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Cubital tunnel syndrome and ulnar neuropathy.

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1. Chiappinelli VA, Zigmond RE: a-Bungarotoxin blocks
nicotinic transmission in the avian ciliary ganglion. Proc Natl
Acad Sci USA 75:2999-3003, 1978
2. Lepore FE, Sanborn GE, Slevin J T Pupillary dysfunction in
myasthenia gravis. Ann Neurol 6:29-33, 1979
3. Snedecor GW, Cochran WG: Statistical Methods. Sixth edition. Ames, IA, Iowa State University Press, 1967
Frederick E. Lepore, MD, George E. Sanborn, MD,
and John T. Slevin, MD
W e wish to thank D r Bryant for his thoughtful analysis of
the data collected in our study and to address ourselves to
his observations.
When calculating the t statistic to test the null hypothesis
for right and left eye cycle times in patients with myasthenia gravis, we tested for unpaired variates. The t statistic
calculated for paired variates indicates a statistically
significant difference (t = 2.488, 0.010 <: p < 0.025, twotailed). The t statistic calculated from the difference between eyes by pairs in the normal subjects (t = 1.009,O.lO
< p < 0.25, two-tailed) and the steroid-treated control
group (t = 0.642, 0.60 < p < 0.75, two-tailed) is not
significant. As all subjects were tested concurrently, it is
doubtful that the asymmetry in patients with myasthenia
gravis can be ascribed to an order effect in the testing procedure. To date, we are unable to give a pathophysiological
basis either for this phenomenon or for why the cycle time
disparity increases with disease severity.
D r Bryant’s speculation of myasthenic involvement of
the autonomic parasympathetic ganglion as the source of
pupil cycle slowing, though intriguing, must be considered
cautiously due to its extrapolation from a study [l] performed with a-bungarotoxin, which can bind to a variety of
structures now shown to be clinically o r pathologically involved in myasthenia gravis. Additionally, that study was
done o n chicken ciliary ganglion, a structure different from
its mammalian counterpart by virtue of its dual chemical
and ephaptic modes of transmission [ 2 ] as well as its innervation of a striated muscle pupillary sphincter. Regardless,
it should be stressed that the pupil cycle time cannot isolate
dysfunction of a specific structure between the EdingerWestphal nucleus and the pupillary sphincter. With normal
afferent visual function, this test measures the integrity of
the entire efferent limb of the pupillary light reflex.
Department of Pharmacology
The Johns Hopkins University
School of Medicine
Baltimore, M D 21205
1. Chiappinelli VA, Zigmond RE: a-Bungarotoxin blocks
nicotinic transmission in the avian ciliary ganglion. Proc Natl
Acad Sci USA 7512999-3003, 1978
2. Martin AR, Pilar G: An analysis of electrical coupling at
synapses in the avian ciliary ganglion. J Physiol (London)
171~454-475, 1964.
Cubital Tunnel Syndrome
and Ulnar Neuropathy
William F. Brown, MD, Stephen K. Yates,
and Gary G. Ferguson
The paper by Robert G. Miller [3]o n precise localization
of functional abnormalities in the ulnar nerve in so-called
cubital tunnel syndrome was of interest to us. Over the past
five years, we have carried out intraoperative stimulation
of the ulnar nerve at the time of surgical transposition in
more than 30 patients in an attempt to better localize and
characterize the conduction abnormality. Stimulation was
carried out at 1-cm intervals for up to 4 to 5 cm proximal
and 5 cm distal to the medial epicondyle, a length that
clearly included the retroepicondylar segment and cubital
tunnel entrance. In earlier stimulation trials bifocal stimulation was used [ 11, but more recently we have employed a
tripolar (cathode central) electrode to better localize the
level of nerve activation. Careful attention has been paid to
the appearance of the ulnar nerve, and intraoperative
photographs have been taken to document the experimental procedure and the appearance of the nerve, particularly for those nerves in which localized conduction delay
was evident.
T h e most common conduction abnormalities have been
characterized by a localized conduction delay extending over
several centimeters but maximum just proximal to, at the
level of, or within 1 to 2 cm distal to the medial epicondyle.
In no ulnar nerve explored has there been evidence of local
constriction or other deformation of the ulnar nerve at the
entrance to the cubital tunnel, but in over half, a localized
enlargement of the nerve was noted at or just proximal to
the level of the medial epicondyle. In about one-fourth of
the ulnar nerves investigated, an obvious conduction block
was evident over the same segments where the abnormal
increases in conduction time were found. Conduction
block was not detected preoperatively across the cubital
tunnel entrance but was observed to complicate a previous
ulnar nerve transposition, perhaps because of fixation of
the nerve by postoperative scar tissue at or just distal to the
cubital tunnel entrance.
It has been our experience that cubital tunnel ulnar
nerve lesions similar to those originally reported by Feindel
and Stratford [ 2 ] are probably not all that common; but
there is no doubt that cubital tunnel compression can be a
source of ulnar neuropathy, based not only on Feindel and
Stratford’s report but also on the observations of Neary and
Eames [4] and, later, Neary, Ochoa, and Gilliatt [ 5 ] . W e
would be interested to hear about others’ observations on
the importance of cubital tunnel compression in the pathogenesis of ulnar neuropathies.
Department of Clinical Neurological Sciences
University Hospital
PO Box 5339
London, Ont, Canada N 6 A 5A5
Notes and Letters
1. Brown WR, Ferguson GG, Jones MW, et al: The location of
conduction abnormalities in human entrapment neuropathies.
Can Neuro Sci 3:111-122, 1976
2. Feindel W, Stratford J: The role of the cubital tunnel in tardy
ulnar palsy. Can J Surg 1:287-300, 1958
3. Miller RG: The cubital tunnel syndrome: diagnosis and precise
localization. Ann Neurol 6:56-59, 1979
4.Neary D, Eames R: The pathology of ulnar nerve compression
in man. Neuropathol Appl Neurobiol 1:69-88, 1975
5 . Neary D, Ochoa J, Gilliatt RW: Sub-clinical entrapment neuropathy in man. J Neurol Sci, 24:283-298, 1975
Robert G. Miller, M D
The observations by D r Brown and his colleagues stand
in direct contrast to those reported in our paper. In the
series of patients that we described, both local enlargement
of the ulnar nerve and the conduction block extended distal
to the medial epicondyle, a variable distance of 1 to 4 cm.
In the majority of patients, the nerve segment was narrowed and pale under the tight band at the entrance to the
cubital tunnel. W e did not measure conduction delay at
1-cm intervals; however, the responses shown in Figure A
of our paper were quite typical of our series, wherein a
marked slowing of conduction was localized between 2 and
4 cm distal to the medial epicondyle.
It is difficult to reconcile these conflicting observations.
Differences in arm position (flexed versus extended) and
technique of stimulation may be important. Differences in
patient selection between the two series may be more pertinent, however. Our patients with the cubital tunnel syndrome had no history of prior trauma and no evidence of
joint deformity. Six of the 9 patients had bilateral ulnar
neuropathy, and a taut, palpably enlarged ulnar nerve was
found in the ulnar groove in the majority of patients. We
thus excluded patients with tardy ulnar palsy, postsurgical
ulnar neuropathy, and ulnar nerves which were hypermobile and dislocated over the medial epicondyle. In D r
Brown’s reported series of 13 patients, 7 might be sus-
Annals of Neurology
Vol 7
No 3 March 1980
pected of having had recent trauma by virtue of a recent
hospitalization or surgical procedure, o r a history of extensive alcohol intake. Two others had diabetes mellitus and
may have developed a spontaneous mononeuropathy from
a vascular lesion [l]. In this heterogeneous group of patients, the pathophysiology may be different from that in
patients with the cubital tunnel syndrome.
Dr Brown’s observations are of interest, and his technique is elegant. His data suggest that many patients with
ulnar neuropathy at the elbow d o not have the cubital tunnel syndrome, a fact with which we agree.
Precise localization of the lesion has practical implications for selecting appropriate therapy. When the primary
lesion is found at the cubital tunnel, simple decompression
by division of the aponeurosis which forms the roof of the
tunnel is logical treatment. In 11 of 12 patients with progressive cubital tunnel syndrome, we found evidence of
both clinical and electrophysiological improvement following surgical decompression without transposition [21.
Our electrophysiological data, intraoperative observations,
and responses to simple decompression, when considered
with the pathological studies of Neary and co-workers
[3, 41, all constitute an emerging body of evidence that the
cubital tunnel is the site of mischief in an important subgroup of patients with ulnar neuropathy at the elbow.
Neuromuscular Research
Children’s Hospital of San Francisco
PO Box 3805
San Francisco, C A 94119
1. Asbury AK: Proximal diabetic neuropathy (editorial). Ann
Neurol 2:179-180, 1977
2. Miller RG, Hummel EE: The cubital tunnel syndrome: treatment with simple decompression. Ann Neurol (in press)
3. Neary D, Eames R: The pathology of ulnar nerve compression
in man. Neuropathol Appl Neurobiol 1:69-88, 1975
4. Neary D, Ochoa J, Gilliatt RW: Sub-clinical entrapment neuropathy in man. J Neurol Sci 24:283-298, 1975
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cubital, syndrome, neuropathy, ulnar, tunnel
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