Acute Spinal Cord Syndrome Research Articles

Traumatic lumbar hematomyelia causing spinal shock: A case report

Background: Spinal cord hemorrhage or hematomyelia can arise from trauma or non-trauma causes, adverse effect of anticoagulation therapy and ruptured vascular malformation. Bleeding in epidural space is common and complications such as acute spinal cord syndrome can arise due to the compression and destruction of the spinal cord. Symptoms of hematomyelia might be varied depending on location of the lesion, often accompanied with acute radicular pain. In this case study, we reported a case of spinal shock after traumatic lumbar hematomyelia. Case: A 13-year-old girl presented to Dr. Moewardi General Hospital with inferior paraparesis, bladder and bowel incontinence, a day after falling on her gluteus. Physical examination revealed reduced motoric and sensory function below 12th thoracal dermatome, with no patellar and reduced Achilles reflexes. Conventional X-ray was unremarkable and further investigation with MRI showed a hematoma on thoracal 10 to 12 vertebrae. Motor and sensory functions were improved after 12 days administration of corticosteroids and further improvement was seen almost immediately after decompression surgery. Objective: To describe a case of spinal shock caused by traumatic lumbar hematomyelia Method: This is a case report study describing spinal shock which improved after administration of corticosteroid and decompression surgery. Conclusion: Spinal shock could be caused by traumatic lumbar hematomyelia, which is characterized by loss of motor, sensory, and bladder function, and decompression surgery improved the prognosis.

A sign of spinal cord stroke. Vertebral body ischemia

Spine cord infarction is a rare neurological disease. The MRI can show T2 hyperintense signals, and these lesions can be associated with a vertebral body lesion, that supports the ischemic etiology. We present a 54 year-old-woman with an acute spinal cord syndrome, with a final diagnosis of spinal cord infarction. The initial MRI showed no abnormalities, but a second MRI showed increased signal intensity in T2 sequences and DWI, with a decreased in ADC maps, all compatible with an ischemic lesion. Moreover, the MRI revealed a T2 hyperintense signal in adjacent vertebral body, compatible with ischemic nature. Spine cord MRI is an important complementary exploration in the diagnostic of myelitis syndrome. Other sequences, such as diffusion, should be included, as well as consider the coexistence of a lesion in the adjacent vertebral body, which can support the ischemic etiology of the symptoms.

Acute infectious myelopathies.

The patient who presents with an acute spinal cord syndrome with weakness/paralysis of the limbs presents a diagnostic. Two important syndromes are acute transverse myelitis (ATM) and acute flaccid paralysis (AFP). Both can be caused by a number of infectious and noninfectious causes. Since 2014 there have been outbreaks of acute flaccid myelitis (a subgroup of AFP) in the United States, with a national surveillance program underway. In addition, there have been increasing reports of ATM from new and emerging pathogens, and opportunistic infections in immunocompromised hosts. Infectious causes of ATM or AFP need to be ruled out first. There may be important clues to an infectious cause from epidemiologic risk factors, immune status, international travel, MRI, and laboratory findings. We summarize key features for the more common pathogens in this review. Advances in laboratory testing have improved the diagnostic yield from cerebrospinal fluid, including real-time polymerase chain reaction, metagenomic next-generation sequencing, and advanced antibody detection techniques. These tests still have limitations and require clinical correlation. We present a syndromic approach to infectious myelopathies, focusing on clinical patterns that help narrow the diagnostic possibilities.

Diagnostic value of bright spotty lesions on MRI after a first episode of acute myelopathy

Background and purposeTo determine the diagnostic value of bright spotty lesions (BSLs) for aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (NMOSDAQP4+), the predictive value of axial-BSLs for AQP4-IgG seropositivity, and the radio-clinical differences in NMOSDAQP4+ patients with and without axial-BSLs. Materials and methodsRetrospective study that included patients aged≥16 years, with a first acute spinal cord syndrome between 2005 and 2018 and abnormal spinal cord MRI with axial and sagittal T2 sequences. Patients with MRI findings consistent with compressive myelopathy were excluded. All spinal cord MRI were retrospectively evaluated for the presence of BSLs by 2 radiologists blinded to the diagnosis of acute myelopathy. ResultsA total of 82 patients were included; 15 aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder patients (NMOSDAQP4+), and 67 other patients, considered as the other causes of myelopathy (OM) group. The specificity of axial-BSLs for NMOSDAQP4+ patients was 94.0% (95% CI [85.6 to 97.7]). The sensitivity was 40.0% (95% CI [19.8 to 64.3]). In the multivariable analysis, the only MRI characteristic associated with AQP4-IgG positivity was the presence of axial-BSLs (OR: 9.2, 95% CI [1.2 to 72.9]; P=0.022). In NMOSDAQP4+ patients, the median of cord expansion ratio was higher with axial-BSL (1.2, IQR [1.1–1.3]) than without axial-BSL (1.1, IQR [1.0–1.2]; P=0.046). ConclusionAfter a first acute spinal cord syndrome, the presence of axial-BSLs on spinal cord MRI seems very specific for NMOSDAQP4+ and seems to be a predictor radiological marker of AQP4-IgG positivity.

Acute spinal cord syndrome due to spontaneous cervical haematomyelia - An unusual case

Acute spinal cord syndrome due to spontaneous cervical haematomyelia - An unusual case

Acute Paraplegia due to Thoracic Hematomyelia.

Spontaneous intraspinal intramedullary hemorrhage is a rare entity with the acute onset of neurologic symptoms. The etiology of idiopathic spontaneous hematomyelia (ISH) is unknown, and there are few published case reports. Hematomyelia is mostly associated with trauma, but the other nontraumatic etiologies are vascular malformations, tumors, bleeding disorders, syphilis, syrinx, and myelitis. MRI is a good choice for early diagnosis. Hematomyelia usually causes acute spinal cord syndrome due to the compression and destruction of the spinal cord. A high-dose steroid treatment and surgical decompression and evacuation of hematoma are the urgent solution methods. We present idiopathic spontaneous hematomyelia of a previously healthy 80-year-old male with a sudden onset of back pain and paraplegia.

456 Segmental Acute Spinal Cord Syndrome: “As A Bomb”

BackgroundThe segmental spinal cord syndrome is defined clinically as a neurological injury (incomplete or complete) sensory, motor and autonomic.Results13 year old female, previously healthy with a sudden onset of severe...

Bilateral traumatic avulsion of abducens nerve

DISCUSSION Cavernoma is a benign tumor and it is considered a dysplasia of the vessels-forming mesoderm. Cavernous hemangiomas in the vertebral, extradural, intradural extramedullary and intramedullary spaces are responsible for 3 to 16% of spinal vascular anomalies. Extradural cavernous hemangioma represent 4% of all spinal epidural lesions. Modern diagnostic imaging techniques are increasing the number of diagnosis and its frequency may be more than previously reported in the medical literature. There are four clinical syndromes described: slow and progressive spinal cord syndrome, which is the most common form; acute spinal cord syndrome; back pain; and radiculopathy. Imaging diagnostic exams such as spine X-rays, myelography, CT and MRI are important for evaluating the relationship of the lesion with the surrounding anatomic structures. Currently, MRI is the modality of choice. The treatment for these lesions is total removal of the tumor with microsurgical technique. REFERENCES 1. Hatiboglu MA, Iplikcioglu AC, Ozcan D. Epidural spinal cavernous hemangioma-case Report. Neurol Med Chir (Tokyo) 2006;46:455-458. 2. Goyal A, Singh AK, Gupta V, Tatke M. Spinal epidural cavernous haemangioma:a case report and review of literature. Spinal Cord 2002;40: 200-202. 3. Zevgaridis D, Buttner A, Weis S, Hamburger C, Reulen HJ. Spinal epidural cavernous hemangiomas. Report of three cases and review of the literature. J Neurosurg 1988;88:903-908. 4. Saringer W, Nobauer I, Haberler C, Ungersbock K. Extraforaminal, thoracic, epidural cavernous hemangioma:case report with analysis of magnetic resonance imaging characteristics and review of the literature. Acta Neurochir (Wien) 2001;43:1293-1297. 5. Santoro A, Piccirilli M, Bristot R, Norcia V, Salvati M, Delfini R. Extradural spinal cavernous angiomas: report of seven cases. Neurosurg Rev 2005;28: 313-319.

B-Cell Lymphoma of the Thoracic Spine Presenting with Spinal Cord Pressure Syndrome

B-cell lymphomas are the most common type (85%) of non-Hodgkin lymphomas [1]. Diffuse large B-cell lymphoma accounts for a third of these tumors and occurs mostly in older people [1]. NonHodgkin’s lymphomas arising in the spinal cord are extremely rare. Spinal cord compression as the initial manifestation of nonHodgkin’s lymphoma is rare and may occur in advanced stages of the disease [1-3]. It usually looks isointense or low signal (relative to the spinal cord) on T1-weighted images and high signal on T2weighted images [4]. Contrast enhancement is usually intense and homogeneous [4]. A 70-year-old African-American male presented to the emergency room complaining of bilateral mild lower extremity weakness for 2 days. The patient could not bear weight on his legs when he tried to get out of bed in the last two mornings. He also felt numb in both legs. Since then, he has been incontinent of urine but not feces. He denied any back pain or trauma. He also had no weakness or numbness in the upper extremities. His past medical history included chronic obstructive pulmonary disease and aortic regurgitation. He was on Zithromax and Prednisone at Home. He denied using alcohol, tobacco or elicit drugs. The patient had some wheezing and cough in addition to mild abdominal pain. On neurological exam, the patient had weakness in the lower extremities. The strength at the hip and knee was 2/5 on the right side and 3/5 on the left side and 1/5 at the ankle on both sides. Deep tendon reflexes were 2+ in the biceps and triceps symmetrically. His right knee jerk was 1+ and left knee jerk 2+ and both ankle jerks were abscent. He also had absence of position sense in both of his ankles and feet. He had a pinprick sensation at the nipple level (T4) both anteriorly and posteriorly. The initial diagnosis was acute spinal cord syndrome at T4 and the patient was put on Decadron. Thoracic MRI showed an epidural soft tissue mass at the T3, T4 and T5 levels extending from the posterior aspect of the spinal canal causing moderate encroachment upon the spinal cord at T4 with diffuse metastatic disease involving the cervical and lumbar vertebral bodies (Fig. 1-3). After consulting with the patient it was decided to proceed with T3, T4, T5 decompressive laminectomies and excision of tumor from epidural space under microscope. Microscopic examination revealed a diffuse proliferation of

Acute non-traumatic spinal epidural hemorrhage

Two cases of acute non-traumatic spinal epidural hemorrhage are reported. Eight additional cases, four of which had a history of minor indirect trauma, have been collected from the literature. In spite of the apparent rarity of the syndrome awareness of its existence should lead to prompt surgical intervention in an effort to aviod permanent paraplegia. Although the etiology of the non-traumatic form of spinal epidural hemorrhage remains obscure, certain factors suggest that rupture of a weak vascular wall in a pre-existing abnormality of the epidural venous plexus may be the pathogenetic mechanism of this acute spinal cord syndrome. These factors are: (1) pathological evidence of the focal occurrence of two types of vascular abnormalities, venous varicosities and telangiectases in the epidural space; (2) the clinical anatomy of the vertebral venous system, in which the absence of valves permits rapid transmission of increased venous pressure from intra-abdominal and pelvic veins to epidural veins; and (3) the history of some form of straining effort immediately preceding the onset of symptoms in eight of the ten reported cases of spinal epidural hemorrhage.