A female, 48 years old, (height, 161 cm, weight, 61 kg) admitted to the hospital in Taipei, Taiwan. She was complaining of two-week history of pain and weakness affecting her left upper extremity. Her movement was limited in that she could only raise her left arm only with increased effort. Difficulty breathing and shortness of breath (Progressive Dyspnea) were also observed. The medical history was taken and nothing was unusual.
During the physical examination of the patient, everything was regular expect an increased respiratory rate of 25 breaths per minute. While studying the patients breathing patterns, doctors noticed her abdominal wall movement was convoluted. She still maintained normal breathing sounds though. Abnormal red and mucous membrane (erythematous) rash and vesicles were observed around her left upper extremity. It was located around the C5 to C7 dermatomes, around the top of the left forearm. During the examination many physical aliments were found. There was a weakness in the left deltoids and biceps muscles. Also there was a diminished left biceps reflex. Spiral CT scan of the chest with intravenous contrast and radionuclide pulmonary ventilation-perfusion scans were normal.
An MRI was taken that was gadolinium-enhanced, a chemical compound given during MRI to highlight the areas of inflammation. If the gadolinium-enhanced magnetic resonance imaging (MRI) scan actually shows a lesion that indicates that there is a break down in the blood brain barrier and inflammation is current. The MRI was also T1-weighted which can show permanent axonal damage symbolized by dark black holes on the MRI image. The MRI revealed T1-weighted hyperintensity in the left antero-lateral aspect of the spinal cord at the C5 level. Herpes zoster with motor paresis was diagnosed. Herpes zoster, commonly known as shingles, is a viral disease with painful skin rash with blisters, usually on one side of the body. Years after the first infection, the virus may break out of the nerve cells and go down the nerve axons to cause an infection of the skin of that nerve. Zoster can only occur in patients who have previously had the chicken pox.
The patient was treated with orally administered 1000mg Valacyclovir three times a day, for seven days. The patient's pain was cured three months later. Follow ups appointments were attended for the next two years, and there was no further complications. Typically, Herpes zoster effects depend on the area of infection. Some patients may experience mild symptoms like stinging, aching, and numbness, while other may have extreme symptoms such as stabbing pains in the affected area.
PART II: Address Questions
Varicella zoster virus is what causes herpes zoster. Varicella zoster virus is a enveloped, double-stranded DNA virus. It belongs to the Herperviridae family. The genome encodes for about 70 proteins. Humans can acquire varicella zoster virus when it comes in contact with conjunctiva or the mucosa of the respiratory tract. From there it is distributed throughout the body. After the initial infection, the virus travels through the sensory nerve fibers to the dorsal root ganglia where it turns inactive. The initial infection is usually chickenpox.
The varicella zoster virus can stay dormant until death, but in the case of herpes zoster the varicella zoster virus is usually reactivated after decades of the initial infection. The exact cause of the reactivation is unsure but there are some theories. One cause could be external reexposure to the virus. Another thought is emotional stress and medications may reactivate the varicella zoster virus. Another cause could be chronic or acute disease processes. There are many risk factors to herpes zoster. The risks factors in adults and children are varicella zoster virus specific immunity and cell-medicated immunity, Immunosuppression (by HIV or AIDS), Anti-tumor necrosis factor (TNF), and acute lymphocytic leukemia.
There are two syndromes that the varicella zoster virus causes. First is the chickenpox illness and the second beginnings after the reactivation of the varicella zoster virus from the remaining viral particles in the dorsal root. There is a latent period between the two syndromes lasting sometimes decades. During this latent period, the host immunologic mechanism stops replication until the host fails to control the virus. This is the reactivation that leads to herpes zoster. The infected skin cells spread to the sensory nerve ending, then to the ganglia. The mucous rashes due to herpes zoster are caused by a T-cell proliferation. This a long lasting cell-mediated immunity response to varicella zoster virus.
The exact cause of the reactivation is unknown today, but once it is activated in the spinal root or cranial nerve neuron an inflammatory response is triggered. Hemorrhagic necrosis of the nerve cells may occur and it is due to the inflammation in the dorsal root ganglion. This results in fibrosis and neuronal loss. If the varicella zoster virus spreads to the anterior horn cells, cranial nerve palsies, neurogenic bladder, and muscular weakness. If more sections of the spinal cord get infected they can develop into myositis, Guillain-Barre syndrome, and transverse myelitis.
The symptoms vary in their strength. The first symptoms are usually tingling or burning on one side of the body. The burning and pain may be extreme and usually occurs before any rash appears. The rashes start off by red patches that soon form into small blisters. The blisters usually break, forming painful sores that dry and form crusts that fall off in two to three weeks. The rash location depends of the on the area of infection. The rash normal starts in a small area from the spine and travels down to the front of the abdomen or chest area. The rash may move to other places such as ears, eyes, face and mouth.
Other than the rashes, there are more physical symptoms to herpes zoster. The patient may experience chills and a fever, along with a general ill feeling. Headache may occur, while joint pains and swollen lymph nodes are common. This is due to the fact that herpes zoster is inflammatory response disease. Muscle weakness is common but it may affect the patient's face. Reactions include dropping eyelid, loss of eye motion, vision problems, and difficulty moving some muscles of the face, hearing loss, and taste problems.
Herpes zoster can be treated by an antiviral medicine. It prevents complications, reduces pain, and shortens the duration of the disease. For the most effective results, the medications must be taken within 72 hours of the first pain or burning, before the blisters appear. Corticosteroids and other strong anti-inflammatory medicines may be taken to reduce the pain and swelling. In some patients, these medications do not work. A dose of 40-60 mg of corticosteroids is given over a course of a week.
Majority of the patients with herpes zoster experience pain, and usually is the most bothersome symptom. There are medications given to the patient to ease their pain. For example, narcotic and nonnarcotic analgesics (both topical and systemic) can be given. Another drug that can be used is neuroactive agents (eg, trcyclic antidepressents). These treatments have been established and common but not many studies have been done on these medication's affects on herpes zoster specifically. Herpes zoster does not need an extensive follow up. After proper treatment, herpes zoster can be cured in the patient.
The information presented in the journals correlated greatly with the case study. The female patient in the case study had complained of pain and weakness in her left upper extremity and limited movement. According to the journals, this is a normal symptom of herpes zoster. Also rashes and sores were found in the same area indicating that the patient was suffering from the varicella zoster virus. This is a main symptom of herpes zoster as indicated by many journal articles. Another symptom that was noted in numerous articles is that all of the pain and rashes are associated with one side of the body. In the patient's case it was the left side. The rash and pain were on the upper left side along with weakness in the left deltoids and biceps muscles, and diminished left biceps reflex.
There was one significant difference between the literature and the case. In the case the patient was suffering from dyspnea, which is a shortness of breath or abnormal breathing effort. The patient had an increased respiratory rate of 25 breaths/minute. Her breathing pattern was observed as being convoluted in the abdominal wall movement, even though her breathing sounds were fine. Spiral CT scan of the chest with intravenous contrast and radionuclide pulmonary ventilation-perfusion scans were normal. In most the literature, dyspnea was not listed as a symptom of herpes zoster.
Herpes zoster can affect any muscle but it is rarely reported in respiratory muscles. The abnormal abdominal wall movement is an indicating sign that the varicella zoster virus infected the respiratory muscles, specially the diaphragm. The phrenic nerve innervates the diaphragm. It is hypothesized that there was a lesion in the c% level of the spinal cord that caused the motor defects in the patient's left side. This lesion may have been caused by the intense lymphocytic inflammation and vasculitis in nerves. This caused degeneration of the sensory and motor roots and may have spread to the spinal cord. That, in turn, causes demyelination and grey matter necrosis. The patient had a good result after an intense antiviral therapy treatment.
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