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April 16, 2018
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A 76-year-old man with an atypical presentation of extensor lag

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A 76-year-old African-American man presented to the ED after a fall from standing the day prior. His chief complaint was an inability to extend his right knee since the fall. He also reported some weakness he had experienced in his right leg for the past 3 weeks. Before the fall, he ambulated independently. He denied having any numbness or tingling in the affected extremity and any other injuries. His past medical history included hypertension, non-insulin-dependent diabetes mellitus and untreated herpes zoster (shingles) that involved the right leg 3 weeks prior to presentation. His surgical history was significant for right shoulder rotator cuff repair. He denied any recent travel history.

On physical examination, a rash was present over his anteromedial thigh in L2/3 distribution (Figure 1), and he had a minimal knee effusion. No other rash was documented. He was unable to actively extend his knee and had 2/5 quadriceps strength. No definite quadriceps tendon defect was palpable, and his knee was not tender to palpation. He otherwise had 5/5 motor strength throughout the right lower extremity musculature. He had no ligamentous laxity, and his right leg was neurovascularly intact.

Plain radiographs of the right knee were obtained in the ED (Figure 2), and they were unremarkable other than a nonarticular, superior patellar spur. The patient was subsequently diagnosed by emergency medicine physicians as having a ruptured quadriceps tendon, and he was placed in a knee immobilizer. The patient followed up in the orthopedic surgeon’s office the same day with an unchanged exam.

Due to the atypical presentation, further diagnostic studies were ordered including an MRI of the knee (Figure 3) and the lumbosacral spine (Figure 4). The knee MRI showed muscular edema in the rectus femoris and vastus medialis oblique but did not show any evidence of quadriceps tendon tear. His extensor mechanism was intact. The MRI of the lumbar spine displayed a broad-based disc bulge in midline and left of midline at L4/5 with mild spinal stenosis. With concern arising from the atypical presentation of rash and negative imaging, electromyography/nerve conduction velocity was ordered, which showed dense fibrillation potentials in L2/3 and severe right L2/3 radiculopathy. There was no evidence of diabetic neuropathy or plexus injury.

Figure 1. This clinical photograph demonstrates a herpes zoster rash in the L2-3 dermatome.
Figure 2. Shown are the patient’s lateral (a), anteroposterior (b) and sunrise (c) views of the knee, which are unremarkable except for a superior patellar spur.
Figure 3. Shown are T2-weighted (a, b) and T1-weighted (c, d) MRI sagittal cuts through the right knee, which demonstrate an intact extensor mechanism, ACL and PCL.
Figure 4. Shown are T2-weighted cuts of the patient’s lumbar spine. The sagittal cut (a) shows a mild disc bulge at L4-5 and L5-S1 which were stable based on a study done 2 years prior. The axial cuts showed no compromise of the canal or foramina at L2-3 (b), mild uniform disc bulge at L3-4 (c), and broad-based disc bulge in midline and left of midline at L4-5 (d), as well as mild spinal stenosis at L4-5.

Source: Raymond W. Acus III, MD

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Herpes zoster motor neuropathy

Before treatment, our patient exhibited 2/5 quadriceps strength and could not walk without his knee buckling. He was treated with a drop-lock knee brace locked in extension and was able weight-bear as tolerated. Physical therapy was started for strengthening. After 7 months of treatment, he progressed to being able to extend his knee to 30. At 10 months, the patient had 4/5 quadriceps strength and full active range of motion. He was able to ambulate and painlessly perform all activities of daily living.

Discussion

Herpes zoster (HZ) affects nearly 1 million patients annually in the United States with the highest incidence in individuals from the 7th decade onwards. Primary varicella zoster virus infection presents with viral prodrome and a characteristic maculopapular rash in a dermatomal pattern. This rash often progresses into painful vesicles and bullae in 1 to 2 weeks. Other symptoms are pruritus, paresthesias and a viral prodrome of fatigue, malaise and fever. The virus lies dormant in the dorsal root ganglion and may reactivate years later, typically in the fifth to seventh decades of life, as occurred in our patient. Reactivation may be increased in elderly patients secondary to age-related decline in immunity and in those who are immunosuppressed.

This patient’s zoster-associated mononeuropathy (ZAM) with paresis is a rare complication of HZ that is only found in up to 3% of cases. Paresis following HZ eruption has been reported 2 to 3 weeks after dermatic symptoms arise. In one study, the duration of weakness was prolonged (mean 282 days, range 45 to 1,242 days). The mechanism is unknown, but studies have postulated there is a distally mediated neuropathic process. Nerve conduction testing has demonstrated conduction block and fibrillation potentials in affected muscles that eventually resolves, suggesting dysmyelination as a pathophysiological explanation. The mechanism of how the HZ virus reactivates and causes disease is still not well understood. However, most physicians agree the symptoms of weakness and post-herpetic neuralgia can cause significant morbidity for affected patients, and prompt management is critical.

ZAM is more common in elderly individuals, and weakness frequently affects proximal muscle groups (C5-C7 and L2-L4). Primary care providers and orthopedic surgeons should recognize motor neuropathy as a potential complication of shingles. Recent publications demonstrate patients with diabetes may be at a higher risk of developing HZ (1.8-fold to 8.4-fold increase) and an adjusted relative risk of 3.7 (95% CI, 2.0-6.8). The fact that the incidence of diabetes mellitus has increased to 5.8% to 12.9% in the general population highlights that providers must be familiar with the symptoms and presentation of HZ now more than ever. Prognosis is good after ZAM, with complete or almost complete recovery of muscle function in more than 50% of patients within 6 to 12 months.

Disclosures: Acus K, Acus RW and McKernan report no relevant financial disclosures.