**5.2 Case 3: cerebral infarction associated with granulomatous vasculitis**

The patient was a 76-year-old man who developed infarction in the right medial hypothalamus 34 days after the onset of right ophthalmic herpes zoster. He further

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*Neurologic Complications of Varicella-Zoster Virus Infection*

showed stenosis of the left middle cerebral artery.

**6. Cranial polyneuropathy**

cranial nerves [28].

**6.1 Case 5: lower cranial polyneuropathy**

particularly with pain and even without rash.

**6.2 Case 6: lower cranial polyneuropathy**

developed an infarction in the right occipital lobe 73 days after the onset of herpes zoster infection. Although the MRI obtained while the patient presented with herpes zoster rash did not show any abnormal findings, the MRI performed 73 days

The patient was a 52-year-old woman with systemic lupus erythematosus (SLE) who exhibited altered levels of consciousness during immunotherapy for SLE. The CSF test showed pleocytosis, an elevated protein level, and positivity for VZV DNA, and the patient was then diagnosed with VZV meningoencephalitis. Brain MRI showed cerebral infarction in the left cerebral white matter, and MR angiogram

Cranial nerve palsy can sometimes develop in patients with herpes zoster of face or neck regions. Facial nerve palsy accompanying herpes zoster infection is known as Ramsay Hunt syndrome, and those patients often exhibit cranial polyneuropathy [26, 27]. Lower cranial polyneuropathy causes dysphagia, dysarthria, and hoarseness. Furthermore, there was no elevation or constriction in the unilateral soft palate, and tongue deviation and muscular weakness of the sternocleidomastoid and trapezius muscles were observed due to unilateral glossopharyngeal, vagus, accessary, and hypoglossal nerve paralyzes. Cranial polyneuropathy is often accompanied by meningitis, and CSF examination showed pleocytosis and elevated protein levels. In most cases, brain MRI shows no abnormalities. However, contrast MRI sometimes shows enhancement in the affected cranial nerves. As a mechanism of this condition, reactivation of VZV from the geniculate ganglion could result inflammatory process, circulatory disturbance, or edema to involve

A 64-year-old woman developed acute paralysis of the IX, X, XI, and XII nerves

The patient was a 66-year-old man who presented with dysphagia and hoarseness 2 days after the onset of pain in the left occipital region to the shoulder. At an otorhinolaryngology clinic, recurrent nerve paralysis was observed, and lesions of herpes zoster were noted in the left side of the neck. Left glossopharyngeal, vagal, accessory, and hypoglossal nerve paralyzes were observed during neurological examination. CSF examination showed increased cell count and positivity for VZV DNA, and the patient was diagnosed with multiple lower cranial polyneuropathy.

on the left side after experiencing pain in the left ear and throat. CSF examination revealed lymphocytic pleocytosis and elevated protein levels. VZV DNA was detected with PCR using CSF. She was diagnosed with cranial polyneuropathy due to VZV reactivation. After the oral administration of antiviral agent and steroid, all signs and symptoms dramatically improved. Notably, there was no evidence of cutaneous or mucosal rash during the entire course of the disease. VZV reactivation should be included in the differential diagnosis of multiple cranial nerve palsies,

later showed severe stenosis of the posterior communicating artery.

**5.3 Case 4: cerebral infarction associated with granulomatous vasculitis**

*DOI: http://dx.doi.org/10.5772/intechopen.83036*

**Figure 2.** *Clinical course (Case 1).* developed an infarction in the right occipital lobe 73 days after the onset of herpes zoster infection. Although the MRI obtained while the patient presented with herpes zoster rash did not show any abnormal findings, the MRI performed 73 days later showed severe stenosis of the posterior communicating artery.
