Seizures caused by pyridoxine (vitamin B6) deficiency in adults: A case report and literature review

Tong, Yisha

doi:10.5582/irdr.2014.01005

Cited by 30 publications

(15 citation statements)

References 26 publications

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“…Moreover, Pyridoxine (vitamin B6) deficiency is a well-known cause of refractory SE; however, most of the reported cases were in infants and neonates [12,13]. Few adult cases of pyridoxine deficiency related RSE seizures have been reported in the literature [32,33] and the majority were associated with nutritional deficiencies and comorbidities [34][35][36][37] or with pregnancy [38].Vitamin B6 deficiency in adults is rare and may result from dietary deficiency (especially in elderly and alcoholics), and in patients with liver disease, chronic kidney Open Access Journal of Neurology & Neurosurgery disease on dialysis, rheumatoid arthritis, women with type 1 diabetes, as well as during pregnancy and in those patients with HIV who develop an increased risk of vitamin B6 deficiency, despite adequate dietary intakes [26,39,40]. Certain medications can also affect the availability of vitamin B6 in the body or interfere with its' metabolism, such as anticonvulsants, corticosteroids, Isoniazid, Cycloserine, and Penicillamine [41].…”

Section: Discussionmentioning

confidence: 99%

New Onset Refractory Status Epilepticus in an Adult Patient with Autoimmune Encephalitis Responding to Vitamin B6 Pyridoxine

Nadeem¹

2020

OAJNN

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Section: Discussionmentioning

confidence: 99%

New Onset Refractory Status Epilepticus in an Adult Patient with Autoimmune Encephalitis Responding to Vitamin B6 Pyridoxine

Nadeem¹

2020

OAJNN

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“…This leads to decreased levels of GABA and enhanced seizure susceptibility. Moreover, since the decarboxylation reaction involved in GABA synthesis is pyridoxine dependent, INH induced pyridoxine depletion also leads to reduction of GABA concentrations [88,89]. Although seizures have been described in INH toxicity, therapeutic doses may also induce convulsive seizures [90].…”

Section: Isoniazidmentioning

confidence: 99%

Antibiotic-induced epileptic seizures: mechanisms of action and clinical considerations

Wanleenuwat

Suntharampillai

Iwanowski

2020

Seizure

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In recent years, there has been growing interest in the development of epileptic seizures as an adverse effect of antibiotic therapy. The most commonly accepted mechanisms underlying the development of antibiotic-induced seizures include direct-and indirect gamma-aminobutyric acid (GABA) antagonism, inhibition of GABA synthesis, and glutaminergic N-methyl-D-Aspartate (NMDA) receptor agonistic activity. Inhibitory pathway inhibition leads to increased neuronal excitability and lowered seizure threshold. Blockage of myoneural presynaptic acetylcholine release, mitochondrial dysfunction, interference of neural protein synthesis, and oxidative stress caused by the generation of neurotoxic radicals also contributes to the development of neurotoxicity. Patients with pre-existing risk factors such as renal or hepatic insufficiency, central nervous system pathology, neurological diseases, history of epilepsy or seizures, critical illness, and increased age are more susceptible to seizure development as a consequence of antibiotic therapy. Administration of antibiotics, together with antiseizure drugs, may also lead to enhanced seizure risk due to drug interactions, which predisposes to alterations in drug metabolism and therapeutic efficacy.

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“…Vitamin B6 (pyridoxine) is an important cofactor in the process by which glutamic acid decarboxylase (GAD) converts the excitatory, pro-epileptogenic neurotransmitter, glutamate, into the inhibitory, anti-epileptogenic neurotransmitter, gamma-aminobutyric acid (GABA) [ 1 ]. This concept has been established in infants with pyridoxine-dependent epilepsy in addition to other causes of infantile spasms, with vitamin B6 administration resulting in the cessation of seizures [ 2 , 3 ].…”

Section: Introductionmentioning

confidence: 99%

Low Serum Pyridoxine Levels Worsen Seizure Control in Adult Epilepsy Patients

Rane¹,

Elrahi²,

Villarreal³

et al. 2022

Cureus

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Background: Vitamin B6 (pyridoxine) is an important cofactor in the process by which glutamic acid decarboxylase (GAD) converts the excitatory, pro-epileptogenic neurotransmitter, glutamate, into the inhibitory, anti-epileptogenic neurotransmitter, gamma-aminobutyric acid (GABA). This concept has been established in infants with pyridoxine-dependent epilepsy as well as adult patients with other epilepsy subtypes who presented with medication-resistant status epilepticus, with both patient groups experiencing cessation of seizure activity following pyridoxine administration. Given our knowledge of the role of vitamin B6 in the conversion of glutamate to GABA, its effect on seizure control in infants with specific epilepsy subtypes, reports of adult-onset seizures associated with vitamin B6 deficiency, and vitamin B6’s role in terminating status epilepticus in adult patients with other types of epilepsy, we suspect that low vitamin B6 levels in adult epilepsy patients may correlate with poor seizure control across all epilepsy subtypes. This study seeks to determine whether there is a relationship between pyridoxine levels and the level of seizure control in adults with epilepsy, regardless of their seizure type. Methods: After obtaining institutional review board approval, we prospectively enrolled 32 patients (age range: 25-57 years) with epilepsy who presented to our clinic. Patients who did not meet the study criteria or who were diagnosed with psychogenic non-epileptic seizures (PNES) were excluded from the study (n = 2). Patients were classified as well-controlled (WC) or poorly controlled (PC) based on the absence or presence of a seizure within the last three months, respectively. After classification as WC or PC, pyridoxine serum levels and anti-seizure medication (ASM) levels were drawn in that clinic visit, following patient consent. All patients were contacted regarding pyridoxine and serum ASM levels, and patients that were found to be deficient in pyridoxine were treated with appropriate supplementation. At the end of the recruitment period, we performed analyses to determine if there was a statistically significant relationship between PC status and serum pyridoxine levels. Results: Of 32 patients, two patients were diagnosed with psychogenic non-epileptic events and were subsequently excluded. Of 30 patients, 10 had PC epilepsy. Median (interquartile range) serum B6 levels were 35.8 (26.8-54.2) in patients with WC epilepsy and 17.5 (10.1-41.3) in patients with PC epilepsy (P = 0.11). In the PC group, 6/10 (60%) of the patients demonstrated low serum pyridoxine compared to 3/20 (15%) in the WC group (P = 0.03). Conclusion: There was a statistically significant relationship between serum pyridoxine levels and seizure control. If appropriate, pyridoxine supplementation should be considered, especially in critically ill adult patients with refractory or PC seizures despite good adherence to ASMs.

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Seizures caused by pyridoxine (vitamin B6) deficiency in adults: A case report and literature review

Cited by 30 publications

References 26 publications

New Onset Refractory Status Epilepticus in an Adult Patient with Autoimmune Encephalitis Responding to Vitamin B6 Pyridoxine

New Onset Refractory Status Epilepticus in an Adult Patient with Autoimmune Encephalitis Responding to Vitamin B6 Pyridoxine

Antibiotic-induced epileptic seizures: mechanisms of action and clinical considerations

Low Serum Pyridoxine Levels Worsen Seizure Control in Adult Epilepsy Patients

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