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      The Role of Vitamin B 12 in the Management and Optimization of Treatment in Patients With Degenerative Cervical Myelopathy

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          Abstract

          Study Design:

          Narrative review.

          Objectives:

          To discuss the relationship between degenerative cervical myelopathy (DCM) and vitamin B 12 deficiency. Specifically, it is the aim to outline the rational for future research into assessment and therapeutic optimization of vitamin B 12 in the treatment of DCM.

          Methods:

          Literature review.

          Results:

          DCM is the commonest cause of spinal cord impairment, with an average age of presentation in the sixth decade. Patients at this age have also been reported to have a high prevalence of vitamin B 12 deficiency, with estimates of up to 20% in the elderly. Vitamin B 12 deficiency can result in subacute combined degeneration of the spinal cord (SACD), and several case reports have pointed to patients with both DCM and SACD. Both SACD and reversible compressive injury due to DCM necessitate remyelination in the spinal cord, a process that requires adequate vitamin B 12 levels. Basic science research on nerve crush injuries have shown that vitamin B 12 levels are altered after nerve injury and that vitamin B 12 along with dexamethasone or nonsteroidal anti-inflammatory drugs can reduce Wallerian degeneration. Furthermore, it has been suggested that a combination of B-vitamins can reduce glutamate-induced neurotoxicity.

          Conclusions:

          Given the high prevalence of clinical and subclinical vitamin B 12 deficiency in the elderly, the role of vitamin B 12 in myelination, and vitamin B 12 deficiency as a differential diagnosis of DCM, it is important to investigate what role vitamin B 12 levels play in patients with DCM in terms of baseline neurological function and whether optimization of vitamin B 12 levels can improve surgical outcome. Furthermore, the routine assessment of vitamin B 12 levels in patients considered for DCM surgery should be considered.

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          Most cited references49

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          Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis.

          Among 141 consecutive patients with neuro-psychiatric abnormalities due to cobalamin deficiency, we found that 40 (28 percent) had no anemia or macrocytosis. The hematocrit was normal in 34, the mean cell volume was normal in 25, and both tests were normal in 19. Characteristic features in such patients included paresthesia, sensory loss, ataxia, dementia, and psychiatric disorders; longstanding neurologic symptoms without anemia; normal white-cell and platelet counts and serum bilirubin and lactate dehydrogenase levels; and markedly elevated serum concentrations of methylmalonic acid and total homocysteine. Serum cobalamin levels were above 150 pmol per liter (200 pg per milliliter) in 2 patients, between 75 and 150 pmol per liter (100 and 200 pg per milliliter) in 16, and below 75 pmol per liter (100 pg per milliliter) in only 22. Except for one patient who died during the first week of treatment, every patient in this group benefited from cobalamin therapy. Responses included improvement in neuropsychiatric abnormalities (39 of 39), improvement (often within the normal range) in one or more hematologic findings (36 of 39), and a decrease of more than 50 percent in levels of serum methylmalonic acid, total homocysteine, or both (31 of 31). We conclude that neuropsychiatric disorders due to cobalamin deficiency occur commonly in the absence of anemia or an elevated mean cell volume and that measurements of serum methylmalonic acid and total homocysteine both before and after treatment are useful in the diagnosis of these patients.
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            Cervical spondylotic myelopathy: the clinical phenomenon and the current pathobiology of an increasingly prevalent and devastating disorder.

            Cervical spondylotic myelopathy (CSM) is a common disorder involving chronic progressive compression of the cervical spinal cord due to degenerative disc disease, spondylosis, or other degenerative pathology. CSM is the most common form of spinal cord impairment and causes functional decline leading to reduced independence and quality of life. Despite a sound understanding of the disease process, clinical presentation and management, a universal definition of CSM and a standardized index of severity are not currently used universally. Work is required to develop a definition and establish clinical predictors of progression to improve management of CSM. Despite advances in decompressive and reconstructive surgery, patients are often left with residual disability. Gaps in knowledge of the pathobiology of CSM have limited therapeutic advances to complement surgery. Although the histopathologic and pathophysiologic similarities between CSM and traumatic spinal cord injury have long been acknowledged, the unique pathomechanisms of CSM remain unexplored. Increased efforts to elucidate CSM pathobiology could lead to the discovery of novel therapeutic targets for human CSM and other spinal cord diseases. Here, the natural history of CSM, epidemiology, clinical presentation, and current methods of clinical management are reported, along with the current state of basic scientific research in the field.
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              Neurologic aspects of cobalamin deficiency.

              We reviewed 153 episodes of cobalamin deficiency involving the nervous system that occurred in 143 patients seen over a recent 17-year period at 2 New York City hospitals. Pernicious anemia was the most common underlying cause of the deficiency. Neurologic complaints, most commonly paresthesias or ataxia, were the first symptoms of Cbl deficiency in most episodes. The median duration of symptoms before diagnosis and treatment with vitamin B12 was 4 months, although long delays in diagnosis occurred in some patients. Diminished vibratory sensation and proprioception in the lower extremities were the most common objective findings. A wide variety of neurologic symptoms and signs were encountered, however, including ataxia, loss of cutaneous sensation, muscle weakness, diminished or hyperactive reflexes, spasticity, urinary or fecal incontinence, orthostatic hypotension, loss of vision, dementia, psychoses, and disturbances of mood. Multiple neurologic syndromes were often seen in a single patient. In 42 (27.4%) of the 153 episodes, the hematocrit was normal, and in 31 (23.0%), the mean corpuscular volume was normal. Neutropenia and thrombocytopenia were unusual even in anemic patients. In nonanemic patients in whom diagnosis was delayed, neurologic progression frequently occurred although the hematocrit remained normal. In 27 episodes, the serum cobalamin concentration was only moderately decreased (in the range of 100-200 pg/ml) and in 2 the serum level was normal. Neurologic impairment, as assessed by a quantitative severity score, was judged to be mild in 99 episodes, moderate in 39 and severe in 15. Severity of neurologic dysfunction before treatment was clearly related to the duration of symptoms prior to diagnosis. In addition, the hematocrit correlated significantly with severity, independent of the longer duration of symptoms in nonanemic patients. Four patients experienced transient neurologic exacerbations soon after beginning treatment with cyanocobalamin, with subsequent recovery. Followup evaluation was adequate to assess the neurologic response to vitamin B12 therapy in 121 episodes. All patients responded, and in 57 (47.1%), recovery was complete, with no remaining symptoms or findings on examination. The severity score was reduced by 50% or greater after treatment in 91% of the episodes. Residual long-term moderate or severe neurologic disability was noted following only 7 (6.3%) episodes. The extent of neurologic involvement after treatment was strongly related to that before therapy as well as to the duration of symptoms. The percent improvement over baseline neurologic status after treatment was inversely related to duration of symptoms and hematocrit. Some evidence of response was always seen during the first 3 months of treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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                Author and article information

                Journal
                Global Spine J
                Global Spine J
                GSJ
                spgsj
                Global Spine Journal
                SAGE Publications (Sage CA: Los Angeles, CA )
                2192-5682
                2192-5690
                17 May 2018
                May 2019
                : 9
                : 3
                : 331-337
                Affiliations
                [1 ]Department of Neurosurgery, Yale University, New Haven, CT, USA
                [2 ]Department of Neurosurgery, University of Cincinnati, Cincinnati, OH, USA
                [3 ]Department of Neurosurgery, Johns Hopkins University, Baltimore, MD, USA
                Author notes
                [*]Joseph S. Cheng, Department of Neurosurgery, University of Cincinnati College of Medicine, 260 Stetson Street, Suite 2200, Cincinnati, OH 45219, USA. Email: chengj6@ 123456ucmail.uc.edu
                Author information
                https://orcid.org/0000-0002-4965-3059
                Article
                10.1177_2192568218758633
                10.1177/2192568218758633
                6542160
                31192102
                d6c533a8-7b22-42df-9be1-be67e99586f2
                © The Author(s) 2018

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 License ( http://www.creativecommons.org/licenses/by-nc-nd/4.0/) which permits non-commercial use, reproduction and distribution of the work as published without adaptation or alteration, without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Categories
                Review Articles

                nutrition,anemia,subacute combined degeneration,spinal cord,nitrous oxide,cobalamin

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