Abdominal pseudohernia is a condition characterized by the protrusion of abdominal viscera through a weakened area of the abdominal wall without a hernia sac. Various causes, including spinal disorders and trauma, can lead to this condition; however, the most common cause is reported to be herpes zoster. We present a rare case of spontaneous resolution of abdominal pseudohernia following lung cancer surgery. A 71-year-old male presented with left upper abdominal bulging and pain. A CT scan performed at the time incidentally revealed a nodular lesion in the right lower lobe, suspicious for lung cancer. Single-port thoracoscopic surgery was performed, and the final diagnosis was right lower lobe lung squamous cell carcinoma. Following the lung cancer surgery, the left upper abdominal bulging spontaneously resolved within one week. In this case, we hypothesize that the immune dysregulation caused by lung cancer increased the activity of the herpes zoster virus, leading to the development of pseudohernia. The spontaneous resolution of the pseudohernia is thought to be due to the improvement of immune dysregulation after surgery.

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BACKGROUND: Facial herpes is a common form of the herpes simplex virus-1 infection and usually presents as vesicles near the mouth, nose, and periocular sites. In contrast, we observed a new facial symptom of herpes on the entire face without vesicles.
METHODS: A 33-year-old woman with a history of varicella infection and shingles since an early age presented with sarcoidosis of the entire face and neuralgia without oral lesions. The patient was prescribed antiviral treatment with valacyclovir and acyclovir cream. One day after drug administration, facial skin lesions and neurological pain improved. Herpes simplex without oral blisters can easily be misdiagnosed as pimples upon visual examination in an outpatient clinic.
CONCLUSIONS: As acute herpes simplex is accompanied by neuralgia, prompt diagnosis and prescription are necessary, considering the pathological history and health conditions.

UNASSIGNED: Solid organ transplant recipients are at high risk for developing severe zoster-associated neuralgia, and the pharmaceutic therapies of pain management for these patients with limited organ function are challenging. Intravenous lidocaine infusion showed positive analgesic effects and is used for the management of neuropathic pain. This case series reports the safety and effectiveness of intravenous lidocaine infusion in the treatment of intractable zoster-associated neuralgia in solid organ transplant recipients.
UNASSIGNED: Five solid organ transplant recipients suffering from refractory zoster-associated neuralgia (numeric rating scale 8-10, despite using high doses of antiepileptic drugs or combined with opioids) were enrolled. Intravenous lidocaine (5 mg/kg ideal bodyweight) was administered over 1.5 h with the monitoring of vital signs. Pain intensity, patient satisfaction, adverse events, typical liver, and kidney function were evaluated. All subjects reported high satisfaction with their treatment and effective pain relief at the 6-month follow-up. One patient experienced short and mild numbness in the mouth and dizziness after the therapy, but no major adverse reactions were reported.
UNASSIGNED: This case series provides evidence that intravenous lidocaine infusion provided effective pain relief as an analgesic treatment option for transplant patients with intractable zoster-associated neuralgia.

BACKGROUND: We present a case of a 29-year-old male patient without immunodeficiency who suffered from rapid osteonecrosis and tooth exfoliation resulting from herpes zoster (HZ) infection in the left maxillary branch of the trigeminal nerve. Various complications associated with shingles infections have been reported, cases of osteonecrosis and tooth exfoliation due to HZ infection among young people without immunodeficiency are rare. In this case, we focus on the particular manifestation of HZ infection.
METHODS: The patient presented with clusters of erythema and papules, along with non-hemorrhagic blisters on the left face and the loss of the left upper incisor. All lesions were localized to the left side of the face without exceeding the midline. After receiving antibacterial and antiviral treatment, successful control over the infection was achieved; however, he experienced the loss of all upper teeth on the left side except for the first and second upper left molars.
CONCLUSIONS: This case highlights that rapid osteonecrosis and tooth exfoliation may occur among young individuals without immunodeficiency after HZ infection. HZ infection of the face should be taken very seriously to obtain prompt treatment to prevent the rare complications of bone necrosis and tooth loss as much as possible.

BACKGROUND: Herpes zoster is an infectious skin disease caused by the reactivation of the varicella zoster virus (VZV), which has been latent in the posterior root ganglia of the spinal cord or cranial ganglia for an extended period. Neurological complications caused by herpes zoster include aseptic meningitis, white matter disease, peripheral motor neuropathy, and Guillain-Barré syndrome. However, reduced unilateral sweating caused by the VZV is very rare.
METHODS: This article reports the case of a 34-year-old woman who was admitted to our hospital with sore throat, dizziness, and reduced sweating on the left side of her body. Physical examination found herpes lesions on the left upper lip and left external ear canal (scabbed) and reduced sweating on the left side of the body. Head magnetic resonance imaging (MRI) with contrast showed no abnormalities. After a lumbar puncture, the patient was diagnosed with viral meningitis by VZV infection. The electromyographic skin sympathetic reflex indicated damage to the left sympathetic nerve.
CONCLUSIONS: Secondary unilateral sweating reduction is a rare neurological complication of herpes zoster, caused by damage to the autonomic nervous system. Literature review and comprehensive examination indicated that the reduced unilateral sweating was due to the activation of latent herpes zoster virus in the autonomic ganglia which has damaged the autonomic nervous system. For patients who exhibit acute hemibody sweat reduction, doctors should consider the possibility of secondary autonomic nervous system damage caused by herpes zoster.

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A 19-year-old young man presented with prodromal symptoms including fever and sore throat, followed by the development of scattered rashes in the perianal and penile regions. Monkeypox (MPX) was confirmed using polymerase chain reaction (PCR) of lesions. On the third day after complete resolution of the initial rash, the patient developed a new rash, which was diagnosed as secondary herpes zoster (HZ). Therefore, clinicians should not only focus on the accurate diagnosis of monkeypox, but also be alert to secondary herpes zoster.

The varicella-zoster virus reactivates to cause the \"herpes zoster\" (HZ). \'\'Varicella-zoster virus\'\' (VZV) termed as \'\'HHV-3\'\' or \'\'human herpesvirus-3\'\' infection causes herpes zoster. Varicella, the primary form of the virus, is chickenpox, and the secondary form of the virus is herpes zoster also called shingles. During prior chicken pox episodes, this virus enters the body through cutaneous nerve endings and becomes dormant in the dorsal root ganglia. It sometimes affects the orofacial region and appears as unilaterally distributed burning pain, multiple, painful vesicular lesions, and ulcerations. Immunocompromised people are more likely to have disseminated zoster, which is defined as the involvement of three or more dermatomes. These are most likely to occur in elderly, immunocompromised patients, patients undergoing cancer chemotherapy, patients on immunosuppressants, and patients suffering from AIDS. This is a study of a male geriatric patient, aged 74 years, who reported unilateral pain, swelling, as well as multiple ulcerations on the left side of his face, extraorally as well as intraorally. The case was diagnosed as a herpes zoster infection involving V1 and V2 dermatome of the trigeminal nerve.

BACKGROUND: Reactivation of the varicella zoster virus (VZV) results in herpes zoster (HZ), which is a painful unilateral rash with a typical dermatomal distribution. HZ may be followed by postherpetic neuralgia (PHN), vasculopathy, myelopathy, retinal necrosis, and cerebellitis. Vasculopathy can cause ischemic stroke, aneurysms, arterial dissection, transient ischemic attack, and rarely, peripheral arterial disease (PAD). The possible mechanism is that the VZV travels to the arteries through the sensory ganglia, leading to inflammation and pathological vascular remodeling, which result in vasculopathy.
METHODS: Here, we describe a rare case of femoral artery occlusion induced vasculopathy 5 years after HZ. A 65-year-old woman visited our pain clinic with persistent pain following HZ that occurred 3 months earlier. She had several rash scars on the right thigh along with a continuous throbbing, shooting, and sharp pain. The patient was diagnosed with PHN and prescribed with medications that relieved the leg pain. The symptoms remained stationary for almost 5 years. She presented again with complaints of a paroxysmal tingling sensation in the right thigh and claudication due to increased pain, which had begun 6 months prior. She reported leg pain after walking for 10 minutes. Lumbar spine magnetic resonance imaging (MRI) revealed foraminal stenosis at the level of right L2, with no abnormality below L2. Subsequently, the patient was evaluated for vascular diseases. Lower extremity ultrasonography and computed tomography (CT) angiography revealed stenosis and thrombotic occlusions in the right superficial femoral and tibial arteries as well as the left middle femoral and tibial arteries. Surgical revascularization via percutaneous angioplasty was performed bilaterally. The leg pain was relieved after the procedure and the claudication improved.
CONCLUSIONS: Peripheral artery occlusion is a rare phenomenon following HZ. In cases involving changes in HZ symptoms, further evaluation is required for potential vasculopathy.