Scientific Understanding of Consciousness
Consciousness as an Emergent Property of Thalamocortical Activity

Abnormal Function of Brain

Analyzing the abnormal functioning of the brain can be a way to gain insight about brain functions underlying consciousness. Other avenues of research include (1) psychological studies of humans, (2) brain imaging (fMRI, etc.) studies of humans, (3) research with animals such as monkeys and chimps, (4) physiological studies of neurons of lower animals such as sea slugs. Strokes, trauma, diseases such as Alzheimer’s can provide insight into brain and CNS functioning and thereby into the functioning of consciousness.

Anosognosia

Anosognosia: the vehement denial of paralysis in some patients who have suffered a right hemisphere stroke. (Ramachandran; Illusions of Body Image, 29)

Alcohol abuse

Brain withdrawal reactions after alcohol abuse can be depicted via Allan Hobson’s AIM brain model.

 

(paraphrase of Allan Hobson; Pace-Schott; Sleep and Dreaming, p.49)

Dissociations can result from a frag­mentation of normally unified neuromodulatory states. The forebrain, midbrain, and brainstem fail to occupy a single position the AIM state space. Instead, there is a split along the Activation or Input axis, with different brain regions occupying different positions in AIM space. Insight into how these associations might arise comes from the ex­ample of delirium associated with alcohol withdrawal.

Chronic alcohol usage blocks REM and upon withdrawal there is a REM rebound, marked by increased amounts and intensity of REM sleep. It is during this period of REM rebound that delirium occurs. Presumably, the brain reacts dynamically to the alcohol-induced REM deprivation with an increased pressure towards REM sleep. We imagine this as pressure to move the brain lower in the AIM state space, towards lower aminergic and higher cho­linergic neuromodulation. But while this pressure is exerted by the brain, the alcohol blocks the actual movement through the state space.

When alcohol is withdrawn, the REM pressure forces AIM down in the state space causing increased REM sleep, but also causing hallucinations and delirium during waking. These symptoms of psychosis are caused by the release of brain systems which are normally inhibited except in REM sleep. In this case, it is an abnormal shift downward along the "M" axis of the state space which pro­duces the splitting of AIM and causes its dissociation along the "I" axis. The net result is to move the brain-mind close to a position of REM sleep in waking.

(end of paraphrase)

 

Alzheimer’s

In Alzheimer's disease, plaques of an insoluble protein fragment, beta amyloid, accumulate in the cleft between neurons, blocking communication. (Carter; Mapping the Mind, 178)

Alzheimer's, Parkinson's, and Huntington's diseases are characterized by clumps of defective proteins and other cellular trash that the cells fail to clear away. (Horstman; Healthy Aging Brain, 97)

Modified tau protein heaps are the first step toward neurofibrillary tangles, one of the hallmarks associated with Alzheimer's disease. (Horstman; Healthy Aging Brain, 94)

Amblyopia

Discordant vision through the two eyes during an early critical period results in the enduring loss of visual acuity (amblyopia) that reflects aberrant circuit remodeling within primary visual cortex (V1).

Amnesia

Storied patient HM had surgery to control epilepsy; both medial temporal lobes removed in 1953; extensively studied aftermath. (Llinás; I of the Vortex, 185)

HM had surgery to control epilepsy, both medial temporal lobes removed 1953, extensively studied aftermath. (LeDoux; Synaptic Self, 99)

 

(paraphrase of Koch; Quest for Consciousness, 194ff)

HM has no obvious perceptual deficiencies, but suffers from severe memory losses, He is severely amnesic for events that occurred since, a couple of years prior to his operation. He forgets events as soon as they are out of his sight and mind. He can, with effort, retain a three-digit number by continual rehearsal. When he is distracted, though, the number is gone. When a person leaves the room and reenters a few minutes later, H.M. can't recall having met them before. An hour after a meal, he is unable to remember what he had eaten or even whether he had eaten at all.

Nevertheless, HM has no specific intellectual loss, has normal immediate memory, and can learn and retain new skills, although he is unable to remember how he had acquired these abilities. And he is most certainly conscious. He can describe and experience his environment, he cor­rectly answers questions about immediate events, and so on.

The pattern of his deficits proves that declarative memories are acquired and stored at distinct sites from procedural memories.

(end of paraphrase)

 

Damasio concludes that basal (core) consciousness cannot depend on these extensive brain regions: Temporal region damage, hippocampus and medial cortices overlying it, polar temporal region, a sizable sector of the lateral and inferior temporal regions, amygdala. (Damasio; Feeling of What Happens, 121)

Anesthesia

Consciousness is absent in deep sleep, deep coma and in deep anesthesia.  The fact that depth has to be specified clearly implies that basal (core) consciousness is not an all-or-none state. (Baddeley; Working Memory, 302)

Temporal dynamics are far too slow to clarify which region (i.e. thalamus or cortex) is affected first by anasthesia and thus could be considered the primary cause of anesthetic-induced unconsciousness. (Alkire; General Anasthesia, 124)

A number of empirical findings support the hypothesis that the main effect of anasthesia occurs in the cortex. (Alkire; General Anasthesia, 124)

Attention deficit hyperactivity disorder (ADHD)

(Hobson,  Dreaming as Delirium, 177ff)

Rapid disengagement is not necessarily good, as shown by children who have attention deficit disorder. For decades the assumption about kids who didn't pay attention, particularly when in school, was that they were "hyperactive." This was the conclusion because the same kids were usually fidgeting, moving around in their chairs, and tapping their feet on the floor instead of staring in blurry-eyed obedience at the blackboard. Note that their "hyperactivity" consists of motor acts. Focusing their eyes on the blackboard and maintaining their concentration (volition) also depend on motor programs. The problem with such children is not that they can't pay attention to anything, it's that they are paying attention to everything. They rapidly disengage from a given signal in order to engage all the others. They fail to inhibit enough motor signals so they can focus on a few.

Today these children are put on a regimen of a mild amphetamine, a molecule that is similar to norepinephrine (notice that amphetamine is an amine). This boost enables them to inhibit some of the distracting motor movements, allowing them to concentrate better. There are adults who have the same problem and are helped with the same drugs.

The main point is that impairments in attention, whether they occur in the REM-sleep state or the awake state of people with attention deficit disorder, share a common chemical cause: a decrease in output from the norepinephrine system.

(end of paraphrase)

 

Many ADHD patients describe their conscious experience as a blur, or as filled with static. (Ratey; User's Guide to Brain, 130)

 

Autism

Autism might be due to a mutation of homeotic genes that leads to faulty brain construction and connections. (LeDoux; Synaptic Self, 68)

Unique features of human cortical development probably underlie neurodevelopmental disorders that affect the cerebral cortex, such as autism and schizophrenia. (Neocortex Outer Region Subventricular Zone Development)

Typically developing human infants preferentially attend to biological motion within the first days of life. Perception of biological motion may be altered in children with autism from a very early age, with cascading consequences for both social development and the lifelong impairments in social interaction that are a hallmark of autism spectrum disorders.

A small percentage of autism spectrum disorders (ASD) patients carry mutations in genes encoding neuroligins, which are postsynaptic cell-adhesion molecules.

Autistic children -- 'slow learners', information comes in faster than they can process it; state of confusion may result. In engineering signal theory, these are called dropouts or aliasing errors; sampling rate too low for a rapidly-changing incident stimulus. (Schneck & Berger; Music Effect, 85)

 

Link to — Autism Spectrum Disorder

Research Study — Autism Therapy may involve Signaling Pathway that Controls Protein Synthesis

Research Study — Orbitofrontal-Amygdala Circuit and Social-Emotional Behavior

Link to — Embryonic Development of Brain (Oral Language Development)

Research Study — Autism Diagnostic decline in Eye Fixation in Infants

Research Study — Autism and the Transcription of Long Genes

Reference — Severe Autism, Science, 11 October 2013, p.179

 

Blindsight

As a result of brain injury to the primary visual cortex (V1), patient does not see anything in the blind part of the visual field, but somehow the behavioral responses are influenced by the unseen stimuli. (Revonsuo; Inner Presence, 368)

Blindsight first came to light on the battlefields of the First World War when blinded soldiers were seen to.duck bullets even though they had no idea they were doing so. (Carter; Mapping the Mind, 184)

 

Coma; Vegetative state

Coma -- an enduring sleep-like state of immobility with eyes closed from which the patient cannot be aroused. (Tononi & Laureys; Neurology of Consciousness, 388)

Coma, AIM diagram. (Hobson; Dream Drug Store, 176)

Coma is a state of unarousable unconsciousness due to the disfunction of the brain's ascending reticular activating system (ARAS), which is responsible for arousal and the maintenance of wakefulness. (Young; Coma, 137)

A person in a deep coma may lock onto a moving target, so they may seem to be watching those who pass by. They might clutch at things and grimace when pricked with a pin. These actions are purely reflex but nevertheless deeply disturbing for those who see them. (Carter; Mapping the Mind, 184)

 

Research Study — Thalamic Stimulation after Severe Traumatic Brain Injury

 

Concussion

Boxer who suffers a brain concussion may remember going to the sporting event and even climbing into the ring, but everything from them all will be a blank. (Squire & Kandel; Memory, 132)

 

Dementia

Dementia -- a chronic syndrome of heterogeneous aetiology characterized by multiple cognitive deficits that include severe memory impairment. (Dudai; Memory from A to Z, 77)

Depression

Anxiety is the most common of the syndromes that cluster with depression as well as with manic depression. (DePaulo; Understanding Depression, 16)

Electroshock treatment for depression. (Hobson; Dreaming as Delirium, 134)

Electroconvulsive therapy (ECT) for depressive illness. (Squire; Memory and Brain, 206)

Electroconvulsive therapy (ECT) for depression, a procedure that often produces memory disturbances as a side effect. (LeDoux; Synaptic Self, 106)

Subdivisions of the anterior cingulate cortex (ACC) have been consistently implicated in the pathophysiology of depression. (Vogt; Cingulate Neurobiology, 529)

Among depression patients receiving somatic interventions, some respond to treatments that modulate serotonergic function while others only seem to respond to treatments targeting multiple neurotransmitter systems; others only achieve an antidepressant response with interventions with widespread neurophysiological effects (e.g. electroconvulsive therapy). (Vogt; Cingulate Neurobiology, 239)

People who are depressed systematically blocked out the positive aspects of their life, seeing only the negative. When a genuinely negative event occurs for depressed people, they tend to exaggerate its magnitude, significance and consequences.A minor error becomes a major catastrophe.  A normal problem becomes an insoluble dilemma. The result of negative thinking is that an individual feels sad and hopeless, withdraws from other people, and may become suicidal. (Lasley; Cognitive Therapy, 35; Insel, Cerebrum 2009)

In cognitive therapy, depressed patients learn to identify distorted thinking, modify beliefs, relate to others in different ways, and change their behavior. (Lasley; Cognitive Therapy, 36)

With cognitive therapy, patients learn to observe their emotional responses to life events, block the automatic resurgence of distressing memories, and reduce their tendency to brood and overanalyze irrelevant information. Cognitive therapy decreased the activity in the prefrontal areas but increased activity in other areas deeper in the brain such as the anterior cingulate, involved in directed attention and monitoring of emotions, and the hippocampus, involved in memory encoding and consolidation. (Lasley; Cognitive Therapy, 39)

Antidepressants adjust the exchange of chemical messengers at the synapse. With antidepressant therapy, with balance restored among the various chemicals -- typically serotonin, dopamine and norepinephrine -- a chain of events begins that ultimately results in the depressed patient's beginning to feel better. (Lasley; Cognitive Therapy, 38)

 

Research Study — Dopamine Transporter Antidepressant Mechanism

Research Study — Antidepressants action on Biogenic Amine Transporters

Research study — Depression Core Symptoms Mediated by Lateral Habenula

Research study — Amygdalar and Hippocampal substrates of Anxious Temperament — Studies in children demonstrate that anxious temperament (AT) is an important risk factor for the later development of anxiety disorders, depression and comorbid substance abuse. Using 238 young monkeys from a multigenerational single-family pedigree, the study showed that the central nucleus region of the amygdala and the anterior hippocampus are key components of the neural circuit predictive of AT.

 

Dizziness

 

Drug-induced abnormal states

Cocaine causes a massive release of dopamine onto the nucleus accumbens, and the user experiences a sudden 'rush' of extreme pleasure. (Johnston; Why We Feel, 116)

Antianxiety drugs such as Valium work by enhancing GABA's natural ability to regulate glutamate. (LeDoux; Synaptic Self, 56)

Prozac may reduce exaggerated fear and anxiety in psychiatric disorders by enhancing the ability of serotonin to facilitate GABA inhibition. (LeDoux; Synaptic Self, 64)

Long before the days of Prozac, however, alcohol, narcotics, analgesics, and hormones such as estrogens and testosterone had shown that feelings can be altered by chemical substances. (Damasio; Looking for Spinoza, 119)

First-person accounts of some substance abuses -- it felt like a total body orgasm; a relaxed feeling like you get after sex, but better; feels like every cell and bone in your body is jumping with delight; a generalized tingly, warm sensation. (Damasio; Looking for Spinoza, 122)

Drugs such as morphine or aspirin alter the brain's pattern of pain or pleasure.  So do ecstasy and scotch.  So do anesthetics.  So do certain forms of meditation.  So do thoughts of despair.  So do thoughts of hope and salvation. (Damasio; Looking for Spinoza, 124)

Natural rewards and drugs of abuse can alter dopamine signaling.

Chronic drug use can lead to addiction, which is initiated by specific brain circuits. The mystery of how one class of drugs, the benzodiazepines, affects activity in this circuitry has finally been solved.

 

Epilepsy

Epileptic seizures - normal brain activity is disrupted. (Koch; Quest for Consciousness, 222)

In an epileptic fit, the source of the waves is usually high up in the cortex, but during REM sleep down in the base of the brain stem. (Hobson; Dreaming as Delirium, 135)

Epileptic activity may be among the most primitive of all functional states -- a bit like sneezing. (Llinás; I of the Vortex, 63)

Paul's vision on the road to Damascus; van Gogh; Jonathan Swift, Gulliver's Travels; Lewis Carroll, Alice in Wonderland; possible temporal lobe epileptics. (Calvin; Neil’s Brain, 79)

 

Research study — Epilepsy Control by Transcranial Electrical Stimulation — seizure-triggered, feedback transcranial electrical stimulation (TES) can dramatically reduce spike-and-wave episodes in a rodent model of generalized epilepsy.

 

Hemineglect

Syndrome that is classically associated with impaired spatial attention. (Awh; Spatial Working Memory, 361)

Unilateral visual neglect -- a person can lose visual awareness of one half of the visual world but maintain awareness of the other half. Patients with neglect do not respond to information that is contralateral to the side of the lesion. (Robertson; Attention and Parietal Function, 260)

Classical symptoms of neglect (spatial deficit for one half of the field), closely linked to functions of the parietal lobes. (Robertson; Attention and Parietal Function, 261)

Acute stages after stroke, neglect is at its worst; may take up to six months for neurological problems to stabilize. By that time it is more likely than not that clinical symptoms of unilateral neglect are gone. (Robertson; Attention and Parietal Function, 261)

Brains compute spatial information in order to perceive and attend to objects veridically. (Robertson; Attention and Parietal Function, 274)

(see Neglect below)

 

Human Genome Project

Link to — Human Genome Project and Neuropsychiatric Disorders — using large collections of patient DNAs with extensive phenotype information, the past several years have witnessed a series of replicable, credible, and increasingly useful genetic discoveries in autism, schizophrenia, and bipolar disorder.

 

Hypnosis and Meditation

Hypnosis and meditation are voluntary changes of state that rely on dissociation to brain benefits. (Hobson; Dreaming as Delirium, 217)

Hypnosis is characterized by highly focused attention as well as by heightened compliance with suggestions. (Vogt; Cingulate Neurobiology, 383)

Hypnosis and meditation are effective because of dissociation; they enable a person to "tune out" the outside while remaining awake, thus reducing stress. (Hobson; Dreaming as Delirium, 217)

Choosing which states your brain-mind may occupy -- meditation, hypnosis, trance. (Hobson; Dreaming as Delirium, 219)

Manic-depressive

Manic-depressive can be creative (perhaps Vincent van Gogh, Robert Schuman)

Many creative individuals have taken their lives -- Vincent van Gogh, Virginia Woolf, Ernest Hemingway. (Andreasen; Creating Brain, 105)

Migraine Cinematographic Vision

Sometimes manifest during visual migraine;    illusion of motion has been lost,    migraine temporarily inactivated the cortical motion area. (Koch; Quest for Consciousness, 266)

Neglect

Unilateral neglect -- dramatic loss of awareness of one side of space, remains a mystery, because the primary sensory pathways may still be intact, and yet the patient is not aware of the stimulus. (Revonsuo; Inner Presence, 370)

(see Hemineglect above)

 

Nicotine Addiction

Nicotine addiction begins with high-affinity binding of nicotine to acetylcholine (ACh) receptors in the brain.

 

Obsessive compulsive disorder (OCD)

There has emerged a growing consensus that brain circuitry contained within the orbitofrontal cortex, anterior cingulate gyrus and the basal ganglia is intimately involved in the expression of the symptoms of obsessive-compulsive disorder (OCD). (Schwartz; Obsessive Compulsive Disorder, 111)

 

Nature 448, 871-872 (23 August 2007)

Neuroscience: Obsessed with grooming

Steven E. Hyman

Department of Neurobiology, Harvard Medical School, Massachusetts Hall, Cambridge, Massachusetts 02138, USA.

(paraphrase)

Obsessive compulsive disorder (OCD) is one of a spectrum of disorders characterized by obsessions (intrusive, unwanted thoughts) and compulsions (ritualized behaviours intended to overcome the anxiety and tension resulting from the obsessions). Other similar conditions include Tourette's syndrome, which produces several motor, and occasionally vocal, tics, often accompanied by obsessions and compulsions.

The available treatments for OCD are only moderately effective. They include cognitive behavioural psychotherapies and antidepressant drugs that increase levels of the neurotransmitter serotonin at synapses.

Understanding the neurobiology of higher cognition, emotion and control of complex behaviour is still a daunting frontier.

Drugs from the selective serotonin reuptake inhibitor (SSRI) class — which selectively enhance serotonin-mediated neurotransmission throughout the brain — is used to treat OCD. A condition responsive to an enhancer of serotonin neurotransmission does not signify a primary defect in serotonin-mediated signalling; instead, the defect is in glutamate-responsive synapses. Alterations in serotonin seem to modulate glutamate action. Accumulating evidence indicates that OCD and its associated disorders result from abnormalities in neural circuits spanning the frontal, striatal and thalamic regions of the brain.

Striatal origin for OCD-like symptoms would make a lot of sense. The medium spiny neurons of the striatum receive convergent glutamate-mediated inputs from the cerebral cortex, which provide detailed information about the context in which behaviours occur. These neurons also receive dopamine-mediated inputs from the midbrain that report on the significance of the behaviour — for example, whether it yields an unexpected reward.

When something important happens, the striatum stimulates circuits that project via the thalamus to the prefrontal cortex; this leads to the formation of memories that can later guide the planning and control of behaviour. Abnormalities in synaptic function within frontal–striatal–thalamic loops could lead to unintended behaviours or even unintended thoughts.

These disorders, like other major psychiatric diseases, seem to be heterogeneous with complex underpinnings — probably involving several genes — that, in interaction with developmental and environmental factors, could lead to abnormalities in frontal–striatal–thalamic circuits.

(end of paraphrase)

 

Prosopagnosia

Inability to recognize familiar people from their faces. (Revonsuo; Inner Presence, 369)

 

Schizophrenia

Unique features of human cortical development probably underlie neurodevelopmental disorders that affect the cerebral cortex, such as autism and schizophrenia. (Neocortex Outer Region Subventricular Zone Development)

Schizophrenia is a severe mental disorder with a lifetime risk of about 1%, characterized by hallucinations, delusions and cognitive deficits, with heritability estimated at up to 80%. Research on pathogenesis has traditionally focused on neurotransmitter systems in the brain, particularly those involving dopamine. A research study indicates that schizophrenia is significantly associated with single nucleotide polymorphisms (SNPs) in the extended major histocompatibility complex region on chromosome 6.

 

Research Study —  Schizophrenia Mutations in Synaptic Networks

 

Sleep walking

When a person sleepwalks, the cortex of the upper brain remains asleep while the lower brain is awake. (Hobson; Dreaming as Delirium, 217)

During sleepwalking, the eyes are open and staring, patients can speak and answer to questions, usually in an incomprehensible manner. (Bassetti; Sleepwalking, 109)

Split-brain phenomenon

Roger Sperry (Koch; Quest for Consciousness, 289)

Functional lateralization evident in behavioral tests of forebrain commissurotomy (split-brain) patients. (diagram) (Roger W. Sperry, 167)

Research over the past 45 years on split-brain patients have revealed unique specialized processes in each hemisphere, including some recently discovered specialized processes in the right hemisphere. (Gazzaniga; Left Hemisphere/Right Hemisphere, 261)

The experience of split-brain patients is indicative of a conscious system that is comprised of thousands of specialized local circuits. (Gazzaniga; Left Hemisphere/Right Hemisphere, 261)

Patients who have undergone surgical section of the corpus callosum for therapeutic purposes leading to a splitting of the thalamocortical system, consciousness is split. (Pietrini; Consciousness and Dementia, 204)

 

Stroke

Anosognosia: the vehement denial of paralysis in some patients who have suffered a right hemisphere stroke. (Ramachandran; Illusions of Body Image, 29)

 

Transient episodes

Migraine Aura

Transient episodes: interpretations can be fantasy (perhaps: Saint Paul, bright light; Emperor Constantine, vision of the cross) (Calvin; Neil’s Brain, 79)

 

Vegetative States

(paraphrase of Shadlen & Kiani; Nature, 2 August 2007, 539-540)

To be awake is to be in a state of engaging with the environment. To have agency is to interrogate this environment with some goal or purpose. This capacity to engage and interrogate seems to go awry in various disorders that affect cognition. And nowhere is this incapacitation more patent than in coma and related conditions.

Coma. The patient seems to be asleep and cannot be awakened. There is no spontaneous organized behaviour, not even pushing away of an irritant, and there is no evidence of any awareness of sensory cues — no response beyond reflexes mediated by the brainstem and the spinal cord. Most patients in coma do not recover meaningful neurological function, but many do progress to states that are clearly distinguishable from coma, such as:

Persistent vegetative state (PVS). This is similar to coma in all respects except that, at times, the patient does not seem to be asleep. The eyes may be open, and spontaneous, non-purposeful, roving eye movements occur. PVS is probably the result of a return of some of the functions that would govern the sleep–wake cycle, albeit in the absence of a functioning cerebral cortex. As a result, it is only the brainstem and perhaps a few islands of dysfunctional (or disconnected) cortex that regain function.

Minimally conscious state (MCS). In contrast to PVS, patients show occasional signs of arousal and organized behaviour. Nevertheless, for the most part, there is a profound deficit in consciousness. Indeed, functional brain-imaging studies indicate that parts of the cortex may be able to function even when the patient seems to be unconscious. This observation and the differential prognosis of MCS and PVS call for more careful classification of patients, which may currently be biased towards PVS.

(end of paraphrase)

 

Nature 443, 132-133 (14 September 2006)

'Vegetative' patient shows signs of conscious thought

Michael Hopkin

Evidence of brain activity raises issues for neurologists.

The question of whether outwardly unresponsive patients may in fact be aware of their surroundings is one of the most heated debates in clinical neuroscience. The research raises questions about whether the definition of a vegetative state should be changed to allow the possibility of using brain imaging to ascertain awareness. Currently, the condition is diagnosed if patients show no external awareness of themselves or their environment, although, in contrast to coma patients, their sleep–wake cycle is preserved. Typically, after a month the patient is judged to be 'persistently vegetative', and the condition is generally pronounced 'permanent' after a year without signs of recovery.

 

The posterior parietal regions have been noted to show a relative decrease in functioning during altered states of consciousness, such as during the persistent vegetative state and sleep. (Alkire; General Anasthesia, 127)

Coma, Persistent Vegetative State (PVS), Minimally Conscious State (MCS) -- (table) (Schiff; Comatose, 191)

Prognosis for someone in a coma very much depends on the person's age, the amount of structural damage, and whether there is evidence of direct injury to the brain stem. (Schiff; Comatose, 191)

If a patient remains in a vegetative state for more than 30 days, he is deemed to be in a persistent vegetative state (PVS). (Schiff; Comatose, 191)

Comatose state, if uncomplicated of the factors, is typically followed within 7 to 14 days by an indeterminate period during which an eyes-open, "wakeful" appearance alternates with an eyes-closed, "sleep" state. (Schiff; Comatose, 191)

Prospects for recovery of consciousness become grim when the vegetative state becomes chronic or permanent, after three months in the case of anoxic injury, and a year a following traumatic injuries. (Schiff; Comatose, 191)

Patients in a vegetative state, including Terry Schiavo. (Schiff; Comatose, 198)

Seminal 1976 Karen Quinlan case, the New Jersey Supreme Court allowed the removal of life-sustaining therapy because Quinlan was in a vegetative state without any possibility of return to a "cognitive sapient state." (Schiff; Comatose, 199)

Because the futility of any potential treatment was pivotal in justifying the right-to-die for PVS patients, many physicians remain nihilistic about potential interventions in these patients with severely impaired consciousness. (Schiff; Comatose, 199)

 

Drugs of Abuse

Altered states of consciousness

Chemically induced pleasure, typically interact with neurotransmitters and/or their receptors in the brain.

Stroke and Tumor

Consciousness can survive most partial loss of brain functionality. However, damage to some areas of the brain can result in substantial changes in personality.

Spinal Cord Injury

Spinal cord damage resulting in retention of human-type consciousness with virtually no peripheral voluntary movement capability

Locked-In Syndrome

Brain stem damage resulting in retention of core or human-type consciousness with virtually no voluntary movement capability. Typically, the only residual capability is vertical movement of the eyes via the first two cranial nerves. A devastating predicament.

Vegetative State

Brain damage with some residual FAPs and movement, but no consciousness. (Abnormal Function of Brain)

Psychiatric Disorders and Medication

Natural disorders of consciousness, treated with medication. Depression treated with Prosaic, schizophrenia with dopamine.

 

 

    Link to — Consciousness Subject Outline

    Further discussion — Covington Theory of Consciousness