Surgical Treatment of Seizure Disorders

In general, imaging studies are used to determine if a structural lesion (i.e., brain tumor, vascular malformation, or developmental anomaly) is present. If a lesion is identified and seizures can be observed on EEG arising from the same geographic location, the seizures are designated as 'lesional' and surgery should be performed. These patients have a high likelihood of improvement in their seizures. For those patients in whom no lesion can be identified, surgical procedures are classified into three categories: ablative, disconnection and neurostimulation.

Ablative/Resective Hemispherectomy

A variety of hemispherectomy procedures have been developed, but the selection criteria are virtually the same: a hemiplegic patient with intractable seizures arising from the damaged hemisphere. This clinical picture is seen with Rasmussen's encephalitis, infantile hemiplegia seizure syndrome and Sturge-Weber syndrome. Injection of intracarotid amytal into the affected hemisphere with cessation of ictal or interictal spike activity provides preoperative evidence that seizure activity is confined to that hemisphere. Several types of hemispherectomies have been described. The classic, or anatomical, hemispherectomy involves a wide craniotomy (often performed using an osteoplastic flap) and dural opening, with the following steps:

1. Ligation of the middle, anterior and posterior cerebral arteries. The middle cerebral artery is exposed subfrontally and through the Sylvian fissure and clipped distal to the origin of deep perforating arteries. The olfactory tract is divided. The anterior cerebral artery is ligated via an interhemispheric exposure just distal to the genu of the corpus callosum. The temporal lobe is elevated and the posterior cerebral artery is ligated where it crosses the tentorium and passes onto the medial surface of the occipital lobe.

2. The lateral ventricle is entered through the interhemispheric fissure and the corpus callosum. Dissection is performed through the angle made by the corpus callosum and the lateral ventricle. The circular sulcus of the insula is reached laterally. As much of the anterior to posterior extent of the circular sulcus of the insula as possible is dissected in this manner.

3. The trigone of the lateral ventricle is entered posteriorly through the in-terhemispheric fissure by incising the lingual gyrus and underlying white matter. The collateral eminance is incised through the floor of the temporal horn. This incision meets the collateral sulcus as it is carried inferiorly. This maneuver is carried anteriorly until the temporal pole is reached.

4. The bulk of the hemisphere remains attached to the subcortical regions only along the mesial and inferior regions of the frontal lobe. These regions are carefully separated with subpial dissection using a suction and bipolar cautery.

5. Finally, the remaining medial temporal structures, the hippocampus and the amygdala are removed.

Late complications from anatomic hemispherectomy include superficial cerebral siderosis and a high rate of subdural hemorrhage into the created space. Subsequent long-term outcome studies have suggested that classic hemispherectomy may be performed with a late complication rate much lower than previously described when meticulous hemostasis is achieved and the surgical cavity is drained for several days postoperatively.

The modified functional hemispherectomy involves division of the posterior frontal and anterior parietal lobes with their opercula, the insular cortex and the anterior temporal lobe. This leaves the anterior frontal lobe and the occipital lobe with an intact blood supply, but with all projection fibers to the brainstem and spinal cord divided. A corpus callosotomy divides the remaining commisural. It is believed that the reduced volume of space also reduces the rate of hemorrhage. Other modifications include hemidecortication and peri-insular hemispherotomy.

Temporal Lobectomy

Traditionally, temporal lobectomy has been withheld until patients have reached their late teens or early 20s. However, evidence exists showing that deferral of surgery subjects a child to possible intellectual deterioration and behavioral disturbance. Children operated on after puberty demonstrate reduced rates of good outcomes. In general, patients with complex partial seizures, characteristic imaging findings of hippocampal sclerosis, and appropriate EEG findings have an excellent chance of seizure control (greater than 90%) following temporal lobectomy.

Table 8. Commonly used anti-epileptic drugs and their features

Drug

Mechanism

Indications Dose

Oral Levels and

Absorption Metabolism

Protein Adverse Binding Effects

Interactions with other AEDs

Phenytoin (Dilantin®)

Phénobarbital

Blocks sodium channels

Carbamazepine (Tegretol®)

Blocks sodium channels

1 ° and 2° partial 5-8 and generalized mg/kg/day

Barbiturate: potentiates GABA-A inhibition seizures by increasing duration of chloride channel opening

Slow but nearly complete

2° generalized 10-20

seizures, also 1 ° mg/kg/day partial and generalized

1 ° and 2° partial 0.5-3 and generalized mg/kg/day

Slow, but nearly complete

Trough concentration: 10-20 mcg/mL; metabolized by liver

Erratic oral absorption

Trough concentration: 4-12 mcg/mL; metabolized in liver by p450 induction, so steady state levels may drop

Trough concentration: 15-35 mcg/mL

Nystagmus, diplopia, ataxia, behavioral changes, rash, hirsutism Gingival hyper-lasia is common children and adolescents

Aplastic anemia, hepatotoxicity, neutropenia diplopia, ataxia, nausea, vomiting

Highly protein bound drugs may displace phenytoin from albumin binding sites Phenytoin is a cyp450 inducer

Macrolide antibiotics may saturate P450, increase levels of carbamazepine Carbmazepine is a cyp450 inducer

Sedating, Caution with other hepatotoxicity, CNS depressants hematological Phénobarbital is a effects, vertigo cyp450 inducer continued on next page

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