CSF and MRI findings in patients with acute herpes zoster

Haanpää, Maija; Dastidar, Prasun; Weinberg, Adriana; Levin, M. B.; Miettinen, A; Lapinlampi, A; Laippala, Pekka; Nurmikko, Turo

doi:10.1212/wnl.51.5.1405

Cited by 183 publications

(114 citation statements)

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“…Haanpää et al (9) found association between MRI brainstem abnormalities and the development of PHN. In our series, acute pain associated with a skin rush was present in only two patients ( Table 1).…”

Section: Discussionmentioning

confidence: 99%

Can pontine trigeminal T2-hyperintensity suggest herpetic etiology of trigeminal neuralgia?

D’Amico

Russo

Ugga

et al. 2016

Quant. Imaging Med. Surg.

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Background: Trigeminal neuralgia (TN) is usually classified into two different categories: idiopathic and secondary. We have investigated the frequency of brainstem pontine lesions in patients with idiopathic TN without multiple sclerosis (MS) or stroke, and their association with herpes zoster (HZ) infection.Methods: Brain magnetic resonance imaging (MRI) studies of 28 patients with TN were retrospectively reviewed. Results:We found seven patients with clinical suspicion of HZ infection and pontine T2 hyperintense lesions, associated with nerve atrophy in one case. Fifteen patients had a neurovascular conflict (NVC) without brainstem involvement, two of them associated with trigeminal atrophy, while four patients had only volumetric reduction of the nerve. In all patients MRI findings were ipsilateral to the side of TN.Conclusions: Pontine T2 hyperintensities could be considered as a MRI sign of TN in patients without NVCs. This "trigeminal pontine sign" (TPS) is frequently found in association with herpetic infections. Methods MRI brain scans of twenty-eight patients (18F, 10M; mean age 52.8±14 years; range of age 26-80 years) with TN without MS or brainstem infarction were retrospectively reviewed by two neuroradiologists with 20 and 24 years of experience, respectively.Eighteen patients (12F, 6M; mean age 50 years; range of age 26-77 years) had idiopathic TN while ten patients (6F, 4M; mean age 50 years; range of age 34-63 years) had a clinical suspicion of a herpes zoster (HZ) infection; only four of these ten patients performed lumbar puncture that confirmed the diagnosis.In all cases a brain MRI was performed (Gyroscan Intera, 1.5 T, Philips Medical System, Best, The Netherlands), including FLAIR (TR: 8,005 ms, TE: 100 ms, TI: 2,200 ms, matrix: 256×192, slice thickness: 5 mm), Fast Spin-Echo (FSE) T1-and T2-weighted (TR: 583-4,454 ms, TE: 15-100 ms, matrix: 244×194−384×288, slice thickness: 5 mm, respectively) sequences; axial three-dimensional (3D) FSE T2 with a driven equilibrium pulse (DRIVE) sequence (TE: 250; TR: 1,500; flip angle: 90°; matrix: 256×256; slice thickness: 1×1×1 mm; FOV: 130×130) and magnetic resonance angiography (MRA) were performed to depict NVC and nerve atrophy. MRA was performed without contrast medium injection by using a 3-dimensional time-of-flight sequence (3D TOF, TE: 65 ms; TR: 6.9 ms; flip angle: 20°; matrix: 160×160; slice thickness: 1.40 mm; FOV: 175×200 mm). Multi planar reformation (MPR) and maximum intensity projection (MIP) reconstructions were subsequently analyzed.We evaluated the presence of brainstem lesions and their correlation with the side of the pain and the TN category. ResultsSeven patients with HZ infection showed hyperintense pontine areas on turbo spin echo (TSE) T2-weighted and FLAIR images, which we called "trigeminal pontine sign" (TPS), all of them without a NVC. Their data were summarized in Table 1. MRI was always consistent with the side of the pain. These lesions had a linear appearance, involving the pathway from the trigeminal root entry zone (...

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Section: Discussionmentioning

confidence: 99%

Can pontine trigeminal T2-hyperintensity suggest herpetic etiology of trigeminal neuralgia?

D’Amico

Russo

Ugga

et al. 2016

Quant. Imaging Med. Surg.

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“…Cerebrospinal fluid examination reveals white blood cells with lymphocytic predominance, protein is normal or high and glucose level is normal (4,11,16). In a study performed in 50 immunocompetent adults, pleocytosis was found in 21 subjects (42%) and increased protein was found in 12 subjects (24%), although no clinical finding of myelitis, aseptic meningitis or encephalitis was present in any subject (17). The definite diagnosis is made by demonstrating VZV DNA in CSF by PCR together with clinical findings (18).…”

Section: Discussionmentioning

confidence: 97%

Zona zoster enfeksiyonu sırasında gelişen aseptik menenjit

...

2012

Tpa

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Sum maryZona zoster is generally a benign disease in immunocompetent children. In immunocompromised children, there is a risk of dissemination. Zona zoster rarely causes some neurological complications such as myelitis, aseptic meningitis, encephalitis and ventriculitis in both immunocompetent and immunocompromised children. A 17-year-old girl who had bone marrow transplantation for thalasemia major was admitted to our hospital with fever, itchy rash on the right chest and axillary region and diagnosed as zona zoster. She had severe headache and vomiting on follow-up. Lumbar puncture was performed, because of positive neck stiffness and meningeal irritation signs and pleocytosis and protein elevation were detected in the cerebrospinal fluid (CSF). The diagnosis of aseptic meningitis due to zona zoster was confirmed by VZV-PCR in the CSF . She cured without sequelea after the administration of acyclovir treatment for 10 days. If symptoms such as headache and vomiting develop in immunocompromised children with zona zoster, neurological complications including aseptic meningitis should be remembered. (Turk Arch Ped 2012; 47: 142-5)

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“…24,25 Like DPN, PHN has been associated with neuroinflammation and a loss of large and small sensory fibers. 26 The etiology of neuropathic pain states encompasses many other conditions, including prolonged treatment with chemotherapeutic agents, infections such as HIV, and from idiopathic and genetic sources. The common causes of neuropathic pain are listed in Table 2.…”

Section: Neuropathic Pain: Definitions and Clinical Considerationsmentioning

confidence: 99%

“…31,32 Furthermore, MRI studies performed on the spinal cord of patients after a herpes zoster outbreak showed abnormal deafferentation only in those that developed PHN. 26 Neuropathic pain is best considered as a complex set of abnormal physiologic processes incited by trauma, a noxious event or a disease state. 22,33 Accordingly, it should not be considered as a syndrome in and of itself, but as a symptom of other neurologic dysfunctions.…”

Section: Neuropathic Pain: Definitions and Clinical Considerationsmentioning

confidence: 99%

Challenges in the development of novel treatment strategies for neuropathic pain

Ossipov

Porreca

2005

Neurotherapeutics

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Summary:Neuropathic pain might best be considered as a collection of various pain states with a common feature, that being symptoms suggestive of dysfunction of peripheral nerves. The development of therapeutic options for the treatment of neuropathic pain is complicated significantly by several factors. Neuropathic pain may arise from widely diverse etiologies such as physical trauma, disease, infection, or chemotherapy. Symptoms indicative of neuropathic pain may also arise in individuals with no evidence of any type of nerve trauma (idiopathic). Although neuropathic pain is a substantial health care issue, it is relatively uncommon and only occurs in a small fraction (Ͻ10%) of individuals with these initiating factors. Moreover, the efficacy of treatment protocols, even against the same type of symptoms, differ depending on the underlying initiating cause of the neuropathy. Although these observations strongly suggest that there are predisposing factors that may impart susceptibility to the development of neuropathic pain, no common predisposing factors or genetic markers have been satisfactorily identified. Because of these vagaries, treatment of neuropathic pain has been based on trial and error. However, recent progress in the understanding of neurophysiologic changes that accompany peripheral nerve dysfunction indicate that regulation of ion channels that maintain membrane potentials or generate action potentials may provide an important therapeutic approach. Neuropathic pain is accompanied by increased activity of peripheral nociceptors, which is produced in part by changes in levels of specific calcium and sodium channels. The identification of sodium and/or calcium channels subtypes that are expressed almost exclusively on nocicpetors may provide a way of regulating the activity of exaggerated nociceptor function without altering other sensory modalities. Thus, the selective targeting of ion channels may represent a viable therapeutic target for the management of the neuropathic pain state, regardless of etiology.

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CSF and MRI findings in patients with acute herpes zoster

Abstract: Subclinical extension of viral inflammation into the CNS occurs commonly in HZ. This finding may have implications for treatment of HZ and prevention of various associated complications.

Cited by 183 publications

References 10 publications

Can pontine trigeminal T2-hyperintensity suggest herpetic etiology of trigeminal neuralgia?

Can pontine trigeminal T2-hyperintensity suggest herpetic etiology of trigeminal neuralgia?

Zona zoster enfeksiyonu sırasında gelişen aseptik menenjit

Challenges in the development of novel treatment strategies for neuropathic pain

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