Table 1 Demographic and clinical characteristics of patients and healthy controls (HCs).

From: Brain functional and structural alteration following acute carbon monoxide poisoning contribute to delayed neurological sequelae

 

DNS (n = 18)

Non-DNS (n = 26)

HCs (n = 30)

Statistics value

P

Age (y)

49.33 ± 9.92

45.15 ± 11.41

49.20 ± 9.14

F = 1.367

0.262a

Gender, Man

11(61.10%)

13 (50.00%)

17 (56.70%)

χ2 = 0.564

0.754b

Education (y)

11.00 (6.00)

11.00 (5.00)

11.00 (3.00)

H = 1.501

0.472c

Time interval from end of CO exposure to MRI scan (d)

4.00 (2.00)

3.50 (2.00)

NA

Z = -0.630

0.528d

Duration of CO exprosure (h)

8.44 ± 1.46*

5.08 ± 1.67

NA

T = 6.904

< 0.001e

GCS < 9

10 (55.60%)*

2 (7.69%)

NA

χ2 = 12.285

0.002b

Number of HBO sessions

3.00 (2.00)

2.50 (1.00)

NA

Z = -1.325

0.185d

ABLs (%)

11 (61.11%)*

2 (7.69%)

NA

χ2 = 14.581

< 0.001b

  1. Continuous variables are presented as mean ± standard deviation or as median (interquartile range).*P < 0.05 was considered statistically significant.
  2. GCS, Glasgow coma scale; ABLs, acute brain lesions; CO, carbon monoxide; DNS, delayed neurological sequelae; HBO, hyperbaric oxygen therapy; NA, not acquire.
  3. a One-way analysis of variance.
  4. b Chi-square test.
  5. c Kruskal–Wallis test.
  6. d Mann–Whitney U test.
  7. e Independent T test.