EEG Viva Examination

from reportlab.lib.pagesizes import A4
from reportlab.lib.styles import getSampleStyleSheet, ParagraphStyle
from reportlab.lib.units import cm
from reportlab.lib import colors
from reportlab.platypus import (
    SimpleDocTemplate, Paragraph, Spacer, HRFlowable, PageBreak, Table, TableStyle
)
from reportlab.lib.enums import TA_CENTER, TA_LEFT, TA_JUSTIFY

OUTPUT = "/tmp/workspace/eeg-viva/EEG_Viva_QA_MDPsychiatry.pdf"

doc = SimpleDocTemplate(
    OUTPUT,
    pagesize=A4,
    rightMargin=2*cm, leftMargin=2*cm,
    topMargin=2.2*cm, bottomMargin=2.2*cm,
    title="EEG Viva Q&A – MD Psychiatry",
    author="External Examiner"
)

styles = getSampleStyleSheet()

# Custom styles
title_style = ParagraphStyle("TitleStyle", parent=styles["Title"],
    fontSize=20, textColor=colors.HexColor("#1a237e"),
    spaceAfter=6, spaceBefore=0, alignment=TA_CENTER)

subtitle_style = ParagraphStyle("SubTitle", parent=styles["Normal"],
    fontSize=12, textColor=colors.HexColor("#283593"),
    spaceAfter=4, alignment=TA_CENTER)

section_style = ParagraphStyle("Section", parent=styles["Heading1"],
    fontSize=13, textColor=colors.white,
    backColor=colors.HexColor("#1a237e"),
    spaceBefore=14, spaceAfter=6,
    leftIndent=-0.3*cm, rightIndent=-0.3*cm,
    borderPad=5)

q_style = ParagraphStyle("Question", parent=styles["Normal"],
    fontSize=10.5, textColor=colors.HexColor("#b71c1c"),
    fontName="Helvetica-Bold",
    spaceBefore=10, spaceAfter=3, leading=14)

a_style = ParagraphStyle("Answer", parent=styles["Normal"],
    fontSize=10, textColor=colors.HexColor("#1b1b1b"),
    fontName="Helvetica",
    spaceBefore=2, spaceAfter=4, leading=14,
    leftIndent=0.4*cm, alignment=TA_JUSTIFY)

note_style = ParagraphStyle("Note", parent=styles["Normal"],
    fontSize=9, textColor=colors.HexColor("#4a4a4a"),
    fontName="Helvetica-Oblique",
    spaceBefore=0, spaceAfter=0,
    leftIndent=0.4*cm)

# ─────────────────────────────────────────────
# DATA: 60 Q&A
# ─────────────────────────────────────────────

sections = [
    {
        "title": "SECTION A: BASIC QUESTIONS (Q1–Q15)",
        "subtitle": "Expected from every candidate",
        "color": "#1a237e",
        "qas": [
            (
                "1. What does EEG stand for, and what does it record?",
                "EEG stands for Electroencephalography. It is a non-invasive neurophysiological technique that records the spontaneous electrical activity of the brain — specifically the summated postsynaptic potentials (primarily EPSPs and IPSPs) of large populations of cortical pyramidal neurons — via electrodes placed on the scalp. The recorded signals represent voltage fluctuations over time and reflect the functional state of the cerebral cortex."
            ),
            (
                "2. Name the standard electrode placement system and how many electrodes it uses.",
                "The International 10-20 System is the standard. It uses 21 electrodes (19 recording electrodes + 2 reference electrodes — A1 and A2 over the earlobes). The numbers '10' and '20' refer to the 10% and 20% inter-electrode distances measured from standard bony landmarks (nasion, inion, and preauricular points). Extended systems (e.g., 10-10 system) use up to 64-256 electrodes for high-density EEG."
            ),
            (
                "3. What are the four main frequency bands? State their ranges.",
                "Delta: <4 Hz (0.5–3.5 Hz) — seen in deep sleep and encephalopathy.\n"
                "Theta: 4–7 Hz — seen in drowsiness, children, and temporal lobe pathology.\n"
                "Alpha: 8–13 Hz — dominant rhythm of relaxed wakefulness (eyes closed).\n"
                "Beta: >13 Hz (13–30 Hz) — seen with alertness, anxiety, benzodiazepines.\n"
                "Gamma (>30 Hz) is a fifth band recognized in cognitive neuroscience."
            ),
            (
                "4. Which EEG frequency is dominant in a normal awake adult with eyes closed?",
                "Alpha rhythm (8–13 Hz) is the dominant frequency. It is best seen over the occipital (posterior) regions bilaterally, is symmetrical, and has an amplitude of approximately 20–100 µV. It is the hallmark of a relaxed, wakeful state with eyes closed and reflects synchronized thalamocortical activity."
            ),
            (
                "5. What happens to the EEG when a normal adult opens their eyes?",
                "Alpha blocking (also called alpha attenuation or the Berger effect) occurs. On eye opening, the posterior alpha rhythm is suppressed and replaced by lower-amplitude, higher-frequency beta activity. This is a normal physiological response indicating intact thalamocortical reactivity. Absence of this response may suggest cortical dysfunction or visual pathway pathology."
            ),
            (
                "6. Define amplitude in EEG. What is the normal amplitude range for alpha waves?",
                "Amplitude is the voltage difference (measured in microvolts, µV) between the peak and trough of an EEG wave. It reflects the synchrony of the underlying neuronal populations. Normal alpha amplitude ranges from 20–100 µV. Alpha amplitude >100 µV is considered abnormally high; <20 µV is abnormally low and may indicate cortical atrophy or subdural fluid collection."
            ),
            (
                "7. What is a montage in EEG? Name two types.",
                "A montage is a specific arrangement defining how electrode pairs are connected for recording. Two main types:\n"
                "1. Bipolar montage: Each channel records the difference between two adjacent electrodes (e.g., Fp1–F3, F3–C3). Good for localizing sharp transients and seizure onset.\n"
                "2. Referential (common reference) montage: Each electrode is referenced to a single electrode (e.g., linked ears A1–A2, or Cz). Good for assessing amplitude asymmetries and slow wave activity."
            ),
            (
                "8. What is the significance of the 3 Hz spike-and-wave discharge?",
                "A 3 Hz (cycles/second) generalized spike-and-wave complex is the hallmark of childhood absence epilepsy (CAE/Petit mal epilepsy). It arises from bilateral, synchronous thalamocortical oscillations. Clinically, these discharges correlate with brief (5–30 second) lapses of consciousness with no post-ictal confusion. They are activated by hyperventilation and may be suppressed by sleep. Their presence confirms the diagnosis of absence epilepsy."
            ),
            (
                "9. What EEG pattern is classically seen in GTCS?",
                "During a GTCS:\n"
                "Tonic phase: Generalized high-frequency (>10 Hz) polyspike or fast rhythmic activity (epileptic recruiting rhythm).\n"
                "Clonic phase: Repetitive spike-and-slow-wave complexes that gradually decrease in frequency.\n"
                "Post-ictal phase: Diffuse generalized delta slowing (postictal suppression), which gradually resolves over minutes to hours.\n"
                "The overall pattern shows evolution in frequency, morphology, and distribution — a key feature distinguishing true seizure from artifact."
            ),
            (
                "10. What is a photoparoxysmal response?",
                "A photoparoxysmal response (PPR) is an abnormal EEG response to intermittent photic stimulation (IPS). It consists of generalized spike-and-wave or polyspike-and-wave discharges that outlast the photic stimulus. It indicates photosensitive epilepsy (e.g., JME, photosensitive occipital epilepsy). A photic following response (occipital driving) is normal; PPR is pathological. It has population prevalence of ~1–2% and is more common in females."
            ),
            (
                "11. Name at least two sleep-specific EEG patterns in a normal adult.",
                "Stage N1 (Drowsiness): Vertex sharp waves (V-waves) at the Cz electrode; alpha attenuation; theta activity.\n"
                "Stage N2: Sleep spindles (12–14 Hz bursts, 0.5–2 sec duration, maximal at Cz) and K-complexes (large biphasic slow waves at Cz, >0.5 sec).\n"
                "Stage N3 (Slow Wave Sleep): High-amplitude delta waves >75 µV, >20% of epoch.\n"
                "REM sleep: Low-voltage mixed frequency EEG resembling wakefulness; saw-tooth waves."
            ),
            (
                "12. Difference between focal and generalized EEG abnormality?",
                "Focal abnormality: Arises from a restricted region of one hemisphere. Seen in only a subset of electrodes (e.g., temporal lobe spikes in TLE). Implies a structural or functional lesion in that region.\n"
                "Generalized abnormality: Involves both hemispheres simultaneously and symmetrically from the outset. Seen in all or most electrodes (e.g., 3 Hz spike-wave in absence epilepsy). Implies a diffuse or subcortical (thalamocortical) disturbance."
            ),
            (
                "13. In TLE, where do you typically see the epileptiform discharge?",
                "In Temporal Lobe Epilepsy, interictal epileptiform discharges (IEDs) — typically sharp waves or spikes — are maximal at the anterior temporal electrodes: F7/F8 (anterior temporal) and T3/T4 (mid-temporal) in the 10-20 system, or the true anterior temporal (zygomatic/sphenoidal) electrodes. In mesial TLE, discharges may be better captured by sphenoidal electrodes. They may be unilateral or bilateral (bilateral independent temporal discharges in ~30% of cases)."
            ),
            (
                "14. What is an epoch in EEG recording?",
                "An epoch is a fixed-length segment of continuous EEG data selected for analysis. In routine clinical EEG, the standard page display is 10 seconds per epoch (screen). In sleep staging (polysomnography), a 30-second epoch is standard. In quantitative EEG analysis, epochs of 1–4 seconds are often used for spectral analysis. Epochs allow systematic, reproducible review of EEG segments."
            ),
            (
                "15. What are artifacts in EEG? Name two common sources.",
                "Artifacts are signals recorded on EEG that do not originate from cerebral electrical activity. They contaminate the recording and may mimic or obscure pathological patterns.\n"
                "Common sources:\n"
                "1. Physiological artifacts: Eye blink/movement (frontopolar electrodes — large slow deflections), ECG artifact (rhythmic QRS-like spikes), muscle artifact (EMG — high-frequency 20–500 Hz activity), sweat artifact (slow undulating baseline).\n"
                "2. Technical/External artifacts: Electrode pop (single electrode sudden high-amplitude deflection), 50/60 Hz electrical interference (mains), movement artifact, ventilator artifact in ICU."
            ),
        ]
    },
    {
        "title": "SECTION B: GOOD TO PASS (Q16–Q30)",
        "subtitle": "Demonstrates working clinical knowledge",
        "color": "#1b5e20",
        "qas": [
            (
                "16. Describe the normal EEG of a full-term newborn. How does it differ from an adult EEG?",
                "The normal full-term neonate EEG (≥37 weeks GA) shows:\n"
                "- Discontinuous pattern during quiet sleep (trace alternant)\n"
                "- Delta brushes: fast rhythmic activity (8–20 Hz) superimposed on delta waves — most prominent in premature neonates\n"
                "- Sleep cycling present (active vs. quiet sleep)\n"
                "- Interhemispheric synchrony >70% at term\n"
                "- Higher amplitude (100–200 µV) than adults\n"
                "Key differences from adult EEG: no alpha rhythm (develops by age 3), no sleep spindles (appear at 2–3 months), discontinuity is normal, frequencies are slower overall."
            ),
            (
                "17. What is discontinuous EEG activity in neonates and its significance?",
                "Discontinuous EEG in neonates refers to alternating bursts of activity and periods of relative quiescence (interburst intervals, IBIs). It is a normal feature of immature brain and is most prominent in premature infants (<30 weeks GA). In term neonates, discontinuity is normal only during quiet sleep (trace alternant). Pathological discontinuity is characterized by: excessively long IBIs (>10 sec at term), absent activity, invariant pattern across states, or very low-amplitude bursts — suggesting hypoxic-ischemic encephalopathy, metabolic disturbance, or severe brain injury."
            ),
            (
                "18. What is 'trace alternant' and at what gestational age does it appear?",
                "Trace alternant (TA) is a normal neonatal EEG pattern seen during quiet sleep. It consists of high-amplitude bursts (1–3 sec) of mixed frequencies alternating with periods of relative suppression (4–8 sec) of lower amplitude (25–50 µV). It is present at 36–38 weeks gestational age and disappears by 44–46 weeks post-menstrual age as cortical maturation progresses. It is distinct from pathological burst-suppression: TA has defined interburst activity, is state-dependent, and shows normal amplitude bursts."
            ),
            (
                "19. Describe the ictal EEG pattern in an absence seizure. What activates it?",
                "Absence seizure ictal pattern: Sudden onset of 3 Hz (2.5–4 Hz) generalized synchronous spike-and-wave or polyspike-and-wave complexes appearing bilaterally, symmetrically, and simultaneously across all electrodes. Onset and termination are abrupt. Duration: 5–30 seconds. The discharge begins at slightly higher frequency (~3.5 Hz) and slows toward the end (~2.5 Hz).\n"
                "Activating factors:\n"
                "1. Hyperventilation — the most reliable activator (3 minutes of HV provokes absence in ~80% of CAE)\n"
                "2. Drowsiness/NREM sleep\n"
                "3. Photic stimulation in photosensitive cases\n"
                "4. Hypoglycaemia"
            ),
            (
                "20. What is post-ictal slowing after GTCS? Clinical significance?",
                "Post-ictal slowing is the generalized diffuse slow-wave (delta) activity seen on EEG immediately after a GTCS. It results from neuronal exhaustion, adenosine release, and increased GABA-ergic inhibition following the massive depolarization of the seizure. It may last minutes to hours and gradually resolves.\n"
                "Clinical significance:\n"
                "1. Confirms that a true epileptic seizure occurred (vs. psychogenic non-epileptic attack — PNEA)\n"
                "2. Duration correlates with seizure severity\n"
                "3. Persistent focal post-ictal slowing (Todd's paresis correlate) suggests focal onset\n"
                "4. Useful in monitoring recovery in status epilepticus"
            ),
            (
                "21. What are interictal epileptiform discharges (IEDs)? What do they indicate?",
                "IEDs are transient EEG abnormalities — spikes (<70 msec duration), sharp waves (70–200 msec), or spike-wave complexes — occurring between clinical seizures. They are the EEG hallmark of an epileptic brain. They reflect hypersynchronous discharges of a neuron population with paroxysmal depolarization shifts (PDS).\n"
                "Clinical significance: They indicate epileptogenicity but are not diagnostic of epilepsy alone (present in 0.5–2% of normal subjects). Localization of IEDs helps identify the epileptogenic zone. Frequency of IEDs can be used to monitor treatment response."
            ),
            (
                "22. Significance of a normal EEG in a patient with clinical seizures?",
                "A normal EEG does NOT rule out epilepsy. This is a critical clinical point:\n"
                "- Sensitivity of a single routine EEG is only 30–55% in known epilepsy\n"
                "- IEDs are time-dependent; a single 20–30 min recording may not capture them\n"
                "- Deep mesial temporal or frontal foci may not appear on scalp EEG\n"
                "- Epilepsy is a clinical diagnosis; EEG supports but does not confirm or exclude it\n"
                "Action: Repeat EEG (sensitivity increases to ~80–90% with 3 recordings), sleep-deprived EEG, prolonged ambulatory EEG, or video-EEG monitoring."
            ),
            (
                "23. What is a sleep-deprived EEG and why is it used?",
                "A sleep-deprived EEG is performed after partial or complete sleep deprivation (typically keeping the patient awake for 24 hours or allowing only 4–5 hours of sleep). Sleep deprivation:\n"
                "1. Promotes sleep during the recording — NREM sleep activates IEDs (especially in frontal and temporal lobe epilepsy)\n"
                "2. Lowers seizure threshold, increasing yield of epileptiform discharges\n"
                "3. Activates absence seizures and JME discharges on awakening\n"
                "Yield: Increases detection rate by 20–30% over routine EEG. Preferred when routine EEG is normal but clinical suspicion remains high."
            ),
            (
                "24. In TLE, what is the significance of anterior temporal sharp waves?",
                "Anterior temporal sharp waves (maximal at F7/F8 or true anterior temporal electrodes) are the most common interictal EEG finding in TLE. Their significance:\n"
                "1. They are the best scalp EEG predictor of mesial temporal seizure onset\n"
                "2. Unilateral discharges strongly lateralize the seizure focus and are important for surgical planning\n"
                "3. Phase reversal at F7 or F8 confirms anterior temporal maximum\n"
                "4. Sphenoidal electrode recordings can improve sensitivity for mesial TLE by 15–20%\n"
                "5. Bilateral independent discharges suggest bilateral pathology — worse surgical prognosis"
            ),
            (
                "25. What is secondary bilateral synchrony? How does it differ from primary generalized epilepsy?",
                "Secondary bilateral synchrony (SBS) refers to a focal epileptiform discharge from one hemisphere that rapidly propagates to the contralateral hemisphere via the corpus callosum, producing apparently bilateral synchronous discharges.\n"
                "Key differences from primary generalized:\n"
                "- SBS has a 'lead-in' or pre-discharge focal spike preceding the bilateral spread by a few milliseconds (visible on careful analysis)\n"
                "- SBS is associated with structural lesions (frontal or mesial temporal)\n"
                "- SBS does not respond to drugs effective in primary generalized epilepsy (e.g., valproate, ethosuximide)\n"
                "- Correct identification is critical: treating SBS as primary generalized epilepsy leads to drug failure"
            ),
            (
                "26. What are K-complexes and sleep spindles? At what stage do they appear?",
                "Sleep spindles: Bursts of rhythmic 12–14 Hz activity, 0.5–2 seconds duration, spindle-shaped (waxing-waning amplitude), maximal at central (Cz) regions. Generated by thalamic reticular nucleus.\n"
                "K-complexes: Large biphasic slow waves (negative sharp component followed by positive slow wave), >0.5 sec duration, maximal at Cz. Represent a cortical response to stimuli during sleep.\n"
                "Both appear in Stage N2 (NREM Stage 2) sleep. Their presence is used to score N2 epochs in polysomnography. Absence of sleep spindles in infancy after 3 months suggests cortical pathology."
            ),
            (
                "27. What is hypsarrhythmia? Which condition is it associated with?",
                "Hypsarrhythmia is a chaotic, high-amplitude (>200–300 µV), disorganized EEG pattern characterized by continuous random delta and theta waves intermixed with multifocal spikes and sharp waves occurring from all regions, without normal background organization. It is most prominent during NREM sleep.\n"
                "Associated condition: West Syndrome (infantile spasms) — the triad of infantile spasms, hypsarrhythmia on EEG, and intellectual disability. It typically occurs between 3–12 months of age. Modified hypsarrhythmia variants (e.g., with interhemispheric synchrony) also occur."
            ),
            (
                "28. What is the EEG finding in BECTS (Rolandic Epilepsy)?",
                "Benign Childhood Epilepsy with Centrotemporal Spikes (BECTS / Rolandic Epilepsy) shows:\n"
                "High-amplitude biphasic sharp waves or spike-wave complexes in the centrotemporal (rolandic) regions — maximal at C3/C4 and T3/T4. They have a characteristic horizontal dipole (negative at central, positive at frontal).\n"
                "Key features:\n"
                "- Markedly activated during NREM sleep (may disappear in wakefulness)\n"
                "- Often unilateral but can shift sides\n"
                "- Functional (the child's cognitive EEG background is normal)\n"
                "- Discharges disappear by puberty, correlating with remission of seizures"
            ),
            (
                "29. What is burst-suppression pattern? Name two conditions.",
                "Burst-suppression is a severe EEG pattern characterized by alternating periods of high-amplitude bursts of mixed-frequency activity (spikes, sharp waves, delta) and periods of profound suppression (near-isoelectric) lasting seconds. It indicates severe diffuse cortical dysfunction.\n"
                "Conditions:\n"
                "1. Hypoxic-ischemic encephalopathy (post-cardiac arrest) — poor prognostic marker\n"
                "2. Deep anesthesia (induced burst-suppression in neurosurgical cases for brain protection)\n"
                "3. Severe metabolic encephalopathy (hepatic, uremic)\n"
                "4. Ohtahara syndrome (early infantile epileptic encephalopathy)\n"
                "5. High-dose barbiturate/propofol coma"
            ),
            (
                "30. How does hyperventilation affect the EEG? Why is it used as an activation procedure?",
                "Hyperventilation (HV) causes hypocapnia (low CO2) → cerebral vasoconstriction → reduced cerebral perfusion → neuronal hypoxia → increased neuronal excitability and synchrony.\n"
                "EEG effects:\n"
                "- Normal response: Diffuse bilateral slowing (theta and delta activity) — more prominent in children\n"
                "- Abnormal response: Activation of 3 Hz spike-wave in absence epilepsy (most reliable activator), activation of focal slowing, or generalized epileptiform discharges\n"
                "Clinical use: Standard 3-minute HV is performed in every routine EEG. It is the single most effective activator for childhood absence epilepsy, provoking absences in up to 80% of untreated cases."
            ),
        ]
    },
    {
        "title": "SECTION C: TOUGH QUESTIONS (Q31–Q45)",
        "subtitle": "Separates average from good candidates",
        "color": "#e65100",
        "qas": [
            (
                "31. Neurophysiological basis of 3 Hz spike-and-wave in absence epilepsy. Structures involved?",
                "The 3 Hz spike-and-wave arises from abnormal thalamocortical oscillations. The thalamic reticular nucleus (TRN) — a GABAergic structure — normally generates 7–14 Hz sleep spindles via rhythmic inhibition of thalamocortical relay neurons. In absence epilepsy:\n"
                "1. Cortical neurons (layer 5/6 pyramidal cells) fire a burst → activate TRN\n"
                "2. TRN inhibits thalamocortical (TC) relay neurons via GABA-B receptors → hyperpolarization → deinactivation of T-type Ca2+ channels\n"
                "3. T-channel burst fires in TC neurons → re-excites cortex\n"
                "4. This loop oscillates at ~3 Hz generating the spike (cortical excitation) + wave (inhibition)\n"
                "Key structures: Cortex (somatosensory areas 5–6) + thalamic reticular nucleus + thalamocortical relay nuclei (VPL, CM). Genetic mutations in T-type Ca2+ channels (CACNA1A, CACNA1H) and GABA-B receptors underlie many cases."
            ),
            (
                "32. Ictal, interictal, and peri-ictal EEG patterns in TLE.",
                "Interictal: Unilateral anterior temporal sharp waves or spikes (F7/F8, T3); may be bilateral; can occur in isolation or in rhythmic bursts. Present between seizures.\n\n"
                "Pre-ictal (just before seizure): Subtle changes including: focal attenuation, rhythmic theta activity, low-amplitude fast activity over temporal regions. May precede clinical onset by seconds.\n\n"
                "Ictal: Begins with rhythmic theta (5–7 Hz) or alpha-frequency activity unilaterally over the temporal lobe, evolving in frequency and amplitude. Progresses to rhythmic delta with sharp components. Contralateral spread may occur.\n\n"
                "Post-ictal: Focal polymorphic delta slowing over the seizure-onset hemisphere, persisting for minutes to hours. Todd's EEG correlate."
            ),
            (
                "33. EEG evolution during a GTCS (tonic → clonic → post-ictal).",
                "Tonic phase (early): Sudden generalized low-amplitude fast activity (beta/gamma, >20 Hz) — 'electrodecrement' or 'epileptic recruiting rhythm' at 10–25 Hz.\n"
                "Tonic phase (late): High-amplitude generalized polyspike discharges becoming increasingly synchronized.\n"
                "Clonic phase: Repetitive generalized polyspike-and-slow-wave complexes. As clonic jerks slow in frequency, wave complexes slow from ~5 Hz to ~2–3 Hz. Amplitude increases then decreases.\n"
                "End of clonic phase: Gradual cessation of spike components; high-amplitude slow waves.\n"
                "Post-ictal phase: Generalized suppression, then diffuse irregular delta polymorphic slowing, gradually replaced by normal background over minutes to hours."
            ),
            (
                "34. What is EEG coherence? What does it tell about brain connectivity?",
                "EEG coherence is a quantitative measure of the functional coupling between two EEG channels. It is calculated from the cross-spectral density of two signals divided by the product of their individual power spectra, yielding a value between 0 (no correlation) and 1 (perfect phase correlation) for each frequency band.\n"
                "Clinical significance:\n"
                "- High coherence indicates synchronized, coupled activity between two brain regions\n"
                "- Reduced interhemispheric coherence: seen in corpus callosum lesions, schizophrenia (reduced frontal coherence)\n"
                "- Increased local coherence: epileptogenic focus\n"
                "- Used in brain connectivity research, BCI, coma prognosis, and assessing cortical maturation in neonates"
            ),
            (
                "35. EEG differentiation: JME vs. Childhood Absence Epilepsy (CAE).",
                "Feature / CAE / JME:\n"
                "Discharge rate: 3 Hz (classic) / 3.5–6 Hz (faster, irregular polyspike-wave)\n"
                "Morphology: Spike+slow wave / Polyspike+wave (multiple spikes before slow wave)\n"
                "Distribution: Generalized, frontal dominant / Generalized, frontal-central dominant\n"
                "Activation: HV is most effective / Awakening and sleep deprivation more prominent\n"
                "Photic: Less common / Photosensitivity in ~30%\n"
                "Age: 4–10 years / 12–18 years\n"
                "Background: Normal / Normal\n"
                "Prognosis: Often remits / Lifelong in most\n"
                "Key distinguishing point: JME shows polyspike-wave at >3.5 Hz, activated by awakening; CAE shows classic 3 Hz spike-wave activated by hyperventilation."
            ),
            (
                "36. What is FIRDA? Clinical significance?",
                "FIRDA (Frontal Intermittent Rhythmic Delta Activity) consists of rhythmic, sinusoidal or monomorphic delta waves (1.5–2.5 Hz) appearing in runs, predominantly over the frontal regions, bilaterally and synchronously. It is typically intermittent and may alternate with normal background.\n"
                "Clinical significance:\n"
                "- Non-specific marker of diffuse cerebral dysfunction or subcortical/diencephalic disturbance\n"
                "- Causes: metabolic encephalopathy, increased intracranial pressure, deep midline (thalamic, hypothalamic) lesions, hydrocephalus, toxic-metabolic conditions\n"
                "- Can also be seen in some seizure disorders\n"
                "- NOT specific for any single condition; must be correlated clinically\n"
                "- OIRDA (Occipital IRDA) is the childhood equivalent, associated with absence epilepsy"
            ),
            (
                "37. How to differentiate normal discontinuous neonatal EEG from pathological?",
                "Normal discontinuous (term neonate, quiet sleep):\n"
                "- State-dependent (only in quiet sleep)\n"
                "- IBI duration <10 seconds at term (up to 30 sec premature)\n"
                "- IBI minimum amplitude 25–50 µV\n"
                "- Burst content: normal (delta brushes if premature, mixed frequencies)\n"
                "- Normal cycling between active and quiet sleep\n"
                "- Interhemispheric synchrony >70% at term\n\n"
                "Pathological (burst-suppression):\n"
                "- State-independent (continuous, not just quiet sleep)\n"
                "- IBI >30 sec or near-isoelectric (<5 µV) between bursts\n"
                "- Invariant pattern (no state change)\n"
                "- Abnormal burst content (rhythmic spikes)\n"
                "- Poor prognostic indicator (HIE, metabolic, structural)"
            ),
            (
                "38. What are PLEDs? Which conditions produce them?",
                "PLEDs (Periodic Lateralized Epileptiform Discharges) — now renamed LPDs (Lateralized Periodic Discharges) by ACNS — are repetitive, periodic, sharply contoured discharges occurring at regular intervals (0.5–2 Hz), maximal over one hemisphere or focal brain region.\n"
                "They indicate acute focal brain injury and carry a high risk (~50–80%) for clinical seizures.\n"
                "Conditions:\n"
                "1. Acute stroke (most common cause in adults)\n"
                "2. Herpes simplex encephalitis (temporal lobe — classic association)\n"
                "3. Brain tumors (rapidly growing glioma)\n"
                "4. Brain abscess\n"
                "5. Post-traumatic brain injury\n"
                "6. Focal cortical dysplasia"
            ),
            (
                "39. Role of source localization and dipole analysis in epilepsy surgery workup.",
                "Source localization uses mathematical models (dipole fitting, LORETA, beamforming) to estimate the intracranial generator of scalp-recorded epileptiform activity.\n"
                "Dipole analysis: Models each spike discharge as an equivalent current dipole — a point source with direction and magnitude. Phase reversal in bipolar montage identifies the electrode of maximum negativity (surface negative pole of the dipole).\n"
                "Applications in presurgical workup:\n"
                "1. Non-invasive localization of the irritative zone before intracranial EEG\n"
                "2. Guiding placement of intracranial electrode arrays\n"
                "3. EEG-fMRI and MEG co-registration for multimodal localization\n"
                "4. Dipole cluster localization correlates well with electrocorticography in temporal lobe cases\n"
                "Limitations: Accuracy limited by skull conductivity, depth of source, and choice of head model."
            ),
            (
                "40. EEG changes across stages of anesthesia.",
                "Stage 1 (Light sedation/induction): Alpha activity + anterior beta shift; alert pattern lost.\n"
                "Stage 2 (Light anesthesia): Beta and fast spindle activity; paradoxical excitation pattern.\n"
                "Stage 3 (Surgical anesthesia): Anterior dominant delta and theta activity; amplitude increases; spindle-like activity; suppression periods begin.\n"
                "Stage 4 (Deep anesthesia): Burst-suppression pattern — bursts of high-amplitude polyspike/delta alternating with suppression.\n"
                "Stage 5 (Isoelectric/overdose): Flat isoelectric EEG.\n"
                "Depth of anesthesia monitors (BIS, Entropy) use processed EEG parameters to maintain optimal anesthetic depth and reduce awareness."
            ),
            (
                "41. What is SREDA? Why is it a diagnostic pitfall?",
                "SREDA (Subclinical Rhythmic Electrographic Discharge in Adults) is an uncommon, benign EEG pattern of uncertain significance. It consists of rhythmic, sharply contoured theta or alpha-frequency activity (5–7 Hz), appearing bilaterally over posterior or parietal regions, without clinical correlate. Duration: 20 seconds to several minutes. It typically occurs in older adults (>50 years) during drowsiness or relaxed wakefulness.\n"
                "Diagnostic pitfall:\n"
                "- Its rhythmic, evolving appearance mimics an electrographic seizure (absence or non-convulsive status)\n"
                "- Can lead to unnecessary antiepileptic drug treatment\n"
                "- Distinguished by: no clinical correlate, no post-discharge slowing, stereotyped morphology, no true evolution of frequency, age group"
            ),
            (
                "42. Pre-ictal changes in TLE with mesial temporal sclerosis (scalp EEG)?",
                "Pre-ictal scalp EEG changes in mesial TLE (seconds to minutes before clinical onset):\n"
                "1. Focal attenuation over the temporal lobe (ipsilateral)\n"
                "2. Rhythmic delta or theta activity in the anterior temporal region\n"
                "3. Theta hypersynchrony ('pre-ictal theta') over F7/F8 or T3/T4\n"
                "4. Reduced variability of background activity\n"
                "5. Occasionally, contralateral suppression\n"
                "These changes reflect the initial activation of the mesial temporal structures before propagation to neocortex. However, scalp EEG may miss the very earliest mesial hippocampal onset — intracranial depth electrodes are required for definitive onset localization."
            ),
            (
                "43. What is 'EEG negativity' and what does polarity reversal tell you?",
                "By convention, in most EEG display systems, upward deflections on the EEG represent negative voltage at the active electrode. A spike or sharp wave is a surface-negative event (the pyramidal cell apical dendrite generates a negative sink at the cortical surface during a PDS).\n"
                "Polarity reversal: In a bipolar montage, the electrode with maximum negativity is identified by phase reversal — where adjacent channels show deflections in opposite directions. The electrode where the reversal occurs is over the epileptogenic source.\n"
                "Example: If F7–T3 deflects down and T3–T5 deflects up → phase reversal at T3 → maximum negativity at T3 → source is under T3 (mid-temporal)."
            ),
            (
                "44. How to interpret normal EEG in a known epileptic on AEDs? Limitations?",
                "A normal EEG in a patient on antiepileptic drugs (AEDs) must be interpreted cautiously:\n"
                "1. AEDs (phenobarbitone, benzodiazepines, carbamazepine) can suppress IEDs without abolishing seizures\n"
                "2. The EEG represents only a 20–40 min sample of a continuous process\n"
                "3. IEDs are state-dependent (more in drowsiness/sleep) — a waking-only recording may be falsely normal\n"
                "4. Deep sources (mesial temporal, frontal base) may not project to scalp\n"
                "5. Seizure frequency affects IED yield\n"
                "Clinical conclusion: Normal EEG on AEDs does not mean the patient is seizure-free, nor can AEDs be withdrawn based on this alone. Use clinical parameters + ambulatory/video-EEG."
            ),
            (
                "45. What are high-frequency oscillations (HFOs) in EEG? Significance in epilepsy?",
                "HFOs are EEG oscillations with frequencies above the conventional range. Two main subtypes:\n"
                "Ripples: 80–250 Hz — occur in normal hippocampus during memory consolidation (sharp-wave ripples); also mark epileptogenic tissue.\n"
                "Fast ripples: 250–600 Hz — highly specific marker of epileptogenic tissue; rarely seen in normal brain.\n"
                "Significance:\n"
                "- Pathological HFOs (especially fast ripples) identify the seizure-onset zone better than conventional IEDs\n"
                "- Surgical resection of tissue generating fast ripples predicts seizure freedom\n"
                "- Require microelectrodes or high-density intracranial EEG for reliable detection (not visible on routine scalp EEG)\n"
                "- Active area of research for non-invasive detection using MEG and high-density scalp EEG"
            ),
        ]
    },
    {
        "title": "SECTION D: DISTINCTION LEVEL (Q46–Q60)",
        "subtitle": "For the outstanding candidate",
        "color": "#4a148c",
        "qas": [
            (
                "46. Critically evaluate sensitivity and specificity of routine scalp EEG in epilepsy.",
                "Sensitivity: A single routine EEG detects IEDs in only 30–55% of patients with definite epilepsy. With repeat studies (3 EEGs), sensitivity rises to ~80–90%. With sleep deprivation or prolonged recording, it approaches 92%.\n"
                "Specificity: IEDs are seen in 0.5–2% of normal subjects (higher in children). Thus, a single IED does not diagnose epilepsy.\n"
                "Fundamental limitations:\n"
                "1. Sampling problem: A 20–30 min recording captures <0.01% of brain activity\n"
                "2. Spatial limitation: Scalp electrodes are 6 cm apart; sources <6 cm2 of cortex may be invisible\n"
                "3. Signal-to-noise: Skull attenuates signal by 30–40x; deep foci (hippocampus, orbitofrontal) may not project to scalp\n"
                "4. State dependence: IEDs more common in sleep; wake-only recordings underestimate\n"
                "5. Medication effect: AEDs suppress IEDs\n"
                "6. Observer variability: Inter-rater agreement for spike detection is only ~70–80%\n"
                "Conclusion: EEG is a supportive tool; epilepsy is a clinical diagnosis."
            ),
            (
                "47. Scalp EEG vs. intracranial EEG (iEEG). When is iEEG indicated? Types?",
                "Scalp EEG: Non-invasive; records from skull surface; attenuated and smeared signal; limited spatial resolution (~3–6 cm); cannot record from deep structures.\n"
                "Intracranial EEG (iEEG): Electrodes placed directly on or in brain tissue; provides high spatial resolution (<1 mm); direct cortical signal; can record HFOs; guides surgical resection.\n"
                "Indications for iEEG (presurgical evaluation):\n"
                "1. MRI-negative focal epilepsy\n"
                "2. Discordant non-invasive data (EEG, MRI, PET, SPECT disagree)\n"
                "3. Bilateral temporal IEDs requiring lateralization\n"
                "4. Seizure onset near eloquent cortex (language, motor)\n"
                "5. Multi-lobar or extratemporal epilepsy\n\n"
                "Types of iEEG:\n"
                "1. Subdural grids and strips (electrocorticography, ECoG) — surface arrays\n"
                "2. Stereo-EEG (SEEG) — depth electrodes implanted stereotactically; samples deep structures (amygdala, hippocampus, cingulate); becoming standard of care\n"
                "3. Foramen ovale electrodes — semi-invasive; mesial temporal access"
            ),
            (
                "48. Ictal onset zone, irritative zone, symptomatogenic zone — EEG contributions.",
                "Irritative zone: Brain region generating interictal epileptiform discharges (IEDs). Defined by interictal EEG/MEG. It is typically larger than the seizure-onset zone.\n\n"
                "Ictal onset zone (seizure-onset zone, SOZ): Brain region where seizures originate. Defined by ictal EEG (scalp or intracranial). The EEG shows the earliest ictal change. This is the primary surgical target.\n\n"
                "Symptomatogenic zone: Region whose activation produces the ictal semiology (clinical symptoms). Defined by correlating EEG ictal onset with clinical features. It may be at or near the SOZ or propagated.\n\n"
                "EEG contributions: Scalp EEG defines irritative zone (IEDs) and provides approximate SOZ localization. iEEG is required for precise SOZ definition and stimulation mapping of symptomatogenic/eloquent cortex.\n"
                "Surgical success correlates with complete resection of the SOZ (Engel Class I outcome)."
            ),
            (
                "49. Bilateral independent temporal discharges in TLE patient being evaluated for surgery — implications?",
                "Bilateral independent temporal discharges (BITDs) are a major surgical challenge. Implications:\n"
                "1. Suggests bilateral independent temporal lobe foci — bitemporal epilepsy\n"
                "2. Standard unilateral temporal lobectomy has low success rate if truly bitemporal\n"
                "3. Risk of post-surgical memory impairment if resection performed on dominant hemisphere\n\n"
                "Additional investigations required:\n"
                "1. Prolonged video-EEG monitoring: Capture multiple habitual seizures; determine if ictal onset is consistently lateralized\n"
                "2. 3T MRI with dedicated epilepsy protocol: Look for unilateral mesial temporal sclerosis\n"
                "3. FDG-PET: Unilateral hypometabolism supports one side as predominant focus\n"
                "4. SISCOM/Ictal SPECT: Regional hyperperfusion at seizure onset\n"
                "5. Neuropsychology: Memory testing (Wada test or fMRI lateralization of memory) to assess risk\n"
                "6. SEEG (stereo-EEG): Bilateral depth electrode implantation to define whether seizures start unilaterally\n"
                "7. MEG: Non-invasive dipole clustering"
            ),
            (
                "50. What is continuous EEG monitoring (cEEG)? ICU indications?",
                "Continuous EEG (cEEG) monitoring involves prolonged (>24 hours) real-time EEG recording, typically used in critical care or inpatient settings with automated seizure detection algorithms and remote review.\n"
                "ICU Indications (Neurology/Psychiatry interface):\n"
                "1. Comatose patients after cardiac arrest — detect non-convulsive seizures and assess prognosis (burst-suppression, reactivity)\n"
                "2. Non-convulsive status epilepticus (NCSE) detection — up to 20% of comatose patients have subclinical seizures\n"
                "3. Monitoring response to anti-seizure treatment in refractory status epilepticus\n"
                "4. Traumatic brain injury — detect delayed seizures and cortical spreading depression\n"
                "5. Subarachnoid hemorrhage — detect delayed cerebral ischemia (EEG is more sensitive than clinical exam)\n"
                "6. Metabolic encephalopathy — characterize degree of dysfunction\n"
                "7. Autoimmune encephalitis (e.g., Anti-NMDAR) — extreme delta brush pattern"
            ),
            (
                "51. EEG findings in NCSE. Differentiation from encephalopathy?",
                "Non-Convulsive Status Epilepticus (NCSE) EEG criteria (Salzburg criteria):\n"
                "1. Epileptiform discharges >2.5 Hz lasting >10 sec, OR\n"
                "2. Epileptiform discharges ≤2.5 Hz OR rhythmic delta/theta activity with:\n"
                "   a. Subtle clinical ictal phenomena, OR\n"
                "   b. EEG and clinical improvement with IV benzodiazepine\n\n"
                "Differentiation from encephalopathy:\n"
                "Feature / NCSE / Encephalopathy\n"
                "Discharges: Rhythmic, evolving, periodic EDs / Diffuse slow (GRDA, delta)\n"
                "Frequency evolution: Yes (increases then decreases) / No\n"
                "Clinical correlation: Subtle (eye deviation, automatisms) / Decreased GCS, fluctuating\n"
                "Benzo response: EEG + clinical improvement / Clinical improvement without EEG change\n"
                "Background: May preserve reactivity initially / Diffuse suppression/slowing\n"
                "Key teaching: The only definitive way to diagnose NCSE is to treat with IV benzodiazepine and observe simultaneous EEG + clinical response."
            ),
            (
                "52. What is qEEG? Applications and limitations in psychiatric disorders?",
                "Quantitative EEG (qEEG) applies mathematical algorithms (FFT, wavelet analysis, coherence, source localization) to transform raw EEG into numerical measures displayed as topographic brain maps or spectral plots.\n"
                "Applications in psychiatry:\n"
                "1. Depression: Alpha asymmetry (reduced left frontal alpha power in melancholic depression); theta cordance predicts antidepressant response; rTMS/ECT treatment monitoring\n"
                "2. Schizophrenia: Reduced gamma oscillations (40 Hz) in frontal/temporal regions; reduced P300 correlates; reduced coherence\n"
                "3. ADHD: Increased theta/beta ratio — used in some centres to support diagnosis\n"
                "4. Dementia: Slowing of dominant frequency; diffuse theta/delta increase\n"
                "5. Biofeedback/neurofeedback therapy monitoring\n\n"
                "Limitations:\n"
                "- Not standardized across laboratories\n"
                "- Normative databases vary by age/sex\n"
                "- Susceptible to artifact (especially muscle)\n"
                "- Group differences don't translate reliably to individual diagnosis\n"
                "- Not yet a validated diagnostic biomarker for any psychiatric disorder"
            ),
            (
                "53. ACNS standardized critical care EEG terminology — four key descriptors.",
                "The ACNS Standardized Critical Care EEG Terminology (2012, updated 2021) uses a structured nomenclature:\n"
                "1. Location: Generalized (G) vs. Lateralized (L) vs. Bilateral independent (BI) vs. Multifocal (Mf)\n"
                "2. Pattern type:\n"
                "   - Periodic Discharges (PDs): LPDs (formerly PLEDs), GPDs (formerly GPEDS), BIPDs\n"
                "   - Rhythmic Delta Activity (RDA): LRDA, GRDA\n"
                "   - Spike-wave/sharp-wave patterns\n"
                "3. Frequency: Rate of discharges (e.g., 1 Hz, 2 Hz)\n"
                "4. Amplitude: Low (<20 µV), medium, high (>150 µV)\n"
                "Additional descriptors: Plus (+) modifier (superimposed fast activity), triphasic morphology, sharpness (sharp vs. blunt), duration, evolution.\n"
                "Key patterns: LPDs, GPDs, LRDA, GRDA, seizure (any evolving pattern), Status epilepticus on EEG."
            ),
            (
                "54. Pathophysiology of absence epilepsy — thalamocortical network. AED mechanisms?",
                "The thalamocortical loop is the key network:\n"
                "1. Cortical pyramidal neurons (layers 5–6, somatosensory cortex) → excite thalamic relay neurons AND thalamic reticular nucleus (TRN)\n"
                "2. TRN (GABAergic) → inhibits TC relay neurons via GABA-A and GABA-B receptors\n"
                "3. GABA-B activation → K+ channel opening → deep hyperpolarization → deinactivation of T-type (low-threshold) Ca2+ channels\n"
                "4. T-channel burst discharge → excites cortex again → cycle repeats at ~3 Hz\n"
                "5. Cortical hypersensitivity (SWD initiation zone) — perioral somatosensory cortex in rats\n\n"
                "AED mechanisms targeting this:\n"
                "- Ethosuximide: Blocks T-type Ca2+ channels in TC neurons → first-line for pure absence\n"
                "- Valproate: T-channel blockade + GABA enhancement + multiple mechanisms\n"
                "- Lamotrigine: Na+ channel + some T-channel blockade\n"
                "- Benzodiazepines: GABA-A potentiation (acute but not chronic)\n"
                "- Avoid: Carbamazepine, oxcarbazepine, phenytoin, gabapentin — can worsen absence"
            ),
            (
                "55. Role of EEG in ECT. EEG endpoint for adequate seizure?",
                "EEG monitoring is the gold standard for assessing seizure adequacy during ECT:\n"
                "Before ECT: Baseline EEG documents pre-treatment brain activity.\n"
                "During ECT:\n"
                "1. Confirms seizure induction (motor response may be suppressed by muscle relaxants)\n"
                "2. Provides accurate seizure duration measurement\n"
                "3. Detects missed seizures (electrical without motor response)\n"
                "4. Detects ictal pattern quality\n\n"
                "EEG endpoint for adequate seizure (Royal College of Psychiatrists guidelines):\n"
                "1. Duration ≥25 seconds of sustained ictal activity on EEG\n"
                "2. Coherent ictal morphology: generalized high-amplitude polyspike-wave evolving to regular delta\n"
                "3. Post-ictal suppression: marked attenuation/flat EEG for ≥2 seconds after seizure end\n"
                "4. Symmetrical bilateral pattern\n\n"
                "Inadequate seizure: <25 sec, fragmented pattern, lack of post-ictal suppression — indicates need to adjust stimulus parameters (increase dose, change electrode placement)."
            ),
            (
                "56. Ethical and medicolegal implications of EEG in fitness-to-drive assessment.",
                "EEG in the context of driving raises complex ethical and legal issues:\n\n"
                "Clinical issues:\n"
                "- EEG is NOT required for routine driving license assessment after a seizure\n"
                "- A normal EEG does not permit driving if clinical seizure has occurred\n"
                "- Specific IED patterns (e.g., 3 Hz SW in absence, JME polyspikes) may indicate ongoing seizure risk even if patient appears asymptomatic\n\n"
                "Ethical dimensions:\n"
                "1. Confidentiality vs. duty of care to the public — DVLA/RTO disclosure obligations (UK DVLA: physician must advise patient; in some jurisdictions must report directly)\n"
                "2. Accuracy of EEG interpretation — over-reading leads to unnecessary license suspension; under-reading is dangerous\n"
                "3. Informed consent: Patient must be informed of EEG implications for driving\n"
                "4. Occupational consequences: Incorrect EEG interpretation can destroy livelihoods\n\n"
                "Medicolegal:\n"
                "- Physician documenting a normal EEG while knowing the patient has active epilepsy and continues to drive has potential liability\n"
                "- EEG reports should state clearly what the findings do/do not imply for driving"
            ),
            (
                "57. EEG in brain death diagnosis. Technical requirements?",
                "EEG is used as a confirmatory test for brain death (electrocerebral inactivity, ECI or electrocerebral silence, ECS). It supports but does not replace clinical criteria.\n\n"
                "EEG finding: Isoelectric (flat) EEG — no cerebral electrical activity >2 µV across all electrodes.\n\n"
                "AEEGS Technical Requirements for ECI (American EEG Society):\n"
                "1. Minimum 8 scalp electrodes + ground + reference (earlobe)\n"
                "2. Inter-electrode impedances 100–10,000 Ω\n"
                "3. Sensitivity increased to 2 µV/mm (more sensitive than routine)\n"
                "4. Time constant ≥0.3 seconds; HF filter ≥30 Hz\n"
                "5. Record minimum 30 minutes\n"
                "6. Technologist must physically stimulate patient (painful, auditory, visual) during recording\n"
                "7. Two recordings separated by ≥6 hours (or per local protocol)\n"
                "8. Artifacts must be excluded (60 Hz noise, electrode pop, cardiac artifact)\n"
                "9. Must be performed by qualified neurophysiology technologist\n"
                "10. Exclude reversible conditions (hypothermia <35°C, sedatives, metabolic)"
            ),
            (
                "58. Significance of interictal HFOs (ripples vs. fast ripples) in predicting epileptogenic zone. Current evidence?",
                "High-frequency oscillations (HFOs) as epileptic biomarkers:\n\n"
                "Ripples (80–250 Hz):\n"
                "- Occur in normal hippocampus (physiological sharp-wave ripples in memory)\n"
                "- Also mark epileptogenic tissue — less specific than fast ripples\n"
                "- Context-dependent interpretation required\n\n"
                "Fast Ripples (FRs, 250–600 Hz):\n"
                "- Highly specific to epileptogenic tissue; rarely seen in normal brain\n"
                "- Represent out-of-phase firing of small neuron clusters (microseizures)\n"
                "- Surgical resection of FR-generating tissue predicts Engel Class I outcome\n\n"
                "Current evidence (Jacobs et al., 2012; Zijlmans et al., 2012; Frauscher et al., 2017):\n"
                "- Resection of >80% of fast ripple-generating tissue → 80%+ seizure freedom\n"
                "- FRs outperform conventional IEDs in delineating SOZ in MRI-negative epilepsy\n"
                "- Detection requires microelectrodes (not standard clinical electrodes)\n"
                "- Non-invasive detection via MEG and high-density EEG is under active investigation\n"
                "- Not yet in routine clinical use — research tool currently"
            ),
            (
                "59. 7-year-old with staring spells, EEG shows 3 Hz generalized spike-wave. Parental counselling?",
                "This is childhood absence epilepsy (CAE). Counselling framework:\n\n"
                "Diagnosis confirmation: The EEG pattern (3 Hz GSW) + clinical features (brief staring, eye flicker, abrupt onset/offset, activation by HV) confirm CAE. Differentiate from focal onset impaired awareness seizures.\n\n"
                "Prognosis (can they outgrow it?):\n"
                "- Approximately 60–70% of CAE patients achieve complete remission by mid-adolescence (age 12–14)\n"
                "- Predictors of remission: Pure absence only, 3 Hz GSW, no other seizure types, normal IQ, normal neurological exam, no family history of JME\n"
                "- Predictors of persistence/evolution to JME: Myoclonic jerks, GTCS, age >10 at onset, persisting EEG abnormalities, eyelid myoclonia\n"
                "- EEG normalization correlates with remission but is not always prerequisite\n\n"
                "Treatment: Ethosuximide (first-line; superior for attention outcomes per NEAD trial) or valproate. Avoid carbamazepine.\n\n"
                "Safety: No swimming unsupervised, bicycle helmets, shower not bath, avoid heights.\n\n"
                "Academic: Inattention/staring may affect learning; inform school."
            ),
            (
                "60. Resident writes 'EEG is normal, epilepsy ruled out.' Your response as examiner and clinician?",
                "This is a critically dangerous and incorrect statement. As the examiner and clinician, my response would be:\n\n"
                "Immediate correction: A normal EEG does NOT rule out epilepsy. This is one of the most common and clinically dangerous misconceptions in neurology and psychiatry.\n\n"
                "Teaching points:\n"
                "1. Sensitivity problem: A routine 20–30 min EEG detects IEDs in only 30–55% of patients with known epilepsy. A negative result does not exclude the diagnosis.\n"
                "2. Sampling bias: EEG is a brief snapshot. Seizures/IEDs are episodic. No discharge in one recording means 'no discharge captured,' not 'no epilepsy.'\n"
                "3. False negative sources: Deep foci (mesial temporal, frontal), small cortical generators, medication suppression, poor recording quality.\n"
                "4. Epilepsy is a clinical diagnosis — based on history of two or more unprovoked seizures. EEG supports but does not make or exclude the diagnosis.\n"
                "5. 'Normal EEG with clinical seizures' → action required: Repeat EEG, sleep-deprived EEG, prolonged ambulatory EEG, or video-EEG monitoring.\n"
                "6. Correct documentation should read: 'No epileptiform activity was recorded during this study. A normal EEG does not exclude a diagnosis of epilepsy.'\n\n"
                "As examiner: I would use this as a teaching moment — and would also note that this statement could have medicolegal consequences if written in a clinical report."
            ),
        ]
    }
]

# ─────────────────────────────────────────────
# BUILD DOCUMENT
# ─────────────────────────────────────────────

story = []

# Title block
story.append(Spacer(1, 0.3*cm))
story.append(Paragraph("EEG VIVA EXAMINATION", title_style))
story.append(Paragraph("MD Psychiatry | External Examiner", subtitle_style))
story.append(Paragraph("60 Questions with Model Answers", subtitle_style))
story.append(Spacer(1, 0.2*cm))
story.append(HRFlowable(width="100%", thickness=2, color=colors.HexColor("#1a237e"), spaceAfter=8))

# Coverage note
cover_note = ParagraphStyle("CoverNote", parent=styles["Normal"],
    fontSize=9.5, textColor=colors.HexColor("#4a148c"),
    spaceBefore=4, spaceAfter=10,
    leftIndent=0.3*cm, leading=13)
story.append(Paragraph(
    "<b>EEG Types Covered:</b> Normal Adult EEG · Normal Infant/Neonatal EEG · "
    "Temporal Lobe Epilepsy (TLE) · Absence Seizures · Generalized Tonic-Clonic Seizures (GTCS)",
    cover_note))
story.append(HRFlowable(width="100%", thickness=1, color=colors.HexColor("#9e9e9e"), spaceAfter=10))

section_colors = ["#e8eaf6", "#e8f5e9", "#fff3e0", "#f3e5f5"]
section_header_colors = ["#1a237e", "#1b5e20", "#e65100", "#4a148c"]

for sec_idx, section in enumerate(sections):
    hdr_color = colors.HexColor(section_header_colors[sec_idx])
    bg_color = colors.HexColor(section_colors[sec_idx])

    # Section header as a table for colored background
    sec_hdr_style = ParagraphStyle("SH", parent=styles["Normal"],
        fontSize=12, textColor=colors.white,
        fontName="Helvetica-Bold", leading=16, alignment=TA_CENTER)
    sec_sub_style = ParagraphStyle("SS", parent=styles["Normal"],
        fontSize=9, textColor=colors.HexColor("#eeeeee"),
        fontName="Helvetica-Oblique", leading=12, alignment=TA_CENTER)

    sec_content = [[
        Paragraph(section["title"], sec_hdr_style),
        Paragraph(section["subtitle"], sec_sub_style)
    ]]
    sec_table = Table(sec_content, colWidths=[17*cm], rowHeights=[None, None])
    # Flatten to single cell
    sec_cell = Table(
        [[Paragraph(section["title"], sec_hdr_style)],
         [Paragraph(section["subtitle"], sec_sub_style)]],
        colWidths=[17*cm]
    )
    sec_cell.setStyle(TableStyle([
        ("BACKGROUND", (0,0), (-1,-1), hdr_color),
        ("BOTTOMPADDING", (0,0), (-1,-1), 6),
        ("TOPPADDING", (0,0), (-1,-1), 6),
        ("LEFTPADDING", (0,0), (-1,-1), 10),
        ("RIGHTPADDING", (0,0), (-1,-1), 10),
        ("ROUNDEDCORNERS", [5,5,5,5]),
    ]))
    story.append(Spacer(1, 0.3*cm))
    story.append(sec_cell)
    story.append(Spacer(1, 0.2*cm))

    for q, a in section["qas"]:
        story.append(Paragraph(q, q_style))
        # Format answer — handle newlines
        for line in a.split("\n"):
            line = line.strip()
            if line:
                story.append(Paragraph(line, a_style))
        story.append(HRFlowable(width="85%", thickness=0.5,
            color=colors.HexColor("#cccccc"), spaceAfter=2))

    story.append(PageBreak())

# Remove last page break if needed
if isinstance(story[-1], PageBreak):
    story.pop()

# Footer note
story.append(Spacer(1, 0.5*cm))
story.append(HRFlowable(width="100%", thickness=1.5, color=colors.HexColor("#1a237e"), spaceAfter=6))
footer_style = ParagraphStyle("Footer", parent=styles["Normal"],
    fontSize=8.5, textColor=colors.HexColor("#5c5c5c"),
    fontName="Helvetica-Oblique", alignment=TA_CENTER, leading=12)
story.append(Paragraph(
    "This document is intended for educational use in MD Psychiatry examination preparation. "
    "EEG interpretation should always be correlated with clinical findings. "
    "Prepared as a comprehensive viva guide covering: Normal Adult EEG, Normal Infant EEG, TLE, Absence Seizures, GTCS.",
    footer_style))

doc.build(story)
print(f"PDF saved: {OUTPUT}")

Successfully replaced 1 instance(s) of the string in '/tmp/workspace/eeg-viva/generate_eeg_viva.py'