Diffusion tensor imaging in orthostatic tremor: a tract‐based spatial statistics study

Abstract

ObjectiveThe pathogenesis of orthostatic tremor (OT) is unknown. We investigated OT‐related white matter changes and their correlations with scores from a neuropsychological testing battery.MethodsDiffusion tensor imaging measures were compared between 14 OT patients and 14 age‐ and education‐matched healthy controls, using whole‐brain tract‐based spatial statistics analysis. Correlations between altered diffusion metrics and cognitive performance in OT group were assessed.ResultsIn all cognitive domains (attention, executive function, visuospatial ability, verbal memory, visual memory, and language), OT patients’ cognitive performance was significantly worse than that of healthy controls. OT patients demonstrated altered diffusivity metrics not only in the posterior lobe of the cerebellum (left cerebellar lobule VI) and in its efferent cerebellar fibers (left superior cerebellar peduncle), but also in medial lemniscus bilaterally (pontine tegmentum), anterior limb of the internal capsule bilaterally, right posterior limb of the internal capsule, left anterior corona radiata, right insula, and the splenium of corpus callosum. No relationship was found between diffusion measures and disease duration in OT patients. Diffusion white matter changes, mainly those located in right anterior limb of the internal capsule, were correlated with poor performance on tests of executive function, visuospatial ability, verbal memory, and visual memory in OT patients.InterpretationWhite matter changes were preferentially located in the cerebellum, its efferent pathways, as well as in the pontine tegmentum and key components of the frontal–thalamic–cerebellar circuit. Further work needs to be done to understand the evolution of these white matter changes and their functional consequences.

The Phenomenology of Primary Orthostatic Tremor

“…Nevertheless, a certain cerebellar component in the POT gait cannot be excluded entirely as high spatiotemporal gait variability has been shown previously 15 . Moreover, the absence of clinical cerebellar ataxia does not preclude the cerebellum from contributing to the disease mechanism, as several studies have demonstrated functional and structural cerebellar alterations in POT and as several locations structurally connected to the cerebellum have been demonstrated to cause secondary OT 21–23 . Nevertheless based on imaging studies, brain regions other than the cerebellum may be involved as well 22 …”

“… 21 , 22 , 23 Nevertheless based on imaging studies, brain regions other than the cerebellum may be involved as well. 22 …”

“…15 Moreover, the absence of clinical cerebellar ataxia does not preclude the cerebellum from contributing to the disease mechanism, as several studies have demonstrated functional and structural cerebellar alterations in POT and as several locations structurally connected to the cerebellum have been demonstrated to cause secondary OT. [21][22][23] Nevertheless based on imaging studies, brain regions other than the cerebellum may be involved as well. 22 Altogether, cerebellar ataxia seems not to be a clear nor consistent feature of POT.…”

Transcriptomic, cellular, and functional signatures of white matter damage in Alzheimer’s disease

“…In the current study, nodal clustering coe cient and local e ciency were observed to be signi cantly decreased for AD or MCI group within GM or WM regions. Speci cally, these regions are primarily engaged in four functions: sensory-motor (i.e., postcentral gyrus 42 and corticospinal tract 43 ), visualspatial (i.e., parahippocampal gyrus 44 , bilateral sagittal stratum 45 , temporal fusiform cortex 46 , temporal occipital fusiform cortex, supracalcarine cortex 47 , occipital pole, posterior thalamic radiation 48 , and left tapetum 49 ), language (i.e., planum polare, heschls gyrus, planum temporale, and bilateral uncinate fasciculus 50 ), and memory-executive function (i.e., parahippocampal gyrus 44 , anterior limb of internal capsule 51 ). Noticeably, the de cits in these functions are the clinical phenotypes of Alzheimer's disease 52 .…”

Gait and balance in cervical dystonia and dystonic head tremor

“…The cerebellum has been regarded as one of the key sources of pathogenic oscillations in other tremor disorders such as ET and OT [ 36 – 39 ]. In the context of ET, presence of head tremors has been found to predict gait dysfunction and balance abnormalities [ 40 ].…”