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Flashcards in Central Nervous System Deck (178):
1

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

Selective vulnerability of neurons

2

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

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

3

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

IRREVERSIBLE hypoxic/ischemic insult

4

Characteristics of Acute neuronal injury or Red neurons

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

5

What reflects the earliest marker of neuronal cell death?

Acute neuronal injury or Red neurons

6

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

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

7

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

Anterior horn cells of the spinal cord

8

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

1) Cell loss (usually via apoptosis)
2) Reactive gliosis

9

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

Reactive gliosis

10

Viral infection:
INTRANUCLEAR inclusion

Cowdry inclusion
(from herpetic infections)

11

Viral infection
INTRACYTOPLASMIC inclusion

Negri bodies
(from rabies infection)

12

Viral infection
BOTH INTRANUCLEAR AND INTRACYTOPLASMIC inclusion

Cytomegalovirus infection

13

Neurodegenerative
INTRACYTOPLASMIC inclusion

Neurofibrillary tangles - Alzheimer disease
Lewy bodies - Parkinson disease

14

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

Creutzfeldt-Jakob Disease

15

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

Reactive gliosis

16

Reactive Gliosis characteristics:

Both HYPERTROPHY and HYPERPLASIA of astrocytes

17

Astrocyte characteristics

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

18

Gemistocyte or Reactive astrocyte

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

19

Alzheimer Type II Astrocyte

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)

20

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

Rosenthal fibers

21

Rosenthal fibers are found in what states?

Long-standing gliosis
Pilocytic Astrocytoma
Alexander Disease

22

Alexander disease
Characteristics

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)

23

Round, faintly basophilic, PAS +, concentrically lamellated structure

Contain HSPs and ubiquitin

Corpora amylacea or Polyglucosan bodies

24

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

Presence of corpora amylacea or polyglucosan bodies

25

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

Share the same biochemical and structural characteristics with corpora amylacea

Lafora bodies
(seen in Myoclonic epilepsy)

26

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

CR3
CD68

27

Microglial response to injury:

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)

28

Feature of acquired demyelinating disorders and leukodystrophies

Injury/apoptosis of oligodendrocytes

29

INTRANUCLEAR VIRAL INCLUSIONS in OLIGODENDROCYTES

JC Virus
(cause of progressive multifocal leukoencephalopathy or PML)

30

a-syncelin glial cytoplasmic inclusions in OLIGODENDROCYTES

Multiple system atrophy (MSA)

31

Disruption of ependymal lining with proliferation of subependymal astrocytes

Seen in inflammation/marked dilation of ventricles

Ependymal granulations

32

May produce extensive EPENDYMAL injury via viral inclusions

CMV

33

Responses not significant to most forms of CNS injury

Ependymal and Oligodendrocytic injury

34

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

Cerebal edema or Brain parenchymal edema

35

What are the two types of cerebral edema?

Vasogenic edema
Cytotoxic edema

36

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

Vasogenic edema

37

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

Cytotoxic edema

38

What further impairs the resorption of excess CSF?

Paucity of lymphatic system in the CNS

39

Causes of localized edema

Adjacent neoplasia or inflammation

40

Causes of generalized edema

Ischemic injury

41

Gross characterisitcs of generalized edema

Gyri are flattened
Sulci are narrowed
Ventricular cavities are compressed

42

Generalized edema have both:

Vasogenic and Cytotoxic edema

43

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

Cytotoxic edema

44

Interstitial edema or hydrocephalic edema happens usually in what ventricle?

Lateral ventricles

45

Defined as the accumulation of excessive CSF within the ventricular system

Hydrocephalus

46

Production of CSF occurs in the:

Choroid plexus

47

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

Foramina of Magendie and Luschka

48

Involved in the absorption of CSF in the subarachnoid space

Arachnoid granulations

49

Causes of hydrocephalus

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

50

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

Enlargement of the head manifested by an INCREASE IN HEAD CIRCUMFERENCE

51

Types of hydrocephalus

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

52

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

Noncommunicating or Obstructive hydrocephalus

53

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

The entire ventricular system is enlarged

Communicating or Nonobstructive hydrocephalus

54

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

Hydrocephalus ex vacuo

55

Noncommunicating hydrocephalus is usually due to:

Mass in the third ventricle

56

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

Herniation

57

Herniation is mostly associated with

Mass effect

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

58

Displaces the cingulate gyrus under the falx cerebri

subfalcine or cingulate herniation

59

Consequence of subfalcine or cingulate herniation

1) Compression of the anterior cerebral artery

60

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

transtentorial
uncinate
medial temporal herniation

61

Consequences of transtentorial herniation

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)

62

Displacement of the cerebellar tonsils through the foramen magnum

tonsillar herniation

63

Consequence of tonsillar herniation

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

64

Physical forces associated with head injury may result in:

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

65

Characteristic of a DISPLACED SKULL FRACTURE

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

66

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

Frontal portion of the skull

67

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

Occipital portion of the skull

68

Correlates for a SUSPECTED BASAL SKULL FRACTURE

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)

69

Characteristic of a DIASTATIC FRACTURE

This occurs when FRACTURES CROSSES SUTURES

70

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

Concussion

71

Clinical correlates of CONCUSSION

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

Amnesia may persist even if recovery is complete

72

What is the pathogenesis of concussion

It is UNKNOWN.

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

73

Repetitive injuries causing concussion may lead to

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

Presentation of direct parenchymal injury can either be:

a. contusion (analogous to a bruise)
b. laceration (tearing of tissue)

75

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

Subarachnoid space (as sequelae to contusion)

76

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

Crests of gyri
(frontal lobe, temporal lobe, orbital ridge)

77

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

Occipital lobe, brainstem and cerebellum
(unless fractures overlying these areas are present)

78

Contusion at the point of contact is called

coup injury

79

Contusion at the diametrically opposite point of contact

contrecoup injury

80

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

via identification of point of impact

coup and contrecoup injury are microscopically and macroscopically the same

81

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

coup injury only

82

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

both coup and contrecoup injury

83

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

instant death

84

General morphology of contusions

a. wedge-shaped
b. similar regardless of traumatic source

85

Progression of contusions

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

Morphologic evidence of neuronal injury in contusions

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

87

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

plaque jaune

88

Plaque jaune are usually seen in

contrecoup injuries of the:
a. inferior frontal cortex
b. temporal pole
c. occipital pole

89

This refers to injury that affects deep white matter regions

diffuse axonal injury

DEEP = diffuse

90

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

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

Microscopical findings of diffuse axonal injury

a. axonal swelling (indicative)
b. focal hemorrhagic lesions

92

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

diffuse axonal injury

93

Pathogenesis of diffuse axonal injury

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

Morphology of diffuse axonal injury

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

Axonal swelling is best demonstrated by

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

96

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

epidural
subdural
subarachnoid
intraparenchymal

97

These hematomas are usually due to trauma

epidural
subdural

98

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

what hematoma is the most common presentation

subdural hematoma

99

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

AV fistula

100

trauma-related epidural hematoma

- associated with skull fracture in the adult population
- RAPIDLY, evolving neurologic symptoms
- REQUIRES EMERGENGY

101

trauma-related subdural hematoma

- 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

trauma-related subarachnoid hematoma

usually due to CONTUSIONS

103

Vascular abnormality-related
subarachnoid hematoma

- 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

tumor-related
intraparenchymal hematoma

- associated with HIGH-GRADE GLIOMAS
- associatd with METASTASES from RENAL CELL CA, CHORIOCARCINOMA, MELANOMA

105

hypertension-related
intraparenchymal hematoma

- presents in DEEP WHITE MATTER, THALAMUS, BRAINSTEM
- may extent into the VENTRICULAR SYSTEM

106

cerebral amyloid angiopathy
(intraparenchymal hematoma)

- LOBAR hemorrhage (limited in a lobe) involving the CEREBRAL CORTEX
- may extend into the SUBARACHNOID SPACE

107

hemorrhage conversion of an ischemic infarction
(intraparenchymal hematoma)

- PETECHIAL hemorrhage in an area of previously ischemic brain tissue
- follows the CORTICAL RIBBON

108

trauma-related
intraparenchyma hematoma

involves the CRESTS OF GYRI
(frontal, temporal, and orbitofrontal)

109

The most common ruptured vessel leading to epidural hematoma

middle meningeal artery

110

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

children

111

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

temporal skull

112

extravasation of blood occurs rapidly in epidural hematoma due to:

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

113

in reality, dura has two layers

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

these layers separate in subdural hematoma

114

The most common ruptured vessel leading to subdural hematoma

superior sagittal sinus
(venous sinuses are prone to injury because they are fixed to the dura mater)

115

Gross appearance of subdural hematoma

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

116

Progression of subdural hematoma

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

chronic subdural hematoma

- 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

subdural hematoma is most common in what part of the brain

lateral aspect of the brain (10% bilateral)

119

Treatment of epidural hematoma

a neurosurgical emergency requiring DRAINAGE

120

Treatment of subdural hematoma

required DRAINAGE OF BLOOD, and REMOVAL OF ORGANIZING TISSUE

121

Sequelae of traumatic brain injuries

- posttraumatic hydrocephalus
- chronic traumatic encephalopathy
- posttraumatic epilepsy
- risk of CNS infection
- psychiatric illness

122

Spinal cord injuries occur because

- 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

cervical injury will result to

quadriplegia

124

thoracic vertebrae and below

paraplegia

125

above C4

respiratory compromise from paralysis of the diaphragm

126

Injury to the brain as a consequence of ALTERED BLOOD FLOW

cerebrovascular disease REFERS to the disease

STROKE refers to the ACUTE CLINICAL SYNDROME

127

Categories of CVD (based on processes involved)

a. ischemic
b. hemorrhage

128

Process of hypoxia, ischemia, infarction in CVD

- Embolism is a MORE COMMON CAUSE than thrombosis
- Can be either Global or Local

129

Process of hemorrhage in stroke

- results from the rupture of vessels
- include HPN and VASCULAR ABNORMALITIES

130

Brain characteristics

- 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

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

oxygen since brain is an aerobic organ

132

Causes of oxygen deprivation in the brain

- 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

Survival of brain tissue at risk depends on:

- 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

Basic pathologic process of neural tissue ischemia

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

135

Consequences of loss of membrane potential brough by ATP depletion

- 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

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

penumbra

137

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

using anti-apoptotic interventions

138

What is the pathology behind GLOBAL CEREBRAL ISCHEMIA

Generalized reduction of cerebal perfision

139

Causes of GLOBAL CEREBRL ISCHEMIA

- cardiac arrest
- shock
- severe hypotension
- carbon monoxide poisoning

140

CNS cells sensitive to poor oxygenation

- neurons (most sensitive)
- astrocytes
- oligodendrocytes

141

Neurons most sensitive to poor oxygenation

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

142

Characteristics of a "BRAIN DEAD" patient

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

143

Consequence of prolonged mechanical ventilator use

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

144

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

border zone or water shed infarcts

145

border zone with the highest risk for infarction

border zone between the ACA and MCA;

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

usually seen in HYPOTENSIVE EPISODES

146

Morphological process of global ischemia

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

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

Pseudolaminar necrosis

148

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

Focal cerebral ischemia

149

Major collateral flow of brain

Circle of Willis
(supplemented by the external carotid-ophthalmic pathway)

150

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

cortical-leptomeningeal pathway

151

Little, if present, collateral pathway is seen in

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

152

Causes of focal cerebral ischemia

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

Sites of embolism that causes focal cerebral ischemia

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

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

MCA (incidence is equal in 2 hemispheres)

155

shower embolization

- related with fat and amniotic embolism
- generalized dysfunction with higher cortical probelms and consciousness prblems
WITHOUT LOCALIZING SIGNS

156

Thrombotic occlusions that can cause local cerebral ischemia are associated with

atherosclerosis and plaque rupture;

frequent association with systemic diseases such as DM and HPN

157

Most common sites of in situ thrombosis

- carotid bifurcation
- origin of the MCA
- either end of the basilar artery

158

Diseases involved in inflammatory vasculitis causing local cerebral ischemia

- 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

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

a. nonhemorrhagic
b. hemorrhagic

160

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

nonhemorrhagic infarct

161

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

hemorrhagic infarct

162

Thrombolytic therapy is CONTRAINDICATED IN:

hemorrhagic infarcts (may lead to extensive cerebal hematomas)

163

which is more hemorrhagic in presentation: ARTERIAL OR VENOUS THROMBOSIS

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

Cause/s of SPINAL CORD INFARCTION

- hypoperfusion OR
- traumatic interruption of the feeding tributaries from the aorta

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

165

Important effects of HPN CVD

- presence of lacunar infarcts
- presence of slit hemorrhages
- hypertensive encephalopathy
- massive HPN intracerebral hemorrhage

166

Most important primary management for HPN CVD

Aggressive control of HPN

167

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

Lacunar infarcts

168

pathophysiology of lacunar infarcts

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

169

Location of lacunar infarcts

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

lentiform nucleus
thalamus
internal capsule
deep white matter
caudate nucleus
pons

170

Presence of lacunar infarcts is associated with:

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

171

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

Slit hemorrhages

172

Microscopically, the characteristics of slit hemorrhages include:

focal tissue destruction
pigment-laden macrophages
gliosis

173

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

HPN encephalopathy

174

Primary management to reduce progression of symptoms

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

175

Post-mortem, the features of HPN encephalopathy are:

- edematous brain with or without herniation
- petechiae and fibrinoid necrosis in the gray and white matter

176

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

Vascular dementia

177

Causes of vascular dementia:

chronic HPN
cerebral atherosclerosis
vessel thrombosis or embolization

178

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

Binswanger disease or subcortical leukoencephalopathy