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
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
3
Q
Acute neuronal injury or Red neurons are evident by 12-24 hours after introduction of what stimulus?
A
IRREVERSIBLE hypoxic/ischemic insult
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
5
Q
What reflects the earliest marker of neuronal cell death?
A
Acute neuronal injury or Red neurons
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
7
Q
Axonal reaction is best seen in what cell of the body?
A
Anterior horn cells of the spinal cord
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
9
Q
What is the earliest marker of Neurodegeneration or Subacute and Chronic Neuronal Injury?
A
Reactive gliosis
10
Q
Viral infection:
INTRANUCLEAR inclusion
A
Cowdry inclusion
from herpetic infections
11
Q
Viral infection
INTRACYTOPLASMIC inclusion
A
Negri bodies
from rabies infection
12
Q
Viral infection
BOTH INTRANUCLEAR AND INTRACYTOPLASMIC inclusion
A
Cytomegalovirus infection
13
Q
Neurodegenerative
INTRACYTOPLASMIC inclusion
A
Neurofibrillary tangles - Alzheimer disease
Lewy bodies - Parkinson disease
14
Q
Abnormal vacuolization of the perikaryon and neuronal cell processes in the neuropil
A
Creutzfeldt-Jakob Disease
15
Q
What is the most important histopathologic indicator of CNS injury, regardless of etiology?
A
Reactive gliosis
16
Q
Reactive Gliosis characteristics:
A
Both HYPERTROPHY and HYPERPLASIA of astrocytes
17
Q
Astrocyte characteristics
A
Star-shaped, multipolar, branching processes
Contain Glial Fibrillary Acidic Protein (GFAP)
Acts as metabolic buffers, and detoxifies the brain
18
Q
Gemistocyte or Reactive astrocyte
A
Bright-pink, somewhat irregular swath around an eccentric nucleus, from which numerous, stout ramifying processes are found
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)
20
Q
Thick elongated, eosinophilic, irregular structures in astrocytic processes. Contain HSPs (ab-crystallin and HSP27) and ubiquitin
A
Rosenthal fibers
21
Q
Rosenthal fibers are found in what states?
A
Long-standing gliosis
Pilocytic Astrocytoma
Alexander Disease
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)
23
Q
Round, faintly basophilic, PAS +, concentrically lamellated structure
Contain HSPs and ubiquitin
A
Corpora amylacea or Polyglucosan bodies
24
Q
In advancing age, what represent a degenerative change in astrocytes?
A
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
