|Year : 2004 | Volume
| Issue : 1 | Page : 122--123
Recurrent seizures: An unusual manifestation of vitamin B12 deficiency
Neurology Unit, Department of Neurological Sciences, Christian Medical College Hospital, Vellore - 632 004, India
Department of Neurological Sciences, Christian Medical College Hospital, Vellore - 632 004
The present report highlights an unusual presentation of vitamin B12 deficiencyŚ recurrent seizures in a 26-year-old man. His symptoms responded to parenteral vitamin B12 therapy. The relevant literature is reviewed.
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Kumar S. Recurrent seizures: An unusual manifestation of vitamin B12 deficiency.Neurol India 2004;52:122-123
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Kumar S. Recurrent seizures: An unusual manifestation of vitamin B12 deficiency. Neurol India [serial online] 2004 [cited 2023 Mar 31 ];52:122-123
Available from: https://www.neurologyindia.com/text.asp?2004/52/1/122/6721
Vitamin B12 deficiency causing neuropsychiatric manifestations such as peripheral neuropathy, subacute combined degeneration of cord, dementia, ataxia, optic atrophy, psychosis and mood disturbances is well known.,, We report a case with recurrent seizures resulting from vitamin B12 deficiency.
A 26-year-old man presented with recurrent episodes of complex partial seizures of three weeks duration. He had developed behavioral changes one year ago characterized by social withdrawal and memory impairment. Prior to admission, he had neglected self-care, had become severely withdrawn and was disoriented. He was treated with risperidone and carbamazepine.
He had impaired concentration, immediate visual and verbal recall, recent and remote memory, and comprehension for three-step commands. Word output was decreased. He had visuospatial disorientation and constructional apraxia. He had impaired distal sensations, exaggerated deep tendon reflexes except for absent ankle jerks. Plantar reflexes were extensor.
Investigations showed hemoglobin 13.2 g%, reticulocyte count 0.1 %, and mean corpuscular volume 114 fl, hypersegmented polymorphs, and moderate megaloblastic changes on bone marrow. Serum B12 assay was 26 pg/ml and folate was 28 ng/ml. Anti-intrinsic factor antibody was positive. Antral biopsy showed atrophic gastritis. CT scan of the brain showed mild cerebral atrophy. EEG showed left temporal epileptiform activity.
A diagnosis of vitamin B12 deficiency with multiple neuropsychiatric manifestations-dementia, psychosis, seizures, and myeloneuropathy-was considered. He was started on intramuscular vitamin B12 injections with which he showed an excellent therapeutic response. He became independent by the end of the third month. Risperidone and carbamazepine were tapered and stopped by six months. At a follow-up period of 24 months, he had been seizure-free for 23 months and was functionally independent.
Neurological involvement often occurs along with macrocytic anemia but can occur in the absence of anemia or macrocytosis. It is unclear why vitamin B12 deficiency leads to neurological disease in some and hematological disease in others. Methylenetetrahydrofolate reductase (MTHFR) polymorphism has been postulated to protect the vitamin B12-deficient patients against anemia and homozygosity for MTHFR C677T gene could cause the dissociation between hematological and neurological disease seen in some patients with vitamin B12 deficiency.
Methylcobalamin is required in the central nervous system for myelin synthesis. Hence, a lack of cobalamin leads to either the destruction of myelin sheaths or incorporation of abnormal fatty acids in myelin sheaths, thus leading to impaired neural function and/or transmission. This may be the underlying cause of neurological symptoms seen in vitamin B 12 deficiency.
The exact mechanism involved in epileptogenesis due to cobalamin deficiency is not clear. It is likely that cerebral neurons with destroyed myelin sheaths are more susceptible to the excitatory effects of glutamate. Cobalamin deficiency may share similarities with multiple sclerosis in this regard.
In conclusion, seizures rarely occur in patients with vitamin B 12 deficiency. Serum B12 levels should be checked, especially in those patients who present with other known neuropsychiatric features of vitamin B12 deficiency. Early withdrawal of antiepileptic drugs should be attempted as long-term antiepileptic use is not warranted and may be associated with adverse effects in such cases. Chronic carbamazepine therapy has been found to lower the levels of vitamin B12 and folate.
|1||Healton EB, Savage DG, Brust JC, Garrett TJ, Lindenbaum J. Neurologic aspects of cobalamin deficiency. Medicine (Baltimore) 1991;70:229-45. |
|2||Lindenbaum J, Healton EB, Savage DG, Brust JC, Garrett TJ, Podell ER, et al. Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. N Engl J Med 1988;318:1720-8. |
|3||Kvittingen EA, Spangen S, Lindemans J, Fowler B. Methionine synthase deficiency without megaloblastic anemia. Eur J Pediatr 1997;56:925-30.|
|4||Akaike A, Tamura Y, Sato Y, Yokota T. Protective effects of a vitamin B12 analog, methylcobalamin, against glutamate cytotoxicity in cultured cortical neurons. Eur J Pharm 1993;241:1-6. |
|5||Poser CM, Brinar VV. Epilepsy and multiple sclerosis. Epilepsy Behav 2003;4:6-12.|
|6||Karabiber H, Sonmezgoz E, Ozerol E, Yakinci C, Otlu B, Yologlu S. Effects of valproate and carbamazepine on serum levels of homocysteine, vitamin B12 and folate. Brain Dev 25:113-5|