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
2
Q
notochord induces overlying ectoderm to differentiate into what?
A
neuroectoderm and form the neural plate
3
Q
neural plate gives rise to what?
A
the neural tube and neural crest cells
4
Q
notochord becomes what in adults?
A
nucleus pulposus of the intervertebral disc
5
Q
what are the name and function of the dorsal part of the neural tube?
A
Alar plate: sensory
6
Q
what are the name and function of the ventral part of the neural tube?
A
Basal plate: motor
7
Q
what are the three primary vesicles of the developing brain?
A
- Forebrain (prosencephalon) • 2. Midbrain (mesencephalon) • 3. Hindbrain (rhombencephalon)
8
Q
what are the five secondary vesicles of the developing brain?
A
- telencephalon • 2. Diencephalon • 3. Mesencephalon • 4. Metencephalon • 5. Myelencephalon
9
Q
the Forebrain (prosencephalon) gives rise to which secondary vesicles?
A
- Telencephalon • 2. Diencephalon
10
Q
the Midbrain (mesencephalon) gives rise to which secondary vesicles?
A
- Mesencephalon
11
Q
the Hindbrain (rhombencephalon) gives rise to which secondary vesicles?
A
- Metencephalon • 2. Myelencephalon
12
Q
the walls of the telencephalon give rise to what?
A
cerebral hemispheres
13
Q
the cavities of the telencephalon give rise to what?
A
lateral ventricles
14
Q
the walls of the diencephalon give rise to what?
A
thalamus
15
Q
the cavities of the diencephalon give rise to what?
A
third ventricle
16
Q
the walls of the mesencephalon give rise to what?
A
midbrain
17
Q
the cavities of the mesencephalon give rise to what?
A
aqueduct
18
Q
the walls of the metencephalon give rise to what?
A
Pons and Cerebellum
19
Q
the cavities of the metencephalon give rise to what?
A
upper part of fourth ventricle
20
Q
the walls of the myelencephalon give rise to what?
A
medulla
21
Q
the cavities of the myelencephalon give rise to what?
A
lower part of the fourth ventricle
22
Q
what happens in neural tube defect?
A
neuropores fail to fuse (4th week) → persistent connection between amniotic cavity and spinal canal
23
Q
neural tube defects are associated with what?
A
low folic acid intake before conception and during pregnancy
24
Q
what are the lab levels in neural tube defect?
A
- ↑ 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
279
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
287
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
292
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
302
CT scan of epidural hematoma shows what?
biconvex (lentiform), hyperdense blood collection not crossing suture lines. • Can cross falx, tentorium
303
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
