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Neuroscience > Neuroscience Week 3: Spastic Paralysis, Spinal Motor Organization and Brain Stem Supraspinal Paths > Flashcards

Neuroscience Week 3: Spastic Paralysis, Spinal Motor Organization and Brain Stem Supraspinal Paths Flashcards

1
Q

Upper Motor Neurons

A

brain and brain stem supraspinal pathways (use gluatamate to excite LMNs, entire cell body axons and cell bodies reside in the CNS, myelinated by oligodendrocytes

UMNs Activity affects muscle contraction indirectly via connections with LMNs Does NOT include sensory neurons (e.g. DRG neurons) Use glutamate as a neurotransmitter Axons never leave the CNS Lesion: typically contralateral to functional deficit(s)

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2
Q

Lower Motor Neurons

A

brainstem as cranial nerves and spinal cord ventral neurons, myelinated by Schwann cells

LMNs Innervate skeletal (and visceral) muscle directly via axons that leave the CNS; final common path from CNS to muscle Use ACh as neurotransmitter Lesion: typically ipsi lateral to functional deficit(s)

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3
Q

LMN lesions typically cause ipsilateral/contralateral functional deficits

A

Typically cause ipsilateral functional deficits

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4
Q

UMN lesions typically cause ipsilateral/contralateral functional deficits

A

Typically cause contralateral

EXCEPT in the spinal cord they will cause ipsilateral functional deficits

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5
Q

Primary Motor Cortex neuron type

A

First order UMNs in the precentral gyrus

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6
Q

First-order UMN innervate what?

A

Can directly innervate some LMNs but typically innervate interneurons to indirectly affect LMN activity

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7
Q

Homunculus

A

the number of neurons that regulate particular body regions is proportional to its size. More UMNs are needed to control the fingers and lips Fewer are required to control the trunk

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8
Q

Stimulation of a homunculus with an electrode in an area will cause

A

individual muscle contraction

Activity controls speed, force and direction

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9
Q

Corticospinal Tract

A
  • Grey matter of precentral gyrus gives rise to axonal fibers which descend through the posterior limb of the internal capsule and run through some of the basal ganglia and the thalamus
  • then will partially create and travel through the cerebral peduncles
  • axons dive internally into the pons then become external at the pontomedullary junction creating the pyramids
  • decussate at the cervico-medullary junction (caudal medulla) and become an internal fiber pathway in the spinal cord
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10
Q

CST path through the brainstem

A
  • Grey matter of precentral gyrus gives rise to axonal fibers which descend through the posterior limb of the internal capsule and run through some of the basal ganglia and the thalamus
  • then will partially create and travel through the cerebral peduncles
  • axons dive internally into the pons then become external at the pontomedullary junction creating the pyramids
  • decussate at the cervico-medullary junction (caudal medulla) and become an internal fiber pathway in the spinal cord
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11
Q

Pre and post olivary sulcus

A

by the pyramids

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12
Q

Lateral corticospinal tract

A
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13
Q

Corticospinal Homunculus

A

in cervical cord lost face because they will have already synapsed

the fibers that are closest medially are the ones that will synapse in the ventral horns at every level so arm fibers will be most medial in the cervical spine

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14
Q

Identify CST Homunculus

A
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15
Q

Identify CST Homunculus

A
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16
Q

Identify CST Homunculus

A
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17
Q

Premotor cortex

A

Premotor Cortex (PMC)

  • Some fibers project directly to spinal cord, striatum, thalamus (part of CST)
  • Primarily innervate MNs that control
  • paraxial (trunk) muscles during reaching
  • Integrates sensory information from
  • objects close to the body
  • also mirror neurons to mimic other people’s behavior such as smiling at a child and the child smiles back
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18
Q

Supplementary motor (SMA)

A
  • Extensive connections with pre frontal cortex, cerebellum
  • Involved in the planning & execution of complex movements
  • Stimulation causes coordinated movements
  • mouse wanted to go left
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19
Q

Primary sensory cortex

A
  • modulates movement via changes to sensory
  • pathways in the dorsal
  • horns (feedback mechanism); intimately connected with M1
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20
Q

Posterior Parietal cortex (PPC)

A

modulates CST activity during the planning and execution of movements (hands/eyes) apraxia (inability to perform actions when asked

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21
Q

Damage to this area causes apraxia

A

Posterior parietal cortex

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22
Q

Identify

A
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23
Q

of fibers in peduncles and the pyramids

A
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24
Q

Corticobulbar tract CBT

A

the homunculus on this figure is not correct!!!

LMNs that are inervated by corticbulbar fibers are innervated bilaterally (EXCEPTION the face)

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25
Q

LMNs that are inervated by corticbulbar fibers are innervated

A

Bilaterally except for CN VII on the lower face

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26
Q

CN VII lesion UMN vs LMN lesions

A
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27
Q

Alternating Hemiplegia

A
  • ophthalmoplegia ipsilateral to the lesion
  • with contralateral hemiplegia
  • Can have deficits that are contralateral in the body and ipsilateral ophthalmoplegia because corticospinal and corticobulbar
  • if contralateral hemiplegia with no ocular symptoms you might think the lesion is solely in the brain or in the cord but not the brainstem
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28
Q

Alternating Hemiplegia AKA

A

Weber Syndrome

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29
Q

UMN Syndrome Symptoms

A
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30
Q

Tests for UMN disease

A
  • Hyperreflexia
  • clonus
  • Babinski +
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31
Q

Babinski test

A
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32
Q

Spasticity vs. Rigidity

and clasp-knife spasticity

A
  • Spasticity is characteristic of a UNM lesion
  • Rigidity is not characteristic of UMN lesion
  • in UMN lesions the clasp-knife spasticity will give way to transient flaccid paralysis
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33
Q

Rigidity is characteristic of?

A

basal ganglia pathology (parkinsons, huntingtons)

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34
Q

UMN and LMN

A
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35
Q

Cases 1 and 2

A
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36
Q

Cases 3 and 4

A
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37
Q

Cases 5 and 6

A
38
Q

Vitamin B12 Deficiency First AID

A

FIRST AID:

Subacute combined degeneration (

SCD

)

demyelination of

S

spinocerebellar tracts, lateral

C

corticospinal tracts, and

D

dorsal Columns.

39
Q

Vitamin B12 Deficiency Etiology

A

Severe chronic B 12 deficiency (B12 is required for red blood cell

production)

40
Q

Vitamin B12 Deficiency Pathogenesis

A

Cause: absorption deficiency due to lack of Gastric Intrinsic Factor (GIF) caused by autoimmunity, genetic or surgical (resection of stomach/small intestine); others include vegan diet, celiac disease, tapeworm infection.

41
Q

Vitamin B12 Deficiency Early Symptoms

A

Early Symptoms (slowly progressing): weakness and fatigue, breathlessness and dizziness, pale or jaundiced skin, sensations of pins and needles, vision changes, numbness (hands and feet), memory/mood disturbances, fevers

42
Q

Vitamin B12 Deficiency Late Symptoms

A

Late Symptoms: absent ankle reflex, patellar hyperreflexia, Babinski sign, changes to mobility/balance, distal anesthesia}Treatment: supplementation if caught early (pills, nasal spray, injections)

43
Q

Vitamin B12 Deficiency Treatment

A

Treatment: supplementation if caught early (pills, nasal spray, injections

44
Q

Anterior Spinal Artery Syndrome FIRST AID

A

FIRST AID: Spares dorsal columns. Mid-thoracic ASA territory is watershed area, as artery of Adamkiewicz supplies ASA below T8.

45
Q

Anterior Spinal Artery Syndrome Common causes

A

Can be caused by aortic aneurysm repair.

46
Q

Anterior Spinal Artery Syndrome Clinical Presentation

A

Presents with ipsilateral UMN deficit below level of lesion (CST), LMN deficit at the level of the lesions (anterior horn), and contralateral loss of pain and temperature sensation below the lesion (spinothalamic tract)

47
Q

Brown-Séquard Syndrome FIRST AID

A

Ipsilateral UMN signs below the level of the lesion (CST damage)

48
Q

Brown-Séquard Syndrome Clinical Presentation

A

Ipsilateral LMN signs at the level of the lesion

sensory stuff on other lectures i guess

49
Q

Brown-Séquard Syndrome Supplementary Complications and Considerations

A

If lesion occurs above T1 patient may present with ipsilateral Horner’s syndrome

50
Q

Supraspinal Tracts

A

UMNs in the brainstem involved in unconscious movements and posture

51
Q

Vitamin B12 Deficiency Overview

A
52
Q

Anterior Spinal Artery Syndrome Overview

A
53
Q

Brown-Séquard Syndrome Overview

A

majority of spinal cord is supplied by the anterior Spinal Artery

the ver

54
Q

Anterior Spinal Artery Syndrome

A

LMN at the level of the lesion but UMN ipsilateral to the lesion anywhere below the lesion because degeneration of the fiber pathways in the corticospinal pathway below T8

contralateral loss of temperature and pain sensation

55
Q

Reticular formation

A

series of interconnected nuclei and pathways not anatomically well-defined

Ascending Reticular Activating System communication with this system and the cortex is believed to cause consciousness

56
Q

What systems cause consciousness?

A

Ascending Reticular Activating System (ARAS) communication with this system and the cortex is believed to cause consciousness

57
Q

Decorticate posturing

A

lesion closer to cortex

58
Q

Decerebrate Posturing

A

Lower brainstem lesion

59
Q

Vestibular System function

A
  • Detection of head orientation, acceleration
  • Maintain balance
60
Q

Vestibular System dysfunction

A
  • False sense of motion; vertigo
  • causes: idiopathic, trauma, infection or intentional
61
Q

Vestibular System Overview

A
62
Q

How does the Vestibular System interact with the limbs

A
63
Q

Vestibular System Test

A

Romberg Test

remove shoes

stand feet together arms folded 30 seconds eyes open and then eyes closed

the test is positive if the patient cannot maintain balance with eyes closed or if they open eyes or take a step

64
Q

Rubrospinal Tract Origin

A

Red Nucleus (Thalamus) w/cerebellar input

65
Q

Rubrospinal Tract Descends

A

lateral column

66
Q

Rubrospinal Tract Terminates

A

LMNs in the cervical cord

67
Q

Rubrospinal Tract Function

A
  • Primarily facilitates flexors of upper limbs (elbow/forearm)
  • Cortical input largely inhibitory (loss causes (flexion);
  • In Decorticate posturing only not in Decerebrate
  • the cortex inhibits this but when the person is unconscious the cortex is no longer being inhibited and it is allowed to be activated
68
Q

Pontine/Medial Reticulospinal Tract Origin/Pathway

A

Medial longitudinal fasciculus

Ventral funiculus

69
Q

Pontine/Medial Reticulospinal Tract Function

A

Function

Facilitate extensors (anti-gravity), inhibited by cortical centers Influences posture and locomotion

Medullary/lateral(LRST)◦Origin/Pathway

Throughout spinal column (lateral funiculus)

70
Q

Medullary/Lateral Reticulo Spinal Tract (LRST) Function

A

Function

Facilitates upper limb flexors; facilitated by cortical centers

Strong enough to Inhibit reflexes

Influences posture and locomotion, + autonomic functions (respiration, shivering, GI function)

71
Q

Medullary/Lateral Reticulo Spinal Tract (LRST) Origin/Pathway

A

Throughout the spinal column (lateral funiculus)

72
Q

Summary of Supraspinal pathways

A
73
Q

MAKE MORE CARDS ON THIS

A
74
Q

Decorticate vs Decerebrate posturing

A
75
Q

If a patient is Decorticate than showing Decerebrate

A

means the lesion is probably descending towards the respiratory centers of the medulla

76
Q

Can go from Decerebrate to Decorticate

A

could be getting better

77
Q

Recovery from capsular stroke

A

lesion destroying the posterior limb

down in the spinal cord the lateral corticospinal tract strong innervation of digit function while proximal muscles are innervated more by multiple pathways while digit muscles are innervated solely by CST

Relatively more contribution of supraspinal pathways of proximal muscles

78
Q

Acute Phase of capsular stroke

A

Complete contralateral motor hemiparesis (contralateral) including face, arm and leg

sometimes tongue and soft palate are affected due to predominant contralateral innervation by CBT

Volitional movements are absent

May include UMN signs (Babinski, hypertonia, hyperreflexia)

79
Q

Tongue and soft palate are innervated how

A

predominantly contralateral innvervation

80
Q

The Reticulospinal tract is comprised of

A

the medial (pontine) tract and the lateral (medullary) tract.

81
Q

Chronic Recovery from capsular stroke

A
82
Q

Contralateral Spastic Hemiplegia

A

Contralateral Spastic Hemiplegia

  • Postural control recovers, some proximal control recovers
  • Antigravity muscles (ventromedial supraspinal pathways)
  • Tongue and soft palate deficits disappear; ipsilateral CBT inputs compensate for the loss of contralateral inputs
  • Can walk because proximal muscles and can have flexed arms and curled fingers but extended arms and legs much like Decorticate posture
  • Almost never regain fine control of distal muscles (digits) because these are controlled solely by the CST
  • Face won’t be able to smile contralateral to lesion but can raise eyebrows

UMN signs remain or become exaggerated (hypertonia, hyperreflexia)

83
Q

Supraspinal innervation is?

A

Bilateral

84
Q

Question 1

A
85
Q

Question 2

A
86
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Question 3

A
87
Q

Question 4

A
88
Q

Question 5

A
89
Q

Question 6

A
90
Q

Question 7

A
91
Q

Question 8

A

Neuroscience (96 decks)

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