Statusepilepticus complicating intrathecal baclofen overdose

Saltuari, Leopold; Marosi, M.; Kofler, Markus; Bauer, Gerhard

doi:10.1016/0140-6736(92)91697-7

Cited by 28 publications

(10 citation statements)

References 5 publications

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“…This targets the drug on the desired spinal site of action, but the normal bulk flow of CSF toward the brain sometimes leads to CNS side-effects (Kofler, Kronenberg, Rifici, Saltuari, & Bauer, 1994). In overdose, intrathecal baclofen can cause coma and status epilepticus (Nugent, Katz, & Little, 1986;Saltuari, Marosi, Kofler, & Bauer, 1992). Memory disturbance has been described occasionally in patients taking baclofen (Sandyk & Gillman, 1985), including reports, with very limited neuropsychological detail, of two patients with discrete, recurrent episodes of 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 3 memory loss in the context of intrathecal baclofen treatment (Grande, Loeser, & Samii, 2008;Rosenblum & Desan, 2014) This association between baclofen and memory impairment is in keeping with the crucial role of the GABA B receptor, at which baclofen is a selective agonist, in memory processing (Gassmann & Bettler, 2012).…”

Section: Introductionmentioning

confidence: 99%

The GABAB receptor agonist, baclofen, contributes to three distinct varieties of amnesia in the human brain – A detailed case report

Zeman

Hoefeijzers

Milton

et al. 2016

Cortex

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We describe a patient in whom long-term, therapeutic infusion of the selective gamma-amino-butyric acid type B (GABAB) receptor agonist, baclofen, into the cerebrospinal fluid gave rise to three distinct varieties of memory impairment: i) repeated, short periods of severe global amnesia, ii) accelerated long-term forgetting, evident over intervals of days and iii) a loss of established autobiographical memories. This pattern of impairment has been reported in patients with temporal lobe epilepsy, in particular the subtype of Transient Epileptic Amnesia. The amnesic episodes and accelerated forgetting remitted on withdrawal of baclofen, while the autobiographical amnesia persisted. This exceptional case highlights the occurrence of 'non-standard' forms of human amnesia, reflecting the biological complexity of memory processes. It suggests a role for GABAB signalling in the modulation of human memory over multiple time-scales and hints at its involvement in 'epileptic amnesia'.Dear Professor Gilboa, Thank you for your comments on our paper, and for the reviews, which we found stimulating and helpful .We were glad that you found the paper 'of great value' overall.We have done as you suggested, resubmitting as a regular manuscript, as we found that dealing with the points raised by the reviewers required some additions to the main text of the paper and to the reference list.We decided to leave the description of the control experiment alluded to in the Results (section 3.3, final sentence) in the Supplementary data, as we felt that its inclusion in the main text of the paper was unnecessary. If you disagree, however, we would of course be happy to move it into the main text.We could supply a version of the paper with all changes 'tracked' if you wish.We hope that you now find the paper acceptable for publication. In these responses, for ease of navigation, we have left the reviewers' original remarks in plain text, have italicised our responses and have highlighted the resulting changes to the text:Reviewer #1: In this manuscript (MS) an interesting case of a 52 year old woman is described who showed a complex symptomatology of memory impairments which were attributed to her treatment with intrathecal baclofen for spasticity. While the paper is well-written in general, I have several concerns and comments, which I am going to outline below.The results are in my eyes not as straight-forward as the authors interpret them. I would therefore recommend that the authors devote some more room to discussing other possible interpretations.a) Although the control participants were matched to CS (the patient) with respect to "age, education and performance on standard psychometric tests" the question is whether baclofen (additionally) affected other functions than memory. In particular one would like to know if it impacted on attention and concentration, motivation (to be tested), mood (depression?), and executive functions. There were no significant differences between CS and control participants on standard measur...

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Section: Introductionmentioning

confidence: 99%

The GABAB receptor agonist, baclofen, contributes to three distinct varieties of amnesia in the human brain – A detailed case report

Zeman

Hoefeijzers

Milton

et al. 2016

Cortex

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“…Clinical data demonstrated an anti convulsant effect of baclofen [2], seizures af ter baclofen withdrawal [3], as well as a con-vulsant action of its overdose [4,5], A similar diversity can be found in experimental data where the whole spectrum from anticonvul sant [6][7][8][9][10][11][12] through nil [13,14] to proconvulsant effects [15] could be found after systemic administration of baclofen. Some authors de scribed both anti-and proconvulsant effects in relation to the dose of baclofen [16] or to the model used [17,18], There is an agree ment concerning the role of the GABAr sys tem in models of primary generalized seizures of the absence type [19,20], where the GABAr agonist baclofen aggravated seizures [21,22], whereas the GABAr antagonist CGP 35348 exhibited an anticonvulsant action [21,23,24], Developmental data reported by Wurpel et al [25] demonstrated in 16-day-old rat pups an anticonvulsant action of systemically ad ministered baclofen against amygdala kin dling, and when injected into the substantia nigra against fluorothyl-induced seizures [26,27], whereas no such action was found in adult rats.…”

Section: Introductionmentioning

confidence: 55%

Moderate Anticonvulsant Action of Baclofen Does Not Change during Development

1996

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The possible anticonvulsant action of baclofen, a GABAb (γ-aminobutyric acid) receptor agonist, was studied using two types of motor seizures (minimal, clonic and generalized tonicoclonic) elicited by pentylenetetrazol in adult rats and rat pups, 7, 12, 18, and 25 days old. If baclofen was administered intraperitoneally (only in 12- and 25-day-old rats), no effect could be observed in 25-day-old animals. In 12-day-old rats, only the 12-mg/kg dose led to a prolongation of the generalized tonicoclonic seizure latency. Subcutaneous administration of baclofen (3, 6, or 12 mg/kg 30 min before subcutaneous pentylenetetrazol injection) led to a moderate action against the tonic phase of generalized tonicoclonic seizures: the tonic phase of hind limbs was significantly suppressed in all age groups, whereas total suppression of the tonic phase was only outlined. Minimal, i.e., clonic, seizures with preserved righting ability were not influenced by baclofen. The conclusion could be made that the anticonvulsant action of baclofen is dependent on the model of seizures used and that there is no change of baclofen action against pentylenetetrazol-induced seizures during postnatal development in rats.

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“…5 Of note, seizures have also been described in relation to intrathecal baclofen-an agent frequently used to treat spasticity in the TBI population. 9,10 Though EEG studies suggested that our patient's shaking episodes were not epileptic, one can easily imagine how combined therapy with amantadine and baclofen-two potentially epileptogenic drugs-might induce DISCUSSION seizures in other minimally conscious patients. Similarly, one can imagine how improved head and neck mobility in a patient with MCS and chronic contractures might increase susceptibility to aspiration pneumonia.…”

Section: Brief Reportsmentioning

confidence: 93%