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CCP Semester 2 > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the difference between an upper and a lower motor neuron?

A

Upper motor neurons represent central nervous system motor neurons (spinal cord and higher) while lower motor neurons represent the peripheral nerves outside the spinal cord and the muscle they innervate

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2
Q

What is grey matter and what does it do?

A

Grey matter (cerebral cortex) is the portion of the cerebrum in which all the meaningful things in life are processed. It is capable of “original thought” and it contains lots of nuclei of neural cells in order to create these important functions.

Grey matter is located above white matter

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3
Q

Why is white matter white?

A

Because it is mielenated meaning it can transmit impulses fast from grey matter tissue.

It is located beneath the cerebral cortex

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4
Q

What is the purpose of the basal ganglia? Why are they susceptible to hypoxic injury?

A

Basal ganglia provide fluidity of movement, and breakdown of these is what leads to conditions like parkinson’s.

They are susceptible to hypoxic injury because they are at the distal ends of the blood vessels.

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5
Q

What is the purpose of the thalamus?

A

Deep subcorticol grey matter than provide a relay point between cerebral cortex and the brainstem (the AV node of the brain).

Susceptible to global hypoxic injury because it is at the distal end of the brain perfusion

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6
Q

Why is the cortex susceptible to hypoxia?

A

High metabolic activity with no backup energy source

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7
Q

What it the purpose of the frontal lobes?

A

Appropriateness, executive functions,

Can function without one frontal lobe!

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8
Q

What portion of vision does the right occipital lobe control?

A

Left half of left eye and left half of right eye

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9
Q

What is the function of the temporal lobe?

A

Memory

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10
Q

What is the function of the parietal lobe?

A

Sensation, movement, Speech (understanding and producing)

Most important lobe

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11
Q

What side of the parietal lobe does speech understanding and production occur?

A

99% of people left side parietal lobe

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12
Q

What part of the cortex is upper body, legs and face?

A

Face is lateral cortex, upper body/hand is middle and medial is foot/leg

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13
Q

What is the internal capsule?

A

Bundle of fibers that come from cortex and go down to the spinal cord

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14
Q

Why does the right side of brain control left side of body for sensation and movement?

A

Because the internal capsule crosses over just above the midbrain meaning homunculus functions are for the contralateral side

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15
Q

What is the function of the brainstem?

A

1) Relays everything
2) Unconscious part of body (breathing while sleeping)
3) Houses 10 of 12 cranial nerves

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16
Q

Which cranial nerves cross over?

A

7 and 8

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17
Q

What is function of respiratory center?

A

Senses CO2 and triggers unconscious breathing

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18
Q

What does the pupillary constriction test tell you about brainstem?

A

CN II senses the light, CN III constricts the pupil and you know that the majority of the brainstem is intact

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19
Q

How do we test the brainstem reflexes in an intubated patient?

A 
Pupil constriction reflex (II, III)
Cornea reflex (V, VII)
Cough Gag (IX, X)
Respiratory effort (Mode of ventilation, effort) (Respiratory center)
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20
Q

What is the purpose of RAS? Where is it located?

A

RAS is located in the midbrain, it tells the thalamus to wake up repeatedly (thalamus tells the cortex to wake up) and keep us conscious

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21
Q

Why do you get blown pupil on same side as pathology, while the deficits are detected on the other side during uncul herniation?

Is this an early or late sign?

A

Uncus pushing down on 3rd cranial nerve in the midbrain (which doens’t cross over) while the same compression of the midbrain affects motor neurons that cross over just below the midbrain

Early sign because as the herniation progresses, both unci push down on both sides of the midbrain

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22
Q

What is the uncus?

A

Bottom floor of the temporal lobe

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23
Q

What is the risk of sedating an infratentorial pathology?

A

Have to wait for neuro exam and during that delay more brain tissue is lost. DO NOT sedate infratentorial herniation

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24
Q

WHY do you put an infratentorial herniation patient on pressure support?

A

Because pressure support allows you to monitor their herniation syndrome and the respiratory center is impacted early in the course of the disease through tonsilar pressure

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25
Q

What are the components of the neuro exam?

A

Brainstem (PS or not, sedatives, open eyes, suction
GCS
“Other” - Tone, Reflexes

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26
Q

What is the point of everything we are doing in brain injury treatment?

A

Prevent secondary ischemic of hypoglycemic brain injury

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27
Q

What is the formula for the cerebral oxygen deman?

A

CBrDO2 = CBF * CaO2

CBF = CPP/CVR

CaO2 = [Hgb] * 1.34 * SaO2

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28
Q

What is the main determinant of CVR?

A

PaCO2 -

Every 1mm CO2 up -> BF changes by 1%
Every 1mm CO2 down -> BF decreases by 1%

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29
Q

What 4 methods can you use to reduce parenchyma in managing ICP?

A

Sedation - reduce metabolic demand
Temp control - reduce metabolic demand
Seizures - reduce neuronal metabolic demand
Osmotic therapy (Mannitol/HTS) - Redu

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30
Q

Should you use bolus dosing or infusion dosing for ICP?

A

Bolus to prevent brain from adapting

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31
Q

How can your reduce ICP with CSF reduction?

A

EVD is the only way

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32
Q

What are the 6 ways to reduce ICP with blood reduction?

A

Arterial -

1) normalize PaCO2

Venous - Faciliate venous drainage -

2) HOB,
3) Collar
4) ETT Ties loose
5) ACS
6) PEEP < 12

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33
Q

What are considerations in choosing between HTS and Mannitol?

A

HTS ideally through a central line (or IO) while Mannitol may cause large diuresis in transport that can be annoying to have to manage

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34
Q

What should your Hgb target be for brain injured patient?

A

Keep above 90

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35
Q

Why so we target a MAP of 80 in TBI?

A

Because we assume an ICP of 20 and this allows a CPP of at least 60

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36
Q

Why do we say MAP of 80 in brain injured patients?

A

Because we assume the autoregulatory curve has probably shifted to the right (normally 50 to 150 of MAP for autoregulation to manage CBF to normal levels).

Map of 80 keeps autoregulation in the assumed range

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37
Q

What is a traumatic brain injury?

A

It’s NOT a disease, but rather a syndrome

38
Q

Why are the upper targets systolic targets and the lower targets MAP targets in brain injury management?

A

You bleed in systole, while you perfuse in diastole! Reduce bleeding, and maintain perfusion in other words

39
Q

What do the PCAs perfuse?

What does the basilar perfuse?

What do the verts perfuse?

A

PCA - Occipital lobe

Basilar - midbrain/pons

Verts - medulla/cerebellum

40
Q

Why does a basilar artery infarct cause a drop attack?

A

Because the basilar artery supplies blood to the midbrain and pons and sudden insult to the ras in the midbrain and the motor fibers would cause a person to fall

Basilar artery stroke is only thing that causes spontaneous flacid paralysis and abnormal brainstem reflexes

41
Q

Where would the infarct be if the patient had face, arm and leg paralysis?

A

Either internal carotid or internal capsule

42
Q

What are the upper BP goals for ischemic stroke with either thrombolysis or non-thrombolysis

What are BP goals for TBI? (excluding epidural)

A

Thrombolized - max SBP 180
Not thrombolized - max SBP 220

TBI (not epidural) - 160

Epidural and ICH - 140

43
Q

Why do deep arteries bleed more in hemorrhagic stroke?

A

Not as tough as the MCA for example - branches of the MCA bleed more often

44
Q

Why are right sided MCA strokes usually cardioembolic?

A

Because the embolism travelled up the anterior circulation via the carotid (right sided) off the aortic arch as it was the first artery that it came across

45
Q

What is a clinical corelate with a C5 injury?

A

Deltoid

46
Q

What does the saying “have Bi’s, will fly” make sense?

A

Because biceps are supplied by nerves at the level of C6, meaning C5 and above are intact and the diaphragm is not impacted. This means this patients has full diaphgramatic control and does not likely need to be intubated.

47
Q

What are 5 things to look for when deciding whether to intubate a spinal cord patient?

A

1) Nasal flaring
2) SCM use
3) Inability to use biceps
4) Normal PaCO2 with RR > 20
5) Paradoxical breathing

48
Q

What is potential impact of a SCI between T1 to T5?

A

Neurogenic shock

T1 to T5 are where the sympathetic nerves exit the spinal cord meaning unregulated parasympathetic activity would dominate.

Symptoms: bradycardia, decreased inotropy, and decreased preload from profound vasodiation (2 litres immediately!)

49
Q

What is the treatment for neurogenic shock?

A

Replace missing sympathetic stimulation

1) Dopamine!
2) Epi

50
Q

What two things should you evaluate when looking at a SCI patient?

A

1) Do they need intubation?

2) Are they in neurogenic shock?

51
Q

What is the MAP target for SCI and why?

A

85 - higher map to prevent expansion of SCI penumbra upwards causing a higher cord injury - cause signicantly reduct ASIA score

52
Q

What is the ASIA scoring system?

A

Used to quantify degree for SCI - A is worse than E

53
Q

Why should albumin be avoided in brain injured patients?

A

It can leech into brain causing increased edema

54
Q

Describe the creation and flow of CSF

A

CSF is created (20-30ml/hr) in the choroid plexus in the lateral ventricles. It flows through the interventricular foramina to the 3rd ventricle (which is at the level of the thalamus).

From the 3rd ventricle, CSF flows through the cerebral aqueduct to the 4th ventricle (level of the pons).

From the 4th ventricle CSF flows in the subarachnoid space around the cranium and into the spinal column

It is absorbed in the archnoid villi of the superior sagittal vein

55
Q

In order, what are the most common sites of aneurism formation and why?

A

MCA > ACA > PCA > Vertebral/basilar

MCA sees the MOST bloodflow of these systems and this contributes to the weakening over time

56
Q

What are 4 causes of SAH and which is most common?

A

1) Aneurism (most common - 85%)
2) Cocaine
3) AVM
4) Trauma

57
Q

How are SAH diagnosed?

A

1) Thunderclap headache (clinical)
2) Radiographic (CT very specific)
3) LP if not obvious on CT

58
Q

What are two scoring systems used to evaluate SAH?

A

1) Fisher (CT scoring)

2) WFNS (basically GCS)

59
Q

What is the tx for SAH?

A

Surgery - need coiling or clipping to “secure” the aneurism.

Keep SBP < 140 as bleeding occurs preferentially in systole.

If hydrocephalus, is it scoop and run - pt needs EVD

Map less important as its not an ICP problem.

TXA if Sx will be greater than 72 hours.

60
Q

What are 6 complications of SAH?

A

1) Re-bleeding
2) Seizures
3) Cardiogenic shock
4) Hydrocephalus
5) Vasospasm
6) Na disorders

61
Q

What causes cardiogenic shock in SAH? What do these patients die from?

A

Massive sympathetic surge from the insult causes apex to tire (farthest tissue from LAD perfusion)

They typically die from torsades as QT prolongs

62
Q

What is the difference between obstructive hydrocephalus and non-obstructive?

A

Obstructive hydrocephalus occurs WITHIN the cranium causing dilation of the ventricles.

63
Q

Why is nimodipine given in SAH?

A

Prophylaxis for vasospasm which is caused by a reduction in nitric oxide (blood scavenges it)

64
Q

When you should induce hypertension and provide milrinone for SAH?

A

After aneurism is secured in order to prevent vasospasm

65
Q

What are 3 sodium disorders associated with SAH, pathophysiology and treatments for each?

A

1) Diabetes insipidus - Dysfunctional hypothalamus produces no ADH, results in polyuria, hypernatremia from dehydration. Tx: DDAVP
2) SIADH - Dysfunctional hypothalamus producted TOO much ADH, results in anuria, hyponatremia from overhydration. Tx: HTS
3) Cerebral Salt Wasting - Increase in ANP/BNP causes hyponatremia AND polyuria… Tx: HTS and fludrocortisone which helps reabsorb Na in collecting ducts

66
Q

Describe GBS, MG, and Tx’s for both and distinguishing features

A

GBS - Infection leads to autoimmune antibodies attacking myelin on nerves (peripheral first) causing weakness and loss of sensation that evolves into weak diaphragm and ventilation issues. Tx: IVIG or Plex (plasmaphoresis)

MG - No infection, but antibodies attack nicotinic Ach receptors causing muscle weakness in muscles that are frequently used (face, eyes etc), but no loss of sensation. Tx: Steroid (reduce ABs), IVIG, Plex and Perisostigmine (Cholinesterase inhibitor)

67
Q

Why are steroids used in MG but not GBS?

A

Steroids also can cause demyelination which would worsen GBS, but not MG.

68
Q

Why is airway a bigger concern in MG versus GBS?

A

Facial weakness leads to poor secretion management

69
Q

Which disease is associated with 60% chance of thymoma?

A

MG

70
Q

Describe the layers of the meninges, which spaces are arterial/venous and what are the blood pressure goals with a hemorrhage in that space?

A

???? confirm this card

Epidural space - between skull and dura mater, arterial, sbp < 140

Dura mater

Subdural space - between dura and arachnoid, potential space, venous or arterial, sbp < 160

Arachnoid mater

Subarchnoid space - actual space between arachnoid and pia mater, arterial or venous, sbp < 140

Pia mater

Intraparenchymal hematoma/contusion, arterial , sbp < 140

71
Q

What are potential causes of bacterial meningitis? What are signs/symptoms (triad)

A

Infection of adjacent space (ear, dental) or bacteremia from pneumonia etc

Triad: HA, LOC, Fever - need at least one of these thigns to potentially have it, if none of these things, you do not have meningtiis

72
Q

What are kernig and brudzinski’s signs?

A

Brudzinkski - flex neck -> hips and knees flex

Kernig - extend knee that is 90 degrees flexed, increased back pain

Both indicate meningeal irritation

73
Q

What would you expect to find with regards to WBC, Proteins and glucose in the CSF profile of meningitis?

A

High WBC, High protein (byproducts of inflammation), and low glucose (bacteria eating it)

74
Q

What are the 4 bacteria that cause bacterial meningitis, what is the most virulent and treatable, and what are the treatments?

A

Steptococcus Pneumonia
H. Flu
Neisseria
Listeria

Neisseria is most virulent and most treatable

Treatment is ceftrixaone and vancomycin for strept, h flu and neisseria

Ampicillan for listeria

75
Q

What are precautions for transporting meningitis?

A

If ABX is less than 24 hours

AND

Patient on Vent -> Airborne

Patient non on vent -> droplet

76
Q

Why might you see normal CSF with viral encephalitis?

A

Because in the inflammation is in the parenchyma and not in the subarachnoid space

77
Q

What triad of symptoms would you expect to see in virus encephalitis?

A

Fever, Headache and changes in LOC

78
Q

What viruses cause viral encephalitis?

A

Herpes Simplex, Vericella Zoster

79
Q

What is the treatment for viral encephalitis?

A

acyclovir

80
Q

Why are viral encephalitis patients transferred?

A

high incidence of status epilepticus as the inflammation of the temporal lobe is very epileptogenic

81
Q

What is meningoencephalitis?

A

When meningeal infection crosses the blood brain barrier and causes parenchymal inflammation

82
Q

Why do benzo’s work in status epilepticus?

A

Lots of GABA receptors early

83
Q

When should you avoid using phenytoin and why?

A

TCA OD because the Na channel blocking property of phenytoin will worsen TCA OD

84
Q

What are the first, second and third line options for status epilepticus?

A

1) Benzos
2) Phenytoin, Kepra, VPA
3) Infusions: Propofol, Midaz, Ketamine

Also consider ketamine

85
Q

When titrating propofol, what should you be concerned about with high doses and what can you consider as an alternative?

A

Propofol infusion syndrome - Doses over 80mg are risky. Consider switching to ketamine/midazolam combination

86
Q

Why is magnesium used as an epileptic agent in eclamptic seizures?

What target should you aim for in magnesium?

A

Non-toxic to fetus

Aim for magnesium level of 1

87
Q

What are causes of seizures? (DIMSS acronym)

A 
Drugs (non-compliance, or epileptogenic drugs)
Infection (CNS mostly)
Metabolic (Low NA, or Low Glucose)
Structural (Ca, etc)
Seizure disorders
88
Q

What is a teratoma coma?

A

Ovarian tumor that releases NMDA activating antibodies causing seizures - treat with sx and plex

89
Q

How long should you wait in between escalation of seizure medications?

A

Seizure clock:

0 minutes - Benzos
15 minutes - Phenytoin
30 minutes - Infusion: propofol, ketamine, midaz

90
Q

What causes hepatic encephalopathy? What are treatments? How are diagnosed?

A

In chronic or acute liver failure, excessive protein load caused by stagnant bowel or GI bleeds causes a buildup of NH3 to form.

NH3 which is very lipid soluble travels in bloodstream to brain causing encephalopathy.

Treatment is lactulose (converts NH3 to NH4+) or rifaxamin (abx) that kills NH3 producing bacteria

Dx: Clinical, altered LOC with liver cirrhosis

91
Q

What is asterixis?

A

Push extended hands backwards (further extended). Result will be uncontrollable flapping forward motion.

Test for hepatic encepalopathy, renal encepalopathy or CO2 narcosis

92
Q

What are the components of the TBI checklist?

A

A - HOB 30
B - PaCO2 - 35-45, PO2 - 100-150, Peep 5-12
C - Map > 80, SBP < 160
Coag - INR < 1.5, PTT< 40, Platelets > 100, Fibrinogen > 1.0
D - Pupils, GCS, Motor
E - Temp 36-37.5
Labs - Na 140-150, Hemoglobin > 90
Herniation - Hypertonic, Mannitol, Hypervilation PaCO 25-30

CCP Semester 2 (9 decks)

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