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CNS :( Flashcards

1
Q

c. One of the most common changes in neurons is associated with

A

hypoxic/ischemic injury of the brain. This is characterized by loss of ribonucleoproteins and denaturation of cytoskeletal proteins, resulting in cytoplasmic eosinophilia (red neurons), observed in hematoxylin and eosin stained sections.

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2
Q

Neuron morphology

A

d. Morphology: 5-100 µm in size
• Prominent nucleolus
• Nissl substance: granular basophilic cytoplasmic material (RER)
• Radiating axons and dendrites

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3
Q

b. in response to brain injury, the astrocytes react by producing a

A

dense network of cytoplasmic processes surrounding the area of injury. This is somewhat analogous to a fibrous scar occurring elsewhere in the body, and is known as reactive gliosis.

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4
Q

Ependymal cells

A

a. cells that line the ventricles.

b. Vary from ciliated columnar to flattened cuboidal cells

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5
Q

Microglia (phagocytes, macrophages)

a. Microglia derived from

A

circulating monocytes

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6
Q

microglia:

b. serve as

A

antigen presenting cells in inflammatory conditions

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7
Q

Microglia: c. act as scavengers during

A 
tissue necrosis (cells with large, foamy cytoplasm called gitter cells)
d.	In some infections, appear as rod cells
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8
Q

a. Acute “red neurons” see

A

12-24 h after irreversible hypoxic/ischemic insult. See shrinkage of the cell body, pyknosis of the nucleus, loss of nucleolus, loss Nissl substance, red cytoplasm, break down in bloodbrain barrier with acute injuries.

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9
Q

a. Subacute and chronic “degeneration”. More

A

slowly progressive injury e.g. AML amyotrophic lateral sclerosis-often see selective cell loss and reactive gliosis.

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10
Q

a. Axonal reaction-see with

A

regeneration of axon-Nissl substance from center to periphery e.g. anterior horn cells spinal cord when motor axons seriously damaged.

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11
Q

a. Neuronal damage and subcellular changes e.g.

A

lipofuscin, viral inclusions e.g. Herpes-Cowdry body.

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12
Q

a. Intracytoplasmic inclusions-

A

Lewy bodies-Parkinson’s, neurofibrillary tangles-Alzheimer Disease.

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13
Q

a. Astrocytes and injury: Often show

A

astrogliosis (repair and/or scar formation). Increased bright pink cytoplasm, cytoplasmic swelling, formation Rosenthal fibers (thick eosinophilic protein aggregates seen in chronic gliosis)

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14
Q

a. Oligodendrocytes: Function to form

A

myelin around axons. Injury apoptosis seen in demyelinating or leukodystrophic diseases. Limited changes, may see viral inclusions “leukoencephalopathy”

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15
Q

a. Ependymal cells: Line the ventricles. No

A

injury specific response. Inflammation note disruption ependymal lining and proliferation of subependymal astrocytes “ependymal granuloma”. Certain pathogens (e.g. CMV) cause extensive ependymal injury with viral inclusions.

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16
Q

a. Microglia: Fixed macrophages in CNS are

A

CD68 and CR3 positive.

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17
Q

microglia: Can also note

A

blood borne macrophages with inflammation. Proliferation, elongated nuclei (rod cells), foci microglial nodules, neuronophagia.

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18
Q
  1. Focally expanding mass lesions-regardless of etiology-can ALL
A

increase intracranial pressure

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19
Q
  1. Cerebral Edema

a. Increased fluid content within

A

brain parenchyma (trauma, hypoxia, tumor, infection)

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20
Q

cerebral edema: b. Common form of

A

secondary brain damage, occurs in 75% of patients with brain injury
c. Major cause of elevated intracranial pressure.

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21
Q

cerebral edema: d. Clinical Classic indications of raised intracranial pressure are

A

headache, vomiting and papilledema (swelling of optic disc)

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22
Q

Cerebral edema: e. Presents as

A

swollen gyri, narrowed sulci, compressed ventricles, brain shifting

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23
Q

Cerebral edema: f. Vasogenic edema-

A

blood brain barrier disruption and increased vascular permeability-note fluid shift from vascular component to the brain.

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24
Q

Cerebral edema: g. Cytotoxic edema-

A

increased intracellular fluid secondary to neuronal glial or endothelial cell membrane injury e.g. hypoxic or metabolic damage.
h. Often note elements of both types of edema

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25
Q

b. Hydrocephalus=

A

accumulation of excessive CSF within ventricular system

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26
Q

a. Choroid plexus produces

A

CSF. In continuity with ependyma, intraventricular fibrovascular cores lined by epithelial cells.

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27
Q

Hydrocephalus: b. Causes:

A
  • Decreased CSF resorption (CSF flow obstructed by: tumor, hemorrhage or inflammation i.e. meningitis)
  • Increased CSF production (tumors of the choroid plexus; rare)
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28
Q
  1. Increased intracranial pressure and herniation.

a. Can cause

A

displacement of brain tissue from one intracranial compartment to another

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29
Q
  1. Increased intracranial pressure and herniation.

a. Most cases associated with a

A

mass effect either diffuse-generalized (brain edema) or focal (tumors, abscesses, hemorrhage).

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30
Q
  1. Increased intracranial pressure and herniation.

a. Cranial vault is divided by

A

rigid dural folds-localized expansion may cause displacement relative to partitions-if severe-note herniation syndrome.

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31
Q
  1. Increased intracranial pressure and herniation.

a. 3 main types

A

subfalcine
uncinate
tonsillar herniation

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32
Q

• Subfalcine (cingulated):

A

Unilateral or asymmetric expansion of the cerebral hemisphere displaces cingulated gyrus under falx cerebri-may compress anterior cerebral artery.

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33
Q

• Uncinate (transtentorial):

A

Medial aspect temporal lobe compressed-CN III compromised-pupils dilate and impairment ocular movements-may also compress posterior cerebral artery-affecting visual cortex-Duret Hemorrhage-midbrain bleeds.

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34
Q

• Tonsillar herniation:

A

Displacement cerebellar tonsils through foramen magnum-life threatening as the brain stem becomes compromised as the breathing and cardiac regulatory centers are located in the medulla oblongata.

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35
Q

B. CNS trauma:

. Effects of the trauma depend on the

A

site affected e.g. frontal lobe of the brain in the parenchyma-may be silent with no obvious effects while trauma at the spinal cord can be severely disabling or fatal if the brainstem is affected. 25% of accidental deaths.

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36
Q

B. CNS trauma:

2. Physical forces responsible for CNS trauma can include:

A

skull fractures, parenchymal injury, vascular injury (subdural, epidural hematoma) can co-exist.

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37
Q

B. CNS trauma:

3. Magnitude and distribution of the damage dependent on:

A

object shape, force of impact, whether or not the head is in motion.

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38
Q

B. CNS trauma:

4. May be a

A

penetrating or a blunt blow. May note open injury or closed.

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39
Q

B. CNS trauma:
5. Skull fractures-skull bone displaced into cranial cavity, greater thickness bone-displaced skull fracture. Pattern of falls affect the site- if the patient is conscious and falls off a ladder

A

-occipital generally affected, if patient is unconscious-frontal damaged site.

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40
Q

. Parenchymal Injuries-concussion.

a. Concussion: Altered consciousness brought about by sudden change in momentum of head-e.g. moving head hits a rigid surface.
b. Neurologic changes-

A

note transient neurologic dysfunction, loss of consciousness, respiratory arrest, loss of reflexes-develop amnesia for the event-neurologic recovery complete.

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41
Q

Direct parenchymal injuries:

Contusion and laceration:

A

Direct parenchymal injury (disruption and hemorrhage of superficial brain) via either kinetic energy transfer e.g. similar to bruising in soft tissue or penetration and tearing of brain parenchyma in a laceration. Increased contusions with areas of brain in contact with irregular inner skull surface e.g. frontal lobes over orbital ridges and temporal lobes.

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42
Q

Direct parenchymal injuries:

b. Coup injury:

A

Damage occurs at the point of contact.

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43
Q

Direct parenchymal injuries:

c. Contrecoup:

A

Note damage at site diametrically opposed. If head stable-coup injury, if head is mobile-may see both.

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44
Q

Direct parenchymal injuries:

d. Violent posterior or lateral hyperextension neck-may avulse

A

pons from medulla or medulla from cervical cord resulting in death.

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45
Q

Traumatic vascular injury: Frequent component of CNS trauma-dependent upon

A

vascular location. May note hemorrhage at: epidural (arterial-meningeal artery-usually skull fracture (dura peeled off skull), subdural (damage to bridging veins-dura still attached), subarachnoid, intraparenchymal compartments (or combination thereof).

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46
Q
  1. Epidural hematomadural arteries most frequently the
A

mid-meningeal artery
• Usually associated with a skull fracture
• Dura separates from blood accumulation. Rupture of a meningeal artery- arterial bleeding
• “Lucid interval”, then progressive loss of consciousness
• Neurosurgical emergency Need PROMPT DRAINAGE as this is a life-threatening condition.

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47
Q
  1. Subdural hematoma

• Brain can

A

move but venous sinuses are fixed
• Blood between dura and arachnoid membrane
•

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48
Q

Subdural hematoma: See this in the

A

elderly (chronic) with brain atrophy (bridging veins are stretched out) and infants (acute – Whiplash injury, Shaken baby syndrome) (bridging veins are thin-walled)

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49
Q

Subdural hematoma: • Usually note slowly progressive

A

neurologic dysfunction-remove blood and organizing granulation tissue.

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50
Q

Cerebrovascular Disease; 3 categories:

A

1) thrombosis (formation of blood clot)
2) embolism (blood clot now mobile in blood stream)
3) hemorrhage (rupture of blood vessel)

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51
Q

Working definition of stroke:

A

acute onset, non-epileptic, neurological deficit that lasts > 24 hours.

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52
Q

Strokes can arise from two processes:

A

hypoxia (Ischemia, Infarction) and hemorrhage.

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53
Q

Hypoxia, ischemia and infarction-

A

due to impaired blood supply and decreased oxygenation of CNS tissues.

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54
Q

Hemorrhage-rupture of CNS vessels. Most common disorders:

A

global ischemia, embolism, hypertensive, intraparenchymal hemorrhage, subarachnoid hemorrhage, vascular malformations and ruptured aneurysm.

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55
Q

d. Focal cerebral ischemia-major source of collateral blood flow is the

A

circle of Willis which is supplemented by the External Carotid.

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56
Q

Majority vascular occlusions are due to atherosclerotic plaques resulting in thrombosis or embolism and most frequently affecting the

A

middle cerebral artery (MCA). Can also involve fat or air.

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57
Q

f. Types of ischemic injury include

A

global cerebral ischemia e.g. cardiac arrest, shock, severe hypotension versus focal-cessation flow localized portion.

58
Q

During hypotension and resulting low flow-

A

neurons are the most sensitive and will be most affected.

59
Q

Glial cells (oligodendrocytes and astrocytes) are also

A

susceptible to reduced blood flow. Note selective vulnerability.

60
Q

Brain Infarction: evolution

A
  1. Grossly & histologically normal: first 12 hours
  2. 24-36 hours (acute): Red neurons and neutrophil infiltration into the brain parenchyma
  3. 3rd – 5th day (subacute): Involved tissue becomes softer in consistency. Macrophages with foamy cytoplasm begin to infiltrate
  4. 1 month: Soft, irregular, cavitated lesion, loss of brain tissue.
  5. 6 months (chronic): Smooth walled cavity
61
Q

• Intrathecal chemotherapy:

A

specific meds depending on cancer type

62
Q
  1. Hypertensive cerebrovascular disease and intraparenchymal hemorrhage.

Hypertension is the most common underlying cause of

A

primary parenchymal hemorrhage.

63
Q
  1. Hypertensive cerebrovascular disease and intraparenchymal hemorrhage.
    b. Accelerated atherosclerosis in ——- and hyaline arteriolosclerosis in ———- weakens the vessel walls.
A

larger vessels

smaller vessels

64
Q
  1. Hypertensive cerebrovascular disease and intraparenchymal hemorrhage.
    c. Subsequently note wall
A

rupture and hemorrhage, which is most common in the regions of the basal ganglia, followed by pons, thalamus and cerebellum.

65
Q
  1. Hypertensive cerebrovascular disease and intraparenchymal hemorrhage. :
    d. Can be clinically devastating if it affects
A

large portions of brain and extends into ventricular system.

66
Q
  1. Hypertensive cerebrovascular disease and intraparenchymal hemorrhage.
    Symptoms:
A

e. Severe headache, hemiparesis, hemisensory loss

67
Q
  1. Subarachnoid hemorrhage

a. Defined as

A

abrupt onset extravasation of blood in space between arachnoid and pia (arterial bifurcations of the circle of Willis) matter due to rupture of vessels in arachnoid space.

68
Q
  1. Subarachnoid hemorrhage

b. Often are

A

spontaneous, but could also be precipitated by traumatic injury.

69
Q
  1. Subarachnoid hemorrhage

c. Chief complaint of patient

A

“Worst headache of my life”.

70
Q
  1. Subarachnoid hemorrhage

d. Ruptured berry (saccular) aneurysm (of major brain arteries) is the

A

most common cause of non-traumatic hemorrhage.

71
Q
  1. Subarachnoid hemorrhage

e. Most aneurysms arise from branches of the

A

middle cerebral, internal carotid and the junction between the anterior cerebral and anterior communicating arteries.

72
Q
  1. Subarachnoid hemorrhage

f. Probably represents an

A

acquired, degenerative process, aggravated by

hypertension.

73
Q
  1. Subarachnoid hemorrhage:

g. Subarachnoid hemorrhage i.e. blood in CSF may be seen together with

A

intraparenchymal hemorrhage.

74
Q

Vascular malformations.

a. Etiology:

A

most commonly from abnormal angiogenesis in developing brain.

75
Q

Vascular malformations:

b. Types are

A

arteriovenous malformation (AVM), cavernous angioma, capillary telangiectasias and venous angioma.

76
Q

Vascular malformations:

c. AVMs

A

(Collection of abnormal blood vessels of variable caliber) are most common and most likely to result in intraparenchymal and/or subarachnoid bleeds.

77
Q
  1. Routes for microbes to reach CNS include:
A

hematogenous (most common), direct implantation (trauma) and local extension of infections (sinusitis, middle ear or dental infections, or along peripheral nervous system e.g. Herpes zoster and rabies).

78
Q
  1. Hematogenous spread is the most common route by which microbes reach the
A

brain.

79
Q
  1. Common brain infections include
A

acute bacterial meningitis, cerebral abscess and encephalitis.

80
Q
  1. Acute bacterial meningitis:

a. Infections resulting in inflammation of the

A

leptomeninges and subarachnoid space. Brain is swollen. Purulent exudate under subarachnoid space, over the cerebral hemispheres. Purulence within the ventricles

81
Q
  1. Acute bacterial meningitis:

b. Acute purulent meningitis is cased by

A

pyogenic bacteria e.g. E. coli, group B streptococci, H. influenza, Neisseria meningitidis).

82
Q
  1. Acute bacterial meningitis:

c. Chronic leptomeningitis is caused by both

A

bacterial e.g Mycobacterial tuberculosis and fungal e.g. Cryptococcus neoformans organisms.

83
Q
  1. Acute bacterial meningitis:

d. Risk factors to develop include:

A

extremes of age, poor hygiene, crowded living conditions, and debilitation.

84
Q
  1. Acute bacterial meningitis:

e. Symptoms include

A

neck stiffness, neurologic impairment, headache, photophobia.

85
Q
  1. Acute bacterial meningitis:

f. Lumbar puncture:

A

increased pressure; bacteria, PMNs, necrotic cellular debris, decreased glucose in the CSF.

86
Q
  1. Tuberculous Meningitis (chronic meningitis)
A

a. > 2-3 weeks of headache, lethargy, nausea & vomiting
b. Cranial nerve palsies, epilepsy
c. Gelatinous exudate, may appear nodular.

87
Q

Tuberculous meningitis:

d. Histology:

A

Lymphocytes, macrophages, and multinucleated giant cells form granulomas. Mycobacteria may be demonstrable by acid fast stain

88
Q
  1. Cryptococcal Meningitis (chronic meningitis)
A

a. Spherical budding yeast, found in soil and bird excrement
b. Low grade fever, debility, headache
c. Slimy exudate, capsular material
d. Both healthy and immunocompromised hosts (e.g. HIV+) can be affected

89
Q
  1. Brain abscess:

a. Usually caused by

A

bacteria which include streptococci, staphylococci and anaerobic organisms.

90
Q
  1. Brain abscess:

b. Cavity contains

A

pus, surrounded by a thick wall of granulation tissue and fibrosis

91
Q
  1. Brain abscess:

c. 50% are spread from

A

adjacent infections (dental, ear or sinus). Streptococcus milleri is most common identified organism.

92
Q
  1. Brain abscess:

d. Usually

A

solitary, may be multiple.

93
Q
  1. Brain abscess:

e. Clinical features:

A

headaches, fever, neck rigidity, increased intracranial pressure and focal neurologic deficits.

94
Q
  1. Brain abscess;

f. Extremes of age is a

A

poor prognostic factor, mortality is approximately 20%.

95
Q

Encephalitis.

a. Diffuse inflammation of the

A

brain parenchyma caused by a number of viral agents e.g. HSV most common, HIV, cytomegalovirus and also many arthropod-borne encephalitis viruses.

96
Q

Encephalitis. :

b. Clinical symptoms:

A

headache, neck stiffness, pyrexia (fever) and focal seizures.

97
Q

Encephalitis. :

c. Without treatment,

A

usually fatal.

98
Q

Encephalitis. :

d. Microscopically can note

A

perivascular lymphocytosis, microglial nodules and neuronophagia. May also note viral inclusions e.g. Cowdry A and Negri bodies.

99
Q
  1. Multiple sclerosis:
A

Autoimmune (T-cell mediated), demyelinating disease. Most common demyelinating disease of the brain.

100
Q
  1. Multiple sclerosis:

Usually presents in

A

young (reproductive aged) adults, female predilection (2:1) over males.

101
Q
  1. Multiple sclerosis:

b. Note waxing and waning

A

signs and symptoms, depending upon area of brain affected.

102
Q
  1. Multiple sclerosis:

c. Common manifestations include:

A

visual disturbances, speech and gait abnormalities, paresthesias and emotional disturbances.

103
Q
  1. Multiple sclerosis:

d. Characteristic lesion is an

A

irregular area of demyelination called a MS plaque. Plaques can arise anywhere in the brain and spinal cord, most common sites are periventricular white matter and optic nerve.

104
Q
  1. Multiple sclerosis:

e. Microscopically plaques demonstrate areas of

A

demyelination, accompanied by perivascular lymphocytosis and infiltration by foamy macrophages.

105
Q
  1. Alzheimer’s Disease
A

b. Mostly sporadic, about 10% family history. Etiology unknown.
c. Note brain atrophy (loss volume and weight) and dilation of the ventricular system.
d. Microscopically note Neuritic (senile) plaques (aggregates of thickened, tortuous processes with central amyloid deposits) and neurofibrillary tangles (filamentous aggregates within neuronal cytoplasm)
e. Often see cerebral amyloid angiopathy.
f. Clinical features: Memory disturbances, language deficits, loss math skills, loss learned motor skills. These losses are non-reversible.

106
Q
  1. Parkinson Disease.

a. Parkinsonism:

A

Rigidity, decreased facial expressions, stooped posture, slowness voluntary movement, pill rolling tremor, gait change.

107
Q
  1. Parkinson Disease. :

b. Cause is degeneration of the

A

dopamine secreting pigmented neurons of the substantia nigra in the midbrain. Etiology unknown.

108
Q
  1. Parkinson Disease.

c. Most cases are

A

sporadic and occur in sixth decade (patient in their 50s).

109
Q
  1. Parkinson Disease.

d. Grossly, brain may appear slightly

A

atrophic.

110
Q
  1. Parkinson Disease.

e. Diagnostic microscopic features:

A

Intracytoplasmic eosinophilic inclusion bodies known as Lewy bodies, within pigmented neurons of the substantia nigra and locus ceruleus.

111
Q
  1. Parkinson Disease.

f. Parkinson disease-

A

pallor of substantia nigra, loss of the pigmented catecholinergic neurons, compromised filaments densely packed at core.

112
Q
  1. Parkinson Disease.

g. Also note impairment cognitive functions-

A

may note dementia. L-DOPA responsiveness decreases over time.

113
Q
  1. Huntington’s disease

a. Hereditary, progressive disorder characterized by

A

spontaneous involuntary movements called chorea and also dementia.

114
Q

Huntingtons

c. Etiology:

A

mutations in the huntingtin gene located on the short arm of chromosome 4

115
Q

Huntingtons:

d. Note atrophy of the

A

basal ganglia (e.g. caudate nucleus, putamen and in advanced cases, the globus pallidus)

116
Q

Huntingtons:

e. Microscopically note

A

severe neuronal loss in the basal ganglia, accompanied by fibrillary gliosis.

117
Q

F. Neoplasms within the Central Nervous System.

Primary:

A
  • Arise from cells of the brain, spinal cord or their coverings
  • Symptoms more reflective of site of origin than tumor type [e.g., increased intracranial pressure (headache), focal deficits, seizure, hydrocephalus etc.]
  • Location is more important than tumor type
  • Even most malignant gliomas rarely metastasize outside the CNS.
118
Q

F. Neoplasms within the Central Nervous System.

• Increased intracranial pressure is often a complication of a

A

large tumor.

119
Q

F. Neoplasms within the Central Nervous System.

• Tumors can also hemorrhage which accentuates the

A

mass effect, and subsequently blow the flow or reabsorption of CSF, resulting in hydrocephalus.

120
Q

F. Neoplasms within the Central Nervous System.

• Brain tumors have varying

A

pathology, but due to their critical location, even histologically benign brain tumors can kill the patient.

121
Q

F. Neoplasms within the Central Nervous System.

• Generally-tumors of CNS account for

A

20% of pediatric cancers. 70% of pediatric cancers arise in the posterior fossa. 70% of adult CNS cancers arise in cerebral hemisphere above tentorium.
• Pediatric brain tumors: Pilocytic Astrocytoma (Grade I tumor). Usually in the cerebellum, often cystic. Astrocytes with thin, hair like processes (Rosenthal fibers)

122
Q

F. Neoplasms within the Central Nervous System.• Subarachnoid space provides an area for

A

intracranial spread.

123
Q

• WHO classification-segregates tumors into

A

Grades I to IV. Lesions of different grade are given a different name. Grade I (least aggressive) to Grade IV (most aggressive).

124
Q
  1. Gliomas

a. Astrocytomas (infiltrating) comprise

A

80% of adult tumors. Symptoms include seizures, headaches and focal neurologic deficits.

125
Q

Gilomas:

b. In adults, mostly affects the

A

cerebral hemisphere

126
Q

Gilomas:

c. Pilocytic astrocytoma (Grade I) →

A

Astrocytoma (Grade II) → Anaplastic astrocytoma (Highly cellular with mitotic figures, Grade III) → Glioblastoma (Necrosis and microvascular proliferation, Grade IV). Glioblastoma → note endothelial cell proliferation.

127
Q

Gilomas:

d. Clinical features-

A

may remain “silent” until increase in growth. Treatment consists of surgical resection, then radiation and chemotherapy. ~ 15 month survival.

128
Q

Gilomas:

e. Pilocytic astrocytoma:

A

Less aggressive, often in pediatric patients, usually located in the cerebellum.

129
Q
  1. Oligodendroglioma.
A

. Patients often have several years of neurologic symptoms including seizures.

b. Mostly cerebral hemisphere.
c. Well circumscribed, often calcified. Cells with uniform, round nuclei and perinuclear halo (fried egg look)
d. Generally better prognosis than astrocytoma.

130
Q
  1. Ependymoma.

a. Arise most often next to

A

ependymoma-lined ventricles-including obliterated central canal of the spinal cord.

131
Q

Ependymoma:

b. Typically occurs near the

A

4th ventricle.

132
Q

Ependymoma:

c. May manifest with

A

hydrocephalus secondary to obstruction of the ventricle. May also have CSF dissemination.

133
Q

Ependymoma;

d. Well-circumscribed lesions, arising from

A

ventricular wall. Elongated cells with processes radiating around blood vessels (perivascular pseudorosettes)
e. Generally low-grade lesions (Usually Grade II).

134
Q
  1. Meningioma.

a. Derived from the

A

arachnoid matter

b. Female predominance
c. Firm, lobulated lesions with a pushing border into underlying brain

135
Q

Meningioma:

d. Microscopically:

A

cellular whorls and psammoma bodies are common

136
Q
  1. Medulloblastoma.

a. Primarily seen in

A

pediatric patients in cerebellum (by definition).

137
Q

Medulloblastoma:

b. Rapid growth with cells disseminating through CSF. May block

A

CSF flow-note hydrocephalus.

138
Q

Medulloblastoma:

c. Cells form

A

Homer-Wright rosettes

139
Q

Medulloblastoma:

d. Very aggressive (Grade IV tumor) but

A

radiosensitive. Surgical excision and radiation. Five year survival as high as 75%.

140
Q
  1. Mets to brain.

a. Most common sites for primary tumors:

A

lung, breast, skin (melanoma), kidney, GI tract (comprise approximately 80% of all mets).

141
Q

b. Mets to brain may be initial presentation of

A

the occult primary cancer.

c. Quality of life benefit to localized treatment for solitary brain metastatic lesions.

142
Q

d. Metastases to the brain are

A

far more common than metastases from the brain

Gen Path Final (18 decks)

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