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1/13. Jugular foramen syndrome caused by varicella zoster virus infection in a patient with ipsilateral hypoplasia of the jugular foramen.

    We report a patient with acute cranial polyneuropathy with unilateral involvement of the ninth, tenth, and eleventh cranial nerves. Although this patient lacked a typical cutaneous herpetic manifestation, elevated levels of IgM and IgG antibodies to varicella zoster virus (VZV) in both the serum and cerebrospinal fluid confirmed the clinical diagnosis of VZV infection and zoster sine herpete. Coexisting hypoplasia of the ipsilateral jugular foramen was detected using three-dimensional, surface-rendering displays reconstructed from the cranial helical CT scan. The patient recovered almost completely following treatment with an anti-inflammatory corticosteroid. Anatomical narrowing of the jugular foramen in this patient may have contributed to entrapment of the affected nerves at their passage through the foramen. ( info)

2/13. Varicella zoster meningoencephalitis following treatment for dermatomal zoster in an alloBMT patient.

    herpes zoster infections are frequently observed after allogeneic bone marrow transplantation (alloBMT). In the majority of cases, the infection is restricted to specific dermatomes and responds to oral acyclovir, without visceral dissemination. We report the case of a 40-year-old male who developed dermatomal herpetic infection 8 months post alloBMT. The herpetic rash responded well to treatment with high-dose oral acyclovir. However, within a week of cessation of therapy, the patient re-presented with dermatomal zoster and meningoencephalitis. Although the cutaneous lesions resolved with intravenous acyclovir, clinical features of meningoencephalitis persisted, along with evidence of varicella zoster virus (VZV) dna in cerebrospinal fluid (CSF). A satisfactory response to treatment was observed only after the addition of intravenous foscarnet to acyclovir. Based on our experience with this patient, we suggest that in a subset of alloBMT recipients, late dermatomal herpes zoster infections may respond only partially to treatment with standard oral acyclovir. The use of oral acyclovir preparations with higher bioavailability (valacyclovir) or intravenous acyclovir early on may prevent the considerable morbidity associated with disseminated zoster infection. bone marrow transplantation (2000) 26, 795-796. ( info)

3/13. Varicella-zoster virus limbic encephalitis in an immunocompromised patient.

    A case of limbic encephalitis in a patient who had undergone prolonged immunosuppressive treatment with i.v. cyclophosphamide and oral prednisolone for a microscopic polyangeitis is reported. A brain MRI scan revealed symmetric mesial temporal lobe lesions. Studies of cerebrospinal fluid (CSF) revealed a positive PCR for varicella-zoster virus (VZV) dna in 2 separate samples. Owing to a delay in diagnosis, intravenous acyclovir was initiated only after 11 d of symptoms. PCR of CSF for VZV dna became negative on day 14 of treatment while brain lesions had resolved on subsequent MRI scans. limbic encephalitis is a novel form of VZV infection. When brain imaging is suggestive of limbic encephalitis in an immunocompromised patient, PCR of CSF for VZV dna should be performed, as early antiviral treatment may improve the outcome. ( info)

4/13. Varicella-zoster virus acquired at 4 months of age reactivates at 24 months and causes encephalitis.

    Varicella-zoster virus (VZV) reactivation in the brain caused encephalitis in a 2-year-old immunocompetent child who had chickenpox 20 months before. Radiologic findings were consistent with large to medium-vessel-vasculitis. VZV-dna was detected in cerebrospinal fluid. Early acquisition of VZV may predispose to major neurologic complications that can occur years after the primary infection. ( info)

5/13. Encephalitis related to primary varicella-zoster virus infection in immunocompetent children.

    INTRODUCTION: Encephalitis is a rare complication of primary varicella-zoster virus (VZV) infection in immunocompetent children. methods: The clinical and laboratory findings of two girls with VZV-related encephalitis are reported. RESULTS: Both children presented with focal epileptic seizures, corresponding to cortical/subcortical as well as white matter lesions. The first showed a typical vesicular skin rash. She was easily diagnosed and made a rapid recovery during acyclovir and steroid treatment. In the second girl, a preceding measles-mumps-rubella virus vaccination and the absence of skin vesicles were misleading with respect to the diagnosis, which was finally proven by IgG seroconversion and intrathecal synthesis of IgG antibodies to VZV. She developed left parieto-occipital tissue necrosis and recovered only transiently during initial acyclovir/steroid treatment. Eight weeks after onset, progressive white matter demyelination and the occurrence of erythema nodosum in the lower limbs necessitated a second 4-month course of oral steroids. The VZV PCR from cerebrospinal fluid was negative in both children. CONCLUSIONS: Primary VZV infection may cause severe encephalitis that may occur without skin vesicles and lead to a chronic course with systemic vasculitis. The coincidence of vaccination and neurologic diseases offers no proof per se of a causal relationship. ( info)

6/13. Existence of acute lymphoblastic leukemia and osteosarcoma in a child.

    The existence of acute lymphoblastic leukemia (ALL) and osteosarcoma is described. An 8-year-old girl had osteosarcoma diagnosed on radiologic and pathologic examination during ALL maintenance treatment. Cytogenetic analyses in primary cell culture of osteosarcoma tissue from the patient showed complex chromosomal abnormalities including t(1;19), usually seen in B precursor cell ALL, and del 13, found in a great majority of primary osteosarcomas. To show the possibility of the existence of the genetic susceptibility caused by gene rearrangements, we used molecular technique. But we could not determine any association between gene and genetic susceptibility. ( info)

7/13. Striatal encephalitis after varicella zoster infection complicated by Tourettism.

    We describe a case of encephalitis after primary varicella zoster infection with localised basal ganglia imaging abnormalities. The patient subsequently developed a chronic tic disorder with attention deficit disorder. This case furthers the proposed association between Tourettism and the basal ganglia. ( info)

8/13. Subdural empyema and herpes zoster syndrome (Hunt syndrome) complicating removal of third molars.

    We report a case of subdural empyema and herpes zoster syndrome (Hunt syndrome) complicating routine removal of third molars. Subdural empyema is an extremely rare but life-threatening complication of dental sepsis arising spontaneously or after dental surgery. The clinician should be familiar with its presentation and have a high index of suspicion, because late recognition and delay in its treatment can increase the associated morbidity and mortality. Surgical procedures and in particular maxillofacial surgery have also been known to trigger varicella zoster reactivation resulting in Hunt syndrome. Some patients develop the characteristic rash several days after the onset of facial weakness, so that Hunt syndrome may initially be misdiagnosed as Bell's palsy. We highlight the difficulties in diagnosing Hunt syndrome and argue the case for early treatment of all patients with Hunt syndrome and Bell's palsy with a combination of systemic steroids and antiviral drugs. ( info)

9/13. Varicella-zoster virus encephalitis in an AIDS patient.

    A 37-year-old man with a three-year history of acquired immunodeficiency syndrome was admitted with impaired consciousness, seizures and fever. He was on highly active antiretroviral therapy and on neurotoxoplasmosis secondary prophylaxis. Laboratory exams from two months before showed a CD4 cell count of 37/microL and a viral load of 230,000 copies/mL. Three months before admission he developed herpetic skin rash in the right trunk and acyclovir was added to his treatment regimen. On physical exam he was drowsy and had motor and sensory aphasia. The patient had elevated protein levels and normal pressure in the cerebrospinal fluid (CSF). Contrast enhanced computed tomography scan of the brain showed a hypodense lesion in the left parietal lobe, with poorly defined margins and no contrast enhancement. The magnetic resonance scan (MRI) showed multiple hyperintensities in T2-weighted image in white and grey matters and hypointense products of hemorrhage in both hemispheres and in the cerebellum. He was empirically treated with intravenous acyclovir and prednisone. Viral dna of Varicella-zoster virus (VZV) was detected in the CSF by means of polymerase chain reaction (PCR) analysis. acyclovir was continued for 10 days and the patient became well, with improvement of aphasia.We present a case of VZV encephalitis, confirmed by nested PCR, in a patient with suggestive MRI findings, who succeeded with treatment. VZV encephalitis is a rare opportunistic infection, occurring in 0.1 to 4% of AIDS patients with neurological disease; it is related to severe immunodeficiency and has a high mortality. ( info)

10/13. Fatal varicella associated with selective natural killer cell deficiency.

    A 2-year-old girl with recurrent severe varicella infections had a fatal outcome. Studies of cellular and humoral immunity were normal. No natural killer (NK) cells were detected, and NK activity was markedly decreased. The interleukin (IL)15/IL15R signaling pathway was intact. This case emphasizes the role of NK cells in controlling herpes viral infection. ( info)
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