Clinical spectrum and prognosis of neurological complications of reactivated varicella-zoster infection: the role of immunosuppression.

Immunosuppressed patients are at higher risk for developing herpes zoster (HZ), and neurological complications are frequent in them. However, the influence of immunosuppression (IS) on the severity and prognosis of neurological complications of varicella-zoster virus (VZV) reactivation is unknown. We studied retrospectively patients with neurological complications due to VZV reactivation who attended our hospital between 2004 and 2019. We aimed to assess the clinical spectrum, potential prognostic factors, and the influence of the immune status on the severity of neurological symptoms. A total of 98 patients were included (40% had IS). Fifty-five patients (56%) had cranial neuropathies which included Ramsay-Hunt syndrome (36 patients) and cranial multineuritis (23 patients). Twenty-one patients developed encephalitis (21%). Other diagnosis included radiculopathies, meningitis, vasculitis, or myelitis (15, 10, 6, and 4 patients, respectively). Mortality was low (3%). At follow-up, 24% of patients had persistent symptoms although these were usually mild. IS was associated with severity (defined as a modified Rankin scale greater than 2) (odds ratio, 4.23; 95% confidence interval, 1.74-10.27), but not with prognosis. Shorter latency between HZ and neurologic symptoms was the only factor associated with an unfavorable course (death or sequelae) (odds ratio, 0.82; 95% confidence interval, 0.71-0.95). In conclusion, the clinical spectrum of neurological complications in VZV reactivation is wide. Mortality was low and sequelae were mild. The presence of IS may play a role on the severity of neurological symptoms, and a shorter time between HZ and the onset of neurological symptoms appears to be a negative prognostic factor.

Can bacterial infection by low virulent organisms be a plausible cause for symptomatic disc degeneration? A systematic review.

STUDY DESIGN: Systematic review and meta-analysis. OBJECTIVE: To review and assess the current evidence from the literature on the potential association between disc infection with the development of symptomatic degenerative disc disease. SUMMARY OF BACKGROUND DATA: The potential relationship between disc infection- and disc degeneration-related symptoms remains controversial, with contradictory evidence available in the literature. Several studies have demonstrated the presence of infected extruded nucleus tissue from first-time disc herniations, implicating the role of disc microbial infection as a pathway for disc degeneration. In contrast, other studies reported very low prevalence of bacterial infection in samples from patients with sciatica, quoting contamination as the predominant source. To summarize the available evidence to date, a systematic review and meta-analysis was conducted. METHODS: A comprehensive search from 6 electronic databases was performed for studies investigating the potential relationship between disc infection as a cause for degenerative disc disease and symptomatic neck/back pain or radiculopathy. Random-effects meta-analysis of proportions and odds ratio with 95% confidence intervals was used to pool the available evidence. RESULTS: Nine relevant studies involving 602 patients with degenerative disc disease or pain were identified. From 6 studies supporting the role of infection in the pathophysiology of disc degeneration, the pooled infection prevalence was 45.2% (34.5%-56.0%). Overall pooled prevalence in all studies was 36.2% (24.7%-47.7%). Proportion of disc infections was higher in patients with symptomatic disc disease than in patients without (37.4% vs. 5.9%; odds ratio, 6.1; 95% confidence intervals, 1.426-25.901). The majority of infections were due to Propionibacterium acnes in 59.6% (43.2%-76.1%). CONCLUSION: From the limited evidence available, the possibility that disc infection may be linked with disc degeneration should not be ruled out. There is a need to investigate this further through larger, adequately powered multi-institutional studies with contaminant arm to control for specimen contamination. LEVEL OF EVIDENCE: 2.

PNET spine: morbid and mortal, but ignored till late.

Spinal primitive neuroectodermal tumor (PNET) is rare. We present clinical, radiologic profile and treatment outcome of 15 spinal PNET patients from June 2003 to March 2010 treated with chemoradiotherapy. Median duration of backache was 6.5 months; all had features of myelopathy and/or radiculopathy; 5/15 (33.3%) patients were diagnosed initially as spinal tuberculosis. The event-free survival (EFS) was 24.73% at a median follow-up of 22 months. Complete functional recovery to treatment significantly predicted better EFS; 4 patients discontinued treatment because of poor functional recovery. It is important to recognize spinal PNET early to prevent permanent neurological damage, which in turn would improve compliance, quality of life, and perhaps EFS.

Eosinophilic radiculomyeloencephalitis: an angiostrongyliasis outbreak in American Samoa related to ingestion of Achatina fulica snails.

For the first time in American Samoa an outbreak of eosinophilic radiculomyeloencephalitis was related to eating giant African snails (Achatina fulica) infected with Angiostrongylus cantonensis. Among 24 Korean fisherman sharing the same infective meal, 16 who ate raw or partially cooked snails became ill; five who ate boiled snails and three who ate none remained well. The ensuing illnesses began within 1-6 days, persisted up to 10 weeks, and were characterized by both peripheral blood and spinal fluid eosinophilia, severe pains, weakness and hyporeflexia of the legs, and dysfunction of the bladder and bowels. Eight patients also had transient hypertension and/or lethargy, and three became comatose. One man died 17 days after eating the infected snails, and maturing larvae of A. cantonensis were found in his spinal cord. Enzyme-linked immunosorbent assay titers for antigens of A. cantonensis were elevated to 1:64 or greater (mean 1:128) in all 10 patients tested. Treatment with thiabendazole had no appreciable effect on the clinical course of the illness.