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. 2020 Feb 4;10:1783. doi: 10.1038/s41598-020-58687-z

Table 1.

Demographics and baseline clinical data of the sample under consideration.

ALS N = 158 Controls N = 86 Statistics
Age in years 61 (31–82) 62 (33–82) Z = −0.4, p = 0.7a
Male sex, n (%) 100 (63) 52 (62) χ²(1) = 0.1, p = 0.8b
Height in cm 172 [10] 174 [9] t(140) = −0.7, p = 0.5c
Weight in kg 75 [14] 79 [14] t(126) = −1.0, p = 0.3c
Definite ALS1 / Probable ALS1 / Possible ALS1 / Suspected ALS1 / PLS, n (%) 12 (8) / 66 (42) / 43 (27) / 28 (18) / 9 (6) N/A N/A
Classic ALS / LMND ALS / UMND ALS / PLS, n (%) 108 (68) / 27 (17) / 14 (9) / 9 (6) N/A N/A
Limb- / bulbar-onset, n (%) 110 (71) / 45 (29)* N/A N/A
Disease duration (months) 16 (3–272) N/A N/A
ALSFRS-R total score 39 (14–48) N/A N/A
Sporadic / familial ALS, n (%) 49 (78) / 14 (22)** N/A N/A
No NIV / NIV, n (%) 122 (77) / 16 (10)*** N/A N/A

Unless otherwise reported, mean [SD] or median (range) is given. For group comparisons a Mann-Whitney U testa, χ² testb, or an independent-samples t testc was conducted.

ALS, amyotrophic lateral sclerosis; ALSFRS-R, revised ALS functional rating scale; LMND, lower motor neuron dominant; N, number; N/A, not applicable; NIV, non-invasive ventilation; PLS, primary lateral sclerosis; UMND, upper motor neuron dominant. 1, according to the El Escorial criteria and its revisions1416. Data were missing in *3, **95 and ***20 patients, respectively. **Of the 14 familial ALS cases, 7 (11%) had mutations in the SOD1 gene and 7 (11%) in the C9orf72 gene. P-values ≤ 0.05 were deemed statistically significant.