Cause Of Myelopathy Research Articles

Spinal cysticercosis: a rare cause of myelopathy

BackgroundNeurocysticercosis is a neuroinfectious disease caused by the larval stage of the tapeworm Taenia solium. Isolated spinal cysticercosis is rare, with limited cases having been reported in the literature. This entity poses great diagnostic and therapeutic challenges.MethodsThis retrospective study included seven patients pathologically diagnosed with spinal cysticercosis. The clinical manifestations, radiological features on magnetic resonance imaging (MRI), treatment, and outcomes were analyzed.ResultsThis case series consisted of four male and three female patients, with an average age of 34.9 ± 10.9 years. Clinically, six patients manifested with localization-related myelopathy. There were four solid lesions, one cystic-solid lesion, and three cystic lesions. The solid and cystic-solid lesions showed characteristic MRI features: 1) within the lesion, there was a mural nodule with isointensity on T1WI and iso- to hyperintensity on T2WI; 2) the signals at the periphery of the mural nodule were variable, ranging from hypointense to hyperintense on T2WI; and 3) ring-like or cyst wall enhancement could be present, and dot-like enhancement could be noted in the mural nodule. Complete resection of the responsible lesion was achieved in all patients, and oral albendazole was administered in a patient with one more suspected homologous lesion. After a mean follow-up period of 56.7 ± 35.1 months, the patient’s symptoms mostly regressed.ConclusionSpinal cysticercosis is an extremely rare cause of myelopathy. Characteristic MRI features can facilitate preoperative diagnosis. Clinicians should be aware of this entity, and it should be included in the differential diagnosis of myelopathy.

Progressive Myelopathy With Acute Worsening After Steroids and Lumbar Puncture.

We present the case of a 73-year-old woman with a 3-month history of non-traumatic thoracic myelopathy. Initial MRI showed a T6-conus T2 signal hyperintensity. Based on this presentation, and given a personal and family history of autoimmune disease, our patient was first managed as an inflammatory transverse myelitis. Subsequent worsening after lumbar puncture and steroids prompted re-evaluation, ultimately identifying the cause as a thoracic spinal dural AV fistula. Both investigation of possible transverse myelitis with lumbar puncture and empiric treatment with steroids may not only result in diagnostic delays but also precipitate venous infarction and irreversible harm. While the MRI often provides the initial diagnosis, clinical suspicion for this under-diagnosed cause of myelopathy should be raised in older patients with a more progressive thoracic myelopathy with worsening after lumbar puncture and/or steroids. Definitive and time-sensitive treatment by interventional neuroradiology or neurosurgery results in stabilization or improvement of disability in most cases.

Dorsal Cord Herniation with DiastematomyeliaA Rare Case

Transdural spinal cord herniation is rare and under reported. Ventral or ventro-lateral cord herniation is relatively more common and a well described entity. Dorsal or posterior spinal cord herniation is very rare, only five cases in the cervical spine, as per our knowledge. It is nonetheless a recognised cause of myelopathy, either acquired postsurgery or post-trauma or idiopathic in cause and congenital. The authors are reporting a rare case of a 47-year-old male patient who underwent Magnetic Resonance Imaging (MRI) spine. The MRI showed cord with diastematomyelia from C3 to C5 levels with kinking of cord at this level attached to the posterior dura. Posterior subarachnoid space at this level is completely effaced with no evidence of Cerebrospinal Fluid (CSF) posterior to the cord and hence, the patient was subsequently diagnosed as postoperative dorsal spinal cord herniation and myelomalacia in the cervical spine associated with diastematomyelia. Patient is being managed conservatively till date.

Potential benefit of olive leaf extract in cervical spondylotic myelopathy model

IntroductionCervical spondylosis is the most common cause of myelopathy in the cervical due to chronic compression of the spinal cord in patients aged 55 years or older. Recent studies suggest that olive extracts suppress inflammation and reduce stress oxidative injury. The purpose of this study was to determine the potential neuroprotective effects of olive leaf extract (OLE) in an experimental cervical spondylotic myelopathy model. MethodsThis study was divided into 6 groups; Control Negative (Sham-Operated) Group, Control Positive 1 & 2 (early chronic and chronic), Treatment Groups 1, 2 & 3 (prophylactic, concomitant & late). Olive leaf extract (OLE) give 350 mg/kg BW and spinal cord sample was taken at the compression level C5. Histopathological assessment and immunohistochemistry of Amyloid-β, p-Tau, TDP-43 dan CD-68 dan evaluation of functional motoric outcome was done before animals were terminated. ResultsChronic spinal cord compression increased the expression of Amyloid-β, p-Tau, TDP-43 dan CD-68. OLE 350 mg/kg BW decreased the expression of these biomarkers and increased functional motoric outcome, especially as prophylactic dan concomitant treatment. DiscussionThese findings indicate that OLE may be effective in protecting cervical spondylotic myelopathy.

Clinical heterogeneity of low flow spinal arteriovenous fistulas; a case series

BackgroundSpinal AVF (SAVF), a potentially treatable cause of myelopathy, remains a challenging diagnosis. Its rarity and non-specific imaging findings often result in misdiagnosis despite a high index of clinical suspicion. The classically described high T2 signal in the spinal cord or prominent vascular flow voids in the intradural space were not infrequently missed on initial imaging, only to be picked up at follow-up imaging after progression of symptoms. Additionally, small sized fistulas(< 1 mm) and SAVF involving less frequent locations like the craniocervical junction in a patient presenting with paraplegia further complicates the diagnosis. On rare occasions, acute atypical presentation following a surgery adds to the conundrum. Definite diagnosis with spinal angiography, the gold-standard modality requires the expertise of highly skilled interventionists which may otherwise lead to false negative findings. We describe four SAVF patients with unconventional presentations, highlighting less described clinical findings.Case presentationFirst was a 50-year-old man presented with spastic paraparesis and was found to have an AVF at the cervical region arising from the vertebral artery. Second, a 45-year-old man with acute paraplegia post-operatively, initially treated for a transverse myelitis before lumbar region AVF was detected. Thirdly, a 27-year-old man presented with subacute lower thoracic myelopathy and deteriorated after corticosteroid treatment. The last patient, who initially appeared to have conus medullaris/cauda equina syndrome had a SAVF at the mid thoracic level. Presentation varied with some exhibiting acute deterioration mimicking other spinal cord pathology such as inflammatory disorders. All patients eventually underwent endovascular treatment with successful embolization of SDAVF. None of them exhibited further neurological deterioration after embolization.ConclusionSuccessful treatment of SAVF is possible provided the diagnosis is made early, allowing timely intervention. Certain clues may aid the diagnosis. Firstly, arteriovenous fistula can be located distant to the clinical localization of myelopathy resulting in the unexpected longitudinally extensive spinal cord signal change. This clinical-radiological discrepancy can be a useful clue in diagnosing SAVF. Secondly, an acute myelopathic presentation immediately post-surgery may be related to SAVF. Other SAVF feature of note includes progressive myelopathy mimicking immune-mediated myelitis among young adults below 30 years of age refractory to immune therapy.

A Case of Subacute Combined Degeneration as a Manifestation of Pernicious Anaemia

Vitamin B12 deficiency affects multiple systems, including the central and peripheral nervous systems, producing a vast spectrum of neurological symptoms. It is particularly important due to its insidious presentation and because it can evolve to spastic paraplegia with permanent sequelae. The authors describe a case of a woman with asthenia, bilateral lower limb weakness, urinary retention, and faecal incontinence, with no structural cause on imaging studies. Blood tests showed anaemia (haemoglobin: 6.8 g/dL) and vitamin B12 deficiency (&lt;100 pg/mL). After upper digestive endoscopy compatible with chronic atrophic gastritis and positive for anti-intrinsic factor antibodies was obtained, the diagnosis of subacute combined degeneration due to vitamin B12 deficiency in the context of pernicious anaemia was admitted. Although this entity is a rare cause of myelopathy, it is a frequent manifestation of vitamin B12 deficiency. Clinical suspicion is fundamental since the reversibility of the neurological lesion is dependent on early treatment.

Progressive spinal cord compression technique in experimental rabbit animal model for cervical spondylotic myelopathy

IntroductionCervical spondylotic myelopathy (CSM) presently estimated at 54% population, commonly cause of myelopathy due to chronic compression of the spinal cord in older people. Physiological injuries caused by static and dynamic forces including compressed, pinched, and pulled out inducing secondary injuries at the molecular level. MethodsWe examined the rabbit model approach with the clinical case of spondylotic myelopathy, in which the disk and facet maintained the cervical spine mobility, and compression was given 0.5 mm per week three times in this model. In this study, a group of 14 days was made (early into the chronic phase) and the 21 day group had a chronic process for 1 week, that period can be categorized as a chronic process and CSM is a chronic process. By examining motor scores, histological examination and immunohistochemistry of the spinal cord, this model efficiently produces myelopathy. The distribution of microglia expressing GFAP, S100-β, and Neurofilaments were observed by immunohistochemical techniques. ResultsThere was a significant difference in the number of cells expressing GFAP between the control group and the 21-day compression group (p = 0.001). There is a decrease in S100-β expression of spinal cord tissue after receiving compression exposure. There was a significant difference in the number of cells expressing NF between the control group, the 14-day compression group (p = 0.04) and 21-day compression group (p = 0.04). DiscussionNeurons have the intrinsic ability to regenerate after injury, although not spontaneously. Cervical spondylotic myelopathy causes permanent neurological disorders, partly due to glial scar formation consisting of astrocytes and microglia. The difference between our study and previous research methods is that we perform compression of the spinal cord in stages (0.5 mm, 1.0 mm & 1.5 mm) so that it is more like the natural occurrence of chronic spinal cord compression. ConclusionAn increasing of GFAP value in this study indicates the presence of astrocyte activity which can be associated with chronic spinal cord injury. There is a decrease in S100-β expression of spinal cord tissue neuron cells after receiving compression exposure. The expression of NF decreased indicating degenerative axons.

Use of residual neural network for the detection of ossification of the posterior longitudinal ligament on plain cervical radiography.

Ossification of the posterior longitudinal ligament (OPLL) causes serious problems, such as myelopathy and acute spinal cord injury. The early and accurate diagnosis of OPLL would hence prevent the miserable prognoses. Plain lateral radiography is an essential method for the evaluation of OPLL. Therefore, minimizing the diagnostic errors of OPLL on radiography is crucial. Image identification based on a residual neural network (RNN) has been recognized to be potentially effective as a diagnostic strategy for orthopedic diseases; however, the accuracy of detecting OPLL using RNN has remained unclear. An RNN was trained with plain lateral cervical radiography images of 2,318 images from 672 patients (535 images from 304 patients with OPLL and 1,773 images from 368 patients of Negative). The accuracy, sensitivity, specificity, false positive rate, and false negative rate of diagnosis of the RNN were calculated. The mean accuracy, sensitivity, specificity, false positive rate, and false negative rate of the model were 98.9%, 97.0%, 99.4%, 2.2%, and 1.0%, respectively. The model achieved an overall area under the curve of 0.99 (95% confidence interval, 0.97-1.00) in which AUC in each fold estimated was 0.99, 0.99, 0.98, 0.98, and 0.99, respectively. An algorithm trained by an RNN could make binary classification of OPLL on cervical lateral X-ray images. RNN may hence be useful as a screening tool to assist physicians in identifying patients with OPLL in future setting. To achieve accurate identification of OPLL patients clinically, RNN has to be trained with other cause of myelopathy.

Myelopathies from Neoplasms.

Benign and malignant tumors can be an important cause of myelopathy. Patients may present with a wide range of neurologic symptoms including back and neck pain, weakness, sensory abnormalities, and bowel and bladder dysfunction. Management can be challenging depending on the location and underlying biology of the tumor. Neuroimaging of the spine is an important component of diagnostic evaluation and patient management both during initial evaluation and when monitoring after treatment. This article provides a systematic and practical review of neoplasms that can cause myelopathy. Unique imaging and biological features of distinct tumors are discussed, and their management strategies are reviewed.

Metabolic and Toxic Myelopathies.

Metabolic and toxic causes of myelopathy form a heterogeneous group of disorders. In this review, we discuss the causes of metabolic and toxic myelopathies with respect to clinical presentation, pathophysiology, diagnostic testing, treatment, and prognosis. This review is organized by temporal course (hyperacute, acute, subacute, and chronic) and etiology (e.g., nutritional deficiency, toxic exposure). Broadly, the myelopathies associated with dietary toxins (neurolathyrism, konzo) and decompression sickness present suddenly (hyperacute). The myelopathies associated with heroin use and electrical injury present over hours to days (acutely). Most nutritional deficiencies (cobalamin, folate, copper) and toxic substances (nitrous oxide, zinc, organophosphates, clioquinol) cause a myelopathy of subacute onset. Vitamin E deficiency and hepatic myelopathy cause a chronic myelopathy. Radiation- and intrathecal chemotherapy-induced myelopathy can cause a transient and/or a progressive syndrome. For many metabolic and toxic causes of myelopathy, clinical deficits may stabilize or improve with rapid identification and treatment. Familiarity with these disorders is therefore essential.

Vascular Spinal Cord Disorders.

Vascular disorders of the spinal cord are uncommon yet under-recognized causes of myelopathy. Etiologies can be predominantly categorized into clinical and radiographic presentations of arterial ischemia, venous congestion/ischemia, hematomyelia, and extraparenchymal hemorrhage. While vascular myelopathies often produce significant morbidity, recent advances in the understanding and recognition of these disorders should continue to expedite diagnosis and proper management, and ideally improve patient outcomes. This article comprehensively reviews relevant spinal cord vascular anatomy, clinical features, radiographic findings, treatment, and prognosis of vascular disorders of the spinal cord.

Hereditary Myelopathies.

Hereditary myelopathies are an important and likely underappreciated component of neurogenetic disease. While previously distinctions have been made by age of onset, the growing power and availability of high-quality neuroimaging and next-generation sequencing are increasingly expanding classical phenotypes and diminishing the utility of age-based classifications. Increasingly, cases of "atypical" disease presentations are challenging past assumptions regarding the age of onset and survival in many disorders and identifying allelic syndromes in others. Despite this, there is poor awareness of the potential for spinal involvement in many diseases that typically affect the brain. Broadly speaking, congenital myelopathies can be neuroanatomically grouped into motor neuron, axonopathy, spinocerebellar, cerebroleukodystrophy, and pan-neuraxis (generally central nervous system predominant with associated axonopathy) disorders.Here, we review hereditary causes of myelopathy, organized by neuroanatomy, and highlight atypical presentations. We discuss findings concerning an underlying genetic etiology for myelopathy, as well as practical, technical, and ethical considerations of diagnostic genetic testing.

Vascular Myelopathies.

Neurologists should be able to identify clinical and neuroimaging features that distinguish vascular disorders from other causes of myelopathy. Although certain clinical features suggest a vascular etiology in acute and chronic myelopathy settings, accurate MRI interpretation within the clinical context is key. Recent studies have shown vascular myelopathies are frequently misdiagnosed as transverse myelitis, and recognition of this diagnostic pitfall is important. Many different vascular mechanisms can cause myelopathy; this article provides a comprehensive review that simplifies disease categories into arterial ischemia, venous congestion/ischemia, hematomyelia, and extraparenchymal hemorrhage. It is important to recognize and manage vascular disorders of the spinal cord as significant causes of acute, subacute, and progressive myelopathy.

Neuroimaging of Spinal Cord and Cauda Equina Disorders.

This article reviews the neuroimaging of disorders of the spinal cord and cauda equina, with a focus on MRI. An anatomic approach is used; diseases of the extradural, intradural-extramedullary, and intramedullary (parenchymal) compartments are considered, and both neoplastic and non-neoplastic conditions are covered. Differentiating imaging features are highlighted. Although T2-hyperintense signal abnormality of the spinal cord can have myriad etiologies, neuroimaging can provide specific diagnoses or considerably narrow the differential diagnosis in many cases. Intradural-extramedullary lesions compressing the spinal cord have a limited differential diagnosis and are usually benign; meningiomas and schwannomas are most common. Extradural lesions can often be specifically diagnosed. Disk herniations are the most commonly encountered mass of the epidural space. Cervical spondylotic myelopathy can cause a characteristic pattern of enhancement, which may be mistaken for an intrinsic myelopathy. A do-not-miss diagnosis of the extradural compartment is idiopathic spinal cord herniation, the appearance of which can overlap with arachnoid cysts and webs. Regarding intrinsic causes of myelopathy, the lesions of multiple sclerosis are characteristically short segment but can be confluent when multiple. Postcontrast MRI can be particularly helpful, including when attempting to differentiate the long-segment myelopathy of neurosarcoidosis and aquaporin-4 (AQP4)-IgG-seropositive neuromyelitis optica spectrum disorder (NMOSD) and when characterizing spinal cord tumors such as primary neoplasms and metastases. Spinal dural arteriovenous fistula is another do-not-miss diagnosis, with characteristic MRI features both precontrast and postcontrast. Tract-specific white matter involvement can be a clue for diseases such as subacute combined degeneration, paraneoplastic myelopathy, and radiation myelitis, whereas gray matter-specific involvement can suggest conditions such as cord infarct, viral myelitis, or myelin oligodendrocyte glycoprotein (MOG)-IgG associated disorder. Knowledge of the neuroimaging findings of the many causes of spinal cord and cauda equina dysfunction is critical for both neurologists and neuroradiologists. A structured approach to lesion compartmental location and imaging feature characterization is recommended.

Atypical HIV-vacuolar myelopathy: a case report

BackgroundHere, we report an atypical HIV-vacuolar myelopathy and search the available medical literature about atypical presentations of human immunodeficiency virus associate vacuolar myelopathy (HIV-VM) and immunoglobulin therapy response.CaseA 26-year-old lady who was 4 weeks postpartum presented to us with acute flaccid quadriparesis, with no sensory level. Extensive workup ruled out other causes of myelopathy. She developed a stage 3 acute kidney injury, and MRI showed diffuse cord atrophy involving the lower cervical and thoracic cord. The patient received IV-immunoglobulin, ARVs, and supportive therapy with inadequate response. Unfortunately, she developed nosocomial pneumonia and died.DiscussionIn HIV-VM, there is spinal cord atrophy, which mainly involves the thoracic cord. In our case, this pathological process also affected the spinal cord's cervical region, leading to flaccid tetraplegia, with high CD4 level, without response to the treatment, including intravenous immunoglobulin.KeynotesVacuolar myelopathy, HIV, Immunoglobulin therapy, flaccid tetraplegia, hypokalaemia. Renal failure.

Spondylotic and Other Structural Myelopathies.

This article highlights both common structural causes of myelopathy, such as spondylotic disease, and infrequent but treatable causes, such as syringomyelia, spinal cord herniation, arachnoid cyst, arachnoid band and web, epidural lipomatosis, Hirayama disease, and arachnoiditis. Neuroimaging improvements and availability have uncovered many structural abnormalities in the spines and spinal cords of patients who were asymptomatic or minimally symptomatic. Recent published clinical series have improved our knowledge of the natural history of structural abnormalities and the risks of intervention versus conservative management. Myelopathy from a suspected structural cause is a common reason for neurologic consultation. Correlation between the history, examination, and imaging are especially important to determine whether intervention is necessary or conservative management is the best option.

Skeletal Fluorosis With Thoracic Myelopathy: A Report of 2 Cases.

To report 2 different presentations of thoracic myelopathy with ossification of ligamantum flavum (OLF) due to fluorosis. Two females presented with thoracic myelopathy secondary to spinal stenosis with OLF due to fluorosis. On examination, the first patient had a grade 4 power in both lower limbs with altered sensation below L1 dermatome. She had segmental OLF on magnetic resonance imaging and computed tomography and was treated with posterior thoracic laminectomy and recovered well. The second patient had a history of a prior thoracic laminectomy at another institution and presented with paraplegia with bladder involvement. Radiological investigations revealed a 3-column injury at the level of D8/D9. This patient was treated with decompression and stabilization. The first patient recovered neurologically and regained independent ambulation while the second patient had a reduction in spasticity but no recovery of power or bladder function. Different presentations and causes of myelopathy due to OLF should be recognized and treated. An unstable injury is very rare and should not be missed.

Clinical-radiological approach to nontraumatic myelopathy

Diseases of the spinal cord often have devastating consequences and imaging studies are indispensable for their diagnosis. The fundamental imaging technique to evaluate these diseases is magnetic resonance imaging of the spine. The diagnostic approach must be based on the clinical context, the time elapsed since the onset of symptoms and signs, and the imaging findings; for this reason, it sometimes necessary to broaden the study to include the brain. The first step in the diagnostic algorithm is to rule out spinal cord compression before evaluating other causes of myelopathy, which sometimes has multiple causes. This paper includes a broad review of the different diseases that can cause myelopathy, their imaging manifestations, their differential diagnoses, and diagnostic algorithms. Using an appropriate radiological approach will result in better management and prognosis of these patients.

Enfoque clínico-radiológico de la mielopatía no traumática

Diseases of the spinal cord often have devastating consequences and imaging studies are indispensable for their diagnosis. The fundamental imaging technique to evaluate these diseases is magnetic resonance imaging of the spine. The diagnostic approach must be based on the clinical context, the time elapsed since the onset of symptoms and signs, and the imaging findings; for this reason, it sometimes necessary to broaden the study to include the brain. The first step in the diagnostic algorithm is to rule out spinal cord compression before evaluating other causes of myelopathy, which sometimes has multiple causes. This paper includes a broad review of the different diseases that can cause myelopathy, their imaging manifestations, their differential diagnoses, and diagnostic algorithms. Using an appropriate radiological approach will result in better management and prognosis of these patients.

HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis Overlapping Ossification of the Ligamentum Flavum

AbstractHTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is an important cause of nontraumatic and noncompressive chronic myelopathy which generally has no improvement regardless of treatment. On the other hand, ossification of the ligamentum flavum (OLF) is also a cause of myelopathy; however, it can improve in some cases when surgical treatment is well applied. In this case report, we presented a case of a patient with HAM/TSP overlapping OLF which showed some improvement with surgical treatment.