Thalamic infarct presenting with thalamic astasia

Lee, Phil Hyu; Lee, J. H.; Joo, U. S.

doi:10.1111/j.1468-1331.2004.01020.x

Cited by 27 publications

(28 citation statements)

References 11 publications

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“…These agree with findings in patients with ischemic posterolateral thalamic lesions (Dieterich and Brandt 1993b;Dieterich et al 2005;Lee et al 2005). The ventrolateral parts of the thalamus receive signals from the superior and medial vestibular nucleus (Shiroyama et al 1999) and the contralateral half of the cerebellum via the superior cerebellar peduncle as well as the ipsilateral globus pallidus (Hyam et al 2012).…”

Section: Multiple Vestibular Relay Stations In the Thalamussupporting

confidence: 85%

Structural and functional connectivity mapping of the vestibular circuitry from human brainstem to cortex

et al. 2015

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Structural and functional interconnections of the bilateral central vestibular network have not yet been completely delineated. This includes both ipsilateral and contralateral pathways and crossing sites on the way from the vestibular nuclei via the thalamic relay stations to multiple "vestibular cortex" areas. This study investigated "vestibular" connectivity in the living human brain in between the vestibular nuclei and the parieto-insular vestibular cortex (PIVC) by combined structural and functional connectivity mapping using diffusion tensor imaging and functional connectivity magnetic resonance imaging in 24 healthy right-handed volunteers. We observed a congruent functional and structural link between the vestibular nuclei and the ipsilateral and contralateral PIVC. Five separate and distinct vestibular pathways were identified: three run ipsilaterally, while the two others cross either in the pons or the midbrain. Two of the ipsilateral projections run through the posterolateral or paramedian thalamic subnuclei, while the third bypasses the thalamus to reach the inferior part of the insular cortex directly. Both contralateral pathways travel through the posterolateral thalamus. At the cortical level, the PIVC regions of both hemispheres with a right hemispherical dominance are interconnected transcallosally through the antero-caudal splenium. The above-described bilateral vestibular circuitry in its entirety takes the form of a structure of a rope ladder extending from the brainstem to the cortex with three crossings in the brainstem (vestibular nuclei, pons, midbrain), none at thalamic level and a fourth cortical crossing through the splenium of the corpus callosum.

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Section: Multiple Vestibular Relay Stations In the Thalamussupporting

confidence: 85%

Structural and functional connectivity mapping of the vestibular circuitry from human brainstem to cortex

et al. 2015

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“…Thus, we consider this manifestation as an astasia. Astasia, which is the inability to stand unsupported despite normal strength, resembles the marked balance impairment observed in patients with vestibulocerebellar disease 1. Masdeu and Gorelick2 first described the cases of patients with thalamic astasia, and their patients fell toward the side contralateral to the side of lesions.…”

Section: Discussionmentioning

confidence: 99%

“…Astasia, which is the inability to stand unsupported despite normal strength, resembles the marked balance impairment in patients with vestibulocerebellar disease 1. Astasia is an uncommon manifestation of thalamic syndrome2, and its duration is transient when it occurs 3.…”

Section: Introductionmentioning

confidence: 99%

Isolated astasia in acute infarction of the supplementary-motor area

Wada

2010

Case Reports

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Astasia, which is the inability to stand in the absence of motor weakness or marked sensory loss, is an uncommon clinical feature of stroke in the thalamic ventrolateral region. The authors describe a patient with a unilateral supplementary motor area (SMA) infarction presenting with contralateral astasia. On neurological examination, he would lean to the left side and would fall unless supported. He showed no muscle weakness, sensory deficits or cerebellar ataxia. Magnetic resolution imaging of the brain showed acute infarction only involving the right SMA. On the basis of the anatomy that the SMA is connected to the vestibulocerebellar system through the ventrolateral nucleus of the thalamus, the authors concluded that contralateral astasia probably resulted from disruption of this connection following infarction of the SMA.

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“…The disturbance differs from cerebellar ataxia in that gait is not broad-based or lurching. It resembles the marked balance impairment of patients with vestibulocerebellar disease [4] . The responsible anatomical region for astasia or astasia-abasia has been known to be related to the thalamic lesion affecting mainly the medial ventrolateral nucleus of the thalamus because the fastigial fibers of the vestibulocerebellar pathway project to the medial ventrolateral nucleus, and disruption of this pathway may cause thalamic astasia [6] .…”

Section: Discussionmentioning

confidence: 99%

“…Unilateral asterixis may be caused by a focal structural brain lesion including stroke involving the thalamus, parietal lobe, frontal lobe, midbrain, basal ganglia and internal capsule, although asterixis was classically associated with metabolic derangement, particularly hepatic encephalopathy, which occurs usually bilaterally [2][3][4][5] . In addition, concurrent unilateral manifestation of astasia and asterixis due to focal cerebral lesions is extremely rare [2,4] . To our knowledge, sudden concurrent development of asterixis and astasia as a consequence of a rostral midbrain infarction has not yet been reported.…”

mentioning

confidence: 99%