Table of Contents  
CASE REPORT
Year : 2015  |  Volume : 8  |  Issue : 2  |  Page : 276-278

Central cord syndrome


1 Department of Anesthesiology, Intensive Care, and Pain Management, Faculty of Medicine, Ain-Shams University, Cairo, Egypt
2 Department of Orthopedic Surgery, Faculty of Medicine, Ain-Shams University, Cairo, Egypt
3 Department of Orthopedic and Spine Specialist, Nasr City Insurance Hospital, Cairo, Egypt

Date of Submission28-Mar-2015
Date of Acceptance08-Apr-2015
Date of Web Publication8-May-2015

Correspondence Address:
Mohamed Saleh
Department of Anesthesiology, Intensive Care, and Pain Management, Faculty of Medicine, Ain-Shams University, Abbasia, Cairo 11566
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1687-7934.156721

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  Abstract 

Spinal cord injuries (SCIs) are classified as complete or incomplete injuries. Central cord syndrome (CCS) is the most common type of incomplete SCI. The syndrome mostly occurs in older individuals with underlying cervical spondylosis caused by a hyperextension injury. The neurological impairment is characterized by a disproportionate weakness of the upper extremities more than the lower extremities and may also include bladder dysfunction and varying degrees of sensory loss. The natural history of the syndrome varies, with some patients experiencing complete spontaneous recovery and others having persistent neurological deficits. The role of surgical intervention remains controversial. We present a case of an elderly patient with cervical spondylosis who underwent thoracolumbar spine fixation and was complicated by CCS mostly due to hyperextension injury during surgery.

Keywords: spinal cord injury, spondylosis, thoracolumbar spine fixation


How to cite this article:
Ewees B, Magdy H, Saleh M, Morsy A, Ashour MH. Central cord syndrome. Ain-Shams J Anaesthesiol 2015;8:276-8

How to cite this URL:
Ewees B, Magdy H, Saleh M, Morsy A, Ashour MH. Central cord syndrome. Ain-Shams J Anaesthesiol [serial online] 2015 [cited 2021 Apr 17];8:276-8. Available from: http://www.asja.eg.net/text.asp?2015/8/2/276/156721


  Case report Top


A 65-year-old male patient, diabetic and on gliclazide 40 mg twice daily, as well as hypertensive and on captopril 25 mg twice daily, was scheduled for a revision of thoracolumbar spinal fixation. His preoperative data showed a blood pressure of 150/80 mmHg and pulse of 82 bpm. Preoperative investigation showed fasting blood glucose of 150 mg/dl. ECG showed inverted T waves V1-V4. Echocardiography showed ejection fraction 58% as well as diastolic dysfunction. Laboratory findings revealed an Hb of 10 g/dl.

After application of ASA standard monitoring, the patient was premedicated with midazolam 2 mg and morphine 5 mg, and anesthesia was induced with sodium thiopental 300 mg and atracurium besylate 35 mg. An armored endotracheal tube of 8 mm ID was inserted and confirmed by capnography. The patient was connected to controlled mechanical ventilation with the following parameters: tidal volume, 500 ml; and respiratory rate, 12/min. After securing endotracheal tube (ETT), the patient was made to lie in prone position. Anesthesia was maintained with isoflurane 0.8% and atracurium besylate 10 mg every 20 min. Nitroglycerin infusion was started at a dose of 0.5 μg/kg/min and titrated to achieve and maintain deliberate hypotension. Intraoperative vital data showed a heart rate of 80-90 bpm, blood pressure of 95/60 mmHg, end-tidal CO 2 of 35 mmHg, and SpO 2 of 99%. The surgical procedure lasted for 4 hours, during which time intraoperative fluid of 1500 ml crystalloid and 500 ml blood was given. Blood loss was estimated to be 800 ml. Urine output was 500 ml.

At the end of the operation, the patient was made to lie in supine position. The patient could spontaneously open his eyes; therefore, extubation was carried out after reversal of muscle relaxant.

Few minutes later, the patient was noticed to be conscious but agitated. On further examination, the patient was found unable to move both his upper extremities. Breathing pattern was abdominal, and the patient's SpO 2 reduced to 70%. Therefore, a decision of reintubation was established, as incomplete reversal of muscle relaxant (recurarization) was suspected.

Further evaluation showed that the patient was alert and conscious but agitated. Motor examination revealed weakness in both upper limbs more distally than proximally, with normal strength in both lower extremities. Arterial blood gas and blood sugar were sampled, with accepted results. The patient was transferred to the ICU and was sedated, intubated, and ventilated.

In the ICU, the patient was administered mechanical ventilation on continuous positive airway pressure, on FiO 2 50%. Laboratory testing, including complete blood count and basic chemistry panel, was within normal limits. Chest radiograph and electrocardiogram were unremarkable. Computed tomographic scan of the brain without contrast showed no evidence of recent infarction. Computed tomographic scan of the cervical spine showed no evidence of acute bony fracture or subluxation. However, there was severe degenerative disk disease and cervical spondylosis from C4-C5 through the C6-C7 disk levels, causing spinal stenosis at these levels. Subsequently, neurology consultation was obtained and MRI of the cervical spine was performed, which showed severe multilevel degenerative disk disease and stenosis from C4-C5 through C6-C7. There was a significant T2 weighted signal abnormality within the spinal cord consistent with edema. There was also a significant amount of prevertebral soft tissues edema. The patient was diagnosed with acute CCS. Six hours later, the motor strength of both upper limbs improved and weaning from ventilation was started, followed by extubation. After extubation the patient was still complaining of numbness and some weakness in both hands. The patient was recommended to wear an aspen collar at all times and to undergo cervical decompression and fusion surgery in the near future when the spinal cord edema subsided.


  Discussion Top


CCS is the most common type of incomplete SCI, comprising 15-25% of all cases [1],[2],[3] . The American Spinal Injury Association (ASIA) defines complete injury as the absence of sensory and motor injury function below the level of injury. Conversely, with incomplete injury, some neurologic function remains below the level of injury [4] . Schneider et al. [5] first described the syndrome in detail in 1954. The classic description of this syndrome was as follows: 'disproportionately more motor impairment of the upper than the lower extremities, bladder dysfunction with varying degrees of sensory loss below the level of the lesion'. This classic description is not found in all patients, and varying levels of neurological impairments are seen in patients with CCS [5],[6],[7] . CCS typically occurs in elderly patients (aged >60 years) with underlying cervical spondylosis causing cervical stenosis. The mechanism of injury is believed to be hyperextension of the neck with pinching of the spinal cord between a thickened ligamentum flavum and a protruding anterior disk or osteophyte. The hyperextension mechanism often seems to be very mild, but in the setting of cervical spondylosis it can result in marked neurologic injury [4],[5],[8],[9] . In this case, hyperextension probably occurred in this elderly patient with cervical spondylosis intraoperatively during the thoracolumbar fixation surgery. CCS originally was theorized to consist of injury to the central gray matter and the central portion of the long tracts, with preservation of the peripheral structures [5] . However, recent studies have shown that the lateral cortical spinal tract in the mid to upper cervical spine contains the main area of pathologic abnormality [10],[11],[12] . MRI studies have failed to show any evidence of cord hemorrhage, and patients with CCS exhibit  Wallerian degeneration More Details of the axonal tracts distal to the zone of injury in the lateral corticospinal tracts [13],[14],[15] . Thus, injury to the large myelinated axons in the medial part of the lateral corticospinal tract seems to be the main cause of the deficits associated with CCS. This explains the primary involvement of the fine motor movements of the distal upper extremity: the medial part of the lateral corticospinal tracts innervates the upper extremities, whereas the lateral part aspect innervates the lower extremities [4],[11],[13] . CCS presents on a spectrum, from weakness limited solely to the hands and forearms with sensory preservation, to complete quadriparesis with sacral sparing as the only evidence of incomplete SCI [16] . The natural history of CCS resulted in a good neurological recovery. Many patients experience spontaneous complete recovery, whereas some may have persistent deficits. Recovery occurs first in the lower extremity if affected, followed by recovery of bladder function and finally recovery of the upper extremity [4],[8],[16] . Studies showed that spontaneous recovery occurs in 50-80% of patients with CCS. Several risk factors that portend a poor prognosis for complete recovery have been described in many studies, such as age greater than 50 years, severe neurological deficit at the time of initial presentation, presence of cord edema on MRI, cervical canal size less than 14 mm, multiple-level injury, and lack of recovery of function during the first few days following injury [7],[8],[17],[18] . Traditionally, it was thought that surgical intervention provided no benefit and therefore was not indicated [19],[20],[21],[22],[23] . However, subsequent studies have demonstrated that surgical decompression may actually improve neurological outcomes in these patients [23],[24],[25],[26] . Therefore, the patient in his report was recommended to undergo surgical later intervention.


  Acknowledgements Top


Conflicts of interest

None declared.



 
  References Top

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