Unilateral spatial neglect (USN) is a neurological condition caused by damage to either the right or left hemisphere of the brain, resulting in the neglect of stimuli presented on the opposite side. Patients with USN experience challenges in performing activities of daily living, and they may require prolonged hospital stay. Currently, evidence-based training options for neglect recovery are limited due to lesion size and area variations, which cause different symptoms. To develop effective rehabilitation strategies, animal models that can control lesion size and area must be developed. The rodent models of USN, which were developed in the late 1900s, have identified the key brain regions affecting attentional functions. These regions include the medial agranular cortex and posterior parietal cortex. The network involving the superior colliculus, striatum, hypothalamus, and thalamus is also essential for spatial attention and direction selection. Different behavioral tasks and optogenetics have identified detailed brain region functions in USN, and advancements in treatment exploration have been made using rodent models. This review introduced the existing rodent models of USN, focused on the neurological mechanisms responsible for USN, and discussed the potential application of validated treatment methods from rodent models to humans.

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Patients with posterior thalamic hemorrhage typically experience favorable recovery in both sensorimotor deficits and life expectancy. However, research detailing the time course of recovery after the onset is limited. Here, we present the clinical and brain imaging findings of a patient with right posterior thalamic hemorrhage, from the onset to 4 months post-event, as assessed through a range of rehabilitation examination tests. The patient demonstrated substantial improvement in sensorimotor function, particularly in ataxia. Upon discharge, the patient demonstrated minimal dependence in activities of daily living and no discernible issues on dementia tests. Despite these improvements, the patient exhibited residual impairment in generalized attention, including short-term memory, selective attention, and divided or switching attention disorders. These attention impairments appeared to negatively affect the driving simulator evaluation tests conducted at discharge. At the onset, the brain images showed a large hemorrhage area (approximately 21 mL in volume), including the ventral lateral nucleus, ventral posterolateral nucleus, and pulvinar. The lesion area converged to the posterior thalamic region, including a part of the ventral posterolateral nucleus and pulvinar, at 3 months post-event. Based on these imaging findings, this report discusses the factors contributing to the notable improvement in thalamic ataxia and the residual generalized attention disorder resulting in driving impairment. This report underscores the need for comprehensive rehabilitation program planning in cases of posterior thalamic hemorrhage, and highlights the importance of balancing recovery and potential post-discharge risks.

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