J Kalita1, U K Misra. 1. Dept. of Neurology, Sanjay Gandhi Post Graduate Institute of Medical Sciences (PGIMS), Rae Bareily Road, Lucknow, 226014, India. jayanteek@yahoo.com
Abstract
OBJECTIVE: To evaluate cognitive function in B12 deficiency neurological syndromes and response to B12 therapy. METHODS: Patients were diagnosed on the basis of low serum B12 or megaloblastic bone marrow or both. Detailed neurological examination was performed and mental status was evaluated by the Mini Mental State Examination (MMSE). Hemoglobin, RBC indices, blood counts, serum chemistry, HIV, thyroid profile, antiparietal cell antibody and craniospinal MRI were done. Cognitive evoked potential was carried out using the odd ball auditory paradigm and recording was achieved from Fz, Cz and Pz referred to mastoid. P3 latency and amplitude were measured and compared with 33 age and sex matched controls. Three months following B12 therapy, clinical and P3 values were reevaluated and compared with the baseline values. RESULTS: 36 patients, aged 16-80 years were included; 32 patients were above 40 years of age. Their median education level was 14 years. The presenting syndrome was myeloneurocognitive in 9, myeloneuropathy in 10, myelocognitive in 8,myelopathy in 8 and only cognitive in 1 patient.MMSE was abnormal in 17; between 28-19 in 14 and 18-11 in 3 patients. Cranial MRI carried out in 14 patients revealed multiple white matter hyperintensity in T2 in 3 and cortical atrophy in 1. P3 was unrecordable in 7 and latency was prolonged in 8 out of 33 patients. P3 latency was significantly prolonged in patients compared to controls and both MMSE and P3 latency improved significantly at the 3-month follow-up. CONCLUSION: MMSE was abnormal in 47 % and P3 in 45.5% of patients with B12 deficiency neurological syndromes which improved following treatment. SIGNIFICANCE: There is high incidence of reversible cognitive impairment and P3 abnormalities in B12 deficiency neurological syndromes.
OBJECTIVE: To evaluate cognitive function in B12 deficiency neurological syndromes and response to B12 therapy. METHODS:Patients were diagnosed on the basis of low serum B12 or megaloblastic bone marrow or both. Detailed neurological examination was performed and mental status was evaluated by the Mini Mental State Examination (MMSE). Hemoglobin, RBC indices, blood counts, serum chemistry, HIV, thyroid profile, antiparietal cell antibody and craniospinal MRI were done. Cognitive evoked potential was carried out using the odd ball auditory paradigm and recording was achieved from Fz, Cz and Pz referred to mastoid. P3 latency and amplitude were measured and compared with 33 age and sex matched controls. Three months following B12 therapy, clinical and P3 values were reevaluated and compared with the baseline values. RESULTS: 36 patients, aged 16-80 years were included; 32 patients were above 40 years of age. Their median education level was 14 years. The presenting syndrome was myeloneurocognitive in 9, myeloneuropathy in 10, myelocognitive in 8,myelopathy in 8 and only cognitive in 1 patient.MMSE was abnormal in 17; between 28-19 in 14 and 18-11 in 3 patients. Cranial MRI carried out in 14 patients revealed multiple white matter hyperintensity in T2 in 3 and cortical atrophy in 1. P3 was unrecordable in 7 and latency was prolonged in 8 out of 33 patients. P3 latency was significantly prolonged in patients compared to controls and both MMSE and P3 latency improved significantly at the 3-month follow-up. CONCLUSION: MMSE was abnormal in 47 % and P3 in 45.5% of patients with B12 deficiency neurological syndromes which improved following treatment. SIGNIFICANCE: There is high incidence of reversible cognitive impairment and P3 abnormalities in B12 deficiency neurological syndromes.
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