What does Shingles affect?

What does Shingles affect?

Jarrod,
As you have so rightly stated, Shingles is a skin rash caused by the same virus that causes chickenpox. The Varicella zoster virus – VZV which is a double-stranded DNA virus in the Alphaherpesvirinae subfamily. After primary infection, VZV remains dormant in the posterior spinal ganglia or cranial sensory ganglia for life. It may subsequently reactivate as the virus migrates down these sensory nerves, or less commonly along the anterior and posterior horn cells, leptomeninges, and peripheral nerves. Herpes zoster, or shingles, is the most common presentation of reactivated VZV. The vast majority of cases of shingles occur in adults. Patients report a prodromal illness of pain, pruritus, burning, and/or parasthesias. Erythematous macules and papules develop along a single dermatome. The lesions progress to vesicles, crust and heal over. Pain and sensory loss are the most common symptoms, motor weakness may also occur if viral activity extends to involve the motor root. Variant forms exist including zoster multiplex, in which multiple dermatomes are simultaneously involved, and zoster sine herpete, in which neurologic symptoms exist without cutaneous vesicles. Diagnosis is based on the clinical presentation, if in doubt, then a skin scraping with Tzanck smear, viral fluid culture, or polymerase chain reaction (PCR) evaluation can confirm diagnosis. Treatment with antivirals (acyclovir, valacyclovir, famciclovir) reduce the severity and duration of symptoms if initiated within the first 3 days of therapy. Topical therapy with cool water compresses, calamine lotion, and analgesics may provide significant symptomatic relief. Use of corticosteroids is controversial. A varicella zoster vaccine is available reducing the incidence of chickenpox and herpes zoster. Most cases of zoster are mild and self-limited, but in some cases, pain in the affected dermatome may persist long after cutaneous lesions have resolved, termed postherpetic neuralgia (PHN). Risk factors for PHN are advanced age, brachial/trigeminal involvement, severe prodromal pain, and severe rash. Early treatment of zoster has been shown to decrease the incidence of PHN, some believe that active herpes zoster sets up a positive feedback loop, creating a central pain syndrome similar to phantom leg. In some patients, areas of scarring or hypopigmentation may be present. Natural history of PHN is slow resolution of symptoms, but numerous treatment options are available including tricyclic antidepressants, anticonvulsants, anesthetics, analgesics, corticosteroids, and antiviral agents. Combination therapy with gabapentine and nortriptyline is particularly effective. Ramsay Hunt syndrome, or herpes zoster oticus, is a reactivation of VZV involving the facial nerve. Cranial nerves V, VI, VIII, and IX may also be involved. Patients initially report pain deep within the ear that radiates to the pinna. The infection then produces vesiculations and ulcerations of the external ear and ipsilateral anterior two thirds of the tongue and soft palate. Ipsilateral lower motor neuron facial paresis/palsy, vertigo, hearing loss, tinnitus, headaches, otalgia, dysarthria, gait ataxia, fever, and/or cervical adenopathy may also develop. Diagnosis is usually made on clinical grounds. Treatment involves corticosteroids and oral acyclovir. Prognosis is good, but less than 50% of patients have complete recovery of the facial nerve. Herpes zoster ophthalmicus is a latent VZV infection involving the ophthalmic division of the trigeminal nerve. It accounts for 10% to 25% of all cases of shingles. The reactivated VZV may travel down the ophthalmic division to the nasociliary nerve, which innervates the tip of the nose and surface of the globe of the eye. The initial presenting symptoms of ocular involvement may include eye pain, red eye, decreased vision, and tearing. A zoster rash on the tip, side, or root of the nose is referred to as the Hutchinson sign and heralds ocular involvement. Subsequently significant inflammatory changes (eg keratitis, scleritis, iritis, orbital vasculitis), nerve damage (eg ocular motor palsies, neurotrophic keratitis), and tissue scarring (eg lid deformities, neuralgia) may develop and cause vision loss in the affected eye. Treatment typically involves early antiviral therapy and topical steroid eye drops to reduce inflammation. Antibiotics, cycloplegics, and glaucoma medications may be used on a case-by-case basis depending on subsequent complications. VZV may also be responsible for aseptic meningitis and encephalitis following varicella or zoster. VZV has also been identified as the third most common cause after herpes virus and enterovirus. Classic meningeal signs of headache, neck stiffness, and photophobia are present with or without a preceding rash. In VZV encephalitis, patients usually present with delirium days to months after a vesicular eruption. In both VZV meningitis and encephalitis, patients typically have pleocytosis and elevated protein on cerebrospinal fluid analysis (CSF). PCR analysis of CSF may be able to amplify and diagnose VZV infection. Prompt treatment with high-dose intravenous acyclovir on an empiric basis is typically the standard of care. I wish you well with your 'project!'



ALL ANSWERS SHOULD BE THOROUGHLY RESEARCHED, IN ANY FORUM AND ESPECIALLY IN THIS ONE. - MANY ANSWERS ARE FLAWED.

It is extremely important to obtain an accurate diagnosis before trying to find a cure. Many diseases and conditions share common symptoms.


The information provided here should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed physician should be consulted for diagnosis and treatment of any and all medical conditions.


Hope this helps
matador 89

---

Orignal From: What does Shingles affect?