Jacewicz - Coma

Question 1

Why is the presence of a pupillary light reaction a good thing in pts with coma?

Answer 1

• Most often assoc with a metabolic encephalopathy (ME) rather than a structural lesion
  1. REMEMBER: metabolic causes of encephalopathy are often REVERSIBLE
• Because pupillary constrictors get compressed early, this is one of the earliest signs of a change in structural integrity/structural lesion

Question 2

Briefly, how should you treat the pt with ME?

Answer 2

• Support vital signs in ICU (ABC’s: airway, breathing, circulation)
• Then determine etiology and treat
• Want to move as quickly as possible to prevent further brain damage
• NOTE: very last neuro reflex to disappear in deepening coma is pupillary light reflex

Question 3

How can you verify and relieve raised ICP in structural coma?

Answer 3

• Do fundoscopic exam to look for raised ICP: while papilledema takes 6hrs to devo, can look for lack of retinal venous pulsations (bc they are compressed; pulsations would be exaggerated at very low ICP)
• Can temporarily relieve ICP to buy time for neuro-surgery by intubating & hyperventilating pt, reducing amount of BF and blood volume in the remaining normal brain (BF in brain highly redundant, so takes about 50% change to produce neuro effects)
  1. Even small change can be helpful
• Mannitol, hypertonic saline can be used to suck water globally out of brain; pupil will suddenly become reactive again, if you have succeeded

Question 4

What is typically the last neuro reflex to disappear in coma caused by ME?

Answer 4

• Pupillary light reflex

Question 5

What are some ways you can distinguish factitious from “real” coma?

Answer 5

• Depth of coma where nail bed pinching produces no response -> unlikely VITAL SIGNS will be normal
• Can check pupils and for doll’s eyes -> if DOLL’S EYES absent, then may factitious
• OCULOVESTIBULAR REFLEX works bc tonic pushing of eyes toward midline by each side. When you shut down one side with cold water, other side will push eyes over to the cold side. If you induce nystagmus with this, pt is NOT in coma, but awake
• Raise hand over face, and it will fall and “JUST MISS” the eye

Question 6

What are the basic features of locked-in syndrome?

Answer 6

• No horizontal gaze bc PPRF’s knocked out
• All they can really do is blink and move their eyes up and down
• Pts are awake, aware, and can remember things, so be careful what you say at bedside

Question 7

What is an easy way to tell between stupor and coma?

Answer 7

• Eyes opening: not coma, but stupor

Question 8

What 3 things should you always think about in an older person with altered mental status?

Answer 8

Bugs, drugs, dehydration

Question 9

If pt presents with head trauma that produces coma, can you do a head thrust maneuver?

Answer 9

• Not without verifying neck is ok
• Assume neck is broken until proven otherwise

Question 10

What are 2 unique features of subdural hemorrhage?

Answer 10

• One subdural is often associated with another on the other side
• Kernohan’s notch phenomenon: pupil on “wrong” side of the brain may be affected (due to cerebral peduncle indentation associated with some forms of transtentorial herniation)

Question 11

Why is it important to pay attention to symptoms in post-ictal state?

Answer 11

• Post-ictal state = post-seizure
• Paralysis gets better over minutes to days
• Always ask for evidence of seizure, like tongue twitching, incontinence, or seen to stiffen by bystander
• This can show evidence of old strokes due to cortical “reset”
• Case in class: diabetic pt with urosepsis

Question 12

What is lethargy? Hypersomnia?

Answer 12

• LETHARGY: sleepy, but easily aroused
• HYPERSOMNIA: excessively sleepy, but normal cognition when awakened on vigorous stimulation

Question 13

What are obtundation, stupor, coma, and delirium?

Answer 13

• OBTUNDATION: mental blunting, DEC alertness, i.e., lethargy + cognitive dysfunction
• STUPOR: eyes open only briefly after vigorous stimulation before returning to deep sleep; cognition impaired (sever obtundation)
• COMA: eyes remain closed after vigorous stimulation
• DELIRIUM: disoriented, misperception of sensory stimuli, hallucinations -> vacillates bt quiet, sleepy periods and hyper-vigilance/agitation

Question 14

What is abulia vs. akinetic mutism?

Answer 14

• ABULIA: awake, but apathetic pt w/no spontaneity
  1. With vigorous stimulation, cognitive function may be normal
  2. Bilateral frontal lobe disease, lobotomized
• AKINETIC MUTISM: silent, alert-appearing immobility
  1. No mental activity w/vigorous stimulation: disease of frontal lobes AND hypothalamus
• NOTE: pts in coma generally devo eye-opening and sleep-wake cycles after 2-4 wks, regardless of cause of coma

Question 15

What is minimally conscious state vs. vegetative state?

Answer 15

• MINIMALLY CONSCIOUS: fragments of awareness from vegetative state -> may reach for objects, grunt, or gesture in response to command, visually fixate and track, but unable to do much more
• VEGETATIVE: awake, no awareness or meaningful interaction with the environment
  1. Vegetative functions of brainstem maintained: sleep-wake cycles, respirations, heart rate, BP, and visceral autonomic regulation
• NOTE: overlap and transitions exist bt these two conditions -> describe stimuli for arousal and the pt’s response in the chart

Question 16

What are the 2 components of consciousness?

Answer 16

• AROUSAL: sleep-wake cycles, ascending arousal system (reticular activating system) of the rostral brainstem -> disease causes stupor and coma
• CONTENT: awareness of onself and the envo, cortical circuits (cognition, purposeful interaxn with the world; premeditated, not reflex) -> disease causes dementia
• Awareness and cognition are impossible without arousal

Question 17

What is encephalitis lethargica?

Answer 17

• Sleeping sickness where ppl slep 20hrs/d, waking only to eat or use restroom; some died
• Lesions in rostral periaqueductal grey matter and posterior 3rd ventricle
• Some pts developed cataplexy due to lesions in post lateral hypothalamus (bt sleep-promoting area in rostral hypothalamus - ventrolateral preoptic nuclues - and wakefulness promoting area in upper midbrain)

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Question 18

Where do lesions of the brainstem begin to affect wakefulness? How will this change your EEG results?

Answer 18

• Upper pontine/midbrain level
• Lesions at this level in animal models cause synchronized EEG showing high voltage slow waves typical of the pattern seen in sleep and some pts with coma
• Below this, lesions show EEG that is desynchronized brain wave pattern characteristic for awake state

Question 19

What damage is universal to brainstem lesions causing coma?

Answer 19

• Damage to the reticular grey formation, whether found in the thalamus, hypothalamus, midbrain peri-aqueductal grey, or upper 1/3rd of the pons
  1. Damage to these areas is often secondary to herniation syndrome affecting one or both cerebral hemispheres
• The other lesion shown here that can elicit coma is bilateral hemispheric disease (it is unusual to have such extensive global insult w/o affecting the upper brainstem as well)

Question 20

What is the RAS?

Answer 20

• Diffuse aggregations of neurons of different types and sizes, separated by a wealth of fibers traveling in all directions
• Net-like or reticular pattern -> not a diffuse, undifferentiated structure, but rather highly specific organization of connections
• NOTE: sensory pathways on their way to the thalamus send a collateral axon to synapse here (startle response)

Question 21

If the diencephalon are spared injury, what lesions of the brainstem result in coma?

Answer 21

• Most common lesions involve the paramedian tegmental area just ventrral to the aqueduct of Sylvius from the midbrain to the rostral pons
• Lesions confined to the upper pons can cause coma even in the absence of midbrain and thalamic injury -> this explains why some pts with pontine hemorrhage are comatose

Question 22

What is a grim possible consequence of lesions in the caudal pons?

Answer 22

• Lesions below rostral pons disrupt corticospinal, corticobulbar tracts bilaterally (can’t speak, swallow, breathe, move their limbs and face on their own)
• Pt remains conscious, aware, and can see and hear, maintaining some control over vertical eye mvmts and blinking, allowing communication with world
• These pts appear to be in coma, but are actually awake and LOCKED-IN: essential to make correct dx, and treat these pts at bedside as fully conscious and mentally competent

Question 23

Where is the RAS located anatomically? How does this predispose it to structural lesions?

Answer 23

• In the intralaminar nuclei of the thalamus (#31), tegmentum of the midbrain (#27), and tegmentum of upper 1/3rd of pons (#28) -> extends from upper 1/3 of pons through midbrain tegmentum, floor of 3rd ventricle, and into thalami
• Note proximity of medial temporal lobe (#10) and tentorium cerebelli (#30)
• NOTE: RAS can be impaired by structural lesions or diffuse metabolic conditions -> injury of any kind in these areas will suppress wakefulness and cause coma