Online ISSN : 1687-8329

    




Quick Search 
 
Author  
Year    
Title  
Vol:  

 
 
July2007 Vol.44 Issue:      2 Table of Contents
Full Text
PDF


Post-Traumatic Epilepsy: Clinical, Neurophysiological and Neuroimaging Study

Ayman Emam1, Nagia Fahmy2, Nagla El-Khayat2

Departments of Neuroscience, SGHJ, Jeddah, SA1; Neurology, Ain Shams University2

 



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.

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 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).

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

10/M/24

19

RTA

Multiple cerebral contusions

19

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

23/M/45

30

RTA

Multiple cerebral contusions

44

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

 

 

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

 

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

 

(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.

  

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

 

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)

 

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)

 

 

 

 

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.

 

 

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.

 

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% 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 trauma25.

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 foci10 .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. Courville26, 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 TBI27,28.

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.

REEFRENCES

 

1.      Wrightson P, Gronwall D, 1999: Post-traumatic epilepsy. In: Mild head injury. London: Oxford University Press; p. 72-75

2.      Annegers JF, Hauser WA, Coan SP, Rocca WA, 1998: A population based study of seizures after traumatic brain injuries. N Engl J Med; 338:20-24.

3.      Annegers JF, Coan SP, 2000: The risks of epilepsy after traumatic brain injury. Seizure; 9: 453-7.

4.      Semah F, Picot M, Adam C, et al, 1998: Is the underlying cause of epilepsy a major prognostic factor for recurrence? Neurology; 51: 1256-62.

5.      Salazar A, Jabbari B, Vance S, et al, 1985: Epilepsy after penetrating head injury. I. Clinical correlates: a report of the Vietnam Head Injury Study. Neurology; 35: 1406-14.

6.      Iudice A, Murri L, 2000: Pharmacological prophylaxis of posttraumatic epilepsy. Drugs; 59: 1091-9.

7.      Asikainen I, Kaste M, Sarna S, 1999: Early and late posttraumatic seizures in traumatic brain injury rehabilitation patients: brain injury factors causing late seizures and influence of seizures on long-term outcome. Epilepsia; 40: 584-589.

8.      Annegers JF, Grabow JD, Groover RV, et al, 1980: Seizures after head trauma: a population study. Neurology 1980; 30: 683-689.

9.      Mathern G, Babb T, Vickrey b, et al, 1994: Traumatic compared to non-traumatic clinical-pathologic associations in temporal lobe epilepsy. Epilepsy Res; 19: 129-39.

10.    Diaz-Arrastia R, Agostini MA, Frol AB, et al, 2000: Neurophysiologic and neuroradiologic features of intractable epilepsy after traumatic brain injury in adults. Arch Neurol; 57: 1611–1616.

11.    Haltiner AM, Temkin NR,Dikmen SS, 1997: Risk of seizure recurrence after the first late posttraumatic seizure. Arch Phys Med Rehabil; 78: 835-840.               

12.    Englander J, Bushnik T,Duong TT, 2003: Analyzing risk factors for late posttraumatic seizures: a prospective, multicenter investigation. Arch Phys Med Rehabil; 84:365–373.

13.    Vespa PM, et al, 1999: In creased incidence and impact of non-convulsive and convulsive seizures after traumatic brain injury as detected by continuous electroencephalographic monitoring. J Neurosurg; 91: 750-60

14.    Sarah O, 2004: Review of the role of anticonvulsant prophylaxis folloing brain injury, J Clin Neurosci; 11: 1-3

15.    Jennett B, 1975: Epilepsy after non-missile head injuries. Chicago: William Heinmann Medical books.

16.    Yablon SA, 1993: Posttraumatic seizures. Arch phys Med Rehabil; 74: 983-1001

17.    The Brain Trauma Foundation, The American Association of Neurological Surgeons, The Joint section on Neurotrauma and Critical Care, 2000: Role of Antiseizure prophylaxis following head injury. J Neurotrauma; 17: 549-53.

18.    Kuzniecky B and Jackson G, 1995: Magnetic Resonance Imaging in Epilepsy. Raven Press, New York; 107-182.

19.    Rushing E, Barnard J, Bigio E, et al, 1997: Frequency of unilateral and bilateral mesial temporal sclerosis in primary and secondary epilepsy. Am J Forensic Med Pathol; 18: 335-341

20.    Ajmone-Marsan C, 1993: When are non-invasive tests enough? In: Engel J (ed): Surgical Treatment of the Epilepsies. Raven Press, New York, 2nd ed, 313-318

21.    Risinger N, Engel J, van Ness P, et al, 1989: Ictal localoization of temporal lobe seizures with scalp/sphenoidal recordings. Neurology; 39: 1288- 1293.

22.    Engel J, van Ness P, Rasmussen T, et al, 1993: Outcome with respect to epileptic seizures. In: engel J (ed): Surgical treatment of epilepsy. Raven press, New York, 2nd ed. 609-621

23.    Da Silva A, Vas A, ribeiro I, et al, 1990: controversies in post-traumatic epilepsy. Acta Neurochir suppl; 50: 48-51

24.    Marks DA, Kim J, Spencer DD, Spencer SS. Seizure localization and pathology following head injury in patients with uncontrolled epilepsy. Neurology 1995;45:2051–2057.

25.    Schuh L, Henry T, Fromes G, et al, 1998: Influence of head trauma on outcome following anterior temporal lobectomy. Arch Neurol; 55: 1325-1328

26.    Courville C, 1958: traumatic lesions of the temporal lobe as the causative cause of psychomotor epilepsy. In: Baldwin M, Bailey P (eds): Temporal Lobe Epilepsy. Springfield; 220-239.

27.    Kotapka M, Graham D, adams J, et al, 1993: Hippocampal damage in fatal pediatric head injury. Neuropathol Appl Neurobiol; 19: 128-133.

28.    Cook M, Fish D, Shorvon S, et al, 1992: Hippocampal volumetric and morphologic studies in frontal and temporal lobe epilepsy. Brain; 115: 1001-1015

29.    Cascino G, Jack C, Parisi E, et al, 1992: MRI in the presurgical evaluation of patients with frontal lobe epilepsy and children with temporal lobe epilepsy: Pathologic correlations and prognostic importance. Epilepsy Res; 11: 51-59

30.    Evans JH, 1962: Post-traumatic epilepsy. Neurology; 12: 665-657

31.    Caveness WF, 1963: Onset and cessation of fits following craniocerebral trauma. J Neurosurg; 10: 570-582

31.    McIntosh TK,Vink R,Noble L, et al, 1989: Traumatic brain injury in the rat: Characterization of a lateral fluid-percussion model. Neuroscience; 28: 233–244.

32.    Laurer H and McIntosh T, 1999: Experimental models of brain trauma. Curr Opin Neurol; 12: 715-721.

33.    Lowenstein DH, Thomas MJ, Smith DH, et, 1992: Selective vulnerability of dentate hilar neurons following traumatic brain injury: a potential mechanistic link between head trauma and disorders of the hippocampus. J Neurosci; 12: 4846-4853.

34.    Coulter DA, Rafiq A, Shumate M, 1996: Brain injury-induced enhanced limbic epileptogenesis: anatomical and physiological parallels to an animal model of temporal lobe epilepsy. Epilepsy Res; 26: 81-91.

35.    Toth Z, Hollrigel GS, Gorcs T, et al, 1997: Instantaneous perturbation of interneuronal networks by a pressure wave-transient delivered to the neocortex. J Neurosci;17:8106–8117.

36.    Santhakumar V, Bender R, Frotscher M, et al, 2000: Granule cell hyperexcitability in the early posttraumatic rat dentate gyrus: the ‘irritable mossy cell’ hypothesis. J Physiol; 524: 117-134.

37.    Sloviter RS, 1991: Permanently altered hippocampal structure, excitability, and inhibition after experimental status epilepticus in the rat: the “dormant basket cell” hypothesis and its possible relevance to temporal lobe epilepsy. Hippocampus; 1: 41-66.

38.    Santhakumar V, Ratzliff ADH, Jeng J, et al, 2001: Longterm hyperexcitability in the hippocampus after experimental head trauma. Ann Neurol; 50: 708-717.

39.    Prince D and Tseng G, 1993: Epileptogenesis in chronically injured cortex: in vitro studies. J Neurophysiol; 69: 1276-1291.

40.    Hoffman S, Salin P, Prince D, 1994: Chronic neocortical epileptogenesis in vitro. J Neurophysiol; 71: 1762-1773.

41.    D’Ambrosio R, Fender JS, Fairbanks JP, et al, 2005: Progression from frontal-parietal to mesialtemporal epilepsy after fluid percussion injury in the rat. Brain; 128: 174-188.


 

الملخــص العربى

 

يعرف مرض الصرع الناتج عن الاصابات المخية بأنه زملة صرعية متكررة نتيجة للاصابات الشديدة بالمخ. و يختلف العلماء فى تحديد أسباب حدوث الصرع فى هؤلاء المرضى و لكن وجد أن تكلس الفص الأذينى من أهم العوامل التى تزيد من احتمال حدوث الصرع.

وقد كان الهدف من هذا البحث هو الدراسة المستفيضة لهؤلاء المرضى من الناحية الاكلينيكية و الفسيولوجية و كذلك دراسة المخ باستخدام الرنين المغناطيسى. و تمت دراسة٢٣مريض يعانون من مرضى الصرع نتيجة للاصابات المخية ووجد أن  ١٤مريضا(٦٠٫٩٪ ) يعانى من الصرع نتيجة لاصابة القشرة المخية و أن ٨ مرضى(٣٤٫٨٪ )  يعانون الصرع نتيجة لاصابة الفص الأذينى وأن مريض واحد (٤٫٣٪)  يعانى من نوعى الصرع معا.

ولقد تم استئصال الفص الأذينى لستة من هؤلاء المرضى وثبت تحسن حالاتهم. وثبت بالدراسة الباثولوجية دلائل تكلس الفص الاذينى فى خمسة مرضى منهم.

ولهذا فان تشخيص الاصابة بتكلس الفص الأذينى من أهم الأسباب اللازمة لعلاج هؤلاء المرضى حيث أن العلاج الجراحى يساعد على تحسن حالاتهم بدرجة كبيرة.



2008 � Copyright The Egyptian Journal of Neurology,
Psychiatry and Neurosurgery. All rights reserved.

Powered By DOT IT