herpes zoster

Herpes zoster

Herpes zoster is an infectious disease that is caused by the varicella-zoster virus

It is postulated that during the course of primary infection with VZV, the virus migrates to the dorsal root or cranial ganglia

Dr Mehran Rezvani pain fellowship anesthesiologist & acupuncturist

Herpes zoster

In some individuals the virus may reactivate and travel along peripheral or cranial sensory pathways to the nerve endings, producing the pain and skin lesions characteristic of shingles

The reason for reactivation ?decrease in cell-mediated immunity


Risk factorsSuffering from malignancies (particularly lymphoma)Receiving immunosuppressive therapy

(chemotherapy, steroids, radiation)

Generally debilitated by chronic diseasesPatients older than 60 years


SIGNS AND SYMPTOMS

Herpetic pain: 5-7 day before of skin lesions May be accompanied by flu-like symptoms Progresses from a dull, aching sensation to unilateral,

Segmental, band-like dysesthesias and hyperpathia Burning pain , hyperesthesia, allodynia Zoster sine herpete


SIGNS AND SYMPTOMS

From a mild self-limited problem to a debilitating, constantly burning pain that is exacerbated by light touch, movement, anxiety,and/or temperature change

Can lead to suicide


TREATMENT

Relief of acute pain and symptoms

Prevention of complications, includingpostherpetic neuralgia

Earlier treatment less likely postherpetic neuralgia


TREATMENT

Sympathetic neural blockade appears to be the treatment of choice to relieve the symptoms of acute herpes zoster as well as to prevent the occurrence of postherpetic neuralgia

Noordenbos "fiber dissociation"


TREATMENT

Herpes zoster in trigeminal nerve & geniculate, cervical, and high thoracic regions: stellate ganglionblockade with

LA daily basisHerpes zoster thoracic, lumbar, and sacral regions: epidural neural blockade with LA

daily basis


TREATMENT

• If the pain is not as severe, NSAIDs or acetaminophen may be all that is needed

• In acute eruption oral narcotics may be administered in the short term, especially

with (NSAIDs)


TREATMENT

Narcotic analgesics may be useful in relieving the aching pain

Antidepressants will help : Alleviate the significant sleep disturbance Ameliorate the neurotic component of the pain May exert a mood-elevating May cause urinary retention and constipation


TREATMENT

Anticonvulsants

May be of value as an adjunct to sympathetic neural blockade They may be particularly useful in persistent paresthetic or

dysesthetic pain


TREATMENT

Anxiety may be treated

HydroxyzineBehavioral interventions(e.g., monitored relaxation training and hypnosis)


TREATMENT

Antiviral agents:Acyclovir , valacyclovir, famcyclovir and perhaps

interferon have been shown to shorten the course of acute herpes zoster


Zoster sine herpete


Classic zoster sine herpete (ZSH) is defined clinically as dermatomal distribution pain without rash

First defined by Lewis(1958) who described zoster patients with dermatomal distribution pain in areas outside that affected byzoster rash


Gilden and colleagues reported 2 men aged62 and 66 years who had had chronic thoracic

distribution radicular pain in whom PCR-amplifiable VZV DNA was detected in the CSF 5 and 8 months after the onset of pain (1994)

Treatment with IV acyclovir produced marked improvement


A third man over 60 years old withsimilar chronic radicular pain was subsequently

reported in whom the VZV etiology was proved by detection of VZV DNA in blood mononuclear cells (MNCs) (1996)


R. Nau, MD M. Lantsch, MD M. Stiefel, MD T. Polak, MDH. Reiber, PhD


Departments of Neurology and Neuroradiology

University of Gttingen, Germany


42-year-old immunocompetent man no history of herpes zostersuddenly experienced dys- and hypesthesia in

his left handfluctuating paresis of the flexion and extension

of the fingers of the left handincreased tendon reflexes on the left at the

upper and lower extremities were notedDr Mehran Rezvani pain fellowship anesthesiologist & acupuncturist

Within the next 10 days, the hypesthetic region expanded to the fingers and the left forearm, and he noticed progressive distal weakness of his left upper extremity


ESR was 17 mm in the first and 33 mm in the second hour.

Serologic tests (c- and p-ANCA, rheumatoid factor, antibodies against DNA, the Sjogren-associated nuclear antigens SS-A and SS-B, and antibodies against extractable nuclear antigens Sm, RNP, Scl-70, and

Jo-1) and a rectum biopsy did not reveal any evidence for systemic vasculitis


On MRI, multiple ischemic lesions in the territory of the right middle cerebral artery (MCA) were detected


MR angiography revealed a proximal stenosis of the right MCA


Lumbar CSF contained 5 leukocytes/pL (predominantly mononuclear cells), and a normal total protein and lactate concentration

The CSF-to-serum concentration quotient of total IgG, for vzv resulting in an antibody index (AI)


The AI against herpes simplex virus was 3.8The polymerase chain reaction (PCR) for VZV

DNA in CSF was negative


High-dose IV acyclovir (750 mg IV three times daily for 10 days)

corticosteroids (1,000 mg IV daily for 3days, and 100 mg daily for another 10 days)

No immediate improvement but stopped the progression of the disease


During the next 6 months, the motor and sensory functions of the left upper extremity slowly improved


Neurology 76 February 1, 2011D.T. Blumenthal, MDE. Shacham-Shmueli, MDF. Bokstein, MDD.S. Schmid, PhDR.J. Cohrs, PhDM.A. Nagel, MDR. Mahalingam, PhDD. Gilden, MD

From the Oncology Division (D.T.B., E.S.-S., F.B.), Tel-Aviv


In 2008, a 77-year-old man developedright C8-distribution zoster; he was not treated with an antiviral agent or

steroids and his rash and pain resolved completely


One year later he developed colon cancer and was treated

every other week for 7 months with a protocol using leucovorin, 5-fluorouracil, oxaliplatin, and folinic acid


In November 2009, right C7–8-distribution pain recurred, but in the absence of rash

In December 2009, he developed a painless right foot drop

In February 2010, neurologic examination revealed C7–8 thigmesthesia and allodynia and an incidental right peroneal palsy.


All deep tendon reflexes were reduced or absent

Cervical MRI :degenerative changes at C5–6 and C6–7 without root compression

The CSF was acellular; cytology was negative, and CSF protein was 87 mg %


A presumptive diagnosis of ZSH was madehe was treated with valacyclovir, 1 g 3 times daily for 14 days, and pregabalin, 150 mg at night

A few days after treatment, he experienced a dramatic reduction in pain,

and 2 months later, was pain-free


Virologic studies of the CSF and serum obtained before antiviral treatment

revealed no amplifiable VZV DNA and no anti-HSV IgG antibody

In contrast, anti-VZV IgG antibody was presentThe serum/CSF ratio of anti-VZV IgG antibody was markedly reduced


It is important to identifypatients with ZSH since their

symptoms and signs may respond to IV acyclovir


In patients with prolonged radicular pain without rash to verify the diagnosisof zoster sine herpete CSF should be examined for both

VZV DNAanti-VZV IgG antibody


negative PCR for VZV DNA in the CSF does not exclude the diagnosis of VZV vasculopathy

1-Blood MNCs for VZV DNA2- CSF VZV DNA3- CSF Anti-VZV IgG antibody


herpes zoster

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