Module E-02 Flashcards

1
Q

Functions Mediated by PREFRONTAL cortex

A

motor planning, motivation and social restraint

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2
Q

Which is the cortes for Motor Programs

A

Premotor Cortex

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3
Q

Cortexes involved inPathway for Voluntary motor systems

A

Prefrontal cortex Projects to Premotor Cortex which then projects to Primary motor cortex for excitation of lower motor neurons

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4
Q

Brodmann’s area for Primary Motor Cortex

A

Area 4

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5
Q

Regions of the brain that make up the Primary Motor Cortex

A

1) Precentral Gyrus

2) Anterior Paracentral Lobule

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6
Q

The organization of cells in the Primary motor cortex is by

A

Somatotopically, particular areas control contractions in specific parts of the body

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7
Q

Visual representation of the somatotopic map

A

Homunculus

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8
Q

Types of cells in Layer 5 (internal pyramidal layer)

A

Large Pyramidal cells

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9
Q

Areas that provide input to the Primary Motor Cortex

A

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

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10
Q

Brodmann’s area for Primary Somatsensory cortex

A

3,1,2

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11
Q

Brodmann’s area for Posterior Parietal cortex

A

5,7

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12
Q

Areas that provide input to the Premotor Cortex

A

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)

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13
Q

Main function of LATERAL corticospinal tract

A

voluntary contraction and relaxation of muscles but with a slightly stronger influence over flexor muscles

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14
Q

Sensory input from ________, ___________ and _________ are modulated through the Thalamus to the Motor regions

A

Basal ganglia; Cerebellum ; Spinal Cord

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15
Q

Medial Premotor cortex aka

A

Supplementary motor area

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16
Q

During Simple repeated activity like flexion/ extension of finger , which areas of the cortex are active?

A

primary motor cortex and primary somatosensory cortex

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17
Q

During more complex motor activity which areas are active?

A

Supplementary motor area , primary motor cortex and primary somatosensory cortex

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18
Q

During mental rehearsal of the complex sequence, which areas are active?

A

Supplementary motor area

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19
Q

When is lateral Premotor cortex more active than Medial (supplementary) Premotor cortex?

A

• Medial premotor (supplementary) areas involved in
planned sequences
• Lateral premotor areas involved in sensory-guided (eg;visual) movements

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20
Q

Start of the Lateral Corticospinal Tract

A

pyramidal somata of layer 5 of the precentral gyrus and

anterior paracentral lobule (Brodmann’s Area 4).

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21
Q

End of the Lateral Corticospinal Tract

A

the contralateral spinal ventral horn, where the many

corticospinal axons synapse on alpha and gamma lower motor neurons

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22
Q

Route of Corticospinal Tract

A

1) cortex
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

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23
Q

Closer to the Genu of the internal capsule which part of the body’s fibers are carried

A

arm followed by trunk then leg

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24
Q

Why are the corticospinal fibers not visible on the ventral surface of the pons?

A

Because of the presence of superficial transverse pontine fibers, which form the middle cerebellar peduncles

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25
Q

Do all the fibers of the corticospinal tract decussate?

A

No

26
Q

What tract do the non crossing fibers form?

A

Anterior corticospinal tract

27
Q

Where are the lower motor neurons of the anterior and lateral corticospinal tract located?

A

Spinal Ventral Horn

28
Q

Do Corticospinal tract only carry Upper motor neurons ?

A

No, A minority of corticospinal fibers (typically arising from
parietal areas) will terminate in the dorsal spinal gray matter, presumably to regulate sensory inputs

29
Q

Damage to the corticospinal fibers rostral to the pyramidal

decussation produces ________ paresis.

A

contralateral

30
Q

Damage to the lateral corticospinal tract caudal to the decussation produces ________ paresis

A

ipsilateral

31
Q

What is spinal shock?

A

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.

32
Q

Manifestations of Upper Motor Neuron Lesions

A

– 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
– Clonus

33
Q

What is the Extensor Plantar response?

A

Stimulus elicits extension of the big toe and a fanning of the other toes, instead of the normal flexion seen in adults

34
Q

Why is Extensor Plantar response seen in infants under 1 yrs?

A

because the immature lateral corticospinal pathway is weakly myelinated

35
Q

Why is there no muscle wasting in Upper motor neuron lesions?

A

Because the muscles are still innervated by the lower motor neuron

36
Q

What is spasticity?

A

pathologically increased muscle tone (hypertonia) with abnormal posturing

37
Q

Manifestations of Lower Motor neuron Lesions

A
– paralysis (virtually complete loss of movement) or paresis (weakness) occur ipsilateral to site of the lesion
– Hyporeflexia/areflexia
– Flaccid paralysis
– Wasting of muscles 
– Fasciculations (spontaneous twitches)
– Fibrillations (as appear on EMG)
– Hypotonia
38
Q

Why does Hyporeflexia occur in LMN?

A

due to interruption of the efferent (motor) limb of the

reflex arcs

39
Q

eg of Lower motor neuron lesions

A

ALS

Peripheral nerve damage

40
Q

What causes Brown Sequard syndrome?

A

Arises from spinal hemisection

41
Q

What symptoms of the corticospinal tract will a patient exhibit in brown sequard syndrome?

A
Contralateral below the lesion: Normal
Ipsilateral below the lesion: Upper motor neuron syndrome
- Hyperreflexia
- Clonus
- Extensor plantar reflex
- Spastic paralysis
42
Q

What symptoms of the Anterolateral tract will a patient exhibit in brown sequard syndrome?

A

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

43
Q

What symptoms of the Dorsal Column/Medial Lemniscus tract will a patient exhibit in brown sequard syndrome?

A

Contralateral below the lesion: Normal

Ipsilateral below the lesion: No touch, vibration or proprioception

44
Q

What is damaged at the level of the lesion in Brown sequard syndrome?

A

Lower motor neurons in the anterior horn ipsilaterally

45
Q

What symptoms of the lower motor neuron damage at the level of the lesion in brown sequard syndrome?

A
  • Hypo- or areflexia
  • Wasting of muscles
  • Flaccid paralysis
  • Fasciculations
  • Fibrillation
46
Q

When does Paraplegia occur?

A

Bilateral spinal cord injury

47
Q

Manifestations of Paraplegia

A

Bilateral Upper Motor Neuron syndrome:
paraplegia:
-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!

48
Q

Start of Corticobulbar Fibers

A

Layer 5 of the ventrolateral precentral gyrus

49
Q

End of Corticobulbar Fibers

A

Motor nuclei of cranial nerves

50
Q

Route of Corticobulbar Fibers

A

Distinct bundles of corticobulbar fibers take different
routes, depending on which cranial nerve nucleus is
innervated.
- they all come down in the genu of the internal capsule

51
Q

Function of Corticobulbar Fibers

A

Innervation of muscles in the head (including those of the eyes and mouth) and part of the neck.

52
Q

Where are the losses seen in Infarction of the posterior limb of the internal capsule?

A

Damage to the corticospinal tract causes a contralateral
upper motor neuron syndrome.
Somatosensory losses are also contralateral to injury

53
Q

Which fibers are damaged in internal capsule infarction?

A

corticospinal and corticobulbar fibers and somatosensory systems

54
Q

Which nucleus innervates the muscles of the tongue?

A

Hypoglossal nucleus

55
Q

Damage to _______ fibers that project to the hypoglossal nucleus causes a _______ deviation of the tongue during protrusion.

A

corticobulbar; contralateral

56
Q

Damage to the corticobulbar fibers projecting to the contralateral _______ in the caudal pons causes a deviation of both eyes ______ the lesion

A

paramedian pontine reticular formation (PPRF); towards

57
Q

Why is there constant deviation of the eyes in PPRF damage and not just when the patient tries to look in a particular direction?

A

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

58
Q

Which area of the cortex is responsible for horizontal gaze?

A

Frontal eye Field

59
Q

Damage to the corticobulbar fibers innervating the facial nucleus causes a ___________ facial paralysis

A

contralateral LOWER

60
Q

What is different about the innervation of the upper and lower facial nuclei?

A
  • The upper facial nucleus receives bilateral innervation through corticobulbar fibers from the ventrolateral primary
    motor cortex.
  • The lower facial nucleus receives only contralateral projections
61
Q

How can we differentiate central facial lesion From Peripheral facial lesion?

A

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

62
Q

Eg of Peripheral facial lesion

A

Lower motor neuron syndrome, like BELL’s Palsy , which is caused by a viral infection