section name header

Information

Nervous System Disorders

= INTRACEREBRAL HEMATOMA

Etiology:

  1. Very common
    1. Chronic hypertension (50%)
      Age:>60 years
      Location: external capsule and basal ganglia (putamen in 65%) / thalamus (25%), pons (5%), brainstem (10%), cerebellum (5%), cerebral hemisphere (5%)
    2. Trauma
    3. Aneurysm
    4. Vascular malformation: AVM, cavernous hemangioma, venous angioma, capillary telangiectasia
  2. Common
    1. Hemorrhagic infarction = hemorrhagic transformation of stroke
    2. Amyloid angiopathy (20%): elderly patients
    3. Coagulopathy (5%): DIC, hemophilia, idiopathic thrombocytopenic purpura; aspirin, heparin, coumadin
    4. Drug abuse (5%): amphetamines, cocaine, heroine
    5. Bleeding into tumor
      1. primary: GBM, ependymoma, oligodendroglioma, pituitary adenoma
      2. metastatic: melanoma, choriocarcinoma, renal cancer, thyroid cancer, adenocarcinoma
  3. Uncommon
    1. Venous infarction
    2. Eclampsia
    3. Septic emboli
    4. Vasculitis (especially fungal)
    5. Encephalitis

Stages of Cerebral Hematomas!!navigator!!

Progression: hematoma gradually “snowballs” in size, dissects along white matter tracts; may decompress into ventricular system / subarachnoid space

Resolution: resorption from outside toward the center; rate depends on size of hematoma (usually 1–6 weeks)

FALSE-NEGATIVE CT:

  1. Impaired clotting
  2. Anemia
    • iso- / hypodense stage

Hyperacute Cerebral Hemorrhage

Time period: 4–6 hr

Substrate: fresh oxygenated arterial blood contains 95% diamagnetic (= NO unpaired electrons) intracellular oxyhemoglobin (Fe2+) with higher water contents than white matter; oxyhemoglobin persists for 6–12 hr)

NECT:

  • homogeneous consolidated high-density lesion (50–70 HU) with irregular well-defined margins increasing in density during day 1–3 (hematoma attenuation dependent on hemoglobin concentration + rate of clot retraction)
  • usually surrounded by low attenuation appearing within 24–48 hours ← edema, contusion
    1. irregular shape in trauma
    2. spherical + solitary in spontaneous hemorrhage
  • less mass effect compared with neoplasms

MR (less sensitive than CT during first hours):

  • little difference to normal brain parenchyma = center of hematoma iso- to hypointense on T1WI + minimally hyperintense on T2WI
  • peripheral rim of hypointensity (= degraded blood products as clue for presence of hemorrhage)

Acute Cerebral Hematoma

Time period: 12–48 hours

Substrate: paramagnetic (= 4 unpaired electrons) intracellular deoxyhemoglobin (Fe2+); deoxyhemoglobin persists for 3 days

MR:

  • slightly hypo- / isointense on T1WI (= paramagnetic deoxyhemoglobin in intact hypoxic RBCs within blood clot does not cause T1 shortening)
  • very hypointense on T2WI ← progressive concentration of RBCs, blood clot retraction, and fibrin production shorten T2
  • surrounding tissue isointense on T1WI / hyperintense on T2WI ← edema

Early Subacute Cerebral Hematoma

Time period: 3–7 days

Substrate: intracellular strongly paramagnetic (= 5 unpaired electrons) methemoglobin (Fe3+) inhomogeneously distributed within cells

NECT:

  • increase in size of hemorrhagic area over days / weeks
  • high-density lesion within 1st week; often with layering

MR:

  • very hyperintense on T1WI (= oxidation of deoxyhemo-globin to methemoglobin → marked shortening of T1)
    1. beginning peripherally in parenchymal hematomas
    2. beginning centrally in partially thrombosed aneurysm (oxygen tension higher in lumen)

    DDx: melanin, high-protein concentration, flow-related enhancement, gadolinium-based contrast agent
  • very hypointense on T2WI (= intracellular methemoglobin causes T2 shortening)

Late Subacute Cerebral Hematoma

Time period:>1 week

Substrate: extracellular strongly paramagnetic methemoglobin (homogeneously distributed)

NECT:

  • gradual decrease in density from periphery inward (1–2 HU per day) during 2nd + 3rd week

CECT:

  • peripheral rim enhancement at inner border of perilesional lucency (1–6 weeks after injury) in 80% ← blood-brain barrier breakdown / luxury perfusion / formation of hypervascular granulation tissue
  • ring blush may be diminished by administration of corticosteroids

MR:

  • hyperintense on T1WI (= RBC lysis allows free passage of water molecules across cell membrane)
  • hyperintense on T2WI (= compartmentalization of methemoglobin is lost ← RBC lysis)
  • surrounding edema isointense on T1WI + hyperintense on T2WI

Chronic Cerebral Hematoma

Time period:>1 months

Substrate: superparamagnetic ferritin (= soluble and stored in intracellular compartment) and hemosiderin (= insoluble and stored in lysosomes) cause marked field inhomogeneities

NECT:

  • isodense hematoma from 3rd–10th week with perilesional ring of lucency

CT:

  • hypodense phase (4–6 weeks) ← fluid uptake by osmosis
  • decreased density (3–6 months) / invisible
  • after 10 weeks lucent hematoma (= encephalomalacia ← proteolysis and phagocytosis + surrounding atrophy) with ring blush (DDx: tumor)

MR:

  • rim slightly hypointense on T1WI and very hypointense on T2WI (= superparamagnetic hemosiderin + ferritin within macrophages); rim gradually increases over weeks in thickness, eventually fills in entire hematoma = HALLMARK
  • center hyperintense on T1WI + T2WI (= extracellular methemoglobin of lysed RBCs just inside the darker hemosiderin ring); present for months to 1 year
  • surrounding hyperintensity on T2WI (= edema + serum extruded from clot) with associated mass effect; should resorb within 4–6 weeks (DDx: malignant hemorrhage)

Prognosis:

  1. Herniation (if hematoma 3–4 cm in size)
  2. Death (if hematoma >5 cm in size)

Basal Ganglia Hematoma!!navigator!!

= rupture of small distal microaneurysms in lenticulostriate arteries in patients with poorly controlled systemic arterial hypertension

MR Appearance of Intracerebral Hematoma

PhaseAgeCompartmentHemoglobinT1T2Comments
Hyperacute<24 hrintracellularoxyhemoglobiniso~hyperhyperacute bleed in <1 hr
deoxygenation
Acute1–3 dintracellulardeoxyhemoglobin~hypohypowithin clotted intact hypoxic RBCs
extracellulardeoxyhemoglobinisoisoafter lysis of RBCs
Subacuteoxidation
early>3 dintracellularmethemoglobin↑↑hyperhypowithin intact RBCs inside retracting clot
late>7 dextracellularmethemoglobin↑↑hyper↑↑hyperafter lysis of RBCs
Chronic>1 min
centerextracellularhemachromesiso~hypernon–iron-containing heme pigments
rimextracellularhemosiderin~hypo↓↓hypowithin macrophages, present for years
fibrous tissuehypohypo
edemaisohyper

Cx:

  1. Dissection into adjacent ventricles (⅔)
  2. Porencephaly
  3. Atrophy with ipsilateral ventricular dilatation

Outline