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| Journal of the New Zealand Medical Association,
19-May-2006, Vol 119 No 1234
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Neurophysiological findings in a case of cervical anterior
spinal artery syndrome: compound muscle action potentials, a marker for
prognosis
Ming Lu, Dexuan Kang, Dongsheng Fan
Case reportA 40-year-old Chinese man was admitted to our hospital in
November 2004. He was suffered from severe aching of the neck irradiating to his
shoulders followed by weakness in both arms. Thirty minutes later, the weakness
extended to the legs. Three hours after onset, the weakness was steadily
progressing and urinary retention developed. He didn’t complain of
respiratory distress or difficulty in swallowing. There was no personal or
family history of neurological illness, and no history of illicit drug
use.
Initial examination showed a complete flaccid tetraplegia.
Sensory examination showed dissociated loss of pin-prick and temperature
discrimination below C3, with normal appreciation of light touch, vibration, and
joint position. Deep tendon reflexes were absent. Babinski sign was positive
bilaterally.
The MRI obtained 5 days after the onset of the illness
showed an enlargement of the cord from C2 to T3 (Figure
1). Spinal angiography 6 days after the
ictus showed the superior segmental obstruction of the anterior spinal artery
(Figure 2). CSF was clear and colourless,
and the pressure was 160 mmH2O.
The CSF leucocyte count was 8/μL, and the protein
content was 0.72 g/L. Ultrasonic cardiogram showed no abnormal on aortic arch
and the lower segment of thoracic aorta. The plasma concentrations of glucose,
total cholesterol, HDL cholesterol, LDL cholesterol, and the inflammatory
markers (including ESR, HS-CRP, and antinuclear antibody) were all normal. The
serum level of homocysteine was 16.4 μmol/L.
Nerve conduction studies were performed 2 weeks after the
initial symptoms (Table 1). Sensory nerve conduction velocities on all
extremities and motor nerve conduction velocities on the lower extremities were
normal, but no CMAP (the compound muscle action potentials) could be obtained on
either median nerves or ulnar nerves.
F-waves and the motor evoked potentials on upper limbs were
absent bilaterally. However, the
somatosensory-evoked potentials showed normal amplitude and latency of the
brachial plexus and cortex response on median nerve stimulation at the wrist on
both sides, and neither the brainstem auditory evoked potentials nor the visual
evoked potentials were abnormal.
The patient was diagnosed as cervical anterior spinal artery
syndrome (ASAS), and treated with daily intravenous methylprednisolone 120 mg
for 1 week and oral aspirin 200 mg for 6 months. After 2 weeks, he gradually
began moving his legs. The recovery of strength of arms was not obviously. Four
weeks later, atrophy of the small hand muscles became apparent. Physical
examination showed 0/5 strength of both upper limbs and 3/5 on the lower
extremities. The ankle jerks were active and the Babinski signs were positive
while the biceps brachii and triceps brachii reflexes were absent. The
neurological findings did not change during the following 6 months.
Table 1. Nerve conduction studies performed 2 weeks
after the initial symptoms
NCV=nerve conduction
velocity; ND=not
detected.
DiscussionIn the present study, we reported a case of cervical ASAS,
and found that no
CMAP could be obtained in either median
nerves or ulnar nerves. Six months after the onset, there was no any recovery of
strength in both arms of the cervical ASAS patient.
Spinal arteries follow nerve roots to the cord and then
bifurcate into anterior and posterior radicular arteries. The anterior radicular
arteries supply the anterior spinal arteries, and the posterior radicular
arteries feed the posterior spinal arteries.1 There is no anastomotic network
between the single anterior spinal artery and the paired posterior spinal
arteries. The cervical and upper thoracic cord is supplied by the vertebral
artery and radicular arteries of the ascending cervical arteries.2 The ventral
two-thirds of the spinal cord are absolutely dependent upon the patency of the
anterior spinal artery and receive no collateral blood supply from the paired
posterior spinal arteries. Occlusion of the anterior spinal artery will result
in dysfunction of the ventral two-thirds of the cord, including anterior horns,
spinothalamic tracts, and pyramidal tracts.2
ASAS was first described in 1904 by Preobranshenski and
characterised in 1909 by Spiller. It occurs
when the territory of the anterior spinal artery, supplying the ventral
two-thirds of the spinal cord, is involved.3
In acute ASAS, the initial symptom is a local or radicular pain at the
level of the vascular occlusion rapidly followed by complete motor paralysis.
Initially, a flaccid paralysis with loss of tendon reflexes
occurs. As the spinal cord shock resolves, flaccidity is replaced by spasticity
of all muscle groups below the level of occlusion.1 Muscles at the level of
infarction remain flaccid and become atrophic from the necrosis of the anterior
horn cells. Bowel and bladder dysfunction is common.4 There is loss of pain and
temperature sense because of the interruption of the spinothalamic tracts, and
paring of position, vibration, and motion sense owing to the reservation of
posterior columns.5
Nowadays, MRI has been established to be the method in
detecting cervical spinal cord ischaemic lesions including those in the
territory of the anterior spinal artery. But the clinical contribution of
angiography to diagnosis of ASAS may be limited because of its lower
specificity.3,6,7 Since the ischaemic process involves neither the spinal
ganglion nor the dorsal column, abnormal sensory nerve conduction studies and
somatosensory evoked potential findings were absent in our cervical ASAS
patient.
Regarding motor nerve conduction studies, however, Amoiridis
et al had reported a considerable reduction of CMAP in an ASAS
patient.8 But the fully absent CMAP in our
patient has not been observed previously. F-waves represent a simple
electroneurophysiological measures for assessing the proximal segment of a
nerve.8
The absent F-waves in our patient were assumed that the
state of inexcitability of the anterior horn cells. It is tempting to speculate
that Wallerian degeneration of peripheral nerves resulting from necrosis of
cervical anterior horn cells may take responsible for the absent CMAP in median
and ulnar nerves. Six months after the
onset, there was no any recovery of strength in his both arms. In our opinions,
CMAP could be seen a marker of prognosis for ASAS patients, and absent CMAP in
motor nerve conduction studies usually forecasts the bad prognosis.
Author information:
Ming Lu, Neurologist; Dexuan Kang, Professor; Dongsheng Fan, Professor and
Head; Department of Neurology,
Peking University Third Hospital, Beijing, China. Correspondence:
Professor Dongsheng Fan, Department of Neurology, Peking University Third
Hospital, 49 North Garden Road, Haidian District, Beijing 100083, China.
Fax: +86 10 62017691 (ext 2250); email: dsfan@sohu.com
References:
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