SPINE Volume 40, Number 8, pp 584 ©2015, Wolters Kluwer Health, Inc. All rights reserved.
LETTER TO THE EDITOR: Re: Detrusor Overactivity in Patients With Cauda Equina Syndrome e read with great interest the article by Kim et al1 titled “Detrusor Overactivity in Patients With Cauda Equina Syndrome.” The authors are to be congratulated for their case series discussed in the article. But we have some concerns about the diagnosis of the cauda equine syndrome (CES). The authors have classified patients as CES according to the definition proposed by Fraser et al.2 During this classification, they also considered the patients with upper motor neuron signs (such as babinski sign and increased deep tendon reflexes) as CES. In this point, we thought that there is an obvious contradiction. According to the International Standards for Neurological Classification of Spinal Cord Injury, CES involves flaccid paralysis of the muscles of the lower limbs and areflexic bowel and bladder.3 On the contrary, conus medullaris syndrome may clinically be similar to the CES, but the injury in CMS is located proximally in the cord (L1 and L2 areas). Furthermore the manifestation of CMS appears with a mixed picture of upper motor neuron and lower motor neuron symptoms. It means that a patient with a unique upper motor neuron sign such as increased deep tendon reflexes or babinski sign and a conus lesion is diagnosed as conus medullaris syndrome. As a result of their study, the authors concluded that detrusor overactivity (DOA) seen in patients with CES might be due to combined conus medullaris lesion; in other words (DOA), it cannot be explained by pure root injuries in the cauda equine region. As they included patients with upper motor neuron signs, this conclusion cannot be entirely supported. In similar studies, some researchers also have reported DOA in patients with cauda equina lesion and suggested some possible DOA mechanisms in patients with CES, but they did not include patients with signs of an upper motor neuron lesion.
W
Therefore, to suggest any of the other mechanisms as a cause of DOA in patients with CES, authors should exclude patients with upper motor neuron signs. If available, we encourage the authors to present the data on DOA by excluding patients with upper motor neuron signs. Ibrahim Gündog˘du, MD Ankara Diskapi Yıldırım Beyazıt Training and Research Hospital Ankara, Turkey Elif Yalcin, MD Ankara Physical Medicine and Rehabilitation Training and Research Hospital Ankara, Turkey [email protected] Erhan Arif Ozturk, MD Ankara Diskapi Yıldırım Beyazıt Training and Research Hospital Ankara, Turkey Mufit Akyuz, MD Ankara Physical Medicine and Rehabilitation Training and Research Hospital Ankara, Turkey
References
1. Kim SY, Kwon HC, Hyun JK. Detrusor overactivity in patients with cauda equina syndrome. Spine 2014;39:E955–61. 2. Fraser S, Roberts L, Murphy E. Cauda equina syndrome: a literature review of its definition and clinical presentation. Arch Phys Med Rehabil 2009;90:1964–8. 3. Kirshblum SC, Burns SP, Biering-Sorensen F, et al. International standards for neurological classification of spinal cord injury. J Spinal Cord Med 2011;34:535–46.
The manuscript submitted does not contain information about medical device(s)/drug(s). No funds were received in support of this work. No relevant financial activities outside the submitted work. DOI: 10.1097/BRS.0000000000000802
584
www.spinejournal.com
April 2015
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited. SPINE140124LTE_LR 584
16/03/15 3:07 PM
Copyright of Spine is the property of Lippincott Williams & Wilkins and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
LETTER TO THE EDITOR: Re: Detrusor Overactivity in Patients With Cauda Equina Syndrome e read with great interest the article by Kim et al1 titled “Detrusor Overactivity in Patients With Cauda Equina Syndrome.” The authors are to be congratulated for their case series discussed in the article. But we have some concerns about the diagnosis of the cauda equine syndrome (CES). The authors have classified patients as CES according to the definition proposed by Fraser et al.2 During this classification, they also considered the patients with upper motor neuron signs (such as babinski sign and increased deep tendon reflexes) as CES. In this point, we thought that there is an obvious contradiction. According to the International Standards for Neurological Classification of Spinal Cord Injury, CES involves flaccid paralysis of the muscles of the lower limbs and areflexic bowel and bladder.3 On the contrary, conus medullaris syndrome may clinically be similar to the CES, but the injury in CMS is located proximally in the cord (L1 and L2 areas). Furthermore the manifestation of CMS appears with a mixed picture of upper motor neuron and lower motor neuron symptoms. It means that a patient with a unique upper motor neuron sign such as increased deep tendon reflexes or babinski sign and a conus lesion is diagnosed as conus medullaris syndrome. As a result of their study, the authors concluded that detrusor overactivity (DOA) seen in patients with CES might be due to combined conus medullaris lesion; in other words (DOA), it cannot be explained by pure root injuries in the cauda equine region. As they included patients with upper motor neuron signs, this conclusion cannot be entirely supported. In similar studies, some researchers also have reported DOA in patients with cauda equina lesion and suggested some possible DOA mechanisms in patients with CES, but they did not include patients with signs of an upper motor neuron lesion.
W
Therefore, to suggest any of the other mechanisms as a cause of DOA in patients with CES, authors should exclude patients with upper motor neuron signs. If available, we encourage the authors to present the data on DOA by excluding patients with upper motor neuron signs. Ibrahim Gündog˘du, MD Ankara Diskapi Yıldırım Beyazıt Training and Research Hospital Ankara, Turkey Elif Yalcin, MD Ankara Physical Medicine and Rehabilitation Training and Research Hospital Ankara, Turkey [email protected] Erhan Arif Ozturk, MD Ankara Diskapi Yıldırım Beyazıt Training and Research Hospital Ankara, Turkey Mufit Akyuz, MD Ankara Physical Medicine and Rehabilitation Training and Research Hospital Ankara, Turkey
References
1. Kim SY, Kwon HC, Hyun JK. Detrusor overactivity in patients with cauda equina syndrome. Spine 2014;39:E955–61. 2. Fraser S, Roberts L, Murphy E. Cauda equina syndrome: a literature review of its definition and clinical presentation. Arch Phys Med Rehabil 2009;90:1964–8. 3. Kirshblum SC, Burns SP, Biering-Sorensen F, et al. International standards for neurological classification of spinal cord injury. J Spinal Cord Med 2011;34:535–46.
The manuscript submitted does not contain information about medical device(s)/drug(s). No funds were received in support of this work. No relevant financial activities outside the submitted work. DOI: 10.1097/BRS.0000000000000802
584
www.spinejournal.com
April 2015
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited. SPINE140124LTE_LR 584
16/03/15 3:07 PM
Copyright of Spine is the property of Lippincott Williams & Wilkins and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
