434 Neuroanatomy: Draw It to Know It
Apraxia & Neglect ( Advanced )
Here, we will learn about the anatomy of the apraxias
and the phenomenon of neglect. Overall, apraxias are
more common with left brain injuries and neglect is
more common with right brain injuries; therefore, we
will use a sagittal view of the left lateral hemisphere to
draw the anatomy of the apraxias and a sagittal view of
the right lateral hemisphere to draw the anatomy of
neglect. However, we need to accept that apraxias can
occur from right brain injury and neglect can occur from
left brain injury, and we need to accept, as well, that
although the laterality of the aff ected limb in the aprax-
ias is oft en contralesional, it is variable. In simple terms,
an apraxia is an inability to perform a purposeful action
in the setting of preserved overall neurologic function.
Broadly, the apraxias can be divided into the frontally
based executive apraxias, which aff ect movement, and
the posterior apraxias, which aff ect sensory skills and
sensorimotor planning.^10
First, in the left hemisphere, draw the following ana-
tomic landmarks: the precentral sulcus, central sulcus,
and intraparietal sulcus. Now, in regards to the executive
apraxias, fi rst, show that limb-kinetic apraxia occurs
from injury to the premotor area. In limb-kinetic apraxia,
there is impairment in fi nely graded fi nger movements
and awkwardness of the arm and hand, manifesting with
an inability to rhythmically open and close the aff ected
hand. In speech apraxia, which is a slowing and incoordi-
nation of speech in the presence of otherwise normal
language and sound vocalization, there is injury to what
is referred to in this context as the left precentral g yrus of
the insula (not shown).^10
In regards to the posterior apraxias, fi rst, show that
injury to the left hemispheric temporoparietal junction
produces ideational apraxia and then that left inferior
parietal lobule injury produces ideomotor apraxia. Note
that ideomotor apraxia also occurs through disconnec-
tion phenomena from injury to the premotor cortex and
anterior corpus callosum. Variations in the defi nitions
of ideational and ideomotor apraxia exist, but by at least
one accepted defi nition, ideational apraxia is an inabil-
ity to correctly conceptualize an action. For instance,
patients with ideational apraxia might brush their teeth
with a spoon or may be unable to sequence a complex
action, meaning , for instance, rather than putting a letter
into an envelope and sealing it, they might seal the enve-
lope and then try to stuff the letter into it. Ideomotor
apraxia is a failure to know how to perform a complex
motor movement; gestures, such as waving goodbye, are
more severely aff ected than concrete movements, such as
using an actual tool.^18 – 21
Now, let’s show an example of a more restricted poste-
rior apraxia. Indicate that injury to the superior parietal
lobule has traditionally been considered the site of optic
ataxia (aka visuomotor ataxia); note, however, that the
actual lesion site for optic ataxia may lie more infero-
posterior at the parieto-occipital junction. Optic ataxia
manifests with an inability to accurately reach for objects
due to visual guidance impairment. Optic ataxia is
one of three important features of Balint syndrome,
which is due to bilateral occipitoparietal lesions. Th e
other two features of Balint syndrome are gaze apraxia
(aka oculomotor apraxia or optic apraxia), which is an
inability to direct the eyes toward the intended target
(instead the eyes fi xate on random objects or wander
aimlessly), and simultagnosia, which is the visual fi xa-
tion on a part of an object and an inability to see the
object for its whole.^7 , 22 , 23
Gerstmann syndrome occurs from injury to the
left hemispheric inferior parietal lobule with specifi c
involvement of the angular g yrus. It is a four-part syn-
drome of left –right disorientation; fi nger agnosia, which
is a fi nger naming disorder; dyscalculia, which is a
calculation disorder; and dysgraphia, which is a writing
disorder.^24