Unusual Case of Spinal Deformity: Post Herpetic Scoliosis
The patient is a 72-year-old female presenting with approximately 1.5 years of progressive coronal and sagittal deformity following an episode of herpes zoster. She reports that less than 2 years prior to presentation, she experienced sudden onset of urinary retention and constipation followed by a characteristic rash distributed to the left gluteal and sacral regions.
Following admission to her local hospital, the patient was diagnosed with herpes zoster and symptomatically treated for bladder and bowel dysfunction. Shortly after improvement in bladder dysfunction, the patient reported that she developed progressive low back pain associated with sagittal and coronal deformity.
Over the course of several months thereafter, her pain and deformity increased significantly, ultimately limiting all her activities of daily living, and ability to ambulate entirely.
A recent DEXA scan revealed a T-score of -3.0. She is 1.63m and weighs 48.1kg.
- Symptomatic low back pain for ~1.5 years
- The patient rates her low back pain as severe; L>R; 9 on a 10-point scale associated with postural pain in the shoulders and thighs; she denies paresthesias, wasting and weakness; she does note moderate relief of symptoms with the use of narcotics and when supine.
- Prior to development of pain, the patient had an unlimited exercise tolerance. However, at the time of presentation to our practice, she is nonambulatory and requires assistance transferring to a wheelchair.
- Lumbar range of motion is limited in flexion and extension.
- Range of motion in hips is full though moderately painful.
- Bilateral muscle strength is 5/5 in ankle dorsi and plantar flexors.
- Bilateral negative straight-leg raise.
- Reflexes 2+ throughout.
- Sensory intact to pinprick throughout.
Figure 1. Full body anteroposterior
Figure 2. Full body lateral
Figure 3. Anteroposterior
Figure 4. In clinic photographs of the patient
- A trial of trigger point injections did not reduce the patient's symptoms.
- A course of physiotherapy produced minimal benefits.
- Pain was moderately improved with narcotics.
- Severe kyphoscoliosis
- Right convex deformity Cobb 51°
- SVA approximately 150 mm
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Given the very unusual etiology and progression of deformity in this case, a full neurologic workup was deemed necessary prior to consideration of surgical correction. Numerous studies have demonstrated increased operative and postoperative complication rates in patients with progressive neuromuscular disease combined with diminished outcomes. It was therefore, crucial to confirm the diagnosis of post herpetic scoliosis prior to surgery.
After referral to neurology and confirmation of diagnosis, the patient underwent a posterior fusion from T4–pelvis with iliac fixation following facetectomies. Fusion was accomplished with autograft from the patient’s bilateral iliac crests, and supplemented with allograft and BMP from L4-S1. She required a complex flap by plastic surgery for closure.
Estimated blood loss was 750cc with a total operative time of about 8 hours. There were no intraoperative complications. The patient was observed in the medical intensive care unit for reasons related to medical comorbidities and discharged to sub acute rehab on postoperative day 7.
Figure 5. Full body anteroposterior
Figure 6. Full body lateral
At the time of this case presentation, the patient is 3 months postoperative. She reports resolution of low back pain and corrected posture. She can ambulate independently more than 250 feet without pain. Her neurologic exam remains unchanged with full strength, sensation and reflexes.
Figure 7. Postoperative in clinic photographs of the patient
Drs. Cruz and Errico present a fascinating case of post herpetic kyphoscoliosis requiring a long construct fusion with correction. While post herpetic shingles is extremely common, muscular weakness and spinal deformities following its occurrence is rare.
This case involves a 72-year-old female who developed progressive spinal deformity with coronal and sagittal malalignment following an episode of shingles. A thorough neurological workup was performed, and an attempt at nonsurgical management failed to improve her condition. Due to the severity of the deformity, surgical treatment was recommended. The authors performed a T4 to the pelvis posterior instrumented fusion and achieved an excellent correction of this severe deformity without complication.
Few case reports or only small case series have been reported on post herpetic paralysis, and none have reported on the development of adult scoliosis.1 Regardless of the etiology, severe spinal deformity, in particular, sagittal plane deformity is associated with poor physical function.2
Correction of sagittal imbalance, whether compensated or uncompensated, yield significant improvement in pain and function.3 I congratulate the authors on an excellent surgical correction of a difficult problem arising from a rare condition.
1. Kawajiri S, Tani M, Noda K, Fujishima K, Hattori N, Okuma Y. Segmental zoster paresis of limbs: report of three cases and review of literature. Neurologist. 2007 Sep;13(5):313-7.
2. Glassman SD, Berven S, Bridwell K, Horton W, Dimar JR. Correlation of radiographic parameters and clinical symptoms in adult scoliosis. Spine (Phila Pa 1976). 2005;30(6):682-688.
3. Smith JS, Singh M, Klineberg E, Shaffrey CI, Lafage V, Schwab FJ, et al. International Spine Study Group. Surgical treatment of pathological loss of lumbar lordosis (flatback) in patients with normal sagittal vertical axis achieves similar clinical improvement as surgical treatment of elevated sagittal vertical axis: clinical article. J Neurosurg Spine. 2014;21(2):160-70.
The case presentation suggests a 72-year-old woman developed progressive kyphoscoliosis related to an acute event of herpes zoster. In the case report, symptoms progressed over 1.5 years. Eventually, the patient underwent a T4 to the pelvis fusion surgery with excellent radiographic and clinical results.
I would suggest there is no mechanism for herpes zoster (shingles) to cause scoliosis. Additionally, the scoliosis was mainly thoracic/lumbar and the alleged herpes zoster occurred in the sacral area. Since herpes zoster is a relatively common condition in the elderly, the herpes zoster was just an incidental finding and not causative in this case.
The postoperative radiographic images are impressive, but I do not believe these results are typical of degenerative thoracolumbar scoliosis in the elderly population, and I would be careful regarding extrapolating these results to all patients with degenerative thoracolumbar scoliosis.
While these authors concede that reports of post herpetic scoliosis are exceptionally rare,1 the acute and rapid nature of deformity in the absence of neuromuscular pathology, combined with its temporal relationship to Herpes Zoster, create a compelling (though controversial) argument for its etiology.
Herpes Zoster is unquestionably common, affecting nearly 1 in 3 people in their lifetime. Known complications of Zoster such as peripheral nerve palsies, however, are strikingly rarer.2 Furthermore, we would argue that a plausible mechanism of deformity secondary to Zoster exists, analogous to those demonstrated by neuromuscular pathologies such as spinal muscular atrophy3 or even anterior horn injury such as seen with West Nile virus infection.4 Though current practice gives little credence to the role of the muscular envelope in skeletal deformity, we must acknowledge that the relationship between the two remains largely unsettled.
1. Tashiro S, Akaboshi K, Kobayashi Y, Mori T, Nagata M, Liu M. Herpes zoster-induced trunk muscle paresis presenting with abdominal wall pseudohernia, scoliosis, and gait disturbance and its rehabilitation: A case report. Arch Phys Med Rehabil. 2010;91(2):321-325.
2. Yaszay B, Jablecki CK, Safran MR. Zoster paresis of the shoulder. Case report and review of the literature. Clin Orthop. 2000;377:112-118. 3. Tisdale S, Pellizzoni L. Disease mechanisms and therapeutic approaches in spinal muscular atrophy. J Neurosci. 2015;35(23):8691-8700. 4. Shrestha B, Gottlieb D, Diamond MS. Infection and injury of neurons by West Nile encephalitis virus infection and injury of neurons by West Nile encephalitis virus. J Virol. 2003;77(24):13203-13213.