Neurogenic disturbances of cardiac rhythm

Arrhythmias are disturbances of electrical activation of the heart and are commonly encountered clinical conditions. Although typically associated with cardiac pathology, they have also been described in stroke and epilepsy. Two closely related structures, the insula and the temporal lobe, particularly the mesial region, have been implicated. Derangement of central autonomic control appears to be a key driver in neurogenic arrhythmogenesis and both these structures appear to play some role in influencing autonomic activity. Our understanding of this phenomenon is only in its infancy, and more research will be necessary to further it.peer-reviewe

Optimisation of anticoagulation in patients with atrial fibrillation

Atrial fibrillation is a common cardiac arrhythmia associated with debilitating complications, one of which is stroke. Anticoagulants (warfarin and the non-vitamin K antagonist oral anticoagulants) are recommended for stroke prophylaxis, their utilisation however requires stroke risk reduction to be balanced against hemorrhage risk. Current review of the literature suggests that despite the presence of risk stratification tools such as the CHADS2 and the newer CHA2DS2-VASc, clinicians often find it challenging to anticipate the risk-benefit ratio of anticoagulation. This results in both the underuse and overuse of anticoagulation in patients as well as uncertainty over whether to use anticoagulation in paroxysmal AF. This review looks at optimising anticoagulation by improving the assessment of bleeding risk and by improving the assessment of stroke risk. The percutaneous occlusion of the left atrial appendage is an emerging alternative to oral anticoagulation therapy.peer-reviewe

Is low cardiac ejection fraction a risk factor for stroke?

Background and Purpose: Reduced ejection fraction (EF) ?35% has been suggested as a criterion for anticoagulation in persons with heart failure in sinus rhythm, but the literature supporting EF as an independent stroke risk factor is conflicting. We here review the status of reduced EF as a stroke risk factor. Methods: We performed a Medline search combining terms for stroke and heart failure (HF) or cardiac left ventricular systolic dysfunction and reviewed evidence that reduced EF increases the risk of stroke. We also reviewed clinical and epidemiological HF studies that included data on stroke and EF. Results: Two of three longitudinal cohort studies found reduced EF (<50%) to be a stroke risk factor but did not find an inverse relationship between EF level and degree of stroke risk. Exploratory analyses of three clinical studies found an inverse relationship between EF level and degree of stroke risk but only in specific subgroups and vascular risk factors appeared to attenuate this relationship. Three analyses suggested an increased stroke risk with EF ?20%. Conclusion: Reduced EF (<50%) probably increases stroke risk but this is not consistently demonstrated in all populations studied. Reduced EF of any degree may be a surrogate for atherosclerotic cerebrovascular disease and in these patients traditional vascular risk factors may be more important for stroke risk than EF. There is no evidence to support EF ?35% as a specific stroke risk factor. Research is needed to determine if very reduced EF (?20%) is a specific stroke risk factor.peer-reviewe

TIA-like presentations of cerebral amyloid angiopathy

Transient focal neurological episodes (TFNEs ) are transient ischemic attack (TIA)-like episodes that may occur in patients with cerebral amyloid angiopathy (CAA). The duration of TFNEs is typically similar to TIAs with most symptoms resolving in minutes. Symptoms, similar to those of TIAs include sensory or visual disturbances, motor weakness and language impairment and there may be limb jerking or associated headache. TFNEs have a more gradual onset and tend to spread slowly to contiguous body parts like a migraine aura. TFNEs may occur repeatedly throughout the day and attacks may continue over several months. TFNEs are typically associated with focal cortical subarachnoid hemorrhage or with focal cortical superficial siderosis. They may also be seen in patients with CAA-related lobar hemorrhage, microhemorrhage or leukoencephalopathy. Migraine prophylactic agents such as verapamil and topiramate may be useful in stopping frequent recurrent TFNEs. TFNEs are an under-recognized cause of apparent TIAs. It is important to keep TFNEs in the differential diagnosis when a patient presents with a presumed TIA as thrombolysis or anticoagulation is relatively contraindicated in CAA. Gradient echo MRI should be performed to exclude microhemorrhages when TFNEs are suspected. Clinicians most frequently associate cerebral amyloid angiopathy (CAA) with intracerebral hemorrhage or with a clinical picture of vascular cognitive impairment.1 There have however, been increasing clinical reports documenting that CAA may cause a variety of acute clinical neurological manifestations.2 Although these phenomena are superficially similar to TIAs and may be mistaken for them, they have clinical time profiles and progressions that can distinguish them from TIAs clinically. They appear to be caused by different manifestations of the complications of CAA and are now known as transient focal neurological episodes (TFNE).2,3 CAA frequency increases with age with approximately 50 % of individuals over the age of 75 being affected. The exact cause of CAA remains uncertain however increased production and/or decreased breakdown of amyloid proteins may have a role. CAA predominantly affects occipital regions of the brain followed by frontal and temporal areas. Cerebellar vessels are less commonly affected.3The Boston criteria is the current standard criteria for diagnosis of CAA. In this review, we attempt to classify and describe the different causes of TFNE’s in CAA.peer-reviewe

Behavioural Improvement in Minimally Conscious State After Caloric Vestibular Stimulation: Evidence from two single case studies.

Objective: To investigate whether caloric vestibular stimulation, a non-invasive form of neuro-modulation, alters level of awareness in people residing in minimally conscious state. Design: Single-case (n=2), prospective, controlled (ABAB) efficacy study. Setting: Tertiary, neuro-rehabilitation in-patient ward within a university hospital Participants: Two individuals in minimally conscious state Intervention: Left ear caloric vestibular stimulation was performed in two four/five-week blocks interleaved with two four/five-week blocks of sham stimulation. Session duration and frequency gradually increased within each block from once per day for 10 minutes (week 1) to once per day for 20 minutes (week 2) to 20 minutes twice per day in the remaining weeks. Measures: Wessex Head Injury Matrix, JFK Coma Recovery Scale – Revised. Results: Both participants’ Wessex Head Injury Matrix scores indicated a transition from involuntary (i.e. mechanical vocalization) to voluntary (i.e. gesture making, selective responses to family members) behaviour that was time-locked to the onset of active stimulation. In one participant, this improvement persisted for at least 4 weeks after active stimulation while in the other it diminished 2 weeks after stimulation. Allied, although less dramatic, changes were seen on the arousal and auditory subscales of the JFK Coma Recovery Scale – Revised. Conclusion: The data provide the first evidence that vestibular stimulation may help improve outcome in low awareness state although further studies are needed to replicate effect and determine longer-term benefit

CHA2 DS2 -VASc score and adverse outcomes in patients with heart failure with reduced ejection fraction and sinus rhythm

AIMS: The aim of this study was to determine whether the CHA2 DS2 -VASc score can predict adverse outcomes such as death, ischaemic stroke, and major haemorrhage, in patients with systolic heart failure in sinus rhythm. METHODS AND RESULTS: CHA2 DS2 -VASc scores were calculated for 1101 patients randomized to warfarin and 1123 patients randomized to aspirin. Adverse outcomes were defined as death or ischaemic stroke, death alone, ischaemic stroke alone, and major haemorrhage. Using proportional hazards models, we found that each 1-point increase in the CHA2 DS2 -VASc score was associated with increased hazard of death or ischaemic stroke events [hazard ratio (HR) for the warfarin arm = 1.21, 95% confidence interval (CI) 1.13-1.30, P < 0.001; for aspirin, HR = 1.20, 95% CI 1.11-1.29, P < 0.001]. Similar increased hazards for higher CHA2 DS2 -VASc scores were observed for death alone, ischaemic stroke alone, and major haemorrhage. Overall performance of the CHA2 DS2 -VASc score was assessed using c-statistics for full models containing the risk score, treatment assignment, and score-treatment interaction, with the c-statistics for the full models ranging from 0.57 for death to 0.68 for major haemorrhage. CONCLUSIONS: The CHA2 DS2 -VASc score predicted adverse outcomes in patients with systolic heart failure in sinus rhythm, with modest prediction accuracy