160

tion with improved gesture production in a real contextual environment [11].

Recently, the term swallowing apraxia has been
used in the dysphagia literature to describe a subtype of
dysfunction in the oral stage of swallowing. It has been
characterized as either a delay in initiation of bolus transfer with no lingual movement or by lingual searching
motions before initiating oral transfer [12]. Robbins and
Levine [1] described swallowing apraxia as a lack of
coordination of labial, lingual, and mandibular movement during the oral stage (p. 14). Deglutition moves
from more to less volition as the bolus moves from the
mouth to the pharynx [13]. Whereas the pharyngeal stage
is primarily involuntary and driven predominantly by
the brainstem, supratentorial regions modify and integrate with the brainstem to control the pharyngeal phase
of swallowing. The oral stage of swallowing is more
volitional, can be voluntarily augmented, and is primarily controlled by the cortex.
Because deglutition is a semivegetative function,
it has been questioned if swallowing apraxia is a true
form of apraxia [4,5,14]. The focus of this article, therefore, is to elucidate this disorder of swallowing apraxia
and determine whether it is truly a disorder of the praxis
system or more of an elemental motor dysfunction. Although limited, a review of the swallowing apraxia literature will be provided. Swallowing apraxia will be
compared and contrasted with the other forms of apraxia,
speech, buccofacial, and limb, to highlight behavioral
and neuroanatomic aspects. Once elaboration of this information is completed, final summaries, thoughts, and
future directions for possible research will be explored.

Literature Review
Tuch and Nielson [15] were the first to use the term
apraxia of swallowing to describe a patient with a sudden
inability to swallow or speak. Neurologically, the patient
presented with intact sensation and motor skills except
slight right facial asymmetry and buccofacial apraxia.
The investigators reported a complete inability to swallow, even saliva, although they did not indicate whether
swallowing was impaired for oral transfer or pharyngeal
motility. Dynamic swallowing tests were not completed.
Postmortem examination showed infarction of the left
lower portions of the pre- and postcentral gyri (Brodmanns areas 4 and 3-1-2).
Using cineradiography, Meadows [14] described
three patients with delays in oral transfer with lingual
and palatal incoordination. Extended durations of oral
transfer were reported clinically and confirmed with radiographic evaluation. Buccofacial apraxia was not evident. Radiographic testing showed right hemispheric in-

S.K. Daniels: Swallowing Apraxia

volvement in all three patients: two patients presented

with tumors and one with an abscess. Of the two surviving patients, swallowing returned to normal after surgical
intervention. Meadows disregarded the term apraxia of
swallowing that had previously been used by Tuch and
Nielson [15] to describe these patients because he felt
that this swallowing deficit was more of an elemental
motor impairment rather than a disturbance of the praxis
system.
In prospective studies of consecutive unilateral
stroke patients, Robbins and Levine and Robbins et al.
[1,2] described a subset of patients with left hemispheric
damage (LHD) who presented with incoordination of
labial, lingual, and mandibular musculature during bolus
transfer. These patients also presented with concomitant
buccofacial and speech apraxia. Robbins and Levine and
Robbins et al. [1,2] indicated that the overall long pharyngeal transit durations exhibited by the LHD patients
were due to extended oral transfer times in this group.
Although they did not comment on extended periods of
oral transfer for patients with right hemispheric damage
(RHD), analysis of their 1988 data [1] show delays in
oral stage transfer also for this group. If one used a score
lower than 2 standard deviations below the mean for the
controls as criterion for abnormal delay in oral transfer,
abnormalities for oral transfer would calculate to longer
than 0.9 sec for liquids and longer than 3.1 sec for paste.
Using this metric, 41% of the LHD patients presented
with abnormal delays for oral transfer of liquids and 38%
had delays with paste. Although not as prominent, 33%
of the patients with RHD had abnormal delays for oral
transfer of liquids and 32% had delays for paste. Because
delay in oral stage transfer is not the hallmark feature for
swallowing apraxia, it is difficult to ascertain whether
any apraxic-type features were evident in the RHD
group as delayed response characteristics were not described. In another prospective study of unilateral stroke
patients (n 79), Shanahan et al. [3] identified swallowing apraxia in a small subset of LHD patients, They
noted that 3 of 37 patients with LHD presented with
swallowing apraxia (4% of the total sample), whereas none
of the 42 RHD patients had evidence of this disorder.
Conversely, in a retrospective study of lesion localization in a small sample of acute stroke patients with
dysphagia (n 16), Daniels et al. [16] found that oral
dysmotility, defined as delayed initiation of oral transfer
or groping, and effortful lingual movements occurred
with equal frequency after left and right hemispheric
stroke (9 of 16, 56%). In a recent prospective study of
consecutive acute stroke patients (n 59), Daniels et al.
[17] found that hemisphere and anteriorposterior localization did not predict occurrence of lingual discoordination, which was defined as random disorganization of
anteriorposterior tongue movements evident in bolus