Subacute Combined Degeneration Of Cord Research Articles

The other side of funny gas (nitrous oxide – N2O), a case report of subacute combined degeneration of cord

The other side of funny gas (nitrous oxide – N2O), a case report of subacute combined degeneration of cord

V for vitamin, inverted V for lack of it: A rare case of subacute combined degeneration of cord with bladder symptoms and associated multiple Tarlov cysts

Subacute degeneration of cord (SACD) is a rare presentation of a common disease and it should be kept in mind when the patient develops symptoms of peripheral neuropathy. This is a case of a 65-year-old male who presented with pins and needles sensation of bilateral hands and feet and with difficulty in voiding. Neurological examination showed large fiber neuropathy with an exaggerated knee jerk, absent ankle jerk, extensor plantar, and a positive Romberg’s sign. Routine laboratory investigations showed low hemoglobin and low vitamin B12 levels. Magnetic resonance imaging of the spinal cord showed a hyperintense lesion in the posterior aspect of the cervical cord with a classical “inverted V” sign on the axial section which is suggestive of SACD. Coincidentally, there were multiple Tarlov cysts present. Finally, the patient improved with vitamin B12 injections. This case is unique as an association of SACD with Tarlov cysts with a classical inverted V sign has not been reported according to the literature.

Subacute combined degeneration of spinal cord, optic atrophy and thrombocytopenia without anemia secondary to B12 deficiency

Long-standing vitamin B12 deficiency can lead to neurological manifestations such as optic atrophy and subacute combined degeneration of the cord without causing significant anemia. In addition, folic acid supplementation could mask the hematological manifestations of vitamin B12 deficiency and delay the presentation of neurological manifestations We present a case of a 32-year-old vegan woman on long-term sodium valproate and folic acid treatment presenting with progressive weakness of bilateral lower limbs for three months and reduced vision in both eyes for two weeks duration. Further evaluation revealed optic atrophy, combined degeneration of the spinal cord, macrocytosis, thrombocytopenia, and severely deficient serum B12 levels. With B12 replacement therapy, the patient’s overall wellbeing improved.

Subacute combined degeneration of the spinal cord in functional vitamin B12 Deficiency states

Vitamin B12 is an essential enzymatic cofactor in multiple cellular metabolic pathways. Deficiency states can arise as a result of both depletion of absolute systemic levels and pathological processes that block its ability to act as an enzymatic cofactor. The latter is also known as functional vitamin B12 deficiency. This can cause a variety of systemic, haematological, and neurological manifestations, some of which may be irreversible if not promptly treated. Neurological syndromes include subacute combined degeneration of the cord (SCDC), peripheral, optic, and autonomic neuropathies, and neuropsychiatric or cognitive deficits. This review presents a case series of vitamin B12 deficiencies leading to SCDC, and we include the clinical features, significant investigations, treatments, and prognoses.

Vitamin B12 deficiency presenting as acute febrile encephalopathy and retinopathy

Vitamin B12 deficiency causes macrocytic anaemia, peripheral neuropathy, myelin loss in posterior and lateral columns of spinal cord (subacute combined degeneration of cord) and a wide variety of neuropsychiatric symptoms...

Pernicious azotaemia? A case series of subacute combined degeneration of the cord secondary to nitrous oxide abuse

Nitrous oxide abuse is a rare cause of vitamin B12 deficiency and consequent subacute combined degeneration of the spinal cord. Worldwide and Australian statistics indicate that recreational use of nitrous oxide is increasing. We report four cases of females aged 18–24 years presenting with clinical symptoms of subacute combined degeneration of the spinal cord. MRI during admission demonstrated the classic findings of T2 hyperintensity, predominantly within the dorsal columns of the spinal cord, with variable involvement of the lateral corticospinal tracts. These cases highlight the ready availability of nitrous oxide and the fact that heavy prolonged recreational use is occurring in the community. It is important that clinicians in emergency and community settings are alerted to this unusual cause of subacute combined degeneration of the spinal cord because early aggressive vitamin B12 replacement together with behavioural change can reverse this disabling neurological syndrome.

"Inverted V sign" in Sub-Acute Combined Degeneration of Cord.

A 54-year-old male patient presented to the outpatient department of neurology with complaints of tingling and numbness of hands since two months. Neurological examination revealed reduced power and decreased proprioception and vibration sense of hands. Laboratory investigations done showed normal Hb-13.7g/dl (normal range, 13.5-17.5 g/dl).Other routine blood, urine parameters were within normal limits. MRI of cervical spine was advised and performed which showed symmetric T2W hyperintense signals in dorsal columns of cervical spinal cord from C2 to C5 [Table/Fig-1a&b,​,2]2] levels (Characteristic Inverted V sign). A provisional diagnosis of Sub-Acute Combined Degeneration of Cord (SACD) was considered. Retrospective investigations of blood showed reduced serum VITAMIN B12 levels of 78.6pg/mL (Normal-200 to 900pg/mL), mild increased mean corpuscular volume 120fl (normal range, 80-100 fl),elevated serum homocysteine levels. Patient was started on vitamin B12 therapy and showed progressive resolution of clinical symptoms. [Table/Fig-1a&b]: Axial T2W MRI at C3 (A) and C4 (B) vertebral level of the spinal cord showing characteristic “inverted v pattern” hyperintene signal (arrow) in the posterior compartment of the spinal cord [Table/Fig-2]: Sagittal T2W MRI showing linear hyperintense signal (arrows) predominantly in the posterior compartment of the cervical spinal cord extending from C2-C5 vertebral levels of the cord Causes of vitamin B12 deficiency include malabsorption syndromes such as pernicious anaemia, crohns disease, celiac disease, bacterial overgrowth in intestinal blind loops, postgastrectomy and ileal resection. Deficiency of vitamin B12 results in failure of conversion of methyl malonyl coenzyme A to succinyl co A resulting in accumulation of methylmalonic acid which causes myelin toxicity of preferential dorsal/posterior columns of the cord [1]. Pathologically multifocal vacuolated and demyelinating lesions involving the dorsal columns, predominately in the lower cervical and upper thoracic region [1] are seen. Demyelination of posterior columns of thoracic spinal cord appears to be the earliest manifestation of vitamin B12 deficiency.It is also considered as the most reversible pathological stage in a case of SACD. MRI findings in SACD of cord are minimal spinal cord enlargement with dorsal spinal cord hypointensity on T1WI, hyperintensity on T2W images. On sagittal images longitudinal signal changes are noted along the dorsal columns of spinal cord.T2WI – axial images show typically characteristic pattern of symmetric bilateral hyperintense signals in the dorsal columns. This specific MRI appearance has been described as the “Inverted V sign” or “Inverted Rabbit Ears appearance”. Some cases may show T2 hyperintense signal in lateral columns of cord and cerebral white matter. Differential diagnsosis for bilateral posterior column involvement [2] include infectious myelitis, infarction of spinal cord, inflammatory demyelination including multiple sclerosis, acute disseminated encephalomyelitis, acute transverse myelitis, and copper deficiency myelopathy. Once the diagnosis of SACD is suspected, treatment with vitamin B12 injection should be started as early as possible to avoid irreversible neurologic damage [3]. Recognition of the specific MRI pattern of cord involvement together with clinical and laboratory analysis helps in early detection and treatment of the Subacute combined degeneration of the spinal cord.

Subacute Combined Cord Degeneration: A Rare Complication of Nitrous Oxide Misuse

We describe a severe case of subacute combined degeneration of the spinal cord precipitated by overuse of the analgesic Entonox (a 50:50 mixture of nitrous oxide and oxygen) in a 19-year-old female with previously undiagnosed vitamin B12 deficiency. MRI of the spine revealed symmetric abnormal signal in the dorsal and anterolateral columns of the cervical and thoracic cord, correlating with the patient's symptoms. Myeloneuropathy is caused by inactivation of vitamin B12 by nitrous oxide. The patient's condition slowly improved with cessation of nitrous oxide exposure and vitamin B12 replacement therapy.

Psychotic Disorder and Extrapyramidal Symptoms Associated with Vitamin B12 and Folate Deficiency

Vitamin B12 and folate deficiency causing neuropsychiatric and thrombotic manifestations, such as peripheral neuropathy, subacute combined degeneration of cord, dementia, ataxia, optic atrophy, catatonia, psychosis, mood disturbances, myocardial infarction and portal vein thrombosis are well known. This present report highlights an unusual presentation of vitamin B12 deficiency-psychotic disorder, extrapyramidal symptoms in a 12-year-old boy. His symptoms responded to parenteral vitamin B12 therapy. So with this report we emphasized that serum vitamin B12 and folate levels should be measured, especially in those patients who present with other known neuropsychiatric features of vitamin B12 and folate deficiency.

Síndrome neuranêmica. Discussão de um caso com caráter familial e evolução aguda, em jovem

Report of a case of pernicious anemia with subacute combined degeneration of the spinal cord. The symptoms began in 1946, at the age of 18, with paresthesias in the hands and feet and weakness in the legs, but no objective somatic sign was evidenced at a medical examination performed in April 1948. About four months later (last days of July), the patient suddenly presented a clinical picture of transverse myelitis, the level of anesthesia reaching T3; death occurred in September 3rd, with bronchopneumonia. Pathological examination disclosed a typical subacute combined degeneration of the cord. The patient was feeble-minded, and his father suffers also of pernicious anemia and subacute combined degeneration of the spinal cord. The authors discuss the heredofamilial aspect, the early onset and the acute evolution of the disease.

A CASE OF SUBACUTE COMBINED DEGENERATION OF THE SPINAL CORD WITH INTERESTING HEREDITARY FEATURES

Case Reports1 October 1942A CASE OF SUBACUTE COMBINED DEGENERATION OF THE SPINAL CORD WITH INTERESTING HEREDITARY FEATURESS. W. RANSON JR., M.D., SAMUEL REBACK, M.D.S. W. RANSON JR., M.D.Search for more papers by this author, SAMUEL REBACK, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-17-4-738 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptOn January 27, 1938, a man, aged 24, was brought to the Neurological Institute of New York, apparently moribund, suffering with subacute combined degeneration of the spinal cord secondary to pernicious anemia. His mother and paternal uncle had had the same disease. This hereditary background, the abnormally early onset of the illness, and the unusually good response to therapy have prompted the presentation of this case report.Hurst,1Meulengracht,2Johannessohn,3Tscherning,4Ungley and Suzman,5and others have presented instances of subacute combined degeneration occurring in more than one member of a family. Wilkinson and Brockbank6in 1931 reviewed the literature,...Bibliography1. HURST AF: Addison's (pernicious) anemia and subacute combined degeneration of the spinal cord, Brit. Med. Jr., 1924, i, 93. CrossrefGoogle Scholar2. JOHANNESSOHN F: Perniziöse Anämie bei zwei Brüdern, Deutsch. med. Wchnschr., 1925, li, 1953. CrossrefGoogle Scholar3. MEULENGRACHT E: The hereditary factor in pernicious anemia, Am. Jr. Med. Sci., 1925, clxix, 177. Google Scholar4. TSCHERNING R: Biermersche Anämie bei drei Geschwistern, Deutsch. med. Wchnschr., 1926, lii, 707. CrossrefGoogle Scholar5. UNGLEYSUZMAN CCMM: Subacute combined degeneration of the cord: symptomatology and effects of liver therapy, Brain, 1929, lii, 271. CrossrefGoogle Scholar6. WILKINSONBROCKBANK JFW: The importance of familial achlorhydria in the aetiology of pernicious anemia, Quart. Jr. Med., 1931, xxiv, 219. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York, N. Y.*Received for publication September 19, 1940.From the Neurological Institute of New York, New York City. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byA Family Study of Pernicious AnaemiaDistúrbios neurológicos nos estados carenciais aquílicos 1 October 1942Volume 17, Issue 4Page: 738-744KeywordsPernicious anemiaSpinal cord Issue Published: 1 October 1942 PDF downloadLoading ...

THE EFFECT OF THIAMIN ON THE RESIDUAL NEURAL DISTURBANCES OF TREATED PERNICIOUS ANEMIA

Article1 July 1941THE EFFECT OF THIAMIN ON THE RESIDUAL NEURAL DISTURBANCES OF TREATED PERNICIOUS ANEMIAJ. C. ZILLHARDT, M.D., KEITH MACLEAN, M.D., WILLIAM P. MURPHY, M.D.J. C. ZILLHARDT, M.D.Search for more papers by this author, KEITH MACLEAN, M.D.Search for more papers by this author, WILLIAM P. MURPHY, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-15-1-33 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptBy supplying sufficient amounts of anti-pernicious anemia substance it is possible to control the neural disturbances of uncomplicated Addisonian anemia. Certain residual neural manifestations are apt to remain, however, in spite of adequate liver therapy. This is particularly true in patients with advanced nervous system involvement and in those who have not been adequately treated at the onset.Considerable thought has been given the various vitamins1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11in connection with pernicious anemia and its associated neural disturbances. At the blood clinic of the Peter Bent Brigham Hospital interest became focused on...Bibliography1. CONNOR HM: Improvement of neurologic manifestations of pernicious anemia, Proc. Staff Meet. Mayo Clin., 1928, iii, 454. Google Scholar2. GARVEYLEVINGULLER PHPMEI: The effect of liver therapy on the neurologic aspects of pernicious anemia, ANN. INT. MED., 1933, vi, 1441. Google Scholar3. GILDEAKATTWINKELCASTLE EFEEWB: Experimental combined system disease, New Eng. Jr. Med., 1930, ccii, 523-527. CrossrefGoogle Scholar4. GILDEACASTLEGILDEACOBB MCWBEFS: Neuropathology of experimental vitamin deficiency, Am. Jr. Path., 1935, xi, 669. Google Scholar5. BERGEL A: Ein Behandlungserfolg bei funikulärer Myelose mittels Vitamin B1 (Betabion), Deutsch. med. Wchnschr., 1936, lxii, 1643. Google Scholar6. LASCH F: Ein erfolgreich mit Vitamin B1 behandelter Fall von schwerer funikulärer Myelose, München. med. Wchnschr., 1936, lxxxiii, 1390. Google Scholar7. WILLIAMSSPIES RRTD: Vitamin B1 and its uses in medicine, 1938, Macmillan Company, New York. Google Scholar8. WINTROBEMITCHELLKOLB MMDMLC: Sensory neuron degeneration in deficiency, Jr. Exper. Med., 1938, lxviii, 207-220. CrossrefGoogle Scholar9. MILLERRHODES DKCP: The experimental production of loss of hematopoietic elements of the gastric secretion and of the liver in swine with achlorhydria and anemia, Jr. Clin. Invest., 1935, xiv, 153. CrossrefGoogle Scholar10. MELLANBY E: The experimental production and prevention of degeneration in the spinal cord, Brain, 1931, liv, 247. CrossrefGoogle Scholar11. SUZMANMULLERUNGLEY MMGLCC: An attempt to produce spinal cord degeneration in dogs fed a high cereal diet deficient in vitamin A, Am. Jr. Physiol., 1932, ci, 529. CrossrefGoogle Scholar12. MURPHY WP: Anemia in practice, 1939, W. B. Saunders Co., Philadelphia. Google Scholar13. GRINKER RR: Neurology, 1937, Charles C. Thomas, Springfield, Ill. Google Scholar14. GREENFIELDO'FLYNN JGE: Subacute combined degeneration and pernicious anemia, Lancet, 1933, ii, 62. CrossrefGoogle Scholar15. COHEN H: Subacute combined degeneration of the spinal cord, Lancet, 1935, i, 1291. CrossrefGoogle Scholar16. GRINKERKANDEL RRE: Results of treatment of the neurologic complications of pernicious anemia, Arch. Int. Med., 1934, liv, 851. CrossrefGoogle Scholar17. BRAIN WR: Subacute combined degeneration, Oxford University Press, New York. Google Scholar18. KENNEDY F: Cecil, Text Book of Medicine, 1937, W. B. Saunders Co., Philadelphia. Google Scholar19. BRAIN WR: Subacute combined degeneration, Brit. Med. Jr., 1935, ii, 1056. CrossrefGoogle Scholar20. GREENFIELDCARMICHAEL JGEA: The peripheral nerves in cases of subacute combined degeneration of the cord, Brain, 1935, lviii, 483. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication March 30, 1940.From the Medical Clinic of the Peter Bent Brigham Hospital. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byPernicious Anemia 1 July 1941Volume 15, Issue 1Page: 33-43KeywordsBloodHospitalsLiverNervous systemPernicious anemiaResearch laboratoriesThiamine Issue Published: 1 July 1941 PDF downloadLoading ...

SUBACUTE COMBINED DEGENERATION OF THE SPINAL CORD

While cases of subacute combined degeneration of the spinal cord following childbirth or occurring during pregnancy have been occasionally mentioned in the literature, cases of this disease in which hemorrhages took place in the epidural spinal space are altogether unknown. In the older literature, hemorrhages in the parenchyma of the spinal cord, especially the gray matter, have been described repeatedly (Minnich, 1 Rothman, 2 Teichmuller, 3 Rheinboldt 4 and others) in subacute combined degeneration of the cord, but they have not been mentioned in the exhaustive studies of later observers (Russel, Batten and Collier, 5 Woltman 6 and Henneberg 7 ). The microscopic effusions of blood occasionally observed in this condition are accidental or agonal. As, in the case to be reported, the foregoing conditions—childbirth, subacute combined degeneration of the cord and epidural hemorrhages—were combined, a discussion of such an unusual combination will be of interest. REPORT OF CASE History. —A

The Effect of Liver Therapy on the Neurologic Aspects of Pernicious Anemia

Article1 May 1933The Effect of Liver Therapy on the Neurologic Aspects of Pernicious AnemiaPAUL H. GARVEY, M.D., PAUL M. LEVIN, M.D., ERASTUS I. GULLER, M.D.PAUL H. GARVEY, M.D.Search for more papers by this author, PAUL M. LEVIN, M.D.Search for more papers by this author, ERASTUS I. GULLER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-6-11-1441 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe treatment of pernicious anemia with liver, introduced by Minot and Murphy1in 1926, after the experimental work of Whipple and his associates, has had a remarkable effect on the clinical course of the disease. The response of the nervous manifestations has been discussed by various authors with considerable difference of opinion. This is due partly to the use of different criteria in evaluating the results of treatment. Some observers have relied on improvement of symptoms not necessarily dependent upon structural restoration, while others have based their conclusions on the rigid interpretation of abnormal neurologic signs. Another cause for confusion...Bibliography1 MINOTMURPHY GRWP: Treatment of pernicious anemia by a special diet, Jr. Am. Med. Assoc., 1926, lxxxvii, 470-476. CrossrefGoogle Scholar2 CONNER HM: Improvement of neurologic manifestations of pernicious anemia; report of case, Proc. Staff Meet., Mayo Clinic, 1928, iii, 454. Google Scholar3 GILDEAKATTWINKELCASTLE EFEWB: Experimental combined system disease, New Eng. Jr. Med., 1930, ccii, 523-527. CrossrefGoogle Scholar4 MELLANBY E: The experimental production and prevention of degeneration in the spinal cord, Brain, 1931, liv, 247-290. CrossrefGoogle Scholar5 HALLHIRSCH GWEF: Paraplegia in flexion, with subacute combined degeneration of cord, Arch. Neur. and Psychiat., 1930, xxiii, 257-265. CrossrefGoogle Scholar6 CURSCHMANN H: Die Nervenstörungen der Biermerschen Anämie und die Lebertherapie, Deutsch. Ztschr. f. Nervenh., 1929, cxi, 151-159. CrossrefGoogle Scholar7 UNGLEYSUZMAN CCMM: Subacute combined degeneration of the cord: symptomatology and effects of liver therapy, Brain, 1929, lii, 271-294. CrossrefGoogle Scholar8 SMITHBURNZERFAS KCLG: The neural symptoms and signs in pernicious anemia: the effects of liver extract, Arch. Neur. and Psychiat., 1931, xxv, 1100-1110. CrossrefGoogle Scholar9 NEEDLES W: Neurologic complications of pernicious anemia; effects of treatment with liver; a preliminary report, Arch. Neur. and Psychiat., 1931, xxvi, 346-358. CrossrefGoogle Scholar10 DAVISON C: Subacute combined degeneration of the cord: changes following liver therapy; a histopathologic study, Arch. Neur. and Psychiat., 1931, xxvi, 1195-1219. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Rochester, New York*Received for publication July 29, 1932.†From the Department of Medicine, University of Rochester School of Medicine, and the Medical Clinic of the Strong Memorial and Rochester Municipal Hospitals. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDie Erkrankungen des erythrocytären SystemsFunikuläre Spinalerkrankungen 1 May 1933Volume 6, Issue 11Page: 1441-1448KeywordsHospital medicineLiverLiver diseasesPernicious anemia ePublished: 1 December 2008 Issue Published: 1 May 1933 PDF downloadLoading ...

The Common Picture of Sprue, Pernicious Anemia, and Combined Degeneration

I. Summary It is our purpose to show that a common clinical entity is embraced by the accepted diagnoses of tropical sprue, pernicious anemia, and subacute combined degeneration of the spinal cord. Review of published case records of these diseases and a study of our own cases point strongly to there being different intensities of manifestation of a common toxin. This toxin seems to attack the three systems, i.e., the blood, the gastro-intestinal tract and the cord, to varying degrees although nearly always, in cases fully studied, all three systems afford evidence of damage under any one of the three clinical diagnoses. For example, typical sprue may show evidence of cord changes and pernicious features in the blood. Typical Addisonian anemia shows evidence of sprue-like gastro-intestinal changes and of cord degeneration. And finally, subacute combined degeneration of the cord is always associated with a progressive anemia which tends to become pernicious in character, and frequently with achylia and other gastro-enteric lesions. We suggest further that the toxin is more likely a group or type toxin than a unit chemical substance, and that its place of origin is in the digestive canal. Such a conception of these large disease groups means that sprue and pernicious anemia can not be considered as unit diseases with a constant classical and characteristic type. But each is a group of variable clinical syndromes just as we know to be the case in the group of what is called beriberi. This holds true to a lesser degree for combined degeneration.