Comsciousness Flashcards
What is consciousness ?
- 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
What are the levels of consciousness?
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
What is loss of consciousness?
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
Summarize the levels of unconsciousness
Levels of unconsciousness:
– lethargic (patient can be fully aroused)
– obtunded (patient cannot be fully aroused)
– stuporous(sleep-likestatus)
– comatose (no purposeful response to stimuli)
What are the inputs into RAS?
Major inputs to the RAS arise from:
- Association cortices
- Limbic system
- Sensory pathways
- Thalamic reticular nucleus (inhibitory GABAergic pathways)
- Brain stem and hypothalamic circuits controlling circadian rhythms
What is the importance of the brainstem and consciousness?
Important role for:
- Background conditions for consciousness
- Attentive vigilance
- Wake-sleeprhythm
• Lesion to either of the 2 branches can impair consciousness
What are the cholinergic pathways of the brainstem and basal formation?
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.
What’s the impact of the thalamus and consciousness?
- 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
What’s the impact of transmission mode in wakefulness?
Describe the vegetative state (awake coma)
-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
Illustrate CT of a person on a vegetative state
What is Locked-In Syndrome?
• 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
Illustrate a CT scan of Locked In syndrome
What is brain death?
• Irreversible loss of all brain functions
• Etiology – Anoxia – Ischemia – Intracranial hemorrhage – Trauma – Brain tumors – Increased intracranial pressure and uncal herniation
How is brain death diagnosed?
- 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
What are the causes of a coma?
- 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)
What supratentorial mass lesions can cause a coma?
Supratentorial mass lesions: – Epidural hemorrhage – Subdural hemorrhage – Intracerebral hemorrhage – Cerebral infarction – Brain tumor – Brain abscess
What subtentorial lesions can cause a coma?
Subtentoriallesions:
– Brain stem infarction
– Brain stem tumor
– Brain stem hemorrhage
What are the metabolic and diffuse cerebral disorders lead to a coma?
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
Describe Glasgow Coma scale
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
How do we assess arousability and motor response in a comatose patient?
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
Describe pupillary dilation
- Sympathetic stimulation of adrenergic receptors causes contraction of and pupillodilator muscle
- Conversely, parasympathetic stimulation of the circular muscle causes pupillary constriction
Summarize the pupillary light response
- Metabolic encephalopathy, drug ingestion, or diffuse pressure on the diencephalon: pupils are slightly smaller than normal but respond to light
- Pressure on the pretectal area (pineal tumor) : no pupillary constriction, causing large, unreactive pupils
- Lesion of oculomotor (Ill) nerve (uncal herniation): unilateral fixed dilated pupil.
- 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
What are the Oculomotor exams in a comatose patient?
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
What are the components of a pupillary light response?
What are the postures of a comatose patient decorateposturing?
What are the postures of a comatose patient decerebate posturing?
What is the respiratory pattern of a comatose patient?
What are the brain waves of a comatose patient?
What are the inputs of RAS?
