scholarly journals Deep brain stimulation may reduce tremor by preferential blockade of slower axons via antidromic activation

2011 ◽  
Author(s):  
Miriam R. Garcia ◽  
Mark Verwoerd ◽  
Barak A. Pearlmutter ◽  
Peter E. Wellstead ◽  
Richard H. Middleton
Keyword(s):  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Antidromic Activation ◽  
Deep Brain

scholarly journals Deep Brain Stimulation of the Nucleus Accumbens Shell Attenuates Cocaine Reinstatement through Local and Antidromic Activation

2013 ◽  
Vol 33 (36) ◽  
pp. 14446-14454 ◽  
Author(s):  
F. M. Vassoler ◽  
S. L. White ◽  
T. J. Hopkins ◽  
L. A. Guercio ◽  
J. Espallergues ◽  
...  
Keyword(s):  
Deep Brain Stimulation ◽  
Nucleus Accumbens ◽  
Brain Stimulation ◽  
Nucleus Accumbens Shell ◽  
Antidromic Activation ◽  
Deep Brain ◽  
Stimulation Of ◽  
Cocaine Reinstatement

scholarly journals Activation of subthalamic neurons by contralateral subthalamic deep brain stimulation in Parkinson disease

2011 ◽  
Vol 105 (3) ◽  
pp. 1112-1121 ◽  
Author(s):  
Harrison C. Walker ◽  
Ray L. Watts ◽  
Christian J. Schrandt ◽  
He Huang ◽  
Stephanie L. Guthrie ◽  
...  
Keyword(s):  
Deep Brain Stimulation ◽  
Parkinson Disease ◽  
Brain Stimulation ◽  
Low Frequency ◽  
High Frequency Stimulation ◽  
Antidromic Activation ◽  
Local Inhibition ◽  
Frequency Stimulation ◽  
Stn Dbs ◽  
Deep Brain

Multiple studies have shown bilateral improvement in motor symptoms in Parkinson disease (PD) following unilateral deep brain stimulation (DBS) of the subthalamic nucleus (STN) and internal segment of the globus pallidus, yet the mechanism(s) underlying this phenomenon are poorly understood. We hypothesized that STN neuronal activity is altered by contralateral STN DBS. This hypothesis was tested intraoperatively in humans with advanced PD using microelectrode recordings of the STN during contralateral STN DBS. We demonstrate alterations in the discharge pattern of STN neurons in response to contralateral STN DBS including short latency, temporally precise, stimulation frequency-independent responses consistent with antidromic activation. Furthermore, the total discharge frequency during contralateral high frequency stimulation (160 Hz) was greater than during low frequency stimulation (30 Hz) and the resting state. These findings demonstrate complex responses to DBS and imply that output activation throughout the basal ganglia-thalamic-cortical network rather than local inhibition is a therapeutic mechanism of DBS.

scholarly journals Therapeutic Deep Brain Stimulation Disrupts Subthalamic Nucleus Activity Dynamics in Parkinsonian Mice

2021 ◽  
Author(s):  
Jonathan S Schor ◽  
Isabelle Gonzalez Montalvo ◽  
Perry W.E. Spratt ◽  
Rea J Brakaj ◽  
Jasmine A Stansil ◽  
...  
Keyword(s):  
Deep Brain Stimulation ◽  
Basal Ganglia ◽  
Subthalamic Nucleus ◽  
Brain Stimulation ◽  
Electrophysiological Recording ◽  
Free Calcium ◽  
Motor Symptoms ◽  
Antidromic Activation ◽  
Stn Dbs ◽  
Deep Brain

Subthalamic nucleus deep brain stimulation (STN DBS) relieves many motor symptoms of Parkinson Disease (PD), but its underlying therapeutic mechanisms remain unclear. Since its advent, three major theories have been proposed: (1) DBS inhibits the STN and basal ganglia output; (2) DBS antidromically activates motor cortex; and (3) DBS disrupts firing dynamics within the STN. Previously, stimulation-related electrical artifacts limited mechanistic investigations using electrophysiology. We used electrical artifact-free calcium imaging to investigate activity in basal ganglia nuclei during STN DBS in parkinsonian mice. To test whether the observed changes in activity were sufficient to relieve motor symptoms, we then combined electrophysiological recording with targeted optical DBS protocols. Our findings suggest that STN DBS exerts its therapeutic effect through the disruption of STN dynamics, rather than inhibition or antidromic activation. These results provide insight into optimizing PD treatments and establish an approach for investigating DBS in other neuropsychiatric conditions.

scholarly journals Resonant Antidromic Cortical Circuit Activation as a Consequence of High-Frequency Subthalamic Deep-Brain Stimulation

2007 ◽  
Vol 98 (6) ◽  
pp. 3525-3537 ◽  
Author(s):  
S. Li ◽  
G. W. Arbuthnott ◽  
M. J. Jutras ◽  
J. A. Goldberg ◽  
D. Jaeger
Keyword(s):  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
High Frequency ◽  
Cortical Neurons ◽  
Active Sites ◽  
Cortical Activation ◽  
Oscillatory Activity ◽  
Antidromic Activation ◽  
Stn Dbs ◽  
Deep Brain

Deep brain stimulation (DBS) is an effective treatment of Parkinson's disease (PD) for many patients. The most effective stimulation consists of high-frequency biphasic stimulation pulses around 130 Hz delivered between two active sites of an implanted depth electrode to the subthalamic nucleus (STN-DBS). Multiple studies have shown that a key effect of STN-DBS that correlates well with clinical outcome is the reduction of synchronous and oscillatory activity in cortical and basal ganglia networks. We hypothesized that antidromic cortical activation may provide an underlying mechanism responsible for this effect, because stimulation is usually performed in proximity to cortical efferent pathways. We show with intracellular cortical recordings in rats that STN-DBS did in fact lead to antidromic spiking of deep layer cortical neurons. Furthermore, antidromic spikes triggered a dampened oscillation of local field potentials in cortex with a resonant frequency around 120 Hz. The amplitude of antidromic activation was significantly correlated with an observed suppression of slow wave and beta band activity during STN-DBS. These findings were seen in ketamine-xylazine or isoflurane anesthesia in both normal and 6-hydroxydopamine (6-OHDA)–lesioned rats. Thus antidromic resonant activation of cortical microcircuits may make an important contribution toward counteracting the overly synchronous and oscillatory activity characteristic of cortical activity in PD.

scholarly journals Model-based deconstruction of cortical evoked potentials generated by subthalamic nucleus deep brain stimulation

2018 ◽  
Vol 120 (2) ◽  
pp. 662-680 ◽  
Author(s):  
Karthik Kumaravelu ◽  
Chintan S. Oza ◽  
Christina E. Behrend ◽  
Warren M. Grill
Keyword(s):  
Deep Brain Stimulation ◽  
Subthalamic Nucleus ◽  
Brain Stimulation ◽  
Pyramidal Neurons ◽  
Antidromic Activation ◽  
Long Latency ◽  
Latency Response ◽  
Stn Dbs ◽  
Deep Brain

Parkinson’s disease is associated with altered neural activity in the motor cortex. Chronic high-frequency deep brain stimulation (DBS) of the subthalamic nucleus (STN) is effective in suppressing parkinsonian motor symptoms and modulates cortical activity. However, the anatomical pathways responsible for STN DBS-mediated cortical modulation remain unclear. Cortical evoked potentials (cEP) generated by STN DBS reflect the response of cortex to subcortical stimulation, and the goal of this study was to determine the neural origin of STN DBS-generated cEP using a two-step approach. First, we recorded cEP over ipsilateral primary motor cortex during different frequencies of STN DBS in awake healthy and unilateral 6-OHDA-lesioned parkinsonian rats. Second, we used a detailed, biophysically based model of the thalamocortical network to deconstruct the neural origin of the recorded cEP. The in vivo cEP included short (R1)-, intermediate (R2)-, and long-latency (R3) responses. Model-based cortical responses to simulated STN DBS matched remarkably well the in vivo responses. The short-latency response was generated by antidromic activation of layer 5 pyramidal neurons, whereas recurrent activation of layer 5 pyramidal neurons via excitatory axon collaterals reproduced the intermediate-latency response. The long-latency response was generated by polysynaptic activation of layer 2/3 pyramidal neurons via the cortico-thalamic-cortical pathway. Antidromic activation of the hyperdirect pathway and subsequent intracortical and cortico-thalamo-cortical synaptic interactions were sufficient to generate cortical potential evoked by STN DBS, and orthodromic activation through basal ganglia-thalamus-cortex pathways was not required. These results demonstrate the utility of cEP to determine the neural elements activated by STN DBS that might modulate cortical activity and contribute to the suppression of parkinsonian symptoms. NEW & NOTEWORTHY Subthalamic nucleus (STN) deep brain stimulation (DBS) is increasingly used to treat Parkinson’s disease (PD). Cortical potentials evoked by STN DBS in patients with PD exhibit consistent short-latency (1–3 ms), intermediate-latency (5–15 ms), and long-latency (18–25 ms) responses. The short-latency response occurs as a result of antidromic activation of the hyperdirect pathway comprising corticosubthalamic axons. However, the neural origins of intermediate- and long-latency responses remain elusive, and the dominant view is that these are produced through the orthodromic pathway (basal ganglia-thalamus-cortex). By combining in vivo electrophysiology with computational modeling, we demonstrate that antidromic activation of the cortico-thalamic-cortical pathway is sufficient to generate the intermediate- and long-latency cortical responses to STN DBS.

Deep Brain Stimulation Aids Resistant Depression

2008 ◽  
Vol 41 (19) ◽  
pp. 20
Author(s):  
MICHELE G. SULLIVAN
Keyword(s):  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Resistant Depression ◽  
Deep Brain

Nicht-medikamentöse Optionen zur Behandlung pharmakoresistenter Epilepsien

2018 ◽  
Vol 75 (7) ◽  
pp. 448-454
Author(s):  
Thomas Grunwald ◽  
Judith Kröll
Keyword(s):  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Tiefe Hirnstimulation ◽  
Ketogene Diät ◽  
Deep Brain

Zusammenfassung. Wenn mit den ersten beiden anfallspräventiven Medikamenten keine Anfallsfreiheit erzielt werden konnte, so ist die Wahrscheinlichkeit, dies mit anderen Medikamenten zu erreichen, nur noch ca. 10 %. Es sollte dann geprüft werden, warum eine Pharmakoresistenz besteht und ob ein epilepsiechirurgischer Eingriff zur Anfallsfreiheit führen kann. Ist eine solche Operation nicht möglich, so können palliative Verfahren wie die Vagus-Nerv-Stimulation (VNS) und die tiefe Hirnstimulation (Deep Brain Stimulation) in eine bessere Anfallskontrolle ermöglichen. Insbesondere bei schweren kindlichen Epilepsien stellt auch die ketogene Diät eine zu erwägende Option dar.

The Effect of Deep Brain Stimulation for Movement Disorders on Emotions

2008 ◽  
Author(s):  
Jonathan D. Richards ◽  
Paul M. Wilson ◽  
Pennie S. Seibert ◽  
Carin M. Patterson ◽  
Caitlin C. Otto ◽  
...  
Keyword(s):  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Movement Disorders ◽  
Deep Brain
Sign in / Sign up

Export Citation Format

Share Document