Administration of Recombinant Tissue Plasminogen Activator for Sulcal Artery Syndrome

PRACTICAL IMPLICATIONS

The use of rtPA can result in clinical improvement in symptoms from spinal cord infarction. Spinal cord infarction is a rare type of ischemic stroke and often an elusive diagnosis. The study of recombinant tissue plasminogen activator (rtPA) in spinal cord infarction has been limited due to the rarity of this condition. Here, we present the case of an adult man with spinal cord infarction in a sulcal artery distribution who clinically improved following rtPA administration.

Case

A 58-year-old man with a history of left parietal lobe ischemic stroke, multifocal lacunar infarctions with residual mild right-sided weakness, ongoing tobacco abuse, and hypertension presented to the emergency department with an initial complaint of right-sided throbbing headache and right neck, arm, and leg pain that started acutely 3 hours prior. The patient denied new weakness or numbness from his baseline and was ambulatory. While undergoing triage, he acutely developed right arm and leg flaccid paralysis. On evaluation by the stroke team, he was noted to have an National Institutes of Health Stroke Scale of 11. CT of the head demonstrated chronic infarctions, and CT angiogram of the head and neck did not show large vessel occlusion, dissection, or focal intracranial atherosclerosis. Initial screening labs included complete blood count with differential, glucose, and complete metabolic panel, all within normal range. The patient was administered rTPA and admitted to the neurologic intensive care unit. MRI of the brain without gadolinium did not reveal an acute infarction, but showed known prior left superior middle cerebral artery division stroke and prior lacunar infarctions. On hospital day 1, there was subjective improvement in right hemibody weakness, but also new left-sided sensory deficits. Examination was notable for 4-/5 right upper extremity strength, 5-/5 right lower extremity strength, which was nearly at baseline from prior ischemic stroke, except for increased right intrinsic hand weakness. Sensory examination demonstrated new left-sided diffuse loss to pain and temperature in the upper and lower extremity with bilaterally intact vibration and proprioception.

MRI of the cervical spine was obtained on HD5 due to concern for potential myelopathy, which demonstrated a focal ill-defined T2 hyperintense signal within the right ventral cervical spinal cord at the level of C3. Follow-up MRI cervical spine with gadolinium on HD6 demonstrated ill-defined enhancement and restricted diffusion within the previously visualized lesion (Figure, A–D). A lumbar puncture for cerebral spinal fluid analysis was obtained with no white blood cells and mild elevation in protein to 61 mg/dL. Given symptom onset, improvement with tPA, and imaging consistent with spinal cord infarction, no additional workup was pursued. The patient was discharged home on aspirin and atorvastatin for secondary stroke prevention. The patient was seen in follow-up 3 months later with improved hand strength, but now with moderate spasticity throughout the right upper and lower extremities, worsened from prior stroke. Left lower extremity loss to pain and temperature persisted. Repeat MRI cervical spine 4 months following symptom onset demonstrated interval resolution of abnormal enhancement and diffusion signal abnormality with mild persistent abnormal T2 hyperintensity (Figure, E and F).

Figure. Sulcal Artery Territory Ischemic Spinal Cord Infarction.

MRI of the cervical spine demonstrates a nonspecific focus of increased signal in the right anterior spinal cord at the C3 spinal level on (A) T2-weighted sagittal (black arrow) and (B) axial sequences (white arrow). This lesion corresponds to focus of abnormal signal on (C) diffusion-weighted sequences (black arrowhead) with demonstration of contrast enhancement on (D) T1w postcontrast images. Follow-up imaging at 3 months demonstrates interval decrease in increased signal on (E) T2-weighted image in addition to resolution of contrast enhancement on (F) T1w postcontrast images.

Discussion

We describe a case of sulcal artery syndrome (also known as sulcocommissural artery) treated with rtPA. Spinal cord infarction is a rare manifestation of ischemic stroke, accounting for just 1% of reported cases.¹ Sulcal artery syndrome is an uncommon subtype of spinal cord infarction presenting with an incomplete Brown-Séquard syndrome with ipsilateral paraparesis and contralateral loss to pain and temperature sensation.² Acute-onset back or radicular-like pain as the initial presenting symptom for spinal cord infarction is well documented, as in the index case.^3,4 Differentiating transverse myelitis from spinal cord infarction is often difficult; however, this case has key features most often associated with infarction including the acuity of onset, positive diffusion weighted magnetic resonance imaging with vascular risk factors, improvement with thrombolytics, and an anterior distribution in a known vascular territory.⁴

Spinal cord vascular supply involves a vast network of collaterals. The upper cervical cord is predominantly supplied by the vertebral arteries, which give rise to radiculomedullary arteries to supply the anterior spinal artery. Sulcal arteries are perforating branches of the anterior spinal artery perfusing the anterior two-thirds of the cervical hemicord, with the area of cord perfused limited to one side of the anterior hemicord, but not both; thus, an anterior lateralized short segment infarction occurs through sulcal artery occlusion.^1,5

The use of rtPA for ischemic stroke is established; however, little is known about its use in spinal cord infarctions. The use of rtPA in spinal cord infarction has been reported in limited case reports,⁶ and here, we describe a rare use of rtPA in sulcal artery syndrome. This case highlights the importance of recognizing spinal cord infarction syndromes and the potential therapeutic benefit of rtPA.

Appendix. Authors

Study Funding

No targeted funding reported.

Disclosure

The authors report no disclosures. Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp.