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Block7 > Med Neuro > Flashcards

Med Neuro Flashcards

1
Q

What are the 3 major components and levels of control of the motor system?

A

Cerebral Cortex
Brain Stem
Spinal Cord

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2
Q

What are the 3 levels of the motor system regulated by?

A

Basal Ganglia and Cerebellum

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3
Q

What is the final common pathway of the motor system?

A

The bundle of motor neurons involved in contraction

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4
Q

What are the motor neurons that cause muscle contraction and execute movement?

A

lower motor neuron

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5
Q

What are the two types of interneurons?

A

Project to motor neurons, help connect and coordinate motor neurons that contract as a group
segmental
propiospinal

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6
Q

What are propiospinal interneurons?

A

Interneurons that transmit info between multiple spinal cord levels

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7
Q

What are segmental interneurons?

A

Interneurons that project withina single spinal cord level

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8
Q

What is the medial brainstem pathway and the 3 origins?

A

Reticulospinal, vestibulospinal and tectospinal

provides basic postural control system, influences axial and proximal muscles

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9
Q

What is the lateral brainstem pathways?

A

Rubrospinal tract (red nucleus–spinal cord) Tract descends in dorsolateral white matter and terminates in dorsolateral area of ventral spinal cord. Modulate goal-directed limb movements like reaching and manipulation

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10
Q

What is the role of hte primary motor cotex?

A

executes commands to motor neurons, controls individual finger movement. Coordinates force and direction. Somatically mapped

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11
Q

What is the role of the premotor cortex?

A

integrates motor movements with sensory input. Coordinates complex sequences of movments and is involved in motor learning

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12
Q

What is teh role of the supplementary motor area?

A

Important in internally driven, will driven moveents. Formulates an intention

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13
Q

What are the two descending pathways through which the cerebral cortex acts on motor neurons?

A

lateral corticospinal tract-contralateral limb, digits, goal directed reaching
ventral corticalspinal tract-neck, trunk muscles and postural control

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14
Q

What is teh role of hte lateral corticospinal tract?

A

contralateral limb, digits and goal directed reaching

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15
Q

What is the role of the ventral corticospinal tract?

A

involved in neck, trunk muscles and postural control

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16
Q

What are the three types of movment?

A

Reflex, automatic postural adjustments, and voluntary moveemnts

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17
Q

What are the functions of skeletal muscle?

A

execute voluntary movements, maintain posture, produce tremendou heat and metabolic energy

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18
Q

What are skeletal muscles made up of?

A

Parallel bundles of fasicles

fasicles made of muscle fibers

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19
Q

How can complex action potentials in muscle can be recorded with what?

A

Electromyogram (EMG)

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20
Q

Motor neuron pool

A

1 muscle can be innervated by many motor neurons, in the smae pool

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21
Q

Medial motor nuclei?

A

motor neurons that innervate axial muscles of neck

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22
Q

Lateral motor nuclei?

A

innervate limb muscles, most medial innervate proximal limb muscles
most lateral innervate distal limb muscle

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23
Q

What are slow-twitch motor units?

A

Innervate slow, red, slow-twitch muscle fibers
smaller fibers; small MN; slow contraction; small tension output
specialized for endurance; fatigue resistant

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24
Q

What are fast fatigable motor units?

A

Innervate white, fast-twitch fibers
large fibers, large MN, large contraction
fatigue bc glycogen is rapidly depleted
specialized for strength and speed

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25
Q

What are fast fatigue-resistant fibers?

A

innervate intermediate fibers (btw red and white)
combine fast twitch dynamics and contraction with enough aerobic capacity
specialized for excercise with endurance

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26
Q

Ultimate force exerted by a muscle depends on what?

A

Rate code: frequency of action potentials
recruitment: Number of motor units firing
size principle: smallest motor units fire first; largest fire last
slow twitch: fire first
fast-twitch: fire second

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27
Q

What are the receptors in muscle that monitor length and tension of muscle?

A

Muscle spindles and golgi tendon organs

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28
Q

What do muscle spindles do?

A

made of intrafusal fibers and sense muscle length. Important for propioception. Length of muscle correlates with angle of joints Discharge when muscle stretched

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29
Q

What are the types fo intrafusal fibers in muscle spindle?

A

Dynamic nuclear bag fibers sense change in length

Static nuclear bag and nuclear chain fibers sense static length

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30
Q

What afferent nerve innervates muscle spindle sense length and rate of change in length?

A

Ia–convey fasty dynamic response. Code velocity of stretch, very sensitive

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31
Q

what afferent nerve innervates muscle spindel sense static length?

A

II afferents. Sense static length, slow tonic response. Code duration of stretch

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32
Q

What type of nerve innervates gogli tendon organ?

A

capsule innervated by Ib affarent

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33
Q

Where is the golgi tendon organ located?

A

Located at junction of muscle fiber andtendon, in series with 14-20 extrafussal fibers. Intertwined btw collagen fiber mesh

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34
Q

When does Ib afferent nerve discharge?

A

Innervates golgi tendon and discharges when musccle contracts; precisesly measures force

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35
Q

What is the purpose of golgi tendon reflexes?

A

protects muscle from too much tendon, and gives procise control of musccle force.

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36
Q

What type of motor neuron innervates muscle spindles?

A

gamma motor neuron. In comparison to alpha motor nerutons of extrafusal fibers

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37
Q

What is gamma alpha motor coactivation?

A

During voluntary movment alpha and gamma motor neurons causespindles to shorten keeping them sensitive at al length

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38
Q

What is the stretch reflex?

A

monosynaptic excitatory reflex
“deep tendon reflex”
strike tendon cause muscle contracts very fast

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39
Q

What is teh mechanism of action of stretch reflex?

A

muscle lenthened, spindles excited Ia afferent excited. Excites alpha motor neurons to contract. Monosynaptic contraction
disynaptic inhibits antagonist muscle

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40
Q

What are the clinical causes of decreased or absent deep tendon reflex?

A

indicates problem with component of reflex arc

disease of muscles, neuromusc junction, sensory neurons, lower motor neurons

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41
Q

What are the clincial cause of hyperreflexia?

A

upper motor neuron lesion

loss of descending inhibitory control

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42
Q

What are the purpose of monosynaptic reflexes?

A

maintain appropiate amnt of tension
muscle tone balance
holding still
smoothe out movement

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43
Q

What si teh crossed-extension reflex?

A

Withdrawal from painful stimulus

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44
Q

Mechanism of action of crossed-extension reflex?

A

Adelta nociceptor activated causes excited ipsilateral flexor inhibit ipsilateral extensor
interneurons cross and excite contralateral extensor

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45
Q

What is the golgi tendon reflex?

A

muslce contracts and puts tension on golgi tendon organ
activates Ib afferent and Ib inhib internueron
used to pick up delicate things. Increase in muscle tension
complex, polysynaptic

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46
Q

Inhibitory interneurons do what?

A

help coordinate reflex actions

pupose is to simplify voluntary control

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47
Q

Descending control does what?

A

descending neurons from cortex and brainstem modulate reflexes

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48
Q

What is muscular dystrophy?

A

30 types of a group of chronic hereditary disease, caused by weakness and wasting of skeletal muscles

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49
Q

What is teh most common form of muscular dystrophy in chidlren?

A

Duchenne’s MD, wasting, X-linked

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50
Q

What are the clinical symptoms of Duchenne’s muscular dystrophy?

A

Waddling, lurching gait.

muscle wasting esp at pelvic girdle and hypercontracted muscle fibers

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51
Q

Clinical tests reveal what in Duchenne’s muscular dystrophy?

A

High creatine kinase levels due to muscle damage

elevate before symptoms appear

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52
Q

What is teh cause of Duchenne’s muscular dystrophY?

A

Lack of gene for dystrophin, located on X-chromosome,

protein in cytoskeleton of muscle membrane and stabilizes muscle. Without it muscle shears

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53
Q

What is the tx for Duchenne’s?

A 
PT to keep muscles functioning
posture excercises
surgery for scoliosis correction
Corticosteroids to slow muscle deterioration
Prognosis Death at 20-30
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54
Q

What is myathensia gravis?

A

autoimmune disorder, antibodies to nictonic Ach Receptor in muscle blocking it, crosslinking it triggereing internatlization leading to muscle weakness and easy fatigue

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55
Q

What are teh clinical symptoms of myathensia gravis?

A

Weakness, especiallly cranial muscles and ptosis
fatigue in oropharyngeal muscles–drooling trouble chewing
difficulty breathing

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56
Q

What is teh main treatment for myathensia gravis?

A 
Acetylcholinesterase inhibitor (pyridostigmine) prolongs half life of Ach
Immunosuppressive therapies
Plasmapheresis- remove blood and reinfuse with saline or plasma subsititue
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57
Q

What are the clinical symptoms of lower motor neurons?

A

fasiculations
atrophy of muscles
decreased muscle tone, fatigue
hyporeflexia

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58
Q

What are the clinical symptoms of upper motor neurons?

A

spasticity
incrased muscle tone
hyperreflexia
weakness in muscle but no atrophy of muscle

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59
Q

What is amyotrophic lateral sclerosis?

A

Lou Gherig’s disease; progressive degeneration of upper and lower motor neurons
muscle atrophy and hardness of spinal cord from scarring of lateral tracts

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60
Q

What causes the scarring of ALS?

A

Disease of corticospinal tracts, degenerate progressively
loss of motor nuclei in lower brainstem and loss of motor neurons in ventral spinal cord
loss of betz cells and other pyramidal neurons
usually spares ocular muscles and bladder spphincter

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61
Q

What are teh clinical symptoms of ALS?

A 
progressive weakness
cramps
atrophy of muscles
fasiculations
spacitiy
babinskis sign
respiratory muscle weakness
head droop
dysathria--slurred speech
dysphagia
cognitive and behavioral deficity
pseudobulbar effect: emotional incontinence
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62
Q

What is spared in ALS?

A

eye movemnts, snesory systems, autonomic NS (bladder, Bowels) cognitive and memory sometimes

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63
Q

What is teh ause of ALS?

A

Unkonwn, cases sporadic and low genetic correlation

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64
Q

What is the Tx for ALS?

A

90% die in 6 yrs
Physical therapy
Riluzole: blocks glutamate release to reduce damage
antioxidants

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65
Q

What is guillain-barre syndrome?

A

disorder of peripheral nerve, acute inflammatory demyelinating polyneuropathy
rapid onset 1-2 weeks after viral infection, affects both motor and sensory

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66
Q

Sympotoms of Guillain-Barre syndorm?

A 
Initial:
tingling
insensitiivyt to heat and cold
difficulty moving
rapid onset of weakness
as it progresses
paralysis of breathing muscles
Loss of stretch reflex and plantar reflexes due to motor weakness
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67
Q

What is the Tx of Guillain Barre?

A

Plasmapheresis, Iv immunoglobulin therapy

Good prognosis most recover ina year and most make near full recovery

68
Q

What is the role of the reticular formation?

A

Helps regulate conciousness and contains respiratory and CV centers

69
Q

What is the role of the corticospinal tract?

A

Most important tract; controls voluntary movmeent and fie motor control of limbs

70
Q

What si teh role of the spinothalamic tract?

A

transmits sensory inforamtion

71
Q

What are the somatic motor classification and what do they cover?

A

Innervate skeletal muscles in the head and neck that are derived from myotomes
CN 3,4,6,12

72
Q

What are the branchial motor nuclei?

A 
innervate skeletal muscles derived from branchial arch
motor nucleus of 5
facial nucleus (7)
nucleus ambiguus (9 and 10)
Spinaal Acessory nucleus (11)
73
Q

What are the visceral motor nuclei?

A 
preganglionic parasympathetic innervation
edinger-westphal (3)
Salivatory (7)
Inferior Salivatory (9)
Dorsal motor nucleus of 10 (10)
74
Q

What are the visceral sensory nuclei?

A

special-taste (rostral nuclus solitarius (7,9, and 10))

General-control of carioresp and digestive function (caudal nucleus solitarius (9 and 10))

75
Q

What are the somatic sensory nuclei?

A 
Convey touch, pain, temp posion, vibraion, muscles nad joints
trigeminal nucleus (5,7,9,10)
76
Q

What are the special sensory nuclei?

A

cochlear nucleu and vestibular nucleui (8)

77
Q

What part of the cerebellum influences hte control of axial and proximal limb movments and what tract is it a part of?

A

vermis and part of spinocerebellum

78
Q

What part of the cerebellum controls distal limbs and what tract is part of?

A

intermediate zone and part of spinocerebellum

79
Q

What part of the cerebellum controls planning and initiation of movments?

A

Lateral zone and part of cerebrocerebellum

80
Q

What are the 5 major neruonal types of hte cerebellum and what is the excitatory type?

A 
Purkinje
Golgi
Basket
Stellate
Granule-->excitatory
81
Q

What are the two excitatory afferents of the cerebellar cortex?

A 
Climbing fibers(from contralateral inferior olivary nucleus)--> synapse directly with Purkinje cells
Mossy fibers--> synapse with granule cells which activate Pukinje cells
82
Q

What are the three layers of the cerebellum?

A

Molecular layer, purkinje cell layer and granular layer

83
Q

What does the Molecular layer contain?

A 
Dendrites of Purkinje cells
Parallel fibers of granule cells
climbing fibers from ION
stellate cells
Basket cells
84
Q

What is contained within the purkinje cell layer?

A

Purkinje cells

85
Q

What is contained within the granule layer?

A

granule cells
golgi cells
mossy fibers

86
Q

The deep cerebellar nuclei contains what?

A 
Receives collaterals from climibng and mossy fibers
receive inputs from PUrkinje cells
output is excitatory
Denate nuclei
interposed nuclei
fastigial nuclei
87
Q

What is a denate nuclei?

A

largest and most lateral nuclei of the deep cerebellar nuclei
receive projections from lateral zone

88
Q

What is the interposed nuclei?

A

Emoboliform + blobose; deep cerebellar nuclei receive projections from intermediate zone

89
Q

What are the inhibiotry neurons of the cerebellum?

A

Basket and stellate cells in hte molecular layer inhibit purkinje cell
golgi cells in granular layer inhibit granule cells

90
Q

What does the vesitulocerebellum contain?

A

flocculondodular lobe and inferior vermis

91
Q

What does the vestibulocerebellum control?

A

Control balance and equilibrium while standing or moving. Controls eye movements. Coordinates movements of head and eyes

92
Q

What is part of the spinocerebellum?

A

Vermis and intermedaite zone?

93
Q

What does the spinocerebellum control?

A

Vermis control of azial and proximal muscle
intermediate zone control of distal movements
ongoing execulation of movements

94
Q

What is contained within the cerebrocerebellum?

A

Lateral zone of cerebellum

95
Q

What is the funciton of the cerebrocerebellum?

A

Involved in iniation planning and mental rehearsal of complex motor actions

96
Q

What is the full route of the spinocerebellum major efferents?

A

Intermediate zone to interposed nuclei to either

  • thalamus-motor and premotor cortex and corticospinal tract or
  • brain stem (red nucleus) to lateral descending systems
97
Q

What is the route of the cerebrocerebellum path?

A

nerves initially form contralateral cortex to lateral zones–dentate nucleus–contralateral red nucleus–thalamus– then eithe rpons or spinal cord

98
Q

What is the result of the indirect pathway to the thalamus?

A

movement is inhibited by thalamus inhibition

99
Q

What is the result of the direct pahtway to teh thalamus?

A

Thalamus is disinhibited and movement is facilitated

100
Q

What 2 different types of output neurons does dopamine affect in the striatum?

A

Neurons with D1 dopamine receptors excite direct pathway
Neurons with D2 dopamine receptors inhibit indirect pathway
dopamine therefore facilitates movment

101
Q

What is the cause of parkinsons disease?

A

degeneration of dopaminergic cells in SNc

102
Q

What is the cause of huntington disease?

A

mutation in chromosome 4 leads to degeneration of cholinergic and GABAerigic neurons in striatum

103
Q

What is the cause of Tardive dyskinesia?

A

results from long term of antipsychotic agens. which block DA transmission
involuntary movements of face and tongue

104
Q

What si teh cause of Hemiballismus?

A

lesion of subthalamic nucleus resulting in violent ball-thrwoing movements of cotnralateral arm

105
Q

What are the inputs to the cerebellum?

A

motor information from cord
Visual sensory motor information from cortex
and propioceptive information from the limb

106
Q

What is the path of omotor informationf rom the spinal cord to the cerebellum?

A

cord to VSCT to SCP to cerebelulm

107
Q

What is the path of visual sensory motor information from teh cortex to the cerebellu?

A

cortex to pontine nuclei to MCP to cerebellum

108
Q

What is the path of propioceptive information from the limbs to the cerebellum?

A

limbs to fasciculus gracilus/cuneatus to DSCT and cuneocerebellar tract to ICP to cerebellum

109
Q

What are the three outcomes of cerebellar outputs

A

movement, head/eye control and posture and unconcious motor control

110
Q

Why are symptoms ipsilateral to the cerebellar lesion?

A

inputs are ipsilateral or doublecrossed

111
Q

What is ataxia?

A

uncoordinated muscle movement; problems with speed, range, force and timing

112
Q

What are clinical symptosm of vermian lesion?

A

tibuation=tremor of head or trunk

113
Q

What are a symptoms of flocculonodular lobe lesion?

A

ocular dymetria=overshoot or undershoot of eyes when focusing on target
nystagmus
slow saccades=slow eye movments

114
Q

What do lesions of cortex invovle as far as eye movement?

A

saccades=quick,voluntary eye movements

115
Q

What is a symptom of lesion of lateral hemisphere?

A

scanning ataxic speec=slow,effortful

116
Q

What are the acute causes of cerebellar disorders?

A

cerebellar stroke, alcohol intoxication and drug overdose (ie phenytoin)

117
Q

What are the chronic causes of cerebellar disorder?

A

Essential tremor, spinocerebellar ataxia, tumor (ie astrocytoma)

118
Q

What is an essential tremor?

A

most common movement disorder, bilateral postural and action tremor that is persistant
autosomal dominant
neuodegenerative gradual loss of purkinje cells

119
Q

Chronic alcoholism causes what changes in the cerebellum?

A

cerebellar vermian atrophy and acute EtOH intoxicantion which causes dysfunction of vermis

120
Q

What is the romberg test?

A

aska patient to stand in place, feet together and close eyes; if they need to step to stabilize the dfecit could be due to cerebellar, propioceptive or vestibular disorder

121
Q

What occurs if the lateral hemispheres of the cerebellum are lesioned?

A

influences LCST pathway

and gain appendicular ataxia

122
Q

What occurs if hte intermediate hemisphere is lesioned?

A

influences LCS, rubrospinal tract results in appendicular ataxia?

123
Q

What occurs with a vermis and flocculondoluar lobe lesion?

A

VCST, reticulospinal tract, vestibulospinal tract–>truncal ataxia
and or balance and vestibuloocular reflexes at hte medial longitutudal fasciculus result in nystagmus/slow saccades

124
Q

What si spinocerebellar atazia?

A

gropu of autosomal dominant ataxic disorders caused by degeneration of afferent and efferent cereellar pathways and destruction of purkinje cells

125
Q

What is the striatum composed of?

A

putamen, caudate, nucleus accumbens; large cholinergic internurons are located within striatum

126
Q

What is teh subthalamic nucleus?

A

Only excitatory nucleus in the striatum and releases gluatamte

127
Q

What is the corticostriatl pathway?

A

excitatory path from cortex to striatum mediated by glutamate; cortical input to direct pathway acts like an accelerator and facilitates volitional movment; cortical input to indirect pathway acts like a break

128
Q

What is the nigrostriatal pathway?

A

dopaminergic pathways from substantia nigra to striatum that results in opposing efects
direct pathway results in exciattion fo striatum
indirect pathway results in inhibition of striatum

129
Q

What is the normal striatal affect of activation of the direct pathway?

A

gaba released and inhibits globus pallidus interna and substantia nigra pars reticula and gaba is not released onto VA/VL thalamus with release of inhibition goes to VA/VL thalamus is activated which actavtes motor cortes and facilitates movment

130
Q

What does normal striatal actiavtion of indirect pathway cause?

A

Gaba released and inhibits globus pallidus externa and SNR which means gaba not released onto STN and STN is activated and releases glutamate onto GPi/SNR and this is activated and releases GABA onto thalamus which inbhitis movmet

131
Q

WHat is the cause of parkinsons dsease?

A

loss of dopaminergic neurons in substantia nigra pars compacta (hypokinetic movment disorder)

132
Q

What are the four clinical features of Parkinsons disease?

A

resting tremor
bradykinesia
rigidity
postural instability

133
Q

What is the cause of Huntingtons disease?

A

neurodegenerative disorder with loss of neurons primarily in the caudate (hyperkinetic movment disorder)

134
Q

What are the symptoms of huntingtons disease?

A

dance like near continuous movment of limbs, face and toungue
lesion of caudate is the cause

135
Q

What is hemiballims?

A

brief high amplitude irregular movemnts of a limb; caused by a lesion of subthalamic nucleus

136
Q

What is the definition of encephalopathy?

A

all 3 domains affected but a lesser degree than coma; some alertness maintained

137
Q

What is a coma?

A

loss of alertness, attention, awareness

138
Q

What is altered consciousness?

A

if altered emntation from baseline, then lesion could be in bilateral cerebal hemispheresm, bilateral thalami, brainstem ARAS

139
Q

What is the frontal lobe supplied by?

A

MCA and ACA

140
Q

What is Jacksonian march?

A

seizure that spreads along primary motor cortex

141
Q

Where is broca’s area?

A

inferior frontal lobe usually the leftside

142
Q

What artery supplies Broca’s area and what occurs when a stroke or tumor disrupts brocas area?

A 
MCA
aphasia:
non-fluent
few words, effortful
comprehension intact
repetition impaired
143
Q

What is the role of the prefrontal cortex?

A

provides order
personality
executive function
sequencing, organizing, abstaction, problem solving

144
Q

What is the role of the orbitofrontal cortex?

A

provides restrain
part of limbic system–> memory and emotions
inhibits socially inappropriate behavior
2 most common ways for lesions to this area include head trauma and meningoma

145
Q

What is the frontotemporal dementia?

A

atrophy of the orbitofrontal and prefrontal cotex leading to change in personality, poor judgement, and innappropiate behavior

146
Q

What is the role of hte mesiofrontal cortex?

A

provides initiative, motivation, goal directed behavior

micturition inhibitory center

147
Q

What does a lesion of the mesiofrontal cortex cause?

A

akinetic mutism
abulia
incontinence

148
Q

What is the role of the parietal cortex?

A

primary somatossensory cortex
assocaition cortex
nondominant association cortex

149
Q

What occurs due to a lesion of hte association cortex?

A

loss of stereognosis

graphesthesia

150
Q

What occurs to a lesion of the nondominant association cortex

A

neglect

apraxia

151
Q

Whic association cortex (dominant or non-dominant) drives attention to the world?

A

non-dominant

contains “map of the world”

152
Q

What is praxis?

A

ability to execute a learned skilled task sucha s dressing, riding a bicycle or tying a shoe lace

153
Q

What is apraxia?

A

inability to performa task despite good comprehension and strength

154
Q

What is Gerstmann syndrome?

A 
dominant parietal lobe and angular gyrus
agraphia
acalculia
finger agnosia
R/L confusion
155
Q

What is the result of Wernicke’s aphasia?

A

fluent lots of nonsensical words come out
no comprehension
impaired repetition
smaller branch of MCA stroke

156
Q

What occurs during a conduction aphasia?

A

arcuate fibers damaged due to a smaller branch of MCA stroke

repetition impaired

157
Q

What is global aphasia and cause?

A 
impaired comprehension
impaired repetition
impaired fluency
mute
Full MCA stroke at its proximal end
158
Q

What is Kluver-Bucy syndrome?

A 
bilateral anterior temporal poles and b/l amygdala lesion
hyperorality
innaporpriate sexual displays
irritability/aggression
anterograde amnesia
depression v overactivity
159
Q

Alzheimer’s disease often has what?

A

severe hippocampal atrophy

160
Q

Damage to occipital cortex results in what type of disturbance??

A

homonymous visual field defects

pre

161
Q

presence of a homonymous hemianopia indicates what?

A

cortical or subcortical disease

162
Q

What causes macular sparing?

A

VF deficit with a PCA stroke; macular vision is spared bc crtiical area of brain recieves dual supply

163
Q

What are the aterial supplies of the macula?

A

PCA-primary contribution

MCA-collateral contribution

164
Q

What is the cause of balint syndrome?

A

MCA-PCA watershed infacts; alzheimer’s

165
Q

What is Balint SYndrome?

A

simultanagnosia=inability to perceive the visual field as a whole
optic ataxia=inability to point/reach for object in visual field under visual guidance
ocular apraxia=inability to look at objects in VF using saccades
lesions of bilateral occipital-parietal ccortices

166
Q

What are watershed strokes?

A

defined as ischemia that are localized to border of zones between territories of two major arteries in teh brian

Block7 (10 decks)

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