Leg paralysis due to herpes zoster: segmental paralysis or viral vasculopathy and stroke?

Abstract

Herpes zoster (HZ) is caused by a ubiquitous, exclusively human, highly neurotropic virus called varicella-zoster virus (VZV), which can affect the entire neuraxis. It usually presents with a characteristic unilateral vesicular rash and radicular pain in a dermatomal distribution. Eventhough in most of the cases only a single or two adjacent dermatomes are affected, multiple contiguous dermatomes can be involved in some patients. Somatic and autonomic neuropathy leading to a segmental zoster paresis/paralysis and autonomic motor complications has also been recognized as a part of the herpes zoster syndrome [1]. Other neurological complications such as stroke, transient ischemic attack, and myelopathy have also been described [2, 3]. On the other hand, disseminated HZ is usually defined as a generalized eruption of more than 20 extradermatomal vesicles occurring within a week of classic dermatomal herpes zoster [4]. It occurs mainly in patients with decreased VZV specific cell-mediated immune response, such as elderly individuals, patients with underlying malignancy, patients on immunosuppressive therapy, and patients with acquired immunodeficiency syndrome. Recently, we read an article published in the Internal and Emergency Medicine journal by Nicoli et al. [5] describing a case of herpetic leg paralysis, abdominal ileus, and urinary retention in a patient with idiopathic myelofibrosis. Although the case was very interesting, we have a few concerns regarding the description and discussion of this case. First, in this case report, the authors claim that a systemic widespread VZV infection involving the central nervous system and VZV encephalitic vasculopathy could precipitate the right lower limb paralysis. In adults, the typical clinical presentation of stroke caused by VZV is the occurrence of cranial nerve distribution HZ followed by acute contralateral hemiplegia weeks to months later. This patient had HZ involving the lumbosacral segments. Although the authors did not report a specific dermatomal distribution, judging by the description of the case it appeared as if the L2–L3 dermatomes were affected. Furthermore, a detailed strength examination was not performed to identify muscle weakness in the different muscle groups of the lower and upper limbs. Second, in patients with VZV vasculopathy, brain imaging reveals ischemic or hemorrhagic infarction in virtually all cases [2]. This particular patient had a negative computed tomography scan of the brain, which rules against VZV vasculopathy. Unfortunately, magnetic resonance imaging (MRI) of the brain, which could have added more information regarding the case, was not performed due to the contraindication of the presence of his pacemaker. In addition, MRI of the spinal cord would be another test to possibly assist in the differential diagnosis, as cases of myelopathy, polyradiclopathy, and polyradiculoneuropathy may be detected. Third, this case most likely does not represent systemic disseminated VZV infection, because there was no finding I. Chernev Physical Medicine and Rehabilitation, Beckley Appalachian Regional Healthcare, Beckley, WV, USA