Frontiers Of Neurology And Neuroscience[JOURNAL]
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200 papers
Anatomy of the hippocampal formation.
Schultz C, Engelhardt M
Front Neurol Neurosci · 2014 · PMID 24777126 · Publisher ↗
The hippocampus is one of several brain regions that together comprise the hippocampal formation. The hippocampal formation is a prominent C-shaped structure bulging in the floor of the temporal horn of the lateral ventr...
The hippocampus is one of several brain regions that together comprise the hippocampal formation. The hippocampal formation is a prominent C-shaped structure bulging in the floor of the temporal horn of the lateral ventricle. The hippocampus proper consists of three major subfields (CA1-CA3). The other regions that together comprise the hippocampal formation consist of the dentate gyrus, the subicular complex, and the entorhinal cortex. Based on its extrinsic connectivity, the hippocampal formation receives a vast amount of highly processed multimodal sensory information that is funneled into the hippocampal formation mainly by the entorhinal cortex. The entorhinal cortex is connected to associational neocortical areas in a reciprocal manner. Extensive hippocampal integration of sensory information is established by a largely unidirectional chain of intrinsic hippocampal projections. Our current knowledge on hippocampal connectivity and function is largely based on studies of rodents and monkeys. It still remains to be determined to which extent such neuroanatomical data of experimental animals is applicable to the human hippocampal formation.
Introduction.
Hennerici MG
Front Neurol Neurosci · 2014 · PMID 24777125 · Publisher ↗
Abstract loading — click title to view on PubMed.
Antithrombotic therapy in transient ischemic attack patients.
Held VE, Wolf ME, Hennerici MG
Front Neurol Neurosci · 2014 · PMID 24157563 · Publisher ↗
Historically, studies of antithrombotic therapy in ischemic cerebrovascular disease have included both stroke and transient ischemic attack (TIA). Thus, therapy regimes are very similar. Aspirin (75-325 mg within 48 h af...
Historically, studies of antithrombotic therapy in ischemic cerebrovascular disease have included both stroke and transient ischemic attack (TIA). Thus, therapy regimes are very similar. Aspirin (75-325 mg within 48 h after onset of symptoms) is still the standard antithrombotic treatment because other agents have performed similarly (or worse). Combinations of agents have shown mixed results. Aspirin combined with clopidogrel has failed to show a significant reduction of stroke/TIA recurrences but increased the bleeding risk if taken for more than several months. The combination of aspirin and dipyridamole is slightly better than aspirin alone and in particular reduced nonfatal stroke/TIA - hence it is recommended as an alternative and may be used in patients with recurrent events while on regular aspirin. In contrast, combined treatment is regularly recommended after endovascular interventions and if both cardio- and cerebrovascular diseases are present. Warfarin and similar compounds have long been the standard treatment for most patients with permanent, paroxysmal or intermittent non-valvular atrial fibrillation, for which there is excellent evidence in most patients (CHADS-VASc score >1). New compounds have been approved in recent years and shown to reduce either ischemic events, intracranial bleeding complications or both when compared with warfarin. None of them requires regular therapy monitoring. Because there are no head-to-head comparisons of these newer agents, definite recommendations as to which to choose, and when, are hard to make. However, there are some notable differences as well as new approved entities.
Stroke subtypes and interventional studies for transient ischemic attack.
Lavallée P, Amarenco P
Front Neurol Neurosci · 2014 · PMID 24157562 · Publisher ↗
Transient ischemic attack (TIA) is the most important risk factor for ischemic stroke. The risk is the highest in the first hours after symptom onset, and treatment must be initiated in emergency. In the acute phase, ant...
Transient ischemic attack (TIA) is the most important risk factor for ischemic stroke. The risk is the highest in the first hours after symptom onset, and treatment must be initiated in emergency. In the acute phase, antithrombotic agent is probably the most important treatment, but it is not excluded that lipid-lowering agents and/or antihypertensive drugs are also important. For current guidelines, monotherapy of antiplatelet agent remains the gold standard in emergency. However, most recent data and meta-analysis support a combination therapy of clopidogrel and aspirin. Data on treatment in the very acute phase of TIA in the different etiologic stroke subtypes are also lacking especially for cardioembolic stroke and the potential benefit of anticoagulant. Long-term prevention mainly derived from large trials, in which TIA and minor stroke patients have constituted the largest part. Patients with non-cardioembolic stroke must be treated with antiplatelet agent in monotherapy, and dual antiplatelet therapy such as clopidogrel plus aspirin should be avoided, particularly in lacunar strokes, whereas anticoagulants are the treatment of choice for patients with cardioembolic stroke. Major advances concerning stroke prevention in patients with atrial fibrillation have emerged with new oral anticoagulant agents that are as effective as vitamin K antagonists and safer, especially with regard to the risk of intracranial hemorrhage. At variance with moderate and severe cerebral infarction, oral anticoagulants can be initiated without delay in TIA patients. Left atrial appendage closure seems to be a promising treatment in patients ineligible for anticoagulation. Aggressive management of vascular risk factors, including blood pressure as low as 130/80 mm Hg, intensive statin treatment, smoking cessation and diabetes control, also plays a major role in the prevention of vascular event.
Neurosonological examinations of transient ischemic attack.
Sharma VK, Wong KS
Front Neurol Neurosci · 2014 · PMID 24157561 · Publisher ↗
Cerebrovascular ultrasonography is the only modality that provides real-time information about blood flow in various cervicocerebral arteries. Continuous information can be obtained over extended periods with high resolu...
Cerebrovascular ultrasonography is the only modality that provides real-time information about blood flow in various cervicocerebral arteries. Continuous information can be obtained over extended periods with high resolution and excellent spatial display. Hemodynamic changes in the cerebral circulation due to various physiological or pathological states can be monitored reliably. The information obtained from cerebrovascular ultrasonography carries diagnostic, therapeutic as well as prognostic potential in various conditions. Cervical duplex sonography evaluates blood flow as well as arterial wall characteristics in the major arteries that supply the cerebral vascular bed. Validated criteria for the diagnosis of steno-occlusive disease of carotid or vertebral arteries have high accuracy parameters. Transcranial Doppler (TCD) ultrasonography provides a reliable evaluation of intracranial blood flow patterns in real-time and adds physiological information to the anatomical details obtained from other neuroimaging modalities. Cerebrovascular ultrasonography is relatively cheap, can be performed at bedside, and allows monitoring in acute emergency settings. Extended applications of TCD provide important information about the pathophysiology of cerebrovascular ischemia and risk stratification. Therefore, cerebrovascular ultrasonography has become an integral component of the armamentarium of stroke neurologists for understanding stroke etiopathogenesis, planning and monitoring definitive treatment and determining the prognosis. It has been suggested as an essential component of a comprehensive stroke center. We have reviewed various established applications of ultrasonography in patients with cerebrovascular ischemia.
Radiological examinations of transient ischemic attack.
Tung CE, Olivot JM, Albers GW
Front Neurol Neurosci · 2014 · PMID 24157560 · Publisher ↗
Neuroimaging is critical in the evaluation of patients with TIA. CT and MRI are the two available options for imaging. Head CT is more widely available and commonly used. Diffusion MRI is the recommended modality to imag...
Neuroimaging is critical in the evaluation of patients with TIA. CT and MRI are the two available options for imaging. Head CT is more widely available and commonly used. Diffusion MRI is the recommended modality to image an ischemic lesion. The presence of a diffusion lesion in a patient with transient neurological symptoms is an indicator of a high risk of recurrent stroke. Perfusion imaging with perfusion MRI or CT perfusion may improve the detection of ischemic lesions. Noninvasive vessel imaging may detect a symptomatic vessel lesion associated with an increased risk of stroke.
Guidelines for management of patients with transient ischemic attack.
Uehara T, Minematsu K
Front Neurol Neurosci · 2014 · PMID 24157559 · Publisher ↗
A transient ischemic attack (TIA) is a medical emergency that is associated with a high risk of early ischemic stroke and other vascular events. Several evidence-based guidelines have been published to provide recommenda...
A transient ischemic attack (TIA) is a medical emergency that is associated with a high risk of early ischemic stroke and other vascular events. Several evidence-based guidelines have been published to provide recommendations for the evaluation and treatment of patients with TIA. These guidelines underline the need for the urgent referral of patients with TIA so that they can access expert evaluation and immediate treatment. The distinction between TIA and ischemic stroke has recently become less important because these two conditions share pathophysiological mechanisms and many of the preventive approaches are applicable to both. Therefore, current guidelines are often described without a distinction between TIA and ischemic stroke. However, the applicability of recommendations for applying treatment for ischemic stroke to TIA has not been proven. Further studies are required to determine the effects of urgent intervention or treatment early after TIA.
Symptoms of transient ischemic attack.
Kim JS
Front Neurol Neurosci · 2014 · PMID 24157558 · Publisher ↗
Transient ischemic attack (TIA) is a cerebrovascular disease with temporary (<24 h) neurological symptoms. The symptoms of TIA patients are largely similar to those of ischemic stroke patients and include unilateral limb...
Transient ischemic attack (TIA) is a cerebrovascular disease with temporary (<24 h) neurological symptoms. The symptoms of TIA patients are largely similar to those of ischemic stroke patients and include unilateral limb weakness, speech disturbances, sensory symptoms, visual disturbances, and gait difficulties. As these symptoms are transient, they are frequently evaluated based on patients' subjective reports, which are less precise than those of patients with stroke whose longer-lasting symptoms and signs can be reliably assessed by physicians. Some symptoms, such as monocular blindness, are much more common in TIA than in stroke, and limb shaking occurs almost exclusively in TIA patients. On the other hand, symptoms like hemivisual field defects or limb ataxia are underappreciated in TIA patients. These transient neurological symptoms are not necessarily caused by cerebrovascular diseases, but can be produced by a variety of non-vascular diseases. Careful history taking, examination, and appropriate imaging tests are needed to differentiate these TIA mimics from TIA. Each TIA symptom has a different specificity and sensitivity, and there has been an effort to assess the outcome of the patients through the use of specific clinical features. On top of this, recent developments in imaging techniques have greatly enhanced our ability to predict the outcomes of TIA patients. Perception or recognition of TIA symptoms may differ according to the race, sex, education, and specialty of physicians. Appropriate education of both the general population and physicians with regard to TIA symptoms is important as TIAs need emergent evaluation and treatment.
Epidemiology of transient ischemic attack.
Kokubo Y
Front Neurol Neurosci · 2014 · PMID 24157557 · Publisher ↗
Few epidemiologic data are available regarding the prevalence and incidence of transient ischemic attack (TIA). Here, the incidence of TIA and that of subsequent stroke events were reviewed. The incidences of TIA in Euro...
Few epidemiologic data are available regarding the prevalence and incidence of transient ischemic attack (TIA). Here, the incidence of TIA and that of subsequent stroke events were reviewed. The incidences of TIA in Europe were 0.52-2.37 and 0.05-1.14 in men and women aged 55-64, 0.94-3.39 and 0.71-1.47 in those aged 65-74, and 3.04-7.20 and 2.18-6.06 in those aged 75-84, respectively. The corresponding incidences are similar in the United States, and lower in Japan. Higher incidences were revealed in men compared with women. The incidence of TIA increased very markedly with age, regardless of race or gender. The evidence of risk factors for TIA excluding ischemic strokes is very limited. The ABCD/ABCD(2) score was developed to predict individual risk and to triage patients on the first presentation. In prognostic TIA, the crude rate of stroke risks (%) for general populations were 1.7, 4.8, 6.6, 8.5, and 11.4 at 2 days, 1 week, 1 month, 3 and 6 months, whereas those for hospital patients were 13.7 and 12.4 at 1 and 3 months, respectively. There is very limited evidence of an association between a family history of stroke and the incidence of stroke after TIA, which showed that family history of stroke does not predict the risk of ischemic stroke after TIA. There is also limited evidence of seasonal variation in TIA incidence. TIAs were reported to be most frequent in autumn or spring and less common in winter or spring to summer, and most frequent on Mondays. There seems to be no consensus regarding seasonal differences in TIA incidence.
Risk scores for transient ischemic attack.
Wolf ME, Held VE, Hennerici MG
Front Neurol Neurosci · 2014 · PMID 24157556 · Publisher ↗
The risk of recurrent ischemic stroke after a transient ischemic attack (TIA) has been reported to be 5-10%, and is elevated especially within the first days after the index event. Since TIA primarily has a good outcome...
The risk of recurrent ischemic stroke after a transient ischemic attack (TIA) has been reported to be 5-10%, and is elevated especially within the first days after the index event. Since TIA primarily has a good outcome without persisting new deficits, interest has been growing to predict stroke recurrence after TIA. This has led to the development of scores, initially for long-term prognosis such as the Stroke Prognosis Instrument (SPI) or the Hankey score, which both have shown a good predictive value at 1 or 2 years after TIA. Risk factors such as age, hypertension or cardiovascular disease were integrated in these systems. Since the early risk prediction for stroke in patients presenting within 24 h after onset of symptoms became clinically more and more relevant in emergency stroke units, the ABCD score (for the predictive factors Age, Blood pressure, Clinical symptoms, Duration of symptoms) was developed. Validation was promising, and hence further scores were developed, which entailed a large number of studies trying to validate these systems or to improve them (e.g. ABCD(2), ABCD(2)I, ABCD(3), ABCD(3)I, CIP model, ASPIRE approach, ABCDE+ etc.). The main approaches were to include imaging results (such as DWI positivity) or etiologic considerations (e.g. carotid stenosis or atrial fibrillation). However, these new scores necessitate an extensive diagnostic workup, and therefore can only be used in large stroke centers. Currently, for acute TIA management, the use of ABCD(2) is recommended in several guidelines.
TIA clinic: a major advance in management of transient ischemic attacks.
Lavallée P, Amarenco P
Front Neurol Neurosci · 2014 · PMID 24157555 · Publisher ↗
Patients with transient ischemic attack (TIA) are at very high risk of imminent stroke. This risk could be decreased by 80% if patients are immediately investigated and treated by stroke specialists. However, because TIA...
Patients with transient ischemic attack (TIA) are at very high risk of imminent stroke. This risk could be decreased by 80% if patients are immediately investigated and treated by stroke specialists. However, because TIA workup includes not only specialist advices but also a wide range of investigations such as brain, arterial and cardiac imaging, management of these patients in emergency required well-organized dedicated health care system, such as TIA clinics. Management of TIA patients in outpatient clinics has been shown to be safe and cost-effective avoiding full hospitalization in most of the cases.
Transient ischemic attack as a medical emergency.
Okada Y
Front Neurol Neurosci · 2014 · PMID 24157554 · Publisher ↗
Since transient ischemic attack (TIA) is regarded as a medical emergency with high risk for early stroke recurrence, the underlying mechanisms should be immediately clarified to conclude a definitive diagnosis and provid...
Since transient ischemic attack (TIA) is regarded as a medical emergency with high risk for early stroke recurrence, the underlying mechanisms should be immediately clarified to conclude a definitive diagnosis and provide early treatment. Early risk stratification using ABCD(2) scores can predict the risk of ischemic stroke occurring after TIA. Carotid ultrasonography (US) can evaluate the degree of stenosis, plaque properties and flow velocity of ICA lesions. High-risk mobile plaques can be classified by carotid US, and aortogenic sources of emboli can be detected by transesophageal echocardiography. Cardiac monitoring and blood findings are thought to play a key role in a diagnosis of cardioembolic TIA. Diffusion-weighted imaging (DWI)-MRI and MR angiography are also indispensable to understand the mechanism of TIA and cerebral circulation. To prevent subsequent stroke arising from TIA, antiplatelet and anticoagulant therapies should be started immediately along with comprehensive management of life-style, hypertension, diabetes mellitus, dyslipidemia and other atherosclerotic diseases. Carotid endarterectomy and endovascular intervention are critical for treating symptomatic patients with significant stenosis of ICA. A novel concept of acute cerebrovascular syndrome (ACVS) has recently been advocated to increase awareness of TIA among citizens, patients and medical professionals. TIA should be recognized as the last opportunity to avoid irreversible ischemic stroke and its sequelae. The clinical relevance of the new concept of ACVS is advocated by early recurrence after TIA, analysis of high-risk TIA, treatment strategies and the optimal management of TIA. Raising TIA awareness should also proceed across many population sectors.
The concept of acute cerebrovascular syndrome.
Uchiyama S
Front Neurol Neurosci · 2014 · PMID 24157553 · Publisher ↗
Early after the onset of transient ischemic attack (TIA), patients are at very high risk of stroke. There is no meaning to differentiate TIA in acute settings from acute ischemic stroke (AIS) only by the duration of symp...
Early after the onset of transient ischemic attack (TIA), patients are at very high risk of stroke. There is no meaning to differentiate TIA in acute settings from acute ischemic stroke (AIS) only by the duration of symptoms. Acute TIA and AIS are on the same spectrum of acute ischemic syndrome in the central nervous system. We proposed a new concept termed acute cerebrovascular syndrome (ACVS), which includes TIA in acute settings and AIS. The concept of ACVS is comparable to acute coronary syndrome (ACS), which includes unstable angina and acute myocardial infarction. When a focal symptomatic reversible ischemia occurs in the brain, it is called TIA, and when a focal symptomatic irreversible ischemia occurs in the brain, it is called AIS. Patients with ACS share a single pathophysiological mechanism, that is rupture of unstable plaque followed by formation of platelet-rich thrombi to plug up coronary arteries. Unlike ACS, the mechanism of ACVS is complicated, which is not only large artery atherosclerosis similar to ACS but also cardioembolism or small vessel occlusion. In addition, there are no measurable biomarkers for ACVS, while there are practical biomarkers for ACS. Nevertheless, the concept of ACVS is practical to emphasize the importance of immediate evaluation and starting treatment to prevent subsequent stroke in acute settings of TIA. Therefore, TIA in acute settings as well as AIS should be recognized as ACVS, which is a medical emergency.
History of transient ischemic attack definition.
Mohr JP
Front Neurol Neurosci · 2014 · PMID 24157552 · Publisher ↗
Transient ischemic attacks have been recognized as a clinical entity for well over a century. Efforts before the availability of modern imaging to establish a diagnosis of inferred ischemic stroke led to acceptance of to...
Transient ischemic attacks have been recognized as a clinical entity for well over a century. Efforts before the availability of modern imaging to establish a diagnosis of inferred ischemic stroke led to acceptance of too long a time period (>24 h) compared with the actual typical events lasting <24 min (usually 5-15 min). Revision of the time period has improved diagnostic yield and discovered many whose image-documented acute infarct is associated with a short clinical course.
Clinical recovery from CNS damage. Preface.
Naritomi H, Krieger DW
Front Neurol Neurosci · 2013 · PMID 23859975 · Publisher ↗
Abstract loading — click title to view on PubMed.
Prevention of post-stroke disuse muscle atrophy with a free radical scavenger.
Naritomi H, Moriwaki H
Front Neurol Neurosci · 2013 · PMID 23859973 · Publisher ↗
In spite of appropriate treatment in the acute phase of stroke, quite a few patients with hemiparetic stroke become disabled and stay in a wheelchair or bedridden state in the chronic phase. In stroke patients, gait dysf...
In spite of appropriate treatment in the acute phase of stroke, quite a few patients with hemiparetic stroke become disabled and stay in a wheelchair or bedridden state in the chronic phase. In stroke patients, gait dysfunction results mainly from severe hemiparesis due to ischemic damage to the motor neuron tract and partly from disuse muscle atrophy in paretic and nonparetic legs. Disuse muscle atrophy occurs even in healthy subjects as early as 4 days after bed rest immobilization and progresses further correlating with the duration of immobilization. Although detailed mechanisms of disuse muscle atrophy remain unclear, free radical scavengers are known to play an important role in the development of disuse muscle atrophy. One of the neuroprotective agents, edaravone, a free radical scavenger, succeeded in proving clinical usefulness in a phase III clinical trial in Japan. In this trial, stroke patients were administered edaravone for 14 days consecutively. The results of the edaravone trial are taken to indicate that long-term administration of a free radical scavenger may prevent disuse atrophy thereby improving functional outcome. We performed a randomized pilot study in hemiparetic stroke patients to test the validity of this view. Acute stroke patients were randomly allocated to two groups, one receiving edaravone for 3 days (short-term group) and the other for 10-14 days (long-term group). At 3 months after stroke, the grade of femoral muscle atrophy was significantly milder and the maximum walking speed was significantly faster in the long-term group than in the short-term group. The study suggests that long-term administration of a free radical scavenger may prevent the development of leg disuse atrophy thereby ameliorating locomotor function. Attention should be paid to myoprotective drug therapy in acute stroke, since it may be easier and clinically more effective than neuroprotective therapy from the viewpoint of functional prognosis.
High voltage electric potentials to enhance brain-derived neurotrophic factor levels in the brain.
Yanamoto H, Nakajo Y, Kataoka H … +1 more , Iihara K
Front Neurol Neurosci · 2013 · PMID 23859972 · Publisher ↗
Development of a safe method to increase brain-derived neurotrophic factor (BDNF) levels in the brain is expected to enhance learning and memory, induce tolerance to cerebral infarction or tolerance to depressive state,...
Development of a safe method to increase brain-derived neurotrophic factor (BDNF) levels in the brain is expected to enhance learning and memory, induce tolerance to cerebral infarction or tolerance to depressive state, improve glucose metabolism, and suppress appetite and body weight. We have shown that repetitive applications of high-voltage electric potential (HELP) to the body increase BDNF levels in the brain, improving learning and memory in mice. Here, we investigated the effects of HELP treatment for a chronic period on the BDNF levels in the mouse brain, and on body weight in mice and humans. Adult mice were exposed to 3.1 or 5.4 kV HELP (on the body), 5 h a day for 24 weeks, and BDNF levels in the brain and alterations in body weight were analyzed. Humans [age, 53.2 ± 15.5 years old; BMI, 27.8 ± 5.6 (mean ± SD, n = 6)] were exposed to 3.9 kV HELP (on the body) for 1 h a day, continuing for 33 months (2.8 years) under the monitor of body weight. In mice, the HELP application elevated BDNF levels in the brain at least temporarily, affecting body weight in a voltage- and time-dependent manner. In humans, the HELP treatment reduced body weight compared to the pretreated initial values without any aversive effects (p < 0.002, one-way ANOVA with the post hoc Holm-Sidak test). The results in mice indicated that 3.1 kV HELP was considered insufficient for a continuous elevation of intracerebral BDNF, and 5.4 kV HELP was considered as excessive. HELP with an appropriate voltage can be utilized to increase BDNF levels in the brain for a prolonged period. We anticipate further investigations to clarify the effect of the optimal-leveled HELP therapy on memory disturbances, neurological deficits after stroke, depression, diabetes, obesity and metabolic syndrome.
Influence of therapeutic hypothermia on regeneration after cerebral ischemia.
Yenari MA, Han HS
Front Neurol Neurosci · 2013 · PMID 23859971 · Full text
The protective effect of therapeutic hypothermia in cerebral ischemia is well accepted in experimental models, and some clinical studies show that there is benefit in humans as well. Long-term observations in animal and...
The protective effect of therapeutic hypothermia in cerebral ischemia is well accepted in experimental models, and some clinical studies show that there is benefit in humans as well. Long-term observations in animal and clinical studies have documented recovery of neurological function following hypothermia treatment. Diminished damage by hypothermic protection should contribute to the recovery in many ways, but hypothermia appears to enhance regeneration of brain tissue as well. Since regeneration of the brain after damage initiates within hours and is active days and weeks after stroke, prolonged hypothermia might affect regenerative processes which have been documented to occur in these time frames. As there is a lack of data at the basic and clinical levels, the mechanism of neuroregeneration by hypothermia is unclear. Yet, we speculate that hypothermia enhances regeneration by positively influencing neurogenesis, angiogenesis, gliogenesis and synapse/circuit formation after stroke. In this chapter, we will provide up-to-date data from experimental studies and clinical reports on the effect of therapeutic hypothermia on neuroregeneration, with perspectives on future research.
Role of repetitive transcranial magnetic stimulation in stroke rehabilitation.
Pinter MM, Brainin M
Front Neurol Neurosci · 2013 · PMID 23859970 · Publisher ↗
In recent years, efforts have focused on investigating the neurophysiological changes that occur in the brain after stroke, and on developing novel strategies such as additional brain stimulation to enhance sensorimotor...
In recent years, efforts have focused on investigating the neurophysiological changes that occur in the brain after stroke, and on developing novel strategies such as additional brain stimulation to enhance sensorimotor and cognitive recovery. In the 1990s, repetitive transcranial magnetic stimulation (rTMS) was introduced as a therapeutic tool for improving the efficacy of rehabilitation for recovery after stroke. It is evident that disturbances of interhemispheric processes after stroke result in a pathological hyperactivity of the intact hemisphere. The rationale of using rTMS as a complementary therapy is mainly to decrease the cortical excitability in regions that are presumed to hinder optimal recovery by low-frequency rTMS delivered to the unaffected hemisphere, while high-frequency rTMS delivered to the affected hemisphere facilitates cortical excitability. However, the exact mechanisms of how rTMS works are still under investigation. There is a growing body of research in stroke patients investigating the effect of rTMS on facilitating recovery by modifying cortical and subcortical networks. Clinical trials applying rTMS already yielded promising results in improving recovery of sensorimotor and cognitive functions. Altogether, in combination with conventional therapeutic approaches, rTMS has a potential to become a complementary strategy to enhance stroke recovery by modulating the excitability of targeted brain areas. In future studies, emphasis should be placed on selecting patient populations to determine whether treatment response depends on age, lesion acuteness, or stroke severity. Furthermore, it is important to identify parameters optimizing the beneficial effects of rTMS on stroke recovery, and to monitor their long-term effects.
Novel methods to study aphasia recovery after stroke.
Hartwigsen G, Siebner HR
Front Neurol Neurosci · 2013 · PMID 23859969 · Publisher ↗
The neural mechanisms that support aphasia recovery are not yet fully understood. It has been argued that the functional reorganization of language networks after left-hemisphere stroke may engage perilesional left brain...
The neural mechanisms that support aphasia recovery are not yet fully understood. It has been argued that the functional reorganization of language networks after left-hemisphere stroke may engage perilesional left brain areas as well as homologous right-hemisphere regions. In this chapter, we summarize how noninvasive brain stimulation can be used to elucidate mechanisms of plasticity in language networks and enhance language recovery after stroke. We first outline some basic principles of transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS). We then present evidence from studies in healthy volunteers for a causal role of the right hemisphere in different language functions. Finally, we review recent studies that used TMS or tDCS to promote language recovery after stroke. Most of these studies applied noninvasive brain stimulation over contralateral right-hemisphere areas to suppress maladaptive plasticity. However, some studies also suggest that right-hemisphere regions may beneficially contribute to recovery in some patients. More recently, some investigators have targeted perilesional brain regions to promote neurorehabilitation. In sum, these studies indicate that language recovery after stroke may integrate left- as well as right-hemisphere brain regions to a different degree over the time course of recovery. Although the results of these preliminary studies provide some evidence that noninvasive brain stimulation may promote aphasia recovery, the reported effect sizes are not striking. Future studies on larger patient collectives are needed to explore whether noninvasive brain stimulation can enhance language functions at a level that is clinically relevant.
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