Combined Degeneration Of Spinal Cord Research Articles

Laughing gas abuse causing subacute combined spinal cord degeneration with psychiatric manifestations

Background. Nitrous oxide, a nonirritating gas commonly used as an anesthetic, is increasingly abused by the young population for its euphoric effects due to its seemingly harmless nature. However, its neurological impacts can vary in intensity and sometimes result in permanent damage. Accurate diagnosis and treatment hinge on identifying nitrous oxide use through anamnesis, clinical and paraclinical findings, as demonstrated in the following case report. Case report. A 27-year-old female with psychiatric history presented with progressive paresthesia and walking difficulty, admitting to recent nitrous oxide use, alongside other substances. Clinical examination revealed mild tetraparesis, coordination disturbances, generalized hyporeflexia, and sensory deficits. Electromyography showed severe sensory neuropathy, and spinal MRI indicated subacute combined degeneration (SCD) of the spinal cord. Laboratory tests revealed hyperhomocysteinemia and elevated methylmalonic acid levels, despite normal vitamin B12 levels. Treatment included intramuscular vitamin B12, folic acid, and neurotrophic agents, along with physical rehabilitation. Psychiatric symptoms, possibly exacerbated by nitrous oxide, complicated adherence to therapy. Conclusions. This case underscores the neurotoxic potential of nitrous oxide, particularly its disruption of cobalamin metabolism, and highlights the need for thorough patient histories to uncover substance use contributing to neurological symptoms. Despite treatment, some neurological deficits may persist, emphasizing the importance of early intervention and comprehensive care strategies.

FT4-to-FT3 ratio is a novel prognostic marker in subacute combined spinal cord degeneration patients.

The FT4-to-FT3 ratio (FFR) variations in patients with subacute combined spinal cord degeneration (SCSD) as a potentially useful prognostic indicator are still unknown. This study aimed to investigate the changes of FFR as a potentially valuable prognostic predictor in patients with SCSD. This study included 144 consecutive SCSD patients who received standard diagnostic and therapeutic procedures between January 2015 and December 2021 and were admitted to the Department of Neurology at the First Affiliated Hospital of Bengbu Medical University. At the time of admission, we gathered data on all patients' demographics, daily routines, previous chronic conditions, medication histories, and other clinical details. For the purpose of measuring FFR, blood samples were specifically taken within 48 h of admission. The degree of neurological impairment of patients was assessed using the functional disability scale at the time of admission. At 6 months following discharge, the Modified Rankin Scale (mRS) was used to evaluate the clinical prognosis. To evaluate the relationship between the FFR and the risks of a poor outcome (mRS > 2), univariate and multivariate logistic regression analysis was utilized. The significance of the FT4/FT3 ratio in predicting the clinical outcomes in SCSD patients 6 months after discharge was assessed using the area under curve-receiver operating characteristic (AUC-ROC). About 90 patients (62.5%) of the 144 patients had poor outcomes, while 54 (37.5%) had favorable outcomes. Higher FFR at admission was independently linked to higher odds of a poor outcome, according to a logistic analysis. With an optimized cutoff value of >2.843, the FFR exhibited the maximum accuracy for predicting a poor outcome, according to the AUC‒ROC curve (AUC 0.731, P < 0.001; sensitivity, 77.8%; specificity, 83.3%). FFR was identified as an independent predictor of poor outcomes by multivariate logistic regression (OR, 2.244; 95% CI, 1.74-2.90; P < 0.001). We discovered that in patients who had a bad result 6 months after discharge, the FFR had dramatically increased at the time of admission, providing a unique prognostic marker in patients with SCSD.

Poūmės kombinuotos nugaros smegenų degeneracijos, sukeltos diazoto monoksido („linksminančių dujų”) vartojimo, klinikinio atvejo aprašymas

Although nitrous oxide (N2O) has long been used as an anesthetic, it’s use as a recreational drug has recently increased. As N2O abuse is associated with a number of adverse health effects, it has become a significant public health issue. Chronic abuse can lead to a number of neurological complications, most commonly related to functional vitamin B12 deficiency. One of the most encountered forms of N2O neurotoxicity is a subacute combined degeneration, which can cause permanent neurological damage. The medical community should therefore be aware of the increasing scale of recreational N2O exposure and the possible complications of this drug abuse. Early recognition and treatment of N2O toxicity are crucial. We present the case of an 18-year-old male who was diagnosed with subacute combined spinal cord degeneration related to N2O abuse.

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.

The association between serum total homocysteine and subacute combined degeneration of spinal cord

Objective: The research was aimed to investigate the association between serum total homocysteine (tHcy) and subacute combined degeneration of the spinal cord (SCD). Methods: A retrospective survey of 106 newly diagnosed patients with SCD were enrolled in this research who were treated in the department of neurology of Xijing Hospital from January 2008 to February 2019, meanwhile, 121 patients with spinal cord lesion (not SCD) and 104 neurology mild outpatients were selected as controls. Serum tHcy level was determined by using the chemiluminescent immunoassay assay. A multivariate logistic regression model was used to analyze the risk factors for SCD. The area under the curve (AUC) of the receiver operating characteristic (ROC) curve, sensitivity, specificity and Youden index were used to evaluate the diagnostic efficacy of tHcy. Spearman correlation analysis was used to observe the correlation between tHcy and SCD severity. The SCD patients were categorized into normal or mild tHcy group, moderate tHcy group, and severe tHcy group based on tHcy levels. Clinical symptoms, nerve conduction velocity, magnetic resonance imaging (MRI) findings from the patients were studied. Results: The serum tHcy levels in SCD patients were 64.3(26.5, 98.8) μmol/L, while in patients with spinal cord lesion (not SCD) group were 13.7(10.8, 19.2) μmol/L, neurology mild outpatients were 10.6(8.2, 13.0) μmol/L, which was higher in SCD group (H=112.020,P<0.001), (H=165.525,P<0.001).The multivariate logistic regression model showed tHcy is the impact factor of SCD (OR=1.107, 95%CI:1.077-1.139, P<0.001). At ROC analysis, tHcy showed diagnostic value with an optimal cut-off value of 24.9 μmol/L (AUC 0.913, 95%CI: 0.875-0.951, sensitivity 79.2%, specificity 91.6%). Spearman correlation analysis showed that tHcy was positively correlated with functional disability rating scale (r=0.254, P=0.009). Conclusions: Serum tHcy is the risk factor for SCD and related to its disability. Focus on the increased level of tHcy plays a positive role in the diagnosis of SCD.

Subacute combined degeneration of spinal cord due to chronic nitrous oxide abuse

Subacute combined degeneration of spinal cord due to chronic nitrous oxide abuse

Neurological disorders in vitamin B12 deficiency.

The review discusses thesteps of vitamin B12 metabolism and its role in maintaining of neurological functions. The term "vitamin B12 (cobalamin)" refers to several substances (cobalamins) of a very similar structure. Cobalamin enters the body with animal products. On the peripherу cobalamin circulates only in binding with proteins transcobalamin I and II (complex cobalamin-transcobalamin II is designated as "holotranscobalamin"). Holotranscobalamin is absorbed by different cells, whereas transcobalamin I-binded vitamin B12 - only by liver and kidneys. Two forms of cobalamin were identified as coenzymes of cellular reactions which are methylcobalamin (in cytoplasm) and hydroxyadenosylcobalamin (in mitochondria). The main causes of cobalamin deficiency are related to inadequate intake of animal products, autoimmune gastritis, pancreatic insufficiency, terminal ileum disease, syndrome of intestinal bacterial overgrowth. Relative deficiency may be seen in excessive binding of vitamin B12 to transcobalamin I. Cobalamin deficiency most significantly affects functions of blood, nervous system and inflammatory response. Anemia occurs in 13-15% of cases; macrocytosis is an early sign. The average size of neutrophils and monocytes is the most sensitive marker of megaloblastic hematopoiesis. The demands in vitamin B12 are particularly high in nervous tissue. Hypovitaminosis is accompanied by pathological lesions both in white and gray brain matter. Several types of neurological manifestations are described: subacute combined degeneration of spinal cord (funicular myelinosis), sensomotor polyneuropathy, optic nerve neuropathy, cognitive disorders. The whole range of neuropsychiatric disorders with vitamin B12 deficiency has not been studied well enough. Due to certain diagnostic difficulties they are often regarded as "cryptogenic", "reactive", "vascular» origin. Normal or decreased total plasma cobalamin level could not a reliable marker of vitamin deficiency. In difficult cases the content of holotranscobalamin, methylmalonic acid / homocysteine, and folate in the blood serum should be investigated besides carefully analysis of clinical manifestations.

Rapid healing of a patient with dramatic subacute combined degeneration of spinal cord: a case report

BackgroundPrevalence of cobalamin deficiency is high especially in older patients and an immediate therapy start is necessary to prevent irreversible neurological damages. Unfortunately, the diagnosis of cobalamin deficiency is difficult and at present, there is no consensus for diagnosis of this deficiency. Therefore, we aim to elucidate a meaningful diagnostic pathway by a case report with an initially misleading medical history.Case presentationA 57 year-old Caucasian man suffering from dramatic myelosis of the cervical posterior columns. Apart from associated neurological symptoms (tactile hypaesthesia, reduced vibration sensation, loss of stereognosis and of two-point-discrimination) there were no further complaints; especially no gastrointestinal, haematological or psychiatric disorders were provable. Cobalamin (vitamin B12) serum level was normal. The diagnosis of subacute combined degeneration of spinal cord was confirmed by an elevated methylmalonic acid, and hyperhomocysteinemia. Cobalamin deficiency was caused by asymptomatic chronic atrophic inflammation of the stomach with a lack of intrinsic factor producing gland cells. This was revealed by increased gastrin and parietal cell antibodies and finally confirmed by gastroscopy. Parenteral substitution of cobalamin rapidly initiated regeneration.ConclusionsThis case demonstrates that normal cobalamin serum levels do not rule out a cobalamin deficiency. In contrast, path-breaking results can be achieved by determining homocysteine, holotranscobalamin, and methylmalonic acid.

Can vitamin B12 deficiency manifest with acute posterolateral or posterior cord syndrome?

Vitamin B12 deficiency can cause varied neurological manifestations which are subacute to chronic in onset. Subacute combined degeneration of spinal cord is one such characteristic neurological manifestation of vitamin B12 deficiency. We report a case series of five patients who presented with acute onset (<15 days) neurological manifestations due to vitamin B12 deficiency. Detailed history and clinical examination along with appropriate relevant investigations were done in all patients. Out of the five, two cases were of useless hand syndrome due to involvement of posterior column of the cervical spinal cord, another two patients presented with acute posterolateral cord syndrome causing gait ataxia and one acute posterior cord syndrome presented with acute sensory gait ataxia. Laboratory investigations were compatible with the diagnosis of cobalamin deficiency in all cases. All cases improved after parenteral vitamin B12 supplementation. Vitamin B12 deficiency can present with acute neurological manifestations.

A rare case of gastric carcinoid presenting as subacute combined degeneration of spinal cord

Gastric carcinoids originate from the foregut and are derived from enterochromaffin-like (ECL) cells, which are the main neuroendocrine cells in the gastric mucosa. Gastrin acts directly on ECL cells to induce hyperplasia, dysplasia, and, eventually, neoplasia or carcinoid . In patients with chronic atrophic gastritis, decreased gastric acid secretion stimulates the secretion of gastrin, and ECL cells transform into a carcinoid. Herein we report a case of type I gastric carcinoid presenting as SACD.

Subacute combined degeneration of spinal cord

Subacute combined degeneration of spinal cord

Subacute combined degeneration of spinal cord due to nutritional vitamin B12 deficiency in early childhood

Subacute combined degeneration of spinal cord is a rare neurological manifestation of vitamin B12 deficiency due to inadequate dietary intake in children. We report a case of 4.5-year-old girl who was vegan with developmental regression, hyperpigmentation over extremities and features of subacute combined degeneration of spinal cord, a rarity in children. Laboratory investigations and neuroimaging were confirmatory. She responded well to treatment and she is having no complaints at present.

Correlation of Clinical and MRI Features of Neuropsychiatric Manifestations in Sub-acute Combined Degeneration of Spinal Cord: Neurological Syndrome Associated with Vitamin B12 Deficiency

Vitamin B12 or cynacobalamin is an important water soluble vitamin which plays a key role in erythropoiesis, proper nervous system functioning and for the metabolism of carbohydrate, fat and protein. Patients with cynacobalamin deficiency may present with haematological, gastro-intestinal, oral, dermatological, psychiatric and neurological disturbances. We present a case of sub-acute combined degeneration (SACD) of spinal cord in a fortynine year old female presenting with one month history of progressive symptoms of lower limb paraesthesia, sensory deficit, psychotic symptoms and postural instability. This case report is unusual as it elucidates the characteristic triad, i.e., haematological, psychiatric and neurological symptoms in sub-acute combined degeneration of spinal cord (SACD) associated with B12 deficiency, correlation of its clinical manifestations, electrophysiological signs, laboratory investigations ( especially biomarkers of B12 status) and spinal magnetic resonance (MR) imaging in establishing the diagnosis, treatment outcomes, and potential therapeutic relevance of vitamin B12 replacement therapy in symptoms remission.

IT'S NO LAUGHING MATTER

Background Nitrous oxide abuse is on the increase and can cause neurological dysfunction by inactivation of Vitamin B12 resulting in manifestations such as Sub-acute combined degeneration of spinal cord and Peripheral neuropathy. Case report We report two young patients who presented to emergency neurology clinic with progressive dysasthesia. Both had history of smoking, alcohol and had inhaled nitrous oxide from whipped cream canisters. Examination of both patients revealed unremarkable cranial nerves but case 1 had sluggish reflexes in the lower limbs with thoracic sensory level while case 2 had mild weakness distally in the upper limbs, global areflexia and cervical sensory level. MRI spine in both cases showed posterior cervico-thoracic cord high signal change. Case 1 had low Vitamin B12 and high Methylmalonic acid levels. Case 2 declined blood tests but had a demyelinating sensorimotor neuropathy on nerve conduction studies. Both patients were advised on abstinence from nitrous oxide and treated with Vitamin B12 supplementation. Conclusion Neurological sequelae of Nitrous oxide toxicity are under-recognised. It is a common recreational drug and its use should be specifically sought in young patients presenting with signs of a myelo-neuropathy.

A Case of Sub-acute Combined Degeneration of the Spinal Cord with Associated Pernicious Anaemia

Aim and Objective Vitamin B12 deficiency disease, specially associated with pernicious anaemia is a relatively rare disease in the developing countries. Patients with B12 deficiency may present with hematological, gastro-intestinal and neuro-psychiatric manifestations. Here we discuss a case of a fifty five-year-old lady presented with sub-acute combined degeneration of the spinal cord. Case presentation A fifty five year old female was admitted in Neurology ward in Apollo Hospitals, Dhaka from OPD for progressive quadriparesis with tingling in the hands and feet. She had no associated visual, bulbar symptoms, sphincter incontinence or memory impairment. Investigation revealed mild anaemia, macrocytosis on peripheral blood picture, low Vitamin B12 level with megaloblastic changes in bone marrow examination. Anti-Intrinsic factor antibody and anti-parietal cell antibody was not done, as it is not available here. MRI of dorsal spine shows T2 hyper-intense lesions in the posterior cord. GI Endoscopic biopsy revealed chronic atrophic gastritis. Conclusion We presented this case because of its relatively uncommon occurrence in our country. Sub-acute combined degeneration of spinal cord associated with dietary deficiency is common in Indian sub-continent. High index of suspicion is needed for its early diagnosis as delay in treatment can lead to poor neurological recovery. DOI: http://dx.doi.org/10.3329/pulse.v5i1.20193 Pulse Vol.5 January 2011 p.57-60

Don't forget your hammer if you want to go to work!

SummaryBilateral lower limb paraesthesia is a common diabetic neuropathy presentation in any busy diabetic clinics. We present a case of a 28-year-old man with a long history of type 1 diabetes mellitus presented with bilateral paraesthesia of both feet and unsteady gait. The patient was able to feel a 10 g monofilament. The presence of brisk reflexes and upgoing plantars in this patient were pointers that further evaluation was warranted. Further investigations revealed diagnosis of subacute combined degeneration of spinal cord. The patient had rapid symptomatic improvement with i.m. vitamin B12 injection. The high volume of patients attending the outpatients with diabetes and paraesthesia can blind us to other possible diagnoses. This article emphasizes that peripheral neuropathy in a diabetic may be due to aetiologies other than diabetes.Learning points Pernicious anaemia is known to be more common in patients with type 1 diabetes.Cobalamin deficiency is reversible if detected early enough and treated by B12 replacement.By contrast, diabetic neuropathy is generally a progressive complication of diabetes.Peripheral neuropathy in a diabetic may be due to aetiologies other than diabetes.

Carence en vitamine B12 par toxicité du protoxyde d’azote : une cause méconnue de sclérose combinée de la moelle

IntroductionNitrous oxide is widely used in anesthesia. It is usually safe but may be associated with severe side effects when it is used repeatedly or on a prolonged time. Here, we report a case of drug-induced subacute combined spinal cord degeneration related to cobalamin deficiency. Case reportA 20-year-old man with sickle-cell disease (SS) who was followed for severe recurrent vaso-occlusive crisis with repeated hospital admissions presented with ascending motor and sensitive neurological deficits that were later associated with bladder dysfunction. He was first considered to develop Guillain-Barre syndrome. However, persisting neurological signs despite adequate treatment lately led to diagnose subacute combined medullar degeneration due to abnormal cobalamin (vitamin B12) metabolism induced by repeated use of nitrous oxide during painful episodes of sickle-cell disease. ConclusionInhaled nitric oxide is widely used in the treatment of vaso-occlusive crisis. Clinicians should be aware of possible severe neurologic side effects.

Spastic Quadreparesis - An Unusual Presentation of Sub-acute Combined Degenaration of Spinal Cord

We report a case of a 45-year-old gentleman presenting with numbness of both legs and hands. He has anemia, spastic quadriplegia with exageraterd tendon jerks with lose of vibration and position sense. Investigations revealed combined deficiency anemia with low serum vitamin B12. His MRI of cervicel spine was normal. Endoscopically he had atrophic gastritis. Ultimately he was dignosed as a case of sub-acute combined degeneration of spinal cord due to pernicious anemia. Patient was treated with injection vitamin B12 and well responded. On his followup, he had significant clinical improvement. This is a reversible condition if early diagnosis can be made and vitamin B12 therapy promptly given. Delayed treatment can result in irreversible neurological impairment.DOI: http://dx.doi.org/10.3329/jom.v14i1.14585 J MEDICINE 2013; 14 : 85-87

Teaching Neuro Image : Inverted V sign in subacute combined degeneration of spinal cord

A 60-year-old man presented with 3 months of finger paresthesias. Neurologic examination showed pseudoathetosis in arms, loss of joint position and vibration sensation in toes and fingers, brisk deep tendon reflexes in arms and knees with depressed …

A red tongue and an unsteady gait: MRI in subacute combined degeneration of the spinal cord

We present a case of cobalamin deficiency secondary to chronic autoimmune gastritis resulting clinically in complex combined motor and sensory spinal cord syndrome. Magnetic resonance imaging disclosed increased signal intensity in the dorsal columns of the cervical and thoracic spinal cord on T2-weighted images and the right lateral column stretching from C1 to C6, corresponding with the clinical picture. This is, to our knowledge, the first report of increased signal intensity in lateral columns on T2-weighted images in subacute combined degeneration of spinal cord. The spectrum of clinical symptoms inherent to this disorder, diagnostic tests, with emphasis on magnetic resonance imaging, and treatment are discussed.