ICL 10.9: Evaluation of the Unconscious Patient

Question 1

what is consciousness?

Answer 1

“the state of awareness of self and environment, and normal responsiveness to external stimulation and inner need”

Question 2

what are the qualifications where you would consider someone as conscious?

Answer 2

consciousness is a state in which both of the following are preserved:

1. ability to be aware of oneself and one’s environment
2. ability to respond appropriately to environmental stimuli

Question 3

what are the 5 levels of consciousness?

Answer 3

1. awake/alert: fully attentive, aware and responsive
2. sleepy: awake but appears sleepy with decreased attention and slow responses
3. obtunded: asleep, wakes to verbal or light physical stimulation, falls back to sleep easily if stimulus stops
4. stupor: deep sleep requires noxious and persistent stimulation to maintain arousal/participate in exam
5. coma: eyes closed, unresponsive to external stimuli, with the exception of brainstem and spinal reflexes

Question 4

what is the ascending reticular activating system?

Answer 4

ARAS is a complex poorly defined neural network that involves input &/or output with all of the following:

1. brainstem reticular formation
2. hypothalamus & forebrain
3. thalamus
4. cortical, cerebellar & spinal feedback

ARAS starts in the brainstem reticular formation and it’s located more in the upper brainstem so the upper 1/2 of the pons to the midbrain

it’s divided into 3 functional 4 neurochemical components

Question 5

what are the 3 functional components of the ascending reticular activating system?

Answer 5

1. efferents –> thalamus
2. efferents –> hypothalamus and forebrain
3. direct diffusion projections –> cortex

Question 6

what are the 4 neurochemical divisions of the ascending reticular activating system?

Answer 6

there are key nuclei in the ARAS portion of the reticular formation that produce the main neurotransmitters of consciousness = Ach, serotonin, histamine and norepinephrine

Question 7

what is the function of the hypothalamus in consciousness?

Answer 7

even though it’s considered that arousal starts in the ascending reticular formation, the arousal system includes initiation in the hypothalamus

so the lateral hypothalamus releases orexin 1 and 2 on the various nuclei in the ARAS pathway in the brainstem to stimulate the release of their respective NTs

Question 8

what is the function of cortical, cerebellar and spinal feedback in relation to consciousness?

Answer 8

these are super important because think about how you wake up based on when you perceive light or how you don’t want to sleep when you smell smoke so there’s feedback from all the senses into the ARAS activation system

so there’s visual, auditory, smell, tactic feedback etc. to make sure we have the mechanisms to preserve our survival so we don’t sleep through important things

Question 9

how do we localize impaired consciousness?

Answer 9

1. bilateral cortex problems = ARAS pathway has diffuse output to the cortex so anything that diffusely effects the bilateral cortices can cause impaired consciousness –> usually these are toxibolic syndromes, hyper/hypoglycemia, global ischemia, etc.
2. bilateral thalamus problems = most pathways go through the thalamus so each thalamus communicates its arousal pathways to the ipsilateral cortex so if you knock out both thalami you can impair consciousness
3. contralateral cortex and thalamus = if you were to have a lesion that effects an entire cortex and the contralateral thalamus, you can also impair consciousness that way

so when you’re trying to see what’s causing lost consciousness, you need to try and localize it to the brainstem, thalamus or the cortex?

Question 10

what are the 6 disorders of consciousness?

Answer 10

1. locked-in state
2. catatonia
3. akinetic Mutism
4. minimally conscious State
5. unresponsive wakefulness syndrome
6. coma

Question 11

what causes locked-in syndrome?

Answer 11

classically seen in basilar strokes

but can also be seen in:
1. MS

2. infection
3. tumor
4. hemorrhage
5. trauma

Question 12

what is locked-in syndrome?

Answer 12

aka cerebromedullospinal disconnection OR de-efferented state

it’s where the anterior pons and midbrain are effected usually due to a basilar stroke

the reticular formation and dorsal midbrain are spared though!

Question 13

what are the signs of locked-in syndrome?

Answer 13

because the dorsal motor nuclei are spared that means the oculomotor nerve is spared, they still have vertical eye movements, and can still blink – the reticular activating tracts and sensory tracts are also still in tact!

what’s effected is basically all of their motor outputs

Question 14

what are the 3 forms of locked-in syndrome?

Answer 14

all of these forms include full consciousness, sensation, emotional and startle responses so they’re cognitively still there

1. pure = spares only vertical eye movements & blinking – so this is how a lot of them communicate
2. incomplete = wide range of spared motor function depending on how extensive the stroke or infection was
3. total = no spared function, not even eye movements and blinking – in this case it’s really hard to differentiate them from someone who is comatose

Question 15

how do you differentiate between the locked in state and a comatose patient?

Answer 15

many of these patients initially present with impaired or loss of consciousness so that’s why it’s so important to test the occulocephalic reflex when examining an unconscious patient

so most physicians do the dolls eye test where they move the head side to side to make sure the eyes stay on the target but you also need to move the head up and down and make sure it stays on the target as well so you don’t miss any vertical eye movements before they’re awake and able to blink/move their eyes up and down

this might be the only thing that differentiates them from a comatose patient!!! a locked-in syndrome patient will have spared vertical eye movements

some patients actually feel that they have a reasonable quality of life in the locked in state because they have power chairs and lift systems and are able to communicate with their family and recognize them – this is what really differentiates the patients from coma because some feel that the are still in a meaningful state of life

Question 16

what is catatonia?

Answer 16

a state in which a person appears unresponsive or unconscious

it simulates akinetic mutism, stupor or light coma

it’s often associated with psychiatric disorders, severe depression etc.

Question 17

what will be seen on a PE of a catatonic patient?

Answer 17

1. brainstem reflexes intact
2. oculocephalic testing consistent with awake state = eyes move/track with the head
3. resistance to eye opening
4. waxy flexibility = if you position their limb in a certain way they’ll maintain it for a long time
5. catalepsy = hold uncomfortable postures for a long time
6. adventitious movements like repetitive motor mannerisms or choreiform jerking (consider EEG to make sure it’s not seizures)

Question 18

what is akinetic mutism?

Answer 18

silent & inert – profound apathy

it’s a complete lack of spontaneous speech or movement due to a lack of motivation or drive. Patients are fully aware and visual tracking is preserved

patients are conscious, aware of their surroundings and depending on the localization can register and retain what happens during time in that state

Question 19

what part of the brain is effected with akinetic mutism?

Answer 19

localization can be due to injury to the midbrain, anterior thalamus or uni-/bilateral medial frontal lobe lesions

usually associated with diminished dopamine pathways

we see a lot of this with ACA stroke patients where nurses will say they stopped following commands or they can’t get them to do anything – it’s not that the patient isn’t capable, it’s that they don’t have the motivation to do it

Question 20

what is a minimally conscious state?

Answer 20

it’s a spectrum of states! these people can be anywhere from being comatose to a akinetic mute state

it can be transitional; like people coming out of a coma can go through this spectrum before being totally awake –> or they can get stuck along this spectrum at various severities of impaired consciousness

this is the most important loss of consciousness condition to be aware of because with every day there’s improvements in the patient so you need to look at the subtle changes to be able to identify progression along the different stages

Question 21

how can you identify if someone is in a minimally conscious state?

Answer 21

with every day there’s improvements in the patient so you need to look at the subtle changes to be able to identify progression along the different stages

EYES
dysconjugate –> roving –> midline –> fixation –> tracking

MOTOR
flaccid –> posturing –> withdrawal –> localize –> following

Question 22

what is the unresponsive wakefulness syndrome?

Answer 22

a return of arousal without the return of awareness following a coma –> this is basically what happens if you never make it into a minimally conscious state –> so coma patients will eventually die from medical complications or they’ll transition into an UWS

a person in a vegetative state may open their eyes, wake up and fall asleep at regular intervals and have basic reflexes, such as blinking when they’re startled by a loud noise, or withdrawing their hand when it’s squeezed hard – they’re also able to regulate their heartbeat and breathing without assistance

however, a person in a vegetative state doesn’t show any meaningful responses, such as following an object with their eyes or responding to voices. They also show no signs of experiencing emotions nor of cognitive function.

UWS causes the brain to halt the ability to create thoughts, experience sensation, and remember past events. Patients in a vegetative state are awake, but show no signs of awareness

this is what was previously known as a vegetative state and it’s considered persistent if it goes on for more than 3 months –> with traumatic brain injury it’s considered persist UWS if it persists for more than a year and this is because with traumatic brain injury there’s a lot of axonal damage that could potentially remyelinate over the year so you have to wait before giving them the diagnosis of persistent UWS

Question 23

what is the clinical presentation of someone in an unresponsive wakefulness syndrome?

Answer 23

from a cognitive standpoint, the patient remains unresponsive and mostly unconscious and does not appear to have awareness of self, environment or needs

eyes might open to pain; may progress to spontaneous opening or a diurnal pattern – there might be intermittent blinking or brief fixation/tracking of faces and objects but it’s never consistent and it doesn’t progress into anything more

from a motor perspective they might swallow spontaneously, grind their teeth, front or moan – they can also assume some primitive postures and reflexes of the limb like cortical thumbing that babies do

Question 24

what causes an unresponsive wakefulness state?

Answer 24

1. diffuse cortical injury like from a cardiac arrest
2. diffuse subcortical injury like with diffuse axonal injury from a traumatic brain injury
3. thalamic injury like from influenza

Question 25

what is a coma?

Answer 25

eyes closed, unresponsive to external stimuli, with the exception of brainstem and spinal reflexes

Question 26

what are the levels of coma?

Answer 26

you can classify a coma via:

1. quantitatively – scores: GCS & FOUR
2. qualitatively – exam features
3. electrophysiologically – variety of EEG patterns in comatose individuals

Question 27

what is the Glasgow coma scale? (GCS)

Answer 27

it’s a scale that assesses the level of consciousness of a patient

for adults it’s broken down by eye opening response, verbal response and motor movement

the lowest score you can get is a 3 and that means even to noxious stimuli there’s no response

the highest you can get is a 15 which means your eyes open spontaneously, you’re oriented and conversing, and can obey motor commands

the middle is an 9; less than 8 is considered comatose –> if you open your eyes to painful stimuli, make incomprehensible sounds or have an abnormal posture that’s no longer comatose; the moment you start to withdraw from pain that’s a response to stimuli and the person would no longer be considered comatose!

Question 28

what is the problem with the GCS coma scale?

Answer 28

in intubated patients it’s not very accurate

how are you going to get a verbal response with a trach tube??

you can modify the GCS but it gets really confusing because people use it differently so instead use the FOUR score

the FOUR score means you have the same eye and motor responses but it also takes into account EOM and brainstem reflexes and breathing patterns and this score is better at predicting outcome in intubated patients than the GCS

Question 29

what is brain death?

Answer 29

Legal definition of death based on a clinical diagnosis

it means cessation of all brain AND brainstem function

Unified Determination of Death Act (UDDA) – 1980s

Question 30

what are the components of claiming someone is braindead? Like what are the requirements to say someone is official braindead?

Answer 30

1. evidence of an irreversible causative lesion
2. rule out any potential confounders like metabolic conditions so make sure toxicology, pH, electrolytes, endocrine, temperature are in the normal range
3. neurological exam consistent with brain death
4. apnea test to confirm lack of respiratory effort despite significant hypercapnia (excessive CO2)
5. ancillary testing if either the neurological exam or apnea test cannot be done

Question 31

what are the 3 parts of a brain death exam?

Answer 31

1. level of consciousness
2. brainstem reflexes assessment
3. apnea test

Question 32

how do you assess the level of consciousness during a brain death exam?

Answer 32

1. response to presence
2. response to verbal
3. response to pain

make sure you uncover your patients to make sure you can see any reflexes or movements that are happening

Question 33

how do you assess the brainstem reflexes during a brain death exam?

Answer 33

1. blink to threat (CN 2/3)
2. pupillary light reflex (CN 2/3)
3. corneal reflex (CN 5/7)
4. oculocephalic vertical & horizontal (CN 3, 4, 6, 8 *C-spine)
5. cold caloric (tympanic membrane)
6. gag (CN 9/10)
7. cough (CN 10/10)

Question 34

how do you assess apnea during a brain death exam?

Answer 34

1. get a baseline ABG
2. apneic oxygenation 8-10 mins
3. look for chest rise
4. follow up ABG-PaCO2 > 60 or ⇡20

so provide oxygen but don’t let ventilator run and without ventilation CO2 will rise and once it gets over 60 and there’s no initiation of breath, that would confirm a positive apnea test

Question 35

what are the ancillary tests you can do if the other components of a brain death exam can’t be done?

Answer 35

1. EEG
2. nuclear medicine perfusion test
3. ultrasound

Question 36

what results will you see in a nuclear medicine perfusion test of a braindead patient?

Answer 36

send radionuclei tracer through the blood stream and what you’ll see is the external carotid branches will fill so the nose will look black on the image but the skull will be white meaning that because the brain is dead it’s no longer recruiting perfusion (sagittal sinus will still fill though because the scalp drains into it)

the pituitary gland will also light up because it has collateral from the external carotid circulation so that’s doesn’t mean anything either

Question 37

what results will you see in an EEG of a braindead patient?

Answer 37

you’re checking for electrocerebral silence which is the flatline equivalent of an EKG

Question 38

what results will you see in an ultrasound of a braindead patient?

Answer 38

you ultrasound the middle cerebral artery and you can see a specific pattern that’s consistent with no blood being passed through it to the brain

Question 39

when can’t you check tone and reflexes?

Answer 39

after the patient has been intubated and sedated!

Question 40

what part of the brain does acute apnea localize to?

Answer 40

this is associated with Cushing’s triad that’s seen in tonsillar herniation due to medulla compression!

Question 41

what part of the brain does Biot’s breathing localize to?

Answer 41

Biot’s is irregular cluster breathing

it localizes to the pons

Question 42

what part of the brain does agonal breathing localize to?

Answer 42

medulla

it’s like someone taking one long laborious breath like once a minute; like imagine what you think of when someone is about to die and is taking those slow breaths

Question 43

what part of the brain does hyperpnea localize to?

Answer 43

thalamic and midbrain lesion

Question 44

what part of the brain does bradypnea localize to?

Answer 44

medulla

Question 45

what part of the brain does Cheryne-Stokes breathing localize to?

Answer 45

forebrain or metabolic issues like CHF

it’s a medullary on/off regulation in response to CO2 levels

when there’s a delay in blood flow from the heart to the carotid bodies and the chemoreceptors ramp up until you blow off so much CO2 from the delayed feedback that you go apnic and then CO2 builds up and you ramp up again

so Cheyne Stokes is very rhythmic and sinusoidal

slide 33

Question 46

what part of the brain does apneustic breathing localize to?

Answer 46

pons

looks like a slanted zig-zag line….this signify the force of the breath like sucking in and holding it in then quickly breathing out

Question 47

what does Kussmaul breathing signify?

Answer 47

acidosis

zig zag line because patients breath in deep and then forcefully exhale

Question 48

what does air trapping signify?

Answer 48

COPD

Question 49

what does a lot of sighing indicate?

Answer 49

medulla injury

Question 50

56-year-old patient who was found unresponsive in his room at the start of shift by his nurse. He was last seen well at last-night shift check.

VS: 115 (sinus) 160/95 / 26 (tachypnea) / O2Sat 100% / AF

He grimaces and groans to sternal rub and withdraws all 4 extremities symmetrically to peripheral pain. His pupil are 4 mm and briskly reactive. The remainder of his CN exam is intact. He does not follow any commands. He is hyporeflexic, mute Babinski and normal tone

He is well perfused, skin is warm and he is diaphoretic. Breath and heart sounds are normal. Pulses are thready

work through this: do localization, general exam, history, history, workup and differential

Answer 50

localization: there’s no CN abnormalities, you can’t really localize so it’s non-focal

general exam: hypertensive and tachycardic and are diaphoretic

history: acute
workup: do a metabolic workup but also make sure you’re not missing something wrong with the thalamus higher up past the brainstem

what you end up finding is that the patient has a glucose of 40 so they’re hypoglycemic

maybe just go look at slide 35

Question 51

27-year-old woman brought to ED with history of severe HA/emesis worsening x 4 hours. On arrival is she unresponsive and was intubated for airway protection.

VS: 97 (NSR) / 170/100 / 35 (hyperpnea) / O2Sat 100% / AF

She does not follow any commands, has decorticate posturing & bilateral grimace to pain. Her pupils are 6 mm, unreactive. Vertical EOMI, loss of abduction bilaterally. Remainder of brainstem reflexes intact. She is hypereflexic, with +Babinski and rigid tone

Crackles over anterior lung fields bilaterally, otherwise unremarkable general exam

work through this: do localization, general exam, history, history, workup and differential

Answer 51

decorticate posturing = red nucleus in the midbrain

pupils are dilated and unreactive = CN 3, midbrain

vertical eye movements intact but abduction is impaired = CN 6

everything else is fine except some upper motor neuron signs

so mostly midbrain problems other than CN 6 which was probably stretched in this case instead of being directly compressed

probably an anterior lesion since only CN 6 was effected, CN 7 was fine because there was no facial weakness which is more dorsally located and also since 7 wasn’t effected it supports even more that CN 6 was just stretched instead of something effecting the whole pons

pulmonary edema in a young patient isn’t common….so some differentials would be cerebral venous sinus thrombosis, SAH with hydrocephalus, tumor with hemorrhage, bacterial meningitis

but then you find out she’s on oral contraceptives and smokes so high clotting risk! she has a superior sagittal sinus thrombus which you see in the CT – her brain is super swollen which pushes down on CN 6