Exam 5 (no drugs) Flashcards

(145 cards)

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
Gliomesodermal rxn - occurs when? - appearance on T-1 MR w/ contrast? how does it differ with glioblastoma multiforme?
- occurs when CNS injury involved tissue NECROSIS - subacute and chronic abscesses Imaging - well-defined ring enhancing lesion - GBM ring lesion will be very irregular
26
Resident macrophages of CNS?
microglia
27
Ependymal cells - line the? - what happens when they get destroyed? see with?
-line the ventricular system When destroyed -> ependymal granulations - astrocytes form small nodule underneath area that was destroyed - seen with chronic hydrocephalus
28
Components of anesthesia
* Unconsciousness * Amnesia * Analgesia * Inhibition of autonomic reflexes * Skeletal muscle relaxation
29
Stages of anesthesia
1. Premedication - reduce pain - reduce dose of subsequent anesthetics 2. Induction 3. Maintenance 4. Emergence
30
Characteristics of ideal anesthesia -what's balanced anesthesia?
* Rapid, smooth loss of consciousness * Rapidly reversible * Wide margin of safety balanced anesthesia -> specific drug for each goal limiting the side effects of each
31
Potency of anesthetic is directly proportion to?
Hydrophobicity (not causational)
32
# Define the MAC - MAC relation to potency? | - MAC value at which amnesia occurs?
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
33
How does alveolar concentration relate to speed at which you go to sleep?
higher = faster
34
``` 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 ```
* Inspired concentration – higher = faster (overpressure) * Solubility – lower = faster * Alveolar ventilation – increased = faster * Cardiac output – lower = faster! * Alveolar–venous difference – smaller = faster
35
Define Fa/Fi
Ratio of alveolar concentration to inspired concentration
36
``` Effect of volatile anesthetics on organ systems • Blood pressure • Heart rate • SVR • Tidal volume • Respiratory rate • PaCO2 • Cerebral metabolic rate • Hepatic, renal blood flow ```
Everything decreases except RR, PaCO2 and HR
37
BIS value associated w/ low incidence of recall?
<60
38
Variables that increase the rate of elimination of inhaled anesthetics - solubility - ventilation - cardiac output
– Solubility – lower = faster – Ventilation – greater = faster – Cardiac output – greater = faster
39
1. Another name for stage III astrocytoma is? | 2. Another name for stage IV astrocytoma is?
1. Anaplastic astrocytoma | 2. Glioblastoma mulitforme
40
Histological feature that is seen in grade IV astrocytoma?
Vascular endothelial proliferation
41
What are some gross features seen in oligodendroglioma?
- heterogeneous - calcifications - cysts - focal enhancement
42
Halo cells or fried eggs appearance is a histological feature of which brain neoplasm?
Oligodendroglioma
43
A pituitary adenoma growing in the cavernous sinus has potential for compressing which nerves?
III, IV, V1, V2, VI
44
Signs of parinaud's syndrome? Related to which tumor? How does it cause the syndrome?
1. Hydrocephalus and sunset sign 2. Pineal tumor 3. Hydrocephalus -> compression of cerebral aqueduct Sunset sign -> compression of colliculus (tectum)
45
Pediatric brain tumors - majority primary or 2ndary? - most common location?
- primary | - posterior fossa (cerebellum very common)
46
True rosettes and pseudorosettes - description? - seen in which brain tumor? - what can this tumor cause? - what grade is the tumor?
• 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
47
CSF seeding is very common with which CNS tumor?
medulloblastoma
48
Medulloblastoma in adults is metastasis from?
Lung (seen with smokers)
49
Rosenthal fibers - describe - characteristic of which tumor - is it benign or malignant - grade? - age group affected?
- eosinophilic, “corkscrew” shaped protein globules (which are actually intracellular accumulations) - pilocytic astrocytoma - Grade I -> Benign - 5 to 20
50
Which type of radiation is better for mets to the brain? primary tumors?
stereotactic - giving one large dose fractionated for primary CNS tumor
51
Tx for glioblastoma?
- surgery - radiation - Temozolomide - alkylating agent
52
PCV: Procarbazine/Lomustine or “CCNU”/Vincristine is used to tx?
``` Grade III (anaplastic) astrocytoma -best outcome in people with 1p/19q codeletion ```
53
What drug is effective for primary CNS lymphoma surgery? radiation?
Methotrexate (3-7 years in remission) surgery is not effective radiation can be considered at recurrence
54
Tx for medulloblastoma?
Surgery craniospinal radiation chemo in children for 1 year
55
2 most common mets site to the brain
Lungs and breast
56
3 characteristics of local anesthetic recovery?
spontaneous, predictable and complete
57
Relate the following to local anesthetic sensitivity - fiber diameter - firing frequency - fiber position in nerve bundle
- 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
58
LA's composed of? (4 qualities)
– a lipophilic group (an aromatic ring) – an intermediate chain (an ester or amide) – an ionizable group (a tertiary amine) – The amine group is hydrophilic
59
Ester vs. amide local anesthetic - naming - metabolism - duration of action
Ester - one "i" - hydrolyzed by PLASMA cholinesterase - short duration Amides - two "i's" - hepatic metabolism by Cyt P450 - variable duration of action
60
Arrange rate of metabolism for the amide LA's
prilocaine (fastest) > lidocaine > mepivacaine > ropivacaine > bupivacaine (slowest)
61
How is percentage of LA in uncharged form related to pKa
inversely proportional
62
Which 2 amides are packaged only in the S(+) stereoisomer? Why?
Ropivacaine and Levobupivacaine | -reduced cardiotoxicity
63
Severe cardiotoxicity due to LA overdose can be txed by?
lipid rescue
64
Methemoglobinemia due to LA's - which drugs - mechanism - patient presentation - tx
- 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
Good LA for anesthesia emergent delivery
Chloroprocaine
66
Good LA for epidural anesthesia during labor (2 drugs)
bupivacaine and ropivacaine
67
LA to tx neuropathic pain
IV lidocaine or oral mexiletine
68
What can be added to intensify analgesia effect of LA's when they are administered into the epidural/subarachnoid space? What's the mechanism?
opioids and clonidine -> inhibit release of substance P and reduce neuronal firing
69
Describe the progression of sxs for CNS toxicity due to LA's
numbness and tingling -> lightheadedness -> visual/auditory disturbances -> muscular twitching -> unconsciousness -> convulsions -> coma -> respiratory arrest
70
Why is spinal lidocaine no longer used?
TNS - transient neurological symptoms | -show up upon ambulation
71
Which physiochemical properties are the following aspects of LA's related to? 1. speed of onset 2. potency 3. toxicity and metabolism
1. speed of onset -> pKa 2. potency -> lipid solubility 3. Toxicity and metabolism -> degree of protein binding
72
Following an ischemic stroke which subtype has the highest risk of recurrence? Short term? Long term?
Short term - Large vessel Long term - cardioembolic
73
Tx for symptomatic carotid stenosis > 70%
surgery | -medical management alone not adequate
74
Define the CHAD2 score and it's use
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
What are 4 general locations where an ICH can occur?
1. Lobar • Gray matter • Subcortical white matter ``` 2. Deep • Basal ganglia • Periventricular white matter • Internal capsule • Thalamus • Pure IVH ``` 3. Cerebellum 4. Brainstem - most in the pons
76
What's the biggest risk factor for lobar ICH in elderly people? Describe this condition with regards to: - path - imaging - management
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
Single biggest outcome determinant after ICH
size of hemorrhage (larger = worse outcome) - 20 cc ICH, mortality < 20% - 120 cc ICH, mortality > 90%
78
What is the goal for cerebral perfusion pressure? How do you calculate it? Cerebral ischemia
CPP = MAP - ICP Goal > 60 mmHg Cerebral ischemia > 20 mmHg
79
Which vascular malformation is most commonly associated with ICH?
AVM
80
Cavernous angiomas can present with? (2 things) How to they appear on MRI?
hemorrhage or seizure popcorn like lesions
81
SAH most often caused by? | mortality rate if this happens?
- ruptured berry (saccular) aneurysm | - 25% mortality rate
82
Most important modifiable risk factor for SAH? What are some others?
SMOKING * Hypertension * Heavy alcohol use * Black race (in USA) * Female gender
83
What condition is protective for SAH and ICH?
Hyperlipidemia
84
Protocol for dxing SAH?
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
Describe the relationship b/w vasospasms and SAH - what can it cause - timeframe - management - monitoring
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 ``` 4. Monitoring patients: • Transcranial doppler ultrasound
86
Cardinal manifestations suggesting CNS infection
- fever - headache - AMS - focal neurological signs NOT SPECIFIC FOR INFECTION BUT FOR GENERAL CNS PATHOLOGY
87
Post Infectious syndromes such as Guillain-Barre are presumed to work through which mechanism?
Immunological mediated
88
Term infants and premature infants have what significant difference in their normal CSF values as compared to adults?
percent neutrophils (60 in infants vs. 0 in adults)
89
The most common non-infectious entity that causes non-infectious meningitis is
NSAIDs
90
Vaccination against which agent of meningitis lead to dramatic reduction in cases in the 1 - 23 month age group?
Haemophilus influenzae
91
Which meningitis agent has a bimodal distribution in the old and young?
Listeria monocytogenes
92
In acute meningitis organisms can extend what to form a 2ndary abscess?
Virchow-Robin space
93
Which white cells are seen in chronic meningitis? What do they surround?
Perivascular lymphocytes
94
Bone marrow derived histiocytes that reside in the brain are known as? Appearance on histo?
Microglia spindle shaped
95
Define Charcot joints. Which disease are they seen in?
Clinically, a loss of touch, vibration, and position sense would cause an abnormal gait and could lead to joint injuries Tabes Dorsalis (neurosyphilis)
96
Which area of the brain is often targeted with herpes encephalitis? How does the virus get there? What kind of lesion is seen?
limbic system via retrograde transport of virus from trigeminal ganglion hemorrhagic necrosis
97
Cells from which area are attacked with acute poliomyelitis? What cells are responsible for the attack?
-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
What is a grossly classical pattern for multiple sclerosis?
2 symmetric periventricular lesions
99
What are 3 things that ring enhancing lesions on contrast imaging can indicate?
Abscess, tumor, demyelinating disease
100
In AIDS patients, most lymphomas contain the genome of which virus?
Epstein-Barr virus
101
Describe Plan A for txing bacterial meningitis - patient population - common organisms - treatment
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
Describe Plan A+ for txing bacterial meningitis - patient population - common organisms - treatment
1. Really young/really old and community acquired ``` 2. Organisms –Strep. pneumoniae –Neisseria meningitides (erythematous early, then petechial) –Group B strep. –Listeria monocytogenes ``` 3. Treatment Same as A but ADD IV ampicillin
103
Describe Plan B for txing bacterial meningitis - patient population - common organisms - treatment (reasoning)
1. Neurosurgical, immunocompromised or hospital acquired ``` 2. Organisms – Staph. aureus (MRSA) – Pseudomonas aeruginosa – Listeria – Group B Strep ``` 3. Tx Same as A+ but change out ceftriaxone for ceftazimide (better against pseudomonas)
104
What is the most clear cut difference when comparing CSF findings in bacterial meningitis vs viral meningitis?
Glucose is decreased w/ bacterial but not viral
105
Herpes simplex encephalitis - tx - harbored in - diagnosis (test and imaging)
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
West nile virus - class - causes - commonly attacks which regions - diagnosis - seasonality
1. arbovirus 2. poliomyelitis (LMN sxs) 3. Thalamus and basal ganglia 4. Dx w/ PCR and CFS IgM 5. July - October
107
Arrange the region based arbovirus in order of decreasing severity
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
What are three things needed to make the dx for neurosyphilis?
• Clinical pic • Positive TFA – excellent syphilis serology • Inflammatory CSF - Pleocytosis – increase in WBC count - Elevation in IgG index
109
Tx for neurosyphilis
Parenteral penicillin G for 14 days or more
110
Normal CSF values - Cell count - Glucose - Protein
cell count -normal is 5 or less glucose <45 mg/dL
111
Locked-in syndrome is caused by infarcts in the?
Ventral pons or central pontine myelinolysis
112
Delerium vs. encephalopathy
Delerium -> confused and hyperactive Encephalopathy -> confused and drowsy
113
Cushing's triad is a sign of? what are the 3 signs?
Neurological response to increased ICP HTN Bradycardia Irregular respirations
114
Give the cranial nerves and region of the brainstem tested with following reflexes: 1. Pupillary light reflex 2. Corneal reflex 3. Oculocephalic reflex
1. II and III (midbrain) 2. V and VII (pons) 3. VIII and III/IV/VI (lower pons to midbrain)
115
Causes of coma (VITMIN CD)
- vascular - infections - trauma - metabolic - iatrogenic - neoplastic - congenital - degenerative
116
Describe hypothermia tx of ischemic cerebral injuries | -how long is tx applied and at what temp?
Used for first 24 hours (32-34 C)
117
In the setting of cardiac arrest and hypoxic injury, what would indicate almost no chance of recovery?
Absent pupillary reflex and absent doll's eyes reflex at 24 hours
118
In patients with severe head injury, addition of what 2 factors will double morbidity and mortality?
Hypoxia and shock
119
Kiss of death ICP
> 20mmHg
120
In order, list the 2 most significant factors indicative of outcome following SHI
1. ICP > 20mmHg | 2. BP < 80mmHg
121
Asymmetry in motor strength or type of motor response between one side of the body and the other is indicative of?
Intracranial mass lesion until proven otherwise
122
Emergency tx of raised ICP
* 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
Most common choice to monitor ICP?
intraventricular catheter | -can dain CSF to reduce ICP
124
What's the preferred pharmacological choice for maintaining CPP? which drug class?
NE -> vasopressor
125
Patients that had 2/3 of the which factors had an increased ICP 60% of the time
1. Age > 40 2. Systolic BP < 90mmHg Motor posturing
126
If someone experiences 10/10 headache for 6 yers w/ impact on activities they most likely have?
Tension headaches
127
Additional criteria required to make the dx of migraine?
nausea or vomiting and sonophobia or photophobia
128
Scalp tenderness and jaw claudication seen with?
Temporal arteritis
129
Where is a tumor likely to be present if vomiting is seen?
Posterior fossa tumors
130
Subdural hematoma - presentation - risk factor - diagnosis
- new headache w/ behavioral changes - anticoagulation (warfarin) - CT scan - DO NOT TAP
131
Pseudotumor cerebri - patient population at increased risk - findings - may cause - treated w/ - what can imitate it?
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
Temporal arteritis - patient population - elevation in which lab value - can cause - tx with
- headache of elderly - elevated ESR - can cause blindness - tx w/ prednisone and confirm dx w/ temporal artery bx
133
Describe the presentation and tx for cluster headaches
``` 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
Tension type headaches - time duration - tx
- more than 72 hours and more than 50% of the days | - tx w/ amitriptyline
135
Anencephaly is defined as the
failure of forebrain development due to disruption 28 days gestation
136
Define rachischisis
failure of spinal cord closure that is more extensive than spinal bifida ( myelomeningocele)
137
Chiari Type I associated with?
cervical syrinx - post necrotic cystic cavity
138
What 2 things are associated w/ Chiari type II
Hydrocephalus and lumbar myelomeningocele
139
Converging of what 2 structures marks the torcular
Straight sinus and transverse sinus
140
Compare the genetic defects in neurofibromatosis
Type I - chromosome 17 (neurofibromin) Type II - chromosome 22 (merlin) Both are tumor suppressors
141
Bilateral schwannomas are associated with?
NF-2
142
NF-1 mostly presentes with
mostly cutaneous and soft tissue tumors
143
Compare LIS-1 vs. doublecortin patterns for lissencephaly
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
Compare cortical arousal to cortical awareness based on areas of input to the cortex
Cortical arousal: activity of cortex due to input from ARAS | Cortical awareness: is activity of cortex due to thalamocortical & corticocortical processing (cognition)
145
Sleep atonia - which stage of sleep? - mediated by? - is any muscle spared?
- REM - Locus ceruleus - everything but extraocular muscles and diaphragm