# Update on the Pathophysiology and Management of Tics

**Authors:** Emily Casaletto, Lucy Morse, Darren Miller, Juan Deliz-Gonzalez, Danielle Larson

PMC · DOI: 10.1007/s11910-026-01480-8 · Current Neurology and Neuroscience Reports · 2026-03-04

## TL;DR

This review summarizes recent advances in understanding tics, their genetic and neurological basis, and new treatment options.

## Contribution

The paper collates recent findings on tics, including genetic studies, FTLBs, and novel treatments, with a focus on pandemic-related insights.

## Key findings

- Genome-wide and neuroimaging studies reveal genetic and structural links to Tourette Syndrome.
- Functional tic-like behaviors increased during the pandemic, influenced by social media exposure.
- New treatments like VMAT-2 inhibitors and transcranial stimulation are being explored for tic management.

## Abstract

This review aims to collate takeaways from the most recent and relevant literature related to tics, from genetic studies to case studies elucidating Functional tic like behaviors (FTLBs) and clinical trials of novel drugs in development.

Recent genome-wide association studies (GWAS) and functional neuroimaging studies have enhanced the understanding of genetic and structural links to Tourette Syndrome (TS). The rise of FTLBs during the Covid-19 pandemic heightened our understanding of this phenomenon and led to the identification of social media’s influence on tics. New studies have identified sex-related difference in TS and common psychiatric co-morbidities. Tic treatment is evolving away from traditional anti-psychotics toward newer compounds including VMAT-2 inhibitors, Ecopipam, and cannabinoid formulations, as well as novel transcranial stimulation approaches.

Our understanding of tic etiology and pathophysiology as well tics’ functional counterpart FTLBs and social media impact is expanding along with our ability to manage tics with novel treatments in development.

## Linked entities

- **Diseases:** Tourette Syndrome (MONDO:0007661)

## Full-text entities

- **Genes:** DRD1 (dopamine receptor D1) [NCBI Gene 1812] {aka D1R, DADR, DRD1A}, SLC18A2 (solute carrier family 18 member A2) [NCBI Gene 6571] {aka PKDYS2, SVAT, SVMT, VAT2, VMAT2}
- **Diseases:** memory lapses (MESH:D008569), Mov Disord (MESH:D009358), movement disorders (MESH:D009069), extrapyramidal symptoms (MESH:D001480), Tic (MESH:D020323), cognitive difficulties (MESH:D003072), media (MESH:D010033), hyperkinetic (MESH:D006948), FMD (MESH:C536391), involuntary movements (MESH:D020820), aggressive behaviors (MESH:D010554), fatigue (MESH:D005221), OCD (MESH:D009771), depression (MESH:D003866), distractibility (MESH:C538521), TD (MESH:D004409), weight gain (MESH:D015430), anxiety (MESH:D001007), FTLBs (MESH:D013981), ASD (MESH:D001321), induced (MESH:D000092582), ADHD (MESH:D001289), -psychotics (MESH:D011618), COVID-19 (MESH:D000086382), -morbidities (OMIM:614963), insomnia (MESH:D007319), TS (MESH:D005879), psychiatric (MESH:D001523), headache (MESH:D006261), somnolence (MESH:D006970), tension (MESH:D018781)
- **Chemicals:** atomoxetine (MESH:D000069445), dextroamphetamine (MESH:D003913), risperidone (MESH:D018967), Nabiximols (MESH:C587251), Cannabinoid (MESH:D002186), dopamine (MESH:D004298), desipramine (MESH:D003891), guanfacine (MESH:D016316), valbenazine (MESH:C000603978), selegiline (MESH:D012642), deutetrabenazine (MESH:C000609690), lurasidone (MESH:D000069056), Delta9-tetrahydrocannabinol (MESH:D013759), Ecopipam (MESH:C058081), Aripiprazole (MESH:D000068180), methylphenidate (MESH:D008774), brexpiprazole (MESH:C000591922), tetrabenazine (MESH:D013747), clonidine (MESH:D003000), CBD (-), haloperidol (MESH:D006220)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12960455/full.md

## References

10 references — full list in the complete paper: https://tomesphere.com/paper/PMC12960455/full.md

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Source: https://tomesphere.com/paper/PMC12960455