No abstract available.
Nitrous Oxide* ; Subacute Combined Degeneration*

No abstract available.
Magnetic Resonance Imaging* ; Subacute Combined Degeneration*

No abstract available.
Humans ; Subacute Combined Degeneration ; Vitamin B 12

No abstract available.
Inhalation ; Nitrous Oxide ; Pulmonary Embolism ; Subacute Combined Degeneration

No abstract available.
Magnetic Resonance Imaging* ; Spinal Cord* ; Subacute Combined Degeneration* ; Vitamin B 12 Deficiency

Vitamin B12 deficiency can cause neurologic complications in the spincal cord, brain, and optic and peripheral nerves. Subacute combined degeneration is a rare disease of demyelinating lesions of the spinal cord, affecting mainly the posterior and lateral columns of the thoracic cord. We report the MR imaging findings of a case of subacute combined degeneration of the spinal cord in a patient with vitamin B12 deficiency and mega-loblastic anemia.
Anemia ; Brain ; Humans ; Magnetic Resonance Imaging* ; Peripheral Nerves ; Rare Diseases ; Spinal Cord* ; Subacute Combined Degeneration* ; Vitamin B 12 Deficiency ; Vitamins

Subacute combined degeneration (SCD) of the spinal cord is a neurological complication arising from vitamin B12 deficiency. Typical findings are demyelination and axonal loss of the posterior and lateral columns of the thoracic and cervical spinal cord, leading to sensory ataxia and paresthesia. Clinical and neurological features and MRI findings all contribute to the diagnosis of this entity. In the Korean medical literature, only one case of SCD involving pre-treatment MRI has been reported. We describe one case of SCD in a post-gastrecto-my patient who initially presented with progressive sensory abnormality in both upper and lower extremities and showed T2 hyperintensity in the posterior and lateral columns of the spinal cord; this diminished, with clinical improvement, after vitamin B12 therapy. Our report includes the MR images obtained during follow up.
Ataxia ; Axons ; Demyelinating Diseases ; Diagnosis ; Follow-Up Studies ; Humans ; Lower Extremity ; Magnetic Resonance Imaging* ; Paresthesia ; Spinal Cord* ; Subacute Combined Degeneration* ; Vitamin B 12 ; Vitamin B 12 Deficiency ; Vitamins

Autosomal dominant hereditary spastic paraplegia (AD-HSP) is due to mutations in the "spastin" gene (SPAST gene) encoding the AAA protein. The main clinical features of "pure" HSP are progressive lower-limb spasticity with corticospinal tracts and dorsal column degeneration without peripheral neuropathy. Here we report the case of HSP with novel SPAST gene mutation that misdiagnosed with subacute combined degeneration initially. A 58-year-old man with gait disturbance came to our hospital. He was unable to regulate his steps by himself. The impaired gait began 3 years after he had undergone subtotal gastrectomy and chemotherapy for 6 months. Thereafter, he started feeling tingling sensations in the hands and feet and acquired gait difficulties. He denied having a family history of abnormal gait or developmental problem. We diagnosed him with subacute combined degeneration on the evidence of history of gastrectomy, lower normal limit of vitamin B12 (363 pg/ml), apparent absence of vibration sensations and paresthesia in the feet. He was intramuscularly administered cyanocobalamin regularly. However, there was no improvement in his condition. We reconsidered his symptoms and signs, decided to examine the SPAST gene, which is the most common mutation in HSP. The SPAST gene, c.870+1delG, heterozygote, splicing mutation is detected from the gene sample. There was no previous information of this polymorphism or mutation at this locus. We examined his two children, and the same mutation was founded in his son. We report a patient of novel SPAST gene mutation with AD-HSP which is misdiagnosed with SCD.
Child ; Foot ; Gait ; Gastrectomy ; Hand ; Heterozygote ; Humans ; Muscle Spasticity ; Paresthesia ; Peripheral Nervous System Diseases ; Porphyrins ; Pyramidal Tracts ; Sensation ; Spastic Paraplegia, Hereditary ; Subacute Combined Degeneration ; Vibration ; Vitamin B 12

We report a patient who was diagnosed as subacute combined degeneration (SCD) with elevated homocysteine and methylmalonic acid levels in the situation of a spurious elevation of the vitamin B12 concentration. A false-positive elevation of the vitamin B12 level could lead to a delayed diagnosis and cause irreversible changes in the nervous systems. We therefore suggest that the homocysteine and methylmalonic acid levels should be checked in patients with a normal or elevated vitamin B12 level for whom there is a high clinical suspicion for vitamin B12 deficiency, as a further evaluation for SCD.
Delayed Diagnosis ; Gastritis, Atrophic* ; Homocysteine ; Humans ; Methylmalonic Acid ; Nervous System ; Subacute Combined Degeneration* ; Vitamin B 12 Deficiency ; Vitamin B 12* ; Vitamins*

OBJECT: There have been some controversies about the nature of peripheral neuropathy in patients with subacute comblned degeneration. Mayer concluded that the neuropathy was essentially demyelinating. And other reports which were based on pathologic or electrophyslological filldings have been saying axonopathy. We tried to find the nature of perlpheral neuropathy by doing conventional nerve conduction studies in 19 patients with subacute combined degeneration. SUBJECT AND METHOD: We included 19 patients with subacute combined degeneration, who were diagnosed by decreased serum vitamin B12(200pg/ml) and abnormal neurologic symptoms and/or signs. The patients were between 26 and 86 years of age. Eleven of them were male. We performed conventional nerve conduction studies Including H-reflex, When nerve conduction parameters deviated by more than 2SD from the normal mean value, they were consider as abnormal. RESULTS: nerve conduction studies were abnormal in 13/19. 11/13 with abnormal nerve conduction studies showed the pattern of peripheral polyneuropathy. Ten of them showed decreased amplitudes of sensory nerve action potentials or compound nerve action potentials with/wlthout mild slowing of nerve condcution. The abnormalities of the three patients with nerve conduction parameters of demyelinating range were confined to the distal segments of the median nerves. CONCLUSION: We thought that the results of the nerve conduction studies of our cases were compatible with axonopathy rather than demyelinopathy as a principal ]esion of the peripheral nervous system.
Action Potentials ; H-Reflex ; Humans ; Male ; Median Nerve ; Neural Conduction* ; Neurologic Manifestations ; Peripheral Nervous System ; Peripheral Nervous System Diseases ; Polyneuropathies ; Subacute Combined Degeneration ; Vitamins