Cerebellar ischemia and hypoxia cause ischemic necrosis of local tissues, called cerebellar infarction. It is mainly caused by atherosclerosis, thrombosis or embolism in the posterior circulation (also known as the vertebrobasilar system) that supplies blood to the brain [15]. High-risk factors mainly include high blood pressure, diabetes, dyslipidemia, smoking, lack of exercise, abdominal obesity, heart disease, and poor eating habits [2, 11, 12, 14, 15]. Because of the extensive anastomosis between the cerebellar blood supply arteries, the incidence of cerebellar infarction is low, accounting for about 1.5–3% of ischemic stroke [16]. However, larger cerebellar infarcts are likely to cause hydrocephalus and lower brainstem compression, with severe clinical symptoms and higher mortality. So improving the understanding of the clinical characteristics of cerebellar infarction is essential for early diagnosis, treatment, prevention and assessment of prognosis.
Our research showed that the incidence of cerebellar infarction in men and women was close to 2:1 and there were more patients older than 65 years old. However, smoking and drinking did not seem to be associated with cerebellar infarction. We found that the included patients with cerebellar infarction had multiple underlying diseases, including diabetes, coronary heart disease, hyperlipidemia, carotid atherosclerosis, atrial fibrillation and hypertension. It is showed that hyperlipidemia, hypertension and carotid atherosclerosis were the main underlying causes. Especially, there was the most obvious correlation between carotid atherosclerosis and cerebellar infarction. It is generally believed that the risk factors of cerebellar infarction are consistent with the risk factors of cerebrovascular diseases, and the latter significantly increases the incidence of cerebellar infarction [11, 12, 17]. In terms of clinical manifestations, the incidence of ataxia and brainstem syndrome was relatively high, while the incidence of vestibular syndrome was relatively low. Common clinical manifestations of cerebellar infarction include dizziness/vertigo, nystagmus, limb and gait ataxia, cerebellar dysarthria, etc. Previous studies have found that infarcts in the blood supply area of PICA and AICA are more likely to cause dizziness in patients than infarcts in the SCA area. This is because the structure of the vestibular cerebellar nodules and floccules are mainly supplied by PICA and AICA [18]. The prominent clinical manifestations of SCA are limb and gait ataxia and dysarthria [15]. Due to the limited sample size in this study, it is difficult to clarify the differences in clinical manifestations caused by infarctions in different vascular regions, which needs to be further explored in future. The NIHSS scores of the patients included in this study were mostly less than one point, and the TOAST classification indicated that the SAO and LAA were mostly. Studies have shown that most patients with cerebellar infarction have lower NIHSS scores, and the TOAST etiological classification of cerebellar infarction has a certain relationship with the involved arteries [1, 2, 7, 15, 18].
We analyzed the vascular imaging results of patients with cerebellar infarction and found that the incidence of cerebellar infarction caused by SCA involvement was the highest regardless of whether it was performed by CTA or MRA. In addition to SCA, the probability of PICA involvement is also significantly greater than that of AICA. The involvement of different cerebellar blood vessels will produce different clinical symptoms, which is helpful for the diagnosis and prognosis of the disease. Obstruction of the PICA can lead to a headache and AICA territory infarction often leads to dysmetria, unilateral hearing loss and ipsilateral facial paralysis, and obstruction of the SCA tends to produce more ataxia, dysarthria and nystagmus [15]. By calculating the detection rate, we found that there was no statistical difference in the detection rate of different blood vessels between CTA and MRA. This indicates that if MRA cannot be performed for the patient, enhanced CT angiography and perfusion imaging will provide a good reference for the display of cerebellar infarcted blood vessels [7, 15, 16]. In this study, both CT and MRI examinations showed that the incidence of unilateral cerebellar infarction accounted for more than 80%; and the left hemisphere cerebellar infarction was the main one. This was a sure finding that MRI had an absolute advantage in detecting cerebellar infarction compared with CT. Brain CT scan is the most commonly used examination for cerebral infarction, but it is not sensitive to ultra-early ischemic lesions and small infarcts, especially brain stem. However, MRI can detect cerebral infarction early and has a high sensitivity [15, 16]. One hour after the onset, local gyrus swelling, narrowing of the brain sulcus and abnormal long T1 and long T2 signals can be seen. In particular, MRI is sensitive to lacunar infarcts in the thalamus, cerebellum, and brainstem [7].
Our study found that patients with high NIHSS scores had higher serum concentrations of D-dimer, LDL, and triglycerides than those with low scores, while HDL levels were just the opposite. The increase of D-dimer suggests that it is related to thrombotic diseases caused, and it illustrates the enhancement of fibrinolytic activity. Existing studies generally support that the increase of D-dimer is a risk factor for cerebral infarction, and it has predictive significance for the course of the disease [19–21]. Studies have shown that cholesterol carried by LDL is prone to accumulate on the walls of blood vessels and arteries, forming unstable soft plaques, which blocks the cerebral artery and causes a cerebral infarction [22–24]. The main harm of triglycerides to the human body is mainly to cause atherosclerosis, block blood vessels and form thrombus. It is closely related to the occurrence of cerebral infarction [23, 24]. Our research suggests that the D-dimer, LDL, HDL, and triglycerides can be used as indicators to predict the severity of the NIHSS scores in patients with cerebellar infarction [25]. The TOAST subtype classification standard focuses on the etiological classification, which has good credibility in clinical application [26]. We found that the serum D-dimer concentrations in patients classified as CE was higher than that in patients classified as LAA and SAO. The cardiogenic embolus is detached and embolized in the corresponding cerebral artery with the blood flow, causing ischemic cerebral infarction in the corresponding blood supply area. Among them, atrial fibrillation-related infarctions account for more than 79% of all cardiogenic infarctions [11, 26]. Previous studies have also shown that D-dimer is intrinsically related to cardiogenic cerebral infarction [27, 28]. Our research suggests that patients with cerebellar infarction with elevated D dimer concentrations should focus on the investigation of the possibility of cardiogenic embolism. Our study showed that patients classified as LAA and SAO had higher serum concentrations of LDL than those classified as CE, suggesting that LDL plays a prominent role in vascular embolism caused by atherosclerosis. LDL receptors are distributed on the cell membrane surface of various tissues throughout the body, such as arterial wall cells, and abnormally increased levels can cause atherosclerosis [29].
In the study, all patients with cerebellar infarction underwent cranial CT and MRI. We found that both CT and MRI showed that the serum HDL concentrations of patients with a cerebellar infarct area of less than 20mm in diameter was significantly higher than that of patients with an infarct area greater than or equal to 20mm in diameter. It is known that the high concentrations of HDL has a negative correlation with the occurrence of cardio-cerebral vascular embolism and infarction [30, 31]. Our study suggests that HDL is a protective factor against cerebellar infarction and its high levels can reduce the occurrence of cerebellar infarction, which can also be understood that patients with higher HDL indicate a lower degree of cerebellar infarction and a better prognosis. Studies showed that HDL can bind to lipids attached to the walls of blood vessels to dissolve them. The dissolved products are transformed into excretable metabolites through the liver's biochemical reaction, thereby reducing the occurrence of vascular sclerosis and embolism [32, 33]. Regardless of the result of CT or MRI, we found that the diameter of the cerebellar infarct area of patients with NIHSS scores more than one point was significantly larger than that of patients with NIHSS scores less or equal to 1 point. The tool of NIHSS scores is mainly used to evaluate the neurological status of stroke patients, and has important significance in individualized treatment, prognosis prediction and correct health education. The higher the scores are, the more severe the nerves damage [10, 25]. Our research suggests that the NIHSS scores are positively correlated with the sizes of the cerebellar infarction area, which can indirectly reflect the severity of the infarction. In addition, we found that the cerebellar infarct area of patients classified as LAA by TOAST classification was significantly larger than that of patients classified as SAO and CE, and the measurement results from CT and MRI showed the same trend. The LAA patients often are found with significant stenosis in the carotid artery, anterior cerebral artery, middle cerebral artery, posterior cerebral artery, and vertebrobasilar artery during retrospective examination. Cerebral infarction caused by LAA often manifests as large area, rapid onset and high mortality rate [34, 35].