# Transcranial Magnetic Stimulation in Parkinson’s Disease and Parkinsonian Syndromes: A Narrative Expert Review

**Authors:** Mariagiovanna Cantone, Manuela Pennisi, Rita Bella, Raffaele Ferri, Francesco Fisicaro, Giuseppe Lanza, Maria P. Mogavero, Aurora Palmigiano, Angelica Quercia, Mario Zappia

PMC · DOI: 10.3390/life16020233 · Life · 2026-02-01

## TL;DR

This paper reviews how transcranial magnetic stimulation (TMS) can be used to study and treat Parkinson’s disease and related movement disorders, offering a non-invasive alternative to surgery.

## Contribution

The paper provides a comprehensive narrative review of TMS applications in parkinsonian syndromes, emphasizing clinical potential and research gaps.

## Key findings

- TMS can modulate cortical plasticity and improve motor and non-motor symptoms in Parkinson’s disease.
- TMS is a safe, repeatable, and non-invasive method for investigating neurophysiological changes in parkinsonian syndromes.
- TMS may help distinguish neurophysiological differences in atypical parkinsonisms and offer symptomatic relief.

## Abstract

Transcranial magnetic stimulation (TMS) is a non-invasive brain stimulation tool for investigating the neurophysiology of different neurological and neuropsychiatric disorders, including Parkinson’s disease (PD) and other parkinsonian syndromes and movement disorders. Briefly, TMS enables targeted stimulation of specific cortical regions through externally applied magnetic pulses, avoiding surgical intervention (as it occurs in deep brain stimulation) and making it a safe, repeatable, and well-tolerated approach. Over the past two decades, extensive research has explored the clinical utility of TMS in PD, with particular emphasis on motor cortex excitability, synaptic plasticity, and functional connectivity, which are central contributors to both motor and non-motor symptoms in PD patients. In addition, repetitive TMS and related stimulation paradigms have been shown to positively modulate cortical plasticity, i.e., the brain’s capacity to reorganize neural circuits, suggesting potential benefits for longer-term non-pharmacological management and rehabilitation protocols. More recently, studies have also investigated the role of TMS in atypical and secondary parkinsonisms, indicating that it may help characterize distinct neurophysiological abnormalities and provide symptomatic improvement in selected patients. This narrative expert review provides a comprehensive summary of TMS applications across the wide spectrum of parkinsonian syndromes, highlighting not only clinical potential, but also methodological limitations and future research directions.

## Linked entities

- **Diseases:** Parkinson’s disease (MONDO:0005180)

## Full-text entities

- **Genes:** GFAP (glial fibrillary acidic protein) [NCBI Gene 2670] {aka ALXDRD}, MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}, BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}, PRKN (parkin RBR E3 ubiquitin protein ligase) [NCBI Gene 5071] {aka AR-JP, LPRS2, PARK2, PDJ}
- **Diseases:** akinetic rigidity (MESH:D009127), Supranuclear Palsy (MESH:D013494), gait instability (MESH:D043171), impaired voluntary vertical gaze (MESH:D009155), RBD (MESH:D020187), motor disorder (MESH:D000068079), cognitive and neuropsychiatric symptoms (MESH:D003072), neurological and neuropsychiatric disorders (MESH:D009422), movement and motor disorders (MESH:D009069), callosal damage (MESH:D002145), LID (MESH:D004409), FoG (MESH:D020234), depression (MESH:D003866), sleep fragmentation (MESH:D012892), neuronal degeneration (MESH:D009410), LICI (MESH:C565433), Dementia (MESH:D003704), cortical abnormalities (MESH:D054220), Parkinsonisms (MESH:D010302), involuntary movements (MESH:D020820), corticospinal dysfunction (MESH:D006331), degeneration of the substantia nigra pars compacta (MESH:D015868), ischemic damage (MESH:D017202), attentional and visuospatial deficits (MESH:D001289), PSP (MESH:D011030), organic movement disorders (MESH:D019965), infections (MESH:D007239), aphasia (MESH:D001037), vascular injury (MESH:D057772), cerebrovascular lesions (MESH:D002561), NIBS (MESH:D000093284), alien-hand syndrome (MESH:D055964), hallucination (MESH:D006212), gliosis (MESH:D005911), postural abnormalities (MESH:D054972), dysphagia (MESH:D003680), EDS (MESH:D006970), ocular motility abnormalities (MESH:D015835), cerebellar ataxia (MESH:D002524), tremor (MESH:D014202), akinetic (MESH:D018476), ischemic vascular dementia (MESH:D015140), myoclonus (MESH:D009207), hyperactivity (MESH:D006948), MD (MESH:D003865), neurological disorders (MESH:D009461), olivopontocerebellar atrophy (MESH:D009849), FMD (MESH:C536391), difficulty (MESH:D051346), autonomic dysfunction (MESH:D001342), systemic diseases (MESH:D034721), post-traumatic parkinsonism (MESH:D004834), olfactory dysfunction (MESH:D000857), and cholinergic dysfunction (MESH:C535672), mood disturbances (MESH:D019964), gait disturbances (MESH:D020233), primary lateral sclerosis (MESH:D016472), dysarthria (MESH:D004401), FMDs (MESH:D003291), Fatigue (MESH:D005221)
- **Chemicals:** dopamine (MESH:D004298), glutamine (MESH:D005973), fluoxetine (MESH:D005473), scopolamine (MESH:D012601), pramipexole (MESH:D000077487), melatonin (MESH:D008550), L-DOPA (MESH:D007980), NIBS (-), GABA (MESH:D005680), acetylcholine (MESH:D000109), clonazepam (MESH:D002998), apomorphine (MESH:D001058), vitamin D (MESH:D014807), adenosine (MESH:D000241)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

256 references — full list in the complete paper: https://tomesphere.com/paper/PMC12942502/full.md

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Source: https://tomesphere.com/paper/PMC12942502