basilar part of pons

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basilar part of pons

[TA]
the large bulbous portion of the pons seen on the ventral portion of the brainstem and ventral to the medial lemniscus in a cross section: contains longitudinally oriented fibers (corticospinal, corticopontine, corticoreticular, and others) and the transversely oriented pontocerebellar fibers.
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WD can be secondary to some diseases, especially stroke.[1] It has been reported that WD may occur in the 1st week after stroke (at the earliest), and that corticospinal tracts are commonly involved.[1],[2] The nerve fibers in the pons are concentrated and complex, particularly in the basis pontis. Infarction at this special location may lead to bilateral and symmetrical WD of the middle cerebellar peduncles (MCPs).[3],[4],[5] However, because bilateral lesions of the MCPs may also occur in ischemic, demyelinating, metabolic, other neurodegenerative diseases and intoxication,[6],[7] misdiagnosis in clinical practice may occur; consequently, clinicians need to become more familiar with secondary lesions.
In the case group, MRI revealed that all of the primary infarctions were located above MCPs and extended to the basis pontis, with left in 12 cases (40.0%), right in 18 (60.0%), paramedian pons in 21 (70.0%), and ventrolateral pons in nine (30.0%).
Dysarthria-clumsy hand syndrome is a well-known, but infrequent lacunar syndrome, which generally occurs due to a focal lesion in the basis pontis that damages corticofugal fibers, as well as adjacent pontine neurons or their axons (1,2).
The human basis pontis: motor syndromes and topographic organization.
The site of the lesion is usually in the basis pontis and there may be variable involvement of the pontine tegmentum, medulla and midbrain.
Brain magnetic resonance imaging (MRI), on admission [Figure 1], revealed a high signal intensity lesion involving basis pontis and medulla oblongata on both the T2-weighted image [Figure 1]b and fluid attenuation inversion recovery (FLAIR) [Figure 1]d.
We speculate the possible mechanism of VZV spreading to CNS is the reactivated viruses, which establish latency in geniculate ganglia, upward thread porus acusticus internus along with facial canal, and eventually enter intracranially and firstly invade basis pontis. Meanwhile, VZV may also spread downwards along with general somatosensory fibers to the skin of external auditory canal resulting in herpes zoster formation.
The typical location of CPM is center of dorsal basis pontis and displays a round or oval shape on axial MR sections in acute CPM or a triangular shape in chronic or subacute CPM.