Bell’s Palsy following Cervical Herpes Zoster
Year: 2025
Type: article
Abstract: Dear Editor, Herpes zoster (HZ), triggered by the reactivation of the varicella-zoster virus (VZV), can cause a number of neurological complications ranging from peripheral nerve involvement (cranial nerve involvement, radiculopathy) to central neurological involvement (meningitis, myelitis, meningoencephalitis, stroke, vasculopathy, necrotizing retinitis).[1] Bell’s palsy following non-cranial HZ, however, is unreported. A 54-year-old woman with no associated comorbidities presented with multiple groups of vesicles on an erythematous base on the right side of the neck corresponding to the C3 dermatome. There was no ear pain; or vesicles on the auricle, external auditory meatus, cheek, tongue, or palate. She was diagnosed clinically as HZ of the C3 dermatome (right) and commenced on oral valacyclovir 1000 mg thrice daily for 10 days. The rash resolved with residual pigmented scars. However, 10 days after the commencement of treatment, she noticed asymmetry of her face with restricted facial movements. Examination revealed a frozen forehead on the right side, inability to fully close her right eye with upward rolling of the eyeball (Bell’s phenomenon), obliteration of the right nasolabial fold, drooping of the right side of the mouth, and lateral shifting of the mouth to left [Figure 1]. Examination of other cranial nerves was normal. There was no other motor or sensory deficit. There was no headache, hearing impairment, nystagmus, or vertigo. The parotid glands were normal. Biochemical and hematological investigations were normal. She was diagnosed with Bell’s palsy (right) and commenced on a short, tapering course of oral prednisolone 40mg once daily for 5 days, tapered to 20mg once daily for 5 days followed by 10 mg once daily for 4 days along with the continuation of oral valacyclovir 1000mg thrice daily for seven days. After a follow-up period of one month, the skin lesions healed completely with residual pigmented scars. The motor deficit gradually recovered with physiotherapy and facial muscle exercises.Figure 1: Pigmented scars of healed herpes zoster lesions on the neck along the C3 dermatome right along with ipsilateral Bell’s palsyVaricella-zoster virus (VZV) is a neurotropic, double-stranded DNA alpha-herpesvirus. The primary infection causes varicella generally in children, following which the virus becomes latent in cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia along the entire neuraxis. Reactivation of VZV causes HZ generally in adults. The thoracic dermatomes are most commonly involved, followed by the facial dermatomes. Facial lesions usually present with involvement of the ophthalmic division of the trigeminal nerve (keratitis, Hutchinson’s sign) or with involvement of the facial nerve [weakness of all facial muscles unilaterally, along with rash in the ipsilateral external ear (zoster oticus); constituting the Ramsay Hunt syndrome, RHS]. Peripheral facial nerve palsy refers to lower motor neuron lesion of the facial nerve and can result from viral infections, trauma, parotid gland tumors, Guillain–Barré syndrome, Lyme disease, otitis media, sarcoidosis, etc. Bell’s palsy reportedly accounts for 60 to 70% of all cases of unilateral acute peripheral facial nerve palsy (APFP).[2] While reactivation of herpes simplex virus type 1 (HSV-1) is presumed to be the most common infective cause, VZV and human herpes virus 6 are also common etiological agents of Bell’s palsy. However, VZV reactivation has been reported to be responsible in 88% of patients of APFP who lacked antibodies to HSV.[3] Bell’s palsy needs to be differentiated from RHS. RHS is a late consequence of VZV infection, which causes inflammation of the geniculate ganglion of the seventh cranial nerve. It is characterized by a triad of ipsilateral facial paralysis, otalgia, and vesicles in the auricle or auditory canal but may also be present on the tongue, cheek, or scalp. Generally, otalgia precedes the auricular vesicles. Our case lacked all these features. In retrospect, zosteriform herpes simplex by HSV could be considered as a differential of cervical HZ, though the clinical distinction between them is difficult. Polymerase chain reaction is regarded as the most sensitive and reliable method for VZV or HSV detection. Viral cultures could also be employed as unlike HSV, VZV cannot be cultured from human ganglia.[4] None of these tests were performed in our case. The only motor deficit reportedly associated with cervical zoster is occasional arm weakness; also termed as zoster paresis.[5] However, HZ of the cervical dermatome, followed by Bell’s palsy, is not reported in the literature. A plausible explanation is that in herpes of the vertebral nerves C2 and C3 (also known as herpes occipitocollaris), branches of the vertebral nerves C2 and C3 communicate with cranial nerves 7 and 10, leading to dissemination of the virus to these nerves.[6] A thorough literature search failed to reveal any similar reports linking vertebral sensory ganglia with cranial motor nerve. This case is presented owing to the rarity of this association. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given her consent for her images and other clinical information to be reported in the journal. The patients understand that her name and initials will not be published. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest. Use of artificial intelligence (AI) The preparation of this manuscript was carried out entirely by the author without the use of artificial intelligence technologies.
Authors: Sanjiv Grover, Shubhang Grover
Language: English
Subfield: Neurology
Field: Medicine
Domain: Health Sciences
Open Access status: diamond
OpenAlex ID: W4411493099