and pons in 5 to 12 percent [112]. In the subsequent Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT2) of over 2000 subjects with imaging-confirmed ICH and hypertension, the frequency of affected brain structures was as follows [113]: Putamen/globus pallidus 56 percent Posterior limb of internal capsule 46 percent Anterior limb of internal capsule 5 percent Thalamus 31 percent External capsule 27 percent Lobar 14 percent Cerebellum or brainstem 7 percent Caudate head 2 percent Intraventricular extension of the ICH was identified in 29 percent in this study. Neurologic exam deficits typically correspond to the location of the hemorrhage and associated edema. Patients with deficits not attributable to the hemorrhage should be evaluated for other causes, such as expansion of the hemorrhage, post-ictal symptoms after a seizure, or increased intracranial pressure. The localization of ICH may be associated with typical neurologic exam findings: Putaminal hemorrhage Spread of hemorrhage into the putamen most commonly occurs along white matter fiber tracts, causing hemiplegia, hemisensory loss, homonymous hemianopsia, and gaze palsy. Stupor and coma may develop if the hemorrhage is large. Caudate hemorrhage Hemorrhage typically originating within the head of the caudate nucleus may cause acute-onset confusion, personality changes, or memory impairment as well as transient contralateral weakness or numbness [114]. Headache and drowsiness may also occur, especially if bleeding extends into the adjacent intraventricular space. Internal capsule hemorrhage Small hemorrhages restricted to the internal capsule may cause mild dysarthria, contralateral hemiparesis, and sensory deficit [115]. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 12/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Cerebellar hemorrhage Cerebellar hemorrhage usually originates in the dentate nucleus and may extend into the hemisphere and fourth ventricle and possibly into the pontine tegmentum. These bleeds typically cause an inability to walk due to imbalance, vomiting, and occipital headache. Some patients have referred pain to the neck or shoulder, neck stiffness, gaze palsy, and/or facial weakness. Notably, there is often no hemiparesis. The patient may become stuporous due to obstructive hydrocephalus or brainstem compression. Patients with acute cerebellar hemorrhage may frequently deteriorate and require surgery. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Surgical approaches for selected patients' and "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Cerebellar hemorrhage'.) Thalamic hemorrhage Thalamic hemorrhages may extend in a transverse direction to the posterior limb of the internal capsule, downward to put pressure on the tectum of the midbrain, or medially to rupture into the third ventricle. Symptoms include hemiparesis, hemisensory loss, and occasionally transient homonymous hemianopsia. Pupils may be miotic and unreactive along with a gaze palsy (eg, peering at the tip of the nose, skewed, or "wrong-way eyes" toward the weak side [in contrast with hemispheric cortical injury in which the eyes are deviated away from the hemiparesis]). Aphasia may occur if the bleed affects the dominant hemisphere, while neglect may develop if the bleed affects the nondominant hemisphere. Patients with small anterior thalamic hemorrhages may present with drowsiness, acute confusion, or neuropsychiatric symptoms. Lobar hemorrhage Lobar hemorrhages vary in their neurologic signs depending upon location. They most often affect the parietal and occipital lobes. These bleeds are associated with a higher incidence of seizures. Occipital hemorrhages frequently present with a very dense contralateral homonymous hemianopsia. Hemorrhages in the frontoparietal region will produce a contralateral plegia or paresis of the leg with relative sparing of the arm. Pontine hemorrhage Pontine hemorrhages typically originate in brainstem nuclei and may extend into the base of the pons. These often lead to deep coma over the first few minutes following the hemorrhage, probably due to disruption of the reticular activating system. The motor examination may be marked by bilateral paralysis. The pupils are pinpoint and react to a strong light source. Horizontal eye movements are often absent, and there may be ocular bobbing, facial palsy, deafness, and dysarthria if the patient is awake. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 13/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Seizures Seizures may accompany acute ICH. Seizures in the first days after ICH occur approximately 15 percent of patients [116,117]; they are more common in lobar hemorrhages (affecting cortical tissue) than in deep or cerebellar ICH [118-121]. (See "Overview of the management of epilepsy in adults", section on 'Poststroke seizures'.) Cardiac abnormalities Cardiac abnormalities are commonly associated with spontaneous ICH [122]. The most frequently associated electrocardiographic (ECG) changes are prolonged QT interval and ST-T wave changes. These changes may reflect catecholamine-induced cardiac injury, which is most likely due to a centrally mediated release of excess catecholamines caused by increased intracranial pressure or autonomic disturbance [123]. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy" and "Complications of stroke: An overview", section on 'Neurogenic cardiac damage'.) Mild elevations in serum myocardial enzymes often accompany the ECG changes, including cardiac troponin and beta natriuretic peptide [122]. Echocardiographic abnormalities may involve global or regional wall motion abnormalities and reduced ejection fraction. Ventricular arrhythmias may occur with brainstem compression [124]. BRAIN IMAGING Both computed tomography (CT) or magnetic resonance imaging (MRI) are considered first- choice imaging options for the emergency diagnosis and assessment of ICH ( image 14) [125]. Clinical deficits on neurologic examination can be correlated with impacted brain regions apparent on CT or MRI. Acute imaging also provides information about extension into the ventricular system, the presence of surrounding edema, shifts in brain contents (herniation), impending expansion, and underlying etiology. ICH severity can be assessed by calculating the volume of the hemorrhage. (See 'Estimating hemorrhage volume' below.) Head CT Noncontrast head computed tomography (CT) accurately identifies the presence of acute ICH, distinguishing it from ischemic stroke. Hyperacute blood will appear hyperdense except in rare cases of severe anemia when it might appear isodense. Over weeks, the blood from an acute hemorrhage will typically become isodense and may have a ring-enhancement appearance. Chronically, the blood is hypodense ( image 15). CT angiography that may be performed along with a noncontrast head CT may identify an underlying vascular cause to the ICH [29,126]. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 14/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Noncontrast head CT and CT angiography may also provide additional information regarding propensity for hemorrhagic expansion [127]. (See 'Predicting hemorrhage expansion' below.) Brain MRI Brain magnetic resonance imaging (MRI) is similarly sensitive as CT for detecting acute ICH. Acute ICH can be diagnosed by MRI with up to 100 percent sensitivity and accuracy by experienced readers [128]. In the Hemorrhage and Early MRI Evaluation (HEME) study, 200 patients presenting with focal stroke symptoms were evaluated with MRI including gradient recall echo (GRE) and diffusion-weighted imaging (DWI) sequences within six hours of symptom onset followed by CT [129]. MRI and CT were equivalent for the detection of acute ICH, and MRI was significantly more accurate than CT for the detection of chronic ICH. However, MRI is contraindicated for patients with some metallic implants [130]. Additionally, MRIs are not as readily available on an emergent basis as CT and conventional protocols take longer than CT protocols. Age of hemorrhagic findings MRI may also provide information about the age of the ICH ( table 2). The appearance of intracerebral blood on MRI images varies with time depending on the paramagnetic properties of the various stages of hemoglobin and on the mode of imaging acquisition [131,132]. Of note, these imaging features do not apply to extra-axial or intraventricular hemorrhage. Hyperacute hemorrhage (0 to 3 hours) A hyperacute parenchymal hematoma contains oxyhemoglobin and appears hypo- to isointense on T1-weighted images, hyperintense on T2-weighted images, and hypointense on T2*-weighted (GRE or susceptibility-weighted imaging) sequences ( image 14) [133]. Acute hemorrhage (3 hours to 3 days) Acute ICH can be accurately detected due to the magnetic susceptibility of deoxygenated hemoglobin (deoxyhemoglobin) [128,129,132-136]. This property of superparamagnetic deoxyhemoglobin results in rapid dephasing of proton spins causing signal loss (darkening or hypointensity) that is best seen in T2*-weighted images. Subacute hemorrhage (3 days to 3 weeks) Subacute ICH is recognized by the presence of diamagnetic methemoglobin, which appears as a T1-hyperintense signal, often first along the periphery of the hemorrhage. The appearance on T2-weighted imaging is hypointense in the first week due to magnetic susceptibility but becomes T2 hyperintense in the late subacute stage (one to three weeks) as red blood cells lyse and methemoglobin becomes extracellular. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 15/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Chronic hemorrhage (>3 weeks) The presence of superparamagnetic hemosiderin and ferritin in chronic ICH causes marked hypointensity on T2- and T2*-weighted images. On T1-weighted images, chronic hemorrhage is isointense compared with brain tissue. Nonhemorrhagic findings in acute ICH Brain MRI may show other findings associated with acute ICH. Cerebral edema Tissue damage and subsequent inflammatory response to the presence of intracranial blood can lead to perilesional cerebral edema in ICH [137]. Edema can compress adjacent intracranial structures, causing elevated intracranial pressure (ICP) and leading to hydrocephalus. Cerebral edema may be seen in acute and subacute ICH and typically appears hypointense on T1-weighted images and hyperintense on T2-weighted images. ICH-related cerebral edema often peaks two to three weeks after hemorrhage [7,138]. Acute imaging showing prominent edema along with ICH may indicate subacute age of bleeding or suggest ICH may be due to a specific underlying cause such as cerebral sinus thrombosis ( image 6) or tumor ( image 9). (See "Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis", section on 'Follow-up neuroimaging'.) Diffusion-weighted imaging lesions Brain MRI may show hyperintense diffusion- weighted imaging (DWI) lesions associated with acute ICH. These may indicate hemorrhagic transformation of a primary ischemic infarct ( image 7) or embolism such as from infective endocarditis ( table 3). (See "Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis", section on 'Follow-up neuroimaging'.) Small DWI hyperintense lesions may also be found in patients with primary acute ICH. These lesions are often punctate in size, multifocal in number, and remote from and contralateral to the site of hemorrhage in location ( image 16). They appear to occur most frequently during the first several days after ICH but can also be found on subsequent nonacute imaging [19]. In a systematic review of observational studies that included 5211 patients with acute ICH, the pooled prevalence of DWI lesions on acute brain MRI was 24 percent [139]. DWI lesions are associated with larger ICH volume, subarachnoid bleeding, and elevated blood pressure, suggesting acute changes in cerebral perfusion and/or ICP may contribute to their development [139,140]. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 16/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate MRI may also demonstrate imaging findings that may suggest a specific underlying cause. (See 'Subsequent imaging' below.) Estimating hemorrhage volume An estimate of ICH volume is useful to communicate hemorrhage severity and make early assessments of prognosis. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Clinical prediction scores'.) The formula is calculated using the centimeter scale on the CT (or MRI) images as follows [141]: A is the greatest hemorrhage diameter on the CT slice with the largest area of hemorrhage. B is the largest diameter 90 degrees to A on the same (index) CT slice ( image 17). C is the approximate number of CT slices with hemorrhage multiplied by the slice thickness in centimeters. To calculate C, each CT slice with hemorrhage is visually compared with the index CT slice [141]. An individual hemorrhage slice is counted as one full slice for determining C if the hemorrhage area is >75 percent of the area on the slice with the largest hemorrhage. A slice is counted as one-half if the hemorrhage area is approximately 25 to 75 percent of the area on the largest hemorrhage slice. The slice is not counted if the area is <25 percent of the largest hemorrhage slice. ABC/2 gives the ICH volume in cubic centimeters. In children, ICH volume may instead be measured as a percent of total brain volume as ABC/XYZ, where X is the largest midline axial diameter of supratentorial brain, Y is the largest axial diameter perpendicular to X, and Z is the brain vertical diameter [142]. Predicting hemorrhage expansion Enlargement of the hemorrhage is associated with neurologic deterioration and worse outcomes. These observations indicate that significant improvements in patient outcome from ICH may be achieved by minimizing both secondary brain ischemia and hemorrhage enlargement in the early hours following the onset of bleeding. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on 'Managing hemorrhagic expansion'.) Serial CT scans in patients with hypertensive hemorrhage have shown that the hemorrhage enlarges in the first few hours after presentation in a subset of patients [2,6,143]. In most but not all cases, the bulk of hemorrhage expansion occurs in the first three hours after onset of ICH [2-5,144]. In a prospective series of 103 patients with ICH, significant hemorrhage growth (a >33 percent volume increase) occurred in 38 percent of patients over the first 24 hours [2]. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 17/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate In a patient-level meta-analysis of studies reporting ICH growth, with data on over 5400 subjects, several independent predictors of hemorrhage growth identified [145]: Shorter time from symptom onset to initial imaging ICH volume Antiplatelet or anticoagulant use Contrast extravasation (eg, "spot sign") on initial CT angiography ( image 18) While all patients with ICH should be treated to limit risk for hemorrhage expansion, the presence of specific radiologic findings may trigger a somewhat more aggressive approach to monitoring and treatment. (See 'Subsequent imaging' below and "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis".) Spot sign on CT angiography The spot sign ( image 18) describes the appearance of small focal or multifocal areas of contrast enhancement within a hemorrhage on CT angiography source images [146]. The spot sign has been linked to hemorrhage expansion and poor outcomes, including mortality [127,147]. In a retrospective analysis of 367 patients with acute ICH, a spot sign was found in 19 percent of patients and was independently associated with hemorrhage expansion [148]. Accumulation of contrast extravasation within the hemorrhage on postcontrast CT also predicts subsequent hemorrhage expansion [149]. Although less well-studied, tiny spots of contrast extravasation within the hemorrhage on MRI (the MRI spot sign) have also been detected on postcontrast T1-weighted and dynamic T1-weighted images, particularly when performed in the first six hours after ICH onset [150]. This "MRI spot sign" may be associated with hematoma growth and worse clinical outcomes, but definitive data are lacking [151]. A spot sign score that grades the number of spot signs, their maximum dimension, and attenuation has been found to be a strong predictor of hemorrhage expansion; of these features, the number of spot signs appears to be most predictive [148,152,153]. Signs on noncontrast head CT Irregularity or heterogeneity of the hematoma on noncontrast head CT also suggests ongoing bleeding or risk of hematoma expansion [154,155]. In a systematic review including 25 studies and 10,650 patients with ICH, several imaging features visible on CT were associated with subsequent risk of poor functional outcome [156]. These include ( image 19): Irregular hematoma shape Island sign ( 3 scattered hematomas separate from the main hematoma) https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 18/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Hypodensity (any hypodense focus within the hematoma) Heterogeneous density ( 3 foci of hypodensity within the hematoma) Black-hole sign (focus of hypodensity with a difference of >28 Hounsfield units [HU] from the hematoma) Swirl sign (hypodense region within the hematoma) Blend sign (focus of hypodensity with a difference of >18 HU adjacent to the hematoma) Subarachnoid extension In one study, extension of hemorrhage into the subarachnoid space was associated with subsequent hemorrhagic expansion in patients with acute lobar ICH but not in patients with nonlobar ICH [157]. Intraventricular extension Expansion of ICH into the intraventricular space has been reported in up to 40 to 60 percent of patients in various studies and is associated with neurologic complications and worse outcomes [158-160]. EVALUATION AND DIAGNOSIS ICH is a neurologic and medical emergency because it is associated with a high risk of ongoing bleeding, progressive neurologic deterioration, permanent disability, and death [161,162]. As the diagnostic evaluation is proceeding, patients with ICH may also need acute interventions, possibly including intubation and mechanical ventilation, anticoagulation reversal, blood pressure control, intracranial pressure monitoring and treatment, and consideration of the need for ventriculostomy or surgical hematoma evacuation ( table 1). These issues are discussed in detail separately. (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis".) Initial evaluation Clinical suspicion for ICH is based upon features such as acute onset of gradually worsening symptoms and increasing neurologic deficit, particularly if accompanied by severe headache, vomiting, severe hypertension, and decreased level of consciousness or coma. However, the distinction between brain hemorrhage and ischemia cannot be made on the basis of clinical characteristics alone [162]. Importantly, headache may be absent in some cases of ICH. (See 'Clinical presentation' above.) Neuroimaging with brain computed tomography (CT) or magnetic resonance imaging (MRI) is mandatory to confirm the diagnosis of ICH and to exclude ischemic stroke and stroke mimics as possible causes [162]. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 19/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate Laboratory and other dignostic testing Routine laboratory evaluation to evaluate for underlying causes or associated risks in patients with ICH includes [162]: Complete blood count, electrolytes, blood urea nitrogen, creatinine, and glucose Prothrombin time (with international normalized ratio [INR]) and activated partial thromboplastin time for all patients; thrombin clotting time for patients taking direct oral anticoagulants (and/or ecarin clotting time where available for patients known or suspected to be taking direct thrombin inhibitors) Cardiac-specific troponin Toxicology screen to detect cocaine and other sympathomimetic drugs Urinalysis Pregnancy test in a female of childbearing age An electrocardiogram (ECG) obtained at baseline may help identify patients with ICH and coexistent cardiac dysfunction [163,164]. A repeat ECG is also typically obtained along with an echocardiogram for those with heart failure or hemodynamic instability. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction" and "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy".) An electroencephalogram is reserved for patients with seizures or those with encephalopathy not explained by the location or size of the ICH. (See "Nonconvulsive status epilepticus: Classification, clinical features, and diagnosis", section on 'When to suspect NCSE' and 'Neurologic signs and ICH location' above.) Subsequent imaging Once ICH is confirmed by head CT or MRI, additional imaging is warranted in the event of clinical deterioration to evaluate for ICH expansion or rebleeding. A follow-up imaging study may also be performed to document that the bleeding has stabilized. Subsequent imaging is also typically performed to identify an underlying cause of the ICH to help guide preventive measures to reduce the risk of recurrent hemorrhage. The necessity for further evaluation to determine the cause of ICH varies with the clinical setting. (See "Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis", section on 'Follow-up neuroimaging'.) For some patients, the etiology of the ICH is identified with initial neuroimaging studies, and further imaging studies are not required. An example may include a stable patient with an acute ICH in the putamen suggestive of hypertensive vasculopathy who has a history of longstanding hypertension. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 20/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate For other patients, initial imaging studies do not sufficiently exclude other causes of ICH and follow-up evaluation is required. We obtain follow-up imaging when an underlying cause is suspected by clinical features or initial imaging findings ( table 3) [162]. Initial imaging findings that may suggest a specific underlying cause include: Early perihematomal edema out of proportion to the underlying ICH ( image 9) [165] ICH within arterial vascular territory suggesting primary ischemic infarction ( image 7) Multifocal hemorrhage ( image 20) Isolated intraventricular hemorrhage ( image 21) The assessment of the possible underlying structural pathology may be shrouded and distorted by the hematoma or surrounding edema. In these cases, delayed imaging performed after bleeding and edema have resolved may identify patients with underlying structural abnormalities at high risk for ICH recurrence ( algorithm 1). (See "Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis", section on 'Follow-up neuroimaging'.) Brain MRI with contrast is the preferred modality to help identify the underlying cause of ICH for most patients. For patients who are unable to undergo MRI, head CT with contrast is a less sensitive alternative option. Vascular imaging (eg, CT or MR angiography or digital subtraction angiography) is performed when an underlying vascular lesion is suspected [29,30,126,166]. (See "Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis", section on 'Follow-up neuroimaging'.) SOCIETY GUIDELINE LINKS Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Stroke in adults".) INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." th th The Basics patient education pieces are written in plain language, at the 5 to 6 grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more th th sophisticated, and more detailed. These articles are written at the 10 to 12 grade reading https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 21/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.) Basics topics (see "Patient education: Hemorrhagic stroke (The Basics)" and "Patient education: Arteriovenous malformations in the brain (The Basics)") Beyond the Basics topics (see "Patient education: Stroke symptoms and diagnosis (Beyond the Basics)" and "Patient education: Hemorrhagic stroke treatment (Beyond the Basics)") SUMMARY AND RECOMMENDATIONS Underlying causes Injury to brain parenchyma occurs via hematoma expansion and perilesional edema as well as secondary excitotoxic and inflammatory injury from the breakdown of the blood-brain barrier. Common conditions associated with intracerebral hemorrhage (ICH) include hypertension, cerebral amyloid angiopathy, and ruptured vascular malformation. Other etiologies include cerebral venous thrombosis, vasculopathies, primary or metastatic tumors, and coagulopathies. (See 'Pathogenesis and etiologies' above.) Risk factors Major risk factors for spontaneous ICH include older age, hypertension, and the use of antithrombotic (antiplatelet and anticoagulant) therapy. (See 'Risk factors' above.) Presenting signs and symptoms The signs and symptoms of ICH vary according to the location and size of the hemorrhage ( table 1). Patients typically present with an acute onset of a focal neurologic deficit such as hemiparesis, aphasia, or visual impairment corresponding to the part of the brain affected. The neurologic symptoms and signs may be progressive over minutes or a few hours ( figure 1). Headache, vomiting, and a decreased level of consciousness develop if the hemorrhage is large. Patients may also present with stupor or coma due to associated reversible causes such as acute metabolic derangements or seizure. (See 'Clinical presentation' above.) Initial diagnostic imaging Neuroimaging with head computed tomography (CT) or magnetic resonance imaging (MRI) is mandatory to confirm the diagnosis of ICH and to https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 22/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate exclude ischemic stroke and stroke mimics as alternative causes to symptoms. Acute imaging also provides information about the severity of the hemorrhage, the risk of expansion of bleeding, and the underlying cause of the ICH ( image 19 and table 3). (See 'Evaluation and diagnosis' above and 'Brain imaging' above.) Both CT or MRI are considered first-choice imaging options for the emergency diagnosis and assessment of ICH. CT angiography may be performed along with a noncontrast head CT to help identify an underlying vascular cause to the ICH. (See 'Brain imaging' above.) Predictors of hemorrhage growth associated with neurologic deterioration include a shorter time from symptom onset to initial imaging, initial ICH volume, antithrombotic medication use, and imaging signs of ICH heterogeneity on noncontrast CT or focal contrast extravasation on CT angiography ( image 18 and image 19). (See 'Predicting hemorrhage expansion' above.) Subsequent imaging evaluation Additional imaging may be warranted after the diagnosis of ICH in the event of clinical deterioration to evaluate for ICH expansion or rebleeding and to document that the bleeding has stabilized. (See 'Subsequent imaging' above.) We also obtain follow-up imaging when an underlying cause is suspected by clinical features or initial imaging findings to help guide preventive measures to reduce the risk of recurrent hemorrhage ( table 3). Brain MRI with contrast is the preferred modality to help identify the underlying cause of ICH for most patients. Vascular imaging (eg, CT or MR angiography or digital subtraction angiography) is performed when an underlying vascular lesion is suspected. (See 'Subsequent imaging' above.) Use of UpToDate is subject to the Terms of Use. REFERENCES 1. Xu BN, Yabuki A, Mishina H, et al. Pathophysiology of brain swelling after acute experimental brain compression and decompression. Neurosurgery 1993; 32:289. 2. Brott T, Broderick J, Kothari R, et al. Early hemorrhage growth in patients with intracerebral hemorrhage. Stroke 1997; 28:1. 3. Mayer SA, Brun NC, Begtrup K, et al. Recombinant activated factor VII for acute intracerebral hemorrhage. N Engl J Med 2005; 352:777. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 23/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate 4. Davis SM, Broderick J, Hennerici M, et al. Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage. Neurology 2006; 66:1175. 5. Mayer SA, Brun NC, Begtrup K, et al. Efficacy and safety of recombinant activated factor VII for acute intracerebral hemorrhage. N Engl J Med 2008; 358:2127. 6. Balami JS, Buchan AM. Complications of intracerebral haemorrhage. Lancet Neurol 2012; 11:101. 7. Venkatasubramanian C, Mlynash M, Finley-Caulfield A, et al. Natural history of perihematomal edema after intracerebral hemorrhage measured by serial magnetic resonance imaging. Stroke 2011; 42:73. 8. Staykov D, Wagner I, Volbers B, et al. Natural course of perihemorrhagic edema after intracerebral hemorrhage. Stroke 2011; 42:2625. 9. Li N, Worthmann H, Heeren M, et al. Temporal pattern of cytotoxic edema in the perihematomal region after intracerebral hemorrhage: a serial magnetic resonance imaging study. Stroke 2013; 44:1144. 10. Olivot JM, Mlynash M, Kleinman JT, et al. MRI profile of the perihematomal region in acute intracerebral hemorrhage. Stroke 2010; 41:2681. 11. Oeinck M, Neunhoeffer F, Buttler KJ, et al. Dynamic cerebral autoregulation in acute intracerebral hemorrhage. Stroke 2013; 44:2722. 12. Murai Y, Ikeda Y, Teramoto A, Tsuji Y. Magnetic resonance imaging-documented extravasation as an indicator of acute hypertensive intracerebral hemorrhage. J Neurosurg 1998; 88:650. 13. Aksoy D, Bammer R, Mlynash M, et al. Magnetic resonance imaging profile of blood-brain barrier injury in patients with acute intracerebral hemorrhage. J Am Heart Assoc 2013; 2:e000161. 14. Kidwell CS, Burgess R, Menon R, et al. Hyperacute injury marker (HARM) in primary hemorrhage: a distinct form of CNS barrier disruption. Neurology 2011; 77:1725. 15. Silvera S, Oppenheim C, Touz E, et al. Spontaneous intracerebral hematoma on diffusion- weighted images: influence of T2-shine-through and T2-blackout effects. AJNR Am J Neuroradiol 2005; 26:236. 16. Menon RS, Burgess RE, Wing JJ, et al. Predictors of highly prevalent brain ischemia in intracerebral hemorrhage. Ann Neurol 2012; 71:199. 17. Garg RK, Liebling SM, Maas MB, et al. Blood pressure reduction, decreased diffusion on MRI, and outcomes after intracerebral hemorrhage. Stroke 2012; 43:67. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 24/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate 18. Kang DW, Han MK, Kim HJ, et al. New ischemic lesions coexisting with acute intracerebral hemorrhage. Neurology 2012; 79:848. 19. Auriel E, Gurol ME, Ayres A, et al. Characteristic distributions of intracerebral hemorrhage- associated diffusion-weighted lesions. Neurology 2012; 79:2335. 20. Boulanger M, Schneckenburger R, Join-Lambert C, et al. Diffusion-Weighted Imaging Hyperintensities in Subtypes of Acute Intracerebral Hemorrhage. Stroke 2018; :STROKEAHA118021407. 21. Prabhakaran S, Naidech AM. Ischemic brain injury after intracerebral hemorrhage: a critical review. Stroke 2012; 43:2258. 22. Beslow LA, Licht DJ, Smith SE, et al. Predictors of outcome in childhood intracerebral hemorrhage: a prospective consecutive cohort study. Stroke 2010; 41:313. 23. Cordonnier C, Demchuk A, Ziai W, Anderson CS. Intracerebral haemorrhage: current approaches to acute management. Lancet 2018; 392:1257. 24. Garcia JH, Ho KL. Pathology of hypertensive arteriopathy. Neurosurg Clin N Am 1992; 3:497. 25. Folsom AR, Yatsuya H, Mosley TH Jr, et al. Risk of intraparenchymal hemorrhage with magnetic resonance imaging-defined leukoaraiosis and brain infarcts. Ann Neurol 2012; 71:552. 26. Offenbacher H, Fazekas F, Schmidt R, et al. MR of cerebral abnormalities concomitant with primary intracerebral hematomas. AJNR Am J Neuroradiol 1996; 17:573. 27. Cheng AL, Batool S, McCreary CR, et al. Susceptibility-weighted imaging is more reliable than T2*-weighted gradient-recalled echo MRI for detecting microbleeds. Stroke 2013; 44:2782. 28. Meretoja A, Strbian D, Putaala J, et al. SMASH-U: a proposal for etiologic classification of intracerebral hemorrhage. Stroke 2012; 43:2592. 29. Delgado Almandoz JE, Schaefer PW, Goldstein JN, et al. Practical scoring system for the identification of patients with intracerebral hemorrhage at highest risk of harboring an underlying vascular etiology: the Secondary Intracerebral Hemorrhage Score. AJNR Am J Neuroradiol 2010; 31:1653. 30. van Asch CJ, Velthuis BK, Greving JP, et al. External validation of the secondary intracerebral hemorrhage score in The Netherlands. Stroke 2013; 44:2904. 31. Gross BA, Jankowitz BT, Friedlander RM. Cerebral Intraparenchymal Hemorrhage: A Review. JAMA 2019; 321:1295. 32. Mallon D, Doig D, Dixon L, et al. Neuroimaging in Sickle Cell Disease: A Review. J Neuroimaging 2020; 30:725. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 25/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate 33. Steiner T, Al-Shahi Salman R, Beer R, et al. European Stroke Organisation (ESO) guidelines for the management of spontaneous intracerebral hemorrhage. Int J Stroke 2014; 9:840. 34. Feigin VL, Lawes CM, Bennett DA, et al. Worldwide stroke incidence and early case fatality reported in 56 population-based studies: a systematic review. Lancet Neurol 2009; 8:355. 35. Sacco S, Marini C, Toni D, et al. Incidence and 10-year survival of intracerebral hemorrhage in a population-based registry. Stroke 2009; 40:394. 36. Gebel JM, Broderick JP. Intracerebral hemorrhage. Neurol Clin 2000; 18:419. 37. Flaherty ML, Woo D, Haverbusch M, et al. Racial variations in location and risk of intracerebral hemorrhage. Stroke 2005; 36:934. 38. Labovitz DL, Halim A, Boden-Albala B, et al. The incidence of deep and lobar intracerebral hemorrhage in whites, blacks, and Hispanics. Neurology 2005; 65:518. 39. van Asch CJ, Luitse MJ, Rinkel GJ, et al. Incidence, case fatality, and functional outcome of intracerebral haemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurol 2010; 9:167. 40. Poon MT, Bell SM, Al-Shahi Salman R. Epidemiology of Intracerebral Haemorrhage. Front Neurol Neurosci 2015; 37:1. 41. Broderick JP, Brott T, Tomsick T, et al. Intracerebral hemorrhage more than twice as common as subarachnoid hemorrhage. J Neurosurg 1993; 78:188. 42. Stein M, Misselwitz B, Hamann GF, et al. Intracerebral hemorrhage in the very old: future demographic trends of an aging population. Stroke 2012; 43:1126. 43. Krishnamurthi RV, Feigin VL, Forouzanfar MH, et al. Global and regional burden of first-ever ischaemic and haemorrhagic stroke during 1990-2010: findings from the Global Burden of Disease Study 2010. Lancet Glob Health 2013; 1:e259. 44. Bruno A, Carter S, Qualls C, Nolte KB. Incidence of spontaneous intracerebral hemorrhage among Hispanics and non-Hispanic whites in New Mexico. Neurology 1996; 47:405. 45. Morgenstern LB, Smith MA, Lisabeth LD, et al. Excess stroke in Mexican Americans compared with non-Hispanic Whites: the Brain Attack Surveillance in Corpus Christi Project. Am J Epidemiol 2004; 160:376. 46. Gokhale S, Caplan LR, James ML. Sex differences in incidence, pathophysiology, and outcome of primary intracerebral hemorrhage. Stroke 2015; 46:886. 47. Appelros P, Stegmayr B, Ter nt A. Sex differences in stroke epidemiology: a systematic review. Stroke 2009; 40:1082. 48. Woo D, Sauerbeck LR, Kissela BM, et al. Genetic and environmental risk factors for intracerebral hemorrhage: preliminary results of a population-based study. Stroke 2002; https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis/print 26/70 7/5/23, 12:25 PM Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis - UpToDate 33:1190. 49. Woo D, Haverbusch M, Sekar P, et al. Effect of untreated hypertension on hemorrhagic stroke. Stroke 2004; 35:1703. 50. Feldmann E, Broderick JP, Kernan WN, et al. Major risk factors for intracerebral hemorrhage in the young are modifiable. Stroke 2005; 36:1881. 51. Zia E, Hedblad B, Pessah-Rasmussen H, et al. Blood pressure in relation to the incidence of