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Articles by B. R. Bloem
Total Records ( 2 ) for B. R. Bloem
  R. C Helmich , H. R Siebner , N Giffin , S Bestmann , J. C Rothwell and B. R. Bloem

Episodic ataxia type 2 and familial hemiplegic migraine are two rare hereditary disorders that are linked to dysfunctional ion channels and are characterized clinically by paroxysmal neurological symptoms. Impaired regulation of cerebral excitability is thought to play a role in the occurrence of these paroxysms, but the underlying mechanisms are poorly understood. Normal ion channels are crucial for coordinating neuronal firing in response to facilitatory input. Thus, we hypothesized that channel dysfunction in episodic ataxia type 2 and familial hemiplegic migraine may impair the ability to adjust cerebral excitability after facilitatory events. We tested this hypothesis in patients with episodic ataxia type 2 (n = 6), patients with familial hemiplegic migraine (n = 7) and healthy controls (n = 13). All subjects received a high-frequency burst (10 pulses at 20 Hz) of transcranial magnetic stimulation to transiently increase the excitability of the motor cortex. Acute burst-induced excitability changes were probed at 50, 250, 500 and 1000 ms after the end of the burst. This was done using single-pulse transcranial magnetic stimulation to assess corticospinal excitability, and paired-pulse transcranial magnetic stimulation at an interstimulus interval of 2 and 10 ms to assess intracortical inhibition and facilitation, respectively. The time course of burst-induced excitability changes differed between groups. Healthy controls showed a short-lived increase in excitability that was only present 50 ms after the burst. In contrast, patients with episodic ataxia type 2 showed an abnormally prolonged increase in corticospinal excitability that was still present 250 ms after the transcranial magnetic stimulation burst. Furthermore, while controls showed a decrease in intracortical facilitation during the 1 s period following the transcranial magnetic stimulation burst, patients with episodic ataxia type 2 had increased intracortical facilitation 1000 ms after the burst. Intracortical inhibition was unaltered between groups. Patients with familial hemiplegic migraine were not significantly different from either controls or patients with episodic ataxia type 2. Together, these findings indicate that patients with episodic ataxia type 2 have an excessive increase in motor cortex excitability following a strong facilitatory input. We argue that this deficient control of cortical excitability may set the stage for the emergence of paroxysmal neural dysfunction in this disorder.

  L. B Oude Nijhuis , J. H. J Allum , G. F Borm , F Honegger , S Overeem and B. R. Bloem

Support-surface movements are commonly used to examine balance control. Subjects typically receive a series of identical or randomly interspersed multidirectional balance perturbations and the atypical "first trial reaction" (evoked by the first perturbation) is often excluded from further analysis. However, this procedure may obscure vital information about neurophysiological mechanisms associated with the first perturbation and, by analogy, fully unexpected falls. We studied first trial reactions, aiming to clarify their directional impact on postural control and to characterize the underlying neurophysiological substrate. We instructed 36 subjects to maintain balance following support-surface rotations in six different directions. Perturbations in each direction were delivered in blocks, consisting of 10 serial stimuli. Full body kinematics, surface reactive forces, and electromyographic (EMG) responses were recorded. Regardless of direction, for the very first rotation, displacement of the center of mass was 15% larger compared with the ensuing nine identical rotations (P < 0.0001). This first trial reaction immediately reemerged whenever a new perturbation direction was introduced. First trial reactions (and near-falls) were greatest for backward-directed rotations and smallest for laterally directed rotations. This directional dependence coincided with early changes in vertical head accelerations. First trial reactions in EMG responses involved larger amplitudes in general and earlier muscle response onsets in upper body muscles. These findings show that first trial reactions are associated with significantly increased postural instability, mainly due to increased response amplitudes. Although rapid habituation occurs following presentation of identical stimuli, subjects immediately become unstable again when the perturbation direction suddenly changes. Excessive responses due to a failure to combine proprioceptive and vestibular cues effectively may explain this instability seen with first trials, particularly when falling backward.

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