Vestibular agnosia in traumatic brain injury and its link to imbalance.
Vestibular agnosia in traumatic brain injury and its link to imbalance.
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DOI：
10.1093/brain/awaa386
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发表时间：
2021-02-12
期刊：
影响因子：
--
通讯作者：
Seemungal BM
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文献类型：
--
作者：
Calzolari E;Chepisheva M;Smith RM;Mahmud M;Hellyer PJ;Tahtis V;Arshad Q;Jolly A;Wilson M;Rust H;Sharp DJ;Seemungal BM
Calzolari等人表明，急性创伤性脑损伤可能导致“前庭失认症”。这通过右颞叶的白色物质束损伤直接介导失衡，并通过降低临床医生对常见的可治疗前庭诊断的认识间接介导失衡。前庭功能障碍，导致头晕和失衡，是TBI患者常见但知之甚少的特征。内耳、神经、脑干、小脑和大脑半球的损伤都可能影响前庭功能，因此，需要从反射到感知的多层次评估。在以前的报告中，姿势不稳定是行走的急性TBI患者最常见的神经系统特征。在病房评估期间，我们还经常观察到急性TBI患者的眩晕感丧失，常见的内耳疾病和相关的强烈前庭眼反射性眼球震颤，提示“前庭失认症”。前庭失认症的患者也更不平衡;然而，前庭失认症和不平衡之间的联系被内耳疾病的存在所混淆。我们通过对保留外周前庭功能的患者进行前庭功能（从反射到感知）的前瞻性实验室评估，研究了急性TBI失衡的脑机制、其与前庭失认症的联系以及潜在的临床影响。评估包括：前庭反射功能、参与者报告的在黑暗中被动偏转旋转的前庭感知、通过姿势描记术的客观平衡、通过问卷的主观症状和结构神经成像。我们前瞻性筛选了918例急性入院，评估了146例，招募了37例。与37名匹配的对照组相比，患者显示前庭感知阈值升高（患者12.92°/s对3.87°/s），但前庭眼反射阈值正常（患者2.52°/s对1.78°/s）。前庭感知阈值升高的患者[高于对照组平均值3个标准差（SD）]被指定为前庭失认症患者，与非前庭失认症患者相比，其姿势图表现更差，尽管前庭症状评分没有差异。仅在姿势控制受损的患者中（高于对照组平均值3 SD），全脑弥散张量体素分析显示右颞叶下纵束的平均弥散度升高（且各向异性分数趋势较低），与前庭失认严重程度相关。因此，平衡障碍和前庭失认症共同定位于右颞叶的下纵束。最后，一项临床审计显示，临床上明显的前庭失认症急性患者中，临床医生对常见外周前庭疾病（良性阵发性位置性眩晕）的识别率降低了7倍。前庭失认症患者表现出更差的平衡，但没有增加头晕症状，这解释了为什么临床医生可能会错过这些患者的可治疗的前庭诊断。总之，前庭失认通过右颞叶的白色物质束损伤直接介导创伤性脑损伤的不平衡，并通过减少常见的可治疗的前庭诊断的临床识别间接介导创伤性脑损伤的不平衡。
Calzolari et al. show that acute traumatic brain injury may cause a ‘vestibular agnosia’. This mediates imbalance both directly via white matter tract damage in the right temporal lobe, and indirectly by reducing clinician recognition of common, treatable vestibular diagnoses. Vestibular dysfunction, causing dizziness and imbalance, is a common yet poorly understood feature in patients with TBI. Damage to the inner ear, nerve, brainstem, cerebellum and cerebral hemispheres may all affect vestibular functioning, hence, a multi-level assessment—from reflex to perception—is required. In a previous report, postural instability was the commonest neurological feature in ambulating acute patients with TBI. During ward assessment, we also frequently observe a loss of vertigo sensation in patients with acute TBI, common inner ear conditions and a related vigorous vestibular-ocular reflex nystagmus, suggesting a ‘vestibular agnosia’. Patients with vestibular agnosia were also more unbalanced; however, the link between vestibular agnosia and imbalance was confounded by the presence of inner ear conditions. We investigated the brain mechanisms of imbalance in acute TBI, its link with vestibular agnosia, and potential clinical impact, by prospective laboratory assessment of vestibular function, from reflex to perception, in patients with preserved peripheral vestibular function. Assessment included: vestibular reflex function, vestibular perception by participants’ report of their passive yaw rotations in the dark, objective balance via posturography, subjective symptoms via questionnaires, and structural neuroimaging. We prospectively screened 918 acute admissions, assessed 146 and recruited 37. Compared to 37 matched controls, patients showed elevated vestibular-perceptual thresholds (patients 12.92°/s versus 3.87°/s) but normal vestibular-ocular reflex thresholds (patients 2.52°/s versus 1.78°/s). Patients with elevated vestibular-perceptual thresholds [3 standard deviations (SD) above controls’ average], were designated as having vestibular agnosia, and displayed worse posturography than non-vestibular-agnosia patients, despite no difference in vestibular symptom scores. Only in patients with impaired postural control (3 SD above controls’ mean), whole brain diffusion tensor voxel-wise analysis showed elevated mean diffusivity (and trend lower fractional anisotropy) in the inferior longitudinal fasciculus in the right temporal lobe that correlated with vestibular agnosia severity. Thus, impaired balance and vestibular agnosia are co-localized to the inferior longitudinal fasciculus in the right temporal lobe. Finally, a clinical audit showed a sevenfold reduction in clinician recognition of a common peripheral vestibular condition (benign paroxysmal positional vertigo) in acute patients with clinically apparent vestibular agnosia. That vestibular agnosia patients show worse balance, but without increased dizziness symptoms, explains why clinicians may miss treatable vestibular diagnoses in these patients. In conclusion, vestibular agnosia mediates imbalance in traumatic brain injury both directly via white matter tract damage in the right temporal lobe, and indirectly via reduced clinical recognition of common, treatable vestibular diagnoses.
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影响因子：
3.4
作者：
Cronin T;Arshad Q;Seemungal BM
通讯作者：
Seemungal BM
DOI：
10.1093/cercor/bht266
发表时间：
2015-02
期刊：
Cerebral cortex (New York, N.Y. : 1991)
影响因子：
--
作者：
Nigmatullina Y;Hellyer PJ;Nachev P;Sharp DJ;Seemungal BM
通讯作者：
Seemungal BM
影响因子：
3.1
作者：
Kirsch, V.;Keeser, D.;Dieterich, M.
通讯作者：
Dieterich, M.
影响因子：
5.3
作者：
Bonnelle, Valerie;Leech, Robert;Sharp, David J.
通讯作者：
Sharp, David J.
影响因子：
6
作者：
Agosta, Federica;Galantucci, Sebastiano;Filippi, Massimo
通讯作者：
Filippi, Massimo