Management of Status Epilepticus (PART 3)

ANESTHETIC CONSIDERATION IN SE:(1)
After all standard therapy has failed or has been determined to have unacceptable side effects most neurology textbooks recomend consulting an anesthesiolo
gist for administration of general anesthesia to manage SE.Under these situations what anesthetic should be given ?
Unfortunately no controlled clinical studies have been conducted to adequately answer this question.
Anesthetic drugs that have been used successfully to stop SE include barbitutates,benzodiazepine,propofol,etomidate ketamine,isoflurane,enflurane,and halothane. 
If general anesthesia is needed to manage SE a patient outcome is thought to corelate more with the underlying diseases than the success in terminating seizures.

One factor in this is the delay in beginning general anesthesia caused by the need to first try less potent drugs and the logistic problems in starting an anesthetic in an intensive care unit.
Prolonged used of high dose of barbiturate (i.e.for days or weeks) has been associated with barbiturate tolerance which may exacerbate the underlying seizure problem.
In one case report,isoflurane was used to facilitate the withdrawal of barbiturate.In addition,the neurochemical effects of such prolonged anesthetic used can result in substantial increases in brain glycogen after only a few hours. Moreover the potential for prolonged volatile anesthesia to be organotoxic or to induce tolerance is unknown.

The effects of isoflurane,thiopental,ketamine and midazo 
lam were assessed in rats undergoing mercaptopropionic acid induced or flurothyl induced seizures. 
Midazolam resulted in less damaged in the substantia nigra after seizures.
No protective effect was suggested with isoflurane or thiopental and although a protective effect was suggested with ketamine,it was statistically unsignificant.  
Unfortunately this study revealed nothing about the anes
thetic effects or seizure induce damage in the lymbic system.The ketamine data however are supported by other reports of anticonvulsant or neuroprotective of ketamine in the lymbic system during seizures in rodents. 
For the reasons previously given the therapeutic approach in choosing an anesthetic agent for SE should first involve increasing dosis of benzodiazepine or barbiturate. 
Only after this therapy failed should volatile anesthetic drugs be considered.

Volatile anesthetics have the advantage of allowing continuous realtime titration to maintain a spesific blood anticonvulsant level based on entidal gas monitoring.
In one patient the monitoring of end tidal volatile anesthetic concentration facilitated titration of the anti
convulsant anesthetic against EEG.
In another patient,isoflurane use facilitated withdrawal of a prolonged barbiturate infusion on which the patient was thought to be dependent.
Thus volatile anesthetics may have a role in closely titrating anticonvulsant therapy for seizures in situation where a general anesthesia is to use as little as possible while observing the patient closely for cessation of seizure and for hemodynamic compromise.

Such patient must be intubated and mechanical ventilated .
Optimally continuous EEG shoul be monitored through anesthetic procedure.If thiopental is used 50 to 500 mg iv can be given as a loading dose in adult,followed by an iv infusion,the infusion rate initially should be higher
and then should be decreased as indicated by EEG.
After the loading dose the infusion rate could be set initially at 500-1000 mg/h and then decreased as indicated to the lowest rate feasible.
Repeated boluses,100-500 mg,might be needed initially to mantain close titration.
If isoflurane is used it should be started at 0,2-0,3% inspired concentration (6L/min gas flow initially) and inreased over 10 to 20 min as indicated by EEG and hemodynamic tolerance.

Determining the end point to guide drug titration can be difficult. For example,burst occuring within a burst suppression pattern on EEG can resemble epileptic discharges.
The decision about seizure control and EEG interpretation should be jointly with the refering neurologist or epileptologist.
After seizures are controlled and if the source is still unclear reversible causes should be sought and corrected,
after which,anesthesia should be stopped. 
Otherwise the anesthetic dose should be decreased periodically to permit assessment. 
If seizures continue to recur on anesthetic discontinuation the next decision is wether to continue anesthesia considering the many unknown effects,bioethical concerns and logistic and economic issues of prolonged anesthetic administration compared with drawing life support. Nothing,the trend toward end tidal concentrations at which seizures recur,a real time seizure thresold,over such 
assessment may contribute to such decision.

Summary :
Status epilepticus can be defined as a condition in which prolonged or recurrent seizures or epileptic events persist for more than 30 minutes.
SE is most often seen with drug withdrawal (including antiepilepticmedication and alcohol),drug intoxication
metabolic disarray and structural lesion from stroke,tumor,
abscess and trauma.

Morbidity and mortality from SE are related to three factors 
1.the damage to the CNS caused by the acute insult 
    precipitating the SE.
2.systemic stress from repeated seizures.
3.the injury from repetitive electrical discharges with the 
   CNS.

The most important clinical factors determining outcome are etiology, and the time from onset of SE until treatment is initiated.
The worst prognosis is found in those in whom status results from a serious intracranial process such as encephalitis, 
stroke or cerebral hemorhage.The best prognosis is seen in patients without structural lesions.

Generalized convulsive status epilepticus is considered  
a neurologic emergency.
To prevent brain damage seizure must be stopped as soon as possible optimally within 30 minutes of onset.
Initial treatment of SE starts with basic life support.
In addition the management of SE is best carried out using a predetermined protocol.
After all standard therapy has failed or has been deter mined unacceptable side effects neurology textbooks recomend consulting anesthesiologist for administration of general anesthesia to manage status epilepticus.

Reference :
1.Koffke Andrew W et all: Status Epilepticus,Anesthesia for 
   Epileptic Patients ;Cottrell E James;Anesthesia and 
   Neurosurgery;4th edit,Mosby Company,St Louis, 
   London,Philadelphia,2001,pp 477-8.

2.Trop Davy,Oliver Andre:The Problem of Status Epilepti
    cus,Albin S M;Textbook of Neuroanesthesia ,The McGraw 
    Hill Company,Newyork,1997,pp.684-7.

3.Chang JW,Bleck P Thomas:Status epilepticus;Stone DJ
   Sperry JR;the Neuroanesthesia Handbook,Mosby,St louis
   Baltimore,1966.pp.452-5

4.Namara MC Brian,Boniface J Simon:The EEG in Status   
   Epilepticus;Matta F Basil;Textbook of Neuroanesthesia 
   and Critical Care,Greenwich Medical Media Ltd,London
   2000,pp.78-80.

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Management of Status Epilepticus (PART 2)

MANAGEMENT OF TONIC- CLONIC  SE:(1,2)
Time from initiation
of observation and
treatment (min)          Procedure
=================================================
        0                         Assesss cardiorespiratory function
                                   as the presence of tonic clonic sta
                                   tus is verified.If ensure of diagnosis
                                   observe one tonic-clonic attack and
                                   verify the presence of unconcious
                                   ness after the end of the tonic clo
                                   nic attack.Insert oral airway and ad
                                   minister 02,if necessary.Insert an in
                                   travenous catheter.Draw venous 
                                   blood to determine anticonvulsant
                                   levels,glucose,BUN,electrolytes,and
                                   complete blood count stat.Draw ar
                                   terial blood for stat pH,PO2,PCO2,
                                   HCO3-.Monitor respiration,blood 
                                   pressure,and electrocardiograph.
                                   If possible monitor encephalograph.


        5                         Start iv infusion with NS contain- 
                                   ing with B complex. Give a bolus    
                                   injection of 50 ml of 50% glucose.


     10                          Infuse 1 mg lorazepam over 5 mi  
                                  nutes also give fosphenytoin to a
                                  total of 17 mg/kg(level >20 mcg
                                  per ml). If hypotension develops
                                  slow infusion rate.Phenytoin 50
                                  mg/ml in propyleneglycol may be
                                  placed in a 100 ml volume control
                                  set and diluted with normal saline.     
                                  the rate of infusion should be 
                                  watched. Alternatively phenytoin  
                                  may be injected slowly by iv.


    20                         If seizures persist give 1mg lorazepam 
                                 intravenously.


    30                         If seizures persist consider pseudo 
                                seizures if no CNS infection or   
                                trauma.Otherwise, phenobarbital 20 
                                mg/kg iv no faster than 100 mg/min  
                                until seizures stop or to a loading of 20 
                                mg/kg(level > 40 mcg/ml).


  60                          If seizure continue, general anesthesia  
                               with pentobarbital is instituted.


120                          If SE continue a neurologist and 
                               anesthesiologist with expertise in SE    
                               should be consulted. Advice from a 
                               regional epilepsy center on the 
                               management of intractable SE also 
                               should be sought Push pentobarbital      
                               until seizures stop or hypotension 
                               arises.With cessation of seizures if
                               still twitching assess EEG to rule out
                               subtle SE.


Generalized convulsive SE is considered a neurologic emergency.
Treatment to secure the airway, provide oxygen,and maintain circulation must be initiated within the first fiew minutes to prevent complications such as hypoxaemia,
systemic hypertension,tachydysrythmia.


Protocols for the treatment of convulsive SE remain somewhat individualized by institution and specialty.
Recent trends have pushed aggressive treatment beginning as soon as 10 minutes into continuous convulsive state. 
In practice this intervention can rarely be effected except in hospital. One of many approaches to control SE is shown as mention above. 
This protocol reflects the current widespread use of lorazepam titrated to effect (0,03 to 0,22 mg/kg) as a subtitute for diazepam.
Parke Davis has withdrawn phenytoin(Dilantin) in favor of the prodrug fosphenytoin(Cerebyx).This a water soluble preparation with pH of 9 is converted in 15 minutes to the active drug phenytoin by tissue phosphatases. It is equally as effective as phenytoin but without complications of the propyleneglycol solvent and higher alkalinity (pH 12).
It can be delivered intramuscularly and more stable in the iv form but it can also precipitate hypotension if adminis-
tered too rapidly.


Phenobarbital as alternative drug when seizure persist after lorazepam. Physicians are using thiopental much earlier in the treatment of SE when phenobarbital is not available.
When phenytoin and phenobarbital are ineffective, a benzodiazepine is often suggested. Midazolam and diazepam have a shorter onset time than lorazepam although lorazepam generally has a longer duration of action with a lower likelihood of severe respiratory depression making it the preferred agent of some clinicians.


Diazepam is the fastest onzet (1-3 minutes) and hystoricaly was the treatment of choice because is known as the fastest  medication to terminate seizures. However because of its lipholicity diazepam has a very short duration in CNS (10-20 min). For this reason lorazepam has replaced diazepam as the drug of choice. Its onset in only slower (2-3 min) but its anticonvulsant action typically last for more than 4 hours.
Diazepam has been reported to be effective rectally, and midazolam to be effective intramuscularly and intranasally in children.
If seizures continue to be refractory to treatment with the previously noted drugs, pentobarbital  usually can be used some times thiopental.


Alternatively,volatile anesthetics can also be used. 
Intravenous valproate (depakene) is now available which being tried in refractory status. Any of the other non iv formulated AEDs can be administered via nasogastric tube.
Propofol has been used in ambulances for patient refractory to iv benzodiazepine, given in 30 mg boluses every 30 seconds until the seizure are terminated.There may be a future role for alpha 2 agonist therapy as such drugs become clinically available. 
Dexmedetomidine confered brain protection in an animal
seizure model.


Other protocol for tonic clonic generalized SE based on stage :


Stage             General measures            AEDs  Usual route of adm
Premonitory   Continued neurolo           Diazepam 10mg iv bolus                                                                
                     gic observation,dia         max 5mg/min
                     agnostic SE by ob           Lorazepam 4mg iv bolus                                       
                     serving continued           max 2mg/min                                                    
                     seizure activity of          Midazolam 5mg iv bolus                                                                                               
                     one additional sei           max 4m/min 
                     zure.                             Paraldehyde 5- 10 ml in
                                                         5- 1 ml water or oil
                                                         by rectal First line


Early              Ensure adequate           Diazepam 10mg iv bls
(0-30 mins)     cardiorespiratory          Lorazepam 4- 8mg iv
                     function,iv line,ad-             
                     minister 02,initiate      Second line
                     regular ECG,and BP      Midazolam  5-10 mg iv
                     monitoring,draw         Phenytoin 15-18 mg/kg
                     blood for emergen-     iv loading                  
                     cy investigations,in-    dose(max.               
                     tubation may be          50mg/min.
                     considered.                Paraldehyde solution 4%                                        
                                                      in saline,50-100ml/h                                                                                  
                                                      iv solution
                                                      Lidocaine:iv bolus and
                                                      short infusion.


Established     Set second iv line         First line                 
                     (large veins)admi-        Phenytoin repeate                        
                     nister thiamine 100       7mg /kg iv.                                
                     mg iv and glucose         Phenobarbital                                    
                     D50W-50 ml iv,           10-20 mg/kg iv         
                     treat acidosis,estab      loading dose                                         
                     lished etiology,admis-  (<100mg/m)
                     sion to ICU,intubation   second line        
                     ICU,intubation has to    Diazepam iv infusion       
                     be considered,EEG/     Midazolam iv infusion
                     ECG monitoring.          Paradeldehyde iv infusion


Refractory   Full anesthesia needed    First line
(>120 min)   EEG/ECG monitoring,ar-  Pentobarbital iv/infus
                   terial line,initiate pres-   Propofol iv/infusion           
                   sor therapy when requi-        
                   red monitoring of AEDs    Second line
                   levels intracranial pres-    Isoflurane inhalation      
                   sure monitoring where 
                   appropriate.


In a patient who is actively seizing a lateral position may help prevent aspiration.The choice of iv fluids should include normal saline if phenytoin will be used because phenytoin will precipitate in glucose containing solution 


After 8 mg of lorazepam if seizures have not been aborted
use of another anticonvulsant medication is indicated.
If benzodizepine are effecive in seizure control further seizures need to be prevented with a long acting anticonvulsant.


A loading dose of phenytoin is 18-20 mg /kg ,even at the recomended rate of administration (50mg/min),hypotension is the most common side effect and mandates decreasing the infusion rate.


to be continued

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Management of Status Epilepticus (PART 1)

DEFINITION:(1,2)
Status epilepticus(SE) is a condition characterized by an epileptic seizure that are so frequently repeated or so prolonged as to produce a fixed and lasting epileptic condition.
Clinically this should be interpreted as any patient who has convulsive activity for more than 30 minutes or who has a 30 minutes of repetitive seizures without rousing to full awareness and clear mental status.
The 30 minutes interval has come from recent animal and human studies that show significant neuronal damage occuring after this time.


Therefore,to prevent brain damage, seizure should be terminated as soon as possible optimally within 30 minutes of onset.
Repeated events associated with impaired conciousness should be considered to represent SE when the recurrence rate does not permit return of conciousness. Non convulsive SE can be considered "electromechanical dissociation" of the CNS where electrographic seizures have no overt clinical manifestation except a diminished mental status.


EPIDEMIOLOGY AND ETIOLOGY:(2,3)
It occurs more frequently in children and in the elderly and in patients with structural cerebral  pathology.The most commonly reported form of SE is tonic-clonic (or convulsive status),which accounts for about 40 to 50% of the total. In the USA alone,convulsive status affects more than 50.000
people each year and in a great proportion of patients the episode of SE represents the initial manifestation of their epilepsy (12 to 18%).


SE occurs relatively frequently during the neonatal period often due to metabolic infectious disorders.It is more common in mentally retarded patients probably because of diffuse cerebral abnormality. The annual incidence of SE in general population is estimated to be about 450 to 650 cases per 1000.000 persons in the USA and SE accounts for
1 to 5% of all hospital admissions for epilepsy.


The frequency of status is greatest in children and most episodes occur before 5 years age.In the first year 75% of episodes of SE were in the context of an acute illness whereas this number falls to 28% in children over 3 year of age.In older children and adults frequent causes of SE
include poor anti epileptic drugs compliance,or drug withdrawal (31%),ethanol related status(28%),drug toxicity or abuse and withdrawal(9%) CNS infections(8%),metabolic disorders(14%),cerebrovascular diseases(10%),cerebral tumor(7%),trauma(10%),fibrile SE(12%),almost exclusively found in children.No etiology is identified in about 20% of events resulting in a diagnosis of idiopathic or cryptogenic SE.


SE can be devided in stages :(1,2)
Premonitory stage    
Usually in patients with established  epilepsy. May last several hours. 


Early status 
This is the stage where(0-30 min)mechanism compensate
for the greatly enhanced metabolic activity(adaptative
or early compensated phase).                                          


Established status
Defines as status that has continued (30-120 min) for 30
minutes in spite of early stage treatment.Physiologic decompensation has begun (maladaptative or late decompensated phase).


Refractory status
Seizures continue after initiation of (>120 min) therapy
Prognosis is worse and there is a high mortality.                    


PATHOPHYSIOLOGY OF SE:(1)
It has been noted that during tonic clonic SE especially motor seizures are frequently restricted in their distribution. In addition focal or lateralized convulsive activity does not necessarily indicate that a localized structural lesion is responsible for the status.
At later stages in the sequence of events,motor activity diminishes or even disappears.Therefore,the end stage may consist of ongoing epileptiform discharges recorded by EEG without motor accompaniment or a form of electromecha-
nical discociation between motor events and brain dischar-
ges.Status epilepticus both convulsive and non convulsive can lead lifethreatening,systemic,metabolic,and physiolo-
gic disturbances.These factors usually account for the poor prognosis associated with this disorder. Status itself,how 
ever,independent of metabolic and physiologic disturbances may lead to lasting brain dysfunction and prolinged status may result in permanent neuronal damages.


Tonic clonic status is often preceded by a premonitoring stage during which seizure activity progressively increases from its habitual levels, resulting in clinical deterioration. 
In patients who have an acute  symptomatic events however,status often starts abruptly.
Physiologic changes in tonic clonic SE are usually divided into two phases with an early compensated phase I, and a late decompensated phase II. The transition from early to late phase occurs often about 30 min, that is why that 30 minutes is the time limit usually defined to represent SE.


During early compensated phase cerebral matabolism is greatly increased due to seizure activity but physiologic mechanism are sufficient to meet the metabolic demands and cerebral tissue is protected from hypoxia or other metabolic damages.The major physiologic changes are related to the increased CBF and metablism(hyperglycae
mia,lacticacidosis), autonomic activity cardiovascular changes(including hypertension, tachycardia,cardiac arrhythmia,hypersecretion and  perspiration,hyperpyrexia vomiting, and incontinence).
Later, if not controlled the status enters a phase of decompensation during which the increased cerebral metabolic demands cannot be fully met,resulting in hypoxia,failure cerebral autoregulation,hypoglycaemia
cerebral edema,resulting in rising ICP;altered systemic metabolic patterns (electrolyte disturbance,metabolic and respiratoric acidosis,multiorgan failure)


THE EEG AND SE (4)
The EEG is important tool in the management of both convulsive or non vulsive SE.While SE is a medical emergency and treatment should not be delayed,if an EEG is not available,clinical examination alone may result
in misdiagnosis of SE for two reasons :
First,psychogenic status,is a common cause of diagnostic confusion.
In one study 20% of patients presenting to an emergency department of a tertiary referral centre with intractable convulsive movements had psychogenic seizures.


Second,non convulsive status is under recognized and patients with non convulsive status are often mislabelled as being confused or postical.


In sedated patients treated with general anesthesia continuous EEG monitoring allows immediate recognition and treatment of seizures.
Seizure activity increases CMRO2 and causes excitotoxic cell damage. Continuous EEG monitoring facilitates adequate seizure control without over treatment in SE and reduces this risk of excitotoxic cell damage.
Mortality in SE increases with the duration of seizures.
It is therefore reasonable to assume that early detection of subclinical seizures in the ICU reduces morbidity and mortality.
Where continuous EEG monitoring is not available it is reasonable to obtain an EEG daily while the patient remains unconcious and to consider performing an EEG before making significant alterations to therapy.
Also continuous EEG monitoring is essential to titrate medications to burst suppression.


to be continued

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Anesthesia For Epilepsi Surgery (PART 5)

ANESTHETIC MANAGEMENT (CONCIOUS ANALGESIA):(1,2,3)
One must be assessed the ability of an individual patient to tolerate the procedure awake.There is significant associated discomfort and possibly pain which must be explained very clearly to the patient.
In ability to comprehend this (e.g.in mentally retarded  patients or children ) is a relative contra indication to awake craniotomy.
The upper airway should be assessed;a patient in whom 
difficulty with tracheal intubation is predicted may not be
suitable candidate for awake craniotomy because intuba-
tion sometimes is needed emergently even with the patient
in the akward position required for surgery.


Another factor is the anesthesiologist experience;local anesthesia with concious sedation should not be used without proper training.
The patient must be concious and alert while electrical stimulation is being carried out. On the day of surgery only steroid are given prior to admission to the operating suite Anxiety should be dealt with without use of pharmalogic means. Unneccessary verbal comments and noise should be kept to a minimum.The temperature in the room should be comfortable for the patient. Anesthesia equipment and medication for control of a seizure episode should be at hand. After transfer to the table patient's position them selves on the operating table so that they are as comfortable as possible.
Although they are need to be restrained, a small amount of movement should be allowed to maintain comfort throughout  this long procedure. 


The lateral position is preferred because freedom of the airway is easier to maintain.
Careful attention is paid to the protection of pressure points which should be padded.
At this time an iv lines is secured at once,an a saline infusion started at a low flowrate which will be maintained through the procedure.
To limit the discomfort of a full bladder the drip rate is a adjusted to 1 ml/kg per hour. An indwelling urinary catheter is inserted although some prefer to limit the amount of iv fluids and withhold the catheter.
Oxygen is delivered through nasal prongs while capnography can be performed via an 18-20 g Teflon catheter in one nasal prong.


Before surgical incision local anesthesia is injected subcutaneously into the scalp.Some patients dont require futher sedation at incision.
However,the painful parts of the procedure should be anticipated. They mostly occur early during surgical exposure.Using a neurolept analgesia technique has demonstrated that adequate ventilation could be maintain in such conditions.
An infusion of propofol (8mg/ml)mix with alfentanil
(50 mcg/ml) and lidocaine (2 t0 4mg/ml)is begun at 
100 to 200mcg/kg/min,reading the propofol dosage 
(alfentanil is simultaneously administered at a ratio
of 1:160 (i.e.when propofol is 80 mcg/kg,alfentanil
is 0,5 mcg/kg/min).
This dose is occasionally supplemented with bolus doses through the infusion pump to achieve sedation.
The patient has little or no response to these manouvers yet ventilated and oxygenated well.
The infusion is typically decreased to 50 to 80 mcg per kg per min propofol while the patient is unstimulated.


Trap has described in detail about concious sedation analgesia. Before the surgeon starts skin preparation and aplication of the drapes fentanyl 0,5-0,75 mcg/kg and dropridol 0,15 mg/kg are given intravenously.Immediately before the episodes the patients need reassurance and
possibly,supplementation of sedation analgesia with fentanyl 25 to 100 mcg/kg per min,titrated to maintain a comfortable level of analgesia and respiratory rate of 12 breaths/min.


More recently Rosa et all and Silbelger et all have reported similar view using propofol. A bolus of propofol (0,3 to 1 mg/kg) is used followed by a continuous infusion at 75 to 100 mcg/kg per min.


In case of insufficient sedation,supplementary boluses at 0,5 mg/kg are added and the infusion rate is gradually increased to 125 mcg/kg/min.
Small increments of fentanyl (1 mcg/kg) are injected at 3 min intervals. A minute amount of dropridol (0,015 mcg/kg) is given for prevention of nausea and vomiting. 
An appropriate level of sedation is achieved on the average within 10 minutes.


Most patients tolerate the procedure especially when the anesthesiologist has been able to established good communication and is able to predict and control painful stimulation. 
Possible complication of awake craniotomy include rest-
lessness and agitation, with a good rapport with the patient in the preoperative period and at times a change in the level of sedation will resolve this complications.


A three pin Mayfield head holder is applied after infiltration of the sites of pin placement with local anesthesia.
Not only are patients able to tolerate the head holder well, but the head remains secure even during seizure.
Craniectomy and dural stimulation sometimes require additional bolus dosing of iv anesthesia.
A fairly large craniotomy incision is usually needed, extending down to the zygoma for maximum visualization of the tip of the temporal lobe and the inferior temporal circumvolution.
Local anesthesia is achieved with a mixture of bupivacaine 0,25% and lidocaine 1,0% both with 1:200.000 epinephrine.
Optimal points of injection for scalp anesthesia include the origin of the greater and lesser occipital nerves below superior nuchal line,the auriculo temporal nerve just in front of the ear and the supraorbital nerve above the eye brow. Finally an injection made into the subctaneous tissue of the anterior temporal region will join the zygomatic are with the lateral part of the superior orbital ridge.
To optimize the homeostasis the injections must be made into the subcutaneous tissue of the scalp and not exclusively into the subgaleal region.
At least 10 to 15 ml of solution must be injected into the deep part of the temporalis muscle extending from the supraorbital ridge through to the posterior part of the zygoma.
Intracranial structures that are painful to touch and traction include the dura and meningeal vessels.
Once the dura is exposed pain sensation is blocked by intradural injection of small amounts of local anesthetic on each side of the middle meningeal artery and its mayor branches.
The patients are usually awakened before opening the dura.
The propol infusion was titrated down from its original rate so as  to maintain a grade 3 to 4 sedation score is now set to zero.


Sedation scores according Wilson et al :
Grades                              Degree of sedation
    1.                             Fully awake and oriented
    2.                             Drowsy
    3.                             Eyes closeed but rousable to   
                                    command
    4.                             Eyes closed but rousable to mild     
                                    physical stimulation.
    5.                             Eyes closed and unrousable to mild 
                                    physical stimulation.


Patients wake up and within 5 to 10 minutes, are able to speak and answer commands.
At least 30 minutes before ECoG the propofol is stopped although some anesthesiologist will wait until tha last
few minutes.
The patients usually awaken abruptly and demonstrated no lingering confusion.


Spontaneous seizures sometimes have occured in severe epileptic asleep with propofol,methohexital may be 
needed to control the seizure.
With the patient awake and the brain exposed direct cortical readings are performed.The goal of ECoG recording is to delineate the full extent of interictal epileptiform activity, Draps must be placed in a way that allows access to the face and also allows the anesthesiologist to converse with the patient.
Face and arm must be clearly visible and permit monitoring the peripheral response to cortical stimulation.


Following recording of spontaneous electrical activity the exposed cortex is stimulated to map out important neurologic areas.
Depending on the degree of surgical confidence and on the location of the planned resection only topographyc landmarks are used for identification of the central sulcus and the central area.
Stimulation of motor cortex results involuntary movements of the face and extrimities.The area representing the face and the mouth is at the inferior portion of the precentral gyrus (motor cortex) just above temporal lobe.
Although the patient is usually aware of the involuntary movements direct observation is important.


Stimulation of the post central gyrus (sensory cortex) may result in paresthesia. Tingling or prickly sensation in tongue,gums,face and extrimities. It is important to instruct the patient prior to the procedure to report any unusual feeling.
The patient may also be asked to perform certain task during stimulation.Usually the effect of stimulation on speech is evaluated during counting or reciting such familiar concepts as days of the week or months of the year.


Stimulation of speech area is signaled by an abrupt interuption in speech, which will resume immediately upon cessation of the stimulation. If localization of the seizure focus is still in doubt after cortical recording depth electrodes are positioned toward deeper structures in the vicinity of the amygdala and the hypocampus.Spontaneous activity is again recorded followed by stimulation.


Activation of epileptic activity is attempted by adminis-
tration of a 0,5mg/kg of methohexital and its effect on the ECoG is observed.
Resection is initiated after the epileptogenic focus is identified and functional areas of the exposed brain have been mapped out.


To relief anxiety and pain with unwanted side effects for instance tachycardia and hypertension,movements,the profol infusion is reinitiated and additional amounts of fentanyl administered especially when there is traction or coagulation blood vessels.
The continuous infusion of propofol during resection of an epileptogenic focus under local anesthesia has considerably facilitated the anesthetic management of procedure. If the propofol is not available,neurolept analgesia has proved to be a safe technique. Intra operative nausea and vomiting is rare with the use of propofol.
However the potential pharmacologic interference with the intraoperative ECoG tracings recently has been demonstra-
ted such as beta activity triggered by propofol.
Seizure control is occasionally necessary;methohexital (1 mg/kg) or benzodiazepine (midazolam) is effective.
At the completion of the surgery all patients are taken to the recovery room awake and responsive.


MONITORING:(3)
Non invasive monitoring is used as a rule for concious sedation analgesia. The oxygenation status of the patient is monitored with a pulse oximeter. Et CO2 is continuously sampled at the nose and the information is utilized essentially as a means to monitor respiration rate.
Non invasive blood pressure measurements are displayed every 5 minutes.
ECG tracing displayed continuously on the video screen to monitor hemodynamic parameter.
Blood loss is estimated and corrected when it approaches 20% of circulating blood volume.


COMPLICATION OF EPILEPSY SURGERY:(1,3)
General complication include acute post operative hemor-
rhage,infection and hydrocephalus.
Spesific complication may be subdivided in transient and permanent deficits which relate directly to the nature the original lesion,the location of the epileptogenic focus and the extent of the surgical removal.
During concious sedative  analgesia the intraoperative problems included convulsions,nausea and vomiting,exces-
sive sedation,tight brain and local anesrthetic toxicity.   
However as stated by Girvin,the most frequent and promi-
nent risk of epilepsy surgery is the failure to achieve the goal of the investigation and treatment.


SUMMARY :
Epilepsy is a common disease that has major effect both on individuals carrying the diagnosis and society as a whole.
Approximately 10% of  the epilepsy patient have medically intractable seizure resulting in progressive neurologic impairment.
These patients may benefit from surgical therapy which should be carried out in a medical center with well organized program consisting neurologist,neurosurgeon and anesthesiologist and experienced electro encephlographer necessary to perform prolonged electroencephaloraphy
studies and resultant neurologic procedures.
One of the most important toll for the investigation of seizures and epilepsy is the EEG.
One of the more important of these concerns is the most appropriate anesthetic approach for surgery that's wether to use general anesthesia or concious analgesia with local anesthesia.
Other disputed area include the optimal anesthetic technique, wether anesthetic induced seizure activity can cause brain damage and the appropriateness of inducing a seizure with an anesthetic drug during ECoG.
Concious sedation analgesia remains a useful technique when approaching an epiloptogenic lesion in crucial zones such as the motor and speech areas.When preoperative anatomic and electrophysiologic studies have clearly demarcated the epileptogenic zone in the non crucial area,general anesthesia can be used quite satisfactorily.


REFERENCES :
1.Johnson O Joel: Anesthesia for epilepsy surgery;Stone 
   JD,Sperry JR:The Neuroanesthesia Handbook,Mosby Year 
   Book Company,Newyork inc,1989,pp 201-9.


2.Kofke Andrew W,Tempelhoff Rene,Dasheeff Richard:
   Anesthesia for epileptic patients and for epilepsy 
   surgery;Cottrel E James,Smith S David: Anesthesia and 
   Neurosurgery ;4th edition,Mosby Company,St Louis
   London,Philadelphia, Sydney,Toronto.2001 pp.474-90


3.Dure S Lean :Seizures and epilepsy;Albin S Maurice,
   Textbook of Neuroanesthesia with Neurosurgical  and 
   Neuroscience perspectives; McGraw Hill,USA,1997.
   pp.613-17


4.Stoelting K Robert,Dierdarf F Stephes: Epilepsy Aneshesia
   and coexisting disease,3rd edit,Churchill Livingstone
   Newyork,Melbourne,1993,pp.232-4.


5.Mc Namara Brian,& Boniface J Simon:Electrophysiological 
   Monitoring of The Central Nervous System; Matta F Basil,
   Menon K David,Turner M John:Textbook of Neuroanesthe
   sia and Critical Care,Greenwich Medical Media,1st edition
   London,2000.pp.69-83


Ltd.,London,2000.pp.69-76.

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