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Flashcards in Principles in Neurology_1 Deck (351):
1

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

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

2

notochord induces overlying ectoderm to differentiate into what?

neuroectoderm and form the neural plate

3

neural plate gives rise to what?

the neural tube and neural crest cells

4

notochord becomes what in adults?

nucleus pulposus of the intervertebral disc

5

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

Alar plate: sensory

6

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

Basal plate: motor

7

what are the three primary vesicles of the developing brain?

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

8

what are the five secondary vesicles of the developing brain?

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

9

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

1. Telencephalon • 2. Diencephalon

10

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

1. Mesencephalon

11

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

1. Metencephalon • 2. Myelencephalon

12

the walls of the telencephalon give rise to what?

cerebral hemispheres

13

the cavities of the telencephalon give rise to what?

lateral ventricles

14

the walls of the diencephalon give rise to what?

thalamus

15

the cavities of the diencephalon give rise to what?

third ventricle

16

the walls of the mesencephalon give rise to what?

midbrain

17

the cavities of the mesencephalon give rise to what?

aqueduct

18

the walls of the metencephalon give rise to what?

Pons and Cerebellum

19

the cavities of the metencephalon give rise to what?

upper part of fourth ventricle

20

the walls of the myelencephalon give rise to what?

medulla

21

the cavities of the myelencephalon give rise to what?

lower part of the fourth ventricle

22

what happens in neural tube defect?

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

23

neural tube defects are associated with what?

low folic acid intake before conception and during pregnancy

24

what are the lab levels in neural tube defect?

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

25

why is it that AChE can be measured in NTD?

fetal AChE in CSF transudates across defect into the amniotic fluid

26

what is spina bifida occulta?

failure of bony canal to close, but no structural herniation

27

spina bifida occulta is usually seen where?

lower vertebral levels

28

status of dura in spina bifida occulta?

intact

29

spina bifida occulta is associated with what?

tuft of hair or skin dimple at level of bony defect

30

what is meningocele?

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

31

what is meningomyelocele?

meninges and spinal cord herniate through spinal canal defect

32

what are the types of forebrain anomalies?

anencephaly • holoprosencephaly

33

what happens in anencephaly?

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

34

what are the clinical findings in anencephaly?

↑AFP, polyhydramnios

35

why is there polyhydramnios in anencephaly?

no swallowing center in the brain

36

anencephaly is associated with what?

maternal diabetes type I

37

what decreases the risk of anencephaly?

folate supplementation

38

what is holoprosencephaly?

failure of left and right hemispheres to separate

39

when does holoprosencephaly happen?

usually occurs during weeks 5-6

40

what is the etiology of holoprosencephaly?

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

41

what is the spectrum of severity of holoprosencephaly?

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

42

what are the posterior fossa malformations?

Chiari II (Arnold-Chiari malformation) • Dandy Walker

43

what is an Arnold Chiari malformation?

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

44

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

thoraco-lumbar myelomeningocele and paralysis below the defect

45

what is a Dandy-Walker malformation?

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

46

Dandy Walker malformation is associated with what?

hydrocephalus and spina bifida

47

what is syringomyelia?

cystic enlargement of central canal of spinal cord

48

which fibers of spinal cord are damaged first in syringomyelia?

crossing fibers of spinothalamic tract

49

syringomyelia results in what?

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

50

syringomyelia is associated with what?

Chiari I malformation

51

what is Chiari I malformation?

>3-5mm cerebellar tonsillar ectopia

52

where is syringomyelia most common?

C8-T1

53

which embryonic structures form the tongue?

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

54

muscles of the tongue are derived from what?

occipital myotomes

55

which nerves carry taste?

CN VII, IX, X (solitary nucleus)

56

which nerves carry tongue pain?

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

57

which nerve is responsible for motor function of tongue?

CN-XII

58

neuroectoderm gives rise to which neural tissue?

CNS neurons • ependymal cells • oligodendroglia • astrocytes

59

neural crest gives rise to which neural tissue?

PNS neurons • schwann cells

60

mesoderm gives rise to which neural tissue?

Microglia

61

which are the signal transmitting cells of the nervous system?

neurons

62

how often do neurons divide?

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

63

what are neurons?

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

64

cell bodies and dendrites of neurons can be stained how?

via the Nissl substance (stains RER)

65

why doesn't Nissl stain the axon?

RER is not present in the axon

66

what happens if an axon is injured?

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

67

what are the functions of astrocytes?

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

68

how do astrocytes respond to injury?

reactive gliosis

69

what is the astrocyte marker?

GFAP

70

what are microglia?

CNS phagocytes • Scavenger cells of CNS

71

what is the germ layer origin of microglia?

mesoderm

72

how do microglia stain with Nissl?

not readily discernable in Nissl stains

73

what is the function of microglia?

respond to tissue damage by differentiating into large phagocytic cells

74

what happens to microglia in HIV?

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

75

what is the function of myelin?

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

76

the function of myelin results in what action?

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

77

what makes myelin in the CNS?

oligodendrocytes

78

what makes myelin in the PNS?

Schwann cells

79

Each oligodendrocyte myelinates how many CNS axons?

multiple (up to 50 each)

80

how do oligodendroglia appear in Nissl stain?

much smaller nuclei with dark chromatin and little cytoplasm

81

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

oligodendrocyte

82

oligodendroglia are destroyed in which disease?

MS

83

how do oligodendroglia look in H&E stain?

like fried eggs

84

each Schwann cell myelinates how many PNS axons?

only 1

85

Schwann cells also promote what?

axonal regeneration

86

Scwhann cells are derived from what?

Neural crest

87

Schwann cells are destroyed in which disease?

Guillan-Barre syndrome

88

what is Acoustic neuroma?

type of Schwannoma typically located in internal acoustic meatus CNVIII

89

what are the 2 types of free nerve endings?

C • Aδ

90

what type of fibers are C fibers?

slow, unmyelinated fibers

91

what type of fibers are Aδ fibers?

fast, myelinated fibers

92

what are the locations of C fibers and Aδ fibers?

All skin, epidermis, some viscera

93

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

Pain and temperature

94

what type of fibers are Meissner's corpuscles?

Large, myelinated fibers that adapt quickly

95

what is the location of Meissner's corpuscles?

glabrous (hairless) skin

96

what are the senses carried by Meissner's corpuscles?

dynamic, fine/light touch; position sense

97

what type of fibers are Pacinian corpuscles?

Large, myelinated fibers

98

what is the location of Pacinian corpuscles?

deep skin layers, ligaments, and joints

99

what are the senses carried by pacinian fibers?

vibration • pressure

100

what type of fibers are Merkel's discs?

Large, myelinated fibers that adapt slowly

101

what is the location of Merkel's discs?

hair follicles

102

what are the senses carried by Merkel's discs?

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

103

what is the endoneurium of a peripheral nerve?

invests single nerve fiber layers

104

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

Guillain-Barre

105

which part of the peripheral nerve forms the permeability barrier?

Perineurium

106

the perineurium of a peripheral nerve surrounds what?

a fascicle of nerve fibers

107

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

Perineurium

108

what is the epineurium of a peripheral nerve?

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

109

how does NE change in disease?

↑ in anxiety • ↓ in depression

110

where is NE synthesized in the brain?

Locus ceruleus (pons)

111

how does dopamine change in disease?

↑ in schizophrenia • ↓ in Parkinsons • ↓ in depression

112

where is dopamine synthesized in the brain?

Ventral tegmentum and SNc (midbrain)

113

how does 5-HT change in disease?

↓ in anxiety • ↓ in depression

114

where is 5HT synthesized in the brain?

Raphe nucleus (pons)

115

how does ACh change in disease?

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

116

where is ACh synthesized in the brain?

Basal nucleus of Meynert

117

how does GABA change in disease?

↓ in anxiety • ↓ in Huntingtons

118

where is GABA made in the brain?

Nucleus accumbens

119

Functions of the Locus ceruleus?

stress and pain

120

functions of the nucleus accumbens and septal nucleus?

reward center • pleasure • addiction • fear

121

Blood brain barrier does what?

prevents circulating blood substances from reaching the CSF/CNS

122

blood brain barrier is formed by which 3 structures?

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

123

can glucose and amino acids cross BBB?

glucose and amino acids cross slowly by carrier mediated transport mechanism

124

do nonpolar/lipid soluble substances cross BBB?

cross rapidly via diffusion

125

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

area postrema- vomiting after chemo • OVLT- osmotic sensing

126

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?

neurohypophysis- ADH release

127

besides BBB what are the other notable barriers?

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

128

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

vasogenic edema

129

how do hypothalamic inputs and outputs get to their target?

they permeate the BBB

130

BBB helps prevent what?

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

131

what are the functions of the hypothalamus?

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

132

what are the inputs to the hypothalamus?

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

133

supraoptic nucleus of the hypothalamus makes what?

ADH

134

paraventricular nucleus of hypothalamus makes what?

oxytocin

135

Lateral area of hypothalamus controls what?

hunger

136

destruction of lateral area of hypothalamus → what?

anorexia, failure to thrive

137

lateral area of the hypothalamus is inhibited by what?

leptin

138

ventromedial area of the hypothalamus controls what?

satiety

139

what can destroy the ventromedial nucleus of the hypothalamus?

craniopharyngioma

140

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

hyperphagia

141

ventromedial area of the hypothalamus is stimulated by what?

leptin

142

anterior nucleus of hypothalamus controls what?

cooling, parasympathetic

143

posterior nucleus of hypothalamus controls what?

heating, sympathetic

144

the suprachiasmatic nucleus of the hypothalamus controls what?

circadian rhythm

145

posterior pituitary receives hypothalamic axonal projections from where?

supraoptic (ADH) and paraventricular (oxytocin) nuclei

146

what is the function of the thalamus?

major relay for all ascending sensory information except olfaction

147

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

spinothalamic and dorsal columns/medial lemniscus

148

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

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

149

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

1° somatosensory cortex

150

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

trigeminal and gustatory pathway

151

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

face sensation and taste

152

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

1° somatosensory cortex

153

what is the input to the LGN of the thalamus?

CN II

154

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

vision

155

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

Clacarine sulcus

156

what is the input to the MGN of the thalamus?

superior olive and inferior colliculus of tectum

157

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

hearing

158

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

auditory cortex of the temporal lobe

159

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

basal ganglia

160

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

motor

161

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

motor cortex

162

what is the limbic system?

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

163

limbic system structures include what?

hippocampus • amygdala • fornix • mammillary bodies • cingulate gyrus

164

limbic system is responsible for what?

Feeding • Fleeing • Fighting • Feeling • Sex

165

cerebellum modulates what?

movement; aids in coordination and balance

166

what is the input to the cerebellum?

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

what is the output from the cerebellum?

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

168

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

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

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

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

170

function of lateral cerebellar nuclei?

voluntary movement of extremities

171

function of the medial nuclei of cerebellum?

balance, truncal coordination

172

what happens when lateral nuclei of cerebellum are injured?

propensity to fall toward injured (ipsilateral) side

173

basal ganglia are important in what?

voluntary movements and making postural adjustments

174

basal ganglia do what?

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

175

what makes up the Striatum?

putamen (motor) + caudate (cognitive)

176

what makes up the lentiform nucleus?

putamen + globus pallidus

177

what happens in the excitatory pathway of basal ganglia?

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

178

what happens in the inhibitory pathway of basal ganglia?

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

179

what are the effects of dopamine in the basal ganglia?

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

180

what is PArkinson's disease?

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

181

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

α-synuclein- intracellular inclusion

182

what happens to your body in Parkinsons?

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

183

what is the inheritance of Huntington's disease?

autosomal dominant

184

what causes Huntington's?

trinucleotide repeats • CAG • Caudate loses ACh and GABA

185

Huntington's is characterized by what?

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

186

Neuronal death in Huntingtons is via what?

NMDA-R binding and glutamate toxicity

187

what can be seen on imaging in huntingtons?

atrophy of striatal nuclei (main inhibitors of movement)

188

what is the presentation of hemiballismus?

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

189

what is the characteristic lesion causing hemiballismus?

contralateral subthalamic nucleus (e.g. lacunar stroke)

190

what is the presentation of Chorea?

sudden, jerky, purposeless movements

191

what is the characteristic lesion causing chorea?

Basal ganglia (e.g. Huntington's)

192

what is the presentation of athetosis?

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

193

what is the characteristic lesion causing athetosis?

Basal ganglia (e.g. huntingtons)

194

what is the presentation of myoclonus?

sudden, brief, uncontrolled muscle contraction

195

what is the typical picture of myoclonus?

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

196

what is the presentation of dystonia?

sustained, involuntary muscle contractions

197

what are the typical pictures of dystonia?

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

198

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

action tremor; exacerbated by holding posture/limb position

199

what causes essential tremor?

genetic predisposition

200

patients with essential tremor typically self medicate with what?

alcohol, decreases tremor amplitude

201

what is the treatment for essential tremor?

β blockers, primidone

202

what is the presentation of Resting tremor?

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

203

what is the characteristic lesion causing resting tremor?

Parkinsons disease

204

what is the presentation of intention tremor?

slow, zigzag motion when pointing/extending toward a target

205

what is the characteristic lesion causing intention tremor?

cerebellar dysfunction

206

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

anterior cerebral artery

207

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

Kluver-Bucy syndrome

208

what are the clinical features of Kluver-Bucy syndrome?

hyperorality • hypersexuality • disinhibited behavior

209

Kluver-Bucy syndrome is associated with what?

HSV-1

210

what are consequences of frontal lobe lesions?

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

211

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

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

212

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

reduced levels of arousal and wakefulness (coma)

213

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

Wernicke-Korsakoff syndrome

214

what are the clinical features of Wernicke-Korsakoff syndrome?

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

215

Wernicke Korsakoff syndrome is associated with what?

thiamine deficiency and excessive EtOH use

216

how can Wernicke Korsakoff syndrome be precipitated?

giving glucose without B1 to a B1 deficient patient

217

what are the consequences of a basal ganglia lesion?

may result in tremor at rest, chorea, or athetosis

218

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

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

219

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

truncal ataxia, dysarthria

220

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

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

221

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

contralateral hemiballismus

222

what are the consequences of a lesion to the hippocampus ?

anterograde amnesia

223

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

eyes look away from the lesion

224

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

eyes look toward lesions

225

what are the clinical features of central pontine myelisnosis?

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

226

central pontine myelinosis can cause what?

locked in syndrome

227

what is central pontine myelinosis?

massive axonal demyelination in pontine white matter tracts

228

what causes central pontine myelinosis?

commonly iatrogenic, caused by overly rapid correction of Na levels

229

what is aphasia?

higher order inability to speak (language deficit)

230

what is dysarthria?

motor inability to speak (movement deficit)

231

what is Broca's aphasia?

nonfluent aphasia with intact comprehension

232

where is Broca's area?

inferior frontal gyrus of frontal lobe

233

what is Wernicke's aphasia?

fluent aphasia with impaired comprehension

234

where is Wernicke's area?

superior temporal gyrus of temporal lobe

235

what is global aphasia?

nonfluent aphasia with impaired comprehension

236

what areas are affected in global aphasia?

both Broca's and Wernicke's

237

what is conduction aphasia?

poor repetition but fluent speech, intact comprehension

238

conduction aphasia can be caused by what?

damage to arcuate fasciculus

239

anterior cerebral artery supplies what?

anteromedial surface of cortex

240

middle cerebral artery supplies what?

lateral surface of cortex

241

posterior cerebral artery supplies what?

posterior and inferior surface of cortex

242

where are the watershed zones in cerebral circulation?

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

243

watershed areas of cerebral circulation are damaged in what?

severe hypotension

244

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

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

245

cerebral perfusion is primarily driven by what?

pCO2

246

what is the effect of therpeutic hyperventilation on brain?

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

247

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

MCA • ACA • Lateral striate artery

248

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

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

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

contralateral paralysis- upper limb and face

250

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

contralateral loss of sensation- upper limb and face

251

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

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

252

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

1. Motor cortex-lower limb • 2. Sensory cortex- lower limb

253

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

contralateral paralysis- lower limb

254

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

contralateral loss of sensation- lower limb

255

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

striatum • internal capsule

256

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

striatum, internal capsule→ contralateral hemiparesis/hemiplegia

257

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

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

258

what is ACA?

anterior cerebral artery

259

what is AComm?

Anterior Communicating Artery

260

what is AICA?

Anterior Inferior Cerebellar artery

261

what is MCA?

middle cerebral artery

262

what is PCA?

Posterior cerebral artery

263

what is PComm?

posterior communicating artery

264

what is PICA?

posterior inferior cerebellar artery

265

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

ASA • PICA • AICA • PCA

266

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

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

267

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

contralateral hemiparesis- lower limbs

268

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

↓contralateral proprioception

269

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

inpsilateral hypoglossal dysfunction (tongue deviates ipsilaterally)

270

what is the relative side frequency of ASA strokes?

commonly bilateral

271

Medial medullary syndrome is caused by what?

infarct of paramedian branches of ASA and vertebral arteries

272

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

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

273

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

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

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

Lateral medullary (Wallenberg's) syndrome

275

which symptoms are specific to a PICA lesion?

nucleus ambiguus effects: • "Don't pick a (PICA) horse (hoarseness) that can't eat (dysphagia)"

276

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

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

277

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

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

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

ataxia • dysmetria

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

lateral pontine syndrome

280

which symptoms are specific to AICA lesions?

facial nucleus effects • "Facial droop means AICA's pooped"

281

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

occipital cortex • visual cortex

282

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

contralateral hemianopia with macular sparing

283

what are the communicating arteries of the brain circulation?

AComm • PComm

284

lesions of AComm are typically what?

aneurysms not strokes

285

AComm is a commone site of what lesions?

saccular (berry) aneurysm

286

saccular (berry) aneurysm of AComm → what?

impingement on cranial nerves

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symptoms of a berry aneurysm of AComm?

visual field defects

288

lesions of PComm are typically what?

aneurysms, not strokes

289

PComm is a common site of what lesion?

saccular (berry) aneurysm

290

what are the symptoms of PComm berry aneurysm?

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

291

berry aneurysms occur where?

at the bifurcations in the circle of Willis

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most common site of berry aneurysm?

bifurcation of AComm

293

what is the most common complication of berry aneurysm?

rupture

294

rupture of berry aneurysm leads to what?

SAH or hemorrhagic stroke

295

rupture of berry aneurysm can cause which symptoms?

bitemporal hemianopia via compression of optic chiasm

296

berry aneurysms are associated with what?

ADPKD • ED • Marfan's syndrome

297

other risk factors for berry aneurysm include what?

advanced age • htn • smoking • black race

298

Charcot-Bouchard microanerysm is associated with what?

chronic hypertension

299

charcot-bouchard microanerysm affects what?

small vessels in basal ganglia, thalamus

300

what causes epidural hematoma?

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

301

how does epidural hematoma present clinically?

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

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CT scan of epidural hematoma shows what?

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

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what causes subdural hematoma?

rupture of bridging veins

304

how does subdural hematoma present clinically?

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

305

subdural hematoma is seen in whom?

elderly individuals • alcoholics • blunt trauma • shaken baby

306

predisposing factors to subdural hematoma include what?

brain atrophy • shaking • whiplash

307

how does subdural hematoma look on CT?

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

308

what causes subarachnoid hemorrhage?

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

309

what is the clinical presentation of subarachnoid hemorrhage?

rapid time course • WHOML • bloody or yellow spinal tap

310

risk 2 or 3 days after SAH?

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

311

Intraparenchymal hemorrhage is most commonly caused by what?

systemic hypertension

312

intraparenchymal hemorrhage is also seen with what?

amyloid angiopathy • vasculitis • neoplasm

313

where does intraparenchymal hemorrhage typically occur?

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

314

in ischemic brain disease/stroke irreversible damage begins when?

after 5 minutes of hypoxia

315

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

hippocampus • neocortex • cerebellum • watershed areas

316

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

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

how does stroke look on diffusion weighted MRI?

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

318

how does stroke look on noncontrast CT?

dark in ~24 h

319

in stroke, bight areas on noncontrast CT indicate what?

hemorrhage (tPA contraindicated)

320

what does atherosclerosis do to the brain?

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

321

what happens in hemorrhagic stroke?

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

322

hemorrhagic stroke can be secondary to what?

ischemic stroke followed by reperfusion (↑ vessel fragility)

323

what happens in ischemic stroke?

atherosclerotic emboli block large vessels

324

etiologies of ischemic stroke include what?

atrial fibrillation • carotid dissection • patent foramen ovale • endocarditis

325

lacunar strokes block what?

small vessels

326

lacunar strokes may be 2° to what?

hypertension

327

what is the treatment for ischemic stroke?

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

328

what is a transient ischemic attack?

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

329

;deficits in TIA are due to what?

focal ischemia

330

what are dural venous sinuses?

large venous channels that run through the dura

331

what do dural venous sinuses do?

drain blood from cerebral veins and receive CSF from arachnoid granulations

332

dural venous sinuses empty into where?

jugular vein

333

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

superior sagital sinus

334

Inferior sagital sinus drains to what?

straight sinus

335

superior sagital sinus drains to what?

typically becomes right transverse sinus or confluence of sinuses

336

straight sinus drains to what?

typically becomes left transverse sinus or confluence of sinuses

337

occipital sinus drains to what?

confluence of sinuses

338

confluence of sinuses drain to what?

right and left transverse sinuses

339

sphenoparietal sinuses drain to what?

cavernous sinuses

340

lateral ventricles drain to what?

3rd ventricle via right and left intraventricular foramina of Monro

341

3rd ventricle drains to what?

4th ventricle via cerebral aqueduct of Sylvius

342

4th ventricle drains to what?

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

343

CSF is made by what?

ependymal cells of choroid plexus

344

CSF is reabsorbed by what?

arachnoid granulations and then drains into dural venous sinuses

345

what are the 3 types of nonobstructive hydrocephalus?

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

346

what happens in communicating hydrocephalus?

↓ CSF absorption by arachnoid granulations

347

Communicating hydrocephalus can lead to what?

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

348

normal pressure hydrocephalus results in what?

↑subarachnoid space volume but no increase in CSF pressure

349

in normal pressure hydrocephalus, expansion of ventricles does what?

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

350

what is hydrocephalus ex vacuo?

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

351

clinical presentation in hydrocephalus ex vacuo?

intracranial pressure is normal; triad is not seen