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Diane H . Russell, P h D
In our brief communication “Altered Muscle Polyamine Levels in Human Neuromuscular Diseases” (Ann
Neurol9:605-607, 1981), it is not apparent that the mean
2 S D and range at the bottom of the table on page 606
refer to controls and not, as it appears in the article, to
statistics related to the biopsy levels of polyamines in various neuromuscular diseases.
Department of Pharmacology
The University of Arizona
Health Sciences Center
Tucson, A2 85724
Nature of the Decussated
Innervation of the
Norman Geschwind, M D
The article by Balagura and Katz [l]in the January, 1980,
issue of Annals o f Neurology states that there is an undecussated innervation to the sternomastoid muscle. They point
out that in patients with hemiplegias of cerebral origin the
head is turned away from the hemiplegic side, and if there
is weakness of a sternomastoid, it is o n the side opposite to
the hemiplegia. In favor of an ipsilateral innervation is the
fact that in patients with seizures the head turns away from
the focus, a movement which requires innervation of
the sternomastoid ipsilateral to the focus. O n e finds in
hemiballismus that the head movements are primarily toward the thrashing limbs and that these result from contraction of the sternomastoid on the side opposite the abnormal limb movements.
These authors did not stress the possibility, however,
that there is a doably decussated (rather than undecussated)
innervation of the sternomastoid. An apparently ipsilateral
innervation can be achieved by at least three mechanisms.
The first possibility is that the innervation is truly ipsilateral, i.e., it is mediated by a pathway descending purely ipsilaterally from the hemisphere which controls the movement. A second possibility is that the movement originates
in one hemisphere and is then transmitted across the corpus callosum to the opposite hemisphere, which in turn
controls a movement o n the contralateral side, i.e., the side
ipsilateral to the hemisphere from which the movement
T h e third possibility, and the one most relevant to control of the sternomastoid muscle, is that which depends o n
a double decussation. In this case, the multisynaptic pathway along which the movement is mediated crosses from
one hemisphere to the opposite side of the brainstem o r
the spinal cord and then undergoes a decussation back to
the side ipsilateral to the hemisphere of origin. Thus, a lesion of the hemisphere may lead in the acute stage to conjugate gaze weakness to the opposite side, i.e., a failure to
innervate simultaneously the opposite lateral rectus muscle
and the ipsilateral medial rectus muscle. As is well known,
this is the result of damage to a pathway that crosses from
the hemisphere to the opposite side of the pons and then
recrosses to the medial rectus nucleus o n the same side as
the lesion.
It is recognized that there are pyramidal fibers originating in one hemisphere which cross in the usual fashion in
the medulla to the opposite spinal cord, but which then
cross back to the side of the cord ipsilateral to the hemisphere of origin. I know of n o evidence at present that such
a pathway mediates ipsilateral innervation of the sternomastoid. Definite evidence has been reported by Bender, Shanzer, and Wagman [2], however, which supports
the view that the responsible pathway crosses from the
hemisphere to the opposite pons and then returns to the
side of the cord ipsilateral to the hemisphere of origin.
These authors showed that stimulation in the cerebrum and
upper brainstem produced head-turning to the opposite
side. O n the other hand, stimulation in the pontine tegmentum resulted in deviations of the head to the ipsilateral
side. Lesion experiments produced deficits which were
consistent with these stimulation experiments.
These results of Bender and his colleagues clearly show
that there is a decussation in the brainstem for innervation
of head turning. Since the sternomastoid is a major component of this movement, and since that muscle is controlled
ipsilaterally, there must be a second decussation. Although
I know of no formal studies o n this point, I presume that
the second decussation is located in the decussation of the
T h e results of these studies also point to a valuable clinical feature. Hemiplegia accompanied by sternomastoid
weakness on the opposite side is typical of hemispheric lesions, while a hemiplegia with weakness of the sternomastoid on the same side implies a lesion at the pontine level o r
Neurological Unit
Beth Israel Hospital
330 Brookline Awe
Boston, M A 02215
1. Balagura S, Katz RG: Undecussated innervation to the sternocleidomastoid muscle: a reinstatement. Ann Neurol 7:848 5 , 1980
2. Bender MB, Shanzer S, Wagman IH: On the physiologic decussation concerned with head turning. Confin Neurol
24:169-181, 1964
Saul Balagura, MD, PhD
D r Geschwind is a thoughtful man. His comments should
generate inquiry into the complex neural circuits subserving the innervation of the sternocleidomastoid muscle.
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