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Discussion Starter · #1 ·
What part of the brain is responsible for consciousness? All of it, say most authors, with the cortex in the leading role but profoundly influenced by operations in the limbic system (emotions) and the reticulate formation (RF: attention, sleep-wake cycles, control of the body's physiological functions). {11}. But Eugene Shea {12} places consciousness in the reticulate formation, which he views as a servomechanism for the brain, and an interface between the brain and the organs of perception. By regulating sensory input through the reticular activating system, the RF decides which inputs need to be processed in consciousness, which should be inhibited, and which can be handled by unconscious stock responses.

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Discussion Starter · #2 ·
reticular activating system (RAS), a working system in the brain that controls levels of consciousness, attention, and concentration. A group of nerve fibers in many parts of the brain (thalamus, hypothalamus, brain stem, and cerebral cortex) ar...

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Discussion Starter · #3 ·
States of consciousness

1) Central nervous system governs sleeping, dozing daydreaming and full alertness

2) Neurons of the reticular activating system control the changing levels of consciousness by releasing serotonin

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Discussion Starter · #4 ·
Control of Consciousness

Ascending projections from the reticular formation terminate in the thalamus, subthalamus, hypothalamus, and basal ganglia.
The functions of most of these are poorly understood, but those to the thalamus seem to be particularly important.
They terminate in the intralaminar nuclei, which in turn project to widespread areas of the cortex.
Activity in this pathway is essential for the maintenance of a normal state of consciousness.
Bilateral damage to these fibres as they traverse or originate in the midbrain reticular formation results in prolonged coma.

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Discussion Starter · #5 ·
Consciousness can be broken down into AWARENESS and AROUSAL. Arousal generally reflects activity of the ARAS (ascending reticular activating system) and indicates a level of responsiveness to stimuli. Awareness includes, additionally, the ability to interpret these stimuli and produce meaningful responses, as well as a sense of oneself in relation to one?s environment.

Levels of consciousness can be assigned, for clinical consideration, by a system such as this one:


Fully awake, alert, oriented to environment (e.g., knows season of the year)
Spontaneous (voluntary) speech at a normal rate.
Normal voluntary and reflex somatic motor activity.
Eyes open; normal oculomotor activity.

Ability to respond to stimuli is intact, but inattentive
Spontaneous sentences, spoken slowly.
Decreased speed of voluntary motor activity.
Eyes open; decreased oculomotor activity.


Spontaneous words, spoken infrequently.
Decreased speed and coordination of voluntary motor activity
Eyes open or closed; decreased oculomotor activity.
Motor defenses are intact.

Vocalization only to stimuli that cause pain.
Markedly decreased spontaneous motor activity.
Eyes generally closed; some spontaneous eye movements.
Motor defenses still intact.

No vocalization.
Appropriate defensive movements, generally flexor,
to stimuli that cause pain
Eyes generally closed.

(Light coma)
No vocalization.
Only primitive mass movements to stimuli that cause pain.
Eyes closed; decreased spontaneous conjugate eye movements.
Abnormal body posturing.


No vocalization.
Decerebrate posturing to stimuli that cause pain, or no response.
Eyes closed; absent spontaneous eye movements.

Brain death
See below.

Persistent vegetative coma ? arousal without awareness. Eye movements appear normal, EEG shows normal sleep-wake cycle, but no real response to environment.

Note: lesion resulting in loss of corticobulbar/corticospinal paths, but intact ARAS, can lead to state of awareness with no ability to respond, other that with eye movements, ("Locked-in syndrome").

Transient loss of consciousness (fainting or syncope) is caused by a loss of oxygen or glucose supply to the brain which can be caused by a reduction in cerebral blood flow due to occlusion of blood vessels or a drop in blood pressure. When autoregulatory processes increase blood flow (and thus oxygen and glucose supplies), consciousness is regained.

When major damage occurs to the brain, a loss of consciousness for an extended period (coma) can occur. Two general types of cortical damage lead to coma. One type, apallic (without pallium or cortex), consists of widespread damage to the cerebral hemispheres. The other type is a more localized damage to the brain stem (reticular formation) and thalamus. Damage can occur by: (1) infratentorial lesions which affect the central core of the brain stem; (2) supratentorial lesions that indirectly compress deep diencephalic structures; and (3) metabolic disorders that affect wide areas of the brain.

Cerebral concussion is a loss of consciousness resulting from a blow to the head which does not cause gross cerebral damage. Loss of consciousness is transient lasting from seconds to about 30 minutes. It is thought that a concussion results from small hemorrhages in the brain.

Anesthetics are drugs which produce a reversible loss of consciousness which is dose dependent, predictable, and controllable in duration and depth. Four stages of anesthesia have been described during which there is a progressive slowing of EEG activity, spontaneous motor activity, and reflex activity. The mechanism of anesthesia is not known, although these drugs do depress synaptic transmission and may disrupt gap junctions.

Stage 1 ? Stage of Analgesia. Reduced pain sensation.

Stage 2 ? Stage of Delirium. Involuntary increase in activity due to removal of inhibition.

Stage 3 ? Stage of Surgical Anesthesia. Respiration automatic and regular. Depression of reflex activity to noxious stimuli.

Stage 4 ? Stage of Respiratory Paralysis. Respiratory arrest.

Assessment of level of consciousness, possible region of deficit:

A number of easily performed tests can help reveal:

whether an apparently unconscious individual is physiologically unconscious, as opposed to malingering (faking) or hysterical loss of consciousness.
whether a deficit is more likely metabolic or structural. (Metabolic disorders are likely to present with symmetrical symptoms. Unilateral symptoms are more likely due to a lesion.)
where a deficit may be located.
Assume that the individual is supine (lying face up), has a pulse, and is breathing.

Raise patient?s hand over his face. Drop the hand. Did it miraculously miss hitting his face? If so, the problem may not be disrupted neurologic function.
Is breathing normal?
Cheyne-Stokes (periodic) ? cerebral hemispheres compromised, bilateral lesion or metabolic disorder.
Hyperpnea/hyperventilation ? mesencephalon compromised
Ataxic breathing (gasping) ? medulla oblongata compromised.
Look at posture:
decorticate posturing (Arm flexion, adduction. Leg extension.) ? cerebral hemispheres compromised.
decerebrate rigidity (Arm extension, adduction. Leg extension.) ? lesion of brainstem below middle of mesencephalon.
Test pupil size and response to light:
Bilaterally fixed and dilated ? structural damage to mesencephalon? atropine poisoning? Barbiturate O.D.?
Bilateral pinpoint ? structural damage to pons? Narcotic O.D.? (treat with naloxone ? narcotic antagonist)
Asymmetric dilation ? structural lesion? Ipsilateral oculomotor nerve compression? ? warning! possible life-threatening uncal herniation.
Induced eye movements:
Doll?s Eye Reflex ? so called because dolls eyes tend to maintain a position with respect to gravity (move the head, the eyes retain same position in space). Test: rotate patient?s head to the side. Do eyes lag, as though staring at a fixed point above head?
Small reflex.?Normal awake response:
Large reflex ? lethargy or semicoma, brainstem ok.
NO reflex ? coma.
Unilateral reflex ? brain stem lesion.
Caloric test ? squirt ice water into ear canal (make sure tympanic membrane is intact).
Normal awake response: nystagmus away from that ear (after which he will probably hit you with something heavy). "Normal" unconscious patient: slow deviation of eyes towards ear. Brain stem ok.
No response: barbiturate coma? Compromised brain stem? Unilateral response: brain stem lesion?
Note: warm water has opposite effect: COWS (cold opposite, warm same).

Brain death (cerebral death)


All appropriate diagnostic and therapeutic procedures have been performed.
Criteria to establish brain death:

Coma. Cerebral lesion, no response, even to pain. Irreversible widespread damage
No toxins, etc present to account for symptoms. i.e., no barbiturates, tranquilizers, no liver or kidney failure.
Body temperature above 90? F (32? C)
Apnea (patient makes no effort to override respirator for 15 min)
Pupils fixed and dilated.
No cephalic reflexes (includes pupillary, corneal, oculovestibular, etc.). Spinal reflexes may persist.
If above criteria present for over 6 hours, or for 30 min at least 6 hours after onset of coma):

Isoelectric EEG
No brain stem evoked potentials

Table 1. Representative listing of the final diagnosis in patients with an initial diagnosis of "coma of unknown etiology"


Supratentorial mass lesions

Epidural hematoma

Subdural hematoma

Intracerebral hematoma

Cerebral infarct

Brain tumor

Brain abscess









Subtentorial lesions

Brain stem infarct

Brain stem tumor

Brain stem hemorrhage

Cerebellar hemorrhage

Cerebellar abscess








Metabolic and diffuse cerebral disorders

Anoxia or ischemia

Concussion and postictal states

Infection (meningitis and encephalitis)

Subarachnoid hemorrhage

Exogenous toxins

Endogenous toxins and deficiencies









Psychiatric disorders

A seizure is an abnormal electrical discharge within the brain. As such, it is symptomatic; there could be a number of underlying causes. A generalized seizure begins bilaterally (in both hemispheres) while a partial (focal or localized) seizure begins in one site within one hemisphere. A partial seizure may, of course, extend to involve both hemispheres, in which case it is termed a secondary generalized seizure.

Overview of seizure classifications:

I. Generalized = bilateral

1) Absence seizure ? momentary loss of consciousness

2) Atonic seizure ? loss of axial muscle tone, collapse

3) Convulsive seizure ?

tonic = tonic muscle contraction
tonic-clonic = alternating muscle contraction/relaxation
myoclonic = synchronous bilateral muscle jerks
II. Partial = focal

1) may progress to generalized

2) Simple ? no loss of consciousness. Can be sensory or motor.

3) Complex ? partial or complete loss of consciousness. Also called psychomotor. Temporal lobe involvement.

"Ictus" = seizure. "Interictal" = period between seizures.

Sleep is an active process, not simply the absence of wakefulness. Parts if the ARAS (ascending reticular activating system) are necessary to maintain wakefulness. Damage to these areas (roughly mid-collicular) results in coma. However, more caudal ARAS is necessary to permit sleep! Damage here causes wakefulness. Sleep can be divided into two states which can be distinguished on EEG, by behavior, and pharmacologically, in that they are differently affected by commonly available agents (e.g., alcohol, Valium, barbiturates). One state is known as slow wave sleep and consists of 4 progressively deeper stages, accompanied by progressively larger and slower EEG waves. Postural adjustments are common. Heart rate, blood pressure, and respiration are generally stable and may be decreased from waking. The other sleep state goes by many names, including REM sleep. REM sleep is particularly interesting in that brain activity is similar to that of an awake, alert, and active individual while body activity is inhibited to the point of paralysis. At the same time, there may be large swings in heart rate and blood pressure and respiration.

All organisms undergo daily alternations between rest and activity over the 24-hour cycle of day and night. These alternations continue with near 24-hour regularity even in constant conditions, and thus are true circadian rhythms, timed by the body?s biological clock. This pattern of rest and activity is also regulated by homeostatic processes, which are expressed as a tendency for the resting state to restore something used during activity. The function of these major state changes is not yet known. What is known is that the resting or sleep state is characterized by global changes in brain activity. Many brain sites contribute, but few sites are known that control sleep. We will study what is known about changes in both global and region active states. These are useful in diagnosis. The next few years will see great advances in our understanding of the process of sleep, how it changes with depression, organic disease, damaging and aging, and the contribution of regulatory sites. These advances will improve our ability to ameliorate the range of acute and chronic complaints that comprise sleep disorders

Many living things appear to sleep, i.e., they become quiescent. Even snails and scorpions manage this. Moving along the phylogenetic ladder, we find reptiles and amphibians with slow-wave rhythms of brain activity of the sort we associate with sleep. In birds and mammals, we find two distinct types of brain wave rhythm emerging during sleep: slow wave and active.

Slow wave sleep is a quiet sleep, characterized by high voltage, low frequency, synchronized brain waves (EEG). The individual can move, and often does, shifting position roughly every 20 minutes. By and large, parasympathetic activity dominates, leading to decreases in heart rate, blood pressure, and respiration. Sleepwalking occurs in slow wave sleep. In man, we can divide slow wave into 4 stages, aptly named stages 1, 2, 3, and 4, with progressively lower frequency and higher voltage waves. Stage 2 presents with waves and intermittent bursts or "spindles" of activity, and is sometimes called "spindle sleep." Stages 3 and 4 are referred to, collectively, as "delta sleep." Stage 4 sleep is the most difficult level to interrupt. Stage 4 slow wave sleep can be suppressed by benzodiazepines, which is useful as it provides a way to control night terrors that can occur in stage 4 sleep.

Active sleep, also known as paradoxical sleep (because brain activity looks a lot like the awake state), desynchronized sleep (because brain waves are no longer synchronized) and (here?s the one you?ll recognize) REM (Rapid Eye Movement) sleep (because they do?in phasic bursts of 50?60 per minute). This state is characterized by a low voltage, fast activity pattern in brain waves (EEG). In fact, brain metabolism can be higher during REM than when awake. There is a rise in brain temperature and a sympathetic activation which produces increases in heart rate, blood pressure, respiration, and gastrointestinal movements. REM is accompanied by general muscle atonia ? i.e., motor output is inhibited and the sleeper, to all intents and purposes, is paralyzed, with the exception of the muscles of the eye and middle ear. This paralysis originates from the dorsal pons.

REM sleep is when you do most of your memorable dreaming. It is also a) the deepest sleep

state ? hardest from which to awaken someone, and b) the lightest sleep state ? the one from which you are most likely to spontaneously awaken. REM is suppressed by alcohol and barbiturates. If you record at various sites around the brain during REM sleep, you find bursts of electrical activity preceding each eye movement. These bursts can be found particularly in nuclei in the pons, in the lateral geniculate of the thalamus, and in the visual and auditory cortex, earning them the tag of pontine ? geniculate ? occipital (PGO) spikes.

Non-REM and REM sleep cycle throughout the night. Typically, there are four to six periods which occur at 90 minute intervals. During periods of light sleep (stage 1), there is a transition to REM sleep. There is actually an orderly progression in sleep, from stage 1 through to 4 and back, hitting REM briefly. Then back down towards 4, back up for a longer visit in REM, and back down again. Note that after a couple passes, you begin to drop out stage 4 and then stage 3. By the end of the night, you are mostly switching between stage 2 and REM. Intervals between successive REM periods decrease throughout the night and REM periods become longer.

REM sleep occupies about 20?25% of total sleep. Stage 1 about 5%, Stage 2 about 50%, Stage 3 about 5% and Stage 4 about 15%. These sleep patterns change through the life span. Total sleep time decreases until early adulthood with corresponding decreases in the percentage of REM and Stage 4 non-REM sleep.

Contrary to initial theories sleep is not a period of neural inactivity, but rather, is a periodic active process. Sleep is a transient loss of consciousness, but exhibits many characteristics different from the typs of unconsciousness described above. The neural mechanism is not yet clearly understood, but seems to be an active inhibition of the ascending reticular (ARAS) and hypothalamic activating systems. Sleep is cyclic, or circadian, with a biological rhythmicity, in man, of approximately 25 hours, which is usually adjusted to the 24 hour daily cycle.

Early (1930s) studies showed that a mid-collicular transection resulted in a sleep-like EEG, while a lower transection allowed a fairly normal sleep-wake cycle. Conclusion: with no sensory input, the brain goes to sleep. WRONG. Later (1949), discrete lesions of ascending sensory pathways were shown to not cause sleep, while lesions of the reticular formation produced a sleep-like state. Conclusion: the tonically active reticular activating system keeps the brain awake. Decreasing RAS input allows sleep, i.e., passive approach to sleep. WRONG AGAIN. By 1959, it was demonstrated that RAS transections just caudal to those mentioned above actively prevented sleep. BOTTOM LINE: parts of the more rostral reticular formation are required to maintain wakefulness, while parts of the more caudal reticular formation are necessary to permit sleep.

The caudal region probably works by inhibiting the rostral activating reticular formation. This caudal region includes the raphe nuclei, as destruction of the raphe produces complete insomnia, while administration of drugs that increases serotonin levels increases the amount of non-REM sleep. Another area, the nucleus of the solitary tract, also seems to be involved in regulating activity of the ARAS (through inhibition) and, thus, can also induce sleep.

Nuclei of the brainstem reticular formation (PPT = pedunculopontine tegmental and LDT = laterodorsal tegmental) project monosynaptically to thalamic neurons and excite them. Thalamic neurons project to many cortical locations and excite them. The PPT/LDT (cholinergic neurons) fire during the desynchronization of EEG both during waking and REM. In addition, Locus Coeruleus (LC) neurons fire during waking to excite cortical and thalamic structures.

What happens at the transition to slow wave (synchronized) sleep? In part, these populations become quieter, so the thalamic and cortical targets become less activated, less responsive.

Of particular importance, there is a group of neurons, the reticular thalamic nucleus (RE) which is actively inhibited during waking. At the transition to SWS (slow wave sleep), these neurons are released from inhibition. Why does this matter? Because the RE is the pacemaker for spindle oscillations (stage 2 sleep). Spindle oscillations produce long-lasting inhibitory potentials in the thalamocortical neurons. This, in turn, decreases the thalamic transfer function (i.e., thalamus doesn?t pass on all the information it receives.) BOTTOM LINE: Since information from the periphery to the cortex is processed through the thalamus, inhibiting thalamic relay neurons means the higher brain is cut off from outside interruptions.

Sleep Disorders/Disturbances
Insomnia is the chronic inability to induce sleep or to achieve sufficient amounts of sleep. The causes of insomnia are unknown, but may involve: (1) disruption of normal circadian rhythms (e.g., jet lag); (2) aging (see decrease in sleep time during senescence in graph); and (3) psychological disturbances (both anxiety and depression can cause insomnia). Treatment is usually through administration of barbiturates or benzodiazepines; however, they are both addictive and disrupt normal REM sleep.

Sleep apnea is a frequent periodic cessation of respiration which occurs in some patients during sleep. The causes may be quite varied and occurs both in patients with insomnia and hypersomnia. Sleep apnea has been proposed as a possible cause for sudden infant death (crib death) syndrome (SIDS). The cessation of respiration appears to be through a suppression of activity of the medullary reticular respiratory center, but the mechanisms are unknown.

Narcolepsy is characterized by sudden, irresistible attacks of sleep. These attacks can occur without warning and often at inappropriate times (e.g., driving a car). After a short period of sleep (from minutes to hours), the patient awakes refreshed. However, unlike the sleepiness experienced by a normal, but sleep-deprived individual, narcoleptic sleepiness cannot be prevented by increasing the amount of sleep obtained per day.

Other symptoms which can accompany narcolepsy include:

(1) cataplexy, an abrupt, brief, loss of muscle tone and postural reflexes, not associated with any change in consciousness. It can be mild (muscle weakening) or severe (complete paralysis). Attacks are responsive to tricyclic antidepressants.

(2) sleep paralysis, inhibition of muscle tone during the onset of sleep or awakening;

(3) hypnagogic hallucinations, dreamlike experiences, often accompanying sleep paralysis. More like hallucinations than dreams in that the experiences are overlayed on an awareness of ones actual surroundings.

(4) sleep-onset REM, in which narcoleptic patients enter directly into REM sleep.

(5) decreased voluntary sleep latency, in which narcoleptics can fall asleep quickly upon request in comparison to normal subjects (2 min versus 15 min).

(6) lowered concentration of homovanillic acid in CSF

(7) frequent nocturnal wakenings

The causes and mechanisms of narcolepsy have not been fully elucidated. Drug treatment using stimulants has only met with mixed results.

NOTE ADDED IN PROOF: Narcolepsy has now been traced to abnormalities in the hypothalamic neuropeptide, hypocretin, or its receptor. Treatments are improving yearly.

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Discussion Starter · #6 ·
The Raphe Nuclei (Serotonin, 5-HT) ? This is a collection of nuclei distributed throughout the brainstem in the midbrain, Pons and medulla. They project widely throughout most of the central nervous system. The rostral nuclei project to the cerebral cortex and thalamus, while the more caudal nuclei project to the cerebellum and spinal cord. The neurons in the rostral structures are active during the waking state, and quite during sleep. The cells in the Raphe nuclei use Serotonin as a neurotransmitter. The chemical name for Serotonin is 5-hydroxytryptamine and it is often referred to as 5-HT for short. Hypoactivity in this system is thought to play a major role in depression (Fig. 15-12 in Bear et al.).

no offense but this post reminds me of something that i read out of my Anatomy Book last year.

I didn't do that well in Anatomy either

But i did get exempt from the Zoology final :)

663 Posts
Discussion Starter · #8 ·
levels of conciousness, sleep wake cycles, reticular activating system etc. Hmm....Is there a common denominator?
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