Classification and etiology
The vast majority of parenchymal hemorrhages are primary and associated with the rupture of small perforating arteries in elderly individuals.
- Hypertensive hemorrhages: typically located in the striatocapsular region, thalamus, pons, and cerebellum. Large basal ganglia hematomas tend to rupture into the ventricles.
- Amyloid angiopathy: presents as lobar or peripheral lesions, often multifocal.
Secondary hemorrhages develop in the setting of coagulopathies, illicit drug use (cocaine, ecstasy), vasculitis, or hemorrhagic transformation of infarctions. Hemorrhage from a ruptured aneurysm is usually subarachnoid, but may form an isolated intracerebral hematoma if the basal cisterns were walled off by a prior episode.
CT and MRI findings
In the acute phase, non-contrast CT is the imaging modality of choice, where the hematoma appears as an area of hyperdensity (increased density) with a thin hypodense rim.
- The presence of a fluid-fluid level indicates uncoagulated blood (e.g., in coagulopathies).
- After a few days, the primary hematoma gradually loses density from the periphery to the center, while vasogenic edema of the white matter increases.
On MRI, hematoma visualization depends entirely on the timing. Susceptibility-weighted sequences (T2 gradient-echo and SWI) are best for detecting microhemorrhages. On spin-echo sequences, the signal changes following the degradation of blood products:
| Grade | Age | Hemoglobin form | T1-weighted signal | T2-weighted signal |
|---|---|---|---|---|
| Hyperacute | hours | Oxyhemoglobin | Isointense | Hyperintense |
| Acute | 1–3 days | Deoxyhemoglobin | Iso/Hypo | Markedly hypo |
| Early subacute | 3–7 days | Methemoglobin (intracellular) | Markedly hyper | Markedly hypo |
| Late subacute | weeks | Methemoglobin (extracellular) | Markedly hyper | Markedly hyper |
| Chronic | months–years | Ferritin/hemosiderin | Hypointense | Markedly hypo |
Vascular malformations as a cause of hemorrhage
If hemorrhage occurs in a young patient without arterial hypertension, the presence of a vascular anomaly must be ruled out. Malformations are divided into shunting and non-shunting:
- Arteriovenous malformations (AVMs): a tangle of vessels (nidus) with direct arteriovenous shunting without capillaries. MRI shows serpiginous areas of signal void (flow void). Rupture risk is increased in the presence of intranidal aneurysms or deep venous drainage.
- Dural fistulas: acquired shunts between meningeal arteries and sinuses. Can cause reflux into cortical veins with subsequent hemorrhage.
- Cavernomas: vascular cavities without intervening normal brain parenchyma. On MRI, they resemble "popcorn" due to hemorrhages of varying ages with a dark hemosiderin rim.
- Developmental venous anomalies (DVAs): benign venous ectasias producing a "caput medusae" appearance on angiography (caput medusae).
Dural venous sinus thrombosis
Sinus thrombosis can lead to parenchymal hemorrhages, whose specific location (e.g., in the temporoparietal region) suggests involvement of the vein of Labbe or the lateral sinus.
On non-contrast CT, the thrombus is visualized as a hyperdense cord within the sinus. On CT venography, the sinus walls enhance while the thrombus in the center does not, forming the "empty delta sign" (empty delta sign). On MRI, the primary criterion is the loss of the normal flow void (flow void). To differentiate thrombosis from congenital sinus aplasia, the presence of a bony sulcus on the occipital bone is evaluated (CT).
Briefly: answers to topical questions
What factors increase the risk of arteriovenous malformation (AVM) rupture?
The risk of arteriovenous malformation rupture is increased by anatomical, angiographic, and anamnestic factors. The main predictors include:
- Deep location — location of the malformation itself within deep brain structures.
- Venous drainage patterns — drainage into deep cerebral veins, exclusive deep venous drainage, single draining vein, venous reflux, as well as stenosis and varices of the outflow vessels.
- Presence of aneurysms — extra- and intranidal aneurysms (risk directly correlates with their size).
- History — presence of prior hemorrhages.
What complications can develop in the acute period of intracerebral hemorrhage?
In the acute period of intracerebral hemorrhage, the following may develop:
- Blood breakthrough — extension of the hematoma into the ventricles or subarachnoid space.
- Perifocal vasogenic edema in the surrounding white matter.
What are the indications for surgical removal of an intracerebral hematoma?
Indications for surgical removal of an intracerebral hematoma depend on its size, resulting complications, and etiology. Surgery is indicated for:
- Relief of mass effect — when it is necessary to relieve brain compression and shift, as well as to resolve obstructive hydrocephalus.
- Reduction of intracranial pressure — in cases of severe intracranial hypertension, hematoma evacuation is supplemented by decompressive craniectomy.
- AVM treatment — simultaneous removal of the hematoma and AVM is indicated for small malformations with a compact structure and a high risk of re-rupture. Removal of the hematoma alone is performed for AVMs > 3 points on the Spetzler-Martin scale.
Which clinical scales are used to assess the severity of intracerebral hemorrhage?
The ICH Score is used to assess the severity and predict the outcome of intracerebral hemorrhage. It takes into account the level of consciousness according to the Glasgow Coma Scale, hematoma volume, presence of intraventricular hemorrhage, subtentorial location, and patient age.
The Spetzler-Martin scale is used to evaluate AVMs and select the scope of surgical intervention, rather than to assess the severity of intracerebral hemorrhage.
Class and exam questions
How to distinguish hypertensive hemorrhage from amyloid angiopathy on MRI?
In hypertension, microbleeds are located predominantly in central structures (basal ganglia, thalamus), whereas in amyloid angiopathy they are localized peripherally, in lobar regions.
What to do if a hematoma is isodense to the brain on CT?
This pattern is occasionally seen in patients with severe anemia (hematocrit below 20%). The diagnosis is confirmed by the clinical presentation and subsequent MRI, which is more sensitive to blood degradation products.
When is angiography indicated for hemorrhage?
It is mandatory in young normotensive patients or when a vascular malformation/aneurysm is suspected (including in cases of recreational drug use). In stable patients, the study is better postponed, as an acute hematoma can compress small anomalies, yielding a false-negative result.
What else to study on this topic
- Criteria for choosing between CT angiography and digital subtraction angiography (DSA)
- Differences between acute and chronic subdural hematomas
- Genetics and familial forms of cerebral cavernous malformations
- MRI sequences: spin-echo vs. SWI in neuroimaging
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