Neuroscience Exam 4: Room 101

Front 1

Motor Control Systems basic fxn

Back 1

i. Function is to tell LMN (alpha & gamma MN) what to do.
ii. The end result is to instruct LMN to fire or not to fire.

Front 2

two major motor control systems

Back 2

(that cannot really work in isolation, highly integrated)
1. Pyramidal: initiated, voluntary skeletal m activity.
2. Extrapyramidal: involuntary skeletal m activity..

Front 3

Supplemental motor area location

Back 3

pyramidal system; located in frontal lobe
1. Anterior to pre-central gyrus (PCG)
2. Superior to the motor cortex

Front 4

supplemental motor area fxns

Back 4

3. Functionally, it is an association area for pre central gyrus (finesse)
a. Important for initiation of movement
b. Involved w/ orientation of the eyes & head (i.e., extrinsic eye m coordination)
c. Planning sequential & bi-manual movements.

Front 5

supplemental motor area sends UMN where?

Back 5

4. Interacts w/ pre-central gyrus & sends UMN to the
a. cranial N (CN) motor nuclei (via corticobular tract) &
b. ventral horns of SC where UMN synapse w/ LMN. (via cortiospinal tract)

Front 6

pre motor area location

Back 6

pyramidal system
1. located in the frontal lobe
2. Anterior to the PCG

Front 7

Pre-motor area fxns

Back 7

3. Functionally, it is an association area
a. Controls trunk, pelvic, & pectoral girdle musculature (i.e., changing posture; stabilization)
b. Involved w/ anticipatory postural control & adjustments (stability)

Front 8

pre-motor area interacts with and sends UMN where?

Back 8

4. Interacts with pre-central gyrus, as well as sending UMN to the CN nuclei in the brain stem (via cortiobulbar tract) & sends UMN to the ventral horns (via cortiospinal tract)

Front 9

Broca's area characteristics

Back 9

pyramidal system; located in the frontal lobe
1. Anterior to PCG
2. Functionally, it is an association area.
a. 1° (primary) function is to instigate speech

Front 10

Corticospinal tract characteristics

Back 10

-pyramidal system
-contralateral skeletal m activity from the extremities & trunk (Head and neck NOT included here)
-Unilateral

Front 11

two corticofugal motor tracts

Back 11

corticospinal tract

corticobulbar tract

Front 12

corticospinal tract cell bodies location

Back 12

1. Cell bodies of UMNs are located in the Pre-central gyrus of frontal lobe (Pre motor cortex)

Front 13

corticospinal tract pathway

Back 13

2. Descend through white matter -> posterior limb of the internal capsule (PLIC) -> Through the crus cerebri of the cerebral peduncles of the midbrain -> Through the ventral pons and into the ventral medulla

Front 14

corticospinal pathway decussation

Back 14

i. 90% decussate in the pyramids of the medulla.
1. Descend the contralateral lateral white column of the SC & are called the lateral corticospinal tract (Still UMNs)
2. Synapse w LMN in ventral horn -> exits to become spinal nerve

Front 15

corticospinal pathway no decussation

Back 15

ii. 10% do not decussate in the pyramids
1. Continue ipsilateral descent via the ventral white column of the SC
a. Ventral corticospinal tract (UMN)
2. Decussate via the anterior white commissure (ventral spinal cord) to the contralateral side.
3. Synapse w/ LMN in the ventral horn  peripheral nerve

Front 16

Result of corticospinal tract's 90/10 decussation pattern

Back 16

corticospinal tract never experiences a complete lesion. (Complete paralysis)

Front 17

corticobulbar tract characteristics

Back 17

pyramidal system

Bilateral except for CN VII and CN XII

Front 18

corticobulbar tract fxns

Back 18

voluntary contralateral skeletal mm activity of the:
a. head & neck
b. mm of facial expression
c. extrinsic eye mm
d. tongue, mastication,
e. neck, pharynx, larynx,
f. & scalp.

Front 19

corticobulbar tract cell bodies location

Back 19

located in the PCG (precentral gyrus) of the frontal lobe.

Front 20

corticobulbar tract pathway

Back 20

a. Descend through the posterior limb of internal capsule (PLIC)
b. They may pass through the crus cerebri of the cerebral peduncles of the midbrain
c. Depending on which part of the brain stem they are going, some go to the midbrain, some continue coursing through the ventral pons and some continue on into the medulla (CN 3-4 midbrain, CN 5-8 pons, CN 9-12 medulla)
d. Decussate in the region of the brain stem to which they are going.
e. Synapse w/ LMN in the CN motor nuclei in the tegmentum of the brain stem
f. LMN then become part of the cranial N

Front 21

Bilateral projection pattern: (III, IV, V, VI, IX, X, XI) of corticobulbar tract advantage

Back 21

do not lose function if it becomes damaged b/c there is input from both sides of the brain.
i. EXCEPTION: CN VII (facial) & XII (hypoglossal) have a unilateral decussating pattern

Front 22

unilateral pattern characteristics

Back 22

1. In a unilateral pattern, the L side controls the L & the R controls the R.
a. Will see a stroke affect CN VII & XII b/c there is no compensation by a bilateral projection pattern.

Front 23

only cranial nerves which do not have motor input

Back 23

CN I (olfactory), II (optic), VIII (vestibulocochlear)

Front 24

2 cranial nerves which have unilateral projection patterns

Back 24

They are CN VII (facial) & XII (hypoglossal)

Front 25

Oculomotor N (CN III) LMN originate where?

Back 25

LMN originate in oculomotor nucleus

Front 26

Oculomotor N (CN III) receives bilateral input from where?

Back 26

1. Bilateral input from UMN in corticobulbar tract

Front 27

2. Oculomotor nuclear complex contains

Back 27

contains cell bodies of LMN in tegmentum of the midbrain

Front 28

Oculomotor N (CN III) motor innervations

Back 28

Innervates extrinsic eye mm (superior rectus, medial rectus, inferior rectus, & inferior oblique) & the levator palpebrae superioris

Front 29

occulomotor nerve parasympathetic innervations

Back 29

4. Innervates iris & ciliary body (parasympathetic - controlled by hypothalamus; not UMN); extrapyramidal system b/c involuntary movement)

Front 30

occulomotor nerve parasympathetic innervations pathway

Back 30

a. Preganglionic parasympathetic neurons begin in the Edinger-Westphal nucleus in the tegmentum of the midbrain.
i. Not part of corticobulbar tract bc it is a reflex, not a bilateral innervation pattern
b. Synapse w/ postganglionic parasympathetic neurons in ciliary ganglia.
i. Innervate the iris (miosis – contraction of the pupil) & the ciliary body of the lens (accommodation).

Front 31

Trochlear nerve (CN IV) characteristics

Back 31

1. Innervates superior oblique extrinsic eye m
2. Bilateral input from UMN in corticobulbar tract.
3. Trochlear motor nucleus contains cell bodies of LMN in tegmentum of the midbrain.

Front 32

Trigeminal nerve (CN V) V3 (mandibular; mixed nerve) innervates

Back 32

1. Innervates the mm of mastication (medial & lateral ptyergoid, masseter, & temporalis mm).

Front 33

Trigeminal nerve (CN V) V3 (mandibular; mixed nerve) characteristics

Back 33

2. Bilateral input from UMN in corticobulbar tract.
3. Motor nucleus of V contains cell bodies of LMN in tegmentum of the pons.
4. All LMN are contained in mandibular nerve (V3).
5. Decussates to contralateral side in the pons at the motor nucleus of V.

Front 34

abducens nerve characteristics

Back 34

1. Innervates the lateral rectus extrinsic eye m (abduct the eye).
2. Bilateral input from UMN in corticobulbar tract.
3. Abducens motor nucleus contains cell bodies of LMN in tegmentum of the pons.

Front 35

Facial nerve (CN VII) skeletal muscule innervations

Back 35

Innervates the mm of facial expression (dilators & constrictors of mouth, orbits, & nasal apertures)

Front 36

facial motor nucleus cell bodies where?

Back 36

the pons

Front 37

Upper ½ of facial nerve corticobulbar tract receives bilateral input from and innervates

Back 37

bilateral input from R and L UMN of corticobulbar tract.
1. innervates muscles above a horizontal line across the eye orbit
2. Usually still work b/c bilateral input

Front 38

lower 1/2 of facial nerve corticobulbar tract receives unilateral input from and innervates

Back 38

ii. Lower ½ receives unilateral input from contralateral corticobulbar tract.
1. innervates muscles below a horizontal line across the eye orbit.
2. Usually show paralysis b/c unilateral input, if injury to the contra lateral side

Front 39

Parasympathetic function of VII:

Back 39

Innervation of the submandibular, sublingual, & lacrimal glands.

Front 40

Parasympathetic VII pathway

Back 40

a. Preganglionic parasympathetic neurons originate in salivatory nuclei in the tegmentum of the medulla (shared w/ CN IX)
b. Synapse w/ postganglionic parasympathetic neurons in the submandibular & pterygopalatine ganglia.
i. Submandibular gland & sublingal glands – submandibular ganglia
ii. Lacrimal gland – pterygopalatine ganglia
c. Nothing to do with corticobulbar tract

Front 41

Glossopharyngeal nerve (CN IX) skeletal mm innervation

Back 41

Innervates the stylopharyngeus m of the pharynx.

Front 42

Glossopharyngeal nerve (CN IX) skeletal mm innervation pathway

Back 42

a. Bilateral input from both corticobulbar tract.
b. Nucleus ambiguus contains cell bodies of LMN in tegmentum of the medulla.
i. Shares nucleus ambiguus w/ CN X (Vagus), XI (Spinal Accessory).

Front 43

Glossopharyngeal nerve (CN IX) parasympathetic innervation

Back 43

2. Innervation of the parotid gland (parasympathetic).

Front 44

Glossopharyngeal nerve (CN IX) parasympathetic innervation pathway

Back 44

a. Preganglionic parasympathetic neurons in salivatory nuclei in tegmentum of the medulla. (travels w CN VII)
b. Synapse w/ postganglionic parasympathetic neurons in otic ganglia in the neck.
c. Not part of corticobulbar tract

Front 45

Vagus nerve skeletal mm innervations

Back 45

1. Innervation of mm of the larynx, pharynx, & soft palate

Front 46

Vagus nerve parasympathetic innervation

Back 46

c. Innervation of viscera of the thorax, abdomen, & pelvis. (PARASYMPATHETIC)

Front 47

Vagus nerve motor pathway

Back 47

a. Bilateral input from both corticobulbar tract.
b. Nucleus ambiguus contains cell bodies of LMN in tegmentum of the medulla.
i. Shared w/ CN IX (Glossopharyngeal) & XI (Spinal Accessory).

Front 48

Vagus nerve parasympathetic pathway

Back 48

i. Preganglionic parasympathetic neurons originate in the dorsal motor nucleus in tegmentum of medulla.
ii. Synapses w/postganglionic parasympathetic neurons in numerous ganglia located near the organ being innervated (usually behind the organ)
iii. NOT involved w/cortocobulbar tract

Front 49

Spinal accessory nerve receives input from where?

Back 49

1. Bilateral input from corticobulbar tract

Front 50

Spinal accessory nerve cervical portion characteristics

Back 50

Spinal motor nucleus contains cell bodies of LMN
i. Nuclei are located in the rostral cervical regions of SC.
ii. Innervates the sternocleidomastoid & trapezius.

Front 51

Spinal accessory nerve cranial portion characteristics

Back 51

nucleus ambiguus contains cell bodies of LMN
i. Nucleus located in tegmentum of the medulla.
ii. Innervates the intrinsic laryngeal mm
iii. Nucleus ambiguus shared w/ CN IX (Glossopharyngeal) & X (Vagus).

Front 52

Hypoglossal nerve characteristics

Back 52

1. Unilateral input from corticobulbar tract. (R receives from L and L receives from R)
2. Hypoglossal motor nucleus contains cell bodies of LMN located in tegmentum of the medulla.
3. Innervates extrinsic (move tongue around) & intrinsic (change tongue shape) mm of tongue via the genioglossus m.

Front 53

Modulatory descending motor tracts definition

Back 53

pathways that subserve the corticospinal tract in that they refine & finesse the activity of LMN receiving input from UMN

Front 54

Rubrospinal tract pathway

Back 54

1. Cell bodies of UMN are located in the red nucleus of the midbrain.
a. Decussate in the midbrain.
2. Terminate in the ventral horns of the SC.

Front 55

Rubrospinal tract fxn

Back 55

3. Excite flexor activity & inhibit extensor activity

Front 56

Tectospinal tract pathway

Back 56

1. Cell bodies of UMN are located in the superior colliculus of the midbrain.
a. Decussate in the midbrain.
2. Terminate in the ventral horns of the upper cervical SC.

Front 57

Tectospinal tract fxn

Back 57

3. Reflex postural movements of the head, neck, & upper extremities in response to visual stimulus

Front 58

iii. Vestibulospinal tract pathway

Back 58

1. Cell bodies of UMN are located in the vestibular nuclei in the tegmentum of the pons.
a. NO DECUSSATION.
2. Terminate in the ventral horns of the SC.

Front 59

Vestibulospinal tract fxn

Back 59

3. Involved w/ “righting reflexes” in response to vestibular equilibrium stimuli (ie. Postural adjustments due vestibular system activation)

Front 60

iv. Reticulospinal tract characteristics

Back 60

1. Cell bodies of UMN are located in multiple reticular nuclei throughout the brainstem.
2. Has primarily ipsilateral function.
3. Excites extensor activity & inhibits flexor activity.
a. Opposite of rubriospinal tract

Front 61

damage to which tracts is most damanging clinically?

Back 61

a. Cortical spinal & corticobulbar cause the most damage

Front 62

b. Classical signs of UMN damage

Back 62

i. Paresis: weakness b/c skeletal mm are receiving less input.
ii. Paralysis: loss of movement and function
iii. Exaggerated DTR: hyperreflexia.
iv. Clonus
v. Spastic paralysis
vi. Hypertonia

Front 63

i. Paresis definition

Back 63

weakness b/c skeletal mm are receiving less input

Front 64

iv. Clonus definition

Back 64

spasms w/ alterations of contractions & relaxation in rapid succession of antagonistic & agonistic mm (Classic sign of UMN damage)
1. Due to hyperreflexia of spinal reflexes

Front 65

spastic paralysis definition

Back 65

characterized by involuntary contraction of 1 or more mm w/ loss of function.
1. Simultaneous contraction of agonist and antagonist -> Limits function

Front 66

vii. Contralateral effects vs ipsilateral effects

Back 66

vii. Contralateral effects prior to decussation & ipsilateral effects after decussation.

Front 67

c. What accounts for spastic paralysis,hyperreflexia, hypertonia, , & clonus?

Back 67

i. Due to: Excessive uncontrolled or spontaneous LMN discharge due to loss of supraspinal control

Front 68

1. Damage to UMN characteristics

Back 68

LMN is getting no supraspinal instruction (i.e., corticospinal tract is no longer influencing LMN activity).
2. Gamma damage impact is greater than alpha damage impact

Front 69

3. LMN is still intact w/ reflex arc characteristics

Back 69

a. Skeletal m is still innervated
b. Reflex arc runs amuck due to lack of superior control.
i. Causing increased DTR & hypertonicity

Front 70

ii. Babinski test for UMN lesion characteristics

Back 70

run an object up the lateral side of the foot
1. Normal Babinski: toes will plantarflex
2. Positive Babinksi: toes will dorsiflex & the great toe fans.

Front 71

CN w/ UMN (corticobulbar tract) which have bilateral input:

Back 71

1. CN III, IV, V, VI, VII (only top half of the orbits), IX, X, XI (Have motor nuclei w LMN; need UMN to tell them what to do)

Front 72

2. Parasympathetic LMN characteristics

Back 72

(Need UMN to tell them what to do)
a. III, VII, IX, X – NOT corticobulbar tract

Front 73

Compensatory mechanism of CN w/ UMN (corticobulbar tract

Back 73

damage to one side & still getting information from the other side.
a. Why you don’t see spastic paralysis in these CN if you have a stroke on one side or the other.

Front 74

2 cranial nerve exceptions to bilateral input

Back 74

CN VII and XII

Front 75

Damage to corticobulbar tract can lead to problems w/ the:

Back 75

-tongue, CN XII
d. Spastic paralysis b/c UMN event, stroke on R side affects the L side of the tongue. It is not getting any input from the R tract (corticobulbar). Person can stick tongue out but will deviate to the L b/c of spastic paralysis on L. Deviates to paralyzed (contralateral) side b/c healthy side pushes the tongue to paralyzed side b/c there is no resistance on that side

Front 76

Damage to R corticobulbar effect on facial nerve

Back 76

i. Superior (bilateral) will not be damaged
ii. Inferior ½ will have facial spastic paralysis

Front 77

Classical signs of LMN damage

Back 77

i. Damage to the cell body or the axon
ii. CN involved w/ LMN paralysis( Any CN w/ motor funtion)
iii. LMN can be alpha or gamma motor neurons
vi. Paresis
vii. Flaccid paralysis
viii. Hypotonia
ix. Decreased or absent DTR
x. Atrophy
xi. Fibrillations/fasciculations

Front 78

LMN found in:

Back 78

Motor nuclei of CN

Ventral horns of SC

Front 79

How do LMN get damaged?

Back 79

1. Can damage the ventral horn itself
2. Ventral roots
3. Spinal nerve
4. peripheral N (will probably also damage sensory N)

Front 80

LMN paresis characteristics

Back 80

weakness; not innervating skeletal muscle resulting in a dramatic weakness; also occurs with UMN damage.
1. When peripheral nerve is cut – NMJ is no longer functioning, so skeletal muscle function is lost.

Front 81

flaccid paralysis characteristics

Back 81

total loss of muscle tone w/resultant loss of function.
1. Lost the instructions from LMN
2. Different from UMN damage b/c you still have innervation from LMN but you have lost the control.

Front 82

hypotonia characteristics

Back 82

-decreased muscle tone.

-No reason for the muscle to contract b/c it lost the source that makes the muscle contract.

Front 83

Decreased or absent DTRj due to

Back 83

wiped out LMN part of reflex arc

Front 84

atrophy characteristics

Back 84

reduction in size of skeletal muscle as a result of decreased tone (decreased actin & myosin fibers).
1. Cut a peripheral nerve you no longer contract the muscle (not in use) therefore the actin & myosin starts to deteriorate b/c you don’t need it anymore.
2. Don’t get this w/UMN b/c the muscle cells are still contracting but it is spastic

Front 85

Fibrillations/fasciculations characteristics

Back 85

spontaneous activity of skeletal muscle.

Physiological (chemical) response, not neurological

Front 86

xii. Symptoms will always be ______ with LMN damage

Back 86

ipsilateral

Front 87

symptoms will always be ipsilateral w/ LMN damage, why?

Back 87

1. Ipsilateral and contralateral is ALWAYS in reference to the lesion
2. b/c the cell body of LMN is in the ventral horn of the SC or the motor nucleus of a CN w/motor function.
3. There is no decussating of LMN - therefore it will always be ipsilateral

Front 88

Cranial nerves involved with LMN damage

Back 88

III, IV, V, VI, VII, IX, X, XI, XII (innervate skeletal muscle)

Front 89

Spinal reflex responses characteristics

Back 89

1. Segmental in nature
2. May be involved w propriospinal loops (circuits)
3. Can be modulated by supraspinal influences

Front 90

Brainstem reflexes characteristics

Back 90

1. Counterpart of SC reflexes
2. Noxious reflexes
3. DTR

Front 91

posture and muscle tone fxn

Back 91

1. Stabilization & setting a foundation for other movements.
2. Results from constant adjustments by your mm to the shifts in gravity; proprioception.

Front 92

central pattern generators characteristics

Back 92

-used to delineate rhythmic patterns
-neural networks that produce rhythmic patterned outputs w/out sensory feedback. Involuntary and maintained in CNS
-Hardwired systems set up the above structures
-Make a new central pattern generator each time you learn a new motor task.

Front 93

central pattern generators associated with/maintained in

Back 93

i. Basal ganglia
ii. SC
iii. Brainstem
iv. Cerebellum

Front 94

4 fundamental anatomical parts to a SC reflex

Back 94

i. Receptor organ on distal end of a sensory organ.
ii. Afferent sensory neuron w/ receptor at distal end.
iii. An efferent motor neuron w/ an effector organ at its distal end.
iv. An effector organ

Front 95

Spinal cord reflexes characteristics

Back 95

a. Segmental in nature: May involve 1 segment or several adjacent segments.
b. May involve propriospinal loops or circuits.
i. Located close to midline of SC, Communicate b/w different levels, Located in gray matter.
c. Can be modulated by supraspinal influences:
i. Rubrospinal tract, Reticulospinal tract

Front 96

Flexor reflexes characteristics

Back 96

activated by Type III & IV fibers (A delta and C fibers, see pain notes from section III)(acute & chronic fibers), protective withdrawal, always involves flexor mms

Front 97

DTR/myotactic/stretch reflex definition

Back 97

contraction of agonistic & synergistic mm following the stretching of agonistic mm

Front 98

DTR/myotactic/stretch reflex characteristics

Back 98

i. MM stretch caused by hitting quadriceps tendon.
ii. Activates type Ia fibers
iii. Travel to dorsal root to then synapse w/ LMN that returns to same mm that was stretched.
iv. Important for mm tone (posture)
v. 2 neuron pathway

Front 99

Sensory receptor organ of DTR/myotactic/stretch reflex?

Back 99

muscle spindle (neuromuscular bundle)

Measures length & rate of change of length in extrafusal fibers

Front 100

b. The modified cells inside the muscle spindle are called

Back 100

intrafusal fibers

Front 101

intrafusal fibers of muscle spindle

Back 101

i. Dynamic nuclear bag: Ia
ii. Static nuclear bag: II
iii. Nuclear chain fiber: II

Front 102

intrafusal fibers of muscle spindle fxn

Back 102

1. All of the above function to differentiate b/w static & dynamic change in length & rate of change in length of skeletal mm.

Front 103

non-contractile portion of DTR/myotactic/stretch reflex?

Back 103

middle of intrafusal fiber that does not contract.

Front 104

annulospiral ending of non-contractile portion characteristics

Back 104

wrapped around the noncontractile portion

The receptor organ of the Ia fiber

Front 105

Flower spray ending of non-contractile portion characteristics

Back 105

located laterally on either side of the annulospiral ending. They are the endings of the secondary fibers (type II – nuclear chain fibers), of intrafusal fibers

Front 106

Type Ia fibers (dynamic nuclear bag w/ annulospiral ending) synapse characteristics

Back 106

become the primary fiber and monosynaptically synapse in SC w/ alpha motor neuron(LMN) which innervate the same (homonymous) (extrafusal fibers) of the mm or synergistic (heteronymous) mm.

Front 107

Type II fibers (static nuclear bag or nuclear chain fiber w/ flower spray endings) characteristics

Back 107

become the secondary fiber and only synapse w/ alpha motor neurons that attach to the extrafusal fibers of the same (homonymous) mm

Front 108

efferent component of a DTR?

Back 108

3. Alpha motor neurons

Front 109

alpha motor neurons of DTR characteristics

Back 109

a. Cell bodies in ventral horns.
b. Innervate extrafusal fibers.
c. Can get inhibition of antagonistic mm activity using Renshaw cells (reciprocal inhibition).

Front 110

renshaw cells definition

Back 110

inhibitory neurons in the gray matter of the SC & are associated w/ alpha motor neuron; they choose to inhibit 1 mm & excite 1

Front 111

GTO reflex characteristics

Back 111

autogenic inhibition
i. Encapsulated receptor at the junction b/w the m & tendon.
ii. Separately arranged in a series, however muscle spindles are parallel
iii. Proprioceptive reflex
iv. Type Ib fibers (afferent)
v. Measure tension & rate of change of tension in tendon.

Front 112

GTO fxns

Back 112

1. Adjust m activity in concert w/ information from muscle spindle & descending controls.
2. Prevents the tearing of mm by keeping the antagonistic m from being excessively stretched or contracted.
3. Causes a loss of MM tone and sometimes functionally gives way
4. sometimes doesn't work ie. tear Achilles tendon

Front 113

Muscle tone definition

Back 113

partial state of contraction of extrafusal fibers

Front 114

Muscle tone characteristics

Back 114

a. Everyone needs some m tone.
b. Much more efficient to contract a m that is already partially contracted
c. Posture is a consequence of m tone
i. It’s also a result of constant responses to proprioception input from adjustment of mm to shifts in gravity.
ii. Adjust to have a steady platform on which to function

Front 115

3 primary factors which influence muscle tone

Back 115

ii. Intrinsic characteristics of extrafusal fibers
iii. Gravity pulling on skeletal mm & activating stretch reflexes (Ia & Alpha Motor Neurons)
iv. Gamma bias-finessing system of m tone.

Front 116

Gamma bias-finessing system of m tone due to

Back 116

1. Due to supraspinal descending pathways influencing gamma motor neurons(a LMN)
2. These influences originate from:
a. Cerebellum
b. Reticular formation of brainstem

Front 117

Gamma motor neurons location

Back 117

cell bodies located in ventral horn of SC

Front 118

Gamma motor neurons characteristics

Back 118

a. They innervate contractile portion of intrafusal fibers
b. They are smaller than alpha motor neurons
c. Tend to discharge spontaneously

Front 119

Things gamma motor neurons don't do

Back 119

i. Not excited monosynaptically by Ia fibers
ii. Do not respond to Type II
iii. GTOs (Ib) do not influence gamma motor neuron activity
iv. Don't respond to peripheral input
v. Not involved w/ Renshaw cell activity
vi. Large number of things they don't do really

Front 120

effect of gamma motor neurons

Back 120

-their job is to alter the sensitivity of the muscle spindle by altering the length of the intrafusal fiber and the tension they exert
-When they do fire, they cause skeletal mms aspect of intrafusal fiber to contract. Makes it easier for Ia fibers to fire, b/c it is more sensitive to fire.
i. This can also work in opposite manner, making it harder to fire Ia fibers. Intrafusal fiber becomes slacked
-Gamma Bias primes skeletal m tone when you anticipate something
i. Ex: waiting in the blocks as a sprinter

Front 121

How do you get hypotonia?

Back 121

i. By eliminating LMN (i.e. transected N); no reflex arc
ii. Eliminate afferent sensory input, alpha motor neurons don't know what to do/when to contract
iii. Lesions of the cerebellum

Front 122

Spasticity characteristics

Back 122

i. Characterized by hyper-reflexia of DTR due to UMN damage
ii. Increased resistance to passive movement
iii. "Clasp Knife Phenomenon": an initial increase in resistance followed by a sudden disappearance of resistance (or all of a sudden relaxation).

Front 123

Rigidity characteristics

Back 123

Characterized by increase in m tone in all mm, although the strength & reflexes are not affected (Systemic effect)

Front 124

"lead pipe rigidity" (plastic) definition

Back 124

rigidity is uniform throughout the ROM. (Usually associated w basal ganglia dysfunction)

Front 125

"cog-wheel" rigidity definition

Back 125

which rigidity is a series of jerks during the ROM. (Seen in Parkinson’s disease, due to basal ganglia dysfunction)

Front 126

1° Functions of the cerebellum

Back 126

i. Coordinates Voluntary mm activity (pyramidal system)
ii. Coordinates equilibrium activity
iii. Influence mm tone
iv. Cerebellum does not project directly to the SC and initiate voluntary skeletal muscle activity. If you damage the cerebellum, you can still have movement b/c it indirectly projects to SC

Front 127

b. Information the cerebellum needs

Back 127

-unconscious proprioception information
-The equilibrium state of the body
-Information being sent via the corticobulbar & corticospinal tracts to skeletal mm of the body

Front 128

unconscious proprioceptive info definition

Back 128

-position, state of contraction, and activity of mm and joints
-Occurs via the anterior (enters cerebellum through the superior peduncle) & posterior (inferior peduncle) spinocerebellar tracts

Front 129

equilibrium state of the body occurs how?

Back 129

1. Occurs via the vestibulocerebellar tract (vestibular nuclei [90% are in pons, 10% are in medulla]enters the cerebellum through the inferior peduncle  pons)
2. Transmits unconscious proprioception

Front 130

Information being sent via the corticobulbar & corticospinal tracts to skeletal mm of the body transmitted via

Back 130

Transmitted to cerebellum via the inferior & middle cerebellar peduncles

Front 131

Characteristics of cerebellar control of the body:

Back 131

i. Each hemisphere controls information on the ipsilateral side i.e., R hemisphere controls R body
ii. Clinically, cerebellar symptoms will be ipsilateral (b/c cerebellum has several double decussation patterns)
iii. The cerebellum does not initiate voluntary movement.
1. Initiation comes from corticospinal/corticobulbar tracts.
2. Thus, there is no paralysis in a cerebellar injury.

Front 132

Cerebellum damage is always effects which side?

Back 132

If you have damage to the lobes the damage will always be on the same side. Ipsilateral ataxia on the R side of your body due to R sided posterior lobe damage:

Front 133

i. Anterior (spinocerebellum paleocerebellum fxn

Back 133

maintains m tone, posture, gross voluntary movement, & gait. This is a bilateral structure.

Front 134

posterior cerebellar lobe fxn

Back 134

coordination of fine, voluntary movement.

Front 135

iii. Flocculonodular cerebellar lobe fxn

Back 135

maintenance of equilibrium

Front 136

general ataxia definition

Back 136

abnormality in muscular coordination leading to abnormality of voluntary movement.

Front 137

Anterior Lobe of cerebellum damage characteristics

Back 137

i. MM contract weakly & irregularly
ii. Unsteady or drunken gait
iii. broader BOS
iv. Lean or lurch to affected side
v. Hypotonia: loss of m tone
1. DTR: pendular swinging after DTR is diagnostic for cerebellar dysfunction
2. Diminished resistance to passive movement b/c mm tone has been reset at a lower level

Front 138

Posterior Lobe of cerebellum damage characteristics

Back 138

i. Intentional tremor/terminal tremor– may occur when approaching a target. Closer you get to the target the more you shake.
ii. Dysmetria: inability to stop a m movement at a desired point
iii. Dyssynergia: voluntary movements are jerky & tremor like
iv. Dysdiadokinesia: inability to perform rapid, alternating movements
1. I.e., rapid pronation/supination of forearm quickly
v. Dysarthria: slurred or hesitant type of speech. “scanning speech”

Front 139

Flocculonodular lobe of cerebellum damage characteristics

Back 139

i. Nystagmus: ataxia of the eyes due to influence of the cerebellum on the extrinsic eye mm; rapid & slow tracking phase
1. Rapid = saccades
2. Slow = slow tracking

Front 140

basal ganglia characteristics

Back 140

a. Extrapyramidal system
b. Involuntary, instinctive skeletal m activity (don’t have to think about).
c. Deep seated nuclei w/in white matter of cerebral hemispheres
d. Combines w/ red nucleus (midbrain), substantia nigra (midbrain), & subthalamic nucleus (diencephalon) to form the extrapyramidal system.
e. Has no direct connection w/ the SC, meaning it has an indirect relationship to LMN.

Front 141

3 primary players of basal ganglia

Back 141

Caudate nucleus, lenticular nucleus, which is made up of the putamen & globus pallidus

Front 142

basal ganglia reticulospinal tract characteristics

Back 142

BG send info to reticular formation  ventral horns of SC
1. Biased toward extensor activity

Front 143

basal ganglia corticospinal tract characteristics

Back 143

BG send info to pre-central gyrus
1. Influcenes UMN in precentral gyrus

Front 144

basal ganglia nigroreticular tract characteristics

Back 144

BG send info to substantia nigra in midbrain to reticular formation to reticulospinal tract

Front 145

basal ganglia thalamocortical tract characteristics

Back 145

BG send info to thalamus which then sends info to cortex

Front 146

Fxns of basal ganglia

Back 146

i. Intimately integrated w/ pyramidal system. The 2 cannot work in isolation of one another.
ii. Assists in inhibiting co-contraction in antagonistic mm of the limbs.
1. Ex: thalamocortical influence (info is from thalamus to caudate nucleus to precentral gyrus).
iii. Assists in adjusting the body position during movement for a specific task.
iv. Works at a subconscious or reflexive level

Front 147

basal ganglia inhibitory mechanisms

Back 147

i. Determines direction, speed, force of movement.
1. Ex: If you want to hit someone with a pillow, you would use your BG so it can recruit the UMN to tell LMN to work.
ii. Involved w/ CPG (central pattern generators)
1. Where they are remembered. Start as voluntary & w/ repetition they become remembered.

Front 148

Hypokinesia (akinesia) definition

Back 148

-reduction in the initiation, implementation, & facilitation of execution of movement (slow movement)

-Movements initiated slowly & stop w/ difficulty

Front 149

h. Clinical Synopsis of Basal Ganglia: Characteristics of Basal Ganglia damage:

Back 149

Hypokinesia (akinesia)
1. Hypertonia – reason they’re moving slower. Increase in m tone w/ resistance to PROM.
2. Rigidity: associated w/ hypokinesia & hypertonia, implying that the entire body presents w/ it.
3. Common w Parkinson’s:
a. Conscious movements may be suppressed w/ hypokinesia.
b. Abnormal postures may be assumed (stooped, lean to one side)
c. Reciprocal arm swing during gait is absent.
d. DTR are usually normal.
e. Facial expression may be masked. Hard to laugh or smile, etc. b/c it requires motor function.

Front 150

Pathology of Parkinson’s Disease characteristics

Back 150

1. Degeneration of substantia nigra of midbrain.
a. Normally there are neurons in the substantia nigra that release dopamine (an inhibitory NTM) to the basal ganglia.
2. Decreased amounts of neurons leads to a dopamine-depleted basal ganglia.
a. Decreased levels of dopamine = decreased inhibition.
3. Disinhibition: basal ganglia cannot be inhibited & will do things in an uncontrolled manner.
a. Thus, causing activity that you do not want (i.e., hypotonia), involuntary movements.
b. Disinibition Phenomenon = involuntary movement b/c BG is no longer inhibiting the movement.

Front 151

Static tremor characteristics

Back 151

hallmark of basal ganglia dysfunction; rhythmic, fine, involuntary tremor when the extremity is in a fixed position. Associated w/ Parkinson’s.
i. Differentiate b/w cerebellar dysfunction (intentional tremor – tremor starts as you approach a target) & basal ganglia dysfunction (static tremor).
ii. Due to substantia nigra dysfunction.

Front 152

b. Alternating tremor characteristics

Back 152

-due to alternating contraction of opposing mm groups; “pill rolling”. Hyperkinesia characterized by regular, symmetrical, to & fro movements produced by patterned, alternating contraction of mm & their antagonists. When pt’s are doing a voluntary skeletal mm activity, then the tremor will stop. It also usually stops during sleep.
i. Due to caudate nucleus dysfunction.

Front 153

c. Athetosis characteristics

Back 153

involuntary movement characterized by slow, writhing (squirmy), worm-like movements of the fingers. (not associated w/ Parkinson’s)
i. May occur at rest or during involuntary or voluntary movement.
ii. Indicates putamen dysfunction

Front 154

d. Chorea characteristics

Back 154

sudden, involuntary, jerky movements w/ grimacing or twitching of facial mm & faulty vocalization.
i. Huntington’s chorea: autosomal dominant disorder. Indicative of damage to caudate nucleus.
1. Caudate nucleus atrophies or breaks down.
2. Becomes disinhibited
3. Doesn’t usually manifest until the fourth decade of life.
ii. May occur at rest or voluntary movement.
iii. Indicates caudate nucleus dysfunction

Front 155

ballism characteristics

Back 155

involuntary movements of an entire limb; begins proximally & proceeds distally. . Movements are quite dramatic.
i. May involve 1 limb or more than 1 extremity on the same side (monoballism-1 limb, hemiballism- both limbs on one side)
ii. Indicative of subthalamic stroke (dysfunction of subthalmic nucleus)
1. Not part of BG, but still part of the extrapyramidal system which helps w/ voluntary movements

Front 156

excitatory basal ganglia NT/NM

Back 156

a. ACh – acetylcholine
b. Glutamate
c. Aspartate

Front 157

inhibitory basal ganglia NT/NM

Back 157

a. GABA
b. Dopamine
c. Glycine

Front 158

i. If you damage a cranial N (LMN ) then all effects are which side?

Back 158

ipsilateral

Front 159

ii. Olfactory (CN I) damage characteristics

Back 159

each tract decussates via the anterior commissure.
1. Anosomia: loss of smell out of the particular nostril
a. This does not occur w/ a unilateral lesion.
i. Damage to 1 side causes a loss in 1 nostril.
ii. There is a bilateral projection pattern so you can still smell.
b. Not as devastating if you damage 1 of the NN.

Front 160

iii. Optic (CN II) damage characteristics

Back 160

1. Blindness: a loss of R & L visual fields.
2. Occurs w/ damage to ipsilateral optic N.
3. L visual field will be perceived in my R occipital lobe & vice versa.
a. If you cut L optic tract then you will no longer be able to see the R visual field.
i. Often w/ stoke victims (Tract cut  Lose all of that visual field, half from each eye)
b. If you cut R optic nerve, then you will be blind in the R eye. (Nerve cut Lose both visual fields in that eye)

Front 161

iv. Oculomotor (CN III) damage characteristics

Back 161

1. LMN paralysis: flaccidity of the ipsilateral extrinsic eye mm & levator palpebrae superioris.
2. Physical signs (Next slide)

Front 162

Physical signs of Oculomotor (CN III) damage

Back 162

ptosis
diploplia
abduction of the eye
strabismus
Mydriasis
Unresponsiveness of the pupillary light reflexes

Front 163

a. Ptosis definition

Back 163

drooping of upper eye lid due to dysfunction of the levator palpebrae superioris

Front 164

diploplia definition

Back 164

double vision; occurs when the extrinsic eye mm are paralyzed.
i. Eyes are no longer coordinated in vertical & horizontal axes.
ii. Generally happens w/ damage to midbrain. (CN III, IV, VI)

Front 165

abduction of the eye from CN III damage characteristics

Back 165

due to inability of the eye to move medially, upward, & downward (i.e., lateral rectus [ CN VI] & superior oblique are unopposed by the medial rectus). CN III isn’t innervating well, but CN VI is working.

Front 166

strabismus definition

Back 166

eyes are crossed and not synchronized during movement.
i. Extrinsic eye mm are not properly innervated.
ii. Eye mm themselves are damaged.
iii. Damage to CN III, IV, VI

Front 167

Mydriasis characteristics

Back 167

dilated pupil; loss of preganglionic parasympathetic fibers in the N.
i. Lack of parasympathetic input to the iris (Edinger-Westphal nucleus).
ii. Anisocoria: pupils of unequal size; due to 1 iris being innervated & 1 not due to loss of preganglionic parasympathetic fibers of the affected N. (Mydriasis on one eye but not the other)

Front 168

f. Unresponsiveness of the pupillary light reflexes characteristics

Back 168

loss of preganglionic parasympathetic fibers in the N w/ the resultant loss of innervation of the iris which controls pupil size.
i. Usually if something is going on… it’s a problem w/ the midbrain
1. Direct reflex – one eye reflexes w/light shined into it
3. Ex: shine light in R eye & do not get a direct reflex in R eye but getting consensus reflex in L eye
a. CN II of R eye is intact & sending sensory information.
b. Assume R CN III (occulomotor) is not working b/c that one causes the R pupil to constrict.
4. Ex: Shine a light in R eye & do not get direct or consensus reflex
a. R CN II (optic) is not working – no afferent sensory information.

Front 169

direct pupillary reflex definition

Back 169

one eye reflexes w/light shined into it
a. No reflex then problems w/CN II (sensory) or III (Motor)

Front 170

indirect pupillary reflex definition

Back 170

– both eyes reflex w/light in one of the eyes.
a. Collateral of CN II goes to edinger westphal nuclei of opposite eye then goes to CN III of that eye & causes it to reflex – CN II talks to both eyes

Front 171

trochlear cranial nerve damage characteristics

Back 171

1. LMN paralysis: superior oblique extrinsic eye m
2. Diplopia: pt may tilt head toward the shoulder of the side opposite the paralyzed m in order to compensate for the double vision. This is characteristic to damage of CN IV.
3. Strabismus not included bc other occulant nerves compensate

Front 172

trigeminal cranial nerve damage characteristics

Back 172

1. Loss of general sensation
2. LMN paralysis
3. Loss of direct & consensual corneal reflexes

Front 173

LMN paralysis of trigeminal nerve characteristics

Back 173

mm of mastication on ipsilateral side (masseter, temporalis, medial & lateral pterygoids)
a. Jaw deviates & points to the paralyzed side
b. Loss of ipsilateral jaw jerk reflex
c. Fibrillation, weakness, & atrophy of mm of mastication

Front 174

trigeminal nerve damage- Loss of direct & consensual corneal reflexes

Back 174

-Loss of input from the cornea from V1
-Corneal reflex causes your eye to shut if you touch the cornea with a cotton swab
-Touch cornea w/ cotton swab -> Sensory input through V1 (ophthalmic N) of trigeminal -> main sensory nucleus of trigeminal where it synapses w/ motor nucleus of facial N CN VII -> tells orbicularis oculi to contract. If you damage V1, then you won’t get a reflex b/c you won’t get sensory info in (touch cornea, & eye doesn’t close, then you injured V1).

Front 175

trigeminal nerve direct reflex pathway

Back 175

Sensory info from V1 -> main sensory nucleus of V in pons -> medial longitudinal fasiculus in pons -> motor nucleus of facial nerve (VII) -> synapses w/LMN (alpha motor neurons) -> CN VII goes to orbicularis oculi muscle & causes it to close.

Front 176

trigeminal nerve consensus reflex pathway

Back 176

Sensory info from V1 -> sends of collateral to main sensory nucleus of V in pons of L eye -> MLF in pons of L eye -> motor nucleus of facial nerve VII -> synapses with LMN -> CN VII goes to orbicularis oculi muscle & closes L eye.

Front 177

c. Touch R cornea & R doesn’t close but L does means that

Back 177

i. Sensory information is getting into the brain stem so nothing wrong with V1
ii. Nothing wrong with CN VII on L side since closing.
iii. R CN VII is not working since R eye is not closing

Front 178

d. Touch R cornea & no direct or consensus means that

Back 178

i. V1 is not sending sensory information to brain stem so not getting any response in either eye.

Front 179

vii. Abducens (CN VI) damage characteristics

Back 179

innervates lateral extrinsic rectus m.
1. Diplopia: double vision due to loss of innervation of lateral rectus.
2. Adducted eye: ipsilateral (affected) eye will be adducted toward the nose due to unopposed action of the medial rectus. Therefore, CN III will override CN VI (which controls the lateral rectus), so the eye will be adducted since CN VI is damaged.

Front 180

viii. Facial (CN VII) damage characteristics

Back 180

1. LMN paralysis: Bell’s palsy
2. Loss of tearing
3. Loss of Salvation
4. Loss of taste perception on the anterior 2/3 of tongue: ipsilaterally

Front 181

Bell's palsy characteristics

Back 181

a. Forehead may be immobile.
b. Corner of mouth sags
c. Facial lines are lost
d. Nasolabial folds of the face are flat
e. Saliva may drip from the affected corner of the mouth
f. Cannot whistle or puff due to the affected buccinator m
g. Smiling: normal mm draw up appropriately, but the corner of the mouth continues to sag
h. Corneal sensitivity remains, but the pt is unable to close or blink the involved eyelid (direct corneal reflex is not possible, but consensual is)
i. Sensory portion is ok but the efferent limb on the paralyzed side is not working

Front 182

CN VII damage loss of tearing characteristics

Back 182

ipsilateral side due to loss of preganglionic parasympathetic neurons w/ subsequent loss of innervation of the lacrimal glands.
a. Cornea is dry & painful
b. Opthalmologic problems

Front 183

CN VII damage loss of salivation characteristics

Back 183

on ipsilateral side due to loss of preganglionic parasympathetic neurons w/subsequent los of innervation of sublingual & submandibular glands.
a. Dryness of mouth
b. Difficulty in swallowing

Front 184

ix. Vestibulocochlear (CN VIII) damage characteristics

Back 184

1. Loss of hearing (cochlear): ipsilateral ear
2. Loss of equilibrium input (semicircular canals): ipsilateral ear (vestibular)

Front 185

x. Glossopharyngeal (CN IX) damage characteristics

Back 185

1. Loss of general sensation: ipsilateral posterior 1/3 of tongue & adjacent areas
2. Loss of taste perception: ipsilateral posterior 1/3 of tongue
3. Ipsilateral loss of gag reflex: (pharyngeal reflex) due to loss of general sensation input from post 1/3 of tongue, tonsilar region, & soft palate.
4. Ipsilateral loss of palatal & uvular reflexes: see #3
a. If you lose the afferent aspect then you lose the ability to constrict
5. Dysphagia: difficulty in swallowing due to loss of ipsilateral innervation of the soft palate & stylopharyngenus mm
6. The affected uvula & soft palate will deviate to the unaffected side b/c they are unopposed.
7. Ipsilateral loss of salivation: parotid gland; loss of preganglionic parasympathetic neurons

Front 186

xi. Vagus (CN X) damage characteristics

Back 186

1. LMN paralysis: ipsilateral soft palate
a. Twang when speaking
2. Dysphagia: flaccid paralysis of pharyngeal mm
3. LMN paralysis of laryngeal mm
a. Vocal cord becomes fixed & partially adducted
b. Voice is hoarse (dysphonia) & reduced to a whisper
4. Loss of gag reflex: ipsilateral due to loss of LMN innervation to soft palate & pharyngeal mm.
5. Loss of palatal and uvular reflexes: see #4
6. Transient tachycardia: (increased HR) reduced parasympathetic input to the heart.
a. Lose the ability to slow down the heart (parasympathetic); instead the sympathetic system can speed it up all it wants
7. GAG REFLEX – CN IX is responsible for sensory, CN X responsible for motor response

Front 187

xii. Spinal accessory (CN IX) damage characteristics

Back 187

1. LMN paralysis: flaccidity of the ipsilateral SCM
a. Inability to rotate the head, so that the chin points to the opposite side of the lesion. (Can’t turn towards the lesion)
2. LMN paralysis: flaccidity of the trapezius m
a. Downward & outward rotation of the scapula

Front 188

xiii. Hypoglossal (CN XII) damage characteristics

Back 188

1. LMN paralysis: flaccidity of the ipsilateral intrinsic & extrinsic tongue mm
a. Tongue will point to the paralyzed side due to the normal side being unopposed
2. Paralyzed side will atrophy & become wrinkled
3. Dysphagia

Front 189

Broca’s area characteristics

Back 189

: located around the inferior frontal gyrus in the frontal lobe
1. Primary cortex for motor speech
2. Association area of frontal lobe that finesses the precentral gyrus
3. Damage causes Broca’s aphasia (often done in a stroke)

Front 190

a. Aphasia definition

Back 190

language disorders (reading, writing, speaking, or comprehension of written and spoken words)

Front 191

broca's aphasia definition

Back 191

(Motor aphasia, non-fluent aphasia), generally in stroke of middle cerebral A; pt has difficulty forming words even though vocal cords & innervations are normal *cerebral cortex dysfunction*
i. Speech/Writing is slow & deliberate; must concentrate.
ii. VERBALLY & GRAPHICALLY COMPROMISED
iii. 90% of humans are L hemisphere dominant, w/ Broca’s area strongest on the L hemisphere. Therefore, a pt presenting w/ stroke & affected R-side will have severe damage to Broca’s area.
iv. Non-fluent: words do not flow, despite the ability to perceive language & organize thought processes.
v. Pts are usually aware & they get very frustrated.
vi. 3 symptoms usually appear together – Broca’s aphasia, hemianopsia, paralysis of facial mm on R
1. B/c the optic pathway & internal capsule are close to Broca’s area

Front 192

b. Language cortex: Wernicke’s area characteristics

Back 192

i. 90% Located in the posterior part of the superior temporal gyrus
ii. Controls comprehension of spoken words & written & auditory language.
1. 10% extends into parietal lobe
a. Though still considered a function of the temporal lobe
iii. L hemisphere is more dominant over the R

Front 193

iv. Wernicke’s aphasia characteristics

Back 193

(fluent aphasia, receptive aphasia); involved w/ comprehension of spoken & written language. Able to speak & write words but the sequence is not normal, so they don’t make sense. A pt will be aware that they do not make sense & will be frustrated
1. LINGUISTICALLY COMPROMISED
2. If large lesion, then visual & linguistic ability is compromised.
3. Empty speech: speaking but it does not make sense
a. Paraphasia: substitute one word for another.
b. Neologisms: create new & meaningless words & put them into sentences.
c. Jargon aphasia: words & phrases are strung together with no meaning. Speech is incomprehensible but seems logical to the pt.
4. Same A feeds Broca’s and Wernicke’s areas – middle cerebral A
v. Conduction aphasia: occurs when something impairs the conduction from

Front 194

v. Conduction aphasia characteristics

Back 194

occurs when something impairs the conduction from Wernicke’s (language comprehension) to Broca’s (speech formation).
1. The 2 areas are not specifically damaged, but the lesion destroys the arcuate fasciculus
2. Characteristics:
a. Less fluent in language than pts w/ Wernicke’s aphasia.
b. May make paraphasic errors (substitution of 1 word for another)
c. Comprehension is good, ability to repeat is limited/poor.
d. Naming is impaired
e. Reading aloud is impaired, but pt can read silently w/ good comprehension.
f. Writing (function of Broca’s) is abnormal w/ misspelled & omitted words.

Front 195

global aphasia characteristics

Back 195

Most severe form of aphasia: inability to use language in any form due to extensive damage to Broca’s, Wernicke’s, & arcuate fasciculus; LINGUISTICALLY & VERBALLY compromised – unable to read/write well, unable to comprehend speech, unable to produce intelligible speech.
1. Generally occurs in the L hemisphere

Front 196

apraxia definition

Back 196

impairment of voluntary skeletal m activity which is not due to lack of comprehension, innervation or mm physiology. (something wrong w/ specific part of cortex… that means it’s horizontal issues)

Front 197

agnosia definition

Back 197

impairment of ability to comprehend a sensory stimuli due to lesions of the cerebrum.

Front 198

Homonymous Hemianaopia (hemianopsia) definition

Back 198

loss of visual fields in each eye is ½. Due to strokes that damage the optic tract.

Front 199

R and L sided neglect due to

Back 199

(L side neglect -> R parietal lobe)

Front 200

X. Regeneration of the NS characteristics

Back 200

i. PNS: Very successful
1. Surrounding the peripheral nerve is the epineurium, surrounding the vesicles is the perieurium, surround each axon is the endoneurium (endoneurium tube), which is connective tissue **
ii. CNS: Not very successful

Front 201

regeneration definition

Back 201

-replacement of cells or tissue w/ identical cells or tissue

-want regeneration, not repair

Front 202

Repair definition

Back 202

-replacement of living cells or tissue w/ cells or tissue of a more primitive nature

-We want regeneration, not repair

Front 203

d. PNS regeneration- motor or sensory neurons characteristics

Back 203

ii. A transected peripheral N will cut motor & sensory properties.
1. If the cell body is not permanently damaged, then regeneration can occur.
2. No regeneration will occur in the CNS or PNS if the cell body is damaged.

Front 204

wallerian degeneration happens when

Back 204

occurs after a lesion in a peripheral N

Front 205

wallerian degeneration characteristics

Back 205

1. Everything distal to the cut degenerates in a predictable manner
a. Axons
b. Schwann cells (take longer)
2. There is also an inflammatory process
a. Autolysis
b. Phagocytosis
3. Endoneurial tube stays in place (up to 30 days after the initial injury) despite degeneration of axons & Schwann cells
4. Axon starts to form a filopoda (distal end of the proximal segment) at the area of the lesion

Front 206

wallerian degeneration- Axon starts to form a filopoda (distal end of the proximal segment) at the area of the lesion

Back 206

a. 1 filopoda becomes a dominant extension & the others disappear
b. Extension enters & grows down the endoneurial tube
i. Growth is facilitated by NGF produced by target structures & Schwann cells
ii. Schwann cells remyelinate down the endoneurial tube
iii. CNS Oligodendrocytes -> 1st order sensory neuron -> Schwann Cells (NGF, BDNF, Neurotrophins) -> Target Recognition Signals from Target Cells (NG, BDNF, Neurotrophins)

Front 207

iv. Rate of regeneration is variable based on the area of the body characteristics

Back 207

1. upper forearm: 2.5 mm/day; distal forearm: 2 mm/day; distal wrist/ hand: 1 mm/day

Front 208

What determines the success of neural regeneration?

Back 208

1. Crush: endoneurial tubes are better preserved, they are only squished & the tube integrity is maintained.
2. Transect: interrupts the integrity of the NN; there is an immediate inflammatory process w/ scar tissue; Resultant environment is difficult for regenerating axons
3. Length of time b/w injury & repair work by surgeon
4. General nutritional status & health of the individual affected.

Front 209

e. CNS regeneration characteristics

Back 209

regeneration is not as successful. Occurs in brain & SC
i. No mitosis occurs in the CNS
ii. Damage neurons = damage axons
1. This interferes with the development of synapses b/w axons & dendrites
iii. Inability to regenerate is thought to be an intrinsic characteristic
iv. There is evidence to support that this is not true

Front 210

evidence on CNS regeneration implies that

Back 210

1. There are no characteristics about the CNS environment that prevent significant regeneration as compared to regeneration in the PNS.
2. The failure to regenerate is not due to intrinsic characteristics of the neurons as previously thought.

Front 211

evidence of CNS regeneration characteristics

Back 211

1. Ramon y Cajal (1928) & Tello (1911) showed that CNS neurons could regenerate in vitro if the environment was conditioned.
2. Aguayo (1980) repeated the same experiment w/ new techniques & definitely showed that CNS neurons can regenerate.

Front 212

So why don't nerves regenerate in the CNS?

Back 212

a. There are CNS environmental characteristics which prevents significant regeneration as compared to regeneration in the PNS.
b. Recent research has shown that the oligodendrocytes produce inhibitory chemicals (NOGO factors), which prevent regeneration. Thus the problem is environmental, not genetic

Front 213

vi. So, what constitutes successful regeneration in the CNS?

Back 213

1. It is a multi-step process including the following:
a. The injured neuron must survive (cell body intact)
i. Cells in the cortex die, the cell bodies die
ii. Cell in white matter, will be ok b/c cell bodies are still intact
b. The damaged axon must extend across the cut or damaged process to original neuronal target.
c. Once contact is made w/ target structures, the axon needs to be remyelinated & functional synapses need to form on the surface of target neurons.

Front 214

Learning can be done through

Back 214

1. Conditioned responses (unpleasant odors associated w/ something)
2. Repetitive learning: going over & over the information again & again
3. Aversion learning: use w/ smoking or dieting. Avoid an activity. Rubber band snaps if you cuss.
4. Conceptual learning: the big picture
5. Integration learning: association

Front 215

How is memory stored in the CNS?

Back 215

i. Only a very small portion of information is stored & retained. Only if important to us
ii. We constantly process our environment, but we don’t usually remember all of it.
iii. There are many parts of the brain that process info, but 2 most important are:
1. Amygdaloid nuclear process & Hippocampus
a. Both bilateral structures
b. All experiences go through here & are processed for retention
c. Form neural circuits to other parts of the brain (to & from)
d. Both are located deep in the temporal brain

Front 216

i. Memory trace definition

Back 216

the neural circuit, that connects a sensory event w/ a learned behavioral response, is altered in some way to support the learning. (Ex: Dr. Garrison getting pulled over by a cop; he may not remember what other cars are around him, but he remembers the cop. )

Front 217

ii. Memory consolidation definition

Back 217

occurs if the experience is somewhat permanently retained. (Ex: Dr. Garrison retelling his story numerous times to faculty & students. )
1. Can occur quickly or take long periods of time

Front 218

variables that influence memory consolidation?

Back 218

a. Catecholamine (adrenaline) levels in the body
i. Important events that you’re very excited about (or dangerous events – car accident), you have high adrenaline levels so you’re more likely to remember.
b. Motivation (context learning) – learn better if you’re interested in what you’re learning.
i. This is our main way of learning.
c. Physiological states may influence learning. poor memory consolidation.
i. Shock (decreased BP), trauma, emotional trauma
ii. Sleep deprivation – adversely affects learning b/c you don’t go through the consolidation process.
iii. All physiological states preclude long-term potentiation.

Front 219

iii. Long-term potentiation (LTP) characteristics

Back 219

[molecular basis of memory due to synapses]
1. Occurs at the cellular level involving cell membrane. Physiological/biological process.
2. Original studies & most current studies use neurons (synapses) in the hippocampus
a. Dissect neurons of hippocampus & put them in petri dishes or do fMRI.

Front 220

hebbian processing

Back 220

Extensive research in animals shows that following a heavy train of stimulation (real fast stimulation), the postsynaptic excitatory potentials have an increase in amplitude which can last for varying periods of time (days or weeks).

Front 221

Hebbian Processing- how it works

Back 221

b. If the postsynaptic amplitude is increased for weeks, then the neuron is different.
i. There is an increase firing of postsynaptic neuron (glutamate is the NTM) due to a variety of stimuli.
ii. Increased firing rate is associated w/ increased activation of glutamate receptors.
iii. These ligand gated channels open  influx of Ca.
iv. The increased Ca enhances enzymatic cascades in the postsynaptic cell. This activity modulates the nature of the postsynaptic membrane receptors & makes them more sensitive (a change in the cell membrane has occurred).
v. In addition nitric oxide is formed & diffuses back across the synapse to increase the effectiveness of the presynaptic membrane. (making the glutamate release easier)

Front 222

iv. Long-term depression (LTD) definition

Back 222

similar to LTP, but w/a reverse effect (you lose memory)

Front 223

Long-term depression (LTD) characteristics

Back 223

1. Biochemical changes - decreases the effectiveness of synapses
2. Anatomical changes – increase in # and types of synapses & increase in function; associated with an increase in activity
a. Use it or lose it principle
b. Membranes lose sensitivity & proper synapses are not in place
c. Dendritic spines wither away when not used reducing the number of synapses

Front 224

i. Declarative memory characteristics

Back 224

(conscious, explicit, cognitive)
1. Remembering facts, events, concepts, & locations
a. Can be easily verbalized
b. Requires attention during recall

Front 225

a. First stage of declarative memory characteristics

Back 225

Immediate memory (1-2 sec) similar to trace memory
i. Used to plan a response to some stimulus

Front 226

2nd stage of declarative memory characteristics

Back 226

Short-term memory/working memory/primary memory
i. Memory may last only minutes or days unless reinforced. Doesn’t last forever.
ii. Usually involves prefrontal cortex – primary intellectual area.
iii. Involves associated areas of primary functional cortical area. (association areas of all cortices)
1. Ex: Visual association area = visual memory

Front 227

3rd stage of declarative memory characteristics

Back 227

Long-term memory/ remote memory
i. Involves short term memory which has been permanently consolidated & stored in the area which 1st processed it
1. Stored in hippocampus or amygdala
2. Visual or auditory stimulus – ultimately processed through hippocampus & association area. Then if consolidated & stored permanently, then it is stored in the primary cortical area.
a. Superior temporal gyrus – if you heard a great song

Front 228

episodic memory characteristics

Back 228

people remember their own experiences as they happened in a specific place & time in their own history (ex: can’t tell the story unless they go through the whole process)
i. Also a type of long term memory

Front 229

semantic memory characteristics

Back 229

Form which deals w/ general knowledge
i. Learning in school (ex: neuroscience information)
ii. Provides the database required for thinking/ knowledge base allows you to think & make decisions
iii. Also a type of long term memory
iv. Very explicit information: if it’s super specific then it’s semantic memory

Front 230

semantic memory pathway

Back 230

v. First processing something  it will go to hippocampus or amygdala  then stored in the prefrontal cortex  then through the consolidation process (study over and over again)  this puts it into long term memory in either 1. Back to hippocampus OR 2. The area of the brain that first processed it (so if it was sight, then it would go back to occipital lobe).

Front 231

ii. Non-declarative Memory characteristics

Back 231

(implicit memory/ procedural memory/ unconscious memory/ skill & habit memory):
1. The person has no previous awareness of memory; cannot describe the learned information except through behavior & cannot necessarily remember how, when, or where the learning occurred.
2. These will be stored in things like cerebellum, basal ganglia, & amygdala. Stored in central pattern generators. B/c these are learned motor activities. Ventral horns of gray matter.

Front 232

amnesia characteristics

Back 232

loss of long term memory
1. Retrograde: loss of memory prior to trauma or disease
2. Anterograde: loss of memory of events which follow trauma or disease
a. Amygdala & hippocampus are damaged and are not processing information
3. Both involve declarative & nondeclarative memory.

Front 233

neuroplasticity definition

Back 233

i. Refers to the brain’s ability to change structure & function.
1. Structure: reestablish synapses.
ii. The pattern of functional & structural changes in responses to environmental, physiological, or pathological events
iii. Refers to changes that occur in the organization of the brain, & in particular changes that occur to the location of a specific information processing functions, as a result of the effect of learning & experience

Front 234

d. What stimulates neuroplasticity in CNS?

Back 234

i. Loss or modified afferent input to CNS
1. If you lose afferent/peripheral input then the CNS can’t be stimulated.
ii. Damage to CNS (stroke or cancer)
1. Neuroplasticity takes palce
iii. Chemical stimulation (drugs, meds)
1. Some drugs can enhance neuroplasticity
iv. Environmental or training stimulation
1. This isn't a pathological thing. Ex: learning to play banjo; motor skill training. Increasing sensory input ex: teaching someone how to smell wines.

Front 235

theories for neural plasticity

Back 235

i. Stem cell activation – produces new neurons.
ii. Sparing: remaining cells (the ones that are spared) become more active.
iii. Redundancy of systems
1. Many parallel systems in CNS. If one portion is damaged, the other portion can take over.
2. Damage to the spinothalamic tract  pt is told they only live for a certain time frame. Then the dorsal column tract takes over
iv. Unmasking secondary areas – association areas become more important & compensate
-Structural morphological changes- main reason for neural plasticity

Front 236

Structural (morphological) changes for neural plasticity characteristics

Back 236

1. Increase in synapses (connectivity) – important if you want any permanent memory or rehab
2. Modification of synapses – need chemical changes to change synapses sensitivity.
3. Increase in dendrites (dendritic sprouting & spines) – since the neuron isn’t getting input from a certain area anymore, it needs to become more receptive, so it increases the dendrites & spines, which increases surface area, which increases synapses.
4. Dendritic & axonal remodeling – the way the dendrites & axons reconnect to form synapses

Front 237

Research on neural plasticity characteristics

Back 237

i. Cellular conditioning studies examine the direct induction of plastic changes at an intermediate level by documenting changes in selective responses of single neurons as a result of short-term conditioning protocols, memory, & learning.
ii. A decade & a half of research has shown that cortical maps are not static in adults, but in fact undergo plastic changes in response to both peripheral manipulations & behaviorally important experience throughout life. Within certain limits, the cortex can allocate cortical area in a use-dependent manner.
1. Ex: Blind individuals -> Primary visual cortex becomes dedicated to perception of general sensation due to reading of brail

Front 238

Evaluation of neuroplasticity characteristics

Back 238

i. Need to be able to differentiate b/w neuroplasticity mechanisms at work & the ability of the organism to compensate:
ii. Motor ex: picking up a pen. Pt’s will compensate by using other muscle groups, twisting differently, etc. Cognitively figuring out how to do it in another way (Not neuroplasticity!)
iii. W/ neural plasticity, new synapses have been formed (Not as much cognitive requirements to figure out how to do the task)

Front 239

h. What influences neuroplasticity?

Back 239

i. Environmental stimuli (constraining the good limb forces use of the affected limb)
ii. Complex is more effective than simple (functional & something they will be using, no pegs in holes!) Applies to motor, cognitive, and sensory rehab.
iii. Less effective as age increases (Plasticity is age dependent)
iv. Most effective immediately following CNS insult (the longer you wait for intervention, the harder it will be to regain functionality)
v. Neurotrophins

Front 240

Environmental stimuli effect on neural plasticity characteristics

Back 240

(constraining the good limb forces use of the affected limb)
1. Environmental stimuli results in contralateral affects as confirmed w/ PET & fMRI studies as well as neurochemical tracer studies
a. Morphological changes, Neurochemical tracer studies

Front 241

neural plasticity- Neurotrophins characteristics

Back 241

1. Can help increase neuroplasticity
2. Products of glial cells & neurons
3. Some are activity dependent

Front 242

neurosplasticity park example

Back 242

kids in the park. 15 kids playing on the square. 4 kids playing on the rectangle. 5 kids playing on the triangle. 10 kids playing on the star. Park manager takes away the star, so those 10 kids now have to go play on the other shapes. Now you have more kids on each shape, they’re adapting. In neuroplasticity, when the nearby cells die, the one’s around it adapt.