Week 5 Gems Flashcards

0
Q

Staring spells, sudden onset, no post ictal state, hyperventilation can induce spell, improve as patient ages

A

Absence seizures

Idiopathic or primary

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1
Q

No focal Sx. Seizures begins suddenly, post ictal state

A

Generalized tonic clonic seizures

Tend to be primary - inborn genetics or
Drug intoxication or withdrawal or
Metabolic abnormalities or
Encephalities

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2
Q

Focal lesion or disease affecting brain. Without alternation in state of awareness

A

Simple partial seizures

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3
Q

Focal lesion or disease affecting brain. With alternation in state of awareness.

A

Complex partial seizures

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4
Q

Sx of wilson’s disease

A

Movement disorders
psychiatric
Liver

Tx: zinc

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5
Q

2 basic types of neurons

A

UMN

  • Control movement
  • cerebral cortex
  • brainstem

LMN

  • control muscles
  • brainstem
  • spinal cord
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6
Q

Where is LMN in spinal cord and brainstem?

A

Ventral horn in spinal cord

Facial nucleus and oculomotor nuclei in brainstem

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7
Q

Where are UMN cell bodies

A

In cerebral Cortex: planning and initiating movement

  • primary motor cortex
  • premotor cortex
  • posterior cingulate cortex

In brainstem: regulation of muscle tones, movements of eye, H&N

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8
Q

Initiation of movement - posterior cortex

A

Specifies movement goals

Send info to temporal cortex, prefrontal cortex and M1

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9
Q

Inititation of movement - prefrontal cortex

A

generate plans for movement

send info to premotor Cx

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10
Q

initiation of movement - premotor cortex

A

contains lexicon of movement
can recognize movement of others
can send info to motor Cx

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11
Q

initiation of movement - primary motor cortex

A

contains lexicon of more elementary movements

contributes to the recruitment of LMN

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12
Q

random motor system hierarchy

A

over 30% of CST are from premotor cx
some areas of premotor and SMA DON’T have direct connection with motor cx
areas in M1 can have higher cognitive functions
motor cx and some premotor cx can coordinate complex movement

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13
Q

2 proposed motor system hierarchy

A
  1. simple serial

2. several layer association with interconnection at each level

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14
Q

what does a intracortical microstimulation tell you?

A

organized movement is stimulated rather than individual muscles

e.g if you injure the thumb area of M1, you will get weakness of thumb as well as the other fingers and arm –> because it is affecting the movement (pincer grip) not only the thumb muscle

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15
Q

What is a muscle field?

A

the peripheral muscles controlled by a single UMN

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16
Q

what are the secondary motor cortexes?

A

premotor cx - ventrolateral
SMA - dorsalmedial
cingulate area - important for facial expression of emotions

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17
Q

SMA vs premotor cx

A

similarities:
mediate selection of movements, involvement with whole body movement

differences:
SMA - in response to external cues - closed loop
premotor - activated bilaterally, in response to internal cues - open loops

18
Q

primary VS secondary motor cx

A

differences:
strength of direct connections to LMNs
primary - initiation of specific movements, lesions causes contralateral weakness
secondary - selection of movements, lesions impair ability to develop appropriate strategy (apraxia), no weakness

19
Q

What is the function of Frontal Eye Fields (FEF)? clinical presentation if lesion?

A

for saccadic eye movement
in area 6 –whatever
lesion result in BOTH eyes deviating TOWARDS side of lesion

20
Q

3 principles of descending pathways and their organization

A
  1. parallel functional organization - medial and lateral
  2. direct and indirect projections (via brainstem) from cortex
  3. monosynaptic and polysynaptic connections between descending pathways and LMNs (interneurons)
21
Q

somatotropic organization of ventral horn

A

Dorsal MNs innervate flexor muscles
Ventral MNs innervate extensor muscles
Medial MNs innervate proximal/ axial muscles - trunk muscles
Lateral MNs innervate distal/ appendicular muscles - fingers

22
Q

Medial Pathway of descending motor control

A

E.g. medial VST
for posture and balance
terminate bilaterally
long intersegmental interneurons within spinal cord with ipsilateral and bilateral connections

23
Q

Lateral Pathway of descending motor control

A

e.g. CST
involve in skilled movement
terminate unilaterally
short intersegmental interneurons within spinal cords unilaterally ( intermediate zone of the spinal grey)

24
Q

4 brainstem motor control center (UMN) and their functions

A
  1. vestibular nuclei - postural activity in response to inner ear signals
  2. reticular formation - limb movements to maintain posture & balance
  3. red nucleus - connects to cerebellum & upper limb movements
  4. tectum of midbrain - reflex turning of head in response to sights & sounds
25
Q

Medial VS lateral VST

A

medial VST:
- MVN terminate bilaterally in the UPPER spinal cord (cervical)
- regulate head position in response to input from semicircular canals
- vestibulo-cervical reflex
-extensor biased
Lateral VST:
-LVN terminates ipsilaterally in UPPER and LOWER spinal cord (SC all levels)
-innervates proximal muscles and axial musculature
-activates extensor muscles in response to input from saccule and utricle
-vestibulo-spinal reflex

26
Q

Tectospinal projection to the spinal cord

A

From the superior colliculus, which is part of the tectum of midbrain. it helps to orient movements of head and eyes. and terminates in the UPPER spinal cord (cervical spinal cord)

-extensor biased (medial pathway)

27
Q

Functions of Reticular Formation

A
  • nuclei founds at all levels of brainstem
  • sleep/wakefulness, cardiovascular and respiratory centers, eye movements
  • ***coordination of limb and trunk movement
28
Q

Reticulospinal tract porjection

A
  • terminates in motor neurons pools innervating axial musculatuire and proximal limb muscles
  • input from cortex, hypothalamus and brainstem
  • IMPORTANT IN ANTICIPATORY POSTURAL ADJUSTMENTS
29
Q

Indirect pathways from motor cortex to spinal cord

A

Cortical neurons have direct pathway to the motorneurons BUT…
they can also terminate on UMN in RF that mediate posture. These UMN are located medially in the ventral horn

30
Q

Feedforward VS Feedback mechanism of postural control

A

Feedforward: (reticulospinal tract) responses are preprogrammed and procede the onset of limb movement

Feedback: responses are initiated by sensory inputs that detect postural instability. Rely on INDIRECT pathway from the cortex

31
Q

special processing of myelin

A
  • fixed in glutaraldehyde & embedded in epoxy resin

- fixed and stained with osmium

32
Q

origins of CSTs and their terminations

A
  • frontal lobe: terminate in ventral spinal grey (spinal enlargements & lateral ventral horn)
    1/3 from primary motor cx
    1/3 from secondary motor cx

-parietal lobe: terminate in dorsal spinal grey (deep dorsal horn, not UMNs)
1/3 from S1 cx mostly

33
Q

Lateral vs Ventral CST from frontal lobe

A

lateral CST

  • terminates in more lateral parts of spinal VH
  • control proximal & distal muscles

Ventral CST

  • terminates bilaterally in more medial parts of spinal VH
  • control truncal muscles
34
Q

Lateral vs Medial Reticulospinal tracts

A

Lateral RST:

  • medulla RF –> SC all levels
  • flexor biased

Medial RST:
-Pons RF –> SC all levels
extensor biased - medial pathway

35
Q

Rubrospinal Tract

A

Red nucleus –> SC cervical levels

Flexor biased - lateral pathway

36
Q

Reticulospinal vs vestibulospinal MNs termination

A

reticulospinal: gamma MN
vestibulospinal: alpha MN

37
Q

Decrebration

A
  • brainstem transection in upper pons/lower midbrain (above vestibular nuclei, below RN)
  • results in extensor rigidity (clinical spasticity) (CST & RuSt -severed/ Lat VST & Medial ReST is intact)
  • muscle tons is mediated by gamma MNs, which is under control of ReSt with excitatory predominates. The lesion disrupt the inhibitory signals from basal ganglia to RF, causing a loss of inhibition on gamma MNs, which increases extensor muscle tones
38
Q

Decortication

A
  • lesion above midbrain
  • CST is lesioned, RuST & medial ReSt are intact
  • RuST opposes extensor UMNs to cervical levels
39
Q

Respiratory patterns in different level of brain dysfunction

A
forebrain - cheyne-stokes
Midbrain - hyperventilation
rostral pons - apneustic
lower pons - ataxia
medulla - respiratory arrest
40
Q

decerebrate rigidity vs spasticity vs clinical rigidity

A

decerebrate rigidity & clinical defined spasticity
-increased muscle spindle reflexes & increased extensor tone

clinical rigidity

  • increased muscle tone in basal ganglia disease: PD
  • NO hyperactive MSRs
41
Q

Tx of spasicity

A

Baclofen

  • GABA agonists which reduces activity in spinal afferents of hyperactive reflexes that generate hypertonia
  • oral / intrathecal as muscle relaxant
42
Q
Lesions affecting lateral gaze: Patient ask to gaze right
L FEF
L INO
L CN III palsy
R CN VI palsy
L vestibular nerve damage
abducens/PPRF
A

L FEF - both eyes gaze L
L INO - L MLF lesion, R nystagmus, L won’t move
L CN III palsy - L out and down with ptosis
R CN VI palsy - R won’t move, L adduct
L vestibular nerve damage - R nystagmus
abducens/PPRF - both won’t move

43
Q

Gaze preference of cortical and brainstem lesions, seizures

A

cortical: towards lesion
brainstem: away from lesion
seizures: away from lesion