|
|
IMAGES |
|
Year : 2017 | Volume
: 4
| Issue : 3 | Page : 222-223 |
|
Imaging and differential diagnosis of tectal plate gliomas
Reddy Ravikanth
Department of Radiology, St. John's Medical College, Bengaluru, Karnataka, India
Date of Web Publication | 13-Jul-2017 |
Correspondence Address: Reddy Ravikanth St. John's Medical College, Bengaluru - 560 034, Karnataka India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/cjhr.cjhr_125_16
How to cite this article: Ravikanth R. Imaging and differential diagnosis of tectal plate gliomas. CHRISMED J Health Res 2017;4:222-3 |
Description | |  |
A 12-year-old male child was brought by his family with complaints of movement disorder since birth, increased in the past 1 month with frequent headaches and vomiting episodes. Vitals were stable and blood parameters were within normal limits. Magnetic resonance imaging (MRI) brain revealed T1 hypointense dorsal exophytic [Figure 1], T2/T2 FLAIR hyperintense lesion [Figure 2] measuring 8.5 mm × 8.5 mm, involving the tectal plate of the midbrain causing mass effect on the aqueduct and causing moderate hydrocephalus [Figure 3]. There was no enhancement of the lesion on contrast administration. He underwent ventriculoperitoneal shunt placement achieving adequate control and improvement of the symptoms and was advised follow-up. | Figure 1: Sagittal T1-weighted magnetic resonance image showing a well-defined hypointense lesion (arrow) in the tectum of the midbrain.
Click here to view |
 | Figure 2: Axial T2 FLAIR magnetic resonance image obtained in a 12-year-old male child showing a hyperintense lesion involving the tectal plate causing mass effect on the aqueduct (arrow).
Click here to view |
 | Figure 3: Sagittal contrast enhanced T1-weighted magnetic resonance image showing an exophytic mass lesion dorsally extending from the quadrigeminal plate causing moderate hydrocephalus in the ventricular system. No enhancement occurred with contrast administration.
Click here to view |
Discussion | |  |
Brainstem glioma, pilocytic astrocytoma, and medulloblastoma are the most frequent infratentorial tumors in patients under 18 years, representing 10%–30% of brain tumors in children.[1] Tectal plate gliomas represent approximately 5% of pediatric brainstem gliomas, have a favorable prognosis, and remain clinically and radiologically stable for years after cerebrospinal fluid diversion due to hydrocephalus secondary to enlargement of the tectal plate and obstruction of the cerebral aqueduct. They are usually infiltrative lesions, and only a small number (dorsal exophytic) have a favorable prognosis. They occur mostly in childhood and adolescence (77% in ages below 20 years). MRI demonstrates a focal, well-circumscribed, bulbous lesion deforming the quadrigeminal plate above the cerebral aqueduct that may have a posterior exophytic component that extends beyond the tectal plate. The histopathology is commonly benign which includes nonneoplastic hamartoma as well as low-grade astrocytomas such pilocytic and nonpilocytic astrocytomas and mixed gliomas and rarely more aggressive tumors such as anaplastic astrocytomas. Resected tectal plate lesions in order of incidence were pilocytic astrocytoma being the most common, followed by fibrillary astrocytoma (21%), oligoastrocytoma (14%), ganglioglioma (7%), and high-grade astrocytomas.[2] The most common clinical symptoms are diplopia, visual deficits, decreased school performance, nystagmus, and seizures. Association is noted with Parinaud syndrome and neurofibromatosis (NF).[3] Because of the benign nature of the lesion, generally MRI follow-up is required. When the tectum is near-normal, then the differential diagnosis is largely limited to aqueductal stenosis (no mass lesion) or a focal stenosis with the web. With larger lesions, where the mass is not definitely arising from the tectal plate, then the differential is essentially that of a pineal region mass and therefore includes pineal parenchymal tumors, germ cell tumors, pineal cysts, meningiomas, cerebral metastasis, and cavernous malformations.[4] In patients with NF1, a hamartoma should also be considered which tends to have variable T1 hyperintensity.[5] Tectal plate is a rare location for a tumor. Among tumors found in the tectal plate, the most common is the astrocytoma, but other types have been described, such as oligodendroglioma, ependymoma, ganglioglioma, medulloblastoma, primitive neuroectodermal tumors, metastasis, as well as lipoma, melanoma, dysembryoplastic neuroepithelial tumor, cavernomas, abscess, and periaqueductal gliosis. Tectal tumors may extrude from the tectum into the lumen of the cerebral aqueduct and subsequently protrude to the third ventricle, pushing away the posterior commissure and enlarging the orifice. The radiologic investigation of these tumors has been upgraded with better visualization of the tectal region on computed tomography (CT)/MRI; however, the majority of lesions continue to appear as obstructive hydrocephalus alone although calcification or a hypodense lesion on the tectal plate can be observed on CT. MRI of these tumors reveals tectal distortion or thickening caused by a localized mass, leading to aqueductal compression and hydrocephalus; characteristic T1 hypointensity and T2 hyperintensity. MRI is an accurate and noninvasive method of diagnosis that can be indicated in all cases of late-onset hydrocephalus and aqueductal obstruction, especially in adults. In endemic countries with prevalence of tuberculosis, central tuberculomas in the tectum are the result of hematogenous spread of Mycobacterium infection. Tuberculomas present as multiple lesions and show a ring enhancement pattern. Active tuberculomas may show central region of hypointensity on T2-weighted MR images with surrounding perilesional edema. On spectroscopy, tuberculomas show lipid peak along with choline peak and decrease in N-acetyl-aspartate peak.
Although intrinsic tectal lesions in children are clinically indolent, the initial management consists of CSF diversion and long-term follow-up with serial MRI. Endoscopic third ventriculostomy (ETV) has been used in patients with tectal gliomas, both as an initial procedure and after shunt failures. Conventionally, CSF diversion has been accomplished with shunt procedures. Nevertheless, because of the failure rates and complications associated with ventricular shunt placement, other methods of CSF diversion have been investigated recently. ETV provides a more physiological solution to the problem of obstructive hydrocephalus and may be performed with low morbidity and high shunt-free success rates. Furthermore, shunt placement procedures have the following known complications such as subdural hematoma, shunt dependence, infection, mechanical failure, disconnection, and migration, whereas ETV can be performed with minimal accompanying morbidity.[6] Another advantage of ETV is the possibility of performing an endoscopic biopsy procedure at the time of ventriculostomy.[7]
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | May PL, Blaser SI, Hoffman HJ, Humphreys RP, Harwood-Nash DC. Benign intrinsic tectal “tumors” in children. J Neurosurg 1991;74:867-71.  [ PUBMED] |
2. | Bowers DC, Georgiades C, Aronson LJ, Carson BS, Weingart JD, Wharam MD, et al. Tectal gliomas: Natural history of an indolent lesion in pediatric patients. Pediatr Neurosurg 2000;32:24-9. |
3. | Squires LA, Allen JC, Abbott R, Epstein FJ. Focal tectal tumors: Management and prognosis. Neurology 1994;44:953-6. |
4. | Robertson PL, Muraszko KM, Brunberg JA, Axtell RA, Dauser RC, Turrisi AT. Pediatric midbrain tumors: A benign subgroup of brainstem gliomas. Pediatr Neurosurg 1995;22:65-73. |
5. | Wang C, Zhang J, Liu A, Sun B, Zhao Y. Surgical treatment of primary midbrain gliomas. Surg Neurol 2000;53:41-51. |
6. | Blount JP, Campbell JA, Haines SJ. Complications in ventricular cerebrospinal fluid shunting. Neurosurg Clin N Am 1993;4:633-56. |
7. | Daglioglu E, Cataltepe O, Akalan N. Tectal gliomas in children: The implications for natural history and management strategy. Pediatr Neurosurg 2003;38:223-31. |
[Figure 1], [Figure 2], [Figure 3]
|