Ideational Apraxia 
P. Reynolds

The underpinnings of human behavior have led several
theorists to develop unique models that allow for
universal similarities and the internal components
believed to influence behavior.  These models in their
own rite, are not always parallel.  Each model brings
forth a different level to explain the fundamental
aspects concerning human behavior.  Just as each behavior
from each individual is different, so are the theories
which explain them. When proposing the mechanics involved
in cognitive function, it may be described as an
abstract, internal understanding of behavior.  In this
sense, the behavior of investigation is relative to other
observed behaviors and has been developed by comparing
the characteristics of proposed dysfunction in patients
to those of normal behavior.
     
Apraxia is a disorder which most often occurs after
insult to the left hemisphere of the brain.  The general
definition of Apraxia states it as a disorder involving
speech (Rosenbek et al.,1984).  It prevents the execution
of voluntary and commanded motor activity involved in
speaking, despite normal muscle ability (Rosenbek, 1984). 
There are several types of Apraxia, each uniquely
involved in of motor/speech behavior.  I plan to focus on
Ideational Apraxia.  
     
Ideational Apraxia is the inability to plan and
discriminate between gestures (Barbieri & Renzi, 1988). 
These patients have the inability to initiate gestures
appropriate for the utilization of most objects (Renzi,
1985).  Although these subjects are able to comprehend
and identify most objects and their use, when asked to
imitate use of these objects or to actually use these
objects, they exercise this request incorrectly (Poeck,
1985).  It is a disturbance in the concept involved with
the organization of action (Rosenbek, 1984).  Patients
with ideational apraxia would most likely perform poorly
when asked to distinguish correct vs. incorrect gesture
use in photographs (Rosenbek, 1984).  Their disability is
most evident when the patient must design the action and
would be very invisible when a model is provided for them
based on verbal instruction (Faglioni & Basso, 1985,
Mackay, 1985).  Imitation and mimicking movements are
also easy for these patients simply because they may use
tactile cues, visual information and reference points
(Motomura & Yamadori, 1994).  As the desired action
becomes more difficult by addition steps in a sequence of
movements, the disorder becomes more severe (Hecean &
Albert, 1978).  
          
The disabilities proposed in ideational apraxia are best
reflected in a sequence of motions rather than a single
one or two step action of object bound movement (Platz, &
Mauritz, 1995).  These patients' errors are sequential in
nature.  Errors shown by these patients have a wide range
of variability.  For instance, these individuals may stop
after the first partial act has been committed (Hecean &
Albert, 1978).  They may confound the order of the steps
by omitting one or several intermediate steps (Hecean &
Albert, 1978).  A similar action may often times be
substituted for a desired action (Hecean & Albert, 1978).
And lastly, a part of the required action may be omitted
or executed using an incorrect object (Poeck, 1985)  In
all cases, hesitation to a movement is frequent and it is
usually repeated during self correction. This indicates
the patient is aware of the inadequacy of the motor
performance but still performs inappropriately (Poeck,
1985).  
          
"There is no standardized battery of tests available to
examine motor apraxia" (Poeck, 1986). There is, however a
system of dividing up movements into two broad categories
called transitive and intransitive gestures(Renzi, 1985). 
Transitive movements are gestures which direct the
manipulation of objects (Renzi, 1985).  Intransitive
movements are gestures which mean to express ideas or
feelings (Renzi, 1985). Transitive gestures are primary
for establishing  a dysfunction in the sequences and
conception of actions. Intransitive gestures readily
measure the ability to repeat and mimic well practiced
actions or movements (Renzi, 1985). Ideally both are
inhibited or disrupted in ideational apraxia (Ellis &
Young, 1993).
     
Many models of cognition apply different explanations for
ideational apraxia and its fundamental existence.  One of
the biggest controversies rests in the question of
connectionism or serial processing theories (Solso,
1995).  Connectionism is defined as "a theory of the mind
that posits a large set of simple units connected in a
parallel distributed network" (Solso, 1995).  A lesion in
a particular area would therefore be the stem of
dysfunction in apraxia (Rosenbek, 1984).  It would be the
disconnection caused by a lesion which would then  define
impairment.  This would result in damage to the cortical
center responsible for formulation and programming of
speech (Hecean & Albert, 1978).  Connectionism maintains
the conclusion that dysfunction is then a result of
damage to a functional center or unit within a
system(Rosenbek et al., 1984)  In apraxia, this theory
would result in a disconnection between centers and
interrupt the flow of information pertinent for
satisfactory in the role of language behavior (Rosenbek
et al., 1984).  A lesion causing apraxia would disconnect
the systems of actions from systems of speech (Hecean &
Albert, 1978).  

"A coalition or associative theory might suggest that the
brain areas function together to accomplish particular
objectives but that any one structure within this
coalition may also play a role in other coalitions of
behavior" (Rosenbek et al., 1984).  This theory assumes
that without coalitions, the behavior will disappear. 
Ideational apraxia would then be due to a disturbance in
the association elaboration of various inputs with motor
programs and be based on a disturbance in conceptual
motor movements (Poeck, 1985).  Behavioral affects are
reflected by functional coalitions of neuronal structures
which may cross traditional boundaries (Rosenbek et al,
1984).  The advantage to this model is that behavior can
become explainable by referring to anatomical structures
and their cooperation and interaction with multiple
substructures (Rosenbek et al., 1984).  
     
Since ideational apraxia often is seen with both
ideomotor apraxia and agnosia many different theories are
used to explain apraxia and may demonstrate the influence
of categorical inference.  Ideational apraxia is viewed
by some scientists as an independent category, unrelated
to other types of dysfunction (Renzi, 1985)  The
independent diagnosis states "it emerges when a patient
is required to manipulate an object and shows a loss of
the ability to evoke and organize appropriate gestures
(Renzi, 1985).  
     
It has also been defined as a severe case of ideomotor
apraxia (Miller, 1986).  The proposal  states; "gestures
are affected on command, then in imitation, and finally
at the most basic level in the very use of objects"
(Miller, 1986).  This view has been counter argued by the
presence of ideation apraxia in patients with no
ideomotor symptoms.(Renzi, 1985).  Most often a
ideational apractic is able to mimic gestures with no
problem and will display a bilateral rather than
unilateral effect on the limbs in respect to this
disorder.  This is clearly not the case with ideomotor
patients (Leiguarda et al., 1994).  

Other researchers are convinced that it is a sub
component of agnosia.  "A simple language based
explanation would predict a massive associative 
agnosia affecting generic identification simultaneously
in all modalities" (Goldberg, 1990). He also states that
other researchers have found this model is too simplistic
and fails to "operationalize" specific types of deficits
and was to test for them.  It states that "the
lateralization of language is fundamental and the
lateralization of other cognitive functions is secondary
to and derivative from it" (Goldberg, 1990).  

Nonetheless, the area within the brain which is damaged
in ideational apraxia is the one aspect which shows
similarities by almost all researchers.  It is damage to
the left hemisphere which is shown in to coincide with
ideational apraxia (Faglioni & Basso, 1985).  More
specifically, the posterior parietal lobe (Leiguarda et
al., 1994).The parietal cortex is responsible for evoking
and organizing motor patterns (Rosenbek et al., 1984). 
Most cases cite the left angular gyrus region and
associated subcortical structures as the areas of
degradation is these patients (Mackay, 1985).  There has
also been reports of ideational apraxia occurring in
patients with a lesion on the temporal branch of angular
artery between the posterior part of the Sylvan
fissure(Miller, 1986).  This apraxia results from large
lesions that are more diffuse and include the posterior
parietal locus (Hecean & Albert, 1978).      

     Ideational apraxia has been a wide area of research
for many investigators.  There have been countless
attempts to delegate one theory which would most readily
underlie biological function.  Although new theories
emerge almost daily, the perfect solution is still years
away.  A map of the entire cognitive realm deduced from
human behavior will most likely allow for the most
appropriate explanations and work towards reaching a
model congruent with biological aspirations. 

References

Barbieri, C., & De Renzi, E., (1988) The executive and
ideational components of apraxia, Cortex, 24: 535 to 543.

De Renzi, E., (1985) Methods of limb apraxia examination
and their bearing on the interpretation of the disorder,
Neuropsychological Studies of Apraxia and Related
Disorders, E. A. Roy (ed.). New York: Elsevier Science
Publishers B. V. pp. 45 to 62. 


Ellis, A., & Young, A., (1993) Human Cognitive
Neuropsychology. Hillsdayle: Lawrence Erlbaum associates.
pp. 259 to 268.

Faglioni, P., & Basso, A., (1985) Historical perspectives
on neuroanatomical correlates of limb apraxia, 
Neuropsychological Studies of Apraxia and related
disorders, E. A. Roy (ed.) New York: Elsevier Science
Publishers B. V.  pp. 3 to 34.   

Goldberg, E., (1990) Associative agnosias and the
functions of the left hemisphere, Journal of Clinical and
Experimental Neuropsychology, 12: 467 to 484.

Hecean, H., & Albert, M., (1978) Human Neuropsychology.
New York: Wiley Interscience. pp.
97 to 107.


Leiguarda, L., Merello, S., Marsden, C., (1994)  The
nature of apraxia in corticobasal degeneration, Journal
of Neurology, Neurosurgery, and Psychiatry, 57: 455 to
459. 

Miller, N., (1986)  Dyspraxia and its management. 
Rockville, Maryland:  Aspen.  pp. 17 to 25, 37 to 45.  

Makay, D., (1985) A theory of the representation,
organization and timing of action with implications for
sequencing disorders, Neuropsychological Studies of
Apraxia and Related Disorders; E. A. Roy (ed.). New York:
Elsevier Science Publishers B. V. pp. 267 to 306.

Motomura, N., & Yamadori, A., (1994) A case of ideational
apraxia with impairment of object use and preservation of
object pantomime.  Cortex, 30: 167 to 170. 

Platz, T., & Mauritz, K., Human motor planning, motor
programming, and use of new task relevant information
with different apraxic syndromes, European Journal of
Neuroscience, 7: 1536 to 1547. 

Poeck, K. (1985) Clues to the nature of disruptions to
limb praxis, Neuropsychological Studies of Apraxia and
Related Disorders; E. A. Roy (ed.).  New York: Elsevier
Science Publishers B. V. pp. 99 to 107.

Poeck, K.  (1986) The clinical examination for motor
apraxia, Neuropychologia, 24: 129 to 134.


Rosenbek, J., McNeil, M., & Aronson, A., (1984) Apraxia
of Speech: Physiology, Acoustics, Linguistics,
Management. San Diego: College Hill Press. pp. 21 to 50. 

Solso, R., (1995)  Cognitive Psychology.  Needham
Heights: Allyn & Bacon.  pp. 231 to 241.   
 

Copyright © 1997, Dr. John M. Morgan, All rights reserved - This page last edited March 17, 1997
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