Page 352 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Consciousness
We become conscious of only a fraction of the ARAS (→ A5), such as NMDA receptor antago-
information reaching our brain. The conscious nists, alcohol, narcotics, hypnotics, psychoac-
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contents are stored in associative cortical areas tive drugs, anticonvulsives, Na /K -ATPase in-
that specialize in this task (→ p. 346). Con- hibitors (cardiac glycosides), heavy metals. Ex-
scious awareness requires not only that the treme excess or lack of hormones (e.g T 3 , T 4 ,
Systems specific afferents have been transmitted to the parathyroid hormone, adrenocorticoid hor-
mones, pheochromocytoma) as well as mas-
cerebral cortex, but also nonspecific activation
sive neuronal excitation, for example, caused
by the ARAS through which neurons from the
by pain or psychogenic disease (schizophre-
reticular formation activate wide areas of the
Neuromuscular and Sensory the thalamus (→ A). Lastly, neuronal excitability can also be so se-
nia), can lead to loss of consciousness (→ A6).
cerebral cortex via intralaminar neurons of
Damage to large areas of the cortex and/or
verely impaired by hyperthyroidism, hypo-
thermia, inflammatory (e.g., meningitis) or
breakdown of the ARAS brings about loss of
mechanical damage, and neurodegenerative
consciousness. In addition, there may be pri-
mary causes influencing neuronal excitability
disease that it could lead to loss of conscious-
in the above-mentioned neuronal structures.
ness (→ A7).
Loss of consciousness can be divided into
Ischemia (e.g., atherosclerotic vascular occlu-
the patient can still be roused and will re-
pair excitability directly or by cell swelling.
spond; in a stupor (profound sleep) patients
Swelling of glial cells impairs, among other
10 sion) or hypoxia (e.g., suffocation) (→ A1) im- several stages (→ A): in a state of drowsiness
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can be awakened by vigorous stimuli; when
and
functions, their capacity to take up K
thus to keep down the concentration of extra- in a coma this is no longer possible. In so-
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cellular K . This has an indirect effect on neu- called “coma dépassé” vital functions will also
ronal excitability. Part of the effect of tumors, have ceased (e.g., respiratory arrest).
abscesses, or bleeding is also exerted via ische- The split brain represents a special abnor-
mia or hypoxia (→ A1) in that they raise the mality of consciousness (→ B). Uniform con-
cerebral pressure and thus impair cerebral per- sciousness presupposes communication be-
fusion by narrowing the blood vessels. Hypo- tween the two cerebral hemispheres. This
glycemia also modifies excitability, partly via takes place along large commissural fiber bun-
cellular swelling (→ A2). Hyponatremia and dles through the corpus callosum and the
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ammonia (NH 4 ) also act via this mechanism. anterior commissure. In treating uncontrolla-
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The rise in NH 4 in hepatic encephalopathy ble epilepsy the commissural fibers have been
(→ p.174) causes the formation of glutamine transected in some patients, stopping this
from α-ketoglutarate and glutamate in glial communication between the two hemi-
cells; the accumulation of glutamine causes spheres. The two hemispheres now produce
them to swell. At first this swelling is counter- two distinct kinds of consciousness: if an ob-
acted by the removal of osmolytes, seen in ject (e.g., a saucepan) is placed into the right
magnetic resonance imaging as a decrease in hand or placed in the right visual field, the pa-
the cerebral concentration of inositol. When tient can correctly name the object. But if the
this compensatory mechanism is exhausted, object is placed into the left hand or projected
consciousness is lost. into the left visual field, the patient is able to
The excitability of neurons is also affected recognize the object and, for example, find the
by epilepsy (→ p. 338), hyperosmolarity (hy- appropriate saucepan cover with the left hand,
pernatremia, hyperglycemia; → A3) as well as but will not be able to name it.
2+
2+
2–
by disorders of electrolyte (Ca , Mg , HPO 4 )
and acid-base metabolism (→ A4). Uremia (in
renal failure) and diabetes mellitus act partly
via changes in extracellular osmolarity and
342 electrolyte composition. Numerous sub-
stances can impair the excitability of the
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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