Comsciousness

Question 1

What is consciousness ?

Answer 1

• Ability to be aware of oneself and one’s place in the environment
• Ability to respond appropriately to environmental stimuli

Conscious perception relies on both “bottom-up” and “top-down”
activation

“Top-down” selection is facilitated by long range bidirectional re- entrant / recursive association fibers connecting prefrontal and parietal regions to sensory regions

Question 2

What are the levels of consciousness?

Answer 2

Background conditions- Level of Consciousness: Arousal
Reticular activating system

Full consciousness experience- Conscious awareness: Higher-order thalamic nuclei, synchronous firing of broad, heteromodal cortical network

Precept: Content of consciousness- specific thalamic relay nuclei, content-specific sensory regions

Question 3

What is loss of consciousness?

Answer 3

Coma is a non-sleep loss of consciousness that (unlike syncope) lasts for an extended period.

• Patient is incapable of being aroused by external stimuli or inner need
• Continuum of altered arousal between wakefulness and coma

Question 4

Summarize the levels of unconsciousness

Answer 4

Levels of unconsciousness:
– lethargic (patient can be fully aroused)
– obtunded (patient cannot be fully aroused)
– stuporous(sleep-likestatus)
– comatose (no purposeful response to stimuli)

Question 5

What are the inputs into RAS?

Answer 5

Major inputs to the RAS arise from:

1. Association cortices
2. Limbic system
3. Sensory pathways
4. Thalamic reticular nucleus (inhibitory GABAergic pathways)
5. Brain stem and hypothalamic circuits controlling circadian rhythms

Question 6

What is the importance of the brainstem and consciousness?

Answer 6

Important role for:

• Background conditions for consciousness
• Attentive vigilance
• Wake-sleeprhythm

• Lesion to either of the 2 branches can impair consciousness

Question 7

What are the cholinergic pathways of the brainstem and basal formation?

Answer 7

The major cholinergic nuclei in the RAS are:

• Pedunculopontine nucleus
• Laterodorsal tegmental nucleus

Cholinergic pathways arising from the RAS project to:
• Thalamus (intralaminar nuclei) to cortex
• Basal forebrain to cortex

The brain stem and basal forebrain cholinergic systems work together to abolish cortical slow wave activity and promote an alert state.

Question 8

What’s the impact of the thalamus and consciousness?

Answer 8

• Some thalamic nuclei are mainly relay stations (LGN-vision, MGN-audition; VPL- somatosens) with localized connectivity (specific contents of consciousness)
• Other thalamic nuclei (intralaminar, midline thalamic nuclei, pulvinar) have dense connectivity with widespread cortical regions (levels of consciousness)
• The thalamic reticular nucleus projects back to the specific thalamic relay stations, modifying activity of thalamocortical loops
• The thalamic reticular nucleus also has inhibitory pathways to the upper brainstem RAS nuclei, modifying arousal levels

Question 9

What’s the impact of transmission mode in wakefulness?

Answer 9

Question 10

Describe the vegetative state (awake coma)

Answer 10

-Develops after coma
• Loss of ability to think, speak, and respond

• No awareness of environment
• What functions remain intact?
• Breathing and circulation • Autonomic functions
• Non-cognitive functions • Normal sleep patterns
• Spontaneous emotional expressions

Question 11

Illustrate CT of a person on a vegetative state

Answer 11

Question 12

What is Locked-In Syndrome?

Answer 12

• Blockage of basilar artery —> pons infarction
• Tetraplegia: paralysis of all voluntary muscles with
exception of vertical eye movements

• What remains intact?
• Fully aware of environment
• Cognition: thinking, remembering, visualizing
• EEG and cortical metabolic activity are typically normal

Question 13

Illustrate a CT scan of Locked In syndrome

Answer 13

Question 14

What is brain death?

Answer 14

• Irreversible loss of all brain functions

• Etiology
– Anoxia
– Ischemia
– Intracranial hemorrhage
– Trauma
– Brain tumors
– Increased intracranial pressure and uncal herniation

Question 15

How is brain death diagnosed?

Answer 15

• Not responsive to speech, pain or other stimuli
• Nospontaneousrespiration
• Pupils dilated, not reactive to light
• No vestibulo-ocular reflex (ice water in ear, ‘dolls eyes’)
• No corneal reflex
• Isoelectric EEG

Question 16

What are the causes of a coma?

Answer 16

• Small lesions in mesencephalon (paramedian reticular formation)
• Lesion of posterior lateral hypothalamus (pathway through hypothalamus)
• Lesion of thalamus

• Bilateral impairment to both hemispheres
(trauma, metabolic)

Question 17

What supratentorial mass lesions can cause a coma?

Answer 17

Supratentorial mass lesions: 
– Epidural hemorrhage
– Subdural hemorrhage
– Intracerebral hemorrhage
 – Cerebral infarction
– Brain tumor 
– Brain abscess

Question 18

What subtentorial lesions can cause a coma?

Answer 18

Subtentoriallesions:
– Brain stem infarction
– Brain stem tumor
– Brain stem hemorrhage

Question 19

What are the metabolic and diffuse cerebral disorders lead to a coma?

Answer 19

Metabolic and diffuse cerebral disorders
– Anoxia or ischemia (embolic disease, diffuse intravascular coagulation,
vasculitis)
– Concussions
– Ongoingseizuresandpostictalstates
– Infection (meningitis and encephalitis)
– Subarachnoidblood(vasospasm)
– Hypoglycemiaorhyperglycemia
– Hyponatriemiaorhypernatriemia
– Hypothyroidism
– Drugs and alcohol
– Liver failure
– Sepsis
-hypercortisolism 
-hypercarbia
-renal failure

Question 20

Describe Glasgow Coma scale

Answer 20

Patients who score:
≤ 8: 90% are in coma
≥ 9: not in coma

8 is the critical score

≤ 8 at 6 hours: 50% will die
9-11 = moderate severity
12 – 15: minor injury

Question 21

How do we assess arousability and motor response in a comatose patient?

Answer 21

2.Levelofarousabilityandmotorresponse a. Ability to verbal instruction
b. Response to local painful stimulus:
- Damage upper midbrain (bilateral)
Decorticate posturing:

• Damage upper pons or lower midbrain (bilateral):
  Decerebrate posturing
  asymmetric motor responses, asymmetric muscle stretch reflexes, Babinski sign→
  focal injury to the descending motor system

Question 22

Describe pupillary dilation

Answer 22

• Sympathetic stimulation of adrenergic receptors causes contraction of and pupillodilator muscle
• Conversely, parasympathetic stimulation of the circular muscle causes pupillary constriction

Question 23

Summarize the pupillary light response

Answer 23

1. Metabolic encephalopathy, drug ingestion, or diffuse pressure on the diencephalon: pupils are slightly smaller than normal but respond to light
2. Pressure on the pretectal area (pineal tumor) : no pupillary constriction, causing large, unreactive pupils
3. Lesion of oculomotor (Ill) nerve (uncal herniation): unilateral fixed dilated pupil.
4. Lesion in pons: pinpoint pupils, responding slightly to light (magnifying lens). Pontine injury lesion affects the descending sympathetic pathway but also the ascending inputs to Edinger- Westphal nucleus that inhibits its tone

Question 24

What are the Oculomotor exams in a comatose patient?

Answer 24

Oculomotor responses
a. Metabolic encephalopathy
– Dolls head maneuver:
Eyes roll counter head movement
– Cool water in ear:
Eyes turn to ipsilateral side

→ Brain Stem intact

Question 25

What are the components of a pupillary light response?

Answer 25

Question 26

What are the postures of a comatose patient decorateposturing?

Answer 26

Question 27

What are the postures of a comatose patient decerebate posturing?

Answer 27

Question 28

What is the respiratory pattern of a comatose patient?

Answer 28

Question 29

What are the brain waves of a comatose patient?

Answer 29

Question 30

What are the inputs of RAS?

Answer 30