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Published on: December 13, 2017
Study on the pathogenesis of Holmes tremor by multimodal 3D medical imaging: case reports of three patients
Min Shi1, Anrong Wang1, Yu Fang1
1Department of Neurology, Hospital of Chengdu University of Traditional Chinese Medicine, No. 39 Shi-er-qiao Road, Sichuan Province, 610072, Chengdu, P R China.
Insights
This study used 3D imaging to analyze Holmes tremor (HT), finding damage to multiple thalamic nuclei. Different lesion patterns suggest varied causes and treatment responses for this tremor.
Area of Science:
- Neurology
- Medical Imaging
- Neuroscience
Background:
- This study presents the first examination of Holmes tremor (HT) imaging characteristics using multimodal 3D medical imaging.
- Investigated three patients with HT to summarize clinical and imaging data.
Observation:
- Holmes tremor in two patients resulted from hypertensive cerebral hemorrhage; the third had hemorrhage from a ruptured brain arteriovenous malformation.
- Lesions consistently involved the thalamus, affecting various nuclei and nerve fiber tracts, with symptoms appearing 1-24 months post-onset.
Findings:
- Multimodal 3D imaging revealed damage to multiple thalamic nuclei in all patients.
- Specific damaged nuclei and nerve tracts varied between patients, correlating with different clinical presentations and therapeutic outcomes.
- One patient responded well to pramipexole, another to clonazepam, while one showed poor response to both.
Implications:
- The findings suggest potentially multiple pathogeneses for Holmes tremor.
- Highlights the utility of advanced imaging in understanding complex movement disorders.
- Individualized treatment approaches may be necessary based on specific lesion patterns.
Background:
We examined for the first time the imaging characteristics of Holmes tremor (HT) through multimodal 3D medical imaging.
Case Presentation:
Three patients with Holmes tremor who visited the Affiliated Hospital of Chengdu University of TCM from August 2018 to April 2021 were retrospectively investigated to summarize their clinical and imaging data.
Results:
Holmes tremor in two of the three patients was caused by hypertensive cerebral hemorrhage and in the third patient induced by hemorrhage due to ruptured brain arteriovenous malformations. HT occurred 1 to 24 months after the primary disease onset and manifested as a tremor in the contralateral limb, mostly in the upper portion. Cranial MRI showed that the lesions involved the thalamus in all three patients. The damaged thalamic nuclei included the ventral anterior nucleus, ventral lateral nucleus and ventromedial lateral nucleus, and the damaged nerve fibers included left thalamocortical tracts in one patient. In the other two patients, the damaged thalamic nuclei included the centromedian and dorsomedial nucleus, and the damaged nerve fibers included left cerebellothalamic and thalamocortical tracts. One patient showed significant improvement after treatment with pramipexole while the other two patients exhibited a poor response, one of whom had no response to the treatment with pramipexole and was only significantly relieved by clonazepam.
Conclusion:
We used multimodal 3D medical imaging for the first time to analyze the pathogenesis of HT and found that multiple thalamic nuclei were damaged. The damaged nuclei and nerve fiber tracts of two patients were different from those of the third patient, with different clinical manifestations and therapeutic effects. Therefore, it is speculated that there may be multiple pathogeneses for HT.
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