Shingles (Post-Herpetic Neuralgia)

Shingle is an infectious disease caused by the reactivation of the Varicella Zoster virus. The virus responsible for chickenpox contracted in childhood infects sensory nerve ganglia. It remains there in a latent state for many years. 

Reactivated thanks to a decrease in immunity (advanced age, drugs, stress, cancer, HIV, etc.), it manifests itself in the form of shingles, a dermatosis characterized by a vesicular rash in the distribution territory of a sensory nerve. Often preceded by prodromes (headache, fatigue, fever, nausea, paraesthesia, pain), the skin lesions appear in successive outbreaks, in the form of red papular patches, clusters of vesicles, and crusty lesions, which usually disappear within a few weeks.

Unlike chickenpox, where itching is predominant, shingles are characterized by stabbing pain, burning, stinging and electric shocks which can be very intense. Pain is often associated with allodynia and hyperalgesia in affected areas.

Zonas occur most often in the thorax (50-60%), in the cervical region (10-20%), in the face (10-20%), in the lumbar areas (5-10%), and sacred (<5%).

The rash is unilateral, spreads over several dermatomes in 20% of cases, and hardly ever crosses the midline. The simultaneous involvement of several non-contiguous dermatomes generally only appears in immunocompromised patients. Likewise, the dissemination of the virus in the deep organs (lung, brain, liver) is in principle only seen in weakened subjects but is associated with a mortality rate of around 10%.

 

Epidemiology of postherpetic neuralgia

 

A frequent complication of shingles, postherpetic neuralgia (PHN) is the prime example of neuropathic pain. It is defined by pain (VAS> 3), which persists for three months after the rash has healed. In the general population, it accompanies 10 to 15% of zonas, while it is present in more than 50% of elderly patients (> 60 years). Among the proven risk factors for developing PHN, we note in particular the intensity of the pain during the rash, advanced age, and the thoracic and ophthalmic locations 2. The severity of the rash and the presence of prodromes are probable risk factors, while the preventive role of antiviral treatment or nerve blocks remains controversial. No studies have demonstrated the usefulness of corticosteroids in the prevention of PHN.

 

Pathophysiology of postherpetic neuralgia

 

The pathophysiology of NPH presumably involves central and peripheral mechanisms. Replication of the virus causes an inflammatory reaction in the peripheral nerves, dorsal roots, spinal ganglia, and spinal cord, accompanied by the release of pro-inflammatory mediators (TNF-alpha, substance P). These reactions cause posterior horn atrophy, fibrosis of the posterior spinal ganglia, and degeneration of cell bodies and primary afferent axons. These changes may explain a disparate clinical picture, associating hypoaesthesia secondary to loss of skin innervation,

 

Postherpetic neuralgia clinical presentations

 

Patients typically describe shooting pain, burning, stinging, throwing, or electric shock, present intermittently or continuously—over 90% of patients present with hyperalgesia as well as mechanical and thermal allodynia in affected dermatomes. Adjacent dermatomes often reveal hypoaesthesia. The associated sleep and mood disorders negatively influence the quality of life of patients.

 

Topical treatments: lidocaine or capsaicin

 

Patches and ointments are generally devoid of systemic side effects and drug interactions. They are, therefore, particularly interested in elderly patients. However, their use is limited by the skin condition and the extent of the areas to be covered. 5% lidocaine patches (Neurodol ®) are recommended as first-line treatment (NNT 2). The application of 8% capsaicin (Qutenza ® ) is effective in NPH, with an NNT between 7 and 12. The handling of highly concentrated capsaicin plasters requires precautions which means that this treatment is generally offered in a hospital environment. The application can be renewed at three monthly intervals depending on the evolution of symptoms.

 

Botulinum toxin A

 

Local and peripheral injection of botulinum toxin A (BTX-A) leads to a reduction in the release of various substances involved in the regulation of nociception and inflammation (glutamate, substance P, peptide linked to the calcitonin gene (calcitonin gene –Related peptide or CGRP)). Studies have recently evaluated the effectiveness of the administration of BTX-A in the form of 20 and 190 IU divided into numerous intradermal injections distributed in a chessboard in the painful area. Pain, sleep, and quality of life improve significantly soon after administration, and this benefit can last for 2 and 4 months.

 

Epidural injection

 

While epidural injections of local anesthetics and corticosteroids are effective in the acute pain of shingles, there is no evidence to support a lasting effect in PHN.

 

Intrathecal injection

 

Methylprednisolone intrathecal injection (4 weekly injections of 60 mg) was described in a Japanese study involving 270 patients with NPH (excluding cranial nerves). The analgesic effect was excellent (NNT 1.1). However, these results could not be replicated until day 9. Since intrathecal injection of methylprednisolone involves significant risks of arachnoiditis, lumbar radiculitis, transverse myelitis, or even aseptic meningitis, this approach is not recommended in the absence of additional studies.

 

Spinal cord stimulation and peripheral subcutaneous stimulation

 

In two retrospective studies of 10 and 28 patients, spinal cord stimulation’s medium and long-term efficacy was 60% and 82%, respectively. In addition, a small series of peripheral subcutaneous stimulation in the trigeminal nerve territory describes the technique as effective.

However, neuromodulation techniques are often limited in NPH due to the sensory deficit found in the majority of patients.

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