Introduction
Herpes zoster is caused by varicella-zoster virus (VZV), which colonizes the dorsal root ganglion after infection and reactivates when the patient is in immunocompromised state. The most common neurological symptom after a herpes zoster infection is neuropathic pain, which is known as postherpetic neuralgia; however, it can occasionally lead to muscle weakness or paralysis. Previous research has identified plexopathy as the most common cause of limb paresis associated with herpes zoster, with less frequent instances of radiculopathy and mononeuropathy [1]. This report details a unique case of a patient exhibiting both brachial plexopathy and cervical radiculopathy due to herpes zoster infection, thereby demonstrating a combination of preganglionic and postganglionic manifestations.
Case Report
A 62-year-old man presented to a neurosurgery outpatient clinic, reporting sudden-onset right upper limb weakness that had occurred 2 months ago. One week before the onset of weakness, he had been diagnosed with herpes zoster at a local clinic and was subsequently prescribed antiviral medication and topical ointment. His medical history included hypertension and hyperlipidemia.
A neurological examination of the patient's right upper limb, conducted using the Medical Research Council (MRC) scale, revealed muscle weakness graded as 1/5 in shoulder flexion, 2/5 in elbow flexion, and 4/5 in wrist extension. The patient reported paresthesia in his right thumb and index finger, with pin-pricking pain rated as 4 on a numerical rating scale. Initially, eschars were observed on the right lateral upper arm and lateral forearm, which were fully healed 2 months after the onset. To determine the cause of the right upper limb paresis, a comprehensive diagnostic plan was formulated, including nerve conduction study (NCS), electromyography (EMG), computed tomography (CT) of the cervical spine, and magnetic resonance imaging (MRI) of the brachial plexus.
NCS and EMG were performed 2 months following the onset of weakness. Sensory NCS showed reduced amplitudes of sensory nerve action potentials in right lateral antebrachial cutaneous and radial nerves (Table 1). Motor NCS showed reduced amplitudes of compound muscle action potentials in right radial nerve recording at the extensor indicis proprius muscle, right axillary nerve recording at the deltoid muscle, and right musculocutaneous nerve recording at the biceps brachii muscle.
Needle EMG showed abnormal spontaneous activities at rest in the right C4-T2 paraspinalis, supraspinatus, infraspinatus, teres major, deltoid, biceps, extensor digitorum communis, and flexor carpi radialis muscles (Table 2). However, the right extensor indicis proprius muscle showed normal findings. Single interference patterns were shown on maximal volition in the right biceps muscle, while no motor unit action potentials were observed in the right supraspinatus, infraspinatus, teres major, and deltoid muscles. Consequently, the electrodiagnostic findings were consistent with a diagnosis of right brachial plexopathy, predominantly affecting the upper trunk and the posterior cord, and appeared to be associated with lesions in the middle to lower cervical roots.
After performing NCS and EMG, a radiologic evaluation was executed. Cervical spine CT showed mild bulging discs at C3-4 and C5-6, but without root compression. Brachial plexus MRI showed edema and enhancement of the right C5 and C6 nerve roots, as well as edema of the upper trunk and the posterior cord of the right brachial plexus, compared to the left side (Fig. 1), corresponding to the localization of lesions indicated in NCS and EMG.
Following an electrophysiological diagnosis of right radiculoplexopathy, the patient was prescribed gabapentin and amitriptyline to relieve sensory symptoms, and he underwent rehabilitation for his right arm, which included strengthening exercises and electrical stimulation therapy targeting shoulder flexors and abductors. Four months after the onset of weakness, he revisited the outpatient clinic for evaluation. At this time, his right upper limb muscle strength exhibited a slight improvement in shoulder flexion with the MRC scale of 2/5, but the MRC scale for elbow flexion remained unchanged at 2/5. The paresthesia in the right thumb persisted. Seven months after the onset of weakness, the patient showed no significant improvement in muscle strength of the right upper limb.
Written informed consent by the patient was waived due to a retrospective nature of our study.
Discussion
Approximately 5% to 30% of patients with herpes zoster may develop motor weakness, usually within the first 2 weeks following the skin eruption [2]. Notably, motor nerve involvement may not always align with the same dermatome of the rash [3]. Li and Feng [4] have identified age, pain severity, and involvement of C6 or C7 nerve roots as potential risk factors for zoster paresis. Conversely, Tang et al. [5] have argued that age and pain severity are not significant factors, instead suggesting that upper limb involvement and comorbidities are more critical risk factors.
Zoster-induced radiculoplexopathy is rare, with only a few cases reported in the literature [1,6]. Liu et al. [1] conducted retrospective review of 1,393 patients infected with herpes zoster and identified eight cases of zoster-associated paresis. Among these, two cases categorized as radiculopathy exhibited favorable prognoses, achieving full motor recovery within 3 months without treatment, while the other two cases categorized as plexopathies and three cases categorized as radiculoplexopathies demonstrated poor prognoses, varying from partial recovery after 1 year to no motor recovery observed even after 2 years [1].
Jones et al. [6] reviewed 49 cases of zoster-induced paresis, providing a comparative analysis of preganglionic and postganglionic lesions localized by electrophysiological evaluation. The findings revealed that postganglionic lesions were associated with a greater severity of weakness than preganglionic lesions [6]. The mean minimum duration of weakness was 166.3 days in preganglionic lesions and 210.3 days in postganglionic lesions [6].
Castro et al. [7] reviewed 19 cases of zoster-induced paresis, in which six patients reported partial recovery, while other patients reported full recovery. Excluding two cases of abdomen involvement, the case reports reporting partial recovery exhibited reduced amplitude or a failure to evoke the sensory nerve action potential, implying postganglionic involvement. The longest time to evaluate partial recovery in a postganglionic lesion case was 2 years. Consequently, zoster-induced paresis tends to exhibit more severe muscle weakness and a poorer prognosis in instances involving postganglionic lesions than preganglionic lesions.
This tendency is evident not only in cases of zoster infection but also in neuropathies with other causes. Radiculopathy, which is defined as compression or irritation of nerve roots from the spine, generally has a more favorable prognosis than plexopathy. Previous studies have shown that functional outcomes in patients with radiculopathy, including chronic conditions, improve with appropriate treatment [8]. In contrast, plexopathy, which is defined as damage to brachial or lumbosacral plexuses, requires more caution. The etiology is variable, potentially including trauma, neoplasm, or radiation; therefore, its pluralistic nature requires a more detailed history, along with more complex imaging, and electrodiagnostic studies [9]. Extensive nerve involvement complicates the diagnosis, leading to delayed decision-making regarding treatment.
In this case, initial clinical presentation suggested radiculopathy; however, subsequent findings revealed additional postganglionic involvement. Although the patient exhibited a 1-grade improvement in shoulder flexion on the MRC scale 4 months post-onset, no further changes in the MRC scale were observed 7 months after onset. This outcome aligns with previous research documenting that a poor prognosis is associated with postganglionic involvement [1].
While there is a lack of studies directly comparing instances of zoster-induced radiculoplexopathy and plexopathy in isolation, it is presumed that concurrent preganglionic and postganglionic involvement suggests a poor prognosis. This assumption is based on the pathophysiology of VZV, which spreads from the dorsal root ganglion to distal nerves [10]. Further investigation is warranted to comprehensively compare concurrent and singular lesions in zoster-induced paresis, considering the limitation of a restricted number of available cases.
The current study highlights a rare case of zoster-induced radiculoplexopathy, emphasizing its long-term progression. Differentiating the lesion locations in zoster-induced neuropathy can assist clinicians in predicting patient outcomes. Therefore, we recommend that clinicians conduct NCS and EMG in patients presenting with zoster-induced paresis to better anticipate disease progression.
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