Deep Brain Stimulation

Department of Neurology, Washington University School of Medicine, Washington University, St. Louis, Missouri 63110, USA.
Annual Review of Neuroscience (Impact Factor: 19.32). 02/2006; 29(1):229-57. DOI: 10.1146/annurev.neuro.29.051605.112824
Source: PubMed


Deep brain stimulation (DBS) has provided remarkable benefits for people with a variety of neurologic conditions. Stimulation of the ventral intermediate nucleus of the thalamus can dramatically relieve tremor associated with essential tremor or Parkinson disease (PD). Similarly, stimulation of the subthalamic nucleus or the internal segment of the globus pallidus can substantially reduce bradykinesia, rigidity, tremor, and gait difficulties in people with PD. Multiple groups are attempting to extend this mode of treatment to other conditions. Yet, the precise mechanism of action of DBS remains uncertain. Such studies have importance that extends beyond clinical therapeutics. Investigations of the mechanisms of action of DBS have the potential to clarify fundamental issues such as the functional anatomy of selected brain circuits and the relationship between activity in those circuits and behavior. Although we review relevant clinical issues, we emphasize the importance of current and future investigations on these topics.

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Available from: Jonathan W Mink, Oct 03, 2015
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    • "Deep brain stimulation (DBS) has been shown to be effective in the treatment of movement disorders, such as Parkinson's disease and tremor (Kleiner-Fisman et al. 2006; Perlmutter & Mink, 2006). It has also been used in conditions as diverse as chronic pain and Tourette's syndrome (Bittar et al. 2005; Steeves et al. 2012). "
    American Psychiatric Association 168th annual conference, Toronto, Canada; 05/2015
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    • "The increasing adoption of DBS as a clinical tool for the treatment of a diverse range of pathological conditions has intensified interest in answering this question. The emerging consensus is that DBS primarily activates afferent and efferent axonal elements within the vicinity of the electrode tip in both the orthodromic and antidromic directions (Perlmutter & Mink 2006, Kringelbach et al. 2007, Deniau et al. 2010). Glial cell activation resulting in the release of adenosine, which could inhibit synaptic transmission in nearby neurones, may be another contributory factor (Bekar et al. 2008, Tawfik et al. 2010, Vedam-Mai et al. 2012, Fenoy et al. 2014). "
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    ABSTRACT: To understand how deep brain stimulation of the midbrain influences control of the urinary bladder. In urethane-anaesthetized male rats saline was infused continuously into the bladder to evoke cycles of filling and voiding. The effect of electrical (0.1-2.0ms pulses, 5-180Hz, 0.5-2.5V) compared to chemical stimulation (microinjection of D,L-homocysteic acid, 50nl 0.lM solution) at the same midbrain sites was tested. Electrical stimulation of the periaqueductal grey matter and surrounding midbrain disrupted normal co-ordinated voiding activity in detrusor and sphincters muscles and suppressed urine output. The effect occurred within seconds, was reversible and not secondary to cardiorespiratory changes. Bladder compliance remained unchanged. Chemical stimulation over the same area using microinjection of DLH to preferentially activate somatodendritic receptors decreased the frequency of micturition but did not disrupt the co-ordinated pattern of voiding. In contrast, chemical stimulation within the caudal ventrolateral periaqueductal grey, in the area where critical synapses in the micturition reflex pathway are located, increased the frequency of micturition. Electrical deep brain stimulation within the midbrain can inhibit reflex micturition. We suggest that the applied stimulus entrained activity in the neural circuitry locally, thereby imposing an unphysiological pattern of activity. In a way similar to the use of electrical signals to 'jam' radio transmission, this may prevent a synchronised pattern of efferent activity being transmitted to the spinal outflows to orchestrate a co-ordinated voiding response. Further experiments to record neuronal firing in the midbrain during the deep brain stimulation will be necessary to test this hypothesis. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Acta Physiologica 03/2015; 214(1). DOI:10.1111/apha.12491 · 4.38 Impact Factor
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    • "In this context we note that several factors may make the human brain more susceptible to electric fields, including larger sensitivity of individual neurons (due to size; Radman et al. 2009) and higher number of synaptic connections compared with our in vitro preparation (sensitivity to fields may increase with the number of synaptic inputs a neuron receives; Reato et al. 2013). Either way, our field amplitudes are still much below those generated with transcranial magnetic stimulation (Pascual-Leone et al. 2002) or deep brain stimulation (Perlmutter and Mink 2006), estimated in the order of 100 V/m (Salinas et al. 2009 "
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    ABSTRACT: Transcranial Direct Current Stimulation (tDCS) is emerging as a versatile tool to affect brain function. While acute neurophysiological effects of stimulation are well understood, little is know about the long term effects. One hypothesis is that stimulation modulates ongoing neural activity which then translates into lasting effects via physiological plasticity. Here we used carbachol-induced gamma oscillations in hippocampal rat slices to establish whether prolonged constant current stimulation has a lasting effect on endogenous neural activity. During 10 minutes of stimulation, power and frequency of gamma oscillations, as well as multi-unit activity were modulated in a polarity specific manner. Remarkably, the effects on power and multi-unit activity persisted for more than 10 minutes after stimulation terminated. Using a computational model we propose that altered synaptic efficacy in excitatory and inhibitory pathways could be the source of these lasting effects. Future experimental studies using this novel in-vitro preparation may be able to confirm or refute the proposed hypothesis. Copyright © 2014, Journal of Neurophysiology.
    Journal of Neurophysiology 12/2014; 113(5):jn.00208.2014. DOI:10.1152/jn.00208.2014 · 2.89 Impact Factor
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