Upper & Lower Motor Neurons Fall 24-25 ST PDF

Upper Motor Neurons That Maintain Balance and Posture “Motor Control Centers in the Brainstem” Vestibular nuclei as upper motor neurons in brain stem;  The projections from the vestibular nuclei that control axial muscles and those that influence proximal limb m...

Upper Motor Neurons That Maintain Balance and Posture “Motor Control Centers in the Brainstem” Vestibular nuclei as upper motor neurons in brain stem;  The projections from the vestibular nuclei that control axial muscles and those that influence proximal limb muscles originate from different cells and take different routes (called the medial and lateral vestibulospinal tracts).  Other upper motor neurons in the vestibular nuclei project to lower motor neurons in the cranial nerve nuclei that control eye movements (the third, fourth, and sixth cranial nerve nuclei). This pathway produces the eye movements that maintain fixation while the head is moving. Functional significance; Direct projections from the vestibular nuclei to the spinal cord ensure a rapid compensatory response to any postural instability detected by the inner ear. Reticular formation as upper motor neurons in brain stem;  The reticular formation is a complicated network of circuits located in the core of the brainstem that extends from the rostral midbrain to the caudal medulla and is similar in structure and function to the intermediate gray matter in the spinal cord.  The neurons within the reticular formation have a variety of functions, including cardiovascular and respiratory control, governance of myriad sensory motor reflexes, the organization of eye movements, regulation of sleep and wakefulness.  The skeletomotor control by reticular formation is the temporal and spatial coordination of movements. The descending motor control pathways from the reticular formation to the spinal cord are similar to those of the vestibular nuclei; they terminate primarily in the medial parts of the gray matter where they influence the local circuit neurons that coordinate axial and proximal limb muscles. Functional significance; the motor centers in the reticular formation are controlled largely by other motor centers in the cortex or brainstem. The relevant neurons in the reticular formation initiate adjustments that stabilize posture during ongoing movements via feedforward mechanism “predicts” the resulting disturbance in body stability and generates an appropriate stabilizing response.  Upper Motor Neurons That Initiate Complex Voluntary Movements “The Primary Motor Cortex” Origin of pyramidal tract; The upper motor neurons in the cerebral cortex reside in several adjacent and highly interconnected areas in the frontal lobe, which together mediate the planning and initiation of complex temporal sequences of voluntary movements. These cortical areas all receive regulatory input from the basal ganglia and cerebellum via relays in the ventrolateral thalamus, as well as inputs from the somatic sensory regions of the parietal lobe. A primary motor cortex Brodmann’s area 4, which is located in the precentral gyrus has the pyramidal cells of cortical layer V (also called Betz cells) which are the upper motor neurons of the primary motor cortex. Course of pyramidal tract; Their axons descend to the brainstem and spinal motor centers in the corticobulbar and corticospinal tracts passing through the internal capsule of the forebrain to enter the cerebral peduncle at the base of the midbrain. They then run through the base of the pons, where they are scattered among the transverse pontine fibers and nuclei of the pontine gray matter, coalescing again on the ventral surface of the medulla where they form the medullary pyramids. The components of this upper motor neuron pathway that innervate cranial nerve nuclei, the reticular formation, and the red nucleus (that is, the corticobulbar tract) leave the pathway at the appropriate levels of the brainstem. At the caudal end of the medulla, most, but not all, of the axons in the pyramidal tract cross (or “decussate”) to enter the lateral columns of the spinal cord, where they form the lateral corticospinal tract. The lateral corticospinal tract forms the direct pathway from the cortex to the spinal cord and terminates primarily in the lateral portions of the ventral horn and intermediate gray matter A smaller number of axons enters the spinal cord without crossing; these axons, which comprise the ventral corticospinal tract, terminate either ipsilaterally or contralaterally, after crossing in the midline (via spinal cord commissure). The ventral corticospinal pathway arises primarily from regions of the motor cortex that serve axial and proximal muscles. The indirect pathway to lower motor neurons in the spinal cord runs from the motor cortex to two of the sources of upper motor neurons in the brainstem: the red nucleus and the reticular formation. In general, the axons to the reticular formation originate from the parts of the motor cortex that project to the medial region of the spinal cord gray matter, whereas the axons to the red nucleus arise from the parts of the motor cortex that project to the lateral region of the spinal cord gray matter.  Upper Motor Neurons That Initiate Complex Voluntary Movements “The Premotor Cortex” Site A complex mosaic of interconnected frontal lobe areas that lie rostral to the primary motor cortex. The upper motor neurons in this premotor cortex influence motor behavior both through extensive reciprocal connections with the primary motor cortex, and directly via axons that project through the corticobulbar and corticospinal pathways to influence local circuit and lower motor neurons of the brainstem and spinal cord. Components; The functions of the premotor cortex are usually considered in terms of the lateral and medial components of this region. A. Lateral premotor cortex; In contrast to the neurons in the primary motor area that initiate the motor movement the lateral premotor area seem to be involved in the selection of movements based on external events (visual cue) and fire prior to primary motor area. Patients with frontal lobe damage have difficulty learning to select a particular movement to be performed in response to a visual cue or heard verbal command. B. Medial premotor cortex; like the lateral area, mediates the selection of movements. However, this region appears to be specialized for initiating movements specified by internal rather than external cues. In contrast to lesions in the lateral premotor area, the injury in medial premotor area reduces the number of self-initiated or “spontaneous” movements the patient makes, whereas the ability to execute movements in response to external cues remains largely intact. The upper diagram reveals he primary motor cortex and The upper diagram demonstrates midsagittal view of the the premotor area in the human cerebral cortex as seen in brain showing the longitudinal extent of the reticular lateral (A) and medial (B) views. The primary motor cortex formation and highlighting the broad functional roles is located in the precentral gyrus; the premotor area is performed by neuronal clusters in its rostral (blue) and more rostral. caudal (red) sectors. Descending Tracts  The Upper Motor Neuron Syndrome “Damage of the descending Motor Pathways” Injury of upper motor neurons is common because of the large amount of cortex occupied by the motor areas, and because their pathways extend all the way from the cerebral cortex to the lower end of the spinal cord. Damage to the descending motor pathways anywhere along this trajectory gives rise to a set of symptoms called the upper motor neuron syndrome. Spinal shock stage; Hyotonia and hyporeflexia; Damage to the motor cortex or the descending motor axons in the internal capsule causes an immediate flaccidity of the muscles on the contralateral side of the body and face due to hypotonia.The initial period of “hypotonia” after upper motor neuron injury is called spinal shock, and reflects the decreased activity of spinal circuits suddenly deprived of input from the motor cortex and brainstem. The acute manifestations tend to be most severe in the arms and legs: If the affected limb is elevated and released, it drops passively, and all reflex activity on the affected side is abolished. In contrast, control of trunk muscles is usually preserved, either by the remaining brainstem pathways or because of the bilateral projections of the corticospinal pathway to local circuits that control midline musculature. Recovery stage; After several days, however, the spinal cord circuits regain much of their function. Thereafter, a consistent pattern of motor signs and symptoms emerges are: The Babinski sign; The normal response in an adult to stroking the sole of the foot is flexion of the big toe, and often the other toes. Following damage to descending upper motor neuron pathways, however, this stimulus elicits extension of the big toe and a fanning of the other toes. Spasticity; it is an increased muscle tone, hyperactive stretch reflexes, and clonus (oscillatory contractions and relaxations of muscles in response to muscle stretching). Extensive upper motor neuron lesions may also be accompanied by rigidity of the extensor muscles of the leg and the flexor muscles of the arm (called decerebrate rigidity). Spasticity is probably caused by the removal of inhibitory influences exerted by the cortex on the postural centers of the vestibular nuclei and reticular formation. Spasticity is also eliminated by sectioning the dorsal roots, suggesting that it represents an abnormal increase in the gain of the spinal cord stretch reflexes due to loss of descending inhibition. This increased gain is also thought to explain clonus. A loss of the ability to perform fine movements; If the lesion involves the descending pathways that control the lower motor neurons to the upper limbs, the ability to execute fine movements (such as independent movements of the fingers) is lost.  Patterns of Facial Weakness The signs and symptoms pertinent to the cranial nerves and their nuclei are of special importance to clinicians seeking to pinpoint the neurological lesions that produce motor deficits. Lower motor neuron facial weakness; Damage to the facial motor nucleus or its nerve affects all the muscles of facial expression on the side of the lesion. Upper motor neuron facial weakness; unilateral injury to the motor areas in the lateral frontal lobe (primary motor cortex, lateral premotor cortex), as occurs in strokes that involve the middle cerebral artery. Most patients with such injuries have difficulty controlling the contralateral muscles around the mouth but retain the ablility to symmetrically raise their eyebrows, wrinkle their forehead. Why, in upper motor neuron lesion of facial nerve, a patient retains the ablility to symmetrically raise their eyebrows, wrinkle their forehead, and squint? The old belief was assumed that this pattern of inferior facial paresis with superior facial sparing could be attributed to (presumed) bilateral projections from the face representation in the primary motor cortex to the facial motor nucleus The recent interpretation is that strokes involving the middle cerebral artery spare the superior aspect of the face because the relevant upper motor neurons are in the cingulum, which is supplied by the anterior cerebral artery. Superior facial sparing in these situations may arise because this cingulate motor area sends descending projections through the corti_x0002_cobulbar pathway that bifuracte and innervate dorsal facial motor cell columns on both sides of the brainstem. Upper Motor Neuron Vs Lower Motor Neuron Lesions  Summary Two sets of upper motor neuron pathways make distinct contributions to the control of the local circuitry in the brainstem and spinal cord. One set originates from neurons in brainstem centers—primarily the reticular formation and the vestibular nuclei—and is responsible for postural regulation.  The reticular formation is especially important in feedforward control of posture (that is, movements that occur in anticipation of changes in body stability).  In contrast, the neurons in the vestibular nuclei that project to the spinal cord are especially important in feedback postural mechanisms (i.e., in producing movements that are generated in response to sensory signals that indicate an existing postural disturbance). The other major upper motor neuron pathway originates from the frontal lobe and includes projections from the primary motor cortex and the nearby premotor areas.  The primary motor cortex is responsible for movement execution.  The premotor cortices are responsible for planning and selecting movements. The motor cortex influences movements by;  Directly by contacting lower motor neurons and local circuit neurons in the spinal cord and brainstem via corticospinal and corticobulbar tracts (pyramidal tract).  Indirectly by innervating neurons in brainstem centers (the reticular formation and red nucleus) that in turn project to lower motor neurons and circuits via reticulospinal, vestibulospinal and rubrospinal tracts (extrapyramidal tracts). Although the brainstem pathways can independently organize gross motor control, direct projections from the motor cortex to local circuit neurons in the brainstem and spinal cord are essential for the fine, fractionated movements of the distal parts of the limbs, the tongue, and face that are especially important in our daily lives.