A signal intensity on T1-weighted images that is similar to the surrounding brain parenchyma.
In the acute phase of hemorrhage (1-3 days), the hematoma consists primarily of intracellular deoxyhemoglobin.
Deoxyhemoglobin does not significantly shorten the T1 relaxation time, resulting in a signal that is isointense, or sometimes slightly hypointense, relative to gray matter.
Parizel PM, et al. European Radiology. 2001.
T2 dark (hypointense)
A signal intensity on T2-weighted images that is significantly lower (darker) than the surrounding brain tissue.
Intracellular deoxyhemoglobin is paramagnetic and creates local magnetic field inhomogeneities.
This leads to a process called T2 shortening, causing a rapid loss of signal and resulting in the characteristic dark appearance of the acute hematoma on T2-weighted and especially on T2*-weighted gradient-echo (GRE) sequences.
Linfante I, et al. Stroke. 1999.
DWI dark (hypointense)
A signal on Diffusion-Weighted Imaging (DWI) that is lower than the surrounding brain tissue.
The strong magnetic susceptibility effect from intracellular deoxyhemoglobin in an acute hematoma overwhelms the diffusion signal.
This effect, known as “T2 blackout,” causes the hematoma core to appear dark on DWI, masking the underlying diffusion characteristics.
Kang BK, et al. Korean Journal of Radiology. 2001.
ADC bright (hyperintense)
A signal on the Apparent Diffusion Coefficient (ADC) map that is higher (brighter) than the surrounding brain parenchyma, indicating increased water diffusivity.
This finding typically represents vasogenic edema in the parenchyma surrounding the hematoma, rather than the hematoma core itself.
Vasogenic edema is an accumulation of extracellular fluid due to the breakdown of the blood-brain barrier, which allows for less restricted movement of water molecules, resulting in high ADC values.
An acute intracerebral hemorrhage (ICH) is a form of stroke characterized by the sudden extravasation of blood into the brain parenchyma, which may extend into the ventricular system. It represents a medical emergency, as it can lead to significant morbidity and mortality.
Cause
The most common cause of spontaneous ICH is chronic hypertension, which leads to arteriosclerotic damage and rupture of small, deep perforating arteries (Charcot-Bouchard aneurysms).
Cerebral amyloid angiopathy (CAA) is another primary cause, particularly for lobar hemorrhages in individuals over 55, resulting from amyloid deposition in vessel walls.
Secondary causes include trauma, rupture of vascular malformations like aneurysms or arteriovenous malformations (AVMs), bleeding diathesis, coagulopathy (including therapeutic anticoagulation), brain tumors, and illicit drug use (e.g., cocaine, amphetamines).
Pathophysiology
ICH induces a biphasic brain injury. The primary injury occurs immediately from the mechanical disruption and compression of brain tissue by the expanding hematoma, leading to increased intracranial pressure (ICP).
Secondary injury unfolds over the subsequent hours to days and is driven by a complex cascade involving the release of cytotoxic blood components from the hematoma. This cascade includes excitotoxicity, oxidative stress from iron release and hemoglobin breakdown, a robust inflammatory response, and disruption of the blood-brain barrier, which together cause perihematomal edema and further neuronal death.
Structural Result
The hematoma acts as a space-occupying lesion, exerting mass effect on adjacent brain structures. This can lead to midline shift, brain herniation syndromes, and compression of critical structures like the brainstem.
If the hemorrhage extends into the ventricular system (intraventricular hemorrhage, or IVH), it can obstruct cerebrospinal fluid (CSF) flow, resulting in obstructive hydrocephalus and a further rise in ICP.
Perihematomal edema, a form of vasogenic edema, contributes significantly to the mass effect and is associated with worsened neurological outcomes.
Functional Impact
Neurological deficits are determined by the location and volume of the hematoma.
Hemorrhages in the basal ganglia or thalamus commonly cause contralateral hemiparesis or hemisensory loss due to involvement of the internal capsule.
Cerebellar hemorrhages can result in ataxia, vertigo, and nystagmus, and may lead to life-threatening brainstem compression or hydrocephalus.
Lobar hemorrhages produce focal deficits corresponding to the affected cortical area, such as aphasia or visual field defects.
Severe elevations in intracranial pressure can lead to a depressed level of consciousness, coma, and death.
Imaging
Non-contrast computed tomography (CT) is the primary diagnostic modality in the emergency setting, rapidly identifying acute blood as a hyperdense collection within the brain parenchyma.
On Magnetic Resonance Imaging (MRI), the appearance of hemorrhage evolves over time depending on the biochemical state of hemoglobin.
In the acute stage (1 to 3 days), the hematoma consists of intracellular deoxyhemoglobin. This is paramagnetic and causes magnetic field inhomogeneity, resulting in a characteristic signal that is:
T1-weighted: Isointense to slightly hypointense relative to gray matter.
T2-weighted: Markedly hypointense (dark).
Gradient-echo (GRE) / Susceptibility-weighted imaging (SWI): Profoundly hypointense (“blooming” artifact) due to high sensitivity to magnetic susceptibility effects, making these sequences exceptionally sensitive for detecting hemorrhage.
A surrounding rim of hyperintensity on T2-weighted and FLAIR images represents vasogenic edema.
Labs
A complete blood count (CBC) is required to assess for anemia and thrombocytopenia.
Coagulation studies, including prothrombin time (PT/INR) and activated partial thromboplastin time (aPTT), are critical to identify and guide the reversal of any underlying coagulopathy.
For patients on direct oral anticoagulants (DOACs), an anti-Factor Xa activity level may be indicated.
A basic metabolic panel, toxicology screen, and blood alcohol level can identify metabolic derangements or substance use that may have contributed to the hemorrhage.
Treatment
Initial management focuses on medical stabilization (ABCs) and preventing hematoma expansion.
Aggressive blood pressure reduction is a cornerstone of acute management, with guidelines often recommending a target systolic blood pressure of <140 mmHg.
Urgent reversal of any anticoagulation is paramount, using specific reversal agents such as prothrombin complex concentrate (PCC) for warfarin, idarucizumab for dabigatran, or andexanet alfa for Factor Xa inhibitors.
Management of elevated intracranial pressure may involve head-of-bed elevation, osmotic therapy (mannitol or hypertonic saline), and sedation.
Surgical intervention, including craniotomy for hematoma evacuation or placement of an external ventricular drain (EVD) for hydrocephalus, may be indicated based on hematoma location (e.g., cerebellum), volume, and the patient’s neurological status. Prophylactic antiseizure medications are generally not recommended unless there is clinical or electrographic evidence of seizures.
Prognosis
The prognosis for ICH is often poor, with a 30-day mortality rate reported to be between 35% and 50%; half of these deaths occur within the first 48 hours.
Key predictors of poor outcome include a low initial Glasgow Coma Scale (GCS) score, large hematoma volume (>30-60 mL), presence of intraventricular hemorrhage, infratentorial location, and advanced age.
The ICH Score is a validated clinical grading scale that incorporates these variables to predict 30-day mortality.
Fewer than 20% of survivors regain functional independence at 6 months. Survivors are at a sustained increased risk for recurrent ICH, ischemic stroke, and other vascular events.
The term “hemorrhage” originates from the Latin haemorrhagia, which itself is derived from the Greek haimorrhagia.
This Greek term is a composite of haima (“blood”) and rhēgnynai (“to break, burst”), vividly describing a “violent bleeding.”
The word “acute” is used to describe conditions with a sudden onset.
AKA / Terminology
Historically, the clinical presentation of a sudden neurological deficit was termed “apoplexy,” from the Greek apoplexia, meaning “to strike away.”
This term was used for any sudden death preceded by a loss of consciousness.
Over time, as autopsy became more common, distinctions were made.
Giovanni Battista Morgagni in 1761 separated apoplexy into apoplexia serosa and apoplexia sanguinea.
Today, the term “stroke” has largely replaced “apoplexy” in medical literature, and intracranial hemorrhage is further classified by its specific location, such as intracerebral, subarachnoid, subdural, or epidural.
Historical Notes
The understanding of cerebrovascular disease has evolved over approximately 2,500 years.
For centuries, from antiquity through the Renaissance, the concept of apoplexy was based purely on clinical observation without a clear understanding of the underlying pathology.
The advent of autopsies in the 17th century, and particularly the work of Morgagni, began to shed light on the structural changes in the brain associated with apoplexy.
A pivotal moment in understanding the vascular nature of some strokes came from Rudolf Virchow in the mid-19th century.
In 1856, he published his work on thrombosis and embolism, introducing these terms and demonstrating that clots could originate in the peripheral vascular system and travel to obstruct vessels in the lungs or brain.
While Virchow’s Triad (alterations in blood flow, endothelial injury, and a hypercoagulable state) is often cited as the cause of thrombosis, his original work focused more on the consequences of a dislodged thrombus.
The 20th century brought revolutionary diagnostic tools.
The introduction of X-rays, and later, computed tomography (CT), allowed for the in-vivo diagnosis of intracranial hemorrhage for the first time.
Sir Godfrey Hounsfield, an English electrical engineer, developed the first CT scanner in the late 1960s, with the first clinical use in 1971 to identify a brain tumor.
This invention transformed neurosurgery and the management of acute neurological events by allowing physicians to differentiate between ischemic and hemorrhagic strokes rapidly.
Cultural or Practice Insights
Historically, the sudden and dramatic nature of apoplexy led to various cultural interpretations.
In some Ghanaian communities, for example, stroke has been viewed as a “ghost illness” or the result of a curse or witchcraft.
Similar non-biomedical beliefs, such as stroke being linked to “destiny” or strong emotions, have been noted in Korean-American and other communities.
These cultural views can influence how and when individuals seek medical care.
Even in North America in the 1970s, a diagnosis of stroke sometimes connoted hopelessness, a terminal stage where little could be done.
In the Middle Ages, faith healing and patron saints were sometimes sought for conditions like apoplexy.
Notable Figures or Contributions
Giovanni Battista Morgagni (1682-1771): Through his extensive work in pathological anatomy, he was among the first to systematically correlate clinical symptoms of apoplexy with postmortem findings of both serous and sanguineous effusions in the brain.
Rudolf Virchow (1821-1902): A German physician who is considered the “father of modern pathology.” He elucidated the mechanisms of thromboembolism, coining the terms “thrombosis” and “embolism,” which are fundamental to understanding both ischemic and some hemorrhagic events. His work on cellular pathology shifted the focus of medicine to the microscopic level.
Harvey Cushing (1869-1939): Known as the “father of modern neurosurgery,” Cushing made monumental contributions to the surgical treatment of brain lesions. He significantly reduced surgical mortality by introducing blood pressure monitoring during operations, developing techniques to control bleeding like silver clips, and meticulously classifying brain tumors.
Sir Godfrey Hounsfield (1919-2004): An English electrical engineer who invented the CT scanner. This non-invasive imaging technique revolutionized medicine by allowing detailed visualization of intracranial structures, making the rapid diagnosis of acute bleeds possible and earning him the 1979 Nobel Prize.
Quotes and/or Teaching Lines
“The physician is the natural attorney for the poor.” – Rudolf Virchow
“Start by doing what’s necessary; then do what’s possible; and suddenly you are doing the impossible.” — St. Francis of Assisi, often used in stroke recovery encouragement.
“Our greatest glory is not in never falling, but in getting up every time we fall.” – Confucius, a quote used to motivate stroke survivors.
“If you’re going through hell, keep going.” – Winston Churchill, another quote frequently shared with patients undergoing rehabilitation.
1. Which state of hemoglobin is paramagnetic, found within intact red blood cells in the acute phase of hemorrhage (1-3 days), and is primarily responsible for T2 shortening due to magnetic susceptibility effects?
A. Oxyhemoglobin B. Deoxyhemoglobin C. Intracellular methemoglobin D. Extracellular methemoglobin
2. The initial step in the formation of a primary platelet plug at a site of vascular injury is mediated by the binding of which of the following?
A. Thrombin to fibrinogen B. Von Willebrand factor (vWF) to exposed collagen C. Tissue factor to Factor VII D. Plasmin to fibrin
3. A 70-year-old male with a history of poorly controlled hypertension presents with a spontaneous deep intracerebral hemorrhage in the basal ganglia. What is the most likely underlying pathophysiology?
A. Rupture of a saccular aneurysm B. Cerebral amyloid angiopathy C. Arteriovenous malformation D. Lipohyalinosis of small penetrating arteries
4. Which of the following components is NOT part of the original ICH Score used for prognostication in spontaneous intracerebral hemorrhage?
A. Glasgow Coma Scale (GCS) score B. Presence of intraventricular hemorrhage C. Serum creatinine level D. Infratentorial origin of hemorrhage
5. Given MRI findings of a hematoma that is T1 isointense and T2 hypointense, what is the most likely age of the bleed and the predominant hemoglobin product?
A. Hyperacute (<24 hours), Oxyhemoglobin B. Acute (1-3 days), Deoxyhemoglobin C. Early Subacute (3-7 days), Intracellular Methemoglobin D. Chronic (>2 weeks), Hemosiderin
6. A lesion appears bright on DWI and bright on the corresponding ADC map. This phenomenon, which can be seen in subacute hematomas, is best described as:
A. True restricted diffusion B. T2 shine-through C. T2 blackout effect D. T1 shortening
7. Which MRI sequence is most sensitive for the detection of blood products, particularly in chronic microhemorrhages, due to its accentuation of magnetic susceptibility effects?
A. T1-weighted post-contrast B. Fluid-Attenuated Inversion Recovery (FLAIR) C. Diffusion-Weighted Imaging (DWI) D. Susceptibility-Weighted Imaging (SWI)/Gradient Echo (GRE)
Part B
1. Which state of hemoglobin is paramagnetic, found within intact red blood cells in the acute phase of hemorrhage (1-3 days), and is primarily responsible for T2 shortening due to magnetic susceptibility effects?
A. Oxyhemoglobin
✗
Incorrect. Oxyhemoglobin, found in arterial blood and hyperacute hemorrhage, is diamagnetic and does not cause significant T2 shortening.
It is associated with T2 hyperintensity.
B. Deoxyhemoglobin
✓
Correct. Deoxyhemoglobin is a paramagnetic molecule that predominates in the acute phase (1-3 days) of hemorrhage.
Because it is concentrated within intact red blood cells, it creates significant local magnetic field inhomogeneities, leading to accelerated T2 dephasing and marked hypointensity on T2-weighted images (T2 shortening).
Hemphill JC 3rd, et al. Stroke. 2001.
C. Intracellular methemoglobin
✗
Incorrect. Intracellular methemoglobin is found in the early subacute phase (3-7 days).
While it is paramagnetic, its primary effect at this stage is T1 shortening, causing T1 hyperintensity.
D. Extracellular methemoglobin
✗
Incorrect. Extracellular methemoglobin is seen in the late subacute phase (>7 days).
It is paramagnetic but is now diluted in the extracellular space, resulting in both T1 and T2 hyperintensity.
2. The initial step in the formation of a primary platelet plug at a site of vascular injury is mediated by the binding of which of the following?
A. Thrombin to fibrinogen
✗
Incorrect. The conversion of fibrinogen to fibrin by thrombin is the final step of secondary hemostasis, which stabilizes the platelet plug, rather than initiating its formation.
B. Von Willebrand factor (vWF) to exposed collagen
✓
Correct. Primary hemostasis is initiated upon endothelial injury, which exposes subendothelial collagen.
Von Willebrand factor (vWF) binds to this exposed collagen and then captures circulating platelets via their GpIb receptor, leading to platelet adhesion and subsequent activation and aggregation.
Palta, S., et al. J Lab Physicians. 2014.
C. Tissue factor to Factor VII
✗
Incorrect. The binding of tissue factor to Factor VII initiates the extrinsic pathway of the coagulation cascade (secondary hemostasis), leading to the generation of thrombin.
D. Plasmin to fibrin
✗
Incorrect. Plasmin is the enzyme responsible for fibrinolysis, the breakdown of clots after tissue repair has occurred.
It is not involved in clot formation.
3. A 70-year-old male with a history of poorly controlled hypertension presents with a spontaneous deep intracerebral hemorrhage in the basal ganglia. What is the most likely underlying pathophysiology?
A. Rupture of a saccular aneurysm
✗
Incorrect. Saccular (berry) aneurysms are the most common cause of non-traumatic subarachnoid hemorrhage, not deep intraparenchymal hemorrhage.
B. Cerebral amyloid angiopathy
✗
Incorrect. Cerebral amyloid angiopathy (CAA) is characterized by amyloid deposition in cortical and leptomeningeal vessels, typically leading to lobar hemorrhages, particularly in older, normotensive patients.
C. Arteriovenous malformation
✗
Incorrect. While arteriovenous malformations (AVMs) are a cause of intracerebral hemorrhage, particularly in younger patients, hypertensive vasculopathy is far more common in older patients with deep hemorrhages.
D. Lipohyalinosis of small penetrating arteries
✓
Correct. Chronic hypertension induces degenerative changes, including lipohyalinosis and the formation of Charcot-Bouchard microaneurysms, in the small penetrating arteries that supply deep brain structures like the basal ganglia, thalamus, and pons.
Rupture of these weakened vessels is the most common cause of spontaneous, deep intracerebral hemorrhage.
Takeuchi, S., et al. Brain and Nerves. 2014.
4. Which of the following components is NOT part of the original ICH Score used for prognostication in spontaneous intracerebral hemorrhage?
A. Glasgow Coma Scale (GCS) score
✗
Incorrect. The patient’s GCS score on admission is a critical component of the ICH score, with lower scores contributing more points.
B. Presence of intraventricular hemorrhage
✗
Incorrect. The presence of blood within the ventricles (intraventricular hemorrhage) is a component of the ICH score and confers one point.
C. Serum creatinine level
✓
Correct. The five components of the original ICH score are: GCS score, age (≥80 vs. <80), ICH volume (≥30 cm³ vs. <30 cm³), presence of intraventricular hemorrhage, and infratentorial origin.
Renal function, as measured by serum creatinine, is not a component of this prognostic score.
Hemphill JC 3rd, et al. Stroke. 2001.
D. Infratentorial origin of hemorrhage
✗
Incorrect. Hemorrhage originating in an infratentorial location (cerebellum or brainstem) is a component of the ICH score and confers one point.
5. Given MRI findings of a hematoma that is T1 isointense and T2 hypointense, what is the most likely age of the bleed and the predominant hemoglobin product?
A. Hyperacute (<24 hours), Oxyhemoglobin
✗
Incorrect. Hyperacute hemorrhage contains diamagnetic oxyhemoglobin and is classically T1 isointense and T2 hyperintense.
B. Acute (1-3 days), Deoxyhemoglobin
✓
Correct. In the acute stage, hemoglobin becomes deoxygenated to form deoxyhemoglobin.
Deoxyhemoglobin is paramagnetic and, while contained within red blood cells, causes marked T2 shortening (hypointensity) due to magnetic susceptibility effects.
It does not significantly alter T1 relaxation, so the hematoma remains isointense on T1-weighted images.
Bradley WG Jr. Radiology. 1993.
C. Early Subacute (3-7 days), Intracellular Methemoglobin
✗
Incorrect. Early subacute hemorrhage is characterized by intracellular methemoglobin, which causes significant T1 shortening, appearing hyperintense on T1-weighted images.
D. Chronic (>2 weeks), Hemosiderin
✗
Incorrect. Chronic hemorrhage is characterized by hemosiderin and ferritin deposition, which causes profound T2 shortening and appears dark on both T1- and T2-weighted images.
6. A lesion appears bright on DWI and bright on the corresponding ADC map. This phenomenon, which can be seen in subacute hematomas, is best described as:
A. True restricted diffusion
✗
Incorrect. True restricted diffusion, as seen in cytotoxic edema from acute ischemia, is characterized by high signal on DWI and low signal on the ADC map.
B. T2 shine-through
✓
Correct. DWI signal is a function of both water diffusion and T2 relaxation time.
T2 shine-through occurs when a lesion with a very long T2 relaxation time (e.g., vasogenic edema, cysts, late subacute hemorrhage) appears bright on DWI, not because of restricted diffusion, but because its inherent T2 brightness ‘shines through.’
This is confirmed by high signal on the ADC map, which indicates facilitated, not restricted, diffusion.
Silvera S, et al. AJNR Am J Neuroradiol. 2005.
C. T2 blackout effect
✗
Incorrect. T2 blackout is the opposite phenomenon, where profound T2 shortening from paramagnetic substances (like acute or chronic blood products) causes such extreme signal loss that it overwhelms any diffusion signal, appearing dark on both DWI and ADC maps.
D. T1 shortening
✗
Incorrect. T1 shortening is a phenomenon related to T1-weighted imaging, causing hyperintensity on T1 images, and is not the term used to describe this specific DWI/ADC appearance.
7. Which MRI sequence is most sensitive for the detection of blood products, particularly in chronic microhemorrhages, due to its accentuation of magnetic susceptibility effects?
A. T1-weighted post-contrast
✗
Incorrect. This sequence is primarily for evaluating blood-brain barrier disruption and vascularity; it has poor sensitivity for chronic blood products.
B. Fluid-Attenuated Inversion Recovery (FLAIR)
✗
Incorrect. FLAIR is excellent for detecting parenchymal edema and is sensitive to subarachnoid hemorrhage, but it is not the most sensitive sequence for detecting hemosiderin from old microhemorrhages.
C. Diffusion-Weighted Imaging (DWI)
✗
Incorrect. While DWI can show signal changes in hemorrhage depending on the stage, it is susceptible to T2-blackout effects and is less sensitive than susceptibility-based sequences for chronic hemosiderin deposition.
D. Susceptibility-Weighted Imaging (SWI)/Gradient Echo (GRE)
✓
Correct. GRE sequences, and particularly SWI which combines magnitude and phase data, are highly sensitive to the magnetic field inhomogeneities (susceptibility effects) caused by paramagnetic blood products like hemosiderin.
This causes a signal loss or ‘blooming’ artifact, making these sequences superior for detecting chronic microhemorrhages.
