Neuro Block 3

Front 1

3 levels of control for motor systems

Back 1

-cerebral cortex
-brainstem
-spinal cord (ventral horn grey matter)

Front 2

Subcortical structures the modulate motor systems

Back 2

-basal ganglia (caudate nucleus, putamen, etc)
-cerebellum (motor learning)

Front 3

thalamus and motor info

Back 3

-relay system for info from
basal ganglia--> cortex
and
cerebellum--> cortex

Front 4

spinal cord role in motor systems

Back 4

- execute movement
-bottom of hierarchy
-motor neurons and interneurons

Front 5

lower motor neurons

Back 5

-in ventral horn, project to muscles and ultimately cause muscle contraction
-somatotopics: medial=proximal mm; laterla= distal mm

Front 6

Interneurons from spinal cord

Back 6

-in intermediate zone btw dorsal and ventral horns
-segmental (project within a level) and propriospinal (project between levels to motor neurons)
-form circuits that help connect and coordinate motor neurons that contract groups of muscles for specific tasks

Front 7

brainstem role in motor systems

Back 7

- modulates the action of spinal motor circuits
- motor nuclei with motor neurons that directly innerv facial mm
-groups on neurons that project down and terminate on neurons in spinal cord grey matter -- upper motor neurons --> medial and lateral descending brainstem pathways

Front 8

medial brainstem pathways

Back 8

-reticulospinal, vestibulospinal, tectospinal tracts
-descend in medial ventral white matter and terminate in ventromedial area of ventral spinal cord
-axial, proximal mm for basic postural control

Front 9

lateral brainstem pathways

Back 9

-rubrospinal tract
-descends in dorsolateral white matter and temrinates in dorsolateral area of the ventral horn
-distal muscles of limbs for goal-directed limb movements like reaching and manipulating

Front 10

cerebral cortex and motor systems

Back 10

-modulates action of motor neurons in the brainstem and spinal cord
-top of hierarchy
-gives ability to organize complex motor acts
-primary motor cortex, premotor cortex, supplementary motor area
-also primary somatosensory cortex and posterior parietal cortex

Front 11

primary motor cortex

Back 11

-executes commands to motor neurons-- command center
-coordinates force and direction
-somatotopic map
-contralateral

Front 12

premotor cortex

Back 12

-integrates motor movements with sensory input (mainly from visual system)
-coordinates complex sequences of movement (motor learning)

Front 13

Supplemental motor area

Back 13

-internally-driven, will-driven movements
-planning
-will have an increase in blood flow just thinking about performing a complex action

Front 14

primary somatosensory cortex (SI)

Back 14

-regulates incoming sensory info in the dorsal horn

Front 15

posterior parietal cortex

Back 15

-helps localize where an object is with respect to body
(helps motor system reach in correct direction for an object)

Front 16

Cerebral cortex acts on motor neurons via:

Back 16

-two descending pathways
-lateral corticospinal
-ventral corticospinal

Front 17

lateral corticospinal tract

Back 17

-descending pathway from cortex to contralateral limb/digits
-goal-directed reaching

Front 18

ventral corticospinal tract

Back 18

-descending pathways from cortex to neck/trunk muscles
-postural control

Front 19

hierarchy of motor systems

Back 19

-cortex--> brainstem--> spinal cord--> muscle movement
-lower structures=more simple tasks like reflexes
-cognitive motor= slow, but more options

Front 20

parallel motor systems

Back 20

-motor pathway between cortex and spinal cord
-motor pathways between cortex-brainstem-spinal cord
-if one is lesioned, other can partially compensate
-redundancy gives flexibility and plasticity

Front 21

3 general types of movements

Back 21

-reflex
-automatic postural adjustments
-voluntary movements

Front 22

Reflex movement

Back 22

-simple, involuntary coordinated patterns of muscle contract and relax d/t peripheral stimuli
-spinal cord, motor neurons, sensory neurons, brainstem neurons sometimes

Front 23

Automatic postural adjustments

Back 23

-more complex and flexible than reflexes
-involve brainstem, spinal cord, motor neurons
-posture info to vestibular system--> descending pathways from brainstem to spinal cord make compensatory shifts
-contextual controlled

Front 24

voluntary movements

Back 24

-goal-directed
-cerebral cortex, brainstem, spinal cord, motor neurons
-most complex and flexible
-improve with practice
-much longer response time

Front 25

skeletal muscle

Back 25

-execute vol movement, maintain posture, produce heat and metabolic energy
-parallel bundles of fascicles- fascicles made of fibers

Front 26

Motor unit

Back 26

-one motor neuron and all of the muscle fibers it innervates
-smallest functional element of the motor system
-provides smallest increment of tension that can be generated

Front 27

alpha and gamma motor neurons

Back 27

-alpha: extrafusal muscle fibers
-gamma: muscle spindles

Front 28

motor units in normal muscle

Back 28

-motor neuron innervates many muscle fibers in DIFF fascicles within one muscle
-efficiently activate entire muscle
-recruit more units as more force is needed to create smooth movement

Front 29

what does the CNS recognize with regards to muscle

Back 29

-motor units-- uses them as increments of force generation to produce smooth, fluid, energy-efficient movement

Front 30

Motor unit innervating many muscle fibers within ONE fascicle

Back 30

-indicates pathology where deinnervation-reinnervation occurred
-produces jerky movements that are too powerful for force needed

Front 31

Electromyogram

Back 31

-record motor unit action potentials while patient contracts muscles
-a large single motor unit can mean denervation-reinnervation

Front 32

neuropathic disorders on EMG

Back 32

-fasciculations
-denervation causes adjacent neurons to sprout and innervate larger area--> larger motor units
-large EMG
-reduced interference pattern because of reduced total number of motor units

Front 33

Motor neuron organization

Back 33

-in vertical columns called motor nucleus
-motor neurons innervating same muscle are found in same motor nucleus
-1 muscle can be innervated by many motor neurons in one nucleus

Front 34

medial motor nuclei

Back 34

-axial muscles of neck, back
-connect across many segments by propriospinal neurons (long axons, branch extensively)

Front 35

lateral motor nuclei

Back 35

-limb muscles
-most medial innerv proximal limb muscles
-most lateral innerv distal limb mm
-connected across few segments by propriospinal neurons (short axons, less branching)

Front 36

flexors and extensors

Back 36

-flexors closer to center of spinal cord
-extensors are more peripheral

Front 37

upper motor neurons

Back 37

-neurons that originate in brainstem and motor cortex
-descend and synapse on lower motor neurons to convey descending control of movement
-"premotor" neurons

Front 38

upper motor lesions

Back 38

-weakness
-no atrophy
-no fasciculations
-increased reflexes and tone

Front 39

lower motor lesions

Back 39

-weakness
-atrophy
-fasciculations
-decreased relfexes and tone

Front 40

slow-twitch motor units

Back 40

-innerv red, slow, type 1 fibers
-smaller fibers, small MN, slow contraction
-oxidative metabolism: use glucose and O2 via mitoch and myoglobin
-small tension for long duration without fatigue

Front 41

fast fatigable motor units

Back 41

-innerv white, fast type IIb fibers
-large fibers, large MNs
-fast, large contraction
-anaerobic catabolism from glycogen stores-- lactic acid
-specialized for speed and strength

Front 42

fast fatigue-resistant motor units

Back 42

-innerv intermed IIa fibers
-combines fast twitch with enough aerobic capacity to resist fatigue for several minutes
-exercise with endurance

Front 43

ultimate force exerted depends on:

Back 43

-rate of firing (freq of APs in a single MN)
-recruitment (number of motor units firing)
-size principle

Front 44

Size principle

Back 44

-smallest motor units fire first (low threshold for firing)
-largest motor units fire last (high threshold for firing)

Front 45

Motor unit recruitment order

Back 45

-smallest-->largest
-small force: slow twitch fibers recruited
-more force: fast fatigue-resist units recruited
-max force: fast fatigable units
-fibers stop firing in reverse order

Front 46

advantages of size principle

Back 46

-allows a smooth increase in force output by muscle
-minimizes fatigue
-keeps power in reserve until needed
-allow appropriate recruitment of fibers for job

Front 47

general components of a reflex

Back 47

-sense status of muscle via spindles and golgi tendon organs
-cause an effect via efferent motor neurons
-sometimes modify info via interneurons and descending neurons

Front 48

muscle spindle

Back 48

-parallel to extrafusal fibers
-sense muscle LENGTH
-key for proprioception
-discharge best when muscle is stretched
-silent when muscle shortens
-composed of intrafusal fibers

Front 49

types of intrafusal fibers

Back 49

-dynamic nuclear bag fibers: sense change in length
-static nuclear bag fibers and nuclear chain fibers: sense steady response over time

Front 50

Ia afferents

Back 50

-innervate all 3 types of intrafusal fibers
-sense muscle length and rate of change of length
-convey fast, phasic, dynamic response of muscle fibers
-velocity of stretch, very sensitive to small changes

Front 51

II afferent (spindle)

Back 51

-innervate static bag and nuclear chain fibers
-sense muscle length, not rate
-convey slow, tonic, static responses
-code duration of stretch

Front 52

when intrafusal fibers are stretched....

Back 52

-sensory endings are stretched and increase firing rate

(when fibers are not stretched, sensory endings stop firing)

Front 53

why do we need dynamic and static intrafusal fibers in the muscle spindle

Back 53

-need to know angle of joint
-dynamic sense when muscle is changing and static fibers sense when muscle has stabilized at a new length
-both are sensitive to small changes
-CNS uses muscle spindles to sense and correctly change position of body segments

Front 54

golgi tendon organ

Back 54

-@ jx btw extrafusal muscle fibers and tendon
-sense muscle TENSION
-innervated by a single Ib afferent neuron which branches and intertwines with collagen fibers

Front 55

golgi tendon organ and muscle contraction

Back 55

-stretches tendon--> straightens collagen--> compress nerve endings--> AP firing
-very sensitive
-precisely measures force in contracting muscle

Front 56

why do we need golgi tendon organs

Back 56

-continuously measure tension from force in a contracting muscle
-gives NS precise info about state of contraction
-protects muscle from too much muscle tension

Front 57

gamma motor neurons

Back 57

-dynamic: innervate dynamic nuclear bag fibers
-static: innervate static nuclear bag and nuclear chain fibers
-activation causes shortening of intrafusal fibers, stretches central region of intrafusal fibers, increases firing of afferent fibers

Front 58

role of gamma motor neurons

Back 58

-adjust dynamic and static sensitivity of muscle spindle and their afferents
-keep spindles sensitive

Front 59

alpha-gamma co-activation

Back 59

-both are activated during voluntary movement
-maintains spindle sensitivity
-automatically maintains muscle spindle sensitivity over all muscle lengths

Front 60

Monosynaptic excitatory reflex (deep tendon reflex)

Back 60

-stim= stretch of muscle increases its length--> activation of spindles
-afferent= Ia from spindle
-spinal cord=Ia to alpha MNs that control same muscle and project to/excite synergistic mm
-efferent= alpha MNs fire and cause contraction of homoymous and synergistic mm

Front 61

why do we need the monosynaptic reflex

Back 61

-maintain muscle tone for posture
-allows us to hold still
-smooths out movements
-increases efficiency for locomotion

Front 62

Flexion and crossed extension reflex (Flexor Reflex)

Back 62

-role= withdrawal from painful stimulus; polysynaptic
-stim=activation of Ad nociceptors
-spinal cord=nociceptors excite ipsi flexors and inhibit extensors; interneurons cross cord and excite contra extensors and inhibit flexors

Front 63

Golgi tendon reflex

Back 63

-inhibits alpha MN via inhibitory interneuron
-stim= tensions on Golgi tendon activates Ib inhib interneuron--> inhibits original muscle that was stretched = autogenic inhibition
-adjust forces (ie picking up a delicate object wo/crushing it) and prevents overly forceful movements

Front 64

Inhibitory interneurons modulating spinal reflexes

Back 64

-help coordinate reflex actions
-mediate reciprocal innervation
-receive many convergent inputs from muscle afferents and descending pathways

Front 65

inhibitory interneurons in stretch reflex

Back 65

-Ia interneurons inhibit antagonist muscles

Front 66

inhibitory interneurons in golgi tendon reflex

Back 66

-Ib interneurons receive input from Golgi tendon organs, muscle spindles, joint, and cutaneous receptors and descending pathways
-inhibit agonist muscles

Front 67

descending control modulating spinal reflexes

Back 67

-regulate the strength of reflex by changing the tonic level of activity
-sites for modulation: alpha MNs, interneurons, and presynaptic terminals of afferent fibers

Front 68

myopathic diseases

Back 68

diseases arising from intrinsic abnormalities in the skeletal muscle (ie DMD)

Front 69

neuropathy

Back 69

diseases that cause abnormalities in peripheral nerves; symptoms more pronounced distally

Front 70

neurogenic

Back 70

disease that interrupts normal innervation of muscle (dennerv or reinnerv); abnormality in muscle is secondary to abnormality in nerve; ie guillain-barre

Front 71

Duchenne's

Back 71

most common for children; xlinked recessive; usually onset at walking age

Front 72

Duchenne's clinical symptoms

Back 72

waddling or lurching; muscle wasting; lordosis; scoliosis; contractures in gastrocnemius

Front 73

Duchenne's diagnostic test

Back 73

Gowers maneuver-- push up from ground; high creatine kinase in blood before clinical symptoms

Front 74

Duchenne's cause

Back 74

lack of gene for protein dystrophin which anchors actin in cytoskel membrane to stabilize sarcolemma, allowing influx of Ca2+ and necrosis

Front 75

Duchenne's treatment

Back 75

no cure; PT, surgery, corticosteroids to slow rate of muscle degeneration

Front 76

Myasthenia gravis- autoimmune form pathophysiology

Back 76

-ab's made against nicotinic Ach RECEPTOR;
-cross links receptors and triggers internalization and degradation of receptor;
-reduced junctional fold size, larger synaptic cleft

Front 77

Myasthenia gravis net effect of reduced functional Ach receptors

Back 77

-reduced amplitude of end-plate potentials;
-APs fails to fire in some muscles;
-Ach depletes with repeated firing;
-muscle power is reduced

Front 78

mysathenia gravis clinical symptoms

Back 78

-weakness and fatigue in muscles esp cranial and oropharyngeal like ptosis;
-unstable or waddling gait;
-severity varies over day and day-day;
-assoc with other autoimmune diseases

Front 79

Myasthenia gravis and thymus gland

Back 79

-tumors;
-lymphocytes in thymus produce ab's against Ach receptor;
-myoid cells in thymus express Ach receptors and are antigenic

Front 80

Myasthenia gravis treatment

Back 80

-Achase inhibitors;
-corticosteroids to suppress ab production;
-plasmaphoresis to remove ab's

Front 81

disorders of lower motor neurons

Back 81

atrophy, fasciculations, decreased muscle tone, loss of tendon reflexes (weak, wasted, twitching muscles)

Front 82

disorders of upper motor neurons

Back 82

spasticity, overactive tendon reflexes, abnormal plantar extension reflex (Babinski)

Front 83

Amyotrophic lateral sclerosis

Back 83

progressive degeneration of both upper and lower MN's; hardness from proliferation of astrocytes, scarring of lateral columns of spinal cord

Front 84

pathophysiology of ALS

Back 84

-disease of corticospinal tracts;
-loss of MN's in ventral horn of spinal cord;
-loss of motor nuclei in lower brainstem;
-loss of Betz and pyramidal cells in layer V of cortex;
-usually spares ocular muscles and bladder sphincters

Front 85

spinal cord of ALS

Back 85

-lightened lateral and ventral corticospinal tract and ventral horn indicating loss of neuronal cell bodies

Front 86

ALS symptoms

Back 86

-Upper (spasticity, hyperreflexemia, Babinski, dysarthria- slow clumsy speech, dysphagia);
-Lower (progressive weakness, atrophy, fasciculations, cramps);
-brainstem MN's (resp muscle weakness/fatigue, head droop);
-pseudobulbar affect

Front 87

ALS causes

Back 87

-unknown, could be accumulation of oxidative free radicals, 90% die within 6 years of onset

Front 88

ALS treatment

Back 88

-riluzole: blocks glutamine release to protect MN's;
-neurotrophic/GFs, antioxidants

Front 89

Guillain-Barre

Back 89

-acute inflamm demyelinating polyneuropathy;
- often 1-2 weeks after viral infection

Front 90

G-B pathophysiology

Back 90

-inflamm cells and ab's attack myelin sheath around peripheral nerves --> myelin breaks down --> axons damaged

Front 91

G-B symptoms

Back 91

-paresthesia, rapid onset loss of motor in legs/arms; weakness/paralysis of breathing muscles;
-loss of stretch reflex

Front 92

G-B causes

Back 92

-unknown, may be microbial resp or GI infection, autoimmune mechanisms, inappropriate activation of immune system by virus/bact

Front 93

G-B treatment

Back 93

plasmaphoresis; most recover weeks to months and return to normal life

Front 94

Ataxia

Back 94

-lack of order
-uncoordinated movements indicating cerebellar injury

Front 95

Cerebellum blood supply

Back 95

-Superior cerebellar a
-PICA
-AICA

Front 96

Cerebellar lobes

Back 96

-Anterior (in front of primary fissure)
-Posterior (behind primary fissure, with tonsils)
-Flocconodular lobe (1 nodule part of vermis, 2 flocculi-- separated from posterior lobe by posterolateral fissure)

Front 97

Flocculonodular lobe

Back 97

-1 nodule, 2 flocculi
-forms the vestibulocerebellum
-control of equilibrium, balance, and eye movements (VOR)

Front 98

Vermis

Back 98

-along the midline
-part of the spinocerebeelum → control of axial and proximal limb movements

Front 99

Intermed zone of cerebellar hemisphere

Back 99

-part of spinocerebellum
-controls distal limb movement

Front 100

Lateral zone of cerebellar hemisphere

Back 100

-part of cerebrocerebellum
-planning and initiation of movements

Front 101

5 major cell types of cerebellum

Back 101

-Purkinje cells, granule cells, golgi cells, basket cells, stellate cells

Front 102

Purkinje cells

Back 102

-inhibitory
-major output neurons of cerebellar cortex
-largest neurons in brain

Front 103

Granule Cells

Back 103

-excitatory
-only cell type in cerebellum thats excitatory

Front 104

Basket cells

Back 104

-inhibitory
-inhibit Purkinje cell bodies

Front 105

Golgi cells

Back 105

-inhibitory

Front 106

Stellate cells

Back 106

-inhibitory
-inhibit Purkinje cell dendrites

Front 107

Climbing fibers

Back 107

--one afferent fiber type in cerebellum
-from contralateral inferior olivary nucleus

Front 108

Mossy fibers

Back 108

-one afferent fiber type in cerebellum
-from all sources except contralateral inferior olivary nucleus

Front 109

Molecular layer of cerebellum

Back 109

-dendrites of Purkinje cells
-parallel fibers from axons of granule cells (excitatory)
-climbing fibers from inf olivary nucleus (excitatory)
- stellate cells (inhibit Purkinje cell dendrites)
-basket cells (inhibit Purkinje cell bodies)

Front 110

Purkinje layer of cerebellum

Back 110

-Purkinje cells- inhibitory, GABA

Front 111

Granular cell layer of cerebellum

Back 111

-Granule cells- excitatory
-Golgi cells- inhibitory (inhibit synpase btw mossy fiber input)
-Mossy fiber (excitatory)- glomeruli

Front 112

Deep cerebellar nucleus

Back 112

-Major output neurons of the cerebellum
-Excitatory

Front 113

Where do deep cerebellar nuclei receive input from?

Back 113

-Receive collaterals from extrinsic afferents to cerebellar cortex
-receive input from the cerebellar cortex

Front 114

Dendate nucleus

Back 114

-largest
-most lateral

Front 115

Emboliform and Globose nuclei

Back 115

-part of interposed nuclei

Front 116

Fastigial nucleus

Back 116

most medial

Front 117

climbing fibers synaptic circuits

Back 117

- climbing fibers (excitatory) → Purkinje cells (inhibitory) → deep cerebellar nuclei

Front 118

mossy fibers synaptic circuits

Back 118

- mossy fibers (excitatory) → granule cells (excitatory) → parallel fibers (excitatory) → Purkinje cells (inhibitory) → deep cerebellar nuclei

Front 119

inhibitory interneurons

Back 119

-Basket and stellate cells in the molecular layer
-Golgi cells in the granule cell layer

Front 120

Major cerebellar afferent: vestibular nuclei

Back 120

- vestibular nuclei → vestibulocerebellum
-from ipsilateral vestibular labyrinth and vestibular nuclei to vestibulocerebellum or flocculonodular lobe

Front 121

Major cerebellar afferent: visual centers

Back 121

- superior colliculus and visual cortex → pons → vestibulocerebellum to control eye movements

Front 122

Inferior cerebellar peduncle (restiform body)

Back 122

-spinal cord → spinocerebellum
-dorsal spinocerebellar tract (from ipsilateral spinal cord and lower medulla)
-cuneocerebellar track (from ipsilateral spinal cord and lower medulla → upper arm and neck info)
-olivocerebellar tract (from CONTRAlateral inf olivary nucleus)

Front 123

Superior cerebellar peduncle (brachium conjunctivum)

Back 123

-spinal cord → spinocerebellum
-Ventral spinocerebellar tract (from CONTRAlateral spinal cord, projects to contralateral spinocerebellum)

Front 124

Lesion of superior cerebellar peduncle

Back 124

-double crossing results in ipsilateral effects

Front 125

Middle cerebellar peduncle (brachium pontis)

Back 125

-cortex → cerebrocerebellum
-cortico-ponto-cerebellar tract → cerebrocerebellum (from contralateral cortex, via pontine nuclei to cerebrocerebellum)

Front 126

Monoaminergic fibers from the brainstem

Back 126

-serotoninergic fibers from raphe nuclei (along midline)
-noradrenergic fibers fro locus ceruleus

Front 127

Major cerebellar efferent: floccuonodular lobe

Back 127

-flocc lobe → vestibular nuclei
-reciprocal connections
-controls eye movements and body equil while standing or moving

Front 128

Major cerebellar efferent: cerebellar cortex

Back 128

- cerebellar cortex → deep cerebellar nuclei → superior cerebellar peduncle
-input from neck and trunk
-vermis → fastigial nucleus → brainstem regions → medial descending systems → axial and proximal muscles
-vermis → fastigial nucleus → thalamus → motor and premotor cortex
-axial and proximal motor control
-control ongoing execution of movement

Front 129

Major cerebellar efferent: intermediate zones

Back 129

-input from limbs
-intermediate zones → interposed nucleus → brainstem regions (red nucleus) → laterla descending tract → distal limb muscles
-intermed zones → interposed nucleus → thalamus → motor and premotor cortex → corticospinal tract → distal limb muscles
-distal motor control; controls ongoing execution of movements

Front 130

Major cerebellar efferent: lateral zones

Back 130

-lateral zones → dentate nucleus → red nucleus or directly → thalamus → motor and premotor cortex → corticospinal tract → spinal cord or corticopontine tract → back to lateral zone
-initiation, planning, timing of voluntary movements

Front 131

General functional significance of cerebellum

Back 131

-control of balance and eye movement
-regulates movement and posture indirectly by modulating the output of major descending motor systems
-compares intention with actual movement and compensates for errors
-function is changed by experience- motor learning

Front 132

Corticopontocerebellar tract

Back 132

-how cerebellum receives info about plans for movement from motor and premotor cortex

Front 133

Ventral spinocerebellar tract

Back 133

-how the cerebellum monitors the integration of descending and peripheral info regarding movement in the spinal cord

Front 134

Dorsal spinocerebellar tract

Back 134

-how the cerebellum receives feedback info from sensory periphery

Front 135

Dentatorubrothalamic tract

Back 135

-how the cerebellum projects to motor centers that send fibers to the spinal cord to adjust output of the motor system

Front 136

Cerebellar lesions

Back 136

-disruption of coordinated limb and eye movements, impaired balance, reduced muscle tone
-IPSIlateral
-can impair motor learning
-ataxia, hypotonia, intentional tremor, dysdiadochokinesia, dysmetria, nystagmus, titubation

Front 137

Components of basal ganglia

Back 137

-striatum (caudate nucleus and putamen)
-globus pallidus (GPi and GPe)
-subthalamic nucleus
-substantia nigra (SNc and SNr)
-nucleus accumbens

Front 138

Basal ganglia blood supply

Back 138

-anterior cerebral
-middle cerebral
-posterior communicating

Front 139

Basal ganglia direct pathway

Back 139

-Striatum (GABA and substance P) → inhibits Gpi and Snr (GABA) → less inhibition → thalamus → premotor and SMA
-thalamus is disinhibited (excited) = movement facilitated

Front 140

Basal ganglia indirect pathway

Back 140

-striatum (GABA and enkephalin) → inhibits Gpe (GABA) → no inhibition of subthalamic nucleus (glutatmate) → activates Gpe, Gpi, and Snr (GABA) → inhibit thalamus → premotor and SMA
-thalamus is inhibited = movement inhibited

Front 141

Nigrostriatal pathway

Back 141

-dopaminergic
-facilitates movement by acting on both direct and indirect pathways

Front 142

Dopamine effect on D1 dopamine receptors

Back 142

-involved in exciting the direct pathway → facilitates movement

Front 143

Dopamine effect on D2 dopamine receptors

Back 143

-involved in inhibiting the indirect pathway → facilitates movement

Front 144

Acetylcholine in striatum

Back 144

-only acts within striatum
-inhibits direct pathway and excited indirect → inhibition of movement
-Huntington's = Ach path destroyed so no inhibition of movement

Front 145

Extrinsic inputs to basal ganglia come from:

Back 145

-cerebral cortex (motor, sensory, association, limbic): topographical projections, corticospinal pathway
-intralaminar nuclei of thalamus (topographic, thalamostriate pathway)
-terminate in striatum

Front 146

Extrinsic output from basal ganglia

Back 146

-arise from globus pallidus and SNr
-project to motor nuclei of thalamus or superior colliculus of midbrain (for eye movement)

Front 147

Caudate and putamen connections within basal ganglia

Back 147

-project to globus pallidus (striatopallidal pathway)
-reciprocally connected with substantia nigra (SNc → striatum → SNr)

Front 148

Subthalamic nucleus connections within basal ganglia

Back 148

-receives input from the motor and premotor cortices
-reciprocally connected with the globus pallidus
-projects to SNr

Front 149

Substantia nigra connections within basal ganglia

Back 149

-receives info and projects to striatum

Front 150

General functional significance of basal ganglia

Back 150

-regulates movement through direct and indirect connections with cerebral cortex
-forms major component of extrapyramidal motor system
-involved in control of eye movements and in the memory of orientation in space
-contributes to cognition
-related to limbic functions

Front 151

Basal ganglia disorders causes

Back 151

-usually a disruption of transmitter metabloism
-abnormal movements are often from release of system from inhibition

Front 152

Symptoms of basal ganglia disorder

Back 152

-involuntary movements: tremor at rest, athetosis, chorea, ballism, dystonia
-akinesia and bradykinesia
-changes in posture and muscle tone, muscular rigidity

Front 153

Parkinson's

Back 153

-disease of basal ganglia
-degeneration of dopaminergic cells in Snc
-tremor at rest, rigidity, bradykinesia

Front 154

Huntington's

Back 154

-degeneration of cholinergic and GABAergic neurons in the striatum
-inherited, mutation in chrom 4 causing lots fo CAG repeats
-chorea, athetosis, dystonia

Front 155

Tardive dyskinesis

Back 155

-results from longterm use of antipsychotic agents that block dopamine transmission
-involuntary movement of tongue and face

Front 156

Hemiballismus

Back 156

-lesion of subthalamic nucleus
-uncontrollable “ball-throwing” movement
-contralateral

Front 157

Cerebellum and spinal cord

Back 157

-direct input
-no direct output

Front 158

Basal ganglia and spinal cord

Back 158

-no input or direct output

Front 159

Cortex input and cerebellum vs basal ganglia

Back 159

-cerebellum: indirect input from cortex
-basal ganglia: direct input from cortex

Front 160

Output of cerebellum/ basal ganglia

Back 160

-cerebellum: excitatory
-basal ganglia: inhibitory

Front 161

Cerebellar lesion in general

Back 161

-ipsilateral symptoms
-ataxia, impaired balance, intentional tremor

Front 162

Basal ganglia lesion in general

Back 162

-often contralateral symptoms, or bilateral
-too much or too little movements
-tremor at rest

Front 163

Basal ganglia general function

Back 163

-planning and execution of complex motor strategies
-amplitude and velocity of movements

Front 164

Cerebellum general function

Back 164

-coordinates the execution of movements
-compares intended with executed

Front 165

Cerebellum integration

Back 165

-integrates input from multiple regions of cortex, brainstem, and spinal cord
-vision, proprioception, muscle strength, muscle tone, vestibular, pressure

Front 166

Patients with a suspected cerebellar disorder must first be examined to rule out:

Back 166

-muscle weakness
-vestibular dysfunction
-impaired proprioception

Front 167

Appendicular ataxia

Back 167

-agonist/antagonist muscles aren't coordinated
-movements are jerky, irregular, not smooth
-affected extremity is IPSIlateral to cerebellar lesion

Front 168

Dysdiadochokinesia

Back 168

-pt is asked to rapidly alternate one hand between supination and pronation
-pts with cerebellar disorder will be clumsy with the hand that is IPSIlateral to the lesion

Front 169

Titubation

Back 169

-patients are unable to sit upright
-unable to coordinate agonist/antagonist muscles of trunk to maintain an upright posture
-irregular, jerky movements of head and thorax
-localizes lesion to vermis/flocculonodular lobe (midline lesion)

Front 170

Suppression of VOR

Back 170

-VOR is normally suppressed by vermis when you are watching a moving object so you can continue to fixate on it

Front 171

Impaired suppression of VOR

Back 171

-midline cerebellar lesions
-can't suppress VOR → unable to fixate on a moving object without it becoming blurred from intermittent triggering of the VOR

Front 172

Gait imbalance

Back 172

-patients have wobbly and erratic gaits due to combinations of leg ataxia and impaired suppression of VOR

Front 173

Scanning dysarthria

Back 173

-Patients asked to repeat multi-syllable words
-Cerebellar dysfunction will mean clipped words, slight hesitations between each syllable

Front 174

Examples of cerebellar disorders

Back 174

-tumors (ie hemangioblastoma)
-ischemic stroke (ie embolism to PICA)
-hemorrhage (ie secondary to arterio-venous malformation)
-infectino (ie abscess)
-atrophy (ie alcoholic or idiopathic)

Front 175

Pt with ischemic stroke, ataxia of R upper extremity and R lower extremity, cannot suppress VOR when object moves from R to L, what was damaged?

Back 175

-R lateral cerebellar hemisphere and L vermis

Front 176

R cerebellar injury, can't watch vehicles moving in which direction?

Back 176

Left to Right

Front 177

Lesion in basal ganglia direct pathway

Back 177

Hypokinesis (no thalamus stimulation)

Front 178

Lesion in basal ganglia indirect pathway

Back 178

Hyperkinesis (no thalamus inhibition)

Front 179

Gross pathological changes seen in Huntington's

Back 179

-caudate and putamen atrophied
-very large ventricles (butterfly shaped instead of boomerang)
-indirect pathway problems → hyperkinetic

Front 180

Events in lesion in indirect pathway

Back 180

dec GABA from striatum → more active Gpe → inc GABA from Gpe → inhibits STN → less glutamate release by STN → inhibits Gpi → no GABA release from Gpi → thalamus is not inhibited → hyperkinesis

Front 181

Huntington's disease characteristics

Back 181

-progressive
-invol movements, chorea, athetosis
-memory loss and cognitive dysfunction
-psychiatric disturbances
-autosomal dominant

Front 182

Parkinson's clinical triad

Back 182

-Tremor at rest (resolves with kinesis)
-rigidity
-bradykinesis

Front 183

Parkinson's characteristics and treatment

Back 183

- loss of dopaminergic neurons in the Snc
-treated with dopamine-replacing medications to improve bradykinesia

Front 184

What kind of surgery can be performed for bradykinesia and rigidity?

Back 184

-Pallidotomy: Create lesion to indirect pathway by burning globus pallidus
or
-Deep brain stimulation: inhibits STN, facilitates movement

Front 185

What kind of surgery can be performed for severe tremor?

Back 185

-Thalamotomy
-Create lesion on thalamus to dampen excessive movement

Front 186

Motor circuits in spinal cord are regulated by input from:

Back 186

-primary motor cortex
-prefrontal cortex
-somatosensory and parietal assoc cortex
-basal ganglia
-cerebellum
-thalamus
-brainstem

Front 187

Lateral motor pathways

Back 187

-goal directed limb movement
-lateral corticospinal tract
-rubrospinal tract

Front 188

Medial motor pathways

Back 188

-posture, head and neck movement, eye movement
-Ant. corticospinal tract
-Lat vestibulospinal tract
-Med vestibulospinal tract
-corticotectal and tectospinal tract
-reticulospinal tract

Front 189

Somatotopy of primary motor cortex

Back 189

-feet-legs-hip-trunk-arm-hand-forehead-chin-tongue

-disproportionally large representation for hand for fine motor movements

Front 190

Corticospinal tract main characteristics

Back 190

-primary motor cortex connects to alpha LMNs
-innervate particular muscle for voluntary control of distal extremities
-allows for skilled movements
-excites flexors
-inhibits extensors

Front 191

CST axons arise from...

Back 191

-primary motor cortex
-Betz cells
-premotor cortex and supplementary motor cortex
-parietal lobe

Front 192

CST axons pass through...

Back 192

-corona radiata
-post limb of internal capsule
-middle of cerebral peduncle (crus cerebri)
-medullary pyramids

Front 193

Where do 90% of CST fibers descend-- Lateral CST?

Back 193

-in pyramidal decussation and descend in lateral funiculus to all sp cd levels

Front 194

Where do 10% of CST fibers descend-- Medial CST?

Back 194

-do NOT decussate in pyramids
-descend in anterior funiculus
-decussate in ventral white commissure to thoracic spinal cord

Front 195

What do lesions to CST above pyramidal decussation result in?

Back 195

- CONTRAlateral weakness

Front 196

What do CST lesions BELOW the pyramidal decussation result in?

Back 196

IPSIlateral weakness

Front 197

CST lesion in cortex

Back 197

-contralateral paresis of a particular part of body corresponding to area of cortical damage

Front 198

CST lesion in the posterior limb of internal capsule

Back 198

-contralateral hemiplegia

Front 199

CST lesion in the cerebral peduncle (crus cerebri)

Back 199

-Weber Syndrome (occlusion of PCA)
-contralateral paralysis of lower face, tongue, arm, leg
-ipsilateral CN III damage (eye deviates laterally, ptosis, pupil dilated and fixed)

Front 200

Possible cause of Weber syndrome

Back 200

-occlusion of PCA

Front 201

CST lesion in medullary pyramid

Back 201

-medial medullary syndrome (occlusion of ant spinal or vertebral aa)
-contralateral hemiparesis, sparing face
-ipsilateral CN XII lesion (paralysis and atrophy of tongue)
-medial lemniscus injury (contralateral loss of touch, vibration, proprioception)

Front 202

CST lesion in spinal cord

Back 202

-ipsilateral spastic paralysis
-ipsilateral Babinski sign

Front 203

Rubrospinal tract function

Back 203

-cerebral cortex and cerebellum indirectly influence motor activity in the spinal cord
-excites motor neurons innervating distal flexors in upper limb

Front 204

Red nucleus

Back 204

-locates in tegmentum of midbrain at sup colliculus
-receives input from cortex and cerebellar nuclei

Front 205

Where does rubrospinal tract decussate and descend?

Back 205

-decussates in ventral tegmentum
-descends in lateral brainstem and lateral funiculus (intermingles with corticospinal tract)

Front 206

Where does the rubrospinal tract project to and terminate?

Back 206

-projects to spinal cord and brainstem nuclei
-terminates directly and indirectly on alpha-LMNs and gamma-LMNs

Front 207

Decorticate Posturing/rigidity

Back 207

-injury to cerebral cortex or internal capsule
-upper limbs flexed at elbow, lower limbs extended
-no cortical input to red nucleus
-do have cerebellar input to red nuc and rubrospinal tract

Front 208

Benedikt's syndrome

Back 208

-unilateral lesion of red nucleus
-CN III injury (ipsilateral occulomotor injury)
-contralateral tremor

Front 209

T1-weighted MRI

Back 209

-shows anatomical resolution highest
-good grey/white matter differentiation
-not as good at showing some types of pathology
-called SPGR also

Front 210

Fluid Attenuated Inversion Recovery (FLAIR) image

Back 210

-multiparameter imaging
-highlights tumors better
-also show edema
-less defined grey/white matter

Front 211

Threshold FLAIR + SPGR

Back 211

-allows detailed anatomy from SPGR and better image of tumor from FLAIR overlayed

Front 212

Functional MRI

Back 212

-highly localized changes in blood flow and oxygenation that are driven by changes in the net neural activity due to a sensory, motor, or cognitive event

Front 213

Blood Oxygenation Level Dependent (BOLD) mech for fMRI

Back 213

-neural activty--> local vasodilation --> highly oxygenated Hb
-water protons within blood are induced to emit radio freq that are high when the local magnetic field created by the scanner is undisturbed but are low when the local field is disrupted by presence of highly oxygenated Hb
-thus, neural activity --> increased blood flow--> removes poorly oxyg Hb --> allows protons to emit strong signal

Front 214

Caveats to BOLD fMRI

Back 214

-how neural activity triggers the blood flow change is not fully understood
-fMRI signals are slow compared to neural events

Front 215

fMRI mapping of the visual field

Back 215

-visual stim consisting of flickering, checkered annulus slowly expands
-colors identify locations in the visual field not the amplitude of the fMRI response

Front 216

MRI and "no-fly zone"

Back 216

-grey and white matter structures within 5-10 mm of a resection site are likely to be at risk for damage caused by the surgery

Front 217

Therapeutic brain stimulation

Back 217

-use 3D CT scans to show a set of 6 surface markers to guide surgeon
-use fMRI to identify optimal location for stimulating electrode placement

Front 218

Intra-op guidance

Back 218

-can track location of surgical instruments relative to images of brain

Front 219

Shapes radiation treatment

Back 219

-shaping of radiation to maximally impact tumor while minimizing dosage to eloquent cortex nearby

Front 220

Lateral vestibulospinal tract

Back 220

-maintain upright posture and balance
-excites neurons for extensors (antigravity) mainly of lower limb

Front 221

Lateral vestibulopsinal tract path

Back 221

Lateral vestib nucleus --> ipsilateral projection to all levels of spinal cord, synapsing on more medial part of ventral horn --> alpha and gamme LMNs that innervate extensors of trunk and limbs

Front 222

Modifying lateral vestibulopsinal tract

Back 222

-input form cerebellum (floccular and nodular lobes)
-sensory receptors in utricle, saccule, semicircular canals via CN VIII

Front 223

Lesion of vestibular nerve or vestibular nuclei

Back 223

-stumbling or falling toward side of lesion

Front 224

Causes of lateral medullary syndrome of Wallenberg

Back 224

-vertebral artery or PICA occlusion

Front 225

Lateral medullary syndrome of Wallenberg

Back 225

-IPSI: dysphagia, dysarthria (nucleus ambiguus CN XI and X), loss of pain and temp from face (spinal tract of V), vertigo, nasea, nystagmus (vestib nuc)
-CONTRA: loss of pain and temp from body (anterolateral system)

key: checkerboard loss of pain temp (ipsi face/ contra body)

Front 226

Medial vestibulospinal tract functions

Back 226

-adjusts head position in response to posture changes
-coordinates eye movements with each other
-VOR

Front 227

medial vestibulospinal tract path

Back 227

medial vestibular nuc --> axons project bilaterally --> ventral horn of cervical spinal cord and LMNs assoc with spinal accessory nerve --> axonds descend in MLF to inhibit alpha and gamma LMNs controlling neck and axial mm

Front 228

Modulating medial vestibulopsinal tract

Back 228

-sensory info to medial vestib nuclei modulates pathway to adjust head in response to posture changes

Front 229

Superiorly projecting axons from medial vestibular nuclei

Back 229

-in MLF to nuclei of CNs III, IV, VI
-coordinates eye movement with each other and VOR

Front 230

Internuclear opthalmoplegia (INO)

Back 230

-lesion in MLF
-side of lesion: eyes can't adduct
-contralat: eye has nystagmus
-from interruption of input to medial rectus btw abducen nuclei and contra occulomotor nuc
-often from MS, pontine infarcts, tumor, trauma

Front 231

VOR afferent and efferents

Back 231

-afferent: neck proprioception and CN VIII
-efferent: MVST projects to abducens nuclei and via MLF to occulomotor nucleus

Front 232

Lesion of R CN VI

Back 232

eye deviates medially (no lateral rectus)

Front 233

lesion of R CN III

Back 233

eye deviates laterally (no medial rectus)

Front 234

Lesion of R abducens nucleus

Back 234

-lose R lateral rectus
-lose info along MLF to contralateral occulomotor nuc
-thus, can't turn eyes to R

Front 235

Corticotectal tract

Back 235

-fibers arise in retina, visual cortex and inf parietal lobe
-project to superior colliculus
-facilitate reflexive turning of eye and head

Front 236

Tectospinal tract

Back 236

-fibers arise in sup colliculus
-decussate in dorsal tegmentum
-terminate in contralateral cervical spinal cord (CN XI nuc= SCM)
-facilitate reflexive head and eye movements and upward gaze

Front 237

Parinaud's syndrome/ dorsal midbrain syndrome/ Collicular syndrome

Back 237

-lesion in sup colliculi or posterior commissure = eye abnormalities
-impaired vertical gaze
-large, irreg pupils
-eyelid abnormalities
-convergence- retraction nystagmus
-from pineal gland tumors or hydrocephalus

Front 238

Reticular formation

Back 238

-scattered groups of neuron cell bodies and fibers that extend throughout interior of brainstem
-input from widespread areas of cerebral cortex

Front 239

Reticulospinal tracts (lateral/medullary and medial/pontine)

Back 239

-help maintain upright posture by influencing voluntary and reflexive movements
-inhibit (LRST) or excite (MRST) motor neurons innervating axial muscles
-convery autonomic info

Front 240

Lateral (medullary) reticuospinal tract

Back 240

-axons descend bilaterally through lat funiculus
-suppresses extensors--> mellow
-ascending fibers project to intralaminar and thalamic nuclei for arousal/sleep

Front 241

Medial (pontine) reticulospinal tract

Back 241

-axons descend ipsilaterally in ant funiculus to all spinal cord levels
-excite axials mm and leg extensors
-pumped up

Front 242

Decerebrate posturing/ rigidity

Back 242

-increased muscle tone
-extension of limbs
-removal of excitatory input to the inhibitory LRST --> only MRST intact--> facilitation of extensors

Front 243

Locked in syndrome

Back 243

patient is aware and awake but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body except for the eye

Front 244

Corticonuclear/ corticobulbar tract functions

Back 244

controls muscles of head and face

Front 245

Corticonuclear path

Back 245

fibers from precentral gyrus --> through corona radiata, internal capsule genu, cerebral peduncle --> project bilaterally --> terminate on brainstem motor nuclei of CNs V, VII, XII, nuc ambigus (X and XI), access nuc

-VII and XII are contralateral, not bilateral

Front 246

Pseudobulbar palsy

Back 246

-bilateral lesion of corticobulbar tract
-dysphagia, dysarthria, paresis of tongue, loss of emotional control, jaw jerk reflex
-from brainstem infarcts, MS, ALS

Front 247

Corticonuclear pathway to facial nucleus

Back 247

-upper portion receives bilateral innervation
-lower portion only receives contralateral innerv

Front 248

LMN lesion: Peripheral CN VII

Back 248

-Bell's palsy
-ipsilateral face, entire half
-lesion occurs after nucleus

Front 249

UMN lesion: central CN VII

Back 249

-upper half still receives some cortical input
-results in CONTRAlateral lower quadrant weakness

Front 250

UMN corticonuclear tract lesion to XII nucleus

Back 250

-contralateral tongue weakness

Front 251

Peripheral lesion of CN XII

Back 251

-ipsilateral tongue weakness

Front 252

Midbrain CN

Back 252

-CN III (eye movement problems)

Front 253

Pons CN

Back 253

-CN V at midpoint (chewing problems)
-bottom= CN VI, VII, VIII

Front 254

Medulla CN

Back 254

-CN IX, X, XI
-difficult swallowing, drooping palate
-further down: CN XII (tongue movement)

Front 255

Midbrain contents

Back 255

-sup and inf colliculi
-PAG and cerebral aqueduct
-red nucleus
-cerebral peduncle (tegmentum, sustantia nigra, crus cerebri)
-corticospinal tract
-spinothalamic tract
-oculomotor nucleus

Front 256

Pons contents

Back 256

-4th ventricle
-corticospinal tract
-medial lemniscus
-spinothalamic tract
-sensory and motor nuc of V
-spinal nuc of V
-facial nuc
-abducens nuc
-lateral vestibular nuc

Front 257

Medulla contents

Back 257

-4th ventricle
-central canal
-hypoglossal nuc
-inf olivary nuc
-dorsal motor nuc of X
-nucleus ambiguus
-vestibular nuc
-spinal nuc of V
-corticospinal tract
-spinothalamic tract
-medial lemniscus
-nucleus gracilis
-nucleus cuneatus
-decussation of pyramids

Front 258

Foveation

Back 258

-highest visual acuity
-the purpose of eye movements is to maintain it

Front 259

functional classes of eye movements

Back 259

-pursuits (slow, steady)
-saccades (very fast, pizza hamburger)
-vestibular
-vergence (maintain focus as objects approach/recede)
-optokinetic (stabilize)
-fixation (maintain foveation on stationary object)

Front 260

Smooth pursuits

Back 260

-follow my finger as I move it
-eyes should track with smooth, uninterrupted movements

Front 261

Smooth pursuit lesion

Back 261

-ipsilateral occipital-temporal lobe
-jerky pursuits on gaze to R = R hemisphere lesion

Front 262

Saccades

Back 262

-initiated by frontal eye fields in frontal lobe
-pt wants to look R--> L frontal eye field sends impulse to contra PPRF in pons --> subnucleus for CN VI for R LR muscle and subnuc for VI to activate MLF to CN III nuc for L MR muscle

Front 263

Hypoactive eye field

Back 263

-ie from infarct
-eyes deviate towards affected eye field

Front 264

Hyperactive eye field

Back 264

-ie from seizure
-eyes deviate away from affected eye field

Front 265

Eyes deviate to L, R hemiparesis, where's the lesion?

Back 265

-L frontal eye field and L motor cortex

Front 266

Eyes deviate to R and R hemiparesis, where's the lesion?

Back 266

-damage to brainstem: L CN VI nucleus or PPRF and to L corticospinal tract

Front 267

How can you determine whether the lesion involves CN VI or the PPRF?

Back 267

-check VOR
-if intact, lesion is in PPRF
-VOR: CN VIII nucleus sends signal to CN VI nucleus, bypasses PPRF

Front 268

If patient can look up and down, what does this indicate?

Back 268

-CN III and IV are intact

Front 269

One-and-a-half syndrome

Back 269

-cannot gaze R at all
-R eye cannot adduct to look L

-R CN VI nuc or PPRF (R eye abduction, L eye adduction) and R MLF (R eye adduction)

Front 270

Locked-in syndrom

Back 270

-infarct in anterior pons
-damages corticopsinal tracts and CN VI nerves
-CN III and IV (in midbrain) and reticular formation are spared
-can look up and down and understand (but that's all)

Front 271

How many motor neurons are involved in the transmission of a nerve impulse from cortex to a muscle fiber?

Back 271

Two:
-UMN
-LMN

Front 272

Where does synpase btw UMN and LMN take place?

Back 272

-ventral horn of spinal cord aka anterior horn cell

Front 273

When are UMNs and LMNs firing?

Back 273

-LMN is always firing, tonically stimulating muscle to contract
-UMN inhibits LMN, allowing muscle to relax

Front 274

What is the pathway for the stretch (deep tendon) reflex?

Back 274

-afferent limb sends sensory stimulus back to integration center
-efferent limb transmits a motor command in response to sensory stimulation

Front 275

Why do patients with diabetic peripheral neuropathy have reduced ankle reflexes?

Back 275

-the sensory nerve (afferent limb) is damaged
-no weakness, but don't get the sensory input

Front 276

What is the UMN pattern of weakness?

Back 276

-Arms: extensors more affected, flexors=stronger --> tonically flexed at elbow, wrist, fingers
-Leg: flexors are less affected, extensors=stronger --> tonically extended at knee, ankle

Front 277

What are the possible localization for a LMN lesion?

Back 277

-anterior horn cell = neuronopathy (ALS, polio, spinal musc atrophy)
-nerve root (disc herniation)
-nerve plexus (brachial plexitis, Pancoast's tumor, lumbosacral plexopathy)
-Peripheral nerve (carpal tunnel)
-NMJ (myasthenia gravis, Lambert-Eaton, botulism)
-muscle (myopathy, myositis)

Front 278

ACA stroke signs

Back 278

-leg weakness more prominent
(midline of cortex where leg motor signals come from is more affected)

Front 279

MCA stroke signs

Back 279

-face and arm weakness more prominent
(periphery of cortex where these motor signals come from is more affected)

Front 280

What distribution will the weakness be in an ACA-MCA watershed stroke

Back 280

-arm>leg weakness

Front 281

A pt suffers from R paresis of arm and leg with no other effects, diagnosis?

Back 281

-Lacunar stroke in medulla
(if in frontal lobe, internal capsule or pons would see facial weakness as well)

Front 282

Testing CN I

Back 282

-unilaterally with a commonly recognized odor

Front 283

Bilateral anosmia after falling

Back 283

-most likely shearing of nerves at cribiform plate
-could be an olfactory groove mass

Front 284

Pt with seizure disorder smells strange odor prior to onset, aura localizes where?

Back 284

Piriform/periamygdaloid/entorhinal cortex (Uncus)

Front 285

CN 3, 4, 5

Back 285

-function to keep both eyes fixated on the same object
-images from each retina fused together to relay the perception of a single object

Front 286

Horizontal diplopia, which CN is dysfunctional

Back 286

CN VI

Front 287

Oblique diplopia, which CN is dysfunctional?

Back 287

-CN III or IV

Front 288

Headache, binocular diplopia, massive ptosis, eye deviates out, large pupil

Back 288

CN III (down and out)

Front 289

CN III supplies what and what is the main finding in a lesion?

Back 289

-SR, MR, IR, IO, levator palpebrae, sphincter pupillae

-down and out, with ptosis

Front 290

Aneurysms and CN III

Back 290

-CN III btw PCA and SCA
-will press on parasymp for pupil dilation then CN III palsy
-common for post communicating artery to outpouch and compress

Front 291

Pupillary-sparing CN III palsy

Back 291

-down and out, massive ptosis, no pupil dilation
-ischemia of CN III fascicles from vasa nervorum
-parasymp's have diff blood supply

Front 292

CN V supplies

Back 292

-facial sensation
-muscles of mastication (x buccinator= VII): BITEM

Front 293

How to examine masseter muscle

Back 293

-have patient clench teeth
-feel bulge over angle of jaw
-try to pry open jaw by pressing down on chin

Front 294

how to examine temporalis muscle

Back 294

-have patient clench teeth
-feel bulge over temple
-try to pry open jaw by pressing down on chin

Front 295

What muscle are you testing when you try to CLOSE a pt's open jaw?

Back 295

-lateral pterygoid (lowers manible, opens jaw, helps move side-side)

Front 296

Medial pterygoid

Back 296

-elevates mandible
-closes jaw
-helps move jaw side-side

Front 297

Vascular decompression surgery

Back 297

-Janetta procedure
-fat/ teflon between affected nerve and artery to protect nerve

Front 298

CN VII functions

Back 298

-facial expression mm
-dampen loud sounds (stapedius)
-lacrimation
-salivatoin
-taste ant 2/3 tongue

Front 299

Testing CN VII

Back 299

-Frontalis: wrinkle forehead
-Orbicularis oculi: close eyes tight and don't let me open them
-Buccinator: pull back corners of your mouth like smiling
-Platysma: wrinkle skin on neck, pull down hard on corners of mouth

Front 300

What features should you pay attention to when assessing facial weakness?

Back 300

-Naso-labial fold
-palebral fissure
-forehaed?
-buried eyelases with eyelid closure

Front 301

Functions of CN IX

Back 301

-stylopharyngeus
-pharyngeal constrictors
-post 1/3 tongue taste and pharynx
-somatic senationof TM, eust tube, mastoid region
-carotid body
-parotid gland

Front 302

Functions of CN X

Back 302

-sensation of concha, dura of post fossa
-pharynx and soft palate mm
-taste for epiglottis, palate, pharynx
-cricothyroid muscle
-sensation to larynx
-all other laryngeal muscles
-cardiac, pulm, esophageal, abdominal visceral plexi

Front 303

Glossopharygneal neuralgia can be caused by

Back 303

compression by R internal carotid artery

Front 304

PICA can compress...

Back 304

-CN IX (neuralgia) or X (asystole)

Front 305

CN XI supplies

Back 305

SCM and trapezius

Front 306

Pt tries to rotate their head against your hand on the their L cheek but you can push their head back to the R, which SCM is weak?

Back 306

R SCM (b/c it's attached to post part of the skull)

Front 307

Arm elevation about the horizontal

Back 307

-limited by the acromion
-requires a functional trapezius to rotate scapula superiorly so that deltoid can continue working

Front 308

Shrugging shoulders

Back 308

-doesn't tell you if CN XI is working properly because levator scapulae (C3-5) can elevate shoulder without a functioning trap
-must have them raise arm above horizontal

Front 309

Cavernous Sinus Thrombosis

Back 309

-Chemosis/proptosis: congested opthalmic vein
-Blindness: compression of central retinal artery
-deficits of CN 3, 4, V1, V2, 6
-usually secondary to mastoiditis or sinusitis