The Central Nervous System Organization of Behavior
Rolland S. Parker in Concussive Brain Trauma, 2016
Corticospinal: The corticospinal tract originates in the motor cortex and the frontal and parietal lobes. Corticospinal motor information is modulated by sensory information and information from other motor regions. Accurate and properly sequenced voluntary movement is enhanced by tactile, visual, and proprioceptive stimuli (Amaral, 2000a). The corticospinal tract is the upper motor neurons (UMNs). These descend through the internal capsule to form the corticospinal tract (pyramids), with 90% decussating in the medulla. Two percent form the uncrossed lateral corticospinal tract, while 8% form the uncrossed anterior corticospinal tract (Parent, 1996, pp. 384–385). The uncrossed fibers descend as the anterior corticospinal tract and descend in the spinal cord. The remaining fibers descend in the ipsilateral ventral corticospinal tract via the internal capsule to synapse on motor neurons of the nucleus ambiguus (special visceral motor; medulla). Many of its motor functions can be taken over by the rubrospinal tract. The corticospinal tract, together with the rubrospinal tract controls fine, skilled manipulations of the extremities. The pyramidal tract contributes collaterals to extrapyramidal pathways. Thus, signals to the spinal cord to elicit a movement are accompanied via collateral signals via the extrapyramidal tract.
Brain Motor Centers and Pathways
Nassir H. Sabah in Neuromuscular Fundamentals, 2020
In humans, the rubrospinal tract is of less importance than in lower animals because of the development of a direct corticospinal projection on motoneurons. The rubrospinal tract is involved in controlling muscles of the shoulder and the upper arm, facilitating flexion in the upper extremities, as in arm swinging during walking. It is not involved in the leg muscles, as the tract terminates in the superior thoracic region of the spinal cord.
Physiology of the nervous system
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2015
The rubrospinal, vestibulospinal and reticulospinal tracts form the extrapyramidal tract. These tracts maintain postural tone and direct voluntary movement. The rubrospinal tract arises from cells in the red nucleus, crosses contralaterally in the brainstem, receives input from the cerebral cortex and runs down the spinal cord. The lateral vestibulospinal tract arises from the lateral vestibular nucleus and does not cross to the contralateral side.
Split phenomenon of antagonistic muscle groups in amyotrophic lateral sclerosis: relative preservation of flexor muscles
Published in Neurological Research, 2021
Jingwen Liu, Zhili Wang, Dongchao Shen, Xunzhe Yang, Mingsheng Liu, Liying Cui
The pattern of split phenomena in our study is consistent with the weak distribution that occurs as the pyramidal tract is damaged, suggesting that pyramidal tract impairment due to UMN lesions may play a role to some extent. Besides the corticospinal tract, there are other indirect pathways, including the reticulospinal tract and the rubrospinal tract that control movement [24]. Experiments with macaques confirmed that after lesioning the corticospinal tract, the connection strength from the brainstem to motor neurons (probably due primarily to the reticulospinal tract) that innervate the forearm flexors is increased significantly, but the path innervating the forearm extensors does not change. This imbalance reflects the phenomenon that the extensor is weaker than the flexor following pyramidal tract lesioning [25]. For example, the flexor predominates over the extensor in patients during the recovery phase after stroke. Moreover, the lower limb is typically held in extension with predominant plantar flexion at the ankle following UMN injury, which makes the patient appear as the foot drop posture (a common symptom of ALS) [10]. In ALS, when both UMN and LMN degeneration is observed, and the split phenomenon appears, the flexor was stronger than the extensor, which conforms to the general manifestation of cortical motor neuron pathway damage.
Endoscopic endonasal resection of a medullary cavernoma: a novel case
Published in British Journal of Neurosurgery, 2019
Puya Alikhani, Sananthan Sivakanthan, Ramsey Ashour, Mark Tabor, Harry van Loveren, Siviero Agazzi
Recent advancements in neuroimaging, namely diffusion tensor tractography, have provided surgeons additional information to aid in operative decision making. It has been demonstrated that the cerebellar peduncles, corticospinal tract, corticopontine tracts, medial lemniscus, lateral lemniscus, spinothalamic tract, rubrospinal tract, central tegmental tract, medial longitudinal fasciculus, and dorsal longitudinal fasciculus can all be reliably and reproducibly tracked using diffusion tensor imaging.11 With this anatomical information, direction of fiber pathway displacement can now be utilized to supplement traditional imaging to formulate the best operative approach. In our case, both location of the cavernoma at the anterior surface of the medulla and the posterolateral deflection of the brainstem tracts was a key factor that contributed to the decision to undertake a purely ventral entry zone into the brainstem, thereby ignoring the classic safe entry zone location into the medulla oblongata. An expanded endoscopic transclival approach was chosen to access the ventral medulla (Figure 2).
Better understanding the neurobiology of primary lateral sclerosis
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2020
P. Hande Ozdinler, Mukesh Gautam, Oge Gozutok, Csaba Konrad, Giovanni Manfredi, Estela Area Gomez, Hiroshi Mitsumoto, Marcella L. Erb, Zheng Tian, Georg Haase
In an effort to better understand the mechanisms of neurodegeneration in PLS, numerous mouse models were generated based on PLS-linked mutations, such as ALS2/Alsin, C9Orf72, DCTN/Dynactin 1, FIG4/Phosphoinositide 5-phosphatase, OPTN/Optineurin, SETX/Senataxin, SPG7/Paraplegin or UBQLN2/Ubiquilin 2 (17). However, generation and characterization of a mouse model for an UMN disease is challenging. Humans heavily depend on their Betz cells for the initiation and modulation of voluntary movement and there are direct projections from Betz cells to the spinal motor neurons. In mice, in addition to the corticospinal tract, the rubrospinal tract also plays an important role and the circuitry within the spinal cord includes an interneuron component (24). Therefore, when humans have defects in their corticospinal tract, they may be paralyzed, whereas mice will be able to move, albeit with loss of their ability for fine movement. During evolution, humans have become more specialized in fine movement in the expense of making themselves vulnerable to significant spinal cord injuries. Rodents, however, have better capabilities to recover from an injury, but they are not as skilled as humans when it comes to dexterity (24,44). Moreover, there are no good outcome measures, which can quantitatively assess the timing and the extent of UMN degeneration in mouse models of PLS. Despite these two limitations the UMNs in mice and human share many common cell biological features and display similar pathologies at a cellular level (26,27,45). Hence, many different labs generated mouse models for genes that had been found mutated in PLS patients. Albeit most mouse lines did not have a prominent phenotype at a species level (46), detailed cellular investigations of their UMNs began to reveal the underlying problems.
Related Knowledge Centers
- Brainstem
- Lateral Corticospinal Tract
- Lateral Funiculus
- Midbrain
- Nervous System
- Spinal Cord
- Extrapyramidal System
- Magnocellular Red Nucleus
- Tegmentum
- Corticospinal Tract