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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTE1NjgwOC1vdmVydmlldw==\nDrugs & Diseases > Neurology\nParaneoplastic Autonomic Neuropathy\nAuthor: Stacy E Dixon, MD, PhD; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS more...\nSections Paraneoplastic Autonomic Neuropathy\nFurther Outpatient Care\nInpatient & Outpatient Medications\nDeterrence/Prevention\nAutoimmune paraneoplastic autonomic neuropathy is a rare paraneoplastic neurological syndrome (PNS), which manifests as disturbance in sympathetic and/or parasympathetic nervous system function. Most often, autonomic problems in cancer patients are attributable to prolonged bed rest, neurotoxic chemotherapy, high-dose analgesics, and malnutrition. However, paraneoplastic autonomic neuropathy should be considered in all cancer patients who present with signs or symptoms of autonomic nervous system dysfunction. Patients may develop autonomic disturbances at any time relative to the diagnosis of cancer. The autonomic problems can precede the cancer diagnosis, and a high level of suspicion is then required to identify the underlying neoplasm.\nAn international expert group established diagnostic criteria in 2004 that divided patients with a suspected paraneoplastic neurological syndrome into \"definite\" and \"probable\" categories. [1] These criteria are based on the presence or absence of cancer, the presence of well-characterized paraneoplastic (onconeural) antibodies, and the type of clinical syndrome.\nThe clinical syndromes are divided into classical and non-classical categories. [1]\nClassical paraneoplastic neurological syndromes include:\nSubacute cerebellar degeneration\nOpsoclonus-myoclonus\nSubacute sensory neuronopathy\nChronic gastrointestinal pseudo-obstruction\nThe most common non-classical paraneoplastic neurological syndromes include:\nBrainstem encephalitis\nCancer- or melanoma-associated retinopathy\nNecrotizing myelopathy\nAcute sensorimotor neuropathies (ie, Guillain-Barre syndrome or brachial neuritis)\nSubacute/chronic sensorimotor neuropathies\nNeuropathies associated with paraproteinemia or vasculitis\nAutonomic neuropathies\nAcquired neuromyotonia\nAcute necrotizing myopathy\nPatients with a definite PNS include those with the following:\nA classical syndrome and cancer that develops within 5 years of the diagnosis of the neurological disorder, regardless of the presence of paraneoplastic antibodies,\nA nonclassical syndrome that objectively improves or resolves after cancer treatment, provided that the syndrome is not susceptible to spontaneous remission,\nA nonclassical syndrome with paraneoplastic antibodies (well characterized or not) and cancer that develops within 5 years of the diagnosis of the neurological disorder, or\nA neurological syndrome (classical or not) with well-characterized paraneoplastic antibodies (ie, anti-Hu, anti-Yo, anti-Ri, antiamphiphysin, anti-CV2, anti-Ma2), and no cancer.\nPatients with a possible PNS include those with the following:\nA classical syndrome without paraneoplastic antibodies and no cancer but at high risk to have an underlying tumor (eg, smoking history),\nA neurological syndrome (classical or not) without cancer but with partially characterized paraneoplastic antibodies, or\nA nonclassical neurological syndrome, no paraneoplastic antibodies, and cancer that presents within 2 years of the neurological syndrome.\nThe main paraneoplastic syndromes associated with autonomic dysfunction include paraneoplastic autoimmune autonomic gangliopathy (AAG), paraneoplastic sensory neuropathies and neuronopathies, paraneoplastic encephalomyeloneuropathies, and Lambert-Eaton myasthenic syndrome (LEMS). Each one of these disorders may have other distinct symptoms and findings in addition to autonomic disturbances.\nIt has long been known that patients with small-cell lung cancer [2] develop neurological signs and symptoms with increased frequency [3] ; however, many cancers including other lung tumors [4] , thymoma, Hodgkin disease [5] , other lymphomas [6] , testicular, ovarian, and breast carcinoma can also cause paraneoplastic neurological syndromes. [7]\nExactly how cancers result in paraneoplastic neurological symptoms is incompletely understood. The development of these syndromes are not due to direct tumor invasion. Expression of onconeural antigens by the cancer cells resulting in autoimmunity appears to be the mechanism. The classical paraneoplastic antibodies are directed at intracellular antigens [8] and may not be directly pathogenic. Passive transfer experiments have generally been unsuccessful. However, antibodies directed against exposed antigens, namely ganglionic acetylcholine receptors and voltage-gated calcium and potassium channels, appear more directly pathogenic. With these antibody types, several passive transfer experiments have been positive, confirming the antibodies direct pathogenic effect.\nAutoantibodies to these extracellularly exposed membrane proteins often occur without an underlying malignancy. A search for a malignancy should still be undertaken, but these conditions may occur through an idiopathic autoimmune process.\nMany antineuronal antibodies have been described to date, and new antibodies are described each year. Sometimes, more than 1 type of antibody is found in a single patient, and the same type of antibody may be associated with very different syndromes in other patients. [9] It is also entirely possible that a patient who lacks identifiable autoantibodies but has a tumor known to express epitopes similar to neuronal structures (eg, small-cell lung cancer), may suffer from paraneoplastic autonomic dysfunction due to an antibody that has not been identified.\nAutonomic dysfunction can occur when this autoimmune process causes sufficient damage to the autonomic nervous system. Limited data are available regarding the immune attack on preganglionic neurons or central autonomic pathways. Typical pathological changes include lymphocytic infiltrates [10] and vascular cuffing; as is shown in the image below from a case of anti-Hu encephalomyeloneuropathy. Similar attacks on autonomic postganglionic and myenteric neurons can occur with antineuronal antibodies.\nParaneoplastic autonomic neuropathy. Central nervous system sections from a patient with autonomic failure, oat-cell carcinoma of the lung, and positive titer of anti-HU antibodies stained with hematoxylin and eosin (H&E). (a) Inferior olive showing a cluster of mononuclear cells (arrowhead); (b) hippocampus showing perivascular mononuclear infiltrate (arrowhead); (c) midbrain section showing a vessel encased in a mononuclear infiltrate; (d) ventral horn of the thoracic spinal cord showing clusters of mononuclear cells around degenerating motor neurons (arrowheads). Magnification bars indicate 100 mm. The bar in b applies also to a and the bar in d also applies to c.\nView Media Gallery\nThe best understood syndromes involving paraneoplastic autonomic dysfunction are paraneoplastic autoimmune autonomic gangliopathy (AAG), paraneoplastic sensory neuropathy and/or neuronopathy, paraneoplastic encephalomyeloneuropathy, and Lambert-Eaton myasthenic syndrome.\nAnti-ganglionic acetylcholine receptor antibodies\nThese antibodies directed at nicotinic acetylcholine in receptors containing the α3 subunit expressed on sympathetic and parasympathetic ganglia cause paraneoplastic AAG. [11] Ganglionic acetylcholine receptor antibodies do not bind to muscle acetylcholine receptors and are not known to cause myasthenia gravis (MG). These anti-ganglionic acetylcholine receptor antibodies are likely directly pathogenic and have an associated clinical picture that is usually characterized by autonomic failure. Only about 20% of cases with AAG appear to be paraneoplastic in origin [12] , relating to small-cell lung carcinoma, thymoma, bladder carcinoma, and rectal carcinoma [13] ; many of the remaining cases appear to be postinfectious analogues to Gullian-Barre syndrome. A case of paraneoplastic AAG coexisting with antibodies against muscle acetylcholine receptors has been reported. [14]\nAnti-Hu\nAnti-Hu antibodies (which are also called antineuronal nuclear antibody type 1 [ANNA-1]) [2] are the second most pertinent to autonomic dysfunction; and are often seen in the setting of small-cell lung cancer. These antibodies can also be seen in non–small-cell lung cancer, neuroblastoma, and malignant disorders of the gastrointestinal tract, prostate, breast, bladder, kidney, pancreas, testicle, and ovary. [15, 13, 16] The autoimmune response is directed to the Hu antigen, an AU-rich 3′-untranslated m-RNA sequence that is expressed by many small-cell lung cancer cells and by all neurons.\nAntibodies to the Hu onconeuronal antigen can affect almost any portion of the central nervous system (CNS) or peripheral nervous system. [17] The anti-Hu antibody is most often associated with a paraneoplastic sensory neuronopathy, which involves destruction of primary sensory neurons. [18] When anti-Hu is present, about 25% of patients have some form of dysautonomia, most frequently gastrointestinal manifestations. [19] This antibody is diagnostically useful, but the exact role of humoral immunity in causing neural degeneration remains uncertain.\nAnti-NMDA receptor\nA recently discovered antibody to the NMDA receptor has been found to be associated with psychosis, seizures, and autonomic instability. In a case series, it was found to be the cause of 4% of encephalitis cases. [20] The antibody is found in cerebrospinal fluid (CSF) in 94% of cases. [21] In one case series, 55% of patients were found to have a teratoma containing neural tissue with NMDA receptors expressed. [22] Typically, the tumor is an ovarian teratoma; however, testicular germ cell tumors, neuroblastoma, and Hodgkin lymphoma have also been reported. [21] There is some evidence that NMDA-receptor antibody encephalitis may result in centrally mediated sinus node dysregulation, including cardiac arrest. [23, 24]\nAnti-VGCC\nIn Lambert-Eaton myasthenic syndrome (LEMS), antibodies against P/Q type voltage-gated calcium channels (VGCC) are present. These antibodies lead to impaired presynaptic calcium release at the neuromuscular junction, resulting in predominantly proximal muscle weakness. These antibodies not only block the voltage-gated calcium channels at the neuromuscular junction but also block them at parasympathetic and sympathetic nerve terminals, thus creating autonomic insufficiency and autonomic symptoms. This syndrome is associated with malignancy 50-60% of the time, typically small-cell lung cancer, but also non–small-cell lung cancer, malignant thymoma, lymphoma, leukemia, and carcinomas of the breast, prostate, larynx, and gallbladder. [15, 25, 19] Autonomic dysfunction in LEMS is normally mild.\nOther paraneoplastic antibodies\nCollapsin response-mediator protein (CRMP-5), also known as CV-2, is another paraneoplastic antibody that has associated autonomic dysfunction in 33% of cases. [19] CRMP-5 is most often seen with small-cell lung cancer. Purkinje cell antibody-2 (PCA-2) frequently causes cerebellar degeneration but can also be associated with autonomic failure. [26] Antibodies against synaptophysin may be associated with lung cancer and gastrointestinal disturbances from the myenteric plexus. [27] Voltage-gated potassium channel (VGKC) antibodies [28] have been reported to cause autonomic failure in 33% of cases. VGKC antibodies are associated with neuroendocrine tumors including small-cell lung carcinoma, retinoblastoma, oligodendroglioma, melanoma, leiomyosarcoma, and hematologic malignancies. [29] . There is a VGKC antibody-complex associated with contractin associate protein 2 (CASPR2) that has been observed with autonomic dysfunction with thymoma or small cell lung cancer. [30]\nGastric dysmotility paraneoplastic disorders can often be seen with antibodies such anti-Yo, anti-Hu, anti-ganglionic acetylcholine receptor, CRMP-5, anti-VGCC, anti-VGKC, GAD65, islet cell antigen 512 (IA-2), gastric parietal cell, muscle striational, thyroid peroxidase, or thyroglobulin autoantibodies. [31] . One case report documents a patient with functional colonic obstruction ultimately resulting from paraneoplastic ocular myasthenia associated with a thymoma. [32]\nStiff person syndrome, when caused by a paraneoplastic disorder (about 5% of cases), has been reported to associate with anti-GAD65, amphiphysin antibodies, anti-Ri (ANNA-2 antibodies), anti-gephyrin, anti ICA 105, and anti-17-B-hydroxysteroid dehydrogenase type 4. Associated tumors are found in breast, thymus, lung, and kidney cancers as well as multiple myeloma. [33]\nProgressive encephalomyelitis with rigidity and myoclonus (PERM) has been found to have a paraneoplastic cause in 20% of patients associated with anti-Ri (ANNA-2), anti-amphiphysin, and anti-GAD65. Autonomic symptoms such as pyrexia and diaphoresis are exhibited in 66% of patients with PERM. [33]\nAnti-Yo, also known as Purkinje cell antibody 1 (PCA-1) is associated with breast, ovarian, fallopian tube, or uterine cancers. [9] It targets an intracellular antigen called CDR2. The typical presentation is gastric dysmotility. [15]\nMany other autoantibodies may also play a role in paraneoplastic dysautonomia, with more being found every year. Recent examples include synaptophysin, SOX, ZIC, anti-AMPA, and anti-GABA, and antibodies to inositol 1,4,5-trisphosphate receptor type 1 (ITRP1) and dipeptidyl-peptidase-like protein-6 (DPP6, also known as DPPX). [34, 35, 36, 37]\nThe autoimmunity in paraneoplastic neurological syndromes does appear to confer some degree of antitumor effect. Inflammation similar to what is seen in the nervous system also affects the tumor.\nThere have been several reported cases in which Hu antibody has occurred with classical paraneoplastic symptoms that spontaneously resolved without an underlying tumor being identified. [38] This could be due to a spontaneous cure of the underlying cancer, possibly due to an anti-tumor effect of the paraneoplastic antibodies.\nIn the United States, the precise incidence of paraneoplastic autonomic disorders in patients with cancer is not known, but the current best estimate is that less than 1% of patients with solid tumors develop any kind of PNS.\nIn the United Kingdom, a national screening program found 63 patients with paraneoplastic neurological symptoms (not including LEMS) from 2000-2001. [7]\nMortality/Morbidity\nMorbidity and death can result from severe failure of autonomic function. However, milder autonomic disturbances may be obscured by prominent symptoms of systemic cancer, anticancer therapy, or other peripheral nervous system and CNS damage.\nNo data suggests differences in frequency or outcomes based on race.\nConflicting evidence exists with many case series suggesting higher frequency in women [7, 39] but others suggesting higher frequency in men.\nPNS can occur at any age, many case series have recorded median age of onset in the sixth [7] or seventh decade. Anti-NMDA receptor antibodies tend to affect much younger patients with a median age in the early 20s. [22]\nGraus F, Delattre JY, Antoine JC, et al. Recommended diagnostic criteria for paraneoplastic neurological syndromes. J Neurol Neurosurg Psychiatry. 2004 Aug. 75(8):1135-40. [Medline].\nAnderson NE, Rosenblum MK, Graus F. Autoantibodies in paraneoplastic syndromes associated with small-cell lung cancer. Neurology. 1988 Sep. 38(9):1391-8. [Medline].\nElrington GM, Murray NM, Spiro SG. Neurological paraneoplastic syndromes in patients with small cell lung cancer. A prospective survey of 150 patients. J Neurol Neurosurg Psychiatry. 1991 Sep. 54(9):764-7. [Medline].\nVeilleux M, Bernier JP, Lamarche JB. Paraneoplastic encephalomyelitis and subacute dysautonomia due to an occult atypical carcinoid tumour of the lung. Can J Neurol Sci. 1990 Aug. 17(3):324-8. [Medline].\nBlaes F, Strittmatter M, Schwamborn J, et al. Antineuronal antibody-associated paraneoplastic neuropathy in Hodgkin's disease. Eur J Neurol. 1998 Jan. 5(1):109-112. [Medline].\nFicker DM, Hammack JE. Primary central nervous system lymphoma presenting as autonomic dysfunction. J Neurooncol. 1995. 23(3):245-8. [Medline].\nCandler PM, Hart PE, Barnett M, et al. A follow up study of patients with paraneoplastic neurological disease in the United Kingdom. J Neurol Neurosurg Psychiatry. 2004 Oct. 75(10):1411-5. [Medline].\nAltermatt HJ, Rodriguez M, Scheithauer BW, Lennon VA. Paraneoplastic anti-Purkinje and type I anti-neuronal nuclear autoantibodies bind selectively to central, peripheral, and autonomic nervous system cells. Lab Invest. 1991 Oct. 65(4):412-20. [Medline].\nPittock SJ, Kryzer TJ, Lennon VA. Paraneoplastic antibodies coexist and predict cancer, not neurological syndrome. Ann Neurol. 2004 Nov. 56(5):715-9. [Medline].\nPanegyres PK, Reading MC, Esiri MM. The inflammatory reaction of paraneoplastic ganglionitis and encephalitis: an immunohistochemical study. J Neurol. 1993 Feb. 240(2):93-7. [Medline].\nVernino S, Adamski J, Kryzer TJ. Neuronal nicotinic ACh receptor antibody in subacute autonomic neuropathy and cancer-related syndromes. Neurology. 1998 Jun. 50(6):1806-13. [Medline].\nVernino S, Low PA, Fealey RD. Autoantibodies to ganglionic acetylcholine receptors in autoimmune autonomic neuropathies. N Engl J Med. 2000 Sep 21. 343(12):847-55. [Medline].\nFreeman R. Autonomic peripheral neuropathy. Lancet. 2005 Apr 2-8. 365(9466):1259-70. [Medline].\nPeltier AC, Black BK, Raj SR, Donofrio P, Robertson D, Biaggioni I. Coexistent autoimmune autonomic ganglionopathy and myasthenia gravis associated with non-small-cell lung cancer. Muscle Nerve. 2010 Mar. 41(3):416-9. [Medline].\nLorusso L, Hart IK, Ferrari D, Ngonga GK, Gasparetto C, Ricevuti G. Autonomic paraneoplastic neurological syndromes. Autoimmun Rev. 2007 Jan. 6(3):162-8. [Medline].\nde Beukelaar JW, Sillevis Smitt PA. Managing paraneoplastic neurological disorders. Oncologist. 2006 Mar. 11(3):292-305. [Medline].\nLucchinetti CF, Kimmel DW, Lennon VA. Paraneoplastic and oncologic profiles of patients seropositive for type 1 antineuronal nuclear autoantibodies. Neurology. 1998 Mar. 50(3):652-7. [Medline].\nCamdessanche JP, Antoine JC, Honnorat J. Paraneoplastic peripheral neuropathy associated with anti-Hu antibodies. A clinical and electrophysiological study of 20 patients. Brain. 2002 Jan. 125(Pt 1):166-75. [Medline].\nVernino S. Antibody testing as a diagnostic tool in autonomic disorders. Clin Auton Res. 2009 Feb. 19(1):13-9. [Medline].\nGranerod J, Ambrose HE, Davies NW, Clewley JP, Walsh AL, Morgan D. Causes of encephalitis and differences in their clinical presentations in England: a multicentre, population-based prospective study. Lancet Infect Dis. 2010 Dec. 10(12):835-44. [Medline].\nLancaster E, Martinez-Hernandez E, Dalmau J. Encephalitis and antibodies to synaptic and neuronal cell surface proteins. Neurology. 2011 Jul 12. 77(2):179-89. [Medline]. [Full Text].\nDalmau J, Gleichman AJ, Hughes EG, Rossi JE, Peng X, Lai M. Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies. Lancet Neurol. 2008 Dec. 7(12):1091-8. [Medline].\nNazif TM, Vázquez J, Honig LS, Dizon JM. Anti-N-methyl-D-aspartate receptor encephalitis: an emerging cause of centrally mediated sinus node dysfunction. Europace. 2012 Feb 15. [Medline].\nMillichap JJ, Goldstein JL, Laux LC, Nordli DR Jr, Stack CV, Wainwright MS. Ictal asystole and anti-N-methyl-D-aspartate receptor antibody encephalitis. Pediatrics. 2011 Mar. 127(3):e781-6. [Medline].\nMahadeva B, Phillips LH 2nd, Juel VC. Autoimmune disorders of neuromuscular transmission. Semin Neurol. 2008 Apr. 28(2):212-27. [Medline].\nVernino S, Lennon VA. New Purkinje cell antibody (PCA-2): marker of lung cancer-related neurological autoimmunity. Ann Neurol. 2000 Mar. 47(3):297-305. [Medline].\nTschernatsch M, Klotz M, Probst C, Hosch J, Valtorta F, Diener M, et al. Synaptophysin is an autoantigen in paraneoplastic neuropathy. J Neuroimmunol. 2008 Jun 15. 197(1):81-6. [Medline].\nTan KM, Lennon VA, Klein CJ, Boeve BF, Pittock SJ. Clinical spectrum of voltage-gated potassium channel autoimmunity. Neurology. 2008 May 13. 70(20):1883-90. [Medline].\nVincent A, Bien CG, Irani SR, Waters P. Autoantibodies associated with diseases of the CNS: new developments and future challenges. Lancet Neurol. 2011 Aug. 10(8):759-72. [Medline].\nDhamija R, Tan KM, Pittock SJ, Foxx-Orenstein A, Benarroch E, Lennon VA. Serologic profiles aiding the diagnosis of autoimmune gastrointestinal dysmotility. Clin Gastroenterol Hepatol. 2008 Sep. 6(9):988-92. [Medline].\nMalhotra K, Georgiades IB, Davies J. Functional colonic obstruction in an adult as a presenting feature of thymoma. Ann R Coll Surg Engl. 2011 Sep. 93(6):e61-3. [Medline].\nDuddy ME, Baker MR. Stiff person syndrome. Front Neurol Neurosci. 2009. 26:147-65. [Medline].\nGraus F, Saiz A, Dalmau J. Antibodies and neuronal autoimmune disorders of the CNS. J Neurol. 2010 Apr. 257(4):509-17. [Medline].\nTschernatsch M, Klotz M, Probst C, Hosch J, Valtorta F, Diener M. Synaptophysin is an autoantigen in paraneoplastic neuropathy. J Neuroimmunol. 2008 Jun 15. 197(1):81-6. [Medline].\nSven Jarius, Marius Ringelstein, Jurgen Hass, Irina I. Serysheva, Lars Komorowski, Kai Fechner, et al. Inositol 1,4,5-trisphosphate receptor type 1 autoantibodies in paraneoplastic and non-paraneoplastic peripheral neuropathy. Journal of Neuroinflammation. Oct 24, 2016. 13:278. [Medline].\nWilliam Oliver Tobin, Vanda A. Lennon, Lars Komorowski, Christian Probst, Stacey Lynn Clardy, Allen J. Aksamit, et al. DPPX potassium channel antibody; frequency, clinical accompaniments, and outcomes in 20 patients. Neurology. Nov. 11, 2014. 83:1797-1803. [Medline].\nByrne T, Mason WP, Posner JB, et al. Spontaneous neurological improvement in anti-Hu associated encephalomyelitis. J Neurol Neurosurg Psychiatry. 1997 Mar. 62(3):276-8. [Medline].\nChalk CH, Windebank AJ, Kimmel DW, McManis PG. The distinctive clinical features of paraneoplastic sensory neuronopathy. Can J Neurol Sci. 1992 Aug. 19(3):346-51. [Medline].\nChinn JS, Schuffler MD. Paraneoplastic visceral neuropathy as a cause of severe gastrointestinal motor dysfunction. Gastroenterology. 1988 Nov. 95(5):1279-86. [Medline].\nDalmau J, Graus F, Rosenblum MK. Anti-Hu--associated paraneoplastic encephalomyelitis/sensory neuronopathy. A clinical study of 71 patients. Medicine (Baltimore). 1992 Mar. 71(2):59-72. [Medline].\nTitulaer MJ, Soffietti R, Dalmau J, Gilhus NE, Giometto B, Graus F, et al. Screening for tumours in paraneoplastic syndromes: report of an EFNS Task Force. Eur J Neurol. 2010 Sep 29. [Medline].\nOh SJ, Dropcho EJ, Claussen GC. Anti-Hu-associated paraneoplastic sensory neuropathy responding to early aggressive immunotherapy: report of two cases and review of literature. Muscle Nerve. 1997 Dec. 20(12):1576-82. [Medline].\nKhurana RK, Koski CL, Mayer RF. Autonomic dysfunction in Lambert-Eaton myasthenic syndrome. J Neurol Sci. 1988 May. 85(1):77-86. [Medline].\nMaddison P, Lang B. Paraneoplastic neurological autoimmunity and survival in small-cell lung cancer. J Neuroimmunol. 2008 Sep 15. 201-202:159-62. [Medline].\nMamdani MB, Walsh RL, Rubino FA. Autonomic dysfunction and Eaton Lambert syndrome. J Auton Nerv Syst. 1985 Apr. 12(4):315-20. [Medline].\nBlock MS, Vassallo R. Lack of FDG uptake in small cell carcinoma associated with ANNA-1 positive paraneoplastic autonomic neuropathy. J Thorac Oncol. 2008 May. 3(5):542-4. [Medline].\nParaneoplastic autonomic neuropathy. Histopathology of peripheral nerve and sympathetic ganglion from a patient with autonomic failure, oat-cell carcinoma of the lung, and positive anti-HU antibody titer. (a) Peripheral nerve in longitudinal section stained with Luxol fast blue-periodic acid-Schiff (PAS) showing scattered wallerian degeneration (arrowheads). (b) Low-power view of a paravertebral sympathetic ganglion stained with hematoxylin and eosin (H&E). Arrowhead indicates perivascular mononuclear infiltrates. (c) High-power view of the same sympathetic ganglion showing degenerating neurons (single arrowheads) and mononuclear infiltrates (double arrowhead). Magnification bars in a and b indicate 100 mm; c is 50 mm.\nParaneoplastic autonomic neuropathy. Hematoxylin and eosin (H&E)–stained sections from dorsal root ganglion showing the hallmark histopathology of anti-HU disease; a and c are from a healthy patient; b and d are from a patient with autonomic failure, oat-cell carcinoma of the lung, and positive titer of anti-HU antibodies. The arrowheads in b and d indicate degenerating sensory neurons. Also note the interstitial hypercellularity and decreased numbers of neurons in b and d. Magnification bar in b indicates 100 mm and applies also to a. Similarly, the magnification bar in d indicates 50 mm, which also applies to c.\nStacy E Dixon, MD, PhD Assistant Professor of Neurology, University of Colorado School of Medicine\nStacy E Dixon, MD, PhD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, Colorado Society of Clinical Neurologists\nDisclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Biogen; Genetech.\nDianna Quan, MD Professor of Neurology, Director of Electromyography Laboratory, University of Colorado School of Medicine\nDianna Quan, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Neurological Association\nDisclosure: Received research grant from: Alnylam; Pfizer; Cytokinetics; Momenta.\nJorge C Kattah, MD Head, Associate Program Director, Professor, Department of Neurology, University of Illinois College of Medicine at Peoria\nJorge C Kattah, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, New York Academy of Sciences\nTarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS Professor Emeritus of Neurology and Psychiatry, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Neuroscience Director, Department of Neurology, Crouse Irving Memorial Hospital\nTarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS is a member of the following medical societies: American College of International Physicians, American Heart Association, American Stroke Association, American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners Institute, National Association of Managed Care Physicians, American College of Physicians, Royal College of Physicians, Royal College of Physicians and Surgeons of Canada, Royal College of Surgeons of England, Royal Society of Medicine\nRonald G Wiley, MD, PhD Professor of Neurology and Pharmacology, Vanderbilt University, Chief of the Neurology Service, Veterans Affairs Tennessee Valley Healthcare System\nRonald G Wiley, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Association for the Advancement of Science, New York Academy of Sciences, Society for Neuroscience\nBjorn E Oskarsson, MD Assistant Professor, Department of Neurology, University of California, Davis, School of Medicine\nBjorn E Oskarsson, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine\nDisclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Flex Pharma<br/>Serve(d) as a speaker or a member of a speakers bureau for: Grifols<br/>Received research grant from: Neuraltus, Glaxo, Eisai, Cytokinetics, Genentech,.\nDaniel Mordechai Goldenholz, MD, PhD Resident Physician, Department of Neurology, University of California Davis Medical Center\nDaniel Mordechai Goldenholz, MD, PhD is a member of the following medical societies: American Academy of Neurology\nencoded search term (Paraneoplastic Autonomic Neuropathy) and Paraneoplastic Autonomic Neuropathy\nImaging in Lung Cancer Staging\nSmall Cell Lung Cancer Staging\nNon-Small Cell Lung Cancer (NSCLC) Imaging\nNon-Small Cell Lung Cancer (NSCLC) Staging\nThe Expression Level of HJURP has an Independent Prognostic Impact and Predicts the Sensitivity to Radiotherapy in Breast Cancer\n'Unprecedented' Drop in US Cancer Deaths, Driven by Lung Cancer\nOncology and Hematology Clinical Practice Guidelines - 2019 Year in Review\nTop News From ASCO 2019: Slideshow\n2001 /viewarticle/923703 News\nNews Step Count Predicts Outcomes in Lung Cancer\nNews Age No Excuse Not to Treat Lung Cancer, Even in 'Oldest Old'\nNews Auricular Acupressure May Reduce Fatigue During Lung-Cancer Chemo\nNews AstraZeneca's Imfinzi Gets Speedy FDA Review for Small Cell Lung Cancer"