Epilepsy & Seizures
Comprehensive integrative medicine approach for lasting healing and complete recovery
Understanding Epilepsy & Seizures
Epilepsy is a chronic neurological disorder characterized by a predisposition to generate recurrent seizures due to abnormal, excessive, or synchronous neuronal activity in the brain. It affects approximately 50 million people worldwide and is defined by the International League Against Epilepsy (ILAE) as a disease of the brain defined by any of the following conditions: (1) at least two unprovoked (or reflex) seizures occurring more than 24 hours apart; (2) one unprovoked (or reflex) seizure and a probability of further seizures similar to the general recurrence risk after two unprovoked seizures (approximately 75% or greater); or (3) diagnosis of an epilepsy syndrome. Seizures are classified as focal (originating within networks limited to one hemisphere) or generalized (involving both hemispheres from onset), with numerous subtypes within each category.
Recognizing Epilepsy & Seizures
Common symptoms and warning signs to look for
Recurrent, unprovoked seizures of any type
Sudden, uncontrolled muscle jerking (tonic-clonic seizures)
Brief loss of awareness or consciousness (absence seizures)
Temporary confusion and disorientation following seizures (postictal state)
Loss of muscle control during episodes (atonic or drop attacks)
What a Healthy System Looks Like
In a healthy individual, the brain maintains precise electrochemical balance through inhibitory GABAergic neurons and excitatory glutamatergic neurons working in concert. The neuronal membrane potential is maintained at approximately -70mV through active ion channel function (sodium, potassium, calcium, chloride). Synaptic transmission is finely regulated with appropriate neurotransmitter release and receptor binding. The blood-brain barrier protects the CNS from circulating toxins and pathogens. Cerebral autoregulation maintains consistent blood flow despite systemic blood pressure changes. Glial cells (astrocytes and oligodendrocytes) support neuronal function through nutrient transport, myelin formation, and metabolic support. The brain's intrinsic anticonvulsant mechanisms—including adenosine release, endogenous cannabinoid signaling, and hyperpolarizing potassium currents—prevent pathological synchronization of neuronal firing.
How the Condition Develops
Understanding the biological mechanisms
Epilepsy results from an imbalance between excitatory and inhibitory neurotransmission in the brain, leading to hyperexcitability and hypersynchronization of neuronal networks. Key mechanisms include: (1) Ion Channel Dysfunction - mutations in voltage-gated sodium channels (SCN1A, SCN2A), potassium channels (KCNQ2, KCNQ3), and calcium channels (CACNA1A) cause abnormal neuronal firing patterns; (2) GABAergic Inhibition Failure - reduced GABA synthesis (via GAD enzyme deficiency), impaired GABA receptor function, or decreased benzodiazepine binding sites diminish inhibitory signaling; (3) Glutamatergic Excitotoxicity - excessive NMDA/AMPA receptor activation, particularly from mesial temporal sclerosis, leads to calcium influx and neuronal damage; (4) Cortical Malformations - focal cortical dysplasia, heterotopias, and cortical tubers create abnormal neuronal circuits prone to seizures; (5) Neuroinflammation - activated microglia release pro-inflammatory cytokines (IL-1beta, IL-6, TNF-alpha) that lower seizure thresholds; (6) Mitochondrial Dysfunction - impaired ATP production affects ion pump function and promotes oxidative stress; (7) Astrocyte Dysfunction - failure to clear extracellular glutamate leads to excitotoxicity; (8) Network Hyperexcitability - structural lesions, altered connectivity, and impaired inhibitory interneurons create self-sustaining seizure networks.
Key Laboratory Markers
Important values for diagnosis and monitoring
| Test | Normal Range | Optimal | Significance |
|---|---|---|---|
| EEG (Electroencephalogram) | Normal background rhythms, no epileptiform discharges | Normal with well-organized alpha rhythm 8-12 Hz | Detects epileptiform discharges (spikes, sharp waves), slowing, and seizure patterns; gold standard for epilepsy diagnosis |
| Anti-NMDA Receptor Antibodies | Negative | Negative | Autoimmune encephalitis marker; presence indicates antibody-mediated epilepsy |
| GAD65 Antibodies (Glutamic Acid Decarboxylase) | <5 IU/mL | Negative | Elevated in autoimmune epilepsy and stiff-person syndrome; indicates immune-mediated seizure disorder |
| VGKC Complex Antibodies (LGI1, Caspr2) | <1:10 titer | Negative | LGI1 antibodies cause limbic encephalitis with seizures; Caspr2 associated with neuromyotonia and seizures |
| Thyroid Antibodies (TPO, Tg) | <35 IU/mL (TPO) | <20 IU/mL | Autoimmune thyroid disease can co-occur with epilepsy; Hashimoto's encephalopathy presents with seizures |
| Vitamin B6 (Pyridoxine) | 5-50 mcg/L | 20-50 mcg/L | B6 deficiency can cause refractory seizures; required for GABA synthesis |
| Magnesium (Serum) | 1.5-2.5 mg/dL | 2.0-2.5 mg/dL | Hypomagnesemia lowers seizure threshold; essential for NMDA receptor regulation |
| Homocysteine | 5-15 micromol/L | <8 micromol/L | Elevated homocysteine associated with epilepsy; affects neuronal excitability and methylation |
| CBC with Differential | WBC 4,000-11,000/mcL | WBC 5,000-8,000/mcL | Elevated WBC may indicate infection-triggered seizures; eosinophilia suggests parasitic infection |
| Folate (Serum) | 3-20 ng/mL | 10-20 ng/mL | Folate deficiency associated with seizures; required for DNA synthesis and methylation |
| Prolactin | M: 2-18 ng/mL, F: 2-25 ng/mL | M: <10, F: <15 ng/mL | Post-ictal prolactin elevation can help distinguish generalized tonic-clonic from psychogenic non-epileptic seizures |
| MRI Brain with Epilepsy Protocol | No structural abnormalities | Normal with hippocampal symmetry | Identifies structural causes: mesial temporal sclerosis, cortical dysplasia, tumors, vascular malformations, scars |
Root Causes We Address
The underlying factors contributing to your condition
{"cause":"Genetic Mutations","contribution":"40%","assessment":"Family history; genetic testing for SCN1A, SCN2A, KCNQ2, DEPDC5, PCDH19, and epilepsy gene panels; consider WES/WGS for unexplained cases"}
{"cause":"Structural Brain Abnormalities","contribution":"30%","assessment":"MRI brain with epilepsy protocol (thin-cut coronal FLAIR, T1 MPRAGE); identifies cortical dysplasia, hippocampal sclerosis, tumors, vascular malformations"}
{"cause":"Autoimmune Encephalitis","contribution":"20%","assessment":"Antibody panel (anti-NMDA, LGI1, CASPR2, GAD65, AMPAR, GABABR); CSF analysis for oligoclonal bands; PET shows limbic hypermetabolism"}
{"cause":"Traumatic Brain Injury","contribution":"15%","assessment":"Detailed trauma history; CT/MRI shows contusions, gliosis, or contusional necrosis; latency period of months to years post-injury"}
{"cause":"Stroke and Cerebrovascular Disease","contribution":"10%","assessment":"MRI brain with diffusion-weighted imaging; MRA/CTA to identify vascular lesions; hemorrhagic stroke has higher epilepsy risk"}
{"cause":"Neuroinflammation","contribution":"25%","assessment":"CSF analysis (cell count, protein, oligoclonal bands); serum inflammatory markers (CRP, ESR); consider PET imaging for neuroinflammation"}
{"cause":"Infections (CNS)","contribution":"10%","assessment":"Infection history (meningitis, encephalitis, neurocysticercosis); CSF PCR for viral/bacterial pathogens; serology for parasitic infections"}
{"cause":"Metabolic Disorders","contribution":"15%","assessment":"Metabolic panel, ammonia, lactate, pyruvate, B6, B12, folate, homocysteine; consider inborn errors of metabolism in refractory cases"}
{"cause":"Neurodegenerative Diseases","contribution":"5%","assessment":"Age of onset; progressive cognitive decline; consider Alzheimer disease, Lewy body disease, frontotemporal dementia in appropriate clinical context"}
Risks of Inaction
What happens if left untreated
{"complication":"Sudden Unexpected Death in Epilepsy (SUDEP)","timeline":"Ongoing risk, peaks ages 20-40","impact":"SUDEP accounts for 10-50% of epilepsy deaths; risk factors include generalized tonic-clonic seizures, nocturnal seizures, poor seizure control, lack of supervision; estimated incidence 1-2 per 1000 patient-years"}
{"complication":"Status Epilepticus","timeline":"Medical emergency, can occur at any time","impact":"Prolonged seizure (>5 minutes) or repeated seizures without recovery; mortality 10-20%; causes irreversible neuronal damage; requires immediate treatment; risk increases with seizure frequency"}
{"complication":"Traumatic Injuries","timeline":"During seizure events","impact":"Falls, burns, drowning, head injuries, fractures, dental trauma; estimated 1-2% annual risk of significant injury; driving restrictions often required; safety precautions at home and work"}
{"complication":"Cognitive Decline","timeline":"Progressive, especially with uncontrolled seizures","impact":"Memory impairment, attention deficits, executive dysfunction; chronic seizures cause hippocampal sclerosis and cortical atrophy; progressive decline with ongoing uncontrolled seizures; impact on work and quality of life"}
{"complication":"Psychiatric Comorbidity","timeline":"Progressive","impact":"Depression affects 30-50% of epilepsy patients; anxiety in 20-30%; suicide risk 2-3x higher than general population; stigma and social isolation compound mental health burden"}
{"complication":"Refractory Epilepsy Development","timeline":"Months to years","impact":"Seizures not controlled with first two appropriate medications (30-40% of patients); increased risk of status epilepticus; limited treatment options; surgical evaluation becomes necessary"}
{"complication":"Medication Side Effects","timeline":"Ongoing with pharmacotherapy","impact":"Antiepileptic drugs cause cognitive impairment, mood changes, weight changes, bone loss, organ toxicity; drug interactions; teratogenicity; some side effects progressive with cumulative exposure"}
How We Diagnose
Comprehensive assessment methods we use
{"test":"Detailed History and seizure classification","purpose":"Establish diagnosis and guide treatment","whatItShows":"Seizure type (focal/generalized), triggers, frequency, duration, semiology; ILAE classification; identify potential causes and precipitants"}
{"test":"EEG (Electroencephalogram)","purpose":"Confirm epileptic nature and localize seizure focus","whatItShows":"Interictal epileptiform discharges (spikes, sharp waves), slowing, seizure patterns; hyperventilation and photic stimulation activate abnormalities; sleep-deprived EEG increases yield"}
{"test":"MRI Brain with Epilepsy Protocol","purpose":"Identify structural causes and surgical candidates","whatItShows":"Cortical dysplasia, hippocampal sclerosis, tumors, vascular malformations, gliosis, cysts; thin-cut coronal images essential for mesial temporal sclerosis"}
{"test":"Video-EEG Monitoring","purpose":"Capture events for diagnosis and localization","whatItShows":"Correlation of ictal EEG with clinical semiology; distinguishes epileptic from PNES; localizes seizure onset zone for surgical planning"}
{"test":"Autoimmune Epilepsy Panel","purpose":"Identify antibody-mediated epilepsy","whatItShows":"Anti-NMDA, LGI1, CASPR2, GAD65, GABABR, AMPAR antibodies in serum and CSF; associated with immunotherapy-responsive epilepsy"}
{"test":"Prolactin (Postictal)","purpose":"Support diagnosis of generalized tonic-clonic seizures","whatItShows":"Postictal prolactin elevation (>2x baseline) suggests epileptic seizure; not elevated in PNES or syncope; must be drawn within 30-60 minutes"}
{"test":"PET Scan (Interictal)","purpose":"Metabolic imaging for localization","whatItShows":"Hypometabolic areas corresponding to seizure focus; particularly useful for temporal lobe epilepsy; helps identify candidates for epilepsy surgery"}
{"test":"SPECT (Ictal)","purpose":"Blood flow during seizures for localization","whatItShows":"Hyperperfusion at seizure onset zone during ictal SPECT; SISCOM technique improves localization for surgical planning"}
{"test":"Comprehensive Metabolic Panel","purpose":"Rule out metabolic triggers","whatItShows":"Electrolytes, glucose, liver function, renal function, ammonia, calcium, magnesium; metabolic disorders can cause or contribute to seizures"}
{"test":"Genetic Testing","purpose":"Identify genetic causes and guide treatment","whatItShows":"Epilepsy gene panels, WES, WGS; identifies SCN1A (Dravet syndrome), KCNQ2, PCDH19, DEPDC5, and many others; informs prognosis and treatment selection"}
Our Treatment Approach
How we help you overcome Epilepsy & Seizures
Phase 1: Acute Stabilization and Diagnosis (Weeks 1-4)
{"phase":"Phase 1: Acute Stabilization and Diagnosis (Weeks 1-4)","focus":"Establish diagnosis, classify seizure type, identify triggers and underlying causes","interventions":"Detailed history and seizure classification per ILAE criteria. Comprehensive blood workup (CBC, CMP, metabolic panel, autoimmune panel, vitamin levels). EEG (routine and sleep-deprived if needed). MRI brain with epilepsy protocol. Initiate appropriate antiepileptic drug (AED) based on seizure type. Safety education: driving restrictions, water precautions, seizure first aid. Establish seizure diary for tracking triggers and response. Baseline cognitive testing if indicated. Address immediate safety concerns and quality of life.\n"}
Phase 2: Optimization and Root Cause Treatment (Weeks 4-16)
{"phase":"Phase 2: Optimization and Root Cause Treatment (Weeks 4-16)","focus":"Maximize seizure control, treat underlying causes, minimize medication side effects","interventions":"Titrate AED to optimal dosing or transition to alternative medication if needed. Initiate specific treatment for identified cause: immunotherapy for autoimmune encephalitis, surgical evaluation for structural lesions, dietary modifications for metabolic triggers. Evaluate for epilepsy surgery candidacy if pharmacoresistant. Address comorbidities: sleep disorders, mood disorders, cognitive issues. Begin ketogenic diet if indicated (particularly for GLUT1 deficiency, Doose syndrome). Vagus nerve stimulation evaluation if indicated. Optimize lifestyle factors: sleep hygiene, stress management, trigger avoidance. Monitor AED levels and side effects. Many patients achieve seizure freedom with appropriate pharmacotherapy.\n"}
Phase 3: Maintenance and Functional Restoration (Months 4-12)
{"phase":"Phase 3: Maintenance and Functional Restoration (Months 4-12)","focus":"Sustain seizure control, optimize function, support quality of life","interventions":"Continue optimized AED regimen with monitoring. Gradual return to activities as seizure control permits. Address residual cognitive or mood issues. Physical therapy/occupational therapy if needed for post-seizure deficits. Driving evaluation and rehabilitation if applicable. Social support and counseling for adaptation to chronic condition. Vocational counseling if needed. Monitor for treatment-emerging psychiatric symptoms. Support groups and patient education. Most patients achieve meaningful seizure reduction with comprehensive care; 60-70% achieve seizure freedom with appropriate treatment.\n"}
Phase 4: Long-Term Management (Year 1+)
{"phase":"Phase 4: Long-Term Management (Year 1+)","focus":"Maintain optimal seizure control, monitor for complications, support long-term wellbeing","interventions":"Regular follow-up with seizure monitoring and medication adjustment as needed. Periodic imaging and EEG monitoring as clinically indicated. Long-term AED management with attention to cumulative side effects, bone health, metabolic effects. Screening and treatment of comorbidities (depression, anxiety, cognitive issues). Consider medication withdrawal in selected patients who are seizure-free for extended periods. SUDEP risk counseling and mitigation strategies. Annual review of driving eligibility. Ongoing psychosocial support. Address treatment-resistant cases with surgical evaluation, device therapy (RNS, VNS, DBS), or dietary therapy. Many patients achieve durable seizure control and excellent quality of life with comprehensive management.\n"}
Diet & Lifestyle
Recommendations for optimal recovery
Lifestyle Modifications
Strict sleep hygiene: 7-9 hours consistent sleep; sleep deprivation is a major seizure trigger, Stress management: chronic stress raises cortisol and lowers seizure threshold; meditation, yoga, mindfulness, Regular exercise: improves overall health, reduces stress, may have anticonvulsant effects; avoid exercise alone if seizures poorly controlled, Seizure first aid training for family and coworkers, Safety modifications at home: padded floors, shower instead of bath, no swimming alone, helmet for at-risk activities, Driving regulations: know local laws; typically requires seizure-free period (6 months to 1 year in most jurisdictions), Medical alert identification: wear bracelet or carry card, Technology aids: seizure detection devices, smartphone apps for tracking, Avoid flashing lights if photosensitive: certain seizure types triggered by visual stimuli (3% of epilepsy), Occupational safety: discuss with employer; may need workplace modifications, Travel preparation: carry medication, medical records, seizure action plan
Recovery Timeline
What to expect on your healing journey
Phase 1 (Weeks 1-4): Comprehensive diagnosis with history, EEG, MRI, and laboratory evaluation; classification of seizure type; initiation of appropriate antiepileptic medication; safety education; seizure diary establishment; some patients notice initial improvements as seizure triggers identified and medication initiated.
Phase 2 (Weeks 4-16): Medication optimization; treatment of identified underlying causes; evaluation for alternative therapies if needed; 60-70% of patients achieve seizure freedom with first appropriate medication; 40-50% may need medication adjustments or second-line treatments.
Phase 3 (Months 4-12): Sustained treatment; return to normal activities as seizure control permits; management of any residual symptoms or medication side effects; psychological support; most patients who respond to treatment achieve meaningful seizure reduction and improved quality of life.
Phase 4 (Year 1+): Long-term management with monitoring; many patients maintain seizure freedom with ongoing treatment; regular follow-up to adjust to life changes; surgical candidates identified and treated if pharmacoresistant; ongoing support for comorbidities; majority of patients achieve excellent quality of life with appropriate management.
How We Measure Success
Outcomes that matter
Seizure freedom (complete cessation of seizures)
Reduction in seizure frequency (target: 50%+ decrease)
Reduction in seizure severity
Decreased medication side effects
Improved quality of life scores
Restored driving privileges
Return to work/school function
Resolution of interictal EEG abnormalities
Improved mood and cognitive function
Reduced emergency room visits and hospitalizations
Successful management of comorbidities
Frequently Asked Questions
Common questions from patients
What is the difference between focal and generalized seizures?
Focal seizures originate in networks limited to one cerebral hemisphere and may or may not impair consciousness. They can cause localized symptoms (twitching, sensory disturbances, emotional changes) or evolve into bilateral tonic-clonic seizures (focal to bilateral tonic-clonic). Generalized seizures involve both hemispheres from onset and always impair consciousness. Types include: absence (brief staring), myoclonic (brief jerks), tonic (stiffening), clonic (rhythmic jerking), tonic-clonic (stiffening and jerking), and atonic (drop attacks). Accurate classification is essential for appropriate treatment selection.
Can epilepsy be cured or only controlled?
The answer depends on the underlying cause. Approximately 60-70% of patients achieve complete seizure control with appropriate medication. Some epilepsy syndromes (childhood absence epilepsy, benign rolandic epilepsy) are age-limited and may resolve. If a structural cause is identified and surgically removable, potential cure exists. However, many patients require long-term management. Studies show that after 2 years seizure-free, approximately 50-60% remain seizure-free after medication withdrawal. The goal shifts from 'cure' to achieving optimal quality of life with minimal side effects.
What triggers seizures in people with epilepsy?
Common triggers include: sleep deprivation (most common), stress, alcohol (especially binge drinking and withdrawal), flashing lights (photosensitivity in 3%), illness/fever, hormonal changes, low blood sugar, certain medications that lower seizure threshold, irregular sleep patterns, and extreme heat. Each person has individual triggers that can be identified through seizure diary tracking. Avoiding triggers significantly reduces seizure frequency in many patients.
When is epilepsy considered 'refractory' or 'pharmacoresistant'?
Epilepsy is considered refractory when seizures fail to achieve sustained seizure freedom after two appropriately chosen, well-tolerated antiepileptic drug trials (whether as monotherapies or in combination). This affects approximately 30-40% of patients with epilepsy. Refractory epilepsy requires comprehensive evaluation including video-EEG monitoring, advanced imaging, and consideration of surgical options (resective surgery, laser ablation, RNS), device therapy (VNS, RNS, DBS), or dietary therapies (ketogenic diet). A second opinion at a specialized epilepsy center is recommended for all patients with pharmacoresistant epilepsy.
Is it safe to exercise with epilepsy?
Yes, regular exercise is encouraged and may actually reduce seizure frequency. However, safety precautions are important: swim only with direct supervision, use protective gear for cycling/contact sports, avoid climbing or heights if seizures uncontrolled, consider medical alert ID during exercise. Many Olympic athletes and professional sports figures have epilepsy. Exercise reduces stress, improves sleep, and enhances overall wellbeing. Discuss activity restrictions with your neurologist based on your specific seizure type and control.
What should I do if someone has a seizure?
1) Stay calm and note the time. 2) Prevent injury: move dangerous objects away, put something soft under the head, do NOT put anything in the mouth. 3) Turn the person on their side to prevent choking. 4) Do NOT restrain the person. 5) Speak calmly and reassure others. 6) After the seizure, the person may be confused or sleepy; stay with them until fully recovered. 7) Call emergency services if: seizure lasts more than 5 minutes, person doesn't wake up between seizures (status epilepticus), person is pregnant or has diabetes, person is injured during seizure, first-time seizure, or seizure occurs in water.
Medical References
- 1.Fisher RS, Acevedo C, Arzimanoglou A, et al. ILAE official report: a practical clinical definition of epilepsy. Epilepsia. 2014;55(4):475-482. doi:10.1111/epi.12550. PMID: 24730690
- 2.Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology. Epilepsia. 2017;58(4):512-521. doi:10.1111/epi.13709. PMID: 28276062
- 3.Kwan P, Brodie MJ. Early identification of refractory epilepsy. N Engl J Med. 2000;342(5):314-319. doi:10.1056/NEJM200002033420503. PMID: 10660394
- 4.Thijs RD, Surges R, O'Brien TJ, Sander JW. Epilepsy in adults. Lancet. 2019;393(10172):689-701. doi:10.1016/S0140-6736(18)32596-0. PMID: 30686584
- 5.Devinsky O, Vezzani A, O'Brien TJ, et al. Epilepsy. Nat Rev Dis Primers. 2018;4:18024. doi:10.1038/nrdp.2018.24. PMID: 29713784
- 6.Hitiris N, Mohanraj R, Norrie J, Brodie MJ. Mortality in epilepsy. Epilepsy Behav. 2007;10(3):363-376. doi:10.1016/j.yebeh.2007.01.005. PMID: 17337247
Ready to Start Your Healing Journey?
Our integrative medicine experts are ready to help you overcome Epilepsy & Seizures.