The clinical and neuroimaging studies in Holmes tremor

Gajos, Agata; Bogucki, Andrzej; Schinwelski, Michał; Sołtan, Witold; Rudzińska, Monika; Budrewićz, Sławomir; Koszewicz, Magdalena; Majos, Agata; Górska-Chrząstek, Magdalena; Bieńkiewicz, Małgorzata; Kuśmierek, Jacek; Sławek, Jarosław

doi:10.1111/j.1600-0404.2009.01319.x

Cited by 38 publications

(62 citation statements)

References 20 publications

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“…Head trauma accounted for almost 20% of the cases in previous publications, 1,[3][4][5]7,8,,e1-e52 while we found 17.24% traumatic cases in our series (table e-1).…”

Section: Opportunistic Infection In Aidscontrasting

confidence: 39%

“…3,7 In one of them, 2 blind raters could not find asymmetry in DaTSCAN SPECT, and the quantitative measurements of radiotracer uptake demonstrated only minimal differences between both sides, with slightly worse uptake contralateral to HT. 7 In 6 of their 10 patients, levodopa was administered, and only 2 improved: one had a mild response and the other moderate improvement. 7 The authors concluded that the dopaminergic deficit on DaTSCAN SPECT could be a predictor of levodopa responsiveness.…”

Section: Opportunistic Infection In Aidsmentioning

confidence: 99%

“…7 In 6 of their 10 patients, levodopa was administered, and only 2 improved: one had a mild response and the other moderate improvement. 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.…”

Section: Opportunistic Infection In Aidsmentioning

confidence: 99%

“…6 As it is a symptomatic tremor, imaging studies are usually abnormal, although in some cases no lesion can be demonstrated. 7,8 Tremor commonly develops between 1 and 24 months after a CNS insult. This delayed onset might be due to neuronal plastic changes.…”

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confidence: 99%

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Holmes tremor

et al. 2016

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Objective: To describe the clinical features, etiology, findings from neuroimaging, and treatment results in a series of 29 patients with Holmes tremor (HT).Methods: A retrospective study was performed based on review of medical records and videos of patients with HT diagnosis.Results: A total of 16 women and 13 men were included. The mean age at the moment of CNS insult was 33.9 6 20.1 years (range 8-76 years). The most common causes were vascular (48.3%), ischemic, or hemorrhagic. Traumatic brain injury only represented 17.24%; other causes represented 34.5%. The median latency from lesion to tremor onset was 2 months (range 7 days-228 months). The most common symptoms/signs associated with HT were hemiparesis (62%), ataxia (51.7%), hypoesthesia (27.58%), dystonia (24.1%), cranial nerve involvement (24.1%), and dysarthria (24.1%). Other symptoms/signs were vertical gaze disorders (6.8%), bradykinesia/rigidity (6.8%), myoclonus (3.4%), and seizures (3.4%). Most of the patients had lesions involving more than one area. MRI showed lesions in thalamus or midbrain or cerebellum in 82.7% of the patients. Levodopa treatment was effective in 13 out of 24 treated patients (54.16%) and in 3 patients unilateral thalamotomy provided excellent results. Conclusions:The most common causes of HT in our series were vascular lesions. The most common lesion topography was mesencephalic, thalamic, or both. Treatment with levodopa and thalamic stereotactic lesional surgery seems to be effective.

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“…Head trauma accounted for almost 20% of the cases in previous publications, 1,[3][4][5]7,8,,e1-e52 while we found 17.24% traumatic cases in our series (table e-1).…”

Section: Opportunistic Infection In Aidscontrasting

confidence: 39%

Section: Opportunistic Infection In Aidsmentioning

confidence: 99%

Section: Opportunistic Infection In Aidsmentioning

confidence: 99%

mentioning

confidence: 99%

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Holmes tremor

et al. 2016

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“…Rubral tremor is a coarse resting tremor, which usually exacerbates while active (3). It is usually associated with the diseases that cause lesions in superior cerebellar peduncle, midbrain tegmentum, and posterior thalamus.…”

Section: Introductionmentioning

confidence: 99%

Rubral Tremor Associated with Klinefelter Syndrome; a Case Report and Literature Review

et al. 2017

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Introduction: Previous case series suggested an association between Klinefelter syndrome (KS) and tremor, but most reported cases had ET-like tremor. Also, previous studies did not suggest any suitable treatments for the tremor. Case Presentation: The current report presented a case of KS that his rubral tremor led to the KS diagnosis at the age of 43. Regular anti-tremor medication was immediately started along with testosterone therapy; none of which were effective on the tremor. Next, a table of KS patients was provided with a tremor to elucidate the type of tremor and medical treatments in the patients. The result of the literature review of the most effective therapy for tremor in such patients showed that primidone, propranolol, gabapentin, and levetiracetam were not always effective, while deep brain stimulation of the ventral intermediate nucleus showed promising results. Conclusion: Since tremor in KS has an unknown origin, it may not be responsive to regular anti-tremor medication; therefore, deep brain stimulation (DBS) of the ventral intermediate (VIM) may be the best therapy for such patients

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Mapping holmes tremor circuit using the human brain connectome

Joutsa

Shih

Fox

2019

Annals of Neurology

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Objective Holmes tremor is a debilitating movement disorder with limited treatment options. Lesions causing Holmes tremor can occur in multiple different brain locations, leaving the neuroanatomical substrate unclear. Here, we test whether lesion locations that cause Holmes tremor map to a connected brain circuit and whether this circuit might serve as a useful therapeutic target. Methods Case reports of Holmes tremor caused by focal brain lesions were identified through a systematic literature search. Connectivity between each lesion location and the rest of the brain was computed using resting state functional connectivity magnetic resonance imaging data from 1,000 healthy volunteers. Commonalities across lesion locations were identified. This Holmes tremor circuit was then compared to neurosurgical treatment targets and clinical efficacy. Results We identified 36 lesions causing Holmes tremor, which were scattered across multiple different brain regions. However, all lesion locations were connected to a common brain circuit with nodes in the red nucleus, thalamus, globus pallidus, and cerebellum. In cases with effective neurosurgical treatment, the treatment target was connected with the lesion location, indicating that a second hit to the same circuit might be beneficial. Commonly used deep brain stimulation targets such as the ventral intermediate nucleus and subthalamic nucleus fell outside our Holmes tremor circuit, whereas the globus pallidus target was close, consistent with published clinical response rates for these targets. Interpretation Lesions causing Holmes tremor are part of a single connected brain circuit that may serve as an improved therapeutic target. ANN NEUROL 2019;86:812–820

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The clinical and neuroimaging studies in Holmes tremor

Abstract: It is open to debate whether nigrostriatal pathway damage is crucial for the phenomenology of HT. Alternative hypothesis is presented that HT represents the heterogeneous spectrum of tremors with similar phenomenology, but different pathophysiology.

Cited by 38 publications

References 20 publications

Holmes tremor

Holmes tremor

Rubral Tremor Associated with Klinefelter Syndrome; a Case Report and Literature Review

Mapping holmes tremor circuit using the human brain connectome

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