Holmes’ tremor following midbrain Toxoplasma abscess: clinical features and treatment of a case

Pezzini, Alessandro; Zavarise, Paola; Palvarini, Laura; Viale, Pierluigi; Oladeji, O.; Padovani, Alessandro

doi:10.1016/s1353-8020(01)00013-x

Cited by 28 publications

(10 citation statements)

References 31 publications

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“…According to one report (Raina et al 2016 ) 13 out of 24 patients treated with levodopa improved and in seven tremor disappeared almost completely. In some subjects even single dose of levodopa produced dramatic response (Raina et al 2007 ; Vélez et al 2002 ) and with daily doses between 750 and 1000 long term improvement was achieved (Kim et al 2009 ; Raina et al 2007 ; Vélez et al 2002 ; Pezzini et al 2002 ). A good response to levodopa (100 mg tid) persisted for 4 years was reported in a case of HT related to midbrain dysplasia (Boelmans et al 2012 ).…”

Section: Discussionmentioning

confidence: 99%

“…In one patient 750 mg of levodopa failed to be effective, but 2 mg of cabergoline significantly alleviated all components of tremor (Akkus and Diramali 2006 ). In some patients dopaminergic therapy was more effective in reducing resting tremor than the kinetic one (Kim et al 2009 ; Strecker et al 2007 ; Raina et al 2016 ; Pezzini et al 2002 ) but in others levodopa improved resting, postural and kinetic tremor (Raina et al 2007 ). Only limited data concerning the effectiveness of dopaminergic therapy in subjects with dopaminergic dysfunction confirmed by SPECT are available.…”

Section: Discussionmentioning

confidence: 99%

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Is nigrostriatal dopaminergic deficit necessary for Holmes tremor to develop? The DaTSCAN and IBZM SPECT study

et al. 2017

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Holmes’s tremor (HT) is assumed to be the result of coexistence of nigrostriatal dopaminergic system impairment and the lesion of cerebello-thalamic pathways. It was suggested that dopaminergic deficiency is responsible for rest tremor, and lack of compensatory cerebellar function leads to spill of tremor into voluntary movements. Cases of HT with and without abnormalities of the presynaptic part of dopaminergic nigrostriatal were published and these findings raised the question of possibility of the postsynaptic lesion. Three patients with HT diagnosed according to criteria of Consensus Statement on Tremor were studied. In all of them SPECT imaging with ligands of presynaptic (I 123-FP CIT—DaTSCAN) and postsynaptic (I 123-iodobenzamide—IBZM) nigrostriatal dopaminergic neurons was performed. Indices of uptake in caudate and putamen normalized to nonspecific uptake in occipital cortex and indices of asymmetry for each whole striatum as well as for putamen and caudate separately were calculated. SPECT studies did not reveal asymmetry of DaTSCAN and IBZM binding in striatum in all studied subjects. The current clinical diagnostic criteria of HT are presumably insufficiently specific and when using them we identify patients both with and without the involvement of dopaminergic system. These two groups may represent tremor disorders of similar phenomenology but of different pathomechanism.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Is nigrostriatal dopaminergic deficit necessary for Holmes tremor to develop? The DaTSCAN and IBZM SPECT study

et al. 2017

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“…It becomes more pronounced with a fixed posture, and further increases in amplitude with intentional voluntary movement (Vidailhet et al 1998). Some authorities believe that it is actually a cerebellar postural tremor plus a parkinsonian tremor (Vidailhet et al 1998), and can be caused by multiple sclerosis (MS) (Poser and Brinar 2004), vascular insults (Tan et al 2001), tumours (Leung et al 1999), head trauma (Krack et al 1994), neuroleptic exposure (Friedman 1992), and toxoplasma abscess (Pezzini et al 2002).…”

Section: Introductionmentioning

confidence: 99%

Unilateral rubral tremor following treatment with risperidone

Shen

2009

The World Journal of Biological Psychiatry

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Rubral tremor is a rare movement disorder that occurs typically with midbrain damage. The main features of this tremor are its low frequency, irregular rhythm, presence at rest, and acceleration during posture and active movement. Antipsychotic agent-induced tremors are usually bilateral parkinsonian tremors. We found no previous reports of unilateral rubral tremor in the literature. A 23-year-old man had unilateral rubral tremors as a result of a midbrain lesion plus risperidone exposure for treatment of manic symptoms. After we stopped the use of risperidone, the tremor became less apparent and then disappeared. This case highlights the importance of being aware of this rare complication in susceptible patients receiving risperidone treatment.

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“…Strecker and al [6] reported on a case of mesencephalic toxoplasmic abscess involving the red nucleus and extending to the cerebellar peduncle. In the case reported by Pezzini [1], multiple nodular lesions were found in the post-central gyrus, in the right frontal superior gyrus, in the inferior parietal lobule and more importantly in the thalamus extending to the midbrain. There is one report of a patient with Holmes' tremor and toxoplasmic abscess in the left posterior thalamic region and in the posterior arm of the internal capsule [7].…”

Section: Discussionmentioning

confidence: 95%

“…Holmes tremor is a rare symptomatic movement disorder [1]. It has a predominantly proximal distribution in the limbs and is characterized by its large amplitude, low frequency (less than 4 Hz), and postural and action patterns that worsen during movement and markedly increase in goal directed movements [2,3].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2010

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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.

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Holmes’ tremor following midbrain Toxoplasma abscess: clinical features and treatment of a case

Cited by 28 publications

References 31 publications

Is nigrostriatal dopaminergic deficit necessary for Holmes tremor to develop? The DaTSCAN and IBZM SPECT study

Is nigrostriatal dopaminergic deficit necessary for Holmes tremor to develop? The DaTSCAN and IBZM SPECT study

Unilateral rubral tremor following treatment with risperidone

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

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