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Hemorrhagic stroke

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Mehrsefat, M.D. [2]Tarek Nafee, M.D. [3]

Synonyms and keywords:

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Overview

References


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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Mehrsefat, M.D. [2]

Overview

Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis. In 1658, in his Apoplexia, Johann Jacob Wepfer (1620–1695) identified the cause of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding in their brains.[1]

Historical perspective

  • Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis.
  • Apoplexy, from the Greek word meaning “struck down with violence,” first appeared in Hippocratic writings to describe this phenomenon.[1]
  • As early as 1599, the word stroke was used as a synonym for apoplectic seizure and is a fairly literal translation of the Greek term.[2]
  • In 1658, in his Apoplexia, Johann Jacob Wepfer (1620–1695) identified the cause of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding in their brains.[1]


References

  1. ↑ 1.0 1.1 1.2 Thompson JE (1996). “The evolution of surgery for the treatment and prevention of stroke. The Willis Lecture”. Stroke. 27 (8): 1427–34. PMID 8711815.
  2. ↑ R. Barnhart, ed. The Barnhart Concise Dictionary of Etymology (1995)


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Classification

Classification

CT scan showing an intracerebral hemorrhage.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Mehrsefat, M.D. [2]

Overview

There are two types of stroke, ischemic and hemorrhagic. Hemorrhagic strokes are less common, only 10-15% of all strokes are hemorrhagic, but they are responsible for about 40 percent of all stroke deaths.[1]

Based on location of the hemorrhage, hemorrhagic stroke may be classified into intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH)

Classification

Main articles: Intracranial hemorrhage and intracerebral hemorrhage

Based on location of the hemorrhage, hemorrhagic stroke may be classified into:

 
 
 
 
 
 
 
 
Stroke
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Ischemic stoke (85%)
 
 
 
 
 
 
 
 
 
 
 
Hemorrhagic stroke (15%)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Aneurysmal SAH (4%)
 
 
Intracerebral hemorrhage (7%)
 
 
Others (4%)

References

  1. ↑ Roger VL, Go AS, Lloyd-Jones DM, Adams RJ, Berry JD, Brown TM; et al. (2011). “Heart disease and stroke statistics–2011 update: a report from the American Heart Association”. Circulation. 123 (4): e18–e209. doi:10.1161/CIR.0b013e3182009701. PMC 4418670. PMID 21160056.


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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Mehrsefat, M.D. [2]

Overview

Pathophysiology

A hemorrhagic stroke, or cerebral hemorrhage, is a form of stroke that occurs when a blood vessel in the brain ruptures or bleeds. Like ischemic strokes, hemorrhagic strokes interrupt the brain’s blood supply because the bleeding vessel can no longer carry the blood to its target tissue. In addition, blood irritates brain tissue, disrupting the delicate chemical balance, and, if the bleeding continues, it can cause increased intracranial pressure which physically impinges on brain tissue and restricts blood flow into the brain. In this respect, hemorrhagic strokes are more dangerous than their more common counterpart, ischemic strokes. There are two types of hemorrhagic stroke: intracerebral hemorrhage, and subarachnoid hemorrhage. Amphetamine abuse quintuples, and cocaine abuse doubles, the risk of hemorrhagic strokes.

Intracerebral hemorrhage

The exact cause of brain damage following intracerebral hemorrhage is unknown. It is thought that ICH may result in brain injury by following mechanisms:[1][2]

Intraparenchymal hemorrhage

  • High blood pressure and aging blood vessels are the most common causes of intracerebral hemorrhage (intraparenchymal hemorrhage).Hyperten­sive Intracerebral hemorrhage (ICH) usually results from spontaneous rupture of a small artery deep in the brain.[3][4] Breaks in the vessel wall usually occurs following chronic hypertension. Prolonged hypertentsion usually result in intimal hyperplasia and hyalinosis, which may result in focal necrosis and cause in vessel wall breaks. Massive hemorrhage may occur when the patients have a bleeding disorder and clotting system is unable to control the bleeding.[5]
  • Intracerebral hemorrhage can also caused by an arteriovenous malformation (AVM). AVM occurs as a result of abnormal connection between arteries and veins in the brain and can result in vessels break and bleed into the brain.

Anatomical locations

The most common sites include:

The small arteries in these areas seem more sensitive to hypertension and as a result, it may progress to vascular injury.

If intracerebral hemorrhage (ICH) occurs in other brain areas or in non hypertensive patients, the other causes of intracerebral hemorrhage should be considered such as:

Intraventricular hemorrhage

Intraventricular hemorrhage (IVH) can be:[6][7]

  • Primary, confined to the ventricles
  • Secondary, originating as an extension of an ICH

Most IVH is secondary and related to hypertensive hemorrhages involving the basal ganglia and thalamus.

Microbleeds

It is a clinically silent cerebral microbleeds directly into the brain tissue. It is thought that intimal hyperplasia and hyalinosis following hypertension and amyloid disposition may result in pseudoaneurysm formation and blood vessel leakage.[8][9]

Associated conditions

Anatomical locations

The microbleeds anatomical locations are varies with their etiology:[9]

  • Hypertensive microbleeds
    • Deep subcortical and infratentorial regions
  • Amyloid microbleeds
    • Superficial lobar regions of the cerebral hemispheres

Subarachnoid hemorrhage

Subarachnoid hemorrhage

Subarachnoid hemorrhage is considered a stroke when it occurs spontaneously (not result from external forces and head trauma).

A spontaneous hemorrhage in the brain usually results from:

  • Sudden rupture of an aneurysm in an artery in the brain
    • Congenital aneurysms
    • Secondary to prolonged hypertension (occurs when an artery branches in a weakened area of artery’s wall)
  • Rupture of an abnormal connection between arteries and veins (arteriovenous malformation AVM)
  • Inflamed artery (Septic emboli) travels to an artery that supplies the brain, and causes inflammation and as a result the inflamed artery may weaken and rupture

Gross pathology

The following are images associated with gross pathology of cerebral hemorrhage:

  • Cerebral hemorrhage
    Cerebral hemorrhage
  • Intracerebral hemorrhage
    Intracerebral hemorrhage
  • Subarachnoid hemorrhage gross pathology
    Subarachnoid hemorrhage gross pathology

References

  1. ↑ Lee KR, Kawai N, Kim S, Sagher O, Hoff JT (1997). “Mechanisms of edema formation after intracerebral hemorrhage: effects of thrombin on cerebral blood flow, blood-brain barrier permeability, and cell survival in a rat model”. J Neurosurg. 86 (2): 272–8. doi:10.3171/jns.1997.86.2.0272. PMID 9010429.
  2. ↑ Mendelow AD (1993). “Mechanisms of ischemic brain damage with intracerebral hemorrhage”. Stroke. 24 (12 Suppl): I115–7, discussion I118-9. PMID 8249006.
  3. ↑ Folsom AR, Yatsuya H, Mosley TH, Psaty BM, Longstreth WT (2012). “Risk of intraparenchymal hemorrhage with magnetic resonance imaging-defined leukoaraiosis and brain infarcts”. Ann Neurol. 71 (4): 552–9. doi:10.1002/ana.22690. PMC 3377969. PMID 22522444.
  4. ↑ Delgado Almandoz JE, Schaefer PW, Goldstein JN, Rosand J, Lev MH, González RG; et al. (2010). “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. 31 (9): 1653–60. doi:10.3174/ajnr.A2156. PMC 3682824. PMID 20581068.
  5. ↑ Garcia JH, Ho KL (1992). “Pathology of hypertensive arteriopathy”. Neurosurg Clin N Am. 3 (3): 497–507. PMID 1633473.
  6. ↑ Engelhard HH, Andrews CO, Slavin KV, Charbel FT. Current manage- ment of intraventricular hemorrhage. Surg Neurol. 2003;60:15–21.
  7. ↑ Huttner HB, Hartmann M, Köhrmann M, Neher M, Stippich C, Hähnel S, Kress B. Repeated digital substraction angiography after perimesencephalic subarachnoid hemorrhage? J Neuroradiol. 2006;33:87–89.
  8. ↑ Altmann-Schneider I, Trompet S, de Craen AJ, van Es AC, Jukema JW, Stott DJ; et al. (2011). “Cerebral microbleeds are predictive of mortality in the elderly”. Stroke. 42 (3): 638–44. doi:10.1161/STROKEAHA.110.595611. PMID 21233474.
  9. ↑ 9.0 9.1 Liu W, Liu R, Sun W, Peng Q, Zhang W, Xu E; et al. (2012). “Different impacts of blood pressure variability on the progression of cerebral microbleeds and white matter lesions”. Stroke. 43 (11): 2916–22. doi:10.1161/STROKEAHA.112.658369. PMID 22949472.
  10. ↑ Poels MM, Ikram MA, van der Lugt A, Hofman A, Krestin GP, Breteler MM; et al. (2011). “Incidence of cerebral microbleeds in the general population: the Rotterdam Scan Study”. Stroke. 42 (3): 656–61. doi:10.1161/STROKEAHA.110.607184. PMID 21307170.
  11. ↑ Klarenbeek P, van Oostenbrugge RJ, Rouhl RP, Knottnerus IL, Staals J (2013). “Higher ambulatory blood pressure relates to new cerebral microbleeds: 2-year follow-up study in lacunar stroke patients”. Stroke. 44 (4): 978–83. doi:10.1161/STROKEAHA.111.676619. PMID 23449261.
  12. ↑ Goos JD, Henneman WJ, Sluimer JD, Vrenken H, Sluimer IC, Barkhof F; et al. (2010). “Incidence of cerebral microbleeds: a longitudinal study in a memory clinic population”. Neurology. 74 (24): 1954–60. doi:10.1212/WNL.0b013e3181e396ea. PMID 20548041.
  13. ↑ Jeerakathil T, Wolf PA, Beiser A, Hald JK, Au R, Kase CS; et al. (2004). “Cerebral microbleeds: prevalence and associations with cardiovascular risk factors in the Framingham Study”. Stroke. 35 (8): 1831–5. doi:10.1161/01.STR.0000131809.35202.1b. PMID 15155954.


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Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Causes

Intracerebral hemorrhage

The two major causes of intracerebral hemorrhage include:[1][2][3][4][5]

Other causes of intracerebral hemorrhage include:[1][2][3][4][5]

Subarachnoid hemorrhage

Common causes of subarachnoid hemorrhage include:

Common locations based on casualty

Cause Common Location
Hypertensive hemorrhage
Arteriovenous malformation (AVM)
Transformation of prior ischemic infarction
Aneurysm
Drug
  • Any
  • Lobar
  • Subarachnoid
Coagulopathy[6]
  • Any
  • Supratentorial
  • Intraparenchymal
Metastatic brain tumor
  • Lobar
Amyloid angiopathy
  • Lobar
Cavernous angioma
  • Intraparenchymal
Head trauma
  • Intraparenchymal
  • Frontal lobes, anterior temporal lobes, subarachnoid, extra-axial (subdural, epidural)
Capillary telangiectasias
Dural arteriovenous fistula

References

  1. ↑ 1.0 1.1 Meretoja A, Strbian D, Putaala J, Curtze S, Haapaniemi E, Mustanoja S; et al. (2012). “SMASH-U: a proposal for etiologic classification of intracerebral hemorrhage”. Stroke. 43 (10): 2592–7. doi:10.1161/STROKEAHA.112.661603. PMID 22858729.
  2. ↑ 2.0 2.1 Hart, Robert G., Bradley S. Boop, and David C. Anderson. “Oral anticoagulants and intracranial hemorrhage facts and hypotheses.” Stroke 26.8 (1995): 1471-1477.
  3. ↑ 3.0 3.1 Knudsen, Katherine A., et al. “Clinical diagnosis of cerebral amyloid angiopathy: validation of the Boston criteria.” Neurology 56.4 (2001): 537-539.
  4. ↑ 4.0 4.1 Lovelock, C. E., A. J. Molyneux, and P. M. Rothwell. “Change in incidence and aetiology of intracerebral haemorrhage in Oxfordshire, UK, between 1981 and 2006: a population-based study.” The Lancet Neurology 6.6 (2007): 487-493.
  5. ↑ 5.0 5.1 Rümke CL (1975). “Letter: Implications of the statement: No side effects were observed”. N Engl J Med. 292 (7): 372–3. PMID 1117973.
  6. ↑ Uglietta JP, O’Connor CM, Boyko OB, Aldrich H, Massey EW, Heinz ER (1991). “CT patterns of intracranial hemorrhage complicating thrombolytic therapy for acute myocardial infarction”. Radiology. 181 (2): 555–9. doi:10.1148/radiology.181.2.1924804. PMID 1924804.


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Differentiating Stroke form other Diseases

Differentiating Stroke form other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Differential diagnosis

It is clinically difficult to distinguish an ICH from an ischemic stroke. However, the symptoms like headache, nausea, vomiting, and depressed level of consciousness should raise the suspicion for a hemorrhagic event compared to ischemic stroke.[1][2]

Disease Findings
Ischemic stroke
  • Occurs when a clot or a mass clogs a blood vessel and cutting off the blood flow to the brain
  • Present as a
    • Thrombotic stroke (thrombus develops at the clogged part of the vessel)
    • Embolic strokes (blood clot that forms at another locations usually the heart and large arteries of the upper chest and neck, and travels to the brain)
  • Urgent evaluation with brain / neurovascular imaging (such as MRI, CT, CTA, MRA), cardiac, and metabolic evaluation is often necessary
transient ischemic attack (TIA)
  • Caused by a temporary clot which often called a “mini stroke”
  • Occurs rapidly and presents as a sudden onset of a focal neurologic symptom/sign lasting less than 24 hours
  • Urgent evaluation with brain / neurovascular imaging (such as MRI, CT, CTA, MRA), cardiac, and metabolic evaluation is often necessary
Acute hypertensive crisis/Malignant hypertension
  • Presents as significantly elevated blood pressure (systolic pressure ≥180 and/or diastolic pressure ≥120 mmHg) with or wihout acute end-organ injury
  • Urgent evaluation with MRI and CT of the brain, serum creatinine, urinalysis, cardiac (EKG, chest x ray, and cardiac enzymes) and metabolic evaluation is often necessary
Sentinel headache[3]
  • Caused by small aneurysmal leaks into the subarachnoid space
  • Presents as a episode of headache similar to that accompanying subarachnoid hemorrhage (days to weeks prior to aneurysm rupture) and focal neurologic symptoms and signs are usually absent
Sinusitis
  • Presents with acute and subacute headaches and facial pain
Hypoglycemia
    Pituitary apoplexy[4]
    • Caused by pituitary gland infarct or hemorrhage secondary to pitutiery adenoma
    • Presents with acute headache, change in mental status, ophthalmoplegia, and decreased visual acuity
      • Brain CT and MRI are the preferred imaging techniques
    Cerebral venous thrombosis[5][6]
    • Presents with isolated gradual onset headache or in combination with papilledema, seizures, bilateral focal deficits, and change in mental status
    • Brain MRI with venography should be considered
    Colloid cyst of the third ventricle[7]
    • Caused by an acute obstructive hydrocephalus secondary to sudden obstruction in cerebrospinal fluid flow by the cyst
    • Presents with an acute onset fronto-parietal or fronto-occipital headache which relieved by taking the supine position and may be associated with nausea, vomiting, mental status changes, seizures, coma
    • Head CT or MRI of the brain are usually diagnostic
    Cervical artery dissection[8][9]
    • It usulay occurs spontaneously or after head and neck injury
    • Presents with gradual onset head and neck pain with a local manifestations (such as Horner syndrome, pulsatile tinnitus, bruit, or cranial neuropathies)
    • Neuroimagings are usually preferred (brain MRI with MRA and cranial CT with CTA)
    Reversible cerebral vasoconstriction syndrome
    • Occurs spontaneously and trigerred by sexual activity, exertion, emotion, and constriction of the cerebral arteries
    • Presents with acute severe headache with or without focal deficits or seizures that resolves spontaneously within 12 weeks
    Spontaneous intracranial hypotension[10][11]
    • Presents with orthostatic headaches, nausea, vomiting, dizziness, diplopia, interscapular pain
    • Caused by cerebrospinal fluid (CSF) leakage from spinal meningeal defects or dural tears
    • Brain MRI is the preferred imaging techniques


    Differential Disease Symptoms Signs Laboratory findings Diagnostic modality Management
    Thunderclap headache Sentinel headache[3] Absent of focal neurologic symptoms and signs Absent of focal neurologic signs
    Pituitary apoplexy[4] Acute headache

    Change in mental status

    		Decreased visual acuity

    Ophthalmoplegia

    		Brain CT and MRI are the preferred imaging techniques
    Cerebral venous thrombosis[5][6] – Brain MRI with venography should be considered
    Colloid cyst of the third ventricle[7] – Head CT or MRI of the brain are usually diagnostic
    Cervical artery dissection[8][9] – Brain MRI with MRA and cranial CT with CTA)
    Reversible cerebral vasoconstriction syndrome –
    Spontaneous intracranial hypotension[10][11] Brain MRI is the preferred imaging techniques
    Stroke Ischemic stroke
    transient ischemic attack (TIA)
    Infection Sinusitis
    Others Hypoglycemia Headache,

    Loc

    Abnormal sensation

    Palpitations, sweating, dizziness

    		Speech difficulty

    Gait abnormality

    		Low blood glucose

    Electrolyte imbalance

    Acute hypertensive crisis/Malignant hypertension Urgent evaluation of serum creatinine, urinalysis, metabolic and cardiac evaluation (EKG, chest x ray, and cardiac enzymes) Urgent evaluation with MRI and CT of the brain
    Brain tumor[12] Headache Cachexia Sensory and motor deficit, Gait abnormality and speech difficulty


    Diseases Diagnostic tests Physical Examination Symptoms Past medical history Other Findings
    Na+, K+, Ca2+ CT /MRI CSF Findings Gold standard test Motor Deficit Sensory deficit Speech difficulty Gait abnormality Cranial nerves Headache LOC Motor weakness Abnormal sensations
    Brain tumour[12] ✔ Cancer cells[13] MRI ✔ ✔ ✔ ✔ ✔ ✔ Cachexia
    Hemorrhagic stroke ✔ Xanthochromia[14] CT scan without contrast[15][16] ✔ ✔ ✔ ✔ ✔ ✔ ✔ ✔ Hypertension Neck stiffness
    Subdural hemorrhage ✔ CT scan without contrast[15][16] ✔ ✔ ✔ ✔ ✔ ✔ ✔ ✔ Trauma/fall Confusion, dizziness, nausea, vomiting
    Neurosyphilis[17][18] ✔ ↑ Leukocytes and protein CSF VDRL-specifc

    CSF FTA-Ab -sensitive[19]

    		✔ ✔ ✔ ✔ ✔ ✔ ✔ STIs Blindness, confusion, depression,

    Abnormal gait

    Complex or atypical migraine Clinical assesment ✔ ✔ ✔ Family history of migraine Presence of aura, nausea, vomiting
    Conversion disorder Diagnosis of exclusion ✔ ✔ ✔ ✔ ✔ ✔ ✔ ✔ Tremors, blindness, difficulty swallowing
    Electrolyte disturbance ↓ or ↑ Depends on the cause Confusion, seizures
    Meningitis or encephalitis ↑ Leukocytes,

    ↑ Protein

    ↓ Glucose

    		CSF analysis[20] ✔ ✔ Fever, neck

    rigidity

    Multiple sclerosis exacerbation ✔ ↑ CSF IgG levels

    (monoclonal bands)

    		Clinical assesment and MRI [21] ✔ ✔ ✔ ✔ ✔ ✔ ✔ History of relapses and remissions Blurry vision, urinary incontinence, fatigue
    Seizure ↓ or ↑ Clinical assesment and EEG [22] ✔ ✔ ✔ ✔ Previous history of seizures Confusion, apathy, irritability,
    Hypoglycemia or hyperglycemia ↓ or ↑ Serum blood glucose

    HbA1c

    		✔ ✔ ✔ ✔ ✔ History of diabetes Palpitations, sweating, dizziness

    Hemorrhagic stroke must be differentiated from other causes of headache, seizures and loss of consciousness.

    Diseases Symptoms Physical Examination Past medical history Diagnostic tests Other Findings
    Headache ↓LOC Motor weakness Abnormal sensory Motor Deficit Sensory deficit Speech difficulty Gait abnormality Cranial nerves CT /MRI CSF Findings Gold standard test
    Meningitis + – – – – + + – – History of fever and malaise – ↑ Leukocytes,

    ↑ Protein

    ↓ Glucose

    		CSF analysis[20] Fever, neck

    rigidity

    Encephalitis + + +/- +/- – – + +/- + History of fever and malaise + ↑ Leukocytes, ↓ Glucose CSF PCR Fever, seizures, focal neurologic abnormalities
    Brain tumor[12] + – – – + + + – + Weight loss, fatigue + Cancer cells[13] MRI Cachexia, gradual progression of symptoms
    Hemorrhagic stroke + + + + + + + + – Hypertension + – CT scan without contrast[15][16] Neck stiffness
    Subdural hemorrhage + + + + + – – – + Trauma, fall + Xanthochromia[14] CT scan without contrast[15][16] Confusion, dizziness, nausea, vomiting
    Neurosyphilis[17][18] + – + + + + – + – STIs + ↑ Leukocytes and protein CSF VDRL-specifc

    CSF FTA-Ab -sensitive[19]

    		Blindness, confusion, depression,

    Abnormal gait

    Complex or atypical migraine + – + + – – + – – Family history of migraine – – Clinical assesment Presence of aura, nausea, vomiting
    Hypertensive encephalopathy + + – – – – + + – Hypertension + – Clinical assesment Delirium, cortical blindness, cerebral edema, seizure
    Wernicke’s encephalopathy – + – – – + + + + History of alcohal abuse – – Clinical assesment and lab findings Ophthalmoplegia, confusion
    CNS abscess + + – – + + + – – History of drug abuse, endocarditis, immunosupression + ↑ leukocytes, ↓ glucose and ↑ protien MRI is more sensitive and specific High grade fever, fatigue,nausea, vomiting
    Drug toxicity – + – + + + – + – – – – Drug screen test Lithium, Sedatives, phenytoin, carbamazepine
    Conversion disorder + + + + + + + + History of emotional stress – – Diagnosis of exclusion Tremors, blindness, difficulty swallowing
    Metabolic disturbances (electrolyte imbalance, hypoglycemia) – + + + + + – – + – – Hypoglycemia, hypo and hypernatremia, hypo and hyperkalemia Depends on the cause Confusion, seizure, palpitations, sweating, dizziness, hypoglycemia
    Multiple sclerosis exacerbation – – + + – + + + + History of relapses and remissions + ↑ CSF IgG levels

    (monoclonal bands)

    		Clinical assesment and MRI [21] Blurry vision, urinary incontinence, fatigue
    Seizure + + – – + + – – + Previous history of seizures – Mass lesion Clinical assesment and EEG [22] Confusion, apathy, irritability,


    References

    1. ↑ Linn FH, Rinkel GJ, Algra A, van Gijn J (1998). “Headache characteristics in subarachnoid haemorrhage and benign thunderclap headache”. J Neurol Neurosurg Psychiatry. 65 (5): 791–3. PMC 2170334. PMID 9810961.
    2. ↑ Markus HS (1991). “A prospective follow up of thunderclap headache mimicking subarachnoid haemorrhage”. J Neurol Neurosurg Psychiatry. 54 (12): 1117–8. PMC 1014694. PMID 1783930.
    3. ↑ 3.0 3.1 Polmear A (2003). “Sentinel headaches in aneurysmal subarachnoid haemorrhage: what is the true incidence? A systematic review”. Cephalalgia. 23 (10): 935–41. PMID 14984225.
    4. ↑ 4.0 4.1 Dodick DW, Wijdicks EF (1998). “Pituitary apoplexy presenting as a thunderclap headache”. Neurology. 50 (5): 1510–1. PMID 9596029.
    5. ↑ 5.0 5.1 de Bruijn SF, Stam J, Kappelle LJ (1996). “Thunderclap headache as first symptom of cerebral venous sinus thrombosis. CVST Study Group”. Lancet. 348 (9042): 1623–5. PMID 8961993.
    6. ↑ 6.0 6.1 Bousser MG, Chiras J, Bories J, Castaigne P (1985). “Cerebral venous thrombosis–a review of 38 cases”. Stroke. 16 (2): 199–213. PMID 3975957.
    7. ↑ 7.0 7.1 KELLY R (1951). “Colloid cysts of the third ventricle; analysis of twenty-nine cases”. Brain. 74 (1): 23–65. PMID 14830663.
    8. ↑ 8.0 8.1 Mitsias P, Ramadan NM (1992). “Headache in ischemic cerebrovascular disease. Part I: Clinical features”. Cephalalgia. 12 (5): 269–74. PMID 1423556.
    9. ↑ 9.0 9.1 Touzé E, Gauvrit JY, Moulin T, Meder JF, Bracard S, Mas JL; et al. (2003). “Risk of stroke and recurrent dissection after a cervical artery dissection: a multicenter study”. Neurology. 61 (10): 1347–51. PMID 14638953.
    10. ↑ 10.0 10.1 Rando TA, Fishman RA (1992). “Spontaneous intracranial hypotension: report of two cases and review of the literature”. Neurology. 42 (3 Pt 1): 481–7. PMID 1549206.
    11. ↑ 11.0 11.1 Schievink WI, Wijdicks EF, Meyer FB, Sonntag VK (2001). “Spontaneous intracranial hypotension mimicking aneurysmal subarachnoid hemorrhage”. Neurosurgery. 48 (3): 513–6, discussion 516-7. PMID 11270540.
    12. ↑ 12.0 12.1 12.2 Morgenstern LB, Frankowski RF (1999). “Brain tumor masquerading as stroke”. J Neurooncol. 44 (1): 47–52. PMID 10582668.
    13. ↑ 13.0 13.1 Weston CL, Glantz MJ, Connor JR (2011). “Detection of cancer cells in the cerebrospinal fluid: current methods and future directions”. Fluids Barriers CNS. 8 (1): 14. doi:10.1186/2045-8118-8-14. PMC 3059292. PMID 21371327.
    14. ↑ 14.0 14.1 Lee MC, Heaney LM, Jacobson RL, Klassen AC (1975). “Cerebrospinal fluid in cerebral hemorrhage and infarction”. Stroke. 6 (6): 638–41. PMID 1198628.
    15. ↑ 15.0 15.1 15.2 15.3 Birenbaum D, Bancroft LW, Felsberg GJ (2011). “Imaging in acute stroke”. West J Emerg Med. 12 (1): 67–76. PMC 3088377. PMID 21694755.
    16. ↑ 16.0 16.1 16.2 16.3 DeLaPaz RL, Wippold FJ, Cornelius RS, Amin-Hanjani S, Angtuaco EJ, Broderick DF; et al. (2011). “ACR Appropriateness Criteria® on cerebrovascular disease”. J Am Coll Radiol. 8 (8): 532–8. doi:10.1016/j.jacr.2011.05.010. PMID 21807345.
    17. ↑ 17.0 17.1 Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG; et al. (2012). “Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients”. J Neurol Sci. 317 (1–2): 35–9. doi:10.1016/j.jns.2012.03.003. PMID 22482824.
    18. ↑ 18.0 18.1 Berger JR, Dean D (2014). “Neurosyphilis”. Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
    19. ↑ 19.0 19.1 Ho EL, Marra CM (2012). “Treponemal tests for neurosyphilis–less accurate than what we thought?”. Sex Transm Dis. 39 (4): 298–9. doi:10.1097/OLQ.0b013e31824ee574. PMC 3746559. PMID 22421697.
    20. ↑ 20.0 20.1 Carbonnelle E (2009). “[Laboratory diagnosis of bacterial meningitis: usefulness of various tests for the determination of the etiological agent]”. Med Mal Infect. 39 (7–8): 581–605. doi:10.1016/j.medmal.2009.02.017. PMID 19398286.
    21. ↑ 21.0 21.1 Giang DW, Grow VM, Mooney C, Mushlin AI, Goodman AD, Mattson DH; et al. (1994). “Clinical diagnosis of multiple sclerosis. The impact of magnetic resonance imaging and ancillary testing. Rochester-Toronto Magnetic Resonance Study Group”. Arch Neurol. 51 (1): 61–6. PMID 8274111.
    22. ↑ 22.0 22.1 Manford M (2001). “Assessment and investigation of possible epileptic seizures”. J Neurol Neurosurg Psychiatry. 70 Suppl 2: II3–8. PMC 1765557. PMID 11385043.


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    Epidemiology and Demographics

    Epidemiology and Demographics

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Mehrsefat, M.D. [2]

    Overview

    In 2013, the prevalence of hemorrhagic stroke was estimated at 116.6 cases per 100,000 individuals.[1] Intracerebral hemorrhage (ICH) constitutes 10,000 to 15,000 cases per 100,000 individuals with all kind of strokes and has a higher risk of morbidity and mortality than cerebral infarction or subarachnoid hemorrhage.

    Epidemiology Intracerebral hemorrhage Subarachnoid hemorrhage
    Incidence.[2][3]
    • The overall incidence of ICH ranges from 12 to 31 per 100,000 population
    • The incidence of SAH was estimated 10.5 per 100 000 populations
    Age[4][5]
    • The incidence gets doubled every 10 years after age 35 every
    • Usually occurs at a relatively young age
    • The incidence of aneurysmal SAH increases with age
    Gender[5][6]
    • The prevalence and incidence does not vary by gender
    • Women are slightly more affected with aneurysmal SAH than men
    Race[7][8]
    • Highest in Asians, follow by Blacks, Mexican Americans , and non-Hispanic whites
    • Usually affects individuals of African Americans populations
    Case fatality rate[9][10]
    • Ranges from 37,000 to 52,000 cases per 100,000 individuals
    • Was estimated to be 32,000 cases per 100,000 individuals.

    Epidemiology and demographics

    Prevalence

    In 2013, the prevalence of hemorrhagic stroke was estimated at 116.6 cases per 100,000 individuals.[1]

    Incidence

    In 2013, the age-adjusted incidence of hemorrhagic stroke was estimated 54.3 cases per 100,000 individuals.[1]

    Intracerebral hemorrhage

    Subarachnoid hemorrhage

    Age

    Intracerebral hemorrhage

    • The incidence of intracerebral hemorrhage (ICH) increases with age, after age 35 every 10 years, the risk of having ICH is getting doubled.[4]
    • Primary lobar hemorrhages, due to cerebral amyloid angiopathy, are typically seen in elderly. Younger patients may also develop lobar hemorrhages, but in such cases they usually have an underlying lesion such as cerebral arteriovenous malformation (AVM).[11]

    Subarachnoid hemorrhage

    Gender

    Intracerebral hemorrhage

    The prevalence and incidence of intracerebral hemorrhage does not vary by gender.[6]

    Subarachnoid hemorrhage

    Race

    intracerebral hemorrhage

    • The incidence of intracerebral hemorrhage is the highest in Asians, follow by blacks, and is the lowest in whites.
    • In African Americans, the incidence of hemorrhagic stroke (intracerebral hemorrhage) is 48 cases per 100,000 persons.
    • In whites, the incidence of hemorrhagic stroke (intracerebral hemorrhage) is 48 cases per 100,000 persons. [7]
    • The incidence of Intracerebral hemorrhage is higher in Mexican Americans than non-Hispanic whites.[13]

    Subarachnoid hemorrhage

    Geographic region

    Subarachnoid hemorrhage (SAH)

    Case fatality rate

    intracerebral hemorrhage

    • The 30-day case fatality rate of intracerebral hemorrhage (ICH) ranges from 37,000 to 52,000 cases per 100,000 individuals.[9][10]
    • Death at 1 year for intracerebral hemorrhage (ICH) varies by hemorrhage location:[18]
      • Brain steam 65,000 cases per 100,000 individuals
      • Lobar ICH 57,000 cases per 100,000 individuals
      • Deep ICH 50,000 cases per 100,000 individuals
      • Cerebellar ICH 42,000 cases per 100,000 individuals

    Subarachnoid hemorrhage

    References

    1. ↑ 1.0 1.1 1.2 Global Burden of Disease Study 2013 Collaborators (2015). “Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013”. Lancet. 386 (9995): 743–800. doi:10.1016/S0140-6736(15)60692-4. PMC 4561509. PMID 26063472.
    2. ↑ 2.0 2.1 Gebel JM, Broderick JP (2000). “Intracerebral hemorrhage”. Neurol Clin. 18 (2): 419–38. PMID 10757834.
    3. ↑ 3.0 3.1 van Gijn J, Rinkel GJ (2001). “Subarachnoid haemorrhage: diagnosis, causes and management”. Brain. 124 (Pt 2): 249–78. PMID 11157554.
    4. ↑ 4.0 4.1 Stein M, Misselwitz B, Hamann GF, Scharbrodt W, Schummer DI, Oertel MF (2012). “Intracerebral hemorrhage in the very old: future demographic trends of an aging population”. Stroke. 43 (4): 1126–8. doi:10.1161/STROKEAHA.111.644716. PMID 22282880.
    5. ↑ 5.0 5.1 5.2 5.3 Rinkel GJ, Djibuti M, Algra A, van Gijn J (1998). “Prevalence and risk of rupture of intracranial aneurysms: a systematic review”. Stroke. 29 (1): 251–6. PMID 9445359.
    6. ↑ 6.0 6.1 van Asch CJ, Luitse MJ, Rinkel GJ, van der Tweel I, Algra A, Klijn CJ (2010). “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. 9 (2): 167–76. doi:10.1016/S1474-4422(09)70340-0. PMID 20056489.
    7. ↑ 7.0 7.1 Flaherty ML, Woo D, Haverbusch M, Sekar P, Khoury J, Sauerbeck L; et al. (2005). “Racial variations in location and risk of intracerebral hemorrhage”. Stroke. 36 (5): 934–7. doi:10.1161/01.STR.0000160756.72109.95. PMID 15790947.
    8. ↑ 8.0 8.1 Broderick JP, Brott T, Tomsick T, Huster G, Miller R (1992). “The risk of subarachnoid and intracerebral hemorrhages in blacks as compared with whites”. N Engl J Med. 326 (11): 733–6. doi:10.1056/NEJM199203123261103. PMID 1738378.
    9. ↑ 9.0 9.1 Dennis, Martin S., et al. “Long-term survival after first-ever stroke: the Oxfordshire Community Stroke Project.” Stroke 24.6 (1993): 796-800.
    10. ↑ 10.0 10.1 Kleindorfer D., Broderick J., Khoury J., et al: The unchanging incidence and case-fatality of stroke in the 1990s: a population-based study. Stroke 2006; 37: pp. 2473-2478
    11. ↑ Falcone GJ, Biffi A, Brouwers HB, Anderson CD, Battey TW, Ayres AM; et al. (2013). “Predictors of hematoma volume in deep and lobar supratentorial intracerebral hemorrhage”. JAMA Neurol. 70 (8): 988–94. doi:10.1001/jamaneurol.2013.98. PMC 3808840. PMID 23733000.
    12. ↑ de Rooij NK, Linn FH, van der Plas JA, Algra A, Rinkel GJ. Incidence of subarachnoid haemorrhage: a systematic review with emphasis on region, age, gender and time trends. J Neurol Neurosurg Psychiatry. 2007;78:1365–1372.
    13. ↑ Morgenstern LB, Smith MA, Lisabeth LD, Risser JM, Uchino K, Garcia N; et al. (2004). “Excess stroke in Mexican Americans compared with non-Hispanic Whites: the Brain Attack Surveillance in Corpus Christi Project”. Am J Epidemiol. 160 (4): 376–83. doi:10.1093/aje/kwh225. PMC 1524675. PMID 15286023.
    14. ↑ Shea AM, Reed SD, Curtis LH, Alexander MJ, Villani JJ, Schulman KA (2007). “Characteristics of nontraumatic subarachnoid hemorrhage in the United States in 2003”. Neurosurgery. 61 (6): 1131–7, discussion 1137-8. doi:10.1227/01.neu.0000306090.30517.ae. PMID 18162891.
    15. ↑ Ingall T, Asplund K, Mahonen M, Bonita R. A multinational com- parison of subarachnoid hemorrhage epidemiology in the WHO MONICA stroke study. Stroke. 2000;31:1054 –1061.
    16. ↑ de Rooij NK, Linn FH, van der Plas JA, Algra A, Rinkel GJ (2007). “Incidence of subarachnoid haemorrhage: a systematic review with emphasis on region, age, gender and time trends”. J Neurol Neurosurg Psychiatry. 78 (12): 1365–72. doi:10.1136/jnnp.2007.117655. PMC 2095631. PMID 17470467.
    17. ↑ Ingall T, Asplund K, Mähönen M, Bonita R (2000). “A multinational comparison of subarachnoid hemorrhage epidemiology in the WHO MONICA stroke study”. Stroke. 31 (5): 1054–61. PMID 10797165.
    18. ↑ Woo, Daniel, and Joseph P. Broderick. “Spontaneous intracerebral hemorrhage: epidemiology and clinical presentation.” Neurosurgery clinics of North America 13.3 (2002): 265-279.
    19. ↑ Feigin, Valery L., et al. “Stroke epidemiology: a review of population-based studies of incidence, prevalence, and case-fatality in the late 20th century.” The Lancet Neurology 2.1 (2003): 43-53.


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    Risk Factors

    Risk Factors

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

    Overview

    Risk Factors

    Intracerebral hemorrhage

    Common risk factors in the development of intracerebral hemorrhage (ICH) include:[1][2][3]

    New anticoagulant medications such as dabigatran, rivaroxaban, and apixaban appear to be associated with a lower risk of ICH than VKAs. [4]

    Subarachnoid hemorrhage

    Common risk factors in the development of subarachnoid hemorrhage (SAH) include:[5][6][7][8][9]

    References

    1. ↑ Huhtakangas J, Tetri S, Juvela S, Saloheimo P, Bode MK, Hillbom M. Effect of increased warfarin use on warfarin-related cerebral hemor- rhage: a longitudinal population-based study. Stroke. 2011;42:2431– 2435. doi: 10.1161/STROKEAHA.111.615260.
    2. ↑ Rådberg JA, Olsson JE, Rådberg CT. Prognostic parameters in sponta- neous intracerebral hematomas with special reference to anticoagulant treatment. Stroke. 1991;22:571–576. doi: 10.1161/01.STR.22.5.571.
    3. ↑ Flaherty ML, Kissela B, Woo D, Kleindorfer D, Alwell K, Sekar P, Moomaw CJ, Haverbusch M, Broderick JP. The increasing incidence of anticoagulant-associated intracerebral hemorrhage. Neurology. 2007;68:116–121. doi: 10.1212/01.wnl.0000250340.05202.8b.
    4. ↑ Chatterjee S, Sardar P, Biondi-Zoccai G, Kumbhani DJ. New oral anticoagulants and the risk of intracranial hemorrhage: traditional and Bayesian meta-analysis and mixed treatment comparison of random- ized trials of new oral anticoagulants in atrial fibrillation. JAMA Neurol. 2013;70:1486–1490. doi: 10.1001/jamaneurol.2013.4021
    5. ↑ van Gijn J, Rinkel GJ (2001). “Subarachnoid haemorrhage: diagnosis, causes and management”. Brain. 124 (Pt 2): 249–78. PMID 11157554.
    6. ↑ Bromberg JEC, Rinkel GJE, Algra A, Greebe P, van Duyn CM, Hasan D, et al. Subarachnoid haemorrhage in first and second degree relatives of patients with subarachnoid haemorrhage. BMJ 1995; 311: 288–9.
    7. ↑ Schievink, Wouter I., et al. “Saccular intracranial aneurysms in autosomal dominant polycystic kidney disease.” Journal of the American Society of Nephrology 3.1 (1992): 88-95.
    8. ↑ Van den Berg, J. S. P., M. Limburg, and R. C. M. Hennekam. “Is Marfan syndrome associated with symptomatic intracranial aneurysms?.” Stroke 27.1 (1996): 10-12
    9. ↑ Teunissen LL, Rinkel GJE, Algra A, van Gijn J. Risk factors for subarachnoid hemorrhage – a systematic review. Stroke 1996; 27: 544–9.


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    Natural History, Complications and Prognosis

    Natural History, Complications and Prognosis

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

    Overview

    Natural history

    In intracerebral hemorrhage (ICH), underlying small vessel disease may result in acute vessel rupture. This acute vessel rupture can progress can result in brain injury by folllowing mechanisms:

    All of these mechnisems can lead to perihematomal edema formation and secondary brain injury. Additionally, continued bleeding, or hematoma expansion, occurs in many patients—either continued bleeding from the primary source or secondary bleeding at the periphery of the hemorrhage.

    Intracerebral hemorrhage also can result in dysphagia and aspiration. These two are the major risk factors for the development of pneumonia in patients with stroke.[1] Heart failure can occur as the result of myocardial ischemia, infarction, stress-induced cardiomyopathy, or uncontrolled hypertension in the setting of acute Intracerebral hemorrhage (ICH).[2][3]

    Complications

    The frequency of medical complications after acute stroke is high, although there is substantially more information reported for ischemic stroke than intracerebral hemorrhage (ICH).

    The most common complications following intracerebral hemorrhage (ICH) include:[4][5][6]

    Approximately 50% of deaths after stroke are attributed to medical complications, usually after 7 days of hospitalization. Stroke patients who experience medical complications while in the hospital have increased mortality up to 4 years after the initial event.

    Prognosis

    Wide range of factors associated with outcome after acute hemorrhagic stroke. Identification of these factors result in the development of models to predict mortality and functional outcome. These prediction models include individual patient characteristics such as:[7][8][9][10]

    Prognostic factors

    Intracranial hemorrhage

    • Despite aggressive and newer management strategies, the prognosis of patients with intracerebral hemorrhage is very poor. However, some studies suggested that excellent medical care has a direct impact on intracerebral hemorrhage (ICH) morbidity and mortality.[11]
    • Case-fatality at 1 month is over 40 % and has not improved in last few decades.[12]

    Prognsostic factors in Intracerebral hemorrhage include:[9]

    Poor prognostic factors Associations
    Fever[13]
    • Associated with early neurologic deterioration
    Higher initial blood pressure[14]
    • Associated with early neurologic deterioration and increased mortality
    Higher creatinine[15]
    Higher serum glucose[14]
    • Associated with hematoma expansion and worse outcome
    Warfarin-related hemorrhages[16][17]
    • Associated with an increased hematoma volume, greater risk of expansion, and increased morbidity and mortality
    Warfarin therapy with an INR >3[18]
    • Associated with larger initial hemorrhage volume as well as poorer outcomes
    Intraventricular hemorrhage[19][20]
    • IVH occurs in approximately 45% of patients with spontaneous ICH and is an independent factor associated with poor outcome

    Subarachnoid hemorrhage

    The Hunt and Hess scale describes the severity of subarachnoid hemorrhage, and is used as a predictor of survival.[21]

    Grading Associations Survival
    Grade 1
    • Asymptomatic
    • Minimal headache and slight neck stiffness
    • 70% survival
    Grade 2
    • 60% survival
    Grade 3
    • Drowsy
    • Minimal neurologic deficit
    • 50% survival
    Grade 4
    • 20% survival
    Grade 5
    • 10% survival

    2015 AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage[22]

    Outcome Prediction and Withdrawal of Technological Support: Recommendation

    Class III (Harm)
    “1. Current prognostic models for individual patients early after ICH are biased by failure to account for the influence of withdrawal of support and early DNAR orders. DNAR status should not limit appropriate medical and surgical interventions unless otherwise explicitly indicated (Level of Evidence: C)”
    Class IIa
    “1. Aggressive care early after ICH onset and postponement of new DNAR orders until at least the second full day of hospitalization is probably recommended. Patients with preexisting DNAR orders are not included in this recommendation (Level of Evidence: B)”

    References

    1. ↑ Lyden PD, Shuaib A, Lees KR, Davalos A, Davis SM, Diener HC, Grotta JC, Ashwood TJ, Hardemark HG, Svensson HH, Rodichok L, Wasiewski WW, Ahlberg G; CHANT Trial Investigators. Safety and tolerability of NXY-059 for acute intracerebral hemorrhage: the CHANT Trial. Stroke. 2007;38:2262–2269. doi: 10.1161/STROKEAHA.106.472746.
    2. ↑ Gattringer T, Niederkorn K, Seyfang L, Seifert-Held T, Simmet N, Ferrari J; et al. (2014). “Myocardial infarction as a complication in acute stroke: results from the austrian stroke unit registry”. Cerebrovasc Dis. 37 (2): 147–52. doi:10.1159/000357799. PMID 24481543.
    3. ↑ Maramattom BV, Manno EM, Fulgham JR, Jaffe AS, Wijdicks EF (2006). “Clinical importance of cardiac troponin release and cardiac abnormalities in patients with supratentorial cerebral hemorrhages”. Mayo Clin Proc. 81 (2): 192–6. doi:10.4065/81.2.192. PMID 16471073.
    4. ↑ Elmer J, Hou P, Wilcox SR, Chang Y, Schreiber H, Okechukwu I; et al. (2013). “Acute respiratory distress syndrome after spontaneous intracerebral hemorrhage*”. Crit Care Med. 41 (8): 1992–2001. doi:10.1097/CCM.0b013e31828a3f4d. PMC 3752686. PMID 23760151.
    5. ↑ Oleinik A, Romero JM, Schwab K, Lev MH, Jhawar N, Delgado Almandoz JE; et al. (2009). “CT angiography for intracerebral hemorrhage does not increase risk of acute nephropathy”. Stroke. 40 (7): 2393–7. doi:10.1161/STROKEAHA.108.546127. PMC 2726774. PMID 19461032.
    6. ↑ Malhotra A (2007). “Low-tidal-volume ventilation in the acute respiratory distress syndrome”. N Engl J Med. 357 (11): 1113–20. doi:10.1056/NEJMct074213. PMC 2287190. PMID 17855672.
    7. ↑ Bernstein RA, Hemphill JC. Critical care of acute ischemic stroke. Curr Neurol Neurosci Rep. 2001;1:587–592.
    8. ↑ Rost NS, Smith EE, Chang Y, Snider RW, Chanderraj R, Schwab K, FitzMaurice E, Wendell L, Goldstein JN, Greenberg SM, Rosand J. Prediction of functional outcome in patients with primary intracerebral hemorrhage: the FUNC score. Stroke. 2008;39:2304–2309. doi: 10.1161/ STROKEAHA.107.512202
    9. ↑ 9.0 9.1 Tuhrim S, Horowitz DR, Sacher M, Godbold JH. Volume of ventricular blood is an important determinant of outcome in supratentorial intracere- bral hemorrhage. Crit Care Med. 1999;27:617–621.
    10. ↑ Broderick JP, Brott TG, Duldner JE, Tomsick T, Huster G. Volume of intracerebral hemorrhage: a powerful and easy-to-use predictor of 30-day mortality. Stroke. 1993;24:987–993.
    11. ↑ Hemphill JC, Newman J, Zhao S, Johnston SC (2004). “Hospital usage of early do-not-resuscitate orders and outcome after intracerebral hemorrhage”. Stroke. 35 (5): 1130–4. doi:10.1161/01.STR.0000125858.71051.ca. PMID 15044768.
    12. ↑ Apanasenko BG, Kunitsyn AI, Isaev GA, Khodyrev LP (1976). “[Determination of the weight of disemulsified lipid circulating in the blood as a method of diagnosis of fat embolism]”. Lab Delo (1): 41–3. PMID 0056489.
    13. ↑ Leira R, Dávalos A, Silva Y, Gil-Peralta A, Tejada J, Garcia M; et al. (2004). “Early neurologic deterioration in intracerebral hemorrhage: predictors and associated factors”. Neurology. 63 (3): 461–7. PMID 15304576.
    14. ↑ 14.0 14.1 Sawyer GJ, Fabre JW (1997). “Indirect T-cell allorecognition and the mechanisms of immunosuppression by allogeneic blood transfusions”. Transpl Int. 10 (4): 276–83. PMID 9249937.
    15. ↑ Miller CM, Vespa PM, McArthur DL, Hirt D, Etchepare M (2007). “Frameless stereotactic aspiration and thrombolysis of deep intracerebral hemorrhage is associated with reduced levels of extracellular cerebral glutamate and unchanged lactate pyruvate ratios”. Neurocrit Care. 6 (1): 22–9. doi:10.1385/NCC:6:1:22. PMID 17356187.
    16. ↑ Cucchiara B, Messe S, Sansing L, Kasner S, Lyden P, CHANT Investigators (2008). “Hematoma growth in oral anticoagulant related intracerebral hemorrhage”. Stroke. 39 (11): 2993–6. doi:10.1161/STROKEAHA.108.520668. PMID 18703803.
    17. ↑ Broderick JP, Diringer MN, Hill MD, Brun NC, Mayer SA, Steiner T; et al. (2007). “Determinants of intracerebral hemorrhage growth: an exploratory analysis”. Stroke. 38 (3): 1072–5. doi:10.1161/01.STR.0000258078.35316.30. PMID 17290026.
    18. ↑ Flaherty ML, Tao H, Haverbusch M, Sekar P, Kleindorfer D, Kissela B; et al. (2008). “Warfarin use leads to larger intracerebral hematomas”. Neurology. 71 (14): 1084–9. doi:10.1212/01.wnl.0000326895.58992.27. PMC 2668872. PMID 18824672.
    19. ↑ Bhattathiri PS, Gregson B, Prasad KS, Mendelow AD; STICH Investigators. Intraventricular hemorrhage and hydrocephalus after spon- taneous intracerebral hemorrhage: results from the STICH trial. Acta Neurochir Suppl. 2006;96:65–68.
    20. ↑ Hallevi H, Albright KC, Aronowski J, Barreto AD, Martin-Schild S, Khaja AM, Gonzales NR, Illoh K, Noser EA, Grotta JC. Intraventricular hemorrhage: anatomic relationships and clinical implications. Neurology. 2008;70:848–852. doi: 10.1212/01.wnl.0000304930.47751.75.
    21. ↑ Hunt WE, Hess RM (1968). “Surgical risk as related to time of intervention in the repair of intracranial aneurysms”. J Neurosurg. 28 (1): 14–20. doi:10.3171/jns.1968.28.1.0014. PMID 5635959.
    22. ↑ 2015 AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage http://stroke.ahajournals.org/content/early/2015/05/28/STR.0000000000000069 Accessed on November 10, 2016


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    Diagnosis

    Diagnosis

    History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | CT | MRI | Echocardiography | Ultrasound | Other Imaging Findings

    Treatment

    Treatment

    Early assessment | Medical Therapy | Surgery | Rehabilitation | Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

    AHA/ASA Guideline Recommendations For Prevention of Stroke in Women (2014)

    AHA/ASA Guideline Recommendations For Prevention of Stroke in Women (2014)

    Overview

    Risk Factors

    Sex-Specific Risk Factors

    Pregnancy and Complications | Cerebral Venous Thrombosis | Oral Contraceptives | Menopause and Postmenopausal Hormonal Therapy

    Risk Factors Commoner Among Women

    Migraine with Aura | Obesity, Metabolic Syndrome, and Lifestyle Factors | Atrial Fibrillation

    Prevention

    Case Studies

    Case Studies

    Case #1

    ar:سكتة zh-min-nan:Tiòng-hong ca:Accident vascular cerebral de:Schlaganfall da:Apopleksi el:Εγκεφαλικό επεισόδιο eo:Apopleksio ko:뇌경색 hr:Moždani udar io:Vaskulala cerebrala stroko id:Stroke is:Heilablóðfall it:Ictus he:שבץ מוחי la:Ictus (morbus) hu:Agyvérzés mk:Мозочен удар ms:Angin ahmar nl:Beroerte no:Hjerneslag sl:Možganska kap fi:Aivoverenkiertohäiriö sv:Slaganfall

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