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Herpes Zoster Research Paper

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HERPES ZOSTER
Herpes zoster (shingles) is a relatively common neurological disorder. Its estimated annual incidence is 3-4 per 1,000 of the general population. The incidence is significantly higher in older people and immunocompromised subjects (irrespective of their age).

Herpes zoster is caused by the varicella zoster virus and, typically, develops many years after the patient had recovered from chickenpox. It is thought that at the time of infection with chickenpox the virus migrates from the skin to the sensory ganglia via the axons of peripheral nerves and remains dormant in the ganglia, usually for many years. Activation of the virus occurs when the subject’s cell immunity is reduced. The activated virus travels along the sensory nerve …show more content…
The rash is usually preceded by local itching, tenderness and hyperaesthesia. Mild systemic symptoms, consisting of fever and malaise, are also present. Initially the skin rash consists of erythematous papules. Within a day or two the papules evolve into vesicles and then pustules. By the end of the second week the pustules dry leaving a crust and, later, a scar.

The rash distribution corresponds to the dermatomes of one or more of the sensory nerves. Most frequently the rash occurs in the thoracic region. It is frequently unilateral but may involve both sides of the body in immunocompromised patients.

Infection spreading from the trigeminal ganglion along the ophthalmic division of the trigeminal nerve (ophthalmic herpes zoster) occurs in about 20% of patients. The distribution of the skin rash is in the forehead. Ophthalmic herpes zoster often causes serious eye complications, including keratitis, conjunctivitis, iritis, scleritis and retinal necrosis.

Herpes zoster may also affect other cranial nerves. Ophthalmoplegia due to oculomotor nerves involvement and facial palsy accompanied by a vesicular rash in the external auditory canal (Ramsay Hunt syndrome) occur in some patients. Chronic radiculopathy without a skin rash has also been …show more content…
However, the artemisinin derivatives (artemether, arteether, artesunate, and dihydroartemisinin) have proved to be as effective as quinine and have less adverse effects. Furthermore, in some areas the malaria parasite has developed resistance to quinine. Nowadays artesunate is the drug of first choice for the treatment of cerebral malaria. It is given by intravenous injection in a dose of 2.4mg/kg body weight twice daily on the first day followed by 2.4 mg/kg once daily for another 6 days. If the artemisinin drugs are not available quinine should be used. Quinine loading dose (20 mg salt/kg body weight over 4 hours) should be given intravenously as soon as possible. Eight hours after the loading dose treatment is continued with the intravenous infusion of 30 mg salt/kg per day. Quinine treatment requires careful monitoring as the drug may cause hypoglycaemia and hypotension.

The clinical outcome also depends on the timely and appropriate management of acute complications of cerebral malaria, including cerebral oedema, hypoglycaemia (especially when quinine is used because it causes insulin release from pancreatic cells), shock, hyponatraemia, acidosis, pulmonary oedema, and acute renal

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