Corticoreticular fibers

The corticoreticular fibres (a.k.a. the corticoreticular tract) are descending cortical nerve fibres that connects areas of the cerebral cortex with the reticular formation of the brainstem. These constitute the cortical component of the corticoreticulospinal system, through which cortical motor commands can influence spinal motor activity via the reticulospinal tracts.

The corticoreticular fibres originates mainly from the premotor cortex, although contributions have also been demonstrated from the primary motor cortex, primary somatosensory cortex and prefrontal cortex.

From the cerebral cortex, the fibres descend through the corona radiata and posterior limb of the internal capsule. At the level of the subcortical white matter, the corticospinal fibres lies generally anteromedial to the corticospinal tract, although portions of the two pathways may overlap. It then passes through the mesencephalic tegmentum and pontine reticular formation before terminating in the pontomedullary reticular formation.

Functional correlate

Through its connections with the reticulospinal tracts, the corticoreticular fibres are particularly associated with the control of axial and proximal limb muscles and contributes to gait and postural stability. This contrasts with the lateral corticospinal tract, which is more strongly associated with control of distal limb movements.

Clinical correlate; upper motor neuron lesion

Damage to the corticoreticular tract is particularly associated with proximal and axial motor impairment, including weakness of muscles acting at the shoulder and hip, together with impaired gait and postural stability. If the corticospinal tract remains intact, distal limb movements may be relatively preserved, and corticoreticular injury alone would not normally cause complete limb paralysis.

In an upper motor neuron lesion, involvement of corticoreticular fibres can contribute to hyperreflexia, spasticity and abnormal motor synergies, although damage to the corticoreticular tract does not necessarily produce these features by itself. Normally, spinal stretch-reflex excitability is regulated by a balance between inhibitory influences from the dorsal (medullary) reticulospinal tract and excitatory influences from the medial (pontine) reticulospinal and vestibulospinal tracts. The motor cortex facilitates the inhibitory (medullary) reticulospinal system through the corticoreticular pathway. Therefore, loss of corticoreticular input may reduce this inhibitory influence, leaving the excitatory descending systems relatively less opposed. The resulting increase in spinal motor-neuron and stretch-reflex excitability can contribute to hyperreflexia and spasticity. Thus, these positive upper motor neuron signs are best understood as resulting from an imbalance among interacting descending motor systems, rather than as a direct consequence of damage to the corticoreticular fibres alone.