Diagnosis and Rehabilitation of Visual Field Defects in Stroke Patients: A Retrospective Audit

Objective: Visual field defects (VFD) after stroke can cause significant disability and reduction in quality of life. Adequate diagnosis of VFD and referral to visual rehabilitation are important to improve outcome. Our aim was to conduct a retrospective clinical audit to investigate how neurologists detect and follow up VFD in stroke patients in a university hospital in Norway. Methods: All patients registered in the Bergen NORSTROKE Registry from February 2006 to May 2009 with (1) occipital lobe infarctions and (2) non-occipital infarction and clinically detected VFD were included in the study. Their medical records were reviewed for referral to perimetry for examination of VFD and for referral to a visual rehabilitation program within the first year after brain injury. Results: Of 353 patients, 34 (9.6%) were referred to perimetry and 8 (2.3%) to visual rehabilitation. Patients referred to perimetry were younger (65.1 vs. 74.7 years, p Conclusions: Only few patients were referred to perimetry, and even fewer were offered visual rehabilitation. Age and gender were negative predictors for referral. Neurologists’ awareness of the significant disability related to VFD must be increased. Focused diagnostics on visual impairment and early referral to a visual rehabilitation program should be mandatory in stroke unit services

Erratum: Diagnosis and Rehabilitation of Visual Field Defects in Stroke Patients: A Retrospective Audit

<i>Objective:</i> Visual field defects (VFD) after stroke can cause significant disability and reduction in quality of life. Adequate diagnosis of VFD and referral to visual rehabilitation are important to improve outcome. Our aim was to conduct a retrospective clinical audit to investigate how neurologists detect and follow up VFD in stroke patients in a university hospital in Norway. <i>Methods:</i> All patients registered in the Bergen NORSTROKE Registry from February 2006 to May 2009 with (1) occipital lobe infarctions and (2) non-occipital infarction and clinically detected VFD were included in the study. Their medical records were reviewed for referral to perimetry for examination of VFD and for referral to a visual rehabilitation program within the first year after brain injury. <i>Results:</i> Of 353 patients, 34 (9.6%) were referred to perimetry and 8 (2.3%) to visual rehabilitation. Patients referred to perimetry were younger (65.1 vs. 74.7 years, p < 0.001), had lower modified Rankin Scale scores (2.53 vs. 3.47, p = 0.003), and scored lower on the National Institutes of Health Stroke Scale upon admission (6.68 vs. 13.90, p < 0.001). Men were more often referred to perimetry than women (73.5 vs. 26.5%, p < 0.001), and those referred were younger (61.2 vs. 75.8 years, p = 0.03). <i>Conclusions:</i> Only few patients were referred to perimetry, and even fewer were offered visual rehabilitation. Age and gender were negative predictors for referral. Neurologists’ awareness of the significant disability related to VFD must be increased. Focused diagnostics on visual impairment and early referral to a visual rehabilitation program should be mandatory in stroke unit services

A Pellino-2 variant is associated with constitutive NLRP3 inflammasome activation in a family with ocular pterygium–digital keloid dysplasia

Ocular pterygium–digital keloid dysplasia (OPDKD) is a rare hereditary disease characterized by corneal ingrowth of vascularized conjunctival tissue early in life. Later, patients develop keloids on fingers and toes but are otherwise healthy. In a recently described family with OPDKD, we report the presence of a de novo c.770C > T, p.(Thr257Ile) variant in PELI2 in the affected individual. PELI2 encodes for the E3 ubiquitin ligase Pellino-2. In transgenic U87MG cells overexpressing Pellino-2 with the p.(Thr257Ile) amino acid substitution, constitutive activation of the NLRP3 inflammasome was observed. However, the Thr257Ile variant did not affect Pellino-2 intracellular localization, its binding to known interaction partners, nor its stability. Our findings indicate that constitutive autoactivation of the NLRP3 inflammasome contributes to the development of PELI2-associated OPDKD

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