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Exam 5 (no drugs) Flashcards

1
Q

Describe the key differences b/w necrosis and apoptosis.

  • cause
  • mechanism
  • effector molecules
A 
1. Cause
APOPTOSIS
-DNA damage
-inflammation
-neurodegeneration

NECROSIS
-acute, severe, injury (energy failure, trauma)

  1. Mechanism
    APOPTOSIS
    -Mediators activate caspases

NECROSIS

  • glutamate induced excitotoxicity
  • accumulation of intracellular calcium
  • oxidative stress
  1. Effector molecules
    APOPTOSIS
    -caspases

NECROSIS
-calcium activated phospholipases, proteases and endonucleases

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2
Q

Characteristics of cytotoxic edema

there are 6

A

• Minutes to hours
• Swelling of cellular elements
• Ion pumps fail
• Rapid accumulation of sodium within cells
• Water follows the sodium to maintain osmotic
equilibrium
• Leads to glutamate excitotoxicity

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3
Q

Characteristics of vasogenic edema (3)

A
  • Hours to days
  • Increase in extracellular fluid volume resulting from increased permeability of brain endothelial cells to macromolecular serum proteins
  • Brain herniation
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4
Q

Most dangerous period for cerebral infarct and why?

A

3-4 days -> maximal edema

-risk for herniation

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5
Q

Describe mechanism of glutamate excitotoxicity

A
  • reuptake pumps responsible for removing glutamate from synaptic cleft
  • ischemia/hypoxia depletes ATP which shuts off reuptake pump
  • Glutamate can’t be removed from NMDA receptor which leads to non-stop influx of calcium
  • calcium activates the proteases that ultimate cause the cell death
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6
Q

Central core vs penumbra in cerebral infarct

A

CENTRAL CORE

  • total ischemia and tissue necrosis
  • irreversible

PENUMBRA

  • zone of borderline ischemic tissue
  • receives collateral circulation
  • damage is reversible if blood flow is restored w/in 3-4 hours
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7
Q

Describe central chromatolysis

A

regenerative response to axonal injury

  • cell swells
  • dispersion of Nissl substance - RNA
  • nuclear displacement
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8
Q

Neuronophagia

  • what is it?
  • often seen with?
A
  • phagocytosis of damaged neurons by microglia and monocytes
  • associated w/ rapid cell death: most often seen w/ viral infections
  • microglia surround tissue to form nodule
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9
Q

Neurofibrillary tangles seen in?

A

Alzheimer’s and old age

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10
Q

Granulovacular bodies

  • what/where are they?
  • seen in?
A
  • autophagic lysosomal vesicles - cytoskeletal components being degraded
  • mainly in hippocampus
  • seen in AD but not pathognomonic
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11
Q

Lewy body

  • describe
  • location
  • disease association
A
  • inclusion w/ eosinophilic laminated core and halo
  • substantia nigra, locus coeruleus
  • Seen in parkinson’s and lewy body dementia
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12
Q

Hirano bodies

  • describe
  • associated with?
A
  • dense hyaline mass
  • eosinophilic
  • alzheimer’s
  • Creutzfeldt-Jacob
  • fx of age w/out obvious underlying neurodegeneration
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13
Q

Negri bodies are pathognomonic for?
what is the stain against?
where are the found?

A

Rabies
stains ribonuclear viral proteins
purkinje cells, CA-1 hippocampus

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14
Q

Psammoma bodies pathognomonic for?

A

Meningioma

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15
Q

Verocay bodies pathognomonic for?

what do they look like?

A

Schwannoma

palisading nuclei - lined up around clear areas

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16
Q

What’s left behind after Wallerian degeneration is complete?

A

Endoneurial tube - plays part in repair

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17
Q

Dying back (distal axonopathy) is seen with what conditions?

Histo findings?

A
  • most common type of pathologic rxn in generalized polyneuropathies
  • often attributed to a metabolic etiology (DIABETES)

HISTO

  • myelin fragments
  • ellipsoids
  • axonal fragments
  • macrophages w/ phagocytosed lipid
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18
Q

Diffuse axonal injury/axonal spheroids

  • cause
  • contents of the spheroids
A
  • disruption of cytoskeleton
  • stretching/tearing of axon -> battered baby syndrome

-spheroids contain accumulation of organelles being brought down by cell body

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19
Q

What causes withdrawal of presynaptic neuron terminals?

A

Blocking NGF from being delivered to the postsynaptic neuron

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20
Q

Axonal regeneration can occur after transection of axon only if?

A

Integrity of endoneurial tube is maintained

IN THE PNS

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21
Q

Neuropraxia

  • cause
  • can recovery occur
A
  • Block in conduction
  • Recovery takes place without Wallerian degeneration
  • Biochemical lesion caused by a concussion or shock-like injury to the nerve fiber

Common examples
• Peroneal paralysis from prolonged cross-legged position
•Radial or Saturday night paralysis caused by compression of the axilla

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22
Q

Axonotmesis

  • cause
  • can recovery occur
A
  • Involves loss of the relative continuity of the axon and its covering of myelin
  • Preservation of the connective framework of the nerve – endoneurial tube
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23
Q

Neurotmesis

  • cause
  • can recovery occur
A
  • This results from more severe contusion, stretch, or laceration and not only axons, but the investing connective tissues lose their continuity
  • Both the endoneurial and perineurial connective tissue layers and the axon are disrupted
  • Regenerating axons reach the distal stump but fail to find their preinjury pathwyas
  • No functional regeneration
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24
Q

Gliosis (astrocytosis)

  • response to?
  • what happens?
  • prevents?
  • what produced?
  • over time
  • seen in?
A
  • response to injury
  • gliotic tissue formation -> walling off of damaged area
  • prevents regeneration in CNS b/c axons can’t get through
  • GFAB to form the wall
  • scar formation due to astrocytic cytoplasm (NOT FIBROBLAST)

seen in

  • seizures
  • infarcts
  • chronic degeneration
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25
Q

Gliomesodermal rxn

  • occurs when?
  • appearance on T-1 MR w/ contrast? how does it differ with glioblastoma multiforme?
A
  • occurs when CNS injury involved tissue NECROSIS
  • subacute and chronic abscesses

Imaging

  • well-defined ring enhancing lesion
  • GBM ring lesion will be very irregular
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26
Q

Resident macrophages of CNS?

A

microglia

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27
Q

Ependymal cells

  • line the?
  • what happens when they get destroyed? see with?
A

-line the ventricular system

When destroyed -> ependymal granulations

  • astrocytes form small nodule underneath area that was destroyed
  • seen with chronic hydrocephalus
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28
Q

Components of anesthesia

A
  • Unconsciousness
  • Amnesia
  • Analgesia
  • Inhibition of autonomic reflexes
  • Skeletal muscle relaxation
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29
Q

Stages of anesthesia

A
  1. Premedication
    - reduce pain
    - reduce dose of subsequent anesthetics
  2. Induction
  3. Maintenance
  4. Emergence
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30
Q

Characteristics of ideal anesthesia

-what’s balanced anesthesia?

A
  • Rapid, smooth loss of consciousness
  • Rapidly reversible
  • Wide margin of safety

balanced anesthesia -> specific drug for each goal limiting the side effects of each

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31
Q

Potency of anesthetic is directly proportion to?

A

Hydrophobicity (not causational)

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32
Q

Define the MAC

  • MAC relation to potency?

- MAC value at which amnesia occurs?

A

MAC - minimum alveolar concentration

  • Alveolar partial pressure of an inhaled anesthetic that prevents movement of 1⁄2 the subjects in response to a noxious stimulus
  • The lower the MAC, the more potent the drug
  • MAC’s of individual drugs are additive
  • Amnesia occurs at 0.2 – 0.4 MAC
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33
Q

How does alveolar concentration relate to speed at which you go to sleep?

A

higher = faster

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34
Q 
Relate anesthetic uptake to variables affecting alveolar concentration. What should be done to each of the following to achieve a higher alveolar concentration?
•  Inspired concentration
•  Solubility
•  Alveolar ventilation
•  Cardiac output 
•  Alveolar–venous difference
A
  • Inspired concentration – higher = faster (overpressure)
  • Solubility – lower = faster
  • Alveolar ventilation – increased = faster
  • Cardiac output – lower = faster!
  • Alveolar–venous difference – smaller = faster
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35
Q

Define Fa/Fi

A

Ratio of alveolar concentration to inspired concentration

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36
Q 
Effect of volatile anesthetics on organ systems
•  Blood pressure 
•  Heart rate
•  SVR
•  Tidal volume
•  Respiratory rate
•  PaCO2
•  Cerebral metabolic rate 
•  Hepatic, renal blood flow
A

Everything decreases except RR, PaCO2 and HR

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37
Q

BIS value associated w/ low incidence of recall?

A

<60

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38
Q

Variables that increase the rate of elimination of inhaled anesthetics

  • solubility
  • ventilation
  • cardiac output
A

– Solubility – lower = faster
– Ventilation – greater = faster
– Cardiac output – greater = faster

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39
Q
  1. Another name for stage III astrocytoma is?

2. Another name for stage IV astrocytoma is?

A
  1. Anaplastic astrocytoma

2. Glioblastoma mulitforme

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40
Q

Histological feature that is seen in grade IV astrocytoma?

A

Vascular endothelial proliferation

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41
Q

What are some gross features seen in oligodendroglioma?

A
  • heterogeneous
  • calcifications
  • cysts
  • focal enhancement
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42
Q

Halo cells or fried eggs appearance is a histological feature of which brain neoplasm?

A

Oligodendroglioma

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43
Q

A pituitary adenoma growing in the cavernous sinus has potential for compressing which nerves?

A

III, IV, V1, V2, VI

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44
Q

Signs of parinaud’s syndrome?
Related to which tumor?
How does it cause the syndrome?

A
  1. Hydrocephalus and sunset sign
  2. Pineal tumor
  3. Hydrocephalus -> compression of cerebral aqueduct
    Sunset sign -> compression of colliculus (tectum)
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45
Q

Pediatric brain tumors

  • majority primary or 2ndary?
  • most common location?
A
  • primary

- posterior fossa (cerebellum very common)

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46
Q

True rosettes and pseudorosettes

  • description?
  • seen in which brain tumor?
  • what can this tumor cause?
  • what grade is the tumor?
A

• True rosettes
-Tumor cells surround empty lumen

• Pseudorosette

  • AKA perivascular rosettes
  • Surround blood vessels but leave some space

Seen in EPENDYMOMA
-causes non-communicating hydrocephalus

Grade II

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47
Q

CSF seeding is very common with which CNS tumor?

A

medulloblastoma

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48
Q

Medulloblastoma in adults is metastasis from?

A

Lung (seen with smokers)

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49
Q

Rosenthal fibers

  • describe
  • characteristic of which tumor
  • is it benign or malignant
  • grade?
  • age group affected?
A
  • eosinophilic, “corkscrew” shaped protein globules (which are actually intracellular accumulations)
  • pilocytic astrocytoma
  • Grade I -> Benign
  • 5 to 20
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50
Q

Which type of radiation is better for mets to the brain? primary tumors?

A

stereotactic - giving one large dose

fractionated for primary CNS tumor

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51
Q

Tx for glioblastoma?

A
  • surgery
  • radiation
  • Temozolomide - alkylating agent
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52
Q

PCV: Procarbazine/Lomustine or “CCNU”/Vincristine is used to tx?

A 
Grade III (anaplastic) astrocytoma 
-best outcome in people with 1p/19q codeletion
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53
Q

What drug is effective for primary CNS lymphoma
surgery?
radiation?

A

Methotrexate (3-7 years in remission)

surgery is not effective

radiation can be considered at recurrence

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54
Q

Tx for medulloblastoma?

A

Surgery
craniospinal radiation
chemo in children for 1 year

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55
Q

2 most common mets site to the brain

A

Lungs and breast

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56
Q

3 characteristics of local anesthetic recovery?

A

spontaneous, predictable and complete

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57
Q

Relate the following to local anesthetic sensitivity

  • fiber diameter
  • firing frequency
  • fiber position in nerve bundle
A
  • smaller diameter = more sensitive
  • firing frequency = Rapidly/repetitively firing fibers more sensitive than resting fibers
  • fiber position in nerve bundle = outer fibers more sensitive than inner
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58
Q

LA’s composed of? (4 qualities)

A

– a lipophilic group (an aromatic ring)
– an intermediate chain (an ester or amide)
– an ionizable group (a tertiary amine)
– The amine group is hydrophilic

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59
Q

Ester vs. amide local anesthetic

  • naming
  • metabolism
  • duration of action
A

Ester

  • one “i”
  • hydrolyzed by PLASMA cholinesterase
  • short duration

Amides

  • two “i’s”
  • hepatic metabolism by Cyt P450
  • variable duration of action
60
Q

Arrange rate of metabolism for the amide LA’s

A

prilocaine (fastest) > lidocaine > mepivacaine > ropivacaine > bupivacaine (slowest)

61
Q

How is percentage of LA in uncharged form related to pKa

A

inversely proportional

62
Q

Which 2 amides are packaged only in the S(+) stereoisomer? Why?

A

Ropivacaine and Levobupivacaine

-reduced cardiotoxicity

63
Q

Severe cardiotoxicity due to LA overdose can be txed by?

A

lipid rescue

64
Q

Methemoglobinemia due to LA’s

  • which drugs
  • mechanism
  • patient presentation
  • tx
A
  • prilocaine or benzocaine overdosage
  • o-toluidine -> metabolite of prilocaine oxidizes hemoglobin to methemoglobin
  • patient appears cyanotic and at 85% O2 sat regardless of PaO2
  • tx with methylene blue
65
Q

Good LA for anesthesia emergent delivery

A

Chloroprocaine

66
Q

Good LA for epidural anesthesia during labor (2 drugs)

A

bupivacaine and ropivacaine

67
Q

LA to tx neuropathic pain

A

IV lidocaine or oral mexiletine

68
Q

What can be added to intensify analgesia effect of LA’s when they are administered into the epidural/subarachnoid space? What’s the mechanism?

A

opioids and clonidine -> inhibit release of substance P and reduce neuronal firing

69
Q

Describe the progression of sxs for CNS toxicity due to LA’s

A

numbness and tingling -> lightheadedness -> visual/auditory disturbances -> muscular twitching -> unconsciousness -> convulsions -> coma -> respiratory arrest

70
Q

Why is spinal lidocaine no longer used?

A

TNS - transient neurological symptoms

-show up upon ambulation

71
Q

Which physiochemical properties are the following aspects of LA’s related to?

  1. speed of onset
  2. potency
  3. toxicity and metabolism
A
  1. speed of onset -> pKa
  2. potency -> lipid solubility
  3. Toxicity and metabolism -> degree of protein binding
72
Q

Following an ischemic stroke which subtype has the highest risk of recurrence?

Short term?
Long term?

A

Short term - Large vessel

Long term - cardioembolic

73
Q

Tx for symptomatic carotid stenosis > 70%

A

surgery

-medical management alone not adequate

74
Q

Define the CHAD2 score and it’s use

A

CHAD2 score - assess risk of stroke in patients with stroke risk

1 point for the each of the following

  • CHF
  • age >75
  • HTN
  • DM

2 points for:
-previous ischemic stroke or TIA

Total score of 1 -> border zone (may not need anticoagulants)

Total score > 2 -> tx w/ anticoagulants

75
Q

What are 4 general locations where an ICH can occur?

A
  1. Lobar
    • Gray matter
    • Subcortical white matter
2. Deep 
•  Basal ganglia
•  Periventricular white matter
•  Internal capsule
•  Thalamus
•  Pure IVH
  1. Cerebellum
  2. Brainstem
    - most in the pons
76
Q

What’s the biggest risk factor for lobar ICH in elderly people? Describe this condition with regards to:

  • path
  • imaging
  • management
A

Cerebral amyloid angiopathy - Apo E2/E4

  • path -> destruction of normal cortical vasculature
  • imaging -> microbleeds on MRI

management -> don’t give them anticoagulants and antithrombotics

77
Q

Single biggest outcome determinant after ICH

A

size of hemorrhage (larger = worse outcome)

  • 20 cc ICH, mortality < 20%
  • 120 cc ICH, mortality > 90%
78
Q

What is the goal for cerebral perfusion pressure? How do you calculate it?
Cerebral ischemia

A

CPP = MAP - ICP

Goal > 60 mmHg

Cerebral ischemia > 20 mmHg

79
Q

Which vascular malformation is most commonly associated with ICH?

80
Q

Cavernous angiomas can present with? (2 things)

How to they appear on MRI?

A

hemorrhage or seizure

popcorn like lesions

81
Q

SAH most often caused by?

mortality rate if this happens?

A
  • ruptured berry (saccular) aneurysm

- 25% mortality rate

82
Q

Most important modifiable risk factor for SAH?

What are some others?

A

SMOKING

  • Hypertension
  • Heavy alcohol use
  • Black race (in USA)
  • Female gender
83
Q

What condition is protective for SAH and ICH?

A

Hyperlipidemia

84
Q

Protocol for dxing SAH?

A

Clinical presentation
• “Worst Headache of my life!”
• “Thunderclap headache”
• Loss of consciousness, vomiting, vertigo, nausea, meningeal signs

Imaging
• CT Scan will detect 95%+ of SAH
• If strong suspicion but negative CT, check
lumbar puncture
• Xanthrochromia develops after 6-12 hours and lasts a few weeks

85
Q

Describe the relationship b/w vasospasms and SAH

  • what can it cause
  • timeframe
  • management
  • monitoring
A
  1. Ischemic stroke
  2. Days 3-16 (peak 8) following SAH
3. Management
• ‘Triple H’ – hypertension, hypervolemia
and hemodilution.
• Nimodipine: Calcium channel blocker 
• Intra-arterial verapamil
• Transluminal angioplasty
  1. Monitoring patients:
    • Transcranial doppler ultrasound
86
Q

Cardinal manifestations suggesting CNS infection

A
  • fever
  • headache
  • AMS
  • focal neurological signs

NOT SPECIFIC FOR INFECTION BUT FOR GENERAL CNS PATHOLOGY

87
Q

Post Infectious syndromes such as Guillain-Barre are presumed to work through which mechanism?

A

Immunological mediated

88
Q

Term infants and premature infants have what significant difference in their normal CSF values as compared to adults?

A

percent neutrophils (60 in infants vs. 0 in adults)

89
Q

The most common non-infectious entity that causes non-infectious meningitis is

90
Q

Vaccination against which agent of meningitis lead to dramatic reduction in cases in the 1 - 23 month age group?

A

Haemophilus influenzae

91
Q

Which meningitis agent has a bimodal distribution in the old and young?

A

Listeria monocytogenes

92
Q

In acute meningitis organisms can extend what to form a 2ndary abscess?

A

Virchow-Robin space

93
Q

Which white cells are seen in chronic meningitis? What do they surround?

A

Perivascular lymphocytes

94
Q

Bone marrow derived histiocytes that reside in the brain are known as?

Appearance on histo?

A

Microglia

spindle shaped

95
Q

Define Charcot joints. Which disease are they seen in?

A

Clinically, a loss of touch, vibration, and position sense would cause an abnormal gait and could lead to joint injuries

Tabes Dorsalis (neurosyphilis)

96
Q

Which area of the brain is often targeted with herpes encephalitis? How does the virus get there?
What kind of lesion is seen?

A

limbic system via retrograde transport of virus from trigeminal ganglion

hemorrhagic necrosis

97
Q

Cells from which area are attacked with acute poliomyelitis? What cells are responsible for the attack?

A

-Anterior horn cells in the spinal cord (motor neurons)

  • lymphocytes, microglia and few neutrophils
  • formation of microglial nodules and destruction of the neurons (neurophagocytosis)
98
Q

What is a grossly classical pattern for multiple sclerosis?

A

2 symmetric periventricular lesions

99
Q

What are 3 things that ring enhancing lesions on contrast imaging can indicate?

A

Abscess, tumor, demyelinating disease

100
Q

In AIDS patients, most lymphomas contain the genome of which virus?

A

Epstein-Barr virus

101
Q

Describe Plan A for txing bacterial meningitis

  • patient population
  • common organisms
  • treatment
A
  1. Healthy patient/community acquired
  2. Organisms
    Streptococcus pneumoniae
    Neisseria meningitidis
  3. Treatment
    - IV Ceftriaxone + vanc + dex
    - blood cultures, CBC and renal profile
    - CT -> if no head masses then get CSF
102
Q

Describe Plan A+ for txing bacterial meningitis

  • patient population
  • common organisms
  • treatment
A
  1. Really young/really old and community acquired
2. Organisms
–Strep. pneumoniae
–Neisseria meningitides (erythematous early, then petechial)
–Group B strep.
–Listeria monocytogenes
  1. Treatment
    Same as A but ADD IV ampicillin
103
Q

Describe Plan B for txing bacterial meningitis

  • patient population
  • common organisms
  • treatment (reasoning)
A
  1. Neurosurgical, immunocompromised or hospital acquired
2. Organisms 
–  Staph. aureus (MRSA)
–  Pseudomonas aeruginosa
–  Listeria
–  Group B Strep
  1. Tx
    Same as A+ but change out ceftriaxone for ceftazimide (better against pseudomonas)
104
Q

What is the most clear cut difference when comparing CSF findings in bacterial meningitis vs viral meningitis?

A

Glucose is decreased w/ bacterial but not viral

105
Q

Herpes simplex encephalitis

  • tx
  • harbored in
  • diagnosis (test and imaging)
A
  1. Tx
    - IV acyclovir
  2. Harbored in
    - olfactory ganglion cells in the inferior and mesial temporal lobes
  3. Diagnosis
    - PCR (not biopsy)
    - MR -> increased intensity in medial temporal lobe
106
Q

West nile virus

  • class
  • causes
  • commonly attacks which regions
  • diagnosis
  • seasonality
A
  1. arbovirus
  2. poliomyelitis (LMN sxs)
  3. Thalamus and basal ganglia
  4. Dx w/ PCR and CFS IgM
  5. July - October
107
Q

Arrange the region based arbovirus in order of decreasing severity

A

Severity decreasing as you move from east to west

– Eastern equine (80% severe sequelae)
– LaCrosse (15% epilepsy)
– St. Louis (intermediate)
– California (very Californian – benign)

108
Q

What are three things needed to make the dx for neurosyphilis?

A

• Clinical pic
• Positive TFA – excellent syphilis serology
• Inflammatory CSF
- Pleocytosis – increase in WBC count
- Elevation in IgG index

109
Q

Tx for neurosyphilis

A

Parenteral penicillin G for 14 days or more

110
Q

Normal CSF values

  • Cell count
  • Glucose
  • Protein
A

cell count
-normal is 5 or less

glucose
<45 mg/dL

111
Q

Locked-in syndrome is caused by infarcts in the?

A

Ventral pons or central pontine myelinolysis

112
Q

Delerium vs. encephalopathy

A

Delerium -> confused and hyperactive

Encephalopathy -> confused and drowsy

113
Q

Cushing’s triad is a sign of? what are the 3 signs?

A

Neurological response to increased ICP

HTN
Bradycardia
Irregular respirations

114
Q

Give the cranial nerves and region of the brainstem tested with following reflexes:

  1. Pupillary light reflex
  2. Corneal reflex
  3. Oculocephalic reflex
A
  1. II and III (midbrain)
  2. V and VII (pons)
  3. VIII and III/IV/VI (lower pons to midbrain)
115
Q

Causes of coma (VITMIN CD)

A
  • vascular
  • infections
  • trauma
  • metabolic
  • iatrogenic
  • neoplastic
  • congenital
  • degenerative
116
Q

Describe hypothermia tx of ischemic cerebral injuries

-how long is tx applied and at what temp?

A

Used for first 24 hours (32-34 C)

117
Q

In the setting of cardiac arrest and hypoxic injury, what would indicate almost no chance of recovery?

A

Absent pupillary reflex and absent doll’s eyes reflex at 24 hours

118
Q

In patients with severe head injury, addition of what 2 factors will double morbidity and mortality?

A

Hypoxia and shock

119
Q

Kiss of death ICP

120
Q

In order, list the 2 most significant factors indicative of outcome following SHI

A
  1. ICP > 20mmHg

2. BP < 80mmHg

121
Q

Asymmetry in motor strength or type of motor response between one side of the body and the other is indicative of?

A

Intracranial mass lesion until proven otherwise

122
Q

Emergency tx of raised ICP

A
  • Maintain neutral neck position (C collar)
  • HOB elevated 30 degrees if possible ???
  • 250ml IV bolus of 3% hypertonic saline
  • Hyperventilate
  • Mannitol .25 – 1.0 gram/kg IV bolus
123
Q

Most common choice to monitor ICP?

A

intraventricular catheter

-can dain CSF to reduce ICP

124
Q

What’s the preferred pharmacological choice for maintaining CPP? which drug class?

A

NE -> vasopressor

125
Q

Patients that had 2/3 of the which factors had an increased ICP 60% of the time

A
  1. Age > 40
  2. Systolic BP < 90mmHg
    Motor posturing
126
Q

If someone experiences 10/10 headache for 6 yers w/ impact on activities they most likely have?

A

Tension headaches

127
Q

Additional criteria required to make the dx of migraine?

A

nausea or vomiting and sonophobia or photophobia

128
Q

Scalp tenderness and jaw claudication seen with?

A

Temporal arteritis

129
Q

Where is a tumor likely to be present if vomiting is seen?

A

Posterior fossa tumors

130
Q

Subdural hematoma

  • presentation
  • risk factor
  • diagnosis
A
  • new headache w/ behavioral changes
  • anticoagulation (warfarin)
  • CT scan
  • DO NOT TAP
131
Q

Pseudotumor cerebri

  • patient population at increased risk
  • findings
  • may cause
  • treated w/
  • what can imitate it?
A
  1. women of child bearing age who are above ideal body weight
  2. Findings
    - papilledema
    - Normal CT
    - elevated CSF < 200mm
  3. BLINDNESS
  4. Tx
    - repeated LPs
    - acetazolamide
    - weight loss
    - optic nerve sheath fenestration
  5. Sinus vein thrombosis - do MRV
132
Q

Temporal arteritis

  • patient population
  • elevation in which lab value
  • can cause
  • tx with
A
  • headache of elderly
  • elevated ESR
  • can cause blindness
  • tx w/ prednisone and confirm dx w/ temporal artery bx
133
Q

Describe the presentation and tx for cluster headaches

A 
o	Most commonly occur in the night
o	Averages around 30 min
o	Occurs behind the eye
o	Male predominant
o	Lacrimation, facial sweating, ptosis and red eye
o	Consider glaucoma

o Tx with
• O2
• Prednisone/verapamil - most efficient way
• Lithium
• Sumatriptan (SQ) – metoclopramide + ASA

134
Q

Tension type headaches

  • time duration
  • tx
A
  • more than 72 hours and more than 50% of the days

- tx w/ amitriptyline

135
Q

Anencephaly is defined as the

A

failure of forebrain development due to disruption 28 days gestation

136
Q

Define rachischisis

A

failure of spinal cord closure that is more extensive than spinal bifida ( myelomeningocele)

137
Q

Chiari Type I associated with?

A

cervical syrinx - post necrotic cystic cavity

138
Q

What 2 things are associated w/ Chiari type II

A

Hydrocephalus and lumbar myelomeningocele

139
Q

Converging of what 2 structures marks the torcular

A

Straight sinus and transverse sinus

140
Q

Compare the genetic defects in neurofibromatosis

A

Type I - chromosome 17 (neurofibromin)
Type II - chromosome 22 (merlin)

Both are tumor suppressors

141
Q

Bilateral schwannomas are associated with?

142
Q

NF-1 mostly presentes with

A

mostly cutaneous and soft tissue tumors

143
Q

Compare LIS-1 vs. doublecortin patterns for lissencephaly

A

LIS-1 and doublecortin appear same in males
-polymicrogyria

In females - Doublecortin mutation will lead to migration of some neurons to the cortex while others won’t

144
Q

Compare cortical arousal to cortical awareness based on areas of input to the cortex

A

Cortical arousal: activity of cortex due to input from ARAS

Cortical awareness: is activity of cortex due to thalamocortical & corticocortical processing (cognition)

145
Q

Sleep atonia

  • which stage of sleep?
  • mediated by?
  • is any muscle spared?
A
  • REM
  • Locus ceruleus
  • everything but extraocular muscles and diaphragm

BMB (15 decks)

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