We present a case of lower motor neuron upper limb weakness due to infarction of the anterior horn cells of the spinal cord following diving. To our knowledge, this is the first report of an isolated lower motor neuron syndrome following diving-related decompression

Henderson, Robert D.

Pender, Michael P.

University of Queensland eSpace

Neurology, February 14, 2006; 66(3); 451-452. 
Lower motor neuron weakness after diving-related decompression 
Robert D. Henderson, FRACP; and Michael P. Pender, MD 
 
Myelopathy is a recognized complication of diving and usually presents with upper motor 
neuron weakness and sensory loss of the lower limbs due to thoracic spinal cord damage.1,2 
Here we present a case of lower motor neuron upper limb weakness due to infarction of the 
anterior horn cells of the spinal cord following diving. To our knowledge, this is the first report 
of an isolated lower motor neuron syndrome following diving-related decompression. 
 
A 46-year-old woman was referred for electromyography (EMG) with a clinical diagnosis of 
ALS. Two months earlier, she had noted weakness in her right hand without sensory symptoms. 
The patient was a recreational scuba diver and recalled diving to 90 ft, 1week prior to the onset 
of weakness. She ascended quickly but not in violation of her diving table and 20 hours later 
took an international flight. There was no significant past medical history. 
 
On examination, there was wasting of the small muscles of the right hand and a prominent 
inability to extend the right middle finger. Scattered fasciculations were seen in the small 
muscles of the right hand. There was mild weakness of right elbow extension, forearm 
pronation, wrist extension and thumb abduction, and moderate weakness of finger extension 
and abduction. Left finger abduction was mildly weak, but power was otherwise normal in the left 
upper limb. The biceps, supinator, and triceps jerks were normal bilaterally. The upper limb 
sensation, cranial nerves, and lower limb examination were normal. 
 
Nerve conduction studies showed low amplitude right ulnar and median compound muscle 
action potentials (CMAPs) with normal conduction velocities, F waves, and corresponding 
sensory studies. No conduction block was present. The right radial CMAP recording over the 
extensor digitorum was normal. The EMG showed fibrillations and fasciculations in the right 
first dorsal interosseous and opponens pollicis muscles with reduced recruitment of complex 
large motor units. There was increased size of motor units in the right deltoid, triceps, pronator 
teres, and lower cervical paraspinal muscles. Large motor units were also present in the left first 
dorsal interosseous and opponens pollicis muscles. 
 
MRI of the cervical spine at the time of the clinical examination showed increased signal in the 
spinal cord from C3 to C7 vertebral bodies on sagittal T2 imaging. On T2 axial cuts, the 
increased signal was predominantly in the right anterior horn, with hypointensity on T1imaging 
(figure). T2 hyperintensity was also present to a lesser extent in the left anterior horn. No 
enhancement occurred following the injection of gadolinium. The MRI was consistent with 
focal infarction of the cervical spinal cord. On follow-up, 4 months after the onset of weakness, 
her neurologic condition was unchanged. 
 
Our patient’s hand weakness is explained by infarction involving the anterior horn cells in the 
spinal cord due to diving-related decompression. Spinal cord damage following diving is 
recognized,1-5 but our case is unusual because of the cervical cord involvement with lower 
motor neuron weakness of the upper limb, in contrast to the more typical thoracic spinal cord 
involvement with upper motor neuron weakness of the lower limbs and sensory loss.1-3 In our 
case, this presentation had led to the initial diagnosis by a neurologist of ALS. 
 
Spinal cord infarction is usually reported with type II decompression sickness1 but can occur in 
the absence of clinical signs of decompression sickness.5 In a study of goats with different 
diving exposures, the presence of spinal cord lesions did not correlate with the typical features of 
decompression sickness.5 Spinal cord involvement may occur following dives conducted in 
accordance with US Navy decompression tables.1,4 Rapid ascent has been associated with spinal 
cord involvement.1,5 
Copyright © 2006 by AAN Enterprises, Inc. 
Neurology, February 14, 2006; 66(3); 451-452. 
 
Figure. (A) Axial T2 MRI of the spine at C3 to C4 level with hyperintensity of the right anterior horn and to a lesser 
extent of the left anterior horn. (B) Corresponding T1 scan showing hypointensity of the right anterior horn consistent 
with infarction. 
The most likely mechanism responsible for decompression-related myelopathy is spinal cord 
ischemia due to congestion of the epidural vertebral venous system by nitrogen gas bubbles. The 
epidural vertebral venous system (Batson plexus) can be obstructed by gas bubbles that collect, 
coalesce, and grow, when other major veins do not become obstructed, because the system 
functions as a valveless relatively stagnant venous lake in which the direction of flow changes 
frequently, in contrast to the unidirectional conduit function of other veins.6 In addition to 
mechanically obstructing venous outflow, gas bubbles in the venous bed may accelerate 
coagulation, leading to more complete venous obstruction.6 
 
From the Department of Neurology, Royal Brisbane and Women’s Hospital, School of Medicine, 
University of Queensland, Australia. 
 
Disclosure: The authors report no conflicts of interest. 
References 
1. Kimbro T, Tom T, Neuman T. A case of spinal cord decompression sickness presenting as partial Brown– 
Sequard syndrome. Neurology 1997;48:1454–1456. 
2. Hierholzer J, Tempka A, Stroszczynski C, et al. MRI in decompression illness. Neuroradiology 2000;42:368– 
370. 
3. Manabe Y, Sakai K, Kashihara K, Shohmori T. Presumed venous infarction in spinal decompression sickness. 
AJNR Am J Neuroradiol 1998;19: 1578–1580. 
4. Aharon-Peretz J, Adir Y, Gordon CR, Kol S, Gal N, Melamed Y. Spinal cord decompression sickness in sport 
diving. Arch Neurol 1993;50:753– 756. 
5. Blogg SL, Loveman GA, Seddon FM, et al. Magnetic resonance imaging and neuropathology findings in the 
goat nervous system following hyperbaric exposures. Eur Neurol 2004;52:18–28. 
6. Hallenbeck JM, Bove AA, Elliott DH. Mechanisms underlying spinal cord damage in decompression 
sickness. Neurology 1975;25:308–316. 
Copyright © 2006 by AAN Enterprises, Inc. 


Lower Motor Neuron Weakness After Diving-Related Decompression

Myelopathy is a recognized complication of diving and usually presents with upper motor neuron weakness and sensory loss of the lower limbs due to thoracic spinal cord damage.1,2 Here we present a case of lower motor neuron upper limb weakness due to infarction of the anterior horn cells of the spinal cord following diving. To our knowledge, this is the first report of an isolated lower motor neuron syndrome following diving-related decompression. A 46-year-old woman was referred for electromyography (EMG) with a clinical diagnosis of ALS. Two months earlier, she had noted weakness in her right hand without sensory symptoms. The patient was a recreational scuba diver and recalled diving to 90 ft, 1week prior to the onset of weakness. She ascended quickly but not in violation of her diving table and 20 hours later took an international flight. There was no significant past medical history. On examination, there was wasting of the small muscles of the right hand and a prominent inability to extend the right middle finger. Scattered fasciculations were seen in the small muscles of the right hand. There was mild weakness of right elbow extension, forearm pronation, wrist extension and thumb abduction, and moderate weakness of finger extension and abduction. Left finger abduction was mildly weak, but power was otherwise normal in the lef

Lower Motor Neuron Weakness After Diving-Related Decompression

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