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Principles in Neurology_1 Flashcards

1
Q

what happens in neural development between day 18 and day 21?

A

neural plate + notochord → neural crest → neural tube and neural crest cells

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2
Q

notochord induces overlying ectoderm to differentiate into what?

A

neuroectoderm and form the neural plate

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3
Q

neural plate gives rise to what?

A

the neural tube and neural crest cells

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4
Q

notochord becomes what in adults?

A

nucleus pulposus of the intervertebral disc

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5
Q

what are the name and function of the dorsal part of the neural tube?

A

Alar plate: sensory

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6
Q

what are the name and function of the ventral part of the neural tube?

A

Basal plate: motor

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7
Q

what are the three primary vesicles of the developing brain?

A
  1. Forebrain (prosencephalon) • 2. Midbrain (mesencephalon) • 3. Hindbrain (rhombencephalon)
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8
Q

what are the five secondary vesicles of the developing brain?

A
  1. telencephalon • 2. Diencephalon • 3. Mesencephalon • 4. Metencephalon • 5. Myelencephalon
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9
Q

the Forebrain (prosencephalon) gives rise to which secondary vesicles?

A
  1. Telencephalon • 2. Diencephalon
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10
Q

the Midbrain (mesencephalon) gives rise to which secondary vesicles?

A
  1. Mesencephalon
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11
Q

the Hindbrain (rhombencephalon) gives rise to which secondary vesicles?

A
  1. Metencephalon • 2. Myelencephalon
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12
Q

the walls of the telencephalon give rise to what?

A

cerebral hemispheres

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13
Q

the cavities of the telencephalon give rise to what?

A

lateral ventricles

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14
Q

the walls of the diencephalon give rise to what?

A

thalamus

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15
Q

the cavities of the diencephalon give rise to what?

A

third ventricle

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16
Q

the walls of the mesencephalon give rise to what?

A

midbrain

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17
Q

the cavities of the mesencephalon give rise to what?

A

aqueduct

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18
Q

the walls of the metencephalon give rise to what?

A

Pons and Cerebellum

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19
Q

the cavities of the metencephalon give rise to what?

A

upper part of fourth ventricle

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20
Q

the walls of the myelencephalon give rise to what?

A

medulla

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21
Q

the cavities of the myelencephalon give rise to what?

A

lower part of the fourth ventricle

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22
Q

what happens in neural tube defect?

A

neuropores fail to fuse (4th week) → persistent connection between amniotic cavity and spinal canal

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23
Q

neural tube defects are associated with what?

A

low folic acid intake before conception and during pregnancy

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24
Q

what are the lab levels in neural tube defect?

A
  1. ↑ AFP in amniotic fluid and maternal serum • 2. ↑ AChE in amniotic fluid is a helpful confirmatory test
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25
Q

why is it that AChE can be measured in NTD?

A

fetal AChE in CSF transudates across defect into the amniotic fluid

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26
Q

what is spina bifida occulta?

A

failure of bony canal to close, but no structural herniation

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27
Q

spina bifida occulta is usually seen where?

A

lower vertebral levels

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28
Q

status of dura in spina bifida occulta?

A

intact

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29
Q

spina bifida occulta is associated with what?

A

tuft of hair or skin dimple at level of bony defect

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30
Q

what is meningocele?

A

meninges (but not the spinal cord) herniate through spinal canal defect

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31
Q

what is meningomyelocele?

A

meninges and spinal cord herniate through spinal canal defect

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32
Q

what are the types of forebrain anomalies?

A

anencephaly • holoprosencephaly

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33
Q

what happens in anencephaly?

A

malformation of anterior neural tube resulting in no forebrain, open calvarium (frog like appearance)

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34
Q

what are the clinical findings in anencephaly?

A

↑AFP, polyhydramnios

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35
Q

why is there polyhydramnios in anencephaly?

A

no swallowing center in the brain

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36
Q

anencephaly is associated with what?

A

maternal diabetes type I

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37
Q

what decreases the risk of anencephaly?

A

folate supplementation

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38
Q

what is holoprosencephaly?

A

failure of left and right hemispheres to separate

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39
Q

when does holoprosencephaly happen?

A

usually occurs during weeks 5-6

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40
Q

what is the etiology of holoprosencephaly?

A

complex multifactorial etiology that may be related to mutations in sonic hedgehog signaling pathway

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41
Q

what is the spectrum of severity of holoprosencephaly?

A

moderate form has celf lip/palate, most severe form results in cyclopia

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42
Q

what are the posterior fossa malformations?

A

Chiari II (Arnold-Chiari malformation) • Dandy Walker

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43
Q

what is an Arnold Chiari malformation?

A

Significant cerebellar tonsillar and vermian herniation through foramen magnum with aqueductal stenosis and hydrocephalus

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44
Q

Chiari II (Arnold-Chiari) malformation often presents with what?

A

thoraco-lumbar myelomeningocele and paralysis below the defect

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45
Q

what is a Dandy-Walker malformation?

A

Agenesis of cerebellar vermis with cystic enlargement of 4th ventricle (fills the enlarged posterior fossa)

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46
Q

Dandy Walker malformation is associated with what?

A

hydrocephalus and spina bifida

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47
Q

what is syringomyelia?

A

cystic enlargement of central canal of spinal cord

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48
Q

which fibers of spinal cord are damaged first in syringomyelia?

A

crossing fibers of spinothalamic tract

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49
Q

syringomyelia results in what?

A

cape like bilateral loss of pain and temperature sensation in upper extremities (fine touch sensation is preserved)

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50
Q

syringomyelia is associated with what?

A

Chiari I malformation

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51
Q

what is Chiari I malformation?

A

> 3-5mm cerebellar tonsillar ectopia

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52
Q

where is syringomyelia most common?

A

C8-T1

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53
Q

which embryonic structures form the tongue?

A

1st branchial arch forms anterior 2/3 • 3rd and 4th branchial arches form posterior 1/3

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54
Q

muscles of the tongue are derived from what?

A

occipital myotomes

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55
Q

which nerves carry taste?

A

CN VII, IX, X (solitary nucleus)

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56
Q

which nerves carry tongue pain?

A

CN V3 (ant 2/3), IX, X

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57
Q

which nerve is responsible for motor function of tongue?

A

CN-XII

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58
Q

neuroectoderm gives rise to which neural tissue?

A

CNS neurons • ependymal cells • oligodendroglia • astrocytes

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59
Q

neural crest gives rise to which neural tissue?

A

PNS neurons • schwann cells

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60
Q

mesoderm gives rise to which neural tissue?

A

Microglia

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61
Q

which are the signal transmitting cells of the nervous system?

A

neurons

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62
Q

how often do neurons divide?

A

permanent cells- do not divide in adulthood (and, as a general rule, have no progenitor stem cell population)

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63
Q

what are neurons?

A

signal relaying cells with dendrites (receive input), cell bodies, and axons (send output)

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64
Q

cell bodies and dendrites of neurons can be stained how?

A

via the Nissl substance (stains RER)

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65
Q

why doesn’t Nissl stain the axon?

A

RER is not present in the axon

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66
Q

what happens if an axon is injured?

A

undergoes Wallerian degeneration- degeneration distal to the injury and axonal retraction proximally

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67
Q

what are the functions of astrocytes?

A

Physical support • repair • K+ metabolism • removal of excess neurotransmitter, maintenance of blood-brain barrier

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68
Q

how do astrocytes respond to injury?

A

reactive gliosis

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69
Q

what is the astrocyte marker?

A

GFAP

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70
Q

what are microglia?

A

CNS phagocytes • Scavenger cells of CNS

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71
Q

what is the germ layer origin of microglia?

A

mesoderm

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72
Q

how do microglia stain with Nissl?

A

not readily discernable in Nissl stains

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73
Q

what is the function of microglia?

A

respond to tissue damage by differentiating into large phagocytic cells

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74
Q

what happens to microglia in HIV?

A

HIV-infected microglia fuse to form multinucleated giant cells in the CNS

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75
Q

what is the function of myelin?

A

Wraps and insulates axons: ↑ space constant and ↑ conduction velocity

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76
Q

the function of myelin results in what action?

A

saltatory conduction of action potentials between nodes of Ranvier, where there are high concentrations of Na + channels

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77
Q

what makes myelin in the CNS?

A

oligodendrocytes

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78
Q

what makes myelin in the PNS?

A

Schwann cells

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79
Q

Each oligodendrocyte myelinates how many CNS axons?

A

multiple (up to 50 each)

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80
Q

how do oligodendroglia appear in Nissl stain?

A

much smaller nuclei with dark chromatin and little cytoplasm

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81
Q

what is the predominant type of glial cell in white matter?

A

oligodendrocyte

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82
Q

oligodendroglia are destroyed in which disease?

A

MS

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83
Q

how do oligodendroglia look in H&E stain?

A

like fried eggs

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84
Q

each Schwann cell myelinates how many PNS axons?

A

only 1

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85
Q

Schwann cells also promote what?

A

axonal regeneration

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86
Q

Scwhann cells are derived from what?

A

Neural crest

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87
Q

Schwann cells are destroyed in which disease?

A

Guillan-Barre syndrome

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88
Q

what is Acoustic neuroma?

A

type of Schwannoma typically located in internal acoustic meatus CNVIII

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89
Q

what are the 2 types of free nerve endings?

A

C • Aδ

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90
Q

what type of fibers are C fibers?

A

slow, unmyelinated fibers

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91
Q

what type of fibers are Aδ fibers?

A

fast, myelinated fibers

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92
Q

what are the locations of C fibers and Aδ fibers?

A

All skin, epidermis, some viscera

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93
Q

what are the senses carried by C fibers and Aδ fibers?

A

Pain and temperature

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94
Q

what type of fibers are Meissner’s corpuscles?

A

Large, myelinated fibers that adapt quickly

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95
Q

what is the location of Meissner’s corpuscles?

A

glabrous (hairless) skin

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96
Q

what are the senses carried by Meissner’s corpuscles?

A

dynamic, fine/light touch; position sense

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97
Q

what type of fibers are Pacinian corpuscles?

A

Large, myelinated fibers

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98
Q

what is the location of Pacinian corpuscles?

A

deep skin layers, ligaments, and joints

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99
Q

what are the senses carried by pacinian fibers?

A

vibration • pressure

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100
Q

what type of fibers are Merkel’s discs?

A

Large, myelinated fibers that adapt slowly

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101
Q

what is the location of Merkel’s discs?

A

hair follicles

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102
Q

what are the senses carried by Merkel’s discs?

A

Pressure, deep static touch (shapes, edges) position sense

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103
Q

what is the endoneurium of a peripheral nerve?

A

invests single nerve fiber layers

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104
Q

the endoneurium of peripheral nerve contains inflammatory infiltrate in which condition?

A

Guillain-Barre

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105
Q

which part of the peripheral nerve forms the permeability barrier?

A

Perineurium

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106
Q

the perineurium of a peripheral nerve surrounds what?

A

a fascicle of nerve fibers

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107
Q

which part of a peripheral nerve must be rejoined in microsurgery for limb reattachment?

A

Perineurium

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108
Q

what is the epineurium of a peripheral nerve?

A

dense connective tissue that surrounds the entire nerve (fascicles and blood vessels)

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109
Q

how does NE change in disease?

A

↑ in anxiety • ↓ in depression

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110
Q

where is NE synthesized in the brain?

A

Locus ceruleus (pons)

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111
Q

how does dopamine change in disease?

A

↑ in schizophrenia • ↓ in Parkinsons • ↓ in depression

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112
Q

where is dopamine synthesized in the brain?

A

Ventral tegmentum and SNc (midbrain)

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113
Q

how does 5-HT change in disease?

A

↓ in anxiety • ↓ in depression

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114
Q

where is 5HT synthesized in the brain?

A

Raphe nucleus (pons)

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115
Q

how does ACh change in disease?

A

↓ in Alzheimers • ↓ in Huntingtons • ↑ in REM sleep

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116
Q

where is ACh synthesized in the brain?

A

Basal nucleus of Meynert

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117
Q

how does GABA change in disease?

A

↓ in anxiety • ↓ in Huntingtons

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118
Q

where is GABA made in the brain?

A

Nucleus accumbens

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119
Q

Functions of the Locus ceruleus?

A

stress and pain

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120
Q

functions of the nucleus accumbens and septal nucleus?

A

reward center • pleasure • addiction • fear

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121
Q

Blood brain barrier does what?

A

prevents circulating blood substances from reaching the CSF/CNS

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122
Q

blood brain barrier is formed by which 3 structures?

A
  1. tight junctions between nonfenestrated capillary endothelial cells • 2. basement membrane • 3. astrocyte foot processes
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123
Q

can glucose and amino acids cross BBB?

A

glucose and amino acids cross slowly by carrier mediated transport mechanism

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124
Q

do nonpolar/lipid soluble substances cross BBB?

A

cross rapidly via diffusion

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125
Q

what are the specialized areas of the brain with fenestrated capillaries and no BBB that allow molecules in the blood to affect brain function?

A

area postrema- vomiting after chemo • OVLT- osmotic sensing

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126
Q

what are the specialized areas of the brain with fenestrated capillaries and no BBB that allow molecules in the blood to affect neurosecretory products to enter circulation?

A

neurohypophysis- ADH release

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127
Q

besides BBB what are the other notable barriers?

A

blood-testis barrier • maternal-fetal blood barrier of placenta

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128
Q

what happens when infarction and/or neoplasm destroys endothelial cell tight junctions of the BBB?

A

vasogenic edema

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129
Q

how do hypothalamic inputs and outputs get to their target?

A

they permeate the BBB

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130
Q

BBB helps prevent what?

A

bacterial infection from spreading into the brain • also restricts drug delivery to the brain

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131
Q

what are the functions of the hypothalamus?

A

TAN HATS: • 1. Thirst and water balance • 2. Adenohypophysis control • 3. Neurohypophysis releases hormones produced in the hypothalamus • 4. Hunger • 5. Autonomic regulation • 6. Temperature regulation • 7. Sexual urges

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132
Q

what are the inputs to the hypothalamus?

A

OVLT (senses changes in osmolarity) • area postrema (responds to emetics)

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133
Q

supraoptic nucleus of the hypothalamus makes what?

A

ADH

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134
Q

paraventricular nucleus of hypothalamus makes what?

A

oxytocin

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135
Q

Lateral area of hypothalamus controls what?

A

hunger

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136
Q

destruction of lateral area of hypothalamus → what?

A

anorexia, failure to thrive

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137
Q

lateral area of the hypothalamus is inhibited by what?

A

leptin

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138
Q

ventromedial area of the hypothalamus controls what?

A

satiety

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139
Q

what can destroy the ventromedial nucleus of the hypothalamus?

A

craniopharyngioma

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140
Q

destruction of the ventromedial area of the hypothalamus leads to what?

A

hyperphagia

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141
Q

ventromedial area of the hypothalamus is stimulated by what?

142
Q

anterior nucleus of hypothalamus controls what?

A

cooling, parasympathetic

143
Q

posterior nucleus of hypothalamus controls what?

A

heating, sympathetic

144
Q

the suprachiasmatic nucleus of the hypothalamus controls what?

A

circadian rhythm

145
Q

posterior pituitary receives hypothalamic axonal projections from where?

A

supraoptic (ADH) and paraventricular (oxytocin) nuclei

146
Q

what is the function of the thalamus?

A

major relay for all ascending sensory information except olfaction

147
Q

what is the input to the VPL nucleus of the thalamus?

A

spinothalamic and dorsal columns/medial lemniscus

148
Q

what is the info conveyed via the VPL of the thalamus?

A

pain and temperature; • pressure, touch, vibration, and proprioception

149
Q

what is the destination of the information conveyed via the VPL nucleus of the thalamus?

A

1° somatosensory cortex

150
Q

what is the input to the VPM nucleus of the thalamus?

A

trigeminal and gustatory pathway

151
Q

what is the info conveyed via the VPM nucleus of the thalamus?

A

face sensation and taste

152
Q

what is the destination of the information conveyed by the VPM nucleus of the thalamus?

A

1° somatosensory cortex

153
Q

what is the input to the LGN of the thalamus?

154
Q

what is the info conveyed via the LGN of the thalamus?

155
Q

what is the destination of the info conveyed by the LGN of the thalamus?

A

Clacarine sulcus

156
Q

what is the input to the MGN of the thalamus?

A

superior olive and inferior colliculus of tectum

157
Q

what is the info conveyed by the MGN of the thalamus?

158
Q

what is the destination of the info conveyed by the MGN of the thalamus?

A

auditory cortex of the temporal lobe

159
Q

what is the input to the VL nucleus of the thalamus?

A

basal ganglia

160
Q

what is the info conveyed via the VL nucleus of the thalamus?

161
Q

what is the destination of the info conveyed via the VL nucleus of the thalamus?

A

motor cortex

162
Q

what is the limbic system?

A

collection of neural structures involved in emotion, long-term memory, olfaction, behavior modulation, ANS function

163
Q

limbic system structures include what?

A

hippocampus • amygdala • fornix • mammillary bodies • cingulate gyrus

164
Q

limbic system is responsible for what?

A

Feeding • Fleeing • Fighting • Feeling • Sex

165
Q

cerebellum modulates what?

A

movement; aids in coordination and balance

166
Q

what is the input to the cerebellum?

A
  1. contralateral cortex via middle cerebellar peduncle • 2. ipsilateral proprioceptive information via inferior cerebellar peduncle from the spinal cord (input nerves=climbing and mossy fibers)
167
Q

what is the output from the cerebellum?

A
  1. purkinje fibers to deep nuclei • 2. sends information to contralateral cortex to modulate movement
168
Q

what are the features of the system of output nerves emerging from the cerebellum?

A

output nerves= purkinje fibers send information to deep nuclei of cerebellum, which in turn sends information to the contralateral cortex via the superior cerebellar peduncle

169
Q

what are the deep nuclei of the cerebellum lateral → medial?

A

Dentate • Emboliform • Globose • Fastigial • (don’t eat greasy foods)

170
Q

function of lateral cerebellar nuclei?

A

voluntary movement of extremities

171
Q

function of the medial nuclei of cerebellum?

A

balance, truncal coordination

172
Q

what happens when lateral nuclei of cerebellum are injured?

A

propensity to fall toward injured (ipsilateral) side

173
Q

basal ganglia are important in what?

A

voluntary movements and making postural adjustments

174
Q

basal ganglia do what?

A

receives cortical input and provides negative feedback to cortex to modulate movement

175
Q

what makes up the Striatum?

A

putamen (motor) + caudate (cognitive)

176
Q

what makes up the lentiform nucleus?

A

putamen + globus pallidus

177
Q

what happens in the excitatory pathway of basal ganglia?

A

cortical inputs stimulate the striatum, stimulating the release of GABA, which disinhibits the thalamus via the Globus pallidus internus/Substantia Nigra reticulata (↑ motion)

178
Q

what happens in the inhibitory pathway of basal ganglia?

A

cortical inputs stimulate the striatum, which disinhibits Subthalamic nucleus via Globus pallidus externus and STN stimulates GPi/SNr to inhibit the thalamus (↓ motion)

179
Q

what are the effects of dopamine in the basal ganglia?

A

Dopamine binds to D1 receptors, stimulating the excitatory pathway, and to D2, inhibiting the inhibitory pathway → ↑ motion

180
Q

what is PArkinson’s disease?

A

degenerative disorder of the CNS associated with Lewy bodies and loss of dopaminergic neurons of the substantia nigra pars compacta

181
Q

Lewy bodies in Parkinson’s disease are composed of what?

A

α-synuclein- intracellular inclusion

182
Q

what happens to your body in Parkinsons?

A

it becomes a TRAP • Tremor at rest • cogwheel Rigidity • Akinesia • Postural instability

183
Q

what is the inheritance of Huntington’s disease?

A

autosomal dominant

184
Q

what causes Huntington’s?

A

trinucleotide repeats • CAG • Caudate loses ACh and GABA

185
Q

Huntington’s is characterized by what?

A

chorea, agression, depression, and dementia (sometimes initially mistaken for substance abuse)

186
Q

Neuronal death in Huntingtons is via what?

A

NMDA-R binding and glutamate toxicity

187
Q

what can be seen on imaging in huntingtons?

A

atrophy of striatal nuclei (main inhibitors of movement)

188
Q

what is the presentation of hemiballismus?

A

sudden, wild flailing of 1 arm +/- ipsilateral leg

189
Q

what is the characteristic lesion causing hemiballismus?

A

contralateral subthalamic nucleus (e.g. lacunar stroke)

190
Q

what is the presentation of Chorea?

A

sudden, jerky, purposeless movements

191
Q

what is the characteristic lesion causing chorea?

A

Basal ganglia (e.g. Huntington’s)

192
Q

what is the presentation of athetosis?

A

slow writhing movements; epecially seenin fingers • writhing snake like movement

193
Q

what is the characteristic lesion causing athetosis?

A

Basal ganglia (e.g. huntingtons)

194
Q

what is the presentation of myoclonus?

A

sudden, brief, uncontrolled muscle contraction

195
Q

what is the typical picture of myoclonus?

A

jerks; hiccups; common in metabolic abnormalities such as renal and liver failure

196
Q

what is the presentation of dystonia?

A

sustained, involuntary muscle contractions

197
Q

what are the typical pictures of dystonia?

A

writer’s cramp; • blepharospasm (sustained eyelid twitch)

198
Q

what is the presentation of essential tremor (postural tremor)?

A

action tremor; exacerbated by holding posture/limb position

199
Q

what causes essential tremor?

A

genetic predisposition

200
Q

patients with essential tremor typically self medicate with what?

A

alcohol, decreases tremor amplitude

201
Q

what is the treatment for essential tremor?

A

β blockers, primidone

202
Q

what is the presentation of Resting tremor?

A

uncontrolled movement of distal appendages (most noticeable in hands); tremor alleviated by intentional movement

203
Q

what is the characteristic lesion causing resting tremor?

A

Parkinsons disease

204
Q

what is the presentation of intention tremor?

A

slow, zigzag motion when pointing/extending toward a target

205
Q

what is the characteristic lesion causing intention tremor?

A

cerebellar dysfunction

206
Q

lower extremity deficit in sensation or movement may indicate involvement of what?

A

anterior cerebral artery

207
Q

what are the consequences of a bilateral lesion of the amygdala?

A

Kluver-Bucy syndrome

208
Q

what are the clinical features of Kluver-Bucy syndrome?

A

hyperorality • hypersexuality • disinhibited behavior

209
Q

Kluver-Bucy syndrome is associated with what?

210
Q

what are consequences of frontal lobe lesions?

A

disinhibition and deficits in concentration, orientation, and judgement; • may have reemergence of primitive reflexes

211
Q

what is the consequence of a lesion in the right parietal lobe?

A

spatial neglect syndrome (agnosia of the contralateral side of the word)

212
Q

what are the consequences of a lesion to the reticular activating system (midbrain)?/

A

reduced levels of arousal and wakefulness (coma)

213
Q

what are the consequences of bilateral lesion to the mamillary bodies?

A

Wernicke-Korsakoff syndrome

214
Q

what are the clinical features of Wernicke-Korsakoff syndrome?

A

confusion, ophthalmoplegia, ataxia; memory loss (anterograde and retrograde amnesia), confabulation, personality changes

215
Q

Wernicke Korsakoff syndrome is associated with what?

A

thiamine deficiency and excessive EtOH use

216
Q

how can Wernicke Korsakoff syndrome be precipitated?

A

giving glucose without B1 to a B1 deficient patient

217
Q

what are the consequences of a basal ganglia lesion?

A

may result in tremor at rest, chorea, or athetosis

218
Q

what are the consequences of a lesion in the cerebellar hemisphere?

A

intention tremor • limb ataxia • damage →ipsilateral deficit. fall toward side of lesion

219
Q

what are the consequences of a lesion to the cerebellar vermis?

A

truncal ataxia, dysarthria

220
Q

what is the difference between lesions to the cerebellar hemispheres and cerebellar vermis?

A

cerebellar hemispheres are laterally located- affect lateral limbs • vermis is centrally located- affects central body

221
Q

what are the consequences of a lesion to the subthalamic nucleus?

A

contralateral hemiballismus

222
Q

what are the consequences of a lesion to the hippocampus ?

A

anterograde amnesia

223
Q

what are the consequences of a lesion to the paramedian pontine reticular formation?

A

eyes look away from the lesion

224
Q

what are the consequences of a lesion to the frontal eye fields?

A

eyes look toward lesions

225
Q

what are the clinical features of central pontine myelisnosis?

A

acute paralysis • dysarthria • dysphagia • diplopia • loss of consciousness

226
Q

central pontine myelinosis can cause what?

A

locked in syndrome

227
Q

what is central pontine myelinosis?

A

massive axonal demyelination in pontine white matter tracts

228
Q

what causes central pontine myelinosis?

A

commonly iatrogenic, caused by overly rapid correction of Na levels

229
Q

what is aphasia?

A

higher order inability to speak (language deficit)

230
Q

what is dysarthria?

A

motor inability to speak (movement deficit)

231
Q

what is Broca’s aphasia?

A

nonfluent aphasia with intact comprehension

232
Q

where is Broca’s area?

A

inferior frontal gyrus of frontal lobe

233
Q

what is Wernicke’s aphasia?

A

fluent aphasia with impaired comprehension

234
Q

where is Wernicke’s area?

A

superior temporal gyrus of temporal lobe

235
Q

what is global aphasia?

A

nonfluent aphasia with impaired comprehension

236
Q

what areas are affected in global aphasia?

A

both Broca’s and Wernicke’s

237
Q

what is conduction aphasia?

A

poor repetition but fluent speech, intact comprehension

238
Q

conduction aphasia can be caused by what?

A

damage to arcuate fasciculus

239
Q

anterior cerebral artery supplies what?

A

anteromedial surface of cortex

240
Q

middle cerebral artery supplies what?

A

lateral surface of cortex

241
Q

posterior cerebral artery supplies what?

A

posterior and inferior surface of cortex

242
Q

where are the watershed zones in cerebral circulation?

A

between anterior cerebral/middle cerebral, posterior cerebral/middle cerebral arteries

243
Q

watershed areas of cerebral circulation are damaged in what?

A

severe hypotension

244
Q

consequences for the watershed areas of cerebral circulation of severe hypotension?

A

upper leg/upper arm weakness, defects in higher-order visual processing

245
Q

cerebral perfusion is primarily driven by what?

246
Q

what is the effect of therpeutic hyperventilation on brain?

A

↓pCO2 helps ↓ICP in cases of acute cerebral edema (stroke, trauma) via decreasing cerebral perfusion

247
Q

what are the vessels of the anterior circulation of the brain?

A

MCA • ACA • Lateral striate artery

248
Q

what is the functional distribution of the areas supplied by the MCA?

A
  1. Motor cortex- upper limb and face • 2. Sensory cortex- upper limb and face • 3. Temporal lobe (Wernicke’s area); frontal lobe (broca’s area)
249
Q

what are the symptoms of a stroke to the motor cortex supplied by the MCA?

A

contralateral paralysis- upper limb and face

250
Q

what are the symptoms of a stroke to the sensory cortex supplied by the MCA?

A

contralateral loss of sensation- upper limb and face

251
Q

what are the symptoms of stroke to the temporal lobe and/or frontal lobe supplied by the MCA?

A

aphasia fi in dominant (usually left) hemisphere. • hemineglect if lesion affects nondominant (usually right) side

252
Q

what are the functional distributions of the areas supplied by the ACA?

A
  1. Motor cortex-lower limb • 2. Sensory cortex- lower limb
253
Q

what are the symptoms of a stroke affecting the area of the motor cortex supplied by the ACA?

A

contralateral paralysis- lower limb

254
Q

what are the symptoms of a stroke affecting the area of the sensory cortex supplied by the ACA?

A

contralateral loss of sensation- lower limb

255
Q

what are the structures that are supplied by the lateral striate artery?

A

striatum • internal capsule

256
Q

what are the symptoms of a stroke to the area supplied by the lateral striate artery?

A

striatum, internal capsule→ contralateral hemiparesis/hemiplegia

257
Q

what are the strokes common to the area supplied by the lateral striate artery?

A

striatum and internal capsule are common locations of lacunar infarcts, 2° to unmanaged hypertension

258
Q

what is ACA?

A

anterior cerebral artery

259
Q

what is AComm?

A

Anterior Communicating Artery

260
Q

what is AICA?

A

Anterior Inferior Cerebellar artery

261
Q

what is MCA?

A

middle cerebral artery

262
Q

what is PCA?

A

Posterior cerebral artery

263
Q

what is PComm?

A

posterior communicating artery

264
Q

what is PICA?

A

posterior inferior cerebellar artery

265
Q

what are the arteries of the posterior circulation of the brain?

A

ASA • PICA • AICA • PCA

266
Q

what are the structures supplied by the anterior spinal artery (ASA) that are vulnerable to stroke?

A
  1. Lateral corticospinal tract • 2. Medial lemniscus • 3. Caudal medulla- hypoglossal nerve
267
Q

what are the symptoms of an ASA stroke of the lateral corticospinal tract?

A

contralateral hemiparesis- lower limbs

268
Q

what are the symptoms of an ASA stroke in the medial lemniscus?

A

↓contralateral proprioception

269
Q

what are the symptoms of an ASA stroke in the caudal medulla- hyposglossal nerve?

A

inpsilateral hypoglossal dysfunction (tongue deviates ipsilaterally)

270
Q

what is the relative side frequency of ASA strokes?

A

commonly bilateral

271
Q

Medial medullary syndrome is caused by what?

A

infarct of paramedian branches of ASA and vertebral arteries

272
Q

what are the structures supplied by the PICA that are vulnerable to stroke?

A

Lateral Medulla- • - vestibular nuclei • - lateral spinothalamic tract • - spinal trigeminal nucleus • - nucleus ambiguus • - sympathetic fibers • - inferior cerebellar peduncle

273
Q

what are the symptoms of a PICA stroke in the lateral medulla?

A
  1. vomiting • 2. vertigo • 3. ↓ pain and temperature sensation to limbs/ face • 4. dysphagia • 5. hoarseness • 6. ↓ gag reflex • 7. ipsilateral horner’s syndrome • 8. ataxia • 9. dysmetria
274
Q

what is the name of the disease state caused by PICA stroke to lateral medulla?

A

Lateral medullary (Wallenberg’s) syndrome

275
Q

which symptoms are specific to a PICA lesion?

A

nucleus ambiguus effects: • “Don’t pick a (PICA) horse (hoarseness) that can’t eat (dysphagia)”

276
Q

what are structures supplied by the AICA that are vulnerable to stroke?

A
  1. Lateral pons- cranial nerve nuclei; vestibular nuclei, facial nucleus, spinal trigeminal nucleus, cochlear nuclei, sympathetic fibers • 2. middle and inferior cerebellar peduncles
277
Q

what are the symptoms of AICA stroke in the lateral pons?

A
  1. vomiting • 2. vertigo • 3. nystagmus • 4. paralysis of face • 5. ↓ lacrimation, salivation • 6. ↓ taste from anterior 2/3 of tongue • 7. ↓ corneal reflex • 8. Face- ↓ pain & temperature sensation • 9. Ipsilateral ↓ hearing • 10. ipsilateral horner’s syndrome
278
Q

what are the symptoms of AICA stroke in the middle and inferior cerebellar peduncles?

A

ataxia • dysmetria

279
Q

what is the name of the disease state caused by a stroke of the AICA?

A

lateral pontine syndrome

280
Q

which symptoms are specific to AICA lesions?

A

facial nucleus effects • “Facial droop means AICA’s pooped”

281
Q

what are the structures supplied by the PCA that are vulnerable to stroke?

A

occipital cortex • visual cortex

282
Q

what are the symptoms of a PCA stroke in the occipital cortex, visual cortex?

A

contralateral hemianopia with macular sparing

283
Q

what are the communicating arteries of the brain circulation?

A

AComm • PComm

284
Q

lesions of AComm are typically what?

A

aneurysms not strokes

285
Q

AComm is a commone site of what lesions?

A

saccular (berry) aneurysm

286
Q

saccular (berry) aneurysm of AComm → what?

A

impingement on cranial nerves

287
Q

symptoms of a berry aneurysm of AComm?

A

visual field defects

288
Q

lesions of PComm are typically what?

A

aneurysms, not strokes

289
Q

PComm is a common site of what lesion?

A

saccular (berry) aneurysm

290
Q

what are the symptoms of PComm berry aneurysm?

A

CNIII palsy- eye is down and out with ptosis and pupil dilation

291
Q

berry aneurysms occur where?

A

at the bifurcations in the circle of Willis

292
Q

most common site of berry aneurysm?

A

bifurcation of AComm

293
Q

what is the most common complication of berry aneurysm?

294
Q

rupture of berry aneurysm leads to what?

A

SAH or hemorrhagic stroke

295
Q

rupture of berry aneurysm can cause which symptoms?

A

bitemporal hemianopia via compression of optic chiasm

296
Q

berry aneurysms are associated with what?

A

ADPKD • ED • Marfan’s syndrome

297
Q

other risk factors for berry aneurysm include what?

A

advanced age • htn • smoking • black race

298
Q

Charcot-Bouchard microanerysm is associated with what?

A

chronic hypertension

299
Q

charcot-bouchard microanerysm affects what?

A

small vessels in basal ganglia, thalamus

300
Q

what causes epidural hematoma?

A

rupture of middle meningeal artery (branch of maxillary artery), often 2° to fracture of temporal bone

301
Q

how does epidural hematoma present clinically?

A

lucid interval→ • rapid expansion under systemic arterial pressure → transtentorial herniation, CNIII palsy

302
Q

CT scan of epidural hematoma shows what?

A

biconvex (lentiform), hyperdense blood collection not crossing suture lines. • Can cross falx, tentorium

303
Q

what causes subdural hematoma?

A

rupture of bridging veins

304
Q

how does subdural hematoma present clinically?

A

slow venous bleeding (less pressure= hematoma develops over time)

305
Q

subdural hematoma is seen in whom?

A

elderly individuals • alcoholics • blunt trauma • shaken baby

306
Q

predisposing factors to subdural hematoma include what?

A

brain atrophy • shaking • whiplash

307
Q

how does subdural hematoma look on CT?

A

crescent shaped hemorrhage that crosses suture lines. midline shift. Cannot cross falx, tentorium

308
Q

what causes subarachnoid hemorrhage?

A

rupture of an aneurysm (such as a berry [saccular] aneurysm, as seen in Marfan’s, ED, ADPKD) or an AVM

309
Q

what is the clinical presentation of subarachnoid hemorrhage?

A

rapid time course • WHOML • bloody or yellow spinal tap

310
Q

risk 2 or 3 days after SAH?

A

risk of vasospasm due to blood breakdown (not visible on CT, treat ith nimodipine) and rebleed (visible on CT)

311
Q

Intraparenchymal hemorrhage is most commonly caused by what?

A

systemic hypertension

312
Q

intraparenchymal hemorrhage is also seen with what?

A

amyloid angiopathy • vasculitis • neoplasm

313
Q

where does intraparenchymal hemorrhage typically occur?

A

in basal ganglia and internal capsule (Charcot-Bouchard aneurysm of lenticulostriate vessels), but can be lobar

314
Q

in ischemic brain disease/stroke irreversible damage begins when?

A

after 5 minutes of hypoxia

315
Q

which parts of the brain are most vulnerable to ischemic brain disease/stroke?

A

hippocampus • neocortex • cerebellum • watershed areas

316
Q

what are the findings in the different stages of the progression of irreversible neuronal injury?

A
  1. red neurons (12-48 h) • 2. necrosis and neutrophils (24-72h) • 3. macrophages (3-5 days) • 4. reactive gliosis and vascular proliferation (1-2 weeks) • 5. glial scar (>2weeks)
317
Q

how does stroke look on diffusion weighted MRI?

A

bright in 3-30min and stays bright for 10 days

318
Q

how does stroke look on noncontrast CT?

A

dark in ~24 h

319
Q

in stroke, bight areas on noncontrast CT indicate what?

A

hemorrhage (tPA contraindicated)

320
Q

what does atherosclerosis do to the brain?

A

thrombi lead to ischemic stroke with subsequent necrosis→ cystic cavity with reactive gliosis

321
Q

what happens in hemorrhagic stroke?

A

intracerebral bleeding, often due to hypertension, anticoagulation, and cancer (abnormal vessels can bleed).

322
Q

hemorrhagic stroke can be secondary to what?

A

ischemic stroke followed by reperfusion (↑ vessel fragility)

323
Q

what happens in ischemic stroke?

A

atherosclerotic emboli block large vessels

324
Q

etiologies of ischemic stroke include what?

A

atrial fibrillation • carotid dissection • patent foramen ovale • endocarditis

325
Q

lacunar strokes block what?

A

small vessels

326
Q

lacunar strokes may be 2° to what?

A

hypertension

327
Q

what is the treatment for ischemic stroke?

A

tPA within 4.5 hours (so long as patient presents within 3 hours of onset and there is no major risk of hemorrhage)

328
Q

what is a transient ischemic attack?

A

Brief, irreversible episode of focal neurologic dysfunction typically lasting < 1 hour without acute infarction (-) MRI

329
Q

;deficits in TIA are due to what?

A

focal ischemia

330
Q

what are dural venous sinuses?

A

large venous channels that run through the dura

331
Q

what do dural venous sinuses do?

A

drain blood from cerebral veins and receive CSF from arachnoid granulations

332
Q

dural venous sinuses empty into where?

A

jugular vein

333
Q

what is the main location of CSF return via arachnoid granulations?

A

superior sagital sinus

334
Q

Inferior sagital sinus drains to what?

A

straight sinus

335
Q

superior sagital sinus drains to what?

A

typically becomes right transverse sinus or confluence of sinuses

336
Q

straight sinus drains to what?

A

typically becomes left transverse sinus or confluence of sinuses

337
Q

occipital sinus drains to what?

A

confluence of sinuses

338
Q

confluence of sinuses drain to what?

A

right and left transverse sinuses

339
Q

sphenoparietal sinuses drain to what?

A

cavernous sinuses

340
Q

lateral ventricles drain to what?

A

3rd ventricle via right and left intraventricular foramina of Monro

341
Q

3rd ventricle drains to what?

A

4th ventricle via cerebral aqueduct of Sylvius

342
Q

4th ventricle drains to what?

A

subarachnoid space via: • foramina of Lushka= Lateral • foramen of Magendie= medial

343
Q

CSF is made by what?

A

ependymal cells of choroid plexus

344
Q

CSF is reabsorbed by what?

A

arachnoid granulations and then drains into dural venous sinuses

345
Q

what are the 3 types of nonobstructive hydrocephalus?

A
  1. Communicating hydrocephalus • 2. Normal pressure hydrocephalus • 3. Hydrocephalus ex vacuo
346
Q

what happens in communicating hydrocephalus?

A

↓ CSF absorption by arachnoid granulations

347
Q

Communicating hydrocephalus can lead to what?

A

↑ ICP, papilledema, herniation (e.g. arachnoid scarring post-meningitis)

348
Q

normal pressure hydrocephalus results in what?

A

↑subarachnoid space volume but no increase in CSF pressure

349
Q

in normal pressure hydrocephalus, expansion of ventricles does what?

A

distorts the fibers of the corona radiata and leads to the clinical triad of urinary incontinence, ataxia, cognitive dysfunction (sometimes reversible)

350
Q

what is hydrocephalus ex vacuo?

A

appearance of ↑ CSF in atrophy (e.g. AD, HIV, Pick’s disease)

351
Q

clinical presentation in hydrocephalus ex vacuo?

A

intracranial pressure is normal; triad is not seen

► Med Notes (62 decks)

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