Brainstem hemorrhage

David S Liebeskind MD (

Dr. Liebeskind of the University of California, Los Angeles, received consulting fees from Cerenovus, Genentech, Medtronic, and Stryker.

Steven R Levine MD, editor. (

Dr. Levine of the SUNY Health Science Center at Brooklyn has no relevant financial relationships to disclose.

Originally released February 28, 1995; last updated December 2, 2020; expires December 2, 2023


Brainstem hemorrhage may be a devastating disorder presenting with a broad range of symptoms. Bleeding may be due to trauma, stroke, underlying vascular malformations, or a spectrum of rare disorders. CT and MRI have expanded diagnosis and our understanding of this disorder. Management considerations are highlighted in this overview of brainstem hemorrhage.

Key points


• Brainstem hemorrhage is often a devastating condition.


• Clinical manifestations may range from isolated deficits to coma.


• Hypertension is the most common risk factor.


• MRI may provide further detail and aid prognosis.


• Surgery is reserved for select cases in which specific expertise is available.

Historical note and terminology

Brainstem hemorrhage was first described by Cheyne in 1812 (Cheyne 1812) in a pathological study of patients presenting with lethargy and coma. In 1877 Bode reviewed findings of 67 patients reported in the literature (Bode 1877). Gowers noted that loss of consciousness was not an essential feature and that patients frequently presented with seizures (Gowers 1893). In 1900 Oppenheim described the clinical features of pontine hemorrhage in detail (Oppenheim 1905). The chronological history of brainstem hemorrhage has been reviewed (Thompson and Salcman 1988; Haines and Molman 1993).

Reports on brainstem hemorrhages outside the pons were rare prior to the CT scan era, perhaps because the condition was mild and often confused with brainstem infarction. Clinical and pathological description of hemorrhages in the midbrain and medulla were described after the introduction of cranial CT scanning. Even with CT, detection of small Duret hemorrhages may be limited (Marupaka and Sood 2008). CT also brought awareness of "benign variants" of brainstem hemorrhages (Shuaib 1991).

The underlying mechanism producing the hemorrhage is secondary to vascular damage, most commonly from hypertension (Dinsdale 1964). The resulting hemorrhage leads to severe destruction of the brainstem and often carries a grave prognosis (Chen et al 2019). In young individuals, hemorrhages may develop in the absence of hypertension. Such lesions are frequently secondary to vascular malformations (Mangiardi and Epstein 1988). The hematomas are often small and produce milder deficits. In many patients with such vascular lesions, surgical evacuation of the hematoma may result in early improvement (Mangiardi and Epstein 1988; Stea et al 1994). Surgical excision may prevent recurrences. Rarely, small hemorrhages may be secondary to lacunar disease (type II lacunae) (Challa and Moody 1989). The clinical picture in such patients is similar to ischemic lacunar involvement of the brainstem (Challa and Moody 1989). Brainstem hemorrhage, in order of frequency, is seen in the pons, midbrain, and medulla.

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