Motor cortex cortical motor areas and pyramidal tracts Dr. Dina Merzeban http://facebook.com/physiology.dina
In order to perform motor activity , we need 2 sets of neurons : Upper motor neuron (UMN): arise from cortical or subcortical areas to the anterior horn cells or cranial motor nuclei. They are further divided into pyramidal and extrapyramidal. Lower motor neuron (LMN): these are the motor nerves to the skeletal muscles i.e. cranial motor nuclei (3,4,5,6,7,9,10,11and 12) orAHCs and their nerves.
MOTOR AREAS OF THE SPINAL CORD (1)the primary motor cortex. (2)the premotor area. (3)the supplementary motor area. (4)Some Specialized Areas .
1)Primary Motor Cortex Site : infront of the central sulcus. It is called motor area 4 in relation to Brodmann’s classification of the brain cortical areas. It contains the large excitable Betz cells.
Body representation : The body is represented contralaterally The body is represented unilaterally except the upper half of the face which is represented in both cerebral hemispheres. The body is represented in an inverted manner The size of representation area depend on the degree of complexity of skilled movements performed by the part e.g. lips and fingertips have wide areas of representation.
Function: i.Control of fine skilled movements e.g. fingers. ii.Facilitatory to stretch reflex
2)Premotor Area Site : Immediately anterior to the primary motor cortex. This cortex forms a portion of Brodmann’s area 6 The body is also represented in an inverted manner. Function : Stimulation in this cortex, typically produces movements that involve large groups of muscles. For example, the arm and shoulder may be activated to place the hand in the position of writing.
3)Supplementary Motor Area Site : The supplementary motor area is located in the Brodmann’s area 6 just anterior to motor area 4 and above the premotor area. Function : It may be involved in programming of complex motor activity.
4) Some Specialized Areas of Motor Cortex a)Broca’s area (the motor speech area) Site : lies just anterior to the face portion of the primary motor cortex near the sylvian fissure. It is present in the dominant hemisphere. Function : Activity in this area produce a coordinated pattern of the musculature, needed to convert simple vocal utterances into whole words and complete sentences.
4) Some Specialized Areas of Motor Cortex b)The frontal eye field (Brodmann’s area 8) : Site :lies just anterior to the precentral gyrus, above than Broca’s area. Function : This cortical region controls the conjugate eye movements required to shift gaze from one object to another.
4) Some Specialized Areas of Motor Cortex c)A head rotation area: Site: Lies above the frontal eye field area. Function: serves to enable movements of the head correlated with eye movement.
4) Some Specialized Areas of Motor Cortex d)Hand skills area: Site : is located in the premotor cortex just anterior to the hand region of area 4. Function : the control of fine movements of the hand. When this area is damaged, the muscles of the hand are not paralyzed, but certain hand movements are lost; this is called motor apraxia.
Connections of the motor cortex Afferent Pathways: i.The somatosensory cortex ii.Fibers from a variety of thalamic nuclei that carry information from the ascending somatosensory pathways, cerebellum, basal ganglia, and reticular activating system.
Connections of the motor cortex Efferent pathways: Transmission of signals from the motor cortex to the muscles occurs by 2 ways: I.Corticospinal (Pyramidal) Tract II.Extrapyramidal tracts
I.Pyramidal system A.Corticospinal Tract: Primary Output Pathway From the Motor Cortex. Origin : the primary motor cortex (30 percent) the premotor cortex (30 percent) the remainder is divided among several other areas the primary somatosensory cortex (postcentral gyrus), supplementary cortex, N.B. The largest fibers in the pyramidal tract originate from Betz cells and represent only about 3 percent of the entire tract.
I.Pyramidal system A.Corticospinal Tract: Course: After leaving the cortex -------> posterior limb of the internal capsule ----> ventral surface of the brain stem to medullary pyramids. At the junction of the medulla and spinal cord: most of the fibers cross the midline to form the lateral corticospinal tract, which extends throughout the length of the cord. The fibers that do not cross continue as far as the thoracic spinal cord as the ventral corticospinal tract.
Pyramidal tracts Lateral and medial motor systems: The motor neurons (AHCs) in the anterior horn of the spinal cord are divided into lateral and medial motor neurons. The Lateral motor system: the lateral corticospinal tract supplies the lateral motor neurons that supply distal limb muscles that perform fine skilled movements ( hands and fingers). The medial motor system: the ventral corticospinal tract supplies the medial motor neurons that supply muscles of the trunk that perform gross movements (axial ms. and proximal limb ms.)
Pyramidal tracts B.Corticobulbar tract: Has the same origin as corticospinal but when they reach the brain stem they cross to the opposite side and relay on cranial motor nuclei 5, 7, 9, 10, 11 and 12 in pons and medulla. Their axons in-turn supplies ms. Of the head. C.Cortico nuclear tract: originate from area 8 and cross to the opposite side in the brain stem to supply cranial nuclei 3,4,6 that in turn supply extraocular ms.
II.Extrapyramidal tracts The term extrapyramidal motor system has been used in clinical circles to denote all the portions of the brain and brain stem that contribute to motor control but are not part of the corticospinalpyramidal system. The descending extrapyramidal tracts arise from the basal ganglia, the reticular formation of the brain stem, the vestibular nuclei, and often the red nuclei to the AHCs of the spinal cord. No specific neurophysiological functions to the extrapyramidal system as a whole. In fact, the pyramidal and extrapyramidal systems are extensively interconnected and interact to control movement.
Upper motor neuron lesion Lower motor neuron lesion Cause: Interruption of the pyramidal tract along its course e.g. stroke due to thrombosis of arteries supplying the internal capsule Cause: interruption of the Lower motor neuron (cranial nuclei in the brain stem &/or AHCs of spinal cord and their nerves. e.g. poliomyelitis (destruction of some AHCs) or diabetes (degeneration of peripheral nerves) Clinical manifestations State of muscle No wasting ( or only mild wasting in long standing cases)Muscles can contract reflexly (spasticity due to exaggerated stretch reflex ) No fasciculations Clinical manifestations Marked muscle wasting due to disuse atrophyMuscles are completely denervated Presence of fasciculations: in irritative lesions of the anterior horn cells. Tone: Hypertonia ( clasp Knife spasticity) Hypotonia or atonia ( flaccidity)Due to interruption of the stretch reflex arc Power : Paralysis on the opposite side of the body Flaccid paralysis in the muscles supplied by the affected segments on the same side of the lesion Reflexes: Deep reflexes Hyperreflexia Hyporeflexia or areflexia Superficial reflexes: Absent on the affected sideAbsent abdominal and cremastric reflexes. Extensor plantar reflex Absent in the affected segments Electric excitability: Normal Faradic current: Produce tetanic contractionGalvanic current:Chronaxie is normal Abnormal Faradic current: No responseGalvanic current:Chronaxie is prolonged
Effect of Lesions in the Motor Cortex or the Corticospinal Pathway Causes: 1.The “Stroke”: Lesion in the Motor Cortex or the Corticospinal Pathway due to cerebrovascular causes (intracranial hemorrhage or Thrombosis). 2.Tumours 3. Infilmmatory conditions ( brain abscess ) .
Lesions in the Motor Cortex when lesions involves the primary motor cortex only (origin of the corticospinal tract), there is loss of voluntary control of discrete movements involving the distal portions of the extremities, particularly the fingers and hands. This does not necessarily mean that the muscles are completely paralyzed but rather that the control of fine movements is lost. Furthermore, postural movements or gross positioning of the limbs may not be affected.
Lesions in the Corticospinal Pathway with or without lesion in motor cortex: hemorrhagic or ischemic cortical strokes typically involve more territory than just the primary motor cortex. When the tissue damage extends beyond the primary cortex and involves neurons that project to the caudate, putamen, or reticular formation, characteristic symptoms such as hyperreflexia, hypertonia, and spasticity occur.
Muscle Spasticity Caused by Lesions That Damage Large Areas Adjacent to the Motor Cortex. The primary motor cortex normally exerts a continual tonic stimulatory effect on the motor neurons of the spinal cord; when this stimulatory effect is removed, hypotonia results. Spasticity results mainly from damage to accessory pathways from the nonpyramidal portions of the motor cortex that normally inhibit the vestibular and reticular brain stem motor nuclei. When “disinhibited”, they become spontaneously active and cause excessive spastic tone in the involved muscles.
The effect of a lesion in the internal capsule (Capsular Stroke): 1) Typical hemiplegia: UMNL of the opposite side of the body including the face and limbs 2) Hemianaethesia : loss of somatic sensations on the opposite side of the body due to injury to sensory radiation. 3 )Contralateral homonymous hemianopia: due to injury to optic radiation. 4) Mild to moderate sensori-neural hearing loss : due to injury of auditory radiation. there is no deafness due to bilateral representation of auditory cortex.