Rapidly Progressive Numbness and Weakness After Soft-Tissue Abscess

2021 ◽  
pp. 7-9
Author(s):  
Elia Sechi ◽  
Dean M. Wingerchuk

A previously healthy 45-year-old man had development of neck pain and swelling, followed 1 week later by fevers, chills, and night sweats. Cervical computed tomography showed a left-sided cervical soft-tissue abscess. The patient was treated with oral cephalexin for 10 days, without benefit. Fine-needle aspiration biopsy of the mass showed granulomatous inflammation and a heterogeneous lymphocyte population without evidence of malignancy. Meropenem and gentamicin were started. Ten days later, he had development of acute urinary retention, numbness and weakness in the lower extremities, and numbness in the upper extremities. At symptom nadir 2 days later, he required the aid of a walker to ambulate. Lhermitte sign and erectile dysfunction were also present. The patient was admitted to the hospital. Spinal cord magnetic resonance imaging showed a longitudinally extensive, nonenhancing, T2-hyperintense lesion predominantly affecting the ventral and lateral parenchyma of the cervical and thoracic spinal cord. Cerebrospinal fluid examination showed a white blood cell count of 581 cells/µL with 42% neutrophils, 35% lymphocytes, and 22% monocytes, increased protein concentration (109 mg/dL), and normal glucose concentration. A diagnosis of postinfectious idiopathic transverse myelitis was made. The patient was treated with intravenous immunoglobulin, intravenous methylprednisolone, and broad-spectrum antibiotics, with improvement of both the abscess and his neurologic symptoms. After discharge, he was able to walk unassisted. At follow-up evaluation 6 months after the initial evaluation, neurologic examination showed only mild weakness of the left iliopsoas muscle and brisk reflexes in the lower extremities. Acute transverse myelopathies are a heterogeneous group of spinal cord disorders characterized by acute or subacute signs and symptoms of spinal cord dysfunction, typically a combination of sensory, motor, and autonomic manifestations. Underlying causes include vascular, infectious, neoplastic, postirradiation, traumatic, and inherited/metabolic, and inflammatory processes.

BMC Neurology ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Fangfang Qu ◽  
Zhenzhen Qu ◽  
Yingqian Lv ◽  
Bo Song ◽  
Bailin Wu

Abstract Background Transverse myelitis (TM) is due to inflammatory spinal cord injury with bilateral neurologic involvement, which is sensory, motor, or autonomic in nature. It may be associated with autoimmune disease, vaccination, intoxication and infections. The most common infection cause of TM is Coxsackie virus and Mycoplasma pneumoniae. The cryptococcosis is rare. We present the case of disseminated cryptococcosis revealed by transverse myelitis in an immunocompetent 55-year-old male patient. The literature review is also stated. Case presentation The 55-year-old man suffered from gradual numbness, weakness in both lower limbs and finally paralyzed in the bed. The thoracic spine Computed tomography (CT) was normal, but multiple nodules in the lung were accidentally discovered. Thoracic Magnetic Resonance Imaging (MRI) showed diffused thoracic spinal cord thickening and extensively intramedullary T2 hyper intensity areas. Gadolinium contrast enhanced T1WI showed an intramedullary circle-enhanced nodule at 9th thoracic level. Diagnosis was made by histological examination of the bilateral lung biopsy. The patient was treated successfully with systemic amphotericin B liposome and fluconazole and intrathecal dexamethasone and amphotericin B liposome. Conclusions This is a patient with disseminated cryptococcosis involving the lung, spinal cord and adrenal glands, which is rare in the absence of immunodeficiency.


2021 ◽  
pp. 242-245
Author(s):  
Nicholas L. Zalewski

A 25-year-old man was transferred for evaluation and management of severe transverse myelitis. He had no pertinent past medical history. His symptoms started approximately 6 months earlier with new, substantial low back pain for 2 days, followed by a 3-day history of lower extremity weakness. He could only ambulate with the help of a rolling chair and had to discontinue work because of the severity of the weakness, but his symptoms resolved spontaneously within a few days. Findings of repeated spinal cord magnetic resonance imaging were consistent with evolution of a recent hemorrhage in the lower thoracic spinal cord. Digital subtraction angiography of the spinal canal showed normal findings, without evidence of arteriovenous malformation. Additional thorough evaluations for bleeding diatheses, drugs of abuse, thorough skin evaluation to exclude melanoma, and systemic imaging with computed tomography of the chest, abdomen, and pelvis and testicular ultrasonography were all normal. Given the clinical timeline, the lobulated hemorrhagic appearance of the lesion with a surrounding T2-hypointense rim and heterogeneous T1 and T2 signal indicating recent hemorrhage, no pattern on imaging to suggest a neoplasm, with negative systemic evaluation and normal digital subtraction angiography, a diagnosis of hematomyelia due to intramedullary spinal cavernous malformation was made. No neurosurgical management was recommended given the complete cross-sectional spinal cord injury at the level of hemorrhage, with potential risk of surgery with resection of the intramedullary spinal cavernous malformation. Short-interval follow-up imaging 3 weeks later showed expected evolution of the recent hemorrhage secondary to intramedullary spinal cavernous malformation. Hematomyelia may be caused by several potential mechanisms. The most common nontraumatic causes are attributable to cavernous malformations and arteriovenous malformations. Hematomyelia most commonly presents with acute back pain referable to the site of hemorrhage and myelopathy deficits with a range of severity (often severe).


2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi149-vi149
Author(s):  
rusha Shah ◽  
Vyshak Venur ◽  
Tresa McGranahan

Abstract Cortical and subcortical neurotoxicity from CAR-T therapy is a well described complication in literature, with over 40% of patients experiencing at least one neurologic side effect. However, spinal cord toxicity from CAR-T therapy is less well described. To our knowledge, this is the first reported case of a spinal cord infarct following CAR-T therapy. A 44 year old male with primary refractory DLBCL without CNS involvement, which was refractory to R-CHOP, R-ICE, and hyperCVAD part B underwent CD-19 CAR-T treatment. The day after infusion he developed grade 1 cytokine release syndrome (CRS) with fever and up trending inflammatory markers. Infectious work up was negative and he was treated with tocilizumab and dexamethasone. His fever resolved and markers down trended. On day 5 post CAR-T, he became encephalopathic, developed severe back pain, and was unable to move his bilateral lower extremities. He was treated with 2nd and 3rd doses of tocilizumab, dexamethasone and was started on anakinra. Patient’s mental status cleared by day 7 and he was found to have a dermatome sensory level at T10 with flaccid bilateral lower extremity paralysis. MRI Brain was unremarkable, but a spinal MRI showed longitudinally extensive cord edema and diffusion restriction at T10. Due to an initial question of transverse myelitis, he was treated with a 3-day course of IV methylprednisolone, with no improvement in symptoms. CSF studies were unable to be obtained due to his thrombocytopenia. Repeat MRI obtained 10 days after initial imaging showed resolution of cord edema, but continued areas of FLAIR hyperintensity at T10 through the conus. Despite aggressive rehabilitation services, four months later, patient remained paralyzed in his lower extremities with an indwelling foley catheter. He remains in a complete remission.


2019 ◽  
Vol 17 (4) ◽  
pp. E161-E161
Author(s):  
Siri Sahib S Khalsa ◽  
Yamaan S Saadeh ◽  
Brandon W Smith ◽  
Jacob R Joseph ◽  
Mark E Oppenlander

Abstract Spinal cord herniation is an uncommon surgically treatable cause of thoracic myelopathy and progressive paraplegia. The thoracic spinal cord focally protrudes through a defect in the dura, resulting in progressive weakness, numbness, and spasticity affecting the lower extremities, in addition to possible urinary symptoms. In this video, we present the case of a 69-yr-old female who presented with 3 yr of progressive thoracic myelopathy due to a thoracic spinal cord herniation at T4-T5. We demonstrate the surgical steps to lyse arachnoid webs, mobilize the spinal cord, reduce the spinal cord herniation, and repair the dural defect. Appropriate patient consent was obtained.


2021 ◽  
Vol 15 (2) ◽  
pp. e0009161
Author(s):  
Angus de Wilton ◽  
Dinesh Aggarwal ◽  
Hans Rolf Jäger ◽  
Hadi Manji ◽  
Peter L. Chiodini

Background Neuroschistosomiasis is a severe complication of schistosomiasis, triggered by the local immune reaction to egg deposition, with spinal cord involvement the most well recognised form. Early treatment with praziquantel and high dose steroids leads to a reduction of neurological sequelae. The rarity of this condition in returning travellers to high income countries can result in delayed diagnosis and treatment. We aimed to evaluate the diagnosis and management of neuroschistosomiasis in a UK national referral centre. Materials/Methods A retrospective review of confirmed clinical cases of spinal schistosomiasis referred to the Hospital for Tropical Diseases, UK, between January 2016 and January 2020 was undertaken. Electronic referral records were interrogated and patient demographic, clinical, laboratory, and radiological data collected. Results Four cases of neuroschistosomiasis were identified. The median age at diagnosis was 28 (range 21 to 50) with three male patients. All patients had epidemiological risk factors for schistosomiasis based on travel history and freshwater exposure; two in Uganda (River Nile), one in Malawi and one in Nigeria. All patients presented with features of transverse myelitis including back pain, leg weakness, paraesthesia and urinary dysfunction. The mean time from presentation to health services to definitive treatment was 42.5 days (range 16–74 days). Diagnosis was confirmed with CSF serology for schistosomiasis in all cases. Radiological features on MRI spine included enhancement focused predominantly in the lower thoracic spinal cord in three cases and the conus in one patient. All patients received a minimum of three days of oral praziquantel and high dose steroids. At three-month follow-up, one patient had complete resolution of symptoms and three had residual deficit; one patient was left with urinary and faecal incontinence, another had urinary retention, and the final patient has persistent leg pains and constipation. Conclusion We observed a marked delay in diagnosis of neuroschistosomiasis in a non-endemic country. We advocate undertaking a thorough travel history, early use of imaging and CSF schistosomal serology to ensure early diagnosis of neuroschistosomiasis in patients presenting with consistent symptoms. If schistosomal diagnostics are not immediately available, presumptive treatment under the guidance of a tropical medicine specialist should be considered to minimize the risk of residual disability. We advocate for consensus guidelines to be produced and reporting to be performed in a uniform way for patients with spinal schistosomiasis.


2001 ◽  
Vol 45 (4) ◽  
pp. 353 ◽  
Author(s):  
Sung Chan Jin ◽  
Seoung Ro Lee ◽  
Dong Woo Park ◽  
Kyung Bin Joo

2018 ◽  
Vol 46 (05) ◽  
pp. 323-329 ◽  
Author(s):  
Nele Ondreka ◽  
Sara Malberg ◽  
Emma Laws ◽  
Martin Schmidt ◽  
Sabine Schulze

SummaryA 2-year-old male neutered mixed breed dog with a body weight of 30 kg was presented for evaluation of a soft subcutaneous mass on the dorsal midline at the level of the caudal thoracic spine. A further clinical sign was intermittent pain on palpation of the area of the subcutaneous mass. The owner also described a prolonged phase of urination with repeated interruption and re-initiation of voiding. The findings of the neurological examination were consistent with a lesion localization between the 3rd thoracic and 3rd lumbar spinal cord segments. Magnetic resonance imaging revealed a spina bifida with a lipomeningocele and diplomyelia (split cord malformation type I) at the level of thoracic vertebra 11 and 12 and secondary syringomyelia above the aforementioned defects in the caudal thoracic spinal cord. Surgical resection of the lipomeningocele via a hemilaminectomy was performed. After initial deterioration of the neurological status postsurgery with paraplegia and absent deep pain sensation the dog improved within 2 weeks to non-ambulatory paraparesis with voluntary urination. Six weeks postoperatively the dog was ambulatory, according to the owner. Two years after surgery the owner recorded that the dog showed a normal gait, a normal urination and no pain. Histopathological diagnosis of the biopsied material revealed a lipomeningocele which confirmed the radiological diagnosis.


Author(s):  
Fedorova Jana ◽  
Kellerova Erika ◽  
Bimbova Katarina ◽  
Pavel Jaroslav

AbstractSpontaneous recovery of lost motor functions is relative fast in rodent models after inducing a very mild/moderate spinal cord injury (SCI), and this may complicate a reliable evaluation of the effectiveness of potential therapy. Therefore, a severe graded (30 g, 40 g and 50 g) weight-compression SCI at the Th9 spinal segment, involving an acute mechanical impact followed by 15 min of persistent compression, was studied in adult female Wistar rats. Functional parameters, such as spontaneous recovery of motor hind limb and bladder emptying function, and the presence of hematuria were evaluated within 28 days of the post-traumatic period. The disruption of the blood-spinal cord barrier, measured by extravasated Evans Blue dye, was examined 24 h after the SCI, when maximum permeability occurs. At the end of the survival period, the degradation of gray and white matter associated with the formation of cystic cavities, and quantitative changes of glial structural proteins, such as GFAP, and integral components of axonal architecture, such as neurofilaments and myelin basic protein, were evaluated in the lesioned area of the spinal cord. Based on these functional and histological parameters, and taking the animal’s welfare into account, the 40 g weight can be considered as an upper limit for severe traumatic injury in this compression model.


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