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Table 1 Pathology groups and clinical data

From: Evidence for mTOR pathway activation in a spectrum of epilepsy-associated pathologies

 

Pathology group

Case

Age of onset of seizure (years)

Age at resection (years)/Gender

Outcome

Resection site/Procedure

Main pathology features in section

N = number of cases

(Seizure type)

Epilepsy-lesional pathology

HS N = 4

1

4 (PS, GS)

34 M

SF

Right ATL

HS ILAE type I: neuronal loss in CA1, CA4, gliosis, granule cell dispersion; mossy fibre sprouting confirmed in 3 cases.

2

6 (PS, GS)

43 F

NSF

Right ATL

3~

1 (PS)

55 F

NSF

Left ATL

4

31 (PS, GS)

46 M

NSF

Left ATL

HS With dysmorphic neurones n = 5

5

UK

30 F

NSF

Left ATL

Hippocampal sclerosis (ILAE type I) with dysmorphic neurones in CA4 and balloon cell glia in DG: mossy fibre sprouting confirmed in 3 cases.

6

12

42 F

NSF

Right ATL

7

7 (PS, GS)

31 F

SF

ATL

8

25 (GS)

42 F

SF

Right ATL

9

14 (PS, GS)

54 F

NSF

Right ATL

FCDIIA N = 1

10~

7 (PS, GS)

18 F

NSF

Right parietal resection

Dysmorphic neurones; no balloon cells.

FCDIIB N = 5

11~

UK (PS, GS)

26 M

SF

Right temporal lobectomy

Dysmorphic neurones, cortical dyslamination and balloon cells

12

11 months (PS)

24 F

SF

Left parietal resection

13~

7 (GS)

34 F

SF

Right frontal resection

14

15 months (PS)

33 F

NSF

Right parietal resection

15

5 (PS, GS)

18 M

NFS

Right parietal resection

FCD IIIA N = 5

16

12 (PS)

54 F

SF

Right ATL

Neuronal loss in outer cortical layers with gliosis and reorganisation of layer II neurones

17

2 (PS)

34 M

SF

Right ATL

18

18 (PS, GS, SE)

44 M

SF

Left ATL

19

8 (PS, GS)

40 M

SF

Left ATL

20

3 (PS, GS)

19 F

SF

Left ATL

FCD IIIB N = 3

21

10 months (PS, GS)

27 F

SF

Left temporal lobectomy

Cortex adjacent to a long-term epilepsy associated tumour (LEAT/DNT)

22

6 (PS, GS)

23 M

SF

Right ATL

23

7 (PS)

31 F

SF

Temporal lobectomy

FCD IIID N = 3

24

3 (PS, GS)

18 F

NSF

Right hemispherectomy

Cortical disorganisation adjacent to an early infarct

25

4 (PS)

23 M

NSF

Left ATL

26

11 (PS, GS)

18 F

NSF

ATL

Rasmussen’s Encephalitis N = 5

27

11

18/F

NSF

Right sided brain biopsy

Active encephalitis* + gliotic atrophic cortex

28

3 (FS, GS)

30 M

SF

Right hemispherectomy

Active encephalitis* + neuronal hypertrophy

29

14 (FS, GS, EPC)

18 M

SF

Temporal lobe resection and hemispherectomy

Active encephalitis* + normal cortex and atrophic cortex and frequent dysmorphic neurones

30

UK

9 F

NSF

Left temporal lobe resection

Burnt out encephalitis, atrophic cortex

31

UK

UK

NSF

Cortical resection

Burnt out encephalitis, atrophic cortex

Cortex adjacent to Cavernoma

32

27 (FS)

30 M

SF

Right temporal lobe resection

Cavernoma with reactive gliosis including ‘balloon cell’ like glia

Control-non lesional

Acute ICE injury N = 5

11~

12 (S, GS)

26 M

SF

Right temporal lobectomy

Organising electrode track cavity of 8 days

33

15

30 F

SF

Left ATL

Organising electrode track cavity of 8 days

10~

7 (FS, GS)

18 F

NSF

Right parietal resection

Organising electrode track cavity of 8 days

12~

11 months (FS)

24 F

SF

Left parietal resection

Organising electrode track cavity of 10 days

13~

7 (GS)

34 F

SF

Right frontal resection

Organising electrode track cavity of 10 days

Epilepsy: Paired samples from different regions according to intracranial recordings. N = 4

34

6 (GS)

39M

NSF

Right frontal resection:

No specific pathology- focal inflammation

Sample 1. Ictal onset zone

Sample 2. Peripheral samples in CUSA specimen

35

7 (PS, GS)

25 F

SF

Left frontal lobe resection

No specific pathology

Sample 1. Seizure onset zone

Sample 2. Frontal pole; spreading of EEG activity

36

16 (PS)

33 M

SF

Right frontal lobe resection

No specific pathology

Sample 1. Ictal onset zone

Sample 2. Inferior fronto-orbital; spreading of activity

37

8 (PS,GS)

37 M

SF

Right frontal lobe resection

Focal inflammation only

Sample 1. Ictal onset zone

Sample 2. Spreading of EEG activity

Epilepsy: Pathology negative

38

12 (GS)

18 M

NSF

Frontal lobe cortex

Pathology negative

39

18 (PS, GS)

31M

NSF

40

6 (PS, GS, SE)

34 M

SF

Temporal lobe cortex

No pathology in temporal lobe; HS in other sample

41

6 (PS, GS)

43 F

SF

3~

1 (PS)

55 F

NSF

42

31 (PS, GS)

46 M

NSF

43

UK

40M

UK

44

6 (PS)

48 F

NSF

45

7 (PS, GS)

48 M

SF

Non-Epilepsy Cortex N = 3

46

NA

37M

NA

Left temporal lobectomy

Metastatic carcinoma

47

NA

30M

NA

Left temporal lobectomy

Low grade oligo-astrocytoma

48

NA

74M

NA

Right temporal lobectomy

High grade astrocytoma

  1. ICE = Intracranial electrode, FCD = focal cortical dysplasia, HS = hippocampal sclerosis, DG = dentate gyrus, GS = generalised tonic clonic seizures, PS = partial of focal seizures (no distinction made between complex and simple type), SE = status epilepticus, EPC = Epilepsy partialis continua, SF = completely seizure free at follow up, NSF = not seizure free at follow up (includes nocturnal seizure and rare seizures/auras) [Follow up periods vary between 1 year to 15 years and status taken at last follow up], ATL = anterior temporal lobectomy including hippocampectomy, DNT = dysembryoplastic neuroepithelial tumour, ICE = intracranial electrode injury, CUSA = ultrasonic tissue aspirator, DG = dentate gyrus, UK = unknown. *Active encephalitis was determined by the presence of microglial nodules/neuronophagia and lymphocytic infiltrates on H&E as well as HLADR and CD163 labelling. ~These cases had more than one lesion in different regions of the surgical resection.