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Neuro- Farrah stuff > Test 3 Motor Systems CC > Flashcards

Test 3 Motor Systems CC Flashcards

1
Q

Damage to LMN- what type of neuron, 4 signs?

A

LMN= alpha motor neurons

  1. Flaccid paralysis==> atrophy
  2. Fibrillations or fasciculations
  3. Hypotonia
  4. Hyporeflexia or areflexia
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2
Q

Areflexia

A

Loss of reflexes, from damage to LMN

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3
Q

Myasthenia Gravis

A

Autoimmune disease of neuromuscular junction. Form Ab to AchR. Ocular muscles first affected (sometimes limited to extraocular muscles)

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4
Q

Myasthenia Crisis

A

Weakness of respiratory muscles==requires rapid intervention

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5
Q

Muscle stretch reflex

A

Ia spindle afferent==> excitatory connection with alpha motor neurons

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6
Q

Reciprocal Inhibition

A

Ia fibers (afferent stretch) activate Ia interneurons= inhibition of antagonistic muscles

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7
Q

Crossed Extensor Reflex

A

Interneurons activate extensors and inhibit flexors on opposite side so that when you withdraw the limb, the opposite side is ready for it.

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8
Q

Blocking AchR

A

Causes: myasthenia gravis, curare, alpha bungaro toxin, curare, Treatment: Achesterase inhibitors= neostigmine

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9
Q

According to Dr. Bridges…drooping eyelids is characteristic of?

A

Myasthenia gravis

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10
Q

+ babinksi sign

A

corticospinal tract problem

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11
Q

Apraxia

A

inability to preform complex motor tasks (ex: dressing). Damage to motor or association cortex.

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12
Q

Blocking cholinesterase

A

Nerve gases: Saran, Soman, Tabun, VX- death by asphyxiation

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13
Q

Blocking Ach Release

A

Botulinum toxin

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14
Q

Explosive Ach Release

A

Black widow= alpha-latrotoxin Convulsion–> paralysis (when run out of Ach) 1) Prevents fusion at synaptic vesicle followed by 2) triggered Ach Release.

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15
Q

Rubrospinal system

A

UE, no influence on LE

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16
Q

Supratentorial lesions

A

=central/transtentorial lesions Unopposed hyperactivity of extensor muscles= decerebrate rigidity

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17
Q

Noxious stimulus to decerebrate patient

A

exacerbate decerebrate rigidity or evoke it if it isn’t apparent

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18
Q

Diencephalic stage=

A

during central herniation (transtentorial), before herniation through notch Sx= decreased level of consciousness, lethargy, small and poorly reactive pupils. Withdraw reflex is intact. Bilateral babinski response. Weak extremeties==>decorticate on ipsilateral side then both sides.

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19
Q

Part 2 of central herniation

A

=herniation through tentorial notch Sx: decerebrate, comotose, dilated fixed puils without light reaction. No eye movement. As it reaches midbrain, respiration stops

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20
Q

Cheyne Stokes

A

Damage to brain stem during central/transtentorial herniation:

abnormal pattern of breathing characterized by progressively deeper and sometimes faster breathing, followed by a gradual decrease that results in a temporary stop in breathing called an apnea.

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21
Q

Decerebrate condition

A

=gamma rigidity. flexor muscles are inactive (corticospinal and corticorubrospinal input) Extensor muscle tracts not effected

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22
Q

Extensor muscle tracts

A

reticulospinal (gamma motor neurons) and vestibulospinal

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23
Q

Flexor muscle tracts

A

corticospinal and corticorubrospinal tracts

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24
Q

Decerebrate condition

A

=gamma rigidity (mostly reticulospinal) flexor muscles are inactive (corticospinal and corticorubrospinal input) Extensor muscle tracts not effected

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25
Q

Flexor muscle tracts

A

corticospinal and corticorubrospinal tracts

26
Q

Decerebellate rigidity

A

=alpha rigidity (mostly vestibulospinal) loss cerebellar anterior lobe= no purkinje cell inhibition to vestibular nuclei and of fastigial neurons.

27
Q

Decorticate rigidity- Symptoms?

A

Sx:

  • flexion of upper extremities (intact rubrospinal);
  • extensor hypertonus (intact reticulospinal);
  • altered state of consciousness, respiration, oculomotor deficits, weakness
28
Q

Upper Motor neuron damage- Symptoms? do they change ove time?

5 total

A
  1. Initially weak and flaccid
  2. Become spastic
  3. Hypertonia- resistance to passive movement
  4. hyprereflexia
  5. Babinksi sign=dorsiflexion of great toe (normal is plantar)
29
Q

Spasticity- clinical symptoms? Most obvious muscles?

A

Spasticity

Increased resistance to passive movement or manipulation. Velocity dependent: increased resistance the faster the examiner moves the extremity.

  • upper extremitiy: proximal flexors
  • Lower extremity: extensors
30
Q

Clasp Knife Effect

A

Clasp Knife Effect

After brief period of applied force (during exam for spasticity), the increased resistance collapses. –the spasticity stops

31
Q

Clonus

A

Clonus: Observed in UMN lesion

  • Repetitive sequential contractions of flexors and extensors following flexion/extension.
  • Usually accompanied by spasticity
32
Q

Corticospinal lesions cause ipsilateral/contralateral deficits?

A

Corticospinal tract lesions

Ipsilateral= below motor decussaiton

Cotralateral deficit= above decussation

33
Q

Infarction of primary motor cortex=

A

infaction of MI (= primary motor cortex)= usually paralysis

34
Q
  1. Infarction of premotor cortex=
  2. Infarction of supplementary motor cortex
A
  1. Lesion to premotor cortex= Contralateral apraxia
    • normal strenght and tone
    • Inability to perform voluntary action (ex: picking up pencil)
  2. Lesion to supplementary motor cortex= ability to corrdinate actions on both sides of the body
    • normal strength and tone
35
Q

Posterior limb of internal capsule

  1. Blood supply
  2. Damage causes
A

Posterior limb of internal capsule- has corticospinal fibers

  1. Blood= Lenticulostriate branches of M1
  2. Symptoms: Transient flaccid paralysis followed by spastic paralysis in contralateral UE/LE. never resolves.
36
Q

Fiber bundles found in posterior limb of internal capsule

A
  • Posterior limb of internal capsule:
    • Corticospinal= motor loss
    • thalamocortical= hemisensory loss, homonymous hemianopia
37
Q

Corticospinal fibers in the midbrain are found?

A

Midbrain corticospinal fibers are found in the middle third of the crus cerebri.

UE= medial; LE=lateral

38
Q

Weber’s Syndrome

A

Weber’s Syndrome= Damage to medial 2/3 of crus cerebri-

  • Causes: Hemorrhage of posterior communicating artery and paramedial branches of P1
  • Symptoms: superior alternating hemiplegia, crossed deficit
    • Corticospinal fibers-contralateral hemiparesis
    • Frontopontine/corticobulbar fibers-deviation of ipsilateral eye (down and out); possible loss of direct, consensual light reflex and loss of accomodation
39
Q

Corticospinal fibers in pons are supplied by ____ a.

Symptoms of occlusion to the artery? What is the general condition called? what is the specific name for it?

A

FOVILLE SYNDROME

Blood supply: Paramedian branches of the basilar a

Symptoms: MIDDLE alternating hemiplegia, crossed deficit

  • Hemiplegia, UMN sign
  • Damage to abducens fibers=ipsilateral lateral rectus paralysis
  • possible damage to medial lemniscus
40
Q

Corticospinal fibers in the medulla

  • Blood supply
    • What else is supplied by this artery-sx if occluded?
  • Symptoms if occluded?
  • Name of syndrome?
A
  • Blood supply in Medulla= Anterior spinal artery
    • hypoglossal nerve=ipsilateral flaccid paralysis of tongue (LMN); deviation to side when protruded
    • medial lemniscus=contralateral loss of two point discriminations
    • pyramids= Contralateral hemiparesis
  • Dejerine Syndrome= inferior alternating hemiplegia
41
Q

Damage to ROSTRAL half of motor decussation=

A

Damage to ROSTRAL half of motor decussation=

  • Ipsilateral hemiparesis in UPPPER extremity
  • Contralateral hemiparesis in LOWER extremity
42
Q

Anterior vs lateral corticospinal tract

A

Anterior corticospinal tract= does not decussate

Lateral corticospinal tract- decussates in pyramids

43
Q

Damage to corticospinal tract in upper cervical cord

A

Corticospinal tract damage in cervical part=

  • hyperreflexia
  • Babinski sign
  • spastic hemiplegia in ipsilateral LE and UE
44
Q

Lesion of cervical enlargement

A

Lesion of cervical enlargement​

  • LMN signs in ipsilateral UE
  • UMN signs in ipsilateral LE
45
Q

Clinical symptoms if patient has corticospinal damage AND damage to anterior horn?

A

Clinical symptoms if patient has corticospinal damage AND damage to anterior horn?

LMN signs

46
Q

Central Cord Syndrome

A

Central Cord Syndrome- hyperextension of the neck-can damage cord or occlude sulcal branches of ASA.

  • bilateral hemiparesis of UE (medial region of both lateral corticospinal tracts)
  • urinary retention
  • bilateral patchy loss of pain and temp below injury
47
Q

Blood supply to

  1. Medial part of lateral corticospinal tract
  2. Lateral part of lateral corticospinal tract
A

Blood supply to

  1. Sulcal branches of ASA=Medial part of lateral corticospinal tract=UE
  2. Penetrating branches of ASA= Lateral part of lateral corticospinal tract= LE
48
Q

Brown Sequard Syndrome

A

Brown Sequard Syndrome=hemisection of spinal cord

  • Ipsilateral loss of two point discrimination (posterior columns)
  • Contralateral loss of pain, temp, crude tough (ALS)
  • Ipsilateral paralysis (corticospinal tract)
49
Q

Corticonuclear fibers course (start in cortex)- blood supply in each region? –list nuclei it innervates in order

A

Innervates 5 nuclei

  • Start in Layer V of face part of motor cortex= MCA
  • Go through genu of internal capsule= lenticulostriate arteries
  • Midbrain: medial part of crus cerebri=paramedian branch of basilar a.
  • Pons: trigeminal ==>facial motor nuclei
  • Medulla: Hypoglossal, nucleus ambiguous==> Accessory motor nucleus
50
Q

Unilateral damage to corticonucluear fibers?

A

Equal innervation from both sides to motor V and upper muscles of motor VII.

  • No visisble weakness of muscles of mastication
  • No visisble weakness of upper facial muscles
  • contralateral weakness of lower facial muscles (if rsotral to motor nucleus)
51
Q

Central facial paralysis

A

Central facial paralysis: Lesion of corticonulcear fibers rostral to facial motor nucleus=

  • CONTRALATERAL drooping of muscles at corner of the mouth and lower portion of face on the side opposite to the lesion
52
Q

Bell’s Palsy

A

Damage to ROOT of facial nerve= flaccid paralysis of all muscles on IPSILATERAL side

53
Q

Corticonuclear fiber damage at mid-medullary levels

A

contralateral weakness to palatal arch muscles (nucleus ambiguous), failure to elevate on weak side and deviation of uvula to side of lesion

54
Q

Damage to root of vagus nerve

  • what can cause this?
  • clinical manifestations
A

Root=LMN lesion

  • can happen in jugular foramen syndromes
  • weakness and slight drooping of the arch on same side, deviation of uvula to contralateral side of lesion
  • (uvula deviates to STRONG side)
55
Q

Hypoglossal muscles- damage to fibers before vs after nucleus

A

damaged corticonuclear fibers= UMN, deviation of tongue during protrusion to opposite side of lesion (to weak side). May also have symptoms associated with damaged genu of internal capsule (central seven, uvula deviation)

damaged hypoglossal nerve- LMN= atrophy of tongue, deviates to side of lesion.

56
Q

Damage to corticonuclear fibers to accessory nucleus

A

IPSilateral weakness. Cannot shruf or elevate shoulder on side of lesion, cannot turn head away from lesion

57
Q

Lenticulostriate A hemorrhage=

A

Lenticulostraite artery= genu and posterior limb of internal capsuel

Corticospinal damage=contralateral spastic hemiparesis

Corticonuclear damage= contralateral central facial paralysis, deviation of uvula to side of lesion, deviation of tongue to contralalteral side of lesion, inability to turn head away from lesion, raise shoulders on side of lesion

58
Q

Uncal herniation

A

Damage to occulomotor nerve and crus cerebri on side of herniation

CN III= ipsilateral paralysis of eye movement, diplopia, dilated pubul

Corticospinal= contralateral hemiplegia

59
Q

Kernohan Syndrome

A

Kernohan Syndrome=midbrain displaced against edge of tentorium on side CONTRALATERAL to the herniation

  • IPSilateral occulomotor nerve palsy (expected)
  • IPSilateral hemiplegia (false localizing sign, caused by compression of crus CONTRAlateral to herniation)
60
Q

Corticorubral system

  • where does it start?
  • function?
A

Corticorubral system

  • From area 4 and 6 of cortex
  • can partially compensate for loss of corticospinal tract
  • flexion of upper extremity

Neuro- Farrah stuff (16 decks)

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