1,721,087 research outputs found
Brainstem avenues in Parkinson's disease research
No full textReflex blinking is a relatively simple and stereotyped motor act.Despite this, a complex neuroanatomical framework, comprisingbrainstem circuitries as well as descending effects from subcorticaland cortical areas, intervenes in the neural control of reflex eyelidmovements (Cruccu et al., 2005; Valls-Sole, 2012; Bologna et al.,2013). Thus, investigations on reflex blinking represent a valuabletool in the field of clinical and experimental neurophysiology, inboth healthy subjects and neurological conditions. For example,studies on the blink reflex in patients with Parkinson’s diseaseand other parkinsonian syndromes have provided evidence inthese conditions of the pathophysiological involvement of thebrainstem, resulting from either neurodegenerative changes orindirect basal ganglia effects on blink reflex circuits due to alteredcentral dopaminergic activit
Distinguishing essential tremor from Parkinson’s disease: clinical and experimental tools
No full textIntroduction: Essential tremor (ET) and Parkinson's disease (PD) are the most common causes of tremor and the most prevalent movement disorders, with overlapping clinical features that can lead to diagnostic challenges, especially in the early stages. Areas covered: In the present paper, the authors review the clinical and experimental studies and emphasized the major aspects to differentiate between ET and PD, with particular attention to cardinal phenomenological features of these two conditions. Ancillary and experimental techniques, including neurophysiology, neuroimaging, fluid biomarker evaluation, and innovative methods, are also discussed for their role in differential diagnosis between ET and PD. Special attention is given to investigations and tools applicable in the early stages of the diseases, when the differential diagnosis between the two conditions is more challenging. Furthermore, the authors discuss knowledge gaps and unsolved issues in the field. Expert opinion: Distinguishing ET and PD is crucial for prognostic purposes and appropriate treatment. Additionally, accurate diagnosis is critical for optimizing clinical and experimental research on pathophysiology and innovative therapies. In a few years, integrated technologies could enable accurate, reliable diagnosis from early disease stages or prodromal stages in at-risk populations, but further research combining different techniques is needed
The cerebellum and dystonia
No full textDystonia is a heterogeneous disorder characterized by involuntary muscle contractions, twisting movements, and abnormal postures in various body regions. It is widely accepted that the basal ganglia are involved in the pathogenesis of dystonia. A growing body of evidence, however, is challenging the traditional view and suggest that the cerebellum may also play a role in dystonia. Studies on animals indicate that experimental manipulations of the cerebellum lead to dystonic-like movements. Several clinical observations, including those from secondary dystonia cases as well as neurophysiologic and neuroimaging studies in human patients, provide further evidence in humans of a possible relationship between cerebellar abnormalities and dystonia. Claryfing the role of the cerebellum in dystonia is an important step towards providing alternative treatments based on noninvasive brain stimulation techniques
Cerebellum: an explanation for dystonia?
Full text linkDystonia is a movement disorder that is characterized by involuntary muscle contractions, abnormal movements and postures, as well as by non-motor symptoms, and is due to abnormalities in different brain areas. In this article, we focus on the growing number of experimental studies aimed at explaining the pathophysiological role of the cerebellum in dystonia. Lastly, we highlight gaps in current knowledge and issues that future research studies should focus on as well as some of the potential applications of this research avenue. Clarifying the pathophysiological role of cerebellum in dystonia is an important concern given the increasing availability of invasive and non-invasive stimulation techniques and their potential therapeutic role in this condition
Low-Intensity Transcranial Ultrasound Stimulation: Mechanisms of Action and Rationale for Future Applications in Movement Disorders
Full text linkLow-intensity transcranial ultrasound stimulation (TUS) is a novel non-invasive brain stimulation technique that uses acoustic energy to induce changes in neuronal activity. However, although low-intensity TUS is a promising neuromodulation tool, it has been poorly studied as compared to other methods, i.e., transcranial magnetic and electrical stimulation. In this article, we first focus on experimental studies in animals and humans aimed at explaining its mechanisms of action. We then highlight possible applications of TUS in movement disorders, particularly in patients with parkinsonism, dystonia, and tremor. Finally, we highlight the knowledge gaps and possible limitations that currently limit potential TUS applications in movement disorders. Clarifying the potential role of TUS in movement disorders may further promote studies with therapeutic perspectives in this field
Evolving concepts on bradykinesia
No full textBradykinesia is one of the cardinal motor symptoms of Parkinson's disease and other parkinsonisms. The various clinical aspects related to bradykinesia and the pathophysiological mechanisms underlying bradykinesia are, however, still unclear. In this article, we review clinical and experimental studies on bradykinesia performed in patients with Parkinson's disease and atypical parkinsonism. We also review studies on animal experiments dealing with pathophysiological aspects of the parkinsonian state. In Parkinson's disease, bradykinesia is characterized by slowness, the reduced amplitude of movement, and sequence effect. These features are also present in atypical parkinsonisms, but the sequence effect is not common. Levodopa therapy improves bradykinesia, but treatment variably affects the bradykinesia features and does not significantly modify the sequence effect. Findings from animal and patients demonstrate the role of the basal ganglia and other interconnected structures, such as the primary motor cortex and cerebellum, as well as the contribution of abnormal sensorimotor processing. Bradykinesia should be interpreted as arising from network dysfunction. A better understanding of bradykinesia pathophysiology will serve as the new starting point for clinical and experimental purposes
The effect of L-dopa in Parkinson's disease as revealed by neurophysiological studies of motor and sensory functions
No full textNTRODUCTION:
This review will first discuss evidence of motor and sensory abnormalities as yielded by neurophysiological techniques in patients with PD. It will then go on to describe the effects of L-dopa replacement on motor and sensory abnormalities in PD as assessed by neurophysiological studies.
AREAS COVERED:
We analyzed papers in English using Pubmed with the following keywords: L-dopa, dopamine, bradykinesia, basal ganglia, kinematic analysis, TMS, motor cortex plasticity, motor cortex excitability, somatosensory discrimination threshold, pain Expert commentary: L-dopa improves the amplitude and speed of upper limb voluntary movements, but it does not restore abnormalities in the sequence effect or voluntary facial movements. L-dopa only partially normalizes changes in motor cortex excitability and plasticity and has also contrasting effects on the sensory system and on sensory-motor integration. The neurophysiological studies reviewed here show that PD is more than a hypo-dopaminergic disease, and non-dopaminergic mechanisms should also be considered
Effects of subthalamic nucleus deep brain stimulation and l-dopa on blinking in Parkinson's disease
No full textIn this study we asked whether subthalamic nucleus deep brain stimulation (STN-DBS) alone, or in combination with L-dopa, modifies voluntary, spontaneous and reflex blinking in patients with Parkinson's disease (PD). Sixteen PD patients who underwent STN-DBS were studied in four experimental conditions: without STN-DBS and without L-dopa, STN-DBS alone, L-dopa alone and STN-DBS plus L-dopa. The results were compared with those obtained in 15 healthy controls. Voluntary blinking was assessed by asking participants to blink as fast as possible; spontaneous blinking was recorded during two 60 s rest periods; reflex blinking was evoked by electrical stimulation of the supraorbital nerve. Blinking were recorded and analysed with the SMART motion system. STN-DBS increased the peak velocity and amplitude for both the closing and opening voluntary blink phases, but prolonged the inter-phase pause duration. L-dopa had no effects on voluntary blinking but reversed the increased inter-phase pause duration seen during STN-DBS. Spontaneous blink rate increased after either STN-DBS or L-dopa. Reflex blinking kinematics were not modified by STN-DBS or L-dopa. The STN-DBS effects on voluntary blinking kinematics and spontaneous blinking rate may occur as results of changes of cortico-basal ganglia activity. The prolonged pause duration of voluntary blinking indicates that STN-DBS has detrimental effects on the cranial region. These results also shed light on the pathophysiology of eyelids opening apraxia following STN-DBS. (C) 2012 Elsevier Inc. All rights reserved
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