Intracerebral hemorrhage
Intracerebral hemorrhage, or hemorrhagic stroke, is a sudden, dramatic event where blood unexpectedly ruptures into the delicate tissues of the brain, or its fluid-filled ventricles. This internal bleeding creates immediate pressure and damage, posing a severe threat to neurological function and life itself. Understanding this critical condition is vital, as it represents a significant medical emergency with complex causes and outcomes. Intracerebral hemorrhage is a severe form of stroke caused by bleeding within the brain, leading to rapid neurological decline. High blood pressure and weakened blood vessels are primary risk factors, making early diagnosis via CT scans crucial for survival. Treatment focuses on immediate blood pressure control, managing intracranial pressure, and sometimes surgery, though outcomes can vary significantly.
AI Summary
Intracerebral hemorrhage, or hemorrhagic stroke, is a sudden, dramatic event where blood unexpectedly ruptures into the delicate tissues of the brain, or its fluid-filled ventricles. This internal bleeding creates immediate pressure and damage, posing a severe threat to neurological function and life itself. Understanding this critical condition is vital, as it represents a significant medical emergency with complex causes and outcomes.
- Intracerebral hemorrhage is a severe form of stroke caused by bleeding within the brain, leading to rapid neurological decline.
- High blood pressure and weakened blood vessels are primary risk factors, making early diagnosis via CT scans crucial for survival.
- Treatment focuses on immediate blood pressure control, managing intracranial pressure, and sometimes surgery, though outcomes can vary significantly.
What is Intracerebral Hemorrhage?
Imagine a pipe bursting deep within the most intricate control center you know—your brain. That's essentially an intracerebral hemorrhage, or ICH, also known as a hemorrhagic stroke. It's a sudden, critical event where a blood vessel ruptures, spilling blood directly into the brain's delicate tissues, called the parenchyma, or into its fluid-filled chambers, the ventricles.
This internal bleeding can occur with terrifying speed, rapidly disrupting brain function and creating dangerous pressure. Unlike an ischemic stroke, which is caused by a blockage, an ICH is a 'leak'—and it poses an immediate medical emergency where every second truly counts.
The Roots of Rupture
What makes a blood vessel in the brain suddenly give way? Often, it's a pre-existing vulnerability. Conditions like arteriolosclerosis, where small arteries harden and lose their elasticity, or cerebral amyloid angiopathy, which weakens vessel walls with protein deposits, are common culprits in spontaneous hemorrhages. Think of them as tiny, ticking time bombs within the brain's delicate vascular network.
Beyond these degenerative changes, other structural issues can trigger an ICH. Malformed blood vessels, like arteriovenous malformations (AVMs), or balloon-like bulges called aneurysms, are particularly dangerous. Even brain tumors or severe head trauma can sometimes lead to these devastating internal bleeds, underscoring the many pathways to this critical condition.
Identifying the Risks
Among all the potential triggers, sustained high blood pressure—or hypertension—stands out as the single most significant risk factor for spontaneous ICH, increasing the risk by two to six times. Over time, this constant strain can severely damage and weaken the brain's tiny arteries, making them prone to rupture. It's a silent threat, often without obvious symptoms until it's too late.
Other factors can also increase your vulnerability. Chronic alcohol use, certain blood thinners (anticoagulants), and even illicit drug use like cocaine can heighten the risk. Additionally, conditions like amyloidosis, which involves abnormal protein deposits in blood vessels, can also weaken vessel walls, setting the stage for a bleed.
The Critical Diagnosis
When a hemorrhagic stroke is suspected, time is of the essence. The primary diagnostic tool is a computed tomography, or CT, scan of the brain. This rapid imaging technique allows doctors to quickly visualize the fresh blood within the brain tissue, as it appears distinctly brighter than the surrounding structures, confirming the diagnosis and guiding immediate next steps.
Immediate Intervention
Treating an intracerebral hemorrhage is a race against time, typically requiring admission to an intensive care unit (ICU). A critical first step is meticulously controlling blood pressure. Doctors aim for specific targets, often using powerful medications to either lower or, in some cases, carefully maintain it, all to prevent further bleeding and protect the brain from additional damage.
Beyond blood pressure, other immediate concerns include reversing the effects of any blood thinners the patient might be taking. Swelling and fluid buildup within the brain, known as hydrocephalus, can also elevate intracranial pressure, sometimes necessitating the placement of an external ventricular drain, or EVD, to relieve the dangerous pressure. Interestingly, corticosteroids, once thought helpful for brain swelling, are now generally avoided due to evidence suggesting worse outcomes.
Surgical Considerations
In some cases, directly removing the accumulated blood—the hematoma—through surgery can be a life-saving measure. This is often considered when the hematoma is large, exceeding 3 cm, or when there's an underlying structural cause like an aneurysm that can be repaired simultaneously. The goal is to alleviate pressure and reduce direct damage to brain tissue.
The Human Impact
Intracerebral hemorrhage, first distinguished from ischemic strokes in 1823, is thankfully less common than other types of stroke, affecting about 24.6 people per 100,000 each year. However, its impact is profound. It tends to strike more often in older individuals, with those 85 or older being 9.6 times more likely to experience one than middle-aged adults, reflecting age-related changes in blood vessel health.
The statistics for ICH are sobering. Approximately 44% of those affected unfortunately succumb to the condition within a month, with half of those deaths occurring in the first two days. Even for survivors, a truly good outcome—meaning significant functional independence—is achieved in only about 20% of cases, highlighting the severe, long-lasting consequences of this devastating brain injury.
Where the Bleeding Strikes
Not all brain bleeds are alike, and their location profoundly impacts the outcome. One major category is Intraparenchymal Hemorrhage (IPH), where bleeding occurs directly within the brain's parenchyma—its functional tissue. This is the most common form of ICH and is particularly dangerous, responsible for a higher rate of death and severe disability compared to other stroke types or subarachnoid hemorrhages.
Inside the Ventricles
Another critical type is Intraventricular Hemorrhage (IVH), a bleed within the brain's ventricular system. These fluid-filled chambers produce and circulate cerebrospinal fluid, essential for brain health. While some IVHs originate directly in the ventricle, most are "secondary," meaning they occur as an extension of a larger intraparenchymal or subarachnoid hemorrhage. Either way, blood here can block CSF flow, leading to a dangerous buildup of pressure throughout the brain, often signaling a widespread and severe injury.
The Body's Alarm Bells
The brain is a master map of the body, and the symptoms of an ICH often directly correspond to the functions controlled by the damaged area. These "localizing signs" can appear rapidly, sometimes within minutes, making immediate medical attention absolutely crucial. While perhaps not as instantaneous as some ischemic strokes, every second counts.
Recognizing a Stroke: FAST
To help the public quickly identify a potential stroke, organizations worldwide advocate the "FAST" mnemonic. It stands for: Facial droop, Arm weakness, Speech difficulty—and Time to call emergency services. Recognizing these signs can mean the difference between life and irreversible brain damage, though it's important to note FAST is less reliable for strokes in the brain's posterior circulation.
When Pressure Builds
As blood accumulates, it creates a growing mass effect, leading to a dangerous rise in intracranial pressure (ICP). This escalating pressure can manifest as severe headaches, relentless nausea and vomiting, and a progressive decrease in consciousness—from confusion to stupor. If unchecked, this can lead to brain herniation, a dire displacement of brain tissue that compresses vital structures and is often a precursor to irreversible damage or death.
Location, Location, Location
The exact location of the bleed dictates specific neurological deficits. A hemorrhage in the basal ganglia or thalamus, for example, which accounts for about 65% of cases and are critical relay stations for movement and sensation, frequently causes weakness or paralysis on the opposite side of the body, alongside sensory loss. These can also cause issues with eye movement, known as gaze palsies.
Bleeding in the cerebellum, at the back of the brain, can disrupt coordination, causing severe dizziness, imbalance, and incoordination of limbs. A more dangerous scenario is a brainstem hemorrhage, especially in the pons, which often leads to life-threatening issues with breathing, consciousness, and multiple cranial nerve deficits, presenting with a grim prognosis due to damage to the reticular activating system.
Unpacking the Causes Further
While we touched upon primary risk factors, let's delve deeper into the origins of these devastating bleeds. Uncontrolled hypertension remains the overwhelming cause for spontaneous ICH, constantly stressing and weakening the delicate cerebral arteries. Another significant contributor, particularly in older adults, is cerebral amyloid angiopathy, where amyloid proteins accumulate in vessel walls, making them fragile and prone to rupture.
Beyond chronic conditions, certain medications and lifestyle choices play a role. The use of anticoagulants (blood thinners) and antiplatelet drugs significantly elevates ICH risk, which is why their careful management is critical. Curiously, even very low levels of "bad" cholesterol (LDL) and chronic kidney disease have been linked to an increased risk, though the precise mechanisms are still being explored. Smoking, while harmful, has a weaker direct link to ICH.
Not all ICHs are "spontaneous." Severe head trauma, such as that from falls or accidents, can also directly cause bleeding. These traumatic hemorrhages can occur immediately at the time of injury, known as acute hematomas. In some cases, surprisingly, they can develop hours to even several weeks later—these are called delayed traumatic hematomas, further complicating diagnosis and treatment.
Advanced Diagnostics
While a standard CT scan confirms the presence of blood, more advanced imaging like CT angiography (CTA) or magnetic resonance angiography (MRA) can provide crucial additional information. These scans can identify underlying vascular malformations or aneurysms that might have caused the bleed, and sometimes even reveal a "spot sign"—a small, enhancing area of contrast within the hematoma—which indicates ongoing active bleeding, guiding urgent intervention.
The Expanding Threat: Edema
A growing concern after an ICH is the development of perihematomal edema—swelling that forms around the blood clot. This edema isn't just passive swelling; it actively contributes to brain injury, worsening neurological function and prognosis. It rapidly expands in the first 48 hours, peaking around two weeks post-hemorrhage, driven by the breakdown products of the spilled blood, which are toxic to surrounding brain tissue.
Beyond CT scans, new techniques like transcranial ultrasound are emerging as valuable tools. By using sound waves, doctors can non-invasively monitor the progression of the hematoma, estimate its volume, and potentially identify patients with active bleeding who might benefit most from immediate intervention. This method also offers the advantage of reducing radiation risk to the patient compared to repeated CT scans.
Nuances in Treatment Strategies
Intensive care for ICH involves a delicate balance. While rapid blood pressure lowering can improve functional recovery at 90 days post-hemorrhage, the optimal target remains a subject of active research, with some guidelines recommending a systolic blood pressure (SBP) of 140 mmHg. The goal is to reduce hematoma expansion without compromising blood flow to vital, yet vulnerable, brain tissue.
Counteracting Coagulation Issues
For patients on blood thinners, immediate reversal of anticoagulation is paramount. Specific antidotes like idarucizumab or andexanet alfa exist for newer oral anticoagulants, while prothrombin complex concentrates or vitamin K are used for older ones like warfarin. However, some treatments, like administering Factor VIIa, or platelet transfusions for those on antiplatelet medication, can carry their own risks, such as increasing the chance of new clots, and are carefully weighed based on individual patient circumstances.
Seizures can occur after an ICH, both overtly and subclinically. Yet, anticonvulsants are generally reserved only for patients with clear clinical seizures or confirmed seizure activity on EEG, as their routine use can ironically increase mortality risk. Additionally, medications like H2 antagonists or proton pump inhibitors are often given to prevent stress ulcers, a common complication in critically ill patients.
Surgical Pathways
When surgery is deemed necessary, options range from minimally invasive to open procedures. Catheter-based techniques can navigate the brain's vasculature to treat underlying lesions, while stereotactic surgery or endoscopic drainage can aspirate the hematoma through small incisions. For larger, life-threatening bleeds, a decompressive craniectomy, which involves temporarily removing a section of the skull, may be performed to relieve critical intracranial pressure, though its long-term neurological benefits are debated.
Article
Intracerebral hemorrhage
Intracerebral hemorrhage (ICH), also known as hemorrhagic stroke, is a sudden bleeding into the tissues of the brain (i.e. the parenchyma), into its ventricles, or into both. An ICH is a type of bleeding within the skull and one kind of stroke (ischemic stroke being the other). Symptoms can vary dramatically depending on the severity (how much blood), acuity (over what timeframe), and location (anatomically) but can include headache, one-sided weakness, numbness, tingling, or paralysis, speech problems, vision or hearing problems, memory loss, attention problems, coordination problems, balance problems, dizziness or lightheadedness or vertigo, nausea/vomiting, seizures, decreased level of consciousness or total loss of consciousness, neck stiffness, and fever.
Hemorrhagic stroke may occur on the background of alterations to the blood vessels in the brain, such as cerebral arteriolosclerosis, cerebral amyloid angiopathy, cerebral arteriovenous malformation, brain trauma, brain tumors and an intracranial aneurysm, which can cause intraparenchymal or subarachnoid hemorrhage.
The biggest risk factors for spontaneous bleeding are high blood pressure and amyloidosis. Other risk factors include alcoholism, low cholesterol, blood thinners, and cocaine use. Diagnosis is typically by CT scan.
Treatment should typically be carried out in an intensive care unit due to strict blood pressure goals and frequent use of both pressors and antihypertensive agents. Anticoagulation should be reversed if possible and blood sugar kept in the normal range. A procedure to place an external ventricular drain may be used to treat hydrocephalus or increased intracranial pressure, however, the use of corticosteroids is frequently avoided. Sometimes surgery to directly remove the blood can be therapeutic.
Cerebral bleeding affects about 2.5 per 10,000 people each year. It occurs more often in males and older people. About 44% of those affected die within a month. A good outcome occurs in about 20% of those affected. Intracerebral hemorrhage, a type of hemorrhagic stroke, was first distinguished from ischemic strokes due to insufficient blood flow, so called "leaks and plugs", in 1823.
Epidemiology
Intracerebral hemorrhage
The incidence of intracerebral hemorrhage is estimated at 24.6 cases per 100,000 person years with the incidence rate being similar in men and women. The incidence is much higher in the elderly, especially those who are 85 or older, who are 9.6 times more likely to have an intracerebral hemorrhage as compared to those of middle age. It accounts for 20% of all cases of cerebrovascular disease in the United States, behind cerebral thrombosis (40%) and cerebral embolism (30%).
Types
Intraparenchymal hemorrhage
Intraparenchymal hemorrhage (IPH) is one form of intracerebral bleeding in which there is bleeding within brain parenchyma. Intraparenchymal hemorrhage accounts for approximately 8-13% of all strokes and results from a wide spectrum of disorders. It is more likely to result in death or major disability than ischemic stroke or subarachnoid hemorrhage, and therefore constitutes an immediate medical emergency. Intracerebral hemorrhages and accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause elevation of intracranial pressure (ICP) and potentially fatal herniation syndromes.
Intraventricular hemorrhage
Intraventricular hemorrhage (IVH), also known asintraventricular bleeding, is a bleeding into the brain's ventricular system, where the cerebrospinal fluid is produced and circulates through towards the subarachnoid space. It can result from physical trauma or from hemorrhagic stroke.
30% of intraventricular hemorrhage (IVH) are primary, confined to the ventricular system and typically caused by intraventricular trauma, aneurysm, vascular malformations, or tumors, particularly of the choroid plexus. However 70% of IVH are secondary in nature, resulting from an expansion of an existing intraparenchymal or subarachnoid hemorrhage. Intraventricular hemorrhage has been found to occur in 35% of moderate to severe traumatic brain injuries. Thus the hemorrhage usually does not occur without extensive associated damage, and so the outcome is rarely good.
Signs and symptoms
Intracerebral hemorrhage
People with intracerebral bleeding have symptoms that correspond to the functions controlled by the area of the brain that is damaged by the bleed. These localizing signs and symptoms can include hemiplegia (or weakness localized to one side of the body) and paresthesia (loss of sensation) including hemisensory loss (if localized to one side of the body). These symptoms are usually rapid in onset, sometimes occurring in minutes, but not as rapid as the symptom onset in ischemic stroke. While the duration of onset may not be as rapid, it is important that patients go to the emergency department as soon as they notice any symptoms as early detection and management of stroke may lead to better outcomes post-stroke than delayed identification.
A mnemonic to remember the warning signs of stroke is FAST (facial droop, arm weakness, speech difficulty, and time to call emergency services), as advocated by the Department of Health (United Kingdom) and the Stroke Association, the American Stroke Association, the National Stroke Association (US), the Los Angeles Prehospital Stroke Screen (LAPSS) and the Cincinnati Prehospital Stroke Scale (CPSS). Use of these scales is recommended by professional guidelines. FAST is less reliable in the recognition of posterior circulation stroke.
Other symptoms include those that indicate a rise in intracranial pressure caused by a large mass (due to hematoma expansion) putting pressure on the brain. These symptoms include headaches, nausea, vomiting, a depressed level of consciousness, stupor and death. Continued elevation in the intracranial pressure and the accompanying mass effect may eventually cause brain herniation (when different parts of the brain are displaced or shifted to new areas in relation to the skull and surrounding dura mater supporting structures). Brain herniation is associated with hyperventilation, extensor rigidity, pupillary asymmetry, pyramidal signs, coma and death.
Hemorrhage into the basal ganglia or thalamus causes contralateral hemiplegia due to damage to the internal capsule. Other possible symptoms include gaze palsies or hemisensory loss. Intracerebral hemorrhage into the cerebellum may cause ataxia, vertigo, incoordination of limbs, and vomiting. Some cases of cerebellar hemorrhage lead to blockage of the fourth ventricle with subsequent impairment of drainage of cerebrospinal fluid from the brain. The ensuing hydrocephalus, or fluid buildup in the ventricles of the brain leads to a decreased level of consciousness, total loss of consciousness, coma, and persistent vegetative state. Brainstem hemorrhage most commonly occurs in the pons and is associated with shortness of breath, cranial nerve palsies, pinpoint (but reactive) pupils, gaze palsies, facial weakness, coma, and persistent vegetative state (if there is damage to the reticular activating system).
Causes
Intracerebral hemorrhage
Axial CT scan showing hemorrhage in the posterior fossa
Intracerebral bleeds are the second most common cause of stroke, accounting for 10% of hospital admissions for stroke. High blood pressure raises the risks of spontaneous intracerebral hemorrhage by two to six times. More common in adults than in children, intraparenchymal bleeds are usually due to penetrating head trauma, but can also be due to depressed skull fractures. Acceleration-deceleration trauma, rupture of an aneurysm or arteriovenous malformation (AVM), and bleeding within a tumor are additional causes. Amyloid angiopathy is not an uncommon cause of intracerebral hemorrhage in patients over the age of 55. A very small proportion is due to cerebral venous sinus thrombosis.
• Hypertension (high blood pressure) • Diabetes mellitus • Menopause • Excessive alcohol consumption • Severe migraine
Hypertension is the strongest risk factor associated with intracerebral hemorrhage and long term control of elevated blood pressure has been shown to reduce the incidence of hemorrhage. Cerebral amyloid angiopathy, a disease characterized by deposition of amyloid beta peptides in the walls of the small blood vessels of the brain, leading to weakened blood vessel walls and an increased risk of bleeding; is also an important risk factor for the development of intracerebral hemorrhage. Other risk factors include advancing age (usually with a concomitant increase of cerebral amyloid angiopathy risk in the elderly), use of anticoagulants or antiplatelet medications, the presence of cerebral microbleeds, chronic kidney disease, and low low density lipoprotein (LDL) levels (usually below 70). The direct oral anticoagulants (DOACs) such as the factor Xa inhibitors or direct thrombin inhibitors are thought to have a lower risk of intracerebral hemorrhage as compared to the vitamin K antagonists such as warfarin.
Cigarette smoking may be a risk factor but the association is weak.
Traumatic intracerebral hematomas are divided into acute and delayed. Acute intracerebral hematomas occur at the time of the injury while delayed intracerebral hematomas have been reported from as early as 6 hours post injury to as long as several weeks.
Diagnosis
Intracerebral hemorrhage
Spontaneous ICH with hydrocephalus on CT scan
Both computed tomography angiography (CTA) and magnetic resonance angiography (MRA) have been proved to be effective in diagnosing intracranial vascular malformations after ICH. So frequently, a CT angiogram will be performed in order to exclude a secondary cause of hemorrhage or to detect a "spot sign".
Intraparenchymal hemorrhage can be recognized on CT scans because blood appears brighter than other tissue and is separated from the inner table of the skull by brain tissue. The tissue surrounding a bleed is often less dense than the rest of the brain because of edema, and therefore shows up darker on the CT scan. The oedema surrounding the haemorrhage would rapidly increase in size in the first 48 hours, and reached its maximum extent at day 14. The bigger the size of the haematoma, the larger its surrounding oedema. Brain oedema formation is due to the breakdown of red blood cells, where haemoglobin and other contents of red blood cells are released. The release of these red blood cells contents causes toxic effect on the brain and causes brain oedema. Besides, the breaking down of blood-brain barrier also contributes to the odema formation.
Apart from CT scans, haematoma progression of intracerebral haemorrhage can be monitored using transcranial ultrasound. Ultrasound probe can be placed at the temporal lobe to estimate the volume of haematoma within the brain, thus identifying those with active bleeding for further intervention to stop the bleeding. Using ultrasound can also reduces radiation risk to the subject from CT scans.
Location
When due to high blood pressure, intracerebral hemorrhages typically occur in the putamen (50%) or thalamus (15%), cerebrum (10–20%), cerebellum (10–13%), pons (7–15%), or elsewhere in the brainstem (1–6%).
Treatment
Intracerebral hemorrhage
Treatment depends substantially on the type of ICH. Rapid CT scan and other diagnostic measures are used to determine proper treatment, which may include both medication and surgery.
• Tracheal intubation is indicated in people with decreased level of consciousness or other risk of airway obstruction. • IV fluids are given to maintain fluid balance, using isotonic rather than hypotonic fluids.
Medications
Rapid lowering of the blood pressure using antihypertensive therapy for those with hypertensive emergency can have higher functional recovery at 90 days post intracerebral haemorrhage, when compared to those who undergone other treatments such as mannitol administration, reversal of anticoagulation (those previously on anticoagulant treatment for other conditions), surgery to evacuate the haematoma, and standard rehabilitation care in hospital, while showing similar rate of death at 12%. Early lowering of the blood pressure can reduce the volume of the haematoma, but may not have any effect against the oedema surrounding the haematoma. Reducing the blood pressure rapidly does not cause brain ischemia in those who have intracerebral haemorrhage. The American Heart Association and American Stroke Association guidelines in 2015 recommended decreasing the blood pressure to a SBP of 140 mmHg. However, later reviews found unclear difference between intensive and less intensive blood pressure control.
Giving Factor VIIa within 4 hours limits the bleeding and formation of a hematoma. However, it also increases the risk of thromboembolism. It thus overall does not result in better outcomes in those without hemophilia.
Frozen plasma, vitamin K, protamine, or platelet transfusions may be given in case of a coagulopathy. Platelets however appear to worsen outcomes in those with spontaneous intracerebral bleeding on antiplatelet medication.
The specific reversal agents idarucizumab and andexanet alfa may be used to stop continued intracerebral hemorrhage in people taking directly oral acting anticoagulants (such as factor Xa inhibitors or direct thrombin inhibitors). However, if these specialized medications are not available, prothrombin complex concentrate may also be used.
Only 7% of those with ICH are presented with clinical features of seizures while up to 25% of those have subclinical seizures. Seizures are not associated with an increased risk of death or disability. Meanwhile, anticonvulsant administration can increase the risk of death. Therefore, anticonvulsants are only reserved for those that have shown obvious clinical features of seizures or seizure activity on electroencephalography (EEG).
H2 antagonists or proton pump inhibitors are commonly given to try to prevent stress ulcers, a condition linked with ICH.
Corticosteroids were thought to reduce swelling. However, in large controlled studies, corticosteroids have been found to increase mortality rates and are no longer recommended.
Surgery
Surgery is required if the hematoma is greater than 3 cm (1 in), if there is a structural vascular lesion or lobar hemorrhage in a young patient.
A catheter may be passed into the brain vasculature to close off or dilate blood vessels, avoiding invasive surgical procedures.
Aspiration by stereotactic surgery or endoscopic drainage may be used in basal ganglia hemorrhages, although successful reports are limited.
A craniectomy holds promise of reduced mortality, but the effects of long‐term neurological outcome remain controversial.
Prognosis
Intracerebral hemorrhage
About 8 to 33% of those with intracranial haemorrhage have neurological deterioration within the first 24 hours of hospital admission, where a large proportion of them happens within 6 to 12 hours. Rate of haematoma expansion, perihaematoma odema volume and the presence of fever can affect the chances of getting neurological complications.
The risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the injury occurs in the brain stem. Intraparenchymal bleeds within the medulla oblongata are almost always fatal, because they cause damage to cranial nerve X, the vagus nerve, which plays an important role in blood circulation and breathing. This kind of hemorrhage can also occur in the cortex or subcortical areas, usually in the frontal or temporal lobes when due to head injury, and sometimes in the cerebellum. Larger volumes of hematoma at hospital admission as well as greater expansion of the hematoma on subsequent evaluation (usually occurring within 6 hours of symptom onset) are associated with a worse prognosis. Perihematomal edema, or secondary edema surrounding the hematoma, is associated with secondary brain injury, worsening neurological function and is associated with poor outcomes. Intraventricular hemorrhage, or bleeding into the ventricles of the brain, which may occur in 30–50% of patients, is also associated with long-term disability and a poor prognosis. Brain herniation is associated with poor prognoses.
For spontaneous intracerebral hemorrhage seen on CT scan, the death rate (mortality) is 34–50% by 30 days after the injury, and half of the deaths occur in the first 2 days. Even though the majority of deaths occur in the first few days after ICH, survivors have a long-term excess mortality rate of 27% compared to the general population. Of those who survive an intracerebral hemorrhage, 12–39% are independent with regard to self-care; others are disabled to varying degrees and require supportive care.