Aaem case report #23: Acute paralytic poliomyelitis

AAEM CASE REPORT #23

A 56-year-old man with acute paralytic poliomyelitis is described. The illness started with fever and diarrhea after an overseas trip, and an enterovirus other than poliovirus was isolated from the patient's stool. The onset of weakness was rapid and asymmetric, with primary involvement of the lower extremities. Nerve conduction studies revealed low amplitude motor responses after the first week, with normal results for sensory studies. Serial electromyographic studies were performed, documenting acute denervation followed later by reinnervation in the distribution of multiple segments. The clinical and electrodiagnostic features of acute poliomyelitis are reviewed.Key words: poliomyelitis motor neuron disease enterovirus electromyography nerve conduction study MUSCLE & NERVE 14:1159-1164 1991

AAEM CASE REPORT #23: ACUTE YUEN T. SO, MD, PhD, and RICHARD K. OLNEY, MD

Paralytic poliomyelitis is a clinical syndrome most frequently caused by enteroviruses, although herpes, mumps, and other viruses have been implicated occasionally.8 Before the advent of the poliovirus vaccine, virtually all cases of poliomyelitis in the United States were due to poliovirus, accounting for more than 15,000 cases per year between 1951 and 1955. The widespread use of vaccination resulted in a dramatic decline in incidence to only 9 cases per year between 1980 and 1984. T h e majority of recent cases are due to exposure to the live-attenuated virus in oral polio vaccine, either in vaccine recipients o r in household contacts of vaccinated individuals. With the decline in incidence of poliovirus infection, other enteroviruses such as coxsackievirus, echovirus, and enterovirus 7 1, have emerged as relatively important causes of paralytic poliomyelitis.

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CASE REPORT

A 56-year-old Caucasian man developed a fever of 40°C and watery diarrhea on the day he returned from a trip to Madagascar.

Clinical History.

From the Department of Neurology, School of Medicine, University of California, San Francisco, California. Address reprint requests to American Association of Electrodiagnostic Medicine (formerly the American Association of Electromyography and Electrodiagnosis), 21 Second Street S.W., Suite 306, Rochester, MN 55902. Accepted for publication December 12, 1990. CCC 0148-639)(/91/01201159-06 $04.00 0 1991 Yuen T. So, MD, PhD, and Richard K. Olney, MD Published by John Wiley & Sons, Inc.

AAEM Case Report #23: Acute Poliomyelitis

Seven days later, he awoke with a cramping discomfort in his left foot and could not move his left ankle. Milder weakness developed in his right leg the next day. Leg weakness progressed over 2 days to the point that he was unable to walk. His bladder and bowel function and lower extremity sensation were normal. With the exception of a dull frontal headache, there were no other neurologic symptoms. His past medical history was unremarkable. He had received an oral booster vaccine to poliovirus approximately 4 years previously, but had never received a primary vaccination. T h e rectal temperature was 38.6"C. There was pain with flexion of the neck. Tests of higher cortical function and cranial nerves were normal. Fasciculations were infrequently observed in several lower extremity muscles. The tibialis anterior, tibialis posterior, peroneus longus, and toe dorsifllexors on the left did not have any visible or palpable contraction. The gastrocnemius, toe plantar-flexors, quadriceps, hamstrings, and iliopsoas on the left were severely weak (MRC, grade 3), and the glutei and other proximal left leg muscles were moderately weak (grade 4). The right leg muscles below the knee had moderate weakness (grade 4), whereas the right thigh and hip girdle muscles had normal strength. Intrinsic hand muscles and wrist extensors on the left were mildly weak (grade 4+). Other muscles in the upper extremities had normal strength. Muscular bulk was normal in all muscles, and tone was reduced only in the left leg.

Physical Examination.

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December 1991

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Needle electromyography (EMG) was performed with a concentric needle electrode that had an active recording area of 0.07 mm'. Fibrillation potentials and positive sharp waves were graded from 0 to 4+ according to commonly accepted criteria: 0 = none; 1+ = persistent single trains in at least 2 areas; 2+ = moderate numbers of fibrillations in 3 o r more areas; 3+ = many in all areas; 4 + = filling the baseline in all areas.' A semiquantitative analysis of recorded motor unit action potentials (MUAPs) was employed. The amplitude and duration of early recruited MUAPs (from the first 3 to 5 in the recruitment order) were measured from the digitally stored oscilloscope images with bandpass filter at 20 Hz to 10 kHz. Amplitude was measured peak to peak, and duration was for the total width of the potential. Approximately 10 MUAPs were measured in each muscle, and the results were reported as a range of minimum to maximum.

Sensory examination was normal. Deep tendon reflexes were depressed, but present at the left knee and at both ankles, and were normal elsewhere. Plantar responses were flexor bilaterally. Laboratory Test. Complete blood cell count, routine serum, and urine studies were normal. Magnetic resonance imaging revealed no abnormal signal in the conus and the lower thoracic spine and no evidence of disk disease. Lumbar puncture on admission (3 days after onset of weakness) showed an opening pressure of 150 mm H,O, and clear, colorless cerebrospinal fluid (CSF) with 62 white blood cells/mm3 (27% polymorphonuclear cells, 56% lymphocytes, and 17% monocytes), total protein of 42 mg/dL, and glucose of 62 mg/dL. CSF cultures were negative. Stool cultures grew out echovirus type 4. Acute and convalescent titers for antibodies to poliovirus types 1, 2, and 3 were negative. ELECTRODIAGNOSTIC EXAMINATION

Nerve Conduction Studies. NCSs were performed initially 4 days after the onset of weakness (Table 1). Amplitude of the CMAPs was reduced only for the right extensor digitorurn brevis following right peroneal nerve stimulation at all sites. Motor nerve conduction velocities (NCVs) were normal, and there was no sign of conduction block in any nerve. F responses were unobtainable from 3 of the 4 nerves in the legs. Normal results were obtained with all sensory NCSs. NCSs were repeated 1 week later, 11 days after the onset of weakness. These studies demonstrated a reduction in CMAP amplitude by 58% to 100% of the previous values for all 4 intrinsic foot muscles. Distal motor latencies, motor NCVs, and the results of sensory NCSs remained normal.

We used a Dantec 1500 EMG System for all electrodiagnostic studies. Nerve conduction studies (NCSs) were performed using conventional techniques of surface recording and percutaneous supramaximal stimulation. Amplitudes of compound muscle action potentials (CMAPs) were measured from the baseline to negative peak, whereas amplitudes of sensory nerve action potentials (SNAPS)were measured from preceding positive peak to the negative peak. Sensory conduction velocities were calculated using the latency to onset of the sensory potentials. The minimal F-wave latency for each nerve was determined from a series of 10 distal (ankle or wrist) stimulations. Methods.

Table 1. Electrodiagnostic nerve conduction studies performed 4 days after the onset of clinical weakness.

Distal latency (ms)*

Amplitude (mV or pV) Stimulate Motor Peroneal F wave Tibia1 F wave Sensory Sural Superficial Peroneal

Record

Right

Left

Normal

Right

Left

Normal

Right

Left

Normal

EDB ED6 AH AH

0.5

2.2

>2

>37

>3