3. • 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.
4. MOTOR AREAS OF THE SPINAL CORD
(1)the primary motor cortex.
(2)the premotor area.
(3)the supplementary motor area.
(4)Some Specialized Areas .
5. 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.
6. 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.
10. 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.
11. 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.
12. 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.
13. 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.
14. 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.
15. 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.
16. 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.
17. 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
18. 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.
19. 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:
1. most of the fibers cross the midline to form the lateral
corticospinal tract, which extends throughout the length of the
cord.
2. The fibers that do not cross continue as far as the thoracic spinal
cord as the ventral corticospinal tract.
20.
21. 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.)
22. 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.
23. 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 corticospinal-
pyramidal 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.
24. 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 muscleNo 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
denervatedPresence 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 reflexesHyperreflexia Hyporeflexia or areflexia
Superficial reflexes: Absent on the affected
sideAbsent abdominal and cremastric reflexes.
Extensor plantar reflex
Absent in the affected segments
Electric excitability: NormalFaradic current: Produce
tetanic contractionGalvanic current:Chronaxie is
normal
AbnormalFaradic current: No responseGalvanic
current:Chronaxie is prolonged
25. 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 )
.
26. 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.
27. 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.
28. 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.
29. 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.