The document provides information on epilepsy classification, diagnosis, and treatment. It discusses:
1. The 2017 ILAE classification system for seizures, which categorizes seizures as focal or generalized based on onset and includes motor and non-motor seizure types.
2. Factors that can help diagnose epilepsy including EEG, MRI/CT scans, and seizure description/videos. An EEG is most valuable within 24 hours of a seizure.
3. Treatment considerations like using broad-spectrum anti-epileptic drugs (AEDs) like levetiracetam as first-line due to few drug interactions and cognitive side effects. AED treatment should begin after the first seizure in adults.
Author: Danielle Cassidy, Pharm.D., BCPS
Audience: Third year pharmacy students at University of Colorado School of Pharmacy
Background: describes common causes of seizures, differentiates dosing of antiepileptic drugs in pediatrics vs. adults, common risk factors associated with febrile seizures, treatment of febrile seizures, treatment of status epilepticus (inpatient & outpatient), & how to dispense/counsel parents on the administration of Diastat.
Author: Danielle Cassidy, Pharm.D., BCPS
Audience: Third year pharmacy students at University of Colorado School of Pharmacy
Background: describes common causes of seizures, differentiates dosing of antiepileptic drugs in pediatrics vs. adults, common risk factors associated with febrile seizures, treatment of febrile seizures, treatment of status epilepticus (inpatient & outpatient), & how to dispense/counsel parents on the administration of Diastat.
On the occasion of National Epilepsy Day 2014, Dr. V Natarajan gave a talk titled "New Trends in Epilepsy Management" at the Epilepsy Knowledge Forum in Chennai organised by Neurokrish & Trimed and Sponsored Medall.
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On the occasion of National Epilepsy Day 2014, Dr. V Natarajan gave a talk titled "New Trends in Epilepsy Management" at the Epilepsy Knowledge Forum in Chennai organised by Neurokrish & Trimed and Sponsored Medall.
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Abstract: Epilepsy is a serious and common chronic neurological disorder characterized by recurrent seizures, which are caused by abnormal synchronized neuronal disorders. It is a relatively common condition (up to 2% of the population) which can affect anyone at any age. Epilepsy can be controlled in a number of ways. The most common way to treat epilepsy is with anti-epileptic drugs. These AEDs can control but not cure epilepsy. Surgery can also be a possible treatment. Curative epilepsy surgery can only be performed in patients in whom the epileptogenic focus can be localized and does not overlap with eloquent brain areas. In the other patients with bilateral or multiple epileptogenic foci, with epilepsy onset in eloquent areas, or with no identifiable epileptogenic focus, treatments such as ketogenic diet, vagus nerve stimulation can be offered. VNS is an available procedure of which the mechanism of action is not understood, but with established efficacy for refractory epilepsy and low incidence of side-effects. The ketogenic diet is a high-fat, moderate protein, low carbohydrate diet used to treat intractable epilepsy, primary in the pediatric population. Hippocampal Deep Brain Stimulation has been used to treat patients with refractory epilepsy. Complementary and Alternative Medicine for epilepsy such as apuncture, aromatherapy, yoga etc may be used for lessening seizures, for alleviating related symptoms and for reducing side effects. Gene therapy aims to utilize viral and non-viral vectors in the delivery of DNA to target areas for the treatment of patients before their disease progresses. Gene therapy has delivered promising results in animal trials and pre-clinical settings and can be used for neurological disorders such as epilepsy.
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Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
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7. 7
1. Epilepsy with brain dysfunction
(2ry) MOSTLY RESISTANT
as GDD, CP, postmeningitis ,etc
Prevalence up to 30-50%
Often intractable
Often mixed
Frequency and severity are proportion of
degree of the disorder
CT/MRI
Treatment is challenging
BROAD SPECTRUM AED
POLYTHERAPY
NEUROPROTECTIVE
ANTIEPILEPTOGENIC
10. 10
5- 10% of normal persons have
abnormal EEG
10% of non epileptic persons have
abnormal EEG
Migraine
Anxiety
Depression
FC
BHS
Tension child
ADHD
11. 11
Up to 30% of epileptic patients with
normal EEG
30-60 minutes
Sleep deprivation,
HV,
IPS
Generalized slowing
activity
12. 12
One normal EEG does not exclude epilepsy
A second EEG performed during sleep in
sleep deprived patients reveals epileptiform
abnormalities in half of patients whose first
EEG was normal
13. 13
3. When EEG is of valuable?
Same day
After 2 weeks from the attack
After 4 weeks from the attack
14. 14
EEG is most valuable within 24 h of the
seizure
Arch Neurol. 2010 Jul 12.
Optimizing Electroencephalographic Studies for
Epilepsy Diagnosis in Children With New-Onset Seizures.
17. Some Seizure Onsets can be Focal or Generalized
Focal Onset Generalized Onset
atonic
clonic
epileptic spasms
myoclonic
tonic
tonic-clonic
atonic
clonic
epileptic spasms
myoclonic
tonic
tonic-clonic
18. Classification according to EEG
findings. ILAE 1981
Generalized Focal
Both Cerebral
Hemispheres
Only a part of a
hemisphere
Loss of Consciousness No loss of
consciousness
Treated by Valproate Treated by
Carbamazipine
MRI
Focal with
2ry G
19. Motor
Tonic-clonic
Other motor
Non-Motor (Absence)
Unknown Onset
Motor
Non-Motor
focal to bilateral tonic-clonic
Generalized OnsetFocal Onset
Motor
Tonic-clonic
Other motor
Non-Motor
ILAE 2017 Classification of Seizure Types Basic Version 1
Unclassified 2
1 Definitions, other seizure types and descriptors are listed in the accompanying paper & glossary of terms
2 Due to inadequate information or inability to place in other categories
Aware
Impaired
Awareness
From Fisher et al. Instruction manual for the ILAE 2017
operational classification of seizure types. Epilepsia doi:
10.1111/epi.13671
20. Motor
tonic-clonic
clonic
tonic
myoclonic
myoclonic-tonic-clonic
myoclonic-atonic
atonic
epileptic spasms2
Non-Motor (absence)
typical
atypical
myoclonic
eyelid myoclonia
Unknown Onset
Motor Onset
automatisms
atonic2
clonic
epileptic spasms2
hyperkinetic
myoclonic
tonic
Non-Motor Onset
autonomic
behavior arrest
cognitive
emotional
sensory
focal to bilateral tonic-clonic
Generalized OnsetFocal Onset
Aware
Impaired
Awareness
Motor
tonic-clonic
epileptic spasms
Non-Motor
behavior arrest
ILAE 2017 Classification of Seizure Types Expanded Version1
Unclassified3
1 Definitions, other seizure types and descriptors are listed in the
accompanying paper and glossary of terms.
2 These could be focal or generalized, with or without alteration of awareness
3 Due to inadequate information or inability to place in other categories
From Fisher et al. Instruction manual for the ILAE 2017
operational classification of seizure types. Epilepsia doi:
23. 23
Brain CT/MRI
1. every patient with a newly diagnosed focal
epilepsy should undergo CT/MRI
2. RESISTANT EPILEPSY
3. SECONDARY EPILEPSY
24. 24
Identify structural causes of epilepsy as
cortical malformation, traumatic brain injury,
brain cyst or tumour, and cerebrovascular
disease
Repeat MRI in case of drug-resistant epilepsy
as a first step to explore surgical options
25. WHEN U START AED ?
AFTER ONE SEIZURE
AFTER TWO SEIZURES IN SAME DAY
AFTER TWO SEIZURES WITH ONE DAY
APART
AFTER THREE SEIZURES SAME DAY
AFTER THREE SEIZURES A DAY APART
25
26. In adults , after one attack
Because of
• Driving
• Employability
27. 27
Practical points
Aim : to stop attacks
Monotherapy avoid polytherapy
Treat fits but not blood serum level
Start with minimal dose and increase gradually
Stop if side effects appeared
Don’t ask for SGOT ..ONLY If suspect hepatic
dysfunction so ask for SGPT
Don’t withdraw AED suddenly but gradually
Treatment
29. 29
Principles of drug usage
Monotherapy
Least dosage
First choice
Compliance: cost, dosage division, formula
Least S/E especially cognitive functions
30. 30
Impact of Dosing Frequency
on Compliance
Cramer JA, et al. JAMA. 1989;261:3273-3277.
20
40
60
80
100
Patients(%)
QD BID TID QID
87%
81%
77%
39%
EpilepsyIn epilepsy patients
Higher compliance rates
are associated with once-
or twice daily dosing
Noncompliance with AEDs
is a major factor in:
Breakthrough seizures
Recurrence of seizures
N=24 patients followed for 2 to 37 weeks.
increase till max ( or S/E) before changing to other AED
31. 31
5. WHEN TO Withdrawal of
AED?
After 2 years of last attack REGARDELESS
EEG ?
withdraw over 3 months
Same period of AED if it will recur
?? 2ry epilepsy
32. 32
AEDs
First-generation AEDs include: phenobarbital,
phenytoin, carbamazepine, valproic acid,
clonazepam, and primidone
Since early 1990’s: lamotrigine, gabapentin,
oxcarbazepine, levetiracetam, divalproex
sodium, topiramate, zonisamide, vigabatrin,
tiagabine, and felbamate
The latest AEDs to become available are
pregabalin, lacosimide, and rufinimide.
37. Levetiracetam
Dose
Children: weight/10 ( ml) twice
,MAXIMUM x3
{20 – 60 mg/kg/d}
Therapeutic plasma concentration
Not relevant
Indicated for
NEARLY ALL
Comments
No drug interactions described
38. Forms:
Oral: (100mg/1ml)
250, 500, 1000 mg tablets
AMPOULES
Blood Follow up: NONE
Onset of action 24-48HRS
Monotherapy or Add on, no drug
interaction
(Levetiracetam)
39. January 26, 2012
FDA approval for levetiracetam
in infants and children from one
month of age with partial onset
seizures
40. Quick onset of action
No cognitive S/E
Bind specific CNS areas only as hippocampus
Not liver metabolism, not protein binding so not
interact with other AED
The starting dose of 20mg/kg/day was increased
at intervals of 1 week by 10mg/kg/day,
if necessary, up to a maximum dose of 60mg/kg/day.
Steady state: 8hX5
41. Quick onset of action
No cognitive S/E
Not liver metabolism, not protein binding so not
interact with other AED
Steady state: 8hX5
43. 43
Levetiracetam LVT
Bind specific CNS areas only as hypocampus
Pathogenesis:
SV2A* binding site so prevent vesicles
release of its stimulant contents
Not liver metabolism, not protein binding so
not interact with other AED
44. Advantages
Broad spectrum
Not interfere with other AEDs
Same day effect
Prophylaxis after brain operation
Prophylaxis after HIE
Anti-epileptogenic
Neuroprotective
No cognitive S/E
44
45. NEUROPROTECTIVE LVT
IN HIE / NEWBORN /PREMATURE
POST BRAIN SURGICAL TREATMENT
POST I C HGE
NON CLINICAL SEIZURES AS AUTISM
45
70. Partial Seizures (start in one place)
Simple (no loss of consciousness of memory)
Sensory
Motor
Sensory-Motor
Psychic (abnormal thoughts or perceptions)
Autonomic (heat, nausea, flushing, etc.)
Complex (consciousness or memory impaired)
With or without aura (warning)
With or without automatisms
Secondarily generalized
Generalized Seizures (apparent start over wide areas of brain)
Absence (petit mal)
Tonic-clonic (grand mal)
Atonic (drop seizures)
Myoclonic
Other
Unclassifiable seizures
Dreifuss et al. Proposal for revised clinical and
electroencephalographic classification of epileptic
seizures. From the Commission on Classification
and Terminology of the International League
Against Epilepsy. Epilepsia. 1981;22:489-501.
INTERNATIONAL CLASSIFICATION OF SEIZURES 1981
71. New generalized seizures
absence with eyelid myoclonia
epileptic spasms (infantile spasms)
myoclonic-atonic (e.g., Doose)
myoclonic-tonic-clonic (e.g., JME)
New combined seizures
(focal to bilateral tonic-clonic)
Non-Motor
behavior arrest
(autonomic)
(cognitive)
emotional
(sensory)
Motor
atonic
automatisms
clonic
epileptic spasms
hyperkinetic
myoclonic
tonic
New Focal Seizures
(parentheses) indicates prior existence, but renaming
The 2017 ILAE Classification of Seizures
72. O L D T E R M N E W T E R M
Unconscious (still used, not in name) Impaired awareness (surrogate)
Partial Focal
Simple partial Focal aware
Complex partial Focal impaired awareness
Dyscognitive (word discontinued) Focal impaired awareness
Psychic Cognitive
Secondarily generalized tonic-clonic Focal to bilateral tonic-clonic
Arrest, freeze, pause, interruption Behavior arrest
Wording Changes
73. Supportive Information
Seizures are usually classified by symptoms and signs
But supportive information may be helpful, when available:
• Videos brought in by family
• EEG patterns
• Lesions detected by neuroimaging
• Laboratory results such as detection of anti-neuronal ANTIBODIES,
Blood prolactin within 10-15 min
• Gene mutations
• Diagnosis of an epilepsy syndrome diagnosis