Abstract

Dementia is recognized as a healthcare and social burden and remains challenging in terms of proper diagnosis and treatment. Transcranial magnetic stimulation (TMS) is a diagnostic and therapeutic tool in various neurological diseases that noninvasively investigates cortical excitability and connectivity and can induce brain plasticity. This article reviews findings on TMS in common dementia types as well as therapeutic results. Alzheimer’s disease (AD) is characterized by increased cortical excitability and reduced cortical inhibition, especially as mediated by cholinergic neurons and as documented by impairment of short latency inhibition (SAI). In vascular dementia, excitability is also increased. SAI may have various outcomes, which probably reflects its frequent overlap with AD. Dementia with Lewy bodies (DLB) is associated with SAI decrease. Motor cortical excitability is usually normal, reflecting the lack of corticospinal tract involvement. DLB and other dementia types are also characterized by impairment of short interval intracortical inhibition. In frontotemporal dementia, cortical excitability is increased, but SAI is normal. Repetitive transcranial magnetic stimulation has the potential to improve cognitive function. It has been extensively studied in AD, showing promising results after multisite stimulation. TMS with electroencephalography recording opens new possibilities for improving diagnostic accuracy; however, more studies are needed to support the existing data.

Highlights

  • With life expectancy still increasing, dementia has become one of the main healthcare and social burdens in developed countries

  • Depending on the stimulation pattern, induced plasticity may be directed toward long term potentiation (LTP) with the enhancement of synaptic transmission and increased neuronal firing and metabolism or long-term depression (LTD) with opposite changes. repetitive TMS (rTMS) with high frequencies, i.e., five or more stimuli per second, and a more complex pattern called intermittent theta burst stimulation, as well as several other less frequently used patterns, induce predominantly LTP, whereas low-frequency stimulation, continuous theta burst stimulation and several other protocols result predominantly in LTD [37]

  • The search strategy consisted of the following terms used in combination: “transcranial magnetic stimulation”, “TMS”, “dementia”, “cognitive impairment”, “Alzheimer’s disease”, “dementia with Lewy bodies”, “frontotemporal dementia”, “vascular dementia”, “Parkinson’s disease”, “mild cognitive impairment”, “diagnostics”, “diagnosis”, “therapy”, “treatment”, “biomarker”

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Summary

Introduction

With life expectancy still increasing, dementia has become one of the main healthcare and social burdens in developed countries. At the beginning of TMS, which was in 1985, single pulses were used to excite the primary motor cortex (PMC) and, in turn, to induce descending volleys down the pyramidal tract and the peripheral motor pathways and to induce the contraction of skeletal muscles, which was recorded electrophysiologically as the motor evoked potential (MEP) This basic technique was used and still is, primarily in neurology, to assess the conduction in central motor pathways [22]. Paired Pulse TMS ppTMS gives a more detailed and dimensional insight into excitability and inhibition of the motor cortex In this method, the magnetic stimulus elicited to evoke motor response is preceded by a conditioning stimulus. The parameters obtained with ppTMS described below are, the main established measurements of cortical excitability

Short-Interval Cortical Inhibition
Intracortical Facilitation
Long-Interval Intracortical Inhibition
Short-Latency Afferent Inhibition
Repetitive Transcranial Magnetic Stimulation
Materials and Methods
Alzheimer’s Disease
Increased Cortical Excitability in AD
Impaired Cortical Plasticity
Impaired Cortical Inhibition
Diagnostic Sensitivity and Specificity
Therapy with rTMS
Vascular Dementia
Dementia with Lewy Bodies
Frontotemporal Lobar Degeneration
Parkinson’s Disease with Dementia
Mild Cognitive Impairment
Findings
10. Conclusions
Full Text
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