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

Question 1

Upper Motor Neurons

Answer 1

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)

Question 2

Lower Motor Neurons

Answer 2

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)

Question 3

LMN lesions typically cause ipsilateral/contralateral functional deficits

Answer 3

Typically cause ipsilateral functional deficits

Question 4

UMN lesions typically cause ipsilateral/contralateral functional deficits

Answer 4

Typically cause contralateral

EXCEPT in the spinal cord they will cause ipsilateral functional deficits

Question 5

Primary Motor Cortex neuron type

Answer 5

First order UMNs in the precentral gyrus

Question 6

First-order UMN innervate what?

Answer 6

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

Question 7

Homunculus

Answer 7

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

Question 8

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

Answer 8

individual muscle contraction

Activity controls speed, force and direction

Question 9

Corticospinal Tract

Answer 9

• 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

Question 10

CST path through the brainstem

Answer 10

• 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

Question 11

Pre and post olivary sulcus

Answer 11

by the pyramids

Question 12

Lateral corticospinal tract

Answer 12

Question 13

Corticospinal Homunculus

Answer 13

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

Question 14

Identify CST Homunculus

Answer 14

Question 15

Identify CST Homunculus

Answer 15

Question 16

Identify CST Homunculus

Answer 16

Question 17

Premotor cortex

Answer 17

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

Question 18

Supplementary motor (SMA)

Answer 18

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

Question 19

Primary sensory cortex

Answer 19

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

Question 20

Posterior Parietal cortex (PPC)

Answer 20

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

Question 21

Damage to this area causes apraxia

Answer 21

Posterior parietal cortex

Question 22

Identify

Answer 22

Question 23

of fibers in peduncles and the pyramids

Answer 23

Question 24

Corticobulbar tract CBT

Answer 24

the homunculus on this figure is not correct!!!

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

Question 25

LMNs that are inervated by corticbulbar fibers are innervated

Answer 25

Bilaterally except for CN VII on the lower face

Question 26

CN VII lesion UMN vs LMN lesions

Answer 26

Question 27

Alternating Hemiplegia

Answer 27

* 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

Question 28

Alternating Hemiplegia AKA

Answer 28

Weber Syndrome

Question 29

UMN Syndrome Symptoms

Answer 29

Question 30

Tests for UMN disease

Answer 30

* Hyperreflexia * clonus * Babinski +

Question 31

Babinski test

Answer 31

Question 32

Spasticity vs. Rigidity and clasp-knife spasticity

Answer 32

* 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

Question 33

Rigidity is characteristic of?

Answer 33

basal ganglia pathology (parkinsons, huntingtons)

Question 34

UMN and LMN

Answer 34

Question 35

Cases 1 and 2

Answer 35

Question 36

Cases 3 and 4

Question 37

Cases 5 and 6

Question 38

Vitamin B12 Deficiency First AID

Answer 38

 FIRST AID: Subacute combined degeneration ( SCD ) demyelination of **S** spinocerebellar tracts, lateral **C** corticospinal tracts, and **D** dorsal Columns.

Question 39

Vitamin B12 Deficiency Etiology

Answer 39

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

Question 40

Vitamin B12 Deficiency Pathogenesis

Answer 40

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.

Question 41

Vitamin B12 Deficiency Early Symptoms

Answer 41

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

Question 42

Vitamin B12 Deficiency Late Symptoms

Answer 42

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

Question 43

Vitamin B12 Deficiency Treatment

Answer 43

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

Question 44

Anterior Spinal Artery Syndrome FIRST AID

Answer 44

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

Question 45

Anterior Spinal Artery Syndrome Common causes

Answer 45

Can be caused by aortic aneurysm repair.

Question 46

Anterior Spinal Artery Syndrome Clinical Presentation

Answer 46

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)

Question 47

Brown-Séquard Syndrome FIRST AID

Answer 47

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

Question 48

Brown-Séquard Syndrome Clinical Presentation

Answer 48

Ipsilateral LMN signs at the level of the lesion sensory stuff on other lectures i guess

Question 49

Brown-Séquard Syndrome Supplementary Complications and Considerations

Answer 49

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

Question 50

Supraspinal Tracts

Answer 50

UMNs in the brainstem involved in unconscious movements and posture

Question 51

Vitamin B12 Deficiency Overview

Answer 51

Question 52

Anterior Spinal Artery Syndrome Overview

Answer 52

Question 53

Brown-Séquard Syndrome Overview

Answer 53

majority of spinal cord is supplied by the anterior Spinal Artery the ver

Question 54

Anterior Spinal Artery Syndrome

Answer 54

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

Question 55

Reticular formation

Answer 55

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

Question 56

What systems cause consciousness?

Answer 56

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

Question 57

Decorticate posturing

Answer 57

lesion closer to cortex

Question 58

Decerebrate Posturing

Answer 58

Lower brainstem lesion

Question 59

Vestibular System function

Answer 59

* Detection of head orientation, acceleration * Maintain balance

Question 60

Vestibular System dysfunction

Answer 60

* False sense of motion; vertigo * causes: idiopathic, trauma, infection or intentional

Question 61

Vestibular System Overview

Answer 61

Question 62

How does the Vestibular System interact with the limbs

Answer 62

Question 63

Vestibular System Test

Answer 63

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

Question 64

Rubrospinal Tract Origin

Answer 64

Red Nucleus (Thalamus) w/cerebellar input

Question 65

Rubrospinal Tract Descends

Answer 65

lateral column

Question 66

Rubrospinal Tract Terminates

Answer 66

LMNs in the cervical cord

Question 67

Rubrospinal Tract Function

Answer 67

* 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

Question 68

Pontine/Medial Reticulospinal Tract Origin/Pathway

Answer 68

Medial longitudinal fasciculus Ventral funiculus

Question 69

Pontine/Medial Reticulospinal Tract Function

Answer 69

**Function** Facilitate extensors (anti-gravity), inhibited by cortical centers Influences posture and locomotion Medullary/lateral(LRST)◦Origin/Pathway Throughout spinal column (lateral funiculus)

Question 70

Medullary/Lateral Reticulo Spinal Tract (LRST) Function

Answer 70

**Function** Facilitates upper limb flexors; facilitated by cortical centers Strong enough to Inhibit reflexes Influences posture and locomotion, + autonomic functions (respiration, shivering, GI function)

Question 71

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

Answer 71

Throughout the spinal column (lateral funiculus)

Question 72

Summary of Supraspinal pathways

Answer 72

Question 73

MAKE MORE CARDS ON THIS

Question 74

Decorticate vs Decerebrate posturing

Answer 74

Question 75

If a patient is Decorticate than showing Decerebrate

Answer 75

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

Question 76

Can go from Decerebrate to Decorticate

Answer 76

could be getting better

Question 77

Recovery from capsular stroke

Answer 77

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

Question 78

Acute Phase of capsular stroke

Answer 78

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)

Question 79

Tongue and soft palate are innervated how

Answer 79

predominantly contralateral innvervation

Question 80

The Reticulospinal tract is comprised of

Answer 80

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

Question 81

Chronic Recovery from capsular stroke

Answer 81

Question 82

Contralateral Spastic Hemiplegia

Answer 82

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)

Question 83

Supraspinal innervation is?

Answer 83

Bilateral

Question 84

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