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DPT 520 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

where are the cell bodies of LMNs located?

A

in the ventral horn of the SC

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2
Q

are LMN peripheral neurons?

A

yes!

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3
Q

what are the signs of a LMN lesion?

A

hypotonicity

hyporeflexia/areflexia

neurogenic atrophy

fasciculation/fibrillation

paralysis and paresis

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4
Q

do UMNs or LMNs lesions result in neurogenic atrophy?

A

LMN lesions

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5
Q

do UMN or LMN lesions result in disuse atrophy?

A

UMN lesions

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6
Q

what is hypotonicity?

A

low muscle tone (abnormally low resistance to passive motion)

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7
Q

what is muscle tone?

A

resistance to muscle stretch in resting muscle

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8
Q

what is flacidity?

A

more severe where there is an absence of resistance to passive movement

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9
Q

do UMN or LMN lesions result in resting tension close to none?

A

LMN lesions

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10
Q

why can hypotonicity lead to injury?

A

there is ligament laxity and hypermobility of the jts

lack of voluntary muscle control

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11
Q

what is the importance of the phasic stretch reflex/DTR?

A

it determines the integrity of the monosynaptic reflex and SC at different segmental levels

it determines the excitability of the alpha motor pool

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12
Q

is phasic stretch reflex the same thing as tonic stretch reflex?

A

no! tonic stretch reflex is abnormal

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13
Q

what does diminished input from motor neurons to skeletal muscles lead to?

A

hyporeflexia

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14
Q

what is neurogenic muscle atrophy?

A

rapid loss of muscles bulk due to denervation of skeletal muscle associated with LMN lesions

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15
Q

what chain of events lead to neurogenic atrophy?

A

lack of neural stimulation and contraction–>lack of gene expression–> changed protein production–>rapid atrophy

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16
Q

what is this describing?: a ground motor neuron is trying to innervate a lot of motor fibers but can’t support them so they die

A

neurogenic atrophy

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17
Q

what is fasciculation?

A

spontaneous quick twitch of a single motor unit (one motor neuron and all its fibers it innervates) that can be seen

not always pathological like an eyelid twitch

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18
Q

is a fasciculation pathological?

A

not always

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19
Q

when is fasciculation pathological?

A

with atrophy

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20
Q

what are some common causes of fasciculation?

A

too much caffeine

fatigue

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21
Q

what is fibrillation?

A

spontaneous contraction of muscle fibers that can’t be observed with the eye

pathological sign of denervation/electrolyte imbalance

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22
Q

what is fibrillation a sign of?

A

denervation

electrolyte imbalance

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23
Q

is fibrillation pathological?

A

yes!

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24
Q

what causes fibrillation?

A

muscles not getting enough ACh, so the receptors get dispersed and become hypersensitive to ACh

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25
Q

what is paralysis?

A

completely severed nerve with no way of getting signals to the muscles

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26
Q

is paralysis or paresis more common in LMN lesions?

A

paralysis

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27
Q

what is paresis?

A

cut a few nerve fibers w/remaining fibers leads to weaker muscles but not completely paralyzed

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28
Q

how are paralysis and paresis measured?

A

MMT and dynamometer

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29
Q

are these examples of UMN or LMN disorders?:

poliomyelitis

GBS

Erb’s palsy

Klumke’s palsy

myasthenia gravis (not really though)

A

LMN

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30
Q

what is poliomyelitis?

A

polio virus selectively destroys somas of MNs leading to denervation of muscle fibers and weakness of muscles

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31
Q

do poliomyelitis effect one or both limbs?

A

one limb

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32
Q

do the impairment of poliomyelitis last a lifetime?

A

yes:(

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33
Q

can there be some recovery in poliomyelitis? why or why not?

A

yes, bc it is PNS

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34
Q

is poliomyelitis worse in children or adults?

A

adults, it will result in quadriplegia

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35
Q

who is mostly effected by poliomyelitis?

A

children under 5 y/o

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36
Q

doe poliomyelitis have mostly motor or sensory symptoms?

A

mostly motor

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37
Q

what is post-polio syndrome?

A

overextension of surviving MN following poliomyelitis results in death of neurons that tried to take on orphan fibers

occurs years after initial viral infection

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38
Q

what are the s/s of post-polio syndrome?

A

increasing weakness

fatigue

jt and muscle pain from muscles fatigue (achy)

breathing difficulty

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39
Q

t/f: the s/s of the initial infection correlate to the severity of the post-polio symptoms

A

true

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40
Q

t/f: pts with post-polio syndrome are a fall risk

A

true

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41
Q

what is Erb’s palsy?

A

brachial plexus injury from birth trauma or falling in neck lateral flexion resulting in avulsion of C5-6 nerve roots

motor and sensory symptoms

arm paralysis

medial rotation or the shoulder, elbow extension, and wrist flexion

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42
Q

what is the pattern of sensory loss in Erb’s palsy?

A

dermatomal

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43
Q

what is the pattern of motor loss in Erb’s palsy?

A

myotomal

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44
Q

what LMN disorder results in the “waiter’s tip” deformity?

A

Erb’s palsy

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45
Q

what is the prognosis for Erb’s palsy?

A

usually pretty good but depends on severity of the initial injury

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46
Q

if a pt with Erb’s palsy makes a recovery when would this recovery occur?

A

about 9 months after birth

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47
Q

what is Klumpke’s palsy?

A

a brachial plexus injury from traction of an abducted arm that results in avulsion of C8-T1 nerve roots

sensory and motor loss

severe pain in the nerve path

atrophy of hand muscles

hyperextended MCP jts, flexion of PIP and DIP jts (intrinsic plus)

paralysis of intrinsic hand muscles, wrist flexors, and finger flexors/extensors

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48
Q

what LMN disorder results in the “claw hand” deformity?

A

Klumpke’s palsy

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49
Q

what are the UMN tracts?

A

lat/med corticospinal, lat/med vestibulospinal, reticulospinal, and rubrospinal tracts

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50
Q

what does the lat corticospinal tract control?

A

fractionated movement for fine object manipulation

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51
Q

what does the med corticospinal tract control?

A

posture

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52
Q

what UMN tracts come from the BS?

A

vestibulospinals, reticulospinal, and rubrospinal tracts

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53
Q

are the basal ganglia and cerebellum UMNs?

A

no!

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54
Q

what is the corticobulbar (cortico-brainstem) tract?

A

from the primary motor cortex to the CN nuclei in the BS decussation at different levels

controls muscles of the face, tongue, and neck (pharynx and larynx)

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55
Q

describe the innervation of the upper face

A

innervated by 2 UMNs

contralateral and ipsilateral innervation

redundancy bc it’s innervated by both sides of the cortex

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56
Q

describe the innervation of the lower face

A

contralateral innervation only

no redundancy=no compensation with damage to one side

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57
Q

what are the non-specific motor tracts?

A

emotional motor system

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58
Q

what activates the emotional motor system?

A

excessive limbic activity

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59
Q

t/f: there is poorer motor performance with high anxiety

A

true

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60
Q

how does the emotional motor system control movement?

A

modulates the activity of interneurons and LMNs

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61
Q

what is the ceruleospinal tract?

A

fast acting system

NE=induce sympathetic activity

slightly depolarized LMN makes it easier to excite

adrenaline in antinociception that suppresses pain perception

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62
Q

what is the raphespinal tract?

A

serotonin

modulation of LMNs

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63
Q

what are the signs of UMN lesions?

A

hypertonicity

disuse atrophy

abnormal reflexes

abnormal synergies

movement disturbances

impaired postural control

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64
Q

what is disuse atrophy?

A

slower progression of atrophy due to lack of muscle use

more mild than neurogenic atrophy

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65
Q

is paresis or paralysis more common in UMN lesions?

A

paresis

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66
Q

what is hypertonicity?

A

abnormally strong resistance to passive stretch

neuromuscular overactivity and excessive contraction from an UMN lesion

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67
Q

what are the 2 types of hypertonicity?

A

spasticity and rigidity

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68
Q

what is spasticity?

A

velocity-dependent increase in resistance to stretch

increased velocity=increased hypertonicity

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69
Q

should you move a limb slower or faster to avoid spasticity?

A

slower

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70
Q

what are the 2 mechanisms of spasticity?

A

1) hyperreflexia at the level of the SC
2) BS motor tracts overactivity

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71
Q

t/f: muscles shorten secondary to spasticity

A

true

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72
Q

what is rigidity?

A

velocity independent increase in resistance to stretch

constant resistance to passive movement regardless of the speed of the force applied

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73
Q

BS lesions above the red nucleus- produce what?

A

decorticate posture

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74
Q

what is the decorticate posture?

A

“arms to the core”

red nucleus- no longer under cortical inhibition=UE flexion

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75
Q

what is decerebrate posture?

A

results from lesion below the red nucleus but above the vestibular nuclei

no rubrospinal contribution for UE flexion=UE extension

vestibular nuclei no longer under cortical inhibition=UE extension

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76
Q

what is a common feature of both decorticate and decerebrate posture?

A

necks and trunk extension

typically in response to noxious stimulus (sternal rub)

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77
Q

what is reflex irradiation?

A

reflex test performed on one area results in reflex of another adjacent area

ie: reflect test of quad tendon results in hamstring and quad reflexes

ie: one side tendon tap results in rxn on both sides

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78
Q

what are signs of corticospinal tract (CST) damage (UMN)?

A

positive Babinski sign

positive Hoffman sign

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79
Q

what is a positive Babinski sign?

A

toes fan out w/stroking of the lateral plantar side of the foot

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80
Q

what is a positive Hoffman sign?

A

opposition of the thumb and index finger when the examiner flicks the nail of the middle finger down

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81
Q

what is clonus?

A

involuntary, repeating, rhythmic contractions of a single muscle group induced by muscle stretch, noxious stimulus, or voluntary movement

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82
Q

where is clonus commonly seen?

A

at the ankle

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83
Q

what injury commonly results in clonus?

A

SCI

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84
Q

what is the clasp knife response?

A

with slow stretch of paretic muscle, resistance is initially strong and sudden goes away

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85
Q

what is the result of a lesion in the corticospinal tract?

A

disinhibition of the reticulospinal tract

abnormal synergy patterns

loss of fractionation of movement

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86
Q

what is fractionated movement?

A

ability to isolate one jt movement from another

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87
Q

what is abnormal UE flexion synergy?

A

scap retraction, elevation or hyperextension

shoulder abduction and external rotation

forearm supination

wrist and fingers flexion

elbow flexion*

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88
Q

what is abnormal UE extension synergy?

A

scap protraction

shoulder adduction*, internal rotation

forearm pronation

wrist and fingers flexion

elbow extension

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89
Q

what is abnormal LE flexion synergy?

A

hip flexion*, abduction, and external rotation

knee flexion

ankle dorsiflexion

toe flexion

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90
Q

what is abnormal LE extension synergy?

A

hip extension, abduction*, and internal rotation

knee extension*

ankle plantarflexion* and inversion

toe extension

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91
Q

what are the pathological reflexes of UMN lesions?

A

(+) Babinski sign
(+) Hoffman sign
reflex irradiation
clasp knife response

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92
Q

what are the pathological reflexes of LMN lesions?

A

absent reflexes

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93
Q

what are the UMN disorders?

A

spina bifida

Arnold chairi malformation

MS

cerebral palsy

stroke

SCI

trauma (TBI)

tumor

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94
Q

what is the most frequently affected artery in strokes?

A

middle cerebral artery

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95
Q

what the pathology of a stroke?

A

interruption in blood flow to the cerebrum

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96
Q

what tracts are effected by stroke?

A

corticospinal tracts

corticoreticular tract

corticobrainstem tracts

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97
Q

what are the impairments in stroke?

A

contralateral motor impairments

contralateral sensory impairments: all face and body modalities

contralateral UMN signs

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98
Q

where do the upper and lower face get innervation from?

A

corticobulbar tract

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99
Q

if there is a lesion to the cortiobrainstem tract, what is the pattern of loss in the face?

A

UMN

paralysis of the contralateral lower face

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100
Q

if there is a lesion to the facial nerve(CN), what is the pattern of loss in the face?

A

LMN

no motor function on one side of the face

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101
Q

t/f: the raphespinal and ceruleospinal tracts may be able to produce a smile in the paralyzes lower side of the face with a corticobulbar tract lesion

A

true

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102
Q

is ALS an UMN or LMN disorder?

A

both

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103
Q

what is amyotrophic lateral sclerosis (ALS)?

A

selective destruction of motor neurons (LMN) and motor pathways (UMN) causes gradual onset of progressive muscle weakness

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104
Q

is ALS usually idiopathic?

A

yes

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105
Q

when is ALS usually diagnosed?

A

age 40-70

106
Q

what is the life expectancy of someone after an ALS diagnosis?

A

2-5 years

107
Q

are there sensory impairments in ALS?

A

no

108
Q

how is ALS different from SMA?

A

SMA involves lack of SMN gene that leads to death of neurons and is solely LMN

ALS is both UMN and LMN

109
Q

what are the UMN signs associated with ALS?

A

(+) Babinski sign

increased DTR

slow/rapid alternating movements

110
Q

what are the UMN symptoms associated with ALS?

A

lack of movement coordination

poor balance

stiffness w/UE and LE movements

111
Q

what the LMN signs associated with ALS?

A

difficulty squatting and rising from a chair

foot drop

UE and LE atrophy

waddling gait

fasciculations

112
Q

what are the LMN symptoms associated with ALS?

A

muscle cramps

fasciculations

UE and LE weakness

113
Q

what are the disorders of the ANS?

A

Horner’s syndrome

orthostatic hypotension

syncope

autonomic dysreflexia

diabetic autonomic neuropathy

114
Q

what is the central autonomic pathway?

A

the hypothalamospinal tract

115
Q

what is the dysfunction associated with a hypothalamic lesion?

A

metabolic (impaired thermoregulation, obesity, anorexia) and behavior dysfunction

116
Q

what is the dysfunction associated with a limbic lesion?

A

altered autonomic responses to emotion (no longer have sympathetic responses paired with emotional responses)

117
Q

what is the dysfunction associated with a brainstem lesion?

A

loss of descending control of HR, BP, and respiration

autonomic dysfunction associated with CN damage (pupillary control, swallowing, salivation, tear production)

118
Q

what is the dysfunction associated with SC lesions?

A

loss of ascending and descending autonomic signals at and below the lesion

vasomotor, HR control, etc affected (autonomic dysreflexia)

119
Q

what is the dysfunction associated with peripheral nerve lesions?

A

loss of vasomotor control, temp regulation, and sweating bc peripheral nerve contain autonomic fibers

trophic changes (changes in skin elasticity) affecting hair and nail formation-blotchy, red, cyanotic, thin, cold, or hot skin

120
Q

what is Horner’s syndrome?

A

PAM due interruption of sympathetic efferent pathway (hypothalamospinal/brainstem tracts) affecting the ipsilateral face

121
Q

what does PAM stand for in Horner’s syndrome?

A

Ptosis (drooping eyelid)

Anhidrosis (loss of sweating)

Miosis (constricted pupil)

122
Q

why is the pupil contracted in Horner’s syndrome?

A

it is a parasympathetic function from no opposing sympathetic force

123
Q

in Horner’s syndrome, the pupil is >__% smaller than the other side

A

50

124
Q

why do people with Horner’s syndrome have dry red skin?

A

vasodilation (parasympathetic function)

125
Q

what are the causes of Horner’s syndrome?

A

tumor, stroke, trauma, disease affecting area surrounding sympathetic nerve, genetics

126
Q

what is orthostatic hypotension?

A

decrease of greater than or equal to 20 mmHg SBP or 10 mmHg DBP or HR increase of more than 20 bpm during the 1st 3 minutes of standing

127
Q

what is the pathology of orthostatic hypotension?

A

impaired reflex mediated by the arterial baroreceptors that normal constrict vessels when standing

128
Q

what are the s/s of orthostatic hypotension?

A

dizziness, light-headedness, feeling faint, fainting

129
Q

can orthostatic hypotension be neurogenic?

A

yes

130
Q

what are neurologic causes of orthostatic hypotension?

A

SCI

peripheral neuropathy

autonomic degenerative disorders (Parkinson’s)

131
Q

what is postural orthostatic tachycardia syndrome (POTS)?

A

HR increase of greater or equal to 30 bpm within initial 10 minutes of standing

absence of orthostatic hypotension and other explanations tachycardia

132
Q

t/f: POTS is caused by anxiety/psychological factors

A

false

133
Q

what population is frequently affected by POTS?

A

females 15-50 y/o

134
Q

what are causes of POTS (other than prolonged bed rest)?

A

trauma, sympathetic NS overactivity, low blood volume, cardiogenic deconditioning

135
Q

what is syncope?

A

fainting-temporary loss of consciousness bc of inadequate blood flow to the brain

decreased BP and HR

recovery w/o intervention or lingering symptoms

136
Q

what is neurocardiogenic syncope?

A

caused by emotional response

ie. when seeing a needle or lots of blood, getting excited or shocking news

vasovagal syncope

137
Q

what is situational syncope?

A

caused by mechanoreceptor activation on CNs

cough, sneeze, defecation, urination

138
Q

what is carotid sinus sensitivity syncope?

A

caused by pressure on the carotid artery

ie. turning head, tight collar

139
Q

what are causes for syncope?

A

mechanoreceptors triggered to slow the HR

medulla inhibits the sympathetic NS-signal to the vagus nerve

140
Q

what is autonomic dysreflexia?

A

sympathetic overactivity in pts with SCI at/above T6 level

dangerous vasomotor response to noxious stimuli below the level of injury

pain below the lesion can’t be felt and triggers a sympathetic response below the lesion that can’t reach above the lesion and parasympathetic response above the lesion that can’t get below the lesion

decreased HR above the lesion

dissociated sympathetic/parasympathetic activity

141
Q

what are the s/s of autonomic dysreflexia?

A

HTN, bradycardia, excessive sweating above the lesion, flushing of the face, pounding headache

142
Q

should you lay down a pt if you suspect that they have autonomic dysreflexia?

A

NO! THIS WILL KILL THEM BY SENDING MORE BLOOD UP TO THE HEART

143
Q

what is diabetic autonomic neuropathy?

A

damage to the PNS including sympathetic nerves

144
Q

what are the s/s of diabetic autonomic neuropathy?

A

increased sweating in the extremities

trophic changes in the distribution of the peripheral nerve (shiny, hairless, anhidrosis of the skin)

postural (orthostatic) hypotension bc there is a lack of vasoconstriction in the legs bc of loss of sympathetic fxn

decreased ANS fxn following the glove and stocking pattern

impaired motility of the GI tract, gallbladder dysfunction, diarrhea, b/b dysfunction, impotence

145
Q

what are the functions of the cerebellum?

A

movement coordination

feedback/feedforward

comparator

146
Q

what does cerebellar dysfunction affect?

A

posture, automatic movements, eye movements, and voluntary movements

147
Q

a unilateral lesion of the cerebellum will affect what side of the body?

A

ipsilateral bc most pathways projecting from the cerebellum stay ipsilateral or double decussate

148
Q

what is spinocerebellar ataxia?

A

poor hand-eye coordination, poor eye movement, poor balance, poor coordination, and poor speech

149
Q

what does vestibulocerebellar lesion result in?

A

unsteadiness

truncal ataxia

nystagmus

vertigo

150
Q

what is the input of the vestibulocerebellum?

A

vestibular apparatus

151
Q

what is the output of the vestibulocerebellum?

A

vestibular nuclei controlling eye movement and balance/equilibrium

152
Q

what is the nucleus associated with the vestibulocerebellum?

A

the fastigial nucleus

153
Q

what region of the cerebellum is the vestibulocerebellum in?

A

fluculonodular lobe

154
Q

what region of the cerebellum is the spinocerebellum in?

A

vermis and paravermis-

155
Q

what region of the cerebellum is the cerebrocerebellum in?

A

the lateral hemispheres

156
Q

what is the input of the spinocerebellum?

A

visual, auditory, and vestibular inputs

157
Q

what is the output of the spinocerebellum?

A

lateral UMNs

158
Q

what does a lesion in the spinocerebellu result in?

A

truncal ataxia

limb ataxia (dysdiadochokinesia and dysmetria)

ataxic gait

intention tremor

dysarthria

movement decomposition

159
Q

what is dysdiadochokinesia?

A

the inability to make rapid alternating movements like fast pronation/supination

160
Q

what is dysmetria?

A

inability to measure distance of movement, so there is often overshooting and undershooting of targets

161
Q

how is dysmetria tested?

A

nose to finger test

162
Q

what is ataxic gait?

A

wide BOS and instability results from truncal or limb ataxa

163
Q

what is an intention tremor?

A

tremor during movement (cerebellar sign)

164
Q

what is dysarthria?

A

slurred speech

165
Q

what is movement decomposition?

A

segmental movements can’t happens in one motion

166
Q

what is the input of the cerebrocerebellum?

A

cerebral cortex

167
Q

what is the output of the cerebrocerebellum?

A

motor and premotor cortex

168
Q

what does a lesion in the cerebrocerebellum result in?

A

finger ataxia

dysarthria

169
Q

what is the nucleus associated with the spinocerebellum?

A

interposed nucleus

170
Q

what is the nucleus associated with the cerebrocerebellum?

A

dentate nucleus

171
Q

is the paravermis lateral or medial motor?

A

lateral

172
Q

is the vermis lateral or medial motor?

A

medial

173
Q

does the use of vision change gait performance with cerebellar ataxia?

A

no

174
Q

will sensory or cerebellar ataxia have a positive Romberg test?

A

sensory?

175
Q

t/f: cerebellar ataxia limits timing and accuracy of voluntary motor control

A

true

176
Q

what are the characteristics of cerebellar ataxia?

A

delayed, jerky movement

range of movement errors (longer to get from nose to finger)

patterned movement errors (dysdiadochokinesia)

truncal ataxia

gait and limb ataxia

hand and finger ataxia

177
Q

what is spinocerebellar atrophy?

A

an inherited, neurodegenerative, heterogeneous disease subset of cerebellar ataxia

progressive degeneration of the cerebellum caused by CAG nucleotide abnormally repeating expansion that encode polyglutamine

178
Q

what is ACDA 1?

A

cerebellar ataxia

pyramidal features

extra pyramidal features

amytrophy

179
Q

what is ACDA 2?

A

cerebellar ataxia

pigmentary retinal degeneration

180
Q

what is ACDA 3?

A

pure cerebellar ataxia symptoms

181
Q

what are the signs of spinocerebellar atrophy?

A

dystonia

muscles fasciculations

poor hand-eye coordination

slurred speech

learning disabilities

parkinsonism

hyperreflexia

seizures

182
Q

what are the symptoms of spinocerebellar atrophy?

A

difficulty walking

reduced b/b control

involuntary eye movements

difficulty swallowing

muscles weakness, stiffness, and cramps

numbness

183
Q

how is spinocerebellar atrophy diagnosed?

A

genetic testing

neuro imaging

electrophysiologic testing

184
Q

is there a cure for spinocerebellar atrophy?

A

no:(

185
Q

what meds can be used to manage spinocerebellar atrophy?

A

antiepileptic drugs

Botox

beta-blockers

primidone

antidepressants

Levodopa

dantrolene

antisense oligonucleotides

186
Q

what are activity limitations in spinocerebellar atrophy?

A

decreased walking distance and stability

decreased cognition

impaired balance w/surface change and in static posture

187
Q

what are participation restrictions in spinocerebellar atrophy?

A

difficulty w/ambulation and balance for ADLs

withdrawal from social situations

work

188
Q

t/f: PT can delay the need for a WC in spinocerebellar atrophy

A

true!

189
Q

what can PT do for a pt with spinocerebellar atrophy?

A

exercise and balance based therapy to improve motor fxn

accessory respiratory muscles strengthening and diaphragmatic breathing exercises to improve respiratory fxn

190
Q

what are the hypokinetic disorders?

A

Parkinson’s disease

atypical parkinsonism

191
Q

what are the hyperkinetic disorders?

A

Huntington’s disease

dystonia

192
Q

what are the disorders of the basal ganglia?

A

hyperkinetic diseases (Huntingtons and dytonia)

hypokinetic diseases (Parkinson’s, and parkinsonism)

basal ganglia stroke

193
Q

what is hypokinesia?

A

less movement

194
Q

hypokinesia results from down regulation of the ___ pathway and up regulation of the ____ and ___ pathways

A

go, no-go, stop

195
Q

hyperkinesia results from up regulation of the ____ pathway and down regulation of the ____ and ____ pathways

A

go, no-go, stop

196
Q

what are the 2 types of hypokinesia?

A

bradykinesia and akinesia

197
Q

what is bradykinesia?

A

slow movement (decreased velocity of movement)

198
Q

what is akinesia?

A

lack of movement (decreased amount of movement)

199
Q

what is dyskinesia?

A

uncontrolled, irregular, involuntary movement

200
Q

what is cogwheel rigidity?

A

intermittent break in tone

on and off rigidity

201
Q

what lead pipe rigidity?

A

resistance throughout

202
Q

what is the pathology of Parkinson’s disease (PD)?

A

idiopathic neurdegenerative disease that causes loss of dopaminergic neurons in the SNpc

203
Q

when does the onset of PD usually begin?

A

50-60 y/o

204
Q

t/f: men are more affected by PD

A

false, men and women are affected equally

205
Q

there are no s/s of PD until __% of dopaminergic neurons are dead

A

80

206
Q

what is the most common type of PD?

A

postural instability gait difficulty PD (50%)

207
Q

what are the 3 types of PD?

A

postural instability gait difficulty PD

tremor dominant PD

mixed type PD

208
Q

what happens to the GPi in PD?

A

it becomes more inhibitory

209
Q

what is the result of the GPi becoming more inhibitory in PD?

A

the motor thalamus, PPN, and MLR are always inhibited

210
Q

what is the result of the lack of motor thalamus activation from increased inhibition from the GPi

A

bradykinesia and hypokinesia

211
Q

what is the result of the lack of PPN activation from increased inhibition from the GPi?

A

trunk rigidity

212
Q

what is the result of lack of MLR activation from increased inhibition from the GPi?

A

changes in gait

213
Q

what are the characteristics of gait in PD?

A

festinating, freezing gait

hard to start and once started it speeds up

sudden stopping

214
Q

what are the cardinal signs of PD?

A

TRAP:
resting Tremors

Rigidity

Akinesia

Postural instability gait deviations

215
Q

what are resting tremors?

A

a basal ganglia sign

tremor when not doing anything

usually a “pill rolling” tremor

216
Q

what is akathisia?

A

restless feeling

feel like they have to move

can’t stay still

may be the first sign of PD way b4 other signs and dx

217
Q

what are postural instability gait deviations?

A

shuffling gait

decreased arm swing and trunk rotation

retropulsion

stopped posture

poor anticipatory and reactive postural responses

218
Q

what is retropulsion?

A

a tendency to fall or walk backwards with a a slight push back

219
Q

what are the non-motor manifestations of PD?

A

impaired autonomic fxn

insomnia/daytime somnolence

depression

bradyphrenia

difficulty shifting attention

dementia

dysphoria

apathy and psychosis

visuospatial/visuoperceptual impairments

220
Q

why is there impaired autonomic fxn in PD?

A

there’s inadequate NE released leading to thermoregulation dysfunction and neurogenic orthostatic hypotension

221
Q

why is there insomnia in PD?

A

disruption of RAS and circadian rhythm

222
Q

t/f: insomnia in PD can contribute to depression

A

true

223
Q

t/f: depression in PD can be neurogenic or situational

A

true

224
Q

what is bradyphrenia?

A

pathological slowing of cognitive processing

225
Q

what is dysphoria?

A

profound feeling of unhappiness, discomfort, and dissatisfaction towards everything

226
Q

what are the secondary neurologic impairments in PD?

A

impaired communication

masked face (hypomimia-lack of facial expression)

hypokinetic dysarthria (impaired speech) and hypophonia

227
Q

what are secondary impairments of PD?

A

neurologic impairments

impaired oral motor control

impaired fine and gross motor performance

impaired motor learning and planning

228
Q

what are the secondary oral impairments in PD?

A

dysphagia (difficulty swallowing)

sidlorrhea (drooling/excessive salivation)

229
Q

what is a secondary fine and gross motor impairment in PD?

A

micrographia (small writing)

230
Q

how can PD be managed?

A

medications and surgery

231
Q

what medications are used to manage PD?

A

dopamine replacement

232
Q

what surgeries can treat PD?

A

deep brain stimulation and destructive surgery

233
Q

what does deep brain stimulation do in PD?

A

an electrode goes to the thalamus to activate it

234
Q

what does destructive surgery do in PD?

A

destroys the GP to reduce bradykinesia and rigidity

235
Q

what are the additional s/s of atypical parkinsonism?

A

rapid disease progression

signs of cerebellar and corticospinal dysfunction

early postural instability and retropulsion

voluntary gaze dysfunction (supranuclear gaze palsy)

respiratory dysfunction

pseudo-bulbar affect (PBA)

236
Q

what is PBA?

A

uncontrollable/inappropriate emotions

laughing or crying out of context

237
Q

what causes PBA?

A

disinhibition of pathways involving serotonin and/or glutamate

disconnect b/w frontal lobe controlling emotions and cerebellum where emotions are mediated

238
Q

does parkinsonism respond well PD meds?

A

no

239
Q

what is multiple system atrophy (MSA) and its key impairements?

A

progressive disease involving cerebellar signs, CST dysfunction, autonomic dysfunction, cardiac issues, and decreased sweating

240
Q

what are other s/s of MSA?

A

generalized weakness, double vision/visual disturbances, difficulty breathing and swallowing, and sleep disturbances

241
Q

what s/s can set apart PD and MSA?

A

generalized weakness as this is usually present in MSA but is not common in PD

242
Q

what is progressive supranuclear palsy (PSP)?

A

abnormal eye movements with early onset gait instability, freezing gait, axial rigidity, dysarthria, and dysphasia

due to the buildup of tau proteins (like Alzheimer’s)

243
Q

when does PSP usually begin?

A

age 60-70

244
Q

what is a risk factor for PSP?

A

age

245
Q

what is dementia with Lewy bodies?

A

an abnormal accumulation of Lewy bodies inside nuclei of neurons in the brain areas that control motor control and cognition

246
Q

what are the s/s of dementia with Lewy bodies?

A

parkinsonism motor symptoms

early progressive cognitive decline

fluctuations in alertness and attention

visual hallucinations

depression

247
Q

what is corticobasal syndrome?

A

assymetric involuntary movements, apraxia, and cortical sensory deficits that begin in 60s with a life expectancy of 6-8 years after dx

248
Q

what is CTE?

A

abnormal tau protein buildup resulting from recurrent head injury

249
Q

what are the 4 causes of secondary parkinsonism?

A

1) traumatic - chronic traumatic encephalopathy (CTE)

2) toxic

3) infectious

4) drug-induced -antipsychotics, digestive, or MPTP drugs

250
Q

what are the effects of CTE?

A

memory, behavior, personality, speech and language, and balance disturbances

251
Q

what is Huntington’s disease/Huntington’s chorea?

A

an autosomal dominant hereditary disorder that causes degeneration in many areas of the brain (predominantly in the striatum and cerebral cortex)

enlarged ventricles

dementia

252
Q

when is the onset of Huntington’s disease?

A

30-40 y/o

253
Q

after the onset of symptoms, how long do pts with Huntington’s disease have?

A

about 15 years

254
Q

what happens to the PPN in Huntington’s disease?

A

it is disinhibited

255
Q

t/f: Huntington’s disease is a dopamine problem

A

false

256
Q

are D1 or D2 putamen receptors overactive in Huntington’s disease?

A

D1, causing upregulation of the go pathway and down regulation of the no-go pathway

257
Q

what happens to D2 receptors in the putamen in Huntington’s disease?

A

they are degenerated leading to a down regulation of the no-go pathway

258
Q

what happens to the GPi in Huntington’s disease?

A

it has reduced inhibition ???

259
Q

what is the affect of the PPN being overly inhibitory in Huntington’s disease?

A

not enough activation of postural muscles

260
Q

is clonus an UMN sign or LMN sign?

A

UMN sign

DPT 520 (13 decks)

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