Post-stroke dizziness, depression and anxiety.

OBJECTIVE: Vestibular and psychiatric disorders are very closely related. Previous research shows that the discomfort and dysfunction caused by dizziness in patients can affect psychological processes, leading to anxiety and depression, and the irritation of anxiety and depression can aggravate the discomfort of dizziness. But the causal relationship between dizziness in the recovery period of stroke and Post-stroke depression (PSD) / Post-stroke anxiety (PSA) is not clear. Identifying the causal relationship between them can enable us to conduct more targeted treatments. METHODS: We review the epidemiology and relationship of dizziness, anxiety, and depression, along with the related neuroanatomical basis. We also review the pathophysiology of dizziness after stroke, vestibular function of patients experiencing dizziness, and the causes and mechanisms of PSD and PSA. We attempt to explore the possible relationship between post-stroke dizziness and PSD and PSA. CONCLUSION: The treatment approach for post-stroke dizziness depends on its underlying cause. If the dizziness is a result of PSD and PSA, addressing these psychological factors may alleviate the dizziness. This can be achieved through targeted treatments for PSD and PSA, such as psychotherapy, antidepressants, or anxiolytics, which could indirectly improve dizziness symptoms. Conversely, if PSA and PSD are secondary to vestibular dysfunction caused by stroke, a thorough vestibular function assessment is crucial. Identifying the extent of vestibular impairment allows for tailored interventions. These could include vestibular rehabilitation therapy and medication aimed at vestibular restoration. By improving vestibular function, secondary symptoms like anxiety and depression may also be mitigated.

No-reflow after stroke reperfusion therapy: An emerging phenomenon to be explored.

In the field of stroke thrombectomy, ineffective clinical and angiographic reperfusion after successful recanalization has drawn attention. Partial or complete microcirculatory reperfusion failure after the achievement of full patency of a former obstructed large vessel, known as the "no-reflow phenomenon" or "microvascular obstruction," was first reported in the 1960s and was later detected in both experimental models and patients with stroke. The no-reflow phenomenon (NRP) was reported to result from intraluminal occlusions formed by blood components and extraluminal constriction exerted by the surrounding structures of the vessel wall. More recently, an emerging number of clinical studies have estimated the prevalence of the NRP in stroke patients following reperfusion therapy, ranging from 3.3% to 63% depending on its evaluation methods or study population. Studies also demonstrated its detrimental effects on infarction progress and neurological outcomes. In this review, we discuss the research advances, underlying pathogenesis, diagnostic techniques, and management approaches concerning the no-reflow phenomenon in the stroke population to provide a comprehensive understanding of this phenomenon and offer references for future investigations.