Left Lower Extremity Weakness Research Articles

Adult neuromuscular choristoma, a rare peripheral nerve pathology: illustrative case.

Neuromuscular choristomas (NMCs) are rare tumors involving aberrant intercalation of muscle fibers into peripheral nerves, most commonly the sciatic nerve. Although benign, these lesions risk developing into NMCs with desmoid-type fibrosis (NMC-DTFs), aggressive lesions potentially requiring amputation. Currently, information on NMCs and the link between NMCs and NMC-DTFs is limited in adults, with the majority of cases reported in children. We present the case of a 66-year-old male with a sciatic NMC alongside a Preferred Reporting Items for Systematic Reviews and Meta-Analyses-based systematic review of similar cases to better characterize this lesion in the adult population. A male presented with 10 years of progressive left lower-extremity weakness and paresthesia, and a mildly enlarged proximal sciatic nerve was discovered on magnetic resonance imaging. He underwent left sciatic fascicular nerve biopsy, with histopathological examination identifying the lesion as an NMC. The literature review revealed that our case, alongside other cases of adults with NMCs, shared characteristics similar to NMCs in the pediatric population. More comprehensive studies of adults with NMCs are needed, as the current literature contains limited information concerning disease course, diagnostic characteristics, and treatment. Furthermore, NMCs in adults should be handled with care because of the increased likelihood of transformation to NMC-DTF after surgical intervention.

Abstract 102: Pseudo‐Internuclear Ophthalmoplegia in a Patient with an Acute Globus Pallidus Infarct: A Case Report

Introduction Internuclear ophthalmoplegia (INO) is an ocular movement disorder typically due to a lesion in the medial longitudinal fasciculus (MLF). Rarely, similar ocular movement abnormalities can be observed in the absence of an MLF lesion. This case report aims to highlight a potential association between acute globus pallidus (GP) infarct and an ocular movement abnormality resembling INO. Methods N/A Results Case Presentation: A 72‐year‐old male with a medical history significant for chronic myeloid leukemia, prostate cancer, type 2 diabetes mellitus, hypertension, prior stroke, and heart failure presented with dizziness. Examination revealed right INO, skew deviation with right hypertropia, left lower extremity weakness, left upper extremity dysmetria, right facial weakness (prior deficit), and ataxic gait. MRI of brain confirmed an acute lacunar infarct in the right globus pallidus with no apparent brainstem or cerebellar lesion. The patient was started on dual antiplatelet therapy and discharged with home rehabilitation services to improve his balance. Discussion: The patient presented with pseudo‐INO in the setting of an acute globus pallidus infarct. This case introduces the idea that ocular motor abnormalities resembling INO could occur due to a GP lesion, which was not previously reported. The basal ganglia control saccadic eye movements by means of their connection to the superior colliculus (SC). GP was shown to have a role in this connection which may provide a plausible explanation for this observation. Another possible explanation can be based on the concept of diaschisis, where a lesion in a specific area of the brain (GP in this case) can lead to deficits or impairments in various functions associated with that region (the SC and its pathway for controlling saccadic eye movement). Conclusion This case emphasizes that slow adducting saccades and associated nystagmus is not always INO.

Embolic Stroke Following Intravenous Ozone Therapy (P2-5.007)

<h3>Objective:</h3> NA <h3>Background:</h3> Ozone therapy via autohemotherapy has become among the alternative therapies purported to treat chronic lymphocytic leukemia. Ozone gas is injected into blood drawn from the patient, which is mixed then transfused back intravenously. Due to the infrequent use of this modality, it has not been previously reported as a risk factor for stroke. <h3>Design/Methods:</h3> A 62-year-old man with a history of chronic lymphocytic leukemia, chronic migraines, hypertension, and diabetes mellitus type II presented with acute left arm numbness followed by weakness during administration of intravenous (IV) ozone. Shortly after, he developed a migrainous headache, which is typical for him. Neurological examination revealed left upper and lower extremity weakness. CT head and CT angiography were performed and were unremarkable. The patient was treated with IV tPA. He continued to have left-sided weakness and numbness along with a migrainous headache after the intervention. MRI of the brain revealed multiple bilateral frontal and parietal infarcts. Dual antiplatelet therapy was initiated. Echocardiogram revealed a large patent foramen ovale (PFO) with a right-to-left shunt. A transcranial doppler with bubble study revealed multiple high intensity transient signals post valsalva maneuvers, supporting the diagnosis of paradoxical emboli. Patient eventually underwent successful outpatient PFO closure without complications. <h3>Results:</h3> NA <h3>Conclusions:</h3> This case presents a rare cause of stroke following IV injection of ozone. Acute stroke following ozone therapy has not been previously reported in the literature. The pathogenesis remains unknown, although it is theorized that it may have been due to IV administration of ozone-mixed blood in the presence of a PFO. It is imperative to recognize this phenomenon as a potential risk of embolic stroke in patients receiving IV ozone treatment. <b>Disclosure:</b> Dr. Kokash has nothing to disclose. Dr. Zahra has nothing to disclose. Dr. Singh has nothing to disclose. Dr. Yacoub has nothing to disclose. Dr. Leary has received personal compensation in the range of $5,000-$9,999 for serving as a Consultant for Boston Clinical Research Institute. Dr. Leary has received personal compensation in the range of $10,000-$49,999 for serving as a Consultant for Baim Clinical Research Institute. Dr. Leary has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Syneos Health. Dr. Leary has received publishing royalties from a publication relating to health care.

A Case of Progressive Left Leg Weakness and Vision Changes: Focal Inflammatory Cerebral Amyloid Angiopathy Masquerading as a Glioma (P12-5.003)

<h3>Objective:</h3> To emphasize the need to consider tumefactive focal inflammatory cerebral amyloid angiopathy (CAA) in the differential diagnosis of CNS lesions. <h3>Background:</h3> Although classically considered an etiology of cognitive impairment in the elderly, CAA represents a spectrum of disease. CAA-related inflammation (CAA-ri), a distinct CAA phenotype, is characterized by vascular inflammation from amyloid deposition. CAA-ri may rarely appear as a tumefactive lesion, mimicking CNS malignancy. We present a case of biopsy-proven focal CAA-ri initially misidentified as a glioma, with the goal of increasing awareness of this entity. <h3>Design/Methods:</h3> Not applicable <h3>Results:</h3> A 68-year-old man with Parkinson’s disease presented with progressive left lower extremity weakness, word finding difficulty and vision changes. Neurological examination revealed Parkinsonian features, left homonymous superior quadrantanopia and left leg weakness. Brain MRI revealed a non-enhancing FLAIR hyperintensity in the subcortical right parieto-occipital lobe, with numerous susceptibility-weighted foci within this area, consistent with microhemorrhages versus vascular inflammation. Flash frozen pathology was initially suggestive of glioma, prompting lesionectomy. Final pathology revealed inflammation of small and medium sized blood vessels, multinucleated giant cells and positive Congo-red staining, consistent with necrotizing vasculitis and amyloid angiopathy. Treatment with steroids was deferred following risk-benefit analysis. <h3>Conclusions:</h3> We report a unique case of tumefactive CAA-ri, a clinicopathologic variant of CAA, manifesting as a mass-like lesion with distinguishing radiographic features. Our literature review identified only three prior reports of this entity. Clinical presentation depends on lesion size, location, and presence of edema and inflammation. While our patient lacked systemic co-pathologies, uterine involvement and carpal tunnel syndrome have been reported. Management relies on vascular risk modification, and steroids or immunosuppressants for active inflammation. Our case underscores the need to recognize CAA-ri in the differential of mass-like lesions. Recognizing the spectrum of CAA-related disease is key in understanding the natural history of the disease, and potential benefit of future anti-amyloid therapies. <b>Disclosure:</b> Dr. Mohammadi has nothing to disclose. Dr. Lilian has nothing to disclose. Mr. Chen has received research support from National Institues of Health. Michelle Offit, MS has nothing to disclose. Dr. Lin has nothing to disclose. Dr. Streicher has nothing to disclose. Dr. Sabharwal has nothing to disclose.

Transverse myelitis following bivalent COVID‐19 booster vaccine and quadrivalent seasonal influenza vaccine

Transverse myelitis following bivalent <scp>COVID</scp>‐19 booster vaccine and quadrivalent seasonal influenza vaccine

Calcium pyrophosphate deposition disease mimicking spinal neuroarthropathy.

A 75-year-old male with degenerative joint disease status-post T12-L5 fusion five years ago presented with new-onset left lower extremity weakness. He denied any sensory abnormalities, saddle anaesthesia, or dysfunction of the bladder or bowels. Physical examination was notable for 2/5 left quadriceps and gastrocnemius strength, compared with 5/5 on the right side. CT scan shows erosion and sclerosis of the T10 and T11 end plates with gas within the disk space, consistent with Charcot spinal neuroarthropathy (Fig. 1A). Due to the persistent neurological deficits, the epidural mass was resected and a dural patch graft was placed. Histopathology revealed fibrocartilaginous tissue fragments with degenerative changes and deposition of positively birefringent crystals consistent with calcium pyrophosphate deposition disease (CPPD) (Fig. 1B). One month after resection, the patient’s lower extremity weakness had fully resolved. CPPD can mimic many joint pathologies, including gout and osteoarthritis, in atypical locations. In this case, the radiographic appearance of destruction, debris, distention, disorganization, and density changes resembled Charcot neuroarthropathy but in an unexpected location without the typical antecedent sensory neuropathy [1]. This case illustrates that, when radiographic evidence seems to contradict clinical signs and symptoms of joint disease, clinicians should reserve a high index of suspicion for CPPD [2]. Informed consent has been obtained.

1033. Management of Disseminated Nocardiosis in an Immunocompromised Patient Using Multi-Drug Therapy

Abstract Background Nocardiosis may cause fatal infections in immunocompromised and immunocompetent patients. While there are many different species, Nocardia farcinica, has been a clinically important cause but less frequently identified species. We present a case of an immunocompromised patient successfully treated with a multi-drug regimen for disseminated nocardiosis due to Nocardia farcinica. Methods The patient is a 65-year-old male with a history of Autoimmune Hemolytic Anemia (AIHA) who presented with fevers, chills, symptomatic anemia, and new left lower extremity weakness associated with spasms over several days prior to arrival. Results 6 months prior, he had received treatment for AIHA with rituximab, cyclophosphamide, and high dose corticosteroids. Head CT revealed a 1.5cm right posterior frontal lobe mass with surrounding edema. CT thorax revealed innumerable spiculated pulmonary nodules and masses bilaterally. Lung biopsy as well as blood culture were positive for Nocardia farcinica, specimen was sent to reference laboratory for susceptibility testing. He was initially treated with imipenem and IV Bactrim. Subsequently, clinical exam findings were unchanged and repeat MRI brain showed enlarging frontal mass. Linezolid and IV amikacin were added to the regimen based on susceptibility results. Patient was discharged home but returned to hospital shortly after discharge with severe hemolytic anemia, suspected to be due to Bactrim administration. The patient was later discharged home on Imipenem, IV amikacin, oral Linezolid, and oral Moxifloxacin in stable condition without surgical intervention and with improved left lower extremity weakness. Conclusion Disseminated Nocardiosis is known to cause fatal pulmonary and CNS infections in immunocompromised patients and requires aggressive therapy usually with multiple antibiotics. Nocardia farcinica infections are particularly clinically complex given the organism’s multiple inherent resistance mechanisms, interpretation of in vitro susceptibility testing, and possible adverse effect profile of treatment regimen. Disclosures All Authors: No reported disclosures.

394: A CASE OF EXTENSIVE NECROTIZING FASCIITIS DUE TO STRING TEST-NEGATIVE KLEBSIELLA PNEUMONIAE

Introduction: Monomicrobial Klebsiella pneumoniae necrotizing fasciitis is rare in North America. The strain that causes necrotizing fasciitis is thought to be hypermucoviscous or hypervirulent K. pneumoniae (hvKP). hvKP is responsible for increasing numbers of cases within the US due to the prevalence of travel and immigration. Description: A 57-year-old Caucasian female with diabetes and history of IV drug use presented to the emergency room with 3 days of left calf pain. Venous doppler was negative for DVT. She was discharged home with medication for musculoskeletal pain. Eleven days later, she returned with worsening left lower extremity pain, edema, and weakness. Physical exam revealed left lower extremity tenderness to palpation and crepitus with scars from drug injections. The laboratory risk indicator for necrotizing fasciitis (LRINEC) score was 9, indicating high suspicion for necrotizing fasciitis. X-ray of the tibia-fibula and femur revealed subcutaneous gas. Broad spectrum antibiotics were initiated, and the patient underwent emergent surgical debridement. Despite aggressive surgical intervention, she continued to worsen with increasing vasopressor requirements due to septic shock. Imaging of the abdomen and pelvis showed extension of the necrotizing fasciitis. Gas was identified within a complex left perirenal abscess, the epidural space and intervertebral disc space of the lower lumbar spine and sacrum, as well as within the urinary bladder. The patient returned to the operating room for further debridement. Wound, blood, and urine cultures yielded Klebsiella pneumoniae and the lab was directed to perform a string test, which was negative. On hospital day two, she had worsening multiorgan failure, and the family elected to withdraw care. Discussion: hvKP with a negative string test is a unique phenotype that is not well described in the literature. Usually, hvKP is identified by a string test and rarely genotyping. Most cases involve patients of Asian descent or recent travel to Asia. As this patient was Caucasian with no recent travel, we suspect that she contracted the organism through IV drug use. The unique aspects of this case may help us understand this new emerging strain in the US.

Crizanlizumab Use in Recurrent Neurologic Symptoms Attributed to Sickle Cell Disease Induced Moyamoya Syndrome

Sickle cell disease (SCD) is a genetic disorder that affects about 100,000 Americans and carries the risk of significant complications including ischemic stroke. Moyamoya syndrome (MMS), a complication of SCD, is characterized by progressive stenosis of carotid arteries leading to ischemic stroke (Dobson, et al). To reduce these complications, the mainstay of treatment of SCD, until recently, has been transfusion and hydroxyurea. In 2019, the FDA approved the monoclonal antibody crizanlizumab. Crizanlizumab binds and blocks p-selectin to prevent downstream cell to cell interactions, including platelet aggregation, thereby improving blood flow and preventing vaso-occlusion (Ataga, et al). We report a case of a sickle cell patient with recurrent neurological symptoms and MRI findings of MMS that unexpectedly resolved with crizanlizumab treatment. A 26 year old woman with history of vitamin B12 deficiency, HbSS disease complicated by silent cerebral infarct in childhood treated with hydroxyurea and red blood cell (RBC) exchange presented to the hospital with left lower extremity weakness. She reported that her sickle cell crisis typically manifested with left sided weakness rather than pain. Her most recent RBC exchange six days prior had revealed a hemoglobin S level of 11.8%. Her initial workup including MRI brain demonstrated right parietal encephalomalacia and evidence of chronic ischemic change of the right frontal and parietal lobes consistent with previously known silent ischemia of the right middle cerebral artery (MCA). There was no evidence of acute stroke. The patient continued monthly RBC exchange, maintaining a hemoglobin S level less than 36% and continued to experience symptoms of intermittent weakness, typically of the left lower extremity, but also at times involving the bilateral lower extremities and left upper extremity. Repeat MRI brain did not demonstrate any additional acute infarctions. However brain MRA did reveal bilateral stenosis of the MCA arteries and high-grade stenosis of the M1 segment and considered stable from previous MRI, consistent with MMS. Her symptoms continued intermittently and additional evaluation including MRI cervical, thoracic, and lumbar spine was unrevealing. Of note, at one point laboratory evaluation demonstrated a vitamin B12 level of 248 pg/mL, however her symptoms continued in spite of adequate repletion. Approximately 21 months following her initial presentation, the SARS-CoV-2 pandemic began, resulting in limited access to hospital facilities including RBC exchange. Consequently the patient was started on crizanlizumab with intermittent simple transfusion for hemoglobin less than 8 g/dL in an effort to see if this therapeutic measure would alleviate her symptoms. Interestingly, after initiating crizanlizumab, even without continued RBC exchange and a hemoglobin S level of 83%, she had no further episodes of weakness until, due to insurance issues, her crizanlizmab was delayed. Subsequently her symptoms of weakness returned requiring hospital admission. Repeat workup including both MRI and MRA brain were negative for acute ischemia and again consistent with MMS. Resumption of crizanlizumab again alleviated symptoms until infusion was delayed again for insurance reasons. She was readmitted and repeat MRI and MRA of the brain again did not show acute ischemia. Given recurrent issues with insurance and easing of the SARS-CoV-2 pandemic restrictions she was resumed on both red-cell exchange followed by crizanlizumab and continues to do well to this day. SCD carries significant potential neurological morbidity and mortality. SCD patients experience a significantly higher risk of stroke due to repeated vaso-occlusive events leading to cerebral ischemia and the development of MMS. This is the first case we are aware of in which a patient with sickle cell disease and MMS and worsening neurologic symptoms but without acute stroke was successfully was treated with crizanlizumab after failure of RBC exchange. Crizanlizumab targets P-selectin which is implicated in increased platelet aggregation in sickle cell disease. It is possible that crizanlizumab improved the patient's symptoms by reducing the risk of transient cerebral ischemia associated with her underlying abnormal vasculature, which was suspected due to acute cerebral vaso-occlusion secondary to sickle cell disease induced moyamoya syndrome.

Radiographic presentation of a multi-compartmental atypical giant lipoma of the lower extremity

A 61-year-old female with no significant past medical history presented with painless progressive left lower extremity weakness and foot drop resulting in altered gait over the course of two years prior to seeking care. Examination revealed a hypertrophied left lower extremity, steppage gait, and 1 out of 5 strength with left ankle dorsiflexion. Initial x-ray of the affected ankle was unremarkable.

LEFT ATRIAL SEPTAL POUCH IN A PATIENT WITH RECURRENT STROKE

LEFT ATRIAL SEPTAL POUCH IN A PATIENT WITH RECURRENT STROKE

ID:16177 Dorsal Root Ganglion Stimulation for Treatment of CPRS After Failed Spinal Cord Stimulation

Patient is a female with complaints of left foot/ankle pain. She suffered a MVA several years ago and has had multiple foot surgeries since then. Pain is constant, throbbing, and aching in nature. She endorsed paraesthesias as well. Pain was worse with prolonged standing and cold weather. She also endorsed some left lower extremity weakness and numbness. Her history and symptoms were consistent with CRPS. She had been on Fentanyl 50mcg patch and oxycodone 10mg with some pain relief. She continued to have pain despite medications (TCA, SNRI, opioids), physical therapy, massage therapy, acupuncture, steroid injections, SNB all with minimal relief.

Atypical Multiple Sclerosis Presenting as Bilateral Optic Neuritis

Purpose: We report a case of multiple sclerosis with bilateral optic neuritis that was atypical in terms of both the clinical signs and symptoms.Case summary: A 34-year-old female visited the department of neurology with a complaint of sudden-onset, left lower extremity weakness and numbness that had developed 3 weeks prior, and bilateral blurred vision that had commenced 2 weeks prior. The patient was diagnosed with multiple sclerosis and prescribed high-dose intravenous methylprednisolone for 3 days, but the blurred vision did not improve. The patient was referred to the ophthalmology department. The initial best-corrected visual acuity was 0.04 in both eyes, and the relative afferent pupillary defect test was positive for the left eye. The Ishihara color test scores were 1/17 for both eyes. No optic disc swelling was evident on fundus examination. Brain and spine magnetic resonance imaging (T2-weighted) performed during the initial visit revealed lesions of high signal intensity in the frontal, subcortical white matter; the optic chiasm; the left retrobulbar optic segment; the medulla; and the spinal C2-5 processes. Aquaproin-4 immunogloblin G antibody (AQP4-IgG Ab) was not detected in serum. One month after prescription of the oral steroid, the vision improved to 1.0 in the right and 0.8 in the left eye. The patient was lost to follow-up after prescription of interferon-beta for 4 years, without recurrence.Conclusions: Binocular optic neuritis accompanied by severe visual loss is a rare form of multiple sclerosis. A thorough diagnosis (with a focus on exclusion) is required, as is appropriate treatment.

Sleep apnea and unilateral upper and lower extremity allodynia as a result of a large thoracic disc herniation: a case report

BackgroundClinically significant disc herniations in the thoracic spine are rare accounting for approximately 1% of all disc herniations. In patients with significant spinal cord compression, presenting symptoms typically include ambulatory dysfunction, lower extremity weakness, lower extremity sensory changes, as well as bowl, bladder, or sexual dysfunction. Thoracic disc herniations can also present with thoracic radiculopathy including midback pain and radiating pain wrapping around the chest or abdomen. The association between thoracic disc herniation with cord compression and sleep apnea is not well described.Case presentationThe following is a case of a young male patient with high grade spinal cord compression at T7-8, as a result of a large thoracic disc herniation. The patient presented with complaints of upper and lower extremity unilateral allodynia and sleep apnea. Diagnosis was only made once the patient manifested more common symptoms of thoracic stenosis including left lower extremity weakness and sexual dysfunction. Following decompression and fusion the patient’s allodynia and sleep apnea quickly resolved.ConclusionsThoracic disc herniations can present atypically with sleep apnea. We recommend taking into consideration that sleep symptoms may resolve when planning treatment for thoracic disc herniation.

Non-penetrating traumatic psoas muscle hematoma presenting with gross hematuria: a case report

Psoas muscle hematoma is defined as a spontaneous or traumatic retroperitoneal collection of blood involving the psoas muscle. Early symptoms of an iliopsoas hematoma include lower abdominal or severe groin pain. Although psoas hematoma is a known complication of coagulopathy, psoas hematoma caused by non-penetrating trauma is the subject of only scattered reports and its significance has not been well described in the literature, so the aim of this study was to report a case of blunt traumatic psoas hematoma with the fracture of vertebral transverse process with the presentation of gross hematuria. A 65-year-old Iranian man slipped backward to the ground, and the patient complaint of gross hematuria and difficulty in walking. There was severe left costo-vertebral angle (CVA) tenderness, and mild groin tenderness, and the lower back area was painful, and he had some pain with the flexion of the vertebral column, and there was tenderness on lumbar spine, but there was no tingling, paresthesia, and weakness in left lower extremity. Hip flexion was 3/5 in the left lower. We used some diagnostic modalities as x-ray radiography, ultrasonography, computed tomography (CT) scan with intravenous (IV) contrast, CT cystography, and intravenous pyelogram (IVP) IVP to differentiate the diagnoses and also find skeletal and other organ injuries associated with this kind of injury. We can conclude that post-traumatic psoas hematoma is a rare condition. The diagnostic modality of choice is CT scan which allows rapid identification and measurement of the hematoma. The lesion usually treated with non-operative conservative management.

Unruptured aneurysmal clipping complicated by delayed and refractory vasospasm: case report

BackgroundDelayed symptomatic vasospasm is a rare complication following clipping of an unruptured intracranial saccular aneurysm. There have been ten reported cases of delayed symptomatic vasospasm and only two of these occurred after 2 weeks from initial intervention. Our case is the first to document the refractory nature of such vasospasm despite aggressive first line therapy.Case presentationHere, we present a 67-year-old female who had surgical clipping of a 10x7mm right middle cerebral artery (MCA) bifurcation aneurysm. Her surgery and initial postoperative course were uncomplicated, but she presented with acute left hemiparesis, dysarthria, headache and vomiting on post-op day 29 secondary to vasospasm of M2. She was initially stabilized with intra-arterial verapamil then managed with volume expansion, permissive hypertension, and nimodipine. She developed recurrent vasospasm of M2 the following day and was again treated with intra-arterial verapamil. Magnetic resonance imaging (MRI) brain showed an infarction involving the right basal ganglia, frontal lobe, and parietal lobe and her hospital course was complicated by super-refractory status epilepticus. At her follow up appointment she displayed continued left lower extremity weakness, left visual field defect, and left-sided neglect.ConclusionsOverall, cerebral vasospasms associated with unruptured aneurysms remain rare complications and are not often monitored for after initial recovery. Reviewing the documented cases highlights the unpredictability of when these events occur with our current knowledge. Current hypotheses for the mechanisms responsible for delayed and refractory vasospasms include: blood-derived breakdown products, mechanically induced vasospastic responses, and delayed reactions from the trigemino-cerebrovascular system (TCVS). The uncertainly of these events warrants further research and supports a strong argument for monitoring patients with initial surgical clipping up to a month out from their initial procedure.

Symptomatic intraspinal lumbosacral pseudomeningocele, a late consequence of root avulsion injury secondary to a gunshot wound

BackgroundTraumatic pseudomeningocele are usually a late consequence of cervical root avulsion injury and its occurrence in lumbosacral region is rare. This pathology is mostly due to violent blunt traumatic events and usually develops outside of the spinal canal. Occasionally, a pseudomeningocele may grow inside of the spinal canal causing delayed neurological deficit due to compromise of the adjacent neural structures. Case descriptionEvaluation of a delayed left lower extremity weakness in a young man with a history of a gunshot wound injury revealed an extradural pseudomeningocele arising from an S1 root avulsion injury with compressive effect on the adjacent L5 root OutcomeExcision of the cyst wall and reinstitution of the nerve root sheath resulted in an uneventful recovery ConclusionTo the best of our knowledge, the presented case with traumatic pseudomeningocele is the first example secondary to high velocity bullet injury. Furthermore, management of traumatic intraspinal pseudomeningocele subsequent to root avulsion injury has not been paid sufficient attention. In this paper, the surgical strategy will be discussed in detail.

SUN-285 Too Big to Be True, Too Young to Stroke!

BACKGROUND: Lactotroph adenomas are the most common type of pituitary adenomas and can cause infertility and menstrual irregularities in women; hypogonadism and gynecomastia in men.1 Giant prolactinomas are an unusual subset of pituitary macroadenomas with limited literature available on their management.2 We describe an unusual case of giant prolactinoma in a young man who presented with symptoms of stroke, that reversed with treatment with cabergoline. Clinical Case: 25-year old man presented with gradually progressing upper extremity weakness for evaluation of stroke. He reported stumbling into things when walking. There was a question of left sided facial droop and Bell’s palsy in recent past. He reported recent weight gain and erectile dysfunction. He was noted to have left homonymous hemianopsia on exam in addition to left upper and lower extremity weakness. MRI Brain showed an enormous mass that filled the sella turcica, invaded the sphenoid sinus and right side of the skull base, invaginating deep into the base of the right cerebral hemisphere with mass effect on the pons, right-sided midbrain, right temporal lobe and right basal nuclei, measuring 6.3 X 5.5 x 7.5 cm. Pituitary hormonal evaluation showed elevated prolactin (PRL) level with dilution at 13,580 ng/mL, with low testosterone (T) level (total T 42 ng/dL, free T 10 pg/mL, SHBG 15 nmol/L). Thyroid and adrenal axes were intact with normal IGF-1 level. In view of very high PRL level, he was started on cabergoline 0.5 mg daily initially and decreased to every other day after 2 weeks as PRL level began to decline. In 8 months, PRL levels decreased to 1293.07 ng/dl (90% reduction) and prolactinoma decreased to 6.0 x 3.7 x 4.7 cm (56% volume reduction). Total and free T improved to 134 ng/dL and 31 pg/dL respectively. He experienced marked improvement in left hemianopsia, with resolution of weakness and slurred speech. Energy level and erectile dysfunction improved. Currently he is being maintained on 0.5 mg cabergoline every other day Conclusion: Giant prolactinomas are uncommon and can present with compressive symptoms, that can be mistaken as stroke. Treatment with anticoagulation may cause hemorrhage and apoplexy with worsening of symptoms.1,2 There is limited data available regarding first line therapy for giant prolactinomas with 2 case reports where giant prolactinomas have been treated effectively with cabergoline.3,4 It is important to recognize the cause of such symptoms, and treated where possible with effective medical therapy to prevent morbidity.

Intradural Extramedullary Surgical Lysis of an Arachnoid Web of the Spine: 2-Dimensional Operative Video.

Arachnoid web of the spine (AWS) is a rare and subtle lesion that can have severe neurological consequences. Patients typically present with progressive myelopathic symptoms and have no more than a slight indentation of spinal cord on imaging, commonly referred to as the "scalpel sign." A unique feature associated with this lesion is the extent of (and sometimes the rapidity of) the recovery that occurs following treatment. In this operative video, we highlight the treatment of a 32-yr-old male with a history of lumbar spondylosis, who, over a 2 wk period, developed progressive spasticity and weakness of the entire left lower extremity and left foot numbness. Magnetic resonance imaging revealed a T4-T5 "scalpel sign" and spinal cord compression on computed topography myelogram, which was subsequently taken to the operating theater. The major steps in this video include the following: A) a summary of the patient's presentation and preoperative imaging, B) the technical steps in the surgical lysis of the AWS, and C) his postoperative course. The patient tolerated the procedure well, demonstrating a rapid improvement in symptoms postoperative day 1. At the time of most recent follow-up (4 mo), the patient remains neurologically intact with a full return to his neurologic baseline. Surgical lysis of AWS demonstrated to be a curative procedure with rapid neurological recovery, showing no signs of recurrence or regression. Consent was given by the patient for the use of deidentified images and the intraoperative video for educational purposes at the time consent was obtained for the surgical procedure, in accordance with our institution's policy.

Sciatic neuropathy after normal vaginal delivery: A case report

Postpartum neuropathies of the lower extremities are possible complications after delivery, with an estimated incidence of 1%. There are a few case reports about sciatic neuropathy after a caesarean section. However, a sciatic neuropathy after normal vaginal delivery has not been reported till date. This is a case report of a 30-year-old woman who visited our department with a chief complaint of left lower extremity weakness after normal vaginal delivery (at gestational age of 38 + 5 weeks) one month prior. The delivery took place under epidural anesthesia for about 6 h, with no dystocia or perinatal complications. She was primiparous, with a medical history of gestational diabetes. Physical examination revealed a lower extremity we;2akness (MRC grade III of left ankle plantar flexor) and a paresthesia at the left posterior calf and sole. Magnetic resonance imaging, nerve conduction studies, and electromyography were performed, and a diagnosis of left sciatic neuropathy proximal to the branch to the biceps femoris muscle was made. After 3 months, her motor weakness and paresthesia resolved spontaneously. In addition, the follow-up nerve conduction studies and electromyography confirmed a near complete recovery of the left sciatic neuropathy. In conclusion, sciatic neuropathy can occur after normal vaginal delivery even without dystocia and perinatal complications. The sciatic neuropathy in the case presented here had a good prognosis.