Page 356 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Disorders of Memory
Two forms of memory are distinguished: De- pending on the extent and localization of the
clarative, explicit memory (semantic or epi- disorder, the loss can be reversible or irrevers-
sodic) stores memory that can only be recalled ible. In the former case the patient will lose
consciously (→ A). It is needed, for example, in items of memory, but they can be retrieved. In
order to be able to recognize certain things irreversible loss the particular items are per-
Systems (apples, animals, faces). Procedural, implicit manently lost.
memory (→ A3) does not require conscious ac-
Transitory bilateral functional disturbance
tivation for storage and recall. It is required,
of the hippocampus can cause anterograde
and retrograde (days to years) amnesia (tran-
e.g. for learning to play the piano.
Neuromuscular and Sensory formation first of all reaches the correspond- (frequent in chronic alcoholics) both antero-
To form declarative memory (→ A1) the in-
sient global amnesia). In Korsakoff’s syndrome
grade and retrograde amnesia can occur. Pa-
ing association cortex (e.g., the secondary vi-
tients thus affected often try to cover up gaps
sual cortex) via the particular primary sensory
cortical area (e.g., the primary visual cortex).
in memory by means of confabulations.
The procedural (implicit) memory (→ A3) is
From here, via the entorhinal cortex (area 28),
not impaired in lesions of the hippocampus. It
the information reaches the hippocampus,
which is essential for long-term storage of de-
allows imprinting, learning of skills, sensitiza-
ing on the task, cerebellum, basal ganglia,
tures in the diencephalon, basal forebrain, and
amygdala and cortical areas are involved. Both
prefrontal cortex the item is again stored in the
10 clarative memory. With mediation from struc- tion, habituation, and conditioning. Depend-
asssociation cortex. In this way the informa-
the cerebellum and basal ganglia play an im-
tion is first taken up, via the sensory memory, portant role when learning skills. Relevant af-
by the short-term memory, which can hold on ferent impulses reach the cerebellum via oli-
to the content for only a few seconds to min- vary and pontine nuclei. The storage capacity
utes. The information can be transferred to of the cerebellum can be lost by, for example,
the long-term memory, for example, through toxic damage, degenerative diseases, and trau-
being rehearsed (→ A2). Such rehearsal is not ma. Dopaminergic projections of the substan-
an essential precondition for the formation of tia nigra also play a part in the formation of
long-term memory, however. procedural memory.
It is particularly the transfer into long-term The amygdala is important in conditioning
memory that is impaired in lesions of the anxiety reactions. It receives its information
above-named structures in neurodegenerative from the cortex and thalamus and influences
diseases (e.g., Alzheimer’s disease; → p. 348), motor and autonomic functions (e.g., muscle
trauma, ischemia, alcohol, carbon monoxide, tone, palpitations [awareness of tachycardias],
and inflammation. In addition, memory for- goose-pimples) via the reticular formation and
mation can be temporarily stopped by electric hypothalamus. Removal of the amygdala (e.g.,
shock. The most important transmitter in the by trauma or opiates) cancels conditioned
hippocampus is glutamate (NMDA receptors). anxiety reactions. Bilateral removal of the
Memory formation is promoted by norepi- amygdala with portions of the hippocampus
nephrine and acetylcholine (nicotinergic re- and temporal lobe results in amnesia and dis-
ceptors). inhibited behavior (Klüver–Bucy syndrome).
Lesions in the hippocampus or its connec-
tions result in anterograde amnesia (→ A2).
The affected patients will from that moment
on no longer be able to form any new declara-
tive memory. They will remember events prior
to the lesion but none subsequent to it.
Retrograde amnesia (→ A2), i.e., the loss of
346 already stored information, occurs in disorders
in the relevant associative cortical fields. De-
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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