**6. Cranial polyneuropathy**

*Human Herpesvirus Infection - Biological Features, Transmission, Symptoms, Diagnosis...*

tion, reactivates and directly invades the vessels in the CNS.

and she was diagnosed with meningoencephalitis.

**5.1 Case 2: meningoencephalitis**

(average of 7 weeks) [18, 19]. Patients with cerebral infarction often present with stenosis or obstruction in the anterior cerebral artery or middle cerebral artery. Because VZV DNA and antigens are detected in the walls of cerebral arteries, this evidence should provide an anatomic pathway for transaxonal spread of VZV after reactivation from trigeminal ganglia as a mechanism of intracerebral VZV vasculopathy [20–22]. The incidence of stroke increases 6 months after the onset of herpes zoster infection [23], and VZV vaccine and antiviral drug therapy may help reduce the risk of stroke after herpes zoster infection [24]. Cerebral infarction can also develop after varicella infection in children [25]. Although it is rare, it occurs within 6 months after varicella infection, and a similar mechanism as cerebral infarction after varicella zoster infection is considered [25]. In these conditions, VZV, which causes latent infection in the trigeminal ganglion after varicella infec-

The patient was a 77-year-old woman who was admitted to our hospital due to convulsions and impaired consciousness. She presented with a Glasgow Coma Scale score of E1V1M4, and positive nuchal rigidity was observed. The convulsions were treated with the intravenous injection (IV) of diazepam and intramuscular injection of phenobarbital. However, the patient had high fever after admission at the hospital. CSF examination showed increased cell count (125.0 mg/dl), elevated protein level (125.0 mg/dl), and positivity for VZV DNA, and she was then diagnosed with VZV infection. The patient was treated with acyclovir and dexamethasone, and she regained consciousness and was able to talk on the second day of hospitalization. On the seventh day, she recovered with lucid consciousness without sequelae (**Figure 2**). Her MRI showed no abnormal lesions in the brain parenchyma,

**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

**36**

**Figure 2.**

*Clinical course (Case 1).*

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 cranial nerves [28].
