|Year : 2015 | Volume
| Issue : 3 | Page : 235-236
Symmetrical central tegmental tract hyperintensities on magnetic resonance imaging
Paramdeep Singh, Amarpreet Kaur, Rupinderjeet Kaur, Simmi Aggarwal, Ramandeep Singh
Department of Radiology, Paediatrics and Medicine, Guru Gobind Singh Medical College and Hospital, Baba Farid University of Health Sciences, Faridkot, Punjab, India
|Date of Web Publication||18-Sep-2015|
Department of Radiology, Guru Gobind Singh Medical College and Hospital, Baba Farid University of Health Sciences, Faridkot, Punjab
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Singh P, Kaur A, Kaur R, Aggarwal S, Singh R. Symmetrical central tegmental tract hyperintensities on magnetic resonance imaging. J Pediatr Neurosci 2015;10:235-6
The central tegmental tracts (CTT) hyperintensities seen on T2-weighted images (T2-WI) of the brain magnetic resonance imaging (MRI) is an unusual neuroimaging finding of unclear etiology. The CTT predominantly comprises the extrapyramidal tract connecting between the red nucleus and the inferior olivary nucleus. The CTT is one of the earliest regions of myelination; its myelination begins at 9 postconceptional months.  Due to early myelination, the CTT cannot be normally recognized on T2-WI or diffusion weighted image after birth. We described a 1-year-old male patient who presented with cerebral palsy (spastic diplegia) and delayed milestones. MRI revealed CTT lesions in T2-W [Figure 1] and [Figure 2], and diffusion weighted images [Figure 3] as well as the mild paucity of white matter. CTT lesion has been defined as symmetrical hyperintensities on T2-WI and/or diffusion weighted images. Yoshida et al. described CTT lesions among children between 1 and 5 years of age suffering from different underlying conditions, including epilepsy, cerebral palsy, neoplasm, and various neurodevelopmental disorders. In children, CTT hyperintensities are also seen in patients with various metabolic disorders comprising nonketotic hyperglycinemia, mitochondrial disorders, methionine adenosyl transferase deficiency, leukoencephalopathy with vanishing white matter, neonatal intrahepatic cholestasis caused by citrin deficiency, 6-pyruvoyl-tetrahydropterin synthetase deficiency and perinatal asphyxia, signifying an increased susceptibility of the CTT to external or internal injurious agents. Similar lesions have also been described in patients with congenital brain anomalies, in-utero insult, neurodegenerative disorders, metabolic disorders, neuromuscular disorders, and postnatal brain disorders. , However, the importance of the imaging findings and their clinical correlation with prognosis are still not defined. Neuropathological studies revealed that CTT lesions seen in the MRI examinations might be because of gliosis, vacuolization, neuronal loss, demyelination, and necrosis in the CTT.  On the other hand, Takanashi et al. proposed that, these lesions may be due to intramyelinic edema resulting from brain insults in utero in an asymptomatic patient with 6-pyruvoyltetrahydropterin synthetase deficiency,  whereas another study concluded these lesions were mostly transient and may represent a normal, physiological maturational phenomenon.  Even though, the pathophysiology of CTT alteration is not completely understood and needs more research, radiologists, and clinicians should be familiar with the pathologies associated with CTT hyperintensities.
|Figure 1: T2-weighted axial image shows symmetrical hyperintensities in the central tegmental tracts|
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|Figure 2: T2-weighted axial image shows symmetrical hyperintensities in the central tegmental tracts|
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|Figure 3: Diffusion weighted image showing diffusion restriction in the central tegmental tracts|
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[Figure 1], [Figure 2], [Figure 3]