Coma

Question 1

Lethargy

Answer 1

sleepy but easily aroused with stimulation

Question 2

Hypersomnia

Answer 2

excessively sleepy but normal cognition when awake

Question 3

obtundation

Answer 3

mental blunting

Question 4

stupor

Answer 4

eyes open only briefly after vigorous stimulation before returning to sleep

Question 5

Coma

Answer 5

eyes remain closed after vigorous stimulation

Question 6

abulia

Answer 6

Awake but apathetic; with vigourous stimulation cognition may be normal (bilateral frontal lobe disease)

Question 7

akinetic mutism

Answer 7

silent, alert-appearing. no mental activity.

Loss of frontal lobes and hypothalamus

Question 8

minimally conscious state

Answer 8

fragments of awareness

Question 9

vegetative state

Answer 9

awake, no awareness or meaningful interaction with the environment

Question 10

Two components to consciousness

Answer 10

• Arousal
• Content

Arousal is controlled by ascending arousal system of the brainstem. Disease of this region causes stupor and coma

COntent is controlled by cortical units, disease = dimentia

Question 11

Studies in the 1920’s showed that lesions of the brainstem did not affect wakefulness until the lesion reached what level?

Answer 11

Upper pontine and midbrain level. Until this point, EEG showed wakefulness patterns. Once the midbrain was injured however, wakefulness was not achieved.

Question 12

Primary lesions that cause coma were always, in some way, shown to affect what region of the brain?

Answer 12

Reticular Grey formation

Question 13

KNOW»> lesion of the paramedian tegmental area just ventral to the aqueduct of sylvius= coma

Answer 13

THis shows that lesions confined to the upper pons can cause coma even if there is no midbrain or thalamic injury

Question 14

WHat occurs when the lesion is slightyly more caudal to the paramedian tegmental area?

Answer 14

These pts are “locked in”. They have a paralyzed lower face, cannot speak, swallow or breathe, are quadriplegic, yet can see, hear, and control eye movements.

Question 15

THe areas of the reticular formation that produce coma when damaged became known as

Answer 15

RAS- Reticular activating system (upper third of the pons through the midbrain tegmentum (floor of third ventricle) and into the thalami

Question 16

Important to realize that RAS nuclei are not the source of arousal. Rather, injury to this RAS system destroys axons from other nuclei that pass through this territory.

Answer 16

ok

Question 17

What do the two cholinergic wakefullness nuclei do>

Answer 17

They project to the thalamus and inhibit thalamic nuclei firing. Place the thalamuc in transmission mode for filtering and relaying sensroy info to the cortex

Question 18

VLPO

Answer 18

sleep promoting center that when destroyed causes insomnia. Uses GABA and Galanin to inhibit the wakefulness centers.

Question 19

Two types of coma

Answer 19

• Structural: requires surgical intervention. Headache, nausea, vomitting, focal deficits on exam and abnormal imaging
• Metabolic: No focal deficits on exam. Normal imaging

Question 20

In the case of an uncal herniation where the oculomotor nerve is compressed from above, what is the first sign?

Answer 20

Loss of pupillary constriction since the parasympathetic nerve from EW nuclueus lies superiorly

Question 21

Loss of pupillary reaction to light =

Answer 21

EMERGENCY

Question 22

WHat gets caught between a herniating temporal lobe and the brainstem?

Answer 22

Occulomotor nerve

Question 23

Bilateral uncal herniation occurs when?

Answer 23

• Can be due to trauma
• May also be due to metabolic insults such as hypoxia or the cerebral edema that accompanies fulminant liver failure and leads to herniation. Under these circumstances there is pressure both medially and downward to produce such central herniation.

Question 24

Falcine herniation

Answer 24

WHen brain is pushed under the falx cerebri. The big risk here is that one or both anterior cerebral arteries can be compressed

Question 25

How to recognize central herniation

Answer 25

First: reduced consciousness due to pressure on the reticular grey in both thalami

2: Small pupils due to compression of the sympathetic tract and thus unopposed parasympathetic activity
3) Pressure reaches midbrain and EW nucleus fails- pupils now totally unreactive
4) FLexor posturing followed by extensor posturing- late sign
5) Cheyne stokes respirations- apneic spells interspersed with hyperventillation periods- actually an early sign

Question 26

How do you identify primary brainstem lesions

Answer 26

Look for features like:

1) segmental cranial nerve defects
2) contralateral pain and temperature deficits signifying loss of spinothalamic
3) Epicritic deficit
4) Cerebellar signs such as gait ataxia and loss of coordination

Question 27

How will a metabolic encephalopathy present

Answer 27

• neurological defects that are diffuse and global
• CT negative
• Pupils remain reactive to light as other systems fail (pupils are the last to go)
• Asterixes (sudden lapse in muscle tone), multifocal myoclonus (twitching in different areas of the body in an unpatterned sequence), tremor

Question 28

90% of delirum in the elderly caused by

Answer 28

• dehydration
• drug intox
• infection

Question 29

Normal vital signs in coma suggest

Answer 29

psychogenic coma

Question 30

Cheynes Stokes respirations are an early warning sign of

Answer 30

transtentorial or central herniation

Question 31

Glasgow scale scoring

Answer 31

Highest is 15.
12 or better is an excellent prognosis
Below 8 is nursing home care
3 means death