4. Primary motor area
(motor area 4)
Highly excitable (Betz cells)
Controls Sk. M. of opposite side of the body.
Body representation is inverted
Area of representation depends on the motor function
5. Functions of primary motor area:
Primary motor area
(motor area 4)
1- Generates neural impulses that control the execution
of movement. (especially fine discrete movements)
2- Facilitatory to stretch reflex.
7. Premotor Area
(area 6 & 8)
Less excitable (no Betz cells)
Produces programs for complex movements and
sends these programs to primary motor area
8. Primary motor area
Supplementary motor
area
Premotor area
Central
sulcus
Broca’s area
eye movement
Head rotation
Hand skill
Premotor Area
(area 6 & 8)
13. Functions of the pyramidal tract
1- fine skilled movements of hands and face
2- Facilitatory to stretch reflex
14. The Extrapyramidal Tracts
Premotor area
Basal ganglia
Red nucleus
Vestibular nucleus
Reticular formation
Extrapyramidal tracts:
Reticulospinaltracts
Tectospinal tracts.
Rubrospinal tracts.
Vestibulospinal tracts.
Olivospinal tracts.
15. Function of the extrapyramidal tracts:
Gross movements especially of the trunk and proximal
parts of the limbs.
Postural movements and fixation of the body in a
position suitable for the performance of fine movements.
Some extrapyramidal tracts are excitatory to stretch
reflex while some others are inhibitory.
16. Upper motor neuron lesion Lower motor neuron lesion
Cause:
Damage of both pyramidal
and extrapyramidal tracts,
commonly due to
hemorrhage or thrombosis.
Cause:
Damage of anterior horn
cells e.g. poliomyelitis, or
damage of the motor nerve
fibers.
17. Upper motor neuron lesion Lower motor neuron lesion
Paralysis:
- If the lesion is above the level
of pyramidal decussation (e.g.
in internal capsule) there is
paralysis on the opposite side
of the body: contralateral
hemiplegia.
- If the lesion is below the level
of pyramidal decussation, there
is paralysis on the same side
below of the lesion.
- It is characterized by poor
recovery.
Paralysis:
- Affects muscles supplied by the
diseased anterior horn cells or
motor nerves.
- Occurs on the same side of
the lesion.
- Recovery may occur.
18. Upper motor neuron lesion Lower motor neuron lesion
Hypertonia:
- Paralyzed muscles show
hypertonia of the
spastic type (clasp
knife type).
- It is due to loss of
extrapyramidal inhibitory
influence on g-motor
neurons.
Hypotonia or atonia:
- This hypotonia or atonia
of the paralyzed muscle is
referred to as “flaccid
paralysis”.
- It is due to interruption of
the stretch reflex.
19. Upper motor neuron lesion Lower motor neuron lesion
Exaggerated deep
reflexes:
- Observed on the affected
side.
- Clonus is present.
Absent deep reflexes:
- This occurs in muscles
supplied by the affected
segment or motor nerve.
20. Upper motor neuron lesion Lower motor neuron lesion
Loss of superficial reflexes:
- Abdominal and
cremasteric reflexes are
absent.
- Planter reflex shows
dorsi-flexion
(Babinski’s sign).
Loss of superficial reflexes:
- This occurs in muscles
supplied by the affected
segment or motor nerve.
21. Upper motor neuron lesion Lower motor neuron lesion
No significant muscle
wasting:
This is because paralyzed
muscles are still innervated
by anterior horn cells. Motor
neuron exerts a trophic
influence on muscles,
mediated by impulses and by
trophic factors which
influence protein synthesis in
muscle.
Significant muscle wasting:
This is due to loss of motor
neuron trophic influence on
muscles.
22. Upper motor neuron lesion Lower motor neuron lesion
No fasciculation: Fasciculation:
- These are visible
spontaneous contractions
of muscle fibers.
- They are due to
denervation
hypersensitivity.
23. Upper motor neuron lesion Lower motor neuron lesion
Normal electric excitability
of the paralyzed muscles,
chronaxie is normal.
Decreased electric
excitability of the paralyzed
muscles,
chronaxie is prolonged
24. Effects of Lesion in Internal Capsule
Contralateral Hemiplegia:
There is upper motor neuron lesion leading to spastic paralysis affecting the
opposite side of the body.
Contralateral Hemianesthesia:
Lesion of the sensory radiation leads to loss of somatic sensations on the
opposite side of the body.
Crossed Homonymous Hemianopia:
Lesion of the optic radiation leads to loss of vision for objects in the opposite
side visual fields of both eyes.
Decreased auditory acuity in both ears:
Lesion of auditory radiation does not lead to total deafness because each ear
is bilaterally connected to the auditory cortex.
27. Neuronal Connections of the Basal Ganglia
Cortical connections:
Caudate Circuit:
From sensory,
motor, visual &
auditory
association
areas
Caudate
Putamen
Int. Ext.
Globus pallidus
Ventroanterior &
ventrolateral
nuclei of the
thalamus
To prefrontal,
premotor &
supplementary
motor areas
A.Ch.
GABA
28. Neuronal Connections of the Basal Ganglia
Cortical connections:
Putamen Circuit: From premotor &
supplementary
areas
Caudate
Putamen
Int. Ext.
Globus palliduas
ventrolateral &
Ventroanterior
nuclei of the
thalamus
To primary
motor area
A.Ch.
GABA
29. Connection between Striatum and Substantia Nigra:
Neuronal Connections of the Basal Ganglia
Caudate
Putamen
Globus
pallidus
Substantia nigra
Striatum
GABA
Dopamine
Dopamine
30. Efferent Pathways from the basal Ganglia:
Neuronal Connections of the Basal Ganglia
Caudate
Putamen
Globus pallidus
Striatum
Subthalamic
nuclei
Substantia nigra
Reticular formation
Reticulospinal tract
Rubrospinal tract
Vestibulospinal tract
31. Functions of the Basal Ganglia
1- Cognitive control of sequences of motor patterns
caudate circuit + corticospinal tract
to “select” and “put together in sequence” the
movements necessary to achieve a complex goal
32. Functions of the Basal Ganglia
2- Timing and scaling of movements
caudate circuit + the posterior parietal cortex
Determines
how large and how fast
the movement will be
33. Functions of the Basal Ganglia
3- Execution of patterns of motor activity
putamen circuit + the corticospinal tract
4- Initiation and regulation of the gross intentional
movements of the body
e.g. swinging of arms and facial expression
34. Functions of the Basal Ganglia
5- Control of axial and girdle movements
The globus pallidus + the subthalamus + brain stem
6- inhibitory to muscle tone
38. Parkinsonism
Manifestations
3- Bradykinsesia / Akinesia:
Bradykinesia: movements take longer time.
Mask face
Monotonous speech
Gate: short steps + shuffling
loss of swinging arm movements
Hypokinesia: decreased range of movement.
Akinesia: difficulty in initiating movement.
Dysphagia
39. Parkinsonism
Mechanism of the disease
loss of inhibitory dopaminergic influence
Striatum
Cholinergic
+
Rigidity & Tremors
Limbic system
Akinesia
42. Functions of the Cerebellum
I- Control of equilibrium and postural movements:
Vestibulocerebellum
Vestibular apparatus
Vestibulocerebellar tract
proprioceptors
Dorsal spinocerebellar tract
calculates in advance position of different parts
in next fraction of a second
Brain
to guide anticipatory postural movements and reflexes
43. Functions of the Cerebellum
II- Control of distal limb movements:
Spinocerebellum
Brain
intended plan of movement
Corticopontocerebellar tract
Proprioceptors
Performance of movements
Compares
Detects discrepancy before
it occurs
Sends feedback to motor
cortex to correct errors
Damping function
Kinetic (intension) tremors
Spinocerebellar tracts
44. Functions of the Cerebellum
III- Planning, sequencing and timing of movements:
Neocerebellum
Premotor & somatosensory
areas of cerebral cortex
Pons
Dentate nucleus
Thalamus
smooth transmission form one movement to the next
provides timing for each succeeding movement
45. The Neocerebellar Syndrome:
Cause: Damage to the cerebellar cortex and deep
cerebellar nuclei.
Manifestations: On the same side of lesion
I- Hypotonia
II- Ataxia
1- Disturbance of posture and gait: drunken gait
2- Dysmetria: intension tremors
3- Failure of progression of movement: Dysarthria,
Decomposition of movements, Dysdiadochokinesia
4- Rebound phenomenon.
47. Functions of RAS:
1- Maintains conscious state.
2- Integration of motor, cardiovascular and
respiratory responses.
3- Automatic mechanism that brings relevant and
important information to conscious attention.
Editor's Notes
Help pre motor in programming and planning, and execution of movment
Regulate function of caudate and putamen
Substantia neigra send dopamine to caudate and putamen
So Parkinsonism occurs when it can’t release dopamine or receptor has been damaged so we treat it by l- dopa the precursor of dopamine so it can cross blood brain barrier and then form dopamine
