A case of segmental zoster paresis with enhanced anterior and posterior spinal roots on MRI

Herpes zoster is an infectious disease caused by reactivation of the varicella zoster virus (VZV) in the dorsal root ganglia [2]. Neurological complications other than sensory abnormalities such as encephalitis, myelitis, and various lower motor neuron diseases such as polyradiculoneuritis as segmental radiculitis have been reported [7]. Segmental zoster paresis is characterized by focal motor weakness that appears in the same segment where the skin eruptions, neuralgia, and sensory symptoms occur, and is a relatively common complication [1, 3, 6, 7]. We report a patient in whom the radiological findings were consistent with aberration of anterior and posterior spinal roots with zoster paresis. A 73-year-old man developed right shoulder pain and herpes zoster eruptions over the C5 dermatome. Two days later, he found it impossible to lift up the right arm. He was admitted to our hospital with 2-week history of shoulder pain and progressive muscle weakness around the right shoulder. Physical examination on admission showed weakness of the upper extremity in the distribution of the right C5 myotome and sensory disturbance in the right C5 dermatome, but no clinical symptoms of myelitis. Laboratory findings showed VZV-IgM level of 4.30 mg/dl (normal \0.8 mg/dl). Examination of cerebrospinal fluid (CSF) showed 102.8 cells/mm, protein content of 66.8 mg/dl, and elevated varicella zoster virus IgG titer (antibody index [4). Polymerase chain reaction (PCR) of CSF fluid was positive for VZV DNA, but no search for the number of copies was performed. Needle electromyography showed neurogenic changes in the right deltoid and biceps brachii muscles. T1-weighted magnetic resonance imaging (MRI) showed contrast enhancement with gadolinium in the right anterior and posterior C5 spinal roots below the 4th cervical vertebra (Fig. 1b), but no abnormal contrast enhancement of the roots of the 4th and 6th spinal nerves (Fig. 1a, c). Furthermore, T2-weighted MRI showed no abnormal intensity in the cervical spinal cord. The patient was treated with intravenous 1,500 mg acyclovir for 7 days together with rehabilitation. Examination about 1 month later showed improvement of muscle weakness and disappearance of the shoulder pain. The MRI findings suggested VZV reactivation in the dorsal root ganglia, which was localized to the anterior and posterior C5 spinal roots, based on the motor and sensory symptoms of C5 dermatome and myotome. The spread of VZV from the posterior spinal root, or anterior and posterior horn, to the anterior spinal root could have resulted from inflammation. CSF analysis indicated pleocytosis and serologically confirmed VZV. Previous studies reported abnormalities of CSF in 61% of patients with VZV and subclinical extension of viral inflammation into the central nervous system [4]. The clinical symptoms and MRI findings in our patient were not confirmative for myelitis. We postulate the spread of VZV either directly or through the CSF, rather than myelitis, from the posterior spinal root to the anterior spinal root in our patient. The cause of the nerve root enhancement was considered to be due to either viral activation itself or associated inflammation. Previous MRI findings in zoster paresis showed myelitis [3], posterior root with anterior horn [9] and posterior horn [8], suggesting myelitis and anterior root [5], suggesting disruption of the blood–brain barrier. Post mortem M. Yoshioka (&) Y. Kurita M. Hashimoto M. Murakami M. Suzuki Department of Neurology, Aoto Hospital, The Jikei University School of Medicine, 6-41-2 Aoto, Katsushika-ku, Tokyo 125-8506, Japan e-mail: m.yoshioka@jikei.ac.jp