Historically, the corticospinal and corticobulbar tracts were considered to be part of the pyramidal system because their fibers run in the medullary pyramids. More recently, the pyramidal/extrapyramidal nomenclature has been dropped in favor of more descriptive terms such as direct (corticospinal and corticobulbar) and indirect activation pathways in the motor system. Physiologically, the corticospinal and corticobulbar are monosynaptic; an upper motor neuron (UMN) projects and synapses on a lower motor neuron (LMN) which in turn innervates skeletal muscle. Thus, they directly control voluntary motor activity. However, there are numerous other polysynaptic pathways that also influence movement, which were referred to as the extrapyramidal system. For the purposes of this discussion, theses tracts will be identified as indirect pathways. In the indirect system, neuronal activity also begins in the cortex and then project to structures such as the basal ganglia, brainstem nuclei, and cerebellum before synapsing on LMN (). The role of the indirect pathways is to modify or influence neural impulses originating in the cerebral cortex. These pathways include the rubrospinal, reticulospinal, vestibulospinal, and tectospinal tracts as well as the basal ganglia and cerebellum ().
Fig. 17.1 Connections of the cortex with the basal ganglia and cerebellum: programming of complex movements. The pyramidal motor system (the primary motor cortex and the pyramidal tract arising from it) is assisted by the basal ganglia and cerebellum in the planning and programming of complex movements. While afferent fibers of the motor nuclei (green) project directly to the basal ganglia (left) without synapsing, the cerebellum is indirectly controlled via pontine nuclei. The motor thalamus provides a feedback loop for both structures. The efferent fibers of the basal nuclei and cerebellum are distributed to lower structures including the spinal cord. The importance of the basal ganglia and cerebellum in voluntary movements can be appreciated by noting the effects of lesions in these structures. Although diseases of the basal ganglia impair the initiation and execution of movements (e.g., in Parkinson’s disease), cerebellar lesions are characterized by uncoordinated movements (e.g., the reeling movements of inebriation caused by a temporary toxic insult to the cerebellum). (Reproduced with permission from Schuenke M, Schulte E, Schumacher U. THIEME Atlas of Anatomy Second Edition, Vol 3. ©Thieme 2016. Illustrations by Markus Voll and Karl Wesker.)
The brainstem houses several nuclei that are important in movement. UMN in the cortex directly influences spinal cord circuits by synapsing on LMN in the ventral horn of the spinal cord or by synapsing on cranial nerve motor nuclei in the brainstem. Indirectly, some cortical neurons influence movement via polysynaptic pathways involving the red nucleus, vestibular nuclei, reticular nuclei, and from neurons located in the superior colliculus of the midbrain. These nuclei are associated with descending motor tracts that influence movement ().
Fig. 17.2 Descending tracts of the extrapyramidal motor system. The neurons of origin of the descending tracts of the extrapyramidal motor system* arise from a heterogeneous group of nuclei that includes the basal ganglia (putamen, globus pallidus, and caudate nucleus), the red nucleus, the substantia nigra, and even the motor cortical areas. The following descending tracts are part of the extrapyramidal motor system: (A) Rubrospinal tract, (B) Olivospinal tract, (C) Vestibulospinal tract, (D) Reticulospinal tract, (E) Tectospinal tract. These long descending tracts terminate on interneurons which then form synapses onto alpha and gamma motor neurons, which they control. Besides these long descending motor tracts, the motor neurons additionally receive sensory input. All impulses in these pathways are integrated by the alpha motor neuron and modulate its activity, thereby affecting muscular contractions. The functional integrity of the alpha motor neuron is tested clinically by reflex testing. (Reproduced with permission from Schuenke M, Schulte E, Schumacher U. THIEME Atlas of Anatomy Second Edition, Vol 3. ©Thieme 2016. Illustrations by Markus Voll and Karl Wesker.)
The rubrospinal tract is more prominent in species that use limbs for locomotion. In humans, the tract is primarily directed to cervical levels in the spinal cord and its size is somewhat diminished. In lower species, it continues into the lumbar area.
Fig. 17.3 The rubrospinal tract originates from the red nucleus of the midbrain. It receives input from the motor cortex and the cerebellum. It facilitates control of motor neurons supplying flexors of the upper extremity (among other functions). (Reproduced with permission from Alberstone CD, Benzel EC, Najm IM, et al. Anatomic Basis of Neurologic Diagnosis. © Thieme 2009.)
The reticular formation forms the core of the brainstem. It extends from the caudal medulla and continues rostrally to include the midbrain. There are two reticulospinal tracts originating from the reticular formation: the lateral, which arises from the medulla, and the medial, which originates from the pons ().
Fig. 17.4 The reticulospinal tract originates from the reticular formation of the midbrain. Functionally, this tract is involved in preparatory and movement related activities, postural control, and some autonomic responses. (Reproduced with permission from Alberstone CD, Benzel EC, Najm IM, et al. Anatomic Basis of Neurologic Diagnosis. © Thieme 2009.)
Collectively, the reticulospinal tract regulates the sensitivity of the flexor response so that only noxious stimuli will elicit a response. Damage will result in innocuous stimuli such as a gentle touch to cause a reflex response.
The vestibulospinal tract originates in two vestibular nuclei located beneath the floor of the fourth ventricle in the brainstem. Both tracts convey neural impulses from the labyrinth of the inner ear to the spinal cord ().
Fig. 17.5 The vestibulospinal tract originates from vestibular nuclei in the floor of the fourth ventricle. This tract conveys neural impulses from the inner ear to the spinal cord. It is involved in the maintenance of balance and posture. (Reproduced with permission from Alberstone CD, Benzel EC, Najm IM, et al. Anatomic Basis of Neurologic Diagnosis. © Thieme 2009.)
Fig. 17.6 The tectospinal tract originates in the superior colliculus of the midbrain. Although not entirely certain, it is thought to be involved in visual responses. (Reproduced with permission from Schuenke M, Schulte E, Schumacher U. THIEME Atlas of Anatomy. Third edition, Vol 3. © Thieme 2020. Illustrations by Markus Voll and Karl Wesker.)
The function of the tract is not well known. However, due to the fact that the superior colliculus is known to be involved in visual responses, it is likely that this tract facilitates movement of the head in reflex responses to visual stimuli.
The basal ganglia (BG) consist of several subcortical nuclei, subthalamic nucleus, and the substantia nigra (a, b). Damage to these structures or the pathways connecting them with the cortex and spinal cord results in distinct movement disorders. In addition to movement disorders, basal ganglia disease can impact cognitive function and emotions (Clinical Correlation Box 17.1 and 17.2).
Fig. 17.7 (a) Basal ganglia. Transverse section through the cerebrum at the level of the corpus striatum, superior view. The basal ganglia consist of the caudate nucleus, putamen, and globus pallidus and are an essential component of the extrapyramidal motor system, which controls involuntary movement and reflexes and coordinates complex movements (see p.108). The caudate nucleus and putamen, which are separated from each other by the fibrous white matter of the internal capsule, together constitute the corpus striatum. Deficiency of dopamine in the basal ganglia is responsible for Parkinson’s disease. (b) Basal ganglia nuclei and their relationship to other cortical structures. (Fig. 17.7a: Reproduced with permission from Baker EW. Anatomy for Dental Medicine. Second Edition. © Thieme 2015. Illustrations by Markus Voll and Karl Wesker. Fig. 17.7B: Reproduced with permission from Alberstone CD, Benzel EC, Najm IM, et al. Anatomic Basis of Neurologic Diagnosis. © Thieme 2009.)