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Pathophysiology > chapter 15 > Flashcards

chapter 15 Flashcards

1
Q
  • originate in the brain, terminate in the spinal cord
  • send axons down SC tracts
A

upper motor neurons

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2
Q

originate in the spinal cord and terminate in skeletal muscle

A

lower motor neurons

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3
Q

loss of movement

A

paralysis

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4
Q

paresis

A

weakness

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5
Q

stroke or paralysis

A

plegia

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6
Q

mono

A

one limb

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7
Q

hemi

A

both limbs on one side

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8
Q

di- or para-

A

relating to both upper or lower limbs

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9
Q

quadri- or tetra-

A

relating to all four limbs

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10
Q

less than normal muscle tone

A

hypotonia

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11
Q

absent muscle tone

A

flaccidity

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12
Q

descriptors indicating higher than normal muscle tone

A
  • hypertonia
  • rigidity
  • spasticity
  • tetany
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13
Q
  • impulses from pyramidal neurons in precentral gyrus pass through corticospinal tracts
  • descend w/o synapsing and decussate at the medullary pyramids
  • axons synapse w/ interneurons or ventral horn motor neurons
  • regulates fast and fine (skilled) movements
A

direct (pyramidal) pathway

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14
Q

cross sectioning of the spinal cord at any level, results in total motorand sensory loss in regions inferior to the cut

A

transection

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15
Q

transection between T1 and L1 results in

A

paraplegia

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16
Q

transection in the cervical region results in

A

quadriplegia

can result in death if affecting C3-C5 (phrenic nerve that keeps the diaphragm alive)

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17
Q

transient period of functional loss caudal to lesion

A

spinal shock

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18
Q

a neurological condition that causes involuntary and rhythmic muscle contractions and relaxations

A

clonus

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19
Q

parasthesias

A

sensory loss

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20
Q

motor function loss

A

paralysis

spastic or flaccid

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21
Q
  • damage to UMNs of primary motor cortex
  • spinal neurons remain intact
  • muscles are stimulated by reflex activity–no voluntary control
  • muscles often shorten permanently
A

spastic paralysis

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22
Q
  • severe damage to ventral root or ventral horn cells
  • impulses do not reach muscles
  • no involuntary or voluntary control of muscles
  • muscles atrophy
A

flaccid paralysis

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23
Q
  • smoothens and coordinates skillful movements
  • influences voluntary and automatic aspects of movement
  • does NOT initiate activity
  • integrates sensory information concerning position of body parts
  • coordinates skeletal muscle activity
  • maintains posture
A

cerebellum

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24
Q
  • often due to congenital defects, vascular accidents, and a growing tumor
  • results in ataxia, nystagmus, tremor, dysphagia, and dysarithria
A

cerebellar disorders

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25
Q
  • neurological sign that refers to a lack of muscle coordination, which can cause clumsy movements:
  • abnormal eye movements, like nystagmus; changes in speech, like scanning speech; difficulty walking; lack of balance; slurred speech; trouble swallowing
A

ataxia

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26
Q
  • a condition that causes involuntary, rhythmic eye movements
  • movements can be side to side, up and down, or circular
  • can affect one or both eyes, and the movements can be continuous or intermittent
A

nystagmus

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27
Q
  • a speech disorder that makes it difficult to speak clearly due to issues with the muscles, nerves, or brain that control speech
  • makes it difficult to form and pronounce words
A

dysarithria

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28
Q

a neurological procedure that damages the globus pallidus, part of the brain’s basal ganglia

A

pallidectomy

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29
Q
  • often leads to involuntary movement, changes in muscle tone, and disturbances in body posture
  • features: tremors, hypokinetic movements, and hyperkinetic movements
A

basal ganglia disorders

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30
Q

types of hyperkinetic movement

A
  • chorea
  • athetosis
  • ballismus
  • dystonia
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31
Q

jerky movements

A

chorea

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32
Q

continuous twisting movements

A

athetosis

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33
Q

violent flinging movements

A

ballismus

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34
Q

rigidity

A

dystonia

35
Q

TREATMENTS
* cannot use dopamine, as it cannot cross the blood brain barrier
* have to use Levodopa (L-Dopa), as it can cross BBB
* surgical procedures such as a pallidectomy

A

treatments of parkinson’s disease

36
Q

SIGNS AND SYMPTOMS:
* develop slowly usually and start on one side and then proceed to both sides of the body
* motor: tremor (pill rolling at rest), bradykinesia, cogwheel rigidity, difficulty starting and stopping movements, balance and coordination problems, may freeze, lost blinking reflex, forward leaning
* autonomic: excessive sweating, salivation, lacrimation, orthostatic hypotension, depression, and dementia in 15-20% of pts

A

(signs and symptoms of) Parkinson’s Disease

37
Q
  • chronic disorder of basal ganglia funciton characterized by slowness of voluntary movements, rigidity, and tremor
  • degeneration of substantia nigra –> overactive BG –> sends abnormal stimuli to cortex –> motor problems
A

Parkinson’s disease

38
Q
  • damages both UMNs (weakness, lack of motor control esp. over spinal reflexes; stiffness and spasticity) and LMNs (causing irritation due to decreased neuronal firing –> weakness, denervation atrophy, and hyporeflexia
  • results in loss of myelinated fibers in the corticospinal tracts
  • atrophy of precentral gyrus
  • affects mostly men between 40-60 y/o
  • fatal
  • due to degeneration of UMNs in spinal cortex and cell bodies in brainstem and anterior horn cells of the spinal cord
A

Amyotrophic Lateral Sclerosis (ALS)

aka Lou Gherig’s Disease

39
Q

SIGNS AND SYMPTOMS
* when LMNS die, denervation occurs due to lateral sclerosis in SC’s lateral column, results in muscular atrophy
* generalized muscle weakness
* paresis in localized muscle group (which may manifest as muscle cramps in distal legs)

A

Amyotrophic Lateral Sclerosis (ALS)

40
Q

TREATMENT
* antispasmodic drugs
* respiratory support

A

(treatments of) ALS

41
Q
  • damage to many nerves whether by demyelination or axonal degeneration of peripheral nerves
  • longest axons affected first, symptoms begin in distal extremities
  • if ANS is involved –> hypotension, impotence, constipation
A

polyneuropathies

ex: Guillain-Barré Syndrome

42
Q

causes of polyneuropathies

A
  1. immune mechanisms (ex: Guillain-Barré syndrome)
  2. toxic agents (arsenic, lead, alcohol)
  3. metabolic diseases (diabetes mellitus, uremia)
43
Q
  • mostly follows a viral infection (typically either upper RT or GI tract)

SIGNS AND SYMPTOMS
* ascending muscle paralysis of the limbs (symmetric flaccidty and paralysis of respiratory muscles)
* parasthesia and numbness
* ANS involvment (postural hypotension, arrhythmias, sweating abnormalities, urinary retention

A

Guillain-Barré Syndrome

44
Q

TREATMENT
* maintain pt airway
* support respiration
* steroids

A

(treatments of) Guillain-Barré Syndrome

45
Q

damage to one nerve

A

mononeuropathies

eg: Carpal Tunnel Syndrome

46
Q

one single lower motor neuron and all of the skeletal muscle fibers it is controlling

A

motor unit

47
Q

responsible for fine, precise movements

A

small motor units

48
Q

responsible for strength, and force of contraction

A

large motor units

49
Q

a process that occurs when a nerve fiber is damaged, causing the axon distal to the injury to break dow (axon and myelin sheath), causing astroglial scar tissuse to replace it

A

Wallerian Degeneration

50
Q
  • compression of the median nerve as it passes w/ flexor tendons through canal or tunnel made by carpal bones and transverse carpal ligaments
  • due to reduction in size of tunnel or an increase in the volume of tunnel contents
  • caused by wrist injury or wrist overuse
A

carpal tunnel syndrome

51
Q

TREATMENT
* splinting
* rest
* surgery
* anti-inflammatory drugs

A

(treatment of) carpal tunnel syndrome

52
Q

SIGNS AND SYMPTOMS
* pain
* parasthesias
* numbness in thumb and fingers

A

carpal tunnel syndrome

53
Q

potential issues with the motor unit

A
  • NMJ disorders
  • muscular atrophy or dystrophy
  • LMN lesions or infections
  • peripheral nerve injury
54
Q

typical NMJ problems

A
  • decreased ACh release
  • decreased ACh effects on the muscle cell
55
Q

a plant derived substance that affects voluntary muscles by blocking the motor end plate, leading to muscle paralysis

A

curare

56
Q
  • a disease in which antibodies made by a person’s immune system prevent certain nerve-muscle interactions (autoimmune)
  • ACh receptors on muscle cells are destroyed
  • causes weak and easily fatigued muscles
A

myasthenia gravis

57
Q

SIGNS AND SYMPTOMS
* difficulty swallowing and chewing
* drooping eyelids
* ventilator needed if respiratory muscles are affected

A

myasthenia gravis

58
Q

TREATMENT
* drugs that increase the release of acetylcholine (ACh)
* removing thymus gland
* immunosuppressant drugs

A

(treatment of) myasthenia gravis

59
Q

types of peripheral nerve injuries

A
  • demyelination
  • axonal degeneration
60
Q

reasons for demyelination

A
  • schwann cell disorder
  • damage to myelin sheath
61
Q

reasons for axonal degeneration

A
  • damage to LMN cell bodies in the spinal cord
  • damage to axons in the spinal or peripheral nerves
62
Q
  • demyelinating disorder of white matter of brain, spinal cord, and optic nerve
  • occurs mostly in young and middle aged adults
  • females are 2x more at risk than males
  • first symptoms arise at 20-40 y/o
  • remyelination can occur if demyelinating process can be stopped before oligodendrocytes die
A

multiple sclerosis

63
Q

demyelination and gliosis

A

stage 2 multiple sclerosis

64
Q

SIGNS AND SYMPTOMS
* vision disturbances
* fatigue and weakness
* bowel and bladder dysfunction
* vertigo
* tinnitis
* facial weakness

A

multiple sclerosis

65
Q

inflammatory lesions

A

stage 1 multiple sclerosis

66
Q

TREATMENT
* steroids
* immunosuppressive drugs

A

(treatment of) multiple sclerosis

67
Q
  • destruction of ventral horn motor neurons–muscles atrophy
  • death may occur from paralysis of respiratory muscles or cardiac arrest
A

poliomyelitis virus

68
Q

semi-permeable membrane that surround muscle cells, separating the intracellular and extracellular environments

A

sarcolemma

69
Q
  • due to lack of innervation
  • if LMN dies or axon destroyed
  • muscle cells in motor unit go through temporary, spontaneous contractions
  • after a few months, muscle degenerates
  • crushed axons in PNS can regenerate when proper conditions are provided
A

denervation atrophy

70
Q
  • 1 in 3,500 births
  • females are carriers, disease seen mainly in males
  • detection between 2-7 years old
  • death in early 20s
  • muscle fibers lack dystrophin
  • present w/ problems regulating calcium release
A

duchenne muscular dystrophy

71
Q

role of dystrophin

A

stabilizes sarcolemma

72
Q

SIGNS AND SYMPTOMS
* postural hip muscles affected first
* shoulder muscles next
* frequent falling from 3-4 y/o
* death due to respiratory and cardiac muscle wasting

A

signs and symptoms of duchenne muscular dystrophy

73
Q

how is duchenne muscular dystrophy diagnosed

A
  • muscle biopsy
  • EMG
  • gene probes
74
Q

TREATMENT
* prednisone
* myoblast transfer therapy

A

(treatment of) duchenne muscular dystrophy

75
Q
  • originates in the motor cortex and provides control of delicate muscle movement
A

pyramidal motor system

76
Q
  • originates in the basal ganglia
  • provides background for more crude, supportive movement patterns
A

extrapyramidal system

77
Q

what can cause the death of LMNs

A
  • loss of spinal reflexes
  • flaccid paralysis
  • denervation atrophy of muscles
78
Q

an injury to the C7 peripheral nerve results in

A

hand weakness only

79
Q

a spinal cord injury at T12 or lower results in

A

flaccid paralysis to body levels below site

80
Q
  • disruption of communication between muscle and all neural input from spinal cord reflexes
  • causes spontaneous contraction of muscle units
  • can be due to infeciton or inflammation of LMN (e.g. due to poliomyelitis virus)
A

LMN lesions

81
Q
  • weakness and loss of voluntary motion
  • spinal reflexes remain intact but cannot be modulated by the brain
  • increased muscle tone
  • hyperflexia
  • spasticity
A

upper motor neuron lesion

82
Q

lesion at or above the level of the pyramids results in…

A

paralysis on the opposite side

83
Q

SIGNS AND SYMPTOMS
* loss of fine, skilled, voluntary lower limb movement
* reduced bowel and bladder function
* reduced sexual function
* hypertonia

A

L1 UMN lesion (or above)

84
Q

SIGNS AND SYMPTOMS
* loss of fine, skilled, voluntary lower limb movements
* reduced bowel and bladder functiion
* reduced sexual function
* hypertonia
* reduced upper limb movement
* LMN reflexes intact, but no more input from higher brain centers
* immediate weakness–later converts to hypertonicity or spasticity and clonus

A

above C5 UMN lesion

Pathophysiology (7 decks)

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