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Week 4 - Neuro > Week 4 - Neuro Big Ideas > Flashcards

Week 4 - Neuro Big Ideas Flashcards

1
Q

carotid artery on ultrasound

A

laterally on neck, does not compress, pulses, can find bifercation superiorly - dark circle

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2
Q

jugular vein on ultrasound

A

laterally on the neck, compresses, larger than carotid, gets larger when feet are elevated - dark circle

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3
Q

thyroid on ultrasound

A

isthmus medially over trachea, lobes laterally, grainy gray

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4
Q

trachea on ultrasound

A

medial, dark circle, can see cartilage rings

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5
Q

clinical applications of neck ultrasound

A

anthosclerosis, putting in lines, cysts, tumors, thyroid / parathyroid / salivary gland abnormalities

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6
Q

ultrasound usage

A

top of screen = superficial, bottom of screen = deep, orient green dot to same side of body, square probe = deep, rectangular probe = shallower, transvaginal probe = long and thin, increasing usage

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7
Q

muscle receptors (sensory)

A

muscle spindles and golgi tendon organs

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8
Q

muscle spindles

A

sensory afferent, in intrafusal muscle fibers parallel with extrafusal fibers, noncontractile core, attached to contractile units on either end, 2 receptor types in center - 1. primary Ia annulospiral endings, 2. secondary II flower spray, spindle is innervated by gamma motor neurons

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9
Q

gogli tendon organ

A

sensory afferent, at junction of muscle and tendon, in series with extrafusal fibers

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10
Q

extrafusal muscle fibers

A

normal contractile muscle fibers, innervated by alpha motor neurons

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11
Q

intrafusal muscle fibers

A

contains muscle spindle, parallel to extrafusal fibers, innervated by gamma motor neurons

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12
Q

muscle spindles

A

sensory mechanoreceptor, stretch reflex - muscle contracts in response to moderate stretch

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13
Q

coactivation of alpha and gamma motorneurons

A

maintains activity in the spindle and tone in the muscle

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14
Q

golgi tendon organ

A

sensory mechanoreceptor, inverse stretch reflex - strong contraction is followed by muscle relaxation due to GTO activation of inhibitory interneuron

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15
Q

muscle spindle physiology

A

low activity if muscle is relaxed, muscle stretch causes spindle depolarization

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16
Q

muscle spindle primary type Ia response to muscle stretch

A

detect velocity of stretch in dynamic muscle contraction, phasic graded potential that declines with adaptation and theoretically hyperpolarizes completely on muscle contraction release (prevented by gamma motor neurons)

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17
Q

muscle spindle secondary type II response to muscle stretch

A

detect amplitude of stretch in static muscle contraction, graded potential that is tonic and does not adapt, does slightly hyperpolarize when contraction stops

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18
Q

stretch reflex

A

muscle spindle, monosynaptic, muscle stretch causes muscle and spindle contraction, 1. muscle stretches, 2. depolarization of spindle afferent, 3. activation of alpha and gamma motor neurons, 4. contraction of extrafusal fibers via alpha motor neurons stimulation, 5. intrafusal fibers contract to keep tension in spindle (like hair cell tip link adaptation motor) via gamma motor neuron stimulation for continued response - the spindle afferent itself is not contractile but the intrafusal fibers it is in are contractile - key in maintaining muscle tone

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19
Q

muscle tone

A

mediated by muscle spindle stretch reflex, tested by deep tendon reflex tests, if gamma motor neurons are defective = spastic effects

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20
Q

golgi tendon organ physiology

A

inverse stretch reflex, 1. tendon stretch causes gogli tendon depolarization, 2. activation of inhibitory interneuron, 3. decreased alpha and gamma motor neuron activity, 4. muscle relaxation

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21
Q

normal muscle spindle and golgi tendon organ function

A

systems work together to maintain muscle tone

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22
Q

elimination of alpha motor neurons

A

causes falccid paralysis because muscle fibers are not stimulated to contract

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23
Q

overactive gamma motor neurons

A

spastic paralysis due to muscle overcontraction, spindles tell alpha motor neurons to contract more

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24
Q

elimination of descending inhibition from motor cortex

A

spastic paralysis, too much tone in muscles

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25
Q

spinal reflexes - final common pathway

A

alpha motor neuron, not truly final, creates a spindle and GTO feedback loop instead

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26
Q

alpha motor neuron - spindle and GTO feedback loop

A

need because muscles are nonlinear force generators (only create optimal force vs stretch for short time during contraction), reflexes keep muscle in optimal force vs stretch range

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27
Q

reflex arc

A
  1. sensory receptor, 2. 1st order afferent neuron, 3. 1-3 CNS synapses, 4. motor neuron, 5. muscle - can have multiple components that create a complicated pathway and timed delay response in waves
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28
Q

stretch reflex

A

monosynaptic

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29
Q

inverse stretch reflex

A

trisynaptic

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30
Q

recurrent inhibition

A

afferent or motor neuron shuts itself off, ex: motor neuron making closed loop with renshaw cell that inhibits the motor neuron when the motor neuron sends an excitatory message - shuts off the original motor neuron and other touching the renshaw cell

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31
Q

scratch reflex in a dog

A

specific sensory stimulus is adequate for evoking a specific stereotyped response

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32
Q

lengthening reaction (contraction followed by relaxation)

A

light weight -> moderate stretch -> spindle fiber stretch reflex -> contraction that maintains the weight, heavier weight -> activated tendon receptors -> inverse stretch reflex -> muscle relaxation, modulated by gamma motor neurons, allows for controlled contraction with balanced tension

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33
Q

clasp knife reflex

A

problem in lengthening reaction (gamma motor neuron overactivity, spindle problem, decreased in descending inhibition)

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34
Q

withdrawal reflex

A

interaction between reflexes, noxious stimulus -> withdrawal of limb by contraction of flexors (monosynaptic pathway) and relaxation of extensors (disynaptic pathway with inhibitory interneuron)

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35
Q

crossed extensor

A

part of withdrawal reflex, extensors on other side of body contract to counter withdrawal reflex

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36
Q

reflex

A

first level of motor control, defined stimulus causing stereotyped response

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37
Q

spinal integration of motor control

A

built on underlying circuits

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38
Q

remove higher level motor control in circuit (upper motor neuron lesion)

A

behave of lower parts of the circuit becomes apparent, ex: descending control -> reflexes -> central pattern generator (stereotyped response) -> alpha motor neuron, remove higher CNS centers like motor cortex = reveals lower forms of control including nystagmus and clasp knife reflex

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39
Q

spinal cord lesion

A

reflexes and circuits below lesion remain intact, initially after spinal cord injury have period of spinal shock with no reflexes, eventually primitive and then more complicated reflexes return

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40
Q

Snellen test / chart

A

tests visual acuity with letter in rows of decreasing size, placed 20 ft from pt, tests cones in macula mostly

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41
Q

neurological injury and learning

A

easier to relearn something already learned than to learn for the first time after neurological injury

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42
Q

neurological injury and plasticity

A

plasticity - ability of brain to change or take on new function, highest at birth and decreases, improves recovery from neurological injury

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43
Q

ideal time for child neurological injury

A

3-7 years old, development and key learning have happened (language), plasticity is high

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44
Q

developmental stages

A

different anatomy, physiology, and disease onset - neonatal, toddler, childhood, adolescent, adult

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45
Q

timing of pediatric neurological lesions

A

congenital?, static?, progressive?, what is the lesion doing over time?

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46
Q

pediatric neurological H & P

A

hard, nonverbal pt, very observation base, rely on eyes / ears

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47
Q

newborns and locating neurological lesions

A

extrapyramidal system is in control because pyramidal system is not fully developed, extra pyramidal system is dominant first and bilateral, lesion may not show until pyramidal system starts to take over, ex: congenital stroke may not show until 6-12 months old

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48
Q

distinguishing CNS and PNS lesions

A

in both cases muscle tone is low, reflexes are present with CNS lesion, reflexes are not present with PNS lesion

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49
Q

pediatric neurologist tools

A

reflex hammer, play sets, legos, chalk board, eyes - watch reach/draw/squat/walk, ears - listen to speech

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50
Q

gower sign

A

climbing / pushing on things to stand up due to proximal muscle weakness

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51
Q

traction pull

A

pull on lower extremity, baby responds by flexing knee and hip

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52
Q

head control

A

watch head position and ability to hold it up in baby

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53
Q

vertical suspension

A

looks for proximal muscle tone in baby, hang baby vertically and baby pulls legs into sitting position

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54
Q

horizontal suspension

A

looks at pelvic tone and head control, hold baby horizontally under belly, head and butt should be even

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55
Q

galant sign

A

sensory, spine, stroke one side of spine and back will curve in response, should be gone by 4mnths

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56
Q

grasping

A

finger in baby palm hand should clench, foot does same but must distinguish from Babinski sign

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57
Q

thumbs and fisting

A

bad, sign of upper motor neuron spasticity, thumb inside fist abnormal, fist should open with Marrow startle response

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58
Q

rooting reflex

A

run finger on cheek, turn head and start to pucker

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59
Q

morrow repsonse

A

startle response, limbs should go out

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60
Q

skin

A

pediatric neurological exam, tells you a lot, ex: neurofibromatosis with cafe spots in groin and axial areas, myelomeningeocele (tuft of hair), hypomelaninosis of Ito - whorls of white spots on skin, Sturge-Weber with port wine stain in trigeminal region

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61
Q

growth charts

A

pediatric neurological exam, tells you a lot, ex: hydrocephalus (feel for bulging fontaneles), Angelman syndrome (underweight - eat little), Prader-Wili (over weight - eat lots), failure to thrive

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62
Q

basic motor control system

A

primary motor cortex -> ventral horn cells -> muscle, there are many other parts

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63
Q

motor control circuits

A

influence corticospinal tract, cerebellum and basal ganglia, to cortex via thalamus and back from cortex

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64
Q

brainstem motor control centers

A

indirect motor control centers and pathways because cortical motor pathways pass through them, ex: rubrospinal, vestibulospinal, and reticulospinal, tonically activate lower motor neurons esp. to axial and antigravity muscles, neurons in medial ventral horn

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65
Q

corticospinal tract

A

main influence on motor neurons to distal extremities (like hand and foot in lateral ventral horn)

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66
Q

corticospinal tract collaterals

A

modulate and control brainstem centers to create right amount of supporting tone without stiffness

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67
Q

upper motor neuron lesion

A

corticospinal tract and collaterals to brain stem motor nuclei, loss of direct effect on lower motor neurons and loss of control and modulation in brainstem control centers

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68
Q

upper motor neuron lesion clinical findings

A

findings due to loss of direct effect on lower motor neurons -> loss of lower strength, loss of lower dexterity, positive Babinski sign; findings due to loss of control of brain stem centers -> increased tone, hyperreflexia, clasp-knife phenomenon

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69
Q

lower motor neuron lesion clinical findings

A

final common motor neuron pathway, loss of strength, tone, and reflexes with denervated muscle wasting and hypersensitivity fasciculations

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70
Q

upper motor neuron syndrome

A

combination of loss of direct corticospinal tract and indirect brainstem motor control centers

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71
Q

decorticate posture

A

upper motor neuron lesion above red nucleus, thumb tucked, fisted fingers, pronation of forearm, flexion of elbow, lower extremity extension, foot inversion - red nucleus reinforces antigravity flexions of arms

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72
Q

decerebrate posture

A

upper motor neuron lesion below red nucleus and above vestibulospinal and reticulospinal nuclei, arm pronated, arm extended, lower extremity extended - antigravity flexion of red nucleus is gone and reticulospinal/vestibulospinal tract reinforce extension tone in upper and lower extremities

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73
Q

lesion in medulla

A

acutely flaccid, all brainstem motor nuclei and corticospinal tracts cut off, if pt were to survive tone would return via interneuronal spinal cord activity

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74
Q

localizing upper motor neuron lesions

A

above decussation of pyramids (crossing of corticospinal tracts) gives contralateral findings, below decussation of pyramids in spinal cord gives findings on ipsilateral side

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75
Q

spinal cord lesions

A

give upper motor neuron signs below the level of the lesion from effect on corticospinal tract, lower motor neuron signs at level of lesion from effect on ventral horn / nerve root - lower motor neuron signs are good for locating the level of a spinal cord lesion

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76
Q

motor system clinical testing

A

muscle strength, tone, reflexes, pathological reflexes

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77
Q

spasticity (clasp-knife phenomena)

A

type of hypertonia, upper motor neuron lesion, rate dependent resistance with collapse of resistance at end of range of motion

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78
Q

rigidity (lead pipe or plastic-like)

A

type of hypertonia, upper motor neuron lesion, basal ganglia disease, resistance constant throughout range of motion

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79
Q

acute upper motor neuron lesions / upper motor neuron lesions in infants

A

can produce hypotonia first, followed by hypertonia

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80
Q

motor cortical areas

A

frontal lobe - primary motor cortex (area 4), premotor cortex (area 6), supplementary motor cortex (area 6), frontal eye fields (area 8) - internal motor commands, deficits include loss of voluntary movement, paresis, increased tone/stretch reflexes, only way we can communicate

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81
Q

motor projections from motor cortex

A

corticobulbar, corticopontine, corticoreticular, corticospinal - to brainstem and spinal cord

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82
Q

connected to motor cortical areas, help control muscle tone

A

cerebellum, basal ganglia, descending systems

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83
Q

motor cortex characteristics

A
  1. agranular - poorly developed granular layers II and IV, well developed pyramidal layers III and V, giant pyramidal Betz cells in layer IV (cortex has 6 layers, sensory cortex has good granular layers), 2. low intensity stimulus evokes movement
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84
Q

functions of primary motor cortex

A
  1. control individual muscles/force as shown in stimulation studies, 2. control global aspects of movement like direction and amplitude of force - debated
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85
Q

primary motor cortex homunculus

A

lateral/temporal to medial - mouth, face, hand, arm, trunk, hip, leg, foot

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86
Q

primary motor cortex columnar organization

A

vertical columns with sharp boundaries down into cortex, control specific actions, ex: thumb flexion / adduction / abduction

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87
Q

afferent input into primary motor cortex

A

dorsal column nuclei and ventral posterior lateral/medial thalamus, cerebellum, basal ganglia, primary somatosensory cortex, premotor cortex, supplementary motor cortex, posterior partietal cortex (areas 5 and 7)

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88
Q

afferent input from dorsal column nuclei and ventral posterior lateral/medial thalamus to primary motor cortex

A

joint afferents, muscle spindle receptors (type Ia and II) length and velocity of contralateral muscle, cutaneous input from glaborous skin, primary motor cortex intergrates sensory information to execute movements

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89
Q

primary motor cortex outputs

A

from pyramidal neurons in primary motor / premotor / supplementary motor / somatosensory / posterior parietal / frontal eye fields to basal ganglia / red nucleus / pontine nuclei / reticular formation / cranial nerve nuclei / spinal cord; many axons, few are giant Betz cells from cortical layer IV, passes through pyramidal decussation, to lower motor neurons, part of reflex circuits, part of motor programs

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90
Q

primary motor cortex to basal ganglia

A

corticostriate

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91
Q

primary motor cortex to red nucleus

A

corticorubral, involves cerebellum too

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92
Q

primary motor cortex to pontine nuclei

A

corticopontine, involves cerebellum too

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93
Q

primary motor cortex to reticular formation

A

corticoreticular, tone and reflex control

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94
Q

primary motor cortex to cranial nerve nuclei

A

corticobulbar, clinically useful for CNS lesions

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95
Q

primary motor cortex to spinal cord

A

corticospinal

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96
Q

corticobulbar tract to trigeminal motor nucleus (CN V)

A

controls muscles of mastication via V3, medial to trigeminal chief sensory nucleus, in the midpons

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97
Q

corticobulbar tract to facial nucleus (CN VII)

A

lower face controlled by contralateral motor cortex (affected by stroke), upper face controlled by ipsilateral and contralateral cingulate motor cortex (not affected by stroke), facial nucleus is in caudal pons, lower face portion lateral, upper face portion medial

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98
Q

corticobulbar tract to nucleus ambiguus

A

primary motor cortex to laryngeal and upper airway, vagus and glossopharyngeal, bilateral connections, located in rostral medulla dorsal to inferior olive

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99
Q

corticobulbar tract to spinal accessory nerve in cervical spine

A

trapezius and strernocleidomastoid, shrugging shoulders and turning head to side opposite SCM, stronger ipsilateral than bilateral, terminates on cells in medial ventral horn in upper cervical spinal cord

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100
Q

corticobulbar tract to hypoglossal nucleus

A

tongue muscles, nucleus in dorsal rostral medulla in floor of 4th ventricle, stronger contralateral, some bilateral parts, tongue will deviate toward defective side

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101
Q

lower quadrant of face affected

A

lesion in lower face portion of CN VII nucleus

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102
Q

upper half of face affected

A

lesion in upper face portion of CN VII nucleus

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103
Q

frontal eye field

A

project to brainstem gaze centers that project to CN III, IV, and VI nuclei, voluntary eye movement control

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104
Q

corticospinal tract

A

motor cortex to spinal cord, terminates on dorsal horn / intermediate gray / ventral horn, single corticospinal axon diverges into alpha motor neurons of many muscle, corticospinal fibers cross to contralateral at pyramidal decussation, passes through internal capsule, cerebral crus, basilar pons, ventral fasiculus of spinal cord

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105
Q

primary motor cortex cells encode for muscle activation/force

A

experiment - chimp with extensor and flexor loads, specific motor cortex neuron only fires with flexor load and responding flexor action

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106
Q

primary motor cortex cells encode for movement direction

A

experiment - chimp with target in different directions, specific motor cortex neuron only fires in directional movement on one side of circle

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107
Q

population code and primary motor cortex

A

neurons broadly tuned to a movement parameter, fire as a population, each cell contributes to movement

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108
Q

robotic prosthetic arm and primary motor cortex

A

can use muscle and direction coding groups of cells to control robotic prosthetic arm via thoughts from motor cortex - without seeing the monkey can know what the monkey is doing

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109
Q

premotor cortex afferent input

A

prefrontal cortex, supplementary motor area, posterior parietal (area 5 and 7), cingulate motor area, cerebellum and basal ganglia via thalamus

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110
Q

premotor cortex efferent output

A

primary motor cortex (area 4), supplementary motor area, posterior parietal cortex, prefrontal cortex, basal ganglia, red nucleus in brainstem, corticospinal tract

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111
Q

premotor cortex stimulation

A

coordinates turning of contralateral eye and head, eyes go and head follows, synergistic movement - contralateral hand reaches and head turns to watch

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112
Q

premotor cortex functions

A

sensorimotor transformation (sensory cue into motor action), planning and learning, dorsal portion for arm, ventral portion for hand,

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113
Q

premotor cortex function experiment

A

monkey sees yellow block and plans to put hand on it when stimulus light goes on, while planning neurons fire and firing decreases after stimulus light goes on, same neuron is not involved in planning to move hand other direction

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114
Q

dorsal strea

A

pathway by which visual information moves from posterior to anterior via the occipital lobe / posterior parietal lobe / premotor and primary motor cortexes; allows for sensory cues to guide movement

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115
Q

ventral premotor cortex (hand)

A

controls higher levels of grasping, contains mirror neurons that fire when pt grasps or when pt watches another person grasp same object

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116
Q

mirror neurons

A

found in ventral premotor cortex, fire when pt grasps or when pt watches another person grasp same object, functions - imitation, action understanding (use motor system to understand actions of another person), intention (harmful?)

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117
Q

mirror neurons experiment

A

ventral premotor neurons fire when monkey grasps and when monkey watches another monkey or human grasp same object

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118
Q

supplementary motor cortex afferents

A

primary motor cortex (area 4), prefrontal cortex, posterior parietal, basal ganglia, cerebellum

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119
Q

supplementary motor cortex efferents

A

primary motor cortex (area 4), striatum, brainstem, corticospinal tract

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120
Q

supplementary motor cortex stimulation

A

contralateral limb movement across joints, related to postural changes

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121
Q

supplementary motor cortex functions

A

internal generation of movement, sequences of learned movements

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122
Q

supplementary motor cortex homunculus

A

leg most posterior, arm, face most anterior

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123
Q

experiment - involved in learned motor sequences

A

primary motor cortex, supplementary motor area - internally driven movement - part of muscle memory - athletes stimulate the supplementary motor area when they visualize doing something

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124
Q

experiment - not involved in motor action after sensory cue

A

primary motor cortex, premotor area - sensory driven movement

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125
Q

supplementary motor area and internally driven learned movements

A

neuron fires with specific learned sequence but not with same parts of sequence in different order

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126
Q

highly proficient tasks and supplementary motor area

A

as tasks become more proficient and better learned, supplementary motor area reduces activity and primary motor cortex assumes control

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127
Q

cerebellar vermis

A

along midline in cerebellum

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128
Q

cerebellar intermediate zone

A

lateral to vermis in cerebellum

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129
Q

cerebellar lateral zone

A

lateral to intermediate zone in cerebellum

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130
Q

deep cerebellar nuclei

A

lateral to medial - dentate, emboliform, globose, fastigial - don’t eat green frogs - also connected with vestibular nucleus

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131
Q

cerebellar peducles

A

superior, middle, inferior

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132
Q

cerebellar cortical layers

A

outer to inner, molecular, purkinje cell, granular

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133
Q

purkinje cells

A

output neuron of cerebellum, sends inhibitory GABA messages to cerebellar nuclei and vestibular nuclei, receives parallel (excitatory from granule cells) and climbing fiber input (excitatory from inferior olive), dendrites in molecular layer and cell body in purkinje cell layer

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134
Q

granule cells

A

cell body in granular cell layer with parallel fibers to purkinje cells, 1/2 of neurons in the brain, parallel fibers are excitatory with glutamate

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135
Q

inhibitory interneurons of cerebellum

A

Stellate, basket, and Golgi cells - all give off GABA - all excited by parallel fibers with glutamate

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136
Q

carabellar circuits

A
  1. mossy fibers -> granule cells -> purkinje cells, 2. cotralateral inferior olive -> climbing fiber -> purkinje cell, 3. purkinje cell -> cerebellar nuclei and medial / lateral vestibular nucleus, 4. cerebellar nuclei -> many CNS targets
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137
Q

cerebellar afferents

A

mossy fibers afferents and climbing fiber afferents

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138
Q

mossy fiber cerebellar afferents

A

many spinal and brainstem sites of origin, excitatory glutamate synapse with granular cells, produce simple spikes in purkinje cells, high firing frequency, encode temporal and intensity infromation, run in groups horizontally across cerebellum

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139
Q

climbing fiber cerebellar afferents

A

sole source is inferior olive, monosynaptic with purkinje cell, powerful excitation, produces complex spikes in purkinje cell, fires less often, encodes teaching signal, run in vertical groups on cerebellum

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140
Q

cerebellar organization

A

ipsilateral, left cerebellum = left side of body, right cerebellum = right side of body

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141
Q

cerebellar functional divisions

A

vestibulocerebellum, spinocerebellum, cerebrocerebellum

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142
Q

vestibulocerebellum

A

flocculonodular lobe and vermis zone

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143
Q

vestibulocerebellum afferents

A

via mossy fibers, semicircular canals, otoliths, visual (parietal/occipital to pontine nuclei)

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144
Q

vestibulocerebellum efferents

A
  1. medial / lateral vestibular and fastigial nuclei, 2. medial vestibulospinal tract (trunk/neck muscles), 3. lateral vestibulospinal tract (limb muscles), 4. gaze centers in brainstem (eye movements)
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145
Q

spinocerebellum

A

intermediate zone of cerebellum

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146
Q

spinocerebellum afferents / inputs

A

via mossy fibers to granular cells to parallel fibers, vestibular visual/auditory input, spinocerebellar tract inputs, facial somatosensory and proprioceptive input

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147
Q

dorsal spinocerebellar tract

A

spinocerebellar input, peripheral feedback - re-afferent information, in dorsal lateral fasiculus of spinal cord

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148
Q

ventral spinocerebellar tract

A

spinocerebellar input, provides info about state of spinal circuitry - efferent copy, relays muscle motor commands to other parts of nervous system, ventral lateral fasiculus of spinal cord

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149
Q

dorsal spinocerebellar tract path

A

cell body in Clark’s nucleus of dorsal horn, ascends on ipsilateral side into cerebellum via inferior cerebellar peduncle, ascends from cerebellum to ventral lateral and anterior thalamic nuclei to cerebral cortex

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150
Q

ventral spinocerebellar tract path

A

cell body in ventral horn, crosses to contralateral via anterior white commissure in spinal cord, ascends to rostral pons, crosses back to ipsilateral, descends to cerebellum in the superior cerebellar peduncle

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151
Q

rubrospinal tract

A

branch off dorsal spinocerebellar tract as it ascends from cerebellum, goes to red nucleus, descends in dorsal horn

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152
Q

spinocerebellum efferents / outputs - vermis

A

vermis projects to fastigial nucleus, enters reticulospinal tract and vestibulospinal tract

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153
Q

spinocerebellum efferents / outputs - intermediate zone

A

intermediate zone projects to globose and emboliform nuclei, which go to red nucleus that controls rubrospinal tract, goes ventral lateral thalamus and motor cortex that controls that corticospinal tract

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154
Q

cerebrocerebellum

A

lateral zones of cerebellar hemispheres

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155
Q

cerebrocerebellum afferents / inputs

A

pontine nuclei, sensory / motor / premotor / parietal cortices

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156
Q

cerebrocerebellum efferents / outputs

A

to dentate nuclei, projects to ventral lateral thalamic nucleus to motor and premotor cortex (controls corticospinal tract), to prefrontal cortex, to red nucleus (controls rubrospinal tract)

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157
Q

climbing fibers

A

from contralateral superior olive to purkinje cells in cerebellum, orthoganal (right angle) to parallel fibers, run in parasagittal (vertical), projections in cerebellum, source of complex spikes that are teaching signals

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158
Q

functions of the cerebellum

A

produces smooth/coordinated movement (problems in cerebellum cause decomposition of movements and dysmetria), times movements, motor learning, predicts consequences of motor action by receiving information about effects of movements and intended movement

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159
Q

motor learning in cerebellum

A

when presented with new motor learning, climbing fibers stimulate parallel fiber - purkinje cell synapse until learning has happened for a long time and then climbing fiber stimulation decreases giving way to long term depression

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160
Q

motor learning with vestibulo-oculo reflex

A

reflex allows eyes to stays on target even though head is moving, 2x magnifying glasses causes world to move more than head and world slips off fovea (retinal slip), climbing fibers are activated to vestibulocerebellum to reteach reflex, vestibulo-ocular reflex adjusts to magnifying glasses, during learning period climbing fibers cause vestibulo-oculo reflex to have an increased amplitude

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161
Q

long term depression of parallel fibers in cerebellum

A

after climbing fiber teaching for a long time climbing fiber stimulation decreases at synapse of parallel fiber - purkinje cell and synapse gets weaker

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162
Q

dorsal spinocerebellar tract

A

re-afferent about effect of movement, arises from Clarke’s nucleus, from legs and trunk, enters cerebellum through inferior cerebellar peduncle

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163
Q

ventral spinocerebellar tract

A

efference copy (info about intended movement to other parts of brain), arise from ventral horn, from legs and trunk, enters cerebullum through superior cerebellar peduncle

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164
Q

cuneocerebellar tract

A

re-afferent (effect of movement), arises from external cuneate nucleus, from arms, enters cerebellum through the inferior cerebellar peduncle

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165
Q

rostral spinocerebellar tract

A

efference copy (information about intended movement to rest of body), arises from ventral horn, from arms, enters cerebellum through interior cerebellar peduncle

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166
Q

cerebellum predicts consequences of motor action by…

A

comparing re-afferent messages from dorsal spinocerebellar tract (legs/trunk) and cuneocerebellar tract (arms) with efference copy (intended movement) information from ventral spinocerebellar tract (legs/trunk) and rostral spinocerebellar tract (arms) - learning via climbing fibers improves predictions

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167
Q

ethical obligation in field of medicine

A

Huntington case - state law that says that you are obligated to report pt who is a surgeon with Huntington, other law says that we are allowed to break confidentiality when there is a risk to public health (ex: bus driver with HD)

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168
Q

cerebellar output

A

from purkinje cells, has inhibitory synapse on deep cerebellar nuclei

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169
Q

layer V of primary motor cortex

A

contains medium-large pyramidal cells that give rise to corticospinal and corticobulbar axons that pass through ventral pons

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170
Q

neurological exam - station

A

pt should be able to stand with feet less than shoulder width apart

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171
Q

neurological exam - gait

A

normal walk, should be smooth and coordinated, upper extremities should move with walk

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172
Q

neurological exam - heel and toe walks

A

tests balance and strength in distal lower extremities

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173
Q

neurological exam - tandem gait

A

heel to toe walk on straight line, pt should be able to balance without falling or stepping aside

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174
Q

hemiplegic/hemiperetic gait

A

all on one side, extension of leg with internal rotation, shoulder adducted, elbow flexed, wrist pronated, fist with thumb tucked in

175
Q

diplegic/diperetic gait

A

on both sides of body, flexion at hip and knee, ankles extended and internally rotated, knees adducted, arms flexed - looks like swinging side to side, ex: cerebral palsy

176
Q

neuropathic gait - distal lower extremities effected

A

on both sides, inability to dorsiflex the foot (foot drop/drag if don’t step high enough), must raise foot high to clear floor, if unilateral is peripheral nerve injury, if bilateral is something like ALS

177
Q

myopathic gait

A

inability to stabilize the pelvis, pelivis dips toward nonweight bearing leg and hips look tilted, body/head leans toward weight bearing leg to centralize weight, aslo called Trendelenberg, can be caused by muscular dystrophy

178
Q

parkinson gait

A

hypokinetic gate, stooped, bent at waist, trouble initiating gate, small/shuffle steps that speed up to a finestrated gait, hands tremor, turn as though on a block in one place with little shuffles

179
Q

huntington gait

A

hyperkinetic gate, head randomly side to side, arms moving randomly, finger curling, shoulders up and down, legs kicking out to sides, back and forth at the hip

180
Q

ataxic gait

A

wide stance (trouble with normal narrow station), small jerks especially above waist, trouble with tandem walk - falling to sides, cerebellar lesion or drunken

181
Q

neuroaxis

A

all levels contribute to gait, look at upper and lower extremities,

182
Q

neurological exam - upper extremities

A

inspect for bulk and fasciculations, palpate for tenderness/consistency/contractures, tone - passive range of motion (flexion/extension at wrist/elbow), strength from proximal to ditsal and grade 0-5

183
Q

upper extremity strength testing

A

C5 - should extension, C6 - arm flexion, C7 - arm extension, C8 - wrist extension, T1 - hand grasp

184
Q

muscle strength grading

A

0 - no contraction, 1 - slight contraction no movement, 2 - full ROM without gravity, 3 - full ROM with gravity, 4 - full ROM and some resistance, 5 - full ROM and full resistance

185
Q

biceps DTR

A

C5-6

186
Q

brachioradialis DTR

A

C5-6

187
Q

triceps DTR

A

C7

188
Q

finger flexors

A

C8

189
Q

grading deep tendon reflexes

A

0 - absent, 1 - decreased, 2 - normal, 3 - brisk and excessive, 4 - with clonus

190
Q

pronator drift

A

extend arms in front with palms up and eyes closed, watch for pronation or downward drift of arm, indicates corticospinal tract disease if present

191
Q

neurological exam - lower extremities

A

inspect (bulk/fasciculation), palpate (tenderness/consistency/contractures), tone (passive range of motion in flexion/extension of ankle/knee), strength (proximal to distal, graded 0-5), deep tendon reflexes

192
Q

lower extremity strength testing

A

L2 - hip flexion, L3 - knee extension, L4 - knee flexion, L5 - ankle dorsiflexion, S1 - ankle plantar flexion

193
Q

lower extremity deep tendon reflex

A

L2-4 - patellar reflex, S1-2 achilles reflex

194
Q

plantar reflex

A

stroke skin on lateral sole heel to ball to great toe, flexion of all toes is normal, Babinski sign - abnormal extension of great toe and fanning of other toes

195
Q

pathological reflexes

A

reflex pattern that appears when there is damage to frontal lobes and inhibition of primitive reflex is absent

196
Q

snout reflex

A

press tongue blade against lips, abnormal - pouting of lips

197
Q

root reflex

A

stroke lateral upper lip, abnormal - move mouth toward stimuli

198
Q

palmomental reflex

A

stroke palm of hand, abnormal - contraction of ipsilateral mentalis muscle in lower lip

199
Q

lower extremities - upper leg and girdle strength

A

tested by squating and rising

200
Q

lower extremities - foreleg strength

A

tested by heel and toe walks

201
Q

skin sensation dermatomes

A

xxxxxxxxxxxxxx

202
Q

muscle dermatomes

A

xxxxxxxxxxxxxx

203
Q

neurological exam parts

A

mental status, cranial nerves, motor, sensory, reflexes, coordination, gait

204
Q

mental status exam

A

judgement (what would you do if…), orientation (person, place, time), intellect (name last presidents), memory (recall 3 words now and later), remote memory (past event), appearance (hygiene and dress), calculation (serial 3s)

205
Q

upper extremities muscle strength

A

bicep, tricep, deltoid, grip, wrist extension, thumb opposition, intrinsic hand muscles

206
Q

lower extremities muscle strength

A

hip flexion/extension, hip adduction/abduction, knee flexion/extension, foot dorsiflexion/plantar flexion

207
Q

deep tendon reflexes

A

bicep, tricep, brachioradialis, patellar, achilles

208
Q

Babinski

A

if present is positive, stroke lateral sole to ball to great toe, toes should flex, abnormal - toes flare/extend

209
Q

sensory

A

spinothalamic tract (pain and temp) - sharp/dull or coolness; dorsal column (touch, vibration, proprioception) - vibration with tuning fork or position of finger

210
Q

coordination

A

finger-nose-finger, heel-to-shin, rapid alternating movements

211
Q

gait

A

station, normal, tandem, heel, toe

212
Q

Romberg

A

standing with eyes closed for 20 sec w/out support, see if pt waivers to one side

213
Q

pronator drift

A

arms outstretched palms up, drift down suggests corticospinal defect, drift upward suggests position sense problem

214
Q

parts of basal ganglia

A

neostriatum, globus pallidus, substantia nigra, subthalamic nucleus

215
Q

neostriatum

A

receives major inputs, part of basal ganglia, made up of caudate and putamen nuclei - both have spiny neurons

216
Q

spiny neurons

A

in neostriatum (caudate, putamen), have many dendrites, receive major input, primary output, GABA neurotransmitter, two kinds - GABA/substance P and GABA/enkephalin

217
Q

afferent from cortex to neostriatum (corticostriate pathway)

A

cortex has excitatory effect on GABA/SP and GABA/ENK spiny cells in caudate/putamen with glutamate, afferent from premotor/primary motor/supplementary motor area cortices

218
Q

aspiny neurons

A

function as interneurons in neostriatum

219
Q

striatum to thalamus projection (direct pathway) - allows thalamus to act

A

cortex (glutamate/excitatory) -> striatal GABA/SP (GABA /inhibitory) -> globus pallidus internus (GABA/inhibitory) -> ventral anterior and ventral lateral thalamic nuclei via lenticular fasciculus -> returns to cortex as excitatory feedback loop

220
Q

striatum to brainstem projection

A

cortex (glutamate/excitatory) -> striatal GABA/SP (GABA /inhibitory) -> substantia nigra pars reticulata -> ventral anterior and ventral lateral thalamic nuclei via lenticular fasciculus and to brainstem -> superior colliculus for eye movements and pedunculopontine nuclei for locomotion (believed to be part of eye movement problem in parkinson)

221
Q

striatum to thalamus (indirect pathway) - suppresses thalamus

A

cortex (glutamate/excitatory) -> striatum GABA/ENK (GABA/inihibitory) -> globus pallidus externus (GABA/inhibitory) -> subthalamic nucleus (glutamate/excitatory) -> globus pallidus internus / substantia nigra reticulata (GABA/inhibitory) -> thalamus -> excitatory feedback loop to cortex

222
Q

cortex to thalamus (hyperdirect pathway - bypasses striatum) - fast way for cortex to suppresses thalamus

A

cortex (glutamate/excitatory) -> subthalamic nucleus (glutamate/excitatory) -> globus pallidus internus and substantia nigra reticulata (GABA/inhibitory) -> ventral anterior and ventral lateral thalamic nuclei -> excitatory feeback loop to cortex

223
Q

substantia nigra reticulata

A

GABA inhibitory to thalamus

224
Q

substania nigra compacta (dopamine loop)

A

striatum GABA/SP (GABA/inhibitory) via striatonigral projection -> substantia nigra compacta (dopamine) -> excitatory on striatum GABA/SP D1 receptors and inhibitory on striatum GABA/ENK D2 receptors

225
Q

dopamine and GABA/SP D1 receptors

A

excitatory, stimulates the direct pathway from striatum to thalamus allowing thalamus to act on movement, stimulates inhibition of dopamine loop

226
Q

dopamine and GABA/ENK D2 receptors

A

inhibitory, blocks indirection pathway from striatum to thalamus that inhibits the thalamus - allowing the thalamus to act on movement

227
Q

globus pallidus internus / substantia nigra reticulata

A

inhibitory to thalamus, tonically suppresses thalamus and motor activity

228
Q

motor activity

A

requires decreased globus pallidus internus activity so that thalamus is no longer inhibited

229
Q

direct pathway

A

facilitates movement by inhibiting globus pallidus internus that would normally inhibit the thalamus, cortex -> striatum -> globus pallidus internus

230
Q

indirect pathway

A

suppresses movement by suppressing the thalamus, cortex -> striatum -> globus pallidus externus -> subthalamic nucleus -> globus pallidus internus -> thalamus

231
Q

hyperdirect pathway

A

suppresses movement quickly by suppressing the thalamus, cortex -> subthalamic nucleus -> globus pallidus internus -> thalamus

232
Q

basal ganglia circuit example - eye movement via

A

frontal eye fields (excitatory/glutamate) -> caudate nucleus GABA/SP (GABA/inhibitory) -> substantia nigra reticulata (GABA/inhibitory) -> superior colliculus uninhibited (glutamate/excitatory) -> gaze centers in brainstem stimulated (saccade)

233
Q

effect of increased dopamine on direct pathway

A

inhibits GABA/ENK striatum, increasing globus pallidus externus output inhibitory output, excitatory action of subthalamic nucleus on globus pallidus internus decreased, globus pallidus internus is not stimulated to inhibit thalamus, thalamus is allowed to act on movement

234
Q

effect of increased dopamine on indirect pathway

A

excites GABA/SP striatum, increasing inhibition of globus pallidus internus, decreasing inhibition of thalamus - allowing thalamus to act on movement

235
Q

normal globus pallidus internus activity

A

creates inhibitory tonic balance in ventral anterior and ventral lateral thalamus

236
Q

increased dopamine levels (methanphetamine)

A

less excitation of globus pallidus internus by subthalamic nucleus, more inhibition of globus pallidus internus by striatum (putamen), overall less inhibition of ventral anterior and ventral lateral thalamus by globus pallidus internus = MORE MOTOR ACTIVITY

237
Q

movement selection and basal ganglia

A

basal ganglia circuit used to select movement based on reward, dopamine neurons provide estimate of reward

238
Q

postural tone

A

tonic muscle activity that opposes gravity, lower limb extensors, upper limb flexors, due to tonic activity of alpha motor neurons on extrafusal fibers, keep center of gravity directly above support surface, descending tracts and spinal reflexes work together to maintain center of mass

239
Q

increases tone

A

direct increased alpha motor neuron activity, increased gamma motor neuron activity in intrafusal spindle reflex causes increased alpha motor neuron activity via IA fibers

240
Q

vestibulospinal tract and postural tone

A

increases/decreases alpha motor neuron activity directly, medial vestibulospinal tract to axial muscles (neck/spine), lateral vestibulospinal tract to limb muscles, input from vestibular organs and cerebellum

241
Q

medial vestibulospinal tract

A

axial tonic muscle control via direct alpha motor neurons stimulation, starts in medial vestibular nucleus, decends in medial vestibulospinal tract, synpases on alpha motor neuron cell body in medial ventral horn

242
Q

lateral vestibular tract

A

appendicular tonic muscle control via direct alpha motor neurons stimulation, starts in lateral vestibular nucleus, decends in lateral vestibulospinal tract, synpases on alpha motor neuron cell body in lateral ventral horn

243
Q

alpha motor neuron

A

direct tonic muscle control, cell body in ventral horn

244
Q

reticulospinal tract

A

increases/decreases gamma and alpha motor neuron activity (gamma activity causes spindle to fire which causes alpha to fire), two descending systems - pontine reticular formation and medullary reticular formation - activity in this tract explains hypertonic/hyperreflexive changes in upper motor neuron syndrome

245
Q

pontine reticular formation

A

premotor/primary motor/primary sensory cortices -> contralateral pontine reticular formation -> descends in medial reticulospinal tract -> excitatory on gamma motor neuron in ventral horn

246
Q

medullary reticular formation

A

premotor/primary motor/primary sensory cortices -> contralateral medullary reticular formation -> descends in lateral reticulospinal tract -> inhibitory on gamma motor neurons; controls extensors - prevents from being hypertonic

247
Q

tilt head/surface up

A

example of vestibulospinal reflex, vestibulocollic refelxes act on neck, vestibulospinal reflexes act on limbs, neck flexion, arm flexion, extension of legs

248
Q

tilt head/surface down

A

extension of neck, extension of arms, flexion of legs

249
Q

rotation around spinal axial

A

vestibulospinal reflex

250
Q

head / body rolled to right

A

head rotates left, right limbs extend, left limbs flex

251
Q

head / body rolled to left

A

head rotates to right, left limbs extend, right limbs flex

252
Q

vestibulospinal reflex circuit

A

vestibular afferents -> vestibular nuclei -> vestibulospinal (limbs) and vestibulocollic (neck) tracts -> alpha motor neurons of neck and limbs

253
Q

spinal cord transection (spinal cord injury or cerebral palsy)

A

descending corticospinal/vestibulospinal/reticulospinal tracts cut, 1-2 months flaccid and no reflexes, after 2 months hyperreactive reflexes and hypertonic muscles (increased extensor tone), caused by denervation hypersensitivity and spinal interneurons filling void left by inactive descending neurons

254
Q

denervation hypersensitivity

A

leads to hyperreflexia and hypertonia with spinal cord transection, alpha motor neuron receptors upregulated and phosphorylated

255
Q

interneurons filling descending innervation void

A

leads to hyperreflexia and hypertonia with spinal cord transection, interneuron fron muscle spindle to alpha motor neuron grows more sprouts

256
Q

decerebration

A

lesion below red nucleus in spinal cord (mid-collicular), prevents cortex from inhibiting pontine reticular formation (excites gamma motor neuron) and stimulating medullary reticular formation (inhibits gamma motor neuron), allows pontine reticular formation to excite gamma motor neurons -> activating muscle spindle IA fibers -> activating alpha motor neurons -> tensing extensors in arms/legs/neck, sing of increasing pressure in brain, must relieve pressure, emergency

257
Q

removal of cerebral cortex control

A

increases gamma motor neuron activity because the pontine reticular formation is no longer inhibited and has an excitatory effect on gamma motor neurons, overactive stretch reflex and extensors tensed

258
Q

relief of abnormal tone

A

cut dorsal root where muscle spindle IA fiber enters to synapse with alpha motor neuron, used in cerebral palsy

259
Q

decortication

A

lesion above red nucleus, extension of legs, flexion of arms, disinhibition of red nucleus increases flexor motor neuron activity in cervical spine

260
Q

huntington epidemiology

A

1/10,000, white, 35-50 yrs, 1/3 clinical, 2/3 carriers, most common inherited neurodegenerative disorder, 100% penetrance, 15-20 year life expectancy after onset, causes of death - pneumonia, heart disease, falls, suicide, violence

261
Q

huntington gene (Htt)

A

large, widespread in peripheral tissue, expressed in neurons, essential for embyronic development, on chromosome 4

262
Q

huntington protein (Htt)

A

unique, found in many tissues and parts of cell, striatal neurons vulnerable, undergoes post-translational modifications, many functions of wild-type protein (transport, anchoring, signaling)

263
Q

huntington gene mapping project

A

1980s, Lake Maracaibo, Venezuela, Nancy Wexler - her mother had disease

264
Q

huntington gene mutation (Htt)

A

autosomal dominant, expanded CAG repeat in exon 1, CAG codes for glutamine (Q) - poly Q, mutation in germline but continues in somatic cells, normal poly Q < 35, 36-41 poly Q incomplete penetrance, 40-60 poly Q adult onset, >60 poly Q juvenile onset

265
Q

anticipation in huntington

A

age of onset decreases with successive generations, CAG repeat instability during meiosis (egg/sperm) and mitosis (sperm), anticipation more likely with paternal carrier due to higher rate of mutation in sperm

266
Q

huntington modifier genes

A

mostly size of CAG repeat dictates age of onset, but some modifier genes affect age of onset, GluR6 (kainate receptor) = 5 years earlier, ApoE modifies severity, E4 protectively increases age of onset, NMDA receptor variants influence severity

267
Q

sex of parent with huntington

A

earlier onset with paternal transmission

268
Q

environmental factors and huntington

A

omega-3 fish fatty acids protective, omega-6 red meat increased susceptibility, enrichment slows disease

269
Q

triple repeat diseases

A

9 neurodegenerative diseases with polyQ, all auto dominant except one, polyQ protein undergoes proteolytic cleavage liberatining toxic fragements, protein folding defects leading to inclusion aggregates, inverse correlation between number of repeats and age of onset

270
Q

cleavage of huntington protein Htt

A

cleaved by proteases, expanded polyQ in exon 1 enhances rate of protein cleavage nearby, cleaved wildtype Htt is degraded in cytoplasm, cleaved mutant Htt tranlocates to nucleus becoming trapped and forming protein aggregates from remaining toxic fragment, basketlike aggregate traps other proteins

271
Q

neurological inclusion bodies in huntington

A

protein aggregates, in striatum / cortex, appear before symptoms, possible protective against cell death, protective, or just end stage byproduct

272
Q

neurotoxic effects of huntington

A

transcription dysregulation, altered neurotransmitters and excitotoxicity, interferes with wildtype Htt, apoptosis, oxidative stress from mito dysfunction and altered metabolism, gain of function and loss of wildtype function (vesicle transport, synaptic function)

273
Q

clinical timeline in huntington

A

neuronal dysregulation long before motor defects which are long before cell death - psychiatric symptoms may preceded motor onset and cell death by 20 years

274
Q

dysregulation of transcription in huntington

A

altered transcription precedes neurodegeneration, mutant Htt inhibits DNA binding and transactivation of different transcription factors, major target is CBP (histone acetyltransferase) which inhibits transcription, possible Tx histone deacetylase inhibitor to counter effect of mutant Htt on chromatin condensation

275
Q

effects of huntington on neurons and neurotransmitters

A

NT alteration, loss of spiny neurons with GABAergic deficiency, upregulation of NMDA receptors causes exototoxicity (due to chronic glutamate exposure), neuronal cell death from overstimulation

276
Q

increased excitotoxicity in huntington

A
  1. increased glutamate, 2. reduced glia glutamate uptake, 3. hypersensitivity to NMDARs or increased mGluR signaling, 4. altered Ca intracellularly, 5. mitochondrial dysfunction
277
Q

interference with wildtype Htt in huntington

A

Htt needed for embyronic development, mutant can trap wildtype in nucleus or bind in cytoplasm, wildtype function loss leads to defected axonal transport and synaptic dysfunction

278
Q

apoptosis in huntington

A

end stage result, induced by mutant Htt, inhibition of mutant Htt cleavage reduces cell death

279
Q

oxidative stress and huntington

A

excitotoxicity causes huge release of Ca -> mitochondrial dysfunction -> release of cytochrome C -> caspase activation -> cell death, mutant Htt interfers with PGC-1alpha in mitochondrial membrane - may explain metabolic dysfunction of losing weight despite normal caloric intake

280
Q

huntington Tx strategies

A

inhibit protease, inhibit proteasome, inhibit misfolded protein, inhibit protein aggregation, inhibit autophagy of aggregates

281
Q

allele specific siRNA potential tx for huntington

A

siRNA can selectively degrade mRNAs that differe by one nucleotide, 3/4 HD pts heterozygous for panel of SNPs in Htt gene

282
Q

triple repeat diseases

A

9 neurodegenerative diseases with polyQ, all auto dominant except one, polyQ protein undergoes proteolytic cleavage liberatining toxic fragements, protein folding defects leading to inclusion aggregates, inverse correlation between number of repeats and age of onset

283
Q

cleavage of huntington protein Htt

A

cleaved by proteases, expanded polyQ in exon 1 enhances rate of protein cleavage nearby, cleaved wildtype Htt is degraded in cytoplasm, cleaved mutant Htt tranlocates to nucleus becoming trapped and forming protein aggregates from remaining toxic fragment, basketlike aggregate traps other proteins

284
Q

neurological inclusion bodies in huntington

A

protein aggregates, in striatum / cortex, appear before symptoms, possible protective against cell death, protective, or just end stage byproduct

285
Q

neurotoxic effects of huntington

A

transcription dysregulation, altered neurotransmitters and excitotoxicity, interferes with wildtype Htt, apoptosis, oxidative stress from mito dysfunction and altered metabolism, gain of function and loss of wildtype function (vesicle transport, synaptic function)

286
Q

clinical timeline in huntington

A

neuronal dysregulation long before motor defects which are long before cell death - psychiatric symptoms may preceded motor onset and cell death by 20 years

287
Q

dysregulation of transcription in huntington

A

altered transcription precedes neurodegeneration, mutant Htt inhibits DNA binding and transactivation of different transcription factors, major target is CBP (histone acetyltransferase) which inhibits transcription, possible Tx histone deacetylase inhibitor to counter effect of mutant Htt on chromatin condensation

288
Q

effects of huntington on neurons and neurotransmitters

A

NT alteration, loss of spiny neurons with GABAergic deficiency, upregulation of NMDA receptors causes exototoxicity (due to chronic glutamate exposure), neuronal cell death from overstimulation

289
Q

increased excitotoxicity in huntington

A
  1. increased glutamate, 2. reduced glia glutamate uptake, 3. hypersensitivity to NMDARs or increased mGluR signaling, 4. altered Ca intracellularly, 5. mitochondrial dysfunction
290
Q

interference with wildtype Htt in huntington

A

Htt needed for embyronic development, mutant can trap wildtype in nucleus or bind in cytoplasm, wildtype function loss leads to defected axonal transport and synaptic dysfunction

291
Q

apoptosis in huntington

A

end stage result, induced by mutant Htt, inhibition of mutant Htt cleavage reduces cell death

292
Q

oxidative stress and huntington

A

excitotoxicity causes huge release of Ca -> mitochondrial dysfunction -> release of cytochrome C -> caspase activation -> cell death, mutant Htt interfers with PGC-1alpha in mitochondrial membrane - may explain metabolic dysfunction of losing weight despite normal caloric intake

293
Q

huntington Tx strategies

A

inhibit protease, inhibit proteasome, inhibit misfolded protein, inhibit protein aggregation, inhibit autophagy of aggregates

294
Q

allele specific siRNA potential tx for huntington

A

siRNA can selectively degrade mRNAs that differe by one nucleotide, 3/4 HD pts heterozygous for panel of SNPs in Htt gene

295
Q

human genome project ELSI

A

ethical, legal, and social implications - use of info, privacy, confidentiality, stigam, reproductive issues, clinical concerns, testing and therapies, commercialization, patents

296
Q

sequence of events for child born to parent with huntington

A

diagnosis of parent, awareness of risk status, recognition of disease in older relatives, care for children and affected parent, death of effected parent and disability of pt if HD positive, observe siblings develop disease and manage own behavior if HD positive, surviving parent helps care for affected adult child and total dependence if HD positive, birth of pt’s grandchildren and pt’s death

297
Q

suicidal ideation

A

peaks prior to diagnosis by symptoms and again when managing HD behaviors

298
Q

predictive genetic testing

A

assess risk, intended to reduce morbidity and mortality, valuable if there is prevention or tx , can be pre-natal to assure non-affected child

299
Q

huntington predictive testing

A

38+ repeats of Htt gene = 100% chance of getting HD, no tx, personal choid with psycho-social implications, pre and post counseling needed, only 5% choice predictive test

300
Q

huntington exclusionary testing

A

embryos created in vitro, only unaffected embryos implanted, mother/father is never told their HD status

301
Q

clincal issues with huntington

A

pregnancy/children, psychological, family dynamics, advice/counseling

302
Q

huntington and beneficence

A

do good when possible, knowledge is power, planning life

303
Q

huntington and non-maleficence

A

do no harm, emotional, family, social, privacy, confidentiality, indeterminate tests (lower number of CAG repeats <38), when will disease develop

304
Q

huntington and autonomy

A

informed consent before testing, only test after age 18, prenantal testing - mother decides what happens to her body

305
Q

huntington and justice

A

do greatest good for greatest number, is it ethical to test for disease that has no cure, cost of test ($300 diagnostic, $1000 predictive), genetic discrimination

306
Q

triad of huntington symptoms

A

motor - chorea/impersistence/hypotonia/hyperreflexia/dystonia/akinetic-rigid; psychiatric - irritability/depression/agitation/delusions/personality change/suicidal ideation (7% of HD pts); cognitive - dementia/loss of processing speed/executive dysfunction/attention/retrieval/visual-spatial

307
Q

huntington clinical additional symptoms

A

impaired visual saccades with normal smooth pursuit, weight loss, cachexia

308
Q

juvenile huntington symptoms

A

myoclonus, seizures, like parkinsons, cognitive change, chorea often absent

309
Q

huntington diagnosis

A

family hx - none in 8% of cases, paternal anticipation, physical exam, genetic testing, neuroimaging - caudate atrophy

310
Q

huntington tx

A

there are no disease modifying agents, but there are tx given to lessen symptoms

311
Q

memory enhancing drugs

A

amphetamines, aderol

312
Q

synapse development

A

do form in absence of transmission (as in fetus), but transmission is needed to establish final connections

313
Q

strengthen synapses

A

presynaptic and postsynaptic neurons firing simultaneously

314
Q

weakens synapses

A

presynaptic and postsynaptic activities not linked

315
Q

main learning and memory neurotransmitter

A

glutamate

316
Q

main learning and memory receptors

A

metabotrophic glutamate receptor, ionotrophic - AMPA and NMDA receptors

317
Q

NMDA receptors

A

blocked by Mg2+ at neg resting potential, if presynaptic glutamate release and postsynaptic depolarization coincide Mg2+ is displaced and Ca2+ enters cell - enhances synaptic effectiveness

318
Q

long term potentiation

A

post synpatic response increases to new level following NMDA receptor stimulation because additional AMPA receptors are trafficked to the cell membrane/synapse

319
Q

long term depression

A

weak NMDA receptor activation causes AMPA receptors to be internalized from cell membrane/synapse

320
Q

memory and learning

A

adaptive change in response to environmental input

321
Q

learning

A

acquisition of new information

322
Q

memory

A

retention of learned information

323
Q

memory consolidation

A

sensory input -> short term memory -> consolidation -> long term memory; process of protein synthesis that is inhibited by protein synthesis inhibitors

324
Q

engrum

A

location where memory is residing, some area of brain important to memory formation, memory is an assembly of connected cells

325
Q

H.M. case study

A

seizures, removed hippocampus and rhinal cortex in medial temporal lobe - lost a lot of memory

326
Q

animal memory models

A

sea slugs and fruit flies, identified gene mutations in fruit flies that prevented learning, Ddc, amnesiac, rutabaga, dunce

327
Q

Dcd mutation

A

prevents conversion of L-DOPA into dopamine and 5-hydroxytryptophan into serotonin

328
Q

rutabaga mutation

A

prevents ATP being turned into cAMP

329
Q

dunce mutation

A

prevents cAMP being turned into AMP by phosphodiesterase - which prevents the activation of protein kinase

330
Q

molecular short term memory

A

5HT binds receptor, cAMP phosphorylates protein kinase which opens K+ and Ca2+ channels

331
Q

molecular long term memory

A

transcription factor CREB1 is activated by phosphorylation by protein kinase and removal of CREB2 by MAP kinase, the gene CRE is transcribed early, the genes CAAT and TAAC are transcribed late, proteins are produced for synaptic growth

332
Q

over expression of CaM kinase II

A

enhances activity of protein kinase A, more CREB1 transcription factor phosphorylated, smarter

333
Q

protein kinase M zeta

A

involved in maintenance of late long term potentiation and memory, transcription of gene brought on by NMDA receptor stimulation, Ca inflow, and kinase activation

334
Q

ZIP

A

peptide that abolishes long term potentiation in hippocampus by inhibiting protein kinase M zeta that acts at AMPA receptors, possible tx for PTSD

335
Q

genes linked to intelligence in humans

A

IGF2R, higher IQ with mutation of cathespin D (CTSD), Alzheimers linked to CHRM2 (none = smarter, 1 copy = middle, 2 copies = lowest)

336
Q

four questions for localizing lesions

A

what level is the lesion at - what side is the lesion on - mass / non-mass / indeterminate - pathology

337
Q

what level is the lesion at

A

supratentorial (cerebral and diencephalon), posterior fossa (brainstem, cerebellum), spinal/vertebral, peripheral (plexus, nerves), multiple levels

338
Q

what side is the lesion on

A

right focal, left focal, midline focal, diffuse non-focal

339
Q

is the lesion mass

A

mass - focal and progressive, ex: hematoma / abscess / neoplasm, expansion and compression of tissues

340
Q

is the lesion non-mass

A

focal and non-progressive ex: infarct OR diffuse and progressive ex: meningitis

341
Q

is the lesion indeterminate

A

transient ex: transient ischemic attack

342
Q

lesion temporal profile

A

time over which maximum signs and symptoms develop

343
Q

vascular temporal profile

A

acute, < 24 hours, ex: hematoma

344
Q

inflammatory temporal profile

A

subacute, 1 day - 1 month, ex: meningitis

345
Q

neoplasm temporal profile

A

chronic, >1 month and focal, ex: astrocytoma

346
Q

degenerative temporal profile

A

chronic > 1 month and diffuse, ex: parkinson

347
Q

other causes of brain defects

A

intoxication, congenital, allergic/autoimmune, traumatic, endocrine/metabolic

348
Q

acute, focal, progressive

A

mass, vascular, hematoma

349
Q

subacute, focal, progressive

A

mass, inflammatory, abscess or granuloma

350
Q

chronic, focal, progressive

A

mass, neoplasm

351
Q

acute, focal, non-progressive

A

non-mass, vascular, infarct

352
Q

acute, diffuse, progressive

A

non-mass, vascular, subarachnoid hemorrhage, anoxia

353
Q

subacute, diffuse, progressive

A

non-mass, inflammatory, meningitis, encephalitis

354
Q

chronic, diffuse, progressive

A

non-mass, degenerative

355
Q

diffuse

A

suggest non-mass

356
Q

intersegmetal findings

A

involve major sensory ascending or descending motor pathways, broader effect

357
Q

segmental findings

A

specific components of CNS of PNS, localizing value

358
Q

midbrain

A

CN III / IV

359
Q

pons

A

CN V / VI / VII / VIII

360
Q

medulla

A

CN IX / X / XI / XII

361
Q

brachial plexus

A

C5-T1

362
Q

sacral plexus

A

L2-S3

363
Q

nipple

A

T4

364
Q

umbillicus

A

T10

365
Q

supratentorial

A

right / left cerebral hemispheres

366
Q

posterior fossa

A

cerebellum and brainstem, cranial nerves

367
Q

upper extremity segments

A

C5-T1

368
Q

thoracic/abdominal segments

A

T1-T12

369
Q

lower extremity segments

A

L2-S3

370
Q

sphincter segments

A

S2-S4

371
Q

supratentorial lesion

A

deficits on contralateral head and body

372
Q

posterior fossa lesion

A

ipsilateral head and contralateral body

373
Q

spinal cord lesion

A

ipsilateral (touch) and contralateral (pain/temp) body

374
Q

peripheral nerve lesion

A

ipsilateral body

375
Q

limbic system controls

A

mood, emotion, feelings, motivation, critical for memory

376
Q

difficult to study limbic system

A

all structures anatomically interconnected, hard to measure physiological response

377
Q

limbic system is clinically relevant because…

A

> 50% of pts Tx for mood disorder

378
Q

structures of limbic system

A

amygdala, hippocampus, septal nuclei, nucleus accumbens, medial prefrontal cortex, anterior cingulate cortex, ventral tegmental area, anterior and dorsomedial thalamic nuclei, mammillary nuclei

379
Q

hippocampus to mammillary bodies and septal nuclei

A

limbic pathway, large C shaped via the fornix

380
Q

mammillary body to anterior thalamic nucleus

A

limbic pathway, mamilla-thalamic tract

381
Q

amygdala to septal nuclei

A

limbic pathway, called stria terminalis

382
Q

midbrain to forebrain

A

limbic pathway, via medial forebrain bundle

383
Q

hypothalamus to brain stem / spinal cord

A

limbic pathway, via dorsal longitudinal fasciculus

384
Q

anterior thalamic nuclei to anterior cingulate gyrus and medial prefrontal cortex

A

limbic pathway, via anterior limb of the internal capsule

385
Q

all limbic circuits pass through…

A

hypothalamus, way to connect to autonomic and neuroendocrine pathways

386
Q

limbic innervation

A

monoaminergic and cholinergic axons

387
Q

norephinephrine in limbic system

A

released by locus ceruleus in pons, to cerebellum, brainstem, cortex

388
Q

serotonin in limbic system

A

released by raphe nuclei in pons and midbrain, to cerebellum, brainstem, cortex

389
Q

dopamine in limbic system

A

released by ventral tegmental area (VTA) in the mesolimbic system, from midbrain medial to substantia nigra to limbic system parts (nucleus accumbens, medial prefrontal cortex, amygdala, spetal nuclei)

390
Q

dopamine

A

reward

391
Q

addiction

A

dopamine plays a role due to role in reward

392
Q

cocaine

A

blocks dopamine reuptake

393
Q

amphetamine

A

blocks dopamine reuptake and increases dopamine release

394
Q

lesion of ventral tegmental area / nucleus accumbens / dopamine receptor antagonist

A

decrease drug seeking behaviors

395
Q

natural dopamine rewards

A

food, sex, exercise, produce dopamine reward through mesolimbic system

396
Q

Tx addiction through mesolimbic reward system

A

reduces response to natural rewards

397
Q

acetylcholine

A

released by nucleus basalis and septal nucleus in limbic system to hippocampus, loss of cholinergic neurons in early Alzheimers

398
Q

amygdala

A

fear conditioning, increased activity with conditioned stimulus, lesion = no fear conditioning, inability to pair unconditioned and conditioned stimuli

399
Q

prefrontal cortex

A

Phineas Gage, lesion = loss of goal directed behavior, increased impulsiveness, loss of moral reasoning, prefrontal cortex inhibits amygdala which excites the hypothalamus

400
Q

dorsolateral prefrontal cortex

A

working memory for planning

401
Q

orbital frontal cortex

A

inhibitory output to the amygdala for emotional control

402
Q

hippocampus

A

lesion of hippocampus = anterograde amnesia (no new memories), temporally graded retrograde amnesia (lost memories 2-3 years before surgery, earlier memories intact), lost explicit/declarative memory (facts / events), did not lose implicit procedural nondeclarative memory (motor skills)

403
Q

medial midbrain CN

A

CN III ventrally, CN IV dorsally

404
Q

dorsal medial midbrain

A

CN III, descending pyramidal system with motor tracts, medial lemniscus with ascending sensory tracts

405
Q

lateral midbrain

A

spinothalamic tract, reticulospinal tract

406
Q

medial pons CN

A

CN VI

407
Q

medial pons

A

CN VI, pyramidal system with descending motor tracts, medial lemniscus with ascending sensory tracts

408
Q

lateral pons CN

A

CN V, CN VII, CN VIII

409
Q

lateral pons

A

ascending spinothalamic tract, descending reticulospinal tract, spinal tract of CN V

410
Q

medial medulla CN

A

CN XII

411
Q

medial medulla

A

CN XII, descending pyramidal motor tracts, ascending medial lemniscus sensory tract

412
Q

lateral medulla

A

CN IX, CN X, ascending spinothalamic tract, descending reticulospinal tract, descending spinal tract of CN V

413
Q

rigidity

A

inflexibility and stiffness, resistance to passive stretch, clasp knife or lead pipe

414
Q

dystonia

A

constant muscle contraction, often with pain

415
Q

positive symptoms of parkinson / huntington

A

gain of function, lead pipe rigidity, cogwheel rigidity, athetosis (can’t maintain posture), dystonia (involuntary contraction), chorea, ballismus (violent flinging of arms)

416
Q

negative symptoms of parkinson / huntington

A

loss of function, akinesia, bradykinesia, masked facies, dystonia

417
Q

schizophrenia postive symptoms

A

gain of function, hallucinations, dellusions

418
Q

schizophrenia negative symptoms

A

loss of function, social withdrawal

419
Q

resting tremor

A

parkinson, over-inhibition of thalamus by globus pallidus externus internus and substantia nigra reticulata, causes thalamic cells to go into osscilatory firing, disappears with action

420
Q

intention tremor

A

MS, depressive substance withdrawal, with deliberate movement inadequate motor signaling during voluntary movement

421
Q

nausea from parkinson tx (levodopa)

A

dopamine stimulates chemoreceptor trigger center in CNS, dopamine activates peripheral dopamine receptors - goes away with increased carbadopa

422
Q

myerson’s sign

A

normal - can stop blinking when tapping on forehead, abnormal - can’t stop blinking when tapping on forehead

423
Q

myerson’s sign pathway

A

cortex -> basal ganglia -> cortex -> motor nuclei; basal ganglia normally inhibit, in parkinson basal ganglia inhibition is gone

424
Q

direct basal ganglia motor circuit

A

increases motor activity by uninhibiting the thalamus

425
Q

indirect basal ganglia motor circuit

A

decreases motor activity by inhibiting the thalamus

426
Q

dopamine basal ganglia motor circuit

A

dopamine released by sunstantia nigra compacta, excites the direct pathway, inhibits indirect pathway - overall: motor activity increased with dopamine input

427
Q

hyperkinetic disorder

A

direct pathway excited, indirect pathway inhibited, thalamus uninhibited = more motor activity, dyskinesia and ballismus, huntington

428
Q

hypokinetic disorder

A

direct pathway inhibited, indirect pathway activated, thalamus inhibited = less motor activity, bradykinesia, akinesia, parkinson

429
Q

parkinson tx model

A

imbalance of dopamine / ACh, low dopamine, can tx dopamine deficiency or use ACh receptor antagonist, interneurons signal spiny neurons with ACh, substantia nigra compacta signals spiny neurons with dopamine

430
Q

hypothalamus functions

A

maintains homeostasis (receptor -> hypothalamus -> dorsal longitudinal fasciculus -> brainstem / spinal cord), integrate information for control of endocrine/autonomic/neural system - attached to pituitary gland

431
Q

pituitary gland

A

sella turcica in sphenoid bone - stability

432
Q

anterior pituitary gland

A

adenophysis - endoderm origin, pars tuberalis and distalis

433
Q

posterior pituitary gland

A

neurophysis - ectoderm origin, infundibular stalk and posterior lobe

434
Q

median eminence

A

infundibulum from hypothalamus to pituitary gland

Week 4 - Neuro (5 decks)

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