The BIS value may decrease by cerebral hypoperfusion. We report a case in which the BIS value suddenly decreased during cervical spine surgery, which led us to find cervical screws compressing the vertebral arteries. In a 79-year-old man undergoing cervical spine surgery, the BIS suddenly decreased from about 40 to 10-20, about 4 h after the start of surgery. Intraoperative 3-dementional computed tomography indicated that both the two tips of cervical screws inserted in the 6th cervical vertebra were within bilateral transverse foramens. These cervical screws were removed, and the BIS increased immediately. The cervical screws were re-inserted again thorough the same vertebra into the bilateral transverse foramens, and the BIS decreased immediately. Postoperatively, cerebral hypoperfusion due to compression of bilateral vertebral arteries by two cervical screws was identified. The BIS may be a useful to detect cerebral hypoperfusion due to compression of the vertebral artery by a cervical screw.

Ascending aortic dissection is typically characterized by severe chest or back pain. However, its presentation can be atypical, leading to diagnostic challenges, especially in settings where classic symptomatology may not be evident. In this report, we described the case of a 74-year-old woman who presented to the emergency room of a rural community hospital with chief complaints of vertigo, nausea, and vomiting, without the classic symptoms of chest or back pain associated with aortic dissection. Despite initial treatment for autonomic dysregulation, the patient\'s symptoms persisted. Subsequent comprehensive assessments, including computed tomography angiography, revealed an ascending aortic dissection extending to the bilateral common carotid arteries. This atypical presentation, characterized by cerebral hypoperfusion and systemic hypotension without tachycardia, emphasizes the need to maintain a high suspicion index, even in the absence of hallmark symptoms. This case underscores the importance of considering the possibility of ascending aortic dissection in patients with nontraditional symptoms. Recognizing these atypical presentations is crucial for timely intervention, especially in rural settings with limited advanced diagnostic tools. This case also highlights potential sex disparities in symptom presentation, emphasizing the need for clinicians to recognize nontraditional symptoms in women. Rapid identification, evaluation, and management are imperative to prevent severe outcomes, and a multidisciplinary approach has proven to be the most effective in such cases.

Vascular cognitive impairment and dementia (VCID) is a series of cognitive dysfunction associated with cerebrovascular diseases and currently lacks effective treatments. The white matter, which is essential for neuronal information processing and integration, is nourished by a network of capillaries and is vulnerable to chronic hypoperfusion. Here, we show that metformin, a widely used drug for the treatment of type 2 diabetes, alleviates the white matter damage and improves cognitive impairment in a mouse model of VCID established by bilateral carotid artery stenosis (BCAS)-induced chronic hypoperfusion. Mechanistically, metformin restores the dysfunctions of oligodendrocyte precursor cells (OPCs) under hypoxia. Metformin up-regulates prolyl hydroxylases 2 via activating the AMP-activated protein kinase pathway, leading to hypoxia-inducible factor-1α (HIF-1α) degradation in OPCs. These findings suggest that metformin may have a promising therapeutic role in alleviating cognitive abnormalities by ameliorating white matter damage of VCID.

Vascular cognitive impairment (VCI) refers to all forms of cognitive disorder related to cerebrovascular diseases, including vascular mild cognitive impairment, post-stroke dementia, multi-infarct dementia, subcortical ischemic vascular dementia (SIVD), and mixed dementia. Among the causes of VCI, more attention has been paid to SIVD because the causative cerebral small vessel pathologies are frequently observed in elderly people and because the gradual progression of cognitive decline often mimics Alzheimer\'s disease. In most cases, small vessel diseases are accompanied by cerebral hypoperfusion. In mice, prolonged cerebral hypoperfusion is induced by bilateral carotid artery stenosis (BCAS) with surgically implanted metal micro-coils. This cerebral hypoperfusion BCAS model was proposed as a SIVD mouse model in 2004, and the spreading use of this mouse SIVD model has provided novel data regarding cognitive dysfunction and histological/genetic changes by cerebral hypoperfusion. Oxidative stress, microvascular injury, excitotoxicity, blood-brain barrier dysfunction, and secondary inflammation may be the main mechanisms of brain damage due to prolonged cerebral hypoperfusion, and some potential therapeutic targets for SIVD have been proposed by using transgenic mice or clinically used drugs in BCAS studies. This review article overviews findings from the studies that used this hypoperfused-SIVD mouse model, which were published between 2004 and 2021.

Bilateral carotid artery stenosis (BCAS) is a valid approach for modeling vascular dementia (VaD) in mice as it induces cerebral hypoperfusion and produces white matter degeneration and cognitive impairment. VaD is one of the major causes of cognitive impairment and currently has no approved therapy; hence its preclinical modeling is warranted for investigating potential therapeutic compounds. BCAS enables the characterization of brain pathology and associated cognitive phenotype of VaD. In this chapter, we describe the surgical method of inducing BCAS in mice, using titanium micro-coils, and we report cerebral blood flow changes before and after surgical induction as well as some histological findings in the corpus callosum of diabetic mice subjected to long-term BCAS.

Exposure to hypoxic-ischaemia (HI) is consistently followed by a delayed fall in cerebral perfusion. In preterm fetal sheep this is associated with impaired cerebral oxygenation, consistent with mismatch between perfusion and metabolism. In the present study we tested the hypothesis that alpha-adrenergic inhibition after HI would improve cerebral perfusion, and so attenuate mismatch and reduce neural injury. Chronically instrumented preterm (0.7 gestation) fetal sheep received sham-HI (n = 10) or HI induced by complete umbilical cord occlusion for 25 minutes. From 15 minutes to 8 hours after HI, fetuses received either an intravenous infusion of a non-selective alpha-adrenergic antagonist, phentolamine (10 mg bolus, 10 mg/h infusion, n = 10), or saline (n = 10). Fetal brains were processed for histology 72 hours post-HI. Phentolamine infusion was associated with increased epileptiform transient activity and a greater fall in cerebral oxygenation in the early post-HI recovery phase. Histologically, phentolamine was associated with greater loss of oligodendrocytes and hippocampal neurons. In summary, contrary to our hypothesis, alpha-adrenergic inhibition increased epileptiform transient activity with an exaggerated fall in cerebral oxygenation, and increased neural injury, suggesting that alpha-adrenergic receptor activation after HI is an important endogenous neuroprotective mechanism.

Vascular contributions to cognitive impairment and dementia (VCID) is one of the leading causes of dementia along with Alzheimer\'s disease (AD) and, importantly, VCID often manifests as a comorbidity of AD(Vemuri and Knopman 2016; Schneider and Bennett 2010)(Vemuri and Knopman 2016; Schneider and Bennett 2010). Despite its common clinical manifestation, the mechanisms underlying VCID disease progression remains elusive. In this review, existing knowledge is used to propose a novel hypothesis linking well-established risk factors of VCID with the distinct neurodegenerative cascades of neuroinflammation and chronic hypoperfusion. It is hypothesized that these two synergistic signaling cascades coalesce to initiate aberrant angiogenesis and induce blood brain barrier breakdown trough a mechanism mediated by vascular growth factors and matrix metalloproteinases respectively. Finally, this review concludes by highlighting several potential therapeutic interventions along this neurodegenerative sequalae providing diverse opportunities for future translational study.

OBJECTIVE: Positive visual phenomena, although reported in lesions of visual cortex, are often overlooked in patients with acute neurological conditions. Yet, their occurrence without structural abnormalities or other underlying neurological disorders represents a unique observation. This report aims to raise awareness of these phenomena, their implications for understanding visual consciousness and to propose a practical, structured algorithm for the clinical assessment of visual hallucinations related to neurological conditions.
METHODS: We describe the clinical presentation and imaging findings in two patients with isolated visual hallucinosis secondary to transitory hypoperfusion.
RESULTS: One patient presented with subocclusion of the right posterior cerebral artery and the other with multifocal arterial abnormalities suggestive of reversible cerebral vasoconstriction syndrome (RCVS). Both presented isolated visual hallucinations and hypoperfusion of the right mesial occipito-temporal cortex. Hallucinated images exhibited peculiarities of certain attributes that were recognized only through guided perceptual analysis performed during their occurrence.
CONCLUSIONS: Dysfunctions in the visual and attentional networks due to the uneven impact of hypoperfusion on the regions of the mesial occipito-temporal cortex likely contributed to the occurrence of visual hallucinations. The initial impaired awareness of certain image attributes obscured an altered, non-realistic rendering of the hallucinated images. Enhancement of awareness through clinical guidance indicates improved attentional deployment, modulation of visual information processing and hallucination-background integration. These features of the hallucinatory phenomena highlight the critical role of semiological analysis during their occurrence and question the validity of post hoc inquiries.

Blood pressure variability is an emerging risk factor for stroke, cognitive impairment, and dementia, possibly through links with cerebral hypoperfusion. Recent evidence suggests visit-to-visit (e.g., over months, years) blood pressure variability is related to cerebral perfusion decline in brain regions vulnerable to Alzheimer\'s disease. However, less is known about relationships between short-term (e.g., < 24 hours) blood pressure variability and regional cerebral perfusion, and whether these relationships may differ by age. We investigated short-term blood pressure variability and concurrent regional cerebral microvascular perfusion in a sample of community-dwelling older adults without history of dementia or stroke and healthy younger adults. Blood pressure was collected continuously during perfusion MRI. Cerebral blood flow was determined for several brain regions implicated in cerebrovascular dysfunction in Alzheimer\'s disease. Elevated systolic blood pressure variability was related to lower levels of concurrent cerebral perfusion in medial temporal regions: hippocampus (β = -.60 [95% CI -.90, -.30]; p < .001), parahippocampal gyrus (β = -.57 [95% CI -.89, -.25]; p = .001), entorhinal cortex (β = -.42 [95% CI -.73, -.12]; p = .009), and perirhinal cortex (β = -.37 [95% CI -.72, -.03]; p = .04), and not in other regions, and in older adults only. Findings suggest a possible age-related selective vulnerability of the medial temporal lobes to hypoperfusion in the context of short-term blood pressure fluctuations, independent of average blood pressure, white matter hyperintensities, and gray matter volume, which may underpin the increased risk for dementia associated with elevated BPV.

Postoperative cognitive dysfunction is extremely prevalent following cardiac surgery. The increasing patient age and comorbidity profile increases their susceptibility to cognitive impairment. The underlying pathophysiological mechanisms leading to cognitive impairment are not clearly elucidated. Using the contemporary literature (2015-present), this narrative review has three aims. Firstly, to provide an overview of postoperative cognitive impairment. Secondly, to analyse the predominant pathophysiological mechanisms leading to cognitive dysfunction following cardiac surgery such as inflammation, cerebral hypoperfusion, cerebral microemboli, glycaemic control and anaesthesia induced neurotoxicity. Lastly, to assess the current therapeutic strategies of interest to address these pathophysiological mechanisms, including the administration of dexamethasone, the prevention of prolonged cerebral desaturations and the monitoring of cerebral perfusion using near-infrared spectroscopy, surgical management strategies to reduce the neurological effects of microemboli, intraoperative glycaemic control strategies, the effect of volatile vs. intravenous anaesthesia, and the efficacy of dexmedetomidine.