Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuro > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What is the “silent epidemic”?

A

CNS Trauma, primary cause of death at age 45, need for primary prevention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the mechanism of contact phenomena in CNS injury?

A

Result of object striking the head (low velocity). Damages the tissue that is designed to protect the brain - less damage to the brain itself
Results in local effects (lacerations, fractures, epidural hematomas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the types of skull fractures caused by contact phenomena

A

Linear - straight crack
Depressed - bone depresses inward
Basilar - base of skull, CSF leak
Growing - usually in toddlers, very rare, CSF leaks and pulses into the dura
Only factors in prognosis (esp linear) is mechanism and velocity of impact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the signs of skull base fracture (basilar)

A

Depressed skull fracture, may go across the base. anosmia (if crossing CNI), CSF rhinorrhea, bilateral periorbital haematomas (Racoon eyes), sub conjunctival haemorrhage, Bleeding from external auditory meatus, CSF otorrhea, Batttle sign (behind the ear), Facial nerve palsy (if crossing CN VII)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is characteristic of a epidural hematoma?

A

Associated with skull fracture. Bone fragment can tear the middle meningeal a. causing bleeding between the skull and dura
Contact phenomena, “Lucid interval”, low mortality rate due to little damage to the brain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is a translational acceleration/deceleration injury?

A

High velocity injuries where head moves in a single plane following impact. Causes stretching/tearing of veins between the brain and dura (subdural hematoma) and bruising of the brain (contusion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are cerebral contusions?

A

Translational acceleration injury
Usually Frontal and temporal injuries
Swelling, brain shift, increased intracranial pressure, herniation, low mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a subdural hematoma?

A

Caused by translational acceleration injury

Rupture of bridging veins in subdural space. Associated with brain contusions, high mortality rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why are bridging veins more sensitive to subdural hematomas?

A

Bridging veins are more susceptible to tearing when there is cortical atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a rotational acceleration/deceleration injury?

A

High velocity injury (rumble tumble, MVA) and head moves in more than one plane, stretching projection fibers that can tear (spectrum of injuries; can not see on MRI). Diffuse axonal injury (DAI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the pathomorphology of Diffuse axonal Injury (DAI)?

A

Spheroids appear when coma exceeds 6 hours, most commonly effects corpus callosum and brainstem. Sometimes see hemorrhage on CT/MRI at the grey white junction but generally these scans are unremarkable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is a penetrating cranial injury?

A

Results from a combination of contact phenomena and distant translatoinal injury. Results in direct cranial and cerebral injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the pathophysiology of TBI

A

Mass lesion (ie clot), relationship to blood flow/ischemia and CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is intracranial compensation?

A

Brain is essentially non-compressible so any increase in intracranial volume will decrease CSF and/or CBV
CSF - displace so subarachoid
Blood - displaced into jugular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens when intracranial compensation has been exhausted?

A

Small increases in the volume of the mass cause large increases in ICP -> decreases CBF inappropriately

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ICP that does not rise uniformly across the brain and can cause?

A 
Acute or Chronic
herniation laterally (cingulate herniation, can kink anterior cerebral a.) or downwards (transtentorial herniation), or uncal herniation (occludes posterior cerebral a. or occulomotor n.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does TBI affect the astrocyte response to neuronal activity?

A

Mechanical force of TBI -> widespread depolarization and neurotransmitter release -> increase in CBF (amd mechanical force of TBI) -> disrupts CBF autoregulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Defective autoregulation can lead to?

A

Hyperemia or ischemia. At high arterial pressure, the astrocytes relax the vessels. At lower blood pressures, the vessels constrict

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ischemia causes astrocyte failure to reuptake what?

A

K+ -> extracellular K+ accumulates -> neuron depolarizes -> glutamate is released
can alos see a loss of control over the ECF volume of the BBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

If you suspect a stroke in a patient and they have symptoms presenting in the legs, think of a stroke in which vessel?

A

Anterior cerebral (foot drop, loss of leg use)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

If you suspect a stoke in a patient that is presenting with loss of facial sensation, aphagia etc. Think which vessel?

A

Middle cerebral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

If you suspect a stoke in a patient with vision changes, think which vessel?

A

Posterior cerebral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

If you suspect a stroke in a patient and they present with clumsiness, think?

A

Cerebellar ciruculation (AICA, PICA, SCA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

If a patient can’t do math, distinguish R or L, or identify fingers being held up think?

A

Gerstman’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

5 classics symptoms of lacunar stroke (small vessel strokes)

A

pure motor stroke, pure sensory stroke, ataxic hemiparesis, dysarthria/clumsy hand, mixed sensorimotor stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the less common mechanisms of stroke (that you generally cannot change)

A

Fibromuscular Dyspalsia (cheeto blood vessels)
Moya-Moya diz (“puff of smoke”)
Spontaneous arterial dissection
These tend to occur in young females. Usually in the media or intima. All can be familial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Arterial dissections tend to have what shape on an angio?

A

Flame shape

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Hematological causes of stroke in young patients

A

Protein C, Protein S, Antithrombine, Factor V Leiden, Prothrombin
Tend to be uncommon causes of stroke (and mostly venous). SKE is a more common cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is a carotid endartectomy

A

A procedure that involves using a “rotor router” technique to remove a plaque
Successful for symptomatic patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Why are the newer devices considered more efficacious?

A

Because you can go in and retrieve the clot faster.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Theme of acute cranial trauma

A

Blood (epidural, subdural, subarachnoid, intercerebral)
Edema
Diffuse axonal Injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Themes of chronic cranial trauma (repetitive)

A

Chronic Traumatic Encephalopathy (CTE) (concussions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the dynamic between BAPP and axonal injury?

A

Stretch causes the release of molecules that the neuron doesn’t normally see. BAPP lines the axon and accumulates on the neuron. BAPP then retracts and balls up.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Strokes come in two flavors

A

Hemorrhagic and occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the incidence and epidemiology of brain injury?

A

Peak age group 24-35

M:F 2:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the big 3 activities/incidencts that cause brain injury?

A

MVA
Recreation
Violence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the 4 classes of injuries that can cause brain injuries?

A

Contact phenomena
Acceleration Injury
Penetrating Injury
Secondary Injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What shape do epidural hematomas have on CT?

A

Lenticular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is coup and countercoup injury?

A

When the head collides with an object (coup) anteriorly and then momentum causes the head to accelerate away from the object following the collision (countercoup). Causes contusion in the frontal and cerebellar regions of the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Subdural hematomas tend to have what shape on CT?

A

Crescent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is a concussion in relation to projection fibers?

A

Rotation injury that is milder than DAI and just stretches the projection fibers - no tearing. Just enough to cause a temporary physiological change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Following a tear of the projection fiber, what happens?

A

They form balls “axonal spheroids” at sites where the axon is damaged. Thought to be due to a loss of transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Key characteristics of Alzheimer’s

A

Amyloid plaques + neurofibrillary tangles
ACh deficit
Early memory and visuospatial problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Key characteristics of Huntington’s Dz

A

AD
Increased polyglutamine repeats (CAG) in huntington gene on chr 4
Caudate atrophy
chorea, depression, dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Key characteristics of Parkinson’s

A

Lewy bodies with synuclein protein
DA deficit
Tremor, regidity, bradykinesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Lewy Body dementia

A

Lewy bodies with synuclein protein
DA and ACh deficit
Early parkinsonian features, psychosis, fluctuating consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Damage to the peduncle causes (transetorial herniation)?

A

Contralateral hemiparalysis, contralateral pupil dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Symptoms of Uncal herniation?

A

Contralateral hemiparalysis and ipsilateral pupil dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

If the brain is swelling, put the skull back on or leave off?

A

Leave the skull off. Let the course of brain swelling run its course

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is excitotoxicity?

A

nerve cells are damaged or killed by excessive stimulation by neurotransmitters and similar substances. I.e. NMDA and AMPA are over activated by glutamatergic storm. Also initiated by pathological levels of Ca2+, K+
CCB useful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is CPP and what is it influenced by?

A

CPP = Cerebral perfusion pressure
CPP=MAP - ICP
so decreasing ICP increases CPP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Priorities in treating severe brain injuries

A 
ABCD
Airway Patency
Breathing
Circulation
Disability (like spinal cord damage)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How do you manage elevated ICP?

A

Shunting, surgical techniques, regulate MAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Pupillar reflex tests?

A

CN II, III in the midbrain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Corneal blink reflex tests?

A

CN V, VII in the pons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Cold caloric testing, “dolls eyes” tests?

A

Flushing cold water into the ear on one side

CN VIII, VI, III studies pons -> midbrain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Gag reflex tests?

A

CN IX, X in the medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

If a patient fails the pupillar reflex, corneal blink, cold caloric test, and gag reflex consider if the patient is

A

Brain dead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the relative ICP ranges?

A

Normal 3-15 mmHg
Mild 16-20
Moderate 21-40
Severe >40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is a goal CPP?

A

70 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Subdural hemorrhage looks like which fruit?

A

banana

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Epidural hemorrhage looks like which fruit?

A

Lemon (lens)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

intracerebral (intraparanchymal) hemorrhage looks like which food?

A

pie

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Arachnoid hemorrhage looks like which food?

A

Icing over a cake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is intracerebral hemorrhage

A

Direct bleed into the blood tissue.
8-13% of stroke
35-52% 30-day mortality
No medical/surgical treatment of proven benefit in improving mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Clinical presentation for ICH?

A

Acute focal neurologic deficit (depending on where the hemorrhage in the brain)
Decreased LOC
Vomiting/headache
*Don’t take ASA because we can’t tell if it’s ischemic or hemorrhagic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the common locations for an ICH

A

Basal ganglia
Thalamus
Cerebellum
Pons
Lots of little perforating vessels that are sensitive to HTN
Also lobar hemorrhagers affecting the cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the characteristics of deep ICH?

A

Located where small perforating arteries are
Common locations: basal ganglia, thalamus, pons, cerebellar
Common RF: ~ 2/3 related to HTN, Age
Non - Caucasians higher risk
In general, poor outcome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are the characteristics of Lobar hemorrhages

A 
Frontal> Pareital> Occipital> Temporal
Amyloid Angiopathy
RF's: Age, Dementia, Coagulopathy
~ 1/3 related to HTN
Well Tolerated
Caucasian/Asian at higher risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Do Thalmic ICH affect the ventricles?

A

They can. Blood can pool in the lateral and 3rd ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

“Locked in” symptoms are associated with which type of ICH?

A

Pons ICH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Common causes of Lobar ICH

A

Cerebral Amyloid Angiopathy (Amyloidosis!)
Vascular Malformation
Cerebral Venous sinus thrombosus (from DVT)
Hemorrhagic ischemic infarct
Underlying Tumor (can rupture and bleed)
Moya-Moya (arteriopathy affecting, interior and middle cerebral a.)
Sympahtomimetic drugs
Coagulopathy
CNS vasculitis
Truama

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Charachteristics of subarachnoid hemorrhage

A

5% of strokes
Hemorrhage in the space between the arachnoid mater and the brain
Most common cause: Trauma
Most common nontraumatic cause: Aneurysm (80%), Arteriovenous malformation (15%), Unk (5%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is a brain aneurysm

A

Weak, bulging spot on the wall of a brain a., Artery wall becomes thinner allowing further swelling
1 in 50 people have unruptured aneurysm
Saccular - “berry aneurysm” most common occurring at a. branch points
Fusiform - less likely to rupture
AComm and PComm - most common sites of aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is an aneurysmal SAH?

A 
Sudden severe headache, sometimes focal deficit (suggests bleeding inside the brain), altered LOC
Sudden death in ~ 1/3, hydrocephalus
sympathetic surge -> cardiac arrhythmia
50-60% mortality
15-20% moderate disability
15-20% back to normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What are the RF’s for SAH?

A 
Smoking
HTN..? unclear
Women > Men (3:2)
Family Hx of ruptured aneurysm
ConDz: PKD, Ehlers-Danlos, Marfan, Fibromuscular dysplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

How do we treat aneurysms?

A

Clipping (craniotomy) - prevents the aneurysm from growing and risk of rupture dissipates
Coiling - IR, use catheter to place thrombogenic coils in the aneurysm. In rare cases the aneurysm will start growing again
Pipeline - coiling with a stent, helps to prevent regrowth in the neck of the aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Complications of SAH

A

Rebleed (kind of like temponade)
hydrocephalus
Vasospasm (4-14 days; vasculature is irritated by external blood and will vasoconstrict, risk of ischemic stroke)
Cerebral Salt Wasting (hyponatremia -> seizures)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Arteriovenous malformations are?

A

ABN connection between a. and v. without a capillary bed, can produce upstream aneurysms
Risk for hemorrhage (ICH, IVH, SAH)
Congenital
Can present with: hemorrhage, incidental finding, seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Bleeding risk in AVM?

A

3% bleed per year -> 10% mortality, 50% have a new deficit
Second bleed becomes more likely and more severe
5-10% have aneurysm
RF’s for hemorrhage: age, prior hemorrhage, deep location, exclusive deep drainage
Size isn’t a RF, but does make treatment more difficult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

How to treat AVM’s?

A

Watch and re-evaluate
IR - embolize
Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Describe a subdural hemorrhage

A 
Usually traumatic (even mild)
Tearing of bridging v.
More common in elderly in the presence of cortical atrophy
Low pressure v. hemorrhage - slow bleed
May require drainage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is epidural hemorrhage?

A 
Trauma, associated with skull fracture
Tear middle meningeal a.
High pressure a. hemorrhage
May present with lucid interval followed by LOC with increasing ICP
Surgically drain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Epidemiology of Ischemic stroke?

A 
#4 leading cause of death
20-30% mortality
#1 adult disabler
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is an ischemic stroke?

A

Fixed focal neurological deficit lasting about 24hrs due to a. or v. infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is a TIA?

A

A brief episode of neurological dysfunction caused by focal brain or retinal ischemia with clinical symptoms lasting less than one hour and without evidence of acute infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

3 etiologies of ischemic stroke

A

Vasculature
Heart
Other players (ie platelets)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Causes of ischemic stroke

A

embolism
Thrombosis
Arterial dissection
Vasospasm (drugs (cocaine), HTN, arterial irritation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Ischemic stroke associated with the highest mortality

A

Basilar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is the LOC, course, and onset of stroke?

A 
LOC = ok
Course = slow improvement
Onset = instant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is the LOC, course, and onset of TIA?

A 
LOC = ok
Course = Rapid improvement
Onset = instant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is the LOC, course, and onset of Migraine?

A 
LOC = ok
Course = Rapid improvement
Onset = Minutes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the LOC, course, and onset of seizure?

A 
LOC = Out
Course = Slow improvement
Onset = Instant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

In subcortical lacunar strokes you see symmetrical symptoms in the?

A

Face, Arm, and Leg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are the non-modifiable risk factors for ischemic strokes?

A

Age
Gender
Race
Family Hx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are lacunar strokes?

A

Very small strokes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Treatable RF for ischemic strokes

A 
HTN
Lipid Disorders
Smoking
Obesity
Diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

RF’s for ischemic stroke

A 
Alcohol/substance abuse
Physical inactivity
Congenital hearts (PFO/ASD/VSD), acquired hearts
Vasculitis
Migrains
Venous infarction
Vasospasm witout SAH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

How do yo treat ischemic stroke?

A

Anti-platelet (ASA, clopidogrel)

Anticoagulant (warfarin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

In the event of a stroke, within what time interval can you administer tPA?

A

onset - 4.5 hours

Fragment of plasminogen activator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

After giving tPA what else can you give?

A

MERCI, Penumbra, Solitaire (IR procedures)

Solitaire is the most effective is because it is the fastest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Whats an effective way to control Cerebral edema?

A

Mannitol

Steroids aren’t very effective because they are slow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is a neurofibroid tangle?

A

Caused by amyloid and it “gums down” the soma. Alzheimers. It is a repetitive accumulation, does not happen over night

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Helmets are good at protecting brains from what? But bad at protecting from?

A

Helmets are good at preventing acute bleeds and fractures, but not as successful at protecting from concussions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Best way to manage DAI?

A

Prevention. Not much we can do once it occurs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Middle meningeal a. branches off of which vessel?

A

External carotid a.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Pathogmonic for concussion?

A

Linear hematociterrin stain, abraidment around the olfactory bulb/tract. Anosmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Pathophysiology of HTN infarcts?

A

Lacunar infarcts in the subcortical brain OR

Subcortical hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Atherosclerosis tends to affect which vessels in the brain?

A

The proximal vessels, associated with circle of Willis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Most ischemic strokes are a result of?

A

Atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

How does ischemic stroke change the brain?

A

We do not have fibroblasts in our brain (which is good because there is lower risk of scarring in the brain) but ischemic strokes leave behind holes in the brain tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

If tPA is administered too late (10-20hrs), what happens?

A

You converted an ischemic stroke into a hemorrhagic stroke. This can also have spontaneously from innate clot busters that the patient produces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Under normal conditions, how long will cell death occur following an ischemic stroke

A

Within 5 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Possible causes of sudden neurologic deficit (DDx)

A 
Infarct
TIA
Seizure
Hematoma
Neoplasma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Imaging protocol for possible stroke

A

Non contrast CT - look for contraindications for antithrombilytic therapy (hematomas, infarcts, glioblastoma, etc)
Perfusion CT - Tells us perfusion and time/rate
CT angio - provides detailed vascular anatomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What do we look for on CT of arterial infarcts

A

Is it contained to the vasculature?
See loss of grey matter in 1-6 hours
4-14 days density and swelling can return to normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What are your two choices in the acute treatment of stroke?

A

IV thrombolytics -tPA within 4.5 hrs

IA thrombolytics - Within 6 hours, devices (MERCI, Penumbra, stentrievers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Differentiate between MERCI, penumbra, and stentrievers

A

MERCI - stab the clot and pull out
penumbra - vacuum the clot
Stentrievers - deploy the stent across the clot to open the vessel, and pull the whole apparatus (with the clot) out.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is delirium

A 
"off the track"
Acute confussional state
toxic-metabolic encephalopathy (drugs, hypoglycemia, Renal failure etc)
Fluctuating LOC
Impaired attention
Incoherent speech
Usually reversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is dementia

A 
"Down from the mind"
Chronic
Normal LOC, attention
Aphasia
Typically irreversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What is delirium syndrome?

A 
Rapidly developing disorder characterized by inability to maintain a coherent line of thought
Usually hypoaroused (lethargy, somnolence)
Hyperarousal less common (agitation, restlessness)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Pathophysiology of Delirium

A

State of diffuse brain dysfunction caused by loss of homeostasis. Widespread neuronal dysfunction (cholinergic, dopminergic, etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Etiology of Delirium

A 
Drugs/toxins
Metabolic disorders
Infection, Inflammation
Structural lesions
Seizure disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What is delirium tremons?

A

Delirium from alcohol withdrawl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Work up for Delirium

A 
PE, Hx
Complete Metabolic Panel, CBC, U/A, EKG, CXR
Tox screen
CT/MRI
Lumbar puncture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

How do we treat Delirium

A

Give them ways to orient themselves (clocks, photos, tv)
Adequate sleep (avoid naps, trazodone)
Drugs for agitation (PRN benzodiazepines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What is the syndrome of dementia?

A

Acquired and persistent impairment in intellectural function. Deficit in at least 3 of: memory, language, visuospatial skills, complex cognition, emotion, personaltiy sever enough to interfere with social or occupational function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Most common etiology of dementia?

A

Alzheimers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Etiology of dementia (reversible)?

A 
Drugs, toxins
Mass lesions
Normal pressure hyrdrocephalus
Systemic illness (hypothyroid, B12 deficiency)
Inflammation, infection
Depression
mTBI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

How do you evaluate dementia

A

Hx, PE
CMP, CBC, TSH, B12, RPR (neurosyphillis)
MRI/CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What is alzheimer’s disease in relation to Dementia

A 
Most common cause of dementia (50-70%)
Prevalent in 5-10% over 65
Women
Most common reason for nursing home admission
Amyloid plaques, neurofibrillary tangles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Clinical features of Alzheimer’s

A

mortality 6-12 years after onset
Stage I - amnesia, anomia (word finding), apathy
Stage II - marked amnesia, fluent aphasia (lost speech), visiospatial dys,
Stage III - Severe dementia, global aphasia, incontinence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What is mild cognitive impairment (MCI)?

A

An attempt to identify AD sooner.
Memory Complaint, struggle with new learning
No dementia, intact living activities
Considered the intermediate stage between normal Aging and AD (10-15% convert to AD each year)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Neurophathology of AD

A

Cerebral Atrophy
Cortical neuron/synapse loss
Major damage in limbic system (higher function is the most affected)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Microscopic neurophathology of AD

A

Amyloid plaques and tangles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Etiology of AD?

A

Not sure
Mix of genetics and environment
Higher education and occupational engagement are protective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Genetics of AD in the young?

A

Associated with trisomy 21, overexpress Amyloid precursor protein (APP) due to the extra copy (can have very young onset of AD)
Presenilin-1 (PSEN-1), PSEN-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Genetics of AD in the elderly (>65)

A

Apolipoprotein E (APOE) chr 19

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What is the cholinergic hypothesis of AD?

A

ACh producing neurons in the basal forebrain are disproportionately affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What is frontotemporal Dementia (FTD)?

A

frontal and temporal lobe atrophy
Pick’s dz
Hippocampus (memory) is spared

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

DX of FTD?

A

frontal lobe dysfunction - disinhibition, apathy, executive dys, aphasia, but memory is spared
Often initially dx’d with bipolar
Striking on CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

What is Parkinson’s Dz relationship to dementia?

A

Loss of DA cell in the midbrain substantia nigra

80% develop dementia within 15 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What is Huntington’s Dz relationship to dementia?

A

Dementia and chorea dominate
Onset in mid-life
CAG triplet, chordate atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

What are the white matter dementias?

A 
Genetic (metachromatic, leukodystrophy)
Demylinative (MS)
Infectious (HIV)
Inflammatory (SLE)
Toxic (irradiation, toluene abuse)
Metabolic (B12 deficiency)
Vasculat (Binswanger's Dz)
Traumatic (TBI)
Neoplastic (gliomas)
Hydrocephalic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What is Binswangers Dz?

A

Vascular dementia, white mater ischemia exp in periventricular regions
Associated with uncontrolled HTN
No treatment, death within 5 years
MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

What is normal pressure Hydrocephalus?

A

Classic triad: dementia, gait disorder, urinary incontence
Very large ventricles on CT/MRI
Surgical shunting is effective in some people. More likely to improve gait than dementia. Shunts can cause complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

what is multi-infarct Dementia (MID)?

A

Vascular dementia

Combination of strokes producing dementia due to accumulation of destruction of brain tissure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

What is Creutzfeldt-Jakob Dz?

A

Rapidly progressive dementia with acute confusion, hallucinations and delusions
Acquired prion Dz, 10-15% inherited,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

What is variant CJD?

A

Bovine Spongiform Encephalopathy
Consuming infected beef
Earlier age of onset, but longer duration
Have not seen chronic wasting Dz of deer or elk being transmissible to humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

How do you treat dementia?

A

Reverse the causes (ie B12)
Irreversible causes - regular medical care and counseling
Caution alternative medicine
Avoid nihilism (don’t assume that we can’t help, even if the dz is uncurable)
Use behavioral measures to correct eradicate behaviors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What is the only dementia that has an FDA approved treatment?

A

Alzheimers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

What is the general cause of neurodegenerative Dz?

A

Spontaneous failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Key Early symptoms of Alzheimer’s

A

Early memory and visospatial problems

Can’t remember how to get to places

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Key Early Symptoms of Frontotemporal Dementia (FTD)

A

Early behavioral, executive and/or language

Usually inappropriate sexual comments or judgement but no loss in motor function or memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Key Early Symptoms of Parkinson’s Dz

A

Tremor, rigidity, bradykinesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Key early symptoms of Lewy Body dementia

A

Early parkinsonian features, psychosis (delusions, believe the CIA is coming for them, hallucinations), fluctuating consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Key early symptoms of Progressive supranuclear palsy (PSP)

A

Bradykinesia, rigidity, falls, ABN vertical eye movements (struggle to voluntary move eyes up and down, but the reflex still intact), lose the “righting” reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Key early symptoms of Amyotrophic Lateral Sclerosis?

A

Weakness, atrophy, fasciculations (little muscle twitches), both upper and lower motor neuron signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

Key early symptoms of Huntingtons Dz

A

Dementia (poor decision making, incarciration)
Depression
Chorea (fleeting high velocity movements, usually unaware)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Key early symptoms of Creutzfeldt-Jakob Dz

A 
Rapidly progressive (months, not years) dementia, myoclonus (high velocity twitches)
Prion Dz
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

What is a prion?

A

Proteinaceous infectious particle
No nucleic acid
PrP appears to be expressed in all human tissues with the CNS being the highest
DZ -> conformational change in the PrP
ataxia, ABN movements, neuropsychiatric features
Sporadic, heritable, and transmissible Dz
Uniformly fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What is variant CJD?

A 
Bovine-to-human transmission of BSE.  
Younger onset
Slow progression
Different symptoms at presentation (more depression/anxiety)
Different neuropathology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

How is Kuru acquired?

A

Papua New Guinea
Cannibalism, prion
Early tremor/ataxia, dementia late in dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

What is Gerstmann-Straussler schienker Syndrome?

A

AD, very rare, prion
Cerebellar findings (clumsy, incoordination, gait ataxia, myoclonus)
Dementia
Huge variability of symptoms even among family members

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What is fatal familial insomnia?

A

AD, prion
35-60 y/o at onset
Progressive insomnia (thalamic pathology)
Memory loss, confusion, hallucinations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Why worry about prion dz when it’s so rare?

A

Ongoing research to understand if the prion conformational change is related to other protein disturbances (synuclein, amyloid, and others)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

What are the key characteristics that define neurodegenerative dz?

A

Spontaneous death of neuronal populations and location of these neurons determines presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What is myoclonus?

A

Brief involuntary twitching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

What is the only neurodegenerative dz that is transmissible?

A

CJD (prion dz)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

Tau is associated with

A

FTD, PSP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

Synuclein is associated with

A

Parkinson’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

Ubiquitin is associated with

A

ALS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

Polyglutamine is associated with

A

Huntington’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

Prion Protein is associated with

A

CJD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

Bottom up impairment refers to?

A

Delirium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

Top down impairment refers to?

A

Dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

Compare the onset of
Delirium
Depression
Dementia

A

Delirium - abrupt
Depression - fairly discrete
Dementia - Insidious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

Most common CNS neoplasm in adults?

Kids?

A

Adult - Meningiomas

Kid - astrocytomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

What are the five possible locations of intracranial tumors?

A 
Supratentorial
Infratentorial
Tentorial notch
Tentorial
Foramen magnum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

Occurrence of posterior fossa tumors in adults?

Kids?

A

Adults - 30%

Kids 70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

What are 3 main categories of CNS neoplasms?

A

Neuroectodermal tumors
Meningeal and Mesenchymal tumors
Metastatic tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

Gliomas are a subtype of the neuroectodermal tumors and include?

A

Astrocytomas
Oligodendrogliomas
Ependymoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

Meningeal and Mesenchymal Tumors include?

A

Meningioma
Schwannoma
Neurofibroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

What are the sources of tumors that metastasis to the CNS?

A 
Breast
Lung
Kidney
GI
Melanoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

What are the 6 common types of gliomas?

A 
Set by WHO
Pilocytic astrocytoma I
Diffuse astrocytoma II
Anaplastic astrocytoma III
Oligodendroglioma II
Anaplastic oligodendroglioma III
Glioblastoma IV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

Describe Pilocytic Astrocytoma

A

Most common CNS neoplasm in kids
Found in cerebellum, optic pathway, thalmus, hypothalmus, spinal cord, temporal lobe (locations seem to be determined by genetics)
WHO grade I - minimal tendency to progress to a higher grade over time
Bipolar neoplastic cells with elongated hairlike processes (pilo = hair), well-demarcated cyst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

Genetic background of Pilocytic Astrocytoma

A

BRAF fusion (BRAF:KIAA)
BRAF = mitogen-activated protein kinase (MAPK) in the Ras/RAF/MEK/ERK pathway that controlls cell proliferation
So, fusion -> uncontrolled cell proliferation
KIAA1549:BRAF has favorable prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

What is diffuse astrocytoma

A

30-40 y/os
WHO II - may progress
Found in cerebral hemispheres, rarely posterior fossa
Monotonous cellular infiltrate in patternless array
Lack of well-defined borders, bad candidate for surgical resection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

What is anaplastic astrocytoma?

A

Mean age = 45
WHO grade III
Cerebral hemispheres in adults
High cellularity, increased polymorphism, hyperchromasia, and mitosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

What is the genetics of diffuse astrocytomas?

A

IDH1 mutation + p53/ATRX mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

What is oligodendroglioma?

A

5-15% of gliomas with an age of onset of 42
WHO grade II
Arises in cerebral white matter - risk of seizures
Moderate cellularity, ocasional mitosis, intermediate or mixed oligodendroglial phenotype. Perinuclear halo “fried egg” appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

Genetics of oligodendroglioma?

A

IDH1 mutation followed by genetic mutations that lead to oligo vs. astrocyte lineage (p53, LOH 1p, 19q which creates a fusion protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

Oliogdendrogliomas have the ability to turn on which embryological feature?

A

Migration along the radial glia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

What is anaplastic oligodendroglioma?

A

Rare with an onset of 48 years
WHO grade III
same as classic but with increased cellularity, nuclear atypia, mitosis
Occasional vascular proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

Describe the 1p, 19q codeletions

A

Established marker for oligodendroglial tumors
Unbalanced translocation
Good prognosis, use with FISH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

Genetic differences between Anaplastic oligodendroglioma and anaplastic astrocytoma?

A

Both have IDH mutations
oligodendroglioma - 1p/19q co-deletion, progresses to anaplastic if 9p and 10q are lost
Diffuse Astrocytomas - have a TPS3 mutation with 17 p loss, 9 p loss > anaplastic astrocytoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

What is glioblastoma (GBM)?

A 
15% of intracranial neoplasms
onset primary ~ 62 y/o
Cerebral hemispheres
WHO IV - ~3% 5 year survival rate
Mitotically active, dedifferentiated elements, necrosis, reactivate fetal 
vasularization
Tends to be central in the brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

On T2 CSF is?

A

white

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

Characteristics of Primary GBM

A

De-novo
Older onset (~55 y/o)
Short duration of symptoms ~ 3mos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

Characteristics of Secondary GBM?

A

Progression from a lower grade glioma
Younger onset (~ 45y/o)
Long duration of Symptoms more are IDH-1+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

Mutations associated with primary GBM?

A

10 q loss
PTEN mutation
EGFR amplification
CDKN2A/B deletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

Which mutation is a particularly bad prognosis for GBM?

A

EGFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

Pediatric cases of GBM tend to localize in the?

A

Pons (survival ~ 9 mo), genetically different from adult GBM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

What is IDH?

A

Isocitrate Dehydrogenase
1 point mutation makes a target protein of 2-hydroxyglutarate instead of the normal alpha-ketogluterate
This mutation is only found in neoplasms and the Ab is 100% specific (no false positives)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

What is the prognosis of IDH 1 mutations?

A

IDH1 negative Anaplastic astrocytomas do more poorly than those with IDH1 mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

What would be a co-finding in GBM that would have a positive prognosis?

A

MGMT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

What is ependymoma

A

Not all arise from ependymal lining the intraventricular locations (but most do)
Present in the first 20 years
4th ventricle with obstructive hydrocephalus (kids)
Commonly calcified
Adults tend to have spinal cord epndymomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
208
Q

Describe Medulloblastoma

A

By definition, in cerebellum
Most common malignant pediatric tumor (3-8yr)
~50% survival with treatment (0% without)
Most likely originates from Granule cell development from the EGL
Lack differentiation
chr 17 mutations
White coating on spine - CSF dissemination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
209
Q

What is it about tumors that ultimately makes them kill the patient?

A

Spreading to other sites (metastasis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
210
Q

Who induces External Granule migration in development?

A

SHH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
211
Q

What is papillodema?

A

Swelling of the optic n. and retinal a., v.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
212
Q

What procedure should not be performed when papillodema is observed?

A

Lumbar punctures

The increased CSF pressures may cause the patient to herniate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
213
Q

What is meningioma?

A

WHO I intracranial neoplasm unk etiology
30 y/o’s peaking with women in their 50’s
Solitary from arachnoid cells, can penetrate dura and occlude venous sinuses
Well demarcated, superficial, bulbous mass with pseudopod, and able to remove surgically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
214
Q

What are Schwannoma?

A

Tumors of the nerve lining
Slow growing, rare transformation
found on CNVIII and a few others
Also found on spinal nerve roots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
215
Q

What is an acoustic neuroma?

A

a Schwannoma on CNVIII (Vestibular n.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
216
Q

What are the characteristics of familial tumor syndromes?

A

Genetic
Small % of tumors in each class
Tend to have a younger demographic than sporadic tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
217
Q

What are the familiar tumor syndromes?

A

NF-1, NF-2 (neurofibromatosis type I, II)
Tuberous Sclerosis
Von Hippel Lindau Dz
Cowden Dz
Turcot’s Syndrome
* Most brain tumors are sporadic with unk etiology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
218
Q

Describe metastatic tumors and their relation to CNS tumors

A

Tend to metastasize from breast, lung, kidney, melanoma, GI
Usually discrete tumors
Solid pediatric neoplasms rarely metastasize to brain.
Cerebral: cerebellar 8:1 (about the same as the mass ratio)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
219
Q

What is the nomenclature for the MS phenotype

A

Relapsing-Remitting 85% - multiple attacks over time (younger)
Primary progressive - 15% - continuous progression (older)
Secondary progressive - 15% RRMS conversion to progressive dz
Clinically Isolated syndrome - 1 isolated attack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
220
Q

Epidemiology of MS

A

3/4 between 15-45
2/3 female
Caucasians
Most common inflammatory CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
221
Q

What is the neuropathology of MS

A

Lesions evolve over time - early lymphocyte infiltrate with a glial scar forming later
Grey matter lesions seen early on but also lesions on white mater
Germinal structures with B cells in meninges (esp progressive MS)
RRMS and progressive MS are not “all inflam” or “all degen”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
222
Q

Risk for MS relapse is related to which factors?

A

Age

Years since onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
223
Q

Causes of MS?

A

Genetic - HLA DR2; like to IL-7 receptor, IL-2 receptor mutations, 10-20x increase risk in first degree relatives
Environmental - EBV raises risk, smoking, VitD deficiency, obesity. Salt intake doesn’t but a patient at risk, but makes treatment harder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
224
Q

MS is caused by an inflammatory response involving?

A

Macrophages and Ab’s attacking the myelin. See expression of Nogo following damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
225
Q

How do you diagnose MS?

A

Multiple CNS lesions dispersed in space and time without any other cause identified. Must have 12 months of progression of symptoms
McDonald criteria

226
Q

Early MS symptoms

A

unifocal problems (eye, Spinal cord)

227
Q

Later MS symptoms

A

Multifocal with more symptoms (vision, weakness, tingling, vertigo, fatigue, urinary urgency, constipation, etc)

228
Q

what are some findings on PE that is characteristic of MS?

A

Assymetric findings across multiple parts of the brain (cerebellum, pons, etc)

229
Q

What is seen on MR that suggests MS?

A 
T1 - holes, axonal or BBB damamge
T2 - bright lesions (water)
Focal or global atrophy (ventricles expand in response)
"Dawsons fingers"
MRI is diagnostic and prognostic
230
Q

Describe the lesions found in the spinal cord of MS patients

A

Shorter lesions - about the length of one vertebrae, cigar shaped. Helps to differentiate from NMO

231
Q

What would be poor prognostic findings for MS on MRI

A

grey matter atrophy
Holes on T1/T2
Spinal lesions

232
Q

What is seen on CSF in MS?

A

low protein, WBC, normal glucose

IG in CSF, elevated myelin protein

233
Q

MS Prognosis?

A

Decreased motility within 15-20 years
Lifespan decreased 6-7 years
Suicide is 7x more common
Depressed
Significant cause of disability in young people
Most of the disability occurs after the age of 40 or 50

234
Q

Prognositic factors for MS?

A

Bad - older black male with lots of attacks
Good - young white female with normalish MRI
5% pediatric MS

235
Q

Prognosis with therapy?

A

Long term - decreased mortality with interfuron

Short term - frequency and severity of relapses

236
Q

Goals in MS therapy

A

Life-long brain health
Behavioral changes
Manages acute attacks

237
Q

What are the mechanisms of action for the newer MS therapies?

A

Natalizumab - humanized mAB to alpha4-integrin (antagonist). Sequesters protein and prevents it from crossing the blood brain barrier. However, risk of progressive multifocal leukoencephalopathy AE - JCVirus causes brain infection of oligodendrocytes. This virus is normally easily controlled, but becomes active following immunmodulation

238
Q

New thinking when treating MS?

A

Try the newer (and more effective) medications as the first line defense. Don’t prescribe IFN very often anymore

239
Q

Limitations of current MS therapies?

A

Partial responders
Expensive
AE’s can be risky (Natalizumab)
Difficult to “see or feel” the benefit of the therapy (mild ability to control current symptoms, drugs are designed to slow the progression and onset of new symptoms; not trying to enhance CNS function, just trying to modulate the inflammatory response in the CNS)

240
Q

The sensory system contains 4 special senses

A

Vision (light, photons)
Hearing (changes in pressure)
Chemical (olfaction (volatile molecules), taste (water soluble molecules))

241
Q

What is the receptor of the somatosensory system?

A

Exteroception - touch (vibration), temperature, pain

242
Q

What do all sensory receptor cells have (x3)

A
  1. A soma containing a nucleus
  2. Have a way to communicate with other neurons (synapse with 2nd order neuron)
  3. Sensory ending (detects stimuli)
243
Q

How do the sensory endings of neurons relay (or connect) to their soma

A

Via either a dendrite or a peripheral axon

244
Q

Describe the pathway sensory stimuli take from initial sensation to the 2nd order neuron

A

sensory ending -> dendrite, peripheral axon -> soma -> axon -> 2nd order neuron

245
Q

Describe AP propagation in a photoreceptor

A

sensory receptor -> opens non-voltage sensitive channels (stimulant dependent)

246
Q

Will you see voltage-sensitive channels anywhere in the propagation of a visual stimuli?

A

Yes, in the axon. Na+ (activation and inactivation gated)

247
Q

2 sensory cell types in the retina

A

Cones - color

Rods - night vision

248
Q

What is transduction?

A

When a stimuli is converted into a voltage change

249
Q

What is proprioception?

A

Our ability to understand where parts of our body are oriented in space without using our vision. Dependent on the muscle spindle

250
Q

Transduction in photoreceptors (rod) are mediated by?

A

Second messengers (cGMP). Use cGMP gated channels. Cytosolic cGMP keeps the gate open in the dark. Allows influx of Na+ and outflux of K+. Raises Vm close to 0

251
Q

Describe the structure of a rod

A

proximal end - sensory ending
Soma in the midle
Distal end - synapse
No AP because they are so small, hence why they use second messenger mediated transduction

252
Q

What happens when the rod is exposed to light?

A

Cell will hyperpolarize (-)

253
Q

Describe the disc that is found in the proximal end of the rod and what happens when it encounters photons

A

Disc contains cis-retinal at rest. Photons induces a conformation change to trans-retinal. Transducin (G protein) interacts with something on rential (ie the photoreceptor; rhodopsin) -> transducin binds ATP, becomes active -> degrades cGMP -> gate closes -> cell hyperpolarizes

254
Q

Does it take a lot of photons to activate the rod?

A

No. We see huge levels of amplification. 1 trans-retinal can activate many transducin

255
Q

What is a sensory system that does not use the secondary cascade

A

Mechanoreceptors
Somatosensory system - Touch
Proprioception (muscle stretch)

256
Q

How does touch stimuli become converted to a AP?

A

Proteins in the sensory end are linked. When they are stretched apart they open Non-specific cation channels (Na+ influx, K+ out) ->

257
Q

Which sensory systems use secondary messenger systems?

A

Vision
Olfaction
Taste

258
Q

Which sensory systems use direct systems to generate AP’s?

A

Auditory

Touch

259
Q

Which sensory system does NOT go through the thalamus?

A

Olfaction

260
Q

The lateral thalmus relays which sensory information

A

Vision (lateral geniculate nucleus)

261
Q

What is the relay system of vision?

A

Retina, synapses -> optic n -> lateral geniculate nucleus (thalmus), synapses -> Cortex (V1 primary visual cortex) ->

262
Q

What is the relay system for the auditory system

A

Ear -> multiple steps -> medial geniculate nucleus (thalmus), synapse -> auditory cortex (temporal gyrus)

263
Q

What are the mechanoreceptors of the skin?

A 
Free nerve ending
Merkel's disk
Meissner's corpuscle
Pacinian corpuscle
Hair follicle receptor
264
Q

From deepest to most superficial, what is the layering of mechnoreceptors in the skin?

A

Pacinian corpuscle
Free nerve endings (marfenian?)
Meissner’s corpuscle
Merkel’s Disk

265
Q

Which mechanoreceptor has a large receptor field and fast adaptation?

A

Pacinian corpuscle

266
Q

Which mechanoreceptor has a small receptor field with slow adaptation?

A

Meissner’s corpuscle

267
Q

Which mechanoreceptor has a small receptor field with slow adaptation

A

Merkel’s disk

268
Q

Which mechanoreceptor has a large field and fast adaptation?

A

Free Nerve endings

269
Q

If a mechanorecptor has fast adaptation it can sense

A

Vibrations

270
Q

Is touch (posterior lenmisco) ipsi or contra?

A

ipsilateral below brainstem

contralateral above brainstem

271
Q

The ventral posterior lateral (VPL) nucleus in thalmus relays information to

A

relays information from the body to the somatosensory cortex

272
Q

The ventral posterior medial nucleus (VPM) relays which information through the thalmus?

A

Relays information from the face to the somatosensory cortex

273
Q

Define the functions of each Broadman’s area

A

1, 3 - orientation, speed
2a - proprioception
2b - simple touch
4 - motor cortex
1, 2, 3 - primary somatosensory cortex (2a, 2 b receive the stimuli from the thalmus and relay it toward 1 and 3)
There is also communication from 3 to 4 (connects proprio and touch to the motor system)

274
Q

Describe the layering system of the cortex (applies to each cortex)

A

There are 6 layers with 6 being the deepest, 1 most superficial
Thalamus relays information to layer 4
A lower layer will relay a reponse to the talmus
Layer 3 is inhibitory - helps to relay the information to other cortexs and coordinate a response

275
Q

what is the function of the anterolateral system?

A

Carries information about temperature and pain

276
Q

How is pain detected?

A 
Primary sensory neuron (DRG class AdeltaC)
C= unmyelinated
Adelta = poorly myelinated
277
Q

What is unique about the DRG involved in pain?

A

Biaxonal -> one to the periphery (free nerve endings) and another to the CNS

278
Q

After pain is detected by the primary sensory neuron, where does the stimuli synapse?

A

dorsal horn (Spinal Cord) -> 2nd order neuron, crosses the spinal cord (contralateral) and ascends through anterior lateral column

279
Q

Where does the pain information in the ascending anterolateral system go?

A
  1. spinothalamic tract -> Thalmus (VPL) -> somatosensory cortex
  2. spinoreticular tract -> hypothalmus, amygdala (behavioral and emotional response to pain)
  3. spinomesencephalic tract -> midbrain, important for descending modulatory influences of pain
280
Q

Which sensations are carried in the DCML?

A

Touch, proprioception

281
Q

What type of nueron is the primary sensory neuron for touch and proprioception

A

DRG alpha beta

282
Q

First synapse for anterolateral system?

A

Dorsal horn of the spinal cord

283
Q

First synapse for touch and proprioception?

A

Medulla

284
Q

Where is decussitation occur for anterolateral system?

A

Right away in the spinal cord

285
Q

where is decussitation for the DCML system?

A

Medulla

286
Q

For the anterolateral system, the ascending information will travel on which side?

A

Contrlateral

287
Q

For the DCML system, the ascending information will travel on which side?

A

Ipsilateral and will become contralateral in the medulla

288
Q

what are the two types of temperature receptures

A

Warm receptors - as T increases so does firing

Cool Receptors - as T decreases, firing increases

289
Q

What type of DRG receptors are warm and cool?

A

Cool - mostly alpha delta DRG

Warm - mostly C type

290
Q

What are we most sensitive to when it comes to temperature?

A

We are most sensitive to rapid changes in temperature. Better at this than sensing gradual change or a steady temperature

291
Q

When temperature receptors are activated, what are the two possible responses

A

Transient response - change in temperature/time

Sustained response - Absolute temperature (receptor will reach a steady state level following a change in temperature)

292
Q

What is the ratio of cold:warm receptors in the skin?

A

10:1

293
Q

What are the 3 types of pain?

A

Nociception - acute painful stimulus
Neuropathic - CNS damage, chronic pain
Inflammatory..?

294
Q

What are the 3 types of DRG neurons in pain sensation?

A

Thermal -> Extreme Cold - C, Hot - alpha delta
Mechanical -> intense pressure, alpha delta
Polymodal -> C only, respond to temp, chemicals, pressure (nociceptive stimuli)

295
Q

What are the pain receptors in the nerve ending that are able to detect the stimulus?

A

ASIC - acid sensing ion channel (pH)
P2X - purinergic receptor (ie purines/ATP, senses cell rupture)
VR-1 - vanilloid receptor 1; polymodal in itself to temperature and chemicals (capsaicin)

296
Q

Following tissue damage, a wheel with a red center is formed due to?

A

cell contents cleave kinenogen to form Bradykinin

297
Q

Functions of bradykinin

A

vasodilator (red center), increases capillary permeability (edema/wheel)

298
Q

What is responsible for the flare around tissue damage?

A

Substance P (protein). Released upon REPETITIVE intense stimulation

299
Q

What are two classes of molecules that can act on nociceptors

A

Activators - bradykinin, K+, H+, seratonin

Sensitizors - don’t generate a full AP but bring the neuron closer to threshold. Substance P, Prostaglandin, Seratonin

300
Q

Describe nociception response following tissue damage

A

Bradykinin activates nociceptor -> signal travels to a bifurcation and then activates both axons -> causes repetitive intense stimulation -> substance P is released

301
Q

What is hyperalgessia?

A

Hyper sensitive to pain

302
Q

What is allodynia?

A

Having a pain response to something that isn’t normally painful (i.e. showering with a sunburn)

303
Q

Differentiate between 1st pain and 2nd pain

A

1st pain - Immediate, makes you alert to get away from stimuli. Carried by alpha delta
2nd pain - general “ow” pain. Carried by C fibers

304
Q

Describe the order of DRG’s that can be blocked by pressure stimuli

A
  1. A beta
  2. A delta
  3. C fibers
305
Q

Describe the order of DRGs that are block by local anesthetics

A
  1. C fibers
  2. then Adelta
  3. Abeta
306
Q

Describe the order of DRG’s that are blocked by electrical stimulation

A
  1. A beta
  2. A delta
  3. C fibers but ONLY with repetitive stimulation
307
Q

C fibers travel to the dorsal horn and synapse with?

A

Lamina II (substantia geldinosa) and synapses with a second order neuron

308
Q

What is the cause of referred pain?

A

Convergence of inputs from cutaneous (dominant) and visceral sites

309
Q

What is the receptor for substance P?

A

Neurokinin 1 (NK1) -> G coupled receptor leading to the closure of K+ channels (depolarize)

310
Q

When you bump your elbow and rub it to dull the pain, you are activating which DRGs?

A

a betas

Note: Syphilis patients are losing their a betas. Source of their inability to modulate pain

311
Q

What is the enkephalingic inhibitory interneuron

A

Endogenous opiod like neuron
Inhibits the pain synapse pre synaptically (inhibits Ca2+ channels) and post synaptically (hyperpolarizes by opening K+ channels)
Acts at the dorsal horn 2nd order neuron

312
Q

What is dorsal column stimulation

A

Powerful analgesic by blocking ascending neurons in spinal cord (anterolateral?)

313
Q

Define concussion

A

Immediate and transient impairment of neural function (AOC, distrubance of equilibrium etc) due to mechanical forces

314
Q

What is the lowest possible Flasgow Coma Scale?

A

3

315
Q

What are the hallmarks of mTBI?

A

a concussion with confusion and amnesia (NOT unconciousness)

80% of head injuries

316
Q

What are the common late symptoms of concussion?

A 
Headache, lightheadedness
Decreased attention/concentration
Poor memory
Irritability, depressed, anxiety
sleep disturbance (this must be treated for the mTBI to improve)
317
Q

What are the signs of concussion?

A 
Vacant stare
Delayed responses
Disorientation
Slurred speech
Incoordination
Inappropriate emotionality
Memory problems, LOC
318
Q

Regardless of the direction of the force, which lobes are most affected in mTBI?

A

Frontal and temporal

319
Q

What biochemically happens during a concussion

A

Exocitotoxic release of neurotransmiters driving up cellular metabolism (hyperglycolysis) and lactic acid levels. Failure of Na+/K+ during axonal stretch

320
Q

What would be pathogmonic of concussion on imaging?

A

Iron deposition at the gray white junction on GRE filter. If you can see hemorrhagic lesions, then it is confident that the axons are also damaged because the vessels are tougher

321
Q

What is the concussion grading scale?

A

Grade 1 - transient confusion, no LOC, resolves in 15m
Grade 2 - Transient confusion, no LOC, lasts >15m
Grade 3 - LOC a) being brief b) being prolonged

322
Q

What is important when treating a concussion?

A

Total brain rest, gradually re-enter life experiences. Most people will recover within 7 days

323
Q

What is the pathology of second impact syndrome

A

Catastrophic swelling -> vascular autoregulation dysfunction -> severe ICP

324
Q

What symptoms are associated with both PTSD and TBI

A 
cognitive defects
irritability
insomnia
depression
fatigue 
anxiety
325
Q

What effect does altitude have on mTBI?

A

Increases in altitude correlated with decreased ANAM scores for mTBI compared to the controls.

326
Q

What happens when a peripheral nerve is severed?

A

Stump acumlates a hyperdensity of Na+ channels, this changes this threshold and leads to spontaneous firing

327
Q

What does TTX do? Is it always effective?

A

Blocks sodium channels. But, not always. There are TTX resistant channels that require a much higher TTX does to be blocked. From a pain perspective, blocking the Na+ channel would be effective in subsiding pain.

328
Q

what determines if GABA is inhibitory or excitatory?

A

Cl- channels

KCC2 (potassium chloride channel 2) extrudes GABA

329
Q

Which interaction is associated with sustaining pain sensation (or long lasting pain)?

A

Substance P stimulation of NMDA receptor

330
Q

Epidurals mimic the inhibitory action of?

A

Enkephalinergic inhibition neuron

331
Q

What are the 2 basic types of local anesthetics? Acid or base? What does the intermediate chain tell you?

A

Amide and ester linked
Weak bases (7.7-9)
Intermediate chain determines - onset, duration, potency

332
Q

Local anesthetics generally have what 3 groups?

A 
aromatic moiety (lipophylic)
intermediate chain
amino group (hydrophilic)
333
Q

How can you tell if an anesthetic is an amide or an ester?

A

amides - have 2 i’s

esters - have 1 i

334
Q

Which version of local anesthetics can enter the Nav gate? Cationic or neutral?

A

Cation - pH greatly influences the molecules ability to enter the Na+ channels
The neutral form can cross the membrane directly, become hydrated, and then block the sodium channel (a way to block gates from the inside)

335
Q

What is the action of local anesthetics?

A

Block Nav channels and decreases the propagation of action potentials and dissipates the propagation of pain

336
Q

What is the physical mechanism of anesthetics blocking Nav gates?

A

intracellular side of the gate must be open to allow LA+ to the the channel and bind within to obstruct Na+ through the channel
Since the Nav must be open for the LA block to work, the action is “use-dependent”

337
Q

Local anesthetics preferentially block?

A

alpha delta
Beta
C fibers
This means the patients will be temporarily insensitive to pain/discomfort but motor function will be unaffected

338
Q

What qualities do local anesthetics that have faster onset, higher potency, and longer duration of action?

A

Lower pKa
Higher lipid solubility
Greater protein binding

339
Q

How do you terminate the signal of an anestheitc

A

Esters are hydrolyzed by plasma (pseudocholinesterase) and in the liver
Amides are metabolized in the liver (contrindicated in patients with hepatic insufficiency)
Person to person variation in LA toxicity/sensitivity is due to alpha 1 glycoprotein
Excretion via kidney

340
Q

Tetracaine, lidocaine, and cocaine are?

A

Topical anesthetics (surface only)

341
Q

EMLA creas is?

A

A mix of lidocaine and prilocaine that can penetrate the skin (oil suspension)

342
Q

What would benzocaine be used?

A

Lacks a terminal amino group - low water solubility. Directly apply to woulds for slow absorption

343
Q

Lidocaine, procain, and bupivacaine are?

A

Injectable local anesthesthetics

344
Q

Lidocain and bupivacane can be used as?

A

Nerve block anesthesia (inject near peripheral nerve

345
Q

What is IV regional anesthesia (Bier’s block)?

A

squeeze blood out of a limb via a touniquet and inject LA into the limb. Usually lidocaine

346
Q

What is spinal anesthesia?

A

LA injections into CSF to bate the spinal cord. Anesthetizes large region of the body with only low dosages of the drug. Lower extremity surgeries only. Lidocaine (short), bupivacaine (intermediate), and tetracaine (long)

347
Q

What is epidural anesthesia?

A

LA injection just outside the dura-enclosed spinal canal. requires higher doses of LA than spinal anesthesia. Lidocaine (short) or bupivacaine (Longer)

348
Q

What are some LA’s co-applied with epinephrine?

A

All LA’s (except cocaine) have sympathetic activity and cause vasodialtion. Epinephrine reduces this

349
Q

What happens in LA overdose?

A

Convulsions (inhibition of inhibitory neurons)
ANS dysfunction
Arrhythmia (esp bupivacaine)

350
Q

Toxins that can block Nav in motor fibers?

A

Tetrodotoxin - TTX (puffer fish)

Saxitoxin - STX (red tide)

351
Q

Indication of medication overuse headache

A

Dull or migraine-like headache at least 15 days/month. 1 in 25 overuse pain meds. 1 in 4 of over medicators have medication over use headache

352
Q

In migraines the Trigeminovascular system causes?

A

Releases peptides
inflammation
vasodilation (pain)

353
Q

In migraines sensitization is probably responsible for which clinical symptoms?

A

Throbbing quality of pain
Worsening of pain with coughing, bending, sudden movement
Hyperalgesia
Allodynia

354
Q

What role does serotonin play in the sensitization action of migrains

A

serotonin agonist are important in acute treatment but role in generation of the migraine is unclear (decreased 5HT release leads to vasoconstriction

355
Q

Triptans are useful in treating which aspects of migraines?

A

Symptoms related to the Trigeminovascular system

356
Q

What is useful in treating the sensitization aspect of migraines?

A

NSAIDS (incl. Vasodilation caused by the trigem)

Acetaminophen

357
Q

What is the spreading cortical depression of migraines and which symptoms does it cause?

A

Self-propagating wave of neuronal and glial depolarization hypothesized to:

  1. Cause the aura of migraines
  2. Activate trigeminal afferents
  3. Alter BBB permeability via changes in metalloproteinases
358
Q

Pathophysiology of migraine?

A

Trigeminal neurovascular activation
Release of vasoactive peptides
Neuroinflammation (incl. PG release), vasodilation of pial and dural vessels
Moderate to severe pain

359
Q

What are triptans?

A

Triptan-ergot alkaloid (ergotamine, Dihydroergotamine)

Seratonin receptor agonist

360
Q

Side effect of dihydroergotamine?

A

Blanching, cyanosis, parestesia (tingling)

Other triptans - just paratesis

361
Q

Why aren’t Ergot Alkaloids a first line treatment?

A

Because they have some significant AE’s including vascular occlusion and gangrene (mediated bia alpha 1 adrenergic vasoconstriction)
Sever peripheral ischemia when used with a non-selective b1/b2 blocker

362
Q

How many migraines meet the definition of chronic migraines vs. episodic?

A

Chronic - at least 15 a month

363
Q

Which treatment is effective for Chronic migraines BUT is not recommended for episodic?

A

Botox

364
Q

If a patient has menstrual migraines, recommend?

A

NSAIDs

365
Q

If a patient has migraines with a comorbidity of HTN, angina, anxiety recommend?

A

Beta blockers

CCB’s

366
Q

If a patient has migraines with a comorbidity of depression or insomnia recommend?

A

TCADs

367
Q

In chronic pain syndrome, which neurotransmitter should you try to block?

A

Norepinepherine

368
Q

If a patient has migraines with a comorbidity of seizure disorder of bipolar recommend?

A

Anticonvulsants
If those are ineffective - Beta andrenergic antagonist
If that is ineffective - Botox

369
Q

Valproate and topiramate are?

A

Anticonvulsants

370
Q

Role of Botox in migraine control?

A

inhibits realease of ACh at the neuromuscular junction. Helps the scalp to relax and provide relief

371
Q

Mechanism of methysergide?

A

Serotonin receptor antagonist
Blocks serotonin mediated vasoconstriction
Does have a role in refractory migraine

372
Q

A radiculopathy cuses damage to?

A

The nerve root

373
Q

The cona equina begans at which vertebral level?

A

L1 (ie blow the conus)

374
Q

Symptoms and signs of myelopathy (spinal cord) and radiculopathy (nerve root)

A 
Pain (lermittes - myelopathy; Spurling's sign - nerve root;  lasegue's sign - siatic n. or contributing root)
Parethesia (ABN sensation)
Sensory loss 
Weakness
Disorders of bowel, bladder, sexual
Gait problems
375
Q

hypo or hyperesthesia, or anesthesia

A

decreased or excessive sensation

Or loss of sensation

376
Q

What is parathesia?

A

Numbness, tingling, burning sensations

377
Q

What is dysestesia

A

Same as parathesia but more unpleasant

378
Q

What is paresis?

A

Decreased strength

379
Q

What is plegia?

A

Complete loss of strength

380
Q

Above T1 the cervical root exits the spinal column ________ it’s corresponding vertebrae

A

Above

C1 over C1

381
Q

_____ passes directly above T1

A

C8

382
Q

After T1 the nerve roots pass -_________ their corresponding vertebrae

A

below

383
Q

There are how many cervical nerves? And how many cervical vertebrae?

A

C 1-8 nerve roots

C 1-7 vertebrae

384
Q

Where is the major radicular a. (Adamkiewicz)?

A

Generally Left side around T9 or T12

385
Q

As a general rule, in the spinal column the sacral fibers are _________ and the Cervical fibers are __________

A

Scaral is lateral

Cervical fibers are emdial

386
Q

Seconsory territory of C5?

A

Lateral aspect of upper arm (biceps)

387
Q

Sensory territory of C6?

A

Lateral aspect of forearm

388
Q

Sensory territory of C7?

A

The middle finger

389
Q

Sensory territory of L4

A

Knee cap

390
Q

Sensory territory of L5?

A

Plantar aspect of foot

391
Q

Sensory territory of s1?

A

The heel

392
Q

When the L4 intervertebral disc herniates would it impinge the L4 nerve?

A

No. The L5. The exiting nerve hugs the pedicle, so a herniated disc is more likely to damage the next traversing nerve

393
Q

Sympathetic inn of the bladder comes from the?

A

hypergastric n. (T10-L2)

394
Q

Parasympathetic inn of the bladder comes from the?

A

Pelvic n. (detrussor)
Pudendal n. ( urethral spinchter)
S2-S4

395
Q

Older case with difficulty walking, finds improvement in pain with sitting and leaning forward

A

Spinal stenosis (leaning forward relieves pressure on the nerves

396
Q

What is neurological claudication?

A 
Provoked by standing
Sensory symptoms
Normal pulses
Relieved by sitting (more positional)
Worsens with down hills
397
Q

What are the signs of vascular claudication?

A 
Provoked by exercise
No sensory symptoms
Decreased pulses
Relieved by rest
Worse with uphills
398
Q

What defines cauda equina syndrome?

A 
Outside in (pain early, urinary dysfunction late)
Early root pain, radiating down legs
Leg weakness, decreased DTRs (LMN)
Patchy, asymetric "saddle"
Late bladder, bowel, sexual dysfunction
399
Q

What defines conus medullaris syndrome?

A 
Inside out (urinary/bowel dysfunction early, pain late)
Late pain in thigh and butt
Pelvic floor muscle weakness
Symmetric "saddle" anesthesia
Early bladder, bowel, sexual dysfunction
400
Q

How can you determine if a patient has exited spinal shock

A

bulbocavernous reflex

401
Q

Characteristics of toxic disorders?

A

Acquired
Most don’t have a morphologic
Endocrine disorders, pH, electrolytes, renal failure, heavy metals

402
Q

What are the 3 common acquired metabolic disorders without specific morphology?

A 
Hypoglycemia - similar to anoxia except Purkinje cells are spared
Hyperthermia - Similar to anoxia
Hypothermia
Diabetes - DKA -> cerebral edems
Addisons
Thyroid dz
Pancreatic encephalopathy
403
Q

What is a neurotoxin?

A

Affect neurons, axons, myelin, blood vessels.

404
Q

What effect does alcohol on the brain?

A

Putamin hemorrhage (methanol)
Cerebral edema
Chronic effects - cerebellar degeneration (loss of purkinje), cerebral atrophy (esp white matter), can see fibrosis

405
Q

Describe fetal alcohol syndrome

A

hyperactivity, poor motor skills, learning difficulties, retardation
craniofacial features

406
Q

Neurological effect of liver disease

A

increased ICP due to liver failure
hepatic encephalopathy - elevated ammonia (>200)
In liver failure ammonia is converted to urea

407
Q

What is a secondary source of ammonia?

A

Catabolism of proteins by urease containing bacteria in the colon (can be an issue in GI bleeds). Restrict proteins and place on antibiotics

408
Q

What are the signs of hepatic enchephalopathy?

A

Global confusion
Edema
Asterixis (press on the hand and it vibrates)
Ammonia crosses BBB but it is taken up by astrocytes.

409
Q

What do astrocytes do with ammonia?

A

Ammonia is a substrate for glutamine synthesis which can be overwhelmed with too much ammonia

410
Q

What is chronic hepatic encephalopathy?

A

Irreversible neurological damage due to live failure
Alzheimer II astrocytes ( no connection to AD)
See brain damage in deeper cortical layer and putamen
Chronic acquired non-wilsonian hepatocerebral degeneration

411
Q

What is wilson’s disease?

A

Genetic

liver cirrhosis due to copper toxicity. Jaundice ~ 12 years old presenting with movement disorders

412
Q

What is the effect of protein-caloric malnutrition?

A

kwashiorkor with edema due to hypoproteinemia, ascites, hepatomegaly, hepatic steatosis (fatty)
Brain show loss of volume
If nutrition is restored the child can have normal neurologic development

413
Q

What are 3 vitamin deficiencies?

A

vitamin B1 (Wernicke’s)
Vitamin B12
Vitamin E

414
Q

Vitamin B1 deficiency

A

Thiamine
Wernicke - Korsakoff
Alcoholics, hyperemesis (frequent vomiting)
Ocular motility - nystagmus, ataxia, confusion

415
Q

What is the morphology of Wernicke’s encephalopathy?

A

Mamillary body involvement (hemorrhage, fibrosis, necrosis)

416
Q

How does thiamine deficiency lead to brain damage?

A

low alpha-KGDH activity -> cytotoxic edema, increases astrocyte volume -> increases NO synthesis -> vasogenic edema, lose BBB -> neuronal necrosis

417
Q

What is B12

A

Cobalamin
B12 is in meat and dairy products
B12 binds to intrinsic factor in the illeum for absorption
Issue for vegans

418
Q

Where is intrinsic factor from?

A

parietal cells

419
Q

What is B12 deficiency

A

incorporation of ABN fatty acids into biological membranes -> myelin instability
DNA sysnthesis problems
NO abuse mimics this

420
Q

Does B12 always present the same way?

A

No some are more neurologic (spinal cord), others are more hemologic

421
Q

What is subacute combined degeneration?

A

Vitamin B12 deficiency of the spinal column
Early - lower limb parasthesia, loss of vibration sense
Late - paralysis, sensory deficits
Combined because it affects ascending and descending pathways
If untreated it is permanent

422
Q

What is vitamin E?

A

anti-oxidant

423
Q

What is vitamin E deficiency?

A

Intestinal absorption defect
peripheral neuropathy, ataxio, retinopathy, myopathy
Loss of dorsal root nerve cell
Axonal spheroids in lower medulla

424
Q

What does iatrogenic mean?

A

Damage caused by Radiation therapy

Damages myelin, kills blood vessels (even atherosclerosis)

425
Q

What is central pontine myelinolysis (CPM)?

A

When chronically hyponatremic patients have their sodium rapidly corrected. Ventral pons is vulneralbe due to rich mixture of gray and white mater -> pseudobulbar palsy and quadrapalegia, also can cause locked in syndrome

426
Q

What is locked in syndrome?

A

Can’t move, but you’re conscious. Can move eyes

427
Q

Can you treat CPM?

A

Slowly correct hyponatremia

Can use steroids and organic osmolytes

428
Q

Which demographics have the highest rates of bacterial meningitis?

A

Neonates (number of cases has decreased due to Hib vaccine)

Geriatric

429
Q

Most common causes of meningitis?

A

Pneumococcal meningitis

Meningococal mingitis

430
Q

Meningitis infections occur where in the CNS?

A

subarachnoid space

Inflammation in the cortical tissue causes confussion

431
Q

Pathogenesis of bacterial meningitis

A

Bloodstream
Adjactent intracranial infection (sinusitis, mastoiditis, otitis)
Skull/ spinal defects (congenital, trauma)

432
Q

Subarachnoid space inflammation causes?

A

Increased BBB permeability
infarction from vasculitis
Interferes with CSF circulation
products of pre-inflammatory cytokines

433
Q

Clinical features of bacterial meningitis

A

Classic Triad: stiff neck, fever, altered consciousness

Also headache, seuzures, CN palsies

434
Q

Why is bacterial meningitis an emergency?

A

~20% mortality

Start antibiotics within 60 minutes of walking through the door of the ER

435
Q

What is the work up for meningitis?

A

Blood culture
LP
Empiric antibiotics + corticosteroids

436
Q

what results would make you suspect meningitis from LP?

A 
Opening pressure 200-500
CSF pleocytosis
neutrophil/PMN > 80%
low glucose
high protein
437
Q

Get imaging prior to LP if patient has what?

A

Focal deficits/AOC
Signs of ICP (papilloedema)
Suspected CNS lesion
However, before the imaging do the blood culture and start antibiotics and corticosteroids

438
Q

What are the typical causative organisms for meningitis in the neonate (

A

Group B step (50%)
E. coli (14%)
Streptococcus pneumoniae (pneumococcus) (9%)
Neisseria (meningococcus) (8%)

439
Q

What are the typical causative organisms for meningitis in the infant (2-23 months)

A

Group B strep
E. Coli
H. Influenzae

440
Q

What are the typical causative organisms for meningitis in the 2-35 years

A

Neisseria (meningococcus)

Streptococcus (pneumococcus)

441
Q

What are the typical causative organisms for meningitis > 35

A

pneumococcus
meningococcus
Listeria

442
Q

What do you start neonates on if you suspect meningitis?

A

ampicillin

443
Q

What do you start >2mo and adults on if you suspect meningitis?

A

Ceftriaxone and Vancomyocin

444
Q

What do you start Adults > 50 on if you suspect meningitis?

A

Ceftriaxone, Vanco, and Ampicillin

445
Q

If you start antibiotics, how long do you have to collect CSF and still be sensitive for cultures?

A

About 4 hours

446
Q

What do you administer for corticosteroid therapy in meningitis?

A

Start Dexamethasone prior to antibiotics

447
Q

What are some complications in meningitis

A

Decline in consciousness - meningoencephalitis
Cranial nerve palsy (VIII)
Subdural empyema

448
Q

When do you repeat LPs in meningitis?

A

No response after 48 hours
Penicillin resistant pneumococcus
When GNR is the causative agent

449
Q

what is viral meningitis and encephalitis?

A

Acute, febrile illness with headache
Stiff neck
Altered mental status, focal deficits

450
Q

Most common causes of viral meningitis?

A

Enteroviruses

Herpesviruses (HSV2 in adults)

451
Q

Most common cause of viral enchephalitis?

A

West Nile Virus

Herpes ( HSV1)

452
Q

Profile of labs with viral meningitis?

A

Lymphocytic pleocytosis
Normal glucose, protein
PCR +
CSF positive for IG’s

453
Q

Clues of enterovirus?

A

Rash, GI symptoms, myocarditis

Herpangina (throat lesions) - coxsacie virus

454
Q

HSV meningitis prognosis?

A

Good

455
Q

HSV encephalitis prognosis?

A

Bad

456
Q

What is encephalitis?

A

Inflammation of the brain paranchyma (grey matter)

457
Q

What is autoimmune encephalitis?

A

anti-NMDA receptor - psych symptoms with an ecephalitis CSF profile. Immunesuppress

458
Q

Which CN does HSV travel along?

A

CNI

459
Q

How do you treat herpes virus encephalitis?

A

Acyclovir

460
Q

West nile viruses natural reservoir?

A

Mosquitos and birds

People and horses are accidental infections

461
Q

WNV human infection is considered an iceberg. Why?

A

80% asymptomatic

20% febrile fever

462
Q

symptoms of WNV meningoencephalitis?

A

Fever headache stiff neck, GI complaints
Low back pain
tremor (parkinsonism)
myoclonus, flaccid paralysis similar to polio

463
Q

WNV neuroimaging

A

MRI often normal early

Can see some grey mater (basal ganglis, thalamus) ABN late (subtle)

464
Q

HSV on neuroimaging

A

Temporal lobe lesions on MRI

465
Q

Is PCR effective testing for WNV?

A

No, the viremia drops before the patient is symptomatic, but you do see peaks in IgM and IgG. So, if you do an LP and it is positive for IgM (too big to cross BBB) that is diagnostic of WNV infection

466
Q

CSF in WNV

A

Pleocytosis > 2000 cells
PMNs predominant
Reactive lymphocytosis
Elevated protein

467
Q

Most common cause of sporadic encephalitis?

Epidemic encephalitis?

A

sporadic - Herpes

Epidemic - west nile

468
Q

When a patient has a headache, what is hurting?

A

Meninges
Blood vessels (can be lethal)
Dermis
Other Head or neck structures

469
Q

Headaches are generally transmitted through which nerves?

A

Trigeminal (CNV)

C2-4

470
Q

What are the 2 main classes of headaches?

A

Primary - no underlying pathology

Secondary - underlying pathology (10%)

471
Q

What are the 3 types of primary headaches?

A

Migraine
Tension type headache (90%)
Trigeminal autonomic cephalagias

472
Q

What are the 2 types of secondary headaches

A

Vasuclar disorders

Increased ICP

473
Q

What is a cranial neuralgia?

A

Trigeminal Neuralgia

474
Q

What are the criteria for migraine?

A

5 episodes (3 hours - 3 days)
2 of : unilateral, pulsating, moderate or severe, increases with physical activity
1 of: nausea vomtiting photo & phonophobia
No other explanation

475
Q

How is a migraine brain different?

A

Reacts to light and sound causing a “storm”

476
Q

How do you treat migraines?

A
  1. ASA, acetaminophen, NSAIDs
  2. ibuprofen/caffeine/ASA
  3. Triptans - seratonin agonist
  4. Ergotamine derivative (nonselective sertonin agonist)
477
Q

What can you use to prophylactically treat migraines?

A

Beta Blockers
CCB
Tricyclic antidepressants
Anti-epileptics

478
Q

What are some alternative treatments for migraines?

A

sleep
biofeedback
acupuncture
OTC/herbals (vitamin b2, magnesium, butterbur)

479
Q

What are the criteria for tension-type headache

A 
10 episodes
30m - 7days
2 of: pressing or tightening, mild - moderate, bilateral, not aggravated by PA
Nausea or vomiting
photophobia or phonophobia
480
Q

How do you treat tension type headache?

A

ASA, acetaminophen NSAID

481
Q

How do you prophylactic treat tension type headache?

A

Tricyclic antidepressants
CBT, PT
SSRIs

482
Q

What is a cluster headache?

A

5 episodes
Severe, unilateral, periorbital and/or temporal (15 - 180m)
1 every other day or 8x/day
1 of: red eye, lacrimation, congestion, rinorrhema, facial edema

483
Q

What are the triggers of cluster headache?

A

Alcohol
Vasodialters
men: women 4:1

484
Q

What is the treatment for cluster headache?

A

oxygen, triptan inj, ergots
preventative - CCB, Lithium, Antiepileptics
Can try steroids and nerve blockers during the transitional period

485
Q

What is trigeminal neuralgia

A
486
Q

Red flag for worrisome headaches?

A 
SNOOP
Systemic symptoms (fever, weight loss)
Neurologic symptoms (confusion, LOC)
Onset 
Older
Previous headache history
487
Q

Most common cause of sudden intense incapacitating HA?

A

Subarachnoid hemorrhage

488
Q

What is giant cell arteritis/temporal arteritis?

A

Inflammation of vessel wall
> 60 years
Jaw claudication, vision loss, joint pain

489
Q

How do you test for giant cell arteritis in the lab?

A

ESR
CRP
Biopsy temporal a.

490
Q

How do you treat giant cell arteritis?

A

Glucocorticoids

491
Q

What are the symptoms of elevated ICP?

A 
Exertional headache
Retrobulbar pain
Nausea/vomiting
Pulsatile intracranial noises
Transient visual obscuration
Photopsia
Diplopia
Vision loss
492
Q

Causes of ICP?

A 
Tumor
AVM
Infection
Subarachnoid hemorrhage
Intercerebral hemorrhage
DVT
Minocycline (acne)
Trauma
493
Q

How can you see pseudotumor cerebri?

A

Elevated ICP
Normal neuro exam except papilledema and CNVI
Obese women

494
Q

What are the sources of opiods?

A

Plants (poppies)

Endogenous (enkephalins, endorphins, Dynorphin, endomorphins)

495
Q

What are enkephalins?

A

Peptids acting as neurotransmiters
Small peptides so quickly broken down by peptidases
Tyr-Gly-Gly-Phe
Glycines are kinky

496
Q

What are endorphins?

A

Act as neurotransmitters and neurohormones
Peptide (beta form most active)
found in hypothalmic neurons and pituitary

497
Q

What is dynorpin?

A

Peptied, dynorphin A most active. Not well understood but k selective

498
Q

What are endomorphins?

A

peptide not well understood but mu receptor selecting

499
Q

What is naloxone?

A

Can antagonize enkephalin, endorphin, and dynorphin

500
Q

What are the 3 classes of opioid receptors?

A

mu
delta
kappa
all are Gi or Go coupled

501
Q

What is the main cause of opiod overdose?

A

Respiratory depression. Drugs specific against delta would protect from these accidental deaths

502
Q

When an opioid binds a receptor, what happens?

A

decreases neuronal excitability -> inhibits presynaptic VSCC -> inhibits neurotransmitter release
Can also open K+ channels (GIRK) to hyperpolarize the cell
inhibits cAMP synthesis

503
Q

How do opioids inhibit transmission in pain pathways?

A

Inhibition of ascending pain pathway (synapse at 2nd order neuron in the dorsal horn is a major site of regulation)
Activation of descending pathway mediated by seratonin and norepinephrine

504
Q

Opioids also reduce the subjective response to pain, meaning?

A

Induce tranquility, euphoria

Patient can feel pain but the effect is lessened

505
Q

Opioids are best at preventing what type of pain?

A

2nd pain - the dull constant pain
Nociceptive pain
Less effective on neurogenic/neuropathic pain
Can be combined with an antipyretic (Vicodin)

506
Q

Typical uses of opioids?

A

pasin associated with malignancy
post-operative
patient-controlled analgesia
Cough (low doses)

507
Q

What are the behavioral effects of opioids?

A

euphoria (abuse potential) - mu receptor
Dyphoria (hallucinations) - kappa receptor; “spice” (salvinorin A) is a kappa agonist
Sedation, lethargy
Behavioral excitation (sign of toxicity) - caused by metabolites

508
Q

Dangerous side effect of opioids?

A

Respiratory depression
Even at analgesic doses there is respiratory depression
Due to a decrease in CO2 sensitivity in the brain stem

509
Q

Other side effects of opioids?

A

Nausea/vomiting (but this response can be surpresed in overdose)
Cough suppression
Miosis (pinpoint pupils)
Constipation

510
Q

The dorsal ganglia transmits pain and temperature stimuli from the?

A

Trunk and limbs

511
Q

The trigeminal ganglia transmits pain and temperature stimuli from the?

A

Head and neck

512
Q

First order neurons are?

A

Peripheral

513
Q

Second order neurons are?

A

The CNS neurons receiving information from the periphery

514
Q

what is the purpose of the spinothalmic tracts?

A

Provide an animal with a conscious sense of of temperature

515
Q

What is the spinothalmic tract for temperature from the trunk and limbs?

A

DRG neurons -> first synapse in the dorsal horn of the spinal cord -> thalamus -> somatosensory cortex

516
Q

What is the spinothalmic tract for temperature from the head and neck?

A

Trigem neurons -> first synapse in the spinal trigeminal nucleus -> thalamus -> somatosensory cortex

517
Q

What is the spinoreticular tract

A

relays reticular information to the hypothalmus. Important for the control of body temperature (autonomic function)

518
Q

What is the anterolateral system?

A

Refers to the axons of the dorsal horn’s second order neurons that cross the midline
Includes the spinothalmic, spinoreticular, and spinomesencephalic tracts

519
Q

On which side do the pain and temperature information ascend?

A

Contralaterally through the anterolateral system in the spinal cord

520
Q

How are pain stimuli from the limbs and trunk relayed to the CNS?

A
  1. spinothalmic tract -> pain to the ventrobasal thalamus (incl VPL). Info is processed and projected to somatosensory cortex
  2. Spinoreticular tract - elicits arousal, emotional response (limbic system, cingulate gyrus) in the forebrain
  3. Spinomesencephalic tract -> transmits to the midbrain periawueductal gray region (PAG) to regulate the descending control of pain
521
Q

How is pain from the head and neck relayed to the CNS?

A

Trigeminal system -> pain from head/neck in trigeminal ganglion -> enter CNS at pons -> first synapse at spinal trigeminal neucles (analogous to dorsal horn for the lower half of the body)

522
Q

What are thermal nociceptors?

A

Detect extremes in temperature

43C - alpha delta

523
Q

What are mechanical nociceptors?

A

Sense intense pressure

alpha delta

524
Q

What are polymodal receptors?

A

Detect high-intensity mechanical, chemical, or thermal stimuli
C fibers

525
Q

What is VR-1?

A

Activated by capsaicin (strong) or acids (weak). When activated opens non-selective cation channels -> depolarization

526
Q

Which pain sensations are carried by C fibers?

A 
Polymodal nociceptors
Thermal nociceptors (cold)
Capsaicain can be used as a long term analgesic against C fibers because it depletes substance P
527
Q

IN the periphery, pain and temperature can be carried on which two afferent fibers

A

Either A delta or Ctype

Both are slower than alpha alpha and alpha beta

528
Q

Describe the characteristics of alpha delta afferent fibers

A 
Lightly myelinated (faster than C type).  Therefore, a delta senses first pain, because this will reach the CNS first "pricking pain"
Smaller receptive field (easier to localize where the pain is)
529
Q

Describe the characteristics of C type afferent fibers

A 
no myelination (slower than adelta). Therefore C fibers detect second pain, because they travel slower. "burning diffuse pain"
Larger receptive field
530
Q

alpha alpha and alpha beta are associated with which sensory information

A

mechnosensory and proprioceptive receptors

531
Q

How does pressure (like a bp cuff) affect the peripheral nerves (ie. in which order would they become non conductive)?

A

the anoxia will affect the most metabolically active nerves first.

  1. alpha alpha, alpha beta become nonconductive first (lose sense of touch/vibraition)
  2. alpha delta - only able to sense burning pain
  3. C
532
Q

How does electrical stimulus affect the peripheral nerves (ie. in which order would they become conductive)?

A
  1. alpha alpha, alpha beta - higher sensations of touch
  2. alpha delta - feel pricking pain
  3. C fibers - burn (need high intensity AND repetitive stimulation, subP)
533
Q

So, in what order do anesthetics aim to block afferent pain fibers?

A
  1. C fibers - block burning pain
  2. Alpha delta fibers - block pin prick
  3. a/a, a/b - very high doses, numbing and paralysis
534
Q

Which chemicals are activators of nociception?

A

Bradykinin (a/d, and C)
K+
Acid - ASICS, VR-1
Serotonin

535
Q

What chemicals act as sensitizers of nociception?

A

Prostaglandins
Substance P
ATP, ACh, Serotonin
Decreases the threshold for activation

536
Q

Sensitization of nociception is known as?

A

Primary hyperalgesia

Extreme cases can be allodynia

537
Q

What is the analgesic action of aspirin?

A

cyclooxygenase inhibitor. Blocks conversion of arachidonic acid to protsglandin. By blocking this aspirin prevents nociceptor sensitization

538
Q

What is the triple response?

A

Reddening, wheel, flare
Bradykinin - vasodilator (reddening), increased capillary permeability (edema, wheel). Also activates C fiber producing bidirectional APs, invade collateral terminals and stimulate subP release.
subP - milder vasodilation (flare) “axon reflex”

539
Q

What is substance P?

A

Binds NK1
Classic sensitizer, reducing the AP threshold in nociceptors and collaterals. Can cause hypergesia and allodynia. Encourages behavioral changes to not touch the wound.

540
Q

What is the basis for central sensitization (at the dorasal horn)

A

“wind up”
C fibers can either activate AMPA or AMPA + NMDA depending on the intensity of the of the stimulation.
NMDA is essential for sensitization

541
Q

Where do C fibers synapse in the dorsal horn?

A

Rexed’s lamina II (substantia gelatinosa)

a/d sympase at Lamina I

542
Q

What is referred pain?

A

Convergence of visceral and somatic pain inputs. Somatic pain dominates

543
Q

What are the 2 types of glutamate receptors in the dorsal horn?

A

AMPA - rapid synaptic responses
NMDA - slower
Both ionotropic, allows fast and slow excitatory responses

544
Q

What is the role of AMPA in the dorsal horn?

A

AMPA - rapid synaptic responses, needs only glutamate

C fiber -> activate AMPA

545
Q

What is the role of NMDA in the dorsal horn?

A

NMDA - slower excitatory potential, need glutamate and depolarization
C fibers -> activate NMDA when the simulattion is intese and persistent. Allows for intensification of post-synaptic response
This activation triggers a biochemical cascade of long-lasting changes of excitability (ie. NMDA becomes phosphorylated by PKC - now only needs glutamate to be activated)

546
Q

How does SubP affect central sensitization?

A

Released during intense stimulation at the first synapse.
Binds NK1 -> K+ channels close -> depolarization
Causes enhancement and prolongation of glutamate actions
Note: subP is not terminated for reuptake. Causes it to diffuse to many dorsal horn neurons leading to broad central desinsitization

547
Q

How does PAG in the spinomesenphalic tract modulate pain

A

ONly attenuates pain
PAG nuerons project to raphe magnus (medulla) -> medulla is serotonergic, projects to spinal cord vis dorsal lateral funiculus -> in SC 5HT inhibits 2nd order neurons of the dorsal horn by activating enkaphalin inhibitory inerneuron

548
Q

How do enkaphalin inhibitory neurons inhibit 2nd order neurons in the dorsal horn?

A
  1. pre synaptically - Block voltage gated Ca2+ channels
  2. Post synaptically - open K+ channels
    This is why SSRI’s are sometimes used to treat chronic pain disorders
549
Q

How do opiates work in the anterolateral system?

A

Seem to excite PAG
Inhibit transmission in the dorsal horn
Note: Naloxone inhibits PAG

550
Q

What are the 3 endogenous opiates?

A

“endorphins”
enkephalins
Beta-endorphin
dynorphins

551
Q

What is stess-induced analgesia?

A

Stress -> increased limbic activity -> PAG activation -> 2nd order neurons in the dorsal horn are inhibited.
Naloxone can block some but not all of this analgesia suggesting there are opiod and non-opiod components of stress-induced analgesia

552
Q

What is the placebo effect?

A

Naloxone can block the placebo effect.

cognitive activation of limbic system -> secrete endorphins -> PAG activation -> 2nd order inhibition

553
Q

What is neuropathic pain?

A

Peripheral or centeral nervous system damage that can lead to persistent pain syndromes

554
Q

What is the mechanism of peripheral neuropathic pain?

A

TTX resistant channels play a predominant role. Higher expression of ca2+ channels following damage.

555
Q

What is the mechanism of central neuropathic pain?

A

Reduction of GABA -> reduction of dorsal horn inhibition

556
Q

Free nerve endings carry what information?

A

A delta - pricking 1st pain

C - dull 2nd pain

557
Q

Meissner’s corpuscles carry?

A

Small receptor field

fine touch

558
Q

Pacinian corpuscels carry?

A

Pressure and vibration

559
Q

Markes disc sneses?

A

Static touch and position

560
Q

Ruffini ending sense?

A

Sustained pressure and stretch

Neuro (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions