Multiple sclerosis associated with vitamin B12 deficiency

We describe 10 patients with a previously unreported, to our knowledge, association of multiple sclerosis and unusual vitamin B12 deficiency. The clinical features and the age at presentation were typical of multiple sclerosis, with eight cases occurring before age 40 years, which is a rare age for vitamin B12 deficiency. Nine patients had hematologic abnormalities, but only two were anemic. All six patients examined had low erythrocyte cobalamin levels. Only two patients had pernicious anemia; in the remaining patients the vitamin B12 deficiency was unexplained. A vitamin B12 binding and/or transport is suspected. The nature of the association of multiple sclerosis and vitamin B12 deficiency is unclear but is likely to be more than coincidental. Further studies of vitamin B12 metabolism, binding, and transport in multiple sclerosis are indicated, as these cases may offer a clue to the understanding of a still mysterious neurologic disorder.     

Involuntary movements associated with vitamin B12 deficiency

Involuntary movements are not a known feature of vitamin B12 (vB12) deficiency in adults, though they are a characteristic feature of vB12 deficiency in infants. This case report presents an adult patient with vB12 deficiency in whom, myoclonus-like muscular contractions appeared soon after the initiation of vB12 and disappeared after the first week of this therapy. To our knowledge, this is the first report of involuntary movements in an adult patient with vB12 deficiency. Although the mechanism remains unknown, involuntary movements similar to myoclonus should be considered as one of the extraordinary neurological manifestations of vB12 deficiency in adults.     

Spinal myoclonus associated with vitamin B12 deficiency

We report a 85-year-old female patient with involuntary and regular movements restricted to abdominal muscles, resembling belly dance, with additional clinical features; ataxia, impaired cognition, neuropathy and glossitis. We initially excluded the possible cortical and spinal structural abnormalities with magnetic resonance imagings and performed routine blood analysis which revealed that serum vitamin B12 (vB12) level was under normal ranges. The relation of low serum vB12 level and myoclonus is speculative and very few studies have demonstrated such patients. In this case report, serum vB12 deficiency is discussed in the context of its probable role in the generation of spinal myoclonus.     

Involuntary movements associated with vitamin B12 deficiency

Involuntary movements are not a known feature of vitamin B12 (vB12) deficiency in adults, though they are a characteristic feature of vB12 deficiency in infants. This case report presents an adult patient with vB12 deficiency in whom, myoclonus-like muscular contractions appeared soon after the initiation of vB12 and disappeared after the first week of this therapy. To our knowledge, this is the first report of involuntary movements in an adult patient with vB12 deficiency. Although the mechanism remains unknown, involuntary movements similar to myoclonus should be considered as one of the extraordinary neurological manifestations of vB12 deficiency in adults.     

Delirium associated with vitamin B12 deficiency after pneumonia

A case is presented of a 65-year-old man with chronic schizophrenia who, after four years of remission, developed psychotic symptoms after pneumonia. The patient was found to be deficient in vitamin B12. His psychosis remitted within 5 days of administration of vitamin B12 and folic acid. This case emphasizes the need to measure vitamin B12 in psychogeriatric patients, especially when they present with a severe infection and organic mental symptoms.     

Postural and kinetic tremor associated with vitamin B12 deficiency

We report the case of a 77-year-old patient who presented a postural and kinetic tremor of the upper and lower limbs of sub acute onset, which revealed a vitamin B12 deficiency and resolved rapidly after the treatment. Such a presentation is rare.     

Peripheral neuropathy with vitamin B12 deficiency

Summary Seven patients with neuropathy associated with vitamin B₁₂ deficiency are reported. Four of them had other signs of malabsorption aside from the abnormal Schilling test. The neuropathy was diagnosed on the basis of the whole clinical picture and the neurophysiological findings. The pathogenesis of the peripheral nerve disease is discussed in the light of the evidence in the literature.

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Zusammenfassung Es wird über 7 Patienten mit einer Neuropathie bei gesicherter Vitamin B₁₂ Resorptionsstörung berichtet. Bei 4 Patienten wurden andere Anzeichen einer Malabsorption neben dem pathologischen Schilling Test festgestellt. Die Neuropathie wird aus dem gesamten klinischen Bild und den neurophysiologischen Befunden diagnostiziert. Die Pathogenese der peripheren Nervenschädigung wird anhand der Literatur diskutiert.

     

Orthostatic tolerance in older patients with vitamin B12 deficiency before and after vitamin B12 replacement

Abstract. Orthostatic hypotension (OH) and vitamin B12 deficiency are common disorders in older people. Several case series have reported an association between vitamin B12 deficiency and OH. The effect of vitamin B12 replacement on this dysfunction has not been studied. We prospectively studied responses to head up tilt in patients over 70 years with vitamin B12 deficiency (intervention group) and compared their responses after replacement to those of matched patients with idiopathic OH and normal serum vitamin B12 concentrations (control group). Blood pressure (BP), heart rate (HR) and systemic vascular resistance (SVR) changes during orthostatic stress were evaluated using digital artery photoplethysmography. Eight patients and eight controls were studied. Initial head up tilt produced a mean BP decrease of 44/29 mmHg (s. e. m. 4/4 mmHg) in the intervention group and 33/12 mmHg (s. e. m. 3/2 mmHg) in the control group. Repeat head up tilt 6 months after vitamin B12 replacement produced a mean BP decrease of 15/9 mmHg (s. e. m. 5/2 mmHg) in the intervention group. The mean decrease in the control group was 30/12 mmHg (s. e. m. 2/2 mmHg). The difference in BP decreases between groups was statistically significant for both systolic and diastolic BP (p < 0.001 for both systolic BP and diastolic BP). Mean SVR in the intervention group decreased by 658 dynes/cm⁵/ sec (s. e. m. 74 dynes/cm⁵/sec) during initial head up tilt. Mean SVR during repeat head up tilt decreased by 79 dynes/cm⁵/sec (s. e. m. 12 dynes/cm⁵/sec). Mean SVR in the control group decreased by 158 dynes/cm⁵/sec (s. e. m. 10 dynes/cm⁵/sec) during initial head up tilt and by 258 dynes/cm⁵/sec (s. e. m. 31 dynes/cm⁵/sec). The difference in SVR changes between groups was statistically significant (p = 0.02). We conclude that replacing vitamin B12 in older patients with vitamin B12 deficiency is associated with improved orthostatic tolerance to head up tilt.     

Catatonia and other psychiatric symptoms with vitamin B12 deficiency

OBJECTIVE: To study unusual psychiatric manifestation of vitamin B12 deficiency and related issues. METHOD: A case study of 52-year-old female and review of relevant literature. RESULTS: Complete remission of psychiatric symptoms without recurrence for the next 4 years with vitamin B12 as the only specific therapy instituted. CONCLUSION: Importance of B12 estimation and replacement in patients with varied psychiatric manifestations.     

Somatosensory conduction in vitamin B12 deficiency

We tested the hypothesis that the somatosensory central conduction time (CCT) can reveal central nervous system involvement in vitamin B12-deficient patients when this cannot be established on clinical grounds alone. Three patients with pernicious anemia and without clinical signs of upper motor neuron lesion had a striking increase of CCT. This increase was shown to be reversible in 1 patient who improved over 3 years of treatment. Detailed analysis of the CCT showed that the decrease of conduction velocity occurred in the posterior columns, whereas the conduction was normal at the thalamo-cortical level. We conclude that CCT is a useful parameter to localize and quantify central nervous system disease in vitamin B12 deficiency.     

Evoked responses in vitamin B12 deficiency

Abnormalities of visual, brainstem auditory, and somatosensory evoked responses were demonstrated in two of seven individuals with vitamin B₁₂ deficiency. The evoked response delays correlated directly with the degree of neurological dysfunction. Abnormalities were present in sensory systems without clinical evidence of involvement and were similar to those found in individuals with multiple sclerosis.     

MRI in vitamin B12 deficiency myelopathy

BACKGROUND: Little is known about vitamin B12 deficiency myelopathy's magnetic resonance imaging (MRI) manifestations and their relationship to the onset, evolution, and resolution of neurologic signs and symptoms. METHODS: We present a case and review eleven additional reported cases of subacute combined degeneration of the spinal cord detected by MRI. RESULTS: Our patient had increased T2-weighted signal and gadolinium contrast enhancement of the posterior columns in the cervical and thoracic regions and enhancement of the lateral columns in the high cervical region. This is a case with imaging evidence for lateral column lesions. Two prior reports have shown posterior column enhancement. T1-weighted images may show decreased signal in the posterior columns and sometimes demonstrate reversible spinal cord swelling. MRI abnormalities typically improve after vitamin replacement therapy. However, clinical signs may persist despite resolution of imaging abnormalities, and these abnormalities do not always resolve completely. In addition, symptoms may precede the imaging abnormality. CONCLUSIONS: Vitamin B12 deficiency may produce an increased T2-weighted signal, decreased T1-weighted signal, and contrast enhancement of the posterior and lateral columns of the spinal cord, mainly of the cervical and upper thoracic segments. Because the symptoms may precede any imaging abnormality, it is clear that spinal cord MRI may not be a highly sensitive, early test for subacute combined degeneration.     

Cerebellar ataxia and leukoencephalopathy associated with cobalamin deficiency

We report a patient who presented progressive cerebellar ataxia associated with vitamin B(12) deficiency. Brain magnetic resonance imaging (MRI) demonstrated a diffuse leukoencephalopathy. Six months after the initiation of methylcobalamin therapy, there were clinical improvement and reduction in the MRI abnormalities.     

Autonomic dysfunction and hemodynamics in vitamin B12 deficiency

Orthostatic hypotension in patients with cobalamin (Cbl) deficiency has been reported previously in isolated cases but we are not aware of detailed systematic studies of hemodynamic and autonomic nervous system function in patients with cobalamin deficiency. We investigated hemodynamic and autonomic responses to 60 degrees passive head up tilt (HUT) in 21 patients with vitamin B12 deficiency, 21 healthy age-matched control subjects and 9 age-matched patients with diabetes mellitus (DM) and established diabetic neuropathy. To systematically assess hemodynamic and autonomic nervous system function, we performed measurements of heart rate, beat-to-beat systolic and diastolic blood pressure, stroke index, cardiac index, total peripheral resistance index, total power, low (LF) and high (HF) frequency oscillatory component of heart rate variability, LF/HF ratio and spontaneous baroreflex sensitivity. As compared to controls, we found a significant fall of systolic blood pressure during 60 consecutive beats directly after head up tilt; furthermore, a significantly blunted fall of stroke index, cardiac index and a lack of increase of total peripheral resistance index for the duration of tilt in patients with diabetes mellitus and in patients with vitamin B12 deficiency. As compared to controls, we observed an altered response of spectral indices of sympathetic activation and vagal withdrawal and an impaired modulation of baroreflex sensitivity during head up tilt suggestive of a complex modification in the neural control activities in patients with cobalamin deficiency, which was comparable to that observed in patients with diabetes mellitus and established autonomic neuropathy. The results suggest that vitamin B12 deficiency causes autonomic dysfunction with similar hemodynamic consequences and patterns of autonomic failure as seen in diabetic autonomic neuropathy. Defective sympathetic activation may be the cause for orthostatic hypotension, which is occasionally seen in patients with vitamin B12 deficiency. It is concluded that patients with orthostatic hypotension should be screened for cobalamin deficiency.