Effect of infarct location and volume on cognitive dysfunction in elderly patients with acute insular cerebral infarction

Abstract

BACKGROUND

The aging of the population has become increasingly obvious in recent years, and the incidence of cerebral infarction has shown an increasing trend annually, with high death and disability rates.

AIM

To analyze the effects of infarct location and volume on cognitive dysfunction in elderly patients with acute insular cerebral infarction.

METHODS

Between January 2020 and December 2023, we treated 98 cases of elderly acute insula, patients with cerebral infarction in the cerebral infarction acute phase (3-4 weeks) and for the course of 6 months in Montreal Cognitive Assessment Scale (MoCA) for screening of cognition. Notably, 58 and 40 patients were placed in the cognitive impairment group and without-cognitive impairment group, respectively. In patients with cerebral infarction, magnetic resonance imaging was used to screen and clearly analyze the MoCA scores of two groups of patients with different infarctions, the relationship between the parts of the infarction volume, and analysis of acute insula cognitive disorder in elderly patients with cerebral infarction and the relationship between the two.

RESULTS

The number of patients with cognitive impairment in the basal ganglia and thalamus was significantly higher than that without cognitive impairment (P < 0.05). The total infarct volume in the cognitive impairment group was higher than that in the non-cognitive impairment group, and the difference was statistically significant (P < 0.05). The infarct volumes at different sites in the cognitive impairment group was higher than in the non-cognitive impairment group (P < 0.05). In the cognitive impairment group, the infarct volumes in the basal ganglia, thalamus, and mixed lesions were negatively correlated with the total MoCA score, with correlation coefficients of -0.67, -0.73, and -0.77, respectively.

CONCLUSION

In elderly patients with acute insular infarction, infarction in the basal ganglia, thalamus, and mixed lesions were more likely to lead to cognitive dysfunction than in other areas, and patients with large infarct volumes were more likely to develop cognitive dysfunction. The infarct volume in the basal ganglia, thalamus, and mixed lesions was significantly negatively correlated with the MoCA score.

Key Words: Elderly, Acute insular infarction, Infarction site, Cognitive impairment, Infarction volume

Core Tip: With the increasingly obvious aging of the population, the incidence of cerebral infarction is increasing year by year, which seriously leads to patient death. Most survivors suffer from sequelae such as cognitive dysfunction, aphasia and paralysis. This study aims to investigate the different clinical manifestations of patients with acute island infarction from the perspective of infarct location and volume, and mainly explore the influence of infarct location and volume on cognitive dysfunction in elderly patients with acute island infarction, hoping to evaluate cognitive function score, infarct location and volume. This can provide a basis for the clinical diagnosis and treatment of acute island infarction.

INTRODUCTION

Cerebral infarction, or ischemic stroke[1], refers to a disturbance of the blood supply to the brain for various reasons such as local ischemia and hypoxia in the brain, resulting in necrosis and softening of the brain tissue, and corresponding clinical symptoms and even death in severe cases[2]. The incidence and mortality of cerebral infarction is relatively high worldwide, accounting for 87.00% of the total incidence of cerebral strokes[3]. In China, the annual incidence of cerebral infarction is 150 per 100000[4]. With the rapid development of China's national economy, the aging of the population has become increasingly obvious in recent years, and the incidence of cerebral infarction has shown an increasing trend annually, with high death and disability rates[5]. Most survivors suffer from sequelae, such as cognitive dysfunction, aphasia, and paralysis, which seriously affect their quality of life.

Cognitive dysfunction after cerebral infarction is a common complication of stroke. It is reported that cerebral infarction will increase the risk of cognitive impairment by at least 26-27 times[6], and the incidence of cognitive impairment after cerebral infarction is 10%-40%, which is higher than that of the general population[7]. At present, the pathogenesis of cognitive dysfunction after cerebral infarction is not fully defined[8]. Studies have shown that patients with mild cognitive impairment or dementia are more prone to cognitive decline after cerebral infarction, and their rehabilitation process is relatively slow[9]. In addition, comorbidity is one of the important factors affecting cognitive function after cerebral infarction. Common comorbidity, such as hypertension, cardiovascular disease and diabetes, may aggravate the degree of nerve injury and ischemia in cerebral infarction and then affect the rehabilitation and recovery of cognitive function[10,11]. Drug therapy may also affect cognitive function after cerebral infarction. Some drugs may affect the cognitive function of patients, especially some drugs that affect neurotransmitters or brain function, such as sedatives and antidepressants. At the same time, the adverse reactions and side effects of drugs may also affect the cognitive function of patients, which needs to be fully considered during treatment[12]. In addition, different infarct locations and volumes of acute cerebral infarction may lead to different clinical manifestations, and there is a certain relationship with cognitive dysfunction[13]. Other studies have confirmed that insular cortex infarction is a special sign of cardiovascular autonomic function in patients with acute cerebral infarction, mostly in the middle cerebral artery blood supply area[14]. The insula is a highly ischemic region valuable for predicting cognitive dysfunction, motor ability, and aphasia in patients with cerebral infarction[15].

Therefore, this study aimed to investigate the different clinical manifestations of patients with acute insular infarction from the perspective of infarct location and volume, and mainly explore the impact of infarct location and volume on cognitive dysfunction in elderly patients with acute insular infarction, in the hope that the cognitive function of patients with acute insular infarction can be predicted clinically by assessing the cognitive function scores, infarct location, and infarct volume. This can provide a basis for the clinical diagnosis and treatment of acute insular infarctions.

MATERIALS AND METHODS

Object and grouping

Overall, 98 elderly patients with acute insular infarction who were treated at the Department of Neurology of our hospital between January 2020 and December 2023 were selected from the medical records system. The participants were divided into two groups according to the Montreal Cognitive Assessment Scale (MoCA)[16]. Individuals with a MoCA score ≥ 26 were placed into the non-cognitive impairment group (n = 40) and individuals with a MoCA score < 26 group (n = 58) were placed into the cognitive impairment group.

Inclusion and exclusion criteria

The inclusion criteria[17] were as follows: (1) Age ≥ 60 years; (2) Patients with acute insular infarction diagnosed by craniocerebral magnetic resonance imaging (MRI); (3) Patients with a stable condition and who can cooperate with relevant examinations; and (4) Patients with complete case data and follow-up data.

The exclusion criteria[18] were as follows: (1) Patients with a previous history of brain trauma, clinical stroke, or cognitive impairment before the cerebral infarction event; (2) Other medical diseases leading to cognitive impairment (such as hypothyroidism, vitamin B12 deficiency, and severe infection) or neurological diseases (Parkinson’s disease, Alzheimer’s disease, Lewy body dementia, brain atrophy, and cerebral amyloidosis) that may lead to cognitive impairment; (3) Cerebral microvascular disease that can cause cognitive impairment; (4) Patients complicated by depression, bipolar disorder, and other mental disorders; and (5) Lack of clinical data.

Ethical approval

This study was approved by the Research Ethics Committee, and all patients were informed and voluntarily participated in the study.

Observation indicators and methods

Location screening of cerebral infarction and calculation of the cerebral infarction volume were conducted based on MRI detection[19]: A head MRI was performed to identify the location of cerebral infarction lesions in the acute stage of cerebral infarction (3-4 weeks post-cerebral infarction) and 6 months later.

Statistics on the volume of cerebral infarction: The volume of cerebral infarction was based on the MRI results[20]. Two attending or deputy chief physicians of radiology independently read the head MRI images that met the image quality standards using a double-blind method for independent analysis. If the opinions were divided, a third deputy chief physician of radiology participated until a consensus was reached. The location of the infarct was recorded in patients with acute cerebral infarction, and the infarct volume was measured using fluid-attenuated inversion recovery images at 6 months of the disease course. Post-processing software was used to outline the infarction contour of each layer of cerebral infarction in the sequence related to the head, and the area could be automatically calculated and accumulated layer-by-layer. Finally, the volume of the cerebral infarction was obtained by multiplying the sum of layer thickness and layer distance. The sites of the two MRI infarcts in the same patient were compared, and patients with new infarcts were excluded. Using the results of the volume measured by MRI at 6 months, the infarct volume of all patients in each group was added according to the infarct site to obtain the total volume value of each infarct volume in the groups with and without cognitive impairment, and a comparison was conducted between the groups.

Cognitive function assessment[21]: The patients’ cognitive function was evaluated using the MoCA score. The MoCA score is composed of 12 items, with one point deducted for 12 years of education or less, and a maximum total score of 30. It mainly covers seven cognitive domains, which are subdivided into visual space, executive function, naming, attention, memory, computation, repetition, verbal fluency, abstraction, delayed recall, and orientation, and takes 10–15 min to complete.

Statistical analysis

Statistical analyses were performed using IBM SPSS Statistics for Windows, version 26.0. The MoCA score results were represented by mean ± SD and t-test. The χ² test was used to analyze the data. The correlation between the infarct location, infarct volume, and MoCA score was tested using the rank-sum and Spearman’s rank correlation coefficient tests. A P value < 0.05 indicated that the difference was statistically significant. If the correlation coefficient |r| was greater than 0.6, it was considered that a significant correlation was present between them.

RESULTS

General data comparison

A research flowchart is presented in Figure 1. Among the 58 patients with cognitive impairment, the average age was 65.84 ± 8.13 years, including 41 males and 17 females, 23 patients with a history of smoking, 31 patients with a history of drinking, 27 patients with hypertension, and 15 patients with diabetes, and the average length of education were 5.78 ± 4.72 years. There were 52 right-handed and six left-handed cases. Among the 40 patients in the cognitively normal group, the average age was 63.19 ± 7.57 years, with 28 males and 12 females, 16 patients with a history of smoking, 27 patients with a history of drinking, 19 patients with hypertension, and nine patients with diabetes, and the average length of education were 6.12 ± 4.95 years. There were no statistical differences in the above general data between the two groups (P > 0.05), as shown in Table 1.

Figure 1 Flow chart illustrating the patient selection process.

Table 1 Comparison of general data between two groups of patients.

Variable	Cognitive impairment group, n = 58	Non-cognitive impairment group, n = 40	t/χ2	P value
Sex			0.345	0.557
Male	41	28
Female	17	12
Age in years	65.84 ± 8.13	63.19 ± 7.57	1.673	0.692
Smoking history			0.082	0.783
Yes	23	16
No	35	24
Drinking history			0.367	0.674
Yes	31	27
No	27	23
Complicated with hypertension			0.815	0.363
Yes	27	19
No	31	21
Complicated with diabetes			0.459	0.582
Yes	15	9
No	43	31
Years of education	5.78 ± 4.72	6.12 ± 4.95	3.683	0.062
Handedness			0.175	0.684
Right-handed	52	36
Left-handed	6	4

Comparison of infarct volume

The infarct volume in the cognitive impairment group [711.6 mm³ (309.3, 1156.0)] was significantly larger than that in the non-cognitive impairment group [566.0 mm³ (295.1, 866.9); P < 0.05)], as shown in Figure 2.

Figure 2 Comparison of different infarct volumes between the two groups. ^aP < 0.05.

Comparison of different infarct sites

The comparison of the number of infarct sites (basal ganglia, cortex, brainstem, cerebellum, thalamus, and mixed lesions) between the two groups showed that the number of infarct sites in the thalamus and basal ganglia in the cognitive impairment group was significantly higher than that in the group without cognitive impairment, and the difference was statistically significant (P < 0.05), as shown in Table 2.

Table 2 Comparison of different infarct sites between the two groups.

Variable	Cognitive impairment group, n = 58	Non-cognitive impairment group, n = 40	χ2	P value
Basal ganglia	41 (70.69)	14 (35.23)	12.245	< 0.001
Cortical layer	5 (9.39)	5 (11.95)	0.081	0.776
Brain stem	4 (6.56)	4 (9.00)	0.31	0.86
Cerebellum	5 (9.00)	4 (11.00)	0.015	0.902
Thalamus	23 (39.66)	7 (17.13)	5.471	0.019
Mix	7 (12.83)	6 (15.69)	0.177	0.674

Data are n (%).

Comparison of the infarct volume at different infarct sites

The infarct volumes at different infarct sites in the cognitive impairment group was higher than that in the non-cognitive impairment group, and the differences between the two groups were statistically significant (P < 0.05), as shown in Table 3.

Table 3 Comparison of infarct volume at different infarct sites between the two groups.

Variable	Cognitive impairment group, n = 58	Non-cognitive impairment group, n = 40	t value	P value
Basal ganglia	48.55 ± 1.32	24.76 ± 1.01	96.161	< 0.001
Cortical layer	194.26 ± 3.75	110.02 ± 2.64	122.577	< 0.001
Brain stem	112.23 ± 3.64	72.65 ± 2.03	62.346	< 0.001
Cerebellum	81.05 ± 2.02	31.86 ± 1.04	141.47	< 0.001
Thalamus	15.87 ± 1.02	7.32 ± 0.57	48.045	< 0.001
Mixed lesions	289.84 ± 8.13	163.19 ± 6.53	81.932	< 0.001

Data are presented in mm³.

Correlation analysis between the infarct volume at different infarct locations and the total MoCA score

As shown in Figure 3, the MoCA score of elderly patients with acute insular infarction has a strong negative correlation with the infarct volume of the basal ganglia, thalamus, and mixed lesions, and the correlation coefficients r were -0.67, -0.73, and -0.77, respectively. In other parts of the body, there were no obvious correlations between the volumes.

Figure 3 Correlation between infarct volume and Montreal Cognitive Assessment Scale score at different infarct sites. MoCA: Montreal Cognitive Assessment Scale.

DISCUSSION

It is reported that compared with the Mini-Mental State Examination, the MoCA score is recommended to be used for patients in Asia with an education period of < 6 years[22]. The average education period of the cognitive impairment group in this study was 5.78 ± 4.72 years, so this article used the MoCA score.

Few studies have examined the relationship among the infarct location, infarct volume, and cognitive impairment in elderly patients with acute insular infarction[23-25]. The infarction sites of patients with acute insular infarction mainly involved the basal ganglia, cortex, brainstem, cerebellum, thalamus, and mixed lesions among these sites, with the highest incidence in the basal ganglia (41 cases in the cognitive impairment group and 14 cases in the non-cognitive impairment group), followed by the thalamus (23 cases in the cognitive impairment group and seven cases in the non-cognitive impairment group). This is consistent with the results of Jones et al[26], and the difference in the incidence in the basal ganglia and thalamus between the two groups was statistically significant (P < 0.05)[27].

In addition, the results of this study showed that the occurrence of cognitive impairment in patients with cerebral infarction was related to the infarction volume. The infarction volumes in the basal ganglia, cortex, brainstem, cerebellum, thalamus, and mixed lesions in the cognitive impairment group were larger than those in the non-cognitive impairment group, indicating that these areas were related to cognitive impairment. However, Zhou et al[28] believed that the multiple infarction lesions and specific infarction types were important risk factors for cognitive impairment in patients with a cerebral infarction recovery period. The results of the present study confirm this conclusion. This may be because the cerebral cortex is mainly responsible for cognitive and emotional learning and other advanced functions, and patients with cortical infarction are prone to cognitive dysfunction[29].

Further correlation analysis showed that the infarct volumes of basal ganglia, thalamus and mixed lesion in the cognitive impairment group were strongly correlated with MoCA scores (r = -0.67, -0.73, -0.77), while the infarct volumes of cortex, brainstem and cerebellum were weakly correlated with MoCA scores (r = -0.20, -0.28, -0.34). As the conclusion of the current research on the correlation between the infarct location, infarct volume, and cognitive impairment was controversial. Peng et al[17] showed that thalamic infarction is an independent risk factor for cognitive impairment following cerebral infarction. Li et al[30] believed that the location of cerebral infarction was an independent risk factor for cognitive impairment. The results of this study are basically consistent with those of Peng et al[18] and Li et al[30].

Limitations

This study had a few limitations. First, this was a single-center retrospective study and the number of patients was small, which limited the generalizability and extension of the results. Second, previous studies have shown that male sex, hypertension, diabetes mellitus, and low education are independent risk factors for cognitive impairment in cerebral infarction. However, this study appropriately controlled for these factors to make them comparable, such that it can obtain more accurate results of infarction location and infarction volume on cognitive impairment. Nevertheless, there may also be some potential biases that may affect the conclusions of the study. Third, this study did not conduct a long-term follow-up and lacked data on the long-term prognosis of the patients. Another limitation of this study is that a control group of elderly individuals without cerebral infarction has not been added, and further consideration will be given to adding this control group in the later stage to verify the accuracy of the results. In the future, it will be necessary to conduct a multicenter prospective epidemiological study with a large sample size to fully reflect the impact of infarction location and volume on cognitive dysfunction in elderly patients with acute insular infarction.

CONCLUSION

In summary, the total infarct volume of patients with acute insular infarction has a significant impact on cognitive impairment. The infarct volume in the basal ganglia, thalamus, and mixed lesions had a significant negative correlation with the MoCA score, whereas the infarct volume in the cortex, brainstem, and cerebellum had no significant correlation with the MoCA score. Therefore, it is necessary to conduct cognitive function assessments for patients with infarction in these key parts of the brain or with a large infarction volume to identify cognitive impairment after cerebral infarction early and to select the appropriate intervention measures.

ACKNOWLEDGEMENTS

The authors thank the institution for support and all friends and families.