Links information Subacute degeneration of the spinal cord

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Links information Subacute degeneration of the spinal cord

Postby anotherwithpa » Thu Apr 17, 2008 7:50 am

Links to information about Subacute degeneration of the spinal cord :

Vitamin B-12 Associated Neurological Diseases
http://emedicine.medscape.com/article/1152670-overview


Defenition:

Subacute combined degeneration of the cord ïs a symmetrical neuropathy affecting the legs more than the arms; it causes paraesthesiae and numbness (especially in the feet), unsteadiness, ataxia, and difficulty in walking (with a tendency to fall in the dark).

It was thought that these occurred only with vitamin B12 deficiency, but it is now known that they can also occur with folate deficiency [Green and Miller, 1999]. They may occur even in the absence of anaemia.

Pernicious anaemia and intestinal malabsorption: spinal cord degeneration developing during vitamin B 12 treatment.

http://www.pubmedcentral.nih.gov/pagere ... ageindex=1

edited to remove non working link
Last edited by anotherwithpa on Wed Mar 05, 2014 11:35 am, edited 3 times in total.
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Postby kimks mom » Sun Sep 14, 2008 6:14 pm

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Vitamin B-12 Associated Neurological Diseases

Postby anotherwithpa » Mon Dec 08, 2008 1:45 pm

http://www.emedicine.com/NEURO/topic439.htm

Vitamin B-12 Associated Neurological Diseases
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Managing Peripheral Neuropathy

Postby anotherwithpa » Fri Feb 20, 2009 5:24 pm

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Functional vitamin B12 deficiency, normal serum B12.

Postby anotherwithpa » Wed Jul 29, 2009 9:40 am

http://www.ncbi.nlm.nih.gov/pubmed/1915 ... t=Abstract
Functional vitamin B12 deficiency.

Turner MR, Talbot K.

Department of Neurology, John Radcliffe Hospital, University of Oxford, Oxford, UK.

We describe a case of functional vitamin B12 deficiency where the repeated measurement of a serum B12 level within the normal range led to delay in the diagnosis of subacute combined degeneration of the spinal cord, and possibly permanent neurological damage as a result. Failure of intracellular transport of B12 by transcobalamin-2 can lead to functional B12 deficiency but with apparently normal serum levels, and is suggested by raised levels of either serum methylmalonic acid or homocysteine, associated with low levels of transcobalamin-2. Such patients may respond to repeated high-dose injections of B12.

Publication Types:
Case Reports
Historical Article

PMID: 19151237 [PubMed - indexed for MEDLINE]
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Neuropsychiatric disturbances/late-onset cobalamin C disease

Postby anotherwithpa » Sun Sep 06, 2009 7:23 am



Neuropsychiatric disturbances in presumed late-onset cobalamin C disease.Roze E, Gervais D, Demeret S, Ogier de Baulny H, Zittoun J, Benoist JF, Said G, Pierrot-Deseilligny C, Bolgert F.
Service de Neurologie 1, Groupe Hospitalier Pitié-Salpêtrière, Paris, France.

BACKGROUND: Combined methylmalonic aciduria and homocystinuria cobalamin C type (cobalamin C disease) is an inborn metabolic disorder consisting of an impaired intracellular synthesis of the 2 active forms of vitamin B12 (cobalamin), namely, adenosylcobalamin and methylcobalamin, that results in increased levels of methylmalonic acid and homocysteine in the blood and urine. Most patients present in the first year of life with systemic, hematological, and neurological abnormalities. Late-onset forms are rare and had not been comprehensively characterized. They could be easily misdiagnosed. OBJECTIVE: To describe clinical and biochemical features of the disease in 2 siblings affected with presumed late-onset cobalamin C disease. DESIGN: Case report and review of the literature. SETTING: Neurological intensive care unit of a university hospital. OBSERVATION: We describe 2 patients with neurological deterioration due to presumed cobalamin C disease. A 16-year-old girl was initially seen with psychosis and severe progressive neuropathy requiring mechanical ventilatory support and her 24-year-old sister had a 2-year disease course of subacute combined degeneration of the spinal cord. A metabolic workup displayed increased methylmalonic acid levels, severe hyperhomocysteinemia, and low plasma methionine levels. The diagnosis was then confirmed by demonstration of impaired synthesis of adenosylcobalamin and methylcobalamin in cultured skin fibroblasts and Epstein-Barr virus-infected lymphocytes. Under specific treatment the younger sister's condition dramatically improved. CONCLUSIONS: Although complementation studies have not been conducted, it is most likely these patients had cobalamin C disease. This study emphasizes the possibility of late-onset disease with purely neurological manifestations. Left untreated, this treatable condition can lead to death or irreversible damage to the nervous system. Screening for intracellular vitamin B12 dysmetabolism should, therefore, be considered in the investigation of adults with unexplained neurological disease, particularly when they are initially seen with a clinical picture suggestive of vitamin B12 deficiency.
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Peripheral neuropathy

Postby anotherwithpa » Wed Sep 23, 2009 9:13 am

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subacute combined degeneration with normal serum vitamin B12

Postby anotherwithpa » Sat Oct 24, 2009 9:55 am

A case of subacute combined degeneration with normal serum vitamin B12 level



[A case of subacute combined degeneration with normal serum vitamin B12 level][Article in Japanese]

1: Rinsho Shinkeigaku. 2003 Sep;43(9):552-5.

Nagaishi A, Takashima H, Fukuda Y, Kuroda Y.
Department of Internal Medicine, Sasebo City General Hospital.

A 40-year-old woman was admitted to our hospital because of pancytopenia with megaloblastic anemia. Two months later she complained of rapidly progressive gait disturbance and numbness in the distal part of limbs. She also told that her hair had turned totally gray in the third decade. Neurologically, mental state, cranial nerves and cerebellar functions were normal. Superficial sensations were impaired below the lower thoracic level and deep sensations were completely lost in the lower limbs. Moderate weakness was found in the lower limbs, symmetrically. Deep tendon reflexes were diminished in the upper limbs and absent in the lower limbs. Babinski's reflex was positive bilaterally. MR images of the spinal cord showed hyperintensity in the posterior column below the thoracic cord. Although the serum level of vitamin B12 was within normal range, serum homocysteine level was elevated markedly. Under the diagnosis of subacute combined degeneration (SCD) due to possible vitamin B12 deficiency, the treatment with intravenous injections of 500 micrograms/day of mecobalamin was undertaken. Muscle strength and sensory impairment improved progressively and she became able to walk with a cane. The coloration of her gray hair was also noted. After treatment, pancytopenia and megaloblastic anemia also markedly improved. Vitamin B12 became high in serum concentration and the serum level of homocysteine became normal. These clinical and laboratory findings support the diagnosis of SCD with normal serum level of vitamin B12 in our case, suggesting that the level of vitamin B12 in serum does not always correlate with that in tissue and, therefore, SCD should not be excluded just only by the reason of normal serum vitamin B12 level.

PMID: 14727562 [PubMed - indexed for MEDLINE
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MRI and subacute combined degeneration of the spinal cord

Postby anotherwithpa » Sat Oct 24, 2009 10:04 am

: No Shinkei Geka. 2005 May;33(5):489-95.Links
A case of subacute combined degeneration of the spinal cord diagnosed by characteristic findings of magnetic resonance imaging: case report and review of 22 cases



Morishita A, Tomita H, Takaishi Y, Nishihara M, Kohmura E.
Department of Neurosurgery, Kobe University Graduate School of Medicine, Japan.

Subacute combined degeneration (SCD) is a rare cause of demyelination of the dorsal and lateral columns of the spinal cord, and is a neurogenic complication due to vitamin B12 deficiency. This report concerns a patient with progressive sensory disturbance, but no abnormal neurological findings. A 73-year-old man with gastrectomy presented with a 6-month history of gradually worsening tingling in both hands. Magnetic resonance imaging (MRI) of the cervical spine clearly showed symmetrical high-signal areas on T2WI involving the posterior columns of the cervical cord from C2 through C6. A diagnosis of SCD of the spinal cord was considered and confirmed by laboratory findings. The patient was treated with vitamin B12 supplements and showed gradual improvement in his clinical symptoms. Repeat MRI of the cervical spine after 3 months indicated a slight decrease in the area of the abnormal signal. Among all the possible causes of myelopathy, SCD of the spinal cord, involving neurological complications due to vitamin B12 deficiency, is one of the less often encountered diseases. Nevertheless, SCD should be considered in the differential diagnosis of all spinal cord, peripheral nerve, and neuropsychiatric disorders.

PMID: 15912769 [PubMed - indexed for MEDLINE]

--------------------------

Singapore Med J. 2008 Nov;49(11):e330-2.(pdf)
Reversible myelopathy with vitamin B12 deficiency.



Reversible myelopathy with vitamin B12 deficiency.Senol MG, Sonmez G, Ozdag F, Saracoglu M.
Department of Neurology, GATA Haydarpasa Egitim Hastanesi, Noroloji Servisi, Kadikoy, Istanbul, Turkey. mgsenol@yahoo.com

Vitamin B12 deficiency causes haematological, gastrointestinal, psychiatric and neurological diseases. Subacute combined degeneration (SCD) of the spinal cord, characterised by degeneration of the lateral and posterior columns, is often found due to vitamin B12 deficiency. We report SCD occurring in a 57-year-old man who presented with a 2.5-month history of gradually progressing tingling in the fingers and toes and neck ache. Laboratory data revealed vitamin B12 deficiency and magnetic resonance (MR) imaging of the cervical spinal cord demonstrated abnormal hyperintense signal changes on T2-weighted imaging of the posterior columns. In our case, follow-up MR imaging findings correlated well with clinical outcome after treatment with vitamin B12 supplements. Neurological symptoms in vitamin B12 deficiency are frequent. Early spinal MR imaging assists in the early diagnosis and treatment of the disease.

PMID: 19037544 [PubMed - indexed for MEDLINE]

Link to actual case report:
http://smj.sma.org.sg/4911/4911cr13.pdf

(I'm now just annoyed that the MRI I had was of head only, well that does not help much with diagnosing SCD, but think it was only done to eliminate somethin bad such as tumour..)
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high doses of Methylcobalamin improves nerve regeneration

Postby anotherwithpa » Thu Jan 21, 2010 10:16 am



In a rat sciatic nerve injury model, continuous administration of high doses of methylcobalamin improves nerve regeneration and functional recovery.
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SACD caused by nitrous oxide anaesthesia.

Postby BeeNumber12 » Fri Jul 13, 2012 6:06 pm

http://www.ncbi.nlm.nih.gov/pubmed/19169627 PUBMED
Neurol Sci. 2009 Feb;30(1):75-6. Epub 2009 Jan 24.

Subacute combined degeneration of the spinal cord caused by nitrous oxide anaesthesia.

Renard D, Dutray A, Remy A, Castelnovo G, Labauge P.
Source
Department of Neurology, CHU Nîmes, Hôpital Caremeau, Place du Pr Debré, 30029 Nîmes Cedex 4, France. dimitrirenard@hotmail.com
Abstract
Vitamin B12 deficiency causes haematological, gastrointestinal and neurological diseases. Subacute combined degeneration (SCD) of the spinal cord is characterised by degeneration of the posterior and lateral columns. We report a case of SCD associated with nitrous oxide anaesthesia.
Regards,
Dorothy
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SCD is progressive, not likley simultaneous dengeneration

Postby BeeNumber12 » Fri Jul 13, 2012 6:43 pm

Regards,
Dorothy
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Re: SACD AND faulty B12 assays

Postby BeeNumber12 » Tue Oct 09, 2012 6:07 pm

Regards,
Dorothy
Please independently check any information or advice, by reading from or questioning reputable sources, before acting on it.
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SACD -easy diagnosis, effective treatment

Postby BeeNumber12 » Sat Oct 20, 2012 7:24 pm

Regards,
Dorothy
Please independently check any information or advice, by reading from or questioning reputable sources, before acting on it.
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Re: Links information Subacute degeneration of the spinal co

Postby kimks mom » Tue Jul 23, 2013 2:37 am

MRI Images of SACD..thanks to Andrea for finding this article:
http://www.scielo.br/scielo.php?pid=S00 ... ci_arttext
I am a support person for my daughter who was diagnosed with PA and Folate Anaemia in 1994, at the age of 27. Another daughter diagnosed with Hashimotos 2010 but she doesn't have PA.
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