Cerebral toxoplasmosis in Acquired Immunodeficiency Syndrome (AIDS) patients also provides unifying pathophysiologic hypotheses for Holmes tremor

Abstract

BackgroundHolmes tremor is a rare symptomatic movement disorder. Currently suggested pathophysiological mechanisms of the disease are mostly derived from stroke cases. Although rare, cerebral toxoplasmosis may strengthen the pathophysiologic mechanism of disease.Case presentationA case of Holmes tremor secondary to cerebral toxoplasmosis in an AIDS patient is presented. A relevant literature search was performed, using pubmed and several entries for Holmes tremor as labelled in the literature. The unifying feature of our case and those of the literature is the involvement of either the cerebello-thalamo-cortical and/or the dentato-rubro-olivary pathways. The abscess or the extension of surrounding edema beyond these two circuits may account for the superimposed dysfunction of the nigrostriatal system in some but not all cases. The short delay observed in our observation and the dramatic response to treatment may indirectly support the secondary neuronal degeneration theory in the mechanism of Holmes tremor.ConclusionCases of cerebral toxoplasmosis in AIDS patients also provide arguments for the role of the thalamo-cortical and/or the dentato-rubro-olivary pathways dysfunction in the pathogenesis of Holmes tremor. Involvement of the nigro-striatal pathway may not be crucial in the development of this syndrome. Our case also brings additional indirect arguments for the role of secondary neuronal degeneration in the mechanism of Holmes tremor.

Holmes tremor

“…7 The authors concluded that the dopaminergic deficit on DaTSCAN SPECT could be a predictor of levodopa responsiveness. 7 In another report, 3 the authors mentioned that all their patients improved to varying degrees with levodopa therapy, and they found that 18 F-dopa uptake showed values that were markedly and significantly decreased on the lesion side when compared to healthy controls and the contralateral side. However, some values were lower than those observed in parkinsonian patients.…”

Holmes’ or functional tremor?

“…The latency from lesion to tremor onset is usually about two months and its generation likely relies on a combined involvement of both the dopaminergic nigrostriatal system and the cerebello-thalamo-cortical pathways; however, pathophysiologic heterogeneity may account for a variable delay, as supported by DaTSCAN SPECT studies as well as by different therapeutic responses to levodopa, with only mild to moderate improvement ( Gajos et al, 2010 , Raina et al, 2016 ). Delayed tremor onset may also suggest a secondary neural degeneration along the dentate-rubro-olivary pathways ( Lekoubou et al, 2010 ).…”

Headache and Tremor: Co-occurrences and Possible Associations

“…In the majority of cases it is secondary to Toxoplasma abscesses in the mesencephalon of thalamus 27. Holmes tremor usually is a late feature.…”

“… 26 In the majority of cases it is secondary to Toxoplasma abscesses in the mesencephalon of thalamus. 27 Holmes tremor usually is a late feature. Lekoubou et al 27 describe a patient with a relatively short latency between onset of neurological signs and Holmes tremor, and even in this patient the tremor did not become apparent until 8 days after he first came to medical attention.…”