post-traumatic epilepsy: clinical, neurophysiological and ... · post-traumatic epilepsy: clinical,...

Ayman Emam et al.

737

Post-Traumatic Epilepsy: Clinical, Neurophysiological

and Neuroimaging Study

Ayman Emam1, Nagia Fahmy

2, Nagla El-Khayat

2

Departments of Neuroscience, SGHJ, Jeddah, SA1; Neurology, Ain Shams University

2

ABSTRACT

Post-traumatic epilepsy (PTE) is a recurrent seizure disorder due to traumatic injury of the brain. There is

controversy regarding the precise mechanism by which epilepsy may results from traumatic brain injury. Mesial

temporal lobe sclerosis (MTS) is reported as a major risk factor for intractability of posttraumatic epilepsy. We

aimed from this work to revise patients with post-traumatic epilepsy, to define risk factors, and assess the clinical,

neurophysiological and neuroradiological characteristics. The frequency of mesial temporal epilepsy in contrast

to neocortical epilepsy was also assessed in these patients. Twenty- three patients with post-traumatic epilepsy

were included in this study. Clinical assessment, video EEG monitoring and MRI brain results were reviewed. We

found that 14 patients (60.9%) with neocortical epilepsy (NCE), 8 patients (34.8%) of them had their trauma

below or equal to 10 years and 6 patients (26.1%) had their trauma above 10 years old. We found also 8 patients

(34.8%) with mesial temporal epilepsy (MTE), 5 patients (21.8%) had their trauma below or equal to 10 years and

3 patients (13%) had their trauma above 10 years. There was one patient (4.3%) with mixed neocorical and

mesial temporal epilepsy. Of these patients, 6 had temporal lobectomy with successful post-operative results and

the diagnosis of mesial temporal sclerosis was pathologically definite in 5 patients. We concluded that MTS could

occur in patients with PTE in young or old ages. Detection of MTS is mandatory for all patients with PTE as

resective surgeries of these patients gave a good outcome for the control of their intractable epilepsy. (Egypt J.

Neurol. Psychiat. Neurosurg., 2007, 44(2): 737-749)

INTRODUCTION

Post-traumatic epilepsy (PTE) is defined as

recurrent seizure disorder due to injury to the

brain following trauma1. It is an established

consequence of head injury and its incidence is

highest among young adults as they are more

prone to head injury2,3

. PTE accounts for 20% of

symptomatic epilepsy in the general population

and 5% of all epilepsy patients referred to

specialized epilepsy centers3,4

. In military series,

the incidence of PTE is much higher (up to 50%),

as these studies also include many patients with

penetrating head injuries5.

PTE is classified as immediate seizures (less

than 24 hours after injury), early seizures (less

than 1 week after injury) and late seizures (more

than a week after injury)6. The incidence of

immediate seizure is 1-4%, early seizures 4-25%

and late seizures 9-42% in civilian head injuries5,7

.

Definitions for severity of head injury vary,

but one of the most established paradigms is that

proposed by Annegers et al., in which head injury

is classified as mild, moderate, or severe. Mild

injuries are defined by lack of skull fracture and a

period of posttraumatic amnesia or loss of

consciousness that is 30 minutes or less. Moderate

injuries may or may not be associated with skull

fractures, but there is a period of 30 minutes to 24

hours of posttraumatic amnesia or loss of

consciousness. Severe injuries are characterized

by brain contusion, intracranial hematoma, or 24

hours or more of either unconsciousness or

posttraumatic amnesia8.

Egypt J. Neurol. Psychiat. Neurosurg. Vol. 44 (2) – July 2007

738

It was found in some studies that mesial

temporal lobe epilepsy may result from traumatic

brain injury (TBI) and occurs mainly in young

children, while neocortical epilepsy occurs later in

life. This may be because of the vulnerability of the

developing brain to trauma9,10

. In up to two-thirds

of patients, late post-traumatic seizures are

generalized or focal with secondary generalization,

and often both seizure types may coexist11,12

.

The incidence of subclinical seizure activity

is much higher than that of overt seizures and is

even higher in penetrating brain injuries than in

non-penetrating injuries. In one series, the

reported incidence of combined non-convulsive

seizures and overt seizures was 22%, of these the

incidence of non-convulsive seizures was about

52%.13,14

Much less is known about the characteristics

of TBI, which is associated with increased risk of

seizures. However, certain risk factors have been

consistently identified, placing TBI patients at

significant risk of developing post-traumatic

epilepsy. These risk factors include duration of

loss of consciousness, missile injuries,

intracerebral hemorrhage, diffuse cerebral

contusions, prolonged (3 days) pos-traumatic

amnesia, acute subdural hematoma with surgical

evacuation, early post-traumatic seizures and

depressed skull fracture15,16,17,12

. Brain contusions

and subdural hematomas are the strongest risk

factors for late seizures and this increased risk

persists for up to 20 years2. Individuals with

bilateral or multiple cerebral contusions have

increased risk of developing seizures due to large

amount of tissue destruction12

. Patients with

multiple post-traumatic intracranial surgeries have

also high rates of late PTE12

.

We aimed from this work to revise patients

with post-traumatic epilepsy, to define risk

factors, assess the clinical, neurophysiological and

neuroradiological characteristics. The frequency

of mesial temporal epilepsy in contrast to

neocortical epilepsy was also assessed in these

patients.

PATIENTS AND METHODS

Patients:

They were selected from patients attending

the Epilepsy Unit, Neuroscience Department,

Saudi German hospital Jeddah (SGHJ). Patients

were included if they had moderate or severe head

injury that preceded the onset of epilepsy and was

of sufficient magnitude to result in prolonged loss

of consciousness (30 minutes). Amnesia,

hospitalization or neuroradiologic evidence of

traumatic brain injury12

.

Patients must not have in their past history

other risk factors for epilepsy or family history of

epilepsy.

Clinical assessment:

All patients were subjected for detailed

history and neurological examination. Detailed

history of the head trauma, with revising previous

hospital records of trauma, hospitalization, ICU

admission, surgeries done and onset of seizures.

Semiology of seizures was revised with

family members, attending hospital staff and

prolonged video recordings.

Neurological examination was done and

compared with hospital files at time of trauma.

Anti-epileptic medications, types, doses and

response of patients were revised. Intracranial

surgeries done whether as a management of

traumatic brain injury or as an epilepsy surgery,

were all revised.

Neurophysiological study:

All patients underwent prolonged surface

interictal EEG recording using the international

10-20 system of electrode placement (Machine).

Patients were subjected for continuous video EEG

monitoring for ictal and interictal changes.

Detailed descriptions of seizure semiology and

focus detection were done.

Neuroradiological study:

All patients underwent magnetic resonance

imaging (MRI) of the brain. T1-weighted sagittal

Ayman Emam et al.

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and gradient echo axial images were obtained. T1-

and T2-weighted and Fluid attenuated inversion

recovery (FLAIR) coronal images were obtained

at a 3mm-slice thickness through the region of

hippocampus. Mesial temporal sclerosis (MTS)

was defined by the finding of hippocampal

atrophy, T2- weighted hyperintensity, or bright

FLAIR signal of hippocampus18

.

Pathological study:

Pathological examination was done for en

bloc resections of either temporal or frontal

lobectomy. Criteria for mesial temporal sclerosis

were identified19

. These criteria consisted of

neuron loss in CA1 and CA4 and the presence of

associated reactive gliosis.

RESULTS

Twenty-three patients were included in the

study. There were twenty males (87%) and three

females (13%) (Graph 1). The mean age was 30.5

years, the youngest was 9 years old and the eldest

was 46 years old. The mean age of trauma was

12.7 years. The youngest age of trauma was 3

months while the eldest age of trauma was 30

years (Table 1).

Patients with their trauma below or equal to

10 years were 13 patients (56.5%), while patients

with their trauma above age of 10 years were 10

patients (43.5%) (Table 1).

The exact time of starting seizures could not

be known of some of the patients as patients had

management of head trauma at different hospitals

with lacking of some information. But we could

differentiate between 2 groups of patients.

Patients had onset of seizures within the first week

(early seizures,16 patients, 69.6%) and patients

with onset of seizures after the first week (late

seizures,7 patients, 30.4%). In the latter group,

time of onset of seizures ranged between 6 months

(patient no. 3) and 13 years (patient no. 23)

(Graph 2).

Patients had five types of head trauma. Road

traffic accident (RTA) in 14 patients (60.9%),

falling from height in 3 patients (13%), falling to

ground in 3 patients (13%), direct blunted head

trauma in 2 patients (8.7%) and firearm injury in

one patient (4.4%) (Graph 3).

The seizure semiology, EEG findings and

MRI results of all patients were summarized in

Table (2).

Mesial temporal epilepsy (MTE) was

diagnosed according to: (1) seizure semiology (2)

Ictal EEG change showing onset in temporal lobes

(3) Radiological evidence of atrophy of

hippocampus and T2 signal shortening on high

resolution MRI or both20,21

. These criteria of MTE

is widely accepted and is correlated

pathologically.20

We found 14 patients (60.9%) with

neocortical Epilepsy (NCE), 8 patients (34.8%) of

them had their trauma below or equal to 10 years

and 6 patients (26.1%) had their trauma above 10

years old. We found also 8 patients (34.8%) with

mesial temporal epilepsy (MTE), 5 patients

(21.8%) had their trauma below or equal to 10

years and 3 patients (13%) had their trauma above

10 years. There was one patient (4.3%) with

mixed neocorical and mesial temporal epilepsy

and he had his trauma above 10 years of age

(patient number 9), (Table 3 and Graph 4).

Six patients had temporal lobectomy and one

patient had frontal lobectomy and another patient

had aspiration of frontal cyst. Surgical outcome

according to Engel‟s classification22

showed

successful results as 3 patients had class 1 (Sizure

free, or few residual auras after withdrawal of

antiepileptic drugs) and 5 patients had class 2

(Rare seizure, fewer than three complex partial

seizures per year) (Table 4).

Pathological results confirmed mesial

temporal sclerosis in five of six patients with

temporal lobectomy (neuron loss in CA1 and CA4

and the presence of associated reactive gliosis).


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Table 1. Patient Characteristics, Type of Trauma and Brain Lesion.

Patient

No./Sex/

Age (yrs)

Age of

trauma

(Years)

Type of trauma Type of brain injury

Age of

seizures

(Years)

1/M/20 2 RTA Rt. temporal contusion 2

2/M/34 14 RTA Lt frontal &temporal contusion 14

3/M/25 10 RTA Lt frontal &temporal contusion 10

4/F/19 3 Falling to ground Multiple cerebral contusions 13

5/M/36 7 Falling from height Multiple cerebral contusions 7

6/M/23 5 RTA Bilateral frontal & temporal contusions 5

7/M/35 3 months Falling to ground Bilateral frontal contusions 6

8/M/39 6 RTA Lt. frontal contusion 6

9/M/34 23 RTA Multiple cerebral contusions 23


11/F/20 8 RTA Multiple cerebral contusions 8

12/M/20 6 RTA Rt. Extradural hematoma, evacuated 6

13/F/9 2.5 Falling from height Multiple cerebral contusions 2.5

14/M/46 21 Direct blunted head trauma Brain concussion, brain edema 21

15/M/39 19 RTA Rt. Intracerebral hemorrhage, operated 19

16/M/35 22 Direct head trauma Rt. Intracerebral hemorrhage 22

17/M/46 6 Falling from height Rt. Parietal contusion 6

18/M/37 17 RTA Fracture skull and spine 18

19/M/37 30 Falling to ground Fracture skull, biparietal contusions 30

20/M/31 8 RTA Bifrontal contusions 8.5

21/M/13 7.5 RTA Bifrontal contusions 8.5

22/M/35 25 Fire arm injury Rt. Occipital injury 28


( M: Male, F: Female, RTA: Road traffic accident, Rt.: Right, Lt: Left)

females,

3, 13%

Males,

20, 87%

Graph (1): Number of male and female patients.

Ayman Emam et al.

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Late

seizures; 7;

30%

Early

seizures, 16;

70%

Graph (2): Patients with early and late seizures.

0

10

20

30

40

50

60

70

RTA FFH FTG DT FAI

(RTA: Road traffic accident, FFH: Falling from height, FTG:

Falling to ground, DT: Direct head trauma, FAI: Fire arm injury).

Graph (3): Type of head trauma.

0

1

2

3

4

5

6

7

8

Bel/Equal 10Ys Above 10 ys

MTE

NCE

Mixed

Graph (4): Number of patients with MTE and NCE below and above 10 years of age.


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Table 2: Clinical data, EEG findings and MRI results.

Pat.

No. Seizure Semiology EEG Findings MRI Results

Conclusion (Type of

epilepsy)

1 Epigastric aura, Lt. UL

automatism, Rt dystonia

Rt. Temporal slowing Rt. Inferior temporal sclerosis

(Cortical sclerosis)

Rt. Temporal

neocortical

2 Amnesia, Speech arrest,

GTC

Lt. Temporal slowing Lt. Hippocampal sclerosis● Lt. MTE

3 Epigastric aura, Lt. motor

& Lt. adversive, GTC

Rt. Fronto-temporal

epileptic activity

Rt, Fronto-temporal

encephalomalacia

Rt. Fronto-temoral

neocortical

4 Vertigo, Lt. adversive,

GTC

Bilateral temporal

epileptic activity, more Rt.

Rt. Hippocampal atrophy &

sclerosis●

Rt. MTE

5 Expressive dysphasia, Rt.

Motor & adversive, GTC

Left anterior temporal

epileptic activity

Lt. Mesial temoral sclerosis● Lt. MTE

6 Oral automatism, Rt.

Hand dystonia, GTC

Lt. Temoral epileptic

activity

Lt. temporal & bifrontal

encephalomalacia

Lt. Temporal and

Bifrontal neocortical

7 Fear, oral automatism,

GTC

Lt. ant temporal & frontal

epileptic activity

Lt. frontal cyst Lt. Fronto-temoral

neocortical

8 Lt. motor Lt. frontal slowing Lt. frontal cyst Lt. frontal

neocortical

9 Epigastric, Rt. UL

dystonia, GTC

Lt. temporal epileptic

activity

Rt. Frontal encephalomalacia,

Lt. mesial temporal sclerosis●

Rt. Frontal

neocortical & Lt

MTE

10 GTC Rt. Frontal epileptic

activity

Rt. Frontal encephalomalacia Rt. Frontal

neocortical

11 Vertigo, oral automatism,

Rt. Adversive, GTC

Normal Rt. Hippocampal sclerosis● &

cystic lesion

Rt. MTE

12 Lt. Motor & sensory,

GTC

Rt. Anterior temporal

epileptic activity

Rt. Extradural hematoma

(evacuated), Rt. Temporal

sclerosis●

Rt. MTE

13 Attacks of lost

consciousness

Rt. Temporal epileptic

activity

Rt. Mesial temporal sclerosis● Rt. MTE

14 GTC Generalized dysrhythmia Rt. Mesial temporal sclerosis● Rt. MTE

15 Left motor, GTC Rt. Parietal epileptic

activity

Rt. Prietal hematoma

(evacuated)

Rt. Parietal

neocortical

16 Left motor, Rt. dystonia Rt. Fronto-temporal

epileptic activity

Rt. Frontal hematoma

(resolved)

Rt. Frontal

neocortical

17 Lt. adversive, GTC Rt. Post parietal &

occipital epileptic activity

Rt. Parietal encephalomalacia Rt. Parietal

neocortical

18 Chest compression, GTC Rt. Fronto-temporal

epileptic activity

Rt. Frontal gliosis Rt. Frontal

neocortical

19 GTC Lt. Parietal slowing Lt. Parietal encephalomalacia Lt. Parietal

neocortical

20 Rt. Motor, GTC Lt. frontal epileptic

activity

Lt. frontal encephalomalacia Lt. Frontal

neocortical

21 Lt. motor, GTC Rt. Frontal epileptic

activity

Bifrontal encephalomalacia Bifrontal neocortical

22 Vertigo, flashes of light,

GTC

Rt. Occipital epileptic

activity

Rt. Occipito-parietal

encephalomalacia

Rt. Occipito-parietal

neocortical

23 Rt. adversive, post-ictal

confusion, GTC

Lt. temporal epileptic

activity

Lt. Temporal sclerosis● Lt. MTE

(GTC: Generalized tonic-clonic convulsions, Rt: right, Lt: Left, MTE: Mesial temporal epilepsy)

Ayman Emam et al.

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Table 3. Number of patients with Mesial temporal epilepsy (MTE) & Neocortical epilepsy (NCE).

NCE MTE Mixed NCE &MTE

No. % No. % No. %

Below, equal 10 ys 8 34.8% 5 21.8% --- ---

Above 10 ys 6 26.1% 3 13% 1 4.3%

Total 14 60.9% 8 34.8% 1 4.3%

Table 4. Drug treatment and surgical intervention of all patients.

Patient

No. Drug treatment

Surgical Intervention Outcome after

surgery

(Engel’s class.) Surg. TBI Epilepsy Surg.

1 CBZ, PHT, LTG - Rt. Temporal lobectomy Class 2

2 PHT, CBZ - Lt. Temporal lobectomy Class 1

3 CBZ, VPA, LTG - Rt. Ant. Temporal lobectomy Class 2

4 LTG, CBZ - Rt. Temporal lobectomy Class 1

5 VGT. CBZ, LTG, VPA - Lt. Temporal lobectomy Class 1

6 CBZ, VPA, TPA - Lt. Temporal lobectomy Class 2

7 PHT, VPA, LTG - Drainage of cyst Class 2

8 VPA, CBZ, LTG - Rt. Frontal lobectomy Class 2

9 PHT, TPA, VPA, CBZ - - -

10 CBZ, TPA - - -

11 CBZ, VPA - - -

12 LTG, CBZ, CZM Evacuated Extradural H. - -

13 PHT - - -

14 PHT - - -

15 CBZ, VPA Operated cerebral H. - -

16 VPA, TPA Operated cerebral H. - -

17 CBZ, LMG - - -

18 CBZ, TPA Fixation of fracture spine - -

19 CBZ, PHT - - -

20 LTG - - -

21 CBZ - - -

22 CBZ - - -

23 PHT - - -

(PHT: Phynytoin, CBZ: Carbamazepine, VPA: Valproate, TPA: Topiramate, LTG: Lamotrigine, CZM: Clonazepam,

TBI: Traumatic brain injury, H: Hematoma)


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Fig. (1): Patient with Rt. Temporal sclerosis and lobectomy.

Fig. (2): Patient with Lt temporal sclerosis and lobectomy.

Fig. (3): DEEG showed left temporal focus.

Ayman Emam et al.

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Fig. (4): Patient with Right frontal encephalomalacia

Fig. (5): Patient with right frontal and left temporal encephalomalacia.

Fig. (6): Patient with extensive right parietal encephalomalacia.


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Fig. (7): Patient with bilateral frontal encephalomalacia.

DISCUSSION

In this study, we reviewed twenty-three

patients with post-traumatic epilepsy who had

their head trauma at any age.

We found large percentage of male patients

(87%) as compared to female patients (13%) (Graph

1). This could be explained by the large number of

males who are more prone to RTA than females2.

The most common type of head trauma in

our study was RTA (60.9%), followed by falling

from height and falling to ground, each 13% then

direct head trauma 8.7% and fire arm injury, 4.4%

(Graph 3). This showed the magnitude of road

traffic accidents in civilians as a major risk for

post-traumatic epilepsy.

Early seizure were high in our study as we

found 16 patients (70%) with their seizures in the

first week, while only 7 patients (30%) had their

seizures late, even up to 13 years of trauma (Pt.

No. 23) (Graph 3). In some studies the incidence

of immediate seizure was 1-4%, early seizures 4-

25% and late seizures 9-42% in civilian head

injuries5,7

.Other studies showed higher percentage

as our study as they found approximately 80% of

individuals with TBI had their first seizure within

the first 12 months post injury and more than 90%

by the end of the second year23

.Some patients

were followed up to 15 years and found increased

risk especially in penetrating head injuries to

reach 50%2.

Several studies searched for the percentage

of mesial temporal lobe epilepsy and sclerosis in

patients with post-traumatic epilepsy. Many

studies found higher percentage in patients with

head trauma at young age (Below 5 years) and

others found that MTE could occur also in

patients with head trauma occurred at older ages.

In our study, we found 14 patients (60.9%)

with neocortical Epilepsy (NCE), 8 patients

(34.8%) of them had their trauma below or equal

to 10 years and 6 patients (26.1%) had their

trauma above 10 years old. We found also 8

patients (34.8%) with mesial temporal epilepsy

(MTE), 5 patients (21.8%) had their trauma below

or equal to 10 years and 3 patients (13%) had

their trauma above 10 years. There was one

patient (4.3%) with mixed neocorical and mesial

temporal epilepsy and he had his trauma above 10

years of age (patient number 9). So, by addition of

this patient, we had 9 patients with mesial

temporal epilepsy and sclerosis (39.1%)(Table 3,

Graph 4).

Of these patients, 6 had temporal lobectomy

with successful post-operative results and the

diagnosis of mesial temporal sclerosis was

definite in 5 patients (Table 4). Several groups have studied patients who

underwent anterior temporal lobectomy (ATL) as a therapy for refractory epilepsy. Mathern et al.

9,

studied 259 patients who underwent ATL from 1961 to 1992. They found that 26 (10%) of these patients had TBI as a major risk factor and 50%

Ayman Emam et al.

747

of these patients had hippocampal sclerosis. They emphasized also that the mean±SD of these patients was 6.3±1.6 years.

Marks et al.24

described 25 patients with PTE who were examined in Yale University from 1982 to 1992, 21 of whom treated surgically. They found seventeen patients with mesial temporal lobe epilepsy (MTE) and eight with neocortical epilepsy (NCE). Fourteen of the patients with MTE were treated surgically with ATL. Of these, 6 (35%) had hippocampal sclerosis confirmed pathologically and they had excellent postoperative outcomes. Again, these researchers emphasized that all patients with hippocampal sclerosis had their head trauma younger than 5 years (mean age 3.4 years). Patients with NCE were significantly older at time of head trauma (mean age 18.25 years).

Another surgical series describe 102 patients who underwent ATL at the university of Michigan from 1990 to 1996. Twenty-nine (28.4%) had head trauma as a cause, of which, 20 (69%) had hippocampal sclerosis identified pathologically. But this study didn‟t find correlation between MTS and age of head trauma

25.

These earlier reports focused on highly selected patients who were prepared for resective epilepsy surgery.

Our results were compatible with these previous results and one recent retrospective case series, which studied presence of temporal lobe sclerosis in adult patients with intractable epilepsy following TBI. They found that 35% had foci in the mesial temporal lobe while 48% had neocortical foci

10 .So, this supports the findings

that TBI can lead to hippocampal sclerosis in adults as well as in children.

The pathogenesis of temporal lobe sclerosis was studied by many workers. In humans, direct injury to hippocampus from TBI is uncommon. Courville

26, examined the brains of 108 patients

who had fatal TBI and found contusions in the hippocampus in only 11 (10.2%). Other studies have found neuronal loss primarily in CA1 subfield of the hippocampus, which was frequently bilateral. They presumed that hippocampal sclerosis and MTS resulted from diffuse secondary effects of TBI

27,28.

Because of the retrospective nature of these

studies and our study, we can‟t exclude the

possibility that these patients had pre-existing,

clinically silent hippocampal sclerosis, and that

epilepsy was expressed only after injury. This

explanation is unlikely as hippocampal sclerosis is

rare in non-elderly patients who do not have

temporal lobe epilepsy28,29

.It is possible however,

that patients who develop head injury have genetic

predisposition to hippocampal injury.

Epidemiologic support for this possibility is the

studies showed increased family history for

epilepsy in patients with PTE30,31

.

This was studied in animal models for post-

traumatic epilepsy. Several animal studies

documented clear anatomical changes in the

hippocampus and other brain structures together

with increased excitability of specific networks31-37

.

More recent study demonstrated an increase

in the excitability of CA1 pyramidal cells in

response to stimulation, 3 months after fluid

percussion injury in animal models38

.

Other animal models of direct cortical injury

showed epileptiform potentials arising from area

V of cortex39,40

.

More recent work on animal models showed

that following injury, spontaneous partial seizure

originate from the neocortex at site of injury.

Then seizures became chronic and progressive in

course (electrographically and behaviourally). By

follow-up, they found progression of the

phenotype from neocortical (at site of injury) to a

predominance of mesial temporal seizures at later

time points41

.

So, the Importance of our work is that MTS

could occur in patients with head trauma in young

or old ages. Detection of MTS, clinically,

neurophysiologically and radiologically is

mandatory for all patients with PTE as resective

surgeries of these patients gave a good outcome

for the control of their intractable epilepsy. So, we recommend detailed study of patients

with post-traumatic epilepsy, for proper seizure localization and for detection of mesial temporal sclerosis as the source of epileptic activity. Resective surgeries of temporal lobe sclerosis gave successful results for those patients with intractable epilepsy.


748

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