Trimethoprim-Sulfamethoxazole Exacerbates Posthypoxic Action Myoclonus in a Patient with Suspicion of Pneumocystis jiroveci Infection

Jundt, Franziska; Lempert, Thomas; Dörken, Bernd; Pezzutto, Antonio

doi:10.1007/s15010-004-3011-6

Cited by 12 publications

(2 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Sulfonamides have been associated with multifocal and generalized myoclonus. A causative role of altered dopamine metabolism due to inhibition of dihydrofolate reductase [15] as well as increased phenylalanine levels due to the inhibition of phenylalanine metabolism have been proposed [41]. Multifocal myoclonus that is due to aminoglycosides has been attributed to NMDA receptor activation and subsequent excitotoxicity.…”

Section: Resultsmentioning

confidence: 99%

The clinical heterogeneity of drug-induced myoclonus: an illustrated review

2016

View full text Add to dashboard Cite

A wide variety of drugs can cause myoclonus. To illustrate this, we first discuss two personally observed cases, one presenting with generalized, but facial-predominant, myoclonus that was induced by amantadine; and the other presenting with propriospinal myoclonus triggered by an antibiotic. We then review the literature on drugs that may cause myoclonus, extracting the corresponding clinical phenotype and suggested underlying pathophysiology. The most frequently reported classes of drugs causing myoclonus include opiates, antidepressants, antipsychotics, and antibiotics. The distribution of myoclonus ranges from focal to generalized, even amongst patients using the same drug, which suggests various neuro-anatomical generators. Possible underlying pathophysiological alterations involve serotonin, dopamine, GABA, and glutamate-related processes at various levels of the neuraxis. The high number of cases of drug-induced myoclonus, together with their reported heterogeneous clinical characteristics, underscores the importance of considering drugs as a possible cause of myoclonus, regardless of its clinical characteristics.Electronic supplementary materialThe online version of this article (doi:10.1007/s00415-016-8357-z) contains supplementary material, which is available to authorized users.

show abstract

Section: Resultsmentioning

confidence: 99%

The clinical heterogeneity of drug-induced myoclonus: an illustrated review

2016

View full text Add to dashboard Cite

show abstract

“…HIV/AIDS), medication-induced, or other immunosuppressed states. [62][63][64][65][66][67][68][69] Congenital dihydropteridine reductase deficiency is also associated with neurological sensitivity to SXT, 59 while Fragile X syndrome children are similarly prone to parkinsonism with SXT. 70 In all reported cases, tremor disappeared with SXT discontinuation.…”

Section: Case 4: Polypharmacymentioning

confidence: 99%

Acute movement disorders in the medical setting

Zawar

Mario

Feldman

et al. 2016

Int J Psychiatry Med

View full text Add to dashboard Cite

Objective Psychosomatic medicine psychiatrists are often tasked with the evaluation and treatment of complex neuropsychiatric states which may be motoric in phenotype. Little energy has been dedicated to understanding acute movement disorders in the hospital environment. Method Recognizing the importance of frontal-subcortical (corticostriatothalamocortical) circuitry and basal ganglia structures, we present a case series of acute movement disorder phenotypes resulting from underlying medical conditions, commonly-administered medications, or the interaction of both. We organize these scenarios into neurodegenerative disorders, primary psychiatric disorders, neuroinflammation, and polypharmacy, demonstrating a clinical example of each followed by background references on a variety of clinical states and medications contributing to acute movement disorders. In addition, we offer visual illustration of implicated neurocircuitry as well as proposed neurotransmitter imbalances involving glutamate, gamma aminobutyric acid, and dopamine. Furthermore, we review the various clinical syndromes and medications involved in the development of acute movement disorders. Results Acute movement disorder's involve complex interactions between frontal-subcortical circuits and acute events. Given the complexity of interactions, psychopharmacological considerations become critical, as some treatments may alleviate acute movement disorders while others will exacerbate them. Conclusion Integrating underlying medical conditions and acutely administered (or discontinued) pharmacological agents offers an interactional, neuromedical approach to acute movement disorders that is critical to the work of psychosomatic medicine.

show abstract

Antibacterial Drugs

2010

Meyler's Side Effects of Antimicrobial Drugs

View full text Add to dashboard Cite

Trimethoprim-Sulfamethoxazole Exacerbates Posthypoxic Action Myoclonus in a Patient with Suspicion of Pneumocystis jiroveci Infection

Cited by 12 publications

References 24 publications

The clinical heterogeneity of drug-induced myoclonus: an illustrated review

The clinical heterogeneity of drug-induced myoclonus: an illustrated review

Acute movement disorders in the medical setting

Antibacterial Drugs

Contact Info

Product

Resources

About