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Intracranial Hemorrhage

An intracranial hemorrhage results from rupture of an artery, vein or vein sinus within the cranial vault, which may lead to hypoxic neuronal death. Due to the bony skull surrounding intracranial tissues, hemorrhages are very likely to cause detrimental, pressure-induced brain lesions.


Patients sustaining IH present with headaches, nausea and vomiting, and possibly with seizures, neurological deficits and a reduced general condition. If they don't lose consciousness, they may be confused and have an altered mental state. It is not uncommon to observe an affected individual to lose consciousness, to revive, and to fall back into unconsciousness before deteriorating and dying. This is sometimes referred to as "talk and die" [7].

With regards to neurological deficits, they may indicate the precise site of lesion, although there are numerous overlaps of symptoms. Most IH affect lobar regions or basal ganglia, and bleedings are less likely to occur in diencephalon, pons, midbrain or cerebellum.

  • Contralateral hemiparesis including conjugate gaze palsy and contralateral sensory loss are frequent and unspecific symptoms of hemorrhagic stroke. These symptoms may be observed after lobar or basal ganglia hemorrhages, but also if the thalamus is affected.
  • In contrast, tetraparesis indicates brainstem lesions. In such cases, autonomic functions may be impaired, too.
  • Patients may report homonymous hemianopia after hemorrhages in lobar regions, basal ganglia or diencephalon. Furthermore, such hemorrhagic strokes may provoke aphasia and apraxia.
  • Ataxia is typical for cerebellar damage.
  • Subarachnoid hemorrhages are frequently associated with meningism [8].

An ophthalmological examination of IH patients may reveal anisocoria and retinal hemorrhages.

Decreased Renal Function
  • We report one of the first case reports of severe intracranial hemorrhage associated with rivaroxaban in an elderly patient with decreased renal function.[ncbi.nlm.nih.gov]
Intracranial Hemorrhage
  • […] with intracranial hemorrhage.[ncbi.nlm.nih.gov]
  • Reversal of INR of less than 5 hr was not associated with intracranial hemorrhage evolution; however, reversal of less than 10 hr was found to be associated with a decreased odds ratio for intracranial hemorrhage evolution (p .043).[ncbi.nlm.nih.gov]
  • Immediate postoperative catheter-related intracranial hemorrhage is possibly due to the procedure itself; however, delayed intracranial hemorrhage may have other underlying mechanisms.[ncbi.nlm.nih.gov]
  • Lipophilic statins cross the blood-brain barrier more freely than hydrophilic statins and may therefore increase the risk of intracranial hemorrhage.[ncbi.nlm.nih.gov]
  • The intracranial hemorrhage prevalence in our study is similar to previous reports for patients on warfarin.[ncbi.nlm.nih.gov]
  • A 64-year-old woman presented with sudden-onset motor aphasia. Computed tomography revealed subarachnoid hemorrhage, and intracerebral hemorrhage in the left temporal lobe.[ncbi.nlm.nih.gov]
  • We present a 30-year-old woman with sudden onset of right hemiplegia, global aphasia, and new-onset seizures diagnosed with left transverse and sigmoid sinus thrombosis with intraparenchymal hemorrhage.[ncbi.nlm.nih.gov]
  • LOBAR HEMORRHAGE • occipital hemorrhage - hemianopia; • left temporal hemorrhage,-aphasia and delirium; • parietal hemorrhage - hemisensory loss; • frontal hemorrhage,-arm weakness • Focal headache and vomiting can occur 18.[slideshare.net]
  • Also common is hemiparesis (bleeding extension into the internal capsule) and aphasia. Putamen Hemorrhage: Contralateral hemiparesis/hemiplegia, Contralateral sensory loss, Homonymous hemianopia References: Qureshi AI, Palesch YY, Barsan WG, et al.[foamcast.org]
  • Putamen Hemiplegia, hemisensory loss, homonymous hemianopsia, gaze palsy, stupor, coma Cerebellum Gait imbalance, vomiting, headache, neck stiffness, gaze palsy, facial weakness Thalamus Hemiplegia, hemisensory loss, transient homonymous hemianopsia, aphasia[emdocs.net]
Decorticate Posture
  • Initial emergency room evaluation found the patient to have anisocoria with a fixed and dilated right pupil and demonstrated evidence of decorticate posturing.[ncbi.nlm.nih.gov]


In mild to moderate cases, IH patients may present with a medical history of hypertension, coagulation disorders, head trauma, abuse of alcohol or illegal drugs. However, it may not be possible to obtain such data in more severe cases. Patients may be admitted unconsciously and here, blunted reflexes and other neurological deficits as well as pathological ophthalmological findings are often the sole basis of a tentative diagnosis of central nervous system lesions.

The corresponding workup is based on neuroimaging.

  • In images obtained by means of computed tomography, hemorrhages typically appear as regions of hyperdense signal intensity. In trauma patients, multiple IH may be seen.
  • Magnetic resonance imaging is less sensitive than computed tomography, particularly during the first hours after the onset of bleeding. This is due to the fact that shifts of water from extracellular to intracellular spaces, and eventually from cerebral blood vessels to the parenchyma of the brain don't occur immediately. Cytotoxic and vasogenic edema are readily recognizable in magnetic resonance images, but they don't develop until some time has passed after the onset of IH.
  • Moreover, distinct types of angiography may be applied to depict the ruptured vessel, e.g., computed tomographic angiography, magnetic resonance angiography and digital subtraction angiography. They are particularly indicated if other cerebrovascular diseases are suspected [9].
  • Likewise, vascular risk factors (arterial hypertension, diabetes mellitus, obesity, former vascular event, hyperlipidemia, tobacco consumption and/or hypercholesterolemia) did not differ significantly between both groups.[ncbi.nlm.nih.gov]
Staphylococcus Aureus
  • Native valve infective endocarditis by Staphylococcus aureus is a well-known entity. Metastatic eye abscess and intracranial hemorrhage are rare manifestations of infective endocarditis.[ncbi.nlm.nih.gov]


First, patients admitted with hemorrhagic stroke should be stabilized: Intubation and respiratory assistance are often necessary to assure proper oxygen saturation. With regards to the cardiovascular system, heart rate and blood pressure should be monitored and, if need be, adjusted as far as possible to physiological values. Although a target systolic blood pressure of < 180 mmHg is often cited, it has recently been shown that intensive blood pressure lowering therapy (target < 140 mmHg) is associated with an even better functional outcome [10]. Beta-blockers and angiotensin-converting enzyme inhibitors are most often administered, with nitroprusside reserved for patients who present with contraindications to treatment with the former. Nitroprusside may increase intracranial pressure and may thus exacerbate IH. Blood glucose levels and body temperature should also be monitored and maintained in reference ranges. Patients suffering from seizures benefit from administration of benzodiazepines, and some physicians apply anticonvulsants preventively in stroke patients without seizures.

Surgical intervention may be necessary in moderate to severe cases, in patients who present with neurological deficits or those who deteriorate after initial presentation. Surgery primarily aims at relieving intracranial pressure and thus consists in evacuation of the corresponding hematoma. If IH originate from arteriovenous malformations, surgical clipping or endovascular coiling may be indicated. In less severe cases, osmotic diuretics like mannitol or hypertonic saline may be administered to lower intracranial pressure. It is important to monitor blood pressure and cerebral perfusion if such treatment is chosen. Small, asymptomatic hematomas may be self-limiting, but regular neuroimaging is indicated to recognize possible hematoma growth.


Time is crucial in IH diagnosis and the patient's prognosis largely depends on an early recognition of their condition. Only if treatment is provided during the first hours, brain damage can be limited to the initial site of bleeding. Otherwise, the resulting hematoma grows, exerts pressure on adjacent tissues and triggers further neuronal death. In general, large hematoma are associated with a worse outcome, but depending on the precise location of IH, small hematoma may also have detrimental effects.

Moreover, the accessibility of the site of hemorrhage affects the outcome, and deep IH are related to a less favorable prognosis than superficial bleedings. Additional, unfavorable prognostic factors are unconsciousness upon admission, scores ≤ 3 on the Glasgow Coma Scale, hydrocephalus, hypertension and old age. In sum, up to 50% of affected people die within one month after occurrence of IH even though intense medical care is provided [6]. IH survivors often suffer from persistent neurological deficits and disabilities, and require assistance to manage everyday life. Only 20% of IH patients are expected to recover fully [4].


IH occurs upon rupture of an intracranial vessel. This may happen due to systemic diseases, due to an intrinsic vascular disease, pathological processes in adjacent tissues that eventually compromise the vessel, or the application of an external force.

Hypertension is by far the most common cause of IH. Although intracranial vessels are able to resist rather high blood pressures, at some point they will succumb to hypertension. This is largely facilitated if the vessel's wall is already damaged, possibly by any of the factors mentioned below.

With regards to vascular lesions, inflammatory diseases may debilitate the vessel's wall. Giant cell arteritis, polyarteritis nodosa and Wegener granulomatosis are systemic disorders that may comprise inflammation of intracranial blood vessels. Debilitation of the vessel's wall may initially cause the formation of a cerebral aneurysm, but rupture may also occur without an aneurysm being present. Inflammatory processes may originate from tissues other than blood vessels, although the latter are generally involved in diseases like encephalitis and meningitis. Sinusitis is a very common condition that may eventually spread to the brain. Similarly, neoplasms may infiltrate intracranial vessels.

Moreover, cerebral thrombosis may cause affected arteries, veins or sinuses to rupture. In this context, pre-existing endothelial lesions increase the risk of thrombus formation and adherent thrombi provoke an exacerbation of vessel wall lesions. However, endothelial lesions are not a prerequisite for thrombus formation, since systemic diseases causing thrombophilia may induce similar pathophysiologic events. Thrombophilia, polycythemia and disseminated intravascular coagulation shall be mentioned as examples at this point. On the other hand, patients receiving anti-thrombotic therapy in form of anticoagulants or thrombolytics are also at risk of IH. Here, the coagulation system is unable to prevent leakage of blood even from microlesions. This also applies to hemophilia patients [2]. However, this risk is usually considered to be lower than that of cerebral thrombosis, which is important when deciding for a therapeutic approach to head trauma. Such traumas may or may not be associated with skull fracture and are another common cause of IH.

People who abuse of alcohol or illegal drugs like cocaine are particularly prone to IH [3].


IH and subsequent hemorrhagic stroke account for 10-15% of all strokes and the annual incidence of IH has been estimated to be up to 15 per 100,000 people. Hypertension contributes to the vast majority of IH, and because elevations in blood pressure are more common in the elderly, the incidence of intracranial bleedings increases with age. Furthermore, males and patients of African or Asian descent have been reported to be more susceptible to IH [4]. With regards to blacks, higher prevalence of hypertension in this share of the population is assumed to explain the increased incidence of IH. Causes of susceptibility are less clear in Asians, and genetic and environmental factors have been proposed to account for the observed phenomenon.

Sex distribution
Age distribution


The direct cause of IH is the rupture of an intracranial vessel. Depending on the precise site of the lesion, the following types of IH may be distinguished:

  • Epidural hemorrhage / epidural hematoma
  • Subdural hemorrhage / subdural hematoma
  • Subarachnoid hemorrhage / subarachnoid hematoma
  • Intracerebral hemorrhage / intracerebral hematoma

As has been implied above, the most detrimental consequences of IH are shortage of oxygen and glucose supply to dependent tissues, and hematoma-mediated pressure. Neurons are particularly susceptible to hypoxic damage. Within minutes, ATP-depletion occurs and ion pump function is interrupted. Neurons depolarize, and the ensuing intracellular accumulation of ions is followed by cytotoxic edema [5]. Concomitant impairment of glial cell function eventually causes a local breakdown of the blood-brain barrier. Moreover, pressure may directly provoke cell death, or may hinder circulation through blood vessels in close proximity to the intracranial hematoma. The clinical equivalent to those processes is a cerebrovascular accident, a hemorrhagic stroke.


Since hypertension contributes to the vast majority of IH, an adequate control of blood pressure reduces the individual risk of hemorrhagic stroke. Additionally, consumption of alcohol and drugs should be limited as far as possible, and smoking should be discouraged. Head traumas may be prevented by using safety equipment whenever possible, by responsible driving and by generally taking appropriate precautions.


Although the term intracranial hemorrhage (IH) refers to any bleeding caused by rupture of blood vessels inside the bony skull, it is often used interchangeably with the term intracerebral hemorrhage. This is not only due to the fact that the vast majority of intracranial space is occupied by the brain, but also because virtually any IH directly affects the central nervous system.

IH differ from hemorrhages that may occur elsewhere in the human body because of the special anatomy defining the cranium. The skull is covered by scalp fascia and muscles, and is lined by periosteum. The meninges, i.e., dura mater, arachnoid membrane and pia mater are located directly below the bony skull. Epidural, subdural and subarachnoid spaces lie between those meninges, that do cover the brain. Thus, there is a variety of tissues apart from the brain itself, and all those tissues are supplied with oxygen by arteries and blood is drained by venous vessels. Of course, this also applies to the central nervous system. Rupture of any blood vessel below the bony skull may cause IH, and because the cranium forms a rigid shell around all the aforementioned organs, IH are associated with a local increase of pressure.

Accordingly, three main pathomechanisms contribute to IH morbidity:

  • Shortage of oxygen supply to dependent tissues, and under ischemic conditions, neuronal death occurs within minutes.
  • Local increase of pressure due to hematoma formation directly damages adjacent tissues and further impairs circulation through as of yet unaffected vessels.
  • Blood loss, but due to the restricted intracranial space, blood loss is of minor importance in IH.

IH result in hemorrhagic stroke, which is a life-threatening disease with an associated mortality of up to 50%. Also, patients who survive often continue to suffer from neurological deficits and disabilities [1]. Thus, it is of utmost importance to recognize an IH early, and diagnostic imaging like computed tomography, magnetic resonance imaging and possibly angiography are most helpful to this end. Characteristic clinical symptoms that should prompt such a workup are hemiparesis, tetraparesis and sensory loss. Headaches, nausea and vomiting as well as loss of consciousness may also be observed. Generally, treatment consists of surgical intervention and supplementary drug therapy. The hemorrhage has to be stopped, and nerve tissue needs to be relieved of the increased pressure.

Patient Information

The term intracranial hemorrhage (IH) refers to the rupture of a blood vessel supplying the brain or meninges surrounding the brain.

While IH may be provoked by a variety of factors, most of them occur due to hypertension. Additionally, coagulation disorders, inflammation of blood vessels, brain or meninges, as well as head trauma may cause intracranial arteries or veins to tear. People who abuse of alcohol or illegal drugs like cocaine are particularly prone to IH. In many cases, more than one of the aforementioned risk factors contributes to IH.

IH differ from hemorrhages that may occur elsewhere in the human body because of the special anatomy of the cranium. The bony skull forms a rigid shell that protects the brain from traumatic lesions, but it also impairs expansion of intracranial tissues and pressure equalization. Thus, IH and hematoma formation has the following consequences:

  • Shortage of oxygen and glucose supply to dependent tissues.
  • Local increase of pressure due to hematoma formation directly damages adjacent tissues and further impairs circulation through as of yet unaffected vessels in close proximity.
  • Blood loss, which is of minor importance in IH.

If deprived of oxygen and glucose, neuronal death occurs within minutes. The affected individual will experience symptoms corresponding to hemorrhagic stroke. Of note, the more common form of stroke is ischemic stroke, characterized by occlusion of intracranial vessels and sudden interruption of blood flow.

Most frequently, hemorrhagic stroke is associated with neurological deficits like muscle weakness and sensory loss of one side of the body. Also, IH patients often claim headaches, nausea and vomiting, and suffer from seizures. They may lose consciousness.

It is of utmost importance to recognize the condition and to initiate treatment early. The bleeding needs to be stopped, and nerve tissue has to be relieved of the increased pressure. Unfortunately, despite provision of adequate medical care, the outcome is often unfavorable. Many patients die within a few days after IH, and a considerable share of survivors continues to suffer from neurological deficits and disability.



  1. Testai FD, Aiyagari V. Acute hemorrhagic stroke pathophysiology and medical interventions: blood pressure control, management of anticoagulant-associated brain hemorrhage and general management principles. Neurol Clin. 2008; 26(4):963-985, viii-ix.
  2. Nagel K, Pai MK, Paes BA, Chan AK. Diagnosis and treatment of intracranial hemorrhage in children with hemophilia. Blood Coagul Fibrinolysis. 2013; 24(1):23-27.
  3. Herzig R, Urbanek K, Vlachova I, et al. The role of chronic alcohol intake in patients with spontaneous intracranial hemorrhage: a carbohydrate-deficient transferrin study. Cerebrovasc Dis. 2003; 15(1-2):22-28.
  4. Caceres JA, Goldstein JN. Intracranial hemorrhage. Emerg Med Clin North Am. 2012; 30(3):771-794.
  5. Kaiser M, Penk A, Franke H, et al. Lack of functional P2X7 receptor aggravates brain edema development after middle cerebral artery occlusion. Purinergic Signal. 2016.
  6. Bonsack Ft, Alleyne CH, Jr., Sukumari-Ramesh S. Augmented expression of TSPO after intracerebral hemorrhage: a role in inflammation? J Neuroinflammation. 2016; 13(1):151.
  7. Kim J, Kemp S, Kullas K, Hitos K, Dexter MA. Injury patterns in patients who "talk and die". J Clin Neurosci. 2013; 20(12):1697-1701.
  8. Oji Y, Noda K, Tokugawa J, Yamashiro K, Hattori N, Okuma Y. Spontaneous spinal subarachnoid hemorrhage after severe coughing: a case report. J Med Case Rep. 2013; 7:274.
  9. Xia Y, Ju Y, Chen J, You C. Hemorrhagic stroke and cerebral paragonimiasis. Stroke. 2014; 45(11):3420-3422.
  10. Carcel C, Sato S, Anderson CS. Blood Pressure Management in Intracranial Hemorrhage: Current Challenges and Opportunities. Curr Treat Options Cardiovasc Med. 2016; 18(4):22.

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Last updated: 2019-07-11 20:43