Varicella-zoster virus (VZV) infection
General description
Varicella-zoster virus (VZV) remains latent in the trigeminal ganglia, dorsal root ganglia, and autonomic ganglia following primary varicella infection during childhood. Reactivation of the virus can occur when the host's cellular immunity declines due to aging or malignancy. Typical manifestations of VZV reactivation include meningitis, encephalitis, myelitis, vasculitis, and Ramsay-Hunt syndrome involving the facial nerve.
Ramsay-Hunt syndrome
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Facial nerve
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Vestibulocochlear nerve
In Ramsay-Hunt syndrome, a prominent neuroimaging finding is the contrast enhancement of the vestibulocochlear nerve and facial nerve.
Brainstem lesion
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BrainstemPonsPontine tegmentum
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BrainstemMedullaMedulla tegmentum
In cases of trigeminal nerve involvement by latent varicella-zoster virus reactivation, the virus can spread in an anterograde fashion from the trigeminal ganglia towards the trigeminal nerve nuclei, resulting in clinical manifestations such as pain, paralysis, and impaired pain and temperature sensation. Neuroimaging findings in such cases may include contrast enhancement and T2WI hyperintensities within the tegmentum of the pons and medulla, where the spinal trigeminal nucleus is located.
Myelitis
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Spinal cordSpinal white matterPosterior column
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Spinal cordPosterior root
In cases of varicella-zoster virus reactivation involving the spinal cord, multiple T2WI hyperintensities with associated contrast enhancement are primarily observed within the dorsal columns and horns of the spinal cord.
Vasculitis
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ArteryMiddle cerebral artery (MCA)
Several weeks after being infected with the VZV, some patients experienced hemiparesis. This condition was caused by an infarction in the middle cerebral artery (MCA) region, which resulted from vasoconstriction triggered by vasculitis.
Infarction
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CerebrumFrontal lobe
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CerebrumTemporal lobe
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CerebrumParietal lobe
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CerebrumInsula
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Putamen
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Globus pallidus