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How to Master Pathology - Moey Series > Central Nervous System > Flashcards

Central Nervous System Flashcards

1
Q

Due to different type of neurons, the different locations of these neurons, differences in distribution of their connections, neurotransmitters used, metabolic requirements, and level of electrical activity

A

Selective vulnerability of neurons

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2
Q

Neurons require a continuous supply of oxygen to meet what metabolic needs

A

1) Maintenance of membrane potentials essential for transmission of electric signals
2) Support the extensive dendritic arborization of neurons and axonal formation

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3
Q

Acute neuronal injury or Red neurons are evident by 12-24 hours after introduction of what stimulus?

A

IRREVERSIBLE hypoxic/ischemic insult

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4
Q

Characteristics of Acute neuronal injury or Red neurons

A 
Shrinkage of the cell body
Nuclear pyknosis
Nucleolus disappearance
Loss of Nissl substance
Intense cytoplasmic eosinophilia
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5
Q

What reflects the earliest marker of neuronal cell death?

A

Acute neuronal injury or Red neurons

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6
Q

What is observed in the cell body during regeneration of axons?

A

Axonal Reaction:

Peripheral displacement of the nucleus
Enlargement of nucleolus
Central chromatolysis (dispersion of Nissl bodies from the center to the periphery)
Enlargement and rounding of cell body

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7
Q

Axonal reaction is best seen in what cell of the body?

A

Anterior horn cells of the spinal cord

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8
Q

What are the histopathologic characteristics of Neurodegeneration or Subactue and Chronic Neuronal Injury?

A

1) Cell loss (usually via apoptosis)

2) Reactive gliosis

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9
Q

What is the earliest marker of Neurodegeneration or Subacute and Chronic Neuronal Injury?

A

Reactive gliosis

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10
Q

Viral infection:

INTRANUCLEAR inclusion

A

Cowdry inclusion

from herpetic infections

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11
Q

Viral infection

INTRACYTOPLASMIC inclusion

A

Negri bodies

from rabies infection

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12
Q

Viral infection

BOTH INTRANUCLEAR AND INTRACYTOPLASMIC inclusion

A

Cytomegalovirus infection

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13
Q

Neurodegenerative

INTRACYTOPLASMIC inclusion

A

Neurofibrillary tangles - Alzheimer disease

Lewy bodies - Parkinson disease

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14
Q

Abnormal vacuolization of the perikaryon and neuronal cell processes in the neuropil

A

Creutzfeldt-Jakob Disease

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15
Q

What is the most important histopathologic indicator of CNS injury, regardless of etiology?

A

Reactive gliosis

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16
Q

Reactive Gliosis characteristics:

A

Both HYPERTROPHY and HYPERPLASIA of astrocytes

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17
Q

Astrocyte characteristics

A

Star-shaped, multipolar, branching processes
Contain Glial Fibrillary Acidic Protein (GFAP)
Acts as metabolic buffers, and detoxifies the brain

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18
Q

Gemistocyte or Reactive astrocyte

A

Bright-pink, somewhat irregular swath around an eccentric nucleus, from which numerous, stout ramifying processes are found

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19
Q

Alzheimer Type II Astrocyte

A

Gray matter cell with large (2-3x normal) nucleus
Pale-staining central chromatin
INTRANUCLEAR CHROMATIN DROPLET
Prominent nuclear membrane and nucleolus

Seen in LONG-STANDING HYPERAMMONEMIA:
(Chronic liver disease, Wilson disease, hereditary metabolic disorders of the urea cycle)

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20
Q

Thick elongated, eosinophilic, irregular structures in astrocytic processes. Contain HSPs (ab-crystallin and HSP27) and ubiquitin

A

Rosenthal fibers

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21
Q

Rosenthal fibers are found in what states?

A

Long-standing gliosis
Pilocytic Astrocytoma
Alexander Disease

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22
Q

Alexander disease

Characteristics

A

Leukodystrophy associated wth GFAP gene mutations

Has Rosenthal fibers (in periventricular, perivascular, subpial zones)

Has corpora amylacea/polyglucosan bodies (in astrocytic end processes found in perivascular and subpial zones)

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23
Q

Round, faintly basophilic, PAS +, concentrically lamellated structure

Contain HSPs and ubiquitin

A

Corpora amylacea or Polyglucosan bodies

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24
Q

In advancing age, what represent a degenerative change in astrocytes?

A

Presence of corpora amylacea or polyglucosan bodies

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25
Q

Seen in cytoplasma of neurons, hepatocytes, myocytes, etc, in patients with myoclonic epilepsy

Share the same biochemical and structural characteristics with corpora amylacea

A

Lafora bodies

seen in Myoclonic epilepsy

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26
Q

What surface markers are found in both microglia and peripheral monocytes/macrophages?

A

CR3

CD68

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27
Q

Microglial response to injury:

A

1) Proliferation
2) Developing elongated nuclei (rod cells in neurosyphilis)
3) Forming aggregated around small foci of tissue necrosis (microglial nodules)
4) Congregating around cell bodies of dying neurons (neuronophagia)

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28
Q

Feature of acquired demyelinating disorders and leukodystrophies

A

Injury/apoptosis of oligodendrocytes

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29
Q

INTRANUCLEAR VIRAL INCLUSIONS in OLIGODENDROCYTES

A

JC Virus

cause of progressive multifocal leukoencephalopathy or PML

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30
Q

a-syncelin glial cytoplasmic inclusions in OLIGODENDROCYTES

A

Multiple system atrophy (MSA)

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31
Q

Disruption of ependymal lining with proliferation of subependymal astrocytes

Seen in inflammation/marked dilation of ventricles

A

Ependymal granulations

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32
Q

May produce extensive EPENDYMAL injury via viral inclusions

A

CMV

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33
Q

Responses not significant to most forms of CNS injury

A

Ependymal and Oligodendrocytic injury

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34
Q

The result of increased fluid leakage from blood vessels or injury to various cells of the CNS

A

Cerebal edema or Brain parenchymal edema

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35
Q

What are the two types of cerebral edema?

A

Vasogenic edema

Cytotoxic edema

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36
Q

Caused by disruption of the blood-brain barrier or increased vascular permeability

A

Vasogenic edema

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37
Q

Increase in CSF due to neuronal, glial, or endothelial cell injury

A

Cytotoxic edema

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38
Q

What further impairs the resorption of excess CSF?

A

Paucity of lymphatic system in the CNS

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39
Q

Causes of localized edema

A

Adjacent neoplasia or inflammation

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40
Q

Causes of generalized edema

A

Ischemic injury

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41
Q

Gross characterisitcs of generalized edema

A

Gyri are flattened
Sulci are narrowed
Ventricular cavities are compressed

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42
Q

Generalized edema have both:

A

Vasogenic and Cytotoxic edema

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43
Q

Form of edema expected in someone with generealized hypoxic/ischemic insult or metabolic derangement that prevents maintenance of metabolic ionic systems

A

Cytotoxic edema

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44
Q

Interstitial edema or hydrocephalic edema happens usually in what ventricle?

A

Lateral ventricles

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45
Q

Defined as the accumulation of excessive CSF within the ventricular system

A

Hydrocephalus

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46
Q

Production of CSF occurs in the:

A

Choroid plexus

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47
Q

Foramina involved in the circulation of CSF from the ventricular system to the cisterna magna

A

Foramina of Magendie and Luschka

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48
Q

Involved in the absorption of CSF in the subarachnoid space

A

Arachnoid granulations

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49
Q

Causes of hydrocephalus

A

1) Impaired CSF flow
2) Impaired resorption of CSF
3) Overproduction of CSF (rare, happens when choroid plexus tumors are present)

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50
Q

Before closure of cranial sutures in infants, hydrocephalus will lead to:

A

Enlargement of the head manifested by an INCREASE IN HEAD CIRCUMFERENCE

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51
Q

Types of hydrocephalus

A

1) communicating or nonobstructive hydrocephalus
2) noncommunicating or obstructive hydrocephalus
3) hydrocephalus ex vacuo

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52
Q

Type of hydrocephalus that occurs when ventricular system is obstructed and DOES NOT COMMUNICATE with the SUBARACHNOID SPACE

A

Noncommunicating or Obstructive hydrocephalus

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53
Q

Type of hydrocephalus that occurs when THERE IS COMMUNICATION with the SUBARACHNOID SPACE

The entire ventricular system is enlarged

A

Communicating or Nonobstructive hydrocephalus

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54
Q

Type of hydrocephalus the occurs as a compensatory increase in ventricular volume SECONDARY TO BRAIN PARENCHYMAL LOSS

A

Hydrocephalus ex vacuo

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55
Q

Noncommunicating hydrocephalus is usually due to:

A

Mass in the third ventricle

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56
Q

Refers to the displacement of brain tissue past rigid dural folds (falx and tentorium), OR through opening in the skull because of increased ICP

A

Herniation

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57
Q

Herniation is mostly associated with

A

Mass effect

1) Localized (tumorm abscess, hemorrhage)
2) Diffuse (generalized edema)

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58
Q

Displaces the cingulate gyrus under the falx cerebri

A

subfalcine or cingulate herniation

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59
Q

Consequence of subfalcine or cingulate herniation

A

1) Compression of the anterior cerebral artery

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60
Q

Occurs when the medial aspect of the temporal lobe is compressed against the free margin of the tentorium cerebelli

A

transtentorial
uncinate
medial temporal herniation

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61
Q

Consequences of transtentorial herniation

A

1) Ipsilateral pupillary dilation (CNIII compression)
2) Ipsilateral posterior cerebal artery compression (leading to ischemic injury to the primary visual cortex)
3) Kernohan notch (compression of the CONTRALATERAL CEREBAL PEDUNCLE, resulting in HEMIPARESIS IPSILATERAL TO THE SIDE OF HERNIATION)
4) Duret hemorrhages in the midbrain and poms (secondary hemorrhages, linear/flame-shaped lesions in the midline and paramedian regions due to the disruption/tearing of penetrating A and V supplyinh the upper brainstem)

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62
Q

Displacement of the cerebellar tonsils through the foramen magnum

A

tonsillar herniation

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63
Q

Consequence of tonsillar herniation

A

life-threatening due to brainstem compression that compromises the vital respiratory and cardiac centers of the medulla oblongata

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64
Q

Physical forces associated with head injury may result in:

A

a. skull fracture
b. vascular injury
c. parenchymal injury

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65
Q

Characteristic of a DISPLACED SKULL FRACTURE

A

Bone is displaced INTO the cranial cavity by a DISTANCE GREATER THAN THE THICKNESS OF THE BONE

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66
Q

Most common site of impact on the head of a person falling DUE TO LOSS OF CONSCIOUSNESS

A

Frontal portion of the skull

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67
Q

Most common site of impact on the head of a person falling WHILE AWAKE

A

Occipital portion of the skull

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68
Q

Correlates for a SUSPECTED BASAL SKULL FRACTURE

A

a. lower cranial nerve problems / cervicomedullary region
b. presence of orbital or mastoid hematomas DISTANT from the point of impact
c. typically follows impact to the OCCIPUT or SIDES OF THE HEAD
d. CSF dischargefrom the nose or ear; and infection (meningitis may follow)

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69
Q

Characteristic of a DIASTATIC FRACTURE

A

This occurs when FRACTURES CROSSES SUTURES

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70
Q

A clinical syndrome of altered consciousness secondary to head injury, usually brought by a large change in the head momentum

A

Concussion

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71
Q

Clinical correlates of CONCUSSION

A

a. instantaneous onset of transient neurologic dysfunction
b. temporary respiratory arrest
c. loss of reflexes

Amnesia may persist even if recovery is complete

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72
Q

What is the pathogenesis of concussion

A

It is UNKNOWN.

However, it is probably the dysregulation of the RAAS in the brainstem

73
Q

Repetitive injuries causing concussion may lead to

A

Chronic Traumatic Encephalopathy

a. Accumulation of tau-containing neurofibrillary tangles in the superior frontal and temporal cortices
b. brain atrophy
c. widening of the ventricles of the brain

TAU = TRAUMATIC

74
Q

Presentation of direct parenchymal injury can either be:

A

a. contusion (analogous to a bruise)

b. laceration (tearing of tissue)

75
Q

Contusions (intraparenchymal hematomas) can also cause hematoma formation in what region of the CNS

A

Subarachnoid space (as sequelae to contusion)

76
Q

What part of the brain is most susceptible to direct parenchymal injury

A

Crests of gyri

frontal lobe, temporal lobe, orbital ridge

77
Q

What parts of the CNS are least susceptible to direct parenchymal injury

A

Occipital lobe, brainstem and cerebellum

unless fractures overlying these areas are present

78
Q

Contusion at the point of contact is called

A

coup injury

79
Q

Contusion at the diametrically opposite point of contact

A

contrecoup injury

80
Q

How can one differentiate a coup injury from a contrecoup injury?

A

via identification of point of impact

coup and contrecoup injury are microscopically and macroscopically the same

81
Q

What contusion injury is most likely to occur in an IMMOBILE HEAD

A

coup injury only

82
Q

What contusion injury is most likely to occur in a MOBILE HEAD

A

both coup and contrecoup injury

83
Q

Consequence of violent POSTERIOR or LATERAL NECT HYPEREXTENSION causing avulsion of the pons from the medulla OR avulsion of the medulla from the cervical portion of the spinal cord

A

instant death

84
Q

General morphology of contusions

A

a. wedge-shaped

b. similar regardless of traumatic source

85
Q

Progression of contusions

A

EARLIEST STAGES:
edema and pericapillary hemorrhage

NEXT FEW HOURS:
extravasation of blood throughout the involved tissue, across the width of the cerebral cortext into the white matter and SUBARACHNOID SPACE

86
Q

Morphologic evidence of neuronal injury in contusions

A

a. takes place after 24 hours
b. pyknosis
c. eosinophilia
d. axonal injury
e. disintegration of the cell

87
Q

These are DEPRESSED, RETRACTED, YELLOWISH-BROWN PATCHES on the crests of gyri.

These represent old traumatic lesions that can be EPILEPTIC FOCI

Microscopically, one can see:

a. gliosis
b. residual hemosiderin-laden macrophages

A

plaque jaune

88
Q

Plaque jaune are usually seen in

A

contrecoup injuries of the:

a. inferior frontal cortex
b. temporal pole
c. occipital pole

89
Q

This refers to injury that affects deep white matter regions

A

diffuse axonal injury

DEEP = diffuse

90
Q

Common sites of deep white matter regions affected by diffuse axonal injury

A

a. corpus callosum
b. paraventricular zones
c. supratentorial hippocampus
d. cerebral peduncles
e. brachium conjunctivum
f. superior colliculi
g. deep reticula formation of the brainstem

91
Q

Microscopical findings of diffuse axonal injury

A

a. axonal swelling (indicative)

b. focal hemorrhagic lesions

92
Q

50% of individuals who develop coma after trauma even without cerebral contusions are believed to have

A

diffuse axonal injury

93
Q

Pathogenesis of diffuse axonal injury

A

a. direct action of mechanical forces with subsequent alterations in axoplasmic flow causing axonal injury
b. usually due to ANGULAR ACCELERATION ALONE (even in the absence of infarct)

94
Q

Morphology of diffuse axonal injury

A

a. WIDESPREAD, OFTEN ASYMMETRIC AXONAL SWELLING that appear hours after injury and may persist much longer
b. LATER: increase in microglia in damaged areas in the cerebral cortex, and subsequent degeneration of involved fiber tracts

95
Q

Axonal swelling is best demonstrated by

A

a. silver impregnation techniques

b. immunoperoxidase staining for AXONALLY-TRANSPORTED PROTEINS (amyloid precursor protein and a-synclein)

96
Q

Traumatic vascular injury may occur in different anatomic sites. These may be:

A

epidural
subdural
subarachnoid
intraparenchymal

97
Q

These hematomas are usually due to trauma

A

epidural

subdural

98
Q

In settings of:
coagulopathy
significant cerebral atrophy (stretched vessels)
infants (thin-walled vessels)

what hematoma is the most common presentation

A

subdural hematoma

99
Q

A traumatic tear of the carotid artery where it traverses the carotid sinus may lead to the formation of:

A

AV fistula

100
Q

trauma-related epidural hematoma

A
  • associated with skull fracture in the adult population
  • RAPIDLY, evolving neurologic symptoms
  • REQUIRES EMERGENGY
101
Q

trauma-related subdural hematoma

A
  • usually due to mild trauma
  • SLOWLY, evolving neurologic symptoms
  • often with delay of clinical presentation (after 48 hours)
  • SYMPTOMS ARE NONSPECIFIC (headache and confusion)
102
Q

trauma-related subarachnoid hematoma

A

usually due to CONTUSIONS

103
Q

Vascular abnormality-related

subarachnoid hematoma

A
  • may be due to AV malformations or aneurysms
  • SUDDEN ONSET OF SEVERE HEADACHE (thunderclap headache)
  • rapid neurologic symptom development
  • SECONDARY INJURY MAY ARISE DUE TO VASOSPAMS
104
Q

tumor-related

intraparenchymal hematoma

A
  • associated with HIGH-GRADE GLIOMAS

- associatd with METASTASES from RENAL CELL CA, CHORIOCARCINOMA, MELANOMA

105
Q

hypertension-related

intraparenchymal hematoma

A
  • presents in DEEP WHITE MATTER, THALAMUS, BRAINSTEM

- may extent into the VENTRICULAR SYSTEM

106
Q

cerebral amyloid angiopathy

intraparenchymal hematoma

A
  • LOBAR hemorrhage (limited in a lobe) involving the CEREBRAL CORTEX
  • may extend into the SUBARACHNOID SPACE
107
Q

hemorrhage conversion of an ischemic infarction

intraparenchymal hematoma

A
  • PETECHIAL hemorrhage in an area of previously ischemic brain tissue
  • follows the CORTICAL RIBBON
108
Q

trauma-related

intraparenchyma hematoma

A

involves the CRESTS OF GYRI

frontal, temporal, and orbitofrontal

109
Q

The most common ruptured vessel leading to epidural hematoma

A

middle meningeal artery

110
Q

Temporary displacement of the skull can lead to vessel laceration in the absence of skull fractures can happen in:

A

children

111
Q

Skull fracture in this portion of the head is usually related to epidural hematoma

A

temporal skull

112
Q

extravasation of blood occurs rapidly in epidural hematoma due to:

A

arterial pressure can cause separation of dura mater from the inner surface of periosteum of the skull; has a SMOOTH CONTOUR

113
Q

in reality, dura has two layers

A

a. external collagenous layer
b. inner cell layer with scant fibroblasts

these layers separate in subdural hematoma

114
Q

The most common ruptured vessel leading to subdural hematoma

A

superior sagittal sinus

venous sinuses are prone to injury because they are fixed to the dura mater

115
Q

Gross appearance of subdural hematoma

A

collection of freshly clotted blood along the brain surface WITHOUT EXTENSION INTO THE DEPTHS OF SULCI

116
Q

Progression of subdural hematoma

A

1 week - clot lysis
2 week - growth of fibroblast from dural surface into the hematoma
1 to 3 months - early development of hyaline connective tissue

Lesion can eventually retract as the granulation tissue matures until only a thin layer of reactive connective tissue remain (SUBDURAL MEMBRANE)

117
Q

chronic subdural hematoma

A
  • from multiple, recurrent episodes of bleeding
  • PRESUMABLY FROM THIN-WALLED SUBDURAL MEMBRANE
  • risk of bleeding is greatest in the first few months after the initial hemorrhage
118
Q

subdural hematoma is most common in what part of the brain

A

lateral aspect of the brain (10% bilateral)

119
Q

Treatment of epidural hematoma

A

a neurosurgical emergency requiring DRAINAGE

120
Q

Treatment of subdural hematoma

A

required DRAINAGE OF BLOOD, and REMOVAL OF ORGANIZING TISSUE

121
Q

Sequelae of traumatic brain injuries

A
  • posttraumatic hydrocephalus
  • chronic traumatic encephalopathy
  • posttraumatic epilepsy
  • risk of CNS infection
  • psychiatric illness
122
Q

Spinal cord injuries occur because

A
  • vulnerability of the spinal cord to vertebral fractures
  • associated with transient or permanent displacement of vertebral column
  • histology is similar to the other sites of the CNS
123
Q

cervical injury will result to

A

quadriplegia

124
Q

thoracic vertebrae and below

A

paraplegia

125
Q

above C4

A

respiratory compromise from paralysis of the diaphragm

126
Q

Injury to the brain as a consequence of ALTERED BLOOD FLOW

A

cerebrovascular disease REFERS to the disease

STROKE refers to the ACUTE CLINICAL SYNDROME

127
Q

Categories of CVD (based on processes involved)

A

a. ischemic

b. hemorrhage

128
Q

Process of hypoxia, ischemia, infarction in CVD

A
  • Embolism is a MORE COMMON CAUSE than thrombosis

- Can be either Global or Local

129
Q

Process of hemorrhage in stroke

A
  • results from the rupture of vessels

- include HPN and VASCULAR ABNORMALITIES

130
Q

Brain characteristics

A
  • requires CONSTANT GLUCOSE AND OXYGEN
  • 1-2% body weight
  • 15% cardiac output
  • 20% body’s oxygen consumption
  • cerebral blood flow is constant because it is maintained by AUTOREGULATION of resistance
131
Q

What is the limiting substance in the functioning of the brain?

A

oxygen since brain is an aerobic organ

132
Q

Causes of oxygen deprivation in the brain

A
  • hypoxia due to low partial pressure of oxygen
  • impairment of the carrying-capacity of the blood for oxygen
  • inhibition of oxygen use in brain tissue
  • ischemia due to hypotension or vessel obstruction or both
133
Q

Survival of brain tissue at risk depends on:

A
  • presence of collateral circulation
  • duration of ischemia
  • magnitude and rapidity of reduction in blood flow

all of which is helpful in:

  • identification of the anatomic site
  • identification of the size of lesion
  • localizing neurologic symptoms
134
Q

Basic pathologic process of neural tissue ischemia

A

ischemia -> ATP depletion -> loss of membrane potential -> poor neurotransmission

135
Q

Consequences of loss of membrane potential brough by ATP depletion

A
  • increase in cytoplasmic Ca ions leading to cellular injury

- release of GLUTAMATE which allows excess Ca influx through activation of the NMDA-GLUTAMATE receptor

136
Q

Region of transition between necrotic tissue and normal brain. This can be rescued from irreversible damage

A

penumbra

137
Q

According to animal models, the penumbra can be saved by:

A

using anti-apoptotic interventions

138
Q

What is the pathology behind GLOBAL CEREBRAL ISCHEMIA

A

Generalized reduction of cerebal perfision

139
Q

Causes of GLOBAL CEREBRL ISCHEMIA

A
  • cardiac arrest
  • shock
  • severe hypotension
  • carbon monoxide poisoning
140
Q

CNS cells sensitive to poor oxygenation

A
  • neurons (most sensitive)
  • astrocytes
  • oligodendrocytes
141
Q

Neurons most sensitive to poor oxygenation

A
  • pyramidal cells of the hippocampus (CA1 or Sommer Sector) - MOST COMMON
  • purkinje cells of the cerebellum
  • pyramidal cells of the cortex
142
Q

Characteristics of a “BRAIN DEAD” patient

A
  • evidence of irreversible cortical damage (isoelectric or flat line in EEG)
  • brainstem damage (poor cerebral perfusion, loss of reflexes, absent respiratory drive)
143
Q

Consequence of prolonged mechanical ventilator use

A

autolysis of neurons responsible for respiration -> liquefaction of brain tissue “RESPIRATOR BRAIN”

144
Q

Occur in regions of the brain or spinal cord that lie at the most distant reaches of the arterial blood supply; border zone between two arterial territories

A

border zone or water shed infarcts

145
Q

border zone with the highest risk for infarction

A

border zone between the ACA and MCA;

produces a SICKLE-SHAPED BAND OF NECROSIS over the cerebral convexity

usually seen in HYPOTENSIVE EPISODES

146
Q

Morphological process of global ischemia

A

ONSET: edematous brain

EARLY CHANGES (12-24 hours):

  • red neurons
  • neutrophil infiltration

SUBACUTE CHANGES (24 hours - 2 weeks):

  • monocytic infiltration
  • tissue necrosis
  • reactive gliosis
  • vascular proliferation

REPAIR (after 2 weeks)

  • removal of necrotic tissue
  • loss of normal CNS architecture
  • gliosis
147
Q

Morphology in global cerebral ischemia:
uneven neuronal loss and gliosis;
preservation of some layers, destruction of others

A

Pseudolaminar necrosis

148
Q

This refers to the reduction/cessation of blood flow to a LOCALIZED BRAIN AREA due to ARTERIAL OCCLUSION OR HYPOPERFUSION

A

Focal cerebral ischemia

149
Q

Major collateral flow of brain

A

Circle of Willis

supplemented by the external carotid-ophthalmic pathway

150
Q

partial and inconstant reinforcement over distal branches of the ACA, MCA and PCA

A

cortical-leptomeningeal pathway

151
Q

Little, if present, collateral pathway is seen in

A

deep penetrating arteries of the thalamus, basal ganglia and deep white matter

152
Q

Causes of focal cerebral ischemia

A

a. embolization from a distant site (most common)
b. in situ thrombosis
c. various forms of vasculitides
d. others: (hypercoaguable state, dissecting aneurysms of extracranial vessels in the neck, drug abuse - amphetamines, cocaine, heroin)

153
Q

Sites of embolism that causes focal cerebral ischemia

A

a. cardiac mural thrombi (most common)
- predisposing factors: MI, valvular disease, AFIB
b. atheromatous plaques within carotid arteries
c. paradoxical emboli (children with heart anomalies)
d. emboli associated with cardiac surgery
e. emboli from tumor, fat, and air

154
Q

most common site of embolic infarction due to its direct extension of the ICA

A

MCA (incidence is equal in 2 hemispheres)

155
Q

shower embolization

A
  • related with fat and amniotic embolism
  • generalized dysfunction with higher cortical probelms and consciousness prblems
    WITHOUT LOCALIZING SIGNS
156
Q

Thrombotic occlusions that can cause local cerebral ischemia are associated with

A

atherosclerosis and plaque rupture;

frequent association with systemic diseases such as DM and HPN

157
Q

Most common sites of in situ thrombosis

A
  • carotid bifurcation
  • origin of the MCA
  • either end of the basilar artery
158
Q

Diseases involved in inflammatory vasculitis causing local cerebral ischemia

A
  • In normal patients, syphilis and TB
  • In ICC patients, aspergillosis and CMV enecephalitis
  • polyarteritis nodosa (single/multiple infarcts)
  • primary angiitis of the CNS
    (chronic inflammation, multinucleated giant cells, destruction of vessel wall)
  • granulomatous angiitis of the CNS
    (primary angiitis + presence of granuloma; treated with steroid and immunosupression)
159
Q

Brain infarcts are subdivided into 2 categories based on the presence of hemorrhage:

A

a. nonhemorrhagic

b. hemorrhagic

160
Q

This category of brain infrarcts is the usual presentation when brain tissue begin to lose blood supply

A

nonhemorrhagic infarct

161
Q

This category of brian infarcts is seen secondary to ischemia-reperfusion injury/presence of collaterals;
PRESENTED AS PETECHIAL IN NATURE (confluent/multiple)

A

hemorrhagic infarct

162
Q

Thrombolytic therapy is CONTRAINDICATED IN:

A

hemorrhagic infarcts (may lead to extensive cerebal hematomas)

163
Q

which is more hemorrhagic in presentation: ARTERIAL OR VENOUS THROMBOSIS

A

venous thrombosis (especially in the superior sagittal sinus or other sinuses of the deep cerebral veins)

infections, carcinomas, hypercoaguable states increases the risk for venous thrombosis

164
Q

Cause/s of SPINAL CORD INFARCTION

A
  • hypoperfusion OR
  • traumatic interruption of the feeding tributaries from the aorta

RARE: occlusion of the anterior spinal artery via EMBOLISM or VASCULITIDES

165
Q

Important effects of HPN CVD

A
  • presence of lacunar infarcts
  • presence of slit hemorrhages
  • hypertensive encephalopathy
  • massive HPN intracerebral hemorrhage
166
Q

Most important primary management for HPN CVD

A

Aggressive control of HPN

167
Q

This presentation affects the DEEP PENETRATING ARTERIES AND ARTERIOLES that supply the basal ganglia and hemisphere with white matter and brainstem

A

Lacunar infarcts

168
Q

pathophysiology of lacunar infarcts

A

arterioloar sclerosis leading to occlusion -> development of cavitary lesions known as LACUNES (lakelike, <15mm) -> tissue loss w/ surrounding gliosis

169
Q

Location of lacunar infarcts

A

LENTI, DC PO (from most common to least common)

lentiform nucleus
thalamus
internal capsule
deep white matter
caudate nucleus
pons
170
Q

Presence of lacunar infarcts is associated with:

A

Widening of the perivascular spaces w/o tissue infarction (ETAT CRIBLE)

171
Q

These result from the rupture of small-caliber penetrating vessels and the development of small hemorrhages leaving a slit-like cavity surrounded by brownish discoloration

A

Slit hemorrhages

172
Q

Microscopically, the characteristics of slit hemorrhages include:

A

focal tissue destruction
pigment-laden macrophages
gliosis

173
Q

A clinicopathologic syndrome in the setting of malignant, uncontrolled HPN. It is characterized by a DIFFUSE cerebral dysfunction: headache, confusion, vomiting, sometimes leading to coa

A

HPN encephalopathy

174
Q

Primary management to reduce progression of symptoms

A

Redue the accompanying increased intracranial pressure since syndrome does not remit spontaneously

175
Q

Post-mortem, the features of HPN encephalopathy are:

A
  • edematous brain with or without herniation

- petechiae and fibrinoid necrosis in the gray and white matter

176
Q

Complication of malignant HPN that involves BILATERAL, MULTIPLE, white matter (centrum semiovale) and gray matter (basal ganglia, thalamus, cortex), resulting to:

  • dementia
  • gait abnormalities
  • pseudobulbar signs
A

Vascular dementia

177
Q

Causes of vascular dementia:

A

chronic HPN
cerebral atherosclerosis
vessel thrombosis or embolization

178
Q

A form of small vessel vascular dementia which involves LARGE AREAS OF SUBCORTICAL WHITE MATTER, which includes myelin and axonal loss

A

Binswanger disease or subcortical leukoencephalopathy

How to Master Pathology - Moey Series (3 decks)

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