Anterior Cervical Spinal Cord Infarction from Cardioembolic Source Presenting with Respiratory Failure and Quadriplegia
by Shabna Mottemmal1, Adarsh Iyyavoo2, Nandakumar B Vittal3*,Pradumna P Singh3
1Residency Applicant, Kannur Medical College, Kerala, India
2High School Senior, Cambrian Academy, San Jose, California, USA
3Meharry Medical College at Nashville General Hospital; Nashville, TN 37208, USA
*Corresponding author: Nandakumar B Vittal, Associate Professor, Department of Internal Medicine, Division of Neurology, Meharry Medical College, 1005 Dr. DB.Todd Jr. Blvd, Nashville, TN-37208, USA
Received Date: 18 September 2023
Accepted Date: 22 September 2023
Published Date: 25 September 2023
Citation: Mottemmal S, Iyyavoo A, Vittal NB, Singh PP (2023) Anterior Cervical Spinal Cord Infarction from Cardioembolic Source Presenting with Respiratory Failure and Quadriplegia. Ann Case Report. 8: 1455. https://doi.org/10.29011/2574-7754.101455
A 30-year-old man presented with acute respiratory distress, quadriplegia, and other neurologic symptoms, without evident cause on head CT. Subsequent brain MRI revealed bilateral cerebral infarcts, additionally cervical MRI showed T2 hyperintensity in the anterior spinal cord from C2-C6. There was no clear history of trauma and normal cerebral and cervical vascular imaging indicated no potential sources of vascular embolism. The patient’s acute presentation and atrial fibrillation suggests a cardiac source of thrombus for the cerebrospinal infarcts. The presented case of anterior spinal artery syndrome underscores the importance of considering stroke in acute neurological presentations, even with atypical symptoms.
Keywords: Respiratory Failure; Quadriplegia; Anterior Spinal Cord Infarction; Cervical Spinal Cord Infarction; Cardioembolism.
Spinal cord infarction is not uncommon accounting for 1% of acute stroke hospitalizations . Thoracic portion of the cord is involved mainly due to aortic pathologies and cardiac causes leading to systemic hypotension. Cervical anterior spinal cord infarct is rare and often caused by vertebral artery dissection related to trauma. Cardioembolic source is described for thoracic spinal cord infarct but not for cervical spinal cord infarct . Symptoms in cervical spinal cord infarct can include sudden onset of severe neck pain, quadriparesis, sensory deficits, respiratory distress requiring mechanical ventilation, cardiac dysrhythmias and bowel or bladder dysfunction. Diagnosis involves medical history review, physical examination, and spinal cord and vascular imaging. MRI might not demonstrate the spinal cord infarct early on and imaging is done nonetheless to rule out other structural etiologies of myelopathy . Treatment focuses on managing symptoms, mechanical ventilation and other supportive care measures while promoting rehabilitation. Prognosis depends on the location, extent of infarct and timeliness of the intervention [4,5]. Seeking immediate medical attention is crucial for proper diagnosis and appropriate management of spinal cord infarction. Many patients with spontaneous spinal cord infarct do not receive thrombolytics due to “atypical” presentation and lack of diagnosis that can be missed despite availability of spinal cord MRI imaging.
We present the case of a 30-year-old previously healthy man who presented to the ER on a Sunday morning with acute onset difficulty breathing and weakness in his extremities. He spent most of Friday and Saturday with friends. Earlier that morning he had complained of neck pain and tingling in his hands, which prompted his roommate to bring him to the ER. He was able to walk into the ER, soon after he required assistance to stand up. He now reported, “I can’t move” and “I can’t breathe, I want oxygen”. This was followed by agitation, respiratory distress (Oxygen saturation at 31%) requiring intubation and mechanical ventilation. There was no history of trauma, recent surgical procedures, diabetes, hypertension, heart disease, other significant past medical conditions, and no recent travel history. His vital signs showed normothermia soon followed by hypothermia returning to normothermia (98-degree F; dropping to 94-degree F and 98-degree F over 3 hours), BP 160/98 (then 116/61; followed by 56 mm Hg systolic that improved with fluid boluses. Heart rate was 66/min and later 36/min improving to 80s (36-137 range); EKG showed alternating sinus rhythm and atrial fibrillation with rapid ventricular rate. On day 2 patient failed extubation due to very low tidal volume (80 ml). Chest CT did not show any pathology to explain respiratory failure. His exam revealed quadriplegia and this led to a neurology consultation. Neurological examination showed intact consciousness; he responded to loud verbal and physical stimulation with nods or head shaking. Eye movements initially showed dysconjugate gaze (this resolved in 24 hours), patient exhibited flaccid (0/5) quadriplegia, areflexia and down-going plantar response. He however managed to dislodge the endotracheal tube (ETT) with his tongue movements multiple times. He had normal sensation in his face; below his neck, he had decreased sensation to temperature and pain, but intact light touch and proprioception. Head CT did not show any acute abnormalities. Other investigations on admission revealed normal CBC, CMP; urine drug screen was positive for THC and negative for stimulants, blood EtOH level was < 3. Additional tests included CSF analysis with cell count of 7, normal protein and glucose. CSF culture later came back negative, and he had a normal sed rate (ESR). Brain MRI revealed numerous subcentimeter bilateral cerebellar, posterior temporal and occipital embolic infarcts (Figure 2 A- 2E and Figure 3). Magnetic Resonance Imaging of the cervical spine showed T2 hyperintensity in the territory of the anterior spinal artery extending from C2 to C6 (Figure 1). MRA of the head and neck were normal (Figure 4A and 4B). Transthoracic Echocardiography showed normal ejection fraction, no intracardiac structural abnormalities and no right to left shunt. Transesophageal echocardiography did not reveal any abnormalities in the proximal aorta. CT angiography of head and neck done few days later was normal as well indicating no occlusions or dissections (Figure 5A-5E). He received 1-gram intravenous solumedrol daily for five days based on initial cervical MRI findings in addition to aspirin started after MRI showed acute infarcts. His CSF also showed 14 oligo clonal bands (unclear significance likely secondary to acute ischemia). Hospital course – On day 3 he went into neurogenic shock and multiple episodes of vasovagal bradycardia (HR in the 40s) and demonstrated hemodynamic instability when he was being moved by nursing staff. His exam now showed intact cognition and normal cranial nerve examination. He developed ileus and had frequent episodes of bradycardia (Figure 6), fluctuating blood pressure all part of autonomic dysfunction causing the nurses to panic. He required transvenous pacemaker which was soon replaced with permanent pacemaker. After four weeks his tidal volume improved from 80 ml to 240 ml., he started to regain significant strength in his lower extremities to the point where he was able to stand up and walk up to 25 feet when his vital signs permitted. His upper extremities remained flaccid, areflexic except for his ability to close his hands to gently squeeze a soft ball. Repeat labs including spinal fluid showed similar findings including 14-oligoclonal bands, normal cell count, protein, and glucose. West Nile virus IgM, HTLV-1, HIV, HSV and CSF VDRL testing were all-negative. After eight weeks, his autonomic instability continued to improve and so did his participation in physical therapy sessions. He could now ambulate up to 100 feet using a special walker; however, he remained flaccid in his upper extremities and continued to need intermittent daily ventilator support due to tidal volume at ~300ml. Repeat MRI of his brain and spinal cord was placed on hold due to his pacemaker that requires many weeks for lead maturation.
Figure 1A: MRI Cervical spine - Sagittal T2 sequence showing hyperintensity from C2 to C6 in the anterior portion of the spinal cord (ACA territory). Figure-1B and 1C are axial sections showing lesion in the grey matter region (Owl’s eye appearance).
Figure 2A-E: MRI Brain – Diffusion sequence showing bilateral punctate restricted diffusion; A and B - parietal and occipital infarcts, B-E - Occipital infarcts, D and E – bilateral cerebellar infarcts.