What herniation syndromes are caused by subdural hematoma (SDH)?

Answer

In addition to increasing the ICP, the hematoma deforms and displaces the brain. Eventually, transtentorial or subfalcine herniation can develop as the brain is pushed past the dural folds of the tentorial incisura or falx, respectively.

Tonsillar herniation through the foramen magnum may develop if the whole brain stem is forced down through the tentorial incisura by elevated supratentorial pressure. Although much less common than supratentorial subdural hematoma, infratentorial subdural hematoma can develop and cause tonsillar herniation and brainstem compression.

Characteristic herniation syndromes may develop as the brain shifts. As the medial temporal lobe, or uncus, herniates past the tentorium, it can compress the ipsilateral posterior cerebral artery, oculomotor nerve, and cerebral peduncle. Clinically, the consequent oculomotor nerve palsy and cerebral peduncle compression are often manifested by an ipsilaterally dilated pupil and a contralateral hemiparesis.

The patient also may develop a stroke of the posterior cerebral artery distribution. In approximately 5% of cases, the hemiparesis may be ipsilateral to the dilated pupil. This phenomenon is called the Kernohan notch syndrome and results when uncal herniation forces the midbrain to shift so that the contralateral cerebral peduncle is forced against the contralateral tentorial incisura.

Subfalcine herniation caused by midline brain shift may result in compression of anterior cerebral artery branches against the fixed falx cerebri, leading to infarcts in an anterior cerebral artery distribution.

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Media Gallery

Acute right-sided subdural hematoma associated with significant midline shift (ie, subfalcine herniation) shown on CT scan.
Bilateral chronic subdural hematomas shown on CT scan. Midline shift is absent because of bilateral mass effect. Subdural hematoma is bilateral in 20% of patients with chronic subdural hematoma.
An acute subdural hematoma is shown in this intraoperative photograph. Note the frontotemporoparietal flap used. The hematoma is currant jelly–like in appearance.
A left-sided acute subdural hematoma (SDH). Note the high signal density of acute blood and the (mild) midline shift of the ventricles.
A left-sided chronic subdural hematoma (SDH). Note the effacement of the left lateral ventricle.
Chronic subdural hematomas (SDHs) are commonly bilateral and have areas of acute bleeding, which result in heterogeneous densities. Note the lack of midline shift due to the presence of bilateral hematomas.
An isodense subdural hematoma (SDH). Note that no sulcal markings are below the inner table of the skull on the right side. This hematoma has scattered areas of hyperdense, or acute, blood within it.
Isodense subdural hematoma (SDH) as pictured with MRI. MRI can more readily reveal smaller SDHs, and, on MRI, the imaging of the blood products change characteristically over time.
Atrophy of the brain, resulting in a space between the brain surface and the skull, increases the risk of subdural hematoma (SDH).
An acute subdural hematoma (SDH) as a complication of a craniotomy. Note the significant mass effect with midline shift.
Acute subdural hematoma. Note the bright (white) image properties of the blood on this noncontrast cranial CT scan. Note also the midline shift. Image courtesy of J. Stephen Huff, MD
Subacute subdural hematoma. The crescent-shaped clot is less white than on CT scan of acute subdural hematoma. In spite of the large clot volume, this patient was awake and ambulatory. Image courtesy of J. Stephen Huff, MD.

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Author

Richard J Meagher, MD Attending Neurosurgeon, The Spine Institute of Southern NJ

Richard J Meagher, MD is a member of the following medical societies: American Association of Neurological Surgeons, North American Spine Society, Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

Coauthor(s)

William F Young, MD Attending Neurosurgeon, Fort Wayne Neurological Center

William F Young, MD is a member of the following medical societies: Congress of Neurological Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2; Physician Advisory Board for Coherex Medical; National Leader and Steering Committee Clinical Trial, Bristol Myers Squibb; Abbott Laboratories, advisory group.

Acknowledgements

Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association

Disclosure: Nothing to disclose.

Norman C Reynolds Jr, MD Neurologist, Veterans Affairs Medical Center of Milwaukee; Clinical Professor, Medical College of Wisconsin

Norman C Reynolds Jr, MD is a member of the following medical societies: American Academy of Neurology, Association of Military Surgeons of the US, Movement Disorders Society, Sigma Xi, and Society for Neuroscience

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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