Cardinal Chapter Neuro Flashcards

1
Q

What actually defines coma?

A

Not aware
Not awake
Does not respond to vigrous stimulation (an altered person should respond)

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2
Q

What are the two components of consciousness?

A

Arousal - subcortical (am i awake)
Awareness - cortical (do I know what is going on)

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3
Q

What causes the majority of cases of coma?

A

toxic and metabolite causes (not structural)

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4
Q

3 things that can cause pinpoint pupils that are not opioids?

A

Clonidine
Pontine stroke
Cholinergic medications

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5
Q

What is the thalamus?

A

Thalamus - sits deep in the brain. Sensory information comes into the body and then goes to the thalamus, which directs it to the apporpaite cortex. Also helps with sleep and wakefulness

If you are awake but not aware think of inturuption from the thalamus - because the things that give you an awareness of your body like sight and touch arent coming in, going to thalamus and then going to cortex.

Can also make you less awake becuase it helps with sleep and regulation.

Both this and basal ganglia are subcortical structures

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6
Q

What is the basal ganglia?

A

Basal ganglia are a group of nucleai in both hemispheres that control voluntary movement. (When these get knocked out you get movement disorders like Parkinsons). Also help with reward.

five pairs of nuclei: caudate nucleus, putamen, globus pallidus, subthalamic nucleus, and substantia nigra.

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7
Q

What is the FOUR score and its components? What makes it different from GCS?

A

Full Outline of UnResponsiveness Score

Eye response - more detailed inlcudes tracking
Motor - largely the same
Brainstem reflexes - pupils, cornea, cough/gag
Respiration - Intubated or not and breathing on own

(Each section is worth 4 points)

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8
Q

What do eye movements tell you about where you are worried the lesion is? (This is a rosens screenshot that is still confusing to me)

A
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9
Q

What CN can be tested in severe TBI?

A

Occulocephalic Dolls eyes - CN 3,6,8. If I tilt you head back and forth can you keep looking straight (CN and therefore brainstem needed to move eyes and sense that movement are okay)

Occulovestibular or cold caloric (better) CN 8 - head at 30 degrees, inject cold water into ear
Brainstem intact and awake - Look at cold water and nystagmus with fast phase away (brain = get back here), feel nauseaous, dizzy
Brainstem intact - Look at cold water
Brainstem impaired - no response

Corneal reflex - light touch wisp of cotton CN. then blink would be CN 7

Gag - palate lifts. Sensory CN 9, motor CN 10

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10
Q

3 causes of myoclonus?
3 causes of tremor?
2 causes of myoclonic jerks?

A

Myoclonus - SS, hepetic or renal failure, hypercarbia,NCSE

Parkinson, lithium, ETOH or benzo withdrawl

HypoK or HypoCa

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11
Q

2 things that can elevate ammonia?

A

Valoric acid
Inborn errors of metabolism

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12
Q

Methanol posioning and CO posioning on CT? What are two specific findings?

A

Methanol = putamen
Globus pallidus = CO

(remember both of these structures are in the basal ganglia, both these posioning have neurologic findings including coma)

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13
Q

How can you tell between a verbal response of 4 and 3? What about motor of 6, 5 or 4?

A

For verbal 4 is your are talking but you are just confused, 3 is you are only saying single wrong words and then 2 is just sounds like moans

For motor a perfect 6 is a two part command, 5 is moving hand across body or above clavicle, 4 for withdraw is to bend elbow in a way a normal person would, 3 is flexion which is bending but it looks abnormal (posturing in). Decerebrate is also assessed at the elbow.

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14
Q

How would you actually define confusion?

A

Impairment in high cerebral functions like memory, attention or awareness.
Always a symptoms not an underlying process.
Not to be confused with delirium which has specific criteria.

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15
Q

What do the letters stand for in AEIOUTIPS?

A
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16
Q

List 4 mimics or close but not the same differentials for acute confusion

A

Expressive or receptive aphasia (limited communication even though you know what is happening)
Frontal lobe - personality
Subcortical - decreased LOC
Post-ictal
Atypical migraine

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17
Q

What does aphasia suggest?

A

Lesion in dominent hemisphere (left for most R handed people)
This includes both receptive and expressive aphasia

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18
Q

Outline your approach to bCAM

A

Brief consciousness assessment method

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19
Q

Outline how to use the DTS

A

1 - assess if alert and calm
2 - ask them to spell lunch backwards
If both are normal = no delirium.
If either negative do the BCAM

Delirium triage screen.

Delirium triage screen. This is a highly sensitive test so you do this first. Then you do the bCAM which is more specific
Recall that RASS zero = alert and calm (above is agitated, below is sedated)

20
Q

Who does not get Haldol?

A

Parkinsons disease, increased risk of death
(Dopamine antagonist in someone who already does not have enough dopamine - going to not be able to move or stay awake and fall)

21
Q

What is the incidence of seizures in the general population? How many have another in two years?

A

10% and then 45% will have a recurance within the first two years

22
Q

Three risk factors that someone will have a recurrent seizure?

A

Known brain lesion
HIV
Nocturnal seizure
Neuroimaging or EEG abnormaltiies

23
Q

How long is a post ictal period?

A

Typically less than an hour
If generalized tonic-clonic, longer seizure, or older will also last longer

Post ictal period itself is caused by neuronal exaughstion or the medication you gave

24
Q

Why is that 5 minute mark in seizures so important? What is happening on a cellular level?

A

While you are seizing you have more excitatory or impaired inhibition leading to abnormal firing. It can be deep and cross midline.

The body tries to shut this off on its own by turning down AcH and glutamate (excitatory) and turning up GABA (inhibatory). Once you get over 5 minute mark these have failed = enter into status

In status the GABA receptor subunits go inside cells and excitaory NDMA receptors increase. When this happens refractory to benzos.

25
Q

What are the different thresholds for status based on the type of seizure? Why do these exsist?

A

Status defintion is based on liklihood seizure will continue, fail abortive mechanisms, long term conseuquences. This is different based on type (GTC is shorter than obsence or partial)

26
Q

What is the diencephalon?

A

Central part of the brain that contains the thalamus, hypothalamus and pineal gland

Called diencephalon because of where it comes from in embryology

27
Q

What are three main assocaited symptoms we see with seizures?

A

Motor onset or non motor onset based on what first symptom is
(motor = tonic, atonic, clong, myoclonic, mono-motor = absence, automatisms)

Sympathetic symptoms - tachycardia, HTN, tachypnea
Autnomic discharges - incontinence, tongue biting, vomitting

28
Q

What are automatisms?

A

oral or finger movements lip smacking or yawning. Typically front seizure focus

29
Q

What are cogntivie seizures and where do they come from?

A

Previously reffered to as “auras” - Impair a distinct domain:
Language with aphasia
Abnormal thought - hallucinations, deja vu
Olfactory hallucinations - “burnt toast, occipital frontal region)
Fear or auditoary hallucinations - temporal

30
Q

What are five general properties of ictal events?

A

Abrupt onset
Brief duration
Altered LOC
Purposeless sterotypic movements
Post ictal state

31
Q

What typically does not have a post ictal state?

A

absence

32
Q

What can decrease your seizure threshold?

A

illness, trauma
Drugs or etoh
Sleep deprivation
Drug drug intercations (started antibiotics)
Medication non compliance
Pregnancy

33
Q

What are two things a todds paralysis might signify?

A

Focal origin of event (only a focal section of neurons are burnt out)

OR

underlying structural lesion (ischemic or ICH)

34
Q

Who is higher risk of non-convulsive status?

A

acute or remote brain injury
previous craniotomy
Sepsis, renal, liver patients (think ICU)

35
Q

What can you get a level for?
What can raise ammonia?

A

carbamazipime, pheno
barbital, dilantin, valproic acid
Valproic acid

36
Q

What is an EEG good for?

A

Non-convulsive status
Guide third line seizure mangement
Differentiate seizure from not (pseudo)

37
Q

Differentiate seizure from migraine

A

Migraine slow onset, usually has a history

37
Q

4 things to do during a seizure and one things not to do?

A

Left lateral decubitus positioning, suction, get a glucose, put on oxygen

Dont futz with an oral airway - can lead to gagging, aspiration

37
Q

When should you consider calling neurosurgery for second agent?

A

Prior brain insults
Abnormal EEG
Imaging abnormality (not going to get better)
Noctural seizure
Worried about side effects

38
Q

Who can you send home after a first time seizure? Who can you not send home?

A

Normal exam
Normal CT head
No comorbidities
Good follow-up

Required multiple doses of benzos does not go home

38
Q

Risk factors for RCVS?

A

Epsiodic sudden onset pain
Reccurent episodes
Exposure to adrenergic or serotonergic drugs
Postpartum state

39
Q

What helps you with a headache? What doesnt really?

A

Thunderclap, exertional, trauma, stops when I leave the house

Intensity, location, characterization of pain, assocated symptoms (nausea)

40
Q

5 deadly causes of headache in a pregnant patient

A

Eclampsia
Pre-eclampsia
CVT
RCVS
IIH
Stroke
Pituitary apoplexy (bleeding into an organ or loss of blood flow to an organ)

41
Q

When do you think about medication overuse headache?

A

Taking medications more than 10-15 times per month (once underlying condition is ruled out)

42
Q

What are inclusion and exclusion criteria for SAH rule?

A

Inlcusion: patients >15 years, non traumatic, peak intensity within1 hour

Exclusion: No neuro deficit, prior aneursym, prior SAH, known intracranial mass, chronic recurrent headaches

43
Q

What is the mechanism of metoclopramide for headache?

A

Dopamine antagonist. Alternative agent is prochlorperazine