Shingle Pain: Post Herpetic Neuralgia
[1] The varicella zoster virus of the herpes family, is a highly contagious double-stranded DNA virus. More common during childhood, this virus initially manifests as chickenpox in a non-immune or incompletely immune person. During primary infection, varicella gains entry into the sensory root ganglia near the spine and may remain latent after the chickenpox is resolved. As the cell-mediated immunity decreases in people with advanced age or in those who contracted varicella at an age of less than 18 years, the virus can reactivate, replicate, and migrate down the sensory nerve. This leads to the dermatomal distribution of pain, producing blisters characteristic of shingles. Virus reactivation occurs as a result of diseases like Lymphoma or HIV AIDS, in cases of immunosuppression, or during the management of malignancy such as chemotherapy. Demyelination, Wallerian degeneration, and fibrosis occur due to the associated inflammation in the peripheral nerves. The rash typically occurs in a single, wide stripe on either side of the body or face. After two to four days of rash, there may be tingling or local pain and other symptoms. In poorly immune individuals, the rash may be widespread, even involving the eyes and leading to vision loss or Herpes Zoster Ophthalmicus. The uninhibited and amplified activity in unmyelinated primary afferents leads to pain, also known as post herpetic neuralgia or Shingle Pain. About 20% of the patients with herpes zoster or shingles develop post herpetic neuralgia [1].
Rowbotham et al.[2] in his research, quantified the sensory presentations and proposed three subtypes of post herpetic neuralgia:
The irritable nociceptive group, with mechanical allodynia and normal or hyperalgesic thermal sensation
The central reorganization group with mechanical allodynia and thermal sensory deficits
The deafferentation group with ongoing pain, without allodynia, and profound sensory loss
Rowbotham’s research established that almost half of the patients fell under the central reorganization group and the rest of the patients fell equally under the remaining two subtypes. He also found from his research that the involvement of the peripheral cutaneous nociceptors was more prevalent early in the disease and the central nervous system mechanisms were apparent after almost a year [2].
A complication of shingles, post-herpetic neuralgia affects the quality of life of the patients by causing a loss of physical function. Patients complain of fatigue, anorexia, weight loss, reduced mobility, physical inactivity, sleep disturbances (especially insomnia) and reductions in overall health [3, 4]. Post herpetic neuralgia makes it difficult to carry out simple day-to-day tasks like bathing, dressing oneself up, eating and other activities like travelling, shopping, household chores, etc. [3] . In patients of advanced age, this can lead to institutionalization and a loss of autonomy. [5]
Shingle pain also affects the emotional and psychological well-being of the patients [4, 6]. If patients with Herpes Zoster do not develop Shingle pain, their psychosocial scores improve; however, in patients who do develop Shingle pain, the psychosocial scores are reduced [6]. The intensity of physical pain in these patients is directly related to the risk of depression. Patients with less physical pain are at a lower risk of anxiety and depression as compared to those with intense physical pain [3, 4]. These symptoms are usually treated medically using antidepressants and antianxiety drugs, in addition to the pain medicines for the physical pain. Moreover, such physical, mental and emotional changes often lead to disturbances in the key relationships of these patients. They experience reduced independence and also tend to participate less in social events, thereby leading to a loss of social contact, withdrawal and isolation [3, 5]. Most of these patients fear recurrences of the post herpetic neuralgia symptoms. This further declines the mental status of these patients and sometimes they even develop suicidal tendencies as a direct consequence of post herpetic neuralgia [7].
Shingle pain affects the overall health of the individual. It is imperative to eradicate the disease from the community by controlling and preventing the incidence of herpes zoster with the help of effective vaccination. In those who contract the virus, the primary aim should be to prevent the onset of post herpetic neuralgia since it physically debilitates and mentally distresses the patients for years together. It is also essential to customize the treatment to individual patients by identifying subtypes based on the pathophysiology of post-herpetic neuralgia which holds a key to the development of mechanism-specific therapies.
The lifetime incidence of herpes zoster is 30% and an approximate 12.5% of patients aged 50 or higher develop Shingle pain [8]. An estimated 500,000 to 1 million episodes of zoster notably occur every year in the United States. Half of those who live until age 85 years will develop zoster [1]. Currently there are no known effective disease-modifying therapies for post-herpetic neuralgia. Future research in this field is required to study the invasive pain management techniques in the treatment and prevention of refractory post-herpetic neuralgia.
In Good Health
Priyal Agrawal
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