Zoster Paresis Research Articles

Varicella Zoster Virus and the Neuro-Attenuated Vaccine Necessity

Varicella Zoster Virus and the Neuro-Attenuated Vaccine Necessity

Enforced expression of microRNA-21 influences the replication of varicella-zoster virus by triggering signal transducer and activator of transcription 3.

Varicella-zoster virus (VZV) causes chronic pain and serious complications, including zoster paresis. However, the mechanism of VZV replication, a critical part of VZV pathogenesis, remains largely unknown and was investigated in the present study. The upregulation of microRNA-21 (miR-21) was identified following VZV infection in vitro by quantitative polymerase chain reaction. The hypothesis that the overexpression of miR-21 activates the signal transducer and activator of transcription 3 (STAT3) signaling pathway was validated by measuring the mRNA expression levels of STAT3 and the anti-apoptotic protein survivin in human malignant melanoma (MeWo) and human embryonic lung fibroblast (HELF) cell lines transfected with miR-21-mimic and comparing them with those in cells transfected with miR-control. To further study the interaction of miR-21, STAT3 and VZV replication, the effects of miR-21 overexpression and STAT3 knockdown were evaluated. Higher virus titers were detected when miR-21 was upregulated in vitro. Moreover, it was identified that significantly lower virus titers were present in MeWo cells in which STAT3 was knocked down. In addition, the overexpression of miR-21 did not stimulate VZV replication in the MeWo cell line when the STAT3 gene was silenced. Therefore, the observations of the present study indicate that the enforced expression of miR-21 promotes the replication of VZV by activating STAT3 in vitro.

The variegate neurological manifestations of varicella zoster virus infection.

Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which the virus becomes latent in ganglionic neurons along the entire neuraxis. With advancing age or immunosuppression, cell-mediated immunity to VZV declines, and the virus reactivates to cause zoster (shingles), dermatomal distribution, pain, and rash. Zoster is often followed by chronic pain (postherpetic neuralgia), cranial nerve palsies, zoster paresis, vasculopathy, meningoencephalitis, and multiple ocular disorders. This review covers clinical, laboratory, and pathological features of neurological complications of VZV reactivation, including diagnostic testing to verify active VZV infection in the nervous system. Additional perspectives are provided by discussions of VZV latency, animal models to study varicella pathogenesis and immunity, and of the value of vaccination of elderly individuals to boost cell-mediated immunity to VZV and prevent VZV reactivation.

Complications of varicella zoster virus reactivation.

Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which virus becomes latent in ganglionic neurons along the entire neuraxis. With advancing age or immunosuppression, cell-mediated immunity to VZV declines and virus reactivates to cause zoster (shingles), which can occur anywhere on the body. Skin lesions resolve within 1-2 weeks, while complete cessation of pain usually takes 4-6 weeks. Zoster can be followed by chronic pain (postherpetic neuralgia), cranial nerve palsies, zoster paresis, meningoencephalitis, cerebellitis, myelopathy, multiple ocular disorders and vasculopathy that can mimic giant cell arteritis. All of the neurological and ocular disorders listed above may also develop without rash. Diagnosis of VZV-induced neurological disease may require examination of cerebrospinal fluid (CSF), serum and/ or ocular fluids. In the absence of rash in a patient with neurological disease potentially due to VZV, CSF should be examined for VZV DNA by PCR and for anti-VZV IgG and IgM. Detection of VZV IgG antibody in CSF is superior to detection of VZV DNA in CSF to diagnose vasculopathy, recurrent myelopathy, and brainstem encephalitis. Oral antiviral drugs speed healing of rash and shorten acute pain. Immunocompromised patients require intravenous acyclovir. First-line treatments for post-herpetic neuralgia include tricyclic antidepressants, gabapentin, pregabalin, and topical lidocaine patches. VZV vasculopathy, meningoencephalitis, and myelitis are all treated with intravenous acyclovir.

Zoster-associated segmental paresis in a patient with cervical spinal stenosis

Segmental zoster paresis is a rare complication of herpes zoster, characterized by focal motor weakness that does not always present simultaneously with skin lesions. Zoster paresis can be easily confused with other neuromuscular or spinal diseases. This case report describes the case of a 72-year-old woman with herpes zoster and cervical spinal stenosis at the same spinal level, where it was difficult to distinguish segmental zoster paresis from cervical radiculopathy combined with motor neuropathy. Although segmental zoster paresis in the upper extremity is rare, it should be included in the differential diagnosis of segmental pain and weakness in the extremities, especially in older or immunocompromised patients. Correct diagnosis is required, to avoid unnecessary surgery and allow timely antiviral treatment.

Zoster paresis: Asymptomatic MRI lesions far beyond the site of rash and focal weakness

We describe a patient with zoster paresis and an MRI that revealed extensive spinal cord lesions from the upper cervical to the lower thoracic spinal cord. Importantly, the patient reported considerable spontaneous improvement in strength 2–3weeks after zoster. This report reveals a previously undescribed remarkable preponderance of MRI lesions far beyond the site of zoster rash and focal lower motor neuron weakness.

Abdominal distention and constipation followed by herpes zoster infection

Abdominal distention and constipation followed by herpes zoster infection

An unusual cause of dyspnea in a patient with cervical herpes zoster

Motor involvement in acute herpes zoster does occur,but is rare. Most causes of zoster paresis are due to the extension of the inflammation to the anterior horn and/or anterior motor roots. We report a female patient with an unusual diaphragmatic paralysis caused by cervical herpes zoster. The lesion, diagnosed by MRI, involved the anterior horn of the cervical spinal cord.

A case of segmental zoster paresis with enhanced anterior and posterior spinal roots on MRI

Herpes zoster is an infectious disease caused by reactivation of the varicella zoster virus (VZV) in the dorsal root ganglia [2]. Neurological complications other than sensory abnormalities such as encephalitis, myelitis, and various lower motor neuron diseases such as polyradiculoneuritis as segmental radiculitis have been reported [7]. Segmental zoster paresis is characterized by focal motor weakness that appears in the same segment where the skin eruptions, neuralgia, and sensory symptoms occur, and is a relatively common complication [1, 3, 6, 7]. We report a patient in whom the radiological findings were consistent with aberration of anterior and posterior spinal roots with zoster paresis. A 73-year-old man developed right shoulder pain and herpes zoster eruptions over the C5 dermatome. Two days later, he found it impossible to lift up the right arm. He was admitted to our hospital with 2-week history of shoulder pain and progressive muscle weakness around the right shoulder. Physical examination on admission showed weakness of the upper extremity in the distribution of the right C5 myotome and sensory disturbance in the right C5 dermatome, but no clinical symptoms of myelitis. Laboratory findings showed VZV-IgM level of 4.30 mg/dl (normal \0.8 mg/dl). Examination of cerebrospinal fluid (CSF) showed 102.8 cells/mm, protein content of 66.8 mg/dl, and elevated varicella zoster virus IgG titer (antibody index [4). Polymerase chain reaction (PCR) of CSF fluid was positive for VZV DNA, but no search for the number of copies was performed. Needle electromyography showed neurogenic changes in the right deltoid and biceps brachii muscles. T1-weighted magnetic resonance imaging (MRI) showed contrast enhancement with gadolinium in the right anterior and posterior C5 spinal roots below the 4th cervical vertebra (Fig. 1b), but no abnormal contrast enhancement of the roots of the 4th and 6th spinal nerves (Fig. 1a, c). Furthermore, T2-weighted MRI showed no abnormal intensity in the cervical spinal cord. The patient was treated with intravenous 1,500 mg acyclovir for 7 days together with rehabilitation. Examination about 1 month later showed improvement of muscle weakness and disappearance of the shoulder pain. The MRI findings suggested VZV reactivation in the dorsal root ganglia, which was localized to the anterior and posterior C5 spinal roots, based on the motor and sensory symptoms of C5 dermatome and myotome. The spread of VZV from the posterior spinal root, or anterior and posterior horn, to the anterior spinal root could have resulted from inflammation. CSF analysis indicated pleocytosis and serologically confirmed VZV. Previous studies reported abnormalities of CSF in 61% of patients with VZV and subclinical extension of viral inflammation into the central nervous system [4]. The clinical symptoms and MRI findings in our patient were not confirmative for myelitis. We postulate the spread of VZV either directly or through the CSF, rather than myelitis, from the posterior spinal root to the anterior spinal root in our patient. The cause of the nerve root enhancement was considered to be due to either viral activation itself or associated inflammation. Previous MRI findings in zoster paresis showed myelitis [3], posterior root with anterior horn [9] and posterior horn [8], suggesting myelitis and anterior root [5], suggesting disruption of the blood–brain barrier. Post mortem M. Yoshioka (&) Y. Kurita M. Hashimoto M. Murakami M. Suzuki Department of Neurology, Aoto Hospital, The Jikei University School of Medicine, 6-41-2 Aoto, Katsushika-ku, Tokyo 125-8506, Japan e-mail: m.yoshioka@jikei.ac.jp

An open-label pilot study of vemurafenib in previously treated metastatic melanoma patients with brain metastases.

8548 Background: Melanoma is a common cause of cerebral metastases, and indicates a poor prognosis. The BRAF inhibitor vemurafenib (V; RG7204, PLX4032) has shown dramatic activity in Phase I and II studies in metastatic melanoma harboring V600-mutated BRAF. These studies excluded patients with active brain metastasis. The activity of V for brain metastases is unknown. Methods: Open label, single arm trial of V to evaluate the safety and efficacy of V in patients with metastatic melanoma with BRAF V600 mutations (by the cobas 4800 BRAF V600 Mutation Test) and non-resectable-brain mets, pretreated by radiotherapy and/or chemotherapy. Patients may have symptoms related to their brain mets and be on a stable dose of steroids. V is administered continuously at the dose of 960 mg BID. Twenty patients are planned to be include in this study. Staging (MRI brain and CT thorax/abdomen) is scheduled every 4 weeks in the first 2 months and then every 8 weeks. In addition, the serum S100 levels are determined. Results: Four patients with V600 BRAF positive melanoma metastatic to the brain and pretreated with temozolamide and/or total brain radiotherapy V are on treatment between 2 and 10 weeks to date. All patients are young (between 24 and 48 years), have 3 to more than 10 brain mets, ECOG PS 0-2 and are on dexamethasone. Two patients were taking morphine to control pain and neurological symptoms. There was no dose reduction for V. AEs included rash, fatigue in two patients and disseminated Herpes zoster and mild transient paresis of nervus facialis in one patient. Two patients’ staging reports are currently available. Patient 1 presented an confirmed partial response in brain and body (RECIST) associated with a reduction of S-100 from 141.6µg/l (pre-treatment) to 4.4µg/l (day 43). Dexamethasone and morphine doses were reduced. Patient 2 showed a minor response in brain and body at week 4 associated with a reduction of S-100 from 35.6µg/l (day 1) to 3.26µg/l (day 15). Conclusions: V has been well tolerated in symptomatic patients with melanoma metastatic to the brain to date. There are early but strong indications for activity in brain mets.

Segmental Zoster Paresis of the Left Upper Limb in a Pediatric Patient

Segmental zoster paresis of the left upper limb in a pediatric patient.Segmental zoster paresis is a rare complication of herpes zoster characterized by focal, asymmetrical motor weakness in the myotome that corresponds to the dermatome of the rash. Segmental zoster paresis typically develops within 2-3 wks of cutaneous zoster and predominantly affects the middle-aged and elderly populations. Motor complications rarely develop in children and young adults, but when they do develop, involvement is usually confined to cranial and truncal muscles, with sparing of the limb musculature. A 10-yr-old boy with Fanconi's anemia developed left upper limb weakness because of involvement of C5 motor roots as a complication of herpes zoster. Recognizing motor zoster as a cause of acute motor weakness in a pediatric patient is important in avoiding unnecessary interventions and optimizing treatment.

A Case of Recurrent Herpes Zoster Leg Paresis Without Rash

ABSTRACTAcute herpes zoster neuralgia is a benign infection affecting the sensory part of the nervous system with a painful vesicular eruption. The authors report a case of a 48-year-old woman patient with right leg paresis followed by herpetic rash. Needle electromyography revealed pathologic findings while lumbar magnetic resonance imaging (MRI) revealed no pathologic findings. The patient was managed with strengthening exercises as well as pain relief for neuralgia. The potential role of antiviral pharmacotherapy in such a case is discussed. The authors describe this case because zoster paresis should be one of the differential diagnoses of girdle muscle weakness and because the rash followed the leg paresis. The clinical implications of the case are discussed, since the patient presented from time to time with relapses of the disease without prominent rash.

Pearls: Neuromuscular Disorders

Various brief clinical observations helpful in the evaluation of patients with neuromuscular disorders are discussed and illustrated. These include features of focal neuropathies, including the neurologic thoracic outlet syndrome, apparent ulnar nerve-innervated hand weakness in radial neuropathies, scapula movement in long thoracic compared with spinal accessory neuropathies, and diaphragm paralysis in segmental zoster paresis. Potential diagnostic errors include multifocal motor neuropathy mistaken for nerve tumor, the pseudoconduction block of vasculitic neuropathy leading to a diagnosis of Guillain-Barré syndrome, and leg paralysis in myelopathy mistaken for early ascending paralysis in Guillain-Barré syndrome. Very focal weakness of limb muscles occurs in myasthenia gravis, similar to the more familiar focal cranial muscle involvement. Fluctuation, not fatigability, in myasthenia gravis is discussed. The presentation of Lambert-Eaton myasthenic syndrome as a nonfluctuating subacute myopathy is emphasized. Patterns of weakness in inclusion body myositis and facioscapulohumeral muscular dystrophy are illustrated.

Occurrence of Segmental Zoster Paresis in the Right Arm of an Adult with Multiple Sclerosis: A casereport

Segmental zoster paresis is a rare complication of cutaneous herpes zoster. Clinical diagnosis of segmental zoster paresis depends upon a history of painful vesicular eruptions in a dermatomal distribution, followed by muscle weakness in the related myotomes. We report the case of a 45-year-old woman with opticospinal type multiple sclerosis with recent cutaneous herpes zoster and right shoulder girdle weakness. Differential diagnosis included multiple sclerosis relapse, zoster myelitis, segmental zoster shoulder paresis, cervical radiculopathy, and shoulder joint or soft-tissue disorders. MRI with gadolinium enhancement of the spinal cord 1 week after the onset of symptoms showed neither new multiple sclerosis plaque nor abnormal contrast-enhanced lesion. Right shoulder soft-tissue sonography revealed normal joint and soft tissue. Needle electromyography 3 weeks after the onset of weakness indicated increased spontaneous activity at the right biceps, anterior deltoid, and C4-C7 paraspinal muscles, as well as increased polyphasic waves at the right biceps muscle. These findings were compatible with recent right cervical polyradiculopathies involving at least the C4 to C7 levels. Therefore, the most likely etiology for her right shoulder girdle weakness was segmental zoster paresis. The patient received early antiviral therapy and intensive rehabilitation. Two months later, her shoulder muscle strength improved although it hadn't recovered to her premorbid status. The functional recovery in her right upper limb was good. Segmental zoster paresis is underdiagnosed in patients with segmental weakness. Needle electromyography is a good tool for assisting diagnosis and prognosis and for following up motor recovery. With early diagnosis, antiviral therapy and rehabilitation therapy can hasten neurological and functional recovery.

Zoster Paresis Misconceived as a Radiculopathy due to Herniated Intervertebral Disc

Herpes zoster is a viral disease of the posterior root ganglion and sensory nerve fiber, which presents clinically with vesicular eruption of the skin, radicular pain and sensory changes in the distribution of the affected ganglion. However, involvement of the motor neurons can be seen as well. If classic cutaneous lesions are present, herpes zoster-related motor paresis is easily diagnosed. Otherwise, t he diagnosis may be more difficult and suspicious, especially if weakness occurs as a symptom before cutaneous lesions appear, or abnormal findings on the MRI are consistent with the signs. There have been few reports of sciatica with motor loss preceding skin lesions. Here, we report a patient with herpes zoster-related motor paresis preceding skin lesions. In the preliminary diagnosis, the herpes zoster-related motor paresis was confused for some structural disorder. (Korean J Pain 2009; 22: 181-185)

Segmental Zoster Paresis of Limbs

Segmental zoster paresis is a relatively rare complication characterized by focal motor weakness, which may occur in limbs affected by herpes zoster. We demonstrate the clinical characteristics of segmental zoster paresis by reviewing the cases of 138 patients, including 3 of our patients. We report 3 patients with zoster paresis of the limbs. Patients 1 and 3 showed motor weakness in the left shoulder and arm after developing a herpetic rash in the left C5-C6 dermatomes. Patient 2 showed weakness in the right thigh and groin after a right L2-L3 herpetic eruption. The electromyograms of all 3 patients showed abnormal spontaneous activity in the affected muscles. Intravenous acyclovir and corticosteroid pulse therapy were added to oral antiviral drugs for patients 1 and 2. All 3 patients recovered favorably. Our review of the literature revealed that antiviral treatment may prevent the occurrence of zoster paresis; however, there is insufficient evidence to show what treatment hastens recovery from zoster paresis. Segmental zoster paresis is still underrecognized by neurologists. Awareness of this disorder is important because it may eliminate unnecessary invasive investigations and lead to appropriate treatment. Further studies on the treatment are necessary.

Isolated double herpes zoster paresis involving the left facial nerve and the right peroneal nerve following disseminated herpes zoster

A 72-year-old Japanese male developed disseminated herpes zoster and could not easily walk due to right drop foot and pain. He soon developed numbness and pain on the left side of his face, and noticed difficulty closing his left eye. The left angle of his mouth dropped. The patient was diagnosed as having a double mononeuropathy (a left facial nerve paresis and a right peroneal nerve paresis) following disseminated herpes zoster. Given that the patient was elderly and had diabetes mellitus, the patient appeared to be an immunocompromised host. We also describe other rare complications of herpes zoster from the published work.

Monoparesis With Complex Regional Pain Syndrome–Like Symptoms due to Brachial Plexopathy Caused by the Varicella Zoster Virus: A Case Report

Eyigor S, Durmaz B, Karapolat H. Monoparesis with complex regional pain syndrome–like symptoms due to brachial plexopathy caused by the varicella zoster virus: a case report. Viral invasion of the motoneurons and the subsequent inflammation in the anterior horn cells by the varicella zoster virus results in a weakness in the area of the cutaneous eruption. The exact mechanism of zoster paresis is uncertain. The occurrence of symptoms resembling complex regional pain syndrome (CRPS) is common in subjects where the herpes zoster (HZ) outbreak affects an extremity, particularly if it is the distal extremity that is involved. We report the case of a 54-year-old man with monoparesis, hyperalgesia, allodynia, edema, and both color and skin-temperature changes in his left arm after a skin eruption. Electrophysiologic examination revealed the partial degeneration of the superior, middle, and inferior truncus in the brachial plexus, with evidence of HZ infection. Magnetic resonance imaging of the cervical spine and brachial plexus showed degenerative changes without any evidence of nerve root compression. Brachial plexopathy may be the direct cause of the reversible upper-limb paresis resulting from HZ with CRPS-like symptoms.

Segmental Zoster Paresis in Patient with Cervical Disc Disease and Shoulder Impingement Syndrome - A case report -

Herpes zoster is a disease caused by the varicella zoster virus which affects the sensory nerves or peripheral branches of the cranial nerves. Segmental motor paresis, one of the complications of herpes zoster, is a rare complication which can occur two to three weeks after the skin rash develops and involves the corresponding muscle segments to the skin lesions caused by herpes zoster. We treated a patient with segmental zoster paresis who had a disorder similar to herpes zoster.

Segmental Zoster Paresis of the Upper Extremity: A Case Report

Yoleri Ö, Ölmez N, Öztura İ, Şengül İ, Günaydın R, Memiş A. Segmental zoster paresis of the upper extremity: a case report. Segmental zoster paresis, a rare complication of herpes zoster, is characterized by focal, asymmetric motor weakness in the myotome that corresponds to the dermatome of the rash. The pathogenesis of segmental zoster paresis is inflammation caused by the spread of the herpes virus. Motor damage may affect the root, plexus, or peripheral nerve. A woman in her early seventies with right shoulder pain and shoulder girdle muscle weakness was diagnosed with involvement of the C5–7 motor roots and upper truncus of the brachial plexus as a complication of herpes zoster. Recognition of herpes zoster as a cause of acute motor weakness is important in avoiding unnecessary interventions as well as in determining the treatment and outcome of the patient. This case is presented to emphasize that herpes zoster infection may be complicated by segmental paresis, which should be considered in the differential diagnosis of acute painful motor weakness of the upper extremity.