Hunter syndrome

Introduction Hunter's syndrome, or Ramsay Hunt syndrome, also known as ganglion ganglion inflammation, is a common peripheral facial paralysis, which is second only to Bell's facial paralysis. First reported by Ramsay Hunt in 1907, the name of the disease varicella-zoster virus infection (re-emergence) from the varicella-zoster virus invading the occipital ganglia of the eighth cranial ganglia and facial nerve, producing severe ear pain, Deafness, dizziness and facial paralysis. Blisters can be seen in the auricle and external auditory canal of the facial nerve sensory branch. It often involves other cranial nerves, and is often accompanied by some degree of meningeal inflammation. Lymphocytes appear in cerebrospinal fluid, and the protein content is often increased. Many patients also have mild and extensive encephalitis. Deafness can be permanent, and partial or complete recovery may occur. Dizziness can last for days to weeks. Facial paralysis can be temporary or permanent. Symptoms Mainly manifested as severe pain in one ear, ear herpes, ipsilateral facial facial paralysis may be accompanied by hearing and balance disorders. The disease is caused by the varicella zoster virus that is lurking in the ganglia of the facial nerve, which is caused by the activation of the body's immune function. In addition to invading the geniculate ganglia, it can also involve the adjacent auditory nerve. Low cellular immune function is associated with pathogenesis. Because the infection affects the local meningitis caused by the intracranial, the cerebrospinal fluid often has abnormal therapeutic drugs. 1. Early antiviral drugs such as: acyclovir (Zouvirax), famvir or valaciclovir (lovir); Treatment; 3, anti-inflammatory drugs: corticosteroids (Corticosteroids), such as prednisone, to reduce swelling and pain; 4, diazepam to reduce dizziness. Surgical treatment Some people think that surgery is not effective against viral infection. In fact, this is a natural view. Surgery certainly does not inhibit viral replication, but it can effectively improve the swelling and ischemia of the nerves behind the virus infection. Timely decompression in the acute phase of the neurodegenerative phase can improve the blood circulation and help the inflammation to subside. After strict screening, for some advanced patients, decompression can also provide the necessary conditions for nerve regeneration, but the recovery process of facial paralysis is significantly slower than that of Bell's facial paralysis. For the reduction of tears, surgical decompression often has a miraculous effect. According to experience, the tears on the affected side can be found on the night after surgery, and the secretion of tears is improved in some patients after anesthesia. Because of the long-term tear-free, it may eventually cause blindness. In some patients with very severe lesions and long course of disease, postoperative facial movement recovery may be unsatisfactory, but it is also worthwhile to perform facial nerve decompression surgery for lacrimal gland recovery and prevention of decreased vision. Surgical decompression range: lost segment - stem pores, 15% of patients need to temporarily move the ossicle, 60% of them (9% of all surgical patients) will have postoperative complications, that is, there may be affected side Degree of conductive hearing loss and tinnitus. After the operation, it is necessary to cooperate with the corresponding drugs and physiotherapy.