Bastiaan R. Bloem

Bio: Bastiaan R. Bloem is an academic researcher from Radboud University Nijmegen. The author has contributed to research in topics: Parkinson's disease & Gait (human). The author has an hindex of 52, co-authored 287 publications receiving 9019 citations. Previous affiliations of Bastiaan R. Bloem include University Medical Center Groningen & Radboud University Nijmegen Medical Centre.

The Emerging Evidence of the Parkinson Pandemic.

Abstract: Neurological disorders are now the leading source of disability globally, and the fastest growing neurological disorder in the world is Parkinson disease. From 1990 to 2015, the number of people with Parkinson disease doubled to over 6 million. Driven principally by aging, this number is projected to double again to over 12 million by 2040. Additional factors, including increasing longevity, declining smoking rates, and increasing industrialization, could raise the burden to over 17 million. For most of human history, Parkinson has been a rare disorder. However, demography and the by-products of industrialization have now created a Parkinson pandemic that will require heightened activism, focused planning, and novel approaches.

Pallidal dysfunction drives a cerebellothalamic circuit into Parkinson tremor.

Abstract: Objective: Parkinson disease (PD) is characterized by striatal dopamine depletion, which explains clinical symptoms such as bradykinesia and rigidity, but not resting tremor. Instead, resting tremor is associated with increased activity in a distinct cerebellothalamic circuit. To date, it remains unknown how the interplay between basal ganglia and the cerebellothalamic circuit can result in resting tremor. Methods: We studied 21 tremor-dominant PD patients, 23 nontremor PD patients, and 36 controls. Using functional magnetic resonance imaging, we measured functional connectivity between basal ganglia nuclei (globus pallidus internus [GPi], globus pallidus externus [GPe], putamen, caudate) and the cerebellothalamic circuit. Using electromyography during scanning, we measured tremor-related activity in the basal ganglia and cerebellothalamic circuit. We also quantified striatopallidal dopamine depletion using iodine-123-N-omega-fluoropropyl-2 beta-carbomethoxy-3 beta-(4-iodophenyl)tropane [[I-123]FP-CIT] single photon emission computed tomography. Results: Pallidal (but not striatal) dopamine depletion correlated with clinical tremor severity. The GPi, GPe, and putamen were transiently activated at the onset of tremor episodes, whereas activity in the cerebellothalamic circuit cofluctuated with tremor amplitude. The GPi and putamen of tremor-dominant PD patients had increased functional connectivity with the cerebellothalamic circuit, which was relegated through the motor cortex. Interpretation: Resting tremor may result from a pathological interaction between the basal ganglia and the cerebellothalamic circuit. The cerebellothalamic circuit, which controls tremor amplitude, appears to be driven into tremor generation when receiving transient signals from the dopamine-depleted basal ganglia. This may explain why basal ganglia dysfunction is required for developing resting tremor, although a cerebellothalamic circuit produces it. Our model also clarifies why neurosurgical interventions targeted at either the basal ganglia or the cerebellothalamic circuit can both suppress tremor.

Functional Connectivity of Human Premotor and Motor Cortex Explored with Repetitive Transcranial Magnetic Stimulation

Abstract: Connections between the premotor cortex and the primary motor cortex are dense and are important in the visual guidance of arm movements. We have shown previously that it is possible to engage these connections in humans and to measure the net amount of inhibition/facilitation from premotor to motor cortex using single-pulse transcranial magnetic stimulation (TMS). The aim of this study was to test whether premotor activation can affect the excitability of circuits within the primary motor cortex (M1) itself. Repetitive TMS (rTMS), which is known to produce effects that outlast the train at the site of stimulation, was given for 20 min at 1 Hz over premotor, primary motor, and sensory areas of cortex at an intensity of 80% of the active motor threshold for the motor hand area. The excitability of some corticocortical connections in M1 was probed by using paired-pulse testing of intracortical inhibition (ICI) and intracortical facilitation (ICF) with a coil placed over the motor cortex hand area. rTMS over the premotor cortex, but not other areas, changed the time course of the ICI/ICF for up to 1 hr afterward without affecting motor thresholds or motor-evoked potential recruitment. The cortical silent period was also shortened. The implication is that rTMS at a site distant from the motor cortex can change the excitability of circuits intrinsic to the motor cortex.

Gait disorders and balance disturbances in Parkinson's disease: clinical update and pathophysiology.

Abstract: PURPOSE OF REVIEW: Gait disorders and balance impairments are one of the most incapacitating symptoms of Parkinson's disease. Here, we discuss the latest findings regarding epidemiology, assessment, pathophysiology and treatment of gait and balance impairments in Parkinson's disease. RECENT FINDINGS: Recent studies have confirmed the high rate and high risk of falls of patients with Parkinson's disease. Therefore, it is crucial to detect patients who are at risk of falling and how to prevent falls. Several studies have shown that multiple balance tests improve the prediction of falls in Parkinson's disease. Difficulty turning may be caused by axial rigidity, affected interlimb coordination and asymmetries. Turning difficulties are easily assessed by timed performance and the number of steps during a turn. Impaired sensorimotor integration, inability of switching between sensory modalities and lack of compensatory stepping may all contribute to the high incidence of falls in patients with Parkinson's disease. Similarly, various studies highlighted that pharmacotherapy, neurosurgery and physiotherapy may adversely affect balance and gait in Parkinson's disease. SUMMARY: Insights into the pathophysiology of Parkinson's disease continue to grow.At the same time, it is becoming clear that some patients may in fact deteriorate with treatment. Future research should focus on the development and evaluation of multifactorial fall prevention strategies. Language: en

Parkinson’s disease: clinical features and diagnosis

Abstract: Objective: Parkinson’s disease (PD) is a progressive neurological disorder characterised by a large number of motor and non-motor features that can impact on function to a variable degree. This review describes the clinical characteristics of PD with emphasis on those features that differentiate the disease from other parkinsonian disorders. Methods: A MedLine search was performed to identify studies that assess the clinical characteristics of PD. Search terms included “Parkinson’s disease”, “diagnosis” and “signs and symptoms”. Results: Because there is no definitive test for the diagnosis of PD, the disease must be diagnosed based on clinical criteria. Rest tremor, bradykinesia, rigidity and loss of postural reflexes are generally considered the cardinal signs of PD. The presence and specific presentation of these features are used to differentiate PD from related parkinsonian disorders. Other clinical features include secondary motor symptoms (eg, hypomimia, dysarthria, dysphagia, sialorrhoea, micrographia, shuffling gait, festination, freezing, dystonia, glabellar reflexes), non-motor symptoms (eg, autonomic dysfunction, cognitive/neurobehavioral abnormalities, sleep disorders and sensory abnormalities such as anosmia, paresthesias and pain). Absence of rest tremor, early occurrence of gait difficulty, postural instability, dementia, hallucinations, and the presence of dysautonomia, ophthalmoparesis, ataxia and other atypical features, coupled with poor or no response to levodopa, suggest diagnoses other than PD. Conclusions: A thorough understanding of the broad spectrum of clinical manifestations of PD is essential to the proper diagnosis of the disease. Genetic mutations or variants, neuroimaging abnormalities and other tests are potential biomarkers that may improve diagnosis and allow the identification of persons at risk.