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Systems Path 1 > Central Nervous System > Flashcards

Central Nervous System Flashcards

1
Q

What are some characteristics of reversible injury in the CNS?

A

Decreased axonal trasnport (“spheroids” - swollen cells), swelling of soma, displacement of the Nissl substance (central chromatolysis) - possible axonal sprouting.

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2
Q

What is acute neuronal injury?

A

Irreversible injury

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3
Q

What is the cause of irreversible injury?

A

Result of an acute-hypoxic injury

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4
Q

What are some features of irreversible injury?

A

12-24 hours: soma shrinks, pyknosis, eosinophilia. - “red neurons” - (“red is dead”).

Cerebral edema, loss of Nissl body and nucleolus.

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5
Q

What role to astrocytes (astroglia) play in recovery from injury to the CNS?

A

Involved in the process of “gliosis” - CNS fibrosis.

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6
Q

What are some features of gliosis?

A

Injury -> hypertrophy & hyperplasia. Enlarged nucleus, eosinophilic (stain more pink). Gemistocytic astrocytes.

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7
Q

What are gemistocytic astrocytes?

A

An activated astrocyte, sprouting of glial filaments in the hypertrophy/hyperplasia response to CNS injury.

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8
Q

What CNS cells are most involved in acquired demyelinating disorders and leukodystrophies

A

Oligodendrocytes

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9
Q

What are some characterstics of demyelinating disorders and leukodystrophies?

A

White matter damage = nuclear swelling. Enlarged nucleus. May show viral inclusions.

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10
Q

What is the role of microglia?

A

Resident phagocytes of the CNS

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11
Q

What does injury, infxn, and trauma in the CNS do to microglia?

A

Cause them to proliferate and englarge (demyelination, infarctions, hemorrhage.

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12
Q

What is neuronophagia?

A

The phagocytoses of neurons and glial cells.

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13
Q

What are ependymal cells?

A

Make up the choroid plexus (produces CSF). Line the spinal cord and ventricles.

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14
Q

What infx especially affects ependymal cells?

A

CMV: Cytomegalovirus. Causes irregularities of ventricular surface (ependymal granulations), viral inclusions (evidences of infection).

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15
Q

If animals affected with rabies, what features characteristically appears?

A

Negri bodies

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16
Q

What characteristic histological features is found with CMV?

A

Owl’s eye

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17
Q

What inclusion is associated with Parkinson’s?

A

Lewy bodies

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18
Q

What kind of inclusions are associated with Alzheimer’s?

A

Neurofibrillary tangles, and beta-amyloid plaques (tau proteins, which are associated with degenerative, especially neurodegenerative, conditions).

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19
Q

What kind of inclusion is often noted in aging, lipid accumulating cells?

A

Lipofuscin

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20
Q

What is the primary issue, space wise, in the cranial vault, with edema.

A

Limited expansion, increased ICP (blood, pus, tumor, edema)

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21
Q

What are the 2 types of edema?

A

Vasogenic

Cytotoxic

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22
Q

What are some characteristics of vasogenic (blood-brain barrier disruption) edema?

A

Increased permeability leads to extracellular edema.
Localized: Tumors, infxn, inflammation
Generalized: Severe trauma

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23
Q

What are some characteristics of cytotoxic (neuronal/glial membrane injury) edema

A

Intracellular edema

Hypoxic-ischemic injury, toxic exposure.

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24
Q

What is hydrocephalus?

A

Increased CSF volume in ventricles (from overproducing, or under-resorbing).

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25
Q

What is the MC cause of hydrocephalus?

A

Disturbed flow/resorption.

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26
Q

T/F overproduction of CSF is rare?

A

True

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27
Q

What is the condition that would be most likely to lead to the overproduction of CSF?

A

Choroid plexus tumor

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28
Q

How is non-communicating hydrocephalus different from communicating hydrocephalus?

A

Some sort of mass is blocking flow with noncommunicating hydrocephalus.

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29
Q

What is an observable feature with hydrocephalus is those under 2 years old?

A

Cranial enlargement (sutures haven’t fused yet)

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30
Q

What are some general features of hydrocephalus in those greater than 2 years old?

A

Increased ICP, ventricular enlargement

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31
Q

What causes aquired hydrocephalus?

A

Unknown incidence. 50% idiopathic.

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32
Q

What can happen if hydrocephalus goes untreated?

A

Lethal tonsilar herniation. Increased ICP. Leads to respiratory arrest.

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33
Q

What is the tx for hydrocephalus?

A

Shunting (MC): ventriculo-atrial shunt (into abdominal cavity).

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34
Q

What is hydrocephalus ex vacuo?

A

Compensatory enlargement: infarct, neurodegeneration

Not so much a problem with CSF, but neurons lost that are then replaced by CSF

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35
Q

What are some of the hallmark signs of brain herniation?

A

Intracranial volume: Increased ICP (hemorrhage, edema, tumor, pus)

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36
Q

What will be noticed INITIALLY with brain still herniation?

A

Vessel compression and CSF displacement.

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37
Q

What changes in the cerebrum eventually happen with brain herniation?

A

Cerebrum shifts (herniation) across dura or through foramen magnum.

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38
Q

What structures become compromised (and in what way) with brain cerebral herniation?

A

Compression of neurons and vessels

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39
Q

What dangerous positive feedback loop is noticed with compression of vessels and neurons in brain herniation?

A

Decreased blood supply -> infarction. Injury -> swelling.

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40
Q

What is the MC type of brain herniation?

A

Subfalcine (cingulate): Displaced cingulate gyrus, under falx cerebri.

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41
Q

What physiological consequences are noted with subfalcine brain herniation?

A

Abnormal posturing (indicative of severe CNS damage), coma.

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42
Q

What is the second type of brain herniation?

A

Transtentorial (uncinate)

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43
Q

What is transtentorial (uncinate) brain herniation?

A

Displaced temporal lobe, under anterior tentorium.

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44
Q

What cranial nerve is especially affected by transtentorial herniation, and what abnormalities are noted?

A

C.N III (occulomotor).

“Blown pupil” (mydriasis) - dilated pupil found on the ipsilateral side of injury. Abnormal vision is also noted.

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45
Q

What are some more severe abnormalities associated with transtentorial herniation?

A

Hemiparesis, brain stem compression (with duret hemorrhage)

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46
Q

What is the 3rd type of brain herniation and what are it’s hallmark qualities?

A

Tonsillar herniation: displaced cerebellar tonsils (through FM). Cardiorespiratory arrest, hydrocephalus, headache.

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47
Q

What are some noticeable physical features of decorticate rigidity

A

Brachial rigidity
Extension/internal rotation of legs
Injury between the cortex/red nuclei (midbrain)

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48
Q

What are some noticeable physical feature of decerebrate rigidity?

A

Extension of all 4 limbs
Pronation of arms, plantar flexion
Injury to brainstem: Between red nuclei and vestibular nuclei (more life threatening)

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49
Q

What is a duret hemorrage?

A

Vessels that enter the pons are disrupted by herniation “flame-shaped hemorrhage”

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50
Q

What are the levels of severity of type I and II Arnold-Chiari malformations?

A

Type 1: MC, milder

Type 2: More severe

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51
Q

What are some features of Type 1 Chiari malformations?

A

Low-lying cerebellar tonsils,

Downward extension through FM (adults).

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52
Q

What are some features of Type 2 Chiari malformations?

A

Small posterior fossa,

Downward extention through FM (infants).

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53
Q

What are some possible pathological conditions associated with Chiari malformations?

A

Compress brainstem/medulla
CSF obstruction -> hydrocephalus
Headache (tell tale symptom), cervicalgia

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54
Q

What is the tx for chiari malformations

A

Neurosergical (decompression) therapy.

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55
Q

What is the 3rd leading cause of mortality in US?

A

Cerebrovascular disease

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56
Q

What is the MC cause of CVA?

A

neurologic morbidity

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57
Q

What are the 3 mechanisms producing CVA?

A
  1. Thrombotic occlusion
  2. Embolic occlusion
  3. Vascular rupture (dissection)
58
Q

What is a TIA?

A

Transient ischemic attack “mini stroke”. Temporary neurological dysfunction (<24 hours). NO infarction

59
Q

What are the 4 signs of stroke (in lay terms)?

A

F.A.S.T

Face drooping, arm weakness, speech difficulty, time to call 911

60
Q

What is Bell Palsy?

A

Rapid onset of unilateral facial weakness. Expressionless, inability to close eye

61
Q

What CN is paralyzed in Bell Palsy?

A

CN VII

62
Q

What is the cause of Bell Palsy

A

Idiopathic: viral association (HSV-1). Inflammation of CN VII. Self-limited: 2-8 weeks

63
Q

What is the DDx for Bells Palsy?

A

TIA/stroke, brain tumor, skull fx.

64
Q

What ages are MC affected by Bell Palsy?

A

15-45

65
Q

What is the Tx for Bell Palsy?

A

Monitor for a few days. Facial exercises, eye drops/patch

Meds: corticosteroids, antivirals

66
Q

What are some functional similarities/differences between Bell Palsy and stroke?

A

Both show paralysis of the lower face (mouth/cheek)
Upper half of the face has dual innervation (CN VII and motor cortex in brain)

Strokes commonly produce contralateral lower facial weakness (weak smile). Preserves bilateral upper face motor functions (close eyes tightly, symmetrically wrinkle forehead)

Both will not be able to to move the rigth side of the their lower face, but bells palsy is a shut down of half of the face.

67
Q

What does ischemia/hypoxia in the brain cause?

A

Liquefactive necrosis (infarct)

68
Q

What are the two types of functional hypoxia?

A

Less O2 pressure (hypoxemia): increased altitude

Less 02 availability: CO, anemia, cyanide

69
Q

What causes ischemia?

A

Hypotension, occlusion (clot, chokehold, etc)
Transient = TIA
Permanent = stroke

70
Q

What are some features of widespread ischemic-hypoxic injury?

A 
Decreased perfusion
Cardiac arrest (M.I.), shock, severe hypotension
Mild confusion (TIA) -> severe (stroke)
71
Q

What are some features of widespread neuronal death in global cerebral ischemia?

A 
Cerebral edema, red neurons, gliosis
Neurological impairment, coma, death
Comatose: unconscious, >6 hours
Mechanical ventilation: autolysis (brain liquification)
"Respirator brain"
72
Q

How long with cerebral infarction does it take for neurtrophils to leave?

A

48 hours. Followed by macrophages. Followed by something else (see notes)

73
Q

What happens with arterial occlusion?

A

localized ischemia. If sustained, infarction develops

74
Q

What limits injury?

A 
Collateral flow (circle of Willis)
Deep tissues have minimal collateral supply.
75
Q

What are some features of emboli?

A

MC cause of arterial occlusion. Cardiac mural thrombi, valve disease. Internal carotid artery or middle cerebral artery.

76
Q

What are some features of Thrombi?

A

Atherosclerotic plaques. Carotid artery, aortic arch, middle cerebral artery.

77
Q

What are the 3 stages of cerebral infarction (stroke)

A 
Neurtrophils, red neurons, edema 12-48 hours
Nuclear framentation (karyorrhexis) 48 hours -2 weeks
Macrophages and gliosis (months-years), cavitation (remodeling).
78
Q

What does intracranial hemorrhage develop after?

A

Vessel wall injury - HTN (MC)
Structural malformations
Tumors

79
Q

What are the steps of extravasation in intracranial hemorrhage?

A

Coagulates
Compresses parenchyma
Cavitation

80
Q

What are some features of primary parenchymal brain tumors?

A

Spontaneous (non-traumatic) intraparenchymal bleed.
Rupture of small intraparenchymal vessels
Cerebral “microbleed”

81
Q

What age range are primary parenchymal brain tumros MC seen

A

Mid to late adulthood: MC age 60

82
Q

How obvious are primary parenchymal brain tumors?

A 
Clinically silent (small) -> lethal (large)
15% of death in chronic HTN patients
83
Q

What areas are MC affected by primary parenchymal brain tumors?

A

Deep structures: Thalamus, basal ganglia, pons, cerebellum, etc (dont have to know list).

84
Q

What is the order for destruction of tissue with a primary parenchymal brain tumor?

A

Bleed -> clot -> cavitation

85
Q

What are some features of subarachnoid hemorrage?

A

Bleed with the subarachnoid space. Non traumatic onset, rapid loss of consciousness.
1/3 associated with increased ICP: straining, orgasm

86
Q

What patient statement is associated specifically with subarachnoid hemorrhage?

A

“Worst headache I’ve ever had”. Comes on suddenly like a thunder clap

87
Q

What are the 4 causes of a subarachnoid hemorrhage?

A

Ruptured saccular (berry) aneurysm (MC) Tunica media defect -> aneurysm

Vessel malformation
History of head trauma
Tumor

88
Q

What are the 4 causes of a subarachnoid hemorrhage?

A

Ruptured saccular (berry) aneurysm (MC) Tunica media defect -> aneurysm

Vessel malformation
History of head trauma
Tumor

89
Q

What is arteriovenous malformation?

A

Tangle of arteries and veins (“worm like”). MC cerebrovascular malformation

90
Q

How are arteriovenous malformations connected?

A

Via 1 or more fistulas

91
Q

What are some conditions associated with arteriovenous malformations?

A

Seizure disorders
Headaches: 50% of all cases
Intracerebral or subarachnoid hemorrhages

92
Q

What group is most at risk for arteriovenous malformations?

A

Males (2x), age 10-30

93
Q

What may arteriovenous malformations progress to?

A

High output CHF (in infants).

94
Q

What does HTN do to vessels in the brain?

A

Weakens vessel walls (deep) -> rupture. Basal ganglia, cerebral white matter, brain stem.

95
Q

What are the 4 major conditions associated with Hypertensive cerebral vascular disease

A
  1. Massive parenchymal hemorrhage
  2. Lacunar stroke: Single artery occlusion (deep brain tissues: silent -> devastating).
  3. Slit hemorrhage: Ruptured small cerebral vessels, hemorrhage, “slit-like” cavity remains
  4. Acute hypertensive encephalopathy: Global cerebral dysfunction (diastolic BP >130 Increased ICP)
96
Q

What are the 2 primary types of vasculitis?

A

Polyarteritis nodosa: Systemic, autoimmune vasculitis, fibrinoid necrosis of small arteries.

Primary angiitis of the CNS: Chronic inflammation of parenchymal and subarachnoid vessels

97
Q

What are some features of primary angiitis of the CNS? And what is the tx?

A

Idiopathic
Ischemia, occlusion, aneurysm, hemorrhage (diffuse encephalopathy, decreased congnition)

Tx: Immunosupressive meds

98
Q

Who is most at risk for morbity and mortality from CNS trauma?

A

Males 2x. MVAs, violence, falls

99
Q

What areas of the brain are associated with silent, fatal, and disabling CNS trauma?

A

Silent: frontal
Disabling: cord
Fatal: brainstem

100
Q

What is the vital first step in dealing with CNS trauma?

A

History

101
Q

What should be assessed in CNS trauma?

A

Airways, breathing, circulation, and disability (ABCD)

102
Q

What are the 3 types of traumatic parenchymal injury?

A

Contusion
Laceration
Diffuse axonal injury (DAI)

103
Q

What is a contusion?

A

Tissue displacement, vessel disruption, hemorrhage, tissue injury, edema.

104
Q

What is a contusion at impact site called?

A

Coup

105
Q

What is a contusion contralateral to injury site called?

A

Contracoup

106
Q

What part of the brain is most susceptible to contusion?

A

Gyri (frontal, orbital, temporal lobes).

107
Q

What is a laceration?

A

Tearing of cerebral parenchyma, vascular disruption, hemorrhage. Bullet, knife, fracture fragment, nail, etc.

108
Q

What is a diffuse axonal injury?

A

Movement of 1 region relative to another. Commonly from angular acceleration. Diffuse white matter/axonal damage. Widespread cerebral axon damage (generalized axonal swelling - severe edema).

109
Q

What areas are MC affected by DAI?

A

MC lateral ventricles and brain stem

110
Q

Does DAI ever involve coma?

A

50% of all past-traumatic comas

111
Q

What is a contusion?

A

Trauma to cerebrum injures neurons and disrupts vessles -> hemorrhage (brain bruise).

Wedge shaped injury.

112
Q

What is a contusion contralateral to injury site called?

A

Contrecoup

113
Q

What part of the brain is most susceptible to contusion?

A

Gyri (frontal, temporal lobes).

114
Q

What is a laceration?

A

Tearing of cerebral parenchyma, vascular disruption -> hemorrhage. Bullet, knife, fracture fragment, nail, railroad spike (Phinehas Gage) etc.

115
Q

What is a diffuse axonal injury?

A

Movement of 1 region relative to anothe. Commonly from angular acceleration (torsion of brain inside skull). May not involve physical impact.

Diffuse white matter/axonal damage. Widespread cerebral axon damage (generalized axonal swelling - severe edema).

116
Q

Does DAI ever involve coma?

A

50% of all past-traumatic comas

117
Q

What is concussion?

A

Reversible altered consciousness from head injury in teh absence of contusion.

Neurological dysfunction, secondary to trauma.

118
Q

What are some symptoms of concussion (post concussion syndrome)?

A

Decreased cognition, amnesia, LOC, nausea, depression, anxiety, irritability, HA, dizziness, photophobia.

119
Q

What is a transient concussion?

A

Complete neurologic recovery. 80% recover within 7-10 days without tx.

120
Q

T/F

Standard neuroimaging is abnormal

A

False

it’s normal. CT may be used to rule out hemorrhage

121
Q

T/F

There are no imaging studies that confirma concussion Dx

A

True

122
Q

What are the assessments for concussion?

A

Cognitive assessment: attention/memory

Neurological assessment. Serial monitoring (every 5 min).

123
Q

What are risks with concussion?

A

History of concussion, females, contact sports, equestrian sports.

Upper limb contact with head

124
Q

What is the Dx for concussion?

A

Dx of concussion excludes from return to play

125
Q

What is second-impact syndrome?

A

Second concussion, lethal.

126
Q

What is second-impact syndrome?

A

Second concussion, lethal.

127
Q

What is traumatic vascular injury?

A

Trauma that disrupts the cerebral vessels -> bleed. Confusion, HA, progressive neuro dysxn, coma

128
Q

WhWhat are epidural hematormas?

A

Dural ARTERY damage (epidural space). Compresses brain tissue, licid during bleed. Associated with Fx. Neurosurgical emergency.

129
Q

What is a subdural hematoma?

A

Rapid movements tear VEINS, subdural bleed -> compresses brain.

130
Q

What is affected specifically with a subdural hematoma in infants and geriatrics?

A

Infants: thin vessels
Geriatrics: cerebral atrophy

131
Q

What is affected specifically with a subdural hematoma in infants and geriatrics?

A

Infants: thin vessels
Geriatrics: cerebral atrophy

132
Q

What’s the difference (major) between subdural and epideral hematomas besides location?

A

Epidural: artery
Subdural: vein

133
Q

T/F

Subdural hematomas are less comman that epidural hematomas

A

True

134
Q

What artery is MC involved with epidural hematoma

A

Middle meningeal artery

135
Q

T/F

Venous bleeds are continous until stopped by medical intervention

A

False,

MC self limiting. Still an emergency

136
Q

What are neural tube defects?

A

Nueral tube fails to close. MC CNS malformation (folate deficiency, previous child).

137
Q

What is spina bifida occulta

A

Bony defect, asymptomatic (malformation of upper or lower spine).

138
Q

What is a myelomeningocele?

A

Extension of CNS through (lumbosacral) vertebral defect, LE motor and sensory. Bladder/bowel dysfxn. Infections, ulcers.

139
Q

What is anencephaly?

A

Absence of brain, rostral aspect. Common cause of stillbirth

140
Q

What is an encephalocele?

A

CNS diverticulum through cranium. Usually in occipital region.

Systems Path 1 (9 decks)

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