Primary Motor Cortex

Anatomy

• Precentral gyrus and the anterior paracentral lobule; BA 4. Separated from somatosensory cortex by the central sulcus.
• Somatotopic organization (motor homunculus): leg and foot medially, then trunk, arm, hand (a large area), with face and tongue lowest laterally.
• Giant pyramidal cells (Betz cells) in layer V.
• Blood supply: face–arm region MCA, leg region (medial) ACA.

Functions

• Execution of voluntary movement; corticospinal and corticobulbar tracts.
• Coding of force, direction and speed; fine finger movements.
• Reorganization of the somatotopic map with motor learning (plasticity).

Connections and chemistry

• Corticospinal tract (internal capsule → brainstem → spinal cord)
• Premotor cortex / SMA
• Somatosensory cortex
• Thalamus VL (cerebellar and basal ganglia inputs)
• Putamen

Development

Developmental course through childhood and adolescence.

• Corticospinal myelination is rapid from birth to about age 2; fine motor control develops into adolescence.
• Disappearance of primitive reflexes reflects maturation of cortical inhibition.
• Ipsilateral projections present early on are pruned in infancy.

Clinical

• Cerebral palsy: spasticity and motor delay from perinatal injury. Diagnosis can now be made before 6 months (corrected age): before 5 months, General Movements Assessment (GMA) plus MRI is more than 95% accurate; afterwards, HINE plus MRI more than 90% (Novak et al., 2017). Early diagnosis allows intervention while brain plasticity is at its highest. A
• Tourette syndrome and ADHD: reduced short-interval intracortical inhibition (SICI) in TMS studies.
• Functional (conversion) motor disorders: common in adolescence; positive examination signs in the absence of organic findings.

Treatment

This region from the perspective of medication, psychotherapy and neuromodulation. Letter badges are evidence levels.

• Early, diagnosis-specific intervention in cerebral palsy: constraint-induced movement therapy and intensive bimanual training in unilateral (hemiplegic) involvement; botulinum toxin for spasticity; selective dorsal rhizotomy in selected cases. A
• Functional (conversion) motor disorder: diagnosed by positive signs (e.g. Hoover’s sign); a clear and confident explanation of the diagnosis, physiotherapy and psychotherapy together. B
• TMS measures of cortical excitability (SICI) are research tools in Tourette syndrome and ADHD, not treatments. C

Assessment

Neuropsychological tasks and measures that probe this region's function.

• Finger tapping speed, Grooved Pegboard
• Muscle strength and reflex examination
• Motor evoked potentials and cortical inhibition with TMS (research)

Lesions and damage

Clinical findings expected with damage or dysfunction.

• Contralateral upper motor neuron signs: weakness (especially distal fine movements), spasticity, hyperreflexia, Babinski sign.
• Focal motor seizures and the “Jacksonian march”; postictal Todd’s paralysis.

In the model

How this structure is defined in the 3D model, and the data source.

HCP-MMP1.0 areas (Glasser et al., 2016; MNI volumetric version: Horn, 2016) 4 (posterior precentral gyrus and paracentral lobule); precentral vertices without an HCP match follow the CerebrA gyrus.

References

Full citations for the card; links go to the paper (DOI) or a PubMed search.

1. Novak I et al. Early, accurate diagnosis and early intervention in cerebral palsy: advances in diagnosis and treatment. JAMA Pediatr 2017;171(9):897–907. Search PubMed