Herpes Zoster

 

Shingles is a disease that I have come across several times in the past ten years.  My grandmother had her first Shingles outbreak when she was in her eighties, a thirteen year old year I coached was diagnosed with it, and recently, a family friend in her early fifties was diagnosed with Shingles.  After spending so much time learning about neurons and how action potentials are generated I was interested in doing some research to learn more about Shingles and how it attacks the nervous system.
  
Herpes Zoster, more commonly known as Shingles, affects approximately 50% of people who live to be older than 85 and is the result of an initial infection of the varicella zoster virus, more commonly known as the chickenpox virus, reactivated (1).  Following initial infection, the varicella zoster virus enters the nervous system through the dorsal root ganglia (mechanism of entry is not completely understood) where it remains dormant (1).  This period of dormancy is dependent on the level of specific cell-mediated immunity (helper T-cells, cytotoxic T-cells, natural killer cells, and cytokines) which actively work to suppress varicella zoster from entering an active stage.  If the number of specific cell-related immunity cells decrease due to other diseases such as cancer, diabetes, HIV, or as a natural result of aging, varicella zoster enters a lysogenic cycle, rapidly self replicating and attacking the host's nervous system.  The resulting shingles rash will develop in stages.

The early stage of shingles can last several days to weeks and causes symptoms similar to the flu including: headaches, light sensitivity, and itching, burning, tingling, and pain of the affected area.  Commonly, affected areas include the thoracic and abdominal areas, but can also affect the facial nerves (depending on affected nerve and degree of damage can cause hearing and/or vision loss or loss of motor control) and upper and lower extremities (2).  Following this initial stage, the shingle rash will become present.

The shingles rash is the active stage of the infection and is a result of the virus spreading through peripheral nerves, forming vesicles and causing neuronal damage that causes skin blisters and lesions.  The lesions develop a crust-like covering within 7-10 days and will be sloughed off as the lesions heal.  While the rash of lesions associated with the active stage of shingles is certainly uncomfortable, there are more severe complications such as loss of sensory and motor innervation depending on the degree of neuron damage from the viral outbreak.  The most common and debilitating complication is the development of postherpetic neuralgia.

Postherpetic neuralgia is pain caused from damage to neuronal myelin integrity.  Pain varies in degree and duration, but most patients complain of intermittent, excruciating pain in response to moderate stimulation such as wind or clothing touching affected areas especially forehead and chest.  While the exact cause of pain is not entirely understood, it is most likely due to constant stimulation of nociceptors (sensory receptors responsible for perception of pain.)  Treatment of postherpetic neuralgia is limited to relief through topical analgesics, tricyclic antidepressants, anticonvulsants, narcotics and intervention therapy. 




References:

1.) Osemene N, Herpes Zoster (Shingles) and Postherpetic Neuralgia Management. College of Pharmacy and Health Sciences. 2011; http://www.uspharmacist.com/continuing_education/ceviewtest/lessonid/106103/

2.)  Ashkenazi A, Levin M. Three common neuralgias: how to manage trigeminal, occipital, and postherpetic pain. Postgraduate Medicine. 2004;116(3):16-48.