Reviews in the neurosciences (REV NEUROSCI)

Publications in this journal

• Article: Gait and cognition in Parkinson's disease: implications for rehabilitation.

  Robert Iansek, Mary Danoudis, Nicholas Bradfield
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  ABSTRACT: Abstract An increasing awareness of the interaction between gait and cognition has occurred over recent time. This interaction is even more prominent in Parkinson's disease (PD), where the alteration of striatal dopamine deficiency places a greater emphasis on cognition to compensate for the gait disturbances seen in PD. This dissertation aims to provide an insight into this interaction in PD and demonstrate how normal gait control mechanisms are altered in PD to more cognitive control. Evidence will be provided which demonstrates a shift between attention and automatic gait control mechanisms toward attention. In addition, it will be demonstrated that, because of the cognitive dysfunction that also occurs in PD, the capacity to normalize gait still remains impaired and becomes more subject to the effects of external environmental influences. Further, a rationale will be provided to utilize this interaction in a more beneficial manner, to assist the attention control mechanisms to return gait towards normal. This latter approach is applicable to all aspects of gait disorders in PD and forms a basis for possible intervention therapies.
  Reviews in the neurosciences 05/2013;
• Article: Sleep disorders in Parkinson's disease: a narrative review of the literature.

  Alberto Raggi, Rita Bella, Giovanni Pennisi, Walter Neri, Raffaele Ferri
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  ABSTRACT: Abstract Parkinson's disease (PD) is classically considered to be a motor system affliction; however, also non-motor alterations, including sleep disorders, are important features of the disease. The aim of this review is to provide data on sleep disturbances in PD in the following grouping: difficulty initiating sleep, frequent night-time awakening and sleep fragmentation, nocturia, restless legs syndrome/periodic limb movements, sleep breathing disorders, drug induced symptoms, parasomnias associated with rapid eye movements (REM) sleep, sleep attacks, reduced sleep efficiency and excessive daytime sleepiness. Research has characterized some of these disturbances as typical examples of dissociated states of wakefulness and sleep that are admixtures or incomplete declarations of wakefulness, REM sleep, and non-REM (NREM) sleep. Moreover, sleep disorders may precede the typical motor system impairment of PD and their ability to predict disease has important implications for development of neuroprotective treatment; in particular, REM sleep behavior disorder may herald any other clinical manifestation of PD by more than 10 years.
  Reviews in the neurosciences 04/2013;
• Article: Ambient particulate matter and its potential neurological consequences.

  Clare Loane, Christodoulos Pilinis, Themistocles D Lekkas, Marios Politis
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  ABSTRACT: Abstract Exposure to ambient air pollution has been consistently associated with respiratory and cardiovascular disease. However, the neurological effects of air pollution have received little attention. It is suggested that the components of air pollution, such as particulate matter (PM) and specifically ultrafine particulate matter (UFP), may have the potential to extend beyond pulmonary organs to the central nervous system (CNS) and, ultimately, the brain. The transport mechanisms are not clear, although at least four possible routes have been proposed implicating PM and UFP in neurological disease processes. A limited number of studies have been undertaken to assess the role of PM and UFP in CNS diseases, including migraine, headache, stroke, Alzheimer's disease, and Parkinson's disease. Considering the high prevalence of such CNS diseases, along with the frequent and increasing exposure to ambient air pollution, it is important to highlight possible associations with regards to preventative, monitoring, and control measures. This article aimed to review the literature in relation to translocation routes of PM and UFP and their potential role in neurological disease processes.
  Reviews in the neurosciences 04/2013;
• Article: Optic neuropathies: characteristic features and mechanisms of retinal ganglion cell loss.

  Yuyi You, Vivek K Gupta, Jonathan C Li, Alexander Klistorner, Stuart L Graham
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  ABSTRACT: Abstract Optic neuropathy refers to dysfunction and/or degeneration of axons of the optic nerve with subsequent optic nerve atrophy. A common feature of different optic neuropathies is retinal ganglion cell (RGC) apoptosis and axonal damage. Glaucoma and optic neuritis are the two major degenerative causes of optic nerve damage. Here, we review the anatomy and pathology of the optic nerve, and etiological categories of optic neuropathies, and discuss rodent models that can mimic these conditions. Electrophysiology can reveal signature features of RGC damage using the pattern electroretinogram (PERG), scotopic threshold response (STR) and photopic negative response (PhNR). The amplitude of the visual evoked potential (VEP) also reflects RGC axonal damage. The neurotrophin-mediated survival pathways, as well as the extrinsic and intrinsic cell apoptotic pathways, play a critical role in the pathogenesis of RGC loss. Finally, promising neuroprotective approaches based on the molecular signaling are analyzed for the treatment of optic neuropathies.
  Reviews in the neurosciences 04/2013;
• Article: Hippocampus and consciousness.

  Ralf-Peter Behrendt
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  ABSTRACT: Abstract An important assumption concerning the physiology of consciousness is that all varieties of conscious experience are closely related to each other and, hence, are subserved by the same neural mechanism. There are several considerations that lead us to implicate the hippocampus in the generation of conscious perception and, ultimately, of conscious experiences of all kinds. Firstly, conscious perception of external events is intricately linked with the formation of episodic (declarative) memories, a key function attributed to the hippocampus. Secondly, conscious experience is allocentric and contextualized. Consciousness creates or simulates an image of the world that appears to surround us and to be independent of our observation of it. What is characteristic of wakeful consciousness and dreaming alike is that objects or events are experienced as being embedded in an external, that is, allocentric, frame of space and time. The hippocampus has been implicated in the rapid formation and memorization of allocentric representations that embed objects or events in a world context. Thirdly, the hippocampus is ideally positioned to bind information processed in different sensory association cortices. It is argued that rapidly forming patterns of neuronal ensemble firing in the hippocampus, particularly in region CA3, which encode arbitrary associations between objects and their spatiotemporal and emotional context, that is, associations between information derived from different neocortical processing streams, define the informational content of consciousness. Evidence suggestive of an important contribution of the hippocampus to conscious observation, mental imagery, dreaming, conscious anticipation of outcomes, and hallucinations will be reviewed.
  Reviews in the neurosciences 03/2013;
• Article: Physical exercise and Parkinson's disease: influence on symptoms, disease course and prevention.

  Rita Grazina, João Massano
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  ABSTRACT: Abstract Parkinson's disease (PD) is a common, disabling, neurodegenerative condition, and the disease prevalence is expected to increase worldwide in the next few decades. Symptomatic therapy remains unsatisfactory, and greatly needed neuroprotective therapies have not been successfully developed so far. Physical exercise (PE) has been associated with a lower risk of developing a neurodegenerative disease. The literature has been searched, and results have been systematized and interpreted with regard to the effects of PE in PD. Published data show the following: 1) PE has been associated with a lower risk of developing PD; 2) PE has been shown to improve disease symptoms, mobility, balance, gait and quality of life (in this regard, walking training, tai-chi and tango dancing have demonstrated the highest level of evidence of efficacy); and 3) neuroprotective effects from PE could be expected in PD, although this has been suggested in animal studies only. Further research on this topic should be encouraged. Multidisciplinary cooperation between neurologists, sports physicians and researchers is paramount.
  Reviews in the neurosciences 03/2013;
• Article: 5-HT1A receptor as a key player in the brain 5-HT system.

  Nina K Popova, Vladimir S Naumenko
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  ABSTRACT: Abstract Among an impressive variety of identified serotonin receptors, 5-HT1A attracts particular attention due to its central role in the regulation of 5-HT-ergic neurotransmission and the data on its involvement in the mechanisms of stress response, aggressive behavior, anxiety, and depression. This review concentrates on the cross-regulation between 5-HT receptors and the implication of the 5-HT1A receptor in the genetic control of 5-HT-related behavior. Specifically, it describes the (1) functional interactions between 5-HT1A, 5-HT2A, 5-HT3, and 5-HT7 receptors; (2) cross-talk between 5-HT1A receptor and genes encoding key members of the brain 5-HT system; (3) implication of the 5-HT1A receptor in natural hibernation and genetic predisposition to different kinds of defensive behavior; and (4) role of 5-HT1A autoreceptors and heteroreceptors in anxiety, depression, and suicide, and in the antidepressant effect of serotonin reuptake inhibitors. This review provides converging lines of evidence that the 5-HT1A receptor contributes to the action of other 5-HT receptors, modulating their effect on behavior, and describes new data on the unique role of the 5-HT1A receptor in the indirect regulation of gene expression and in the autoregulation of the brain 5-HT system.
  Reviews in the neurosciences 03/2013;
• Article: Red/near-infrared irradiation therapy for treatment of central nervous system injuries and disorders.

  Melinda Fitzgerald, Stuart Hodgetts, Corinna Van Den Heuvel, Riccardo Natoli, Nathan S Hart, Krisztina Valter, Alan R Harvey, Robert Vink, Jan Provis, Sarah A Dunlop
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  ABSTRACT: Abstract Irradiation in the red/near-infrared spectrum (R/NIR, 630-1000 nm) has been used to treat a wide range of clinical conditions, including disorders of the central nervous system (CNS), with several clinical trials currently underway for stroke and macular degeneration. However, R/NIR irradiation therapy (R/NIR-IT) has not been widely adopted in clinical practice for CNS injury or disease for a number of reasons, which include the following. The mechanism/s of action and implications of penetration have not been thoroughly addressed. The large range of treatment intensities, wavelengths and devices that have been assessed make comparisons difficult, and a consensus paradigm for treatment has not yet emerged. Furthermore, the lack of consistent positive outcomes in randomised controlled trials, perhaps due to sub-optimal treatment regimens, has contributed to scepticism. This review provides a balanced précis of outcomes described in the literature regarding treatment modalities and efficacy of R/NIR-IT for injury and disease in the CNS. We have addressed the important issues of specification of treatment parameters, penetration of R/NIR irradiation to CNS tissues and mechanism/s, and provided the necessary detail to demonstrate the potential of R/NIR-IT for the treatment of retinal degeneration, damage to white matter tracts of the CNS, stroke and Parkinson's disease.
  Reviews in the neurosciences 03/2013;
• Article: The role of serotonin in the antidyskinetic effects of deep brain stimulation: focus on antipsychotic-induced motor symptoms.

  Meaghan C Creed, José N Nobrega
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  ABSTRACT: Abstract Treatment with the classic antipsychotic drugs (APDs), such as haloperidol (HAL), is associated with both acute and chronic motor side effects. Acutely, these drugs may induce extrapyramidal symptoms, whereas a prolonged treatment may result in tardive dyskinesia (TD). Atypical antipsychotics have a lower incidence of motor side effects, which have been partially ascribed to the antagonism of serotonin (5-HT) receptors. Although there is currently no satisfactory pharmacotherapy for TD, deep brain stimulation (DBS) has emerged as a promising therapy. However, the mechanisms underlying its effects remain largely unknown. DBS has been shown to affect several neurotransmitter systems, including 5-HT. In this review, we outline the involvement of 5-HT in the development of HAL-induced catalepsy and TD. We also discuss the evidence for DBS-induced alterations in 5-HT function and the relevance of serotonergic alterations to the antidyskinetic effects of DBS. The evidence suggests that the serotonergic mechanisms may be involved in the acute and chronic motor side effects of APDs as well as in adverse psychiatric effects that have been reported following DBS. However, the current evidence suggests that 5-HT alterations do not play an important role in the effectiveness of DBS in models of dyskinesias induced by chronic APDs.
  Reviews in the neurosciences 02/2013;
• Article: Multiple sclerosis and glutamate excitotoxicity.

  Milos Kostic, Nikola Zivkovic, Ivana Stojanovic
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  ABSTRACT: Abstract The previous understanding of multiple sclerosis was solely related to neuroinflammation and its harmful effects; however, countless data indicate the importance of some inflammation-independent, neurodegenerative mechanisms associated with mitochondria malfunction, iron deposition and oxidative stress. Recently, it has been postulated that glutamate excitotoxicity, a phenomenon that takes place when an excessive amount of glutamate overactivates its cellular receptors and induces cell death, could be a missing link between inflammatory and neurodegenerative processes evident in multiple sclerosis. Glutamate is the major excitatory neurotransmitter of the central nervous system, which has been proven to have a central role in a complex communication network established between all residential brain cells, including neurons, astrocytes, oligodendrocytes and microglia. Thus, the disturbance of glutamate homeostasis could affect practically all physiological functions and interactions of brain cells, leading to heterogeneity of pathological events. The understanding of glutamate excitotoxicity as a valid mechanism of central nervous system damage in multiple sclerosis, requires the revision of the current knowledge about a source of elevated extracellular glutamate, glutamate receptor alterations, alterations of glutamate transporters and metabolizing enzymes, as well as molecular mechanism of excitotoxic damage.
  Reviews in the neurosciences 02/2013; 24(1):71-88.
• Article: Effects of chronic stress on the auditory system and fear learning: an evolutionary approach.

  Alexies Dagnino-Subiabre
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  ABSTRACT: Abstract Stress is a complex biological reaction common to all living organisms that allows them to adapt to their environments. Chronic stress alters the dendritic architecture and function of the limbic brain areas that affect memory, learning, and emotional processing. This review summarizes our research about chronic stress effects on the auditory system, providing the details of how we developed the main hypotheses that currently guide our research. The aims of our studies are to (1) determine how chronic stress impairs the dendritic morphology of the main nuclei of the rat auditory system, the inferior colliculus (auditory mesencephalon), the medial geniculate nucleus (auditory thalamus), and the primary auditory cortex; (2) correlate the anatomic alterations with the impairments of auditory fear learning; and (3) investigate how the stress-induced alterations in the rat limbic system may spread to nonlimbic areas, affecting specific sensory system, such as the auditory and olfactory systems, and complex cognitive functions, such as auditory attention. Finally, this article gives a new evolutionary approach to understanding the neurobiology of stress and the stress-related disorders.
  Reviews in the neurosciences 01/2013;
• Article: The role of the subthalamic nucleus in cognition.

  David B Weintraub, Kareem A Zaghloul
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  ABSTRACT: Abstract Because the complex functions of the basal ganglia have been increasingly studied over the past several decades, the understanding of the role of the subthalamic nucleus (STN) in motor and cognitive functions has evolved. The traditional role in motor function ascribed to the STN, based on its involvement in the cortico-striato-thalamo-cortical motor loops, the pathologic STN activity seen in Parkinson's disease, and the benefits in motor symptoms following STN lesions and deep brain stimulation, has been revised to include wider cognitive functions. The increased attention focused on such nonmotor functions housed within the STN partially arose from the observed cognitive and affective side effects seen with STN deep brain stimulation. The multiple modalities of research have corroborated these findings and have provided converging evidence that the STN is critically involved in cognitive processes. In particular, numerous experiments have demonstrated the involvement of the STN in high-conflict decisions. The different STN functions appear to be related to activity in anatomically distinct subregions, with the ventral STN contributing to high-conflict decision-making through its role in the hyperdirect pathway involving the prefrontal cortex.
  Reviews in the neurosciences 01/2013;
• Article: The role of Ser129 phosphorylation of α-synuclein in neurodegeneration of Parkinson's disease: a review of in vivo models.

  Hiroyasu Sato, Takeo Kato, Shigeki Arawaka
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  ABSTRACT: Abstract Parkinson's disease is the most common neurodegenerative movement disorder. The motor impairments of Parkinson's disease are caused by the loss of dopaminergic neurons in the substantia nigra and associated with the appearance of fibrillar aggregates of α-synuclein (α-syn) called Lewy bodies. Approximately 90% of α-syn deposited in Lewy bodies is phosphorylated at serine 129 (Ser129). In contrast, only 4% or less of total α-syn is phosphorylated at this residue in the normal brain. This suggests that the accumulation of Ser129-phosphorylated α-syn leads to the formation of Lewy bodies and dopaminergic neurodegeneration in Parkinson's disease. Our laboratory and others have performed experiments using in vivo models of Parkinson's disease to elucidate the role of increased Ser129 phosphorylation in α-syn neurotoxicity. However, there has been a lack of consistency among these models. In this review, we summarize the main findings regarding the relationship between Ser129 phosphorylation and α-syn neurotoxicity, and examine the differences among models. We further discuss the role of Ser129 phosphorylation in α-syn aggregation and the future directions to test the potential of Ser129 phosphorylation as a therapeutic target for slowing the progression of Parkinson's disease.
  Reviews in the neurosciences 01/2013;
• Article: The roles of MAGE-D1 in the neuronal functions and pathology of the central nervous system.

  Akihiro Mouri, Yukihiro Noda, Ken Watanabe, Toshitaka Nabeshima
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  ABSTRACT: Abstract Melanoma-associated antigen-D1 (MAGE-D1) was discovered in bone marrow stromal cells. MAGE-D1 is detected in progenitor cells in the neuroepithelia and subventricular regions as well as in the postmitotic neuronal cells in the entire brain in the developing embryo and is also detected in most adult tissues, predominantly in the brain. Herein, we provide an overview of the roles of MAGE-D1 in the central nervous system. MAGE-D1 participates in neurotrophin-induced neuronal differentiation and survival by modulating Trk-dependent phosphorylation. MAGE-D1 regulates Dlx-dependent migration-related transcription by binding to necdin or praja-1. MAGE-D1 regulates a number of apoptotic pathways, each caused by distinct input signals, such as bone morphogenetic protein, p75 neurotrophin receptor, and uncoordinated gene-5 homologue. MAGE-D1 knockout mice show depressive behavior and impairments of circadian rhythm caused by decreased ubiquitylation of serotonin transporter and regulated transcription of RORα, respectively. The gene for necdin, a MAGE-D1-binding protein, has been described as responsible for Prader-Willi syndrome. In conclusion, MAGE-D1 plays important roles in the central nervous system in both developmental and adult stages and would be an invaluable target in the development of novel diagnostic and therapeutic agents for depression and Prader-Willi syndrome and also for providing new insights into the pathogenesis/pathophysiology of these diseases.
  Reviews in the neurosciences 01/2013;
• Article: THE EFFECTS OF OZONE EXPOSURE AND ASSOCIATED INJURY MECHANISMS ON THE CENTRAL NERVOUS SYSTEM

  MARTINEZ-LAZCANO JUAN CARLOS, GONZALEZ-GUEVARA EDITH, RUBIO MARIA DEL CARMEN, FRANCO-PEREZ JAVIER, CUSTODIO VERONICA, HERNANDEZ-CERON MIGUEL, LIVERA CARLOS, PAZ CARLOS
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  ABSTRACT: Abstract Ozone (O3) is a component of photochemical smog, which is a major air pollutant and demonstrates properties that are harmful to health because of the toxic properties that are inherent to its powerful oxidizing capabilities. Environmental O3 exposure is associated with many symptoms related to respiratory disorders, which include loss of lung function, exacerbation of asthma, airway damage, and lung inflammation. The effects of O3 are not restricted to the respiratory system or function - adverse effects within the central nervous system (CNS) such as decreased cognitive response, decrease in motor activity, headaches, disturbances in the sleep-wake cycle, neuronal dysfunctions, cell degeneration, and neurochemical alterations have also been described; furthermore, it has also been proposed that O3 could have epigenetic effects. O3 exposure induces the reactive chemical species in the lungs, but the short half-life of these chemical species has led some authors to attribute the injurious mechanisms observed within the lungs to inflammatory processes. However, the damage to the CNS induced by O3 exposure is not well understood. In this review, the basic mechanisms of inflammation and activation of the immune system by O3 exposure are described and the potential mechanisms of damage, which include neuroinflammation and oxidative stress, and the signs and symptoms of disturbances within the CNS caused by environmental O3 exposure are discussed.
  Reviews in the neurosciences 01/2013;
• Article: Imaging the structure of the human anxious brain: a review of findings from neuroscientific personality psychology.

  Christian Montag, Martin Reuter, Magdalena Jurkiewicz, Sebastian Markett, Jaak Panksepp
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  ABSTRACT: Abstract The emotion of anxiety represents one of the most studied topics in the neurosciences, in part due to its relevance for understanding the evolutionary development of the human brain and its role in the pathogenesis of psychopathological conditions. Structural magnetic resonance imaging (sMRI) has enabled mapping of the anxious human brain and has contributed substantially to the understanding of anxiety. Alongside the fields of clinical psychology/psychiatry, personality psychology aims to support the research endeavor of mapping the anxious brain and has found that individual differences in anxiety-related personality dimensions such as Neuroticism or Harm Avoidance (measured by self-report) are correlated with gray and white matter volumes in different areas of the human brain. This review reveals that structures including parts of the frontal cortex (e.g., the orbitofrontal cortex) and the temporal lobe (e.g., the hippocampus) are often associated with trait anxiety, and it points out the inconsistencies that exist in the personality-sMRI literature on human anxiety. Consequently, we suggest new research strategies to overcome the inconsistencies. This review outlines how results from animal research can guide scientists in developing testable hypotheses in search of the anxious brain. Moreover, genetic imaging is presented as an interesting approach to mapping the anxious brain.
  Reviews in the neurosciences 01/2013; 24(2):167-90.
• Article: Aversive motivation and the maintenance of monogamous pair bonding.

  Shanna L Resendez, Brandon J Aragona
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  ABSTRACT: Abstract Social bonds are important for human health and well-being, and a crucial component of these bonds is the ability to maintain a bond once it has been formed. Importantly, although bond maintenance is required for social attachments, very little is known about the neural mechanisms that mediate this behavior. Recently, laboratory studies utilizing the socially monogamous prairie vole (an excellent animal model for the neurobiology of selective social attachment), have allowed the neural correlates of selective social attachment to begin to unfold. These studies have identified that the activation of both motivational and hedonic processing systems, which mediate other natural rewards, is also important for mediating social behaviors that are characteristic of an established pair bond. These social behaviors include appetitive and positive social interactions with a potential mating partner in sexually naïve prairie voles, the avoidance of novel conspecifics (and sometimes aggressive rejection) that characterizes the established pair bond and, finally, an aversion towards partner separation. The following review will discuss how a balance between opposing endogenous opioid systems - positive (mu-opiod receptors) and aversive (kappa-opioid receptors) - provide essential hedonic signaling that guides socially motivated behaviors.
  Reviews in the neurosciences 12/2012;
• Article: The basal ganglia: motor and cognitive relationships in a clinical neurobehavioral context.

  Gerry Leisman, Robert Melillo
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  ABSTRACT: Abstract New information about the basal ganglia and cerebellar connections with the cerebral cortex has prompted a reevaluation of the role of the basal ganglia in cognition. We know that the relation between the basal ganglia and the cerebral cortical region allows for connections organized into discrete circuits. Rather than serving as a means for widespread cortical areas to gain access to the motor system, these loops reciprocally interconnect a large and diverse set of cerebral cortical areas with the basal ganglia. The properties of neurons within the basal ganglia or cerebellar components of these circuits resemble the properties of neurons within the cortical areas subserved by these loops. For example, neuronal activity within the basal ganglia and cerebellar loops with motor areas of the cerebral cortex is highly correlated with parameters of movement, whereas neuronal activity within the basal ganglia and cerebellar loops with areas of the prefrontal cortex is more related to the aspects of cognitive function. Thus, individual loops appear to be involved in distinct behavioral functions. Studies of the basal ganglia and cerebellar pathology support this conclusion. Damage to the basal ganglia or cerebellar components of circuits with motor areas of the cortex leads to motor symptoms, whereas damage to the subcortical components of circuits with nonmotor areas of the cortex causes higher-order deficits. In this report, we review some of the new anatomic, physiologic, and behavioral findings that have contributed to a reappraisal of function concerning the basal ganglia and cerebellar loops with the cerebral cortex and apply it in clinical applications to obsessive-compulsive disorder, Tourette's syndrome, and attention-deficit/hyperactivity disorder as examples of how compromise at different points in the system may yield similar but different clinical results.
  Reviews in the neurosciences 12/2012;
• Article: A review on the effectiveness of repetitive transcranial magnetic stimulation (rTMS) on post-stroke aphasia.

  Ivy S Y Wong, Hector W H Tsang
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  ABSTRACT: Abstract Background: This evidence-based review reports an updated evaluation and critical appraisal of available studies that investigated the effectiveness of repetitive transcranial magnetic stimulation (rTMS) on post-stroke aphasia rehabilitation. Methods: A literature search was performed to identify studies that investigated the therapeutic effects of rTMS on post-stroke aphasia in various electronic databases, from their inception to 2011. The selected studies were classified according to the types of participants, types of interventions, outcome measures, and results. The methodological qualities of the selected studies were evaluated using the Physiotherapy Evidence Database scale. Results: The current review was based on 12 studies, including open-label designs and controlled trials, that showed a positive effect of rTMS, with or without conventional rehabilitation, on post-stroke aphasia compared with sham or conventional rehabilitation alone. About 41% of the selected studies reported the long-term effect of rTMS on aphasia recovery. No adverse effect was reported. Conclusions: The current review reveals that rTMS with or without conventional rehabilitation has positive effects on post-stroke aphasia. The studies also contributed to the plausible mechanisms of stroke recovery. However, with the concerns over the methodology of the selected studies in this review, a larger-scale, multicenter, well-designed randomized controlled trial involving different phases and types of aphasia needs to be carried out before recommending rTMS as a complementary treatment for post-stroke aphasia.
  Reviews in the neurosciences 12/2012;