Acute Myelopathy Research Articles

Ectatic vertebral artery associated medullary compression treated with microvascular decompression: a case report and review of literature

BackgroundVertebral artery compression syndrome is a rare condition defined as the clinical presentation of dizziness, vertigo, ataxia, dysarthria, dysphagia, progressive or acute paralysis, hemisensory loss, and cervical myelopathy secondary to compression of the medulla and upper spinal cord by the vertebral artery.Case descriptionHere we describe a 57-year-old Mexican–American male with bulbar symptoms, positional vertigo, and diplopia. The patient’s symptoms were managed through microsurgical decompression of the medulla utilizing a far lateral transcondylar approach. The patient reported clinical improvement on follow-up.ConclusionThis case underscores the clinical complexity and heterogeneity of this rare neurovascular pathology and the importance of elucidating the pathophysiological mechanisms underlying the symptomatic presentation of vertebral artery compression syndrome.

Neuroimaging feature in identifying acute myelopathy etiologies: comparison between neuromyelitis optica spectrum disorder and cervical spondylotic myelopathy

ObjectiveThe clinical symptoms of neuromyelitis optica spectrum disorder (NMOSD) and acute cervical spondylotic myelopathy (CSM) may overlap in some cases. This study aimed to investigate the differences in imaging features between NMOSD and CSM in acute myelopathy.MethodsWe included 78 patients in this retrospective study, including 28 NMOSD patients and 50 CSM patients. The demographic characteristics and clinical symptoms of the two groups of patients were compared. The T1 signal intensity, length of the spinal cord involved by T2 hyperintensity, degree of intervertebral disc degeneration, proportion of thoracic and lumbar cord involvement, proportion of brain involvement and lesion enhancement rate in magnetic resonance imaging (MRI) were compared between the two groups of patients. The number, length, location on the sagittal image, pattern on the sagittal image, and distribution on the axial image of the lesions in the contrast-enhanced MRI of the two groups were evaluated.ResultsThere were differences between NMOSD and CSM patients in the proportion of women, the proportion of bowel and bladder symptoms, mRS levels, the length of the spinal cord involved by T2 hyperintensity, degree of intervertebral disc degeneration, the proportion of thoracic and lumbar cord involvement, the proportion of brain involvement, the enhancement rate and number of lesions (p < 0.05). Among NMOSD patients, linear, patchy and ring or semi-ring enhancement were present in 8(30.8%) ,14 (53.8%) and 4(15.4%)patients, respectively, and axial gray and white matter were involved in 17 (65.4%) patients. Among patients with CSM, 9(36.0%) patients showed longitudinal oriented flake, 16 (64.0%) patients showed pancake-like enhancement, and 21 (84.0%) patients showed axial white matter involvement only. The differences in enhancement pattern on sagittal images and axial involvement were statistically significant (p < 0.05).ConclusionsEarly differential diagnosis of NMOSD and CSM in acute myelopathy can be made by analyzing images and the number, length, sagittal enhancement pattern, and axial involvement of gadolinium-enhanced lesions.

Clinical presentation, imaging characteristics, and short-term outcome of eight cats presented with suspected traumatic atlantoaxial hyperflexion.

Traumatic atlantoaxial hyperflexion is considered rare in cats, and only a few case reports have been published. There are other conditions that can result in a peracute onset of neurological signs localized to the cervical spinal cord segments, including acute noncompressive nucleus pulposus extrusion, ischemic myelopathy, or vertebral fractures. Appropriate treatment for these conditions can only be initiated after an accurate diagnosis has been obtained. The aim of this observational, retrospective, single-center, descriptive case series study was to describe the clinical presentation, imaging characteristics, and short-term outcome of eight cats presented with suspected traumatic atlantoaxial hyperflexion. Young male healthy domestic shorthair cats were overrepresented (7/8) and typically presented with a peracute, nonprogressive, nonpainful, nonlateralizing C1-C5 myelopathy (tetraplegia or nonambulatory tetraparesis) following a road traffic accident or head trauma. All MRI studies demonstrated a solitary, focal, ill-defined intramedullary lesion immediately dorsal to the dens of the axis, affecting both grey and white matter. All cats were treated medically. In 50% of the cats, the neurological grade improved at discharge or short-term follow-up, 25% of the cats recovered completely, one cat was static at short-term follow-up, and one cat was euthanized due to persistent forebrain signs and lack of neurological improvement.

Spinal arteriovenous fistula leading to acute paraplegia after a lumbar nerve root block: Successful embolization with complete neurological recovery-a case report.

Spinal arteriovenous fistulas (SAVFs) are the most common type of vascular malformation of the spine in adult patients. They can lead to acute or progressive myelopathy due to venous congestion of the medullary veins. While most SAVFs are acquired, their pathophysiology remains unclear. The natural history of the disease and its clinical presentation are highly influenced by the location of the fistula and various factors may trigger sudden neurological decline. We present a case of a patient who developed a complete spinal cord injury after a lumbar nerve root block, likely due to an undiagnosed SAVF. The patient underwent endovascular embolization, resulting in a complete recovery of neurological function.

Role of digital subtraction angiography in acute cervical spinal cord ischemia.

Ascertaining the etiology of cervical spinal cord dysfunction presents a challenge to clinicians, as the list of differential diagnoses is extensive. Although compressive and inflammatory disorders are common and should be considered immediately, vascular causes are similarly important and acute. The overlap of clinical, magnetic resonance imaging, and cerebrospinal fluid features among the causes of myelopathies may lead to erroneous diagnoses. Such errors may be compounded if routine vascular imaging does not reveal the underlying vasculopathy. We present here three cases in which computed tomography angiography and magnetic resonance angiogram could not clarify the nature of an acute myelopathy, whereas digital subtraction angiography established the diagnosis of spinal cord ischemia.

Clinical, magnetic resonance imaging and computed tomography imaging findings in a young cat with epidural pyogranulomatous steatitis

AbstractA 4‐month‐old male domestic shorthair cat with a 36‐h history of acute and progressive painful paraplegia was referred. The neurological examination was consistent with T3‒L3 myelopathy. Magnetic resonance imaging of the thoracolumbar region revealed an extradural mass at the level of T12‒T13 that caused moderate spinal cord compression. The cat underwent T12‒T13 dorsal laminectomy decompressive surgery, and its neurological signs improved shortly after surgery. A diagnosis of epidural spinal steatitis was reached based on histopathological examination of the compressive mass. To the authors’ best knowledge, this is the first description of the magnetic resonance imaging and computed tomographic findings of histopathologically confirmed idiopathic sterile pyogranulomatous inflammation of epidural fat in a cat. Epidural idiopathic sterile pyogranulomatous steatitis should be included as a possible differential diagnosis in young cats with acute and progressive T3‒L3 myelopathy signs.

Determination of the Efficiency of Magnetic Resonance Imaging in the Evaluation of Compressive Myelopathy.

Background The phrase "compressive myelopathy" refers to compression of the spinal cord, either internally or externally. This compression might arise from various sources such as a herniated disc, post-traumatic compression, and epidural abscess as well as epidural or intradural neoplasms. Magnetic resonance imaging (MRI)plays a crucial role in differentiating between compressive and non-compressive myelopathy. After eliminating compressive lesions, attention is directed toward intrinsic cord-related causes of acute myelopathy including vascular, infectious, and inflammatory pathologies. Aims The study aimed to assess different etiologies of compressive myelopathy, analyze the MRI features of spinal cord compressive lesions, classify the lesions depending on site, and correlate MRI findings with intraoperative findings and histopathology in operated cases. Material &methods A total of 50 patients, who exhibited clinical symptoms indicative of compressive myelopathy sent to the Radiology department, Rangaraya Medical College (RMC), Kakinada for MRI spine were included in the study. It's an observational cross-sectional study. Statistical Package for Social Sciences (SPSS) version 22.0 (IBM Corp., Armonk, USA) was used for statistical calculations. Result Among the 50 cases of compressive myelopathy, the etiologiesare distributed as follows: trauma (22 cases), infection (12 cases), primary neoplasm (eight cases), and secondary neoplasm (eight cases); extradural compressive lesions (84%)and Intradural-extramedullary lesions (16%). Conclusion Utilizing MRI successfully assessed the spinal cord integrity and characterized spinal tumors. Consequently, the study concludes that MRI is a highly definitive, sensitive, and accurate tool for evaluating compressive myelopathy.

Thoracic root-related intradural extramedullary cavernoma presenting with subarachnoid hemorrhage: illustrative case.

Just 5% of all cavernomas are located in the spine. Thoracic root-related subtypes are the rarest, with a total of 14 cases reported in the literature to date. Among them, only 4 presented with subarachnoid hemorrhage (SAH). A 65-year-old female presented after an ictus of headache with no neurological deficits. Computed tomography (CT) demonstrated sulcal SAH, with the remainder of the workup nondiagnostic for etiology. Three weeks later, she re-presented with acute thoracic back pain and thoracic myelopathy. CT and magnetic resonance imaging suggested dubiously a T9-10 disc herniation with spinal cord compression. Surgical decompression and resection were then planned. Intraoperative ultrasound (IUS) demonstrated an intradural extramedullary lesion, confirmed to be cavernoma. Complete resection was achieved, and the patient was discharged a few days postoperatively to inpatient rehabilitation. Although spine imaging is deemed to be low yield in the evaluation of cryptogenic SAH, algorithms can be revisited even in the absence of spine-related symptoms. Surgeons can be prepared to change the initial surgical plan, especially when preoperative imaging is unclear. IUS is a powerful tool to assess the thecal sac after its exposure and to help guide this decision, as in this rare entity.

Outcome of the Use of Clinical Reasoning Alone in Dogs with Acute Thoracolumbar Myelopathy and/or Pain.

Acute thoracolumbar myelopathy is a common neurological presentation in dogs. Although certain spinal conditions present with characteristic clinical pictures, managing such cases with clinical reasoning alone (i.e., without cross-sectional imaging) has never been explored. The aim of this study was to define the outcome of patients with suspected intervertebral disc extrusion (IVDE), ischaemic myelopathy (IM) or acute non-compressive nucleus pulposus extrusion (ANNPE) that were managed with clinical reasoning alone. The database of the Queen's Veterinary School Hospital (Cambridge) was searched for paraparetic or paraplegic dogs with suspected IVDE or IM/ANNPE that were initially managed medically without undergoing imaging. Clinical presentation and outcome were recorded. If cross-sectional imaging was subsequently performed, information about the final diagnosis was collected and compared with the initially suspected diagnosis. A total of 123 IVDE cases were collected: 81% had a successful outcome with no imaging performed; 16% had IVDE confirmed with imaging and successful outcome with surgery or medical management; and just 3% were found to have an alternative diagnosis or were euthanised without imaging. A total of 16 IM/ANNPE cases were collected: 94% had a successful outcome, and one dog was euthanised. Successful outcomes can be obtained by using clinical reasoning alone in most dogs with suspected IVDE or IM/ANNPE.

A rare presentation of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) as acute hemorrhagic longitudinally extensive transverse myelitis

BackgroundMyelin oligodendrocyte glycoprotein antibody-associated disease is usually associated with optic neuritis, acute disseminated encephalomyelitis or transverse myelitis. We are presenting a rare case report wherein myelin oligodendrocyte glycoprotein antibody seropositivity was associated with hemorrhagic longitudinally extensive transverse myelitis. To our knowledge, no such cases were found to be published.Case presentationA 15-year-old female came with complaints of sudden onset paraparesis. MRI was performed within 48 h from the episode of paraparesis, which revealed a long-segment, intramedullary, expansile and heterogeneously enhancing spinal cord lesion extending from T1 vertebral level up to conus medullaris. Few foci of blooming were also noted within the spinal cord on gradient sequences. Laboratory evaluation of cerebrospinal fluid analysis revealed no significant abnormality. Neuromyelitis optica antibodies were negative, and myelin oligodendrocyte glycoprotein antibodies (MOG) showed seropositivity. The patient was started on methylprednisolone and plasmapheresis for the same after which the patient gradually improved and regained her ability to walk. Follow-up MRI was performed after 4 weeks, which revealed significant reduction in the extent of the intramedullary lesion described earlier.ConclusionsHemorrhagic longitudinally extensive transverse myelitis without any involvement of optic nerves and brain may show MOG seropositivity, and it should be considered as one of the differential diagnosis in acute myelopathy.

Abstract 087: Cocaine‐Induced Acute Spinal Cord Ischemia Syndrome

Introduction Acute spinal cord ischemia syndrome (ASCIS) is a rare disease that is thought to comprise roughly only 1.2% of all strokes [1, 2]. These strokes primarily occur in the anterior spinal cord artery (ASA) and/or the posterior spinal cord artery (PCA) territory and can have widely variable clinical presentation. The use of recreational cocaine in young adults is well known to be responsible for acute ischemic and hemorrhagic strokes in individuals who lack other vascular risk factors. What is significantly rarer with few reported cases, however, is cocaine‐related ASCIS as the etiology of non‐traumatic acute spinal cord myelopathy [3‐7]. Methods N/A Results A 40‐year‐old female with a history of type I Diabetes mellitus, bipolar disorder, and polysubstance abuse presented with acute‐onset bilateral lower limb weakness, sensory loss, neck pain, and bladder incontinence. On admission, she reported using intravenous crack cocaine in the evening before admission and experiencing a fall in the bathroom a few hours after. She was unable to move her lower limbs following this fall. On examination, there was flaccid weakness in both lower extremities with decreased pinprick sensation below the T4 level and absent sensation below the thighs on both sides. She had no trauma preceding her symptoms and denied any recent vaccinations or travel history. An urgent CT (computed tomography) scan of the cervical, thoracic, and lumbar spine ruled out any obvious traumatic injury. Her urine drug screen was positive for cocaine, opiate, cannabinoid, and benzodiazepine. MRI (Magnetic Resonance Imaging) of the brain without contrast was unremarkable. MRI of the spine with contrast demonstrated two areas of T2 hyperintensities from C5‐C6 and T4 to the conus with cord expansion. The lesion in the thoracic spinal cord showed contrast enhancement and spared the dorsal column. Lumbar puncture was traumatic and showed elevated protein (&gt;300 mg/dl) as well as elevated glucose (186 mg/dl). CSF studies, including meningitis/encephalitis panel, gram stain and culture, flow cytometry, cytology, and oligoclonal bands were negative. Serum autoimmune myelopathy panel, serum Aquaporin‐4 antibodies and MOG (Myelin Oligodendrocyte Glycoprotein) antibodies were negative. The other etiologies of non‐traumatic myelopathy, including HIV, Treponema pallidum, and HTLV‐I/II antibodies, were negative. A diagnostic spinal angiogram was completed with no evidence of arteriovenous fistula or aortic dissection. She completed five days of plasma exchange without any improvement and was transferred to an acute rehabilitation facility. At four months follow‐up, she continues to be flaccid in her lower limbs and requires a urinary catheter leading to frequent urinary tract infections. Conclusion While cocaine‐related cerebrovascular events are well documented, very few cases of cocaine‐related ASCIS have been described. The mechanism is thought to be multifactorial due vasospasm, cerebral vasculitis, vascular thrombosis, cardioembolism from cocaine‐induced myocardial infarction or cardiomyopathy, and hypertensive surges [9]. Due to the scarcity of these events, the patient outcomes are unclear. Other studies on outcomes of spinal cord ischemia have shown that ASIA Impairment Scale (AIS) score, lesion level, and patient age were the strongest predictors of neurologic and functional outcomes, whereas etiology of the ischemia had no effect on outcomes [10].

Student Competition (Knowledge Generation) ID 1984525

Background Drug-induced myelopathy has been reported widely for heroin use, but less frequently for amphetamines or fentanyl. Hyperglycemia-induced acute myelopathy has not previously been described. Methods We present a case of toxic/metabolic myelopathy secondary to the aforementioned results in a patient presenting for tertiary inpatient rehabilitation. Results A 28-year-old man with Type 1 Diabetes without complications and polysubstance use (fentanyl and crystal methamphetamine) presented to hospital with quadriparesis and anesthesia. Patient reported he fell down a flight of stairs while using substances and remained on the ground for hours-days as he was acutely paralyzed when he awoke. Initial examination demonstrated a C5 motor level. Pan-CT demonstrated no intracranial or spinous abnormalities. MRI with gadolinium showed cord edema from C1-T4 and patchy enhancement from C4-C7 without cord compression. Diffusion restriction and hemorrhagic transformation were later seen in C4-C7. Initial blood glucose was 66 with no serum ketones. Serum toxicology was negative and urine toxicology was positive for amphetamines and fentanyl. Autoimmune and infectious workups were negative. He received 5 days of pulse steroids and 7 sessions of plasmapheresis with minimal functional or neurological improvement. He was admitted to rehabilitation as a C5 AIS-B and did not exhibit further improvement in motor or sensory function over 3 months of active inpatient rehab. Conclusions Given the pattern of cord enhancement with hemorrhagic transformation, this injury most likely represents acute myelitis induced by hyperglycemia and amphetamines/fentanyl. To our knowledge, this is the first case report where hyperglycemia may have contributed to acute myelopathy.

Outcomes in Dogs with Multiple Sites of Cervical Intervertebral Disc Disease Treated with Single Ventral Slot Decompression.

In dogs with acute myelopathy but showing multiple sites of spinal compression from intervertebral disc disease (IVDD) on imaging, one approach is surgical decompression of the single acute disc extrusion while ignoring other previously extruded or protruded discs. However, little is known regarding the outcomes of this approach. This study described the outcomes and investigated prognostic factors in 40 dogs with multiple sites of cervical disc extrusion or protrusion on MRI who underwent ventral slot decompression for the single acute disc. The overall recovery rate was 97.5%. The median recovery time was seven days. The number of affected discs (including disc extrusion and protrusion) and the presence and number of the affected discs causing severe spinal compression did not influence the 30-day outcome. Compared with 23 dogs with single disc extrusion treated surgically, the recovery time and outcomes were similar between the two groups. The total number of affected discs was not associated with recovery time or outcomes. In conclusion, if an acute disc could be identified, ventral slot decompression targeting the single acute disc is a viable management approach for dogs with an acute presentation but diagnosed with multiple sites of spinal cord compression from IVDD.

Van Wyk Grumbach Syndrome and Ovarian Hyperstimulation in Juvenile Primary Hypothyroidism: Lessons From a 30-Case Cohort.

Prolonged hypothyroidism in children commonly causes short stature with delayed bone maturation, and delayed puberty. However, a paradoxical occurrence of peripheral precocious puberty and pituitary enlargement in chronically untreated juvenile hypothyroidism was first reported by Van Wyk and Grumbach in 1960. To create increased awareness and a better understanding of this clinical entity among emergency room physicians, pediatricians, surgeons, gynecologists and oncologists. Case records of children diagnosed with Van Wyk-Grumbach syndrome (VWGS) were analyzed retrospectively. Twenty-six girls and 4 boys were identified (2005-2020). All had profound primary hypothyroidism (total thyroxine [T4]: 2.5-33.5 nmol/L, thyrotropin: > 75-3744μIU/mL). Hypothyroidism was not the referral diagnosis in any of the girls. Among them, 17 were referred for precocious puberty, 5 with a diagnosis of pituitary tumor on magnetic resonance imaging, and others for acute surgical abdomen in 7 girls (painful abdominal mass-2, ovarian tumor-2, ovarian torsion-2, ruptured ovarian cyst-1), acute myelopathy in 1, and menorrhagia with headache in another. All girls were successfully managed with levothyroxine replacement alone, except for the 2 with ovarian torsion, who required surgery. Menstruation ceased promptly with T4 therapy in all girls, occurring at an age-appropriate later date. All boys had testicular enlargement at presentation that regressed partially after T4treatment. Catch-up growth was remarkable during the first treatment year, but the final height was compromised in all. Increased awareness of varied presentations of VWGS is vital among pediatricians to facilitate early diagnosis and targeted investigations, and to help in the initiation of the simple yet highly rewarding T4 replacement therapy to avoid all possible complications.

A Case of Hematomyelia in a Teenager with Behcet’s Disease due to both Warfarin and Intramedullary Cavernous Malformation (P6-5.029)

<h3>Objective:</h3> Highlight the importance of recognizing bleeding of intramedullary cavernous malformation or cavernoma as a cause of spinal cord lesion. <h3>Background:</h3> Intramedullary spinal cord hemorrhage, or hematomyelia, is a rare cause of acute myelopathy. Vascular malformations, anticoagulation therapy, and other bleeding diathesis are the most common causes. Cavernoma is a vascular malformation made of closely clustered, enlarged capillaries with a single layer of endothelium and without the elements of normal vascular structure or normal intervening brain parenchyma. Although they can bleed, cavernomas have a relatively benign prognosis. Hemorrhage of an intramedullary cavernoma during anticoagulation with warfarin was not previously reported. <h3>Design/Methods:</h3> Nineteen-year-old man with Behçet’s disease taking warfarin for intraventricular thrombus and multiple pulmonary emboli complained of acute back pain, unilateral leg weakness, and urinary retention. He had no personal or family history of vascular malformations. Examination was remarkable for paraplegia, a sensory level at T10, lower limb hyporeflexia and Babinski reflex bilaterally. INR was supratherapeutic at 3.6. CT of head, cervical and thoracic spine was unremarkable. <h3>Results:</h3> MRI of spine showed an enhancing intramedullary lesion at T8–T9, 3.8 cm in length, with surrounding edema. The mixed T1 hyperintensity and T2 hypointensity was suggestive of hemorrhage caused by a cavernoma. Warfarin was reversed with prothrombin complex concentrate. He was not a candidate for neurosurgical intervention. At discharge, the patient had not regained any motor or sensory function. <h3>Conclusions:</h3> This case highlights the need to suspect hematomyelia as a cause of acute myelopathy in a patient taking anticoagulation. While anticoagulation is not contraindicated in patients with known cavernoma, there should be a low threshold for considering the presence of a bleeding intramedullary cavernoma in a patient with acute myelopathy. <b>Disclosure:</b> Dr. Sacks has nothing to disclose. Dr. Treidler has nothing to disclose.

Posterior Spinal Cord Infarct: To Make the Diagnosis, Think of the Unthinkable! (P12-5.004)

<h3>Objective:</h3> We report a case of posterior spinal artery (PSA) infarct initially misdiagnosed as transverse myelitis (TM) and highlight some of the differentiating features of this exceedingly rare entity. <h3>Background:</h3> Spinal cord infarcts (SCIs) represent 1% of strokes and 5–8% of acute myelopathy. In a systematic review of 133 cases of SCI collected over two decades, PSAs presented 11% of the total pool. Redundancy in the vascular supply of the posterior portion of the spinal cord accounts for PSA rarity. <h3>Design/Methods:</h3> A single case report. <h3>Results:</h3> A 62-year-old woman with a history of recurrent nephrolithiasis, vitamin B12 deficiency, hypertension, and hyperlipidemia presented painless and rapidly progressive severe numbness and weakness of the legs. Sphincter symptoms were absent. Enhanced Magnetic Resonance Imaging (MRI) of the brain and spinal cord were unremarkable. Cerebral spinal fluid (CSF) was unremarkable. She was diagnosed with TM, given a five-day course of intravenous (IV) steroids, and discharged to a rehabilitation facility with a protracted and incomplete recovery. She presented two years later with fluctuating sensory and motor symptoms in the context of ureteral stent removal. Repeat CSF was unremarkable. However, on repeat thoracic spine MRI, there was interval development of a T2 hyperintensity along the dorsal columns and myelomalacia from T3–T4 disc to T12. She received IV steroids with minimal improvement. She had recurrent myelopathy pseudoexacerbations in the context of concurrent illnesses subsequently. Spinal magnetic resonance angiography, computerized chest, abdomen, pelvis tomography, positron emission tomography scan, and cardiovascular investigations were unremarkable. <h3>Conclusions:</h3> Given its scarcity, PSA infarct can often go misdiagnosed. A high index of suspicion for PSA should be kept in mind, particularly in the case of 1) acute, severe, and rapidly progressive myelopathic symptoms, 2) an extensively normal CSF analysis, and 3) an initially normal MRI of the spinal cord that eventually shows some T2 hyperintensity and cord atrophy. <b>Disclosure:</b> Dr. Solis has nothing to disclose. Dr. Zabad has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Bayer. Dr. Zabad has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Biogen. Dr. Zabad has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Genentech. Dr. Zabad has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Celgene/BMS. Dr. Zabad has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Genzyme. Dr. Zabad has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Merck Serono. Dr. Zabad has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Teva Neurosciences. Dr. Zabad has received personal compensation in the range of $500-$4,999 for serving as a Consultant for TG Therapeutics. Dr. Zabad has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for Teva. Dr. Zabad has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for Novartis. Dr. Zabad has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for Genentech. Dr. Zabad has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for BMS. The institution of Dr. Zabad has received research support from Adamas. The institution of Dr. Zabad has received research support from Biogen. The institution of Dr. Zabad has received research support from Novartis. The institution of Dr. Zabad has received research support from Sun Pharma. The institution of Dr. Zabad has received research support from Parexel &amp; MedDay Pharmaceuticals.

Imaging Spectrum of HTLV-1-Related Neurologic Disease: A Pooled Series and Review.

Human T-cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy (HAM) is a well-recognized neurologic complication of HTLV-1. Beyond HAM, several other neurologic manifestations are increasingly recognized, including acute myelopathy, encephalopathy, and myositis. The clinical and imaging features of these presentations are less well understood and potentially underdiagnosed. In this study, we summarize the imaging features of HTLV-1-related neurologic disease, providing both a pictorial review and pooled series of the less well-recognized presentations. 35 cases of acute/subacute HAM and 12 cases of HTLV-1-related encephalopathy were found. In subacute HAM, cervical and upper thoracic longitudinally extensive tranverse myelitis was noted, while in HTLV-1-related encephalopathy, confluent lesions in the frontoparietal white matter and along the corticospinal tracts were the most prevalent finding. There are varied clinical and imaging presentations of HTLV-1-related neurologic disease. Recognition of these features aids early diagnosis where therapy may have the greatest benefit.

Acute Thoracic Compressive Myelopathy as a Rare Manifestation of Thalassemia: A Case Report

Acute Thoracic Compressive Myelopathy as a Rare Manifestation of Thalassemia: A Case Report

Spinal cord injuries in the absence of post-traumatic radiographic anomalies (SCIWORA): the traumatic moment between patient anterior state and efficient/concurrent causes of injury.

Spinal Cord Injury without Radiographic Abnormality (SCIWORA) represents acute traumatic myelopathy in the absence of instrumental evidence of fractures and/or dislocations of the cervical vertebrae. In this article we present 4 cases of SCIWORA that came to our observation and the medico-legal implications associated with them. In defining the compensation in the context of a private accident policy for traumatic pathologies of the spinal cord, an in-depth medical-legal assessment is essential, based on an accurate examination of the health documentation including the instrumental investigations performed, the anamnesis and an accurate evaluation of the trauma dynamic. The paraphysiological deterioration of organ-tissue structures, identifiable in the concept of "natural variability of biological risk", should be included in the same definition of insured risk by age group, with the consequence that physical conditions that fall within the physiological or paraphysiological definitions, although potentially contributing to injury, do not necessarily exclude compensation.A different concept dominates the variability of the compensation according to a paraphysiological pre-existing condition. The two arguments therefore call for thorough consideration of both the paraphysiological contributing causes of injury and/or impairment as necessarily subject to a preliminary study, which through the clinical and instrumental investigation method, will define the perimeter of functionality.

Natural history of pituitary carcinoma with metastasis to the cervical spine: illustrative case

Pituitary carcinoma is a rare tumor of the adenohypophysis with noncontiguous craniospinal dissemination and/or systemic metastases. Given the rarity of this malignancy, there is limited knowledge and consensus regarding its natural history, prognosis, and optimal treatment. The authors present the case of a 46-year-old woman initially treated with invasive prolactin-secreting pituitary macroadenoma who developed metastatic disease of the cervical spine 6 years later. The patient presented with acutely worsening compressive cervical myelopathy and required posterior cervical decompression, tumor resection, and instrumented arthrodesis for posterolateral fusion. This case underscores the importance of long-term monitoring of hormone levels and having a high clinical suspicion for metastatic disease to the spine in patients presenting with acute myelopathy or radiculopathy in the setting of previously treated invasive secreting pituitary adenoma.