Spinal cord infarction can have a wide variety of symptoms at presentation depending on the vascular territory affected. According to the literature, it is a rare disease, with an estimated incidence of 0.003% of all events and 0.3-2% of all stroke events. [1,2].
In most cases, the etiology is not identified. The causes can be classified into iatrogenic and non-iatrogenic causes; the former may be due to aortic surgery or injury from other surgical procedures, while non-iatrogenic causes include trauma, arteriosclerosis, arteriovenous malformations, thrombotic/fibrocartilaginous emboli, polycythemia vera , vertebral hyperextension, myelitis, infections and/or neoplasms [1,3].
This case report aims to describe a rare case of acute spinal cord ischemia syndrome with an atypical presentation and its management, in particular the treatment and etiologic investigation.
A 39-year-old Caucasian male with a history of smoking, occasional cannabinoid use, and hypertension presented to the emergency department (ED) with spontaneous constrictive pain in the right posterior thoracic region, with onset acute one hour before admission, radiating to the interscapular region and to the upper limbs up to the elbows, with a pain severity of 8/10, with no history of trauma.
On admission to the emergency room, the patient had a blood pressure of 192/113 mmHg, a pulse of 130 beats per minute, a regular rhythm, a temperature of 36.8°C and a respiratory rate of 14 breaths per minute. The physical examination was normal, with cardiac auscultation without murmur, pulmonary auscultation was symmetrical without adventitious murmur, and without peripheral edema. Neurological examination showed no focal deficit. Electrocardiogram (ECG) showed sinus rhythm, with ST segment depression in leads V4-V6. A complete blood count and basal metabolic panel were normal, with no elevation of inflammatory parameters (C-reactive protein 3.2 mg/L) and no increase in cardiac biomarkers (troponin I, creatinine phosphokinase, and myoglobin) at hours zero and six . In addition, he had a B-type natriuretic peptide level of 43 pg/mL. Transthoracic echocardiography was performed with documentation of moderate concentric left ventricular hypertrophy, with no other abnormalities. To rule out aortic dissection, computed tomography angiography (CT angiography) of the chest, abdomen, and pelvis (Figure 1) was performed, showing no abnormality. The patient was admitted for clinical monitoring due to persistent symptoms.
On the second day of hospitalization, the patient began to have neurological deficits and showed a decrease in muscle strength in the left lower limb and both hands with impaired sensitivity in the region corresponding to dermatomes T9-T12, associated with acute urinary retention. Neurological examination revealed miotic pupils, poorly photoreactive, bilateral prehension difficulty, grade 3/5 muscle strength in the left lower limb, decreased abdominal sensitivity below T5 and bilateral hyporeflexia. Due to the use of morphine for pain control, naloxone was administered without reversal of symptoms and physical examination findings. Urgent CT angiography (Figure 2) was performed which showed a lesion area extending from C5 to D2 affecting mainly the left anterior and lateral spaces, suggestive of a subacute ischemic spinal cord infarction. Due to the subacute course and the National Institutes of Health Stroke Scale (NIHSS) score of 3, the patient did not undergo thrombolysis or thrombectomy, respectively. Dual antiplatelet therapy (DAPT) and a high potency statin were initiated. Electromyography performed five days after the initial event revealed increased upper and lower extremity F-wave latency values, findings likely related to involvement of the proximal motor part of the spinal reflex arc. In addition, there were signs of non-recent mild neurogenic dysfunction at C7 bilaterally, with no activation of voluntary motor units at C8, also bilaterally. In addition, hyporeflexia in the upper limbs downstream of C7, as well as areflexia in the lower limbs and at the sensory level at T3, were noted. In summary, these findings indicated spinal cord dysfunction.
A subsequent etiological investigation was carried out. Specific blood tests ruled out autoimmune diseases or hypercoagulable states because antinuclear and antineutrophil cytoplasmic antibodies, lupus anticoagulant, and antiphospholipid antibodies were negative; Protein C, protein S, antithrombin III, fibrinogen and factor VIII were normal; and mutations in the prothrombin gene and factor V Leiden have been noted. In addition, the lipid profile was normal (total cholesterol, 171 mg/dL, high density lipoprotein (HDL) cholesterol, 28 mg/dL, low density lipoprotein (LDL) cholesterol, 95 mg/dL, triglycerides, 237 mg/dL), and glycated hemoglobin was 5.5%. Although the patient was previously described as hypertensive, during hospitalization he maintained a controlled blood pressure profile without the introduction of antihypertensive drugs. Cranioencephalic and neuraxial magnetic resonance imaging (MRI) (Figure 3) confirmed the diagnosis and showed no vascular malformations. Carotid and vertebral Doppler echoes were performed, showing normal light permeability, without atherosclerotic involvement. Transesophageal echocardiography excluded patent foramen ovale, septal abnormalities, or adenoids. On admission, the patient was monitored by electrocardiography for 72 hours without any signs of arrhythmia.
During his hospitalization, he had hospital-acquired pneumonia as a complication, without associated respiratory failure, having completed antibiotic therapy with clinical improvement. Patient started rehabilitation treatment for bladder rehabilitation due to recurrent urinary retention after attempted removal of bladder catheterization and motor training due to quadriplegia grade D on Asia Impairment Scale with neurological level C6 predominantly on the left and a debilitating grip deficit. grasping objects, without altering proprioceptive sensitivity. The patient was discharged after 15 days of hospitalization and referred to a motor and functional rehabilitation center.
Spinal cord infarction is often missed in the emergency department due to its low incidence . In nearly 70% of cases, nonspecific chest pain may be the initial presentation, and in these cases it is localized to the level of the ischemic lesion. . Bladder dysfunction is present in more than half of strokes, but rare in spinal cord infarction; however, when present, it is usually associated with urinary retention .
Predisposing conditions include aortic aneurysms, venous thromboembolism, coagulopathies, and aortic surgeries . The cardiovascular risk factor that appears to be associated with this condition is atherosclerosis, although due to its rare incidence it remains unclear. [2,6]. It was described as a case of patent foramen ovale embolization. . Classic risk factors such as hypertension and diabetes mellitus are associated with more serious spinal cord infarctions .
The evolution of symptoms often occurs within a few hours. In nearly 50% of patients, a biphasic stroke is observed; typically pain radiating between the shoulders preceding acute or transient symptoms of spinal cord sensory deficit. The peak of symptoms can last from 35 to 45 minutes to 24 hours . Initial imaging (CT or MRI) may be normal for several days [3,8].
There are no treatment guidelines for spinal strokes, and they should be treated like strokes . Antiplatelet agents, anticoagulants, when clinically justified, and control of cardiovascular risk factors are the main strategies. Other approaches may be needed and should be considered individually, such as steroids to reduce spinal edema and/or cerebrospinal fluid drainage. There are no clinical trial based data that support the use of fibrinolysis [3,8].
Symptom severity at presentation is the prognostic factor with longer term predictive value . Men and young adults tend to have more severe symptoms; however, they tend to improve more quickly. Rehabilitation programs tend to have a favorable outcome. Autonomic dysfunction and chronic pain are reported in most patients at follow-up [2,4].
The diagnosis of spinal cord infarction is very difficult due to its low incidence and the variety of symptoms that may be present on admission. Biphasic stroke and normal initial imaging, as seen in this case, could be another contributing factor to delayed diagnosis and, therefore, management and treatment. Idiopathic events are frequent despite a long and exhaustive study.
Antiplatelet/anticoagulants, control of cardiovascular risk factors and rehabilitation are the main management and follow-up strategies for these patients. Although fearful, this entity generally has a better long-term outcome.
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