Progressive midbrain clefts after head trauma and decompressive surgery: a report of two patients

Abstract

This report describes two patients with acute-onset ptosis, oculomotor dysfunction, ataxia and drowsiness, referable to the midbrain tegmentum. Both patients had previously suffered severe closed head injuries requiring craniotomy for cerebral decompression. Serial brain scans in both cases revealed a newly developing cleft in the midbrain, with features suggestive of abnormal cerebrospinal fluid (CSF) flow across the aqueduct. A trial of acetazolamide was initiated to reduce CSF production, followed by a third ventriculostomy for CSF diversion in one patient, which resulted in arrested disease progression and partial recovery. There are only two previous reports in the literature of midbrain clefts that developed as remote sequelae of head trauma. We postulate that altered CSF flow dynamics in the aqueduct, possibly related to changes in brain compliance, may be contributory. Early recognition and treatment may prevent irreversible structural injury and possible death.

Keywords: brainstem / cerebellum; cranial nerves; neurological injury; trauma CNS /PNS.

Figure 1

Progressive formation of the midbrain cleft in case 1. A brain CT scan immediately after the trauma (A, B) shows a haematoma involving the left basal ganglia and internal capsule with normal midbrain morphology and no visible midbrain contusions. The patient underwent left frontotemporal decompressive craniectomy and evacuation of the haematoma. Cranioplasty was performed after 2 months, and normal midbrain anatomy is evident during the CT scans done then (C, D). At the onset of the illness 2 years later, a CT of the brain shows a partial midbrain cleft and mild atrophy of the left cerebral peduncle. The enlarged images of this CT show the cleft extending rostrally and ventrally from the aqueduct (G–J).

Figure 2

MRI appearance of the cleft in case 1 (A–C) and case 2 (D–F). T2-DRIVE axial scans through the midbrain of case 1 show a ventral midline cleft extending anteriorly from the cerebral aqueduct of Sylvius to the interpeduncular cistern with a fragile membrane separating the two cerebral peduncles (A–C). Similarly, consecutive T1-weighted axial scans of case 2 show a midbrain cleft extending from the aqueduct of Sylvius to the interpeduncular cistern (d-f).

Figure 3

Exaggerated cerebrospinal fluid (CSF) flow through the aqueduct and the cleft in cases 1 and 2. Altered aqueductal CSF signal owing to increased flow is seen in case 1 (A) and is further exaggerated in case 2 (B, C) with a flow void seen here. Areas of gliosis in the occipital and bilateral basifrontal regions with ex vacuo ventricular dilatation are also present. A single in-plane CSF flow image of case 1 (D) and case 2 (E) shows the anteroposteriorly widened area (between the arrows) that represents the flow of CSF through the midbrain cleft. The normal aqueductal CSF flow signal (F) is shown for comparison.