Neuromotor System Flashcards

1
Q

the basal ganglia can be damaged in what two diseases

A

Parkinson’s and Huntington’s

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2
Q

Lower motor neurons cell bodies are found in what two locations?

A

Brainstem motor nuclei ( gives rise to Cranial motor nerves); Anterior horn of the spinal cord segments (gives rise to spinal motor nerves)

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3
Q

Motor neurons that control limb muscles are normally found in what area of the Spinal cord? What about motor neurons that control the axial muscles?

A

Motor neurons in the lateral motor Spinal cord column control limb muscles and Motor neurons in the medial motor Spinal cord column control axial muscles

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4
Q

what neuron type makes up the prime drivers of muscle contraction?

A

Alpha motor neurons

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5
Q

what is the relationship from alpha motor neuron and muscle fibber?

A

One-To-Many; a single motor neuron may innervate many different muscle fibbers but each muscle fibbers is only innervated by a single motor neuron

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6
Q

what makes up a motor unit?

A

the motor neuron and all muscle fibbers it innervates

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7
Q

what makes up a motor neuron pool?

A

All Motor neurons the collectively control a muscle

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8
Q

what is the neurotransmitter at a neuromuscular junction? What is the receptor of that transmitter? What type are the receptors? What ion is involved?

A

Acetylcholine (Ach); nicotinic Ach Receptor; ion channel; Na+

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9
Q

what are some dysfunctions of the neuromuscular junctions? What is the mechanism of action?

A

Myasthenia gravis (Loss of Ach receptors); Muscular dystrophies (muscle physiology problems); Myotonias (excitability of the muscle fibber can be enhanced or depressed)

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10
Q

what are the three types of muscles? What is interesting about the size of the motor neuron that innervates it?

A

Slow oxidative (type I fibbers) these are innervated by small alpha Motor neurons which innervate a small number of muscle fibbers; Fast oxidative (Type Ia fibbers) these are innervated by medium alpha motor neurons which innervate a larger number of muscle fibbers than the small alpha MNs; Fast fatigable (Type IIb) which are innervated by very large alpha MNs these MNs innervate a large number f muscle fibbers

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11
Q

describe the frequency principle of motor neurons

A

a single motor neurons fire at higher rate -> increased muscle tension in a single motor unit due to fusion (combination) of successive contractions

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12
Q

describe the size principle

A

Small alpha motor neurons easier to excite -> early/initial recruitment of small motor units for fine/graded/weak motion; Larger alpha motor neurons are harder to excite -> larger motor units recruited late for larger/stronger motion

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13
Q

what two factors can happen in a muscle contraction?

A

change in length (isotonic) either in concentric(Shorter) or eccentric (longer); Change in Tension (isometric) no change in length

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14
Q

what is the difference between intrafusal muscle fibbers and extrafusal muscle fibbers?

A

intrafusal muscles are only contractile at their ends they have a non-contractile center; the contractile ends are controlled by gamma fibbers and the non-contractile center contains a sensory neuron wrapped around it

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15
Q

what are the two types of muscle sensors?

A

Muscle spindles (proprioceptive sensors located in fleshy parts of the muscle; intrafusal muscle fibbers; Golgi tendon organs; joint receptors

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16
Q

what are the different types of intrafusal fibbers?

A

Nuclear chain fibbers and static nuclear bag fibbers (sensitive to static changes in length; active a rest changes fire rate based on resting length); information to CNS is sent via 1a and Type II afferent nerve fibbers; innervated by static gamma MNs

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17
Q

describe Dynamic nuclear bag fibbers

A

dynamic nuclear bag fibbers are sensitive to dynamic changes in length; only active when a muscle length is changing; information to CNS is sent via 1a afferent nerve fibbers; innervated by dynamic gamma Mns;

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18
Q

describe Nuclear chain fibbers

A

Nuclear chain fibbers and static nuclear bag fibbers are sensitive to static changes in length; active at rest; changes fire rate based on resting length; information to CNS is sent via 1a and Type II afferent nerve fibbers; innervated by static gamma MNs

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19
Q

what is the function of Gamma Motor neurons?

A

maintain the tension in the intrafusal fibbers allowing it to maintain sensitivity across a wide range of muscle lengths

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20
Q

describe Golgi tendon organs: what do they detect?

A

Golgi tendon organs are located in the junction between muscle fibbers and tendons; they detect changes in muscle tension and are directly activated by muscle stretch; they proved information to the CNS via type 1b afferent nerve fibbers

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21
Q

Describe Joint Receptors

A

free sensory nerve ending in joint capsule; activated by tension or distortion of the joint capsule; prove information about the position of joints in space; thought to only be activated with the joint reaches limits

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22
Q

what are the features of a lower motor neuron lesion?

A

Weakness or paralysis; muscle tone reduced or absent; mitotic reflex strength reduced or absent; rapid muscle wasting

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23
Q

what are some of the cause of lower motor neuron lesion

A

Poliomyelitis (viral infection of CNS); Mote neuron disease; spinal cord injury at segmental level; peripheral nerve dysfunction; muscle issues

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24
Q

what is the purpose of the myotatic reflex?

A

helps maintain muscle tone and resist gravity

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25
Q

describe reciprocal inhibition reflex

A

the same receptor neuron that innervates the stimulated muscle also inhibits the neurons of the antagonist muscle

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26
Q

what drives some semi-automatic movements (walking running chewing breathing)? how do they achieve this?

A

central pattern generators in the spinal cords; use reflex circuit to evoke coordinated activity in different muscle groups

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27
Q

what does the corticospinal tract control?

A

Drives fine or skilled conscious movements; directs excitatory inputs to motor neurons;

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28
Q

where doe most axons cross in the corticospinal tract

A

medulla oblongata ( pyramidal decussation)

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29
Q

where do corticospinal tract neurons synapse? What do they synapse with?

A

direct innervation of alpha motor neurons

30
Q

if you have a lesion above the pyramidal decussation what side will the dysfunction be on? Below?

A

above the pyramidal decussation: Contralateral dysfunction; Below the pyramidal decussation: Ipsilateral dysfunction

31
Q

corticospinal tract damage can cause what?

A

Loss of voluntary fine or skilled movements but not automatic movements

32
Q

where are corticospinal tract nerve fibbers that do not cross over located?

A

ventral white matter of the spinal cord

33
Q

what does the reticulospinal tract control?

A

coordinates automatic postural reflexes; locomotion; other simple movements not requiring dexterity

34
Q

where do crossed reticulospinal tract fibbers descend? Uncrossed?

A

both descend in the lateral and ventromedial spinal cord white matter

35
Q

what are the two main divisions of the reticulospinal tract?

A

Lateral (medullary) reticulospinal tract; medial (pontine) reticulospinal tract;

36
Q

describe the later reticulospinal tract:

A

the lateral or medullary reticulospinal tract suppresses extensor spinal reflex activity bilaterally; normal function is to inhibit the reflexes (damage leads to hyper-refexia)

37
Q

describe the Medial reticulospinal tract:

A

the medial (pontine) reticulospinal tract facilitates ipsilateral extensor spinal reflex activity.

38
Q

what does the vestibulospinal tract do?

A

maintains balance and upright posture including head/neck orientation

39
Q

what are the two main divisions of the vestibulospinal tract?

A

Medial tract; Lateral tract

40
Q

the vestibulospinal tract has inputs from what?

A

labyrinths and cerebellum

41
Q

damage to the vestibulospinal tract leads to?

A

Damage cause loss of tone in ipsilateral head/neck muscles and extensor muscles of trunk and limbs

42
Q

describe the Medial tract of the Vestibulospinal tract

A

Uncrossed axons descend in ventromedial spinal cord white matter to upper cervical segments (head and neck reflexes)

43
Q

describe the lateral tract of the vestibulospinal tract

A

uncrossed axons descend in ventromedial spinal cord white matter to all lower segments

44
Q

what is the purpose of the rubrospinal tract?

A

excites flexor muscle motor neurons and inhibits extensor muscle motor neurons

45
Q

Where does the rubrospinal tract cross?

A

crosses in the pons and descends in the dorsolateral spinal cord white matter

46
Q

where is the origin of the Rubrospinal tract

A

Red nucleus

47
Q

Where does the rubrospinal tract project to?

A

only the cervical levels (upper arm and trunk)

48
Q

damage to the rubrospinal tract cause loss of tone in?

A

contralateral flexor muscles of the upper trunk and arms

49
Q

describe decerebrate rigidity; what cause it?

A

due to separation of the higher motor control centres fro the brain stem; this removes the damping down of the vestibulospinal and reticulospinal pathways; this leas to an increase in tone of lower limb extensors (exaggerated knee jerk)

50
Q

what are some clinical manifestations of upper motor lesion

A

Weakness or paralysis; muscle tone increases (but not acutely); myotatic reflex strength increases (but not acutely); muscle mass maintained; Babinski’s sign (due to increased plantar reflexes

51
Q

what is spinal shock?

A

in the period following an injury to the spinal cord tends to damp down all activity of the spinal cord;

52
Q

what are some causes of upper motor neuron lesions?

A

stroke (Symptoms are contralateral and depend on cortical area affected) ; cord section (symptoms are unilateral and depend on the level of injury

53
Q

what is the normal response to stimulation of deep pressure sense on the weight bearing skin of the foot? What is this reflex called? What is the response in an upper motor lesion ?

A

plantar flexion (curling down) of the toes; this is the plantar reflex; curling up of the toes

54
Q

describe spasticity

A

a group of neurological symptoms that involve; increased tone exaggerated tendon jerks; clonus (oscillating); myotatic reflexes have increased gain; due to loss of reticulospinal tract which normally inhibits spinal motor neurons;

55
Q

describe the typical posture in stoke

A

lower limb is extended and medially rotated due to action on intact vestibulospinal tract; upper limb is flexed at elbow and wrist

56
Q

describe the typical posture in spinal cord section

A

both upper and lower limbs are flexed

57
Q

what are the two mechanisms that help us achieve postural reflexes?

A

Feed back system (compensatory; like reflexes); Feed forward (anticipatory; scale of response can be refined)

58
Q

the postural reflexes are mediated by?

A

Vestibular nuclei; reticular formation; superior colliculus; red nucleus

59
Q

The basal ganglia and the cerebellum modulate?

A

Indirectly modulate movement; through synapsis in the cerebral cortex;

60
Q

the basal ganglia is the go or stop signal? The cerebellum is?

A

Basal ganglia is the stop; cerebellum is the Go

61
Q

the Cerebellum is required for what kind of movement? As well as the?

A

The cerebellum is required for precise movement and correction of ongoing movements

62
Q

the Cerebellum mostly develops?

A

After birth

63
Q

what is the prime function of the cerebellum?

A

It compares intended movement with actual performance of movements; and corrects errors by making adjustments;

64
Q

what are the three mechanisms that allow the cerebellum to function as it does?

A

Internal feedback (corollary discharge); External feed back (reference signal); input to lower motor neurons via cortex

65
Q

what are some overall signs of cerebellar dysfunction?

A

errors in overall planning and execution of movements; poor coordination of movements

66
Q

what are some specific features of cerebellar lesions?

A

Intention tremor; dysmetria (improper measuring of distances in complex muscular acts); dysarthria (slowing or slurring of speech); dysdiadochokinesia (impaired ability to perform rapid alternating movements); nystagmus (Abnormal eye movements); impairment of dexterity

67
Q

the basal ganglia is what up of?

A

an inter connected group of nuclei located in the basal forebrain; caudate and the putamen (collectively called striatum); Globus pallidus; substantia nigra; sub thalamic nucleus;

68
Q

the basal ganglia has inputs from? And outputs to? Does it directly connect to lower Motor neurons?

A

inputs from all cerebral cortex; outputs back to cerebral cortex via the thalamus; and no direct connections to lower motor neurons

69
Q

the main motor control function of the basal ganglia is to?

A

inhibit motor activity

70
Q

what are two common disease that affect the basal ganglia?

A

Parkinson’s and Huntington’s

71
Q

describe Parkinson’s disease

A

degeneration of the nigrostriatal pathway leads to loss of dopamine producing neurons in the substantia nigra; leads to tremors; postural reflex impairment; rigidity; bradykinesia

72
Q

what is the treatment for Parkinson’s?

A

l-dopa (precursor compound enhance natural dopamine production); dopamine receptor agonists or inhibitors of dopamine breakdown; surgical (electrode stimulation); stem cell grafting technologies have been tried but are not long -lasting