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Flashcards in Coma Deck (31):
1

Lethargy

sleepy but easily aroused with stimulation

2

Hypersomnia

excessively sleepy but normal cognition when awake

3

obtundation

mental blunting

4

stupor

eyes open only briefly after vigorous stimulation before returning to sleep

5

Coma

eyes remain closed after vigorous stimulation

6

abulia

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

7

akinetic mutism

silent, alert-appearing. no mental activity.
Loss of frontal lobes and hypothalamus

8

minimally conscious state

fragments of awareness

9

vegetative state

awake, no awareness or meaningful interaction with the environment

10

Two components to consciousness

- 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

11

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

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

12

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

Reticular Grey formation

13

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

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

14

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

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.

15

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

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

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.

ok

17

What do the two cholinergic wakefullness nuclei do>

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

18

VLPO

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

19

Two types of coma

- Structural: requires surgical intervention. Headache, nausea, vomitting, focal deficits on exam and abnormal imaging

- Metabolic: No focal deficits on exam. Normal imaging

20

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

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

21

Loss of pupillary reaction to light =

EMERGENCY

22

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

Occulomotor nerve

23

Bilateral uncal herniation occurs when?

- 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.

24

Falcine herniation

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

25

How to recognize central herniation

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

26

How do you identify primary brainstem lesions

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

27

How will a metabolic encephalopathy present

- 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

28

90% of delirum in the elderly caused by

-dehydration
- drug intox
- infection

29

Normal vital signs in coma suggest

psychogenic coma

30

Cheynes Stokes respirations are an early warning sign of

transtentorial or central herniation

31

Glasgow scale scoring

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