Table 1.
Baseline demographics and characteristicsa
| Variable | First‐line lacosamide monotherapy (n = 98) | Conversion to lacosamide monotherapy (n = 341) |
|---|---|---|
| Age, mean (SD), years | 48.8 (19.0) | 51.1 (18.8) |
| <65 y, n (%) | 73 (74.5) | 238 (69.8) |
| ≥65 y, n (%) | 25 (25.5) | 103 (30.2) |
| Gender | ||
| Male | 47 (48.0) | 163 (47.8) |
| Female | 51 (52.0) | 178 (52.2) |
| Time since diagnosis, median (min, max), years | 0.10 (0.0, 32.7) | 4.80 (0.0, 70.3) |
| Seizure frequency per 28 d, median (min, max) | 0.5 (0, 137) | 0.6 (0, 77) |
| Focal seizures (I, partial‐onset), n (%) | ||
| Aware (IA, simple partial) | 27 (27.6) | 131 (38.4) |
| Impaired awareness (IB, complex partial) | 56 (57.1) | 184 (54.0) |
| Evolving to bilateral tonic‐clonic seizure (IC, partial evolving to secondary generalized) | 53 (54.1) | 121 (35.5) |
| Generalized seizures (II),a n (%) | 0 | 6 (1.8) |
| History of seizure clusters and/or status epilepticus | 3 (3.1) | 17 (5.0) |
| Aetiology not known | 56 (57.1) | 168 (49.3) |
| Idiopathic | 6 (6.1) | 24 (7.0) |
| Cryptogenic | 50 (51.0) | 144 (42.2) |
| Aetiology knownb | 42 (42.9) | 173 (50.7) |
| Cerebrovascular | 18 (18.4) | 46 (13.5) |
| Progressive neurodegenerative | 0 | 36 (10.6) |
| Cranial trauma | 6 (6.1) | 25 (7.3) |
| Cerebral neoplasm | 5 (5.1) | 21 (6.2) |
| Congenital | 6 (6.1) | 13 (3.8) |
| Brain surgery | 4 (4.1) | 14 (4.1) |
| Mesial temporal sclerosis | 2 (2.0) | 16 (4.7) |
| Cerebral infection | 1 (1.0) | 8 (2.3) |
| Perinatal events | 1 (1.0) | 8 (2.3) |
| Otherc | 3 (3.1) | 2 (0.6) |
| Genetic origin | 1 (1.0) | 3 (0.9) |
| Any prior AED, n (%) (taken by >10% of patients in the SS) | 21 (21.4) | 340 (99.7) |
| Levetiracetam | 6 (6.1) | 199 (58.4) |
| Carbamazepine | 2 (2.0) | 102 (29.9) |
| Valproic acid | 4 (4.1) | 80 (23.5) |
| Lamotrigine | 3 (3.1) | 75 (22.0) |
| Oxcarbazepine | 1 (1.0) | 46 (13.5) |
AED, antiepileptic drug; SD, standard deviation; SS, Safety Set.
a
All patients were also experiencing focal seizures.
b
Cortical developmental malformations were not predefined and some of these patients may have been included in congenital or other categories.
c
Other aetiologies were specified in five patients (1.1%) and further described as autoimmune, cortical dysplasia, focal cortical dysplasia, nodular heterotopia and temporal cystic lesion.