Plasticity of Adult Sensorimotor System in Severe Brain Infarcts: Challenges and Opportunities

Functional reorganization forms the critical mechanism for the recovery of function after brain damage. These processes are driven by inherent changes within the central nervous system (CNS) triggered by the insult and further depend on the neural input the recovering system is processing. Therefore these processes interact with not only the interventions a patient receives, but also the activities and behaviors a patient engages in. In recent years, a wide range of research programs has addressed the association between functional reorganization and the spontaneous and treatment-induced recovery. The bulk of this work has focused on upper-limb and hand function, and today there are new treatments available that capitalize on the neuroplasticity of the brain. However, this is only true for patients with mild to moderated impairments; for those with very limited hand function, the basic understanding is much poorer and directly translates into limited treatment opportunities for these patients. The present paper aims to highlight the knowledge gap on severe stroke with a brief summary of the literature followed by a discussion of the challenges involved in the study and treatment of severe stroke and poor long-term outcome

Rate of complications due to carotid angioplasty in a tertiary university hospital

Introduction: Stenoses greater than 50% in the cervical internal carotid artery cause up to 8% of all ischemic strokes. Carotid artery stenting (CAS) is an effective alternative to prevent cerebrovascular events to occur. According to recommendations from the American Heart Association/American Stroke Association, CAS is indicated for symptomatic patients with internal carotid stenosis greater than 70% (measured by non-invasive methods), as long as the risk for periprocedural stroke or death is less than 6%. There is few information about complication rates of CAS in developing countries. Objectives: The primary goal of this study was to evaluate the frequency of any stroke or death until hospital discharge after CAS in symptomatic patients with carotid stenosis in a tertiary university hospital. Other complication rates were also assessed as secondary aims. Methods: A single-center retrospective study based on the analysis of charts from patients submitted to CAS between April 2011 and March 2016. Inclusion criteria were: age ≥ 18 years old, admission and follow-up by neurologists from the Neurology Ward, performance of CAS according to the hospital´s protocol (carotid stenosis ≥70%, patients with transient ischemic attack (TIA), amaurosis fugax or minor stroke in the last 180 days, and life expectancy greater than a year). Patients not followed by neurologists after CAS were excluded. Results: A total of 65 patients were included: 3 (4.6%) suffered stroke or death after CAS. Two of these patients presented ischemic strokes and one, an hemorrhagic stroke that lead to death. Myocardial infarctions were not identified, as well as carotid ruptures or dissections, hyperperfusion syndrome, artery perforations, stent thrombosis or encephalopathy. Minor complication rates were: 12.3% for hypotension, 9.2% for bradycardia, 1.5% for TIA, 3.1% for carotid vasospasm and 6.2% for acute kidney injury. The total rate of minor complications was 23.1%, and none of then led to permanent harm. Conclusions: The rate of stroke or death in a reference tertiary service in a developing country was in line with international recommendations

Rate of complications due to carotid angioplasty in a tertiary university hospital

Introduction: Stenoses greater than 50% in the cervical internal carotid artery cause up to 8% of all ischemic strokes. Carotid artery stenting (CAS) is an effective alternative to prevent cerebrovascular events to occur. According to recommendations from the American Heart Association/American Stroke Association, CAS is indicated for symptomatic patients with internal carotid stenosis greater than 70% (measured by non-invasive methods), as long as the risk for periprocedural stroke or death is less than 6%. There is few information about complication rates of CAS in developing countries. Objectives: The primary goal of this study was to evaluate the frequency of any stroke or death until hospital discharge after CAS in symptomatic patients with carotid stenosis in a tertiary university hospital. Other complication rates were also assessed as secondary aims. Methods: A single-center retrospective study based on the analysis of charts from patients submitted to CAS between April 2011 and March 2016. Inclusion criteria were: age ≥ 18 years old, admission and follow-up by neurologists from the Neurology Ward, performance of CAS according to the hospital´s protocol (carotid stenosis ≥70%, patients with transient ischemic attack (TIA), amaurosis fugax or minor stroke in the last 180 days, and life expectancy greater than a year). Patients not followed by neurologists after CAS were excluded. Results: A total of 65 patients were included: 3 (4.6%) suffered stroke or death after CAS. Two of these patients presented ischemic strokes and one, an hemorrhagic stroke that lead to death. Myocardial infarctions were not identified, as well as carotid ruptures or dissections, hyperperfusion syndrome, artery perforations, stent thrombosis or encephalopathy. Minor complication rates were: 12.3% for hypotension, 9.2% for bradycardia, 1.5% for TIA, 3.1% for carotid vasospasm and 6.2% for acute kidney injury. The total rate of minor complications was 23.1%, and none of then led to permanent harm. Conclusions: The rate of stroke or death in a reference tertiary service in a developing country was in line with international recommendations

Dissecting central post-stroke pain:a controlled symptom-psychophysical characterization

Central post-stroke pain affects up to 12% of stroke survivors and is notoriously refractory to treatment. However, stroke patients often suffer from other types of pain of non-neuropathic nature (musculoskeletal, inflammatory, complex regional) and no head-to-head comparison of their respective clinical and somatosensory profiles has been performed so far. We compared 39 patients with definite central neuropathic post-stroke pain with two matched control groups: 32 patients with exclusively non-neuropathic pain developed after stroke and 31 stroke patients not complaining of pain. Patients underwent deep phenotyping via a comprehensive assessment including clinical exam, questionnaires and quantitative sensory testing to dissect central post-stroke pain from chronic pain in general and stroke. While central post-stroke pain was mostly located in the face and limbs, non-neuropathic pain was predominantly axial and located in neck, shoulders and knees (P < 0.05). Neuropathic Pain Symptom Inventory clusters burning (82.1%, n = 32, P < 0.001), tingling (66.7%, n = 26, P < 0.001) and evoked by cold (64.1%, n = 25, P < 0.001) occurred more frequently in central post-stroke pain. Hyperpathia, thermal and mechanical allodynia also occurred more commonly in this group (P < 0.001), which also presented higher levels of deafferentation (P < 0.012) with more asymmetric cold and warm detection thresholds compared with controls. In particular, cold hypoesthesia (considered when the threshold of the affected side was <41% of the contralateral threshold) odds ratio (OR) was 12 (95% CI: 3.8–41.6) for neuropathic pain. Additionally, cold detection threshold/warm detection threshold ratio correlated with the presence of neuropathic pain (ρ = −0.4, P < 0.001). Correlations were found between specific neuropathic pain symptom clusters and quantitative sensory testing: paroxysmal pain with cold (ρ = −0.4; P = 0.008) and heat pain thresholds (ρ = 0.5; P = 0.003), burning pain with mechanical detection (ρ = −0.4; P = 0.015) and mechanical pain thresholds (ρ = −0.4, P < 0.013), evoked pain with mechanical pain threshold (ρ = −0.3; P = 0.047). Logistic regression showed that the combination of cold hypoesthesia on quantitative sensory testing, the Neuropathic Pain Symptom Inventory, and the allodynia intensity on bedside examination explained 77% of the occurrence of neuropathic pain. These findings provide insights into the clinical-psychophysics relationships in central post-stroke pain and may assist more precise distinction of neuropathic from non-neuropathic post-stroke pain in clinical practice and in future trials