Hypocalcemic seizure in adult: Rare cause of lumbar fracture

Asri, Abad Cherif El; Akhaddar, Ali; Baallal, Hassan; Mostarchid, Brahim El; Boulahroud, Omar; Belfquih, Hatim; Dao, Ibrahim; Naama, Okacha; Gazzaz, Miloudi; Boucetta, Mohamed

doi:10.1016/j.clineuro.2011.12.015

Cited by 7 publications

(7 citation statements)

References 5 publications

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“…Hypocalcemia is a condition arises by reducing serum ionised calcium concentration (normal: 2.1-2.6 mmol/L) [15]. The common hypocalcaemia neurological manifestations include delirium, tetany and seizure, indicating a role of hypocalcaemia in causing neurological abnormalities [5,15,16]. Studies suggested that from inducing neurotransmitters release, to the electrical mechanical coupling in the myocyte, almost every step in the neuromuscular function is predicated on calcium [5,17].…”

Section: Discussionmentioning

confidence: 99%

“…The common hypocalcaemia neurological manifestations include delirium, tetany and seizure, indicating a role of hypocalcaemia in causing neurological abnormalities [5,15,16]. Studies suggested that from inducing neurotransmitters release, to the electrical mechanical coupling in the myocyte, almost every step in the neuromuscular function is predicated on calcium [5,17]. Therefore, management in cases of hypocalcaemia seizures has universally comprised of calcium replacement with or without anticonvulsants [5][6][7]16,18,19].…”

Section: Discussionmentioning

confidence: 99%

“…This phenomenon is typically defined as breakthrough seizure. It is shown to frequently exhibit in patients with predisposing endocrinological abnormalities or renal insufficiency with overall poor calcium homeostasis [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

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Neuraxial Anesthesia for Cesarean Section in the Obese Patient

Lisseth¹

2019

JAICM

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Introduction: Epilepsy is the third most common neurological disorder worldwide, following stroke and Alzheimer's disease. Generally, the recommended effective dose of anticonvulsants was enough in attaining seizure control in 70-80% of the patients. However, there are also occasions where patients who are on stable regimen of anticonvulsants associated with breakthrough seizure either induced directly by hypocalcaemia or resulting from chronic kidney failure induced hypocalcaemia. Current paper presents the therapeutic approach for breakthrough seizure secondary to hypocalcaemia in the case of an adolescent with chronic kidney failure.Case narrative: An epileptic male adolescent was admitted due to fitting lasted for 1 minute, followed by postictal drowsiness. Laboratory tests revealed optimal therapeutic range of Sodium Valproate serum concentration, but low serum calcium level. Hence, calcium replacement therapy was given as the main management plan. Discussion: It is recommended that hypocalcaemia with neurological manifestations, without the underlying cause, should be managed with parenteral calcium. In chronic kidney failure patient, oral calcium and vitamin D should be started as soon as practical and maintained even after discharged. Whereas, anticonvulsants should be reserved only for persistent seizure even after correction of calcium level. Conclusion:The management of breakthrough seizure should be individualised depending on clinical data and general condition of the patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Neuraxial Anesthesia for Cesarean Section in the Obese Patient

Lisseth¹

2019

JAICM

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“…Typical symptoms include tingling, tetany and muscle contractions. Severe hypocalcemia may cause seizures [11][12][13][14][15][16] or be responsible for the paradoxical reaction (seizure intensification) to phenytoin administered as an anti-seizure medication [17]. Neurological and neuromuscular symptoms of hypercalcemia yield a different clinical picture and include changes such as drowsiness, coma, decreased muscle strength, adynamia or periodic muscle paralysis [18].…”

Section: Introductionmentioning

confidence: 99%

TTX-resistant sodium currents in medial prefrontal cortex pyramidal neurons depend on extracellular Ca2+ concentration

Sławińska

Nurowska

Dworakowska

2019

Medical Research Journal

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Background: Previous reports reported the presence of TTX-resistant Nav1.8 and Nav1.9 sodium channels in the cortex pyramidal neurons. A characteristic feature of Nav1.9 channels is activation at voltages close to -70 mV. Therefore, they do not participate directly in the action potential but contribute to the regulation of the resting membrane potential. Their physiological role is modulation of cell excitability.The aim of the study was to investigate, with the use of patch clamp technique, the dependence of the activation thresholds of TTX-resistant sodium currents on the concentration of extracellular calcium in medial prefrontal cortex pyramidal neurons in rats. Results:The recorded values of the threshold of the voltage-dependent sodium currents were in the range of -65 mV to -75 mV. This suggests that the sodium currents may result from the presence of Nav1.9 channels in the rat pyramidal neurons. The threshold for the activation of sodium currents depended on the concentration of Ca 2+ . Increasing the concentration of calcium ions in the extracellular solution by 5 mM caused the depolarizing shift in the activation potential by about 10 mV. The effect of calcium ion concentration on the potential of TTX-resistant currents activation suggests that Nav1.9 channels are modulated by extracellular Ca 2+ concentration. Conclusions:The study has experimentally confirmed that TTX-resistant channels are present in the cell membrane of the rat prefrontal cortex pyramidal neurons and may, therefore, take a physiological role in the conductivity of sodium currents in a manner dependent on the concentration of extracellular ions.

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“…Although hypocalcemic seizures are widely documented in medical literature ( Erdeve et al., 2007 ; Tsai et al., 2009 ; Milman and Epstein, 2010 ; El Asri et al., 2012 ; Kidwell et al., 2013 ; Korkmaz, et al., 2014 ), the underlying mechanism seems counterintuitive. From the presynaptic release of neurotransmitters, to the electrical mechanical coupling in the myocyte, almost every step in the neuromuscular function is predicated on calcium ( Sudhof, 2013 ; Baylor and Hollingworth, 2010 ; Lazarevic et al., 2013 ).…”

Section: Introductionmentioning

confidence: 99%

Hypocalcemia-Induced Seizure

2015

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Calcium is essential for both neurotransmitter release and muscle contraction. Given these important physiological processes, it seems reasonable to assume that hypocalcemia may lead to reduced neuromuscular excitability. Counterintuitively, however, clinical observation has frequently documented hypocalcemia’s role in induction of seizures and general excitability processes such as tetany, Chvostek’s sign, and bronchospasm. The mechanism of this calcium paradox remains elusive, and very few pathophysiological studies have addressed this conundrum. Nevertheless, several studies primarily addressing other biophysical issues have provided some clues. In this review, we analyze the data of these studies and propose an integrative model to explain this hypocalcemic paradox.

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Hypocalcemic seizure in adult: Rare cause of lumbar fracture

Cited by 7 publications

References 5 publications

Neuraxial Anesthesia for Cesarean Section in the Obese Patient

Neuraxial Anesthesia for Cesarean Section in the Obese Patient

TTX-resistant sodium currents in medial prefrontal cortex pyramidal neurons depend on extracellular Ca2+ concentration

Hypocalcemia-Induced Seizure

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