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Neuro > The Brain Exam 1 > Flashcards

The Brain Exam 1 Flashcards

1
Q

the spinal cord has ___ pairs of spinal nerves

A

31

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2
Q

ventral surface of spinal cord blood supply

A
  • single anterior spinal artery that supplies the anterior 2/3 of cord
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3
Q

dorsal surface of spinal cord blood supply

A
  • a pair of posterior spinal arteries
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4
Q

CSF flow

A
  • acts as shock absorber
  • elaborated by choroid plexus in ventricles
  • 1/2 L per day
  • exits though foramina in brain stem then reabsorbed to keep constant volume
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5
Q

location of blood vessels & cerebrospinal fluid

A

subarachnoid space

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6
Q

3 layers of meninges

A
  • dura, arachnoid, pia

- specializations in pia anchor cord to dura (denticulate ligaments & filum terminale)

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7
Q

vertebra function

A
  • normally protective but may become a liability in cases of increased mass due to swelling or tumors
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8
Q

development of spinal cord

A
  • 1st trimester: spinal cord & vertebral column grow at same rate, then sc slows
  • birth: sc ends btwn L2/L3
  • adult: sc ends btwn L1/L2
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9
Q

spinal taps

A
  • performed below L2 (after spinal cord ends)

- needle won’t damage nerve roots

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10
Q

nerve root length

A
  • become progressively longer from cervical to sacral levels stemming from differences in growth of spinal cord & spinal column
  • allows it to exit intervertebral foramen at appropriate level
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11
Q

C1-C7

A
  • exit above vertebra of name
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12
Q

C8-S4

A
  • C8 exits above T1 (no C8 vertebra)

- exit below vertebra of name

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13
Q

spinal cord enlargements

A
  • cervical enlargement: C5-T1
  • lumbar enlargement: L3-S2
  • accommodates neurons required for upper/lower extremities
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14
Q

segmental organization

A
  • segment defined by a pair of spinal nerves
  • dorsal (sensory) & ventral (motor)
  • primary sensory neurons located in dorsal root ganglion
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15
Q

dermatome

A
  • cutaneous territories innervated by spinal nerves (segmental organization)
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16
Q

myotome

A
  • muscles innervated by a single nerve root (segmental organization)
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17
Q

reflex arc

A
  • occur at spinal cord level (segmental organization)
  • stretch reflex
  • can involve multiple neurons (as in reciprocal inhibition, nociception, crossed extension)
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18
Q

gray matter

A
  • contains cell bodies
  • dorsal horn: sensory neurons
  • ventral horn: motor neurons
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19
Q

white matter

A
  • contains axons (myelin stain)

- divided into funiculi (bundle of nerves): dorsal, lateral & ventral

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20
Q

substantia gelatinosa

A
  • caps dorsal horn & contains neurons that deal w/ pain & temperature (poorly myelinated)
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21
Q

transverse sections through spinal cord enlargements

A
  • higher levels of cord have more white matter

- cervical & lumbar enlargements seen in ventral horn expansion

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22
Q

axial muscles are controlled ___ & limb muscles are controlled ___.

A

medially & laterally

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23
Q

autonomic nervous system division

A
  • preganglionic sympathetic neurons: T1-L2

- pregnaglionic parasympathetic neurons: S2-S4

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24
Q

phrenic nucleus

A
  • C3-C5

- motor neurons of diaphragm

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25
Q

longitudinal organization principles

A
  • long tracts bringing info to/from cortex must dessucate during ascent or descent
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26
Q

somatotopic organization

A
  • arranged systematically according to parts of body surface
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27
Q

ascending spinal cord pathways

A
  • 3 neuron pathways
  • 1: 1st order neuron (DRG)
  • 2: 2nd order neuron; crosses midline (SC or BS)
  • 3: 3rd order neuron (thalamus)
  • information then sent to cortex
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28
Q

dorsal column pathway

A
  • position sense, vibration sense, 2 point discrimination
  • fasciculus gracilis & cuneatus
  • ipsilateral to where info entered
  • large neurons w/ heavily myelinated axons
  • irrigated by 2 dorsal arteries
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29
Q

fasciculus gracilis

A
  • medial
  • info from T6 & below
  • 1st order neurons end in gracile nucleus (BS)
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30
Q

fasciculus cuneatus

A
  • lateral
  • info from T5 & above
  • 1st order neurons end in cuneate nucleus (BS)
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31
Q

somatotopic organization of dorsal column pathway

A
  • sacral levels more medial
  • cervical levels more lateral
  • continues to cortex
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32
Q

spinothalamic pathway

A
  • localization of pain & temperature
  • 2nd order neuron in dorsal horn (SC). must then pass through ventral white commissure
  • small neurons w/ poor or no myelination
  • contralateral to where info entered
  • anteriolateral to anterior horn
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33
Q

somatotopic organization of spinothalamic pathway

A
  • lower levels more lateral

- higher levels more medial

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34
Q

dorsal column lesion causes ___ deficit.

A

ipsilateral

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35
Q

spinothalamic column lesion causes ___ deficit.

A

contralateral

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36
Q

deficits caused ___ level of lesion

A

below

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37
Q

suspended sensory loss

A
  • lesions that affect roots (not long tracts)

- reveal band-like distribution of deficit

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38
Q

spinothalamic collaterals

A
  • part of multisynaptic spinal reticular pathway that deals w/ affect of pain
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39
Q

referred pain

A
  • pain seeming to originate from specific area of body surface as a result form damaged internal organ
  • visceral pain is poorly localized to diseased organ
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40
Q

referred pain mechanism

A
  • visceral afferents conducting pain enter same spinal cord segment as afferents that supply skin
  • collaterals from visceral afferents send signals to somatosensory tract that innervates region of referred pain
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41
Q

ascending pathways to the cerebellum

A
  • all end ipsilaterally in the cerebellum (right controls right)
  • dorsal spinocerebellar, ventral spinocerebellar, cuneocerebellar
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42
Q

corticospinal pathway

A
  • voluntary fine movement of distal extremities
  • upper motor neuron in cortex crosses in medulla & travels down lateral corticospinal tract
  • lower motor neuron in ventral horn sends axon to skeletal muscle
  • 15% fibers travel in anterior corticospinal pathway & cross at level of synapse
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43
Q

UMN lesion

A
  • hyperreflexia
  • spastic paralysis
  • increased muscle tone (flexers of upper ex & extensors of lower ex)
  • mild atrophy
  • clasp knife reflex
  • clonus
  • babinski sign present
  • large area of body affected (from level of lesion & below)
  • location: lateral corticospinal tract
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44
Q

clonus

A
  • rapid series of alternating muscle contractions in response to a sudden stress
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45
Q

LMN lesion

A
  • flaccid paralysis
  • loss of deep tendon reflexes
  • decrease in muscle tone
  • pronounced atrophy
  • fasciculations (anterior horn cel involvement)
  • segmental distribution of deficit
  • location: ventral horn
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46
Q

fasciculations

A
  • spontaneous contractions of muscle fibers visible through the skin as small twitches
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47
Q

neuron

A
  • 50%

- neurotransmitter-dependent classification

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48
Q

glia

A
  • function-dependent classification
  • macroglia: astroglia (15-20%), oligodendrocyte (15%), oligodendrocyte precursors (5-10%), ependymal
  • microglia (10-15%): originate from mesoderm
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49
Q

schwann cells

A
  • produce myelin in PNS
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50
Q

stains for brain structure & pathological conditions

A
  • H & E (hemotoxylin/eosin): nucleus/cytoplasm

- Nissl: nucleus, rER/RNA granules (loss of staining w/ degeneration)

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51
Q

basic structure of neuron

A
  • dendrites, cell body (soma), axon, & axon terminals
  • polar: signal transmission is directional; impulses carried away from cell body
  • cell signals are electrical
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52
Q

neuron types

A
  • bipolar (interneuron): axon & dendrites from both sides
  • unipolar (sensory): axon & dendrites from one side
  • multipolar (motoneuron): 1 axon & multiple dendrites
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53
Q

axon hillock

A
  • initial segment of axon

- action potential originates here

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54
Q

nodes of Ranivier

A
  • location of VG Na channels
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55
Q

neuron communication

A
  • through synapses
  • axon terminal releases NT to activate receptors on dendritic spines
  • synapse strength matters; amt NT released, # receptors activated, t of activation, & # receptors available
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56
Q

conserved properties of in vivo mature gray matter astroglia

A
  • non-electrically excitable, very low input resistance (leaky)
  • uptake glutatmate through excitatory aa transporters
  • morphologically ramified & complex
  • extensive intercellular coupling through gap-junctions
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57
Q

tripartite synapse

A
  • has glial component in addition to neural component so glial cell can also sense neuronal signal & respond
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58
Q

glutamate-glutamine cycle

A
  • one way that glutamate is replenished in neurons
  • in synapse, glutamate is taken up by both neuron & glial cells
  • in glial cells, converted to glutamine
  • glutamine taken up by neuron to become glutamate
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59
Q

astrocytes in neurological diseases

A
  • astrocytes become GFAP+ to form glial scars in injury
  • why axons cannot regenerate
  • certain reactive astroglia are toxic & able to induce neuronal cell death
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60
Q

microglia

A
  • immuno cell type
  • surveillance
  • release cytokines following activation
  • cluster around amyloid plaques
  • phagocytosis: clear debris
  • high motility
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61
Q

oligodendrocytes

A
  • myelin formation in CNS
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62
Q

how do you know disease is in spinal cord?

A
  • motor sensory level means sc disease
  • LMN involvement means sc involvement (or root, nerve)
  • suspended sensory loss for pain & temp means spinal cord disease (vwc)
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63
Q

dermatomes: C4, T4, T10, L1, L5, S4-S5

A
  • clavicle
  • nipple line
  • umbilicus
  • inguinal crease
  • lateral calf
  • perianal area
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64
Q

myotomes: C3,C4,C5; C5; C7; C8; L3; S1

A
  • diaphragm
  • biceps brachii
  • triceps
  • intrinsic hand muscles
  • quadriceps femoris
  • gastrocnemius
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65
Q

Brown-Sequard syndrome

A
  • when a lateral half of sc is disrupted
  • ipsilateral loss of position & vibration sense
  • contralateral loss of pain & temperature sense
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66
Q

syringomyelia

A
  • lesion in ventral white commissure
  • syrinx that can start small & grow to be more disruptive
  • progression: suspended sensory loss to LMN weakness
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67
Q

ALS

A
  • amyotrophic lateral sclerosis
  • combined UMN & LMN disease
  • affects corticospinal tract & ventral horn
  • rare, elderly, insidious onset, progressive, average survival 2-3 yrs, death from infection
  • mixed UMN & LMN signs; LMN signs predominate & fasciculations
  • sensory pathways normal
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68
Q

ALS variants

A
  • spinal muscular atrophy (LMN)
  • primary lateral sclerosis (UMN)
  • Bulbar ALS (LMN cranial nerves)
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69
Q

tabes dorsalis

A
  • form of tertiary neurosyphilis
  • affects dorsal roots & ganglia
  • patchy loss of pain & temperature
  • predominant posterior column findings: loss of position/vibratory sense; difficulty maintaining erect posture; romberg sign
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70
Q

Romberg sign

A
  • patient can stand w/ eyes open, but cannot stand w/ eyes closed
  • tests for posterior column dysfunction
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71
Q

subacute combined degerneration

A
  • posterolateral sclerosis
  • vit B12 deficiency; pernicious anemia
  • dorsal columns & corticospinal tract
  • UMN signs & Romberg sign
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72
Q

Poliomyelitis

A
  • viral infection w/ predilections for anterior horn cells

- pure lower motor neuron syndrome in setting of acute febrile illness

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73
Q

post-polio syndrome

A
  • new weakness years after acute olio

- often in same distribution as original weakness

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74
Q

anterior spinal syndrome

A
  • dorsal column preserved
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75
Q

motor axons exit via ___ & sensory axons enter via ___.

A

ventral horn & dorsal horn

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76
Q

what happens during sc injury?

A
  • axons damaged, interrupting efficient nerve conduction
  • small % neurons die
  • damaged neurons release glutamate = excitotoxicity = cell death
  • loss of axon transmission causes neurotrophin-deprived cell death
  • swelling = compression
  • site fills w/ cytokine fluid causing glial cell growth = glial scar
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77
Q

neurotrophin

A
  • nerve cell growth factor

- efficient connection needed in order to deliver to cell body

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78
Q

glial scar

A
  • inhibits regeneration preventing reconnection & restored neural function
  • normally keeps nervous system properly sculpted & prevents inappropriate connections
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79
Q

neuronal survival

A
  • reduce swelling: methylpredisone (approved), surgical decompression, hypothermia
  • apply factors directly or engineered cells
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80
Q

altering terrain

A
  • PNS graft at CNS injury, stops once it reaches CNS
  • CNS to PNS prevents PNS growth across it
  • natural inhibitors in CNS that prevent growth
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81
Q

What interventions could enhance growth & reconnection after spinal cord injury?

A
  • preventing swelling
  • providing permissive substrate for growth
  • blocking myelin & glial scar based inhibitors
  • providing neurotrophins
  • adding local guideposts
  • stem cells
  • neuroengineering
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82
Q

what factors exacerbate severity after spinal cord injury?

A
  • excitotoxicity
  • swelling w/in vertebral column
  • damage at one vertebral level interrupting transmission at all points below
  • subsequent loss of neurotrophins leading to cell death
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83
Q

subtypes of neuropathy

A
  • axonal
  • demyelinating
  • Wallerian degeneration
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84
Q

peripheral nerve

A
  • cell body
  • axon
  • myelin sheath
  • symbiotic but structurally independent relationship btwn axon & myelin sheath
  • highly anastomosing vascular supply of arterial branches
  • connective tissue
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85
Q

PNS

A
  • includes all neural structures outside the pial membrane of sc & brainstem
  • dorsal roots extend into posterior columns & dorsal horns of sc
  • peripheral axons of drg are sensory nerve fibers
86
Q

peripheral fibers divided into different sizes

A
  • type I: larger, heavily myelinated; touch/pressure, spindle afferents
  • type II: smaller, thinly myelinated; sharp & lancinating pain & temperature
  • type III & IV: small, unmyelinated; dull, burning poorly localized pain
87
Q

PNS motor

A
  • efferent roots consist of emerging axons of anterior horn cells, lateral horn cells, & motor nuclei of bs
  • large myelinated fibers terminate on muscle
  • small unmyelinated fibers terminate on sympathetic & parasympathetic ganglia
88
Q

alpha motor units

A
  • cause muscle contraction

- not heavily myelinated

89
Q

gamma motor units

A
  • terminate on muscle spindles

- help maintain tension

90
Q

pre- & postganlionic autonomic units

A
  • slower conduction velocity

- terminate on structure involved in sympathetic & parapsym nervous system

91
Q

axonal transport

A
  • neurotubules or microtubules are means
  • anterograde (away from body) & retrograde
  • requires energy (oxphos)
  • independent of electrical activity
92
Q

anterograde transport importance

A
  • necessary to maintain axon itself & in motor nerves is involved in maintaining muscle
  • denervated muscles atrophy
  • chemo drugs can disrupt neurotubule organization
93
Q

rapid axonal transport

A
  • carries synaptic vesicles & membrane bound proteins like plasma membrane proteins
  • requires kinesin which is thought to link proteins to microtubules & transport them w/ ATP dependent mech
94
Q

slow axonal transport

A
  • carries soluble enzymes & tubulin, used in making microtubules
  • determines rate of recovery from nerve injury
95
Q

retrograde transport

A
  • occurs often w/ nerve injury; thought to carry signals of nerve injury inducing chromatolysis
  • uses dynein
  • used by some neurotropic viruses to infect (polio, herpes, rabies)
96
Q

wallerian degeneration

A
  • dying forward
  • degeneration from point of axonal injury peripherally
  • elements needed to regenerate nerve can’t migrate to nerve
  • chromatolysis, muscle atrophy
97
Q

axonal degeneration

A
  • dying back
  • metabolic derangement results in most distal parts of axon to degenerate in proximal direction
  • longest axons die first
  • chromatolysis, muscle atrophy
98
Q

segmental demyelination

A
  • nothing wrong w/ cell body, axon, or connection
  • impulse dies in middle of nerve: only myelin damaged
  • no chromatolysis OR mucsle atrophy
  • may degererate as primary disease or as secondary effect of axonal disruption
99
Q

nerve conduction studies

A
  • test used to look at peripheral nerves
  • measure nerve function by measuring evoked compound motor or sensory nerve action potentials
  • can help distinguish type of lesion & refines pattern of sensory or motor involvement
100
Q

peripheral nerve injury

A
  • sensory & motor studies will both be abnormal
101
Q

nerve root injury

A
  • abnormal motor study

- normal sensory study

102
Q

reflexes: biceps, triceps, knee jerk, ankle jerk

A
  • C5
  • C7
  • L4
  • S1
103
Q

axonal neuropathy

A
  • usually slow and chronic
  • stocking-glove distribution: loss of reflexes distally & muscle wasting distally
  • low amplitude CMAPS & absent SNAPs
104
Q

axonal neuropathy causes

A
  • metabolic (diabetes)
  • toxic (environmental agents)
  • deficiency (thiamine)
  • genetic
  • paraneoplastic (tumor)
105
Q

Guillain-Barre Syndrome

A
  • primarily motor
  • rapidly progressive ( peaks in 2 weeks)
  • areflexia & ataxia belie an afferent component
  • NCSs show conduction block
  • treatment is w/ “immune modulating” therapies
106
Q

demyelinating polyneuropathy

A
  • autoimmune

- genetic

107
Q

chronic demyelinating neuropathy

A
  • hereditary neuropathies
  • CIPD (chronic inflammatory demyelinating neuropathy)
  • myelin continues to grow over & over again, forming onion bulbs
108
Q

ischemic mononeuritis multiplex

A
  • seen in a number of conditions but especially in polyarteritis nodosa
  • fascicular injury: individual fascicles are injured by interruption of microcirculation of nerve
  • individual nerves picked off one by one
  • widespread looks like generalized neuropathy
  • treat w/ steroids & immune suppressor
109
Q

focal neuropathies

A
  • compressive or otherwise traumatic
  • ischemic, infiltrative, autoimmune
  • wallerian degeneration
110
Q

Seddon’s classification of traumatic nerve injury

A
  • class 1: neurapraxia: compression w/ focal demyelination; no denervation; quick recovery
  • class 2: axonotmesis: axonal damage but intact nerve sheath for sprouting to occur; slower & sometimes incomplete recovery
  • class 3: neurotmesis; scarred or disrupted nerve sheath; no recovery
111
Q

features of neuromuscular junction

A
  • VG Ca channel
  • ACh vesicles
  • post-synaptic membrane folds
  • ACh esterase
  • ACh receptors
112
Q

ACh receptor

A
  • 5 subunits
  • extracellular portion that sticks into synaptic cleft: main immunogenic region (MIR) & ACh binding site
  • 2ACh binding causes opening & Na in/K out
113
Q

Myasthenia Gravis mech

A
  • post-synaptic disorder

- Anti AChR Ab bind MIR & activate complement cascade = ACh receptor destroyed & sometimes membrane

114
Q

MG facts

A
  • genetic predisposition to autoimmune disorders
  • young women & older men
  • 10+% have thymus gland tumor (induces Abs)
115
Q

MG clinical bottom line

A
  • disorder of striated muscle that causes muscle weakness
116
Q

MG diagnostics

A
  • fatiguable muscle weakness usually present
  • characteristic distribution of muscle involvement
  • characteristic examination features
  • supportive lab data
117
Q

MG distribution of muscle involvemnet

A
  • ocular: diplopia, ptosis, ophthalmoplegia
  • oropharyngeal: dysarthria, dysphagia, difficulty chewing, nasal regurgitation, choking
  • limb
  • respiratory (diaphragm)
118
Q

MG examination features

A
  • fatiguable ptosis/ophthalmoplegia
  • fatiguable limb weakness
  • normal sensory exam
  • no CNS signs
119
Q

MG diagnostic work-up

A
  • nicotinic ACh receptor Ab
  • Tensilon test (AChe inhibitor)
  • repetitive nerve conduction studies
  • single fiber EMG
  • chest CT/MRI
120
Q

MG treatment

A
  • medications: decrease ACh destruction, reduce Ab, immunosuppressive, block complement
  • thymectomy
121
Q

Lambert Eaton Myasthenic Syndrome (LEMS) mech

A
  • pre-synaptic disorder
  • pre-s VGCC damage = reduced Ca influx during AP, reduced ACh release, reduced safety factor for PSM depolarization -> muscle weakness
122
Q

LEMS etiology

A
  • Ab mediated

- ~ half associated w/ cancer (SCLC)

123
Q

LEMS clinical features

A
  • slowly progressive proximal muscle weakness most common (shoulder/hip)
  • some cranial nerve involvement such as ptosis & ophthalmoplegia but modest
  • autonomic symptoms: dry mouth
  • weakness can improve w/ repetition
124
Q

LEMS diagnostic testing

A
  • VGCC Ab test

- repetitive nerve stimulation & SF-EMG (increment - amplitude increases)

125
Q

LEMS treatment

A
  • turmor search & treatment
  • symptomatic treatment 3,4 DAP
  • immunosuppressive meds
126
Q

myopathy

A
  • pathological disorder that impairs normal muscle function, usually but not always alteration of muscle structure
127
Q

symptoms of myopathy

A
  • muscle weakness: hip girdle, shoulder girdle, oculomotor, facial, bulbar (throat), trunkal, upper airway
128
Q

when to suspect myopathy

A
  • subacute or chronic symmetric weakness, usually in absence of pain/sensory symptoms
  • proximal
  • no CNS, peripheral nerve, or nerve root pattern
  • may affect cranial nerves awa appendicular & axial
  • usually but not always skeletal muscle
  • may affect muscle alone or other organ systems
129
Q

acquired myopathies

A
  • immune mediated: inflammatory (dermatomyositis, polymyositis, inclusion body myositis) & necrotizing myopathy (drugs)
  • infectious: HIV, influenza
  • toxic/metabolic: steroids, immune checkpoint inhibitors
130
Q

hereditary myopathies

A
  • dystrophies: progressive; Duchenne/Becker, FSH, myotonic
  • congenital: present at or soon after birth; milder
  • metabolic: missing enzyme; glycogen/lipid storage mitochondrial
  • channelopathies: periodic paralysis myotonia congenita
131
Q

dermatomyositis

A
  • any age/gender
  • subacute onset
  • rash
  • weakness: proximal, symmetric, neck flexors, dysphagia
  • associations w/ other CTD & malignancy
  • biopsy: diagnostic or suggestive (perifascicular atrophy)
  • responsive to immunomodulation
132
Q

inclusion body myositis

A
  • > 60 yrs; mostly men
  • chronic; slow onset
  • weakness: quadriceps, wrist/finger flexors, neck flexors, dysphagia
  • associations w/ CTD but rarely malignancy
  • biopsy diagnostic in appropriate clinical context
  • unresponsive to immunomodulating treatment
133
Q

endocrine myopathies

A
  • weakness: limb girdle; hip flexors
  • biopsy: type II muscle atrophy
  • EMG, CK - normal
134
Q

necrotizing myopathy

A
  • toxins (statins), autoimmune, or paraneoplastic
  • weakness: limb girdle
  • biopsy: myofiber necrosis
  • EMG, CK: abnormal
135
Q

muscular dystrophies

A
  • heritable, progressive disorders
  • related to mutations in genes producing proteins requisite for myofiber integrity & function
  • biopsy associated w/ destructive changes in muscle
  • historically referred to by eponym or characteristic pattern of weakness
136
Q

dystrophinopathies

A
  • duchenne’s - beckers
  • x-linked mutation of dystrophin gene
  • symptomatic @ 2-3; life expectancy: end of 30s
  • weakness: limb girdle, calf hypertrophy, tight heel cords
  • associated cardiomyopathy, ventilatory muscle weakness, id
137
Q

fascioscapulohumeral

A
  • AD - types 1 & 2
  • recognition from 1st decade to adulthood
  • weakness: face, scapular fixators, biceps/triceps, foot dorsiflexors
138
Q

myotonic MD

A
  • AD - DM1 (myotonin protein kinase), DM2 (zinc finger protein)
  • DM1 trinucleotide repeat disease, variable age of onset, variable severity
  • weakness: cranial, distal limb weakness, ventilatory
  • associated myotonia & systemic features including cardiac conduction defects, cataracts, smooth muscle involvement, frontal balding
139
Q

congenital myopathy

A
  • heritable, often evident at birth, slow progression
  • AD, AR, X-linked
  • associated dysmorphic & orthopedic features common
140
Q

glycogen storage disease

A
  • Pompe: a-glucosidase, AR, weakness: limb girdle/ventilatory, associated cardiac/liver
  • McArdle: myophosphorylase, AR, exertional muscle pain/cramping/myoglobinuria
141
Q

lipid storage disease

A
  • multiple mutations
  • fixed muscle weakness or dynamic depending on mutation
  • other end-organs may be involved
  • symptoms precipitated by fasting, pregnancy, or intercurrent illness
142
Q

mitochondrial myopathy

A
  • mutations in mito genome or nuclear genes coding for mito proteins
  • variable phenotype w/ involvement of end organs (w/ high energy requirement)
143
Q

characteristics of spinal cord lesions involving long tracts

A
  • effects observed at a level of the body & below
  • pain & temperature loss on side opposite lesion
  • weakness, position sense, & vibration sense lost on side of lesion
144
Q

characteristics of brainstem lesions

A
  • lesions of long tracts in brainstem result in contralateral deficit
  • cranial nerve signs reveal level of lesion in brainstem
  • cranial nerve signs observed onside of lesion
145
Q

corticospinal tract travels through the ___ of the ___ in brainstem.

A

pyramids; medulla

146
Q

the olive is

A
  • a relay station for info heading to cerebellum
147
Q

dorsal column pathways travel under ___ in the brainstem

A

bulges on dorsal aspect

148
Q

medial medullary lesions involve _____.

A

the dorsal column pathways & potentially corticospinal tract

149
Q

motor cranial nerve nuclei receive cortical input via the ___.

A

corticobulbar pathway (except those innervating muscles of eye)

150
Q

corticobulbar pathway

A
  • neurons in cortex

- axons branch off & bilaterally synapse on motor nuclei of brainstem (except lower face neurons)

151
Q

alar plate

A
  • gives rise to sensory neurons
152
Q

basal plate

A
  • gives rise to motor neurons
153
Q

in brainstem, motor nuclei are ____ to sensory nuclei.

A

medial

154
Q

columns of CN nucleai medial to lateral in medulla

A
  • somatic motor (hypoglossal)
  • pharyngeal motor (ambiguous)
  • visceral motor (dorsal X)
  • visceral sensory (solitarius)
  • somatic sensory (spinal V)
  • special senses (vestibular)
155
Q

hypoglossal lesion

A
  • paralysis of tongue on side of lesion
  • fasciculations - LMN sign
  • upon protrusion, tongue deviates to side of lesion
156
Q

nucleus ambiguus lesion

A
  • hoarseness
  • difficulty swallowing
  • arch of soft palate droops on affected side
  • uvula is deviated away from side of lesion
157
Q

dorsal motor nucleus of X

A
  • preganglionic parasym for throacic & abdominal viscera
158
Q

nucleus solitarius

A
  • taste & sensation from viscera via CN VII, IX, X (tongue/epiglottis/glottis)
159
Q

spinal nucleus of V

A
  • pain & temp info from face & oral cavity

- lesions result in ipsilateral defect

160
Q

reticular formation

A
  • contains centers for respiration, HR, BP & reticular activating system important for arousal & consciousness
  • extends through entire bs & forms a core
  • descending pain & motor pathways
  • NT production
  • disruption = coma
161
Q

caudal medulla

A
  • motor decussation

- sensory decussation (superior)

162
Q

rostral medulla

A
  • cranial nerve nuclei
163
Q

columns of CN nuclei from medial to lateral in pons

A
  • somatic motor (abducens)
  • branchial motor (facial n & motor n)
  • visceral motor (superior salivary)
  • visceral sensory (solitarius)
  • somatosensory (spinal V, principal sensory V)
  • special senses (vestibular cochlear)
164
Q

cranial nerve VIII & associated nuclei

A
  • hearing to spiral ganglion to ventral & dorsal cochlear nuclei
  • equilibrium to vestibular ganglion to vestibular nuceli
165
Q

auditory info is distributed:

A
  • bilaterally in the CNS
  • info from cochlear nucleus crosses midline in trapezoid body
  • lesion: difficulty localizing sound/eliminating background noise
166
Q

paramedian pontine reticular formation

A
  • lateral gaze center

- receives input from cortex & communicates via medial longitudinal fasciculus

167
Q

neurons that control the upper face receive ____ innervation. neurons that control the lower face receive ____ innervation.

A
  • bilateral corticobulbar

- only contralateral (paralysis indicates contralateral corticobulbar lesion)

168
Q

nuclei of CN V

A
  • principal sensory: relay touch, position, vibration sense
  • spinal V: relay pain, temp
  • mesencephalic V: relay sensation from mastication muscles
  • motor V: innervates mastication muscles
  • sensory travel via trigeminothalamic pathway
169
Q

locked in syndrome

A
  • results from bilateral damage to base of pons

- lesion of corticospinal & corticobulbar pathways

170
Q

columns of CN nuclei from medial to lateral in midbrain

A
  • somatic motor (trochlear, oculomotor)
  • visceral motor (Edinger-Westphal)
  • somatosensory (mesencephalic nucleus of V)
171
Q

locus coeruleus

A
  • major noradrenergic nucleus of brainstem
  • provides most output to cerebral cortex
  • may play role in maintaining attention & vigilance
172
Q

tectum

A
  • top of bs
  • only in midbrain
  • relevant for inferior & superior colliculi
173
Q

substantia nigra

A
  • area of dopaminergic neurons in midbrain

- loss of these neurons leads to parkinson’s

174
Q

vergence

A
  • converging eyes on 1 target
175
Q

saccade

A
  • rapid eye movement
  • horizontal signal from frontal lobe
  • vertical signal from midbrain
176
Q

pursuit

A
  • follow things moving slowly across environment

- requires a lot of cerebellar input

177
Q

vestibulo-ocular reflex

A
  • gyroscope that keeps eyes steady despite eye movement
178
Q

optokinetics

A
  • identification of things when things move rapidly by

- combined saccades & pursuit

179
Q

exotropia

A
  • fixed separation of eyes

- form of strabismus where eyes deviate outward

180
Q

exophoria

A
  • eyes drift apart
181
Q

horizontal gaze palsy

A
  • damage to PPRF
182
Q

internuclear ophthalmoplegia

A
  • lesion to MLF
  • medial rectus slowing & incomplete movement
  • nystagmus is secondary
183
Q

vestibular nucleus damage

A
  • results in nystagmus
  • the intact vestibular nucleus forces eyes toward damaged side w/ corrective movement(s)
  • lateropulsion & Bruyn’s nystagmus
184
Q

disruption of vertical upgaze

A
  • tumor of midbrain blocks neurons responsible for upgaze
185
Q

accompanying signs: CN lesion inside brainstem

A
  • CN lesion + limb weakness, ataxia, or sensory symptoms
186
Q

accompanying signs: CN lesion in subarachnoid space

A
  • multiple CN lesions withouth long tract signs
187
Q

accompanying signs: CN lesion at skull base or beyond

A
  • multiple CN, contiguous, unilateral
188
Q

CN group lesion patterns

A
  • 3, 4, 5, 6: cavernous sinus
  • 5, 7, 8: CP angle
  • 9, 10, 11, 12: skull base
189
Q

cerebellar peduncle connections

A
  • inferior: medulla; non-cortical (spino/vestibulo) input to cerebellum
  • middle: pons; cortical input to cerebellum
  • superior: midbrain; output from cerebellum
190
Q

cerebellar blood supply

A
  • SCA, AICA, PICA (from vertebrals/basilar)
191
Q

Mollaret’s triangle

A
  • inferior olive, red nucleus, dental nucleus

- lesion causes palatal myoclonus

192
Q

cerebellar cortex layers

A
  • internal granular: densely packed neurons receive input
  • molecular: dominated by tracts
  • purkinje: large neurons
193
Q

what does not synapse at granular cell layer?

A
  • climbing fibers from inferior olive

- goes directly to purkinje cells (skips mossy fiber)

194
Q

deep cerebellar nuclei

A
  • dentate nucleus
  • outputs get modulated
  • purkinje cells synapse here
195
Q

functional cerebellar organization

A
  • vermis (midline) & paramedian: trunkal control & leg coordination
  • lateral: limb (mostly upper) control
  • flocculonodular: balance
196
Q

cerebellar areas

A
  • vestibulocerebellum (flocculonodular): input/output vestibular neuclei
  • spinocerebellum (vermis/paramedian): input/output spinocerebellar tract, olives
  • neocerebellum (most): input from cortex via pontine nuclei/output to cortex via VL thalamus
197
Q

cerebellar syndromes

A
  • vestibulocerebellum: balance & gait ataxia; oculomotor control
  • spinocerebellum: truncal incoordination; leg incoordination
  • neocerebellum: upper extremity dyscoordination
198
Q

hemispheric syndromes (cerebellum)

A
  • incoordination - ataxia
  • dysmetria
  • intention tremor
  • dysdiadochokinesis
199
Q

time course in cerebellar dx

A
  • acute: ischemia, hemorrhage, hypoxia, toxins
  • subacute: alcohol, inflammatory, autoimmune
  • chronic: genetic, neurodegenerative
200
Q

structures of basal ganglia

A
  • striatum
  • globus pallidus
  • subthalamic nucleus
  • substantia nigra
201
Q

striatum

A
  • caudate nucleus
  • putamen
  • receive inputs from cortex
  • blood supply: branches from ACA & MCA
202
Q

globus pallidus

A
  • externa/interna
  • main output to thalamus
  • blood supply: anterior choroidal artery, lateral striate arteries
203
Q

subthalamic nucleus

A
  • key component of indirect pathway

- blood supply: branches of PCA & PCOM

204
Q

substantia nigra

A
  • pars compacta (dopamine)
  • pars reticulata (output to thalamus)
  • key inhibitor/activator of striatal activity
  • blood supply: branches of PCA & PCOM
205
Q

basal ganglia function

A
  • extrapyramidal motor system (facilitates voluntary movement & attenuates involuntary movement)
  • NT: glutamate/dopamine excite; GABA/dopamine inhibit
206
Q

direct pathway (basal ganglia)

A
  • facilitate voluntary movement
  • default: net activation of cortex
  • dopamine activates D1 receptors = net increase in cortical activity
207
Q

indirect pathway (basal ganglia)

A
  • inhibit involuntary movement
  • default: net inhibition of cortex
  • dopamine inhibits D2 receptors = net activation of cortex
208
Q

extrapyramidal disorder

A
  • hypokinetic disorders: parkinsonism (bradykinesia resting tremor, rigidity, postural instability)
  • hyperkinetic disorders: tremor, hemiballismus, myoclonus, chorea, dystonia, tics
209
Q

Parkinson’s

A
  • loss of dopamine producing cells in substantia nigra
  • less dopamine present = decreased net activation of cortex
  • bradykinesia, resting tremor, rigidity, postural instability
  • asymmetry of symptoms
210
Q

Huntington’s

A
  • movement disorder: chorea & later parkinsonism
  • dementia
  • psychiatric: depression; psychosis

Neuro (3 decks)

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