Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/45

Click to flip

45 Cards in this Set

  • Front
  • Back
Define Consciousness as well as define its components.
A state of AWARENESS of self and environment.

Content - sum of one's mental functions

Arousal - a state of behaviorally appearing wakeful
List the neurological exam related to coma. x6
1. Glasgow Coma Scale
2. Responsiveness
3. Eye movements
4. Pupils
5. Motor response
6. Respiratory pattern
Define stupor.
"Coma-like."

A condition of behavioral unresponsiveness appearing externally similar to deep sleep.

Patient may be aroused by vigorous and repeated stimuli.

As soon as stimuli ceases, the patient lapses back into unresponsive state.
Define coma.
The absence of awareness of self and environment, even when externally stimulated.

Unarousable, unresponsive, and eyes closed.
What does the reticular formation do in terms of consciousness?
Important in arousal, vigilance (alertness), maintenance of the conscious state.
Midbrain lesions in the ARAS leads to what symptoms?
coma
What does the reticular formation do in terms of unconsciousness.
Involved in regulating sleep.

Is the target of general anesthetics.
Where does the ARAS project to?
Posterior hypothalamus
Thalamus
Cortex
Presence of coma requires what? x3
1. Diffuse and bilateral impairment of the cerebral hemisphere.

2. Failure of the brainstem ARAS.

3. both
List the three components of the Glasgow Coma scale (include max score).
Eye opening (4pts)

Verbal response (5pts)

Motor response (6pts)
Coma induced by metabolic insults would have what effect on pupils?
Tiny and reactive pupils
Uncal Herniation causes what type of posturing?

a.) Decorticate
b.) Decerebrate
c.) Both
d.) None of the above
c.) Both types of postures
Central Syndrome causes what type of posturing?

a.) Decorticate
b.) Decerebrate
c.) Both
d.) None of the above
a.) Decorticate
Describe the Sympathetic Nervous System involved in pupillary response.

- Begins where?
- Travels to where?
- Causes what pupil action?
Begins in the hypothalamus.

Traverses brainstem
Goes to the IMLCC of the thoracic spinal cord.

Mydriasis
Describe the Parasympathetic Nervous System involved in pupillary response.

- Begins where?
- Travels where?
- Pupil action?
Begins in retinal cells

Follows optic nerve/tract
Goes to Pretectum.
Efferent path follows third nerve to the orbit.

Miosis
Pupillary pathways are relatively resistant to what?
Metabolic insults
Pupillary light reflex is the single most important physical sign for what?
Potentially distinguishing structural from metabolic coma.
Midbrain nuclear lesions interrupt what pathways? What is result to eye?
Both SNS and PNS pathway.

Pupils are:
- midposition
- fixed to light
- irregular/unequal
Respiration is affected by what part of the brain?
Respiratory Center (RC) in the medulla
How is a Temporal (UNCAL) lobe herniation initiated?
Ipsilateral cerebral lesion causes

uncus

to push downward through the tentorium

displacing brainstem, arteries, and nerves.
What is the first sign of Uncal lobe herniation and why?
Dilating pupils.

B/c displaced uncal gyrus will come into contact with the ipsilateral 3rd nerve.
Describe the progression of the pupils in Uncal herniation.
1. Pupils dilate
(sluggishly reactive to light)

2. Pupils fully enlarges with external ophthalmoplegia and signs of brainstem dysfunction.

3. Coma
Why is weakness considered a false localizing sign?
Depending on whether lesion is above or below the crossover (on the corticospinal tract), the weakness can present ipsilateral or contralateral.
The Kernohan's notch:

- Laceration of what?
- Occurs how?
Laceration of the cerebral peduncle (corticospinal tract)

from midbrain compression

against the contralateral free tentorial edge.
Decorticate Posturing

- position of UE
- involves lesion where
Flexed

Compressive lesion above red nucleus to thalamus
Decerebrate Posturing

- position of UE
- involves lesion where
Extended

Below red nucleus to vestibular nucleus
What is the etiology of Early Central Rostrocaudal Deterioration.
Large, bilateral hemispheric lesions compress the whole brain downward.
Signs of Early Central Rostrocaudal Deterioration. x3
1. Pupils tiny and reactive

2. Roving eye movements

3. Progressive motor changes
(as brainstem is compresed and shifts downward)
After the early signs of Central syndrome (rostrocaudal deterioration), describe the progression.
1. Perforating arteries elongate and rupture (infarct and hemorrhage in midbrain, then pons)

2. Upgaze restriction

3. Decorticate posturing

4. Pupils become midsized, unequal, irregular, or pear-shaped.
Decorticate rigidity is due to loss of inhibition of what tracts?
Medial Reticulospinal tract

Vestibulospinal tract

Rubrospinal tract
Decerebrate rigidity is due to loss of inhibition of what tracts?
Medial Reticulospinal tract

Vestibulospinal tract
What areas are damaged in decorticate rigidity?
Large portions of cerebral cortex and/or thalamus
What areas are damaged in decerebrate rigidity?
Rostral brainstem (midbrain)
Clinical features of Decorticate rigidity?

- UMN or LMN
- UE
- LE
- Consciousness?
1. UMN spasticity

2. Hypertonia in flexors of UE

3. Hypertonia in extensors of LE

4. Coma
Clinical features of Decerebrate rigidity?

- UMN or LMN
- UE
- LE
- Consciousness?
1. UMN spasticity

2. Hypertonia in extensors of neck and UE

Medial rotation in UE

3. Hypertonia in extensors of LE

4. Coma
Patient localizes to Noxious stimulus. Where is lesion?
At or above thalamus
Patient has decorticate rigidity. Where is lesion?
Below thalamus, but above red nucleus
Patient has decerebrate rigidity. Where is lesion.
Below red nucleus, but above vestibular nucleus.
Patient exhibits flaccidity and no response to noxious stimuli. Where is lesions?
Medullopontine RF
Describe Cheyne-Stokes Respiration.
Pattern of:

Increasing respiration rate
Decreasing respiration rate
Pause
Describe Central Neurogenic Hyperventilation.
Continous rapid respiration
Describe Apneustic breathing.
Breath in.
Hold breath.
Breath out.
Pause.

(like a cramp)
Describe Cluster breathing.
Irregular breathing

in clusters
Describe Ataxic breathing.
Completely irregular
What etiology causes Cheyne-Stokes respiration? x3

Where is lesion?
Bilateral cortical insults
Metabolic distrubance
Shock therapy

Above thalamus
(or bilateral thalamic dysfunction)