What happens to stroke patients after hospital discharge?

Of 231 stroke patients discharged from hospital, 34 patients (14.7%) had died when reviewed 6 months later. Of 195 survivors, 115 (58%) were independent and living in the community. The remaining 80 (42%) patients were dependent. The majority of dependent patients were in institutional care but 29 (36%) were residing in the community of whom a substantial number were not receiving physiotherapy, occupational therapy or day care. Patients who were dependent in nursing homes were less likely to have received physiotherapy (48% versus 70%) or occupational therapy (28% versus 60%) compared to disabled patients in hospital based extended nursing care. 45 patients (24%) had been re-admitted to hospital although only 48% of patients had been reviewed in hospital outpatients since discharge. 64% of patients were on anti-thrombotic treatment. This survey suggests that 6 months after hospital discharge, most stroke patients are still alive and living in the community. Many of the dependent survivors have ongoing unmet medical and rehabilitation needs.     

Motor learning after stroke: Is skill acquisition a prerequisite for contralesional neuroplastic change?

Limited data directly characterize the dynamic evolution of brain activity associated with motor learning after stroke. The current study considered whether sequence-specific motor skill learning or increasing non-specific use of the hemiparetic upper extremity drive functional reorganization of the contralesional motor cortex after stroke. Eighteen individuals with chronic middle cerebral artery stroke practiced one of two novel motor tasks; a retention test occurred on a separate fifth day. Using the hemiparetic arm, participants performed a serial targeting task during two functional MRI scans (day one and retention). Participants were randomized into either a task-specific group, who completed three additional sessions of serial targeting practice, or a general arm use group, who underwent three training sessions of increased but non-task specific use of the hemiparetic arm. Both groups performed a repeated sequence of responses that may be learned, and random sequences of movement, which cannot be learned. Change in reaction and movement time for the repeated sequence indexed motor learning; shifts in the laterality index (LI) within primary motor cortex (M1) for repeated and random sequences illustrated training effects on brain activity. Task-specific practice of the repeated sequence facilitated motor learning and shifted the LI for M1 as shown by a reduced volume of contralesional cortical activity. Random sequence performance did not stimulate motor learning or alter the LI within the task-specific training group. Further, between-group comparisons showed that increasing general arm use did not induce motor learning or alter brain activity for either random or repeated sequences. Motor skill learning of a repeated sequence altered cortical activation by inducing a more normal, contralateral pattern of brain activation. Our data suggest that task-specific motor learning may be an important stimulant for neuroplastic change and can remediate maladaptive patterns of brain activity after stroke.     

Immune responses in stroke: how the immune system contributes to damage and healing after stroke and how this knowledge could be translated to better cures?

Stroke is one of the leading causes of death and disability worldwide. The long‐standing dogma that stroke is exclusively a vascular disease has been questioned by extensive clinical findings of immune factors that are associated mostly with inflammation after stroke. These have been confirmed in preclinical studies using experimental animal models. It is now accepted that inflammation and immune mediators are critical in acute and long‐term neuronal tissue damage and healing following thrombotic and ischaemic stroke. Despite mounting information delineating the role of the immune system in stroke, the mechanisms of how inflammatory cells and their mediators are involved in stroke‐induced neuroinflammation are still not fully understood. Currently, there is no available treatment for targeting the acute immune response that develops in the brain during cerebral ischaemia. No new treatment has been introduced to stroke therapy since the discovery of tissue plasminogen activator therapy in 1996. Here, we review current knowledge of the immunity of stroke and identify critical gaps that hinder current therapies. We will discuss advances in the understanding of the complex innate and adaptive immune responses in stroke; mechanisms of immune cell‐mediated and factor‐mediated vascular and tissue injury; immunity‐induced tissue repair; and the importance of modulating immunity in stroke.     

Does reading about stroke increase stroke knowledge? The impact of different print materials

The purpose of this study was to determine whether print materials on stroke resulted in increased knowledge in a sample of lay people. One hundred and seventy-seven participants received (at random) one of five versions of a stroke information packet, or a control packet on colorectal cancer. Participants rated the materials on readability, understandability and usefulness immediately after reading. After a delay of 18 days on average, participants answered questions assessing stroke knowledge. Ratings of all packets were generally positive; however, stroke knowledge scores were significantly higher for the stroke information groups compared to the control group only for knowledge of causal mechanisms (stroke pathophysiology). While there was some indication that the fictionalized material on stroke was more effective than the expository materials, overall the impact of print materials on stroke knowledge, measured after a delay of at least 1 week, was minimal at best. Further research is needed to determine whether fictional contexts make some information more memorable.     

1α,25-Dihydroxyvitamin D3 treatment does not alter neuronal cyclooxygenase-2 expression in the cerebral cortex after stroke

The inducible prostaglandin synthase, cyclooxygenase-2, is upregulated in response to cerebral ischemia and contributes to potentiation of oxidative injury. Cyclooxygenase-2 expression is regulated by retinoic acid receptors, which form heterodimers with vitamin D receptors and vitamin D. In addition, vitamin D has been reported to have neuroprotective qualities. The aim of this study was to examine whether the biologically active vitamin D₃-metabolite 1α,25-dihydroxyvitamin D₃ (1,25-D₃), influences the expression of inducible cyclooxygenase-2 in photothrombotically lesioned brain or is part of an independent neuroprotective mechanism. We compared groups of nonlesioned control rats and infarcted animals, which were treated with either 1,25-D₃ or solvent at different times postlesion. In control animals, cyclooxygenase-2 immunoreactivity was readily evident in almost all cortical neurons of layers II/III as well as in a few pyramidal cells in layer V. Following photothrombotic infarction of the right cortical hindlimb area, there was a significant, but transient, increase in cyclooxygenase-2 labeling which was restricted to neurons of the injured hemisphere in both 1,25-D₃-treated and solvent-treated rats. Highest levels of cyclooxygenase-2 immunoreactivity were seen at 12 and 24 h postlesion, followed by a gradual decrease at later time points. However, no significant differences were detected between 1,25-D₃-treated and solvent-treated lesioned rats, indicating that postischemic neuronal cyclooxygenase-2 upregulation is not influenced by 1,25-D₃. It is concluded that the neuroprotective effect of 1,25-D₃ does not depend on modulations of neuronal COX-2 expression caused by postlesional hyperexcitation.     

Developing a stroke intervention program: What do people at risk of stroke want?

OBJECTIVE: There is currently little research examining what individuals who are at risk of a stroke want from an invention program. In order to increase the usefulness of such programs, qualitative research methods were used explore invention design issues such as factors affecting accessibility of programs and preferred health information sources. METHODS: Thirty people, each with at least one stroke risk factor, participated in one of eight focus groups. RESULTS: Broad support was indicated for our proposed intervention. Participants perceived the value and likely success of such a program enhanced if it: (a) was integrated with, and supported by, other respected health services; (b) included social components (particularly important to women); (c) produced long-term benefits; and (d) included information that was personally relevant and practical in terms of implementing change. Three reasons emerged for continuing stroke education campaigns as a component of intervention programs; these were: (a) a lack of awareness among some participants of gaps in their stroke knowledge; (b) participants' explicit requests for specific rather than general information; and (c) the apparent failure of some participants to self-identify as at risk. CONCLUSION: This study yielded a number of important design considerations that should be taken into account when developing stroke intervention programs. PRACTICE IMPLICATIONS: We discuss ways of maximising the personal relevance of stroke prevention information along theoretically important dimensions, and consumers' recommendations for the design and delivery of stroke intervention programs.     

TGFβ signaling in the brain increases with aging and signals to astrocytes and innate immune cells in the weeks after stroke

Background  

TGFβ is both neuroprotective and a key immune system modulator and is likely to be an important target for future stroke therapy. The precise function of increased TGF-β1 after stroke is unknown and its pleiotropic nature means that it may convey a neuroprotective signal, orchestrate glial scarring or function as an important immune system regulator. We therefore investigated the time course and cell-specificity of TGFβ signaling after stroke, and whether its signaling pattern is altered by gender and aging.     

Can we distinguish stroke and stroke mimics via red cell distribution width in young patients?

Introduction

Discrimination of stroke and stroke mimics is problematic in young patients. The aim of the study was to determine whether arterial ischemic stroke and stroke mimics can be differentiated via the red cell distribution width (RDW) value in young patients.

Material and methods

In this retrospective cross-sectional study, a total of 236 patients hospitalized at the neurology ward were investigated. The patients were divided into 3 groups: the 1^st group included young stroke patients, the 2^nd group included patients with epilepsy, and the 3rd group included patients with multiple sclerosis (MS). Complete blood count and computed tomographic brain imaging tests were performed in all patients, and magnetic resonance imaging was done when necessary.

Results

A total of 236 patients were included in this study. Ninety-five (40%) patients were young stroke patients, 71 (30%) had epilepsy and 70 (30%) had MS. The mean RDW values of young patients with stroke were significantly higher than patients with epilepsy or MS (14.9 ±1.2, 13.3 ±1.2, 13.4 ±0.6, p < 0.0001, respectively). The diagnostic power of RDW in the differentiation of patients with stroke is good (area under the curve (AUC) = 0.89). When an RDW cut-off value of 14.05% is accepted for differentiating young patients with stroke from other disorders, the sensitivity, specificity, positive predictive and negative predictive values were 73.7%, 87.9%, 6.1 and 0.043, respectively.

Conclusions

Red cell distribution width is a promising, rapid, easy and inexpensive parameter to distinguish young stroke from stroke mimics (such as epilepsy and MS) in young patients.     

Xenon as neuroprotectant in acute stroke?

Stroke is one of the most common diseases worldwide. A current focus of research is to find neuroprotectants that can be given during acute stroke. One specific target is to find antagonists of the N-methyl-D-aspartate (NMDA) receptor in an attempt to limit glutamate associated neurotoxicity. Xenon has recently been found to be an NMDA receptor antagonist. I suggest that xenon be considered as a neuroprotectant in acute stroke, and discuss methods of testing this proposal.     

Arm–eye coordination test to objectively quantify motor performance and muscles activation in persons after stroke undergoing robot-aided rehabilitation training: a pilot study

Previous findings show an advantage in response speed when stimulus and response correspond spatially (i.e., the Simon effect). Chronic unilateral amputees show altered spatial perception near their affected hand, providing an opportunity to investigate whether experience also affects the visuomotor stimulus–response (S–R) mapping that underlies the Simon effect. We used a two-alternative, forced-choice paradigm to probe the spatial correspondence between visual cues and responses, in 14 unilateral upper limb amputees and 14 matched controls. We presented visual stimuli in 5 different locations within peripersonal space, including the midline, and found a smooth gradient of S–R correspondence effects. This is consistent with the hypothesis that S–R correspondence is represented along a spatial gradient. Unilateral amputees performed indistinguishably from matched controls, regardless of whether stimuli appeared in the hemispace ipsi- or contralateral to their missing limbs. This is inconsistent with the hypothesis that experience-dependent visual distortions entail changes in the S–R mapping; alternatively, it could reflect a complete experience independence of the Simon effect. We propose that the affordance competition hypothesis (Cisek in Philos Trans R Soc B Biol Sci 362:1585–1599, 2007) explains the Simon effect and the underlying gradient of S–R correspondence.     

Is it important to classify ischaemic stroke?

Thirty-five percent of all ischemic events remain classified as cryptogenic. This study was conducted to ascertain the accuracy of diagnosis of ischaemic stroke based on information given in the medical notes. It was tested by applying the clinical information to the (TOAST) criteria. Hundred and five patients presented with acute stroke between Jan-Jun 2007. Data was collected on 90 patients. Male to female ratio was 39:51 with age range of 47-93 years. Sixty (67%) patients had total/partial anterior circulation stroke; 5 (5.6%) had a lacunar stroke and in 25 (28%) the mechanism of stroke could not be identified. Four (4.4%) patients with small vessel disease were anticoagulated; 5 (5.6%) with atrial fibrillation received antiplatelet therapy and 2 (2.2%) patients with atrial fibrillation underwent CEA. This study revealed deficiencies in the clinical assessment of patients and treatment was not tailored to the mechanism of stroke in some patients.     

What education do stroke patients receive in Australian hospitals?

Objective

This study evaluated the educational practices of staff working in acute stroke wards in Australian hospitals, including the coordination and methods of patient education provision, post-discharge education and support services available, and the education and support services that health professionals would like to provide.

Methods

Health professionals who worked in acute stroke wards in Australian hospitals were surveyed about the stroke education practices of staff in their ward. Thirty-four hospitals returned a completed questionnaire via email or fax.

Results

Verbal communication and written materials were the most frequently used methods of information provision. Twenty-three (67.6%) wards developed their own written education materials, five (14.7%) offered group education programs, and 19 (55.9%) offered education or support after discharge. Fourteen (41.2%) wards had a particular staff member responsible for coordinating the provision of education to patients and one (2.9%) ward had a written policy on stroke education. The majority (70.6%) of participants would like to be able to provide more education/support services.

Conclusion

The educational practices of the Australian hospitals surveyed were variable, with improvements needed in the coordination and documentation of patient education and the available follow-up services.

Practice implications

Health professionals need to be aware of the importance of education in the care of patients following stroke. Patients’ informational needs, while in hospital and after discharge, may be better met if staff in acute stroke wards had improved communication and coordination practices and ensured that stroke education was appropriately documented and supported by policy.     

Migraine, stroke and patent foramen ovale--connected or not?

A relationship between migraine with aura and patent foramen ovale (PFO) has been established in clinical studies, and is now related to previous observation that migraine and stroke are connected. Studies have shown that the prevalence of PFO in patients with migraine is about 2.5-fold than in patients without migraine. Up to now, there is no consensus on the treatment of PFO in primary or secondary prevention, so both surgical and conservative methods are used. Most nonrandomized studies (and 1 randomized placebo-controlled study) have shown that migraine attacks are reduced after PFO closure; however, recent studies show that a new onset or worsening of migraine headaches may occur after closure of PFO or atrial septal defects. Therefore, no definite conclusions can be made on the treatment of migraines by PFO closure.     

Is thymus redundant after adulthood?

Thymus is considered to involute with age with a decline in thymic function. However, this generality is not universally and incontrovertibly true. Many studies performed in animals and men have proved to the contrary that thymic activity and function appear to be well maintained in the old age and may be indispensable for T cell reconstitution in different immunological settings. During some clinical situations where T cell pool needs to be regenerated, renewal of thymic activity and mass has been observed in an otherwise dormant thymic remnant. New studies have revealed a dynamic interplay between postnatal thymus output and peripheral T cell pool. Moreover, age-related loss of thymic function appears to be only quantitative and not qualitative. This review, thus, focuses on the different conditions that lead to thymic involution and attempts to bring about the emerging notion and the clinical relevance of continuous thymic activity well beyond the adulthood to optimise the function of the immune system in the context of cancer and infectious diseases.     

Are stroke cases affected by sleep disordered breathings all the same?

Sleep disordered breathings (SDB) worsens the clinical prognosis of stroke patients. Continuous positive airway pressure (CPAP) is a promising effective treatment. Unfortunately, not all patients are compliant with CPAP, suggesting that it is not appropriate for all patients with obstructive sleep apnoea (OSA) after stroke. People with the highest likelihood of benefiting have to be identified. We present a classification of cases with stroke and SDB to be adopted in order to identify the best responders to CPAP treatment. We propose to classify patients in four subgroups: (1) patients who terminate the apnoea by arousing from sleep; these cases are those affected either by an anatomical or a functional obstruction of upper airways that may precede or are the consequence of stroke; (2) cases that alternate OSA to central sleep apnoea (CSA) cause of an altered loop gain; (3) cases in whom ischemic damages have altered the sleep microstructure (CAP); (4) cases that manifest a CSA as the direct consequence of stroke on the central neuronal drive to breath. So far, no study has investigated the consequences of stroke on sleep microstructure. In order to better elucidate these relationships, when reviewing the PSG tracings of stroke patients, the microstructure of sleep should be systematically analysed.     

Hyperhomocysteinemia among ischemic stroke victims in the teaching hospital of Lomé

Hyperhomocysteinemia is an independent vascular risk factor involved in ischaemic stroke. Aim of this study was to evaluate the prevalence of hyperhomocysteinemia and the role of the metabolic determinants in ischaemic stroke. The study concerned 183?patients in the Department of neurology of the teaching hospital of Lome. The diagnosis of stroke was made on clinical and brain CT scan arguments. The dosage of homocysteinemia was carried out by the immunoenzymatic method (Abbott Diagnostic). Among 183?patients, 111 (61%) had a hyperhomocysteinemia. The total average homocysteinemia was of 22.0 μmol/L. The average homocysteinemia among men was of 22.4 μmol/L (5.2-198.0) and 18.80 μmol/L (4.2-50) among women with a positive correlation (P = 0.049 and 0.01) between homocysteinemia and the age among the men and women. The average homocysteinemia was of 17.2 μmol/L in the large ischaemic stroke; 23.0?μmol/L when associated with lacunes and 32.8 μmol/L when associated with lacunes and leucoaraiosis (p = 0.001). In conclusion, the hospital prevalence of the hyperhomocysteinemia was of 61%. Hyperhomocysteinemia was the second vascular risk factor after arterial hypertension in term of prevalence, probably from nutritional cause.     

Middle cerebral artery preponderance in ischemic stroke: A coincidence or fate?

Stroke is the leading cause of disability and the third leading cause of death in the United States. More than 700,000 persons per year suffer a first-time stroke in the United States, with 20% of these individuals dying within the first year after the stroke. Ischemic stroke accounts for majority of cases of stroke and within this subgroup also, anterior circulation stroke involving the middle cerebral artery (MCA) is the commonest one. There has been no speculation so far as to why this anatomical preponderance to middle cerebral artery exists in thrombotic stroke. While the role of nitric oxide (NO) as a vasculoprotective molecule has been well established, understanding the stimulus for its release and anatomical course of middle cerebral artery can provide a good justification for the clinical finding mentioned above. This bench to bedside correlation not only explains the predilection of ischemic thrombotic stroke to MCA but also highlights the significance of NO as a vasculoprotective molecule in cerebrovascular disease which has not been emphasized earlier.