Cervical Spinal Cord Infarction Research Articles

Combining Robotic Therapy with Electrical Stimulation Therapy and Transfer Packages for Upper Limb Paresis in Cervical Spinal Cord Infarction：A Case Report

Combining Robotic Therapy with Electrical Stimulation Therapy and Transfer Packages for Upper Limb Paresis in Cervical Spinal Cord Infarction：A Case Report

Cervical Spinal Cord Infarction as a Rare Complication of Fat Embolism Syndrome Due to Orthopedic Trauma (P8-5.025)

Cervical Spinal Cord Infarction as a Rare Complication of Fat Embolism Syndrome Due to Orthopedic Trauma (P8-5.025)

Anterior Cervical Spinal Cord Infarction from Cardioembolic Source Presenting with Respiratory Failure and Quadriplegia

Anterior Cervical Spinal Cord Infarction from Cardioembolic Source Presenting with Respiratory Failure and Quadriplegia

Unilateral Upper Cervical Posterior Spinal Cord Infarction Caused by Spontaneous Bilateral Vertebral Artery Dissection.

A 41-year-old woman complained of sudden numbness of the left face and limbs without neck pain, paraparesis, urinary retention, or constipation. Neurologic examination revealed onion-skin pattern hemifacial dysesthesia and disturbance of touch and proprioception sensation of the left limbs. T2WI and Diffusion weighted imaging (DWI) showed left posterior spinal cord infarction at the C1 level (Figure, A–D). Magnetic resonance angiography (MRA) demonstrated stenosis of bilateral vertebral arteries (Figure, E–F). High-resolution MRI revealed the high signals of intramural hematoma in bilateral vertebral arteries indicating the diagnosis of dissection (Figure, G-J). Isolated posterior spinal cord infarction is rare, and vertebral artery dissection should be considered as an etiologic mechanism.1

Cocaine-related cervical spinal cord infarction: a\xa0case report and review of the\xa0literature

Study designCase report.ObjectivesTo report a clinical case of spinal cord infarction due to cocaine use.SettingSpinal Center, IRCCS Fondazione S. Lucia, Rome (Italy).Case presentationTwo days after recreational use of cocaine, a 27-year-old Caucasic man was admitted to the emergency department for acute cervical pain, weakness in all four limbs, and urinary retention. A cervical spinal magnetic resonance imaging scan, performed after 2 days, showed a “pencil-like” lesion extending from C4 to T1 metamer, compatible with acute ischemia in the anterior spinal artery territory. Other causes of vascular disorders, as well as inflammatory and infectious disorders were ruled out. At admission in our department, the patient had an incomplete tetraplegia at level C6, an indwelling catheter, and was unable to stand and walk. After 3 months of rehabilitation, he had an AIS score D tetraplegia at level C7, was able to stand and walk using parallel bars, and indwelling catheter was replaced by intermittent catheterization.Discussion and conclusionsThe etiology of medullary infarction may remain unexplained in nearly 30–40% of cases. Even if rare, cocaine-induced ischemic myelopathy should be considered and ruled out in the differential diagnosis of any acute nontraumatic myelopathy, especially in young patients.

Abstract 1122‐000032: Spinal Cord Infarction a Young Patient with a Hypoplastic Vertebral Artery

Introduction : Rare presentation of disease processes is absolutely intriguing to the human mind. Spinal cord infarction is abundantly reported to be secondary to cardiological procedures, patients carrying multiple vascular risk factors and vertebral artery dissections. But for it to happen in a patient who is young, relatively healthy and without vascular risk factors is quite interesting. Herein, we present the case of a patient presented with bilateral upper extremity weakness, who has a hypoplastic right vertebral artery that has coincided with him being a professional gamer with exerting compression from video‐gaming posturing of “forward leaning with neck hyperextension”, resulting in cervical spinal cord infarction. Methods : Case report Results : Vertebral artery dissection was excluded by CTA and MRA. our hypothesis was that the patient is a professional gamer and his posture of leaning forward and neck hyper‐extension had a role in inducing his spinal cord infarction given the fact of him having a hypoplastic right vertebral artery. Conclusions : Vertebral artery disease is a well‐recognized cause of ischemia in the posterior cerebral circulation. Recently, however, cervical cord infarction, albeit being extremely rare, has been increasingly reported as a complication of vertebral artery diseases such as dissection. Awareness must be raised that such condition can also happen in the young population due to compression of the vertebral arteries, especially when one is hypoplastic.

Cervical Spinal Cord Infarction Presenting as Chest Pain in Patients with Acute Cerebellar Infarction

Spinal cord infarction is rare, especially cervical cord infarction is lesser than thoracic and lumbar level. We describe two cases of cervical cord infarction following cerebellar infarction with vertebral artery occlusion, which initially presented with chest pain and dyspnea. Blood supply for the cervical cord comes from anterior and posterior spinal artery, which originated from the distal vertebral or posterior inferior cerebellar arteries. Therefore, occlusion of unilateral vertebral artery could cause a cervical cord infarction.

Transient neurologic deficit with complete recovery due to cervical spinal cord infarction after preoperative embolization for metastatic lesion of malignant pheochromocytoma at proximal thoracic spine

Spinal cord infarction after preoperative transarterial embolization for metastatic spinal lesions is uncommon and usually leads to complete paralysis. Transient neurologic deficit due to spinal cord infarction after preoperative embolization for spinal metastases has never been reported in the literature. A 30-year-old female patient was diseased with malignant pheochromocytoma and multiple metastases to lung and bones. She suffered from refractory pain at upper back and numbness at her body below xiphoid process but no motor deficit was noted at extremities. Magnetic resonance imaging (MRI) revealed paraspinal and epidural lesions originating from T2 to T4 vertebrae with compression to spinal cord. Preoperative embolization was executed to the spinal metastases with the intent to reduce intraoperative bleeding. Embolization procedure was performed to bilateral costocervical trunk, 3rd and 4th intercostal arteries with 400 μm Embozene® microsphere under local anesthesia. The procedure was discontinued immediately after development of severe hypertension that might be related to the pheochromocytoma and was treated with intravenous antihypertensive drug. There was no neurologic deficit until 6.5 hours after the procedure when weakness at right lower extremity and hypesthesia at left arm developed. Emergent MRI showed focal infarcts in spinal cord at right aspect of C5 and left C4 levels. With adequate hydration but no administration of steroid, muscle power gradually recovered in a few hours. Posterior instrumentation, neural decompression and tumor debulking were performed 2 days after embolization as scheduled. One week after the event of spinal cord infarction, she could stand up and walk without aid. Even though it is rare, spinal cord infarction is an important differential diagnosis for sudden decrease of muscle power after preoperative embolization for spinal metastases. Although complete paralysis is more common, transient neurologic deficit with complete recovery could happen in patients with minor infarcts in the spinal cord.

Transient neurologic deficit with complete recovery due to cervical spinal cord infarction after preoperative embolization for metastatic lesion of malignant pheochromocytoma at proximal thoracic spine

Spinal cord infarction after preoperative transarterial embolization for metastatic spinal lesions is uncommon and usually leads to complete paralysis. Transient neurologic deficit due to spinal cord infarction after preoperative embolization for spinal metastases has never been reported in the literature. A 30-year-old female patient was diseased with malignant pheochromocytoma and multiple metastases to lung and bones. She suffered from refractory pain at upper back and numbness at her body below xiphoid process but no motor deficit was noted at extremities. Magnetic resonance imaging (MRI) revealed paraspinal and epidural lesions originating from T2-4 vertebrae with compression to spinal cord. Preoperative embolization was executed to the spinal metastases with the intent to reduce intraoperative bleeding. Embolization procedure was performed to bilateral costocervical trunk, 3rd and 4th intercostal arteries with 400 μm Embozene® microsphere under local anesthesia. The procedure was discontinued immediately after development of severe hypertension that might be related to the pheochromocytoma and was treated with intravenous antihypertensive drug. There was no neurologic deficit until 6.5 hours after the procedure when weakness at right lower extremity and hypesthesia at left arm developed. Emergent MRI showed focal infarcts in spinal cord at right aspect of C5 and left C4 levels. With adequate hydration but no administration of steroid, muscle power gradually recovered in a few hours. Posterior instrumentation, neural decompression and tumor debulking were performed 2 days after embolization as scheduled. One week after the event of spinal cord infarction, she could stand up and walk without aid. Even though it is rare, spinal cord infarction is an important differential diagnosis for sudden decrease of muscle power after preoperative embolization for spinal metastases. Although complete paralysis is more common, transient neurologic deficit with complete recovery could happen in patients with minor infarcts in the spinal cord.

A Patient with Upper Cervical Spinal Cord Infarction Presenting with the Sudden Onset of Severe Occipital Headache Followed by Occipital Neuralgia

A 78-year-old man suddenly developed a severe occipital headache, followed by right greater occipital neuralgia (ON). Brain MR imaging revealed a spinal cord infarction in the territory of the right posterior spinal artery (PSA) at the C2 level without vertebral artery (VA) dissection. Even without VA dissection, upper cervical PSA syndrome could cause severe occipital headache. Furthermore, ipsilateral ON could follow it. The present case suggests that severe occipital headache and ON can occur in a patient with upper cervical PSA syndrome without VA dissection.

Spinal cord infarction with ipsilateral segmental neuropathic pain and flaccid paralysis. A functional role for human afferent ventral root small sensory fibres

This paper illustrates the cases of two patients with an acute onset of right brachial neuropathic pain, flaccid paralysis and contralateral thermal and thermal pain hypoesthesia, without posterior column impairment nor pyramidal signs below the segmental lesion. MRI showed right sided spinal cord infarction, in the anterior spinal artery territory between C1 and C5 in one patient and between C3 and C7 in the other. Contact Heat Evoked Potentials and Quantitative Thermal Sensory testing are consistent with contralateral, but not ipsilateral, spinothalamic tract involvement. Electromyographic results established ipsilateral segmental denervation and somatosensory evoked responses were consistent with dorsal column sparing.Unilateral anterior cervical spinal cord infarction may present with acute ipsilateral segmental neuropathic pain, lower motor neurone-type weakness, contralateral thermoanalgesia and no pyramidal signs. The ipsilateral pain provides novel evidence that in some instances, ventral roots can play a role in nociception in humans. The infarcted territory may result from occlusion of a sulcal commissural artery or a number of more proximal vessels (including a single or duplicated anterior spinal artery, vertebral arteries or feeding radicular arteries).

Neuronopatía isquémica cervical y cardioembolismo: otra causa de síndrome del hombre en el barril

Spinal infarction accounts for 1% of all strokes. Cardioembolism is a rare cause. Common areas of ischemic spinal damage are watershed in the dorsal or lumbar regions; however cervical spinal cord infarction has been reported previously. We present a new case of a man-in-the-barrel syndrome produced by cardiac embolization associated with atrial fibrillation during an acute myocardial infarction, which caused cervical ischemic neuronopathy (infarction of the anterior horn). Classic features of cervical spinal cord ischemia are acute tetraplegia, bladder, bowel and cardiovascular dysfunction and dissociate sensory loss. Incomplete collateralization and anatomical characteristics of the circulation of the anterior spinal artery in the cervical spinal cord, makes of the portion C3 to C5, the most vulnerable portion to ischemic damage, since the radicular arteries supply begins bellow C5 and the pathophysiology of a fast fresh clot lysis produced unique bilateral neuronal horn cells damage.

Post-traumatic Winking Induced by Extension of the Hand: A Case Report of a Novel Synkinesis

Several synkinesis syndromes have been reported in the literature. Synkinesis syndromes are rare and are most commonly congenital or follow post-traumatic reinnervation. We describe a novel synkinesis syndrome that developed several months after cervical spinal cord infarction due to a herniated disc in a 29-year-old woman. When the patient overstretched the extensor muscles of the right hand, the right upper eyelid raised automatically and nasal congestion developed. We hypothesize that aberrant reinnervation of the intermediolateral columns of the spinal cord at level C8–T2 by motor neurons of the extensor muscles of the hand occurred.

Cervical Spinal Cord Infarction Presenting as Unilateral Weakness

Ischemic infarction of the spinal cord usually involves the territory of the anterior spinal artery. The most common clinical abnormalities are bilateral limb weakness and impaired pain and temperature sensation with voiding difficulty. We report a case of cervical spinal cord infarction that was noted to have unilateral limb weakness as the initial manifestation without any other symptoms. The diagnosis of cervical spinal cord infarction should be considered in patients with sudden unilateral weakness, regardless of the extent of sensory or voiding impairment. J Neurocrit Care 2014;7(1):60-62

Cervical Spinal Cord Infarction Presenting as Unilateral Weakness

Cervical Spinal Cord Infarction Presenting as Unilateral Weakness

UNUSUAL COMPLICATION OF VERTEBRAL ARTERIAL DISSECTION

IntroductionVertebral artery dissection (VAD) is a common cause of ischemic stroke in patients younger than 45 yrs of age. VAD is rarely life–threatening but we here present a patient with...

Incomplete Tetraplegia Resulting from Cervical Spinal Cord Infarction of Unknown Etiology: A Case Report

Incomplete Tetraplegia Resulting from Cervical Spinal Cord Infarction of Unknown Etiology: A Case Report

Spinal cord infarction: a rare cause of admission to Internal Medicine Departments but a condition with relevant systemic complications

BACKGROUND Spinal cord infarction is a rare cause of admission to Internal Medicine Departments as it is of infrequent occurrence and it is usually addressed to Neurologic Units. Diagnosis at admission however may be challenging expecially in the elderly because of several co-morbidities and variable presentation. Clinical course is often complicated by autonomic, infective and cardiovascular problems as well as a long stay-in-bed period. Outcome is poor in case of severe motor, autonomic (bladder and bowel) and sensitive impairment at presentation, it’s related to anatomic damage site and extension and it’s worse in case of anterior bilateral infarcts. CLINICAL CASE The authors describe the case of an 81- year-old woman who was admitted to an Internal Medicine Department because of cervical spinal cord infarction. The diagnostic evaluation as well as the management of cardiovascular, infective, rheumatologic and autonomic complications needed skillful internistic competence and a long in-hospital period. MR allowed a correct diagnosis a few hours after presentation, but the pathogenesis was never clearly established. The most invalidating symptoms were loss of bowel control lasting for several weeks during hospitalization and neuropathic pain still present at discharge. As for the outcome, the patient was able to go home after 3 months from admission able to walk with aids, with full bowel and bladder control and no sensitive impairment.

Diffusion weighted imaging with trace diffusion weighted imaging, the apparent diffusion coefficient and exponential images in the diagnosis of spinal cord infarction

A 73-year-old man, with a history of hypertension and left supraclavicular fossa arteriovenous malformation with multiple previous uncomplicated vessel embolisation procedures, presented with acute spastic quadriparesis and urinary retention following upper limb angiography and embolisation. There was no evidence of preceding infection or neurological disease prior to the event. Cerebrospinal fluid analysis was unremarkable. MRI of the cervical spine with a 1.5 Tesla magnet performed 13hours from symptom onset revealed bilateral paramedian intramedullary T2-weighted signal change without gadolinium enhancement limited to the grey matter with corresponding diffusion restriction extending from C5–6 down to the mid-T1. The diagnosis of cervical spinal cord infarction (SCI) was made and the patient was given regular aspirin and atorvastatin. On follow-up at 3months, there was modest improvement with respect to his quadriparesis and was walking unaided. An extensive literature review on the role of MRI in SCI is discussed.

Cervical Spinal Cord Infarction After Decompressive Surgery: A Closer Look

Cervical Spinal Cord Infarction After Decompressive Surgery: A Closer Look