Basal Ganglia · PUT · deep structure
Putamen
Putamen
The entry gate of the motor loop: initiation of movement, habits that become automatic and motor sequence learning.
Anatomy
- The lateral part of the lentiform nucleus (together with the globus pallidus).
- Separated from the claustrum by the external capsule and from the caudate and thalamus by the internal capsule.
- Input: primary motor and somatosensory cortex, SMA (motor loop); substantia nigra pars compacta.
- Blood supply: lenticulostriate arteries (MCA).
Functions
- Initiation and scaling of movement.
- Habits (stimulus–response learning) and automatic behaviors.
- Motor sequence learning and procedural memory.
- Rhythm and timing; speech articulation.
- Receiving dopaminergic reward prediction error signals.
Connections and chemistry
- Motor and somatosensory cortex, SMA
- Globus pallidus (direct/indirect pathway)
- Thalamus VL
- Substantia nigra pars compacta (nigrostriatal dopamine)
Development
Developmental course through childhood and adolescence.
- Habit systems function early; motor automatization accelerates in childhood.
- Putamen volume increases in childhood.
Clinical
- Tourette syndrome and tic disorders: motor loop dysfunction; tics are habit-like behaviors.
- ADHD: in the ENIGMA study, putamen, caudate, accumbens, amygdala and hippocampus volumes were smaller in children (Hoogman et al., 2017).
- ASD: relationship between repetitive motor behaviors and striatal size.
- Wilson disease: may begin with psychiatric symptoms in adolescence; copper deposition in the putamen.
- Antipsychotic-related extrapyramidal side effects (striatal D2 blockade).
Treatment
This region from the perspective of medication, psychotherapy and neuromodulation. Letter badges are evidence levels.
- First line for tics is behavior therapy (CBIT: noticing the urge before the tic and a competing movement incompatible with the tic): in 126 children aged 9–17, marked improvement in 52.5% vs 18.5% with supportive therapy (number needed to treat 3); the effect lasted 6 months in 87% of responders (Piacentini et al., 2010). A
- Tic medications: α2 agonists (guanfacine, clonidine; when ADHD co-occurs), D2 blockers (aripiprazole, haloperidol, pimozide). A
- Ecopipam (D1 antagonist, a new mechanism): in a phase III trial (167 children) relapse among responders was 41.9% vs 68.1% with placebo; no weight or movement disorder side effects. Not yet FDA-approved; the application was accepted for priority review in August 2026, with a decision expected in the first quarter of 2027. B
- Wilson disease: copper chelation (penicillamine, trientine) and zinc; with early diagnosis neurological and psychiatric symptoms can reverse. B
- Antipsychotic-induced tardive dyskinesia: VMAT2 inhibitors (valbenazine, deutetrabenazine) are approved in adults. A
Assessment
Neuropsychological tasks and measures that probe this region's function.
- Serial reaction time task (SRTT — implicit learning)
- Mirror drawing, rhythm synchronization (tapping)
- Rotary pursuit
Lesions and damage
Clinical findings expected with damage or dysfunction.
- Dystonia, parkinsonism (dopamine loss).
- Impaired procedural learning.
In the model
How this structure is defined in the 3D model, and the data source.
CerebrA putamen label.
References
Full citations for the card; links go to the paper (DOI) or a PubMed search.
- Piacentini J et al. Behavior therapy for children with Tourette disorder: a randomized controlled trial. JAMA 2010;303(19):1929–1937. Search PubMed
- Ekopipam DIAMOND faz III, JAMA Neurol (Mayıs 2026) and şirket duyuruları. Search PubMed
Evidence level: A large consortium, meta-analysis or regulatory decision · B replicated studies or classic case · C single or pioneering study, experimental use
This page is for education; it must not be used on its own for diagnosis or treatment decisions.
Last reviewed by the author: 12 October 2026
3D model: built from the MNI ICBM152 average brain and the CerebrA, HCP-MMP1.0, CIT168, Harvard AAN, SUIT and Najdenovska thalamus atlases. License details in the atlas.