Chapter 23 Pharmacology of TMS

doi:10.1016/S1567-424X(09)70226-0

Supplements to Clinical Neurophysiology

Volume 56, 2003, Pages 226-231

https://doi.org/10.1016/S1567-424X(09)70226-0 Get rights and content

Publisher Summary

This chapter reviews the currently available data on the pharmacology of transcranial magnetic stimulation (TMS). Only studies on healthy subjects are considered. The most often used experimental approach is to measure motor cortical excitability before (baseline) and at one or more time points after intake of a single dose of the drug under study (post measurements). The post measurements are then compared with the baseline measurements. Another experimental approach is to test drug effects in a blinded placebo-controlled parallel or crossover design. Testing the effects of central nervous system active drugs (neurotransmitters, neuromodulators) on motor cortical excitability by means of TMS has developed into an important field of research. TMS offers now a wide array of measures of motor cortical excitability that covers many different forms of excitability, such as axon and inhibitory and excitatory synaptic excitability.

References (41)

B. Boroojerdi et al.
Mechanisms influencing stimulus-response properties of the human corticospinal system
Clin. Neurophysiol.
(2001)
V. Di Lazzaro et al.
Comparison of descending volleys evoked by transcranial magnetic and electric stimulation in conscious humans
Electroencephalogr. Clin. Neurophysiol.
(1998)
V. Di Lazzaro et al.
Direct demonstration of the effect of lorazepam on the excitability of the human motor cortex
Clin. Neurophysiol.
(2000)
T.V. Ilic et al.
Complex modulation of human motor cortex excitability by the specific serotonin reuptake inhibitor sertraline
Neurosci. Lett.
(2002)
J. Liepert et al.
Orally administered atropine enhances motor cortex excitability: a transcranial magnetic stimulation study in human subjects
Neurosci. Lett.
(2001)
N. Mavroudakis et al.
Effects of diphenylhydantoin on motor potentials evoked with magnetic stimulation
Electroencephalogr. Clin. Neurophysiol.
(1994)
C. Plewnia et al.
Noradrenergic modulation of human cortex excitability by the presynaptic alpha(2)-antagonist yohimbine
Neurosci. Lett.
(2001)
C. Plewnia et al.
Enhancement of human cortico-motoneuronal excitability by the selective norepinephrine reuptake inhibitor reboxetine
Neurosci. Lett.
(2002)
P. Schwenkreis et al.
Influence of the N-methyl-D-aspartate antagonist mementine on human motor cortex excitability
Neurosci. Lett.
(1999)
H. Tokimura et al.
Short latency facilitation between pairs of threshold magnetic stimuli applied to human motor cortex
Electroencephalogr. Clin. Neurophysiol.
(1996)

S. Wischer et al.

Piracetam affects facilitatory I-wave interaction in the human motor cortex

Clin. Neurophysiol.

(2001)

U. Ziemann et al.

Enhancement of human motor cortex inhibition by the dopamine receptor agonist pergolide: evidence from transcranial magnetic stimulation

Neurosci. Lett.

(1996)

U. Ziemann et al.

Changes in human motor cortex excitability induced by dopaminergic and anti-dopaminergic drugs

Electroencephalogr. Clin. Neurophysiol.

(1997;)

U. Ziemann et al.

Pharmacological control of facilitatory I-wave interaction in the human motor cortex. A paired transcranial magnetic stimulation study

Electroencephalogr. Clin. Neurophysiol.

(1998)

R. Cantello et al.

Magnetic brain stimulation: the silent period after the motor evoked potential

Neurology

(1992)

R. Chen et al.

Effects of phenytoin on cortical excitability in humans

Neurology

(1997)

V. Di Lazzaro et al.

Muscarinic receptor blockade has differential effects on the excitability of intracortical circuits in human motor cortex

Exp. Brain Res.

(2000)

V. Di Lazzaro et al.

Noninvasive in vivo assessment of cholinergic cortical circuits in AD using transcranial magnetic stimulation

Neurology

(2002)

V. Di Lazzaro et al.

Ketamine increases motor cortex excitability to transcranial magnetic stimulation

J. Physiol.

(2003)

R.J. Fisher et al.

Two phases of intracortical inhibition revealed by transcranial magnetic threshold tracking

Exp. Brain Res.

(2002)

Cited by (125)

Identifying novel biomarkers with TMS-EEG – Methodological possibilities and challenges
2022, Journal of Neuroscience Methods
Biomarkers are essential for understanding the underlying pathologies in brain disorders and for developing effective treatments. Combined transcranial magnetic stimulation and electroencephalography (TMS-EEG) is an emerging neurophysiological tool that can be used for biomarker development. This method can identify biomarkers associated with the function and dynamics of the inhibitory and excitatory neurotransmitter systems and effective connectivity between brain areas. In this review, we outline the current state of the TMS-EEG biomarker field by summarizing the existing protocols and the possibilities and challenges associated with this methodology.
Neural mechanisms mediating cross education: With additional considerations for the ageing brain
2022, Neuroscience and Biobehavioral Reviews
CALVERT, G.H.M., and CARSON, R.G. Neural mechanisms mediating cross education: With additional considerations for the ageing brain. NEUROSCI BIOBEHAV REV 21(1) XXX-XXX, 2021. - Cross education (CE) is the process whereby a regimen of unilateral limb training engenders bilateral improvements in motor function. The contralateral gains thus derived may impart therapeutic benefits for patients with unilateral deficits arising from orthopaedic injury or stroke. Despite this prospective therapeutic utility, there is little consensus concerning its mechanistic basis. The precise means through which the neuroanatomical structures and cellular processes that mediate CE may be influenced by age-related neurodegeneration are also almost entirely unknown. Notwithstanding the increased incidence of unilateral impairment in later life, age-related variations in the expression of CE have been examined only infrequently. In this narrative review, we consider several mechanisms which may mediate the expression of CE with specific reference to the ageing CNS. We focus on the adaptive potential of cellular processes that are subserved by a specific set of neuroanatomical pathways including: the corticospinal tract, corticoreticulospinal projections, transcallosal fibres, and thalamocortical radiations. This analysis may inform the development of interventions that exploit the therapeutic utility of CE training in older persons.
Cerebellar inhibition in hepatic encephalopathy
2019, Clinical Neurophysiology
Citation Excerpt :
Inhibition in terms of short-interval intracortical inhibition (SICI) is supposed to be mediated by GABA-A receptors and long-interval intracortical inhibition (LICI) by GABA-B receptors. On the other hand, intracortical facilitation (ICF) and short-interval intracortical facilitation (SICF) are supposed to reflect excitatory glutamatergic circuits (Kujirai et al., 1993; Ziemann et al., 1996; Hanajima et al., 2002; Ziemann, 2003). In the present study, we used another type of paired-pulse TMS called cerebellar inhibition (CBI).
Previous animal work reported that hyperammonemia leads to opposing changes of GABAergic neurotransmission in terms of increase in the cerebellum and decrease in the cerebral cortex. In this study, we investigate GABAergic tone in the cerebellum in patients with hepatic encephalopathy (HE) at different stages of the disease and its relation to critical flicker frequency (CFF) and ataxia.
Cerebellar inhibition using transcranial magnetic stimulation was investigated in 15 patients with different stages of HE and 15 healthy controls. All patients were assessed using CFF and the score for assessment and rating of ataxia (SARA).
Decreased cerebellar inhibition (CBI) was observed in manifest HE at interstimulus interval from 5 to 7 ms. However, the degree of CBI at 7 ms correlated significantly with disease severity measured with SARA and with CFF by trend.
Reduced CBI in HE patients indicates affection of the cerebellar efferent pathway. The disease severity dependent increase of CBI magnitude supports the notion of disease stage dependent increase of GABAergic neurotransmission in Purkinje cells.
The results support previous animal experiments showing increase of GABA-ergic neurotransmission in the cerebellum and decrease in the motor cortex in HE.
Age related changes of the motor excitabilities and central and peripheral muscle strength
2019, Journal of Electromyography and Kinesiology
The purpose was to investigate the age effects on central versus peripheral sources of strength, fatigue, and central neural excitabilities.
42 healthy subjects were recruited as young group (23.73 ± 2.15 years; n = 26) and middle-aged group (57.25 ± 4.57 years; n = 16). Maximum voluntary contraction force (MVC), voluntary activation level (VA), and twitch force of quadriceps were evaluated to represent general, central, and peripheral strengths. Central and peripheral fatigue indexes were evaluated using femoral nerve electrical stimulation. Cortical excitabilities were evaluated using transcranial magnetic stimulation (TMS).
The middle-aged group had lower MVC and twitch force of quadriceps, but not VA, than young group. No between group differences were found in fatigue indexes. The cortical excitability in middle-aged group was different from young group in paired TMS with inter-stimulus interval of 7 ms.
The age-related strength loss at early stage was primarily caused by peripheral muscular strength. The deviation of central neural excitability can be detected but the activation level was not impaired in middle-age adults.
Transcranial Magnetic Stimulation for Adolescent Depression
2019, Child and Adolescent Psychiatric Clinics of North America
Induction of excitatory brain state governs plastic functional changes in visual cortical topology
2024, Brain Structure and Function

View all citing articles on Scopus

View full text