: 10.1370/afm.3050. PMID: 38253509
Jäkel L, De Kort AM, Klijn CJM, Schreuder FHBM, Verbeek MM
Alzheimers Dement 2022 Jan;18(1):10-28. Epub 2021 May 31 doi: 10.1002/alz.12366. PMID: 34057813Free PMC Article
Song TJ, Lee KH, Li H, Kim JY, Chang K, Kim SH, Han KH, Kim BY, Kronbichler A, Ducros A, Koyanagi A, Jacob L, Kim MS, Yon DK, Lee SW, Yang JM, Hong SH, Ghayda RA, Kang JW, Shin JI, Smith L
Eur Rev Med Pharmacol Sci 2021 May;25(9):3519-3529. doi: 10.26355/eurrev_202105_25834. PMID: 34002826
Mitra S, Florez ID, Tamayo ME, Mbuagbaw L, Vanniyasingam T, Veroniki AA, Zea AM, Zhang Y, Sadeghirad B, Thabane L
JAMA 2018 Mar 27;319(12):1221-1238. doi: 10.1001/jama.2018.1896. PMID: 29584842Free PMC Article
van Asch CJ, Luitse MJ, Rinkel GJ, van der Tweel I, Algra A, Klijn CJ
Lancet Neurol 2010 Feb;9(2):167-76. Epub 2010 Jan 5 doi: 10.1016/S1474-4422(09)70340-0. PMID: 20056489

Supplemental Content

Table of contents

    Clinical resources

    Practice guidelines

    • PubMed
      See practice and clinical guidelines in PubMed. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.
    • Bookshelf
      See practice and clinical guidelines in NCBI Bookshelf. The search results may include broader topics and may not capture all published guidelines. See the FAQ for details.

    Consumer resources

    Recent activity

    Your browsing activity is empty.

    Activity recording is turned off.

    Turn recording back on

    See more...