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Objective Evaluation of Infraorbital Nerve Involvement in Maxillary Lesions by Means of the Blink Reflex
Masafumi Ohki, MD;
Naonobu Takeuchi, MD
Arch Otolaryngol Head Neck Surg. 2002;128:952-955.
ABSTRACT
Objective To objectively evaluate the effects of maxillary lesions on the infraorbital
nerve (ION).
Methods We investigated the latencies (R1, R2) of the blink reflex, stimulating
the infraorbital foramen electrically (18 mA, 0.2 millisecond). Twenty-two
patients with unilateral maxillary lesions were enrolled.
Results Ten patients showed delayed or absent R1 on the lesion side. Four of
20 patients showed delayed difference in R2 latency. Ten (77%) of 13 patients
with lesions along the ION pathway showed an abnormal blink reflex. Only 3
patients demonstrated a normal blink reflex despite a lesion along the pathway
of the ION. All patients whose ION pathway was intact showed a normal blink
reflex.
Conclusions These results suggested that lesions along the ION pathway may impair
the afferent pathway of the blink reflex. The blink reflex may be valuable
to evaluate maxillary lesions objectively. Furthermore, R1 is more effective
than R2 in detecting ION defects.
INTRODUCTION
PATIENTS WITH maxillary lesions complain of various symptoms. Some of
the symptoms are derived from trigeminal nerve deficits (eg, pain, tactile
deficits, or temperature sensation). Maxillary lesions (eg, maxillary tumors
and maxillary cysts) sometimes impair the infraorbital nerve (ION), which
supplies sensation to the middle parts of the face. In general, clinicians
examine ION functions subjectively on the basis of tactile sensation or temperature
sensation, as a standard nerve conduction study is not feasible in the ION
for anatomic reasons.
The blink reflex (BR) reflects the function of the trigeminal and facial
nerves. In an attempt to evaluate ION deficits objectively, we investigated
the changes in BR under the influence of maxillary lesions. We used a method
to stimulate the ION supplying sensation to the maxillary region. As far as
we know, there are no reports of the use of the BR to objectively investigate
ION deficits induced by maxillary lesions.
SUBJECTS AND METHODS
Twenty-two patients (14 men and 8 women) with unilateral maxillary lesions,
who gave informed consent, were enrolled. Their ages ranged from 26 to 78
years (median, 58 years). Their maxillary lesions were postoperative maxillary
cysts in 13 patients, maxillary cancer in 3, maxillary papilloma in 1, unilateral
chronic sinusitis in 1, mucocele in 1, chronic sinusitis with orbital cellulitis
in 1, ameloblastoma in 1, and traumatic maxillary injury in 1. None had experienced
facial nerve paralysis. In addition, we enrolled 9 volunteers (7 men and 2
women) without maxillary diseases as control subjects. Their ages ranged from
22 to 40 years (median, 25 years).
Active recording electrodes were placed on the bilateral upper eyelids
while reference electrodes were placed on the bilateral temples. Electrodes
(cathode and anode) for electrical stimulation were placed on the skin over
the infraorbital foramen. A ground electrode was set on the forehead. We used
18-mA (0.2-millisecond) electrical stimulation. Electromyographic activities
were amplified and bandpass filtered (20-2000 Hz). The stimulation was done
4 to 5 times at random and the analysis time was 100 milliseconds. When being
measured, patients were instructed to lie on a bed with their eyes gently
closed. We used evoked potential/electromyographic measuring systems (Neuropack
8; Nihon Kohden Corporation, Tokyo, Japan) to measure the responses. The latencies
of the waves were measured. All patients had a computed tomographic scan of
the sinus.
RESULTS
All 9 control subjects showed ipsilateral early waves (R1) and bilateral
late waves (R2).1 The latency of R1 was 11.2
± 0.7 milliseconds (mean ± SD). The time difference of the R1
latency of the stimulated side was 0.6 ± 0.3 millisecond. The time
difference of the R2 latency on the stimulated side was 1.4 ± 1.1 milliseconds.
For R1, the latencies and time differences of the latencies between
the healthy side and the affected side were evaluated, while for R2, the latencies
of the stimulated side were studied. On the basis of the results from control
subjects, the normal range of R1 latency and the time difference of R1 latency
on the stimulated side and that of R2 latency on the stimulated side were
placed at 9.7 to 12.6 milliseconds (within mean ± 2 SDs), 0 to 1.3
milliseconds (within mean ± 2 SDs), and 0 to 3.6 milliseconds (within
mean ± 2 SDs), respectively.
Two of 22 patients who showed absent R1 bilaterally were excluded from
the following results. Ten (50%) of 20 patients showed delay or absence of
R1 on the affected side (Figure 1
and Table 1). Of these 10, 4 patients
showed delayed R1 and 6 patients showed absent R1. Four (20%) of 20 patients
showed a delayed time difference in R2 (Figure
1). No patients showed absent R2 on the affected side. The R1 tended
to show a more abnormal response than R2.
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Figure 1. Recordings of the blink reflex
in a 79-year-old woman with right maxillary mucocele. The right ipsilateral
early wave (R1) was absent and bilateral late wave (R2) was delayed when the
right side (R) was stimulated, whereas the blink reflex was normal when the
left side (L) was stimulated.
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Seven (78%) of 9 patients with bony destruction of the orbital floor
showed abnormal BR (Figure 1, Figure 2 and Table 1). These 7 patients included 3 with bony destruction in the
anterior half of the orbital floor, 2 in the posterior half, and 2 in both.
The BR seemed to be irrelevant to the site of bony destruction between the
anterior and posterior half of the orbital floor. Eight (73%) of 11 patients
without bony destruction of the orbital floor showed normal BR, while the
other 3 patients showed abnormal BR (Table
1). However, 2 of these 3 had bony destruction of the upper anterior
wall of the maxillary sinus and the other one had tumor invasion into the
pterygopalatine fossa. In other words, these 3 patients with abnormal BR had
lesions along the ION pathway to the maxillary nerve.
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Figure 2. Computed tomographic scan of the
patient in Figure 1. Coronal view shows the right maxillary mucocele compressing
the right orbital floor (arrowheads).
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Only 3 patients showed normal BR, despite lesions along the ION pathway
to the maxillary nerve. Two of these patients had bony destruction of the
orbital floor, and 1 had bony destruction of the upper anterior wall of the
maxillary sinus. On the whole, all patients with intact ION pathways to the
maxillary nerve showed normal BR, while the majority of patients (10/13 [77%])
with lesions along the ION pathway to the maxillary nerve showed abnormal
BR.
Seven (70%) of 10 patients with sensory deficits (ie, tactile deficits,
pain, and temperature sensation) in the maxillary region showed abnormal BR,
while results in the other 3 patients were normal. On the other hand, 7 (70%)
of 10 patients without sensory deficits had normal results, while the other
3 patients had abnormal results without clinical sensory deficits. In all,
the clinical sensory deficits were likely to be compatible with the results
of BR testing.
No apparent relationship was suggested between periods from the onset
of sensory deficits and the BR in this study (Figure 3).
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Figure 3. Interval from the onset of sensory
deficits with blink reflex. No apparent relationship was seen.
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COMMENT
The BR reflects the integrity of the trigeminal and facial nerves. It
is generally examined to evaluate the facial nerve, trigeminal nerve, pontine
lesions, or medullary lesions.1-3
The stimulation elicits 2 separate reflex responses (R1 and R2) of the orbicularis
oculi muscle.1-3
The BR can be evoked by not only the supraorbital nerve but also the ION or
mental nerve.2-3 However, as the
supraorbital nerve can most frequently evoke BR in healthy subjects,2-3 this nerve is, in general, stimulated
electrically or mechanically in clinical examinations. Since the purpose of
this study was to evaluate dysfunction of the ION, we applied a method to
stimulate the ION. We frequently detected R1 in all control subjects and in
the healthy side of 20 (91%) of 22 patients, when attempting to record on
upper lids and stimulating only over the nerve. The R2 was detected in all
control subjects and in the healthy side of all patients. The tendency for
R1 to be evoked less often than R2 is compatible with results of a trial by
Kimura.2-3
The ION passes through the infraorbital foramen and inferior orbital
fissure. This pathway lies in the orbital floor between the maxillary sinus
and orbit. After that, it becomes the maxillary nerve in the pterygopalatine
fossa. In this study, all 10 patients who showed abnormal BR had lesions along
this pathway. It was suggested that lesions along this pathway impaired these
afferent pathways of the BR. Moreover, abnormal BR indicated the presence
of the lesion along this pathway. However, 3 patients showed normal BR despite
lesions along the pathway. This finding may depend on the degree of nervous
impairment.
In this study, all patients with abnormal BR showed abnormal R1, while
R2 was shown to be abnormal in only 40%. This means that R1 tended to become
abnormal more often than R2, and the 2 latencies were not always abnormal
together. This may be why R1 and R2 pass through different characteristic
nerve fibers, although they both share the same root of the ION. The R1 fibers
are concerned with tactile sensation, whereas those of R2 are involved with
pain and temperature sensation.2 The different
kinds of nerve fibers are thought to have a different susceptibility to lesions.4
It is still controversial what kind of nerve fibers are responsible
for R1 and R2. Recently, it was suggested that R1 is mediated by Aß fibers,
while R2 is mediated by Aß and A fibers.5-6
In general, tactile sensation activates the larger fibers in the cutaneous
nerve in the Aß range, while pain and temperature sensation activates
the smaller fibers of the A-to-C range.4
The fibers in descending order from thickest to thinnest are A , Aß,
A, and C. The thicker the fibers are, the more susceptible they are
to compression or inflammation7; the fibers
related to R1 may be more fragile. These facts suggest one reason why R1 becomes
abnormal more frequently.
In practice, patients with sensory deficits were inclined to show a
BR abnormality to some degree in this study. As minor sensory deficits may
not be detected clinically, some patients showed abnormal BR without apparent
sensory deficits. Duration of sensory deficits, in this study, seemed not
to be related to an abnormality of BR. As chronic compression or inflammation
may induce demyelination or axonal degeneration of neurons subclinically,
the appearance of sensory deficits and the grade of a nervous impairment may
not necessarily agree.
These results suggested that the lesions along the ION pathway to the
maxillary nerve impaired the afferent pathway of BR. The BR may be a useful
tool to evaluate maxillary lesions objectively. Furthermore, R1 is more effective
than R2 in detecting ION defects. To our knowledge, this is the first report
to use BR to evaluate the effects of maxillary lesions on the ION. Further
investigation is still needed.
AUTHOR INFORMATION
Accepted for publication December 17, 2001.
Corresponding author and reprints: Masafumi Ohki, MD, Department
of Otolaryngology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo,
Tokyo 113-8655, Japan (e-mail: m-ohki{at}wb4.so-net.ne.jp).
From the Department of Otolaryngology, Kameda Medical Center, Chiba
(Dr Ohki), and Department of Otolaryngology, Faculty of Medicine, University
of Tokyo, Tokyo (Drs Ohki and Takeuchi), Japan.
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