Background We describe the clinical and neuropathological features of a patient with T-cell-mediated paraneoplastic limbic encephalitis, parkinsonism, hypothermia, and narcolepsy-like presentation associated with endometrial carcinoma. Objectives This patient with prominent parkinsonism and narcolepsy broadens the phenotype of known paraneoplastic syndromes and demonstrates the importance of investigation for occult malignancy even in the absence of paraneoplastic antibodies. Methods This is a case report with diagnosis confirmed at postmortem. Results Paraneoplastic antibodies were not detected. The initial improvement with immunosuppression was short lived, and postmortem neuropathological examination demonstrated encephalitis with predominant T-cell infiltration affecting the hypothalamus and extending to the brainstem, suggestive of a paraneoplastic syndrome. Conclusions Although the possibility of a novel antibody cannot be ruled out, consideration must also be given to recent demonstration of purely T-cell-mediated neuronal destruction in the context of paraneoplastic syndromes.

With a prevalence of 6.6/100,000, short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) is a rare headache disorder characterized by moderate to severe unilateral head pain in an orbital, supra-orbital, temporal, or other trigeminal distribution and at least one ipsilateral cranial autonomic symptom including conjunctival injection, lacrimation, nasal congestion, and rhinorrhea. The brevity of the symptoms is a hallmark of SUNCT headache, with attacks typically lasting between 1 and 600 seconds. While often idiopathic in nature, there have been growing reports of SUNCT-like attacks occurring secondary to other pathologies including arteriovenous malformations, viral meningitis, cerebral infarction, and prolactinoma. A 69-year-old male presented with a 2-week history of severe right periorbital swelling, erythema, and blistering lesions over the right forehead and scalp without associated pain. Over the 24 hours prior to presentation, he developed excruciating pain in the same distribution. The pain was sharp and constant, rated 10/10 without relief from analgesia. It radiated to the occiput and neck. He also reported nausea and anorexia. Past medical history was significant for idiopathic pulmonary fibrosis treated with right lung transplantation 12 months earlier, requiring ongoing immunosuppressive treatment with tacrolimus, mycophenolate mofetil, and prednisolone. The only prior headache history he reported was mild tension-type headaches in adulthood. On examination, there was a vesicular rash in the right V1 distribution with severe periorbital edema. Further cranial nerve examination revealed bilateral sensorineural hearing deficits. The only positive findings in the remainder of the neurological examination were a mild intention tremor (likely related to tacrolimus), and signs of a mild length-dependent peripheral neuropathy in the lower limbs. On respiratory examination, there were signs of pulmonary fibrosis (diffuse wheeze and crepitations) in his remaining native lung. Acute herpes zoster was suspected given the clinical picture and the patient was admitted to the lung transplant unit with consultation from neurology services. Intravenous acyclovir and intravenous flucloxacillin were initiated immediately. C-reactive protein was 75 mg/L (normal <7 mg/L) and erythrocyte sedimentation rate was 54 mm/hour (normal 1–10 mm/hour). MRI brain on days 9 and 20 showed diffuse pachymeningeal enhancement (Fig. 1). MR Headache doi: 10.1111/head.13447 © 2018 American Headache Society Published by Wiley Periodicals, Inc. ISSN 0017-8748

Background: Alien limb phenomenon occurs in 50–60% of patients with corticobasal syndrome (CBS) and usually presents with an ''alien hand'' phenomenon. The ''alien foot'' presentation is rarer and may be misdiagnosed, as foot involvement can lead to erroneous localization of the clinical problem to the knee, hip, or back. Subsequently misdiagnoses such as myelopathy, radiculopathy, functional disorder, stiff leg syndrome, neuromyotonia, and painful leg moving toes syndrome may occur. Case report: We describe two patients with alien foot symptoms that resulted in multiple opinions from different specialists, multiple diagnostic and therapeutic procedures, and delayed diagnosis. Eventually a diagnosis of CBS was made in both. Alien foot symptoms may be more common than initially thought and can result in a delayed diagnosis of CBS. Conclusion: The inclusion of this clinical finding in recently proposed diagnostic criteria highlights the need for increased clinical awareness.

Autosomal recessive hereditary spastic paraparesis is rare.We present 4 patients with slowly progressive predominantly lower limb spasticity and ataxia. Only one patient had family history of ataxia but without any underlying diagnosis. All of them proved negative for the mutation of Spinocerebelalr ataxia genes SCA 1,2,3 and 6. All had mutation in the SPG 7 gene suggestive of autosomal recessive hereditary spastic paraparesis. One of the heterozygous mutatnts showed a novel c1617delC, p(Val540fs) frameshift mutation in exon 12 of the SPG 7 gene. SPG7 mutation accounts for 1.5-7% of all the HSP but it is the cause of undiagnosed ataxia in 18.6% in a recent case series. SPG7 mutation should be remembered as an important cause of undiagnosed ataxia especially where next generation sequencing is not widely avaialbale or affordable.

A 72-year-old lady presented to the neurology clinic with a constellation of symptoms that began 2 years previously with nocturnal wandering, erratic driving, and becoming withdrawn. Over the next 2 years, she developed recurrent falls, slowness and stiffness, urinary urgency, and hoarseness of voice. She was a previous heavy smoker. Family history revealed idiopathic Parkinson's disease in her father and motor neuron disease in her brother. Examination showed a broad-based gait, stooped posture, bilateral reduced arm swing, jerky tremor on outstretched hands, mild limb rigidity, and severe symmetric bradykinesia. There was mild proximal weakness of the lower limbs with bilateral extensor plantar responses. There was dysphonia without dysarthria. Extraocular movements were normal. A noncontrast computed tomography (CT) scan of the brain showed atrophy of the caudate nuclei and small-vessel ischemic changes (Fig. 1A). Magnetic resonance imaging (MRI) of the brain revealed small caudate nuclei and nonspecific white matter changes on a T2-weighted sequence (Fig. 1B) with unremarkable susceptibility-weighted (Fig. 1C) and sagittal view fluid-attenuated inversion recovery (Fig. 1) sequences. An 18-fluorodeoxyglucose positron emission tomography (18FDG PET) scan of the brain showed prominent, symmetric hypometabolism in the caudate nuclei and putamina, mild left anterior temporal hypometabolism, and low-normal cerebellar metabolic activity (Fig. 1E,F). Left and right basal ganglia activity was reduced by 6.2 and 4.7 standard deviations below the mean, respectively. Electroencephalography revealed intermittent slowing in the temporal regions. Levodopa (l-dopa) was tried, but her condition did not respond. Three years after initial symptom onset, the patient presented to hospital with dyspnea. A CT-guided biopsy followed by pathologic analysis of a newly discovered right lung mass revealed small cell lung carcinoma. Further tests were performed. Western blot analysis of serum was positive for anticollapsin response mediator protein 5 (CRMP5) antibodies. Other onconeuronal antibodies, specifically, anti-Hu, Yo, Ri, Ma1, Ma2, amphiphysin, Sox-1, Zic-4, and anti-Tr, were negative. Antivoltage-gated potassium channel (anti-VGKC) and anti-N-methyl-D-aspartate (anti-NMDA) receptor antibodies were negative. Oligoclonal immunoglobulin G bands were positive in the cerebrospinal fluid (CSF) but not in the serum, suggesting intrathecal synthesis. Further CSF analysis revealed a raised protein level at 629 mg/L and a normal white cell count of 3 cells/mL. A diagnosis was made of paraneoplastic parkinsonism. The patient commenced carboplatin and etoposide. At the time of this writing, the patient had shown clinical improvement after receiving the first three cycles of chemotherapy over 10 weeks, as demonstrated by enhanced mobility, reduced falls, and resolution of nocturnal wandering. A repeat CT scan of the thorax revealed a significant interval decrease in size of the lung lesion. We report a novel finding of prominent, symmetric caudate and putaminal hypometabolism on 18FDG PET imaging of the brain as a manifestation of paraneoplastic parkinsonism associated with anti-CRMP5 antibodies. Paraneoplastic parkinsonism itself is very rare and is usually associated with anti-Ri or anti-Ma2 antibodies.1 There are only four cases described in the literature of anti-CRMP5 antibody-associated paraneoplastic parkinsonism.2, 3 Several key findings support paraneoplastic etiology. CSF analysis demonstrated an inflammatory process. The patient was poorly l-dopa–responsive but improved with chemotherapy. The lung cancer was detected within 5 years of the diagnosis of the neurological disorder. Our patient fulfils the criteria for definite paraneoplastic neurological syndrome (PNS) based on diagnostic criteria proposed by Graus et al. in 2004.4 Another diagnostic consideration is dual pathology involving a coincidental lung malignancy with a separate Parkinsonian disease, such as that associated with C9Orf72 mutation,5 given the remarkable family history; these alternatives are unlikely, though not further investigated. PNS associated with onconeuronal antibodies (e.g., Hu, Yo, CV2/CRMP5, Ri, Ma2, or amphiphysin) are rare, comprising from 0.1% to 1% of patients with cancer, and likely involve T-cell–mediated pathophysiologic mechanisms.6 Notably, extrapyramidal syndromes are commonly associated with antibodies against neuronal cell-surface antigens, e.g., NMDA receptor-associated encephalitis.1 Although less common, onconeuronal antibody-associated movement disorders have been described.1 Anti-CRMP5 antibodies are usually associated with cerebellar ataxia, chorea, optic neuritis, encephalomyelitis, and sensorimotor neuropathy.3 However, the patient's clinical picture does not fit into these categories. CRMP5 is a neuronal cytoplasmic protein expressed throughout the nervous system and in small cell lung carcinoma.3 One study demonstrated localization of CRMP5 expression in the ganglionic eminence, neocortex, and hippocampus in the developing mouse brain.7 In the assessment of neurodegenerative disease with 18FDG PET, putaminal hypometabolism is described in multisystem atrophy and caudate hypometabolism in Huntington's disease and with progressive supranuclear palsy and widespread cortical hypometabolism in idiopathic Parkinson's disease.8 In our patient, cortical involvement was limited to mild left temporal hypometabolism and may have correlated with her behavioral change. There was no temporal lobe atrophy on brain MRI studies. It was proposed that a functional-anatomic discordance between FDG PET and MRI studies frequently occurs in the investigation of PNS.9 This is an area worthy of further research. In conclusion, this case illustrates a vital point that paraneoplastic syndromes may present unusually and mimic neurodegenerative disease. 18FDG PET may play a role in the investigation of paraneoplastic neurological syndromes. 1. Research Project: A. Conception, B. Organization, C. Execution; 2. Statistical Analysis: A. Design, B. Execution, C. Review and Critique; 3. Manuscript Preparation: A. Writing the First Draft; B. Review and Critique. S.M.Y.: 1A, 1C, 3A, 3B T.L.: 1A, 1C, 3A, 3B P.M.: 1A, 1B, 1C, 3B B.M.: 1A, 1C, 3A, 3B Funding Sources and Conflict of Interest: The authors report no sources of funding and no conflicts of interest. Financial Disclosures for the previous 12 months: The authors report no sources of funding and no conflicts of interest.

A 61-year-old woman with known neurofibromatosis type 1 (NF1) presented with lower back pain, urinary retention, impaired hearing, and tinnitus. Her lower limb deep tendon reflexes were brisk bilaterally with extensor plantar responses. MRI showed extensive dural ectasia, as well as hemosiderin deposition characteristic of superficial siderosis (figures 1 and 2). CSF analysis showed elevated erythrocyte counts, protein, and ferritin. Dural ectasia and meningocele formation are recognized complications of NF1.1 In this case, friable vessels at the site of the ectatic dura are the likely source of chronic bleeding into the CSF,2 resulting in diffuse superficial siderosis.

Objective: To describe a case of superficial siderosis in a neurofibromatosis type-1 (NF-1) patient with extensive dural ectasia Background: Superficial siderosis is characterised by hemosiderin deposition in the leptomeninges and adjacent parenchyma. It typically presents with progressive ataxia, hearing loss, and tinnitus, but can also cause myelopathy. Hemosiderin deposition results from the prolonged exposure of glial cells to blood in the subarachnoid space. This may arise from a neoplasm or vascular malformation, however in most cases no bleeding source is identified. Previous case series report dural pathology (meningoceles/pseudomeningoceles) in more than half of cases. Friable blood vessels at the site of abnormal dura may cause recurrent bleeding. Methods: Case report Results: A 61-year-old woman with NF-1 presented with lower back pain and urinary retention. She also reported impaired hearing and tinnitus. On examination, she had difficulty mobilising due to pain, but was not ataxic. Her lower limb deep tendon reflexes were brisk bilaterally with extensor plantar responses. Power was intact. MRI showed dural ectasia with scalloping of the posterior vertebral bodies extending from T5 to T11. A meningocele at the level of T9 was seen, expanding the left neural exit foramen. A rim of T2 hypointensity around the cord was seen on susceptibility weighted images. There was also loss of signal on gradient echo sequences within the sulci of the cerebral hemispheres bilaterally, and around the brainstem and cerebellum, consistent with hemosiderin deposition. CSF analysis showed elevated red cell counts, protein, and ferritin. Conclusions: This patient had evidence of extensive dural ectasia (a well-known complication of NF-1), which was in this case the most likely source of chronic bleeding into the CSF, resulting in superficial siderosis. This association has not been previously described, and should prompt clinicians to use gradient echo MRI to detect hemosiderin deposition in similar cases.

A 64-year-female smoker presented with a prolonged history of altered behavior, personality changes, and seizures. Anti-HU and anti-RI antibodies were positive. Magnetic resonance imaging demonstrated hyperintensity in the right hippocampal region (Fig. 1A) and corresponding increased radiotracer activity on positron emission tomography–computed tomography (PET-CT) (Fig. 1B, C). This initial PET-CT was negative for malignancy. A follow-up PET-CT 6 months later showed increased uptake in a right hilar node (Fig. 2). This node was sampled with endobronchial ultrasound and fine needle aspirate confirmed small cell carcinoma. Paraneoplastic limbic encephalitis is characterized by clinical presentation, presence of antineuronal antibodies, and imaging findings confirming involvement of the limbic system. Clinical symptoms and imaging abnormalities can predate the detection of malignancy by months to years.1Gultekin SH Rosenfeld MR Voltz R Eichen J Posner JB Dalmau J Paraneoplastic limbic encephalitis: neurological symptoms, immunological findings and tumour association in 50 patients.Brain. 2000; 123: 1481-1494Crossref PubMed Scopus (921) Google Scholar Control and treatment of the primary tumor with chemotherapy or other antineoplastic treatments may result in a neurologic improvement. Immunosuppression with steroids, intravenous immune globulin, plasma exchange, and other immunotherapies may also be of value.2Grisold W Giometto B Vitaliani R Oberndorfer S Current approaches to the treatment of paraneoplastic encephalitis.Ther Adv Neurol Disord. 2011; 4: 237-248Crossref PubMed Scopus (34) Google Scholar Symptomatic treatment should include seizure control with antiepileptic medications and medications to improve autonomic symptoms.2Grisold W Giometto B Vitaliani R Oberndorfer S Current approaches to the treatment of paraneoplastic encephalitis.Ther Adv Neurol Disord. 2011; 4: 237-248Crossref PubMed Scopus (34) Google Scholar

Hintergrund: Ipilimumab kann nachweislich das Gesamtüberleben bei Patienten mit metastasiertem Melanom verbessern; vollständige Remissionen (CRs) bewirkt es jedoch selten. Immunologische Nebenwirkungen betreffen meist die Haut oder den Gastrointestinaltrakt. Neurologische Ereignisse treten weniger häufig auf, sind aber umfassend beschrieben. Fallbericht: Wir berichten hier über den Fall eines 58-jährigen Mannes mit metastasiertem Melanom, bei dem nach einer spinalen Dekompression und Bestrahlung eine Behandlung mit Ipilimumab begonnen wurde. Nach dem 2. Zyklus entwickelte er eine Colitis, und das Ipilimumab wurde abgesetzt. Die Bildgebung zeigte jedoch eine radiologische CR. Acht Wochen später traten bei dem Patienten, trotz weiterhin bestehender CR, eine Paraplegie und Myelitis auf. Die Anwendung von Steroiden bewirkte eine gewisse radiologische Verbesserung, jedoch keine klinische. Schlussfolgerung: Wir berichten über Myelitis mit nachfolgender Paraplegie als potenzielle neurologische, immunvermittelte Nebenwirkung von Ipilimumab. Hierbei beschreiben wir einen Patienten mit einer CR nach 2 Zyklen Ipilimumab im Zusammenhang mit einer Bestrahlung.

Wir berichteten in einer fruheren Arbeit, dass S-777469 [1-([6-Ethyl-1-(4-Fluorbenzyl)-5-Methyl-2-Oxo-1,2-Dihydropyridin-3-Carbonyl]amino)-Cyclohexancarboxylsaure], ein neuartiger Agonist des Cannabin

Mittels einer Kombination aus ATR-FTIR-Spektroskopie (abgeschwächte Totalreflexions-/Fourier-Transformations-Infrarotspektroskopie) und Tape-Stripping-Versuchen in vitro an Schweineohr-Haut wurde die räumliche Verteilung unterschiedlicher Tenside im Stratum corneum (SC) untersucht. Um einen möglichen Zusammenhang zwischen der Größe der gebildeten Mizellen und ihrem Eindringen in die Haut zu ermitteln, wurden außerdem dynamische Lichtstreuungsmessungen der wässrigen Tensidlösungen durchgeführt. Die im Vergleich zu einem Alkylpolyglycosid und Sucroselaurat tiefere Hautpenetration der Aniontenside Natriumlaurylsulfat (sodium dodecyl sulfate; SDS) und Natriumlaurylethersulfat (sodium lauryl ether sulfate; SLES) ließ sich mit einer geringeren Größe der gebildeten Mizellen in Zusammenhang bringen. Neben den Unterschieden in der räumlichen Verteilung wurde auch eine Verbindung zwischen der physischen Präsenz anionischer Tenside im SC und einer Abnahme der Hautfeuchtigkeit festgestellt. Darüber hinaus wurde die Aufnahme von SDS und SLES in das SC selbst nach einem nur kurzen, verbraucherorientierten Waschvorgang mit handelsüblichem Haarshampoo bestätigt. Übersetzung aus Hoppel M, et al: Monitoring the distribution of surfactants in the stratum corneum by combined ATR-FTIR and tape-stripping experiments. Skin Pharmacol Physiol 2015;28:167-175 (DOI: 10.1159/000368444)

Hintergrund: Vitamin D scheint den Verlauf der atopischen Dermatitis (AD) bei Kindern zu beeinflussen. Methoden: Wir untersuchten die Vitamin-D-Konzentrationen im Serum von 39 Kindern mit AD (AD-Gruppe t₀) und von 20 gesunden Kontrollpersonen ohne Allergien (C-Gruppe). Der Schweregrad der AD wurde anhand des AD-Scoring-Systems (SCORAD-Index) beurteilt. Mehrere Zytokin-Serumkonzentrationen (IL-2, IL-4, IL-6, IFN-γ, TNF-α) und Atopie-Biomarker wurden ebenfalls bestimmt. Anschließend wurden die Patienten mittels oraler Supplementierung mit Vitamin D von 1000 IU/Tag (25 mg/Tag) über 3 Monate behandelt. Anschließend ermittelten wir erneut die Vitamin-D-Serumkonzentrationen, die Schwere der AD und die Zytokin-Serumkonzentrationen bei allen behandelten Kindern (AD-Gruppe t1). Ergebnisse: Die Querschnittsanalyse der AD-Patienten (AD-Gruppe t₀) ergab, dass die Ausgangswerte aller untersuchten Zytokine mit Ausnahme von TNF-α höher waren als in der gesunden Kontrollgruppe (C-Gruppe) und außerhalb des Normbereichs lagen. Nach 3-monatiger Supplementierung waren die Vitamin-D-Konzentrationen der Patienten signifikant gestiegen (von 22,97 ± 8,03 ng/ml auf 29,41 ± 10,73 ng/ml; p = 0,01). Außerdem war ein signifikanter Rückgang sowohl des SCORAD-Index (46,13 ± 15,68 beim ersten Termin vs. 22,57 ± 15,28 beim zweiten Termin; p < 0,001) als auch aller auffälligen Zytokinwerte (IL-2, IL-4, IL-6, IFN-γ) festzustellen. Schlussfolgerungen: Diese Studie belegt, dass die ergänzende Gabe von Vitamin D durch die Normalisierung des Th1- und Th2-Interleukin-Musters im Serum eine wirkungsvolle Maßnahme zur Verringerung des Schweregrads der AD bei Kindern darstellt. Übersetzung aus Di Filippo P, et al: Vitamin D supplementation modulates the immune system and improves atopic dermatitis in children. Int Arch Allergy Immunol 2015;166:91-96 (DOI: 10.1159/000371350)

Hintergrund: Wundinfektionen spielen eine wichtige Rolle bei Storungen der Wundheilung. Eine hohe Keimbelastung beeintrachtigt die Heilung und fuhrt zur Chronifiz

Clinical Correspondence Magnetic Resonance Imaging of Temporal Arteritis: A Case Report Albi J. Chalissery MBBS, MD, Corresponding Author Albi J. Chalissery MBBS, MD Department of Neurology, Mater Misericordiae University Hospital, Dublin, IrelandAddress all correspondence to A.J. Chalissery, Eccles Street, Dublin 7, Dublin, Ireland.Search for more papers by this authorTimothy Barry MB Bch BAO, MRCPI, Timothy Barry MB Bch BAO, MRCPI Department of Neurology, Mater Misericordiae University Hospital, Dublin, IrelandSearch for more papers by this authorRosemary Lucey MB Bch, Rosemary Lucey MB Bch Department of Neurology, Mater Misericordiae University Hospital, Dublin, IrelandSearch for more papers by this authorShakya Bhatacharjee MRCPI, Shakya Bhatacharjee MRCPI Department of Neurology, Mater Misericordiae University Hospital, Dublin, IrelandSearch for more papers by this authorPeter De La Harpe Golden MSc, LRCP, SI, MB Bch, BA(Mod), Peter De La Harpe Golden MSc, LRCP, SI, MB Bch, BA(Mod) Department of Pathology, Mater Misericordiae University Hospital, Dublin, IrelandSearch for more papers by this authorEoin C. Kavanagh FFR (RCSI), Eoin C. Kavanagh FFR (RCSI) Department of Neuroradiology, Mater Misericordiae University Hospital, Dublin, IrelandSearch for more papers by this authorBrian Murray MB Msc, Brian Murray MB Msc Department of Neurology, Mater Misericordiae University Hospital, Dublin, IrelandSearch for more papers by this author Albi J. Chalissery MBBS, MD, Corresponding Author Albi J. Chalissery MBBS, MD Department of Neurology, Mater Misericordiae University Hospital, Dublin, IrelandAddress all correspondence to A.J. Chalissery, Eccles Street, Dublin 7, Dublin, Ireland.Search for more papers by this authorTimothy Barry MB Bch BAO, MRCPI, Timothy Barry MB Bch BAO, MRCPI Department of Neurology, Mater Misericordiae University Hospital, Dublin, IrelandSearch for more papers by this authorRosemary Lucey MB Bch, Rosemary Lucey MB Bch Department of Neurology, Mater Misericordiae University Hospital, Dublin, IrelandSearch for more papers by this authorShakya Bhatacharjee MRCPI, Shakya Bhatacharjee MRCPI Department of Neurology, Mater Misericordiae University Hospital, Dublin, IrelandSearch for more papers by this authorPeter De La Harpe Golden MSc, LRCP, SI, MB Bch, BA(Mod), Peter De La Harpe Golden MSc, LRCP, SI, MB Bch, BA(Mod) Department of Pathology, Mater Misericordiae University Hospital, Dublin, IrelandSearch for more papers by this authorEoin C. Kavanagh FFR (RCSI), Eoin C. Kavanagh FFR (RCSI) Department of Neuroradiology, Mater Misericordiae University Hospital, Dublin, IrelandSearch for more papers by this authorBrian Murray MB Msc, Brian Murray MB Msc Department of Neurology, Mater Misericordiae University Hospital, Dublin, IrelandSearch for more papers by this author First published: 11 March 2015 https://doi.org/10.1111/head.12541Citations: 1 Conflict of Interest: None. No financial support towards this work received by any authors. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume55, Issue6June 2015Pages 866-868 RelatedInformation

Background: Ipilimumab has been shown to improve overall survival in patients with metastatic melanoma; however, complete responses (CRs) are uncommon. Immune-related side effects usually involve the skin or gastrointestinal tract. Neurologic events occur less frequently but are well described. Case Report: We report the case of a 58-year-old man with metastatic melanoma who commenced ipilimumab post spinal decompression and radiation. He developed a colitis post cycle 2 and ipilimumab was discontinued. Imaging, however, documented a radiological CR. 8 weeks later, he developed paraplegia and a myelitis despite an ongoing radiological CR. Steroid use resulted in some improvement radiologically, without clinical improvement. Conclusion: We report myelitis with consequent paraplegia as a potential neurological immune-related side effect of ipilimumab. We further describe a patient with a CR after 2 cycles of ipilimumab in the setting of radiation.