Alison Charleston

Not All Patients With Atrial Fibrillation–Associated Ischemic Stroke Can Be Started on Anticoagulant Therapy

Background and Purpose— Ischemic stroke patients in atrial fibrillation (AF) have a 10% to 20% risk of recurrent stroke. Warfarin reduces this risk by two thirds. However, warfarin is underutilized in this patient group. We performed a prospective study to determine the reasons why warfarin is not started in these patients. Methods— All patients with AF-associated ischemic stroke over a 12-month period were identified. Demographic and other data, including whether warfarin was commenced or recommended at discharge, and if not why not, were recorded. Results— Ninety-three of 412 (23%) ischemic stroke patients had paroxysmal or permanent AF. Of these patients, 17 (18%) died, 48 (52%) were discharged home, and 28 (30%) were discharged to institutional care. Only 13 of 64 (20%) patients with known AF were taking warfarin at stroke onset. Warfarin was started (or recommended) in 35 of 76 (46%) survivors. Of those not commenced on warfarin, 32 (78%) were dependent (P<0.001) and 23 (56%) were discharged to institutional care (P<0.001). Warfarin was not started because of severe disability and frailty in 13 (32%), risk of falls in 12 (30%), and limited life expectancy in 4 (10%). Conclusions— In this cohort of patients with AF, warfarin was primarily underutilized before stroke onset, and it was too late to use anticoagulation, in approximately half, once a stroke had occurred. The decision to start or continue anticoagulation requires clinical judgment and should be made on a case by case basis after a complete risk benefit assessment.

Medication compliance in ischaemic stroke patients

Aim: This study aimed to assess the degree of patient compliance with medications prescribed at hospital discharge following ischaemic stroke, and concordance between self‐reported medication use and general practitioner (GP) records.

Changing attitudes to the management of ischaemic stroke between 1997 and 2004: a survey of New Zealand physicians

Aim: In 1997, a survey of New Zealand physicians’ opinions on the management of stroke was carried out. Since then, there have been a number of advances in stroke therapy. We have repeated the 1997 survey to assess changes in physicians’ opinions on stroke management.

C9ORF72 and UBQLN2 mutations are causes of amyotrophic lateral sclerosis in New Zealand: a genetic and pathologic study using banked human brain tissue.

Amyotrophic lateral sclerosis (ALS) is a devastatin g neurodegenerative disease which causes progressive and eventually fatal loss of motor func tio . Here we describe genetic and pathological characterisation of brain tissue banked from 19 ALS patients over nearly 20 years at the Department of Anatomy and the Centre for Brain Research, Unive rs ty of Auckland, New Zealand. We screened for mutations in SOD1, TARDBP, FUS, and C9ORF72 genes, and for neuropathology caused by phosphorylated TDP-43, dipeptide repeats and ubiqui lin. We identified two cases with C9ORF72 repeat expansions. Both harboured phosphorylated TD P-43 and dipeptide repeat inclusions. We show that dipeptide repeat inclusions can incorporate or occur independently of ubiquilin. We also identified one case with a UBQLN2 mutation, which showed phosphorylated TDP-43 and characteristic ubiquilin protein inclusions. This i s the first study of ALS genetics in New Zealand, adding New Zealand to the growing list of countries in which C9ORF72 repeat expansion and UBQLN2 mutations are detected in ALS cases.

Motor neuron disease mortality rates in New Zealand 1992–2013

Abstract Background: We determined the mortality rates of motor neuron disease (MND) in New Zealand over 22 years from 1992 to 2013. Previous studies have found an unusually high and/or increasing incidence of MND in certain regions of New Zealand; however, no studies have examined MND rates nationwide to corroborate this. Methods: Death certificate data coded G12.2 by International Classification of Diseases (ICD)-10 coding, or 335.2 by ICD-9 coding were obtained. These codes specify amyotrophic lateral sclerosis, progressive bulbar palsy, or other motor neuron diseases as the underlying cause of death. Mortality rates for MND deaths in New Zealand were age-standardized to the European Standard Population and compared with rates from international studies that also examined death certificate data and were age-standardized to the same standard population. Results and Conclusion: The age-standardized mortality from MND in New Zealand was 2.3 per 100,000 per year from 1992–2007 and 2.8 per 100,000 per year from 2008–2013. These rates were 3.3 and 4.0 per 100,000 per year, respectively, for the population 20 years and older. The increase in rate between these two time periods was likely due to changes in MND death coding from 2008. Contrary to a previous regional study of MND incidence, nationwide mortality rates did not increase steadily over this time period once aging was accounted for. However, New Zealand MND mortality rate was higher than comparable studies we examined internationally (mean 1.67 per 100,000 per year), suggesting that further analysis of MND burden in New Zealand is warranted.

C9ORF72 and UBQLN2 are genetic causes of ALS in New Zealand: A genetic and pathological study using banked human brain tissue

Amyotrophic lateral sclerosis (ALS) is a devastatin g neurodegenerative disease which causes progressive and eventually fatal loss of motor func tio . Here we describe genetic and pathological characterisation of brain tissue banked from 19 ALS patients over nearly 20 years at the Department of Anatomy and the Centre for Brain Research, Unive rs ty of Auckland, New Zealand. We screened for mutations in SOD1, TARDBP, FUS, and C9ORF72 genes, and for neuropathology caused by phosphorylated TDP-43, dipeptide repeats and ubiqui lin. We identified two cases with C9ORF72 repeat expansions. Both harboured phosphorylated TD P-43 and dipeptide repeat inclusions. We show that dipeptide repeat inclusions can incorporate or occur independently of ubiquilin. We also identified one case with a UBQLN2 mutation, which showed phosphorylated TDP-43 and characteristic ubiquilin protein inclusions. This i s the first study of ALS genetics in New Zealand, adding New Zealand to the growing list of countries in which C9ORF72 repeat expansion and UBQLN2 mutations are detected in ALS cases.

C9ORF72 and UBQLN2 are genetic causes of ALS in New Zealand

Amyotrophic lateral sclerosis (ALS) is a devastatin g neurodegenerative disease which causes progressive and eventually fatal loss of motor func tio . Here we describe genetic and pathological characterisation of brain tissue banked from 19 ALS patients over nearly 20 years at the Department of Anatomy and the Centre for Brain Research, Unive rs ty of Auckland, New Zealand. We screened for mutations in SOD1, TARDBP, FUS, and C9ORF72 genes, and for neuropathology caused by phosphorylated TDP-43, dipeptide repeats and ubiqui lin. We identified two cases with C9ORF72 repeat expansions. Both harboured phosphorylated TD P-43 and dipeptide repeat inclusions. We show that dipeptide repeat inclusions can incorporate or occur independently of ubiquilin. We also identified one case with a UBQLN2 mutation, which showed phosphorylated TDP-43 and characteristic ubiquilin protein inclusions. This i s the first study of ALS genetics in New Zealand, adding New Zealand to the growing list of countries in which C9ORF72 repeat expansion and UBQLN2 mutations are detected in ALS cases.

407: Not all patients with atrial fibrillation associated ischemic stroke can be started on anticoagulant therapy

BACKGROUND AND PURPOSE Ischemic stroke patients in atrial fibrillation (AF) have a 10% to 20% risk of recurrent stroke. Warfarin reduces this risk by two thirds. However, warfarin is underutilized in this patient group. We performed a prospective study to determine the reasons why warfarin is not started in these patients. METHODS All patients with AF-associated ischemic stroke over a 12-month period were identified. Demographic and other data, including whether warfarin was commenced or recommended at discharge, and if not why not, were recorded. RESULTS Ninety-three of 412 (23%) ischemic stroke patients had paroxysmal or permanent AF. Of these patients, 17 (18%) died, 48 (52%) were discharged home, and 28 (30%) were discharged to institutional care. Only 13 of 64 (20%) patients with known AF were taking warfarin at stroke onset. Warfarin was started (or recommended) in 35 of 76 (46%) survivors. Of those not commenced on warfarin, 32 (78%) were dependent (P<0.001) and 23 (56%) were discharged to institutional care (P<0.001). Warfarin was not started because of severe disability and frailty in 13 (32%), risk of falls in 12 (30%), and limited life expectancy in 4 (10%). CONCLUSIONS In this cohort of patients with AF, warfarin was primarily underutilized before stroke onset, and it was too late to use anticoagulation, in approximately half, once a stroke had occurred. The decision to start or continue anticoagulation requires clinical judgment and should be made on a case by case basis after a complete risk benefit assessment.