Patients can have few reflexes, no reactions to sense stimuli or body signals, no awareness, no arousal, no consciousness, no experiences, no voluntary movements, and no waking {coma, mental state} {comatose}|. Patients keep eyes closed. Patients typically do not recover.
causes
Both-hemisphere brainstem-nuclei trauma or oxygen deprivation can cause coma. Posterior upper brainstem arousal-system damage can cause coma. Coma always involves anterior and posterior intralaminar thalamus nuclei damage. Rostral pons and dorsal midbrain damage, or mesencephalic reticular formation and thalamus damage, causes coma for one to seven days. Paramedian thalamic damage causes long-term coma [Giacino, 1997] [Plum and Posner, 1983] [Schiff, 2004] [Schiff and Plum, 2000] [Zafonte and Zasler, 2002] [Zeman, 2001].
Metrazol induces coma but is no longer used in psychiatric treatment. Insulin induces coma.
Patients can sleep and wake, have some sensory reactions, have some voluntary movements, and have some self or environment awareness {stupor} {minimally conscious state}. Stuporous means semi-conscious, semi-aware, and few sensations.
causes
Damage to cortico-striatopallidal-thalamocortical loop disconnects frontal lobes, basal ganglia, and thalamus. Bilateral anterior medial cortex, basal ganglia, and basal forebrain damage causes stupor.
A schizophrenia type involves excitement and then stupor.
types
Bilateral anterior-medial-cortex, basal-ganglia, and basal-forebrain damage, typically from anterior cerebral-artery aneurysm, can cause no motion, except to look around (akinetic mutism). Medial-caudal-thalamus, medial-dorsal-mesencephalon, caudate-nucleus, globus-pallidus, and medial-forebrain-bundle damage can cause no memory, slow behavior {slow syndrome}, and apathy.
Extensive temporal-lobe, parietal-lobe, and occipital-lobe junction damage can prevent self or environment awareness but allow coordinated behavior (hyperkinetic mutism).
Patients can have no voluntary movements, can have no reactions to sense stimulation or body signals, can have intermittent arousal and eye opening, and can sleep and wake {vegetative state}|. They can have reflexes and eye blinks [Celesia, 1997] [Laureys et al., 2000] [Laureys et al., 2002].
causes
Both-hemisphere brainstem-nuclei trauma or oxygen deprivation can cause vegetative state. Permanent vegetative state patients have bilateral thalamic damage but little cerebrum damage.
time
People can stay in vegetative state more than 30 days {persistent vegetative state}. People can stay in vegetative state for much longer {permanent vegetative state}.
People can be in mental states in which they have no voluntary movements, have no sensations, have no perceptions, have no awareness, do not experience sensations, have no event or object memories, and have no functioning mind {unconsciousness, state}|. Unconsciousness is not awakeness, sleeping, coma, stupor, nor vegetative state. Body functions automatically. Unconscious people cannot use habits or perform voluntary behaviors. Unconscious people have no sensations or perceptions. Unconscious people cannot use declarative memories. All mammals can become unconscious, and ability to become unconscious indicates previous consciousness [MacIntyre, 1958].
causes
Unconsciousness occurs when people are asleep and not dreaming, have received a brain concussion, have finished an epileptic episode, have anesthesia, or have fainted.
Trauma from high physical pressure, such as concussion, causes brainstem damage. Low blood-oxygen concentration, low blood-glucose concentration, low blood flow, and low blood pressure affect brainstem. Blood nitrogen-gas bubbles can affect brainstem neurons [Forster and Whinnery, 1988] [Rossen et al., 1943] [Whinnery and Whinnery, 1990].
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Date Modified: 2022.0225