Somatosensory conduction in vitamin B12 deficiency

doi:10.1016/0013-4694(88)90003-X

Electroencephalography and Clinical Neurophysiology

Volume 69, Issue 4, April 1988, Pages 313-318

https://doi.org/10.1016/0013-4694(88)90003-X Get rights and content

Abstract

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.

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Role of B vitamins, thiamine, pyridoxine, and cyanocobalamin in back pain and other musculoskeletal conditions: a narrative review
2021, Semergen
El dolor lumbar, así como otras alteraciones musculoesqueléticas (cervicalgia, artrosis, etc.), son causa muy frecuente de consulta tanto en atención primaria como en otras especialidades hospitalarias y suelen asociarse con una alta discapacidad funcional y laboral. La lumbalgia aguda puede presentar diferentes componentes nociceptivos, neuropáticos y nociplásticos, lo que lleva a considerarlo como un dolor de tipo mixto. La importancia del concepto de dolor mixto obedece a que el alivio sintomático de dichas patologías requiere un enfoque terapéutico multimodal a diversas dianas farmacológicas. Desde hace varias décadas se reconoce el papel antinociceptivo del complejo de vitaminas B, específicamente de la combinación de tiamina, piridoxina y cianocobalamina (TPC). Asimismo, hay evidencia acumulada que indica una acción analgésica adyuvante en el dolor lumbar. El objetivo de la presente revisión es presentar la evidencia existente y los últimos hallazgos sobre los efectos terapéuticos de la combinación TPC en el dolor lumbar. Asimismo, se analizan algunos de los mecanismos de acción más relevantes implicados que pueden explicar dichos efectos. La evidencia revisada indica que el uso combinado de TPC tiene un efecto adyuvante analgésico en el dolor mixto, específicamente en el dolor lumbar y otras alteraciones musculoesqueléticas con componentes nociceptivos y neuropáticos. Dicho efecto puede ser explicado por una acción antiinflamatoria, antinociceptiva, neuroprotectora y neuromoduladora de la combinación TPC sobre el sistema descendente del dolor.
Low back pain, as well as other musculoskeletal disorders (neck pain, osteoarthritis, etc.), are a very frequent cause of consultation both in primary care and in other hospital specialties and are usually associated with high functional and work disability. Acute low back pain can present different nociceptive, neuropathic and nonciplastic components, which leads to consider it as a mixed type pain. The importance of the concept of mixed pain is due to the fact that the symptomatic relief of these pathologies requires a multimodal therapeutic approach to various pharmacological targets. The antinociceptive role of the B vitamin complex has been recognized for several decades, specifically the combination of Thiamine, Pyridoxine and Cyanocobalamin (TPC). Likewise, there is accumulated evidence that indicates an adjuvant analgesic action in low back pain. The aim of the present review is to present the existing evidence and the latest findings on the therapeutic effects of the TPC combination in low back pain. Likewise, some of the most relevant mechanisms of action involved that can explain these effects are analyzed. The reviewed evidence indicates that the combined use of PCT has an adjuvant analgesic effect in mixed pain, specifically in low back pain and other musculoskeletal disorders with nociceptive and neuropathic components. This effect can be explained by an anti-inflammatory, antinociceptive, neuroprotective and neuromodulatory action of the TPC combination on the descending pain system.
Altered neocortical tactile but preserved auditory early change detection responses in Friedreich ataxia
2019, Clinical Neurophysiology
Citation Excerpt :
Increased latency of cSI cortex responses elicited by tactile stimuli is easily explained by the selective loss of large-size fast-conducting primary somatosensory neurons in the DRGs, along with their peripheral and central axonal branches in sensory nerves and in the posterior columns of the spinal cord (Hughes et al., 1968; Zouari et al., 1998; Santoro et al., 1999; Santiago-Perez et al., 2007). Prolonged somatosensory central conduction time is well described in various diseases affecting the posterior columns of the spinal cord, such as multiple sclerosis (Ganes, 1980), vitamin B12 deficiency (Zegers de Beyl et al., 1988), stroke (Tinazzi and Mauguiere, 1995) and medullary compression (Miyoshi and Kimura, 1996), in addition to FRDA (Santiago-Perez et al., 2007). The decrease in cSI cortex responses amplitude to tactile standard stimuli might be due to sensory neuron loss, but also to cerebellar pathology.
To study using magnetoencephalography (MEG) the spatio-temporal dynamics of neocortical responses involved in sensory processing and early change detection in Friedreich ataxia (FRDA).
Tactile (TERs) and auditory (AERs) evoked responses, and early neocortical change detection responses indexed by the mismatch negativity (MMN) were recorded using tactile and auditory oddballs in sixteen FRDA patients and matched healthy subjects. Correlations between the maximal amplitude of each response, genotype and clinical parameters were investigated.
Evoked responses were detectable in all FRDA patients but one. In patients, TERs were delayed and reduced in amplitude, while AERs were only delayed. Only tactile MMN responses at the contralateral secondary somatosensory cortex were altered in FRDA patients. Maximal amplitudes of TERs, AERs and tactile MMN correlated with genotype, but did not correlate with clinical parameters.
In FRDA, the amplitude of tactile MMN responses at SII cortex are reduced and correlate with the genotype, while auditory MMN responses are not altered.
Somatosensory pathways and tactile early change detection are selectively impaired in FRDA.
Vitamin B-12 treatment of asymptomatic, deficient, elderly Chileans improves conductivity in myelinated peripheral nerves, but high serum folate impairs Vitamin B-12 status response assessed by the combined indicator of Vitamin B-12 status
2016, American Journal of Clinical Nutrition
Background: It is uncertain whether vitamin B-12 supplementation can improve neurophysiologic function in asymptomatic elderly with low vitamin B-12 status or whether folate status affects responses to vitamin B-12 supplementation.
Objective: We assessed the effects of a single intramuscular injection of 10 mg vitamin B-12 (which also contained 100 mg vitamin B-6 and 100 mg vitamin B-1) on vitamin B-12 status and neurophysiologic function in elderly community-dwelling Chileans with low serum vitamin B-12 concentrations who were consuming bread fortified with folic acid.
Design: A pretreatment and posttreatment study was conducted in 51 participants (median ± SD age: 73 ± 3 y; women: 47%) with serum vitamin B-12 concentrations <120 pmol/L at screening. Vitamin B-12 status was defined by combining vitamin B-12, plasma total homocysteine (tHcy), methylmalonic acid (MMA), and holotranscobalamin into one variable [combined indicator of vitamin B-12 status (cB-12)]. The response to treatment was assessed by measuring cB-12 and neurophysiologic variables at baseline and 4 mo after treatment.
Results: Treatment increased serum vitamin B-12, holotranscobalamin, and cB-12 (P < 0.001) and reduced plasma tHcy and serum MMA (P < 0.001). Treatment produced consistent improvements in conduction in myelinated peripheral nerves; the sensory latency of both the left and right sural nerves improved on the basis of faster median conduction times of 3.1 and 3.0 ms and 3.3 and 3.4 ms, respectively (P < 0.0001). A total of 10 sensory potentials were newly observed in sural nerves after treatment. Participants with high serum folate at baseline (above the median, ≥33.9 nmol/L) had less improvement in cB-12 (P < 0.001) than did individuals whose serum folate was less than the median concentration (i.e., with a concentration <33.9 nmol/L).
Conclusion: Asymptomatic Chilean elderly with poor vitamin B-12 status displayed improved conductivity in myelinated peripheral nerves after vitamin B-12 treatment and an interaction with folate status, which was detected only with the use of cB-12. This trial was registered at www.controlled-trials.com as ISRCTN02694183.
Polyneuropathy Caused by Nutritional and Vitamin Deficiency
2005, Peripheral Neuropathy: 2-Volume Set with Expert Consult Basic
Polyneuropathy Caused by Nutritional and Vitamin Deficiency
2005, Peripheral Neuropathy
Vitamin B<inf>12</inf> deficiency in patients with chronic-tinnitus and noise-induced hearing loss
1993, American Journal of Otolaryngology--Head and Neck Medicine and Surgery
Introduction: This study examines the incidence of vitamin B₁₂ deficiency in three groups of noise-exposed subjects: patients with chronic tinnitus and noise-induced hearing loss (NIHL), patients with NIHL only, and subjects demonstrating normal hearing.
Materials and Methods: A group of 113 army personnel exposed to military noise was studied. The mean age was 39 years. Chronic tinnitus and NIHL existed in 57 subjects. NIHL alone was observed in 29 subjects, and 27 subjects had normal audiograms. All subjects were queried about noice exposure and dietary habits. Vitamin B₁₂ serum levels were measured.
Results: Patients with tinnitus and NIHL exhibited vitamin B₁₂ deficiency in 47% of cases (blood levels ⩽ 250 pg/mL). This was significantly more (P < .023) compared with NIHL and normal subjects who exhibited vitamin B₁₂ deficiency in 27% and 19%, respectively.
Conclusion: These observations suggest a relationship between vitamin B₁₂ deficiency and dysfunction of the auditory pathway. Some improvement in tinnitus and associated complaints were observed in 12 patients following vitamin B₁₂ replacement therapy. The authors recommend that routine vitamin B₁₂ serum levels be determined when evaluating patients for chronic tinnitus.

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Main articleSomatosensory conduction in vitamin B12 deficiency

Abstract

J. Neurol. Sci.

Electroenceph. clin. Neurophysiol.

J. Neurol. Sci.

Electroenceph. clin. Neurophysiol.

Electroenceph. clin. Neurophysiol.

An ultrastructural study of sub-acute combined degeneration of the spinal cord in vitamin B12-deficient rhesus monkeys

J. Neuropathol. Exp. Neurol.

Nutritional deficiencies and disorders

Generator sources of SEP in man

Main article
Somatosensory conduction in vitamin B12 deficiency