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Deficits in orofacial sensorimotor function in Parkinson's disease.

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Deficits in Orofxial Sensorimotor
Function in Parkmson’s Disease
Jay S. Schneider, PhD, Shirley G. Diamond, BA, and Charles H. Markham, MD
Orofacial sensorimotor function was assessed in patients with Parkinson’s disease and in age-matched controls. Tests
were designed to assess sensory function, motor abilities, and the integration of sensory information for the performance of specific movements. Patients with Parkinson’s disease and normal subjects both made more errors with
increasing age; however, overall, patients with Parkinson’s disease made significantly more errors in our tests than did
normal subjects. Interestingly, patients with Parkinson’s disease showed greater deficits in tests of sensory function and
sensorimotor integration than in tests of motor function. These results suggest that one aspect of Parkinson’s disease
consists of complex deficits in the utilization of specific sensory inputs to organize and guide movements. The results
are further discussed in relation to a proposed sensory gating or filtering schema of basal ganglia motor functioning.
Schneider JS, Diamond SG, Markham CH: Deficits in orofacial sensorimotor function
in Parkinson’s disease. Ann Neurol 19:275-282, 1986
The classic notions of the motor functions of the basal
ganglia have arisen primarily from descriptions of the
sequelae of diseases of the basal ganglia in humans. In
Parkinson’s disease (PD) the major symptoms include
tremor, rigidity, bradylnesia, akinesia, and postural
abnormalilties. In addition to these “motor” problems,
PD patients have some sensory symptoms [22) and
complex sensorimotor disturbances 12, 3). The integration of sensory information with various motor acts
may be defective in PD patients [24].
Results of studies in animals have suggested that a
potent way of influencing the motor system is by modulating sensory information processing 16, 7 ) . By concentrating on interactions between the basal ganglia
and trigeminal sensorimotor system, it has been shown
that structures of the basal ganglia receive complex
trigeminal sensory inputs and influence trigeminal
motor output 119-21). The basal ganglia do not appear to have a direct influence on the activity of trigeminal motor neurons 141; instead, they may gate or
regulate the access of sensory information to these
motor neurons {17J Possibly, when the basal ganglia
are diseased or dysfunctional, certain abnormalities of
movement may result-not from a simple removal of
inhibitory basal ganglia influence on the motor system,
but from a disturbance of the sensory gating systems
of the basal ganglia resulting in abnormal sensory input
to motor areas. A defect in sensorimotor integration
might then result in abnormal movements.
During a vestibular study in which the subject’s head
was positioned and stabilized by means of a bite bar
(Markham CH, Diamond SG, unpublished data,
1782), an interesting phenomenon became evident.
Patients with PD, in contrast to patients with a variety
of other neurological disorders, had great difficulty repositioning their teeth into a dental impression formed
a few minutes earlier. They were seemingly unable to
sense when their teeth were seated properly in the
mold, and unaware when their hold on the bite bar had
slipped by even a grossly visible amount. This finding,
together with previously described findings of complex
basal ganglia-trigeminal interactions in animals, led us
to an investigation of orofacial sensorimotor function
in PD. The goals of this study were: ( I ) to compare
oral-lingual-facial sensory and motor functions in PD
patients with normal controls in a similar age range;
and (2) to assess whether oral, lingual, and head movements become disordered in PD patients when execution of these movements is dependent primarily upon
somatosensory feedback.
From the Department of Neurology, Reed Neurological Research
Center, UCLA School of Medicine, Los Angeles, CA 90024.
Received March 14, 1985, and in revised form July 15. Accepted for
publication Aug 9, 1985.
Address reprint requests to Dr Schneider.
Patients and Methods
The patient population for this study consisted of 15 persons
(9 men and 6 women) who had been previously diagnosed as
having PD of unknown cause. Three patients were in stage I,
8 in stage 11, and 4 in stage 111, as defined by Hoehn and
Yahr [8]. They were thus classified as being mildly impaired.
None had marked akinesia, balance disturbances, or tremor,
including jaw or head tremor. None of the patients was
demented by history or examination. All patients were receiving carbidopa, and about half were receiving low doses of
an anticholinergic drug at the time of study. None of the
patients experienced dopa-related on-off, wearing off,
choreoathetosis, or resistant fluctuations, although several
had had choreoathetosis in the past. Patients ranged in age
from 47 to 83 years, with a mean age of 65.8 +- 9.5. Fifteen
control subjects of similar age (range, 45 to 77 years; mean,
66.0 ? 8.7 years; 9 men and 6 women) with no history of
central nervous system disease and no present signs of dementia were also examined. The general state of oral and
dental health was comparable in both patients and control
subjects. None had temporomandibular joint problems. In
both groups, 11 subjects had their own teeth and 4 had
either partial or full dentures.
Both PD patients and controls were given the following
battery of sensory and motor tests, independently scored by
two observers.
I. Jaw Proprioception
To assess the sense of jaw proprioception, adjustable calibrated calipers fitted with dental bite plates (Fig 1) were
inserted into the patient’s mouth and the patient was instructed to bite down gently on the plates. A trial began with
the investigator saying the word “now” and then either opening or closing the calipers (and thus the jaw) in a standardized
sequence. The patient was instructed to point a finger up if
he felt the jaw open and down if he felt the jaw close, and to
bring the thumb and forefinger together forming a circle if
he was uncertain. Ten trials were performed in which there
was a 1.0-mm change in jaw position, followed by ten trials
in which jaw position was changed by 0.5-mm increments.
Performance was scored as either correct o r incorrect (1
point for each error). This and all other procedures were
performed with the patient’s eyes closed.
2. Tongue Movement in Response to Verbal Command
To evaluate the range and direction of tongue movement on
command, the patient was asked to move his tongue up or
down or right or left in a big movement or a small movement, i.e., “big movement up,” “small movement to right.” A
standard sequence of sixteen randomly selected movements
was scored as either correct or incorrect (1 point for each
F i g I . Caliper used to assess sense of jaw proprioception. Caliper,
fitted with dental bite plates, was inserted into the patienti
mouth. In refwence to a calibration mark on the caliper, the
caliper could be opened or closed 1 .0 mm (90“ rotation of calibration murk) or 0.3 mm (45” rotation of calibration murk).
mance was scored as correct or incorrect (1 point for each
5. Tactile Localization on Tongue
This test was designed to provide a finer analysis of lingual
sensory discrimination. The patient was told that his extended tongue would be touched in various locations (i.e.,
combinations of front, middle, back, and left, middle, right).
The patient was then given a chart depicting his tongue and
the various locations which might be touched. The orientation of the chart was fully explained to the patient. Before
each touch, the patient was instructed to close his eyes and
extend his tongue. The investigator would then say the word
“now” and touch the tongue. Each time the tongue was
touched, the patient was told to open his eyes and point to
the area on the chart corresponding to the location in which
he felt the touch. Ten trials were performed and scored as
correct or incorrect (1 point for each error). Before testing
began, each subject was given a practice demonstration so
that he would know how stimulation at each location would
6. Tactile Localization on Gums
3. Following with Tongue
in Response t o Tactile Stimulation
To assess sensory-triggered movements of the tongue, the
tip of the extended tongue was tapped with a disposable
circular wooden applicator stick at a rate of about one tap per
second. The patient was then instructed to follow the taps
with the tip of his tongue as the applicator was randomly
moved from side to side. The patient’s jaw was held by the
investigator to stabilize the head. Performance on this task
was scored as good (0 points), fair ( 2 points), or poor (4
This test was performed to gain information on sensory discriminative abilities of intraoral structures. With the patient’s
mouth opened widely, a blunt probe was gently touched to
the inner surface of the gum. The areas touched were either
right, middle, or left on the upper gum or right, middle, or
left on the lower gum. Following the touch, the patient was
instructed to place a finger to his face in the location corresponding to where he felt the touch. Twelve randomized
trials were performed and scored as correct or incorrect (1
point for each error).
7. Tactile Localization on Teeth
4. Tongue Sensation
In this test the patient was asked to close his eyes and extend
his tongue, and was told that, after the investigator said the
word “now,” the tongue would be either touched or not
touched. The patient was instructed to point upward if he
felt a touch and downward if he didn’t. Ten randomly interspersed touch and no-touch trials were performed. Perfor-
276 Annals of Neurology Vol 19 No 3 March 1986
The same procedure was followed as for tactile localization
on gums.
8. Targeted Head Movement
on the Basis of Perioral Sensoy Infomation
This assessed ability to accurately perform a head movement
primarily on the basis of p e r i o d somatosensory feedback.
With the subject’s eyes closed, a wooden applicator stick was
briefly touched to the midline of the subject’s upper lip. The
stick was withdrawn, and a different perioral location was
then touched. The patient was instructed to turn his head
and reorient the midline of his upper lip to the new location
of the stick. The task was demonstrated for the patient. Ten
trials in various standardized random perioral locations were
performed, and movements were scored as correct or incorrect (1 point for each error). After completion of the task,
the patient was asked to open his eyes and was tested for
range of head movement by tracking a moving visual
stimulus, verifying that mobility per se, was not impaired.
40 -
9. Tracking Head Movements
on the Basis of Continuous Perioral Sensoy Feedback
This test, similar to the one for perioral sensory information,
was designed to assess head movements made in response to
a constantly moving sensory stimulus. With the patient’s eyes
closed, a small wooden stick was touched to the midline of
the patient’s upper lip, and then slowly and continuously
moved through various locations in the perioral region. The
patient was instructed to move his head and follow the stick
wherever it went, maintaining contact with it on the midline
of his upper lip at all times. A demonstration was performed
to ensure that the patient understood the procedure. The
stick was moved through ten standardized random perioral
locations, and tracking movements were scored as correct or
incorrect (1 point for each error).
10. Two-Point Discrimination Threshoh’s
A two-point caliper was used to test three areas: the middle
of the upper lip (midline), near the corner of the mouth
(perioral), and the middle of the cheek. With eyes closed, the
patient was asked to respond to the tactile stimulus by saying
whether he felt one or two points. The threshold of minimal
recognizable separation was determined and measured in
At the end of testing, the number of errors in tests 1
through 9 were totaled. Means and standard deviations were
calculated on each test for patient and control groups, and on
the two-point discrimination thresholds (test 10). Data on
each test and on the total battery were analyzed by t tests.
PD and control populations each consisted of 9 men
and 6 women. There was no difference between the
ages of subjects in the PD group and those in the
control group. P D patients made significantly more
errors Cp < 0.0005) in the tests than did normal subjects (Fig 2). Performance was not influenced by severity (disease stage) or duration of disease, or by degree
of akinesia or rigidity. Both PD patients and normal
subjects made more errors with increasing age (Fig 3).
Overall, there was also more variability in performance
in the PD group than in the control group. None of
our P D patients reported experiencing any overt orofacial sensory abnormalities, nor did any complain
about trouble chewing or swallowing food. Perfor-
Fig 2. Mean percent ewors on all sensorimotor tests. PatientJ
with Parkinson’s disease made significantly more ewors than did
n o w / subjects. There was also greater variability in peerformnce in the Parkinson’s disease group than in the control
group. Error bars on graphs denote standzrd deviation.
mance on individual sensorimotor tasks is shown in
Figure 4.
1. Jaw Proprioception
PD patients made almost three times as many errors in
judgment of jaw position (mean, 7.3 t 2.5) as did
controls (2.6
1.7), Cp < 0.0001). Both groups had
more difficulty in sensing small jaw displacements (0.5
mm) than larger ones (1.0 mm).
2. Tongzle Movement in Response to Verbal Command
Both PD patients and normal subjects showed no
difficulty in achieving amplitude or direction of tongue
movement on command. Thus, this test did not discriminate between the patient and control population
and showed that tongue mobility was unimpaired in
the P D group.
3. Following with Tongue
in Response to Tactile Stimulation
PD patients had twice as much difficulty (mean, 1.9
1.7) on this task as did normal subjects (mean, 0.8 -+
1.2) Cp = 0.07). These results, though suggestive, were
not statistically significant. While this was not a particu-
Schneider et al: Sensorimotor Function in Parkinson’s Disease
30 -
18 -
the slopes of the two lines (divergence of the two lines with increasing age) may illustrate the more rapid progression of sensorimotor dcjects in Parkinson's disease.
Fig 3. Mean percent ewors on all sensorimotor tests plotted
against age. Both Parkinson's disease (PD) patients and normal
subjects made more ewors with increasing age. The difference in
L T 6
Fig 4. Performance on individual sensorimotor tests: jaw proprioception (JAW PROPRIO.); tongue mmement in response t o verbal command (TONGUE MOVE.); follpwing with tongue in
response t o tactile stimulation (TONGUE FOLLOW.);tongue
sensation (TONGUE SENS.); tactile localization on tongue
(TONGUE LOCAL.); tactile localization on gums (GUM
LOCAL.); tactile localization on teeth (TEETH LOCAL.);
targeted head movement on basis of perioral sensory information
(HEAD TARGET.); and tracking head movements on basis of
Annals of Neurology
Vol 19 N o 3 March 1986
continuous perioral sensory feedback (HEAD TRACK.).
Graphs show the mean number of errors in Performance on each
test for both Parkinson2 disease patients and normAl, agematched controls. Error bars on graphs denote standard dwiation. Tests ofjaw proprioception, tactile localization on tongue,
gums, and teeth, and targeted and tracking head movements on
the basis of sensoy feedback resulted in the greatest differences in
performance between Parkinson's disease patients and normal
larly easy task for normal subjects, PD patients had
more trouble in initiating sensory-mediated tongue
movements. Often P D patients did not move the
tongue at all in response to the tactile stimulus,
whereas normal subjects always moved the tongue in
response to the moving stimulus, sometimes inaccurately.
4. Tongue Sensation
There were no significant differences between PD patients and controls in ability to detect whether the
tongue had been touched or not.
5. Tactile Localization on Tongue
PD patients had distinctly more difficulty in detecting
the location of a tactile stimulus on the tongue (mean,
4.5 ? 2.2) than did normal controls (1.9 -+ 1.3) (p <
6 and 7. Tactile Localization on Gums and Teeth
PD patients made significantly more errors than did
normal controls in assessing the location of a tactile
stimulus on their gums (PD mean, 2.2 zk 1.5; normal
mean, 0.2 ? 0.4) (p < 0.005) or teeth (PD mean, 1.6
? 2.1; normal mean, 0.3 ? 0) (p < 0.05).
8. Targeted Head Movement
on the Basis of Perioral Sensory Information
PD patients were less able to move their heads accurately to orient themselves to a perioral tactile stimulus
(mean score, 1.6 k 2.3) than were normal controls
(mean score, 0.6 t 0.3) (p < 0.05). PD patients often
began to move in the correct direction but failed to
complete the movement and fully orient themselves to
the tactile stimulus. When questioned about their
difficulties, patients acknowledged that they could feel
the stimulus on their face and thought they had indeed
oriented the midline of the upper lip to it, when in fact
they were often several centimeters from the correct
position. Some patients also distinctly overshot the desired position. The most unusual results were those
obtained from patients who moved their heads no
more than a few millimeters in any direction in response to the tactile stimulus. All patients who had
severe difficulties in performing this task had no
difficulty in making a wide range of head movements
in other circumstances.
9. Tracking Head Movements
on the Basis of Continuous Perioval Sensory Feedback
As in the test of targeted head movements, PD patients were less able to accurately track a moving sensory stimulus (mean errors, 3.7 t 4.0) than were normal controls (mean errors, 0.2 +- 0.6) (p < 0.005).
Some P D patients began to move in the proper direction but could not complete the movement. These pa-
tients reported that they felt the stimulus and tracked
it to the best of their ability. Some realized they did
not complete the task, but others thought they had.
The patients again showed no difficulty in performing
head movements in other contexts.
10. Two-point Discrimination Thresholds
Significant differences were found between PD patients and normal subjects in two-point discrimination
thresholds on the midline of the upper lip (PD mean,
6.4 -+ 1.1; normal mean, 5.1 ? 1.5) (p < 0.05) and
near the corners of the mouth (PD mean, 9.8 -+ 1.6;
normal mean, 7.5 4 2.1) (p < 0.005). No statistically
significant difference between the two populations was
found in two-point discrimination on the cheek (PD
mean, 18.2 ? 8.5; normal mean, 13.2 2 5.8) (p =
0.07) (Fig 5). The large variation in responses of both
normal and P D populations, together with the relatively small sample size, may in part account for the
lack of significance on the cheek.
The present results demonstrate that the orofacial sensorimotor system is unquestionably affected in PD.
Although differences between P D patients and normal
subjects were observed on most of the tests, some
tests proved better discriminators than others. Jaw proprioception seemed to be a good discriminator,
whereas tongue sensation did not. Voluntary tongue
movement on command was not a good discriminator
but was a necessary prerequisite test to assess motor
capability before assessing tongue movement in response to a somatosensory stimulus. The latter test did
not turn out to be as good a discriminator as would
have been predicted based on some of the other results. The shortcomings of this test may be due more
to the scoring system than to the test itself. PD patients often performed differently from normals, but
the rating scale (0 = good response, 2 = fair, 4 =
poor) was neither sensitive nor detailed enough to
show differences which were subjectively more apparent than the statistics demonstrated.
The difficulties that PD patients experienced in the
tests of tactile localization on tongue, g u m s , and teeth
could be related to abnormalities in the central processing of these types of peripheral information, or to
the P D patients’ difficulty in translating the sensation
of a tactile stimulus in the mouth to a pointing response. It has been suggested that PD patients have
specific visuospatial deficits. Bowen [33 reported that
PD patients have difficulty in touching parts of their
bodies corresponding to a diagram set before them.
Boller and colleagues C23 have also suggested that PD
produces impairments in visuospatial perception,
defined as difficulty in appreciating the relative position of objects in space, difficulty in integrating those
Schneider et al: Sensorimotor Function in Parkinson’s Disease
objects into a coherent spatial framework, and
difficulty in performing mental operations involving
spatial concepts. None of our “pointing” tasks required
any visuospatial or visuoperceptual tests similar in nature or complexity to those used by other investigators
[2, 33. Difficulty in performing our tasks most probably reflected complex deficits in the use of specific
sensory inputs to organize and guide movements.
Several basal ganglia nuclei in animals have been
shown to process complex uigeminal sensory inputs.
One aspect of this information encoding concerns the
location of a tactile stimulus on the face 120, 213.
Stimulus location on the face appears to be coded
within the basal ganglia, not in an absolute sense but
relative to the front of the face or the midline. In our
human PD group, two-point discrimination thresholds
in the midline and perioral regions were significantly
larger (greater distance between the two points) than
in controls. However, no significant differences between the two groups were found in two-point discrimination thresholds on the cheek. These findings
suggest that, as in lower-order animals, the human
basal ganglia may be more sensitive to events occurring
near the midline or perioral region rather than to those
at more lateral aspects of the face.
Some of the most striking results of the present
study were obtained in the head targeting (No. 8) and
head tracking (No. 9) tests. P D patients had great
difficulty using perioral somatosensory information to
make controlled head movements. These same patients made normal spontaneous, visually guided, or
verbally commanded head movements. This suggests
that they did not have a cervical motor impairment,
per se; more likely, there was a breakdown in the link
between facial somatosensory inputs and cervical
280 Annals of Neurology Vol 19 No 3 March 1986
Fig 5 . Two-point discrimination thresholds. Face diagram shows
locations tested, i.e., midline, perioral (corner of mouth), and
cheek. Corresponding graphs show mean thresholds (and standard deviation error bars) in Parkinson’s disease and control
groaps. Significant differencesbetween the two groups were observed on the midline andperioral area but not on the cheek.
This may indicate a greater disruption of perioral rather than
entire-face sensory functioning in Parkinson’s disease.
motor output. In rats it has been shown that disruption
of basal ganglia outputs produced by lesions of the
globus pallidus causes alterations in trigeminal sensoryinduced reflexive neck muscle activity 1151. If during
normal functioning the basal ganglia are involved in
gating trigeminal sensory inputs to motor areas (e.g.,
trigeminal motor or cervical motor areas) 111, 121, it is
possible in PD that the gating process may shut down
so that appropriate sensory signals do not gain access
to effector regions (Fig 6).
Striatal as well as other basal ganglia neurons are
quite sensitive to sensory stimuli [ 5 , 203. In fact, some
striatal neurons may become responsive to facial tactile
stimulation only when there is accompanying behaviorally important activity such as eating or drinking
1131. Dopamine, instead of functioning as a regulator
of specific movements, may aid in the processing of
such sensory information by the basal ganglia and regulate the access of this information to the relevant
motor control areas. With decreased dopaminergic
function, sensory information may not be readily modulated by the internal gating and filtering system of the
basal ganglia. For example, damage to the ventral
mesencephalic dopamine systems results in inattention
to exteroceptive cues [9, 141. Conversely, with relative
or absolute increased dopaminergic activity, sensory
Sensory &
Motor Info
Trigeminal Sensorymotor System
>/ 1
Rx IN P.D.
/ / -dbq
0= hyperfunctlon B= hypofunction
F i g 6. Basal ganglia sensory-to-motor gating schema of functioning. Hyperfunction and hypofunction refer to the sensoy
filtering or gating mechanism in the basal ganglia. (A) Normal
transmitterfunction maintains a physiological balance within
the basal ganglia so that adequately processed sensory and motor
informution are allowed normal access to areas more immediately
involved in generating movements. This gating function most
probably relies upon presynaptic injluences (right side o f diagram). (B) When the pallidum is lesioned experimentally, relatively ungated sensorimotor information exits from the basal ganglia resulting in the unimpeded access of afferent information to
motor areas and causing a motor hyperexcitability. (C) In the
case of Parkinson's disease, loss of nigrostriatal dopamine enhances the inhibitory sensory gating function of the basal ganglia so that there is a greater than normul inhibition of the
access of sensory information to relevant motor areas, resulting in
a net motor hypoexcitability. (D) With excess dopamine (DOPA
or DA), as in cases of overmedication with L-dopa in Parkinson's disease (P.D.), reduced tonic inhibitoy striatal output and
attenuatedpallihl inhibitory activities may again a l l m unimpeded afferent access to motor systems, resulting in motor hyperexcitability and heightened dyskinetic activities. (E) Similarly, in
Huntington's disease, striatal and pallidal neuronal loss would
lead to reduced inhibitory outfrow of the basal ganglia, ungated
afferent access to motor areas, motor system hyperexcitability, and
unchecked motor activity. For the sake of diagrammatic clarity,
the injluences of the substantia nigra pars reticulata in this
schema of functioning have not been shozun. However, these inhibitoy outputs ofthe substantia nigra pars reticulata must also
be involved in this process and are probabIy influenced in a manner similar to that for pallidal outputs. (See text forfurther
discussion ofthis model.)
information may pass through the system too readily
and may indiscriminately lower thresholds for movement. Abnormal dyskinetic movements may result.
In addition to the effects that a loss of dopamine
would have on striatal sensory processing, loss of
dopamine would cause disinhibition of inhibitory yaminobutyric acid (GABA)-ergic striatal output neurons, resulting in a lessened activity of pallidal and substantia nigra pars reticulata neurons.
As depicted in Figure 6A, during normal functioning, neurotransmitter relationships help maintain a
physiological balance within the basal ganglia so that, in
this example, facial sensory information is adequately
processed and striatal and pallidal outputs are allowed
normal access (by as yet unresolved pathways) to the
trigeminal sensorimotor system. In the case of experimentally induced pallidal lesions (Fig bB), the trigeminal motor system is observed to be hyperexcitable,
apparently resulting from removal of tonic striatal and
pallidal inhibitory influences on trigeminal sensory information or from the linkup between sensory information and the motor system, via a postulated trigeminal presynaptic inhibitory path. This would result in
unimpeded access (lowered threshold) to the motor
area. In the case of dopamine depletion acting on the
striatum (Fig GC), as in PD, the trigeminal motor system (and, as observed in the present study, the cervical
motor system) may become hypoexcitable because of
an enhanced striatal (as well as pallidal and substantia
Schneider et al: Sensorimotor Function in Parkinson's Disease
nigra pars reticulata) inhibitory influence on the processing and gating of certain sensory inputs, which ultimately leads to enhanced inhibition of the trigeminal
reflex arc. This would result in a lack of motor response to particular behaviorally relevant sensory
stimuli but would not totally disturb movements made
in other contexts. This is precisely reflected by the
results of the present study.
Carrying the diagrammatic model further, in PD
(and other basal ganglia diseases in which striatal
dopamine hypersensitivity may exist) excess dopamine
(Fig 6D) may reduce tonic striatal GABAergic output
and attenuate pallidal and nigral GABAergic activities
{ 163 leading ultimately to heightened dyskinetic activity. Similarly, in Huntington’s disease, striatal and pallidal neuronal loss would lead to reduced GABAergic
outflow and ultimately, by currently unknown paths, to
unchecked motor hyperactivity.
Several recent clinical findings support the proposed
presynaptic influence of basal ganglia over sensory access to areas more directly involved in generating
movements. Sandyk 1173 demonstrated that the trigeminal nerves are involved in somatosensory control
of the tongue and the silent period of tongue muscle
activity. Severing these trigeminal nerves results in
abolition of the silent period as well as a disturbance of
nonarticulatory tongue functions (ataxia) [ 173. Similar
tongue disturbances (ataxia, abolished silent period)
have been observed in untreated PD patients E183,
implying that the basal ganglia have an influence on
proprioceptive information to and from the tongue
and somatosensory feedback control of this structure.
Orofacial dyskinesia, characterized by severe involuntary dystonic movements of the facial, oral, and cervical musclature, is usually thought to be a disorder of
the basal ganglia 113. However, some edentulous people with no history of neurological disease show a mild
form of orofacial dyskinesia. Prosthetic dental therapy
has been shown to be effective in this condition {23].
In two studies, when patients with orofacial dyskinesia
C231 or tardive dyskinesia [lo] were fitted with denm e s or when modifications were made to correct existing incorrect denture occlusions (craniomandibular
relations), dramatic reduction of symptoms occurred.
These results demonstrate the importance of regulated
trigeminal sensory inputs in these motor disorders.
We wish to thank Setsuko Kashitani and Dan Stoller for their assistance.
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disease, parkinson, deficit, orofacial, function, sensorimotor
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