Flashcards in Module E-02 Deck (62):
Functions Mediated by PREFRONTAL cortex
motor planning, motivation and social restraint
Which is the cortes for Motor Programs
Cortexes involved inPathway for Voluntary motor systems
Prefrontal cortex Projects to Premotor Cortex which then projects to Primary motor cortex for excitation of lower motor neurons
Brodmann's area for Primary Motor Cortex
Regions of the brain that make up the Primary Motor Cortex
1) Precentral Gyrus
2) Anterior Paracentral Lobule
The organization of cells in the Primary motor cortex is by
Somatotopically, particular areas control contractions in specific parts of the body
Visual representation of the somatotopic map
Types of cells in Layer 5 (internal pyramidal layer)
Large Pyramidal cells
Areas that provide input to the Primary Motor Cortex
1)Primary somatosensory cortex
2) Posterior parietal cortex , which integrates sensory information for motor planning in concert with frontal areas
3) Basal ganglia (via thalamus and premotor area)
4) Cerebellum (via thalamus)
5) Visual and auditory centers
6) Limbic and prefrontal areas
Brodmann's area for Primary Somatsensory cortex
Brodmann's area for Posterior Parietal cortex
Areas that provide input to the Premotor Cortex
1) Prefrontal cortex ( gets input from Limbic association cortex)
2) Posterior parietal area (Brodmann’s areas 5 and 7)
3) Basal ganglia (via thalamus)
4) Cerebellum (via thalamus)
Main function of LATERAL corticospinal tract
voluntary contraction and relaxation of muscles but with a slightly stronger influence over flexor muscles
Sensory input from ________, ___________ and _________ are modulated through the Thalamus to the Motor regions
Basal ganglia; Cerebellum ; Spinal Cord
Medial Premotor cortex aka
Supplementary motor area
During Simple repeated activity like flexion/ extension of finger , which areas of the cortex are active?
primary motor cortex and primary somatosensory cortex
During more complex motor activity which areas are active?
Supplementary motor area , primary motor cortex and primary somatosensory cortex
During mental rehearsal of the complex sequence, which areas are active?
Supplementary motor area
When is lateral Premotor cortex more active than Medial (supplementary) Premotor cortex?
• Medial premotor (supplementary) areas involved in
• Lateral premotor areas involved in sensory-guided (eg;visual) movements
Start of the Lateral Corticospinal Tract
pyramidal somata of layer 5 of the precentral gyrus and
anterior paracentral lobule (Brodmann’s Area 4).
End of the Lateral Corticospinal Tract
the contralateral spinal ventral horn, where the many
corticospinal axons synapse on alpha and gamma lower motor neurons
Route of Corticospinal Tract
2) corona radiata
3) internal capsule (posterior limb)
4) crus cerebri
5) basilar pons
6) pyramid (medulla)
7) pyramidal decussation
8) corticospinal tracts in spinal cord
9) synapses on alpha and gamma motor neurons in spinal ventral horn
Closer to the Genu of the internal capsule which part of the body's fibers are carried
arm followed by trunk then leg
Why are the corticospinal fibers not visible on the ventral surface of the pons?
Because of the presence of superficial transverse pontine fibers, which form the middle cerebellar peduncles
Do all the fibers of the corticospinal tract decussate?
What tract do the non crossing fibers form?
Anterior corticospinal tract
Where are the lower motor neurons of the anterior and lateral corticospinal tract located?
Spinal Ventral Horn
Do Corticospinal tract only carry Upper motor neurons ?
No, A minority of corticospinal fibers (typically arising from
parietal areas) will terminate in the dorsal spinal gray matter, presumably to regulate sensory inputs
Damage to the corticospinal fibers rostral to the pyramidal
decussation produces ________ paresis.
Damage to the lateral corticospinal tract caudal to the decussation produces ________ paresis
What is spinal shock?
In damage to upper motor neurons, Extensive bilateral damage to the motor cortex or its corticospinal and
corticobulbar axons can initially cause muscular flaccidity and areflexia.
This transient state most commonly reflects bilateral spinal injury and, in such cases, is called spinal shock.
Generally after a few weeks, many shock-riddled spinal
circuits caudal to the lesion regain function.
Manifestations of Upper Motor Neuron Lesions
– Lesion above decussation: symptoms contralateral to the lesion
– Lesion below the decussation: symptoms ipsilateral to the lesion
– Hyperreflexia (myotatic, deep tendon reflexes)
– Extensor plantar response
– First flaccid paralysis, later spastic paralysis
– No wasting of muscles
What is the Extensor Plantar response?
Stimulus elicits extension of the big toe and a fanning of the other toes, instead of the normal flexion seen in adults
Why is Extensor Plantar response seen in infants under 1 yrs?
because the immature lateral corticospinal pathway is weakly myelinated
Why is there no muscle wasting in Upper motor neuron lesions?
Because the muscles are still innervated by the lower motor neuron
What is spasticity?
pathologically increased muscle tone (hypertonia) with abnormal posturing
Manifestations of Lower Motor neuron Lesions
– paralysis (virtually complete loss of movement) or paresis (weakness) occur ipsilateral to site of the lesion
– Flaccid paralysis
– Wasting of muscles
– Fasciculations (spontaneous twitches)
– Fibrillations (as appear on EMG)
Why does Hyporeflexia occur in LMN?
due to interruption of the efferent (motor) limb of the
eg of Lower motor neuron lesions
Peripheral nerve damage
What causes Brown Sequard syndrome?
Arises from spinal hemisection
What symptoms of the corticospinal tract will a patient exhibit in brown sequard syndrome?
Contralateral below the lesion: Normal
Ipsilateral below the lesion: Upper motor neuron syndrome
- Extensor plantar reflex
- Spastic paralysis
What symptoms of the Anterolateral tract will a patient exhibit in brown sequard syndrome?
Contralateral below the lesion: No pain or temp perception ( but Lissauer's tract allows there to be sensation 2 to 3 levels below)
Ipsilateral below the lesion: Normal
What symptoms of the Dorsal Column/Medial Lemniscus tract will a patient exhibit in brown sequard syndrome?
Contralateral below the lesion: Normal
Ipsilateral below the lesion: No touch, vibration or proprioception
What is damaged at the level of the lesion in Brown sequard syndrome?
Lower motor neurons in the anterior horn ipsilaterally
What symptoms of the lower motor neuron damage at the level of the lesion in brown sequard syndrome?
- Hypo- or areflexia
- Wasting of muscles
- Flaccid paralysis
When does Paraplegia occur?
Bilateral spinal cord injury
Manifestations of Paraplegia
Bilateral Upper Motor Neuron syndrome:
-Transient flaccid paralysis below the level of the lesion (i.e., related to spinal shock), followed days-to-weeks later by persistent spasticity.
- Increased deep tendon reflexes and clonus.
- Extensor plantar response (Babinski sign).
- Early transient retention of urine with painless distension of the bladder and overflow (reflexive emptying of bladder may return with passage of spinal shock).
- Paraplegia in flexion (physiotherapy is warranted).
- Loss of all somatosensory perception below the lesion!
Start of Corticobulbar Fibers
Layer 5 of the ventrolateral precentral gyrus
End of Corticobulbar Fibers
Motor nuclei of cranial nerves
Route of Corticobulbar Fibers
Distinct bundles of corticobulbar fibers take different
routes, depending on which cranial nerve nucleus is
- they all come down in the genu of the internal capsule
Function of Corticobulbar Fibers
Innervation of muscles in the head (including those of the eyes and mouth) and part of the neck.
Where are the losses seen in Infarction of the posterior limb of the internal capsule?
Damage to the corticospinal tract causes a contralateral
upper motor neuron syndrome.
Somatosensory losses are also contralateral to injury
Which fibers are damaged in internal capsule infarction?
corticospinal and corticobulbar fibers and somatosensory systems
Which nucleus innervates the muscles of the tongue?
Damage to _______ fibers that project to the hypoglossal nucleus causes a _______ deviation of the tongue during protrusion.
Damage to the corticobulbar fibers projecting to the contralateral _______ in the caudal pons causes a deviation of both eyes ______ the lesion
paramedian pontine reticular formation (PPRF); towards
Why is there constant deviation of the eyes in PPRF damage and not just when the patient tries to look in a particular direction?
The PPRFs receive bilaterally equal tonic innervation, which makes it possible to look straight forward. If the innervation of one PPRF is lost, the tonic innervation of the other side
is unopposed, generally causing the deviation of the eyes towards the side of the damaged upper motor neurons
Which area of the cortex is responsible for horizontal gaze?
Frontal eye Field
Damage to the corticobulbar fibers innervating the facial nucleus causes a ___________ facial paralysis
What is different about the innervation of the upper and lower facial nuclei?
- The upper facial nucleus receives bilateral innervation through corticobulbar fibers from the ventrolateral primary
- The lower facial nucleus receives only contralateral projections
How can we differentiate central facial lesion From Peripheral facial lesion?
In central facial lesion , the upper face muscles will still work and the patient will be able to wrinkle the forehead
In Peripheral facial lesion , all the facial muscles of the ipsilateral side will be paralyzed