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1 STEP UWorld neuro+psycho > neuro vascular > Flashcards

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)

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2
Q

When occurs neutrophil infiltration after ischemic stroke?

A

24-72h after damage.

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3
Q

What is the first immune cell that infiltrates brains after ischemic stroke?

A

neutrophils

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4
Q

When occurs macrophage/microglia infiltration and phagocytosis after ischemic stroke?

A

3-7days after ischemic stroke

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5
Q

What happens 1-2 weeks after ischemic stroke in that lesion?

A

reactive gliosis and vascular proliferation around necrotic area

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6
Q

When occurs reactive gliosis and vascular proliferation around the necrotic area after ischemic stroke?

A

1-2 weeks after injury

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7
Q

When occurs glial scar formation after ischemic damage?

A

> 2 weeks

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8
Q

What changes are seen after >2 weeks of ischemic stroke

A

glial scar formation

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9
Q

What cells participate in reactive gliosis?

A

astrocytes

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10
Q

where are formed new vessels when happens angiogenesis after ischemic stroke?

A

in the periphery of the necrotic area

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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)

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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

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13
Q

In CNS repair of injury is performed by ……………

A

astrocytes (eg in peripheral tissues it is done by fibroblasts)

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14
Q

ischemic infarct results form ……… (2)

A

regional hypoperfusion (thrombosis/embolism) or global decline in cerebral blood flow.

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15
Q

When are evident CT findings of ischemic stroke?

A

6-12h after the onset

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16
Q

how looks CT of ischemic stroke? (2)

A

hypoattenuation of tissue and loss of grey-white matter differentiation within the affected region?

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17
Q

microglia is derived from ………………..

A

yolk-sac monocytes

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18
Q

What 3 structures are phagocytized by microglia in ischemic infarct?

A

neurons, myelin, necrotic debris

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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.

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20
Q

What cells release inflammatory mediators after ischemic damage?

A

neutrophils

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21
Q

inflammatory mediators, released after ischemic stroke contriibute to …….

A

hydrolysis of cell in liquedactive necrosis

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22
Q

How looks neutrophils in lipid stain?

A

none. They are not prominent on lipid stain unlike microglia (foamy lipids)

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23
Q

what cells apart microglia would be seen on lipid stain?

A

schwann cell and ependymal cells

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24
Q

when occurs liquefactive necrosis after ischemic damage?

A

1 week-1 month

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25
Q

When occurs gliosis after ischemic damage? what cells?

A

> 1month-years.

Astrocytes and microglia

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26
Q

What are 2 mechanisms of cerebral edema after ischemic stroke?

A

cytotoxic (ionic) and vasogenic edema

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27
Q

What happens in cytotoxic (ionic) edema?

A

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.

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28
Q

When begins cytotoxic (ionic) edema?

A

hours after the ischemic damage

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29
Q

What happens in vasogenic edema?

A

Inflammatory mediators from neutrophils disrupts junctions of BBB –> protein and water leakage into interstitial space.

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30
Q

When begins vasogenic edema?

A

24-48h after ischemic damage

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31
Q

vasogenic phase can cause persistent cerebral edema for …………….. (duration) after the initial injury

A

weeks

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32
Q

What cerebral edema can cause persistent cerebral edema for weeks after the initial injury?

A

vasogenic

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33
Q

Decr. oncotic pressure of in nephrotic. Effect on peripheral and cerebral edema?

A

it causes peripheral edema, but is not significant factor in the development of cerebral edema.

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34
Q

Inadequate absorption of cerebrospinal fluid at the arachnoid granulations can cause…………………

A

communicating hydrocephalus

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35
Q

What ICP and CT changes are in communicating hydrocephalus eg due to inadequate reabsorbtion of CSF in arachnoid granulations?

A

ICP – > increased

CT –> ventriculomegaly

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36
Q

What 2 changes are due to increased hydrostatic pressure in brain?

A

Cerebral edema and increased ICP

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37
Q

Neuro symptoms in patients with increased hydrostatic pressure?

A

gradually worsening headache before development of neurologic abnormalities

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38
Q

Increased ICP cause progressive neurologic impairment through 2 mechanisms?

A

mechanical damage due to brain herniation and direct pressure-induced cell injury

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39
Q

Ependymal cells line …………….. (2 structures)

A

Ventricles and central canal

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40
Q

Function of shwann cells?

A

myelin producing cells that help to guide axonal repair and regeneration in the PNS

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41
Q

Function of oligodendrocytes?

A

myelin producing cells of CNS.

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42
Q

The meninges (eg, pia mater) are separated from the cystic cavity created after ischemic stroke by a …………………………….., which is derived from ……………

A

gliotic tissue layer (derived from the cortex)

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43
Q

origin of astrocytes?

A

neuroectoderm

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44
Q

origin of oligodendrocytes?

A

neuroectoderm

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45
Q

appearance of astorcytes? (2)

A

round vesicular nuclei;

contains glial fibrils (composed of glial fibrillary acidic protein)

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46
Q

function of astrocytes? (5)

A

repair, structural and metabolic support, BBB;

extracellular K buffer, removal of excess neurotrasmiter

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47
Q

appearance of oligodendrocytes? (2)

A

small nuclei surrounded by a pale halo;

fewer processes than astrocytes

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48
Q

function of oligodendrocytes?

A

production of myelin in CNS

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49
Q

appearance of microglia? (2)

A

small alongated nuclei;

mano short branching processes

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50
Q

What is astrocyte marker?

A

GFAP

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51
Q

What happen with microglia in HIV?

A

microglia fuse to form multinucleated giant cells in CNS

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52
Q

function of cilia in ependymal cells?

A

circulate CSF

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53
Q

function of microvili in ependymal cells?

A

helps CSF absorbtion

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54
Q

Myelin vs schwann cells? function

A

myelin - isolates axon to inc. condution velocity;

schwann cells - promote axonal regeneration

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55
Q

In what syndrome are damaged schwann cells?

A

Guillain-Barre

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56
Q

In what syndromes are damaged oligodendrocytes?

A

multiple sclerosis; progressive multifocal leukoencephalopathy (PML), leukodystrophies

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57
Q

origin of schwann cells?

A

neural crest

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58
Q

What is in gray matter and in white matter?

A

gray - bodies of neurons;

white - glial cells (predominantly oligodendrocytes)

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59
Q

What 3 changes in neurons indicate irreversible neuronal damage??

A

shrunken, basophilic nuclei + intensively eosinophilic cytoplasm (red neurons)

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60
Q

What do astrocytes in response to irreversible neuronal injury?

A

astrocytes proliferate at the site of injury to restore tissue intergrity - it is called astrocytosis (or gliosis)

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61
Q

astrocyte perform function analogous to what cell otuside CNS?

A

fibroblasts

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62
Q

what compensation happens to astrocytes in gliosis?

A

hypertrophy and proliferation

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63
Q

What 3 actions are done by proliferated astrocytes to form gliotic scar?

A

they replace lost neurons, compensate for their volume, over time form connected, firm meshwork - a gliotic scar

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64
Q

what process undergo irreversibly injured neurons?

A

cellular necorisi (NOT HYPERTROHPY)

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65
Q

what phagocytozes microglia?

A

dead cells and debris

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66
Q

In neuronal damage is eosinophilic material. Where is eosinophilic material in vascular hyalinization and amyloiud depositions?

A

EXTRACELLULAR!!!

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67
Q

gliosis leads to …………………., which compensates ……………….

A

formation of glial scar, which compensates for volume loss that occurs after neuronal death.

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68
Q

Pulmonary edema + hypotension. What suspect?

A

shock (cardiogenic)

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69
Q

Symetric, bilateral weddge-shaped strips of necrosis over the cerebral convexity. What suspect?

A

global cerebral ischemia - nes bilateral damage, ir cia yra damage in watershed zones

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70
Q

What causes infarct in watershed zones?

A

severe systemic hypotension (eg cardiogenic shock, cardiopulmonary arrest)

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71
Q

What sites are the brain are vulnerable for hypoxic damage? why? (2 groups)

A

Brain regions with HIGH METABOLIC DEMAND - hippocampus, cerebellar Purkinje, neocortex) AND watershed zones - areas supplied by most-distal branches of cerebral arteries

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72
Q

Why watershed zones are vulnerable?

A

because of low baseline perfusion pressure.

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73
Q

Where are located watershed zones? (2)

A

Parallel and a few centimeters lateral to the interhemispheric fissure.
Damage can extend from the frontal to occipital lobe

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74
Q

Global ischemia lasting longer than ………………… can cause irreversible damage to neurons.

A

3-5 min

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75
Q

What cells are primary damaged by hypoxia in CNS? Time?

A

CA1 pyramidal neurons of the hippocampus - 3 min

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76
Q

What cells are second in a row to be damaged by ischemia in CNS? (2). Time?

A

Cerebellar Purkinje cells and neocortex pyramidal neurons - 5-10min.

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77
Q

What unique neurochemical characteristic apart from high metabolic demant have neurons that make them susceptible to ischemia?

A

inability to repolarize after anoxic depolarization

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78
Q

Where is located hippocampus?

A

medial temporal lobe

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79
Q

What role plays hippocampus? (3)

A

memory, spatial processing and response inhibition

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80
Q

Selective damage to the hippocampus is common with …………………

A

transient ischemia

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81
Q

Selective damage to the hippocampus can result in an inability to ……………………….. (2)

A

make new memories (anterograde amnesia) and disorientation to place or time.

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82
Q

Cerebral ischemia results in a rapid depletion of energy stores that triggers a complex cascade of cellular events such as ………………… and …………………, resulting in ……………….

A

cellular depolarization and Ca2+ influx, resulting in excitotoxic cell death.

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83
Q

The critical determinant of severity of brain injury is ………………. and ………………………… and……………

A

duration and severity of the ischemic insult and early restoration of CBF

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84
Q

Embolic infarction vs global ischemia. How differs location of damage?

A

Global - watershed zones - symetric bilateral infarctions

Embolic - multiple scattered infarct in asymmetric pattern - affected multiple different vascular territories

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85
Q

Cerebral amyloid angiopathy leads to ……………….. (ischemia or hemorrhage)

A

hemorrhage

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86
Q

Pterion is a a region where the …………… (4) bones meet in the skull

A

frontal, parietal, temporal and sphenoid bones

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87
Q

What is the thinnest location in the skull?

A

pterion

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88
Q

Fracture to pterion - damage to what artery?

A

middle meningeal artery

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89
Q

damage to middle meningeal artery cause ……………. hematoma

A

epidural

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90
Q

Why is required prompt treatment of epidural hematoma?

A

it is under systemic arterial pressure (middle meningeal artery damage) –> rapid increase of intracranial pressure

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91
Q

Rapid increase of epidural hematoma can lead to ………….. (3)

A

elevated intracranial pressure; brain herniation; death

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92
Q

Elevated ICP in epidural hematoma can cause …………. reflex

A

Cushing

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93
Q

What brain herniation can occur due to epidural hematoma?

A

uncal herniation with oculomotor nerve palsy

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94
Q

Middle meningeal artery is a brach of …………….

A

maxillary artery (which is a branch of external carotid artery)

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95
Q

middle meningeal artery enters the skull via …………

A

foramen spinosum

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96
Q

Middle meningeal artery supplies ………………… (2)

A

dura matter and periosteum

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97
Q

The facial artery is a branch of the ……………………….

A

external carotid artery

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98
Q

what regions supply facial artery? (3)

A

oral, nasal, and buccal regions

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99
Q

what is the course of facial artery?

A

over the mandible anterior to the insertion of the masseter muscle

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100
Q

injury to what artery causes subarachnoid or intracerebral hemorrhage?

A

middle cerebral artery

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101
Q

middle cerebral artery is a branch of ………….

A

internal carotid artery

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102
Q

middle cerebral artery supplies ……………… (2)

A

musch of the parieatl and temporal regions

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103
Q

occipital artery originates from ……………

A

external carotid

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104
Q

occipital artery supplies ………….. (2)

A

posterior scalp and the sternocleidomastoid muscles.

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105
Q

The sphenopalatine artery is a branch of the third part of the ……………………. and supplies much of the ……………….

A

maxillary artery and supplies much of the nasal mucosa

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106
Q

sphenopalatine artery anastomoses with …………….. and …………….. and form ………………………

A

branches of the ophthalmic and facial arteries within the anterior part of the nasal septum in a region known as Kiesselbach’s plexus

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107
Q

too rapid correction of hyperonatremia. drop in serum osmolarity stimulates …………………….. –> … ICP

A

water flow into brain cells –> incr. ICP –> impaired cerebral perfusion and eventual brain herniation

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108
Q

aneurysm due to cystic abnormalities can cause ………….. (hemorrhage).

A

SAH

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109
Q

what causes meningeal irritation in SAH?

A

pooling of the blood in the subarachnoid space –> irritation of meninges (pia matter). Within 24h

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110
Q

When do CT in SAH?

A

within 24h from the onset of symptoms

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111
Q

If CT is negative despite suspicion of SAH, what do?

A

lumbar puncture –> seen xantochromia (bloody or yellow CSP)

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112
Q

What is the most sensitive method to diagnose SAH?

A

lumbar puncture –> xantochromia

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113
Q

CT ins SAH shows blood in …………. (2)

A

cerebral sulci and basal cisterns

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114
Q

Blood in the subarachnoid space can acutely ……………. and ………………….. of cerebral spinal fluid (CSF) by the arachnoid granulations

A

obstruct and impair absorbtion

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115
Q

what causes fibrosis of arachnoid granulations in SAH?

A

blood-induced inflammation

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116
Q

blood-induced inflammation can cause………………… of the arachnoid granulations in SAH

A

fibrosis

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117
Q

What leads to chronic hydrocephalus in SAH?

A

obstruction/impaired absorbtion of CSF;
blood induced inflammation –> fibrosis of arahcnoid granulations –> impaired absorbtion of CSF
Net result: chronic hydrocephalus

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118
Q

the most common complication of SAH?

A

vasospasm (3-12 days) –> ischemic damage

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119
Q

Why there may be vasospasm in SAH?

A

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).

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120
Q

how manifest vasospasm induced delayed cerebral ischemia in SAH?

A

change in mental status and/or new focal neurological deficits 3-12 days after SAH

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121
Q

CT scan of SAH induced vasospasm?

A

no signficant changes

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122
Q

What medication is used to event SAH induced vasospasm?

A

nimodipine

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123
Q

Impaired CSF absorption causes ……………………..

A

communicating hydrocephalus

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124
Q

What ventricles are dilated in hydrocephalus post SAH? Why?

A

all 4;

because a blocked of flow is distal to entire ventricular system (tipo fibrosis of arachidonic granulations)

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125
Q

ventricular enlargement in SAH hydrocephalus leads to …………………………….

A

stretches adjacent nerve fibers and, in the acute setting, leads to deteriorating mental status

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126
Q

Treatment of hydrocephalus?

A

placement of an external ventricular drain to relieve pressure in the ventricular system and subarachnoid space.

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127
Q

What is used to treat chronic hydrocephalus?

A

permanent shunt eg ventriculoperitoneal shunt

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128
Q

What are focal manifestation in SAH?

A

there is no focal neurologic manifestation in SAH (eg aphasia, hemiplegia etc)

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129
Q

Blood breakdown products in SAH cause ………….. (2)

A

obstructing the flow of cerebrospinal fluid or clogging the arachnoid villi.

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130
Q

when can occur rebleeding post SAH?

A

early, <24h post initial bleeding

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131
Q

CT in rebleeding post SAH?

A

Newly extravasated bloodi

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132
Q

Symptoms of rebleeding post SAH?

A

sudden change in consciousness and new nerologic deficit

133
Q

CT of 3 SAH complications?

A

vasospasm - none
hydrocephalus - enlarged ventricles
rebleeding - newly extravasated blood

134
Q

What 2 lesions can increase ICP?

A

hemorrhage, hematoma

135
Q

increased ICP due to hematomas/hemorrhages can manifest as ……………..

A

headache, vomiting, impaired consciousness and ultimately Cushing triad.

136
Q

What indicates Cushing triad after brain injury?

A

imminent brain herniation

137
Q

What is Cushing triad?

A

hypertension, bradycardia and irregular respirations

138
Q

Downward displacement of the brainstem is called ………..

A

central herniation

139
Q

Lesions in the temporal lobe tend to cause ………………….. herniation of the ……….

A

transtentorial herniation of the uncus

140
Q

What compress uncal transtentorial herniation?

A

ipsilateral CN III (because it exits the midbrain at the same level as is tentorium.

141
Q

Compression of CN III due to herniation. Manifestation?

A

ipsilateral CN III palsy with fixed dilated pupil (due to preganglionic parasympathetic nerve fiber damage)

142
Q

What herniation cause paramedian basilar artery branches to rupture?

A

central/downward transtentorial herniation

143
Q

central/downward transtentorial herniation cause rupture of …………..

A

paramedian basilar artery branches

144
Q

Brainstem hemorrhage is called ……………

A

Duret hemorrhages

145
Q

Injury to what arteries cause Duret hemorrhages?

A

paramedian basilar artery branches

146
Q

The most common cause of deep intracranial hemorrhage?

A

hypertensive vasculopathy

147
Q

Mechanism how chronic hypertension can cause hemorrhage in the deep brain.

A

Chronic hypertension –> progressive arteriolar hyalinization and fibrinoid necrosis, weakening the vessel wall –> formation of Charcot-Bouchard aneurysms –> aneurysmal rupture –> hemorrhage

148
Q

What are the most common sites of intraparenchymal hemorrhage?

A

Basal ganglia (putamen), cerebellar nuclei, thalamus, pons.

149
Q

What arteries supply basal ganglia?

A

Lenticulostriate arteries, which are deep, small vessel branches off the middle cerebral arteries.

150
Q

what are neurologic deficits, heahdache and meningeal signs in intraparenchymal hemorrhage due to hypertension?

A

Focal neurologic deficit;
Severe hemorrhage - sometimes presents;
Meningeal signs - no present

151
Q

Hemorrhage in thalamus. Symptoms.

A

Contralateral weakness/numbness and extensor plantar response.
Cia simptomai due to thalamic hemorrhage with edema/mass effect on the internal capsule.

152
Q

Hemorrhage in putamen. Symptoms.

A

Compresses internal capsule –> dysarthria, contralateral hemiparesis, contralateral hemisensory loss

153
Q

What tract fibers are damages in putamen hemorrhage that compresses internal capsule?

A

corticobulbal, corticospinal and somatosensory fibers.

154
Q

Manifestation of increased ICP?

A

headache, nausea/vomiting, altered mental status

155
Q

What 3 vessels changes promotes chronic hypertension?

A

Lipohyalinosis, microatheroma formation, hardening/thickening of the vessels wall (hypertensive arteriolar sclerosis)

156
Q

Hypertensive arteriolar sclerosis leads to…………..

A

progressive narrowing of the arteriolar lumen + predisposes thrombotic vessel occlusion

157
Q

Posterior limb of the internal capsule and/or basal pons. What symptoms?

A

pure motor hemiparesis OR ataxia-hemiplegia syndrome

158
Q

Anterior limb of the internal capsule and/or basal pons. What symptoms?

A

dysarthria-clupsy hand syndrome (ie dysarthria and dysphagia with clumsiness of one hand)

159
Q

Ventroposterolateral or ventroposteromedial thalamus. What symptoms?

A

pure sensory stroke

160
Q

pure motor hemiparesis OR ataxia-hemiplegia syndrome. What part of the brain is damaged?

A

Posterior limb of the internal capsule and/or basal pons.

161
Q

dysarthria-clupsy hand syndrome (ie dysarthria and dysphagia with clumsiness of one hand). What part of the brain is damaged?

A

Anterior limb of the internal capsule and/or basal pons.

162
Q

pure sensory stroke. What part of the brain is damaged?

A

Ventroposterolateral or ventroposteromedial thalamus

163
Q

Lacunar infarct. CT?

A

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
Q

What is lacuna?

A

cavitary spaces filled with CSF and surrounded by scar tissue. Occurs after several weeks of lacunar iinfarct in damages areas.

165
Q

Manifestation of hypertensive encephalopathy? CT?

A

Progressive headache and nausea/vomiting followed by nonlocalizing neurologic symptoms (eg, confusion).
Cerebral imaging may be normal or show parietooccipital white matter edema.

166
Q

Manifestation of hypoxic encephalopathy? CT?

A

decreased consciousness (come, vegetative state); no focal deficit/hemorrhage. CT - may show watershed infarcts.

167
Q

CT of embolic stroke?

A

large-teritory infarctions of the cerebral cortex as large areas of HYPODENSITY

168
Q

Damage to what arteries (general name) cause hemorrhage in basal ganglia?

A

deep penetrating arteries

169
Q

What hemorrhage (location) can be caused by amyloid angiopathy?

A

lobar/cortical

170
Q

pontine arteries are small branches of the …………….

A

basilar arteries

171
Q

location of the pontine hemorrhages?

A

close to the midline –> affect both sides of pons

172
Q

Manifestation of pons hemorrhage? (3)

A

Coma, locked-in syndrome, pinpoint pupils

173
Q

Location of locus ceruleus?

A

the posterior rostral pons near the lateral floor of the fourth ventricle.

174
Q

Function of locus ceruleus?

A

principal site for norepinephrine synthesis in CNS and projects virtually all parts of the CNS.

175
Q

Abnormal activation of the locus ceruleus has been implicated in the pathogenesis of ……………..

A

anxiety disorders, eg panic attacks.

176
Q

Anxiety disorders, eg panic attacks. what part of the brain is abnormaly activated?

A

locus ceruleus

177
Q

Why patients with bilateral pontine hemorrhage typically present with coma?

A

Due to disruption of the reticular activating system

178
Q

disruption of the reticular activating system in pontine hemorrhage leads to ………..

A

coma

179
Q

Pinpoint pupils in pontine hemorrhage. Pathomechanism?

A

descending sympathetic tract damage

180
Q

total paralysis with extensor posturing in pontine hemorrhage due to …………………

A

corticospinal and corticobulbar tract injury

181
Q

descending sympathetic tract damage leads to …………..

A

pinpoint pupils

182
Q

corticospinal and corticobulbar tract injury leads to …………..

A

total paralysis with extensor posturing

183
Q

2 locations of CNS that produce dopamine?

A

ventral tegmental area and substantia nigra pars compacta in the midbrain.

184
Q

What are 3 major dopaminergic pathways in the brain?

A

mesolimbic and mesocortical pathways; nigrostriatal pathway; tuberoinfundibular pathway

185
Q

Mesolimbic and mesocortical pathways regulate …………………

A

cognition and behavior

186
Q

Nigrostriatal pathway regulates …………….

A

coordination of voluntary movements

187
Q

tuberoinfundibular pathway function is ………………

A

inhibits prolactin secretion

188
Q

What is dynorphin?

A

opioid peptide that modulates the pain response

189
Q

Where is produced dynorphin? (3)

A

Periaqueductal gray, rostral ventral medulla, and dorsal horn of the spinal cord

190
Q

Histamine and orexin are produced in the ……………………

A

posterior hypothalamus

191
Q

What 2 substances are produced in posterior hypothalamus?

A

histamine and orexin

192
Q

What is the function of histamine and orexin?

A

arousal and wakefulness

193
Q

Locus ceruleus projects to virtually all parts of the central nervous system and helps control ……………… (5)

A 
mood
arousal (reticular activating system)
sleep-wake states
cognition
autonomic function
194
Q

nonreactive pupils to light stimulation following cardiac arrest carries indicates ……………………

A

anoxic damage to the brainstem at the level of the upper midbrain

195
Q

During the normal pupillary reflex, the retina as well as the optic nerve and tract transmit the light stimulus to the ………………………..

A

midbrain at the level of the superior colliculus

196
Q

What 2 nuclei gets light stimulus in midbrain?

A

pretectal nuclei and then stimuli goes to the bilateral Edinger-Westhpal nuclei.

197
Q

Where goes stimuli from Edinger-Westhpal nuclei?

A

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
Q

Whan happens when light is shone in one eye?

A

both the ipsilateral pupil (direct response) and contralateral pupil (consensual response) constrict.

199
Q

MRI findings in anoxic brain injury?

A

loss of grey-white matter differentiation with sulcal effacement

200
Q

The occipital lobe contains the …………………………

A

primary visual cortex

201
Q

Unilateral occipital lobe damage can cause ………………..

A

contralateral homonymous hemianopia

202
Q

bilateral occipital lesions may result in ………………….

A

cortical blindness

203
Q

cortical blindness is caused by damage in ……………….

A

bilateral occipital lesions

204
Q

contralateral homonymous hemianopia is caused by damage in ………………

A

Unilateral occipital lobe

205
Q

Parietal lobe damage results in difficulties with ………………. and ……………….

A

spatial and visual perception

206
Q

The parietal lobes process and interpret ………….., ……………, and …………….. signals received from other brain areas.

A

visual, auditory, and motor

207
Q

(parietal lobe) Nondominant (eg, right-sided) lesions result in ……………….

A

hemi-neglect and constructional apraxia

208
Q

(parietal lobe) dominant (eg, left-sided) lesions result in ………………….

A

Gerstmann syndrome (eg, right-left confusion, agraphia, acalculia

209
Q

Temporal lobe injury can cause disturbances in ………….. (4)

A

memory (eg, hippocampus); speech (eg, Wernicke area in dominant hemisphere); vision (eg, Meyer loop);
hearing (eg, primary auditory cortex).

210
Q

Bilateral damage to the amygdala results in ……………………..

A

Klüver-Bucy syndrome

211
Q

Klüver-Bucy syndrome manifestation? (3)

A

hyperphagia, hyperorality, hypersexuality

212
Q

What part of the brain contains horizontal gaze center?

A

Pons

213
Q

Bilateral pontine injury results in …………………

A

pinpoint pupils

214
Q

Horizontal gaze center, which helps mediate the ………………………. reflex

A

oculocephalic (doll’s eye)

215
Q

Afferent limb of corneal reflex. What CN?

A

Trigeminal (CN V)

216
Q

Efferent limb of corneal reflex. What CN?

A

Facial (CN VII)

217
Q

Ventral posterolateral nucleus mediates what sensation?

A

Somatic sensation of the body

218
Q

ventral posteromedial nucleus mediates what sensation?

A

Facial sensation and taste

219
Q

the lateral geniculate nucleus mediates …………..

A

vision

220
Q

medial geniculate nucleus mediates ………..

A

hearing

221
Q

Berry aneurysm in anterior communicating artery. What compress?

A

central optic chiasm –> bitemporal hemianopia

222
Q

Berry aneurysm in posterior communicating artery. What compress?

A

oculomotor nerve –> producing ipsilateral mydriasis, ptosis, and “down and out” eye deviation.

223
Q

Basilar artery occlusion –> damage of pons. What limbs affected?

A

quadriplegia

224
Q

Basilar artery occlusion –> damage of pons. What is bulbar dysfunction?

A

facial weakness, dysarthria

225
Q

Basilar artery occlusion –> damage of pons. What is oculomotor deficits?

A

horizontal gaze palsy

226
Q

occlusion of what causes lateral pontine syndrome?

A

anterior inferior cereberal artery

227
Q

occlusion of anterior inferior cereberal artery causes …………………….

A

lateral pontine kazka nx

228
Q

signs of increased ICP?

A

altered mental status, nausea/vomiting, Cushing reflex (bradycardia, hypertension and irregular breathing

229
Q

2 stages of clinical manifestation in epidural hematoma.

A

Transient loss of consciousness and then lucid period, in which patient regains consciousness

230
Q

Diagnostics of epidural hematoma?

A

noncontrast CT - hyperdensi biconvex lesion

231
Q

What is lipohyalinosis in lanucar infarct?

A

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
Q

What is microatheroma in lacunar infarct?

A

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
Q

Emboli most commonly affect what part of the brain?

A

cortex

234
Q

3 characteristics of pats brain necrosis (old cerebral infarct)?

A

cystic cavity, volume loss and enlarged ventricle

235
Q

What releases lysosomal enzymes in brain ischemia?

A

ischemic neurons

236
Q

what releases inflammatory cytokines in brain ischemia?

A

inflammatory cells (neutrophils, macrophages)

237
Q

why eventually there is cavity after brain infarct?

A

phagocytic cells remove necrotic tissue

238
Q

wallerian degeneration results in …………… (2)

A

axonal degenration and breakdown of the myelin sheat distal to the site of injury

239
Q

when begins degeneration of axon after injury?

A

within a few days

240
Q

what cells in PNS sense axonal degeneration?

A

Schwann cells

241
Q

What cells secrete cytokines and chemokines in axonal damage to rectruit macrophages?

A

Schwann cells

242
Q

What cells secrete trophic factor in axonal damage?

A

Schwann cells

243
Q

What does trophic factor in axonal damage?

A

stimulates formation of a growth cone from the stump of the proximal axon and facilitates nerve regeneration

244
Q

Why in CNS phagocytic macrohages/microglia are recruited more slowly than in PNS?

A

due to BBB

245
Q

what happens to oligodendrocytes in axonal CNS injury?

A

myelin-producing oligo becomes inactive or undergo apoptosis

246
Q

how long lasts removal of myelin debrin in CNS after axonal injury?

A

can persist for years in degenerating tracts

247
Q

How is suppresed axonal growth in CNS axonal injury?

A

myelin-associated inhibitory factors

248
Q

What cells in CNS release inhibitory factors in axonal damage?

A

oligo and astrocytes

249
Q

Embolic ischemic strokes have a high risk of undergoing acute hemorrhagic transformation within the first………… days following the ischemic event.

A

7

250
Q

Why there is no axonal regeneration in CNS? (3)

A

Persistence of myelin debris;
secretion of neuronal inhibitory factors;
development of dense glial scar

251
Q

Neutrophilic infiltration progressively increases up to ……..hours after ischemic stroke and then diminishes.

A

48

252
Q

Left leg weakness + vision loss in the right eye. Where is the lesion?

A

Right internal carotid artery

253
Q

Pattern of neurologic deficit in TIA?

A

focal neurologic impairment. TIA most commonly due to emboli originating from atherosclerotic plaques

254
Q

How differ presentation of chronic and acute SDH?

A

acute - profundly depresses mental status at onset

chronic - insidious onset of headache and confusion

255
Q

What 3 conditions predispose SAH?

A

Ehlers-Danlos, aut.dominant polycytic KD, arteriovenous malformations

256
Q

What 2 conditions predisposes berry aneurysms?

A

Ehlers-Danlos and autosom.dom.polycyst kidney disease

257
Q

How clinically looks locked-in syndrome?

A

quadriplegia + speechlessness with preserved eye movements and consciousnes

258
Q

What eye movements are preserved and what not in locked-in syndrome?

A 
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
Q

Why there is consciousness in locked-in syndrome?

A

for consciousness is responsible reticular formation which is in midbrain.

260
Q

preserved or damaged Behavioral arousal and sleep-wake cycles in locked-in?? Why?

A

preserved because the diencephalon–upper brainstem arousal systems are unaffected.

261
Q

Why preserved sensation in locked-in?

A

sensory pathways are not affected and preserved brainstem and spinal reflexes because they do not require cortical input.

262
Q

what 2 motor functions impaired in locked-in? Why?

A

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
Q

Thalamic ventral posterior lateral nucleus receives input from …………………….

A

the spinothalamic tract and dorsal columns

264
Q

ventral posterior medial nucleus receives input from ……………………….

A

the trigeminal pathway

265
Q

Thalamic posterior lateral/medial nuclei send somatosensory information to the ……………….. via ………….

A

to the cortex via thalamocortical fibers

266
Q

Severe proprioceptive defects due to thalamic damage may cause ……….

A

unsteady gait

267
Q

Damage to both thalamic posterior lateral/medial nuclei results in ………….

A

complete contralateral sensory loss (eg touch, pain/temperature, vibration/proprioception)

268
Q

The anterior two-thirds of the posterior limb of the internal capsule is mainly composed of ……………….. fibers (eg ………….. tract),

A

motor fibers (eg, corticospinal tract)

269
Q

The posterior one-third of posterior limb of the internal capsule contains ……………. fibers (eg, ………….. tract).

A

sensory;

thalamocortical

270
Q

motor, sensory and UMN signs in ACA occlusion.

A

Motor - contralateral lower limb weakness;
UMN signs such hyperreflexia, babinski;
Contralateral sensory - occurs in minority of patients

271
Q

Atrial thrombi frequently travel to what brain arteries?

A

ACA and MCA

272
Q

ACA supply what parts of the brain?

A

medial aspects of the frontal and parietal lobes

273
Q

how circle of willi is protective against ischemic injury to the brain?

A

it provides a potential alternate pathways for cerebral arterial blood flow

274
Q

if there is symptomatic ACA stroke, what part of the vessel is more likely obstructed?

A

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
Q

In what part of the brains is micturition reflex center?

A

Medial frontal lobe

276
Q

An embolic occlusion of the anterior spinal artery in the lumbosacral region. Manifestation?

A

Bilateral lower extremity weakness with hyporeflexia, loss of pain and temperature sensation

277
Q

Damage to what structure causes hyporeflexia in embolic occlusion of the anterior spinal artery in the lumbosacral region?

A

ischemia of the anterior horns and corticospinal tracts

278
Q

Damage to what structure causes loss of pain and temperature sensation in embolic occlusion of the anterior spinal artery in the lumbosacral region?

A

ischemia of the spinothalamic tracts

279
Q

inferior frontal, medial frontal, and superior medial parietal lobes. Blood supply?

A

ACA

280
Q

anterior 4/5 of the corpus callosum; Blood supply?

A

ACA

281
Q

olfactory bulb and tract; blood supply?

A

ACA

282
Q

anterior portions of the basal ganglia; blood supply?

A

ACA

283
Q

internal capsule (only anterior portion?). Blood supply?

A

ACA

284
Q

Sensory deficit in ACA occlusion?

A

contralater can occur, bet siaip in a minority of patients

285
Q

Motor and sensory deficits of the right leg (sparing the right arm). Where is damage?

A

medial portions of the left primary motor and somatosensory cortices.

286
Q

Micturition reflex location is supplied by ……….

A

ACA

287
Q

What is location of micturition reflex centers in the brain?

A

frontal micturition center (medial frontal lobe) arba tipo cingulate gyrus

288
Q

The superior division of the MCA supplies blood to ………….

A

frontal lateral cortex

289
Q

The inferior division of the MCA supplies blood to ………….

A

lateral portions parietal and temporal cortices

290
Q

Occlusion of superior division of MCA. What neuro deficit?

A

motor deficit (sometimes sensory deficit in face and arm)

291
Q

Occlusion of inferior division of MCA. What neuro deficit?

A

Sensory deficits of the arm and face (motor function spared)

292
Q

What artery occlusion causes Broca aphasia (in dominant sphere)?

A

superior division of MCA

293
Q

What artery occlusion causes Wernicke aphasia (in dominant sphere)?

A

inferior division of MCA

294
Q

What artery occlusion causes hemineglect (in nondominant sphere)?

A

superior division of MCA

295
Q

What artery occlusion causes PROFUND hemineglect (in nondominant sphere)?

A

inferior division of MCA

296
Q

Oclusion of what division of MCA causes visual defects?

A

inferior division of MCA

297
Q

MCA strokes often associated with ….. (3 neuro manifestation)

A

homonymous hemianopia, aphasia, and hemineglect

298
Q

Why macula is pared in PCA occlusion?

A

due to collateral circulation from the MCA

299
Q

What visual part is spared in PCA occlusion?

A

macula

300
Q

The most common manifestation of PCA occlusion?

A

contralateral hemianopia

301
Q

CT of PCA occlusion?

A

focal parenchymal hypoattenuation and occipital horn effacement.

302
Q

PCA branches of …………. at the level of ………….

A

basilar artery at the level of the pontomesencephalic junction

303
Q

PCA supplies CN……. and CN ……

A

CN III and CN IV (and other structures in the MIDBRAIN)

304
Q

Thalamus. Blood supply?

A

PCA

305
Q

Medial temporal lobe. Blood supply?

A

PCA

306
Q

Splenium of the corpus callosum. Blood supply?

A

PCA

307
Q

Parahippocampal gyrus. Blood supply?

A

PCA

308
Q

Fusiform gyrus. Blood supply?

A

PCA

309
Q

Occipital lobe. Blood supply?

A

PCA

310
Q

If lateral thalamus is involved in PCA occlusion. Manifestation?

A

contralateral paresthesias and numbness (affectin face, trunk and limbs)

311
Q

What 3 cortical symptoms can occur in PCA occlusion?

A

dyslexia, visual agnosia, prosopagnosia

312
Q

What is agnosia?

A

impaired visual recognition of objects

313
Q

How is called impaired visual recognition of objects?

A

agnosia

314
Q

What is prosopagnosia?

A

inability to recognize faces

315
Q

What is inability to recognize faces?

A

Prosopagnosia

316
Q

Anterior choroidal artery branches off ………..

A

internal carotid artery

317
Q

Posterior limb of the internal capsule. Blood supply?

A

anterior choroidal artery

318
Q

optic tract. Blood supply?

A

anterior choroidal artery

319
Q

lateral geniculate body. blood supply?

A

anterior choroidal artery

320
Q

choroid plexus. blood supply?

A

anterior choroidal artery

321
Q

uncus. blood supply?

A

anterior choroidal artery

322
Q

hippocampus. blood supply?

A

anterior choroidal artery

323
Q

amygdala. blood supply?

A

anterior choroidal artery

324
Q

The artery of Percheron branches off either the ……. or ………….

A

right or left PCA

325
Q

The artery of Percheron supplies ………….. (2)

A

bilateral thalami and dorsal midbrain

326
Q

bilateral thalamic or dorsal midbrain strokes. What artery?

A

The artery of Percheron

327
Q

The ACA supply the medial portions of the 2 hemispheres: …………… and ………. lobe

A

frontal and parietal lobes

328
Q

total 4 manifestaion in ACA occlusio?

A

Contralateral motor and sensory deficit of lower extremities, behavioral changes, urinary incontinence

329
Q

behavioral symtoms and incontinence occurs in …………. ……………. occlusion

A

BILATERAL ACA

1 STEP UWorld neuro+psycho (10 decks)

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