Objective
To summarize the 2010 EFNS/MDS‐ES evidence‐based treatment recommendations for the management of Parkinson's disease (PD). This summary includes the treatment recommendations for early and ...late PD.
Methods
For the 2010 publication, a literature search was undertaken for articles published up to September 2009. For this summary, an additional literature search was undertaken up to December 2010. Classification of scientific evidence and the rating of recommendations were made according to the EFNS guidance. In cases where there was insufficient scientific evidence, a consensus statement (‘good practice point’) is made.
Results and Conclusions
For each clinical indication, a list of therapeutic interventions is provided, including classification of evidence.
How pain arises in Parkinson's disease? Defazio, G.; Tinazzi, M.; Berardelli, A.
European journal of neurology,
December 2013, Letnik:
20, Številka:
12
Journal Article
Recenzirano
In recent years, increasing attention has centred on pain in Parkinson's disease (PD). Pain in PD is heterogeneous in quality and body distribution. To clarify how the various pain types relate to PD ...and to propose plausible treatment strategies, in this paper we reviewed psychophysical, neurophysiological and imaging data reported in parkinsonian patients with and without pain. Most available evidence supports abnormal central nociceptive input processing that probably reflects an impairment in the lateral and medial pain pathways. Changes in central pain processing probably underlie all the different pain types and also intervene in patients with PD without pain. Thus, altered pain processing might predispose patients with PD to spontaneous pain that is variable in quality. These background pain‐processing abnormalities may interact with additional factors (such as contractures secondary to marked rigidity/bradykinesia, dystonia and medical conditions associated with painful symptoms), thus causing pain to manifest itself clinically in various ways and providing candidate targets for pain treatment in PD.
Background
A Task Force was convened by the EFNS/MDS‐ES Scientist Panel on Parkinson's disease (PD) and other movement disorders to systemically review relevant publications on the diagnosis of PD.
...Methods
Following the EFNS instruction for the preparation of neurological diagnostic guidelines, recommendation levels have been generated for diagnostic criteria and investigations.
Results
For the clinical diagnosis, we recommend the use of the Queen Square Brain Bank criteria (Level B). Genetic testing for specific mutations is recommended on an individual basis (Level B), taking into account specific features (i.e. family history and age of onset). We recommend olfactory testing to differentiate PD from other parkinsonian disorders including recessive forms (Level A). Screening for pre‐motor PD with olfactory testing requires additional tests due to limited specificity. Drug challenge tests are not recommended for the diagnosis in de novo parkinsonian patients. There is an insufficient evidence to support their role in the differential diagnosis between PD and other parkinsonian syndromes. We recommend an assessment of cognition and a screening for REM sleep behaviour disorder, psychotic manifestations and severe depression in the initial evaluation of suspected PD cases (Level A). Transcranial sonography is recommended for the differentiation of PD from atypical and secondary parkinsonian disorders (Level A), for the early diagnosis of PD and in the detection of subjects at risk for PD (Level A), although the technique is so far not universally used and requires some expertise. Because specificity of TCS for the development of PD is limited, TCS should be used in conjunction with other screening tests. Conventional magnetic resonance imaging and diffusion‐weighted imaging at 1.5 T are recommended as neuroimaging tools that can support a diagnosis of multiple system atrophy (MSA) or progressive supranuclear palsy versus PD on the basis of regional atrophy and signal change as well as diffusivity patterns (Level A). DaTscan SPECT is registered in Europe and the United States for the differential diagnosis between degenerative parkinsonisms and essential tremor (Level A). More specifically, DaTscan is indicated in the presence of significant diagnostic uncertainty such as parkinsonism associated with neuroleptic exposure and atypical tremor manifestations such as isolated unilateral postural tremor. Studies of 123IMIBG/SPECT cardiac uptake may be used to identify patients with PD versus controls and MSA patients (Level A). All other SPECT imaging studies do not fulfil registration standards and cannot be recommended for routine clinical use. At the moment, no conclusion can be drawn as to diagnostic efficacy of autonomic function tests, neurophysiological tests and positron emission tomography imaging in PD.
Conclusions
The diagnosis of PD is still largely based on the correct identification of its clinical features. Selected investigations (genetic, olfactory, and neuroimaging studies) have an ancillary role in confirming the diagnosis, and some of them could be possibly used in the near future to identify subjects in a pre‐symptomatic phase of the disease.
Click here for the corresponding questions to this CME article.
To consider whether the various clinical types of primary late-onset dystonia have a common aetiological background, or are each distinct and separate entities, sharing only the clinical appearance ...of dystonia, we reviewed epidemiological, clinical, neurophysiological and imaging data reported in patients with different forms of primary late-onset dystonia. The epidemiological and clinical features that distinguished the various clinical types and suggest aetiological differences were prevalence, age of onset, sex preference, sensory tricks, and tendency to spread. Likewise, aetiological differences were also supported by the observation that environmental risk factors possibly triggering focal dystonias in predisposed subjects can differ from one form to the other. The fact that different forms of focal dystonia may coexist in the same individual as the result of spread nevertheless suggests that the various focal dystonias are related. Detailed examination of available familial and genetic data indicates that the different forms of primary late-onset dystonia share aetiological factors, most probably genetic. Neurophysiological and imaging studies have demonstrated a number of abnormalities in focal dystonias and some of these are shared by the different clinical types. The shared abnormality of sensorimotor integration (and cortical excitability) beyond the symptomatic body part identified in various clinical types and in unaffected relatives might reflect the genetic abnormality indicating the substrate on which the dystonia develops.
Corticobasal degeneration (CBD) is a neurodegenerative condition characterized by 4R tau protein deposition in several brain regions that clinically manifests itself as a heterogeneous atypical ...parkinsonism typically expressed in adulthood. The prototypical clinical phenotype of CBD is corticobasal syndrome (CBS). Important insights into the pathophysiological mechanisms underlying motor and higher cortical symptoms in CBS have been gained by using advanced neuroimaging and neurophysiological techniques. Structural and functional neuroimaging studies often show asymmetric cortical and subcortical abnormalities, mainly involving perirolandic and parietal regions and basal ganglia structures. Neurophysiological investigations including electroencephalography and somatosensory evoked potentials provide useful information on the origin of myoclonus and on cortical sensory loss. Transcranial magnetic stimulation demonstrates heterogeneous and asymmetric changes in the excitability and plasticity of primary motor cortex and abnormal hemispheric connectivity. Neuroimaging and neurophysiological abnormalities in multiple brain areas reflect asymmetric neurodegeneration, leading to asymmetric motor and higher cortical symptoms in CBS.
Background and purpose
Essential tremor (ET) is a movement disorder primarily characterized by upper limb postural and kinetic tremor. Although still under‐investigated, bradykinesia may be part of ...the phenotypic spectrum of ET. The aim was to evaluate bradykinesia features in ET through clinical examination and kinematic analysis of repetitive finger movements. Data collected in ET patients were compared with those recorded in Parkinson’s disease patients and healthy controls.
Methods
Overall, 258 subjects participated in the study (90 ET patients, 84 Parkinson’s disease patients and 84 healthy controls). Repetitive finger tapping was kinematically recorded using a motion analysis system. Movement velocity, amplitude and decrement (sequence effect) were measured. The three groups were first compared by one‐way analysis of variance. A cluster analysis was also performed to better address the data variability observed in ET patients. Possible relationships between kinematic and clinical data were assessed in ET patients.
Results
Essential tremor patients were slower than healthy controls. Movement slowness in ET did not correlate with postural or kinetic tremor severity. It was also found that movement slowness in ET was not associated with a sequence effect, which instead is a common feature in Parkinson’s disease. Cluster analysis showed that a proportion of ET patients may have movement abnormalities similar to those observed in Parkinson’s disease.
Conclusions
Movement slowness without sequence effect is a common feature in ET patients. The present findings are relevant when interpreted in the context of the new tremor classification system and in the development of a more accurate bradykinesia definition.
Pain is one of the most common and troublesome non‐motor symptoms of Parkinson's disease (PD). It can appear at any time during the disease and is often present before diagnosis. However, there is ...little or no consensus on its definition. An expert group of clinicians with relevant research experience met to review the existing evidence and to identify gaps in our understanding leading towards AUTHOR: ’understanding towards’ has been changed to ’understanding leading towards‘. Please check and confirm that this is appropriate an optimized therapy of pain in PD. Key findings from epidemiologic, neurophysiologic, neuroimaging and clinical studies are reviewed. In each case, the evidence base is limited by wide variations in the definitions of pain applied, study methodologies and populations evaluated. Disease‐related and medical conditions trigger spontaneous pain in patients with PD, which is then abnormally processed and results in painful manifestations in specific body parts. Dopaminergic medications, such as rotigotine, as well as opiate analgesics, such as oxycodone, have shown positive results but future studies with more detailed pain characterization at inclusion are warranted.
Gilles de la Tourette syndrome (GTS) is characterized by motor and vocal tics and often associated with obsessive–compulsive disorder (OCD). Responses to intermittent/continuous theta-burst ...stimulation (iTBS/cTBS), which probe long-term potentiation (LTP)-/depression (LTD)-like plasticity in the primary motor cortex (M1), are reduced in GTS. ITBS-/cTBS-induced M1 plasticity can be affected by brain-derived neurotrophic factor (BDNF) polymorphism. We investigated whether the BDNF polymorphism influences iTBS-/cTBS-induced LTP-/LTD-like M1 plasticity in 50 GTS patients and in 50 age- and sex-matched healthy subjects. In GTS patients, motor and psychiatric (OCD) symptom severity was rated using the Yale Global Tic Severity Scale (YGTSS) and the Yale–Brown Obsessive–Compulsive Scale (Y-BOCS). We compared M1 iTBS-/cTBS-induced plasticity in healthy subjects and in patients with GTS. We also compared responses to TBS according to BDNF polymorphism (Val/Val vs Met carriers) in patients and controls. Fourteen healthy subjects and 13 GTS patients were Met carriers. When considering the whole group of controls, as expected, iTBS increased whereas cTBS decreased MEPs. Differently, iTBS/cTBS failed to induce LTP-/LTD-like plasticity in patients with GTS. When comparing responses to TBS according to BDNF polymorphism, in healthy subjects, Met carriers showed reduced MEP changes compared with Val/Val individuals. Conversely, in patients with GTS, responses to iTBS/cTBS were comparable in Val/Val individuals and Met carriers. YGTSS and Y-BOCS scores were comparable in Met carriers and in Val/Val subjects. We conclude that iTBS and cTBS failed to induce LTP-/LTD-like plasticity in patients with GTS, and this was not affected by BDNF genotype.
PDF
