E. R. Flotte
MD, 2009
Please
send comments and corrections to admin@flotte2.com
General
·
Intractable: failed at least 3 meds.
Occurs in 30%
·
Remission: seizure-free off
medications for 5 or more years
·
Reviews:
Neurosurgical
Focus 9/08
·
Audio: Neurobiology of Epilepsy – During M
Antiepileptics
·
Non-enzyme inducing: Kepra (po only), Lamictal (po only), Depakote (causes bleeding?)
·
Tegretol:
causes leucopenia, hepatitis
Status
Epilepticus
·
30+ minutes seizure activity or
multiple seizures without regaining consciousness
·
Step-wise: ABCs, Thiamine/Glucose IV,
CT when stable
·
Ativan
(4mg x 2 - 0.1mg/kg, IV or rectal) & Dilantin/Fosphenytoin load (20mg/kg then 5mg/kg/d).
·
Phenobarbitol
(<100mg/min up to 20mg/kg) until seizures stop. Watch BP.
·
>30 mins:
Intubate and pentobarbital (or Versed) infusion
or general anesthesia
Hippocampal Sclerosis
·
AKA Ammon’s
Horn Sclerosis (AHS)
·
Correlated with Mesial
Temporal Sclerosis (MTS) on MRI (↑ FLAIR/T2). Hypometabolism
on PET
·
Correlated with febrile seizures
·
Seen with Timm
stain – CA1 & CA3 loss
Hypothalamic
hamartoma
·
Causes gelastic
seizures initially, then complex-partial or generalized. Responds well to
radiosurgery.
o
Gelastic
seizures: laughing fits. Other causes: hypothalamic
glioma, 3rd ventricle tumor, temporal lobe epilepsy, infantile
spasms, etc.
Tumors
·
Seizure focus is usually in the
surrounding brain, not in the tumor
·
Single or controlled seizures – do lesionectomy. Intractable seizures – lesionectomy
plus intraoperative ECOG and resection of seizure focus
Cortical
Dysplasia
·
With complete resection of epileptogenic focal cortical dysplasia, 87% have good
seizure outcome
New Onset Seizures
·
Most
recommend CT and/or MRI. Some repeat in
3-6 months.
·
EEG
performed, and if normal then sleep-deprived EEG
Preoperative Evaluation
·
CNS Course: Identifying
Candidates for Epilepsy Surgery (Kanner AM)
Phase I:
Imaging
·
MRI (FLAIR)
If nonlesional then
proceed with:
·
PET
o
Ictal
PET shows hypermetabolism in focus. Interictal PET shows hypometabolism
in focus in 70%.
o
Sensitvity
in TLE 60-90%
o
Does not correlate with histopathological changes (eg
atrophy)
·
SPECT
o
Subtraction Ictal-Interictal
SPECT
shows hypermetabolism in focus
·
Can
coregister T1 MRI with PET, SPECT, grid xray for image guidance (JN3/04)
·
Possibly
MR Spectroscopy, FMRI triggered spike detection
Scalp
EEG/Video-EEG
·
Dense-array EEG. EEG Dipole Analysis
·
Provocative: hyperventilation
Neuropsychological
Testing
·
Cognitive and functional deficits,
memory reserve
Phase
II:
Invasive
monitoring
Subdural
Grids & Strips:
·
Scalp EEG fails to localize focus in
30%. Used to confirm preoperative hypothesis.
·
Standard: 2 placed perpendicular to
temporal lobe (consider 1 medial & parallel)
·
Electrocorticography
may assist in grid placement
·
Low-amplitude high-frequency activity
at onset correlates with good surgical outcome. Electrodes recording
higher-frequency spikes are closer to focus
·
Stereoelectroencephalography:
Stereotactic placement of depth electrodes
·
Sphenoid and foramen ovale electrodes
used
Depth
Electrodes
WADA
test:
·
Injection of sodium amobarbital into
·
Speech:
arrest not enough, must have naming errors.
·
Memory: Uses:
o
1) Memory localization: less reliable
than speech. (Note hippocampal blood supply mainly
from PCA)
o
2) Focus localization: able to detect
side of eplieptogenic focus in 40-80%, incorrect in
<10%, indeterminate 20-50%. Memory improves
when given on side of focus.
Surgery
Lesionectomy
·
MRI lesion with concordant EEG: 80-90%
seizure-free at 12 months
o
Nonlesional
postop seizure-free 30-50%
Temporal
Lobectomy
·
Complications:
o
Anterior choroidal a. can loop into
choroids plexus – avoid coagulating choroid plexus
o
CNS Course: Complications
of Temporal Lobe Operations for Intractable Epilepsy (Byrne RW)
·
Anterior temporal lobectomy
(corticoamygdalohippocampectomy):
o
70-94% Engle I-II.
o
Wiebe
S NEJM 2001: Only RCT 58% (complex) seizure-free, 8% off
medicine. 10% adverse effects, 55% visual field deficits
o
Diplopia 19% (due to CN4 palsy,
resolves).
o
Extent: 4-5cm in nondominant
lobe, 3.5-4cm dominant lobe.
o
Open choroidal fissure between hippocampus and
choroids plexus (vessels run between choroids plexus & thalamus). Be aware
of basal temporal language area (N5/04)
o
“Temporal
lobotomy”: See N6/04
·
Selective Amygdalohippocampectomy:
Transsylvian approach described by Yasargil & Wieser (1982).
o
74% Engle class I-II in kids. Versus
ATL: No difference in adults, worse control in peds.
o
Pterional craniotomy. Carotid cistern
opened – visualize uncus. Sylvian
fissure opened (anterior 1/3 of insula, 2cm of M2 –
broad opening may cause vasospasm). Incision of limen
insulae just medial to superior temporal gyrus. Enter temporal horn.
o
See Wurm G N6/00 (Neuronav-guided),
·
ATL
vs SelAH: Tanriverdi T JN3/08
Multiple
Subpial Transections
·
Used to make disconnections in
eloquent cortex
·
Used alone: 15% seizure-free, 35%
improved, 50% unchanged. Combined with resection: 40%
seizure-free, 40% improved, 20% unchanged.
·
Used in Landau-Kleffner
Syndrome in which epileptic aphasia develops in previously normal child
Corpus
Callosotomy:
·
Indications:
Secondary generalized, atonic (drop attacks),
infantile hemiplegia, Rasmussens,
Lennox-gastaut.
o
Contraindicated in crossed dominance
(left-handedness with left-sided speech) – obtain WADA in all left-handed patients.
·
Most commonly anterior 2/3rds is
sectioned, interhemispheric approach
·
Complications:
o
Anterior:
¯
spontaneous speech (SMA), nondominant leg paresis
& grasping, urge incontinence (all usually temporary). Permanent speech
deficit with mixed cerebral dominance (speech & motor on opposite sides).
o
Posterior:
interhemispheric disconnection syndrome (¯ tactile sensation & vision on nondominant side, bradyphrenia,
incontinence
o
Complete:
as above + nondominant hand doesn’t perform commands
(can perform antagonistic actions)
Hemispherectomy
·
Indications: Hemiplegia
with intractable seizures: Rasmussen’s disease, cortical dysplasia, hemispheric
infarct.
·
Anatomic:
Complete resection of hemisphere. Complications: hydrocephalus, superficial siderosis.
·
Functional:
Removal of central cortex and temporal lobe, basal ganglia left intact but
disconnected from cortex, disconnection of contralateral hemisphere. 25%
reoperation for recurrent seizures.
·
Other techniques: Hemispherotomy
(JN:P2/04, JN11/04).
Vagal
Nerve Stimulator:
·
Effective on left side only (reason
unknown).
·
Efficacy:
All seizure types equally reduced. 42% reduction in seizures @ 18mo, very few seizure free. Equivalent to adding another medicine.
“50% improvement in 50% of patients”
o
Can be effective after failed
craniotomy (N11/04)
o
Cochrane Database: VNS for partial
seizures appears to be an effective and well tolerated treatment. Adverse
effects of hoarseness, cough, pain, paresthesias, and dyspnea
are associated with the treatment but appear to be reasonably well tolerated as
dropouts were rare.
·
Complications:
Coughing, voice changes, throat pain, drooling, laughing, torticollis, urinary
retention. (No cardiac changes reported.)
Extratemporal Epilepsy Surgery
·
Occipital Epilepsy: about 5%. Visual
auras/hallucinations common. Cortical malformations most common cause. Tandon
N JN2/09
·
CNS Course:
Surgery for Extra-Temporal Lobe Epilepsy (Boling W)
Intraoperative
Electrocorticography
·
Done either with strips or the “Hellraiser”
·
Under general anaesthesia
avoid benzodiazepines and babituates. Under local use
only narcotics (fentanyl) and droperidol.
Perioperative
·
Taper and discontinue AEDs 24hrs
preop. Continue AEDs 1-2 years.
Radiosurgery
·
Dose limited by optic chiasm and
brainstem. Takes >9mos to work; auras
or seizures may increase before decreasing.
May take up to 3yrs before considering retreatment.
·
One
report using 20Gy (N6/04) showed 0/5 improvement with MTS and possibly worsened
cognitive testing. Marseilles group (Regis) report 82% seizure-free and another
12% significantly improved using 25Gy. T2 signal peaks at 1yr.
·
Multicenter
trial (led by UCSF) currently ongoing.
Deep
brain stimulation:
of anterior thalamic nucleus and other areas (centromedian
nucleus, STN, hippocampus) being investigated
Text Copyright 2009
Revised 6/1/09
Please
send comments and corrections to admin@flotte2.com
Disclaimer:
This outline is complied, not original. Sources are being added
retrospectively.
It is
intended for personal educational use by students and residents. It is not intended to guide clinical decision
making. Accuracy and timeliness cannot be guaranteed.