Zoster neuritis of lumbar nerves: A clinical, magnetic resonance imaging, and electrodiagnostic evaluation.

Human herpesviruses, particularly the varicella-zoster virus, are notorious for affecting the central nervous system, especially when secondarily reactivated from a latent state. We present one such case of zoster radiculitis with an ensemble of typical dermatological and neurological features diagnosed on imaging and cerebrospinal fluid (CSF) studies and encourage the consideration of viral (zoster) neuritis as a differential in patients presenting with radicular pain.

Introduction

Varicella-zoster virus, responsible for chickenpox during childhood, tends to remain latent in the sensory nerve root ganglia and cranial nerves. Upon reactivation, this virus produces a typical cutaneous rash known as shingles. The classical appearance of this rash is maculopapular upon an erythematous base, further progressing to vesiculobullous eruptions, and showing gradual resolution.[1] Along with the rash, patients also complain of dysesthesia, pain, and burning, mimicking sciatica due to discogenic causes.[2] The various modalities to confirm the diagnosis of zoster-associated neuritis include MRI imaging, electrodiagnostic tests, CSF culture, and real-time polymerase chain reaction (PCR) for viral deoxyribonucleic acid (DNA). It is essential to initiate antiviral treatment as early as possible to avoid post-herpetic neuralgia or post-zoster neuropathies, both of which have a poor recovery.[2] Hence, the knowledge of various diagnostic parameters of this condition is important in case of the absence of typical findings on any one such diagnostic modality.

Case Report

A 44-year-old male patient presented with chief complaints of right leg pain and episodic loss of sensation along the lateral aspect of the right leg for 20 days. The patient was apparently all right 20 days back when he started developing vesiculobullous rash over his right leg [Figure 1] followed by a loss of sensation, and a few episodes of fall. The patient stated that the pain was radiating in nature. On examination, the patient was noted to have a motor deficit with right thigh and leg power of 4/5. mild reduction in tone was also seen as compared to the left. The patient gave a history of degenerative disc disease and was on antihypertensive medication. No other significant history in terms of fever, recent trauma, diabetes, or immunocompromised state was elicited. A pre- and post-contrast MRI of the lumbar spine was performed. The MRI revealed a sacralized L5 vertebra with loss of lumbar lordosis. Subtle T2 hyperintensity was seen involving right L2, L3, and L4 nerve roots [Figure 2a]. There was also thickening of right L2, L3, and L4 nerve roots with accentuated asymmetric enhancement [Figure 2b and 3a]. Dominant involvement of the L3 nerve root was seen in its entirety [Figure 2c and 3b]. No significant disc bulge was seen. The spinal cord appeared normal. A diagnosis of infective neuritis was made, with supposed viral etiology, and further evaluation was recommended.

Figure 1

Multiple discrete, skin-colored, clear, fluid-filled, vesiculobullous eruptions on erythematous background ranging in size from 2 to 15 mm over the medial aspect of proximal part of the right leg

Figure 2

(a) axial T2-weighted image: right L3 nerve root (arrow) appears bulky with subtle hyperintensity as compared to its left-side counterpart; (b) axial post-contrast image at L3 nerve level: bulky right L3 nerve root (arrow) with accentuated enhancement compared to the contralateral side; (c) note the enhancing thickening along its entire course (dotted arrow)

Figure 3

(a) sagittal post-contrast T1-weighted image showing accentuated enhancement and prominence of L2, L3, and L4 nerve roots (dotted arrows); (b) coronal post-contrast T1-weighted image depicting the difference in the contrast enhancement between the right- (arrows) and left-sided (arrowheads) L2–L4 nerve roots. Note that the enhancement of L3 is seen along its entirety

Electromyography (EMG) and nerve conduction velocity (NCV) studies gave evidence of L2, L3, and L4 active motor axonal degeneration at root level. Needle EMG study showed severe and near-complete axon degeneration affecting right vastus medialis with partial affliction of right iliacus and adductor longus muscles Table 1. Sensory nerve conduction studies showed mild attenuation along the right medial leg. Lumbar puncture was performed with CSF routine demonstrating an increase in the CSF protein levels as well as mononuclear pleocytosis, consistent with infective etiology. Varicella zoster DNA was discovered on CSF real-time PCR studies. Patient was started on pulsed steroidal therapy using methylprednisolone and injection acyclovir. On follow-up after 10 days of initiation of treatment, the patient showed swift recovery on injection of acyclovir 500 mg and oral prednisolone 10 mg therapy.

Table 1

Needle electromyography findings

Name of muscle	Spontaneous activity	Voluntary activity	Interference pattern	Remarks
Left vastus medialis (Femoral nerve L2, 3)	Nil	Normal	Full	Normal
Right vastus medialis (Femoral nerve L2, 3)	Fibs* + 2	Nil	Nil	Complete denervation
Right iliacus (Femoral nerve L2, 3, 4)	Fibs + 2	Large wide polyphasic motor unit potentials	Moderately reduced	Active and chronic partial denervation
Right adductor longus (Obturator nerve L2, 3, 4)	Fibs + 2	Large wide polyphasic motor unit potentials	Mildly reduced	Active and chronic partial denervation
Right peroneus longus (Common peroneal nerve L5, S1)	Nil	Normal	Full	Normal
Right and left gastrocnemius (Tibial nerve S1)	Nil	Normal	Full	Normal

*Fibs = fibrillation potentials

Discussion

There are eight types of human herpesviruses, all of which share a common tendency to reactivate after a latent infection. Another important feature of human herpesviruses is neurotropism. The most common neurological manifestations include meningitis, encephalitis, and myelitis.[3] Varicella-zoster virus resides in the spinal dorsal root ganglion and on reactivation, travels in an antegrade manner to involve nerves and skin.[2] While most reactivations are attributed to immunocompromised states, this is not necessarily true, as in our case. Any form of stress or severe trauma may also precipitate reactivation.[4] Another unusual presentation of our case is the involvement of lumbar nerve roots whereas the literature states that the incidence of reactivation is the highest at the thoracic level (about 50%) and next at the cranio-cervical level.[5] T3–L3 are the most common dermatomes involved.[6]

Radicular pain is most commonly thought to be discogenic in origin. There is extensive literature describing cranial neuritis secondary to herpes infection. However, the involvement of peripheral lumbar nerves is not well studied. Although most studies label the MRI findings of zoster neuritis as non-specific,[7] our patient had clear evidence of nerve root thickening and enhancement secondary to changes of inflammation and vasculitis. A study carried out by Zubair et al.[8] reviewing MR imaging findings of seven patients with zoster-associated limb paresis (ZALP) found that there was an increased nerve T2 signal with nerve root enlargement, however, none of their patients showed the expected nerve root enhancement. The latter was seen in our patient and also in a case reported by Bhushan et al.,[9] wherein the patient had the involvement of L5–S1 dermatome and the MRI demonstrated enlargement, T2 hyperintensity, and enhancement of L5 dorsal root ganglion and nerve root. They also noted that so far there are only two other such cases of nerve root enhancement due to zoster involvement, making ours the fourth such case. Studies have found that high-resolution MR neurography, a relatively novel technique, can be helpful in a clearer depiction of nerve root edema and inflammation.

Herpes zoster presents as pain and rash which tends to be limited to one to three dermatomes in distribution.[3] Post-herpetic neuralgia may occur even in the absence of a rash.[3] Segmental motor paralysis can occur in the overlapping myotomes even about 3–20 days after cutaneous lesions are seen,[6] as is seen in our case. Herpes zoster can affect the motor or sensory nerves. On electrodiagnostic studies, a patient can have reduction or absence of sensory nerve action potential amplitude in case of sensory nerve involvement, or abnormal insertional activity in the form of positive sharp waves and fibrillation potentials.[10] Our patient had predominantly motor degeneration as seen by fibrillations and large wide polyphasic motor unit potentials.

Conclusion

Radiating pain in the presence of a dermatomal rash should prompt investigations for zoster neuritis. Our case demonstrates rare MRI findings of zoster neuritis which in the given clinical settings are pathognomonic, and additionally, EMG and NCV changes of neurodegeneration. Even in the absence of a typical skin rash, zoster neuritis must be considered as a diagnostic possibility in the presence of other findings, as early initiation of antiviral treatment is imperative while awaiting laboratory results.

Declaration of patient consent

The authors certify that appropriate patient consent was obtained.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.