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Rowan Research Day - 2026
Rowan Research Day - 2026
Reference list
Irritability and Related Behavioral Adverse Events Associated With Levetiracetam: A Meta‑Analysis and Meta‑Regression of Randomized Trials
Wearable and Technology‑Assisted Gait and Balance Interventions in Parkinson’s Disease: A Systematic Review and Meta‑Analysis
Trends and Disparities in Mortality Involving Epilepsy and Aspiration Pneumonia Among Older Adults in the United States, 1999–2020
Cerebrospinal Fluid and Serum Manganese Levels in Parkinson’s Disease: A Method‑Stratified Meta‑analysis
Efficacy and Safety of Levetiracetam for Essential Tremor: A Systematic Review and Meta‑Analysis
Prevalence and Clinical Correlates of Restless Legs Syndrome in Neuromyelitis Optica Spectrum Disorder: A Systematic Review and Meta‑analysis
Effects of Subthalamic Nucleus Deep Brain Stimulation on Depressive Symptoms in Patients with Parkinson’s Disease: A Meta‑Analysis
Efficacy and Safety of Droxidopa for Neurogenic Orthostatic Hypotension: A Systematic Review and Meta‑analysis
Focal Status Epilepticus in a Patient with Responsive Neurostimulation: A Rare Complication and Management Insights
Post-concussion syndrome
Post-concussion syndrome
Definition
mTBI ✚ persistent sx ✚ fx impact ✚ exclusion
mTBI
•Head trauma with ± brief loss of consciousness (<30 min)
•± post‑traumatic amnesia (<24 h)
•± confusion/disorientation
•GCS 13–15
•No structural brain injury explaining symptoms
Persistent sx
•One or more post‑concussive sx
•Persisting beyond expected recovery
>4 weeks (children/adolescents)
>3 months (adults)
Sx domains
-Somatic: headache, dizziness, fatigue, photophobia/phonophobia
-Cognitive: attention deficit, memory impairment, slowed processing, executive dysfunction
-Emotional/Behavioral: irritability, anxiety, depression, emotional lability
-Sleep: insomnia, hypersomnia, fragmented sleep
Cannabis use disorder
Cannabis use disorder (CUD)
Note
-DSM-V criteria for CUD
-RCVS
Cannabis withdrawal syndrome
>not life-threatening, but can last 2 wks
Treatment
-Psychosocial tx (CBT)
-OFF-label
>Acetylcysteine (NAC 1200 mg BID)
>Gabapentin
>Mirtazapine
>Dronabinol/nabiximols
Increase Alertness
Increase Alertness
Situations
-Stroke (mainly thalamic)
-PD/ MS
-Consciousness disorder (TBI)
-Narcolepsy/ OSA residual sleepiness
Medications
Base on safety
In-hospital
1st: caffeine, amantadine
2nd: methylphenidate
3rd: levodopa
Outpatient:
-modafinil/ armodafinil, bupropion, atomoxetine
-dextroamphetamine, lisdexamfetamine
Unclear:
-solriamfetol, pitolisant
Safety pearls
-Avoid late‑day dosing → insomnia, agitation
-Monitor BP/HR with methylphenidate, amphetamines, solriamfetol
-Renal adjust amantadine
-Modafinil induces CYP3A4 → ↓ OCP effectiveness
-Start low and titrate weekly
Neuroimaging Acquisition (CTA HN & CTV & DE)
Neuroimaging Acquisition
CTA H&N and CTV and DE
CTA H&N
Note
-1 CTA radiation is equal to 13 mo
Patient preparation
-Large‑bore peripheral IV (usually 18–20 G)
-Preferred site: antecubital vein (2/2 resistance)
Contrast parameters
-Volume: 50–100 mL
-Injection rate: 3–6 mL/s
-Saline flush: 20–40 mL
Timing the scan
Bolus tracking
-A small ROI is placed over a target artery (e.g., aortic arch, carotid)
-The scanner automatically triggers acquisition when attenuation reaches a preset threshold (e.g., 100–150 HU)(our hospital 130); or can manually press ☢️
Graph pressure vs timing
-Maximum pressure: 300 psi (standard)
*peak injection pressure
1, contrast injection; 2, finish of contrast injection
-Arterial phase 20-22s
-Venous phase 45s
-Venous phase 45s
*dependent of cardiac output
CTV acquisition
-Separate imaging
-If more than 3 minutes of last CTA H&N, wait 4h
-Acquisition window 40–60s
Dual Energy (DECT)
-Usual CTH is 120 Kvp
>DE is low (80–90) and high (140–150) energy acquisition
*Low→ iodine; High→ blood
-Creates 2 maps→ iodine (IOM) & non-iodine (VNC-Virtual non-contrast)
>Siemens SOMATOM Force / Drive→ 2 tubes
>Philips Spectral CT→ dual-layer
>GE Revolution→ rapid switch
Epilepsy Monitoring Unit (EMU)
Epilepsy Monitoring Unit (EMU)
How to restart ASM
Lamotrigine
- if < 7d, LMT can be restarted fully no risk of SJS
Stroke - Antiplatelet drugs
Antiplatelet drugs
COX inhibitors
Glycoprotein IIb/IIIa inhibitors
-Integrilin
ADP receptor/P2Y12 inhibitors
-Cangrelor drip
-Prasugrel→ black-box of ICH in pts w/ previous stroke/ TIA
Phosphodiesterase inhibitors
Epileptogenic Zone
Epileptogenic Zone
“Area of cortex that is necessary and sufficient for initiating seizures and whose removal (or disconnection) is necessary for complete abolition of seizures”
Hans Lüders, 1993
History
1884-1935 (Sir John Hughlings Jackson & Victor Horseley)
-1st cortical resections for EPI
-Szs originate from a specific cortical region that can be surgically targeted
Early–Mid 20th Century: Penfield & Jasper
-ECoG to map, now epileptic activity can be recorded & localized
1966: Tailarach & Bancaud
-sEEG based definition
1993: Lüders
-EZ, hypothetical concept
2000s–present
-Focal view to network model
Concepts
EZ
-Minimum amount of cortex to achieve SF
-Inferered it by combining multiple zones
-Minimum amount of cortex to achieve SF
-Inferered it by combining multiple zones
Seizure onset zone (SOZ)
-Szs is actually generated as measured by EEG
Ictal onset zone (IOZ)
-Szs actually begin, as recorded on sEEG
>Often smaller than the EZ
>Sometimes only part of true epileptogenic network
>Sometimes only part of true epileptogenic network
Potential ictal onset zone
-Might be involved in szs onset but are not definitively proven due to limited data
>Common in sEEG when sampling is incomplete
-Might be involved in szs onset but are not definitively proven due to limited data
>Common in sEEG when sampling is incomplete
Irritative zone
-Generates interictal epileptiform discharges as defined by EEG
-Generates interictal epileptiform discharges as defined by EEG
>Usually larger than true EZ
>Helps guide electrode placement but is not sufficient for surgical targeting
Epileptic lesion zone
-Structural abnormality seen on neuroimaging believed to be source of szs
>Not all lesions are epileptogenic, and some EZs occur without visible lesions
Early spread zone
-Region involved immediately after szs onset
>Helps distinguish primary onset from rapid spread
>Spread zones are not necessarily part of EZ
>Spread zones are not necessarily part of EZ
Symptomatogenic zone
-Activation produces clinical sx of szs
>Sx often reflect spread, not onset
>Not removed if overlaping essential function
Eloquent cortex
-Damage causes major, permanent deficits
>Avoid resecting, unless absolutely necessary
Non-eloquent cortex
-Resection is less likely to cause major functional impairment
>Most resections target this area
-Resection is less likely to cause major functional impairment
>Most resections target this area
Putative epileptogenic zone (Resection margins)
-Estimated EZ based on all available data
-Estimated EZ based on all available data
-Area planed to be removed
-Practical, clinically actionable version of theoretical EZ
-Practical, clinically actionable version of theoretical EZ
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