VZV is highly contagious and can be transmitted through respiratory droplets or direct contact with infected skin lesions [9–11]. VZV is neurotropic and which can be lurking in the neurons of the posterior root ganglia of the spinal cord for a long time after infection. When the infected people have lower resistance, tired, or re-infection, the virus can grow and reproduce and move along the nerve fibers to the skin . When VZV causes to a rash, or alongside the nerve into the central nervous system and led to a retrograde infection which can cause complications such as brainstem encephalitis, meningitis, myelitis, and acute cerebrovascular disease. The elderly (greater than 65 years old) or immune dysfunction persons are common in VZV secondary infections [5, 12]. Among the patients in this group, three were elderly patients, three patients with diabetes, and one patient had long-term oral hormones, which basically met the above-mentioned pathogenesis. Nerve VZV can be invaded into the skull through the nerve and can be invaded by meninges and brain parenchyma [13, 14]. Two patients in this group were treated with disturbance of consciousness, two were positive for meningeal irritation, and six patients with MRI showed central nervous system injury, suggesting that both brain parenchyma and meninges were affected. Most patients often have a typical herpes-like rash several days before the onset of the disease. In this group, seven patients had rashes at different locations before the disease, mainly in the cranial nerve distribution area, and the time from herpes to central nervous system damage occurred 3-20d range, basically in line with the body's regular elimination of the virus's immune cycle, suggesting that secondary infection caused by the activation of VZV, early to give adequate, full course of antiviral therapy is necessary. The study found that patients with cranial herpes zoster were more likely to have central nervous system damage. The seven patients in this group were basically consistent with the report. VZV invasion of the cranial nerve can lead to different neurological syndromes, such as RHS syndrome. Typical RHS involved unilateral peripheral facial nerve palsy accompanied by erythematous vesicular lesions on the ear. Frequently the VIII cranial nerve can be also involved, and rarely the V, VI, IX, X, XI, and XII cranial nerves can be affected and cause extraocular movement limitations, facial sensorimotor changes, bulbar dysfunction, and neck weakness [15, 16]. The typical clinical manifestations of this group of five patients with post-auricular pain, posterior herpes zoster, and ipsilateral nerve paralysis meet the diagnostic criteria of RHS, suggesting VZV Transeural nerves and vestibular nerves are the most likely to cause brainstem encephalitis and are considered to be associated with specific anatomical structures of the geniculate ganglia.
Cranial nerve 3D-CISS imaging or enhancement can clearly show the cranial nerve shape and injury, which can significance clearly show the VZV-induced cranial nerve injury segment and location [16, 17]. Patient 2 has RHS as the first symptom. 3D-CISS imaging shows swelling of the left vestibular nerve and facial nerve, thickening; enhancement of the inferior facial nerve and vestibular nerve enhancement in the internal auditory canal, support for the facial nerve and vestibular nerve and the inner auditory canal VZV violation. Transverse hyperintensities in central pons on T2 and FLAIR substantially showed the signal changes in the left vestibular nucleus and along the vestibulocochlear nerve, so patient 2 can also be diagnosed with VZV brainstem encephalitis according to CSF evidence of VZV and pontobulbar involvement on brain MRI. The possible pathogenesis of the patient brainstem encephalitis is that after VZV, which is latent in geniculate ganglia, is activated, retrograde invasion of geniculate ganglia-into the cranial-invading facial nerve, vestibular cochlear nerve - ascending to the facial nucleus, vestibular nuclei, anterior and posterior Nuclear group. The study found that virus invading nerve cells can cause cell swelling and necrosis, which is characterized by diffusion limitation and high signal in the DWI sequence. The DWI imaging of this patient is characteristic, and DWI shows high signal changes in the left intrapontine facial nerve, facial nerve, vestibular nucleus and along the vestibulocochlear nerve, suggesting acute infection of VZV, and also clearly showing the VAS of the acute phase VAV via the vestibular and facial nerves. At the same time, the complex anatomical relationship in the region is clearly demonstrated. In addition, brainstem injuries in 6 patients showed high or slightly higher DWI signals. Patient 4 had no abnormal findings in the MRI scan, but the patient's facial sacral nose test and the knee sac test were not stable, suggesting the possibility of left bridge arm and cerebellum involvement, head MRI plain scan, possible and imaging examination. The timing is related to the selected layer thickness, and it is regrettable that the patient's family refused further magnetic resonance enhancement and thin scan examination due to economic factors. The MRI of patients with patient 3 showed paroxysmal involvement, and the multiple abnormal signals in the brainstem, bridge arm, and cerebellum. Although the patient did not undergo 3D-CISS imaging examination, the bridge arm was severely affected, and it is considered that VZV is more likely to be invaded by facial nerve or vestibular nerve. The patient did not receive any treatment for RHS, the final lesion spread, the patient died. We considering the possibility of the patient's age and the patient's own attention to the RHS syndrome is not enough. The patient 6 and the patient 7 showed an abnormal signal of the bridge arm, suggesting the possibility of viral invasion through the facial nerve or vestibular nerve. Patient 5 had a history of left-sided herpes simplex before the disease. The head MRI showed a patchy long T1 and long T2 signal on the dorsolateral side of the left medulla, Flair showed a high signal, and DWI showed a slightly high signal. The imaging height was similar to dorsolateral medullary syndrome. However, the patient lacks the key symptoms and signs of a medullary dorsolateral syndrome such as dysarthria, dysphagia, and finally, VZV brainstem encephalitis confirmed by lumbar puncture. The patient's medullary magnetic resonance findings were associated with trigeminal semilunar ganglion latent VZV retrograde cranial-induced trigeminal spinal nucleus damage and axons. Patient 1 was diagnosed with difficulty in swallowing. Gastroscope showed multiple ulcers of the esophagus (viral possibility). The head MRI showed patchy long T1 and long T2 signals on the left medulla of the left medulla, Flair showed a high signal, and DWI showed a high signal. The patient's magnetic resonance imaging was also similar to the dorsolateral medullary syndrome, but the patient also had typical features such as painless temperature-sensing disorder, ataxia, and Homer's sign. Left peripheral facial paralysis occurred during treatment. The review head MRI showed that the left side of the bridge arm had a new patchy long T1 and long T2 signal, and the Flair and DWI high signal shadows. Finally, it was confirmed by brainstem encephalitis. The VZV invasion pathway of this patient is not completely clear, and the possible pathogenesis is presumed: (1) VZV is retrograde into the skull through the lingual pharynx and vagus nerve, to the dorsolateral medulla and spread to the dorsal lateral nerve nucleus of the bridge arm. (2) VZV lurks in the trigeminal genic ganglia. After activation, the nerve junction of the facial nerve and the pharyngeal and vagus nerves invades the pharyngeal and vagus nerves. According to Hunt theory, VZV involves both the facial nerve and the vestibular nerve) achieved by the geniculate ganglion. The clinical manifestations and imaging features of the above 2 cases of VZV infection are easily misdiagnosed as a medullary dorsolateral syndrome. Thus, when clinically encountered atypical medullary dorsolateral syndrome lacking key signs such as dysphagia, ataxia, Horner's sign, especially combined when exposure the patient’s who facial herpes, be alert to the possibility of VZV brainstem encephalitis. Comprehensive analysis of the bridge arm, the dorsolateral medulla is vulnerable to VZV invasion, retrograde infection of cranial nerves are facial nerve, the vestibular nerve, and trigeminal nerve.
The cerebrospinal fluid examination is crucial for the diagnosis of this type of patients [18–20]. The cerebrospinal fluid leukocytes in 7 patients are elevated to varying degrees. The cerebrospinal fluid cytology suggests lymphocyte reaction, and the protein is increased to varying degrees, suggesting an inflammatory response. The routine, biochemical, and cytological changes of cerebrospinal fluid in this group of patients were consistent with the typical "viral encephalitis" changes. The number of cells in the rat cerebrospinal fluid increased significantly, the protein increased significantly, the sugar and chloride decreased, and the intracranial pressure was greater than 300. It suggests tuberculous meningitis, but pathogen screening suggests VZV infection. The patient has severe symptoms, multiple intracranial lesions, and eventually die. Considering the causes of cerebrospinal fluid changes similar to tuberculous meningitis in this patient are as follows: (1) The body contains a large amount of poison (VZV detection sequence number 20161), brain tissue damage is serious, blood-brain barrier damage is serious, resulting in increased cell number, protein, and intracranial pressure; low chloride in the cerebrospinal fluid may be associated with low blood chlorine; (2) Is there a possibility of tuberculosis infection, but no evidence is found for pathogen screening and a related tuberculosis screening, but the patient is also treated with anti-tuberculosis during treatment. The routine cerebrospinal fluid examination has little significance for the diagnosis of intracranial infection pathogens. NGS is a novel approach to DNA/RNA sequencing, and it can amplify and sequence the entire DNA content of a sample without using any primers or probes. NGS of CSF is a time-saving, accurate, and specific diagnostic tool for CNS viral infection. Compared with traditional clinical diagnosis, NGS can significantly shorten the diagnosis cycle and achieve an early and accurate diagnosis. Using NGS of CSF, all patients confirmed VZV infection.
At present, there is no fixed pattern for the treatment of such diseases, but early administration of a sufficient amount of antiviral therapy, depending on the degree of damage and severity of the disease, the addition of hormones and intravenous injection of human immunoglobulin is necessary [7, 21, 22]. VZV invasion is different from vascular disease, because of the protective effect of the myelin sheath, early viral infection can’t invade adjacent structures for a while, so the imaging performance is limited, but once the brain stem and brain parenchyma damage occur, the recovery period will be significantly prolonged [23, 24]. According to a case report, these patients have an excellent long-term prognosis and are qualified for daily work. Although six patients in this group had residual or mild or severe neurological deficits at discharge, except for the intracranial spread of Patient 3VZV, most of the patients had no spread of VZV infection, and the clinical prognosis was relatively good. Unfortunately, the patients were not long-term prognosis evaluated accordingly.