Page last updated: 2024-10-26

valproic acid and Atrophy

valproic acid has been researched along with Atrophy in 37 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.

Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes.

Research Excerpts

ExcerptRelevanceReference
"A 44-year-old man with treated neurosyphilis presented with subclinical status epilepticus (SE) refractory to intravenous high-dose lorazepam, phenytoin, and valproic acid over 4 days."7.72Ketamine for refractory status epilepticus: a case of possible ketamine-induced neurotoxicity. ( Lerner, AJ; Maddux, BN; Sagar, SM; Suarez, JI; Ubogu, EE; Werz, MA, 2003)
"A 5-year-old female developed alteration of consciousness during 3 days of long-term treatment with valproic acid for localization-related epilepsy."7.72Reversible altered consciousness with brain atrophy caused by valproic acid. ( Eguchi, M; Imataka, G; Nakagawa, E; Ota, T; Yamanouchi, H, 2003)
"Valproic acid induced coma is presented in an adult patient without a history of metabolic disease."7.68Carbamyl phosphate synthetase-1 deficiency discovered after valproic acid-induced coma. ( Colombo, JP; Straver, JS; van der Vijver, JC; van Woerkom, TC; Verbiest, HB, 1992)
"We evaluated the effect of the divalproex sodium formulation of valproic acid on brain volumes using MRI in people with mild to moderate Alzheimer disease (AD) and assessed for changes associated with behavioral and cognitive effects."5.15Chronic divalproex sodium use and brain atrophy in Alzheimer disease. ( Aisen, PS; Cummings, JL; Fleisher, AS; Jack, CR; Langbaum, JB; Mai, JT; Schneider, LS; Tariot, PN; Thomas, RG; Truran, D; Weiner, MW, 2011)
"Magnetic resonance (MR) multimodality evoked potentials (MEPs) and clinical findings were correlated in a 47-year-old epileptic man in whom parenteral valproic acid (VPA) therapy induced severe comatose hyperammonemic encephalopathy without biological signs of hepatotoxicity (or hepatocytic dysfunction)."3.73Comparison of clinical, magnetic resonance and evoked potentials data in a case of valproic-acid-related hyperammonemic coma. ( Duprez, T; Grandin, C; Guérit, JM; Hantson, P; Nassogne, MC, 2005)
"A 44-year-old man with treated neurosyphilis presented with subclinical status epilepticus (SE) refractory to intravenous high-dose lorazepam, phenytoin, and valproic acid over 4 days."3.72Ketamine for refractory status epilepticus: a case of possible ketamine-induced neurotoxicity. ( Lerner, AJ; Maddux, BN; Sagar, SM; Suarez, JI; Ubogu, EE; Werz, MA, 2003)
"A 5-year-old female developed alteration of consciousness during 3 days of long-term treatment with valproic acid for localization-related epilepsy."3.72Reversible altered consciousness with brain atrophy caused by valproic acid. ( Eguchi, M; Imataka, G; Nakagawa, E; Ota, T; Yamanouchi, H, 2003)
"Valproic acid induced coma is presented in an adult patient without a history of metabolic disease."3.68Carbamyl phosphate synthetase-1 deficiency discovered after valproic acid-induced coma. ( Colombo, JP; Straver, JS; van der Vijver, JC; van Woerkom, TC; Verbiest, HB, 1992)
"Agitation and psychosis are common in Alzheimer disease and cause considerable morbidity."2.76Chronic divalproex sodium to attenuate agitation and clinical progression of Alzheimer disease. ( Aisen, PS; Bartocci, B; Cummings, J; Fleisher, A; Ismail, MS; Jack, CR; Jakimovich, LJ; Loy, R; Porsteinsson, A; Raman, R; Schneider, LS; Tariot, PN; Thal, L; Thomas, RG; Weiner, M, 2011)
"Mood disorders have traditionally been conceptualized as neurochemical disorders, but there is now evidence from a variety of sources demonstrating regional reductions in central nervous system (CNS) volume, as well as reductions in the numbers and/or sizes of glia and neurons in discrete brain areas."2.42The use of mood stabilizers as plasticity enhancers in the treatment of neuropsychiatric disorders. ( Du, J; Gray, NA; Manji, HK; Moore, GJ; Zhou, R, 2003)
"Valproic acid-treated animals developed biochemical evidence of FS as judged by elevated serum gamma-glutamyl transferase (γ-GT), alkaline phosphatase (ALP), creatinine (Cr), and blood urea nitrogen (BUN) along with hypokalaemia, hypophosphataemia, and a decrease in serum uric acid."1.48Mechanism of valproic acid-induced Fanconi syndrome involves mitochondrial dysfunction and oxidative stress in rat kidney. ( Heidari, R; Jafari, F; Khodaei, F; Niknahad, H; Shirazi Yeganeh, B, 2018)
"Although most patients with infantile Alexander disease have epilepsy, infantile spasms are rare."1.39Alexander disease with mild dorsal brainstem atrophy and infantile spasms. ( Hara, T; Ishizaki, Y; Sanefuji, M; Sawaishi, Y; Torisu, H; Yamaguchi-Takada, Y; Yano, T; Yoshikawa, Y, 2013)
" In many situations, the final choice of an antiepileptic drug may need a change due to the agent's side-effect profile."1.37Cerebellar atrophy in a child with valproate toxicity. ( Bhatt, S; Ghosh, VB; Kapoor, S; Prakash, A, 2011)
"We describe a case of catatonia in a 51-year-old man in whom the catatonic symptoms could not be distinguished from symptoms of frontotemporal dementia (FTD) until they were resolved with electroconvulsive therapy (ECT)."1.35A case of catatonia resembling frontotemporal dementia and resolved with electroconvulsive therapy. ( Matsuoka, H; Suzuki, K; Takano, T, 2009)
"Levetiracetam (LEV) treatment was started in combination with VPA in a patient with typical clinical, histological, and biochemical features of MERRF due to a mutation on the tRNA of Phenilalanine gene."1.33Antimyoclonic effect of levetiracetam in MERRF syndrome. ( Filosto, M; Galli, R; Mancuso, M; Murri, L; Pizzanelli, C; Siciliano, G, 2006)
"EEG showed typical hypsarrhythmia in 8 cases, asymmetrical hypsarrhythmia in 1 case and modified hypsarrhythmia in another case."1.30[West's syndrome in patients with cerebral paralysis and periventricular leukomalacia: a good response to treatment]. ( Caraballo, R; Cersósimo, R; Fejerman, N; Intruvini, S; Pociecha, J, 1997)
" Reduction of VPA dosage and subsequent discontinuation 4 months later resulted in disappearance of clinical symptoms with a 20-point improvement at IQ testing and recovery of previous PM score."1.30Reversible pseudoatrophy of the brain and mental deterioration associated with valproate treatment. ( Belmonte, A; Canapicchi, R; Casalini, C; Guerrini, R; Perucca, E, 1998)
"Macro square wave jerks and pendular nystagmus were mildly suppressed after the intramuscular injection of 100 mg of phenobarbital, the oral intake of sodium valproate of 600 mg/day or baclofen of 60 mg/day."1.28[Multiple system atrophy with macro square wave jerks and pendular nystagmus]. ( Fukusako, T; Morimatsu, M; Nogaki, H; Yamamoto, K, 1992)

Research

Studies (37)

TimeframeStudies, this research(%)All Research%
pre-19902 (5.41)18.7374
1990's10 (27.03)18.2507
2000's13 (35.14)29.6817
2010's12 (32.43)24.3611
2020's0 (0.00)2.80

Authors

AuthorsStudies
Lv, Y1
Zhang, N1
Liu, C1
Shi, M1
Sun, L1
Zhang, Y1
Xiang, Z1
Jia, Y1
He, X1
Wang, L1
Cui, W1
Ennaim, N1
Bourrous, M1
Rada, N1
Draiss, G1
Bouskraoui, M1
Ene-Stroescu, V1
Nguyen, T1
Waiblinger, BE1
Bhat, RY1
Kakkar, S1
Prakashini, K1
Lovett, M1
Skidmore, DL1
Mohamed, IS1
Moyal, D1
Sanyal, S1
Khanna, A1
Heidari, R1
Jafari, F1
Khodaei, F1
Shirazi Yeganeh, B1
Niknahad, H1
Abreu, LN1
Issler, C1
Lafer, B1
Ghosh, VB1
Kapoor, S1
Prakash, A1
Bhatt, S1
Tariot, PN2
Schneider, LS2
Cummings, J1
Thomas, RG2
Raman, R1
Jakimovich, LJ1
Loy, R1
Bartocci, B1
Fleisher, A1
Ismail, MS1
Porsteinsson, A1
Weiner, M1
Jack, CR2
Thal, L1
Aisen, PS2
Fleisher, AS1
Truran, D1
Mai, JT1
Langbaum, JB1
Cummings, JL1
Weiner, MW1
Torisu, H1
Yoshikawa, Y1
Yamaguchi-Takada, Y1
Yano, T1
Sanefuji, M1
Ishizaki, Y1
Sawaishi, Y1
Hara, T1
Ubogu, EE1
Sagar, SM1
Lerner, AJ1
Maddux, BN1
Suarez, JI1
Werz, MA1
Gray, NA1
Zhou, R1
Du, J1
Moore, GJ2
Manji, HK2
Yamanouchi, H1
Ota, T1
Imataka, G1
Nakagawa, E1
Eguchi, M1
Hantson, P1
Grandin, C1
Duprez, T1
Nassogne, MC1
Guérit, JM1
Kaur, S1
Sassi, RB1
Axelson, D1
Nicoletti, M1
Brambilla, P1
Monkul, ES1
Hatch, JP1
Keshavan, MS1
Ryan, N1
Birmaher, B1
Soares, JC1
Mancuso, M1
Galli, R1
Pizzanelli, C1
Filosto, M1
Siciliano, G1
Murri, L1
Galimberti, CA1
Diegoli, M1
Sartori, I1
Uggetti, C1
Brega, A1
Tartara, A1
Arbustini, E1
Ferrero, AJ1
Cereseto, M1
Sifonios, LL1
Reinés, A1
Peixoto, E1
Rubio, MC1
Wikinski, S1
Suzuki, K1
Takano, T1
Matsuoka, H1
Papazian, O1
Cañizales, E1
Alfonso, I1
Archila, R1
Duchowny, M1
Aicardi, J1
Baganz, MD1
Dross, PE1
Caraballo, R1
Cersósimo, R1
Intruvini, S1
Pociecha, J1
Fejerman, N1
Guerrini, R1
Belmonte, A1
Canapicchi, R1
Casalini, C1
Perucca, E1
Gelisse, P1
Genton, P1
Raybaud, C1
Thiry, A1
Pincemaille, O1
Alla, P1
Philip, N1
Azulay, JP1
Attarian, S1
Pouget, J1
Straussberg, R1
Kivity, S1
Weitz, R1
Harel, L1
Gadoth, N1
Chen, G1
Sveberg Røste, L1
Taubøll, E1
Berner, A1
Berg, KA1
Aleksandersen, M1
Gjerstad, L1
Vainstein, G1
Korzets, Z1
Pomeranz, A1
Gadot, N1
Yamamoto, K1
Fukusako, T1
Nogaki, H1
Morimatsu, M1
Verbiest, HB1
Straver, JS1
Colombo, JP1
van der Vijver, JC1
van Woerkom, TC1
Walker, RM1
Smith, GS1
Barsoum, NJ1
Macallum, GE1
Takeno, Y1
McLachlan, RS1

Clinical Trials (3)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Treatment of Psychosis and Agitation in Alzheimer's Disease[NCT02129348]Phase 277 participants (Actual)Interventional2014-06-30Completed
A Randomized, Double-Blind, Placebo-Controlled Trial of Valproate to Attenuate the Progression of Alzheimer's Disease (AD)[NCT00071721]Phase 3313 participants (Actual)Interventional2003-10-31Completed
A Pilot Study to Assess the Efficacy of Subanesthetic Doses of IV Ketamine in the Treatment Drug Resistant Epilepsy[NCT05019885]Phase 26 participants (Anticipated)Interventional2022-08-26Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Basic Activities of Daily Living (BADL)

Basic Activities of Daily Living with items for 6 functions: bathing, dressing, toileting, transferring, continence, and feeding. Each item is scored as unimpaired=1, impaired=0. Total score is the measure used, range 0-6; higher scores indicate better functioning. (NCT02129348)
Timeframe: Assessed at Week 0, Week2, Week 4, Week 6, Week 8, Week 10, Week 12

Interventionscore on a scale (Least Squares Mean)
Lithium Treatment Group0.3
Placebo Group0.1

Change in Neuropsychiatric Inventory (NPI) Agitation/Aggression Domain Score

Neuropsychiatric Inventory (NPI) Agitation/Aggression Domain is the measure used that combines symptoms of agitation and aggression. Frequency X Severity rating score, range 0-12. Higher score indicates more agitation and aggressive behavior. (NCT02129348)
Timeframe: Assessed at screening, Week 0, Week 2, Week 4, Week 6, Week 8, Week 10, Week 12

Interventionscore on a scale (Least Squares Mean)
Lithium Treatment Group3.2
Placebo Group2.5

Clinical Global Impression (CGI) Behavior Change

Clinical Global Impression (CGI) Behavior Change score is the measure used to assess change in overall behavior; scoring range 1-7 with higher scores indicating worsening over time and lower scores indicating improvement over time. Scores ranging from 1-3 indicate improvement. Only patients that demonstrated improvement at week 12 were reported; scores for earlier weeks were only used to assess progress throughout the study. (NCT02129348)
Timeframe: Week 12

InterventionParticipants (Count of Participants)
Lithium Treatment Group12
Placebo Group8

Clinical Responder Defined as a 30% Decrease in NPI Core Score (Sum Score of NPI Domains of Agitation/Aggression, Delusions and Hallucinations) Together With a Clinical Global Impression (CGI) Behavior Change Score of 1 or 2

The patient is classified as a responder (score=1) if both criteria are met or as a non-responder (score=0) if both criteria are not met. The first criterion to determine responder status, NPI core score, has a scoring range 0-36; each of the three component scores for symptoms of agitation/aggression, delusions and hallucinations has a scoring range 0-12. For each symptom and the total score, higher score indicates more symptoms. The second criterion to determine responder status, Clinical Global Impression (CGI), is used to assess change in overall behavior; scoring range 1-7 with higher scores indicating worsening over time and lower scores indicating improvement over time. Only patients who met both criteria, assessed as change compared to baseline, were counted as responders; all other patients were non-responders. Patients that demonstrated improvement at week 12 were reported; scores for earlier weeks were only used to assess progress throughout the study. (NCT02129348)
Timeframe: Week 12

InterventionParticipants (Count of Participants)
Lithium Treatment Group12
Placebo Group7

Folstein Mini-Mental Status Exam

30 item questionnaire used to assess degree of cognitive impairment. Orientation, registration, attention/calculation, recall, language, repetitions and commands are assessed. Total score is the measure used; range 0-30, higher scores indicate better global cognitive function. (NCT02129348)
Timeframe: Assessed at Screening, Week 12

Interventionscore on a scale (Least Squares Mean)
Lithium Treatment Group0.9
Placebo Group0.9

Severe Impairment Battery

Neuropsychological test used to assess a patient's cognitive ability. The patient is asked to complete small tasks such as drawing shapes and printing their name. They are also asked to remember certain names and objects, such as a cup and a spoon, and the evaluator's first name. Total score is the measure used; range 0-100, higher scores indicate better cognition. (NCT02129348)
Timeframe: Assessed at Week 0, Week 12

Interventionscore on a scale (Least Squares Mean)
Lithium Treatment Group2.1
Placebo Group-0.0

Simpson-Angus Scale

Simpson Angus Scale for Extrapyramidal Sign requires in-person examination to assess gait, arm dropping, shoulder shaking, elbow rigidity, wrist rigidity, leg pendulousness, head dropping, glabella tap, tremor, and salivation. Total score is the measure used, range 0-40; higher scores indicate increased severity of signs. (NCT02129348)
Timeframe: Assessed at Week 0, Week 2, Week 4, Week 6, Week 8, Week 10, Week 12

Interventionscore on a scale (Least Squares Mean)
Lithium Treatment Group-0.0
Placebo Group0.0

Treatment Emergent Signs and Symptoms

Treatment Emergent Symptom Scale that covers 26 somatic symptoms, each rated as present (score=1) or absent (score=0). Total score is the measure used with scoring range 0-26; higher scores indicate more somatic symptoms. (NCT02129348)
Timeframe: Assessed at Week 0, Week 2, Week 4, Week 6, Week 8, Week 10, Week 12

Interventionscore on a scale (Least Squares Mean)
Lithium Treatment Group0.6
Placebo Group0.7

Young Mania Rating Scale

Young Mania Rating Scale total score is the measure used to assess symptoms that occur in mania; each item is a symptom that is rated for severity. Scoring range 0-60; higher scores indicate more severe symptoms. (NCT02129348)
Timeframe: Assessed at Week 0, Week 2, Week 4, Week 6, Week 8, Week 10, Week 12

Interventionscore on a scale (Least Squares Mean)
Lithium Treatment Group3.1
Placebo Group1.1

Zarit Caregiver Burden Interview

Zarit Caregiver Burden Interview with the caregiver asked to rank 22 items on a scale with responses for each item from 'never' (score 0) to 'nearly always' (score 4). Total score is the measure used; range 0-88 with higher scores indicating greater caregiver burden. (NCT02129348)
Timeframe: Assessed at Week 0, Week 4, Week 8, Week 10, Week 12

Interventionscore on a scale (Least Squares Mean)
Lithium Treatment Group2.8
Placebo Group-0.4

Agitation Measured by the Cohen-Mansfield Agitation Inventory (CMAI), Community Version

The Cohen-Mansfield Agitation Inventory (CMAI) is a 29-item caregiver rating questionnaire for the assessment of agitation in older persons. It includes descriptions of 29 agitated behaviors, each rated on a 7-point scale of frequency. The range of this instrument is 29 to 203 with higher numbers indicating greater impairment. (NCT00071721)
Timeframe: 24 months

InterventionUnits on a scale (Mean)
Valproate10.6
Placebo12.1

Cognitive Performance Assessed by the Alzheimer's Disease Assessment Scale-cognitive Subtest (ADAS-cog)

Alzheimer's Disease Assessment Scale, cognitive sub-scale in points per year (ADAS-cog) is a psychometric measure sensitive to change in mild to moderate AD. The range of this instrument is 0 to 70 with higher numbers indicating greater impairment. (NCT00071721)
Timeframe: 24 months

InterventionUnits on a scale (Mean)
Valproate42.3
Placebo41.9

Functional Performance Assessed by the Alzheimer's Disease Cooperative Study Activities of Daily Living (ADCS-ADL) Inventory

Alzheimer's Disease Cooperative Study Activities of Daily Living Score (ADCS-ADL) is a structured questionnaire about activities of daily living, administered to the subject's caregiver/study partner. The range of this instrument is 0 to 78 with lower numbers indicating greater impairment. (NCT00071721)
Timeframe: 24 months

InterventionUnits on a scale (Mean)
Valproate35.1
Placebo41.0

Global Severity of Dementia Using the CDR Sum of Boxes

Clinical Dementia Rating, Sum of Boxes (CDR-SOB) is a global rating of dementia severity based on the clinician's interpretation of the history and examination. The range of this instrument is 0 to 18 with higher numbers indicating greater impairment. (NCT00071721)
Timeframe: 24 months

InterventionUnits on a scale (Mean)
Valproate12.0
Placebo11.5

Participant's Clinical Condition or Endpoint Assessed With the ADCS-Clinical Global Impression of Change (ADCS-CGIC)

ADCS-Clinical Global Impression of Change (ADCS-CGIC) provides a means to reliably assess global change from baseline. It provides a semi-structured format to allow clinicians to gather necessary clinical information from both the participant and informant, in order to make an overall impression of clinical change. The range of this instrument is 1 to 7 with lower numbers indicating improvement and higher numbers indicating a worsened state. (NCT00071721)
Timeframe: 24 months

InterventionUnits on a scale (Mean)
Valproate5.7
Placebo5.5

Presence of Agitation and/or Psychosis Measured by the Neuropsychiatric Inventory (NPI) Combined With an Assessment of the Clinical Significance of Behavioral Change Rated by the Study Clinician

NPI quantifies behavioral changes in dementia, including depression, anxiety, psychosis, agitation, and others. This is a questionnaire administered to the subject's study partner. The range of this instrument is 0 to 120 with higher numbers indicating greater impairment. To determine whether or not psychosis or agitation is present, there is no cutoff score but is based on the clinician's judgment. In the NPI, the subject responds to 'Yes' or 'No' questions. Then it is determined how often psychosis or agitation occurs and if it is mild, moderate or severe. (NCT00071721)
Timeframe: 24 months

InterventionParticipants (Number)
Valproate25
Placebo29

Reviews

1 review available for valproic acid and Atrophy

ArticleYear
The use of mood stabilizers as plasticity enhancers in the treatment of neuropsychiatric disorders.
    The Journal of clinical psychiatry, 2003, Volume: 64 Suppl 5

    Topics: Anticonvulsants; Apoptosis; Atrophy; Brain; Central Nervous System Diseases; Gene Expression; Genes,

2003

Trials

2 trials available for valproic acid and Atrophy

ArticleYear
Chronic divalproex sodium to attenuate agitation and clinical progression of Alzheimer disease.
    Archives of general psychiatry, 2011, Volume: 68, Issue:8

    Topics: Aged; Alzheimer Disease; Atrophy; Brain; Female; Humans; Magnetic Resonance Imaging; Male; Middle Ag

2011
Chronic divalproex sodium to attenuate agitation and clinical progression of Alzheimer disease.
    Archives of general psychiatry, 2011, Volume: 68, Issue:8

    Topics: Aged; Alzheimer Disease; Atrophy; Brain; Female; Humans; Magnetic Resonance Imaging; Male; Middle Ag

2011
Chronic divalproex sodium to attenuate agitation and clinical progression of Alzheimer disease.
    Archives of general psychiatry, 2011, Volume: 68, Issue:8

    Topics: Aged; Alzheimer Disease; Atrophy; Brain; Female; Humans; Magnetic Resonance Imaging; Male; Middle Ag

2011
Chronic divalproex sodium to attenuate agitation and clinical progression of Alzheimer disease.
    Archives of general psychiatry, 2011, Volume: 68, Issue:8

    Topics: Aged; Alzheimer Disease; Atrophy; Brain; Female; Humans; Magnetic Resonance Imaging; Male; Middle Ag

2011
Chronic divalproex sodium use and brain atrophy in Alzheimer disease.
    Neurology, 2011, Sep-27, Volume: 77, Issue:13

    Topics: Aged; Aged, 80 and over; Alzheimer Disease; Analysis of Variance; Atrophy; Brain; Double-Blind Metho

2011

Other Studies

34 other studies available for valproic acid and Atrophy

ArticleYear
Occipital epilepsy versus progressive myoclonic epilepsy in a patient with continuous occipital spikes and photosensitivity in electroencephalogram: A case report.
    Medicine, 2018, Volume: 97, Issue:15

    Topics: Anticonvulsants; Atrophy; Cerebral Cortex; Diagnosis, Differential; Disease Progression; Electroence

2018
The Notch signaling pathway inhibitor Dapt alleviates autism-like behavior, autophagy and dendritic spine density abnormalities in a valproic acid-induced animal model of autism.
    Progress in neuro-psychopharmacology & biological psychiatry, 2019, 08-30, Volume: 94

    Topics: Animals; Atrophy; Autistic Disorder; Autophagy; Beclin-1; Behavior, Animal; Cerebellum; Dendritic Sp

2019
[Lennox-Gastaut syndrome: Experience of Marrakech University Hospital].
    Archives de pediatrie : organe officiel de la Societe francaise de pediatrie, 2013, Volume: 20, Issue:10

    Topics: Accidental Falls; Anticonvulsants; Asphyxia Neonatorum; Atrophy; Cerebral Cortex; Child; Child, Pres

2013
Successful treatment of catatonia in a young man with schizophrenia and progressive diffuse cerebral atrophy.
    The Journal of neuropsychiatry and clinical neurosciences, 2014,Winter, Volume: 26, Issue:1

    Topics: Adolescent; Amantadine; Anticonvulsants; Antiparkinson Agents; Antipsychotic Agents; Atrophy; Catato

2014
Hemiconvulsion-hemiplegia-epilepsy syndrome: clinical course and neuroradiological features in a 20-month-old girl.
    BMJ case reports, 2014, Mar-10, Volume: 2014

    Topics: Anticonvulsants; Atrophy; Brain; Carbamazepine; Epilepsy; Female; Hemiplegia; Humans; Infant; Syndro

2014
Valproate-induced pseudoatrophy: expanding the clinical and imaging spectrum.
    Pediatric neurology, 2014, Volume: 51, Issue:2

    Topics: Anticonvulsants; Atrophy; Brain; Child; Cognition Disorders; Humans; Magnetic Resonance Imaging; Mag

2014
Valproate induced cerebellar atrophy presenting as movement disorder.
    Schizophrenia research, 2017, Volume: 184

    Topics: Adult; Anticonvulsants; Atrophy; Cerebellum; Electroencephalography; Epilepsy, Tonic-Clonic; Female;

2017
Mechanism of valproic acid-induced Fanconi syndrome involves mitochondrial dysfunction and oxidative stress in rat kidney.
    Nephrology (Carlton, Vic.), 2018, Volume: 23, Issue:4

    Topics: Adenosine Triphosphate; Animals; Atrophy; Disease Models, Animal; Fanconi Syndrome; Glutathione; Kid

2018
Valproate-induced reversible pseudoatrophy of the brain and hyperammonemic encephalopathy in a bipolar patient.
    The Australian and New Zealand journal of psychiatry, 2009, Volume: 43, Issue:5

    Topics: Atrophy; Bipolar Disorder; Brain; Female; Humans; Hyperammonemia; Middle Aged; Neurotoxicity Syndrom

2009
Cerebellar atrophy in a child with valproate toxicity.
    Indian journal of pediatrics, 2011, Volume: 78, Issue:8

    Topics: Anticonvulsants; Atrophy; Cerebellum; Child; Humans; Hyperammonemia; Male; Valproic Acid

2011
Alexander disease with mild dorsal brainstem atrophy and infantile spasms.
    Brain & development, 2013, Volume: 35, Issue:5

    Topics: Alexander Disease; Anticonvulsants; Atrophy; Brain Stem; Brain Waves; Corpus Callosum; DNA Mutationa

2013
Ketamine for refractory status epilepticus: a case of possible ketamine-induced neurotoxicity.
    Epilepsy & behavior : E&B, 2003, Volume: 4, Issue:1

    Topics: Adult; Anticonvulsants; Atrophy; Brain; Electroencephalography; Excitatory Amino Acid Antagonists; H

2003
Reversible altered consciousness with brain atrophy caused by valproic acid.
    Pediatric neurology, 2003, Volume: 28, Issue:5

    Topics: Atrophy; Brain; Child, Preschool; Consciousness Disorders; Electroencephalography; Epilepsy; Female;

2003
Comparison of clinical, magnetic resonance and evoked potentials data in a case of valproic-acid-related hyperammonemic coma.
    European radiology, 2005, Volume: 15, Issue:1

    Topics: Atrophy; Coma; Evoked Potentials; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Rett Syndro

2005
Cingulate cortex anatomical abnormalities in children and adolescents with bipolar disorder.
    The American journal of psychiatry, 2005, Volume: 162, Issue:9

    Topics: Adolescent; Adult; Age Factors; Anticonvulsants; Atrophy; Bipolar Disorder; Brain; Brain Mapping; Ch

2005
Antimyoclonic effect of levetiracetam in MERRF syndrome.
    Journal of the neurological sciences, 2006, Apr-15, Volume: 243, Issue:1-2

    Topics: Activities of Daily Living; Anticonvulsants; Atrophy; Brain; Drug Therapy, Combination; Female; Gene

2006
Brain pseudoatrophy and mental regression on valproate and a mitochondrial DNA mutation.
    Neurology, 2006, Nov-14, Volume: 67, Issue:9

    Topics: Adult; Aged; Anticonvulsants; Atrophy; Brain; Child; Cognition Disorders; Developmental Disabilities

2006
Cytoskeleton of hippocampal neurons as a target for valproic acid in an experimental model of depression.
    Progress in neuro-psychopharmacology & biological psychiatry, 2007, Oct-01, Volume: 31, Issue:7

    Topics: Animals; Antidepressive Agents; Atrophy; Behavior, Animal; Cytoskeleton; Depression; Hippocampus; Im

2007
A case of catatonia resembling frontotemporal dementia and resolved with electroconvulsive therapy.
    The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry, 2009, Volume: 10, Issue:3

    Topics: Anti-Arrhythmia Agents; Anticonvulsants; Antimanic Agents; Atrophy; Atropine; Bipolar Disorder; Cata

2009
Reversible dementia and apparent brain atrophy during valproate therapy.
    Annals of neurology, 1995, Volume: 38, Issue:4

    Topics: Atrophy; Brain Diseases; Child; Child, Preschool; Dementia; Epilepsy; Female; Humans; Magnetic Reson

1995
Valproic acid-induced hyperammonemic encephalopathy: MR appearance.
    AJNR. American journal of neuroradiology, 1994, Volume: 15, Issue:9

    Topics: Adult; Ammonia; Atrophy; Brain Diseases, Metabolic; Cerebral Cortex; Diagnosis, Differential; Epilep

1994
[West's syndrome in patients with cerebral paralysis and periventricular leukomalacia: a good response to treatment].
    Revista de neurologia, 1997, Volume: 25, Issue:145

    Topics: Anticonvulsants; Atrophy; Cerebral Palsy; Cerebral Ventricles; Child; Child, Preschool; Female; gamm

1997
Reversible pseudoatrophy of the brain and mental deterioration associated with valproate treatment.
    Epilepsia, 1998, Volume: 39, Issue:1

    Topics: Atrophy; Brain; Brain Diseases; Child; Cognition Disorders; Diagnosis, Differential; Electroencephal

1998
Benign childhood epilepsy with centrotemporal spikes and hippocampal atrophy.
    Epilepsia, 1999, Volume: 40, Issue:9

    Topics: Atrophy; Cerebral Cortex; Child; Electroencephalography; Epilepsy, Rolandic; Hippocampus; Humans; Ma

1999
[Epilepsy in an adult with chromosome 22q11 micro-deletion].
    Revue neurologique, 1999, Volume: 155, Issue:11

    Topics: Adult; Anticonvulsants; Atrophy; Brain; Chromosome Deletion; Chromosomes, Human, Pair 22; DiGeorge S

1999
Reversible cortical atrophy and cognitive decline induced by valproic acid.
    European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society, 1998, Volume: 2, Issue:4

    Topics: Adolescent; Anticonvulsants; Atrophy; Cerebral Cortex; Cognition Disorders; Electroencephalography;

1998
Clinical and preclinical evidence for the neurotrophic effects of mood stabilizers: implications for the pathophysiology and treatment of manic-depressive illness.
    Biological psychiatry, 2000, Oct-15, Volume: 48, Issue:8

    Topics: Affect; Antimanic Agents; Atrophy; Bipolar Disorder; Brain; Calcium-Calmodulin-Dependent Protein Kin

2000
Morphological changes in the testis after long-term valproate treatment in male Wistar rats.
    Seizure, 2001, Volume: 10, Issue:8

    Topics: Animals; Anticonvulsants; Atrophy; Biomarkers, Tumor; Dose-Response Relationship, Drug; Flow Cytomet

2001
Deepening coma in an epileptic patient: the missing link to the urea cycle. Hyperammonaemic metabolic encephalopathy.
    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2002, Volume: 17, Issue:7

    Topics: Anticonvulsants; Atrophy; Cerebellum; Coma; Epilepsy; Female; Humans; Hyperammonemia; Middle Aged; T

2002
[Multiple system atrophy with macro square wave jerks and pendular nystagmus].
    Rinsho shinkeigaku = Clinical neurology, 1992, Volume: 32, Issue:11

    Topics: Atrophy; Baclofen; Brain Diseases; Diazepam; Electrooculography; Eye Movements; Female; Humans; Midd

1992
Carbamyl phosphate synthetase-1 deficiency discovered after valproic acid-induced coma.
    Acta neurologica Scandinavica, 1992, Volume: 86, Issue:3

    Topics: Adult; Amino Acid Metabolism, Inborn Errors; Ammonia; Atrophy; Carbamoyl-Phosphate Synthase (Ammonia

1992
Preclinical toxicology of the anticonvulsant calcium valproate.
    Toxicology, 1990, Volume: 63, Issue:2

    Topics: Animals; Anticonvulsants; Atrophy; Dogs; Dose-Response Relationship, Drug; Drug Evaluation, Preclini

1990
[Evaluation of bone atrophy by microdensitometry and effect of active vitamin D3 (1 alpha-OH-D3) administration in patients receiving anticonvulsants].
    No to shinkei = Brain and nerve, 1989, Volume: 41, Issue:9

    Topics: Absorptiometry, Photon; Adolescent; Adult; Aged; Anticonvulsants; Atrophy; Bone and Bones; Bone Dens

1989
Pseudoatrophy of the brain with valproic acid monotherapy.
    The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques, 1987, Volume: 14, Issue:3

    Topics: Adolescent; Atrophy; Brain; Cerebral Ventricles; Cognition Disorders; Electroencephalography; Epilep

1987