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Objective:To analyze the abnormal vestibular function of Wernicke encephalopathy (WE) and to explore its diagnostic value.Methods:WE patients who visited the Vertigo Center of the Second Affiliated Hospital of Zhengzhou University from January 2018 to January 2021 were retrospectively collected. All patients were evaluated by clinical neurology. Before treatment, all patients completed video head impulse test (vHIT) and video nystagmusgraphy (VNG) in addition to cranial magnetic resonance and serum thiamine level examination.Results:All 12 patients had a history of eating defects, including 8 cases of alcoholism. All 12 patients had walking instability, 7 cases had dizziness and 8 cases had oscillopsia. Six cases had ophthalmoplegia. All 12 cases showed positive gaze nystagmus. The pathological saccades of bilateral horizontal semicircular canals were found in 12 patients by vHIT before treatment, but there was only 1 patient showing abnormality in vertical semicircular canals, the difference being statistically significant ( P<0.05). All patients could detect bilateral, horizontal, gaze-evoked nystagmus, including 3 cases with vertical nystagmus, 1 case with abnormal saccade test, 3 cases with abnormal smooth tracking test and 1 case with abnormal optokinetic test. There were abnormalities in the caloric test, including 6 cases of bilateral dysfunction and 2 cases of unilateral dysfunction. Conclusions:WE patients may have abnormal vHIT and bilateral, horizontal, gaze-evoked nystagmus, which is similar to the special abnormal signs of simultaneous damage of both peripheral and central vestibular dysfunction.Vestibular function test is valuable for diagnosis of WE, and it is suitable for patients with a history of nutritional disorders who have dizziness or walking instability and suspected WE.
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Objective:To analyze the sleep quality and sleep structure of patients with obstructive sleep apnea hypopnea syndrome (OSAHS) complicated with patent foramen ovale (PFO), and to study the effect of PFO on the sleep structure of OSAHS.Methods:Fifty-six patients with OSAHS complicated with PFO, 64 patients with simple OSAHS and 62 controls were collected from December 2018 to March 2020 in Centre of Sleep Disorders, the Second Affiliated Hospital of Zhengzhou University. Pittsburgh Sleep Quality Index and polysomnography were used to compare the sleep quality and sleep structure of the three groups.Results:Compared with the control group [6/62(9.68%)], OSAHS complicated with PFO group [54/56(96.43%)] and simple OSAHS group [53/64(82.81%)] had higher incidence of poor sleep quality (χ2=112.08, P<0.0l). Furthermore, compared with the control group, the OSAHS complicated with PFO group and simple OSAHS group showed reduced sleep efficiency [PSQI total score was 0.5 (0, 1), 2 (1, 3) and 2 (1, 2) respectively, H=74.549, P<0.01] and reduced proportions of rapid eye movement (REM; 20.45%±3.49%, 12.19%±5.95% and 15.11%±7.21%,respectively, F=21.17, P<0.01) and slow wave sleep (N3; 21.24%±4.12%, 14.15%±6.08%, 17.68%±6.35%, respectively, F=29.51, P<0.01); the N1 (4.47%±2.40%, 9.50%±5.34%, 9.55%±4.61%, respectively, F=30.07, P<0.05) and N2 sleep (53.88%±4.35%, 64.09%±7.49%, 58.14%±6.67% , respectively, F=46.21, P<0.05) were prolonged; the inocturnal lowest oxyhemoglobin saturation (SpO 2) level was lower, mean SpO 2 reduction at night was higher [3.00% (0, 4.00%),6.00% (5.00%, 8.75%) and 4.00% (4.00%, 5.00%), respectively, H=72.24, P<0.05], and periodic leg movement index [16.30(4.80, 32.82), 33.30(9.26, 54.80) and 23.10(8.38, 31.83),respectively, H=17.86, P<0.05], arousal index [11.60(7.73, 17.55), 23.90(14.03, 30.45) and 15.6(11.23, 20.78), respectively, H=22.80, P<0.05] and sleep apnea and hypopnea index (AHI; 1.60±1.38, 23.90±7.27 and 16.24±4.22,respectively, F=136.97, P<0.05) increased. Compared with the simple OSAHS group, the incidence of poor sleep quality was higher, the proportions of slow wave sleep (N3, F=29.51, P=0.047) and REM ( F=21.17, P=0.012) were decreased, N2 sleep ( F=46.21, P=0.000) was prolonged, mean SpO 2 reduction at night ( Z=54.28, P=0.000), wake after sleep onset [116.00(89.88, 143.00) min vs 135.00(118.50, 168.38) min, Z=25.71, P=0.023], arousal times [14.00(8.25, 8.00) vs 17.50(9.00,23.00),respectively, Z=19.68, P=0.041], microarousal ( Z=23.57, P=0.044), and AHI ( F=136.97, P=0.000) were increased in the OSAHS complicated with PFO group. Conclusions:OSAHS complicated with PFO patients had poor sleep quality and high incidence of sleep disorders. They had sleep disorder at night, which was characterized by the decrease of REM sleep and slow wave sleep, the prolongation of N2, the decrease of nocturnal SpO 2 and the increase of awakening times, and the increase of arousal times and AHI. PFO can aggravate the sleep disorder of OSAHS.
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Objective To analyze the distribution of Virchow-Robin spaces (VRS) in migraine by MRI,and to study the effects of the duration of the disease,the attack frequency and the migraine with or without aura on the number of VRS in order to provide imaging support for migraine diagnosis.Methods Fifty migraine patients were enrolled as migraine group and 50 healthy people as control group during January 2013 to December 2016 from Department of Neurology,the Second Affiliated Hospital of Zhengzhou University.The number of VRS in the fronto-parietal subcortical white matter,semioval central,and basal ganglia areas was calculated and compared between groups and within the group by performing a MRI scan of the same sequence,and the impact of the history of migraine,the attack frequency and the migraine with or without aura on the number of VRS was investigated.Results The VRS were found in 48 cases in the migraine group,accounting for 96％,significantly higher than in the control group (41 cases,accounting for 82％),the difference being statistically significant (x2 =5.00,P ＜ 0.05).In the migraine group,the sum of the number of VRS (13.00 (6.75,20.00)) was significantly higher than that of the control group (8.00 (5.00,12.00);Z=3.33,P＜ 0.01).In the migraine group the VRS numbers in the fronto-parietal subcortical white matter,semioval central and basal ganglia areas were 6.00(4.00,12.00),2.00(0.00,4.00)and 4.00 (2.00,6.00) respectively,while the numbers of VRS in the same areas of the control group were 0.00 (0.00,2.00),2.00 (0.75,4.00) and 4.00 (3.50,6.00).The total number of VRS in different areas was significantly different within the two groups (migraine group x2 =39.86,P ＜ 0.01;control group x2 =40.15,P ＜0.01).In the migraine group,the VRS was mainly located in fronto-parietal subcortical white matter,whereas in the control group the VRS was mainly distributed in the basal ganglia.The total number of VRS in the migraine with aura group (20.00 (14.50,26.00)) was more than that in the migraine without aura group (11.00 (6.00,20.00);Z =2.52,P =0.02).The numbers of VRS in the fronto-parietal subcortical white matter,semioval central and basal ganglia areas of the migraine with aura group were 12.00(9.00,14.00),2.00(2.00,6.00) and 4.00(2.50,7.50) respectively;The numbers of VRS in the same areas of the migraine without aura group were 6.00(4.00,10.00),1.00(0.00,4.00) and 4.00 (2.00,6.00) respectively;The numbers of VRS in different areas within the two groups were significantly different (with aura group x2 =16.31,P ＜0.01;without aura group x2 =29.48,P ＜0.01).There were statistically significant differences in the number of VRS among migraine without aura patients with different duration and frequency of episodes.Conclusions The incidence rate of perivascular space in migraine is high.VRS is mainly distributed in the fronto-parietal subcortical white matter,which may provide an imaging assistant basis for the diagnosis of migraine.Migraine with aura is more prone to VRS than those without aura.The disease course and the attack frequency have a certain impact on occurrence of VRS.
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Migraine and cerebral small vessel disease (CSVD) are 2 common neurovascular diseases in clinical practice.Their pathogeneses are still not clear.Migraine may increase the risk of CSVD,and CSVD can also cause migraine attacks by triggering cortical spreading depression and other mechanisms.The relationship between the two diseases is mutual and complex,and is influenced by a variety of factors,but the mechanism of this potential relationship is not yet very clear.With further research,the reports about the relationship between migraine and CSVD are increasing.This article summarizes the pathophysiological mechanisms of migraine and CSVD and the correlation between both.