Page last updated: 2024-10-26

valproic acid and Nerve Degeneration

valproic acid has been researched along with Nerve Degeneration in 18 studies

Valproic Acid: A fatty acid with anticonvulsant and anti-manic properties that is used in the treatment of EPILEPSY and BIPOLAR DISORDER. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of VOLTAGE-GATED SODIUM CHANNELS.
valproic acid : A branched-chain saturated fatty acid that comprises of a propyl substituent on a pentanoic acid stem.

Nerve Degeneration: Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.

Research Excerpts

ExcerptRelevanceReference
" We report here that, while dietary supplementation with high VPA dosage slows down motor neuron death, as assessed by measurement of a specific marker for cholinergic neurons in the spinal cord, it has no significant effect on lifespan."5.35Long-term dietary administration of valproic acid does not affect, while retinoic acid decreases, the lifespan of G93A mice, a model for amyotrophic lateral sclerosis. ( Bonamassa, B; Canistro, D; Contestabile, A; Crochemore, C; Paolini, M; Pena-Altamira, E; Virgili, M, 2009)
"Pentylenetetrazol (PTZ)-induced chronic kindling model and lithium-pilocarpine-induced status epilepticus (SE) model were used in this study."3.81Degeneration and regeneration of GABAergic interneurons in the dentate gyrus of adult mice in experimental models of epilepsy. ( Jiang, W; Wang, Y; Wei, D; Wu, C; Wu, SX; Yang, F, 2015)
"An infant with dysmorphic features was born to an epileptic mother who had taken phenytoin and sodium valproate throughout pregnancy."3.68Neocerebellar hypoplasia in a neonate following intra-uterine exposure to anticonvulsants. ( Hope, PL; Lindenbaum, RH; Squier, W, 1990)
"Spinal muscular atrophy is a devastating disease that is characterized by degeneration and death of a specific subclass of motor neurons in the anterior horn of the spinal cord."1.43Neuron-specific knock-down of SMN1 causes neuron degeneration and death through an apoptotic mechanism. ( Battaglia, GS; Bazzicalupo, P; Castro, S; Chaplin, JC; Di Schiavi, E; Donato, A; Esposito, A; Gallotta, I; Hilliard, MA; Mazzarella, N; Zampi, G, 2016)
" We report here that, while dietary supplementation with high VPA dosage slows down motor neuron death, as assessed by measurement of a specific marker for cholinergic neurons in the spinal cord, it has no significant effect on lifespan."1.35Long-term dietary administration of valproic acid does not affect, while retinoic acid decreases, the lifespan of G93A mice, a model for amyotrophic lateral sclerosis. ( Bonamassa, B; Canistro, D; Contestabile, A; Crochemore, C; Paolini, M; Pena-Altamira, E; Virgili, M, 2009)

Research

Studies (18)

TimeframeStudies, this research(%)All Research%
pre-19901 (5.56)18.7374
1990's2 (11.11)18.2507
2000's7 (38.89)29.6817
2010's8 (44.44)24.3611
2020's0 (0.00)2.80

Authors

AuthorsStudies
Kautu, BB1
Carrasquilla, A1
Hicks, ML1
Caldwell, KA1
Caldwell, GA1
Croce, N1
Bernardini, S1
Caltagirone, C1
Angelucci, F1
Wei, D1
Yang, F2
Wang, Y1
Wu, C1
Wu, SX1
Jiang, W1
Gallotta, I1
Mazzarella, N1
Donato, A1
Esposito, A1
Chaplin, JC1
Castro, S1
Zampi, G1
Battaglia, GS1
Hilliard, MA1
Bazzicalupo, P1
Di Schiavi, E1
Crochemore, C1
Virgili, M1
Bonamassa, B1
Canistro, D1
Pena-Altamira, E1
Paolini, M1
Contestabile, A1
Yamauchi, J1
Torii, T1
Kusakawa, S1
Sanbe, A1
Nakamura, K1
Takashima, S1
Hamasaki, H1
Kawaguchi, S1
Miyamoto, Y1
Tanoue, A1
Kidd, SK1
Schneider, JS1
Penas, C1
Verdú, E1
Asensio-Pinilla, E1
Guzmán-Lenis, MS1
Herrando-Grabulosa, M1
Navarro, X1
Casas, C1
Wang, C1
Luan, Z1
Yang, Y1
Wang, Z1
Cui, Y1
Gu, G1
Bown, CD1
Wang, JF2
Young, LT2
Angehagen, M1
Ben-Menachem, E1
Rönnbäck, L1
Hansson, E1
Brandt, C1
Gastens, AM1
Sun, Mz1
Hausknecht, M1
Löscher, W1
Tsai, LK1
Tsai, MS1
Lin, TB1
Hwu, WL1
Li, H1
Cui, J1
Shao, L1
Sinn, DI1
Kim, SJ1
Chu, K1
Jung, KH1
Lee, ST1
Song, EC1
Kim, JM1
Park, DK1
Kun Lee, S1
Kim, M1
Roh, JK1
Sobaniec-Lotowska, M1
Sobaniec, W1
Schwarcz, R1
Bennett, JP1
Coyle, JT1
Squier, W1
Hope, PL1
Lindenbaum, RH1

Clinical Trials (1)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Regional Anesthesia and Valproate Sodium for the Prevention of Chronic Post-Amputation Pain[NCT01928849]Phase 2128 participants (Actual)Interventional2013-12-31Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Change in Self-Reported Leeds Assessment of Neuropathic Symptoms and Signs Pain Scale (S-LANSS)

The S-LANSS is a self-reported version of the Leeds Assessment of Neuropathic Symptoms and Signs pain scale. It aims to differentiate neuropathic pain from somatic or nociceptive pain. We will analyze the change in numeric average pain score during the past week (range from 0-10) from baseline. Higher scores indicate greater pain. (NCT01928849)
Timeframe: Assessments at enrollment and 3 months or time of final adjudication assessment (up to 6 months)

Interventionscore on a scale (Median)
Cherry Syrup-2
Valproic Acid-2

Number of Patients With Chronic Post-amputation Pain

The primary endpoint is the incidence of chronic pain after surgery. The study team will use the average pain score over the past week as noted on the Self-Reported Leeds Assessment of Neuropathic Symptoms and Signs pain scale (S-LANSS) for the assessment of pain, and define chronic pain as a score greater than or equal to 3. (NCT01928849)
Timeframe: 3 months or time of final adjudication assessment, up to 6 months

InterventionParticipants (Count of Participants)
Cherry Syrup37
Valproic Acid36

Brief Pain Inventory (BPI) Short Form Score

The BPI short form is a multidimensional patient-completed measure that assesses the sensory component of pain intensity. We will analyze the change in average pain score question (ranges 0-10) and the sum of the 7 interference questions (total range 0-70) from baseline. Higher score indicates greater pain and interference. (NCT01928849)
Timeframe: Assessments at enrollment and 3 months or time of final adjudication assessment (up to 6 months)

,
Interventionscore on a scale (Median)
BPI Average Pain ScoreBPI interference question sum
Cherry Syrup-2-15
Valproic Acid-1-7

Defense and Veterans Pain Rating Scale (DVPRS) Score

The DVPRS is a pain assessment tool developed by the military in an effort to improve reliability and interpretability of pain assessment in the military population. It has been found to be an effective and valid tool in this population. We will analyze the change in numeric pain response (range 0-10) and the sum of the four supplemental questions (range 0-40) from baseline. Higher scores indicate greater pain and functional limitations. (NCT01928849)
Timeframe: Assessments at enrollment and 3 months or time of final adjudication assessment (up to 6 months)

,
Interventionscore on a scale (Median)
DVPRS numeric painDVPRS Supplemental Question Sum
Cherry Syrup-2-9
Valproic Acid0-4.5

Effect on Analgesic Requirement

The effect of study drug on perioperative analgesic consumption and corresponding analysis of pain/sedation scales. Outcome defined as total opioid consumption (mg) during each 24-hour periods following surgery. (NCT01928849)
Timeframe: Assessments during hospitalization (0-24 hours and 24-48 hours post-surgery)

,
Interventionmorphine milligram equivalents (Median)
Postoperative hours 0-24Postoperative hours 24-48
Cherry Syrup5949
Valproic Acid3345

Incidence of Pain Sub-types

The incidence of neuropathic limb or post-amputation pain sub-types as defined by adjudication classification at each assessment time point. (NCT01928849)
Timeframe: Assessments at enrollment and 3 months or time of final adjudication assessment (up to 6 months)

,
InterventionParticipants (Count of Participants)
Residual limb painPhantom limb
Cherry Syrup2922
Valproic Acid3126

Richmond Agitation-Sedation Scale (RASS)

The RASS is a commonly used, valid and reliable assessment tool for use in hospitalized patients. Validity testing reveals good inter-rater reliability among medical, surgical, and intensive care units. We will analyze the numeric score at each assessment (range -5 (unarousable) to 4 (combative)). (NCT01928849)
Timeframe: during hospitalization (0-24 hours and 24-48 hours post-surgery)

,
Interventionscore on a scale (Median)
Post-op hours 0-24Post-op hours 24-48
Cherry Syrup00
Valproic Acid00

Other Studies

18 other studies available for valproic acid and Nerve Degeneration

ArticleYear
Valproic acid ameliorates C. elegans dopaminergic neurodegeneration with implications for ERK-MAPK signaling.
    Neuroscience letters, 2013, Apr-29, Volume: 541

    Topics: alpha-Synuclein; Animals; Anticonvulsants; Caenorhabditis elegans; Caenorhabditis elegans Proteins;

2013
Lithium/Valproic acid combination and L-glutamate induce similar pattern of changes in the expression of miR-30a-5p in SH-SY5Y neuroblastoma cells.
    Neuromolecular medicine, 2014, Volume: 16, Issue:4

    Topics: Brain-Derived Neurotrophic Factor; Cell Line, Tumor; Drug Synergism; Gene Expression Regulation; Glu

2014
Degeneration and regeneration of GABAergic interneurons in the dentate gyrus of adult mice in experimental models of epilepsy.
    CNS neuroscience & therapeutics, 2015, Volume: 21, Issue:1

    Topics: Animals; Chronic Disease; Dentate Gyrus; Epilepsy; GABAergic Neurons; Glutamate Decarboxylase; Green

2015
Neuron-specific knock-down of SMN1 causes neuron degeneration and death through an apoptotic mechanism.
    Human molecular genetics, 2016, 06-15, Volume: 25, Issue:12

    Topics: Animals; Animals, Genetically Modified; Caenorhabditis elegans; Disease Models, Animal; Gene Knockdo

2016
Long-term dietary administration of valproic acid does not affect, while retinoic acid decreases, the lifespan of G93A mice, a model for amyotrophic lateral sclerosis.
    Muscle & nerve, 2009, Volume: 39, Issue:4

    Topics: Acetylcholinesterase; Amyotrophic Lateral Sclerosis; Animal Feed; Animals; Antineoplastic Agents; Ch

2009
The mood stabilizer valproic acid improves defective neurite formation caused by Charcot-Marie-Tooth disease-associated mutant Rab7 through the JNK signaling pathway.
    Journal of neuroscience research, 2010, Nov-01, Volume: 88, Issue:14

    Topics: Animals; Cell Line, Tumor; Cells, Cultured; Charcot-Marie-Tooth Disease; Humans; JNK Mitogen-Activat

2010
Protection of dopaminergic cells from MPP+-mediated toxicity by histone deacetylase inhibition.
    Brain research, 2010, Oct-01, Volume: 1354

    Topics: 1-Methyl-4-phenylpyridinium; Acetylation; Analysis of Variance; Animals; Apoptosis; Butyric Acid; Ce

2010
Valproate reduces CHOP levels and preserves oligodendrocytes and axons after spinal cord injury.
    Neuroscience, 2011, Mar-31, Volume: 178

    Topics: Animals; Axons; Cell Count; Cells, Cultured; Dose-Response Relationship, Drug; Endoplasmic Reticulum

2011
Valproic acid induces apoptosis in differentiating hippocampal neurons by the release of tumor necrosis factor-α from activated astrocytes.
    Neuroscience letters, 2011, Jun-22, Volume: 497, Issue:2

    Topics: Aborted Fetus; Anticonvulsants; Apoptosis; Astrocytes; Cell Differentiation; Cells, Cultured; Hippoc

2011
Attenuation of N-methyl-D-aspartate-mediated cytoplasmic vacuolization in primary rat hippocampal neurons by mood stabilizers.
    Neuroscience, 2003, Volume: 117, Issue:4

    Topics: Animals; Antimanic Agents; Bipolar Disorder; Carbamazepine; Cell Survival; Cells, Cultured; Cytoplas

2003
Topiramate protects against glutamate- and kainate-induced neurotoxicity in primary neuronal-astroglial cultures.
    Epilepsy research, 2003, Volume: 54, Issue:1

    Topics: Animals; Animals, Newborn; Anticonvulsants; Astrocytes; Calcium; Calcium Signaling; Cell Membrane; C

2003
Treatment with valproate after status epilepticus: effect on neuronal damage, epileptogenesis, and behavioral alterations in rats.
    Neuropharmacology, 2006, Volume: 51, Issue:4

    Topics: Animals; Anticonvulsants; Behavior, Animal; Body Weight; Cell Death; Disease Models, Animal; Dose-Re

2006
Establishing a standardized therapeutic testing protocol for spinal muscular atrophy.
    Neurobiology of disease, 2006, Volume: 24, Issue:2

    Topics: Animals; Cell Death; Cell Survival; Cyclic AMP Response Element-Binding Protein; Disease Models, Ani

2006
Role of glutathione in neuroprotective effects of mood stabilizing drugs lithium and valproate.
    Neuroscience, 2007, Feb-23, Volume: 144, Issue:4

    Topics: Animals; Antimanic Agents; Brain; Carbamazepine; Cell Death; Cell Line, Tumor; Cells, Cultured; Cere

2007
Valproic acid-mediated neuroprotection in intracerebral hemorrhage via histone deacetylase inhibition and transcriptional activation.
    Neurobiology of disease, 2007, Volume: 26, Issue:2

    Topics: Animals; Apoptosis Regulatory Proteins; Cell Death; Cerebral Hemorrhage; Chemotaxis, Leukocyte; Dise

2007
Effect of chronic administration of sodium valproate on the morphology of the rat brain hemispheres.
    Neuropatologia polska, 1993, Volume: 31, Issue:3-4

    Topics: Animals; Brain; Capillary Permeability; Chemical and Drug Induced Liver Injury; Culture Techniques;

1993
Inhibitors of GABA metabolism: implications for Huntington's disease.
    Annals of neurology, 1977, Volume: 2, Issue:4

    Topics: 4-Aminobutyrate Transaminase; Alkynes; Aminocaproates; Aminocaproic Acid; Animals; Caudate Nucleus;

1977
Neocerebellar hypoplasia in a neonate following intra-uterine exposure to anticonvulsants.
    Developmental medicine and child neurology, 1990, Volume: 32, Issue:8

    Topics: Abnormalities, Drug-Induced; Cerebellum; Drug Therapy, Combination; Epilepsy; Female; Humans; Nerve

1990