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Delayed paralysis of the deltoids due to selective anterior horn necrosis in a patient with traumatic tetraplegia.

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Delayed Paralysis of the
Deltoids Due to Selective
Anterior Horn Necrosis in
a Patient with Traumatic
Tetraplegia
Dominic Foo, MD, Mehdi Sarkarati, MD,
Alain B. Rossier, MD, and Amico Bignami, M D
In spinal cord studies of patients with traumatic paraplegia,
one sometimes observes a second lesion apparently not
related to fracture-dislocation of the spine. We report a
case that is particularly interesting in terms of clinicopathological correlations.
A 49-year-old man sustained multiple injuries in an automobile accident and was immediately unconscious. At
the emergency room he had 3 cardiac arrest but was successfully resuscitated. On the second and fourth days after
injury he had two short episodes of cardiac asystole which
responded to atropine. Four days after the accident the
patient was lethargic but arousable. Pain and touch were
absent below C6 bilaterally. Muscle strength in the upper
extremities was preserved but the hands were paralyzed;
From the Spinal Cord Injury Service and the Spinal Cord Injury
Research and Laboratory Services, West Roxbury Veterans Administration Medical Center, and the Departments of Orthopedic
Surgery and Neuropathology, Harvard Medical School, Boston,
MA.
Accepted for publication May 10, 1979.
Address reprint requests to Dr Foo, West Roxbury Veterans Administration Medical Center, 1400 VFW Pkwy, Boston, MA
02132.
Necrosi.c of the central part of the anterior horns at C5 (arrows). Note the symmetry of the lesion. (Luxol-fast blue.)
the paralyzed lower extremities were flaccid. Roentgenograms of the cervical spine showed fractures of the C7
laminae and of the C4, C5, and C6 spinous processes. O n
the tenth day after injury the patient showed decreased
strength in both deltoid muscles. Two days later, both deltoid muscles had absent function whereas biceps and
triceps functions were present. The neurological state remained otherwise unchanged. The patient died of pneumonia on the twentieth day following injury.
Autopsy of the spinal cord showed massive necrosis at
C8-TI. In view of the bilateral loss of the deltoids with
preservation of the biceps, attention was paid to C5. The
spinal cord between the C4 and C6 roots was cut into four
slices which were embedded separately. Macroscopically,
the C5 level appeared normal except for a slight depression
in the anterior horns in the second and third slices. Histologically, the three upper slices showed neuronal depopulation and chromatolysis of the surviving motor neurons, progressing to frank central necrosis of the anterior
horns with accumulation of lipid macrophages (Figure).
The lower slice was normal except for early wallerian degeneration in the posterior columns. The anterior spinal
artery and its sulcal branches were normal. Above C5, at
C6 and C7, and below T I , the cord was normal except for
early wallerian degeneration. The brain was normal.
The selective necrosis of the anterior horns at C5 with
sparing of two segments above the site of the major
traumatic injury at C8-T1 accounts for a clinical finding
difficult to explain during life, i.e., sparing of the biceps
with complete loss of the deltoids occurring ten days after
injury. The innervation of the deltoid is located at a somewhat higher level in the cord compared with the biceps, and
sparing of the lower part of C5 and of C6 thus accounts for
relative preservation of the biceps in this patient. Selective
necrosis of the anterior horns is a pathological entity distinct from central spinal cord necrosis. Central cord necrosis is a common occurrence in spinal cord injury, probably
due to stretching of the horizontally oriented blood vessels
in anteroposterior compression 121. Selective anterior horn
necrosis is a characteristic experimental lesion in ischemia
of the lumbar spinal cord resulting from temporary occlusion of the thoracic aorta [31.
O u r findings suggest that localized spinal cord ischemia
distant from the site of injury can occur in patients with
traumatic quadriplegia. T h e mechanism of the ischemia
may be difficult to assess in humans but should be amenable to experiments. Selective anterior horn necrosis has
recently been reported in patients suffering from severe
anoxia [ 11. However, the lesions were diffuse throughout
the cord rather than confined to a cervical segment, as in
our patient, and the posterior horns were frequently involved. In addition, contrary to our findings, the brain in
these cases showed severe anoxic changes.
References
Azzarelli B, Roessmann U: Diffuse “anoxic” myelopathy. Neurology (Minneap) 27: 1049- 1057, 1977
Doppman J L The mechanism of ischemia in anteroposterior
compression of the spinal cord. Invest Radio1 10:543-551,
1975
Schneider H, Dralle J: Ultrastructural changes in the rat spinal
cord after temporary occlusion of the thoracic aorta. Act
Neuropathol (Berl) 26:301-315, 1973
Cysticercosis and Spinal
Cord Compression
Jacqueline B. McDonald, MD, Paul T. Turner, MD,
and Alden H . Miller, M D
Involvement of the spinal cord by cysticercus is a rarely
encountered phenomenon, even in countries where cysticercosis is common [ 11. W e have observed this unusual
cause of spinal cord compression and wish to emphasize its
potential for becoming an intraspinal mass [3], as well as to
demonstrate the unique myelographic picture that results
when contrast material is inadvertently injected into the
cyst.
A 53-year-old man had experienced progressive weakness
of his lower limbs for one month. O n admission he was
unable to walk, his bladder was distended, and he complained of numbness and dysesthesias of his lower body.
The patient was a frequent visitor to Chihuahua, Mexico.
Neurological examination revealed flaccid paresis of the
legs. Pinprick sensation was diminished below the inguinal
ligaments, and there was a band of similar hypalgesia in the
midthoracic area. The white blood count was 8,400/mm3
with no eosinophils. At myelography the puncture (L3-4
level) was unusual; upon removal of the stylet, several mil~~
From the Departments of Surgery and Radiology, The University
of New Mexico and the Veterans Administration Hospital, Albuquerque, NM.
Accepted for publication May 18, 1979.
Address reprint requests to Dr Turner, Division of Neurosurgery,
University of New Mexico School of Medicine, Albuquerque,
NM 87131.
Composite roentgenogram showing upper and lower margins of
cyst (arrows) in both head-up and head-down positions; 3 cc of
Pantopaque was introduced at the L3-4 level during the
puncture.
Miters of clear fluid rapidly spewed out, then flow ceased.
Pantopaque, 3 cc, was introduced (Figure).
At laminectomy the cauda equina was shown to be
bound by diffuse arachnoiditis. Three cysts were identified
and excised; the largest of these had been punctured by the
myelogram needle, and it contained Pantopaque. Pathological examination showed a typical three-layered cyst wall
of racemose cysticercosis. The patient was treated with
prednisone, 40 mg per day. Six months after admission he
was able to walk with a cane and had bowel and bladder
control, but complained of lower limb dysesthesias.
Notes and Letters
367
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necrosis, patients, traumatic, selective, due, delayed, paralysis, deltoid, tetraplegia, anterior, horn
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