Pontine hemorrhages are a common form of intracerebral hemorrhage, and usually are a result of poorly controlled long-standing hypertension, although also have other causes. When due to chronic hypertension, the stigmata of chronic hypertensive encephalopathy are often present (see cerebral microhemorrhages). It carries a very poor prognosis.
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Epidemiology
Primary pontine hemorrhage accounts for ~7.5% (range 5-10%) of hemorrhagic strokes and has an incidence of ~3 per 100,000 people 6.
Clinical presentation
Patients present with sudden and precipitous neurological deficits. Depending on the speed at which the hematoma enlarges and the exact location. The clinical presentation may include 1,2:
decreased level of consciousness (most common)
long tract signs including tetraparesis
cranial nerve palsies
seizures
Cheyne-Stokes respiration
Pathology
As is the case with penetrating arteries into the basal ganglia, the penetrating arteries from the basilar artery extending into the pons are subject to lipohyalinosis as a result of poorly-controlled hypertension 1. This renders the vessel wall prone to rupture. The larger paramedian perforators are more commonly the culprit vessels 1.
Hemorrhage into the pons can of course also be secondary to underlying lesions including:
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vascular malformations
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tumors
neuroepithelial (primary) brain tumors
central downward transtentorial herniation (Duret hemorrhages)
supratentorial surgery (remote hemorrhage) 3,4
Radiographic features
CT
CT of the brain is usually the first, and often the only, investigation obtained upon presentation. Features typical of an acute intraparenchymal hemorrhage are noted, usually located centrally within the pons (on account of the larger paramedian perforators usually being the site of bleeding).
The hematoma more frequently extends in a rostrocaudal direction along the traversing long tracts rather than laterally into the middle cerebellar peduncles. Usually the hematoma does not extend beyond the pontomedullary junction inferiorly and the inferior midbrain superiorly 1. These hematomas frequently rupture into the 4th ventricle 1.
There are many predictors of hematoma expansion potentially evident on CT, which are discussed in depth in the main intracerebral hemorrhage article.
MRI
The appearance of hemorrhage on MRI varies with time and to some degree the size of the hematoma (see aging blood on MRI). In patients who have small volume bleeds and who are thought to possibly have an underlying lesion, MRI may be of use (e.g. identification of a vascular malformation), ideally after resolution of the acute hemorrhage.
Treatment and prognosis
Overall, management does not differ for other causes of intracerebral hemorrhage - please see the article on intracerebral hemorrhage for further discussion 7. Notably, open surgical evacuation of the clot is usually not performed, although stereotactic clot aspiration has been advocated by some 5.
Pontine hemorrhages have a poor prognosis, with large bleeds being almost universally fatal. Overall mortality ranges between 30% and 90% 6, with the overall volume of the bleed and initial GCS being related to outcome 2.
Differential diagnosis
The main differential is between a primary pontine hemorrhage and hemorrhages resulting from underlying lesions (see above). Usually, patients present suddenly with severe impairment and the diagnosis is not difficult to make.
In patients where the presentation is not known (e.g. in the exam setting) it is worth considering:
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unruptured/asymptomatic vascular malformations
asymptomatic cavernous malformations (these can periodically have small bleeds resulting in repeated symptoms)
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usually little if any mass effect
serpentine irregular density isodense to intravascular blood elsewhere
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linear, no mass effect
density isodense to intravascular blood elsewhere
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