The Brain Exam 1 Flashcards

(210 cards)

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
longitudinal organization principles
- long tracts bringing info to/from cortex must dessucate during ascent or descent
26
somatotopic organization
- arranged systematically according to parts of body surface
27
ascending spinal cord pathways
- 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
28
dorsal column pathway
- 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
29
fasciculus gracilis
- medial - info from T6 & below - 1st order neurons end in gracile nucleus (BS)
30
fasciculus cuneatus
- lateral - info from T5 & above - 1st order neurons end in cuneate nucleus (BS)
31
somatotopic organization of dorsal column pathway
- sacral levels more medial - cervical levels more lateral - continues to cortex
32
spinothalamic pathway
- 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
33
somatotopic organization of spinothalamic pathway
- lower levels more lateral | - higher levels more medial
34
dorsal column lesion causes ___ deficit.
ipsilateral
35
spinothalamic column lesion causes ___ deficit.
contralateral
36
deficits caused ___ level of lesion
below
37
suspended sensory loss
- lesions that affect roots (not long tracts) | - reveal band-like distribution of deficit
38
spinothalamic collaterals
- part of multisynaptic spinal reticular pathway that deals w/ affect of pain
39
referred pain
- 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
40
referred pain mechanism
- 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
41
ascending pathways to the cerebellum
- all end ipsilaterally in the cerebellum (right controls right) - dorsal spinocerebellar, ventral spinocerebellar, cuneocerebellar
42
corticospinal pathway
- 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
43
UMN lesion
- 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
44
clonus
- rapid series of alternating muscle contractions in response to a sudden stress
45
LMN lesion
- 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
46
fasciculations
- spontaneous contractions of muscle fibers visible through the skin as small twitches
47
neuron
- 50% | - neurotransmitter-dependent classification
48
glia
- function-dependent classification - macroglia: astroglia (15-20%), oligodendrocyte (15%), oligodendrocyte precursors (5-10%), ependymal - microglia (10-15%): originate from mesoderm
49
schwann cells
- produce myelin in PNS
50
stains for brain structure & pathological conditions
- H & E (hemotoxylin/eosin): nucleus/cytoplasm | - Nissl: nucleus, rER/RNA granules (loss of staining w/ degeneration)
51
basic structure of neuron
- dendrites, cell body (soma), axon, & axon terminals - polar: signal transmission is directional; impulses carried away from cell body - cell signals are electrical
52
neuron types
- bipolar (interneuron): axon & dendrites from both sides - unipolar (sensory): axon & dendrites from one side - multipolar (motoneuron): 1 axon & multiple dendrites
53
axon hillock
- initial segment of axon | - action potential originates here
54
nodes of Ranivier
- location of VG Na channels
55
neuron communication
- 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
56
conserved properties of in vivo mature gray matter astroglia
- non-electrically excitable, very low input resistance (leaky) - uptake glutatmate through excitatory aa transporters - morphologically ramified & complex - extensive intercellular coupling through gap-junctions
57
tripartite synapse
- has glial component in addition to neural component so glial cell can also sense neuronal signal & respond
58
glutamate-glutamine cycle
- 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
59
astrocytes in neurological diseases
- astrocytes become GFAP+ to form glial scars in injury - why axons cannot regenerate - certain reactive astroglia are toxic & able to induce neuronal cell death
60
microglia
- immuno cell type - surveillance - release cytokines following activation - cluster around amyloid plaques - phagocytosis: clear debris - high motility
61
oligodendrocytes
- myelin formation in CNS
62
how do you know disease is in spinal cord?
- 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)
63
dermatomes: C4, T4, T10, L1, L5, S4-S5
- clavicle - nipple line - umbilicus - inguinal crease - lateral calf - perianal area
64
myotomes: C3,C4,C5; C5; C7; C8; L3; S1
- diaphragm - biceps brachii - triceps - intrinsic hand muscles - quadriceps femoris - gastrocnemius
65
Brown-Sequard syndrome
- when a lateral half of sc is disrupted - ipsilateral loss of position & vibration sense - contralateral loss of pain & temperature sense
66
syringomyelia
- lesion in ventral white commissure - syrinx that can start small & grow to be more disruptive - progression: suspended sensory loss to LMN weakness
67
ALS
- 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
68
ALS variants
- spinal muscular atrophy (LMN) - primary lateral sclerosis (UMN) - Bulbar ALS (LMN cranial nerves)
69
tabes dorsalis
- 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
70
Romberg sign
- patient can stand w/ eyes open, but cannot stand w/ eyes closed - tests for posterior column dysfunction
71
subacute combined degerneration
- posterolateral sclerosis - vit B12 deficiency; pernicious anemia - dorsal columns & corticospinal tract - UMN signs & Romberg sign
72
Poliomyelitis
- viral infection w/ predilections for anterior horn cells | - pure lower motor neuron syndrome in setting of acute febrile illness
73
post-polio syndrome
- new weakness years after acute olio | - often in same distribution as original weakness
74
anterior spinal syndrome
- dorsal column preserved
75
motor axons exit via ___ & sensory axons enter via ___.
ventral horn & dorsal horn
76
what happens during sc injury?
- 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
77
neurotrophin
- nerve cell growth factor | - efficient connection needed in order to deliver to cell body
78
glial scar
- inhibits regeneration preventing reconnection & restored neural function - normally keeps nervous system properly sculpted & prevents inappropriate connections
79
neuronal survival
- reduce swelling: methylpredisone (approved), surgical decompression, hypothermia - apply factors directly or engineered cells
80
altering terrain
- 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
81
What interventions could enhance growth & reconnection after spinal cord injury?
- preventing swelling - providing permissive substrate for growth - blocking myelin & glial scar based inhibitors - providing neurotrophins - adding local guideposts - stem cells - neuroengineering
82
what factors exacerbate severity after spinal cord injury?
- 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
83
subtypes of neuropathy
- axonal - demyelinating - Wallerian degeneration
84
peripheral nerve
- cell body - axon - myelin sheath - symbiotic but structurally independent relationship btwn axon & myelin sheath - highly anastomosing vascular supply of arterial branches - connective tissue
85
PNS
- 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
peripheral fibers divided into different sizes
- 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
PNS motor
- 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
alpha motor units
- cause muscle contraction | - not heavily myelinated
89
gamma motor units
- terminate on muscle spindles | - help maintain tension
90
pre- & postganlionic autonomic units
- slower conduction velocity | - terminate on structure involved in sympathetic & parapsym nervous system
91
axonal transport
- neurotubules or microtubules are means - anterograde (away from body) & retrograde - requires energy (oxphos) - independent of electrical activity
92
anterograde transport importance
- necessary to maintain axon itself & in motor nerves is involved in maintaining muscle - denervated muscles atrophy - chemo drugs can disrupt neurotubule organization
93
rapid axonal transport
- 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
slow axonal transport
- carries soluble enzymes & tubulin, used in making microtubules - determines rate of recovery from nerve injury
95
retrograde transport
- 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
wallerian degeneration
- dying forward - degeneration from point of axonal injury peripherally - elements needed to regenerate nerve can't migrate to nerve - chromatolysis, muscle atrophy
97
axonal degeneration
- dying back - metabolic derangement results in most distal parts of axon to degenerate in proximal direction - longest axons die first - chromatolysis, muscle atrophy
98
segmental demyelination
- 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
nerve conduction studies
- 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
peripheral nerve injury
- sensory & motor studies will both be abnormal
101
nerve root injury
- abnormal motor study | - normal sensory study
102
reflexes: biceps, triceps, knee jerk, ankle jerk
- C5 - C7 - L4 - S1
103
axonal neuropathy
- usually slow and chronic - stocking-glove distribution: loss of reflexes distally & muscle wasting distally - low amplitude CMAPS & absent SNAPs
104
axonal neuropathy causes
- metabolic (diabetes) - toxic (environmental agents) - deficiency (thiamine) - genetic - paraneoplastic (tumor)
105
Guillain-Barre Syndrome
- 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
demyelinating polyneuropathy
- autoimmune | - genetic
107
chronic demyelinating neuropathy
- hereditary neuropathies - CIPD (chronic inflammatory demyelinating neuropathy) - myelin continues to grow over & over again, forming onion bulbs
108
ischemic mononeuritis multiplex
- 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
focal neuropathies
- compressive or otherwise traumatic - ischemic, infiltrative, autoimmune - wallerian degeneration
110
Seddon's classification of traumatic nerve injury
- 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
features of neuromuscular junction
- VG Ca channel - ACh vesicles - post-synaptic membrane folds - ACh esterase - ACh receptors
112
ACh receptor
- 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
Myasthenia Gravis mech
- post-synaptic disorder | - Anti AChR Ab bind MIR & activate complement cascade = ACh receptor destroyed & sometimes membrane
114
MG facts
- genetic predisposition to autoimmune disorders - young women & older men - 10+% have thymus gland tumor (induces Abs)
115
MG clinical bottom line
- disorder of striated muscle that causes muscle weakness
116
MG diagnostics
- fatiguable muscle weakness usually present - characteristic distribution of muscle involvement - characteristic examination features - supportive lab data
117
MG distribution of muscle involvemnet
- ocular: diplopia, ptosis, ophthalmoplegia - oropharyngeal: dysarthria, dysphagia, difficulty chewing, nasal regurgitation, choking - limb - respiratory (diaphragm)
118
MG examination features
- fatiguable ptosis/ophthalmoplegia - fatiguable limb weakness - normal sensory exam - no CNS signs
119
MG diagnostic work-up
- nicotinic ACh receptor Ab - Tensilon test (AChe inhibitor) - repetitive nerve conduction studies - single fiber EMG - chest CT/MRI
120
MG treatment
- medications: decrease ACh destruction, reduce Ab, immunosuppressive, block complement - thymectomy
121
Lambert Eaton Myasthenic Syndrome (LEMS) mech
- pre-synaptic disorder - pre-s VGCC damage = reduced Ca influx during AP, reduced ACh release, reduced safety factor for PSM depolarization -> muscle weakness
122
LEMS etiology
- Ab mediated | - ~ half associated w/ cancer (SCLC)
123
LEMS clinical features
- 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
LEMS diagnostic testing
- VGCC Ab test | - repetitive nerve stimulation & SF-EMG (increment - amplitude increases)
125
LEMS treatment
- turmor search & treatment - symptomatic treatment 3,4 DAP - immunosuppressive meds
126
myopathy
- pathological disorder that impairs normal muscle function, usually but not always alteration of muscle structure
127
symptoms of myopathy
- muscle weakness: hip girdle, shoulder girdle, oculomotor, facial, bulbar (throat), trunkal, upper airway
128
when to suspect myopathy
- 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
acquired myopathies
- immune mediated: inflammatory (dermatomyositis, polymyositis, inclusion body myositis) & necrotizing myopathy (drugs) - infectious: HIV, influenza - toxic/metabolic: steroids, immune checkpoint inhibitors
130
hereditary myopathies
- 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
dermatomyositis
- 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
inclusion body myositis
- >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
endocrine myopathies
- weakness: limb girdle; hip flexors - biopsy: type II muscle atrophy - EMG, CK - normal
134
necrotizing myopathy
- toxins (statins), autoimmune, or paraneoplastic - weakness: limb girdle - biopsy: myofiber necrosis - EMG, CK: abnormal
135
muscular dystrophies
- 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
dystrophinopathies
- 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
fascioscapulohumeral
- AD - types 1 & 2 - recognition from 1st decade to adulthood - weakness: face, scapular fixators, biceps/triceps, foot dorsiflexors
138
myotonic MD
- 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
congenital myopathy
- heritable, often evident at birth, slow progression - AD, AR, X-linked - associated dysmorphic & orthopedic features common
140
glycogen storage disease
- Pompe: a-glucosidase, AR, weakness: limb girdle/ventilatory, associated cardiac/liver - McArdle: myophosphorylase, AR, exertional muscle pain/cramping/myoglobinuria
141
lipid storage disease
- 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
mitochondrial myopathy
- mutations in mito genome or nuclear genes coding for mito proteins - variable phenotype w/ involvement of end organs (w/ high energy requirement)
143
characteristics of spinal cord lesions involving long tracts
- 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
characteristics of brainstem lesions
- 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
corticospinal tract travels through the ___ of the ___ in brainstem.
pyramids; medulla
146
the olive is
- a relay station for info heading to cerebellum
147
dorsal column pathways travel under ___ in the brainstem
bulges on dorsal aspect
148
medial medullary lesions involve _____.
the dorsal column pathways & potentially corticospinal tract
149
motor cranial nerve nuclei receive cortical input via the ___.
corticobulbar pathway (except those innervating muscles of eye)
150
corticobulbar pathway
- neurons in cortex | - axons branch off & bilaterally synapse on motor nuclei of brainstem (except lower face neurons)
151
alar plate
- gives rise to sensory neurons
152
basal plate
- gives rise to motor neurons
153
in brainstem, motor nuclei are ____ to sensory nuclei.
medial
154
columns of CN nucleai medial to lateral in medulla
- somatic motor (hypoglossal) - pharyngeal motor (ambiguous) - visceral motor (dorsal X) - visceral sensory (solitarius) - somatic sensory (spinal V) - special senses (vestibular)
155
hypoglossal lesion
- paralysis of tongue on side of lesion - fasciculations - LMN sign - upon protrusion, tongue deviates to side of lesion
156
nucleus ambiguus lesion
- hoarseness - difficulty swallowing - arch of soft palate droops on affected side - uvula is deviated away from side of lesion
157
dorsal motor nucleus of X
- preganglionic parasym for throacic & abdominal viscera
158
nucleus solitarius
- taste & sensation from viscera via CN VII, IX, X (tongue/epiglottis/glottis)
159
spinal nucleus of V
- pain & temp info from face & oral cavity | - lesions result in ipsilateral defect
160
reticular formation
- 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
caudal medulla
- motor decussation | - sensory decussation (superior)
162
rostral medulla
- cranial nerve nuclei
163
columns of CN nuclei from medial to lateral in pons
- 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
cranial nerve VIII & associated nuclei
- hearing to spiral ganglion to ventral & dorsal cochlear nuclei - equilibrium to vestibular ganglion to vestibular nuceli
165
auditory info is distributed:
- bilaterally in the CNS - info from cochlear nucleus crosses midline in trapezoid body - lesion: difficulty localizing sound/eliminating background noise
166
paramedian pontine reticular formation
- lateral gaze center | - receives input from cortex & communicates via medial longitudinal fasciculus
167
neurons that control the upper face receive ____ innervation. neurons that control the lower face receive ____ innervation.
- bilateral corticobulbar | - only contralateral (paralysis indicates contralateral corticobulbar lesion)
168
nuclei of CN V
- 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
locked in syndrome
- results from bilateral damage to base of pons | - lesion of corticospinal & corticobulbar pathways
170
columns of CN nuclei from medial to lateral in midbrain
- somatic motor (trochlear, oculomotor) - visceral motor (Edinger-Westphal) - somatosensory (mesencephalic nucleus of V)
171
locus coeruleus
- major noradrenergic nucleus of brainstem - provides most output to cerebral cortex - may play role in maintaining attention & vigilance
172
tectum
- top of bs - only in midbrain - relevant for inferior & superior colliculi
173
substantia nigra
- area of dopaminergic neurons in midbrain | - loss of these neurons leads to parkinson's
174
vergence
- converging eyes on 1 target
175
saccade
- rapid eye movement - horizontal signal from frontal lobe - vertical signal from midbrain
176
pursuit
- follow things moving slowly across environment | - requires a lot of cerebellar input
177
vestibulo-ocular reflex
- gyroscope that keeps eyes steady despite eye movement
178
optokinetics
- identification of things when things move rapidly by | - combined saccades & pursuit
179
exotropia
- fixed separation of eyes | - form of strabismus where eyes deviate outward
180
exophoria
- eyes drift apart
181
horizontal gaze palsy
- damage to PPRF
182
internuclear ophthalmoplegia
- lesion to MLF - medial rectus slowing & incomplete movement - nystagmus is secondary
183
vestibular nucleus damage
- results in nystagmus - the intact vestibular nucleus forces eyes toward damaged side w/ corrective movement(s) - lateropulsion & Bruyn's nystagmus
184
disruption of vertical upgaze
- tumor of midbrain blocks neurons responsible for upgaze
185
accompanying signs: CN lesion inside brainstem
- CN lesion + limb weakness, ataxia, or sensory symptoms
186
accompanying signs: CN lesion in subarachnoid space
- multiple CN lesions withouth long tract signs
187
accompanying signs: CN lesion at skull base or beyond
- multiple CN, contiguous, unilateral
188
CN group lesion patterns
- 3, 4, 5, 6: cavernous sinus - 5, 7, 8: CP angle - 9, 10, 11, 12: skull base
189
cerebellar peduncle connections
- inferior: medulla; non-cortical (spino/vestibulo) input to cerebellum - middle: pons; cortical input to cerebellum - superior: midbrain; output from cerebellum
190
cerebellar blood supply
- SCA, AICA, PICA (from vertebrals/basilar)
191
Mollaret's triangle
- inferior olive, red nucleus, dental nucleus | - lesion causes palatal myoclonus
192
cerebellar cortex layers
- internal granular: densely packed neurons receive input - molecular: dominated by tracts - purkinje: large neurons
193
what does not synapse at granular cell layer?
- climbing fibers from inferior olive | - goes directly to purkinje cells (skips mossy fiber)
194
deep cerebellar nuclei
- dentate nucleus - outputs get modulated - purkinje cells synapse here
195
functional cerebellar organization
- vermis (midline) & paramedian: trunkal control & leg coordination - lateral: limb (mostly upper) control - flocculonodular: balance
196
cerebellar areas
- 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
cerebellar syndromes
- vestibulocerebellum: balance & gait ataxia; oculomotor control - spinocerebellum: truncal incoordination; leg incoordination - neocerebellum: upper extremity dyscoordination
198
hemispheric syndromes (cerebellum)
- incoordination - ataxia - dysmetria - intention tremor - dysdiadochokinesis
199
time course in cerebellar dx
- acute: ischemia, hemorrhage, hypoxia, toxins - subacute: alcohol, inflammatory, autoimmune - chronic: genetic, neurodegenerative
200
structures of basal ganglia
- striatum - globus pallidus - subthalamic nucleus - substantia nigra
201
striatum
- caudate nucleus - putamen - receive inputs from cortex - blood supply: branches from ACA & MCA
202
globus pallidus
- externa/interna - main output to thalamus - blood supply: anterior choroidal artery, lateral striate arteries
203
subthalamic nucleus
- key component of indirect pathway | - blood supply: branches of PCA & PCOM
204
substantia nigra
- pars compacta (dopamine) - pars reticulata (output to thalamus) - key inhibitor/activator of striatal activity - blood supply: branches of PCA & PCOM
205
basal ganglia function
- extrapyramidal motor system (facilitates voluntary movement & attenuates involuntary movement) - NT: glutamate/dopamine excite; GABA/dopamine inhibit
206
direct pathway (basal ganglia)
- facilitate voluntary movement - default: net activation of cortex - dopamine activates D1 receptors = net increase in cortical activity
207
indirect pathway (basal ganglia)
- inhibit involuntary movement - default: net inhibition of cortex - dopamine inhibits D2 receptors = net activation of cortex
208
extrapyramidal disorder
- hypokinetic disorders: parkinsonism (bradykinesia resting tremor, rigidity, postural instability) - hyperkinetic disorders: tremor, hemiballismus, myoclonus, chorea, dystonia, tics
209
Parkinson's
- 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
Huntington's
- movement disorder: chorea & later parkinsonism - dementia - psychiatric: depression; psychosis