neuro vascular Flashcards
1
Q
neurons 12-24h after ischemia?
A
Red neurons - 1. loss of Niss substance + it leads to 2. eosinophilic cytoplasm (due to dissolution of Nissl bodies); 3. pyknotic nuclei (shrunken and deeply basiphilic) + undergo fragmentation (karyorrhexis)
2
Q
When occurs neutrophil infiltration after ischemic stroke?
A
24-72h after damage.
3
Q
What is the first immune cell that infiltrates brains after ischemic stroke?
A
neutrophils
4
Q
When occurs macrophage/microglia infiltration and phagocytosis after ischemic stroke?
A
3-7days after ischemic stroke
5
Q
What happens 1-2 weeks after ischemic stroke in that lesion?
A
reactive gliosis and vascular proliferation around necrotic area
6
Q
When occurs reactive gliosis and vascular proliferation around the necrotic area after ischemic stroke?
A
1-2 weeks after injury
7
Q
When occurs glial scar formation after ischemic damage?
A
> 2 weeks
8
Q
What changes are seen after >2 weeks of ischemic stroke
A
glial scar formation
9
Q
What cells participate in reactive gliosis?
A
astrocytes
10
Q
where are formed new vessels when happens angiogenesis after ischemic stroke?
A
in the periphery of the necrotic area
11
Q
What cells participate in glial scar?
A
there is cystic cavity surrounded by the wall of dense fibers formed by astrocytic processes (glial scar)
12
Q
When is seen first ischemic damage after ischemic stoke on microscope?
A
The first microscopic changes are typically seen 12-24 hours after irreversible ischemic injury
13
Q
In CNS repair of injury is performed by ……………
A
astrocytes (eg in peripheral tissues it is done by fibroblasts)
14
Q
ischemic infarct results form ……… (2)
A
regional hypoperfusion (thrombosis/embolism) or global decline in cerebral blood flow.
15
Q
When are evident CT findings of ischemic stroke?
A
6-12h after the onset
16
Q
how looks CT of ischemic stroke? (2)
A
hypoattenuation of tissue and loss of grey-white matter differentiation within the affected region?
17
Q
microglia is derived from ………………..
A
yolk-sac monocytes
18
Q
What 3 structures are phagocytized by microglia in ischemic infarct?
A
neurons, myelin, necrotic debris
19
Q
What happens with myelin products after they are phagocytized by microglia?
A
breakdown products accumulate in the cytoplasm of microglia as foamy lipids.
20
Q
What cells release inflammatory mediators after ischemic damage?
A
neutrophils
21
Q
inflammatory mediators, released after ischemic stroke contriibute to …….
A
hydrolysis of cell in liquedactive necrosis
22
Q
How looks neutrophils in lipid stain?
A
none. They are not prominent on lipid stain unlike microglia (foamy lipids)
23
Q
what cells apart microglia would be seen on lipid stain?
A
schwann cell and ependymal cells
24
Q
when occurs liquefactive necrosis after ischemic damage?
A
1 week-1 month
25
When occurs gliosis after ischemic damage? what cells?
>1month-years.
| Astrocytes and microglia
26
What are 2 mechanisms of cerebral edema after ischemic stroke?
cytotoxic (ionic) and vasogenic edema
27
What happens in cytotoxic (ionic) edema?
decr. ATP --> failur of ATP-dependent ion pums + release of excitatory AA (eg glutamate) --> accumulation of intracellular Na and H2O in neural and glial cells.
28
When begins cytotoxic (ionic) edema?
hours after the ischemic damage
29
What happens in vasogenic edema?
Inflammatory mediators from neutrophils disrupts junctions of BBB --> protein and water leakage into interstitial space.
30
When begins vasogenic edema?
24-48h after ischemic damage
31
vasogenic phase can cause persistent cerebral edema for ................. (duration) after the initial injury
weeks
32
What cerebral edema can cause persistent cerebral edema for weeks after the initial injury?
vasogenic
33
Decr. oncotic pressure of in nephrotic. Effect on peripheral and cerebral edema?
it causes peripheral edema, but is not significant factor in the development of cerebral edema.
34
Inadequate absorption of cerebrospinal fluid at the arachnoid granulations can cause.....................
communicating hydrocephalus
35
What ICP and CT changes are in communicating hydrocephalus eg due to inadequate reabsorbtion of CSF in arachnoid granulations?
ICP -- > increased
| CT --> ventriculomegaly
36
What 2 changes are due to increased hydrostatic pressure in brain?
Cerebral edema and increased ICP
37
Neuro symptoms in patients with increased hydrostatic pressure?
gradually worsening headache before development of neurologic abnormalities
38
Increased ICP cause progressive neurologic impairment through 2 mechanisms?
mechanical damage due to brain herniation and direct pressure-induced cell injury
39
Ependymal cells line ................. (2 structures)
Ventricles and central canal
40
Function of shwann cells?
myelin producing cells that help to guide axonal repair and regeneration in the PNS
41
Function of oligodendrocytes?
myelin producing cells of CNS.
42
The meninges (eg, pia mater) are separated from the cystic cavity created after ischemic stroke by a ..................................., which is derived from ...............
gliotic tissue layer (derived from the cortex)
43
origin of astrocytes?
neuroectoderm
44
origin of oligodendrocytes?
neuroectoderm
45
appearance of astorcytes? (2)
round vesicular nuclei;
| contains glial fibrils (composed of glial fibrillary acidic protein)
46
function of astrocytes? (5)
repair, structural and metabolic support, BBB;
| extracellular K buffer, removal of excess neurotrasmiter
47
appearance of oligodendrocytes? (2)
small nuclei surrounded by a pale halo;
| fewer processes than astrocytes
48
function of oligodendrocytes?
production of myelin in CNS
49
appearance of microglia? (2)
small alongated nuclei;
| mano short branching processes
50
What is astrocyte marker?
GFAP
51
What happen with microglia in HIV?
microglia fuse to form multinucleated giant cells in CNS
52
function of cilia in ependymal cells?
circulate CSF
53
function of microvili in ependymal cells?
helps CSF absorbtion
54
Myelin vs schwann cells? function
myelin - isolates axon to inc. condution velocity;
| schwann cells - promote axonal regeneration
55
In what syndrome are damaged schwann cells?
Guillain-Barre
56
In what syndromes are damaged oligodendrocytes?
multiple sclerosis; progressive multifocal leukoencephalopathy (PML), leukodystrophies
57
origin of schwann cells?
neural crest
58
What is in gray matter and in white matter?
gray - bodies of neurons;
| white - glial cells (predominantly oligodendrocytes)
59
What 3 changes in neurons indicate irreversible neuronal damage??
shrunken, basophilic nuclei + intensively eosinophilic cytoplasm (red neurons)
60
What do astrocytes in response to irreversible neuronal injury?
astrocytes proliferate at the site of injury to restore tissue intergrity - it is called astrocytosis (or gliosis)
61
astrocyte perform function analogous to what cell otuside CNS?
fibroblasts
62
what compensation happens to astrocytes in gliosis?
hypertrophy and proliferation
63
What 3 actions are done by proliferated astrocytes to form gliotic scar?
they replace lost neurons, compensate for their volume, over time form connected, firm meshwork - a gliotic scar
64
what process undergo irreversibly injured neurons?
cellular necorisi (NOT HYPERTROHPY)
65
what phagocytozes microglia?
dead cells and debris
66
In neuronal damage is eosinophilic material. Where is eosinophilic material in vascular hyalinization and amyloiud depositions?
EXTRACELLULAR!!!
67
gliosis leads to ......................, which compensates ...................
formation of glial scar, which compensates for volume loss that occurs after neuronal death.
68
Pulmonary edema + hypotension. What suspect?
shock (cardiogenic)
69
Symetric, bilateral weddge-shaped strips of necrosis over the cerebral convexity. What suspect?
global cerebral ischemia - nes bilateral damage, ir cia yra damage in watershed zones
70
What causes infarct in watershed zones?
severe systemic hypotension (eg cardiogenic shock, cardiopulmonary arrest)
71
What sites are the brain are vulnerable for hypoxic damage? why? (2 groups)
Brain regions with HIGH METABOLIC DEMAND - hippocampus, cerebellar Purkinje, neocortex) AND watershed zones - areas supplied by most-distal branches of cerebral arteries
72
Why watershed zones are vulnerable?
because of low baseline perfusion pressure.
73
Where are located watershed zones? (2)
Parallel and a few centimeters lateral to the interhemispheric fissure.
Damage can extend from the frontal to occipital lobe
74
Global ischemia lasting longer than ..................... can cause irreversible damage to neurons.
3-5 min
75
What cells are primary damaged by hypoxia in CNS? Time?
CA1 pyramidal neurons of the hippocampus - 3 min
76
What cells are second in a row to be damaged by ischemia in CNS? (2). Time?
Cerebellar Purkinje cells and neocortex pyramidal neurons - 5-10min.
77
What unique neurochemical characteristic apart from high metabolic demant have neurons that make them susceptible to ischemia?
inability to repolarize after anoxic depolarization
78
Where is located hippocampus?
medial temporal lobe
79
What role plays hippocampus? (3)
memory, spatial processing and response inhibition
80
Selective damage to the hippocampus is common with .....................
transient ischemia
81
Selective damage to the hippocampus can result in an inability to ............................. (2)
make new memories (anterograde amnesia) and disorientation to place or time.
82
Cerebral ischemia results in a rapid depletion of energy stores that triggers a complex cascade of cellular events such as ..................... and ....................., resulting in ...................
cellular depolarization and Ca2+ influx, resulting in excitotoxic cell death.
83
The critical determinant of severity of brain injury is ................... and .............................. and...............
duration and severity of the ischemic insult and early restoration of CBF
84
Embolic infarction vs global ischemia. How differs location of damage?
Global - watershed zones - symetric bilateral infarctions
Embolic - multiple scattered infarct in asymmetric pattern - affected multiple different vascular territories
85
Cerebral amyloid angiopathy leads to .................... (ischemia or hemorrhage)
hemorrhage
86
Pterion is a a region where the ............... (4) bones meet in the skull
frontal, parietal, temporal and sphenoid bones
87
What is the thinnest location in the skull?
pterion
88
Fracture to pterion - damage to what artery?
middle meningeal artery
89
damage to middle meningeal artery cause ................ hematoma
epidural
90
Why is required prompt treatment of epidural hematoma?
it is under systemic arterial pressure (middle meningeal artery damage) --> rapid increase of intracranial pressure
91
Rapid increase of epidural hematoma can lead to .............. (3)
elevated intracranial pressure; brain herniation; death
92
Elevated ICP in epidural hematoma can cause ............. reflex
Cushing
93
What brain herniation can occur due to epidural hematoma?
uncal herniation with oculomotor nerve palsy
94
Middle meningeal artery is a brach of ................
maxillary artery (which is a branch of external carotid artery)
95
middle meningeal artery enters the skull via ............
foramen spinosum
96
Middle meningeal artery supplies ..................... (2)
dura matter and periosteum
97
The facial artery is a branch of the ............................
external carotid artery
98
what regions supply facial artery? (3)
oral, nasal, and buccal regions
99
what is the course of facial artery?
over the mandible anterior to the insertion of the masseter muscle
100
injury to what artery causes subarachnoid or intracerebral hemorrhage?
middle cerebral artery
101
middle cerebral artery is a branch of .............
internal carotid artery
102
middle cerebral artery supplies .................. (2)
musch of the parieatl and temporal regions
103
occipital artery originates from ...............
external carotid
104
occipital artery supplies .............. (2)
posterior scalp and the sternocleidomastoid muscles.
105
The sphenopalatine artery is a branch of the third part of the ......................... and supplies much of the ...................
maxillary artery and supplies much of the nasal mucosa
106
sphenopalatine artery anastomoses with ................. and ................. and form ...........................
branches of the ophthalmic and facial arteries within the anterior part of the nasal septum in a region known as Kiesselbach's plexus
107
too rapid correction of hyperonatremia. drop in serum osmolarity stimulates .......................... --> ... ICP
water flow into brain cells --> incr. ICP --> impaired cerebral perfusion and eventual brain herniation
108
aneurysm due to cystic abnormalities can cause .............. (hemorrhage).
SAH
109
what causes meningeal irritation in SAH?
pooling of the blood in the subarachnoid space --> irritation of meninges (pia matter). Within 24h
110
When do CT in SAH?
within 24h from the onset of symptoms
111
If CT is negative despite suspicion of SAH, what do?
lumbar puncture --> seen xantochromia (bloody or yellow CSP)
112
What is the most sensitive method to diagnose SAH?
lumbar puncture --> xantochromia
113
CT ins SAH shows blood in ............. (2)
cerebral sulci and basal cisterns
114
Blood in the subarachnoid space can acutely ................ and ....................... of cerebral spinal fluid (CSF) by the arachnoid granulations
obstruct and impair absorbtion
115
what causes fibrosis of arachnoid granulations in SAH?
blood-induced inflammation
116
blood-induced inflammation can cause..................... of the arachnoid granulations in SAH
fibrosis
117
What leads to chronic hydrocephalus in SAH?
obstruction/impaired absorbtion of CSF;
blood induced inflammation --> fibrosis of arahcnoid granulations --> impaired absorbtion of CSF
Net result: chronic hydrocephalus
118
the most common complication of SAH?
vasospasm (3-12 days) --> ischemic damage
119
Why there may be vasospasm in SAH?
release of vasoconstrictive factors from damaged erythrocytes in the subarachnoid space and the inability of damaged vascular endothelial cells to produce vasodilators (eg, nitric oxide).
120
how manifest vasospasm induced delayed cerebral ischemia in SAH?
change in mental status and/or new focal neurological deficits 3-12 days after SAH
121
CT scan of SAH induced vasospasm?
no signficant changes
122
What medication is used to event SAH induced vasospasm?
nimodipine
123
Impaired CSF absorption causes ..........................
communicating hydrocephalus
124
What ventricles are dilated in hydrocephalus post SAH? Why?
all 4;
| because a blocked of flow is distal to entire ventricular system (tipo fibrosis of arachidonic granulations)
125
ventricular enlargement in SAH hydrocephalus leads to ..................................
stretches adjacent nerve fibers and, in the acute setting, leads to deteriorating mental status
126
Treatment of hydrocephalus?
placement of an external ventricular drain to relieve pressure in the ventricular system and subarachnoid space.
127
What is used to treat chronic hydrocephalus?
permanent shunt eg ventriculoperitoneal shunt
128
What are focal manifestation in SAH?
there is no focal neurologic manifestation in SAH (eg aphasia, hemiplegia etc)
129
Blood breakdown products in SAH cause .............. (2)
obstructing the flow of cerebrospinal fluid or clogging the arachnoid villi.
130
when can occur rebleeding post SAH?
early, <24h post initial bleeding
131
CT in rebleeding post SAH?
Newly extravasated bloodi
132
Symptoms of rebleeding post SAH?
sudden change in consciousness and new nerologic deficit
133
CT of 3 SAH complications?
vasospasm - none
hydrocephalus - enlarged ventricles
rebleeding - newly extravasated blood
134
What 2 lesions can increase ICP?
hemorrhage, hematoma
135
increased ICP due to hematomas/hemorrhages can manifest as .................
headache, vomiting, impaired consciousness and ultimately Cushing triad.
136
What indicates Cushing triad after brain injury?
imminent brain herniation
137
What is Cushing triad?
hypertension, bradycardia and irregular respirations
138
Downward displacement of the brainstem is called ...........
central herniation
139
Lesions in the temporal lobe tend to cause ....................... herniation of the ..........
transtentorial herniation of the uncus
140
What compress uncal transtentorial herniation?
ipsilateral CN III (because it exits the midbrain at the same level as is tentorium.
141
Compression of CN III due to herniation. Manifestation?
ipsilateral CN III palsy with fixed dilated pupil (due to preganglionic parasympathetic nerve fiber damage)
142
What herniation cause paramedian basilar artery branches to rupture?
central/downward transtentorial herniation
143
central/downward transtentorial herniation cause rupture of ..............
paramedian basilar artery branches
144
Brainstem hemorrhage is called ...............
Duret hemorrhages
145
Injury to what arteries cause Duret hemorrhages?
paramedian basilar artery branches
146
The most common cause of deep intracranial hemorrhage?
hypertensive vasculopathy
147
Mechanism how chronic hypertension can cause hemorrhage in the deep brain.
Chronic hypertension --> progressive arteriolar hyalinization and fibrinoid necrosis, weakening the vessel wall --> formation of Charcot-Bouchard aneurysms --> aneurysmal rupture --> hemorrhage
148
What are the most common sites of intraparenchymal hemorrhage?
Basal ganglia (putamen), cerebellar nuclei, thalamus, pons.
149
What arteries supply basal ganglia?
Lenticulostriate arteries, which are deep, small vessel branches off the middle cerebral arteries.
150
what are neurologic deficits, heahdache and meningeal signs in intraparenchymal hemorrhage due to hypertension?
Focal neurologic deficit;
Severe hemorrhage - sometimes presents;
Meningeal signs - no present
151
Hemorrhage in thalamus. Symptoms.
Contralateral weakness/numbness and extensor plantar response.
Cia simptomai due to thalamic hemorrhage with edema/mass effect on the internal capsule.
152
Hemorrhage in putamen. Symptoms.
Compresses internal capsule --> dysarthria, contralateral hemiparesis, contralateral hemisensory loss
153
What tract fibers are damages in putamen hemorrhage that compresses internal capsule?
corticobulbal, corticospinal and somatosensory fibers.
154
Manifestation of increased ICP?
headache, nausea/vomiting, altered mental status
155
What 3 vessels changes promotes chronic hypertension?
Lipohyalinosis, microatheroma formation, hardening/thickening of the vessels wall (hypertensive arteriolar sclerosis)
156
Hypertensive arteriolar sclerosis leads to..............
progressive narrowing of the arteriolar lumen + predisposes thrombotic vessel occlusion
157
Posterior limb of the internal capsule and/or basal pons. What symptoms?
pure motor hemiparesis OR ataxia-hemiplegia syndrome
158
Anterior limb of the internal capsule and/or basal pons. What symptoms?
dysarthria-clupsy hand syndrome (ie dysarthria and dysphagia with clumsiness of one hand)
159
Ventroposterolateral or ventroposteromedial thalamus. What symptoms?
pure sensory stroke
160
pure motor hemiparesis OR ataxia-hemiplegia syndrome. What part of the brain is damaged?
Posterior limb of the internal capsule and/or basal pons.
161
dysarthria-clupsy hand syndrome (ie dysarthria and dysphagia with clumsiness of one hand). What part of the brain is damaged?
Anterior limb of the internal capsule and/or basal pons.
162
pure sensory stroke. What part of the brain is damaged?
Ventroposterolateral or ventroposteromedial thalamus
163
Lacunar infarct. CT?
early - no changes, because infarcts are very small (<15mm). After several weeks - necrotic leasions turns into spaces filled with CSF and surrounded by scar tissues called lacunas
164
What is lacuna?
cavitary spaces filled with CSF and surrounded by scar tissue. Occurs after several weeks of lacunar iinfarct in damages areas.
165
Manifestation of hypertensive encephalopathy? CT?
Progressive headache and nausea/vomiting followed by nonlocalizing neurologic symptoms (eg, confusion).
Cerebral imaging may be normal or show parietooccipital white matter edema.
166
Manifestation of hypoxic encephalopathy? CT?
decreased consciousness (come, vegetative state); no focal deficit/hemorrhage. CT - may show watershed infarcts.
167
CT of embolic stroke?
large-teritory infarctions of the cerebral cortex as large areas of HYPODENSITY
168
Damage to what arteries (general name) cause hemorrhage in basal ganglia?
deep penetrating arteries
169
What hemorrhage (location) can be caused by amyloid angiopathy?
lobar/cortical
170
pontine arteries are small branches of the ................
basilar arteries
171
location of the pontine hemorrhages?
close to the midline --> affect both sides of pons
172
Manifestation of pons hemorrhage? (3)
Coma, locked-in syndrome, pinpoint pupils
173
Location of locus ceruleus?
the posterior rostral pons near the lateral floor of the fourth ventricle.
174
Function of locus ceruleus?
principal site for norepinephrine synthesis in CNS and projects virtually all parts of the CNS.
175
Abnormal activation of the locus ceruleus has been implicated in the pathogenesis of .................
anxiety disorders, eg panic attacks.
176
Anxiety disorders, eg panic attacks. what part of the brain is abnormaly activated?
locus ceruleus
177
Why patients with bilateral pontine hemorrhage typically present with coma?
Due to disruption of the reticular activating system
178
disruption of the reticular activating system in pontine hemorrhage leads to ...........
coma
179
Pinpoint pupils in pontine hemorrhage. Pathomechanism?
descending sympathetic tract damage
180
total paralysis with extensor posturing in pontine hemorrhage due to .....................
corticospinal and corticobulbar tract injury
181
descending sympathetic tract damage leads to ..............
pinpoint pupils
182
corticospinal and corticobulbar tract injury leads to ..............
total paralysis with extensor posturing
183
2 locations of CNS that produce dopamine?
ventral tegmental area and substantia nigra pars compacta in the midbrain.
184
What are 3 major dopaminergic pathways in the brain?
mesolimbic and mesocortical pathways; nigrostriatal pathway; tuberoinfundibular pathway
185
Mesolimbic and mesocortical pathways regulate .....................
cognition and behavior
186
Nigrostriatal pathway regulates ................
coordination of voluntary movements
187
tuberoinfundibular pathway function is ..................
inhibits prolactin secretion
188
What is dynorphin?
opioid peptide that modulates the pain response
189
Where is produced dynorphin? (3)
Periaqueductal gray, rostral ventral medulla, and dorsal horn of the spinal cord
190
Histamine and orexin are produced in the ........................
posterior hypothalamus
191
What 2 substances are produced in posterior hypothalamus?
histamine and orexin
192
What is the function of histamine and orexin?
arousal and wakefulness
193
Locus ceruleus projects to virtually all parts of the central nervous system and helps control .................. (5)
```
mood
arousal (reticular activating system)
sleep-wake states
cognition
autonomic function
```
194
nonreactive pupils to light stimulation following cardiac arrest carries indicates ........................
anoxic damage to the brainstem at the level of the upper midbrain
195
During the normal pupillary reflex, the retina as well as the optic nerve and tract transmit the light stimulus to the .............................
midbrain at the level of the superior colliculus
196
What 2 nuclei gets light stimulus in midbrain?
pretectal nuclei and then stimuli goes to the bilateral Edinger-Westhpal nuclei.
197
Where goes stimuli from Edinger-Westhpal nuclei?
These nuclei projects preganglionic parasympathetic fibers throunght CN III to the ciliary ganglion and then postganglionic fibers innervate sphincter pupillar muscles (constricts the pupil)
198
Whan happens when light is shone in one eye?
both the ipsilateral pupil (direct response) and contralateral pupil (consensual response) constrict.
199
MRI findings in anoxic brain injury?
loss of grey-white matter differentiation with sulcal effacement
200
The occipital lobe contains the ..............................
primary visual cortex
201
Unilateral occipital lobe damage can cause ....................
contralateral homonymous hemianopia
202
bilateral occipital lesions may result in ......................
cortical blindness
203
cortical blindness is caused by damage in ...................
bilateral occipital lesions
204
contralateral homonymous hemianopia is caused by damage in ..................
Unilateral occipital lobe
205
Parietal lobe damage results in difficulties with ................... and ...................
spatial and visual perception
206
The parietal lobes process and interpret .............., ..............., and ................. signals received from other brain areas.
visual, auditory, and motor
207
(parietal lobe) Nondominant (eg, right-sided) lesions result in ...................
hemi-neglect and constructional apraxia
208
(parietal lobe) dominant (eg, left-sided) lesions result in ......................
Gerstmann syndrome (eg, right-left confusion, agraphia, acalculia
209
Temporal lobe injury can cause disturbances in .............. (4)
memory (eg, hippocampus); speech (eg, Wernicke area in dominant hemisphere); vision (eg, Meyer loop);
hearing (eg, primary auditory cortex).
210
Bilateral damage to the amygdala results in ..........................
Klüver-Bucy syndrome
211
Klüver-Bucy syndrome manifestation? (3)
hyperphagia, hyperorality, hypersexuality
212
What part of the brain contains horizontal gaze center?
Pons
213
Bilateral pontine injury results in .....................
pinpoint pupils
214
Horizontal gaze center, which helps mediate the ............................ reflex
oculocephalic (doll's eye)
215
Afferent limb of corneal reflex. What CN?
Trigeminal (CN V)
216
Efferent limb of corneal reflex. What CN?
Facial (CN VII)
217
Ventral posterolateral nucleus mediates what sensation?
Somatic sensation of the body
218
ventral posteromedial nucleus mediates what sensation?
Facial sensation and taste
219
the lateral geniculate nucleus mediates ..............
vision
220
medial geniculate nucleus mediates ...........
hearing
221
Berry aneurysm in anterior communicating artery. What compress?
central optic chiasm --> bitemporal hemianopia
222
Berry aneurysm in posterior communicating artery. What compress?
oculomotor nerve --> producing ipsilateral mydriasis, ptosis, and "down and out" eye deviation.
223
Basilar artery occlusion --> damage of pons. What limbs affected?
quadriplegia
224
Basilar artery occlusion --> damage of pons. What is bulbar dysfunction?
facial weakness, dysarthria
225
Basilar artery occlusion --> damage of pons. What is oculomotor deficits?
horizontal gaze palsy
226
occlusion of what causes lateral pontine syndrome?
anterior inferior cereberal artery
227
occlusion of anterior inferior cereberal artery causes .........................
lateral pontine kazka nx
228
signs of increased ICP?
altered mental status, nausea/vomiting, Cushing reflex (bradycardia, hypertension and irregular breathing
229
2 stages of clinical manifestation in epidural hematoma.
Transient loss of consciousness and then lucid period, in which patient regains consciousness
230
Diagnostics of epidural hematoma?
noncontrast CT - hyperdensi biconvex lesion
231
What is lipohyalinosis in lanucar infarct?
leakage of plasma proteins through damaged endothelium and is characterized by hyaline thickening of the vascular wall, collagenous sclerosis, and accumulation of mural foamy macrophages
232
What is microatheroma in lacunar infarct?
Microatheromas result from atherosclerotic accumulation of lipid-laden macrophages within the intimal layer of a penetrating artery near its origin off the parent vessel.
233
Emboli most commonly affect what part of the brain?
cortex
234
3 characteristics of pats brain necrosis (old cerebral infarct)?
cystic cavity, volume loss and enlarged ventricle
235
What releases lysosomal enzymes in brain ischemia?
ischemic neurons
236
what releases inflammatory cytokines in brain ischemia?
inflammatory cells (neutrophils, macrophages)
237
why eventually there is cavity after brain infarct?
phagocytic cells remove necrotic tissue
238
wallerian degeneration results in ............... (2)
axonal degenration and breakdown of the myelin sheat distal to the site of injury
239
when begins degeneration of axon after injury?
within a few days
240
what cells in PNS sense axonal degeneration?
Schwann cells
241
What cells secrete cytokines and chemokines in axonal damage to rectruit macrophages?
Schwann cells
242
What cells secrete trophic factor in axonal damage?
Schwann cells
243
What does trophic factor in axonal damage?
stimulates formation of a growth cone from the stump of the proximal axon and facilitates nerve regeneration
244
Why in CNS phagocytic macrohages/microglia are recruited more slowly than in PNS?
due to BBB
245
what happens to oligodendrocytes in axonal CNS injury?
myelin-producing oligo becomes inactive or undergo apoptosis
246
how long lasts removal of myelin debrin in CNS after axonal injury?
can persist for years in degenerating tracts
247
How is suppresed axonal growth in CNS axonal injury?
myelin-associated inhibitory factors
248
What cells in CNS release inhibitory factors in axonal damage?
oligo and astrocytes
249
Embolic ischemic strokes have a high risk of undergoing acute hemorrhagic transformation within the first............ days following the ischemic event.
7
250
Why there is no axonal regeneration in CNS? (3)
Persistence of myelin debris;
secretion of neuronal inhibitory factors;
development of dense glial scar
251
Neutrophilic infiltration progressively increases up to ........hours after ischemic stroke and then diminishes.
48
252
Left leg weakness + vision loss in the right eye. Where is the lesion?
Right internal carotid artery
253
Pattern of neurologic deficit in TIA?
focal neurologic impairment. TIA most commonly due to emboli originating from atherosclerotic plaques
254
How differ presentation of chronic and acute SDH?
acute - profundly depresses mental status at onset
| chronic - insidious onset of headache and confusion
255
What 3 conditions predispose SAH?
Ehlers-Danlos, aut.dominant polycytic KD, arteriovenous malformations
256
What 2 conditions predisposes berry aneurysms?
Ehlers-Danlos and autosom.dom.polycyst kidney disease
257
How clinically looks locked-in syndrome?
quadriplegia + speechlessness with preserved eye movements and consciousnes
258
What eye movements are preserved and what not in locked-in syndrome?
```
horizontal - not;
vertical and eyelid elevation - yes.
Horizontal are controled in pons (?)
Vertical + eyelid - in rostral midbrain
locked-in syndrome - due to damage to pons
```
259
Why there is consciousness in locked-in syndrome?
for consciousness is responsible reticular formation which is in midbrain.
260
preserved or damaged Behavioral arousal and sleep-wake cycles in locked-in?? Why?
preserved because the diencephalon–upper brainstem arousal systems are unaffected.
261
Why preserved sensation in locked-in?
sensory pathways are not affected and preserved brainstem and spinal reflexes because they do not require cortical input.
262
what 2 motor functions impaired in locked-in? Why?
motor function of limbs (quadriplegia)ed and oral structures (loss of speech)
DUE TO DESTRUCTION OF CORTICAL SPINAL AND CORTICAL BULBAR PATHWAYS - prevent cranial nerves or the limbs from receiving cortical signals
263
Thalamic ventral posterior lateral nucleus receives input from .........................
the spinothalamic tract and dorsal columns
264
ventral posterior medial nucleus receives input from ............................
the trigeminal pathway
265
Thalamic posterior lateral/medial nuclei send somatosensory information to the .................... via .............
to the cortex via thalamocortical fibers
266
Severe proprioceptive defects due to thalamic damage may cause ..........
unsteady gait
267
Damage to both thalamic posterior lateral/medial nuclei results in .............
complete contralateral sensory loss (eg touch, pain/temperature, vibration/proprioception)
268
The anterior two-thirds of the posterior limb of the internal capsule is mainly composed of .................... fibers (eg .............. tract),
motor fibers (eg, corticospinal tract)
269
The posterior one-third of posterior limb of the internal capsule contains ................ fibers (eg, .............. tract).
sensory;
| thalamocortical
270
motor, sensory and UMN signs in ACA occlusion.
Motor - contralateral lower limb weakness;
UMN signs such hyperreflexia, babinski;
Contralateral sensory - occurs in minority of patients
271
Atrial thrombi frequently travel to what brain arteries?
ACA and MCA
272
ACA supply what parts of the brain?
medial aspects of the frontal and parietal lobes
273
how circle of willi is protective against ischemic injury to the brain?
it provides a potential alternate pathways for cerebral arterial blood flow
274
if there is symptomatic ACA stroke, what part of the vessel is more likely obstructed?
Distal to the origin of the ACom, where collateral blood flow does not occurs.
If occlusion is proximal to the ACom - severity of damage would be limited due to this anastomosis
275
In what part of the brains is micturition reflex center?
Medial frontal lobe
276
An embolic occlusion of the anterior spinal artery in the lumbosacral region. Manifestation?
Bilateral lower extremity weakness with hyporeflexia, loss of pain and temperature sensation
277
Damage to what structure causes hyporeflexia in embolic occlusion of the anterior spinal artery in the lumbosacral region?
ischemia of the anterior horns and corticospinal tracts
278
Damage to what structure causes loss of pain and temperature sensation in embolic occlusion of the anterior spinal artery in the lumbosacral region?
ischemia of the spinothalamic tracts
279
inferior frontal, medial frontal, and superior medial parietal lobes. Blood supply?
ACA
280
anterior 4/5 of the corpus callosum; Blood supply?
ACA
281
olfactory bulb and tract; blood supply?
ACA
282
anterior portions of the basal ganglia; blood supply?
ACA
283
internal capsule (only anterior portion?). Blood supply?
ACA
284
Sensory deficit in ACA occlusion?
contralater can occur, bet siaip in a minority of patients
285
Motor and sensory deficits of the right leg (sparing the right arm). Where is damage?
medial portions of the left primary motor and somatosensory cortices.
286
Micturition reflex location is supplied by ..........
ACA
287
What is location of micturition reflex centers in the brain?
frontal micturition center (medial frontal lobe) arba tipo cingulate gyrus
288
The superior division of the MCA supplies blood to .............
frontal lateral cortex
289
The inferior division of the MCA supplies blood to .............
lateral portions parietal and temporal cortices
290
Occlusion of superior division of MCA. What neuro deficit?
motor deficit (sometimes sensory deficit in face and arm)
291
Occlusion of inferior division of MCA. What neuro deficit?
Sensory deficits of the arm and face (motor function spared)
292
What artery occlusion causes Broca aphasia (in dominant sphere)?
superior division of MCA
293
What artery occlusion causes Wernicke aphasia (in dominant sphere)?
inferior division of MCA
294
What artery occlusion causes hemineglect (in nondominant sphere)?
superior division of MCA
295
What artery occlusion causes PROFUND hemineglect (in nondominant sphere)?
inferior division of MCA
296
Oclusion of what division of MCA causes visual defects?
inferior division of MCA
297
MCA strokes often associated with ..... (3 neuro manifestation)
homonymous hemianopia, aphasia, and hemineglect
298
Why macula is pared in PCA occlusion?
due to collateral circulation from the MCA
299
What visual part is spared in PCA occlusion?
macula
300
The most common manifestation of PCA occlusion?
contralateral hemianopia
301
CT of PCA occlusion?
focal parenchymal hypoattenuation and occipital horn effacement.
302
PCA branches of ............. at the level of .............
basilar artery at the level of the pontomesencephalic junction
303
PCA supplies CN....... and CN ......
CN III and CN IV (and other structures in the MIDBRAIN)
304
Thalamus. Blood supply?
PCA
305
Medial temporal lobe. Blood supply?
PCA
306
Splenium of the corpus callosum. Blood supply?
PCA
307
Parahippocampal gyrus. Blood supply?
PCA
308
Fusiform gyrus. Blood supply?
PCA
309
Occipital lobe. Blood supply?
PCA
310
If lateral thalamus is involved in PCA occlusion. Manifestation?
contralateral paresthesias and numbness (affectin face, trunk and limbs)
311
What 3 cortical symptoms can occur in PCA occlusion?
dyslexia, visual agnosia, prosopagnosia
312
What is agnosia?
impaired visual recognition of objects
313
How is called impaired visual recognition of objects?
agnosia
314
What is prosopagnosia?
inability to recognize faces
315
What is inability to recognize faces?
Prosopagnosia
316
Anterior choroidal artery branches off ...........
internal carotid artery
317
Posterior limb of the internal capsule. Blood supply?
anterior choroidal artery
318
optic tract. Blood supply?
anterior choroidal artery
319
lateral geniculate body. blood supply?
anterior choroidal artery
320
choroid plexus. blood supply?
anterior choroidal artery
321
uncus. blood supply?
anterior choroidal artery
322
hippocampus. blood supply?
anterior choroidal artery
323
amygdala. blood supply?
anterior choroidal artery
324
The artery of Percheron branches off either the ....... or .............
right or left PCA
325
The artery of Percheron supplies .............. (2)
bilateral thalami and dorsal midbrain
326
bilateral thalamic or dorsal midbrain strokes. What artery?
The artery of Percheron
327
The ACA supply the medial portions of the 2 hemispheres: ............... and .......... lobe
frontal and parietal lobes
328
total 4 manifestaion in ACA occlusio?
Contralateral motor and sensory deficit of lower extremities, behavioral changes, urinary incontinence
329
behavioral symtoms and incontinence occurs in ............. ................ occlusion
BILATERAL ACA
