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EC number: 203-445-0
CAS number: 106-94-5
The patient, a 19-year-old Hispanic male without significant past
medical history, was transferred to hospital in February, 1998, after 1
week at another institution. In mid-January he had developed numbness
and mild but progressive weakness of the proximal lower extremities and
right hand. On admission, he could not stand without assistance. Other
symptoms included a transient dysphagia and urinary difficulties. Just
prior to developing these symptoms, he had been employed for 2 months as
a metal stripper. This occupation involved the use of an industrial
solvent used as a degreasing and cleaning agent.
About the time the symptoms began, the man had noted darkening of the
skin of his right hand, which was preferentially exposed to this
solvent. Protective gloves had been used as a precaution, but may not
have been sufficient to keep out the solvent, and may have enhanced
dermal uptake by occlusion effect.
Prior to admission, a brain MRI revealed a non-enhancing lesion, without
mass effect, in the right corona radiata. Lumbar puncture revealed
normal protein, glucose, cell count and the absence of oligoclonal
banding. He was treated with three grams of i.v. solumedrol, for
presumptive multiple sclerosis. This was without effect, but he was
still taking 75 mg of oral prednisone daily on transfer to our hospital.
Neurologic exam on admission revealed the patient to be alert and
oriented. Speech was fluent, and language function was normal.
Extraocular eye movements were full with no nystagmus. The pupils were 4
mm, equal, round and reactive to light and accommodation. The remaining
cranial nerves were grossly intact. Mild (4+/5) weakness of the right
biceps and triceps was present, but all other upper extremity muscle
groups were rated 5/5, and tone was normal. Upper extremity reflexes
were all at 2+.
There was dramatic and symmetric weakness of all lower extremity muscle
groups. Distally the dorsi- and plantar flexors were rated 0/5,
quadriceps 3/5, hamstrings 2+ /5, and iliopsoas 2+ /5. Tone was mildly
increased. The knee reflexes were 3+, while the ankle jerks were
diminished (trace to absent) and the plantar reflexes neutral. Sensation
was profoundly affected in a stocking distribution. Pinprick and
position sense were both markedly decreased-absent at the toes and
ankles. Vibration sense was deficient (the right hand and both lower
extremities, with the right leg being more affected then the left).
A gadolinium enhanced MRI of the brain revealed several patchy areas of
increased T2 signal in the periventricular white matter,
mostly outside the corpus callosum and asymmetrically distributed (more
prominent on the right). There was no evidence of mass effect or
abnormal enhancement, while MRI imaging of the spinal cord revealed
enhancement at multiple thoracic and lumbar levels in the region of the
neural foramina, in the proximity of the nerve root ganglia.
All four extremities were studied using standard nerve conduction
techniques and a Dantec Counterpoint system. These studies included two
motor nerve conductions with F wave response latencies and two sensory
nerve conductions per extremity.
Lower extremity distal motor latencies markedly prolonged (range:
8.0-9.6 ms), but only for the peroneal segment below the knees were the
motor conduction velocities mildly slowed (left: 39.3, right: 38.3 ms).
The right F-EDB and both F-AHs were prologned (57.6 - 62 ms). The left
F-EDB could not be obtained. There was marked slowing of all the lower
extremity sensory conduction velocities sural-left: 36.2, right: 31.8
ms; superficial peroneal-left: 31.2, right: 29.4 ms) but the
corresponding sensory evoked response amplitudes were all normal except
for the left sural (mildly attenuated at 3.1 µV). The lower extremity
motor-evoked response amplitudes were within normal limits.
The distal motor latencies, motor and sensory conduction velocities,
motor evoked response amplitudes and F-response latencies were within
normal limits for both arms. Sensory evoked response amplitudes for the
right arm were within normal limits, but were attenuated compared with
the left (right-median: 10, ulnar: 10.6, left-median: 23.3, ulnar: 23.0
µV). There was no evidence of conduction block or temporal dispersion
for either the upper or lower extremities.
EMG of selected lower extremity muscles revealed increased insertional
activity only in the left extensor digitorum longus, and no sustained
spontaneous activity in any of the muscles studied. Non-quantitative
studies showed a tendency toward prolonged duration (i.e. 17-20 ms) for
numerous MUPs (i.e. motor unit potentials). In several muscles satellite
potentials amplitudes and morphologies varied from discharge to
discharge. No MUPs could be recruited in the right tibialis anterior or
left EDB muscles. In most muscles, recruitment was full, but with a
noticeable lag between the onset of patient effort and muscle
Somatosensory-evoked potential studies revealed normal amplitudes and
latencies for the arms (median nerve stimulation), but no cortical
potentials could be obtained following bilateral peroneal stimulation,
suggesting a lesion at the dorsal column or lemniscal level. The lumbar
latency values (left: 12.2, right: 10.6 ms) suggested an additional
abnormality on the left, at or distal to the lumbar cord. Brainstem
auditory and visual evoked potentials were within normal limits.
Lumbar puncture produced clear colorless fluid with an opening pressure
of 230 mm Hg (31.5 cm H2O). Protein (0.28 g/L), glucose (3.6
mmol/L), and lactic acid (1.6 meq/L) determinations and cell counts (RBC
= 12 c/µL, WBC = 0 c/µL) were all within normal limits, as were myelin
basic protein levels, Lyme titers, CSF ACE level, HSV PCR, and antibody
determinations for CMV, VCA, echo, Coxsackie, and polio viruses, except
for the finding, now, of one oligoclonal band. Lumbar puncture and
serology were negative for VDRL, cryptococcal antigen, CSF bacterial,
fungal and AFB cultures, ANA titer, IgM for EBV, and ANCA C & P
antibodies (IgG for EBV was positive). Serum B12 (1.25 ng/mL)
and folate (17.2 ng/mL) levels were elevated. Total serum cholesterol
was elevated (2.6 and 2.83 g/L).
The patient continued on tapering doses of prednisone. Intermittent
hypertension developed, and was treated with hydrochlorothiazide and
quinapril. He received physical and occupational therapy and by the time
of discharge (3/6/1998) displayed remarkable improvement in lower
extremity strength. Right plantarfiexor strength remained 0/5, left
improved to 2/5, dorsiflexors were both 3/5, iliopsoas muscles 4+ /5,
the quadriceps were 5/5, and hamstring muscles 4/5. Unfortunately
following discharge the patient was lost to follow-up.
A 19-year-old male developed complaints including weakness of the lower
extremities and right hand, numbness, dysphagia and urinary difficulties
following a 2 month exposure to an industrial solvent constituted mainly
of 1-bromopropane, but also containing butylene oxide, 1,3-dioxolane,
nitromethane, and other components. Nerve conduction studies revealed
evidence of a primary, symmetric demyelinating polyneuropathy. Evidence
of CNS involvement came from gadolinium enhanced MRI scans of the brain,
showing patchy areas of increased TZ signal in the periventricular white
matter, similar scans of the spinal cord revealing root enhancement at
several lumbar levels, and SSEP studies. The patient's symptoms had
started to resolve following the discontinuation of the exposure, before
he was lost to follow-up. Similar findings have been reported following
1-bromopropane exposure in rats, leading to a hypothesis that the
patient's symptoms may have been due to 1-bromopropane-induced
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