Download Polyradiculitis and Transverse Myelitis Secondary to Herpes Zoster

Letter to the Editor / Editöre Mektup
193
DOI: 10.4274/npa.y6848
Polyradiculitis and Transverse Myelitis Secondary to Herpes Zoster in a
Liver Transplant Patient
Karaciğer Transpantasyonlu Bir Hastada Herpes Zostere İkincil Poliradikülit ve Transvers Myelit Birlikteliği
Betül ÇEVİK1, Semiha KURT1, Dürdane AKSOY1, Hatice Karaer ÜNALDI1, Özgür GÜNAL2, Volkan SOLMAZ1
1Gaziosmanpaşa University Medical Faculty, Department of Neurology, Tokat, Turkey
2Gaziosmanpaşa University Medical Faculty, Department of Clinical Microbiology and Infectious Diseases, Tokat, Turkey
Dear Editor;
Herpes zoster (HZ) is a common neurocutaneous disease
resulting from reactivation of dormant varicella-zoster virus (VZV) in
sensory ganglions. Factors weakening immune function may
increase HZ and risk of neurological complications (1,2). Infrequent
neurological complications such as transverse myelitis (TM),
encephalitis, radiculoneuritis may develop more frequently in
immune-compromised patients. Rarely, multiple neurological
involvement can occur (1,2,3). Here, we report a case with TM
and polyradiculitis related to HZ while he was under
immunosuppression after liver transplantation.
A 54-year-old man was admitted to our clinic with pain and right
leg weakness complaints. Twenty days ago, he developed burning,
itchy vesicular eruption on his right leg, diagnosed with HZ,
valacyclovir tablet and acyclovir cream was prescribed. Ten days
after the rash, progressive weakness on right leg and numbness in
below waist appeared.
He had chronic hepatitis B virus infection resulting in
hepatocellular carcinoma and underwent liver transplantation
fourteen months ago. He also had type-II diabetes mellitus for oneyear. His medications included prednisolone (10 mg/d), tacrolimus
(20 mg/d), mycophenolate mofetil (2 g/d), insulin, entecavir (0.5
mg/d), ursodeoxycholic acid (1 g/d). High fever, crusted shingles
rash on the right L5-S1 dermatome were determined in physical
examination. There was muscle weakness in the right tibialis
anterior 0/5, right gastrocnemius 3/5 and right quadriceps femoris
4/5. Diminished pain sensation and light touch was noted below T6
dermatome. Proprioception and vibratory sensation were
determined to be lost to the knees. Deep tendon reflexes increased
in the lower extremities. Laboratory findings disclosed as: ESR:40
mm/h (<20); procalcitonin, 0.1 ng/ml (<0.05); white-blood-cells
count, 15300/mm3 with normal cell differentiation. Liver functiontests slightly increased.
Right patella and Achilles reflexes were hypoactive during the
neurologic examination 5 days after admission to our clinic. EMG
was performed revealing reduced amplitudes of compound muscle
action potentials with normal nerve conduction velocity and
prolonged F-wave latencies on bilateral peroneal and posterior
tibial nerves. Bilateral sural nerve conduction studies were normal.
Needle EMG revealed abnormal spontaneous activity and reduced
recruitment in right medial gastrocnemius. Lumbo-sacral magnetic
resonance imaging (MRI) revealed no abnormality.
Cervical-thoracic MRI, performed 22-day after the rash,
showed contrast enhancing T2-hyperintense intramedullary
lesions extending caudally from C2-C3 consistent with myelitis
(Figure 1). The cerebrospinal fluid (CSF) analysis showed normal
opening pressure; 26 WBCs per mm3 of which 90% were
mononuclear cells; 2950 red-blood-cells per mm3; protein 608 mg/L
and glucose 71.5 mg/dL (serum glucose was 219). Acid-fast and
gram stains, bacterial and mycobacterial cultures were negative.
VZV IgG antibody was detected in CSF (VZVIgG:3.98 T.V.). Zoster
Correspondence Address/Yaz›flma Adresi: Betül Çevik MD, Gaziosmanpaşa University Medical Faculty, Department of Neurology, Tokat, Turkey
Gsm: +90 505 858 52 32 E-mail:[email protected] Received/Geliş tarihi: 21.09.2012 Accepted/Kabul tarihi: 30.12.2012
© Archives of Neuropsychiatry, published by Galenos Publishing/ © Nöropsikiyatri Arşivi Dergisi, Galenos Yayınevi taraf›ndan bas›lm›flt›r.
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Çevik et al.
Polyradiculitis and Transverse Myelitis Secondary to Herpes Zoster in a Liver Transplant Patient
myelitis and polyradiculitis was diagnosed and he was treated with
10 mg/kg acyclovir intravenously 3 times daily for two weeks.
The spectrum of VZV myelopathy is broad, ranging from acute
to chronic. HZ myelitis generally occurs at the same time or within
the six-week of rash onset in immune-compromised patients (2).
We observed myelitis at the third-week of the rash onset in our
case. The pathogenesis seems to be abnormal immune response to
infection rather than the direct effect of infectious agent (3). Motor
neuron involvement, referred as segmental zoster paresis, occur in
0.5%–31% of HZ cases (4). Some electrophysiologic abnormalities
were seen in the extremities that have no motor weakness (5).
Although our patient had right leg weakness, bilateral findings were
detected in nerve conduction study.
In liver transplant patients, HZ frequency has been reported as
1.2-18%. Most of the cases occurred within the first year (6,7).
Nöropsikiyatri Arflivi 2013; 50: 193-194
Archives of Neuropsychiatry 2013; 50: 193--194
Underlying malignancy is found 3 times more frequently in patients
with zoster motor paresis than patients with purely cutaneous
zoster (8). We also detected hepatocellular carcinoma recurrence
in our patient.
We would like to emphasize that HZ in post-transplant patients
should be considered as a medical emergency. In severe
immunodeficiency with extended skin lesions or disseminated
central-nerve system, treatment with high dose intravenous
acyclovir and continuous monitoring of renal function are required
(1,2). Despite the delay of systemic acyclovir treatment for 3 weeks
following rash onset in our case, improvement appeared consistent
with a clinical response to this therapy.
In conclusion, neurological complications related to HZ seems
to be increased in patients after organ transplantation and
prolonged steroid treatment, the clinical manifestations may be
unusual and multiple as in our case.
References
1.
A
B
2.
Figure 1 .Distribution of skin lesions due to herpes zoster. (A) Crusted
rash on right L5 dermatomal trace. (B) Crusted rash on L5-S1 dermatomal
traces.
3.
4.
5.
6.
7.
A
B
Figure 2 . Magnetic resonance image of the cervical (A) and throcal (B)
spinal cord. Sagittal T2 fast-recovery fast-spin echo sequence showing
abnormal longitudinal serpiginous contrast enhancing hyperintense
lesions.
8.
Gilden DH, Kleinschmidt-DeMasters BK, LaGuardia JJ, Mahalingam R,
Cohrs RJ. Neurologic complications of the reactivation of varicella-zoster
virus. N Engl J Med 2000; 342:635-645.
Dworkin RH, Johnson RW, Breuer J, Gnann JW, Levin MJ, Backonja M,
Betts RF, Gershon AA, Haanpaa ML, McKendrick MW, Nurmikko TJ,
Oaklander AL, Oxman MN, Pavan-Langston D, Petersen KL, Rowbotham
MC, Schmader KE, Stacey BR, Tyring SK, van Wijck AJ, Wallace MS,
Wassilew SW, Whitley RJ. Recommendations for the management of
herpes zoster. Clin Infect Dis 2007; 44 Suppl 1:S1-26.
Ong OL, Churchyard AC, New PW. The importance of early diagnosis of
herpes zoster myelitis. Med J Aust 2010; 193:546-547.
Conliffe TD, Dholakia M, Broyer Z. Herpes zoster radiculopathy treated
with fluoroscopically-guided selective nerve root injection. Pain Physician
2009; 12:851-853.
Haanpää M, Häkkinen V, Nurmikko T. Motor involvement in acute herpes
zoster. Muscle Nerve 1997; 20:1433-1438.
Herrero JI, Quiroga J, Sangro B, Pardo F, Rotellar F, Alvarez-Cienfuegos J,
Prieto J. Herpes zoster after liver transplantation: incidence, risk factors,
and complications. Liver Transpl 2004; 10:1140-1143.
Gourishankar S, McDermid JC, Jhangri GS, Preiksaitis JK. Herpes zoster
infection following solid organ transplantation: incidence, risk factors and
outcomes in the current immunosuppressive era. Am J Transplant 2004;
4:108-115.
Sørensen HT, Olsen JH, Jepsen P, Johnsen SP, Schønheyder HC,
Mellemkjaer L. The risk and prognosis of cancer after hospitalisation for
herpes zoster: a population-based follow-up study. Br J Cancer 2004;
91:1275-1279.