Validation of a translated, culturally adapted questionnaire. To translate and culturally adapt a Polish version of the Oswestry Disability Index (ODI) and to validate its use in Polish patients. The ODI is among the most popular questionnaires used to evaluate back pain-related disability. To our knowledge no validated Polish version of the index was available at the time our study was initiated. The questionnaire was translated and culturally adapted by 2 independent translators and approved by expert committee. Final version was included in the booklet consisting in addition of a previously validated Roland-Morris disability questionnaire, VAS for low back and leg and 3 Likert scale questions (pain medications, pain frequency, disability). It was tested on 169 patients with chronic low back pain, 164 (97%) of them were enrolled, and 84 of 164 (53%) returned the completed retest booklet within 2 to 14 days after the baseline test. There were no differences between the 2 groups in demographic and clinical parameters. Test-retest reliability, internal consistency, and construct validity were investigated. The mean ODI (standard deviation [SD]) was 48.45 (18.94); minimum 2, maximum 94. The Cronbach α for baseline questionnaires (n = 164) was 0.90. Concurrent validity, measured by comparing ODI responses with the results of the Roland-Morris disability questionnaire score was very good (r = 0.607, P < 0.001). The correlation with VAS back was fair (r = 0.37, P < 0.001) and with VAS leg was good (r = 0.56, P < 0.001). The tested ODI had excellent test-retest reliability, the intraclass correlation coefficient was 0.97 and standard error of measurements was 3.54, the resulting minimal detectable changes at the 95% confidence level was 10. The results of this study indicate that the Polish version of the ODI is a reliable and valid instrument for the measurement of disability in Polish-speaking patients with lower back pain.

The mechanisms responsible for vascular autoregulation in the brain during changes in mean arterial blood pressure are ambiguous. Potentially, adenosine, a purine nucleoside and potent vasodilator, may be involved as earlier studies have documented an increase in brain adenosine concentrations with cerebral ischemia and hypotension. Consequently, we tested the hypothesis that adenosine is involved in vasodilatation during hypotension within the autoregulatory range (>50 mm Hg) by exposing adenosine 2a receptor (A2aR) knockout and wild type (WT) mice to short (2 to 5 mins) periods of hypotension. We found that autoregulation was significantly ( PA2b:10–85>1), ZM-241385, in a dose (1, 5, 10 mg/kg, intraperitoneally)-related manner, attenuated autoregulation in WT mice. In knockout mice treated with ZM-2413585 (5 and 10 mg/kg), autoregulation was further impaired indicating that A2b receptors also participated in cerebral vasodilatation. Treatment with dipyridamole (1.0 mg/kg) that increases extracellular concentrations of adenosine improved autoregulation in the A2aR knockout mice. We would conclude that adenosine through both A2a and A2b receptors is involved in physiologic vascular regulation during hypotension even within the autoregulatory range.

OBJECTIVE: A review article assessing all the risk factors reported in the literature for postoperative cerebellar mutism syndrome (pCMS) among children remains absent. The authors sought to perform a systematic review and meta-analysis to evaluate this issue. METHODS: PubMed, Embase, and Web of Science were queried to systematically extract potential references. The articles relating to pCMS were required to be written in the English language, involve pediatric patients (≤ 18 years of age), and provide extractable data, which included a comparison group of patients who did not develop pCMS. The quality of the included studies was evaluated using the Newcastle-Ottawa Scale. Data were pooled using RevMan 5.4, and publication bias was assessed by visual inspection for funnel plot asymmetry. The study protocol was registered through PROSPERO (ID: CRD42021256177). RESULTS: Overall, 28 studies involving 2276 patients were included. Statistically significant risk factors identified from univariate analysis were brainstem invasion (OR 4.28, 95% CI 2.23–8.23; p < 0.0001), fourth ventricle invasion (OR 12.84, 95% CI 4.29–38.44; p < 0.00001), superior cerebellar peduncle invasion (OR 6.77, 95% CI 2.35–19.48; p = 0.0004), diagnosis of medulloblastoma (OR 3.26, 95% CI 1.93–5.52; p < 0.0001), medulloblastoma > 50 mm (OR 8.85, 95% CI 1.30–60.16; p = 0.03), left-handedness (OR 6.57, 95% CI 1.25–34.44; p = 0.03), and a vermis incision (OR 5.44, 95% CI 2.09–14.16; p = 0.0005). On the other hand, a tumor located in the cerebellar hemisphere (OR 0.23, 95% CI 0.06–0.92; p = 0.04), cerebellar hemisphere compression (OR 0.23, 95% CI 0.11–0.45; p < 0.0001), and intraoperative imaging (OR 0.36, 95% CI 0.18–0.72; p = 0.004) reduced the risk of pCMS. CONCLUSIONS: This study provides the largest and most reliable review of risk factors associated with pCMS. Although some risk factors may be dependent on one another, the data may be used by surgeons to better identify patients at risk for pCMS and for intervention planning.

Objectives: Cervical disc arthroplasty (CDA) has become an alternative treatment for cervical radiculopathy and myelopathy. This technique preserves appropriate motion at both the index and adjacent disc levels and consequently may prevent adjacent segment degeneration (ASD). The authors performed a meta-analysis to compare the safety and efficacy of CDA to those of the gold standard, anterior cervical discectomy and fusion (ACDF). Both surgical and clinical parameters were employed to verify the hypothesis that CDA can reduce the risk of ASD. Methods: The meta-analysis comprised high-quality randomized controlled trials that compared CDA and ACDF treatments of cervical degenerative disc disease. Included papers reported data for at least one of the following outcomes: 1) surgical parameters, 2) questionnaire clinical indices (pre- and postoperative values), and 3) complication rates at 24 months; in addition, for ASD we analyzed 60 month or longer follow-ups. We used mean differences (MDs) or ORs to compare treatment effects between CDA and ACDF. Results: Twenty studies with 3,656 patients (2,140 with CDA and 1,516 with ACDF) met the inclusion criteria. CDA surgery, with mean duration longer than that of ACDF, was associated with higher blood loss. Visual analog scale neck pain score was significantly smaller for CDA (mean difference =-2.30, 95% CI [-3.72; -0.87], P=0.002). The frequency of dysphagia/dysphonia (OR =0.69, 95% CI [0.49; 0.98], P=0.04) as well as the long-term ASD rate for CDA was significantly smaller (OR =0.33, 95% CI [0.21; 0.50], P<0.0001). Conclusion: A significantly lower probability of ASD reoperations in the CDA cohort after a 60-month or longer follow-up was the most important finding of this study. Despite the moderate quality of this evidence, the pooled data corroborated for the very first time that CDA was efficacious in preventing ASD.

The introduction of the term Persistent Spinal Pain Syndrome (PSPS-T1/2), replacing the older term Failed Back Surgery Syndrome (FBSS), has significantly influenced our approach to diagnosing and treating post-surgical spinal pain. This comprehensive review discusses this change and its effects on patient care. Various diagnostic methods are employed to elucidate the underlying causes of back pain, and this information is critical in guiding treatment decisions. The management of PSPS-T1/2 involves both causative treatments, which directly address the root cause of pain, and symptomatic treatments, which focus on managing the symptoms of pain and improving overall function. The importance of a multidisciplinary and holistic approach is emphasized in the treatment of PSPS-T1/2. This approach is patient-centered and treatment plans are customized to individual patient needs and circumstances. The review concludes with a reflection on the impact of the new PSPS nomenclature on the perception and management of post-surgical spinal pain.

We evaluated cerebral blood flow by laser Doppler during 30 secs of hypoxia (0.10 FiO₂) in anesthetized, ventilated adenosine 2a receptor knockout (A2aR KO) and wild-type (WT) mice to test the hypothesis that cerebral hypoxic hyperemia in KO mice would be attenuated. We also studied the effects of selective and nonselective A2aR antagonists. During 30 secs of hypoxia, P_aO₂decreased significantly ( P < 0.05) and to a similar degree in both types of mice, whereas P_aCO₂remained relatively stable. However, mean arterial blood pressure (MABP) decreased to a greater extent ( P < 0.05) during hypoxia in KO mice (58.6 ± 1.5 mm Hg) than in WT animals (76.1 ± 3.2 mm Hg). Consequently, in a separate group of mice, we stabilized and matched MABP during hypoxia. Hypoxic hyperemia was attenuated by 38% ( P < 0.05) in KO animals whose MABP was uncontrolled, and by 81% ( P < 0.05) in KO animals whose MABP changes were matched to the MABP in the hypoxic WT mice. In animals treated with adenosine antagonists, hypoxic hyperemia was decreased by 44% to 48% ( P < 0.05) in WT mice, but was without effect in KO mice. We conclude that adenosine via A2aR is responsible for a significant proportion of the hyperemia during hypoxia.