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We report the case of an adult patient with neurophysiological evidence of persisting conduction block in the forearm segment of the left median nerve and absent responses from the sensory branch of the musculocutaneous nerve (MCN), which had developed during an episode of acute generalised varicella zoster virus (VZV) infection. Clinical manifestations of motor involvement in herpes zoster (HZ) are generally rare and usually due to central nervous system involvement.1 Motor peripheral nervous system manifestations do exist and have been ascribed to nerve root degeneration due to lymphocytic inflammation and vasculitis with possible spread into the spinal cord.2 Recently, conduction block has been identified for the first time as the cause of weakness in an immunocompromised patient with HZ, with evidence of extension of VZV infection along the median nerve on magnetic resonance imaging,3 but persisting conduction block has up to now not been described as a complication of acute VZV infection.
A 29 year old Caucasian electrician was seen for neurophysiological assessment with weakness of his left hand and numbness along the lateral aspect of his left forearm of 9 months’ duration. The numbness had developed 9 days into a severe primary attack of chickenpox, which required hospitalisation. The weakness remained unnoticed by the patient until detection during routine follow up. Oral aciclovir had been commenced 3 days after the onset of the acute illness. No intravenous access had been used in the patient’s left arm. The past medical history included an anecdotal first primary attack of chickenpox at the age of 4, but was otherwise unremarkable.
Findings on neurological examination were confined to the left arm. There was no muscle wasting or fasciculations and deep tendon reflexes were preserved. Muscle testing revealed weakness in the left hand corresponding to median innervated muscles: abductor pollicis brevis (APB) (4/5), opponens pollicis (4/5), and first and second lumbricals (4/5) (MRC rating scale). In addition, there was hypaesthesia for light touch and pinprick in the territory of the sensory branch of MCN.
Magnetic resonance imaging of both forearms was inconclusive with no evidence of significant signal alteration at the proposed site of the conduction block.
Motor nerve conduction studies revealed partial conduction block in the left median nerve between 9.1 and 11.1 cm above the proximal wrist crease (fig 1) with a reduced forearm velocity (34.6 m/s) and absent F-waves. The elbow mixed median nerve potential was smaller on the left than on the right (15.2 v 33.9 µV), thus confirming the presence of a partial conduction block in the forearm segment of the left median nerve. The sensory nerve action potential for the left sensory branch of MCN was absent with normal amplitudes and velocities from the right. Nerve conduction studies were normal for the right median as well as the ulnar and radial nerves bilaterally. Needle electromyography showed normal motor units with a reduced interference pattern and single fasciculation potentials in left APB and was normal in left first dorsal interosseus, flexor pollicis longus, biceps, and extensor digitorum communis.
Conduction block in acute VZV infection has, to the best of our knowledge, never been described before. Partial infarction of a mixed nerve in vasculitic mononeuritis multiplex can cause conduction block by selectively damaging Schwann cells, although axonotmesis with axonal damage and sensory-motor symptoms in the affected nerve would be more typical and should have been apparent during neurophysiological testing. Both the median nerve and the sensory branch of MCN share fibre supply from cervical nerve roots which later form the lateral cord, and they are often in close anatomical proximity in the arm due to frequent anatomical variations. The simultaneous involvement of the median nerve and the sensory branch of MCN might thus indicate a direct spread of the virus between the two nerves. Alternatively, indirect spread from the purely sensory branch of MCN via the spinal cord might have occurred. Autopsies of nervous tissue from HZ patients have shown VZV DNA and antigen to be present in damaged nerve fibres including motor neurons, suggestive of neuronal spread.4 Recently, conduction block in the forearm segment of the median nerve in a case of HZ has speculatively been attributed to local damage of Schwann cells of the motor nerves by direct local invasion or remote allergic mechanisms,3 although the exact pathophysiology in these cases remains to be established.
The patient was found to have fasciculation potentials but no other forms of spontaneous activity in APB, but in none of the other muscles tested. The observed fasciculation potentials most likely represent axonal hyperexcitability at the site of the conduction block in analogy to the presumed mechanism responsible for the occurrence of single and grouped fasciculation potentials in other neuropathies characterised by persistent conduction block.5
Competing interests: none declared
Written confirmation from the Local Research and Ethics Committee in Cardiff was obtained confirming that formal ethical approval was not needed for this case study.
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