Irish Journal of Medical Science

, Volume 180, Issue 2, pp 603–604

Monoparesis secondary to herpes zoster


    • Department of Internal MedicineLouth County Hospital
  • M. Iqbal
    • Department of NeurologyMater Misercordiae University Hospital
  • B. O’Moore
    • Department of NeurologyMater Misercordiae University Hospital
  • J. Alam
    • Department of Internal MedicineLouth County Hospital
  • A. Suliman
    • Department of Internal MedicineLouth County Hospital
Case Report

DOI: 10.1007/s11845-009-0397-2

Cite this article as:
Bilal, S., Iqbal, M., O’Moore, B. et al. Ir J Med Sci (2011) 180: 603. doi:10.1007/s11845-009-0397-2


We describe a 90-year-old woman with right upper limb monoparesis secondary to varicella zoster virus infection as a result of extensive inflammatory involvement of the entire brachial plexus at root level. To our knowledge, this is the first report of entire brachial plexus involvement in a living patient of such advanced age. Despite a delay in presentation and thus initiation of treatment, a favourable clinical response was observed.


Herpes zosterMonoparesisEMGAcyclovirSteroids


Herpes zoster is a relatively common infectious disease. It is caused by the reactivation of the varicella zoster virus (VZV) in the dorsal root ganglia. In the presence of vesicular skin eruptions in a dermatomal distribution, it is seldom difficult to diagnose. Less well known is the fact that muscle weakness of profound degree may be part of the zoster syndrome. A delay in diagnosis may lead to a delay in the treatment. Therefore, it is important for the internists to keep a high index of suspicion for zoster paresis in the differential of acute onset paresis after VZV infection.

Case report

A 90-year-old woman with type-2 diabetes mellitus presented to our department with a 2-week history of weakness in her right shoulder, arm, forearm and hand. There was also a history of skin rash and pain in her right shoulder and arm during her stay in a different hospital where she was investigated for an episode of collapse and was discharged. This occurred 4 weeks prior to the onset of weakness. On admission to our hospital, she had scars and pigmentation over the C4–C6 dermatomes post-herpetic infection. She had motor weakness of (0/5) in the right deltoid, biceps, triceps and hand muscles including flexors and extensors. Deep tendon reflexes were diminished in the right biceps and brachioradialis, in keeping with a lower motor neuron lesion. She had reduced sensation and dysesthesia in dermatomes C4–C6.

The results of routine laboratory tests were normal including well-controlled plasma glucose and HBA1C of 5.20%. Magnetic resonance imaging (MRI) of the brain showed evidence of chronic ischaemic changes. A cervical and brachial plexus MRI was performed to exclude other pathologies. It showed no evidence of compression of the nerve root and localisation of brachial plexus was normal. Nerve conduction studies were normal in right median and ulnar nerves. Needle electromyography (EMG) showed evidence of partial denervation of all muscles examined in the right shoulder and right upper limb. This implied the involvement of the right brachial plexus. The findings pointed to a root involvement between level C5 and T1 on the right. There was evidence of reduced recruitment and polyphasic potentials with unstable and large units were seen in all these muscle groups.

A neurology opinion was sought regarding further management. Five weeks had already elapsed since eruption of skin rash and 3 weeks since onset of right monoparesis. Despite the delay, the patient was treated with 800 mg oral acyclovir QDS along with oral prednisolone 80 mg OD for 5 days then tapered to 60 mg OD for a total of 2 weeks and was then tapered off completely. Physiotherapy was also commenced with medical treatment. Pain was managed with amitriptyline and pregabalin. Hand grip improved after a week and in 2 weeks, there was a marked improvement in the hand and wrist power. In 4 weeks, there was improvement in elbow flexion (1/5), wrist (5/5) and hand (5/5). Right shoulder movements were still restricted (0/5). The patient was discharged to a nursing home with an outpatient ongoing physiotherapy.

On follow-up, 2 months after her discharge, further improvement was noticed in elbow flexion (4/5).


Herpes zoster is a disease not only of the sensory portion of the nervous system, but of its motor portion as well. The reason that some patients develop muscle weakness and others do not is unknown. The pathogenesis remains unclear. Viral spread from the dorsal root ganglion to anterior horn cells or anterior spinal nerve roots results in inflammatory demyelination [1].

The incidence of limb paresis with VZV activation is reported to be 3–5% [2]. Segmental zoster paresis closely parallels cutaneous zoster, predominantly striking the middle aged and the elderly. Children and young adults are rarely affected by motor complications, but if they are, involvement is peculiarly confined to cranial and truncal muscles with seemingly consistent sparing of the extremities.

Muscle involvement almost always follows rather than precedes cutaneous zoster, the time interval between the two commonly being no more than 2–3 weeks. Once begun, zoster paresis peaks within hours or days, after which no further worsening occurs in terms of either exacerbation of existing weakness or spread to other muscles [3]. Zoster-induced motor deficit varies in severity from mild to very profound. Severe pain readily obscures weakness. Appropriate abnormalities in the EMG seem to be the only reliable index of lower motor neuron involvement. It establishes the presence of a neurogenic lesion and also allows a more meaningful prognostic assessment, e.g., a muscle found to be severely denervated cannot be expected to recover for months.

Spinal fluid examination commonly yields abnormal results, but is of limited diagnostic value. Pleocytosis and mild to moderate increase in protein content are seen.

Zoster paresis has a favourable prognosis. In the extremities, complete functional recovery can be estimated to occur in 50% of cases. Only one of five patients will be left with severe and permanent residuals [4].

A higher age at onset significantly correlates with the incidence of segmental zoster paresis and the severity of electrophysiological abnormalities. However, malignant disease, immunosuppression, and diabetes mellitus did not correlate with either the frequency of complications or with the severity of electrophysiological alterations [5].

Antiviral therapy with appropriate dose and duration is associated with a reduced incidence of segmental zoster paresis and a reduced severity of electrophysiological alteration. Patients who develop motor paresis may have more extensive inflammation than that shown in usual cutaneous zoster, which is successfully suppressed by corticosteroid therapy; IV acyclovir therapy and IV corticosteroids, at least at the start should be instituted as soon as zoster paresis is suspected [6].

Early rehabilitation is of utmost importance. Pain should be controlled with medications and other measures including sympathetic and somatic nerve blocks. This will lead to effective rehabilitation.

Learning points

  • VZV reactivation can result in monoparesis of upper or lower limb.

  • Early diagnosis leads to early treatment and better clinical outcome.

  • Pain control measures and physiotherapy are important aspects of management.

Copyright information

© Royal Academy of Medicine in Ireland 2009