An 80-year-old man presents with intermittent headaches and mild confusion. A CT of the head was performed (Fig. 1).
What’s the structure highlighted on this select axial CT image of the head?
a) acute intraventricular hemorrhage
b) large demyelination plaque in the corpus callosum body
c) normal third ventricle
d) cavum septum pellucidum & cavum vergae
e) large pineal region cyst
d) cavum septum pellucidum & cavum vergae
The septum pellucidum is normally a very thin (1-2 mm) structure, which extends from anterior to posterior between the two lateral ventricles. It’s bounded anteriorly by the anterior portion (genu) of the corpus callosum, superiorly by the body of the corpus callosum, posteriorly by the anterior limb and pillars of the fornix, and laterally by the leaflets of the septum pellucidum (Fig. 2).
There’s a potential space between the leaflets of the septum pellucidum, which can expand with fluid. When this occurs, it is termed a cavum septum pellucidum (CSP). This fluid filled structure has been termed “the fifth ventricle” in the past, a misnomer, as it doesn’t communicate with the cerebral ventricles and is not lined by ependymal or choroid plexus cells. A second potential space exists just posterior to the CSP within the same leaflets and when it fills with fluid it’s known as a cavum septum vergae or simply cavum vergae (CV). These two fluid spaces usually communicate with each other.
A cavum septum pellucidum is present in virtually all developing fetuses and almost 100% of premature babies. During brain development, these spaces obliterate from posterior to anterior, such that CSP is more common than CV, and typically the CV is not identified without the adjacent more anterior CSP. The cavum septum is present in about 85% of one-month-old babies, 15-20% of 6-month-olds and between 1-15% of adults (the estimated incidence varies greatly between published series but by personal experience I’d say the number is likely around 5%). Absence of a CSP in antenatal imaging is a concerning sign and often associated with serious CNS anomalies.
In adults, the vast majority of these cavum structures (CSP, CV) are entirely benign and discovered incidentally. When the walls of the cavum space are parallel (as in the case presented), the CSP & CV are typically completely asymptomatic. In our elderly patient, the CSP and CV structures were indeed thought to be unrelated to the presenting symptoms, which resolved spontaneously not long after the scan. The space may measure up to 1 cm in width in these benign cases. In a very small percentage of cases, the cavum space may enlarge and take on a moderately convex outward margination (lateral wall bowing) and lead to intermittent obstructive hydrocephalus with headaches and even occasionally loss of consciousness, not unlike the mechanism of intermittent obstruction noted with colloid cysts of the 3rd ventricle. Treatment of symptomatic cavum septi may include stereotactic cyst puncture, fenestration, ventricular shunting or even radical excision.
Acute intraventricular hemorrhage will appear hyperdense (white) on a CT head study and, the blood being heavier than CSF, will be seen layering out in the posterior horns of the lateral ventricles (as the scans are typically performed in supine position). This choice is definitely incorrect. A large demyelination plaque would be hypodense, but the body of the corpus callosum is not shown at this level so that is also incorrect. The normal third cerebral ventricle resides just below the level of the bodies of the lateral ventricles and is teardrop shaped (Fig. 3) and much smaller than the structure outlined in Fig. 1. A pineal cyst is typically seen at the level of the 3rd ventricle (thus below the image slice in Fig.1) and these can be isodense or slightly hyperdense to surrounding brain tissue, due to proteinaceous material within the cyst fluid. They may contain calcifications within the cyst wall.
|
Figure 2: Diagram of the anatomy in the
region of the septum pellucidum, from a sagittal
perspective. |
References
1. Winter TC et al. J Ultrasound Med 2012;29:427-44.
2. Born CM, et al. Eur Arch Psychiatry Clin Neurosci 2004;254:295-302.
3. Silbert PL, et al. J of Neurology, Neurosurgery and Psychiatry 1993;56:820-2.
4. Shaw CM, Alvord EC. Brain 1969;92:213-24.
5. http://upload.wikimedia.org/wikipedia/commons/4/4d/Gray732.png
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