Acta Neurochir (2014) 156:267–268 DOI 10.1007/s00701-013-1904-9

LETTER TO THE EDITOR - SPINE

Reversible and delayed isolated central sleep apnea after cervical laminectomy: report of the first case Visocchi Massimiliano & Giuseppe Maria Della Pepa & Barbagallo Giuseppe & Spallone Aldo

Received: 19 September 2013 / Accepted: 27 September 2013 / Published online: 30 October 2013 # Springer-Verlag Wien 2013

Dear Editor, The occurrence of breathing disorders after cervical laminectomy has been exceptionally described as a complication after cervical decompressive laminectomy for cervical stenotic myelopathy (CSM). We report the first case of central sleep apnea (CSA) presenting as isolated and delayed transient complication occurring after laminectomy for CSM and the second case of syndromic CSA after cervical laminectomy described in the literature.

Case description A 44-year-old male was admitted to hospital with a diagnosis of cervical stenosis at C3-C6 level (Fig. 1), with bilateral cervicobrachialgia, hyposthenia at lower limbs, and pyramidal signs. A C3-C6-(partial C7) laminectomy was performed according to standard procedures. During surgery, all the parameters monitored were normal. No immediate postoperative respiratory dysfunction was reported. Postoperative course was excellent; lower limbs hyposthenia and cervicobrachialgia improved. Nearly 2 weeks after discharge the patient returned complaining of breathing difficulty during sleep and a sense of pressure in his chest. Postoperative MRI showed a good decompression of the V. Massimiliano : G. M. Della Pepa (*) Institute of Neurosurgery, Catholic University of Rome, Largo A. Gemelli 1, 00168 Rome, Italy e-mail: [email protected] B. Giuseppe Neurosurgical Unit, Department of Neurosciences, Policlinico “G. Rodolico” University Hospital, Catania, Italy S. Aldo Section of Neurosurgery Department of Clinical Neurosciences, Neurological Center of Latium (NCL), Rome, Italy

cervical cord; no pathological intensity signals were found within the cord. Neurophysiological assessments, performed postoperatively, were normal. Pneumological evaluation ruled out mechanical airways obstructions; nevertheless a reduction of the forced vital capacity (FVC: 2.4 l) and forced expiratory volume (FEV: 2.0) were identified. A polysomnographic test showed data consistent with mild CSA syndrome. During the apnea, the arterial blood gas analysis showed a reduction of PO2 and an increase of PCO2 levels compared to eupnea (PO2: 74 mmHg, PCO2: 61 mmHg, pH: 7.33). Continuous positive airway pressure (CPAP) during nighttime was started. One month later, CSA spontaneously, gradually, and stably recovered.

Hypothesis on physio-pathologial mechanisms CSA differs from other forms of sleep-breathing disorders: a loss of normal autonomic response to chemical changes in the blood determines apneas, in absence of airway obstruction [1, 8]. In 1994, Naim-ur-Rahman reported the first case of postoperative CSA following C3-C6 laminectomy, occurring right after surgery and associated with sphincteric incontinence, which spontaneously recovered 3 weeks after onset [5]. CSA has been rarely reported in occipital encephaloceles, Arnold-Chiari type 1 malformation, anterior C1-2 osteochondroma, and os odontoideum [5, 7]. In the present case, onset was delayed from surgery (nearly 2 weeks later) and CSM was not associated with any other neurological sign of spinal cord damage. The mechanisms underlying such a complication are difficult to interpret. Respiratory motor output arises from two distinct, but functionally interacting, rhythmogenic networks: the pre-Bötzinger complex and the retrotrapezoid nucleus/parafacial respiratory group, which is placed in the lower medulla oblongata at the craniocervical junction [2, 4].

268

Acta Neurochir (2014) 156:267–268

decompressive effect on the spinal cord, as seen by the light dorsal migration of the cord, possibly associated with accompanying spasm of the radicular vessels, producing a transient ischemia of the cord, perhaps triggered by neck movements after 1 week from collar removal [5, 7]. The mechanism of central cord syndrome with CSM is thought to be caused by the inward bucking of the ligamentum flavum along with shortening and thickening of the spinal cord while the cervical spine is in extension [3]. Interestingly, animals that have undergone decompressive laminectomies with removal of the epidural ligaments have significant spinal cord deformation with subsequent reduction in blood flow and in MEP when placed in cervical flexion [6]. Does the cervical epidural ligament provide the same protective effect in humans? Although the exact biomechanics of the cervical spine and the spinal cord after decompressive laminectomy remain uncertain, the present experience should enhance the awareness of the spinal surgeon when dealing with CSM. Fig. 1 a Preoperative MR T2-weighted imaging showing a C3—C6 stenosys of the spine (multiple intervertebral disc herniations, osteophytes, and calcified ligamentum flavum) without evident spinal cord lesional pattern. b Postoperative MR T2-weighted imaging showing a C3—C6 posterior decompression of the spinal cord with persistence of multiple intervertebral disc herniations and osteophytes. A central or peripheral lesional pattern of the cord is still not evident

Nevertheless, in our case CSM was definitely anatomically far for the lower medulla to hypothesize a direct compressive/ traumatic mechanism determining a disturbance to the preBötzinger area respiratory centers [2, 4]. We have also critically analyzed whether, after posterior decompression, the spinal cord was displaced posteriorly determining an angular deformation of the lower medulla oblongata that could possibly explain CSA. However, MR imaging did not display any deformation that could justify such a mechanism. Moreover, since there was no diaphragm paralysis, we ruled out a dysfunction of the phrenic nerve nuclea, thus focusing our interest on a possible transient nocturnal sleep-related transmission dysfunction of the reticulospinal fibers directed to these nuclear targets. The delayed modality of presentation could be indicative of “timerelated” neural transmission dysfunction. In fact, decompressive laminectomy provides an immediate

Conflict of interest None.

References 1. Bixler EO, Vgontzas AN, Ten Have T, Tyson K, Kales A (1998) Effects of age on sleep apnea in men: I. Prevalence and severity. Am J Respir Crit Care Med 157:144–148 2. Cinelli E, Robertson B, Mutolo D, Grillner S, Pantaleo T, Bongianni F (2013) Neuronal mechanisms of respiratory pattern generation are evolutionary conserved. J Neurosci 33:9104–9112 3. Dickerman RD, Lefkowitz M, Epstein JA (2005) A traumatic central cord syndrome occurring after adequate decompression for cervical spondylosis: biomechanics of injury: case report. Spine 30(Phila Pa 1976):E611–E613 4. Koizumi H, Koshiya N, Chia JX, Cao F, Nugent J, Zhang R, Smith JC (2013) Structural-functional properties of identified excitatory and inhibitory interneurons within pre-Botzinger complex respiratory microcircuits. J Neurosci 33:2994–3009 5. Naim Ur R (1994) Post-operative central sleep apnoea complicating cervical laminectomy: case report. Br J Neurosurg 8:621–625 6. Shinomiya K, Dawson J, Spengler DM, Konrad P, Blumenkopf B (1996) An analysis of the posterior epidural ligament role on the cervical spinal cord. Spine 21(Phila Pa 1976):2081–2088 7. Vella LM, Hewitt PB, Jones RM, Adams AP (1984) Sleep apnoea following cervical cord surgery. Anaesthesia 39:108–112 8. Villaneuva AT, Buchanan PR, Yee BJ, Grunstein RR (2005) Ethnicity and obstructive sleep apnoea. Sleep Med Rev 9:419–436

Reversible and delayed isolated central sleep apnea after cervical laminectomy: report of the first case.

Reversible and delayed isolated central sleep apnea after cervical laminectomy: report of the first case. - PDF Download Free
117KB Sizes 0 Downloads 0 Views