Organization of theMotor System

Motor Organization – The Big Picture

There are several systems that enable smooth and exact purposeful movements. Thecorticospinal and corticobulbar systems are themost important voluntary motor systems. The motor signals generated in the cerebral cortex are relatively coarse and need modulation, however, as facilitated by the basal ganglia and the cerebellum.Other voluntarily regulated motor pathways are the rubrospinal and the reticulospinal tracts. The two vestibulospinal tracts receive sensory input from the vestibular nuclei but are not directly influenced by the cerebral cortex. They are thus largely involuntary motor pathways. The motor system receives alsosomatosensory input via the muscle spindles, the dorsal column/medial lemniscus pathways, the somatosensory cortex, the anterolaleral system (ALS), and thereticulospinal tracts.

Motor PathwaysThe lateral corticospinal tract is a long motor pathwaybetween the cortex and the spinal cord, several long motorPathways also start in the brainstem and end in the spinal cord.

Start of the Motor Pathways

End of the Motor PathwaysThe descending motor tracts (at spinal levels) are subdivided into the ventromedial (also called anteromedial) and thelateral pathways.The ventromedial tracts are:· Pontine (medial) reticulospinal· Lateral vestubulospinal· Medial vestibulospinal

The lateral tracts are:· Lateral corticospinal· Rubrospinal· Medullary (lateral) reticulospinal

Location of Motor Neurons in Relation to FunctionIn the ventral horn of the spinalcord, flexor and adductorneurons lie dorsal to theextensor and abductorneurons. Cells for distalmuscles lie laterally to thosefor trunk structures (i.e.,proximal muscles).

Relations between Motor Neurons and Spinal Pathways

Lateral Pathways are Biased for Flexion of the Limbs

Medial Pathways are Biased for Extension ofthe Limbs

Corticospinal TractInitiation and Control of Motor ActivityThe corticospinal tract is themost important motorpathway. Prefrontal areas(motor planning) project tothe premotor cortex(production of motorprograms), which thencommunicates with theprimary motor cortex(execution of excitatorydrive for motor activity).

(Brodmann’s area 4)Brodmann’s area 4 is oftencalled the primary motor cortex.

Premotor and Supplementary Cortices (Brodmann’s area 6)

Each distinct area in the primary motor cortex is responsible for the motor controlof a particular partof the body. Therepresentation ofthe body that canbe functionallymapped againstsuch a region iscalled a“homunculus.”

Homunculus

Predominant Role of the Lateral Corticospinal TractThe main function of the lateral corticospinal tract is voluntary contraction of distal flexor muscles of the limbs (e.g., it is thus integral to reaching and walking).Sensory input from the periphery is processed by the cortex, which constantly modifies the signals transmitted by this tract. Inputs into the cortex from the basalganglia and cerebellum via the thalamus also always modulate lateral corticospinal output.

Start of Lateral Corticospinal TractThe origin of the corticospinaltract is the pyramidal cellbodies located in layer 5 ofthe precentral gyrus andanterior paracentral lobule.End of LateralCorticospinal TractThe end of the corticospinaltract is the contralateralanterior horn of the spinalcord, where the axons of theupper motor neuronssynapse with alpha andgamma lower motor neurons

Route of Corticospinal Tract· corona radiata· internal capsule(posterior limb)· crus cerebri· basilar pons· corticospinal tracts inspinal cord· synapses on alpha andgamma neurons inspinal anterior horn

Approximately 90% of the fibers from motor cortex cross over at the pyramidal decussation (caudal medulla) to form the lateral corticospinal tract. Ten percent remain ipsilateral to enter the cord as the ventral (anterior) corticospinal tract.Damage to the lateral corticospinal tract rostral to the pyramidal decussationproduces contralateral hemiparesis.Damage to the lateral corticospinal tract caudal to the decussation producesipsilateral hemiparesis at and below the lesion.

Upper Motor Neurons· Upper motor neurons forming the corticospinal and corticobulbar tracts arise from cell bodies located in layer 5 of the primary motor cortex. The corticospinal fibers project through the corona radiata, internal capsule, crus cerebri, basal pons, and pyramid, entering the spinal cord to terminate (largely) in the contralateralanterior (ventral) horn. Direct or indirect excitatory synaptic contact is made with a second order motor neuron (lower motor neuron).Lower Motor Neurons· The cell bodies of the lower motor neurons dwell in the ventral horn of the spinal cord (receiving inputs from corticospinal fibers) and the motor nuclei of the brainstem (receiving inputs from corticobulbar fibers). They send axons directly to skeletal muscle fibers to effect muscular contractions.

Lower Motor Neuron Lesion

– Symptoms occur ipsilateral to site of the lesion-- Flaccid paralysis (loss of movement)

– Hyporeflexia/areflexia(due to interruption of theefferent (motor) limb of the sensory-motor reflex arcs.

– fasciculations Wasting of muscles,

-- atonia or hypotonia(muscle tone reflects sustained partial contraction of muscular fibers and depends directly on the monosynaptic reflex arc that connects the muscle spindles to the lower motor neurons)

Examples of diseases that involve LMN syndrome are:· Amyotrophic lateral sclerosis· Peripheral nerve damage (traumatic)

Diseases of the Lower Motor Neuron

Amyotrophic Lateral Sclerosis (Lou Gehrig’s Disease)It is a progressive neuromuscular disease that initially affects and later destroys lower motor neurons and eventually also parts of the pyramidal tract and the precentral gyrus (and the anterior portion of the paracentral lobule)ALS patients usually developmuscle weakness and difficultyspeaking and/or swallowing.Sphincter control, sensoryfunction, intellectual ability, andskin integrity are not commonlyaffected.

Upper Motor Neuron Lesion– Lesion above decussation: symptoms contrlateral to the lesion

– Lesion below the decussation: symptoms ipsilateral to the lesion

– Hyperreflexia

– Extensor plantar response

– First flaccid paralysis, later spastic paralysis

– No wasting of muscles (because 2nd motor neuron is not impaired)

Brown–Sequard Syndrome -->Hemisection of the spinal cord

ParaplegiaParaplegia occurs after abilateral spinal cord injury. Inmost cases, a traumaticevent impairs the cells withinthe spinal cord or cuts orcrushes the fibers of the longtracts (through bruising,compression, or laceration).The symptoms ofparaplegia are:· flaccid paralysis belowthe level of the lesion (i.e., related to spinal shock), followed days-to-weeks later by spasticity.· increased deep tendon reflexes and clonus.· extensor plantar response (Babinski sign).· early retention of urine with painless distension of the bladder and overflow, as pressure overcomes the reflex closure of bladder sphincters. Reflexive emptying of bladder accompanies the lifting of spinal shock.· paraplegia in flexion (physiotherapy is warranted).· loss of all somatosensation from below the lesion.

Other Motor Pathways

1. Rubrospinal Tract (Flexor Muscles)

Start: Red nucleus in midbrainEnd: Alpha and gammamotor neurons in the anterior horn of the spinal cord.Function- stimulation of flexors of upper limb.

2. Medullary (Lateral) Reticulospinal Tract (Flexor Muscles)-originates in the nuclei of medulla and ends in anterior horn of spinal cord.- Most fibers of the medullaryreticulospinal pathway facilitate contraction of flexor muscles of thelimbs.

3. Pontine (Medial) Reticulospinal Tract (Extensor Muscles)-originates in the nuclei of medulla and ends in anterior horn of spinal cord.End: anterior horn of the spinal cord.

Most fibers in this pathway facilitatecontraction of extensor muscles of the limbs.

4. Lateral Vestibulospinal Tract (Extensor Muscles)Start: Lateral vestibular nucleus.End: anterior horn of the spinal cord

5. Medial Vestibulospinal Tract (Extensor Muscles)-simillar to lateral vestibulospinal tract.

Decorticate PosturingA lesion rostral to the red nucleus that impairs corticospinal, produces decorticate posturing. After a noxious stimulus or spontaneously, the affected patient will flex the upper limbs and extend the lower limbs.

corticospinal tractinterrupted – mainly flexion impaired• rubrospinal tract intact – flexion of the arms· medullary reticulospinal tract intact – flexion of extremities· pontine reticulospinal tract intact – extension of extremities· vestibulospinal tracts intact – extension of extremities

ArmsIn the arms, the flexor input of the rubrospinal tract is still intact. Hence, there is strong flexor innervation, which is much greater than the extensor input of pontine reticulospinal and vestibulospinal tracts.LegsFor the lower limbs rubrospinal tract has almost no impact, hence the extensor innervation is much more relevant, so the lower limbs are extended.

Decerebrate PosturingA lesion below the red nucleus that impairs thecorticospinal, corticobulbar, and rubrospinal Fibers produces decerebrate posturing. After a noxious stimulus or spontaneously, the patient will extend the upper and lower limbs.

· corticospinal tractinterrupted – mainly flexion impaired· corticobulbar tractinterrupted – paralysis of motor CNs· rubrospinal tract interrupted – no flexion of arms· medullary reticulospinal tract intact – flexion of extremities· pontine reticulospinal tract intact – extension of extremities· vestibulospinal tracts intact – extension of extremities

In the upper and lower limbs, there is flexor input from only the medullaryreticulospinal tract, which is overruled by the extensor innervation of the pontine reticulospinal and vestibulospinal tracts.