Bilateral subdural hematoma caused by spontaneous intracranial hypotension originating from a discogenic microspur successfully treated with duraplasty: A case report

Abstract

Introduction: Discogenic microspurs are calcified outgrowths from the intervertebral disc which can perforate the dura, causing a leak of cerebrospinal fluid (CSF). Spontaneous leaks of the CSF present a recognized cause of spontaneous intracranial hypotension (SIH). Moreover, subdural hematomas (SDH) are a potentially severe complication of SIH.

Research question: We present a case of a bilateral subdural hematoma without orthostatic headaches caused by a discogenic microspur protruding from the T1-2 intervertebral disc. The microspur is conjectured to be the culprit of the leak by ventrally perforating the dura and catalyzing the causal chain leading to the formation of the subdural hemorrhage.

Material and methods: A 79-year woman noticed a progressive gait disturbance accompanied by a decline of short-term memory over several months without experiencing orthostatic headaches. Magnetic resonance imaging (MRI) showed extensive bilateral subdural fronto-parietal hematoma, signs of CSF hypotension (dilated venous compartments), and computed tomography (CT) myelography revealed a CSF leak originating at the T1-2 level.

Results: The leakage site was treated with microsurgical duraplasty leading to a regression of the symptoms and complete resolution of the subdural hematomas within five postoperative months.

Discussion and conclusion: Discogenic microspurs can perforate the dura causing a CSF leak, leading to spontaneous intracranial hypotension, finally resulting in a bilateral subdural hematoma. This constellation of symptoms does not necessarily induce orthostatic headaches and can be treated with microsurgical duraplasty.

Keywords: Cerebrospinal fluid leak; Discogenic microspur; Duraplasty; Spontaneous intracranial hypotension; Subdural hematoma.

Fig. 1

(A) Axial MRI images of the brain displaying the course of regression of a bilateral subdural hematoma in the fronto-parietal region, leading to a compression of both cerebral hemispheres without a midline shift. (Left) Six days preoperative. (Middle) Three weeks postoperative, a slight subsidence of fluid accumulation was observed with a normalization of the ventricular system and reappearance of fronto-parietal cerebral sulci. (Right) Five months postoperative with complete regression of the large subdural hematomas. (B) Sagittal MRI images of the brain showing regression of venous compartment enlargement due to a liquor-leak syndrome. (Left) Four days preoperative. (Middle) Three weeks postoperative. (Right) Five months postoperative.

Fig. 2

(A) CT myelography of the cervicothoracic spine four days preoperative, with a coronal and axial view of a DM out of the intervertebral disc at the T1-2 level, which was assumed to be responsible for the dural leak. (B) MRI of the cervicothoracic spine. (Left) Four days preoperative. (Middle) Three weeks postoperative with fluid extravasation at the T1-2 level. (Right) Five months postoperative with complete regression of the epidural leakage.

Fig. 3

Intraoperative endoscopic view of the tear accessed through an interarcuate fenestration at the T1-2 level (left) and its coating with TachoSil(©), a fibrinogen-thrombin sealant patch (right).