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Neurophysiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Pain

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage

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2
Q

Nociception

A

reception of signals in the CNS evoked by activation of specialized sensory receptors that provide information about tissue damage

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3
Q

Aside from the thalamus cerebral cortex, fibers from the lateral spinothalamic tract also travel where?

A

amygdala, hypothalamus, periaqueductal gray, superior colliculus, and reticular formation

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4
Q

Acute Pain

A

an essential biological signal of the potential for or the extent of injury; lasts or is expected to last a short time.

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5
Q

Chronic Pain

A

arbitrarily defined as pain persisting > 1 month beyond the resolution of an acute tissue injury or pain persisting or recurring for > 3 months

*Chronic pain has no adaptive biological role

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6
Q

What are the components of nociception?

A

transduction (detection of tissue damage by specialized receptors) > transmission (nociceptive information travels from the site of damage along the peripheral nerve) > nociceptive information travels up the spinal cord > modulation (of this information by multiple sites in the brain)

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7
Q

Chemical Nociception

A

algogenic (pain producing) chemicals are released in the region of nerve endings capable of detecting noxious stimuli; occurs in the PRESCENCE of actual tissue damage

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8
Q

Mechanical Nociception

A

pain arising from stretching of collagen fibers and thus squeezing nerve endings between them; occurs in the ABSENCE of actual tissue damage, but when tissue is excessively strained

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9
Q

Mechanical nociception is enhanced by:

A

algogenic chemical sensitization and pre-stressing collagen fibers

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10
Q

A-delta fibers vs. C-fibers

A

A-delta: lightly myelinated; responsible for initial pain (sharp/prickling or stinging type of pain)
C: unmyelinated; responsible for long-lasting pain (dull aching type of pain)

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11
Q

Lamina I receives:

A

C-fibers and A-delta fibers; 2nd order neurons project to thalamus

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12
Q

Lamina II receives:

A

C-fibers and A-delta fibers; synapse on interneurons and dendrites from neurons in Lamina V

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13
Q

Lamina V receives:

A

A-delta fibers only; 2nd order neurons project to brainstem and thalamus

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14
Q

Ectopic Foci

A

myelin damaged; increased production of mechanosensitive and chemosensitive ion channels in demyelinated area; results in abnormal sensitivity to mechanical and chemical stimuli

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15
Q

Ephaptic Transmission

A

crosstalk between nerves (in demyelinated areas); action potential from one neuron may indue an action potential in another neuron

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16
Q

Central Sensitization

A

excessive responsiveness to peripheral input causing alteration in central function; cellular changes may include: increased spontaneous activity, increased responsiveness to afferent inputs, prolonged after-discharge in response to repeated stimulation, and expansion of receptive field

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17
Q

Size Principle

A

slow-twitch muscle fibers are recruited first because they require a smaller threshold, these fibers generate less tension and require less energy expenditure; fast fatigue-resistant fibers are recruited next, followed by fast-fatigable fibers

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18
Q

Muscle Spindles

A

primary endings are velocity sensitive; secondary endings are not velocity sensitive, more important for holding something steady in space

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19
Q

Golgi Tendon Organ

A

located at the musculotendinous junction; sensitive to changes in tension and involved with proprioception and adjusting muscle tension

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20
Q

What do all normal movements require?

A

1) the convergence of information from the peripheral sensors in the spinal cord
2) spinal connections
3) descending pathways onto the cell body and dendrite of the motor neurons, as well as descending control of the interneurons

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21
Q

Phasic Stretch Reflex

A

(DTR, myotatic reflex); Ia afferents and alpha-motor neurons are involved; monosynaptic reflex that DOES NOT involve interneurons

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22
Q

Tonic Stretch Reflex

A

slow, sustained stretch applied to the central muscle spindle facilitates contraction of the muscle; Ia & II afferents and gamma-motor neurons are involed

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23
Q

Reciprocal Inhibition

A

activation of Ia afferents; contraction of homonymous and synergistic muscle groups, and inhibition of antagonistic muscle groups due to activation of Ia inhibitory interneurons; used extensively during voluntary movements

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24
Q

Golgi Tendon Organ Reflex

A

autogenic inhibition; Ib afferents excite antagonistic motor neurons and Ib interneurons inhibit homonymous and synergistic motor neurons; also referred to as reverse myotatic reflex

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25
Q

Flexor Withdrawal Reflexes

A

requires the integration of multiple spinal levels and multiple muscle groups; activates flexor muscles

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26
Q

Cross Extension and Flexor Withdrawal Reflexes

A

requires the integration of multiple spinal levels and multiple muscle groups bilaterally, activates flexors on ipsilateral side and extensors on contralateral side

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27
Q

Upper Motor Neurons that control reflexes

A
  • corticospinal tract: lateral and anterior
  • reticulospinal tract: interacts with spinal interneurons
  • vestibulospinal tract: excitatory to extensor muscles and inhibitory to flexors
  • tectospinal tract: involved with reflexes and head movement
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28
Q

Amyotrophic Lateral Sclerosis (ALS)

A

a disease that destroys only somatic motor neurons and can involve UMN and brainstem, as well as spinal cord LMNs; results in both UMN and LMN sings; astrocytes fail to remove glutamate resulting in excitoxicity

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29
Q

Myasthenia Gravis

A

an autoimmune disorder that destroys Ach nicotinic receptors on muscle cells, affecting the NMJ activity and causing decreased reflexes

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30
Q

Muscular Dystrophy

A

myopathy; muscle fibers degenerate resulting in motor units with fewer muscle fibers than normal and a decreased ability to produce force during contraction; decreased reflexes

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31
Q

Guillian-Barre Syndrome

A

polyneuropathy; an autoimmune disorder that results in acute inflammation and demyelination of peripheral sensory and motor fibers (autonomics fibers can also be affected); patient will get progressively worse for 2-3 weeks and then gradually improve; decreased reflexes

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32
Q

Spasticity

A

velocity dependent increase in tone in response to passive stretch

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33
Q

Hyperreflexia

A

muscle spinal input leading to overactivity in disinhibited and excessively excitable LMNs, resulting in muscle contraction (ie spinal cord)

34
Q

Brainstem UMN overactivity

A

due to excessive reticulospinal and vestibulospinal tract signals to LMNs

35
Q

Cerebral Palsy

A

damage to the CST during development from a decrease in synaptic competition during critical period and persistence of inappropriate connections; abnormal co-contractions and simultaneous activation of agonist and antagonist

36
Q

Stroke-Related Spasticity

A

RST overactivity; decrease in inhibition of RST and increase signaling to spinal LMNs resulting in excessive muscle contraction; exaggerated interlimb neural coupling and can lead to concurrent activation of muscles in the UE and LE

37
Q

Spinal Cord

A

disinhibition of the LMN below the spinal lesion and increased excitability (hyperreflexia); velocity dependent increase in tonic stretch reflex; brisk deep tendon reflex, exaggerated cutaneous reflexes, involuntary flexor and extensor spasms, and clonus

38
Q

What are the components of the motor system?

A

cerebral cortex, brainstem, spinal cord, basal ganglia, and cerebellum

39
Q

What can be affected by movement disorders?

A
  • voluntary muscle force/contraction
  • muscle strength
  • muscle tone
  • muscle size (atrophy)
  • reflexes
  • movement efficacy
  • speed
  • postural control
40
Q

Muscle Tone

A

resistance to stretch of a resting muscle

41
Q

What are the two major types of hypertonia?

A

rigidity and spasticity

42
Q

Rigidity

A

resists stretch independent of velocity

43
Q

Spasticity

A

increased resistance to stretch as velocity increases

44
Q

What are the two types of hypotonia?

A

general hypotonia and flaccidity

45
Q

General Hypotonia

A

abnormally low muscle resistance with passive stretch

46
Q

Flaccidity

A

complete loss of muscle tone

47
Q

Dyskinesias

A

abnormal movement usually due to basal ganglia damage

48
Q

What are the two types of hypokinetic?

A

akinesia and bradykinesia

49
Q

Akinesia

A

inability to initiate movement

50
Q

Bradykinesia

A

slowed movement

51
Q

What are the three types of hyperkinetic?

A

chorea, dystonia, and ballismus

52
Q

Chorea

A

involuntary, jerky, rapid movements

53
Q

Dystonia

A

abnormal postures or twisted repetitive movements caused by sustained muscle contractions

54
Q

Ballismus

A

large amplitude rotary and flinging movements of a large amplitude

55
Q

Truncal Ataxia vs. Appendicular Ataxia

A 
truncal = wide-based unsteady gait
appendicular = uncoordinated movement of extremities
56
Q

Dysarthria

A

poor speech control

57
Q

Dysdiadochokinesia

A

loss of control in rapid alternating movement

58
Q

Dysmetria

A

under or overestimation of distance during movements toward a target

59
Q

Action Tremor

A

shaking of the limb during voluntary movement

60
Q

Fasciculations

A

twitches of muscles visible through the skin via spontaneous firing of alpha motor neurons; may or may not be pathological

61
Q

Fibrillations

A

spontaneous contraction of single muscle fibers from axonal remnants firing spontaneously; ALWAYS pathological

62
Q

Fractionation

A

moving muscles independently of each other in an extremity

63
Q

Paresis

A

partial loss of voluntary contraction/force

64
Q

Paralysis

A

complete loss of voluntary contraction/force

65
Q

Signs of LMN Disorders

A
  • atrophy
  • flaccid paralysis or paresis
  • involuntary muscle contractions: fasciculations or fibrillations
  • hypotonia
  • hyporeflexia
66
Q

Signs of UMN Disorders

A
  • paresis or paralysis
  • spasticity
  • loss of fractionated movement
  • hypertonia
  • hyperreflexia
67
Q

MCA Stroke

A

most common site for cerebrovascular accident; involves damage to the corticospinal, corticoreticular, and corticonuclear tracts; treatment includes drug therapy to reduce spasticity and PT/OT to retrain movement

68
Q

Motor Impairments Associated with MCA Stroke

A
  • spastic paresis of UE
  • spasticity
  • Babinski’s sign
  • Muscle atrophy
  • Contracture
  • Loss of fractionation of movement
  • Decreased movement speed and efficiency
  • Impaired postural control
69
Q

Spinal Cord Injury

A

UMN disorder; can be complete or incomplete; associated with spinal reflexes present below the lesion, contractures form, and spasticity is present

70
Q

Signs of ALS

A
  • paresis
  • spasticity
  • abnormal reflexes: Babinski and clonus
  • Hyper or hyporeflexia
  • Progressive muscle wasting
  • Fasciculations
  • Fibrillations
71
Q

Basal Ganglia Disorders can be either ___________ or ____________

A

hypokinetic; hyperkinetic

72
Q

Basal Ganglia Disorders - Hypokinetic

A

increased inhibitory output of basal ganglia; akinetic/rigig Parkinson’s disease, tremor-dominant Parkinson’s disease, Parkinson-plus syndromes, Parkinsonism

73
Q

Basal Ganglia Disorders - Hyperkinetic

A

decreased inhibitory output of basal ganglia; Huntington’s disease, dystonia, Tourette’s disorder, dyskinetic cerebral palsy

74
Q

Dystonia

A

hyperkinetic disorder and can be either focal or general; characterized by involuntary muscle contractions causing sustained abnormal postures, twisting, or repetitive movements; may increase during stress and activity and is not present during sleep; may also have tremors

75
Q

Focal Dystonia

A

not usually progressive; lack of somatotopic representation specificity in the somatosensory areas of the cortex and thalamus; treatment includes decreasing spasms with modalities, strengthen and teach better movement patterns, and give tools for compensation; stretching is ineffective

76
Q

General Dystonia

A

usually progressive; involuntary twisting postures of limbs and trunk; many times begins as plantarflexion and inversion of foot during gait; treatment includes druge to modulate GABA, Ach, and DA, as well as surgical destruction of motor thalamus

77
Q

Symptoms of Cerebellar Disorders

A

depend on location of lesion and include ataxic gait, dysarthria, dysdiadochokinesia, dysmetria, and action tremor

78
Q

Algogenic Substances

A
  • histamine, potassium ions, serotonin, bradykinins
  • pro-inflammatory cytokines that are produced by WBCs
  • increased expression of NGF and BDNF in inflammatory pain states (increase activity of dorsal horn neurons)
79
Q

Which two chemicals act as neuromodulators in the chemical nociception pathway?

A

prostaglandins and substance P

80
Q

Nociceptors are classified according to:

A

response characteristics (touch, temp, pressure) and type of nerve fiber from which they are derived

Neurophysiology (2 decks)

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