We report two cases of abdominal wall pseudohernia after herpes zoster. Case 1 was a male in his 60s. One week after he experienced lower back pain in the left lumbar abdominal region (T11–T12 thoracic medullary nerve region), blisters with erythema were observed and clinically diagnosed as herpes zoster. On the seventh day of treatment with amenamevir (400mg), the patient noticed a left-sided abdominal bulge. Owing to paralysis of the abdominal muscles and lack of ascites, mass, or hernia in the intestinal tract on computed tomography (CT), the bulge was diagnosed as an abdominal wall pseudohernia. Case 2 was a female in her 70s who had back pain in the left lumbar abdominal region (T11–T12 thoracic medullary nerve region), followed by blisters with erythema in the same region a week later. The patient was treated with amenamevir (400 mg) for seven days. On a follow-up visit 14 days after the initial visit, the doctor noticed a bulge on the left side of the abdomen without any subjective symptoms. Based on patient history and clinical findings, a diagnosis of abdominal wall pseudohernia after herpes zoster was made.
Both patients had only subcutaneous muscle protrusion stiffness in the distended area without subjective symptoms, such as abdominal pain or constipation. Case 1 had pain relief after three months of treatment for sensory neuropathy at the University Hospital Pain Center, and the abdominal wall pseudohernia was also relieved. Case 2 had pain relief after treatment, but the abdominal wall pseudohernia only improved after four months. Sensory neuropathy is a well-known complication of herpes zoster. Dermatologists are familiar with Ramsay-Hunt syndrome, which causes facial paralysis, and muscle weakness of the upper arm, abdominal wall pseudohernia, rectal and bladder disorders by other motor neuropathies. However, although motor neuropathies are well known, practitioners have few opportunities to actually experience them clinically. An abdominal wall pseudohernia is a distension of the abdominal wall resulting from muscle paralysis due to herpetic neuropathy. It is not a true hernia (which are caused by distention of the intestine) but is caused by distension of the abdominal wall due to internal pressure in the abdominal cavity, which is caused by motor neuropathy in the abdominal muscles associated with herpes zoster. The exact mechanism of abdominal paralysis is not well understood, but it is suggested that the motor nerves are involved owing to the spread of inflammation from the dorsal root ganglion to the anterior horn cells and nerve roots. A definitive diagnosis is made using CT, magnetic resonance imaging, or electromyography. However, considering patient history and clinical findings, it is possible to make a pseudohernia diagnosis without conducting a detailed investigation. Reportedly, 79.3% of patients with a pseudohernia usually recover spontaneously (mean, 4.9 months) without active treatment.
A careful clinical follow-up would be justified under the correct diagnosis. When examining patients with herpes zoster in the lumbo-abdominal (T10–T12) region, attention should be paid not only to the skin rash and pain but also to changes in abdominal wall distension.
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