Approach to Coma Flashcards

(49 cards)

1
Q

Lethargy?

A

Sleepy but easily aroused

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Hypersomnia?

A

Excessively sleepy but normal congition when awakened

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Obtundation?

A

Mental blunting, decreased alertness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Stupor?

A

Eyes open only briefly after vigorous stimulation before returning to deep sleep. Cognition impaired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Coma?

A

Eyes remain closed after vigorous stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Delirium?

A

Disoriented, misperception of sensory stimuli, hallucinations. Vacillates between quiet, sleepy periods and hyper-vigilance/agitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When do pts in comas develop eye opening and sleep wake cycles?

A

2-4 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Abulia?

A

Awake but apathetic, no spontaneity. With vigourous stimulation, cognitive function may be normal. (bilateral frontal lobe disease, lobotomized)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Akinetic mutism?

A

Silent, alert-appearing immobility. No mental activity with vigorous stimulation (disease of frontal lobes and hypothalamus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Minimally conscious state?

A

Fragments of awareness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Vegetative state?

A

Awake, no awareness or meaningful interaction with the enviroment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Patients in MCS may do what?

A

Reach for objects, grunt, or gesture in response to a command, Visually fixate and track

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Components of consciousness?

A

Arousal, Content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is arousal achieved?

A

Neural circuits that mediate sleep-wake cycles and involves a specific area of the upper brainstem referred to as the reticular activating system or ascending arousal system of the rostral brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Disruption of the arousal system leads to?

A

Stupor and coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does the content system refer to?

A

Cerebral activity for self-awareness, cognition, and purposeful interactions with the environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Are the content system behaviors premeditative or reflexive in nature?

A

Premeditative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Lesion in encephalitis lethargica?

A

Rostral periaqueductal grey matter and posterior 3rd ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cataplexy?

A

sudden involuntary loss of muscle tone during emotional excitement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Neuropathological patterns associated with coma?

A

A. Extensive, acute bihemispheric disease
B. Lesions of the diencephalon (thalamus and hypothalamus)
C. Lesions of midbrain peri-aqueductal grey matter
D-E. Involvement of upper one third of pontine tegmentum

21
Q

Reticular grey formation?

A

Mediates arousal

22
Q

Route of the reticular grey formation?

A

Upper third of the pons through the midbrain tegmentum, the floor of the third ventricle and into the thalami

23
Q

Injuries to what will cause coma?

A

Reticular grey formation

24
Q

Nuclei responsible for arousal are located where?

A

Ascending arousal system

25
What makes up the ascending arousal system?
Two Cholinergic nuclei | Monoaminergic System nuclei
26
What do the cholinergic nuclei of the AAS do?
Inhibit thalamic firing that increases wakefulness. This puts the thalamus in transmission mode for filtering and relaying sensory info to the cortex.
27
What happens if you did not have the cholinergic projections to the thalamus?
Thalamus would continue their periodic electrical "bursting" and with their widespread connections to the cortex, induce sleep through synchronizing cortical electrical activity.
28
Role of the monaminergic system in the AAS?
It has widespread connections to the cortex, both direct and indirect. Improves signal to noise ratio for messages from the thalamus and thereby prevents any misperception of incoming sensory stimuli
29
What is the sleep promoting center?
The ventro-lateral preoptic nucleus (VLPO)
30
What NT does VLPO use?
GABA
31
Role of VLPO?
Inhibits the many nuclear centers that promote wakefulness and comprise the ascending arousal system.
32
The AAS receives feedback from many sources including?
Thalamus, the Limbic System, the frontal and association cortex
33
Causes of coma?
Structural, Metabolic, Psychogenic (rare)
34
What do you always rule out first in a comatose patient?
Psychogenic coma
35
Structural comas?
Supratentorial mass lesion Acute obstructive hydrocephalus Infratentorial mass lesion
36
Metabolic comas?
``` Reversible injury (sedative OD) Irreversible injury (hypoxia in cardiac arrest) ```
37
What does transtentorial (Uncal) herniation lead to?
Occulomotor entrapment as well as sometimes PCA entrapment.
38
Common cause of transtentorial (Uncal) herniation?
Epidural hematoma from the laceration of middle meningeal artery
39
What does a falcine herniation trap?
One of both ACAs
40
How does a falcine herniation occur?
When mass effect pushes the brain under the falx cerebri
41
How does central herniation present?
Rostral-Caudal deterioration - Diencephalon --> midbrain failure - Reduced conciousness - Small reactive pupils - Decorticate posturing - Cheyne - Stokes respirations - Midbrain failure follows (FIxed mid-position pupils, decerebration)
42
Intrinsic brainstem lesions?
Top of the Basilar Artery ischemic stroke | Pontine hemorrhage
43
Extrinsic brainstem lesions?
Compress and distort the brainstem - Cerebellar hemorrhage - Cerebellar infarction - Cerebellar brain tumor
44
Primary brainstem lesions?
Segmental cranial nerve deficits Ascending (spinothalamic) tract dysfunction Descending (corticospinal, central sympathetic) tract dysfunction Early cerebellar signs
45
Pontine hemorrhage presentation?
``` Abrupt coma Pinpoint pupils Decerebrate rigidity or flaccid quadriplegia Horizontal gaze paresis Ocular bobbing ```
46
Metabolic insult to the brain is?
Global, diffuse, symmetric
47
Neuro-exam shows in pts with metabolic insult?
Does not show any focal or lateralizing deficits
48
What does head CT show in pts with metabolic insult?
Normal
49
What is the state of the pupils in metabolic insult?
Reactive