Dramatic response to zonisamide of post-subarachnoid hemorrhage Holmes’ tremor

Suda, Satoshi; Yamazaki, Mineo; Katsura, Ken‐ichiro; Fukuchi, Takaharu; Kaneko, Norio; Ueda, Masayuki; Nagayama, Hiroshi; Katayama, Yasuo

doi:10.1007/s00415-011-6127-5

Cited by 14 publications

(8 citation statements)

References 10 publications

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“…The present case suggests that this might not be the case, and implies that simple dopamine deficiency did not generate HT. Zonisamide was reported to be effective against HT, but was only partially effective in our patient, and could not restore her daily life. Therefore, we found it necessary to carry out a Vim‐thalamotomy to finally control the tremor.…”

Section: Discussionmentioning

confidence: 99%

Holmes’ tremor caused by coexisting Parkinson's disease in a case of spinocerebellar ataxia type 31

Shimizu

Hanajima

Satou

et al. 2017

Neurology & Clinical Neurosc

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Holmes’ tremor is a low‐frequency resting and intention tremor. Here, we report a case of spinocerebellar ataxia type 31 with an unusual presentation of Holmes’ tremor. We traced it to the development of Parkinson's disease in the patient. L‐dopa was insufficient for tremor, but zonisamide and ventralis intermedius thalamotomy were effective. Both cerebellar and dopaminergic system damage are thus required to express Holmes’ tremor.

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Section: Discussionmentioning

confidence: 99%

Holmes’ tremor caused by coexisting Parkinson's disease in a case of spinocerebellar ataxia type 31

Shimizu

Hanajima

Satou

et al. 2017

Neurology & Clinical Neurosc

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“…Holmes tremor may respond to levodopa, trihexyphenidyl, clonazepam, cabergoline, levetiracetam, bromocriptine, and piribedil, as well as zonisamide, 2,5,12,53,[59][60][61]63 but pharmacotherapy is often unsatisfactory. The success of thalamotomy and chronic thalamic stimulation in essential tremor and parkinsonian tremor led to their application in HT 6,52 and other uncommon tremors.…”

Section: Prior Surgical Approaches To Htmentioning

confidence: 99%

Pallidal stimulation for Holmes tremor: clinical outcomes and single-unit recordings in 4 cases

Kilbane

Ramirez‐Zamora

Ryapolova-Webb

et al. 2015

JNS

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OBJECT Holmes tremor (HT) is characterized by irregular, low-frequency (< 4.5 Hz) tremor occurring at rest, with posture, and with certain actions, often affecting proximal muscles. Previous reports have tended to highlight the use of thalamic deep brain stimulation (DBS) in cases of medication-refractory HT. In this study, the authors report the clinical outcome and analysis of single-unit recordings in patients with medication-refractory HT treated with globus pallidus internus (GPi) DBS. METHODS The authors retrospectively reviewed the medical charts of 4 patients treated with pallidal DBS for medication-refractory HT at the University of California, San Francisco, and San Francisco Veterans Affairs Medical Center. Clinical outcomes were measured at baseline and after surgery using an abbreviated motor-severity Fahn-Tolosa-Marin (FTM) tremor rating scale. Intraoperative microelectrode recordings were performed with patients in the awake state. The neurophysiological characteristics identified in HT were then also compared with characteristics previously described in Parkinson's disease (PD) studied at the authors' institution. RESULTS The mean percentage improvement in tremor motor severity was 78.87% (range 59.9%–94.4%) as measured using the FTM tremor rating scale, with an average length of follow-up of 33.75 months (range 18–52 months). Twenty-eight GPi neurons were recorded intraoperatively in the resting state and 13 of these were also recorded during contralateral voluntary arm movement. The mean firing rate at rest in HT was 56.2 ± 28.5 Hz, and 63.5 ± 19.4 Hz with action, much lower than the GPi recordings in PD. GPi unit oscillations of 2–8 Hz were prominent in both patients with HT and those with PD, but in HT, unlike PD, these oscillations were not suppressed by voluntary movement. CONCLUSIONS The efficacy of GPi DBS exceeded that reported in prior studies of ventrolateral thalamus DBS and suggest GPi may be a better target for treating HT. These clinical and neurophysiological findings help illuminate evolving models of HT and highlight the importance of cerebellar–basal ganglia interactions.

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“…Reported foci include the area superolateral to the red nuclei, rubrothalamic tract, central tegmental tract, superior cerebellar peduncle, and the substantia nigra [2]. Drug therapy including L-dopa, anticholinergic agents, and zonisamide is effective in some cases [3]. This suggests dysfunction of the nigrostriatal tract [4], which is thought to be involved in the onset of rest tremors.…”

Section: Introductionmentioning

confidence: 99%

Vim thalamotomy in a patient with Holmes’ tremor and palatal tremor - Pathophysiological considerations

et al. 2015

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BackgroundWe peformed a ventral intermediate nucleus (Vim) thalamotomy in a patient with Holmes’ tremor and palatal tremor. The frequencies of these movement disorders were 4 Hz and 3 Hz, respectively. Vim thalamotomy stopped the Holmes’ tremor but not the palatal tremor. Our observations suggest different mechanisms for these two involuntary movements.Case presentationA 57-arm 11 months after a pontine hemorrhage. Transoral carotid ultrasonography revealed periodic motion of her posterior pharyngeal wall with a frequency of 3 Hz. Recording of neuronal activities in the thalamus revealed a 4Hz rhythmic discharge time that was associated with her tremor in the contralateral arm. A left Vim thalamotomy was performed. The resting tremor of the upper limb stopped, but the kinetic tremor recurred 6 months after the thalamotomy. No effect was observed on her palatal tremor.ConclusionsThe different effects of Vim thalamotomy on the Holmes’ tremor and palatal tremor suggest different oscillation sources for these two involuntary movements.

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Dramatic response to zonisamide of post-subarachnoid hemorrhage Holmes’ tremor

Cited by 14 publications

References 10 publications

Holmes’ tremor caused by coexisting Parkinson's disease in a case of spinocerebellar ataxia type 31

Holmes’ tremor caused by coexisting Parkinson's disease in a case of spinocerebellar ataxia type 31

Pallidal stimulation for Holmes tremor: clinical outcomes and single-unit recordings in 4 cases

Vim thalamotomy in a patient with Holmes’ tremor and palatal tremor - Pathophysiological considerations

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