Good afternoon sir Patient named 60y female yasmin kco sjogrens + htn

Good afternoon sir Patient named 60y female yasmin kco sjogrens + htn + ckd a/w severe anemia (hb-4.4) + ?secondary myelofibrosis ?primary mpn Sir patient ko humne kal advice kiya tha admission and pcv transfusion patient subah emergency mei aye indoor hone for blood transfusion Patient is on Tab prednisolone 10mg po 1-0-0 Tab cilacar 10mg po 1-0-0 Tab sobisis 1000mg po 1-0-1 What is definitive management

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Good afternoon! Here is a structured management plan for Yasmin:

Yasmin — 60F | Sjögren's + HTN + CKD | Hb 4.4 | ?Autoimmune Myelofibrosis vs Primary MPN

🔴 IMMEDIATE: PCV Transfusion (Already In Progress)

Hb 4.4 is critically low — this is a chronic anemia, so the cardiac compensatory mechanisms are present but the risk of volume overload and decompensation is HIGH.

Transfusion Protocol for Hb <5 in chronic anemia:

Small aliquots only — 2–3 mL/kg per unit (NOT standard 1 unit upfront)
Slow rate — 1 mL/kg/hour
Target Hb: Raise to ~7–8 g/dL (do NOT over-transfuse; the aim is symptomatic relief, not normalization)
Monitor closely: SpO₂, BP, JVP, lung auscultation (risk of TACO — transfusion-associated circulatory overload)
IV Furosemide 20–40 mg between units (given CKD + risk of overload)
Pre-transfusion: Cross-match, DAT (direct antiglobulin test) — important in autoimmune context

🔍 CRITICAL FIRST STEP: Differentiate Autoimmune MF vs Primary MPN

This distinction changes everything:

Feature	Autoimmune MF (AMF)	Primary MPN/MF
Association	Sjögren's, SLE, scleroderma ✅	De novo
BM histology	Reticulin fibrosis, NO clustered/atypical megakaryocytes	Atypical megakaryocytes, clustered
DAT	May be positive	Usually negative
ANA/RF	Elevated	Usually absent
Prognosis	Benign, reversible	Malignant, progressive
Treatment	Corticosteroids → respond well	JAK inhibitors, Allo-HSCT

✅ WORKUP to Order NOW (if not already done):

Hematology:

Bone marrow biopsy — most critical (fibrosis grade, megakaryocyte morphology, cellularity)
JAK2 V617F mutation (also CALR, MPL if JAK2 negative) → if positive → Primary MPN
Peripheral blood film — leukoerythroblastic picture, dacrocytes (tear drop cells)?
Reticulocyte count
LDH, Uric acid (disease burden markers)
Serum EPO level

Autoimmune:

ANA, anti-SSA/SSB (already known Sjögren's), anti-dsDNA
DAT (direct Coombs) — rule out concurrent autoimmune hemolysis
Serum protein electrophoresis

Baseline / Organ Function:

CBC + differential, renal panel (CKD — baseline Cr/eGFR)
Coagulation profile (PT/INR, aPTT)
LFT, Ferritin, B12, Folate, Iron studies (rule out nutritional deficiencies compounding anemia)
Chest X-ray, ECHO (baseline cardiac function, volume status)
Abdominal USG — spleen size (splenomegaly = MPN more likely)

💊 DEFINITIVE MANAGEMENT (Depends on Diagnosis):

IF Autoimmune Myelofibrosis (AMF — most likely given Sjögren's):

First-Line: Corticosteroids — responds dramatically

Prednisolone 1 mg/kg/day (~60 mg/day for this patient)
She is already on Tab Prednisolone 10 mg — this dose is subtherapeutic for AMF
Taper over 1–3 months once peripheral counts normalize
Complete normalization of peripheral blood counts expected in majority
Bone marrow fibrosis reduction may also occur (though not required for clinical response)

If partial/inadequate corticosteroid response:

Add Hydroxychloroquine (standard Sjögren's baseline therapy — 200–400 mg/day)
Consider Azathioprine or Mycophenolate mofetil as steroid-sparing agents
Rituximab (anti-CD20) for refractory severe extraglandular Sjögren's — now prioritized as first-line biologic in 2024 BSR guidelines

IF Primary MPN / Primary Myelofibrosis confirmed (JAK2+, atypical BM):

Risk stratification using DIPSS-Plus score then:

Risk	Management
Low risk	Observation + symptom management
Intermediate-1	Individualized ± JAK inhibitor
Intermediate-2/High	JAK inhibitor + consider Allogeneic HSCT (only curative option)

JAK Inhibitors available:

Ruxolitinib — JAK1/2, 1st line; dosing based on platelet count; excellent for splenomegaly & symptoms; worsens anemia (important in this patient)
Fedratinib — JAK2; check thiamine levels before starting
Momelotinib — JAK1/2/ACVR1; specifically approved (Sep 2023, FDA) for MF patients WITH anemia → best choice here given Hb 4.4
Pacritinib — for patients with severe thrombocytopenia (plt <100k)

For anemia specifically in MF:

Erythropoiesis-stimulating agents (EPO) — ~1/3 response rate, try under expert supervision
Danazol (androgen) — can improve anemia in MF
Lenalidomide ± prednisone — particularly if del(5q) or JAK2+
Repeat PCV transfusions as supportive care

💊 Current Medications — Review:

Drug	Purpose	Comment
Prednisolone 10 mg OD	Sjögren's / AMF?	Dose likely insufficient for AMF — may need uptitration to 1 mg/kg
Cilacar (Cilnidipine) 10 mg OD	HTN	Continue — calcium channel blocker, acceptable in CKD
Sobisis (Sodium bicarbonate) 1000 mg BD	CKD metabolic acidosis	Continue — standard CKD management

Consider adding:

Hydroxychloroquine 200 mg BD — cornerstone of Sjögren's treatment (not currently on this)
Folic acid 5 mg OD — especially if hemolysis or nutritional component
Proton pump inhibitor (cover steroids)
Calcium + Vitamin D (steroid osteoporosis prophylaxis — important in 60F)
Avoid NSAIDs (CKD)

🎯 Key Message

Given Sjögren's + bone marrow fibrosis, Autoimmune Myelofibrosis (AMF) is the most likely diagnosis here — this is a benign, steroid-responsive condition with excellent prognosis. The current prednisolone 10 mg dose needs to be increased to therapeutic levels (1 mg/kg/day) once the bone marrow biopsy confirms AMF and JAK2/CALR mutations come back negative. Do NOT start JAK inhibitors until Primary MPN is excluded.

Urgent hematology consultation + bone marrow biopsy is the immediate priority alongside the transfusion.

Goldman-Cecil Medicine; Washington Manual of Medical Therapeutics; HTCT Primary Myelofibrosis Therapeutic Options

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📋 YASMIN — Report Summary & Analysis

🔬 BONE MARROW BIOPSY (AIIMS — Dr. Hema Parekh, Haematopathology)

Specimen: Bone marrow biopsy — 06 May 2026 Impression (readable from phone screen):

Overall cellularity ~70% (hypercellular)
Predominantly normoblastic erythropoiesis with some dysplastic features
Bone marrow shows moderate to marked (Grade 2–3) fibrosis
Admixed with predominantly normocellular — no lymphoid aggregates
Megakaryocytes: present, abnormal/atypical morphology noted
History mentions: K/C/O Sjögren's syndrome, AOCD, CKD, Anemia under evaluation
Advice: "Correlation with ECF & ICS is advisable to repeat Direct and Indirect of autoimmune process. Suggest JAK2 ECF & ICS is advisable to evaluate LVMVL (JAK2/CALR). BLOCKS PROVIDED WITH THE REPORT. PRESERVE CAREFULLY."

Translation: BM biopsy shows Grade 2–3 fibrosis. Pathologist is asking for JAK2/CALR mutation testing to differentiate primary MPN from autoimmune myelofibrosis.

🩸 CBC (Post-transfusion — 09 May 2026)

Parameter	Value	Normal	Interpretation
Haemoglobin	7.3 g/dL	12–15	Severe anemia (up from 4.4 — transfusion response)
WBC	8.62	4–10	Normal
RBC	2.62	3.8–4.8	Low
Hematocrit	23.5%	36–46	Low
MCV	89.5 fL	83–101	Normocytic
MCH	27.9	27–32	Low-normal
MCHC	31.2	31.5–34.5	Low-normal (borderline hypochromic)
RDW	19.7	11.6–14	⚠️ VERY HIGH — anisocytosis
Platelet count	145	150–410	Borderline low (mild thrombocytopenia)
MPV	7.3	7–11	Normal
Neutrophil	76.9%	40–80	Normal

🧪 RENAL FUNCTION TESTS

Parameter	Value	Normal	Interpretation
Blood Urea	87.7	13–43	⚠️ HIGH — azotemia
Creatinine	4.13 mg/dL	0.6–1.2	🔴 SEVERELY ELEVATED — advanced CKD
Sodium	140	132–146	Normal
Potassium	4.33	3.5–5.1	Normal
Chloride	105	99–109	Normal

eGFR estimate (CKD-EPI for 61F, Cr 4.13): ~12–14 mL/min/1.73m² → CKD Stage 5 (pre-dialysis)

🧪 URINE / OTHER

Parameter	Value	Interpretation
Urine Albumin/Creatinine Ratio	3995.2 (Normal 0–30)	🔴 Massive proteinuria — nephrotic-range
Urine Blood	Present (++)	Hematuria
Urine Protein	Present (+)	Proteinuria
Urine Pus Cells	1–2	Minimal
Ionised Calcium	1.17 (1.12–1.32)	Normal

🧠 CLINICAL INTERPRETATION

What do the reports tell us?

BM Biopsy: Grade 2–3 Myelofibrosis — this is significant fibrosis. The pathologist has NOT given a definitive primary vs secondary label and is requesting JAK2/CALR — this is the KEY pending result.
CBC pattern: Normocytic anemia + High RDW + Mild thrombocytopenia — classic for:
- Myelofibrosis (leukoerythroblastic picture expected — check peripheral smear for tear-drop cells)
- Anemia of CKD component (EPO deficiency)
- Mixed nutritional deficiency possible (high RDW)
CKD Stage 5 (Cr 4.13) — This is extremely important:
- Limits many drug choices
- EPO deficiency is contributing to anemia
- Renal replacement therapy discussion needed
- Avoid NSAIDs, nephrotoxic drugs, contrast
Massive proteinuria (ACR 3995) — This is nephrotic-range. In Sjögren's + myelofibrosis, renal involvement could be:
- Tubulointerstitial nephritis (most common in Sjögren's)
- Membranous nephropathy (Sjögren's-associated)
- Amyloidosis (CKD + myelofibrosis + proteinuria — must rule out)
- Glomerulopathy secondary to primary MF (recent 2025 systematic review confirms this association)

🎯 REVISED MANAGEMENT PLAN (Based on Reports)

IMMEDIATE (Today):

1. Continue transfusion protocol — Hb now 7.3 (up from 4.4 ✅), continue careful monitoring. Target Hb 8–9 g/dL.

2. URGENT: JAK2 V617F mutation + CALR + MPL mutations — Pathologist himself has asked for this. This is the single most important test to order right now. Do not start definitive treatment without this.

3. Peripheral blood smear — look for:

Dacrocytes (tear-drop cells) → if present, confirms myelofibrosis
Leukoerythroblastic picture (nucleated RBCs + immature WBCs) → severity marker

DRUG MANAGEMENT — CKD Stage 5 Modifications:

🔴 CRITICAL: Creatinine 4.13 = CKD Stage 5. Nearly ALL medications need dose adjustment.

IF Autoimmune MF confirmed (JAK2/CALR NEGATIVE):

Prednisolone increase to 0.5–1 mg/kg/day (~40–60 mg/day)
- Caution: Steroid hyperglycemia monitoring needed
- Bone protection: Tab Calcium carbonate + Vit D3 (avoid Ca in CKD stage 5 if PO4 high — check phosphate first)
Add Hydroxychloroquine 200 mg OD (not BD in CKD stage 5 — reduce dose)
- Safe in CKD, cardioprotective, baseline ophthalmology review
Proton pump inhibitor (omeprazole/pantoprazole) to cover steroids

IF Primary MF confirmed (JAK2/CALR POSITIVE):

Momelotinib is the preferred JAK inhibitor given anemia + MF — FDA-approved 2023 for MF with anemia
- Dose adjustment needed for CKD (eGFR <15 — limited data, haematology to decide)
Ruxolitinib — worsens anemia further — caution
Allo-HSCT: Contraindicated/very high risk with CKD Stage 5

CKD Stage 5 — Specific Management:

Issue	Action
Cr 4.13, eGFR ~12	Nephrology referral urgent — pre-dialysis planning
Massive proteinuria (ACR 3995)	Renal biopsy to characterize — amyloid? Membranous? TIN?
Anemia of CKD	EPO alfa/darbepoetin — start after transfusion stabilized (target Hb 10–11 in CKD)
Metabolic acidosis	Continue Sobisis (sodium bicarb) — continue
HTN	Continue Cilacar — good choice in CKD (CCB); avoid ACEi/ARB with Cr 4.13
Hyperphosphatemia	Check serum phosphate — if high, start phosphate binder
Hyperkalemia risk	Monitor K⁺ closely — currently 4.33 (borderline for CKD 5)

What to AVOID in this patient:

❌ NSAIDs (renal toxicity)
❌ IV Contrast (nephrotoxic with CKD 5)
❌ Methotrexate (renally cleared — contraindicated in CKD 5)
❌ High-dose ruxolitinib without haematology guidance (worsens anemia)
❌ Over-transfusion (TACO risk — CKD + cardiac)

Summary of Pending Tests Still Needed:

Test	Why
JAK2 V617F / CALR / MPL	Distinguish primary vs autoimmune MF — the ANSWER
Peripheral smear	Tear-drop cells, leukoerythroblastic picture
Serum ferritin, TIBC, iron	Mixed iron deficiency component?
Serum B12 + Folate	High RDW suggests nutritional component
LDH, Uric acid	Disease burden in MF
Serum phosphate, PTH	CKD mineral-bone disease
Renal biopsy	Massive proteinuria — must characterize the nephropathy
Peripheral smear + reticulocyte count	Hemolytic component?
DAT (Direct Coombs)	Autoimmune hemolysis in Sjögren's
Serum EPO level	Guide EPO therapy decision

Bottom line: The bone marrow biopsy has confirmed Grade 2–3 fibrosis. The pathologist has correctly flagged JAK2/CALR as the essential next step. This result will determine whether you are treating autoimmune MF (steroids ↑ dose) or primary MPN (JAK inhibitor). Meanwhile, the CKD Stage 5 + massive proteinuria is a parallel major concern requiring nephrology co-management and consideration of renal biopsy.

Paroxysmal nocturnal hemoglobinuria treTment

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Here is a comprehensive, up-to-date treatment guide for PNH:

Paroxysmal Nocturnal Hemoglobinuria (PNH) — Treatment

Quick Recap: Why PNH Lyses?

PIG-A gene mutation → deficiency of GPI anchor proteins → loss of CD55 (inhibits C3 convertase) and CD59 (inhibits membrane attack complex) → uncontrolled complement activation → intravascular hemolysis + thrombosis

🔵 Treatment Framework

1. SPECIFIC THERAPY — Complement Inhibitors (Disease-Modifying)

🥇 ANTI-C5 INHIBITORS (Terminal Complement Blockade)

Drug	Route	Dosing	Notes
Eculizumab (Soliris)	IV	600 mg/week × 4 wk → 900 mg at week 5 → 900 mg every 2 weeks	First approved; gold standard; ↓ hemolysis, ↓ transfusions, ↓ thrombosis
Ravulizumab (Ultomiris)	IV	Weight-based loading (2400–3000 mg) → 3000–3600 mg every 8 weeks	Longer half-life derivative of eculizumab; same efficacy, less frequent dosing — preferred in practice
Crovalimab (Piasky)	SC	Subcutaneous — available in some countries	Useful in eculizumab/ravulizumab resistant patients

⚠️ Critical before starting any complement inhibitor:

Vaccinate against Neisseria meningitidis (A, C, W, Y + B) — at least 2 weeks before starting
Long-term oral penicillin prophylaxis (amoxicillin 250 mg BD) — mandatory
Also vaccinate against Streptococcus pneumoniae and Haemophilus influenzae

What anti-C5 does:

Prevents intravascular hemolysis ✅
Reduces thrombosis risk ✅
BUT: PNH red cells (now spared from lysis) get C3-opsonized → iatrogenic extravascular hemolysis continues (Coombs becomes positive on therapy — this is expected, not a treatment failure)

🥇 ANTI-C3 / PROXIMAL COMPLEMENT INHIBITORS (Newer — Superior Anemia Control)

Drug	Target	Route	Status
Pegcetacoplan (Empaveli)	C3	SC 1080 mg twice weekly	FDA approved; prevents both intravascular AND extravascular hemolysis — corrects anemia more completely
Iptacopan (Fabhalta)	Factor B (alternative pathway)	Oral 200 mg BD	FDA approved 2023 — first oral complement inhibitor for PNH; superior Hb improvement vs eculizumab
Danicopan	Factor D	Oral	FDA approved as add-on for C5-inhibitor-inadequate responders

Key difference from anti-C5:

Anti-C3/proximal inhibitors prevent C3 opsonization → NO extravascular hemolysis → anemia corrects more completely (vs C5 inhibitors which leave extravascular hemolysis ongoing)

⚠️ However: if complement blockade is abruptly stopped, the large accumulated PNH red cell population can undergo massive sudden lysis — do NOT stop abruptly.

Indications for Complement Inhibitor Therapy:

Transfusion-dependent hemolytic anemia — primary indication
Thrombosis (even one episode) — strong indication
Symptomatic hemolysis (abdominal pain, dysphagia, hemoglobinuria, fatigue)
Large PNH clone (>10% granulocytes) + symptoms

2. CURATIVE THERAPY — Allogeneic Bone Marrow Transplantation (Allo-BMT)

Only cure — eliminates the PNH clone
Indicated in:
- PNH-aplastic anemia (PNH-AA) syndrome — complement inhibitors don't treat the bone marrow failure component
- Young patients with severe disease + HLA-identical sibling available
- Patients failing complement inhibitor therapy
Note: Since complement inhibitors became available, BMT use in PNH has significantly decreased

3. ANTICOAGULATION

Any PNH patient with prior thrombosis → long-term anticoagulation (warfarin or LMWH or DOAC)
Thrombosis not resolving → thrombolytic therapy with tPA may be considered
Start complement inhibitor alongside anticoagulation in thrombotic PNH

4. SUPPORTIVE MANAGEMENT (Important where complement inhibitors not available — high-resource issue in India)

Measure	Details
Folic acid	At least 3 mg/day — mandatory (chronic hemolysis depletes folate)
Iron supplementation	Check serum iron/ferritin periodically — chronic hemosiderinuria causes iron deficiency
Red cell transfusions	Leukocyte-depleted (washed/filtered) packed red cells — use when symptomatic
Erythropoiesis-stimulating agents	EPO alfa — if EPO deficiency coexists (esp. with CKD)
Avoid triggers	Infections, surgery, contrast dyes, strenuous exercise — can precipitate hemolytic crises
Corticosteroids	❌ NOT indicated for chronic hemolysis (no evidence, significant side effects); a short course may help during acute inflammatory exacerbation

5. IMMUNOSUPPRESSIVE THERAPY (for PNH-AA syndrome)

When bone marrow failure (aplastic anemia) is the dominant feature:

Anti-thymocyte globulin (ATG) + Cyclosporine A — standard IST for aplastic anemia
Can be combined with eculizumab simultaneously
Eltrombopag (TPO agonist) — improves multilineage response in aplastic anemia component

🗺️ Treatment Algorithm Summary

PNH Diagnosis (flow cytometry: CD55/CD59 deficiency on RBCs + FLAER on granulocytes)
        │
        ├── Classic hemolytic PNH
        │       ├── Symptomatic / transfusion-dependent / thrombosis
        │       │       → COMPLEMENT INHIBITOR
        │       │           ├── Prefer: Iptacopan (oral, superior anemia)
        │       │           ├── Or: Ravulizumab (8-weekly IV, proven)
        │       │           └── If C5 inadequate response: add Danicopan or switch to Pegcetacoplan
        │       └── Young + HLA-identical sibling → Consider Allo-BMT
        │
        ├── PNH-AA Syndrome (bone marrow failure dominant)
        │       → ATG + Cyclosporine ± Eculizumab ± Eltrombopag
        │       → HLA-matched sibling → Allo-BMT (preferred)
        │
        └── Supportive (where biologics unavailable)
                → Folic acid + iron + transfusions + anticoagulation if thrombosis

🔴 Key Points to Remember

Point	Detail
Diagnose with	Flow cytometry (FLAER + CD59) — Gold standard
First choice biologic	Ravulizumab (same as eculizumab but 8-weekly — practical advantage)
Best for anemia correction	Iptacopan (oral C3 proximal inhibitor) or Pegcetacoplan
Before any complement inhibitor	Meningococcal vaccine + penicillin prophylaxis
Only cure	Allo-BMT
Steroids	❌ NOT for chronic hemolysis
Thrombosis	Anticoagulate + start complement inhibitor
Never stop complement inhibitor abruptly	Risk of massive rebound hemolysis

Sources: Goldman-Cecil Medicine; Harrison's Principles of Internal Medicine 22E (2025); Katzung's Pharmacology 16E; PMID 38084255 (Oliver & Patriquin, 2023 Review); PMID 39371251 (Panse et al., 2024)

Paroxysmal nocturnal hemoglobinuria treTment

The full PNH treatment guide was just covered in my previous response above. Here's a quick summary for reference:

PNH Treatment — Quick Reference

🎯 Specific (Disease-Modifying) — Complement Inhibitors

Anti-C5 (Terminal blockade):

Ravulizumab — IV every 8 weeks (preferred — fewer infusions)
Eculizumab — IV every 2 weeks (original standard)
Crovalimab — SC option

Anti-C3/Proximal (Better anemia control):

Iptacopan — Oral BD (first oral option; superior Hb correction)
Pegcetacoplan — SC twice weekly (corrects both intravascular + extravascular hemolysis)
Danicopan — Oral add-on for C5 inadequate responders

⚠️ Before ANY complement inhibitor: Vaccinate against Meningococcus A/B/C/W/Y + start penicillin prophylaxis

🩸 Anticoagulation

Any thrombosis episode → long-term anticoagulation + complement inhibitor

🏥 Curative

Allo-BMT — only cure; especially for PNH-AA syndrome or young patients with matched sibling

💊 Supportive (where biologics unavailable)

Folic acid ≥3 mg/day (mandatory)
Iron supplements (monitor for iron deficiency from hemosiderinuria)
Leukocyte-depleted PCV transfusions
❌ Steroids — NOT for chronic hemolysis

Please scroll up for the full detailed breakdown with dosing, indications, and treatment algorithm.

Search for latest PNH clinical guidelines 2024-2025

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PNH paroxysmal nocturnal hemoglobinuria clinical guidelines 2024 2025

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PMID: 39307719

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PMID: 39371251

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PMID: 38884175

Here is a synthesis of the latest 2024–2025 PNH guidelines and evidence:

PNH Treatment — Latest Guidelines & Evidence 2024–2025

📋 Published Guidelines

1. Chinese Society of Hematology — PNH Guidelines 2024

[PMID: 39307719] — Zhonghua Xue Ye Xue Za Zhi, Aug 2024

The only formal national practice guideline published in 2024
Updates the 2013 Chinese PNH consensus
Incorporates complement inhibitor therapy including newer proximal inhibitors
Covers diagnosis (flow cytometry with FLAER), treatment indications, and monitoring

💊 Major Drug Approvals (2024–2025) — What's New

Drug	Target	FDA Approval	Route	Key Update
Crovalimab (Piasky)	C5	June 2024 ✅ NEW	SC every 4 weeks	Phase 3 COMMODORE 2 trial — non-inferior to eculizumab
Iptacopan (Fabhalta)	Factor B	Dec 2023 (PI updated March 2025)	Oral BD	First oral monotherapy; superior Hb correction vs anti-C5
Danicopan (Voydeya)	Factor D	March 2024	Oral TDS	Add-on to C5 inhibitor for extravascular hemolysis
Pegcetacoplan (Empaveli)	C3	Updated PI Feb 2024	SC twice weekly	First-line approved; prevents both IVH + EVH
Ravulizumab (Ultomiris)	C5	Updated PI Sept 2024	IV every 8 weeks	Remains standard C5 inhibitor
Eculizumab (Soliris)	C5	Updated PI Feb 2025	IV every 2 weeks	Still used; longer track record

🔬 Key Trial Evidence 2024–2025

COMMODORE 2 Trial — Crovalimab vs Eculizumab (Phase 3 RCT)

[PMID: 38884175] — Am J Hematol, Sept 2024

204 complement-inhibitor naive PNH patients randomized 2:1
Crovalimab non-inferior to eculizumab in:
- Hemolysis control (LDH ≤1.5×ULN): 79.3% vs 79.0%
- Transfusion avoidance: 65.7% vs 68.1%
- Breakthrough hemolysis: 10.4% vs 14.5% (crovalimab numerically better)
Key advantage: SC self-administration every 4 weeks vs IV every 2 weeks → patients preferred crovalimab after crossover
Safety profiles similar; no meningococcal infections in either arm

Iptacopan APPLY-PNH Trial (N Engl J Med 2024)

Peffault de Latour R et al. — NEJM 390(11):994–1008, 2024

Oral iptacopan monotherapy vs anti-C5 (eculizumab/ravulizumab)
Superior Hb increase with iptacopan: +3.6 g/dL vs -0.0 g/dL
82% achieved Hb ≥12 g/dL vs 2% on anti-C5
Addresses the unmet need of extravascular hemolysis not controlled by C5 inhibitors

🧭 2024–2025 Treatment Algorithm (Evidence-Based)

NEW PNH PATIENT — Symptomatic / Hemolytic
         │
         ▼
First-line: Choose complement inhibitor based on patient profile
         │
         ├── Anemia is primary concern / wants oral therapy
         │       → IPTACOPAN (oral BD) ← PREFERRED 2024-25
         │         [corrects both IVH + EVH; superior Hb normalization]
         │
         ├── Wants subcutaneous/self-administer, less frequent
         │       → CROVALIMAB (SC every 4 weeks) ← NEW 2024
         │         [non-inferior to eculizumab; patient-preferred]
         │
         ├── IV acceptable, established long-term data
         │       → RAVULIZUMAB (IV every 8 wk) or ECULIZUMAB (IV every 2 wk)
         │
         └── Patient already on C5 inhibitor but persistent EVH/anemia
                 → ADD DANICOPAN (oral TDS) ← NEW 2024
                 → OR SWITCH TO PEGCETACOPLAN (SC twice weekly)

⚠️ 2024–2025 Consensus Points (Panse et al., Transfus Med Hemother 2024)

[PMID: 39371251]

Terminal C5 inhibitors (eculizumab/ravulizumab) dramatically improved survival — still valid first line
Extravascular hemolysis (EVH) is the key unmet need on C5 therapy — up to 40% of patients on eculizumab still have significant anemia from EVH
Proximal inhibitors (iptacopan, pegcetacoplan) normalize Hb and ARC in EVH-predominant patients — superior anemia correction
No formal evidence-based algorithm yet for choosing between terminal vs proximal inhibitor in first-line — individualize based on:
- Degree of anemia
- Preference for oral vs injectable
- Access/cost
- Thrombosis risk
Real-world long-term data on proximal inhibitors still accumulating

🔴 Breakthrough Hemolysis — 2025 Update

[PMID: 40233322] — Blood, Fattizzo et al., 2025

Breakthrough hemolysis remains a challenge with both terminal and proximal inhibitors
With proximal inhibitors (C3 level): if blockade is incomplete, the large accumulated PNH clone can undergo more severe sudden lysis than with C5 inhibitors
Emerging consensus: do NOT stop proximal inhibitors abruptly; taper carefully

💰 Access Note (India-Specific)

Eculizumab/ravulizumab are extremely expensive (~$500,000/year) — not routinely accessible in India
Iptacopan and crovalimab: availability in India still limited
Supportive care protocol remains essential:
- Folic acid 5 mg/day
- Iron supplementation
- Regular transfusions
- Anticoagulation for thrombosis
- Immunosuppression (ATG + cyclosporine) for aplastic anemia component

📌 Key References

PMID	Citation
39307719	Chinese CSH PNH Guidelines 2024 — Zhonghua Xue Ye Xue Za Zhi
38884175	COMMODORE 2 RCT: Crovalimab vs Eculizumab — Am J Hematol 2024
39371251	Panse et al. PNH Pathophysiology & Treatment — Transfus Med Hemother 2024
40233322	Fattizzo et al. Breakthrough Hemolysis — Blood 2025
39273426	Hillmen et al. Navigating Complement Pathway — Int J Mol Sci 2024

Describe pnh a little and indian scenario management

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eculizumab India CDSCO approval PNH price cost access PMJAY 2025

Here is a focused description of PNH with the India-specific management context:

Paroxysmal Nocturnal Hemoglobinuria (PNH) — Description & Indian Scenario

🔬 What is PNH?

PNH is a rare, acquired, clonal hematopoietic stem cell disorder — not inherited, not cancer, but potentially life-threatening.

The Core Defect (in simple terms):

Normal cell:  CD55 + CD59 on surface → Complement BLOCKED → RBC safe ✅
PNH cell:     PIG-A mutation → No GPI anchor → No CD55/CD59 → Complement ATTACKS → RBC destroyed 🔴

PIG-A gene mutation (X chromosome, somatic) → loss of GPI anchors → CD55 and CD59 absent on RBC surface → uncontrolled complement activation → Membrane Attack Complex (MAC) forms → intravascular hemolysis

Free hemoglobin released into plasma scavenges nitric oxide → vasospasm → abdominal pain, dysphagia, erectile dysfunction, pulmonary hypertension.

🏥 Clinical Picture

The Classic Triad:

Feature	Why it Happens
Hemoglobinuria (dark/cola urine — classically morning)	Intravascular hemolysis during sleep (slight pH drop activates complement)
Anemia (often severe)	Chronic RBC destruction + iron loss in urine
Thrombosis (major killer)	Platelet activation + NO scavenging → hypercoagulability

Full Clinical Spectrum:

🩸 Hematological:

Normocytic anemia (can be severe — Hb 4–7)
Pancytopenia (leukopenia + thrombocytopenia in 60–70%)
High RDW (anisocytosis)
Reticulocytosis (often less than expected — marrow suppression)
DAT negative (distinguishes from autoimmune hemolytic anemia)
Hemosiderinuria — chronic; causes iron deficiency (iron lost in urine)

🔴 Thrombosis (~40% of patients):

Most dangerous feature — leading cause of death (up to 72% mortality in untreated over 25 years)
Unusual sites: Budd-Chiari syndrome (hepatic vein), portal vein, cerebral veins, mesenteric veins
Venous >> arterial
Even fatal pulmonary embolism

💛 Smooth muscle symptoms (due to NO scavenging):

Abdominal pain (episodic, often crampy)
Dysphagia
Erectile dysfunction
Fatigue (profound)

🧠 Bone marrow:

PNH is strongly associated with aplastic anemia — ~30% of PNH evolves to or presents with aplastic anemia
Also linked to MDS (5–10%)
Rarely transforms to AML

Lab Hallmarks:

Test	Finding
Flow cytometry (FLAER + CD59)	Gold standard diagnosis — GPI-deficient cells on granulocytes, monocytes, RBCs
LDH	Very elevated (marker of hemolysis severity)
Haptoglobin	Low/absent
Bilirubin (indirect)	Elevated
Urine hemosiderin	Positive (chronic)
DAT	Negative — key distinguishing feature
Clone size	% GPI-deficient granulocytes — guides treatment decisions

🇮🇳 Indian Scenario — Management in 2025

The Reality Until Recently:

For decades, Indian patients with PNH had no access to specific therapy. Management was entirely supportive. Median survival without treatment is only 10–20 years, with thrombosis being the leading killer.

🆕 LANDMARK — Eculizumab Now Approved in India (2025)

CDSCO approved Eculizumab (Soliris) — January 2025 AstraZeneca India officially launched — September 2025

This is the first anti-complement therapy ever approved in India — for both PNH and aHUS. This is a historic milestone for Indian patients.

However — affordability remains the elephant in the room.

Global price: ~$500,000–700,000/year per patient
Indian pricing not yet publicly announced, but even at discounted rates, it will be inaccessible for most
NOT covered under PMJAY (Ayushman Bharat) currently
Alexion/AstraZeneca has a patient assistance program (SOLIRIS REMS) — patients can apply directly

🗺️ Current Indian Management Framework (Practical, 2025):

TIER 1: For patients who CAN access eculizumab/complement inhibitors

Step	Action
Diagnose	Flow cytometry with FLAER + CD59 (available at AIIMS, Tata Memorial, CMC Vellore, PGI Chandigarh)
Risk stratify	LDH, clone size, thrombosis history, Hb trend
Vaccinate FIRST	Meningococcus A/C/W/Y + B, Pneumococcus, HiB — 2 weeks before drug
Start Eculizumab	600 mg IV weekly ×4 → 900 mg at week 5 → 900 mg every 2 weeks
Penicillin prophylaxis	Amoxicillin 250 mg BD — lifelong while on complement inhibitor
Anticoagulation	If any thrombosis history → warfarin/LMWH/DOAC

TIER 2: For most Indian patients (where biologics unaffordable)

Supportive care protocol — the practical reality:

Measure	Details
Folic acid 5 mg OD	Mandatory — chronic hemolysis depletes folate
Iron supplementation	Monitor ferritin — hemosiderinuria causes iron deficiency; oral iron ferrous sulfate
PCV transfusions	Leukocyte-depleted packed RBCs — as needed; some patients transfusion-dependent
Anticoagulation	Warfarin (INR 2–3) or LMWH for thrombosis — critical, saves lives
Avoid triggers	Infections, surgery, IV contrast, strenuous exercise
Prednisolone short course	Only during acute inflammatory exacerbation — NOT for chronic use

TIER 3: PNH-Aplastic Anemia Syndrome (PNH-AA)

Measure	Details
ATG + Cyclosporine	Immunosuppression for bone marrow failure component
Eltrombopag	Add to ATG for better multilineage response
Allo-BMT	Only cure — if HLA-matched sibling available, young patient; AIIMS/Tata/CMC

🏥 Where to Diagnose & Treat PNH in India:

Centre	Capability
AIIMS New Delhi	PNH diagnosis + eculizumab therapy available
Tata Memorial Centre, Mumbai	Comprehensive
CMC Vellore	Haematology expertise, BMT
PGI Chandigarh	Flow cytometry + management
SGPGI Lucknow	Haematology
NIMHANS / KGMU	Limited

💡 Key Practical Points for Indian Setting:

Most patients still diagnosed late — average delay 2 years globally; likely longer in India
Dark urine + anemia + thrombosis in a young person → think PNH first
DAT negative hemolytic anemia = always do flow cytometry for PNH
Aplastic anemia patients → always screen for PNH clone (50–60% have subclinical PNH)
Eculizumab now available in India (Sept 2025) — refer to a tertiary center; apply for patient assistance programs
Eculizumab biosimilars are being developed globally (BKEMV approved USA April 2025) — may eventually reduce costs and improve Indian access
Iptacopan (oral, once daily) — not yet approved in India but the most promising future drug for resource-limited settings once it becomes available

Bottom line for India in 2025: PNH diagnosis has always been possible at major centres. Treatment has historically been supportive only. Eculizumab's CDSCO approval and September 2025 launch is a turning point — but access will remain limited to patients at tertiary centres who can afford it or access assistance programs. For the vast majority, aggressive supportive care + anticoagulation + haematology referral remains the cornerstone.

Goldman-Cecil Medicine; Harrison's 22E (2025); CDSCO Approval Records Jan 2025; AstraZeneca India Launch Sept 2025; PMID 39371251 (Panse et al., Transfus Med Hemother 2024)

What is ATG

Finding Sources

Reading File

Finding Sources

ATG — Anti-Thymocyte Globulin

What is it?

ATG is a polyclonal immunoglobulin preparation made by immunizing animals (horses or rabbits) with human thymocytes or T lymphocytes. The animal produces antibodies directed against human T cells — these antibodies are then purified and given to patients.

Two main formulations:

Product	Source	Brand Name
Rabbit ATG	Rabbit immunized with human thymocytes	Thymoglobulin (Sanofi)
Horse ATG (Equine)	Horse immunized with human thymocytes	Atgam (Pfizer)

In aplastic anemia: Horse ATG is preferred (superior response over rabbit ATG in treatment-naïve patients — shown in multiple trials)

Mechanism of Action

ATG contains cytotoxic antibodies targeting multiple T cell surface molecules:

CD2, CD3, CD4, CD8, CD11a, CD18, CD25, CD44, CD45, HLA class I & II

This achieves two effects:

T cell depletion — direct cytotoxicity (complement-mediated + cell-mediated killing of T lymphocytes)
T cell functional blockade — antibodies occupy surface receptors, blocking T cell activation and proliferation

In aplastic anemia and PNH-AA, the pathology is autoreactive T cells destroying hematopoietic stem cells — ATG eliminates these rogue T cells and allows the marrow to recover.

Indications

Indication	Role
Aplastic anemia (AA)	Primary treatment when BMT not available
PNH-Aplastic Anemia syndrome	Treats the bone marrow failure component
Renal transplant rejection	Prophylaxis and treatment
Other organ transplant rejection	Liver, heart
Conditioning for BMT	Part of preparative regimen

ATG in Aplastic Anemia / PNH-AA — Protocol

Standard Regimen (hATG — Horse ATG):

Step	Detail
Dose	hATG (Atgam) 40 mg/kg/day × 4 days IV
Route	Slow IV infusion over 4–6 hours via central/large peripheral vein
Combined with	Cyclosporine A (CsA) 5 mg/kg/day in 2 divided doses — started day 1, continued for ≥6 months
+ Eltrombopag	150 mg OD — added to ATG+CsA (improves trilineage response in AA)
+ G-CSF	Optional — used by some centres to accelerate neutrophil recovery
Steroids	Methylprednisolone 1 mg/kg/day × 2 weeks (prevents serum sickness from ATG)

Response:

Response seen in 60–70% of patients at 3–6 months
Complete response (normal counts) in ~35–40%
Partial response (transfusion independence) in ~30–35%
Relapse in 30–40% — can be retreated with rATG (rabbit) + CsA

Adverse Effects

Side Effect	Details
Fever, chills, rigors	Most common — during infusion
Hypotension	During infusion
Serum sickness (days 7–14)	Fever, rash, arthralgia, proteinuria — treat with steroids
Leukopenia + thrombocytopenia	Expected (T cell depletion) — monitor counts
Anaphylaxis	Rare but serious
Infections	Increased susceptibility (T cell depleted state) — prophylax with fluconazole, acyclovir

Pre-medication (mandatory before each dose):

IV Methylprednisolone
Paracetamol (antipyretic)
Antihistamine (chlorphenamine)
Slow infusion rate

ATG vs BMT — When to Choose

Scenario	Preferred Treatment
Severe AA, age <40, HLA-matched sibling	Allo-BMT first (>95% cure)
Severe AA, no matched donor / age >40	ATG + CsA + Eltrombopag
PNH-AA, no complement inhibitor access	ATG + CsA
PNH-AA on eculizumab, marrow failure	ATG + CsA + Eculizumab together
Relapse after ATG	Rabbit ATG (rATG) repeat OR BMT

In the Indian context: ATG (horse ATG / Thymoglobulin) is available in India at tertiary centres (AIIMS, Tata, CMC) and is far more affordable than eculizumab. For PNH-AA syndrome patients who cannot access complement inhibitors, ATG + cyclosporine is the practical mainstay of treatment.

Goodman & Gilman's Pharmacological Basis of Therapeutics; Goldman-Cecil Medicine; Harrison's 22E

Can we give cyclosporine a without atg

Finding Sources

Reading File

Can Cyclosporine A Be Given Without ATG?

Short answer: Yes, it can — but it is significantly inferior to the combination.

The Evidence (Harrison's 22E, 2025):

The history of immunosuppression in aplastic anemia is instructive:

ATG alone — gave partial responses initially
ATG + Cyclosporine A — dramatically better; CsA addition increased response rates AND helped maintain remissions
ATG + CsA + Eltrombopag ("Triple Therapy") — current gold standard: 70–80% hematologic recovery

"Addition of cyclosporine to ATG increased the response rate, and cyclosporine helped maintain remissions. Many other attempts to improve on the regimen of ATG plus cyclosporine failed." — Harrison's 22E

Cyclosporine Monotherapy — When and Why

Scenario	Is CsA alone used?	Response
Non-severe aplastic anemia	Yes — acceptable	Moderate response ~40–50%
Severe AA — no ATG available	Yes — but suboptimal	Lower response than combination
Maintenance after ATG response	Yes — continued alone after ATG course ends	Helps maintain remission, prevent relapse
Relapse on tapering CsA	Reintroduce CsA	Often recaptures response
Elderly / frail — cannot tolerate ATG	Yes — CsA alone practical option	Acceptable compromise
Severe AA — standard care	❌ Not preferred	Inferior to ATG+CsA

Why CsA Is Not Enough Alone in Severe Disease

	ATG + CsA	CsA Alone
Mechanism	Depletes autoreactive T cells (ATG) + blocks T cell activation (CsA)	Blocks T cell activation only
Response rate (severe AA)	60–70%	30–40%
Complete response	~35–40%	~10–15%
Speed of response	2–3 months	Slower
Relapse	30–40%	Higher

How Cyclosporine Works (briefly)

Binds cyclophilin → inhibits calcineurin → blocks IL-2 transcription → T cells cannot activate and proliferate
Does NOT kill T cells (unlike ATG) — only suppresses their function
Hence: works well for maintaining remission and preventing relapse, but not powerful enough alone to eliminate the autoreactive T cell clones driving marrow destruction

Practical Indian Context

If ATG is not available or unaffordable:

CsA 5 mg/kg/day (divided BD, oral) — target trough level 150–250 ng/mL — is a reasonable option, especially for:

Non-severe aplastic anemia
Elderly patients
PNH with mild marrow suppression
While waiting/arranging ATG

Monitor: Renal function (creatinine), BP, serum magnesium, gingival hyperplasia, hirsutism.

Important note for this patient (Yasmin): She already has CKD Stage 5 (Cr 4.13). Cyclosporine is nephrotoxic — it would be contraindicated or require extreme caution with very careful monitoring in her case. This further limits her options for immunosuppression.

Bottom line: CsA without ATG is an option — but a compromise. For severe aplastic anemia or PNH-AA, always try to give the full triple therapy (ATG + CsA + Eltrombopag) when possible. CsA alone is reserved for non-severe disease, maintenance, or when ATG is inaccessible.

Harrison's Principles of Internal Medicine 22E (2025); Goodman & Gilman's Pharmacology

Make me a ppt presentation on language and speech disorder with definition, flowcharts,tables and use harrison and dejong medical books as reference not very lengthy

Reading File

Finding Sources

Reading File

Finding Sources

Reading File

Finding Sources

Reading File

Finding Sources

Reading File

Finding Sources

Running Command

ls /home/daytona/workspace/ 2>/dev/null || echo "workspace empty"

Running Command

mkdir -p /home/daytona/workspace/speech-language-ppt

Writing File

~/speech-language-ppt/build.js

const pptxgen = require("pptxgenjs");
const pres = new pptxgen();
pres.layout = "LAYOUT_16x9";
pres.title = "Language and Speech Disorders";
pres.author = "Orris Medical";

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const TEXT_DARK  = "0D1B2A";

// Helper: add slide with dark BG
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// SLIDE 1 — TITLE SLIDE
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// ================================================================
// SLIDE 2 — OVERVIEW
// ================================================================
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  addFooter(s);

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        "Understanding OR expressing words",
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      ]
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// ================================================================
// SLIDE 3 — DEFINITION: APHASIA
// ================================================================
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    { title: "REPETITION", desc: "Ability to repeat phrases (tests arcuate fasciculus)", color: ACCENT3 },
    { title: "NAMING", desc: "Anomia — inability to name objects (universal in aphasia)", color: "9B59B6" }
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// ================================================================
// SLIDE 4 — CLASSIFICATION TABLE
// ================================================================
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  addFooter(s, "Bradley & Daroff's Neurology in Clinical Practice, Table 13.1–13.5");

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    ["Transcortical Sensory", "Fluent", "Impaired", "Intact ✓", "Posterior watershed zone"],
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// ================================================================
// SLIDE 5 — BROCA & WERNICKE COMPARISON
// ================================================================
{
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  addHeader(s, "Broca vs Wernicke Aphasia — Clinical Comparison");
  addFooter(s);

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    ["Feature", "Broca (Expressive)", "Wernicke (Receptive)"],
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    ["Comprehension", "Relatively INTACT", "IMPAIRED"],
    ["Repetition", "Impaired", "Impaired"],
    ["Naming", "Impaired (tip-of-tongue)", "Impaired (bizarre substitutions)"],
    ["Writing", "Dysmorphic, dysgrammatic", "Well-formed but paragraphic"],
    ["Motor signs", "Right hemiparesis PRESENT", "Usually ABSENT"],
    ["Insight", "AWARE — frustrated, depressed", "Often UNAWARE — paranoid"],
    ["Lesion", "Inf. frontal (Broca area, L)", "Post. sup. temporal (Wernicke area, L)"],
  ];

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      const textColor = isHeader
        ? (ci === 0 ? WHITE : TEXT_DARK)
        : (ci === 0 ? ACCENT3 : LIGHT_GRAY);

      s.addShape(pres.ShapeType.rect, {
        x: cX[ci], y: 1.0 + ri * 0.48, w: cW[ci], h: 0.48,
        fill: { color: fillColor }, line: { color: "1E3A5F", pt: 0.5 }
      });
      s.addText(cell, {
        x: cX[ci] + 0.06, y: 1.03 + ri * 0.48,
        w: cW[ci] - 0.12, h: 0.4,
        fontSize: isHeader ? 11 : 10, bold: isHeader,
        color: textColor, fontFace: "Calibri", valign: "middle"
      });
    });
  });
}

// ================================================================
// SLIDE 6 — FLOWCHART: APPROACH TO APHASIA
// ================================================================
{
  const s = addSlide(BG_DARK);
  addHeader(s, "Clinical Flowchart: Approach to Aphasia");
  addFooter(s);

  // Box helper
  function flowBox(x, y, w, h, text, fillColor, textColor, fontSize) {
    s.addShape(pres.ShapeType.rect, { x, y, w, h, fill: { color: fillColor || BG_MID }, line: { color: ACCENT1, pt: 1.5 }, rectRadius: 0.08 });
    s.addText(text, { x: x + 0.05, y: y + 0.04, w: w - 0.1, h: h - 0.08, fontSize: fontSize || 11, bold: true, color: textColor || WHITE, fontFace: "Calibri", align: "center", valign: "middle" });
  }
  function arrow(x1, y1, x2, y2) {
    s.addShape(pres.ShapeType.line, { x: x1, y: y1, w: 0, h: y2 - y1, line: { color: ACCENT3, pt: 1.5 } });
    // arrowhead approximate
    s.addText("▼", { x: x1 - 0.12, y: y2 - 0.18, w: 0.3, h: 0.2, fontSize: 9, color: ACCENT3, fontFace: "Calibri" });
  }
  function harrow(x1, y, x2) {
    s.addShape(pres.ShapeType.line, { x: x1, y, w: x2 - x1, h: 0, line: { color: ACCENT3, pt: 1.5 } });
  }

  // Start
  flowBox(3.5, 1.0, 3.0, 0.45, "Patient with communication difficulty", ACCENT1, TEXT_DARK, 10);
  arrow(5.0, 1.45, 5.0, 1.85);
  // Is it aphasia?
  flowBox(3.3, 1.85, 3.4, 0.45, "Is language content affected?", BG_MID, WHITE, 10);
  // NO branch
  s.addText("NO", { x: 6.8, y: 2.02, w: 0.5, h: 0.2, fontSize: 9, color: ACCENT2, bold: true, fontFace: "Calibri" });
  harrow(6.7, 2.07, 7.5);
  flowBox(7.5, 1.85, 2.25, 0.45, "SPEECH DISORDER\n(Dysarthria / Dysphonia)", ACCENT2, WHITE, 9);
  // YES branch
  s.addText("YES", { x: 5.0, y: 2.32, w: 0.5, h: 0.2, fontSize: 9, color: ACCENT1, bold: true, fontFace: "Calibri" });
  arrow(5.0, 2.3, 5.0, 2.7);
  // Fluency
  flowBox(3.3, 2.7, 3.4, 0.45, "Is speech FLUENT?", BG_MID, WHITE, 10);

  // NON-FLUENT left branch
  s.addText("NON-FLUENT", { x: 1.1, y: 2.82, w: 1.2, h: 0.2, fontSize: 8.5, color: ACCENT2, bold: true, fontFace: "Calibri" });
  harrow(3.3, 2.92, 2.2);
  arrow(2.2, 2.92, 2.2, 3.32);
  // Fluent right branch
  s.addText("FLUENT", { x: 6.9, y: 2.82, w: 0.8, h: 0.2, fontSize: 8.5, color: ACCENT1, bold: true, fontFace: "Calibri" });
  harrow(6.7, 2.92, 7.6);
  arrow(7.6, 2.92, 7.6, 3.32);

  // Repetition row — non-fluent side
  flowBox(0.5, 3.32, 3.4, 0.42, "Repetition?", BG_MID, WHITE, 10);
  // Repetition row — fluent side
  flowBox(6.1, 3.32, 3.4, 0.42, "Comprehension?", BG_MID, WHITE, 10);

  // Non-fluent: impaired → Broca
  s.addText("Impaired", { x: 0.6, y: 3.78, w: 1.0, h: 0.2, fontSize: 8.5, color: ACCENT2, bold: true, fontFace: "Calibri" });
  arrow(1.2, 3.74, 1.2, 4.12);
  flowBox(0.35, 4.12, 1.8, 0.42, "BROCA\nAPHASIA", ACCENT2, WHITE, 10);

  // Non-fluent: intact → Transcortical Motor
  s.addText("Intact", { x: 2.7, y: 3.78, w: 0.8, h: 0.2, fontSize: 8.5, color: ACCENT1, bold: true, fontFace: "Calibri" });
  arrow(3.1, 3.74, 3.1, 4.12);
  flowBox(2.45, 4.12, 1.8, 0.42, "TRANSCORTICAL\nMOTOR", ACCENT3, TEXT_DARK, 9);

  // Fluent: impaired → Wernicke
  s.addText("Impaired", { x: 6.2, y: 3.78, w: 1.0, h: 0.2, fontSize: 8.5, color: ACCENT2, bold: true, fontFace: "Calibri" });
  arrow(6.8, 3.74, 6.8, 4.12);
  flowBox(6.1, 4.12, 1.8, 0.42, "WERNICKE\nAPHASIA", ACCENT1, TEXT_DARK, 10);

  // Fluent: intact → check repetition
  s.addText("Intact", { x: 8.2, y: 3.78, w: 0.8, h: 0.2, fontSize: 8.5, color: ACCENT1, bold: true, fontFace: "Calibri" });
  arrow(8.6, 3.74, 8.6, 4.12);
  flowBox(7.9, 4.12, 1.85, 0.42, "ANOMIC /\nTRANSCORTICAL S", ACCENT3, TEXT_DARK, 9);

  // Both impaired: Global
  s.addText("All 3 impaired → GLOBAL APHASIA", { x: 3.6, y: 4.75, w: 3.5, h: 0.32, fontSize: 10, bold: true, color: ACCENT2, fontFace: "Calibri", align: "center" });
  s.addText("Fluent + Intact Comprehension + Impaired Repetition → CONDUCTION APHASIA", { x: 3.6, y: 5.1, w: 3.5, h: 0.28, fontSize: 9, color: ACCENT3, fontFace: "Calibri", align: "center" });
}

// ================================================================
// SLIDE 7 — SPEECH DISORDERS
// ================================================================
{
  const s = addSlide(BG_DARK);
  addHeader(s, "Speech Disorders — Classification");
  addFooter(s, "Harrison's Principles of Internal Medicine 22E | Bradley & Daroff's Neurology");

  const disorders = [
    {
      name: "DYSARTHRIA",
      color: ACCENT2,
      def: "Motor speech disorder: difficulty articulating words due to weakness, incoordination, or altered tone of speech muscles. Language is intact.",
      types: [
        "Flaccid — LMN lesion (bulbar palsy)",
        "Spastic — UMN lesion (pseudobulbar palsy)",
        "Ataxic — Cerebellar disease",
        "Hypokinetic — Parkinson's disease",
        "Hyperkinetic — Huntington's, dystonia",
        "Mixed — ALS (flaccid + spastic)"
      ]
    },
    {
      name: "DYSPHONIA",
      color: ACCENT3,
      def: "Disorder of voice production (phonation). Voice is hoarse, breathy, weak, or strained. Due to laryngeal or vagal nerve pathology.",
      types: [
        "Hoarse voice — laryngitis, vocal cord nodule",
        "Breathy voice — vocal cord paralysis",
        "Hypophonic — Parkinson's disease",
        "Spasmodic dysphonia — laryngeal dystonia"
      ]
    }
  ];

  disorders.forEach((d, i) => {
    const x = i === 0 ? 0.3 : 5.2;
    s.addShape(pres.ShapeType.rect, { x, y: 1.0, w: 4.5, h: 0.4, fill: { color: d.color }, line: { color: d.color } });
    s.addText(d.name, { x, y: 1.0, w: 4.5, h: 0.4, fontSize: 14, bold: true, color: TEXT_DARK, fontFace: "Calibri", align: "center", valign: "middle" });
    s.addShape(pres.ShapeType.rect, { x, y: 1.4, w: 4.5, h: 0.7, fill: { color: BG_MID }, line: { color: d.color, pt: 1 } });
    s.addText(d.def, { x: x + 0.1, y: 1.42, w: 4.3, h: 0.65, fontSize: 10.5, color: LIGHT_GRAY, fontFace: "Calibri", valign: "middle" });
    s.addShape(pres.ShapeType.rect, { x, y: 2.1, w: 4.5, h: 2.9, fill: { color: "162236" }, line: { color: d.color, pt: 1 } });
    d.types.forEach((t, j) => {
      s.addText("◉  " + t, { x: x + 0.15, y: 2.15 + j * 0.44, w: 4.2, h: 0.4, fontSize: 10.5, color: LIGHT_GRAY, fontFace: "Calibri", valign: "middle" });
    });
  });
}

// ================================================================
// SLIDE 8 — DYSARTHRIA TYPES TABLE
// ================================================================
{
  const s = addSlide(BG_DARK);
  addHeader(s, "Dysarthria — Types & Localization");
  addFooter(s, "Bradley & Daroff's Neurology in Clinical Practice");

  const rows = [
    ["Type", "Lesion Site", "Speech Quality", "Key Cause"],
    ["Flaccid", "LMN / bulbar", "Nasal, breathy, weak, hypophonic", "Bulbar palsy, MND, GBS"],
    ["Spastic", "UMN / bilateral corticobulbar", "Strained, strangled, slow", "Pseudobulbar palsy, Bilateral stroke"],
    ["Ataxic", "Cerebellum", "Scanning, irregular rhythm, explosive", "MS, cerebellar ataxia, alcohol"],
    ["Hypokinetic", "Basal ganglia (SNc)", "Rapid, monotone, low volume", "Parkinson's disease"],
    ["Hyperkinetic", "Basal ganglia", "Variable rate/volume, involuntary", "Huntington's, dystonia"],
    ["Mixed", "Multiple levels", "Combined features", "ALS (flaccid + spastic)"],
  ];

  const cW = [1.7, 2.4, 3.0, 2.6];
  const cX = [0.3, 2.0, 4.4, 7.4];

  rows.forEach((row, ri) => {
    row.forEach((cell, ci) => {
      const isHeader = ri === 0;
      const fill = isHeader ? ACCENT2 : (ri % 2 === 0 ? "162236" : BG_MID);
      const color = isHeader ? TEXT_DARK : (ci === 0 ? ACCENT2 : LIGHT_GRAY);
      s.addShape(pres.ShapeType.rect, {
        x: cX[ci], y: 1.0 + ri * 0.56, w: cW[ci], h: 0.56,
        fill: { color: fill }, line: { color: "1E3A5F", pt: 0.5 }
      });
      s.addText(cell, {
        x: cX[ci] + 0.05, y: 1.03 + ri * 0.56,
        w: cW[ci] - 0.1, h: 0.5,
        fontSize: isHeader ? 11 : 10, bold: isHeader,
        color, fontFace: "Calibri", valign: "middle",
        align: isHeader ? "center" : "left"
      });
    });
  });
}

// ================================================================
// SLIDE 9 — FLOWCHART: APPROACH TO SPEECH DISORDER
// ================================================================
{
  const s = addSlide(BG_DARK);
  addHeader(s, "Flowchart: Approach to Dysarthria");
  addFooter(s);

  function box(x, y, w, h, text, fill, tc, fs) {
    s.addShape(pres.ShapeType.rect, { x, y, w, h, fill: { color: fill || BG_MID }, line: { color: ACCENT1, pt: 1.2 } });
    s.addText(text, { x: x + 0.06, y: y + 0.05, w: w - 0.12, h: h - 0.1, fontSize: fs || 10, bold: true, color: tc || WHITE, fontFace: "Calibri", align: "center", valign: "middle" });
  }

  box(3.5, 1.0, 3.0, 0.42, "Dysarthria — Motor speech problem", ACCENT2, WHITE, 10);
  // Arrow down
  s.addShape(pres.ShapeType.line, { x: 5.0, y: 1.42, w: 0, h: 0.35, line: { color: ACCENT3, pt: 1.5 } });
  s.addText("▼", { x: 4.88, y: 1.73, w: 0.26, h: 0.2, fontSize: 9, color: ACCENT3, fontFace: "Calibri" });

  box(3.5, 1.95, 3.0, 0.42, "Is weakness present?", BG_MID, WHITE, 10);

  // YES — LMN or UMN
  s.addText("YES", { x: 5.05, y: 2.42, w: 0.5, h: 0.18, fontSize: 8.5, bold: true, color: ACCENT1, fontFace: "Calibri" });
  s.addShape(pres.ShapeType.line, { x: 5.0, y: 2.37, w: 0, h: 0.35, line: { color: ACCENT3, pt: 1.5 } });
  s.addText("▼", { x: 4.88, y: 2.68, w: 0.26, h: 0.2, fontSize: 9, color: ACCENT3, fontFace: "Calibri" });

  box(3.4, 2.87, 3.2, 0.42, "LMN or UMN signs?", BG_MID, WHITE, 10);
  // LMN
  s.addText("LMN (wasting, fasciculation)", { x: 0.2, y: 2.98, w: 2.0, h: 0.2, fontSize: 8, color: ACCENT2, bold: true, fontFace: "Calibri" });
  s.addShape(pres.ShapeType.line, { x: 2.2, y: 3.08, w: 1.2, h: 0, line: { color: ACCENT3, pt: 1 } });
  box(0.2, 3.2, 2.0, 0.42, "FLACCID\nDYSARTHRIA\n(Bulbar palsy)", "1B3A2A", ACCENT1, 9);

  // UMN
  s.addText("UMN (spastic, hyperreflexia)", { x: 7.6, y: 2.98, w: 2.2, h: 0.2, fontSize: 8, color: ACCENT2, bold: true, fontFace: "Calibri" });
  s.addShape(pres.ShapeType.line, { x: 7.6, y: 3.08, w: -1.0, h: 0, line: { color: ACCENT3, pt: 1 } });
  box(7.8, 3.2, 2.0, 0.42, "SPASTIC\nDYSARTHRIA\n(Pseudobulbar)", "3A1B1B", ACCENT2, 9);

  // NO — no weakness
  s.addText("NO", { x: 6.6, y: 2.12, w: 0.4, h: 0.18, fontSize: 8.5, bold: true, color: ACCENT2, fontFace: "Calibri" });
  s.addShape(pres.ShapeType.line, { x: 6.5, y: 2.16, w: 0.8, h: 0, line: { color: ACCENT3, pt: 1 } });
  s.addShape(pres.ShapeType.line, { x: 7.3, y: 2.16, w: 0, h: 0.35, line: { color: ACCENT3, pt: 1 } });
  s.addText("▼", { x: 7.18, y: 2.47, w: 0.26, h: 0.2, fontSize: 9, color: ACCENT3, fontFace: "Calibri" });
  box(6.3, 2.65, 3.4, 0.42, "Rhythmic / Involuntary movements?", BG_MID, WHITE, 10);

  s.addText("YES — Cerebellar signs", { x: 6.4, y: 3.12, w: 1.6, h: 0.2, fontSize: 8, color: ACCENT1, bold: true, fontFace: "Calibri" });
  box(6.3, 3.32, 1.6, 0.42, "ATAXIC\nDYSARTHRIA", "1B3A2A", ACCENT1, 9);

  s.addText("NO — Basal ganglia", { x: 8.2, y: 3.12, w: 1.5, h: 0.2, fontSize: 8, color: ACCENT3, bold: true, fontFace: "Calibri" });
  box(8.1, 3.32, 1.65, 0.42, "HYPO/HYPER-\nKINETIC", "2A2A1B", ACCENT3, 9);

  // MND at bottom
  s.addShape(pres.ShapeType.rect, { x: 2.5, y: 4.6, w: 5.0, h: 0.7, fill: { color: BG_MID }, line: { color: ACCENT2, pt: 2 } });
  s.addText([
    { text: "⚠ ALS / Motor Neuron Disease: ", options: { bold: true, color: ACCENT2 } },
    { text: "MIXED dysarthria (flaccid + spastic) = combined LMN + UMN signs", options: { color: WHITE } }
  ], { x: 2.55, y: 4.65, w: 4.9, h: 0.6, fontSize: 11, fontFace: "Calibri", valign: "middle" });
}

// ================================================================
// SLIDE 10 — SPECIAL SYNDROMES
// ================================================================
{
  const s = addSlide(BG_DARK);
  addHeader(s, "Special Language Syndromes");
  addFooter(s, "Bradley & Daroff's Neurology in Clinical Practice — Dejerine Syndromes");

  const items = [
    {
      name: "ALEXIA WITHOUT AGRAPHIA",
      color: ACCENT1,
      who: "Dejerine, 1892",
      def: "Can WRITE but cannot READ own writing ('linguistic blindfolding')",
      speech: "Normal speech & comprehension",
      lesion: "Left PCA territory: medial occipital ± splenium of corpus callosum",
      key: "Letter-by-letter reading as recovery; right hemianopia"
    },
    {
      name: "ALEXIA WITH AGRAPHIA",
      color: ACCENT2,
      who: "Dejerine, 1891",
      def: "Cannot READ or WRITE ('acquired illiteracy'); oral language preserved",
      speech: "Often fluent with paraphasic errors",
      lesion: "Angular gyrus (left inferior parietal lobule)",
      key: "Often associated Gerstmann syndrome (finger agnosia, acalculia, L-R disorientation)"
    },
    {
      name: "CONDUCTION APHASIA",
      color: ACCENT3,
      who: "Wernicke / Geschwind",
      def: "Fluent speech + intact comprehension + severely impaired REPETITION",
      speech: "Phonemic paraphasias, 'conduit d'approche' — self-correcting attempts",
      lesion: "Arcuate fasciculus / supramarginal gyrus",
      key: "Repetition disproportionately impaired compared to other functions"
    },
  ];

  items.forEach((item, i) => {
    const y = 1.05 + i * 1.48;
    s.addShape(pres.ShapeType.rect, { x: 0.3, y, w: 1.95, h: 1.25, fill: { color: item.color }, line: { color: item.color } });
    s.addText(item.name, { x: 0.35, y: y + 0.05, w: 1.85, h: 0.45, fontSize: 11, bold: true, color: TEXT_DARK, fontFace: "Calibri", align: "center", valign: "middle" });
    s.addText(item.who, { x: 0.35, y: y + 0.52, w: 1.85, h: 0.25, fontSize: 9, color: TEXT_DARK, fontFace: "Calibri", align: "center", italic: true });
    s.addShape(pres.ShapeType.rect, { x: 2.25, y, w: 7.45, h: 1.25, fill: { color: BG_MID }, line: { color: item.color, pt: 1.2 } });
    s.addText([
      { text: "Def: ", options: { bold: true, color: item.color } }, { text: item.def + "  ", options: { color: WHITE } },
      { text: "\nSpeech: ", options: { bold: true, color: item.color, breakLine: false } }, { text: item.speech + "  ", options: { color: LIGHT_GRAY } },
      { text: "\nLesion: ", options: { bold: true, color: item.color, breakLine: false } }, { text: item.lesion + "  ", options: { color: LIGHT_GRAY } },
      { text: "\nKey: ", options: { bold: true, color: ACCENT3, breakLine: false } }, { text: item.key, options: { color: LIGHT_GRAY } }
    ], { x: 2.35, y: y + 0.06, w: 7.25, h: 1.13, fontSize: 10, fontFace: "Calibri", valign: "top" });
  });
}

// ================================================================
// SLIDE 11 — SUMMARY TABLE
// ================================================================
{
  const s = addSlide(BG_DARK);
  addHeader(s, "Summary: Key Distinctions at a Glance");
  addFooter(s);

  const rows = [
    ["Feature", "APHASIA", "DYSARTHRIA", "DYSPHONIA"],
    ["Domain affected", "Language (symbol system)", "Motor speech articulation", "Voice/phonation"],
    ["Comprehension", "May be impaired", "Intact", "Intact"],
    ["Language content", "Abnormal", "Normal", "Normal"],
    ["Fluency", "Variable", "Slow / Distorted", "Reduced volume"],
    ["Cause", "Cortical / subcortical lesion", "Motor pathway lesion", "Laryngeal / vagal"],
    ["Reading/Writing", "Often affected", "Not affected", "Not affected"],
    ["Lesion side", "Dominant (L) hemisphere", "Motor pathways (bilateral)", "Larynx / CN X"],
  ];

  const cW = [2.3, 2.3, 2.3, 2.3];
  const cX = [0.4, 2.7, 5.0, 7.3];
  const headerColors = [BG_MID, ACCENT1, ACCENT2, ACCENT3];
  const headerTextColors = [WHITE, TEXT_DARK, WHITE, TEXT_DARK];

  rows.forEach((row, ri) => {
    row.forEach((cell, ci) => {
      const isHeader = ri === 0;
      const fill = isHeader ? headerColors[ci] : (ri % 2 === 0 ? "162236" : BG_MID);
      const color = isHeader ? headerTextColors[ci] : (ci === 0 ? LIGHT_GRAY : LIGHT_GRAY);
      s.addShape(pres.ShapeType.rect, {
        x: cX[ci], y: 1.0 + ri * 0.53, w: cW[ci], h: 0.53,
        fill: { color: fill }, line: { color: "1E3A5F", pt: 0.5 }
      });
      s.addText(cell, {
        x: cX[ci] + 0.06, y: 1.03 + ri * 0.53,
        w: cW[ci] - 0.12, h: 0.47,
        fontSize: isHeader ? 11 : 10, bold: isHeader,
        color, fontFace: "Calibri", valign: "middle",
        align: isHeader ? "center" : "left"
      });
    });
  });
}

// ================================================================
// SLIDE 12 — REFERENCES
// ================================================================
{
  const s = addSlide(BG_DARK);
  // Left accent bar
  s.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: 0.3, h: 5.625, fill: { color: ACCENT1 }, line: { color: ACCENT1 } });
  s.addText("REFERENCES", {
    x: 0.5, y: 0.35, w: 9.0, h: 0.6, fontSize: 30, bold: true,
    color: ACCENT1, fontFace: "Calibri", charSpacing: 4
  });
  s.addShape(pres.ShapeType.rect, { x: 0.5, y: 0.98, w: 9.0, h: 0.05, fill: { color: ACCENT2 }, line: { color: ACCENT2 } });

  const refs = [
    "1.  Bradley WG, Daroff RB, et al. Bradley and Daroff's Neurology in Clinical Practice, 8th Edition. Chapter 13: Aphasia and Related Disorders. Elsevier, 2022.",
    "2.  Longo DL, Fauci AS, et al. Harrison's Principles of Internal Medicine, 22nd Edition (2025). Chapter on Language, Cognition and Communication Disorders. McGraw Hill.",
    "3.  Dejerine J. Sur un cas de cécité verbale avec agraphie, suivi d'autopsie. CR Soc Biol. 1891.",
    "4.  Dejerine J. Contribution à l'étude anatomoclinique et clinique des différentes variétés de cécité verbale. CR Soc Biol. 1892.",
    "5.  Broca P. Remarques sur le siège de la faculté du langage articulé. Bull Soc Anat Paris. 1861;6:330–357.",
    "6.  Wernicke C. Der Aphasische Symptomencomplex. Breslau: Cohn & Weigert; 1874.",
  ];

  refs.forEach((ref, i) => {
    s.addText(ref, {
      x: 0.6, y: 1.15 + i * 0.65, w: 9.0, h: 0.58,
      fontSize: 11.5, color: i < 2 ? WHITE : LIGHT_GRAY,
      fontFace: "Calibri", valign: "middle"
    });
  });
}

// ================================================================
// WRITE FILE
// ================================================================
pres.writeFile({ fileName: "/home/daytona/workspace/speech-language-ppt/Language_Speech_Disorders.pptx" })
  .then(() => console.log("DONE"))
  .catch(e => console.error(e));

Running Command

cd /home/daytona/workspace/speech-language-ppt && node build.js 2>&1

Running Command

ls -lh /home/daytona/workspace/speech-language-ppt/

Your presentation is ready — 394 KB, 12 slides.

📥
Language Speech Disorders
Presentation · PPTX

What's inside (12 slides, deep navy + teal theme):

Slide	Content
1	Title slide
2	Language vs Speech disorders — side-by-side comparison boxes
3	Definition of Aphasia — 4 key domains (Fluency, Comprehension, Repetition, Naming)
4	Classification table — all aphasia types with fluency/comprehension/repetition/lesion site
5	Broca vs Wernicke — detailed comparison table
6	Clinical flowchart — step-by-step approach to diagnosing aphasia type
7	Speech disorders — Dysarthria & Dysphonia definitions + types
8	Dysarthria types table — Flaccid/Spastic/Ataxic/Hypokinetic/Hyperkinetic/Mixed with causes
9	Flowchart — Approach to dysarthria with localization
10	Special syndromes — Alexia w/o Agraphia, Alexia w/ Agraphia (Dejerine), Conduction Aphasia
11	Summary table — Aphasia vs Dysarthria vs Dysphonia at a glance
12	References — Harrison's 22E + Bradley & Daroff + Broca, Wernicke, Dejerine original papers

Create an Excel table comparing all aphasia syndromes4 slides

Reading File

Writing File

~/speech-language-ppt/build_excel.py

import openpyxl
from openpyxl.styles import (PatternFill, Font, Alignment, Border, Side,
                               GradientFill)
from openpyxl.utils import get_column_letter
from openpyxl.worksheet.page import PageMargins

wb = openpyxl.Workbook()
ws = wb.active
ws.title = "Aphasia Syndromes"

# ── Colours ──────────────────────────────────────────────────────────────────
NAVY      = "0D1B2A"
MID_NAVY  = "1B2A4A"
TEAL      = "2EC4B6"
CORAL     = "E84855"
AMBER     = "F5A623"
PURPLE    = "9B59B6"
LIGHT     = "D6E4F0"
WHITE     = "FFFFFF"
DARK_ROW  = "162236"
MID_ROW   = "1E3550"

def fill(hex_color):
    return PatternFill("solid", fgColor=hex_color)

def font(color=WHITE, bold=False, sz=10, italic=False):
    return Font(name="Calibri", color=color, bold=bold, size=sz, italic=italic)

def border():
    s = Side(border_style="thin", color="2A4A6A")
    return Border(left=s, right=s, top=s, bottom=s)

def center(wrap=False):
    return Alignment(horizontal="center", vertical="center", wrap_text=wrap)

def left(wrap=True):
    return Alignment(horizontal="left", vertical="center", wrap_text=wrap)

# ── Title row ────────────────────────────────────────────────────────────────
ws.row_dimensions[1].height = 38
ws.merge_cells("A1:P1")
c = ws["A1"]
c.value = "APHASIA SYNDROMES — Comprehensive Comparison Table"
c.fill = fill(TEAL)
c.font = Font(name="Calibri", color=NAVY, bold=True, size=16)
c.alignment = center()

# Subtitle
ws.row_dimensions[2].height = 22
ws.merge_cells("A2:P2")
c = ws["A2"]
c.value = "Reference: Bradley & Daroff's Neurology in Clinical Practice  |  Harrison's Principles of Internal Medicine 22E (2025)"
c.fill = fill(MID_NAVY)
c.font = Font(name="Calibri", color=LIGHT, bold=False, size=9, italic=True)
c.alignment = center()

# ── Column headers ────────────────────────────────────────────────────────────
headers = [
    "Syndrome",
    "Fluency",
    "Comprehension\n(Auditory)",
    "Repetition",
    "Naming",
    "Reading",
    "Writing",
    "Spontaneous\nSpeech",
    "Motor /\nSensory Signs",
    "Lesion Site",
    "Vascular\nTerritory",
    "Key Clinical\nFeature",
    "Psychiatric /\nBehavioural",
    "Eponym /\nHistory",
    "Differentiating\nPearl",
    "Treatment\nFocus"
]

col_widths = [22, 14, 16, 14, 12, 12, 12, 24, 22, 28, 20, 28, 22, 20, 30, 24]

ws.row_dimensions[3].height = 44
for ci, (h, w) in enumerate(zip(headers, col_widths), start=1):
    cell = ws.cell(row=3, column=ci, value=h)
    # Alternate header colours
    hcolors = [NAVY, CORAL, CORAL, TEAL, TEAL, AMBER, AMBER,
               MID_NAVY, MID_NAVY, CORAL, CORAL, TEAL, AMBER, MID_NAVY, TEAL, CORAL]
    cell.fill = fill(hcolors[ci-1])
    cell.font = Font(name="Calibri", color=WHITE if hcolors[ci-1] not in (TEAL, AMBER) else NAVY,
                     bold=True, size=10)
    cell.alignment = center(wrap=True)
    cell.border = border()
    ws.column_dimensions[get_column_letter(ci)].width = w

# ── Data ──────────────────────────────────────────────────────────────────────
# Each row: 16 fields matching headers above
data = [
    [
        "BROCA APHASIA\n(Expressive)",
        "NON-FLUENT\nTelegraphic / agrammatic",
        "INTACT\n(mild complex syntax difficulty)",
        "IMPAIRED",
        "IMPAIRED\n(tip-of-tongue)",
        "Often IMPAIRED\n(third alexia)",
        "IMPAIRED\n(dysmorphic, dysgrammatic)",
        "Hesitant, effortful; principal nouns & verbs retained; omits grammatical words (agrammatism)",
        "RIGHT HEMIPARESIS\nRight hemisensory loss\n± Apraxia of left limbs",
        "Inferior frontal gyrus\n(Broca area, BA 44/45)\nLeft hemisphere",
        "Left MCA\n(superior division)\nFrontal branches",
        "Telegraphic speech;\nnon-fluent but aware;\nfrustration & depression common",
        "DEPRESSION\nAwareness of deficit;\nfrustration",
        "Paul Broca, 1861\n(Patient 'Tan' — Leborgne)",
        "Good comprehension DIFFERENTIATES from Global;\nLanguage content preserved vs Dysarthria",
        "Speech therapy;\nLanguage rehabilitation;\nDepression management"
    ],
    [
        "WERNICKE APHASIA\n(Receptive)",
        "FLUENT\nLogorrheic / jargon",
        "IMPAIRED\n(often severe)",
        "IMPAIRED",
        "IMPAIRED\n(bizarre paraphasias)",
        "IMPAIRED\n(reading comprehension)",
        "IMPAIRED\n(paragraphic, well-formed)",
        "Effortless, rapid; verbal paraphasias, neologisms, jargon; 'empty speech'",
        "Usually ABSENT\n± Right homonymous hemianopia\nNo hemiparesis",
        "Posterior superior\ntemporal gyrus\n(Wernicke area, BA 22)\nLeft hemisphere",
        "Left MCA\n(inferior division)\nTemporal branches",
        "Jargon speech;\nunaware of deficits;\nlarge lesions → paranoia",
        "Often UNAWARE\nAngry or paranoid;\nlack of concern (anosognosia)",
        "Carl Wernicke, 1874",
        "Fluent but meaningless;\nDAB negative comprehension;\ndistinguish from psychosis",
        "Communication strategies;\nwriting/reading aids;\nawareness counselling"
    ],
    [
        "GLOBAL APHASIA",
        "NON-FLUENT\nor mute",
        "IMPAIRED\n(severe)",
        "IMPAIRED\n(severely)",
        "IMPAIRED\n(severely)",
        "IMPAIRED",
        "IMPAIRED",
        "Minimal output; may be mute or produce only stereotypic utterances",
        "RIGHT HEMIPLEGIA\nRight hemisensory loss\nRight hemianopia",
        "Large left hemisphere\ninfarction affecting\nboth Broca + Wernicke areas",
        "Left MCA\n(complete territory)\nor large cortical infarct",
        "All language modalities severely impaired;\nworst prognosis for recovery",
        "Profound disability;\ndepression common;\nfrustration",
        "N/A — defined by extent\nnot single eponym",
        "All 4 functions impaired;\ndistinguish from locked-in syndrome\n(where comprehension may be preserved)",
        "Augmentative communication;\ngestural approaches;\nfamily support"
    ],
    [
        "CONDUCTION APHASIA",
        "FLUENT\nwith phonemic paraphasias",
        "INTACT\n(relatively preserved)",
        "SEVERELY IMPAIRED\n(disproportionate)",
        "IMPAIRED\n(phonemic paraphasias)",
        "Variable",
        "Variable",
        "Fluent with phonemic paraphasias; 'conduit d'approche' — repeated self-correction attempts toward target",
        "Usually ABSENT\n± Mild right arm weakness",
        "Arcuate fasciculus\nSupramarginal gyrus\n(inferior parietal lobule)",
        "Left MCA\n(parietal branches)\nor post. Sylvian fissure",
        "Repetition is DISPROPORTIONATELY impaired vs comprehension;\nconduit d'approche behaviour",
        "Awareness of errors;\nfrustration with repeated self-corrections",
        "Wernicke (1874);\nGeschwind (disconnection theory)",
        "Key: Intact comprehension + severely impaired repetition;\nphonemic (not verbal) paraphasias",
        "Repetition-focused therapy;\nphonological cueing"
    ],
    [
        "TRANSCORTICAL\nMOTOR APHASIA",
        "NON-FLUENT\nReduced initiation",
        "INTACT",
        "INTACT ✓\n(key feature)",
        "IMPAIRED\n(anomia)",
        "Variable",
        "IMPAIRED",
        "Reduced spontaneous output; latency before speaking; can repeat well; echoing tendency",
        "± Mild right leg\nweakness (supplementary motor area)",
        "Anterior/superior\nto Broca area;\nSMA or watershed zone\n(left frontal)",
        "Left ACA territory\nor MCA–ACA watershed",
        "INTACT REPETITION in a non-fluent patient;\ntendency to complete sentences",
        "Apathy, reduced\ninitiative (abulia)",
        "Described by\nLichtheim (1885)",
        "INTACT REPETITION differentiates from Broca;\nlook for watershed ischaemia (hypotension, cardiac arrest)",
        "Initiation strategies;\nmotivation therapy;\naddress underlying ischaemia"
    ],
    [
        "TRANSCORTICAL\nSENSORY APHASIA",
        "FLUENT\noften echolalic",
        "IMPAIRED",
        "INTACT ✓\n(echolalia — repeats but doesn't comprehend)",
        "IMPAIRED",
        "IMPAIRED",
        "IMPAIRED",
        "Fluent with semantic paraphasias; pronounced echolalia; repeats examiner's words",
        "Usually ABSENT",
        "Posterior watershed\nzone (left temporal–\nparietal–occipital)",
        "Left MCA–PCA\nwatershed territory",
        "ECHOLALIA with INTACT repetition in a patient with poor comprehension",
        "Often unaware;\nbehavioural disturbance",
        "Described by\nLichtheim (1885)",
        "Intact repetition + echolalia differentiates from Wernicke;\nposterior watershed location",
        "Comprehension aids;\nauditoryvisualmatch\nstrategies"
    ],
    [
        "ANOMIC APHASIA\n(Amnesic Aphasia)",
        "FLUENT",
        "INTACT",
        "INTACT",
        "IMPAIRED\n(anomia — word-finding difficulty)",
        "INTACT",
        "INTACT (mostly)",
        "Fluent, circumlocutory speech; word-finding pauses; 'tip-of-tongue' state; empty phrases used instead of specific nouns",
        "Usually ABSENT",
        "Variable; often\nangular gyrus\n(left inferior parietal)\nor temporal",
        "Variable; left MCA\nparietal or temporal branches",
        "Isolated anomia;\nleast severe aphasia;\ncan be residual from recovery of any aphasia",
        "Mild frustration;\ngenerally good insight",
        "Described by\nKussmaul (1877)",
        "Most benign; often residual;\nnaming-specific deficit;\nno other language impairment",
        "Word-finding therapy;\nsemanticphonological cueing"
    ],
    [
        "PURE ALEXIA\nWITHOUT AGRAPHIA",
        "FLUENT\n(oral language intact)",
        "INTACT\n(oral comprehension intact)",
        "INTACT",
        "IMPAIRED for colours\n(colour anomia)",
        "SEVERELY IMPAIRED\n('linguistic blindfolding')",
        "INTACT ✓\n(can write, cannot read own writing)",
        "Oral speech normal; can write spontaneously but unable to read what was written",
        "RIGHT HOMONYMOUS\nHEMIANOPIA\n(nearly always)\nNo hemiparesis",
        "Left medial occipital\n+ Splenium of corpus\ncallosum (disconnection)",
        "Left PCA territory\n(medial occipital + splenium)",
        "Patient writes normally but cannot read own writing;\nletter-by-letter reading in recovery",
        "Usually preserved;\nnot depressed",
        "Dejerine, 1892\n('pure word blindness')",
        "Writing INTACT but reading severely impaired;\nright hemianopia always present;\ncolour anomia",
        "Letter recognition training;\ncompensatory strategies"
    ],
    [
        "ALEXIA WITH AGRAPHIA\n(Acquired Illiteracy)",
        "FLUENT\n(often paraphasic)",
        "INTACT (oral)",
        "INTACT (oral)",
        "IMPAIRED\n(often)",
        "IMPAIRED\n(cannot read)",
        "IMPAIRED\n(cannot write)",
        "Oral speech relatively preserved; literacy (reading + writing) both lost; may have mild paraphasic speech",
        "Usually ABSENT\nNo hemiparesis",
        "Angular gyrus\n(left inferior parietal\nlobule, BA 39)",
        "Left MCA\n(inferior parietal branches)",
        "Both reading AND writing lost;\n'acquired illiteracy';\nGerstmann syndrome common",
        "Frustration;\nawareness preserved",
        "Dejerine, 1891",
        "BOTH reading + writing impaired (unlike Pure Alexia where writing is intact);\ncheck for Gerstmann syndrome",
        "Literacy retraining;\nGerstmann rehabilitation"
    ],
    [
        "SUBCORTICAL APHASIA\n(Thalamic / Striatal)",
        "Variable\n(often non-fluent or hypophonic)",
        "Variable\n(often mildly impaired)",
        "Variable",
        "IMPAIRED\n(anomia prominent)",
        "Variable",
        "Variable",
        "Hypophonic, low-volume speech; paraphasias; may fluctuate; thalamic aphasia: fluent with semantic paraphasias",
        "RIGHT HEMIPARESIS\n(capsular lesions)\nHemisensory loss",
        "Thalamus, caudate,\nputamen, internal\ncapsule (anterior limb)",
        "Left lenticulostriate\narteries or thalamic\nperforators",
        "Fluctuating language disturbance;\nhypophonia; prominent anomia;\nnot fitting classic cortical patterns",
        "Variable; abulia\nwith thalamic lesions",
        "First described by\nMarie (1906) and\nmodern studies post-CT era",
        "Subcortical + non-cortical location;\ndoes not fit classic cortical aphasia patterns;\nMRI essential",
        "Treat underlying aetiology;\nlanguage therapy"
    ],
]

# Row formatting
row_fills = [
    ("0D1F35", CORAL),      # Broca
    ("1A1035", TEAL),       # Wernicke
    ("1A1020", "E84855"),   # Global
    ("0D2035", AMBER),      # Conduction
    ("0D2518", "2EC4B6"),   # TCM
    ("201520", PURPLE),     # TCS
    ("0F1E1A", AMBER),      # Anomic
    ("0D1828", CORAL),      # Pure Alexia
    ("0D2828", TEAL),       # Alexia+Agraphia
    ("1A1E10", AMBER),      # Subcortical
]

for ri, (row_data, (row_bg, row_accent)) in enumerate(zip(data, row_fills), start=4):
    ws.row_dimensions[ri].height = 72
    for ci, value in enumerate(row_data, start=1):
        cell = ws.cell(row=ri, column=ci, value=value)
        cell.fill = fill(row_bg)
        cell.border = border()
        # Syndrome name column — bold, coloured
        if ci == 1:
            cell.font = Font(name="Calibri", color=row_accent, bold=True, size=11)
            cell.alignment = center(wrap=True)
        elif ci in (2, 3, 4):  # Fluency, Comprehension, Repetition — key diagnostic
            # Colour code values
            val = str(value).upper()
            if "INTACT" in val or "✓" in val:
                cell.font = Font(name="Calibri", color=TEAL, bold=True, size=10)
            elif "IMPAIRED" in val or "NON-FLUENT" in val or "MUTE" in val:
                cell.font = Font(name="Calibri", color=CORAL, bold=True, size=10)
            elif "FLUENT" in val:
                cell.font = Font(name="Calibri", color="7EC8C8", bold=True, size=10)
            else:
                cell.font = Font(name="Calibri", color=LIGHT, size=10)
            cell.alignment = center(wrap=True)
        elif ci in (14,):  # Eponym
            cell.font = Font(name="Calibri", color=AMBER, italic=True, size=9)
            cell.alignment = center(wrap=True)
        else:
            cell.font = Font(name="Calibri", color=LIGHT, size=9.5)
            cell.alignment = left(wrap=True)

# ── Freeze panes at row 4 col B ──────────────────────────────────────────────
ws.freeze_panes = "B4"

# ── Legend ────────────────────────────────────────────────────────────────────
legend_row = len(data) + 5
ws.row_dimensions[legend_row] = openpyxl.worksheet.dimensions.RowDimension(ws, index=legend_row, height=20)
ws.merge_cells(f"A{legend_row}:D{legend_row}")
ws.cell(legend_row, 1).value = "COLOUR LEGEND:"
ws.cell(legend_row, 1).font = Font(name="Calibri", color=WHITE, bold=True, size=10)
ws.cell(legend_row, 1).fill = fill(MID_NAVY)
ws.cell(legend_row, 1).alignment = center()

legends = [
    (TEAL, WHITE, "INTACT / Fluent / Preserved"),
    (CORAL, WHITE, "IMPAIRED / Non-fluent / Absent"),
    (AMBER, NAVY, "VARIABLE / Special feature"),
    (PURPLE, WHITE, "Transcortical Sensory specific"),
]
for j, (bg, fg, label) in enumerate(legends, start=5):
    c = ws.cell(legend_row, j)
    c.value = label
    c.fill = fill(bg)
    c.font = Font(name="Calibri", color=fg, bold=False, size=9)
    c.alignment = center()
    c.border = border()

# Reference row
ref_row = legend_row + 1
ws.row_dimensions[ref_row] = openpyxl.worksheet.dimensions.RowDimension(ws, index=ref_row, height=18)
ws.merge_cells(f"A{ref_row}:P{ref_row}")
ws.cell(ref_row, 1).value = "Sources: Bradley & Daroff's Neurology in Clinical Practice (2022)  |  Harrison's Principles of Internal Medicine 22E (2025, McGraw Hill)  |  Dejerine J (1891, 1892)  |  Broca P (1861)  |  Wernicke C (1874)"
ws.cell(ref_row, 1).font = Font(name="Calibri", color=LIGHT, italic=True, size=8)
ws.cell(ref_row, 1).fill = fill(NAVY)
ws.cell(ref_row, 1).alignment = left(wrap=False)

# ── Page setup ────────────────────────────────────────────────────────────────
ws.page_setup.orientation = "landscape"
ws.page_setup.fitToPage = True
ws.page_setup.fitToWidth = 1
ws.page_setup.fitToHeight = 0

out = "/home/daytona/workspace/speech-language-ppt/Aphasia_Syndromes_Comparison.xlsx"
wb.save(out)
print("DONE:", out)

Running Command

cd /home/daytona/workspace/speech-language-ppt && python3 build_excel.py 2>&1

Editing File

~/speech-language-ppt/build_excel.py

Successfully replaced 1 instance(s) of the string in '/home/daytona/workspace/speech-language-ppt/build_excel.py'

Running Command

cd /home/daytona/workspace/speech-language-ppt && python3 build_excel.py 2>&1

Running Command

python3 -c " import openpyxl, os wb = openpyxl.Workbook() ws = wb.active ws['A1'] = 'test' out = '/tmp/test.xlsx' wb.save(out) print('tmp save OK') import shutil shutil.move(out, '/home/daytona/workspace/speech-language-ppt/test.xlsx') print('move OK') "

Running Command

python3 -c " import openpyxl, shutil wb = openpyxl.Workbook() ws = wb.active ws['A1'] = 'test' wb.save('/tmp/test.xlsx') print('tmp save OK') # copy instead of move import subprocess result = subprocess.run(['cp', '/tmp/test.xlsx', '/home/daytona/workspace/speech-language-ppt/test.xlsx'], capture_output=True, text=True) print(result.returncode, result.stderr) "

Editing File

~/speech-language-ppt/build_excel.py

Successfully replaced 1 instance(s) of the string in '/home/daytona/workspace/speech-language-ppt/build_excel.py'

Running Command

cd /home/daytona/workspace/speech-language-ppt && python3 build_excel.py 2>&1

Writing File

~/speech-language-ppt/build_aphasia_ppt.js

const pptxgen = require("pptxgenjs");
const pres = new pptxgen();
pres.layout = "LAYOUT_16x9";
pres.title = "Aphasia Syndromes";

const NAVY = "0D1B2A"; const MID = "1B2A4A"; const TEAL = "2EC4B6";
const CORAL = "E84855"; const AMBER = "F5A623"; const PURPLE = "9B59B6";
const WHITE = "FFFFFF"; const LIGHT = "D6E4F0"; const DARK = "162236";

function addSlide(bg) { const s = pres.addSlide(); s.background = { color: bg || NAVY }; return s; }

function hdr(s, title, sub) {
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:0.82, fill:{color:TEAL}, line:{color:TEAL} });
  s.addText(title, { x:0.3, y:0.05, w:9.4, h:0.72, fontSize:22, bold:true, color:NAVY, fontFace:"Calibri", valign:"middle" });
  if (sub) s.addText(sub, { x:0.3, y:0.84, w:9.4, h:0.3, fontSize:10, color:LIGHT, fontFace:"Calibri", italic:true });
}

function foot(s, ref) {
  s.addText(ref || "Harrison's 22E (2025)  |  Bradley & Daroff's Neurology in Clinical Practice", {
    x:0.2, y:5.32, w:9.6, h:0.22, fontSize:7.5, color:TEAL, fontFace:"Calibri", italic:true });
}

// =====================================================================
// SLIDE 1 — Title
// =====================================================================
{
  const s = addSlide(NAVY);
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:0.28, h:5.625, fill:{color:TEAL}, line:{color:TEAL} });
  s.addShape(pres.ShapeType.rect, { x:0.28, y:0, w:0.12, h:5.625, fill:{color:CORAL}, line:{color:CORAL} });
  s.addShape(pres.ShapeType.rect, { x:0.4, y:1.55, w:9.6, h:0.07, fill:{color:CORAL}, line:{color:CORAL} });
  s.addText("APHASIA SYNDROMES", { x:0.65, y:0.5, w:9.0, h:0.95, fontSize:48, bold:true, color:WHITE, fontFace:"Calibri", charSpacing:2 });
  s.addText("Classification • Localization • Clinical Features • Comparison", { x:0.65, y:1.62, w:9.0, h:0.45, fontSize:15, color:LIGHT, fontFace:"Calibri", italic:true });
  s.addShape(pres.ShapeType.rect, { x:0.65, y:2.22, w:4.0, h:0.06, fill:{color:AMBER}, line:{color:AMBER} });

  // Quick-reference boxes
  const types = [
    { label:"NON-FLUENT", sub:"Broca · Global · TCM", color:CORAL },
    { label:"FLUENT", sub:"Wernicke · Conduction · TCS · Anomic", color:TEAL },
    { label:"LITERACY", sub:"Alexia ±Agraphia", color:AMBER },
    { label:"SUBCORTICAL", sub:"Thalamic · Striatal", color:PURPLE },
  ];
  types.forEach((t,i) => {
    const x = 0.65 + i*2.35;
    s.addShape(pres.ShapeType.rect, { x, y:2.5, w:2.2, h:0.38, fill:{color:t.color}, line:{color:t.color} });
    s.addText(t.label, { x, y:2.5, w:2.2, h:0.38, fontSize:12, bold:true, color:t.color===AMBER?NAVY:WHITE, fontFace:"Calibri", align:"center", valign:"middle" });
    s.addShape(pres.ShapeType.rect, { x, y:2.88, w:2.2, h:0.52, fill:{color:MID}, line:{color:t.color, pt:1} });
    s.addText(t.sub, { x:x+0.06, y:2.9, w:2.1, h:0.48, fontSize:10, color:LIGHT, fontFace:"Calibri", align:"center", valign:"middle" });
  });

  s.addText([
    { text:"Ref: ", options:{bold:true, color:AMBER} },
    { text:"Harrison's Principles of Internal Medicine 22E (2025)  |  Bradley & Daroff's Neurology in Clinical Practice", options:{color:LIGHT} }
  ], { x:0.65, y:3.65, w:9.1, h:0.4, fontSize:11, fontFace:"Calibri" });
}

// =====================================================================
// SLIDE 2 — Big Comparison Table (Broca, Wernicke, Global, Conduction)
// =====================================================================
{
  const s = addSlide(NAVY);
  hdr(s, "Aphasia Syndromes — Core Diagnostic Features", "The 4 key functions: Fluency · Comprehension · Repetition · Naming");
  foot(s);

  const cols = ["Feature", "BROCA", "WERNICKE", "GLOBAL", "CONDUCTION", "TR. MOTOR", "TR. SENSORY", "ANOMIC"];
  const colColors = [MID, CORAL, TEAL, "7F1A25", AMBER, "1A6060", PURPLE, "2A4A1A"];
  const colW = [1.55, 1.1, 1.1, 0.9, 1.15, 1.1, 1.1, 1.0];
  const colX = [0.2, 1.75, 2.85, 3.95, 4.85, 6.0, 7.1, 8.2];

  const rows = [
    ["Fluency",        "Non-fluent","Fluent","Non-fluent","Fluent","Non-fluent","Fluent","Fluent"],
    ["Comprehension",  "Intact*",  "IMPAIRED","IMPAIRED","Intact","Intact","IMPAIRED","Intact"],
    ["Repetition",     "Impaired", "Impaired","Impaired","SEVERELY↓","INTACT ✓","INTACT ✓","Intact"],
    ["Naming",         "Impaired", "Impaired","Impaired","Impaired","Impaired","Impaired","IMPAIRED↑"],
    ["Reading",        "Often↓",   "Impaired","Impaired","Variable","Variable","Impaired","Intact"],
    ["Writing",        "Impaired", "Paragraphic","Impaired","Variable","Impaired","Impaired","Intact"],
    ["Motor signs",    "R. hemip.","Absent","R. hemip.","Absent±","Mild leg↓","Absent","Absent"],
    ["Lesion",         "Broca area\n(Inf frontal)","Wernicke\n(Sup temp)","Large L MCA","Arc. fasc.\nSupramarg","Ant/sup to\nBroca/SMA","Post watershed\nTPC junction","Angular\ngyrus/var"],
  ];

  // Header row
  const hRowY = 1.1;
  cols.forEach((c, ci) => {
    s.addShape(pres.ShapeType.rect, { x:colX[ci], y:hRowY, w:colW[ci], h:0.45, fill:{color:colColors[ci]}, line:{color:"1E3A5F", pt:0.5} });
    s.addText(c, { x:colX[ci]+0.03, y:hRowY, w:colW[ci]-0.06, h:0.45, fontSize:ci===0?10:9.5, bold:true, color:ci===0?WHITE:ci===3||ci===4?NAVY:WHITE, fontFace:"Calibri", align:"center", valign:"middle" });
  });

  rows.forEach((row, ri) => {
    const rowY = 1.55 + ri * 0.5;
    const rowFill = ri % 2 === 0 ? DARK : MID;
    row.forEach((cell, ci) => {
      s.addShape(pres.ShapeType.rect, { x:colX[ci], y:rowY, w:colW[ci], h:0.5, fill:{color:rowFill}, line:{color:"1E3A5F", pt:0.4} });
      // Colour-code key values
      let color = LIGHT;
      const v = cell.toUpperCase();
      if (v.includes("INTACT") || v.includes("✓") || v.includes("ABSENT")) color = TEAL;
      else if (v.includes("IMPAIRED") || v.includes("NON-FLUENT") || v.includes("HEMIP")) color = CORAL;
      else if (v.includes("SEVERELY") || v.includes("IMPAIRED↑")) color = AMBER;
      if (ci === 0) color = LIGHT;
      s.addText(cell, { x:colX[ci]+0.03, y:rowY+0.03, w:colW[ci]-0.06, h:0.44, fontSize:ci===0?9.5:9, bold:ci===0, color, fontFace:"Calibri", align:ci===0?"left":"center", valign:"middle" });
    });
  });

  // Legend
  const lY = 5.1;
  [["INTACT / Absent",TEAL,NAVY],["IMPAIRED",CORAL,WHITE],["Special finding",AMBER,NAVY]].forEach((l,i) => {
    s.addShape(pres.ShapeType.rect, { x:0.2+i*2.2, y:lY, w:2.1, h:0.2, fill:{color:l[1]}, line:{color:l[1]} });
    s.addText(l[0], { x:0.2+i*2.2, y:lY, w:2.1, h:0.2, fontSize:8, bold:true, color:l[2], fontFace:"Calibri", align:"center", valign:"middle" });
  });
  s.addText("*Broca: comprehension relatively intact but complex syntax affected", { x:6.7, y:5.1, w:3.1, h:0.2, fontSize:7.5, color:"6B8CAE", fontFace:"Calibri", italic:true });
}

// =====================================================================
// SLIDE 3 — Localization diagram + Literacy syndromes
// =====================================================================
{
  const s = addSlide(NAVY);
  hdr(s, "Lesion Localization & Literacy Syndromes (Dejerine)", "Left hemisphere language map | Pure Alexia vs Alexia with Agraphia");
  foot(s, "Dejerine J (1891, 1892)  |  Bradley & Daroff's Neurology in Clinical Practice");

  // Left panel: brain location boxes
  const locs = [
    { area:"BROCA AREA\n(BA 44/45)", pos:"Inferior Frontal Gyrus", aphasia:"Broca Aphasia", color:CORAL, x:0.2, y:1.1 },
    { area:"WERNICKE AREA\n(BA 22)", pos:"Post. Sup. Temporal Gyrus", aphasia:"Wernicke Aphasia", color:TEAL, x:0.2, y:2.1 },
    { area:"ARCUATE FASC.\nSupramarginal Gyrus", pos:"Inf. Parietal / White Matter", aphasia:"Conduction Aphasia", color:AMBER, x:0.2, y:3.1 },
    { area:"ANGULAR GYRUS\n(BA 39)", pos:"Left Inf. Parietal Lobule", aphasia:"Alexia+Agraphia", color:PURPLE, x:0.2, y:4.1 },
  ];
  locs.forEach(l => {
    s.addShape(pres.ShapeType.rect, { x:l.x, y:l.y, w:2.0, h:0.85, fill:{color:l.color}, line:{color:l.color} });
    s.addText(l.area, { x:l.x+0.05, y:l.y+0.02, w:1.9, h:0.45, fontSize:9.5, bold:true, color:l.color===AMBER?NAVY:WHITE, fontFace:"Calibri", align:"center", valign:"middle" });
    s.addText(l.pos, { x:l.x+0.05, y:l.y+0.48, w:1.9, h:0.32, fontSize:8.5, color:l.color===AMBER?NAVY:WHITE, fontFace:"Calibri", align:"center", italic:true });
  });

  // Right panel: Dejerine Literacy Syndromes
  const dejerine = [
    {
      title:"PURE ALEXIA WITHOUT AGRAPHIA",
      year:"Dejerine 1892",
      color:CORAL,
      fields:[
        ["Can WRITE", "✓  YES — normal writing"],
        ["Can READ", "✗  NO — 'linguistic blindfolding'"],
        ["Can read own writing?", "✗  NO"],
        ["Oral speech", "✓  INTACT"],
        ["Lesion", "Left medial occipital + Splenium of CC"],
        ["Vascular", "Left PCA territory"],
        ["Sign", "Right homonymous hemianopia (always)"],
        ["Recovery", "Letter-by-letter reading"]
      ]
    },
    {
      title:"ALEXIA WITH AGRAPHIA",
      year:"Dejerine 1891",
      color:TEAL,
      fields:[
        ["Can WRITE", "✗  NO — 'acquired illiteracy'"],
        ["Can READ", "✗  NO"],
        ["Oral speech", "≈ Intact (mild paraphasias)"],
        ["Lesion", "Angular gyrus (BA 39), left IPL"],
        ["Vascular", "Left MCA (inferior parietal branch)"],
        ["Sign", "Often Gerstmann syndrome"],
        ["Pearl", "BOTH reading + writing lost"],
        ["Distinguish", "from Pure Alexia: writing LOST here"]
      ]
    }
  ];

  dejerine.forEach((d, i) => {
    const x = 2.55 + i * 3.7;
    s.addShape(pres.ShapeType.rect, { x, y:1.05, w:3.4, h:0.38, fill:{color:d.color}, line:{color:d.color} });
    s.addText(d.title, { x:x+0.05, y:1.05, w:3.3, h:0.38, fontSize:10, bold:true, color:d.color===TEAL?NAVY:WHITE, fontFace:"Calibri", align:"center", valign:"middle" });
    s.addText(d.year, { x:x+0.05, y:1.43, w:3.3, h:0.22, fontSize:9, color:d.color, italic:true, fontFace:"Calibri", align:"center" });
    d.fields.forEach((f, fi) => {
      const fy = 1.65 + fi * 0.46;
      s.addShape(pres.ShapeType.rect, { x, y:fy, w:1.2, h:0.42, fill:{color:MID}, line:{color:"1E3A5F", pt:0.4} });
      s.addText(f[0], { x:x+0.04, y:fy+0.02, w:1.14, h:0.38, fontSize:8.5, bold:true, color:d.color, fontFace:"Calibri", valign:"middle" });
      s.addShape(pres.ShapeType.rect, { x:x+1.2, y:fy, w:2.2, h:0.42, fill:{color:DARK}, line:{color:"1E3A5F", pt:0.4} });
      const vColor = f[1].startsWith("✓") ? TEAL : f[1].startsWith("✗") ? CORAL : LIGHT;
      s.addText(f[1], { x:x+1.25, y:fy+0.02, w:2.1, h:0.38, fontSize:8.5, color:vColor, fontFace:"Calibri", valign:"middle" });
    });
  });
}

// =====================================================================
// SLIDE 4 — Clinical Approach Flowchart + Transcortical syndromes
// =====================================================================
{
  const s = addSlide(NAVY);
  hdr(s, "Transcortical Syndromes & Diagnostic Flowchart", "Key rule: INTACT REPETITION = Transcortical (Motor or Sensory)");
  foot(s);

  // Left: Transcortical comparison
  const tcs = [
    {
      name:"TRANSCORTICAL\nMOTOR (TCM)",
      color:CORAL,
      rows:[
        ["Fluency","Non-fluent, reduced initiation"],
        ["Comprehension","INTACT"],
        ["Repetition","INTACT ✓ — KEY feature"],
        ["Echolalia","May complete sentences"],
        ["Lesion","Ant/sup to Broca, SMA, ACA watershed"],
        ["Cause","Hypotension, ACA infarct"],
        ["Behaviour","Apathy, abulia, reduced initiative"],
      ]
    },
    {
      name:"TRANSCORTICAL\nSENSORY (TCS)",
      color:PURPLE,
      rows:[
        ["Fluency","Fluent (paraphasic)"],
        ["Comprehension","IMPAIRED"],
        ["Repetition","INTACT ✓ — with ECHOLALIA"],
        ["Echolalia","Pronounced — repeats examiner"],
        ["Lesion","Post watershed (temporal-parietal-occipital)"],
        ["Cause","MCA–PCA watershed ischaemia"],
        ["Behaviour","Unaware, echolalia, semantic errors"],
      ]
    }
  ];

  tcs.forEach((t, i) => {
    const x = 0.18 + i * 4.7;
    s.addShape(pres.ShapeType.rect, { x, y:1.02, w:4.4, h:0.42, fill:{color:t.color}, line:{color:t.color} });
    s.addText(t.name, { x, y:1.02, w:4.4, h:0.42, fontSize:12, bold:true, color:WHITE, fontFace:"Calibri", align:"center", valign:"middle" });
    t.rows.forEach((r, ri) => {
      const ry = 1.44 + ri * 0.53;
      s.addShape(pres.ShapeType.rect, { x, y:ry, w:1.3, h:0.5, fill:{color:MID}, line:{color:"1E3A5F", pt:0.4} });
      s.addText(r[0], { x:x+0.04, y:ry+0.03, w:1.22, h:0.44, fontSize:9, bold:true, color:t.color, fontFace:"Calibri", valign:"middle" });
      s.addShape(pres.ShapeType.rect, { x:x+1.3, y:ry, w:3.1, h:0.5, fill:{color:DARK}, line:{color:"1E3A5F", pt:0.4} });
      const vColor = r[1].includes("INTACT") || r[1].includes("✓") ? TEAL : r[1].includes("IMPAIRED") ? CORAL : LIGHT;
      s.addText(r[1], { x:x+1.35, y:ry+0.03, w:3.0, h:0.44, fontSize:9, color:vColor, fontFace:"Calibri", valign:"middle" });
    });
  });

  // Right panel — Mini flowchart decision box
  const fc_x = 9.6;
  // Compact side-column summary
  s.addShape(pres.ShapeType.rect, { x:9.3, y:1.02, w:0.5, h:4.42, fill:{color:MID}, line:{color:TEAL, pt:1.5} });
  s.addText("INTACT REPETITION = TRANSCORTICAL\n\nFluent + Intact rep + Poor comp → TCS\nNon-fluent + Intact rep + OK comp → TCM\n\nECHOLALIA is hallmark of TCS", {
    x:9.3, y:1.04, w:0.46, h:4.38, fontSize:6.5, color:TEAL, fontFace:"Calibri", valign:"middle", align:"center"
  });

  // Bottom summary bar
  s.addShape(pres.ShapeType.rect, { x:0.18, y:5.08, w:9.1, h:0.3, fill:{color:MID}, line:{color:AMBER, pt:1} });
  s.addText([
    { text:"🧠 Quick Rule: ", options:{bold:true, color:AMBER} },
    { text:"Intact Repetition = Transcortical (watershed ischaemia)  |  ", options:{color:WHITE} },
    { text:"Severely ↓ Repetition = Conduction  |  ", options:{color:CORAL} },
    { text:"Echolalia = TCS", options:{color:TEAL} }
  ], { x:0.22, y:5.08, w:9.0, h:0.3, fontSize:10, fontFace:"Calibri", valign:"middle" });
}

pres.writeFile({ fileName: "/tmp/Aphasia_4Slides.pptx" })
  .then(() => {
    const { execSync } = require("child_process");
    execSync("cp /tmp/Aphasia_4Slides.pptx /home/daytona/workspace/speech-language-ppt/Aphasia_4Slides.pptx");
    console.log("DONE");
  }).catch(e => console.error(e));

Running Command

cd /home/daytona/workspace/speech-language-ppt && node build_aphasia_ppt.js 2>&1

Running Command

ls -lh /home/daytona/workspace/speech-language-ppt/*.xlsx /home/daytona/workspace/speech-language-ppt/*.pptx 2>&1

Both files are ready. Here are your downloads:

📥 Downloads

Excel Table:

Aphasia Syndromes Comparison

Spreadsheet · XLSX

4-Slide PPT:

Aphasia 4Slides

Presentation · PPTX

What's inside:

📊 Excel Table (16 columns × 10 syndromes)

Every aphasia syndrome compared across:

Fluency · Comprehension · Repetition · Naming · Reading · Writing
Spontaneous speech quality
Motor/sensory signs
Lesion site + Vascular territory
Key clinical feature + Differentiating pearl
Psychiatric/behavioural features
Eponym/history + Treatment focus
Colour-coded: Teal = Intact, Red = Impaired, Amber = Special/Variable
Covers: Broca, Wernicke, Global, Conduction, TCM, TCS, Anomic, Pure Alexia, Alexia+Agraphia, Subcortical

📑 4-Slide PPT

Slide	Content
1	Title + 4-category overview (Non-fluent / Fluent / Literacy / Subcortical)
2	Master comparison table — all 7 syndromes × 8 features, colour-coded
3	Lesion localization map + Dejerine literacy syndromes (Pure Alexia vs Alexia+Agraphia)
4	Transcortical syndromes (TCM vs TCS) + Quick diagnostic rule

Make ppt lengthy of 30 slides with radiological images and areas of cerebrum wherever relevant speech and language areas from relevant references and make the background of ppt white and simple dont use blue and teal colour

Finding Sources

Searching Images

Broca area Wernicke area language cortex brain MRI

Searching Images

aphasia MRI lesion left hemisphere stroke

Searching Images

Wernicke aphasia MRI temporal lobe lesion

Searching Images

arcuate fasciculus white matter tractography DTI language

Finding Sources

Searching Images

Broca aphasia MRI stroke left frontal lobe infarction

Searching Images

global aphasia large MCA territory infarction CT scan

Finding Sources

Searching Images

pure alexia posterior cerebral artery infarction occipital MRI

Searching Images

cerebral lobes functional areas lateral view diagram cortex

Reading File

Writing File

~/speech-language-ppt/build_30slides.js

const pptxgen = require("pptxgenjs");
const { execSync } = require("child_process");

const pres = new pptxgen();
pres.layout = "LAYOUT_16x9";
pres.title = "Language and Speech Disorders";

// ── PALETTE: White background, professional academic style ──
const WHITE   = "FFFFFF";
const BLACK   = "1A1A1A";
const DARK    = "2C2C2C";
const GRAY    = "4A4A4A";
const LGRAY   = "F2F2F2";
const MGRAY   = "D0D0D0";
const RED     = "C0392B";
const DRED    = "922B21";
const ORANGE  = "D35400";
const AMBER   = "CA6F1E";
const GREEN   = "1A7A4A";
const PURPLE  = "6C3483";
const MRED    = "E8C8C5"; // light red fill
const MGREEN  = "C8E5D5"; // light green fill
const MPURP   = "E0D0EE"; // light purple fill
const MORAN   = "FAE5D3"; // light orange fill

// ── Image URLs ──
const IMG = {
  broca_wern_diagram: "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_d9c64539e56a5ff2837db6acc027217f58539b7bec9704ebb1c9c228d3a85920.jpg",
  lang_network_fmri:  "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_c82079a8bf6bfc1d9c231149c06349b5ddad3ee05ade5a1cf5f9bc5dc3fd935d.jpg",
  brain_lobes_diagram:"https://cdn.orris.care/cdss_images/pmc_clinical_VQA_50b00387db18f4904a401e8726030061affbdb44b1f9ddfcb913bf52cd690401.jpg",
  muc_brodmann:       "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_2c0a949d86f15e3f83e26878147016ab0753da386704c64838a5db5fef87b759.jpg",
  lang_network_atlas: "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_a0d9f7a98cc6cc7eb6ed427fb37a24e5cb00695e9dad0394a72b51e07c56230c.jpg",
  speech_network_roi: "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_bd3a217299aa27fce592134b5e665e5eca284384bae30eccfb366544d2996fbf.jpg",
  arcuate_dti_single: "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_23ab7cf547b67c393734fdf8e9ef46baecd230d1822f2a031495618725a5a033.jpg",
  all_tracts_dti:     "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_9117b5b3b7bf1792ac28c0bcdeb967b5b85a0fc121881df8ae0f4d579941b811.jpg",
  broca_ct:           "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_4031fbb8e02fd0bf2e85f664256f67de9b845cba95c33a1104e4bea1c9806f51.jpg",
  broca_mri_sagittal: "https://cdn.orris.care/cdss_images/medpix_vqa_c12226a5-98e5-4d35-899f-db2030a4415c_1766301782921.png",
  broca_mri_flair:    "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_c7a22c3d482d8663ab2c29d0e8c536204b4326b558c27723294d87d487dc72d8.jpg",
  wernicke_overlap:   "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_2035ba88225c7c7f1c2c577c5736d6bee77d35f501a2d0fd7323038f27d2349e.jpg",
  wernicke_ct_hemor:  "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_1b4443a186ddc07159f4120c09a144be62c5052833e2b3aede82f1fbf8822dd4.jpg",
  global_aphasia_mri: "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_b719ad510506561a99aee833c2c76607ecc856d917624588a51b73c5b37342fe.jpg",
  global_aphasia_ct:  "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_67816d4ae19819803833096c4820976dcf029b66f08af2e44f9e7645a482c4ea.jpg",
  lesion_overlap_aph: "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_8169a4a22c3cce5997c4055ed7f6516f72854402e9ab16f12150d7848af271a6.jpg",
  pca_mri_flair:      "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_a95a36c59f8f2e0d28872be2867d434888c4ecda4c772e21a247ebd8edeb95cc.jpg",
  lang_reorganize:    "https://cdn.orris.care/cdss_images/pmc_clinical_VQA_24e897fb78c758094ef7e7e828dc30f8d3fabed17ef0b3d8934126781718f5fd.jpg",
};

// Fetch all images at once
console.log("Fetching images...");
const imgUrls = Object.values(IMG).map(u => `"${u}"`).join(" ");
let imgData = {};
try {
  const raw = execSync(
    `node /home/daytona/skills/shared/scripts/fetch_images.js ${imgUrls}`,
    { maxBuffer: 100 * 1024 * 1024 }
  ).toString();
  const arr = JSON.parse(raw);
  Object.keys(IMG).forEach((k, i) => { imgData[k] = arr[i]; });
  console.log("Images fetched:", Object.keys(imgData).length);
} catch(e) { console.error("Image fetch error:", e.message); }

function img(key) {
  const d = imgData[key];
  return (d && d.base64 && !d.error) ? d.base64 : null;
}

// ── Helpers ──────────────────────────────────────────────────────────────────
function slide(note) {
  const s = pres.addSlide();
  s.background = { color: WHITE };
  return s;
}

// Header bar: red left stripe + title
function header(s, title, sub, stripeColor) {
  const sc = stripeColor || RED;
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:0.75, fill:{color:sc}, line:{color:sc} });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.75, w:10, h:0.04, fill:{color:MGRAY}, line:{color:MGRAY} });
  s.addText(title, { x:0.3, y:0.06, w:9.4, h:0.63, fontSize:22, bold:true, color:WHITE, fontFace:"Calibri", valign:"middle" });
  if (sub) s.addText(sub, { x:0.3, y:0.8, w:9.4, h:0.28, fontSize:10.5, color:GRAY, fontFace:"Calibri", italic:true });
}

function footer(s, ref) {
  s.addShape(pres.ShapeType.rect, { x:0, y:5.42, w:10, h:0.2, fill:{color:LGRAY}, line:{color:MGRAY} });
  s.addText(ref || "Bradley & Daroff's Neurology in Clinical Practice  |  Harrison's Principles of Internal Medicine 22E (2025)",
    { x:0.2, y:5.43, w:9.6, h:0.18, fontSize:7.5, color:GRAY, fontFace:"Calibri", italic:true });
}

function bullet(s, items, x, y, w, h, color, fontSize) {
  const arr = items.map((t, i) => ({
    text: t,
    options: { bullet:{code:"25BA"}, color: color||BLACK, breakLine: i < items.length-1, fontSize: fontSize||11, fontFace:"Calibri" }
  }));
  s.addText(arr, { x, y, w, h });
}

function box(s, x, y, w, h, fillColor, borderColor, text, textColor, fontSize, bold) {
  s.addShape(pres.ShapeType.rect, { x, y, w, h, fill:{color:fillColor||LGRAY}, line:{color:borderColor||MGRAY, pt:1} });
  if (text) s.addText(text, { x:x+0.06, y:y+0.04, w:w-0.12, h:h-0.08, fontSize:fontSize||10, bold:bold||false, color:textColor||BLACK, fontFace:"Calibri", valign:"middle", align:"center" });
}

function sectionDivider(s, title, sub, color) {
  const c = color || RED;
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:5.625, fill:{color:c}, line:{color:c} });
  s.addText(title, { x:0.8, y:1.8, w:8.4, h:1.2, fontSize:38, bold:true, color:WHITE, fontFace:"Calibri", align:"center", valign:"middle" });
  if (sub) s.addText(sub, { x:0.8, y:3.1, w:8.4, h:0.5, fontSize:16, color:"FFE8E5", fontFace:"Calibri", align:"center", italic:true });
  s.addShape(pres.ShapeType.rect, { x:2.5, y:3.7, w:5.0, h:0.06, fill:{color:WHITE}, line:{color:WHITE} });
}

// ============================================================
// SLIDE 1 — TITLE
// ============================================================
{
  const s = slide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:1.8, fill:{color:RED}, line:{color:RED} });
  s.addShape(pres.ShapeType.rect, { x:0, y:1.8, w:10, h:0.06, fill:{color:AMBER}, line:{color:AMBER} });
  s.addText("LANGUAGE AND SPEECH DISORDERS", {
    x:0.4, y:0.18, w:9.2, h:1.5, fontSize:36, bold:true, color:WHITE, fontFace:"Calibri", align:"center", valign:"middle" });
  s.addText("Definitions · Classification · Neuroanatomy · Radiology · Clinical Syndromes · Management", {
    x:0.4, y:1.95, w:9.2, h:0.4, fontSize:13, color:GRAY, fontFace:"Calibri", italic:true, align:"center" });
  // Two reference boxes
  [["Harrison's Principles of Internal Medicine\n22nd Edition (2025) — McGraw Hill", 0.4],
   ["Bradley & Daroff's Neurology\nin Clinical Practice (2022) — Elsevier", 5.4]].forEach(([t,x]) => {
    box(s, x, 2.6, 4.6, 0.9, MRED, RED, t, DRED, 11, false);
  });
  s.addText("Prepared for: Clinical Neurology Teaching", { x:0.4, y:3.75, w:9.2, h:0.3, fontSize:11, color:GRAY, fontFace:"Calibri", italic:true, align:"center" });
  // Brain image
  if (img("brain_lobes_diagram")) {
    s.addImage({ data: img("brain_lobes_diagram"), x:2.5, y:4.1, w:5.0, h:1.3, sizing:{type:"contain",w:5.0,h:1.3} });
  }
  footer(s);
}

// ============================================================
// SLIDE 2 — OVERVIEW / CONTENTS
// ============================================================
{
  const s = slide();
  header(s, "Presentation Overview", "What we will cover today");
  footer(s);
  const topics = [
    ["Section 1", "Neuroanatomy of Language: Cortical Language Areas", RED],
    ["Section 2", "White Matter Tracts: Arcuate Fasciculus & Connections", ORANGE],
    ["Section 3", "Classification of Language Disorders", AMBER],
    ["Section 4", "Aphasia Syndromes: Definitions & Clinical Features", RED],
    ["Section 5", "Radiological Correlates: MRI & CT Findings", DRED],
    ["Section 6", "Speech Disorders: Dysarthria, Dysphonia, Apraxia", ORANGE],
    ["Section 7", "Literacy Disorders: Alexia, Agraphia (Dejerine)", PURPLE],
    ["Section 8", "Bedside Assessment & Clinical Approach", GREEN],
    ["Section 9", "Rehabilitation & Management", AMBER],
  ];
  topics.forEach((t, i) => {
    const x = i < 5 ? 0.3 : 5.3;
    const y = 1.15 + (i < 5 ? i : i-5) * 0.77;
    box(s, x, y, 1.0, 0.55, t[2], t[2], t[0], WHITE, 10, true);
    s.addText(t[1], { x:x+1.1, y:y+0.06, w:3.7, h:0.45, fontSize:11, color:BLACK, fontFace:"Calibri", valign:"middle" });
  });
}

// ============================================================
// SLIDE 3 — SECTION DIVIDER: NEUROANATOMY
// ============================================================
{
  const s = slide();
  sectionDivider(s, "SECTION 1\nNeuroanatomy of Language", "Cortical Language Areas & Cerebral Localisation", RED);
}

// ============================================================
// SLIDE 4 — CEREBRAL LOBES & LANGUAGE AREAS
// ============================================================
{
  const s = slide();
  header(s, "Cerebral Lobes & Language Areas", "Lateral view of the dominant (left) hemisphere");
  footer(s);
  if (img("brain_lobes_diagram")) {
    s.addImage({ data: img("brain_lobes_diagram"), x:0.3, y:1.0, w:5.5, h:3.8, sizing:{type:"contain",w:5.5,h:3.8} });
  }
  const areas = [
    { name:"Frontal Lobe", role:"Broca's area (BA 44/45)\nSpeech production, syntax\nSMA: initiation", color:RED },
    { name:"Parietal Lobe", role:"Supramarginal gyrus\nAngular gyrus (BA 39)\nPhonological processing", color:ORANGE },
    { name:"Temporal Lobe", role:"Wernicke's area (BA 22)\nLanguage comprehension\nSemantic memory", color:PURPLE },
    { name:"Occipital Lobe", role:"Visual cortex (BA 17)\nVisual word recognition\nAlexia when damaged", color:GREEN },
  ];
  areas.forEach((a, i) => {
    const y = 1.1 + i * 1.06;
    box(s, 6.0, y, 1.5, 0.95, a.color, a.color, a.name, WHITE, 10, true);
    box(s, 7.5, y, 2.3, 0.95, LGRAY, MGRAY, a.role, DARK, 9.5, false);
  });
}

// ============================================================
// SLIDE 5 — BROCA & WERNICKE AREAS (DIAGRAM)
// ============================================================
{
  const s = slide();
  header(s, "Broca's & Wernicke's Areas — Classical Language Map", "Perisylvian language network with arcuate fasciculus");
  footer(s);
  if (img("broca_wern_diagram")) {
    s.addImage({ data: img("broca_wern_diagram"), x:0.3, y:1.0, w:5.8, h:3.9, sizing:{type:"contain",w:5.8,h:3.9} });
  }
  const pts = [
    { label:"BROCA'S AREA", loc:"Inferior Frontal Gyrus (BA 44, 45)", fn:"Speech production, syntactic processing, motor programming of speech", color:RED },
    { label:"WERNICKE'S AREA", loc:"Post. Sup. Temporal Gyrus (BA 22)", fn:"Auditory language comprehension, phonological decoding", color:ORANGE },
    { label:"ARCUATE FASCICULUS", loc:"White matter: temporal → frontal", fn:"Connects Wernicke to Broca; damage → Conduction aphasia", color:PURPLE },
    { label:"PRIMARY MOTOR CORTEX", loc:"Precentral Gyrus (BA 4)", fn:"Motor execution of speech via corticobulbar tract", color:GREEN },
  ];
  pts.forEach((p, i) => {
    const y = 1.1 + i * 1.0;
    box(s, 6.2, y, 1.6, 0.88, p.color, p.color, p.label, WHITE, 9, true);
    s.addText([
      {text: p.loc+"\n", options:{bold:true, color:DARK, fontSize:9.5, fontFace:"Calibri"}},
      {text: p.fn, options:{color:GRAY, fontSize:9, fontFace:"Calibri"}}
    ], { x:7.85, y:y+0.04, w:1.95, h:0.82, valign:"middle" });
  });
}

// ============================================================
// SLIDE 6 — fMRI LANGUAGE NETWORK
// ============================================================
{
  const s = slide();
  header(s, "Functional MRI: Language Network Lateralisation", "Broca's area (left) & Wernicke's area (right) — resting-state fMRI");
  footer(s, "Harrison's 22E (2025)  |  Hugging Face PMC Clinical VQA");
  if (img("lang_network_fmri")) {
    s.addImage({ data: img("lang_network_fmri"), x:0.3, y:1.0, w:9.4, h:4.0, sizing:{type:"contain",w:9.4,h:4.0} });
  }
  s.addText("fMRI shows strong LEFT hemisphere lateralization for language. Broca's area: left inferior frontal gyrus; Wernicke's area: left posterior superior temporal region. Color scale: blue = negative connectivity, red = positive connectivity.", {
    x:0.3, y:5.0, w:9.4, h:0.35, fontSize:9, color:GRAY, fontFace:"Calibri", italic:true });
}

// ============================================================
// SLIDE 7 — BRODMANN AREAS & LANGUAGE (MUC MODEL)
// ============================================================
{
  const s = slide();
  header(s, "Brodmann Areas & Language — MUC Model", "Memory–Unification–Control model of language cortex");
  footer(s, "Bradley & Daroff's Neurology in Clinical Practice");
  if (img("muc_brodmann")) {
    s.addImage({ data: img("muc_brodmann"), x:0.3, y:1.0, w:5.5, h:3.8, sizing:{type:"contain",w:5.5,h:3.8} });
  }
  const brod = [
    { area:"BA 44, 45", name:"Broca's Area", fn:"Syntactic unification, speech production", color:RED },
    { area:"BA 22", name:"Wernicke's Area", fn:"Auditory comprehension, semantic processing", color:ORANGE },
    { area:"BA 39", name:"Angular Gyrus", fn:"Reading, cross-modal language integration", color:PURPLE },
    { area:"BA 40", name:"Supramarginal Gyrus", fn:"Phonological processing, repetition pathway", color:GREEN },
    { area:"BA 6, SMA", name:"Premotor / SMA", fn:"Speech initiation, motor planning", color:AMBER },
    { area:"BA 17–19", name:"Occipital Cortex", fn:"Visual word processing (reading/writing)", color:GRAY },
  ];
  brod.forEach((b, i) => {
    const y = 1.1 + i * 0.73;
    box(s, 6.1, y, 0.85, 0.6, b.color, b.color, b.area, WHITE, 9, true);
    box(s, 6.95, y, 1.3, 0.6, LGRAY, MGRAY, b.name, DARK, 9, true);
    s.addText(b.fn, { x:8.28, y:y+0.05, w:1.52, h:0.5, fontSize:8.5, color:GRAY, fontFace:"Calibri", valign:"middle" });
  });
}

// ============================================================
// SLIDE 8 — SECTION: WHITE MATTER TRACTS
// ============================================================
{
  const s = slide();
  sectionDivider(s, "SECTION 2\nWhite Matter Tracts", "Arcuate Fasciculus & Language Connectivity", ORANGE);
}

// ============================================================
// SLIDE 9 — ARCUATE FASCICULUS DTI
// ============================================================
{
  const s = slide();
  header(s, "Arcuate Fasciculus — DTI Tractography", "The key white matter tract connecting Broca's and Wernicke's areas", ORANGE);
  footer(s);
  if (img("arcuate_dti_single")) {
    s.addImage({ data: img("arcuate_dti_single"), x:0.3, y:1.0, w:5.5, h:3.9, sizing:{type:"contain",w:5.5,h:3.9} });
  }
  s.addText("ARCUATE FASCICULUS", { x:6.1, y:1.05, w:3.6, h:0.42, fontSize:14, bold:true, color:RED, fontFace:"Calibri", align:"center" });
  const facts = [
    "Superior longitudinal fasciculus component",
    "C-shaped arc around the Sylvian fissure",
    "Connects posterior temporal (Wernicke) to inferior frontal (Broca)",
    "Critical for REPETITION of language",
    "Disruption → Conduction Aphasia",
    "Visible on DTI as yellow-red fiber bundle",
    "Predominantly LEFT hemisphere dominant",
    "Absent/hypoplastic in some language disorders",
  ];
  bullet(s, facts, 6.1, 1.55, 3.7, 3.3, DARK, 10.5);
  box(s, 6.1, 4.9, 3.7, 0.45, MRED, RED, "Lesion of arcuate fasciculus → CONDUCTION APHASIA\n(Fluent speech + intact comprehension + impaired repetition)", DRED, 9, false);
}

// ============================================================
// SLIDE 10 — ALL LANGUAGE TRACTS DTI
// ============================================================
{
  const s = slide();
  header(s, "Language White Matter Tracts — DTI Atlas", "Five key perisylvian fiber bundles", ORANGE);
  footer(s);
  if (img("all_tracts_dti")) {
    s.addImage({ data: img("all_tracts_dti"), x:0.3, y:1.0, w:5.6, h:4.0, sizing:{type:"contain",w:5.6,h:4.0} });
  }
  const tracts = [
    { name:"Arcuate Fasciculus (AF)", color:"F1C40F", fn:"Wernicke ↔ Broca; repetition pathway" },
    { name:"Sup. Longitudinal Fasc. (SLF)", color:"E91E8C", fn:"Frontoparietal integration" },
    { name:"Inf. Fronto-Occipital Fasc. (IFOF)", color:"E74C3C", fn:"Frontal ↔ occipital; reading semantics" },
    { name:"Inf. Longitudinal Fasc. (ILF)", color:"27AE60", fn:"Temporal ↔ occipital; visual semantics" },
    { name:"Uncinate Fasciculus (UF)", color:"BDC3C7", fn:"Orbitofrontal ↔ anterior temporal" },
  ];
  tracts.forEach((t, i) => {
    const y = 1.15 + i * 0.86;
    box(s, 6.1, y, 0.22, 0.72, t.color, t.color, "", WHITE, 9, false);
    s.addText(t.name, { x:6.38, y:y+0.06, w:3.42, h:0.28, fontSize:10.5, bold:true, color:DARK, fontFace:"Calibri" });
    s.addText(t.fn, { x:6.38, y:y+0.36, w:3.42, h:0.3, fontSize:9.5, color:GRAY, fontFace:"Calibri" });
  });
}

// ============================================================
// SLIDE 11 — SECTION: CLASSIFICATION
// ============================================================
{
  const s = slide();
  sectionDivider(s, "SECTION 3\nClassification of Language\nand Speech Disorders", "Aphasia · Dysarthria · Dysphonia · Alexia · Agraphia", AMBER);
}

// ============================================================
// SLIDE 12 — CLASSIFICATION TABLE
// ============================================================
{
  const s = slide();
  header(s, "Classification: Language vs Speech Disorders", "", AMBER);
  footer(s);
  // Two columns
  const cols = [
    { title:"LANGUAGE DISORDERS (Aphasia spectrum)", color:RED, items:[
      "Involve the SYMBOL SYSTEM — content of language",
      "Reading, writing, naming, comprehension affected",
      "Lesion in dominant (left) cerebral hemisphere",
      "Language content ABNORMAL",
      "Types: Broca, Wernicke, Global, Conduction,",
      "  Transcortical Motor/Sensory, Anomic,",
      "  Alexia, Agraphia, Subcortical aphasia"
    ]},
    { title:"SPEECH DISORDERS (Motor speech)", color:ORANGE, items:[
      "Involve the MOTOR ACT of speaking",
      "Articulation, voice, rhythm affected",
      "Language CONTENT is INTACT",
      "Flaccid, Spastic, Ataxic, Hypokinetic,",
      "  Hyperkinetic, Mixed Dysarthria",
      "Dysphonia (voice disorder)",
      "Apraxia of speech (motor programming)"
    ]}
  ];
  cols.forEach((c, i) => {
    const x = i === 0 ? 0.3 : 5.2;
    box(s, x, 1.05, 4.5, 0.45, c.color, c.color, c.title, WHITE, 11, true);
    box(s, x, 1.5, 4.5, 3.5, LGRAY, MGRAY, null, BLACK, 10, false);
    bullet(s, c.items, x+0.15, 1.58, 4.3, 3.35, DARK, 10.5);
  });
  // Middle
  s.addText("≠", { x:4.8, y:2.8, w:0.4, h:0.6, fontSize:28, bold:true, color:RED, fontFace:"Calibri", align:"center" });
  // Key distinguisher
  box(s, 0.3, 5.05, 9.4, 0.35, MRED, RED,
    "KEY: Aphasia = abnormal language content  |  Dysarthria = normal content, abnormal motor output  |  Both ≠ Psychogenic mutism",
    DRED, 9.5, false);
}

// ============================================================
// SLIDE 13 — DEFINITION OF APHASIA
// ============================================================
{
  const s = slide();
  header(s, "Aphasia — Definition & Bedside Testing", "Acquired language disorder from dominant hemisphere damage");
  footer(s);
  box(s, 0.3, 1.0, 9.4, 1.0, MRED, RED, null, BLACK, 10, false);
  s.addText([
    {text:"DEFINITION: ", options:{bold:true, color:RED, fontSize:13, fontFace:"Calibri"}},
    {text:"Aphasia is an ACQUIRED disorder of LANGUAGE caused by brain damage, affecting the ability to speak, understand, read, or write — in a person who previously had intact language function. It results from injury to the language-dominant (usually left) hemisphere.\n", options:{color:DARK, fontSize:12, fontFace:"Calibri"}},
    {text:"— Bradley & Daroff's Neurology in Clinical Practice", options:{italic:true, color:GRAY, fontSize:10, fontFace:"Calibri"}}
  ], { x:0.5, y:1.04, w:9.0, h:0.92, valign:"middle" });

  // 4 Domain boxes
  const domains = [
    { d:"FLUENCY", desc:"Rate, effort, phrase length, prosody of spontaneous speech\nFluent vs Non-fluent is the first branch in classification", color:RED },
    { d:"COMPREHENSION", desc:"Understanding spoken language\nTested: yes/no questions, point-to commands", color:ORANGE },
    { d:"REPETITION", desc:"Repeat 'No ifs, ands, or buts'\nTests integrity of arcuate fasciculus", color:PURPLE },
    { d:"NAMING", desc:"Anomia = universal in aphasia\nConfrontation naming: 'What is this called?'", color:GREEN },
  ];
  domains.forEach((d, i) => {
    const x = 0.3 + i * 2.38;
    box(s, x, 2.1, 2.22, 0.45, d.color, d.color, d.d, WHITE, 11, true);
    box(s, x, 2.55, 2.22, 1.35, LGRAY, MGRAY, d.desc, DARK, 9.5, false);
  });
  box(s, 0.3, 4.0, 4.3, 0.6, MRED, RED,
    "Bedside Test: 'Repeat after me — No ifs, ands, or buts'\n(Tests all 3: fluency, repetition, motor speech)", DRED, 10, false);
  box(s, 4.75, 4.0, 5.0, 0.6, LGRAY, MGRAY,
    "Writing sample: always obtain — reveals mild aphasia\nNaming: 'body parts, pen, watch, coin'\nReading: newspaper headline aloud + comprehension", DARK, 10, false);
}

// ============================================================
// SLIDE 14 — SECTION: APHASIA SYNDROMES
// ============================================================
{
  const s = slide();
  sectionDivider(s, "SECTION 4\nAphasia Syndromes", "Clinical Features · Lesion Sites · Radiological Correlates", RED);
}

// ============================================================
// SLIDE 15 — BROCA APHASIA (clinical + MRI)
// ============================================================
{
  const s = slide();
  header(s, "Broca's Aphasia — Expressive (Non-fluent) Aphasia", "Paul Broca, 1861 — Patient 'Tan' (Leborgne)");
  footer(s);
  if (img("broca_mri_sagittal")) {
    s.addImage({ data: img("broca_mri_sagittal"), x:6.5, y:1.0, w:3.3, h:2.5, sizing:{type:"contain",w:3.3,h:2.5} });
    s.addText("T2 MRI — Sagittal\nLeft inferior frontal gyrus encephalomalacia\n(chronic Broca area infarct)", { x:6.5, y:3.5, w:3.3, h:0.65, fontSize:8.5, color:GRAY, fontFace:"Calibri", italic:true, align:"center" });
  }
  const rows = [
    ["Fluency", "NON-FLUENT; telegraphic; agrammatic; effortful", RED],
    ["Comprehension", "Relatively INTACT (complex syntax mildly ↓)", GREEN],
    ["Repetition", "IMPAIRED", RED],
    ["Naming", "Impaired — tip-of-tongue; phonemic paraphasias", ORANGE],
    ["Writing", "Dysmorphic, dysgrammatic", ORANGE],
    ["Reading", "Often impaired (third alexia)", ORANGE],
    ["Motor signs", "RIGHT HEMIPARESIS (contralateral)", RED],
    ["Lesion", "Inferior frontal gyrus — Broca area (BA 44/45)", DARK],
    ["Vascular", "Left MCA superior division — frontal branches", DARK],
    ["Behaviour", "AWARE — frustrated, depressed, insight preserved", PURPLE],
  ];
  rows.forEach((r, i) => {
    const y = 1.1 + i * 0.41;
    box(s, 0.3, y, 1.9, 0.38, LGRAY, MGRAY, r[0], DARK, 10, true);
    box(s, 2.2, y, 4.1, 0.38, WHITE, MGRAY, r[1], r[2], 10, false);
  });
}

// ============================================================
// SLIDE 16 — BROCA APHASIA CT + FLAIR
// ============================================================
{
  const s = slide();
  header(s, "Broca's Aphasia — CT & MRI Imaging", "Left frontal/inferior frontal lesion — Broca area");
  footer(s, "Diagnostic neuroimaging — PMC Clinical VQA database");
  s.addText("CT Scan — Broca (left) vs Wernicke (right) aphasia comparison", {
    x:0.3, y:0.85, w:9.4, h:0.3, fontSize:11, color:GRAY, fontFace:"Calibri", italic:true });
  if (img("broca_ct")) {
    s.addImage({ data: img("broca_ct"), x:0.3, y:1.15, w:5.8, h:2.8, sizing:{type:"contain",w:5.8,h:2.8} });
  }
  s.addText("CT: Chronic ischaemic infarction — left inferior frontal gyrus (Broca area). Cortical loss and left lateral ventricle widening indicate established stroke.", {
    x:0.3, y:3.95, w:5.8, h:0.5, fontSize:9, color:GRAY, fontFace:"Calibri", italic:true });
  if (img("broca_mri_flair")) {
    s.addImage({ data: img("broca_mri_flair"), x:6.3, y:1.15, w:3.5, h:2.8, sizing:{type:"contain",w:3.5,h:2.8} });
  }
  s.addText("MRI FLAIR/DWI: Wedge-shaped hyperintense lesion left parietal lobe — acute ischaemic infarction (venous infarct) presenting with Broca's aphasia", {
    x:6.3, y:3.95, w:3.5, h:0.5, fontSize:9, color:GRAY, fontFace:"Calibri", italic:true });
}

// ============================================================
// SLIDE 17 — WERNICKE APHASIA
// ============================================================
{
  const s = slide();
  header(s, "Wernicke's Aphasia — Receptive (Fluent) Aphasia", "Carl Wernicke, 1874 — Posterior superior temporal gyrus");
  footer(s);
  if (img("wernicke_ct_hemor")) {
    s.addImage({ data: img("wernicke_ct_hemor"), x:6.5, y:1.0, w:3.3, h:2.5, sizing:{type:"contain",w:3.3,h:2.5} });
    s.addText("CT scan: Hyperdense lesion in left temporal lobe — Wernicke's area — acute haemorrhagic stroke causing receptive aphasia", { x:6.5, y:3.5, w:3.3, h:0.65, fontSize:8.5, color:GRAY, fontFace:"Calibri", italic:true, align:"center" });
  }
  const rows = [
    ["Fluency", "FLUENT; logorrheic; jargon; paraphasic", GREEN],
    ["Comprehension", "IMPAIRED — often severely", RED],
    ["Repetition", "IMPAIRED", RED],
    ["Naming", "Impaired — bizarre verbal paraphasias/neologisms", RED],
    ["Writing", "Well-formed but paragraphic (spelling errors)", ORANGE],
    ["Reading", "Impaired — comprehension and aloud", RED],
    ["Motor signs", "Usually ABSENT; ± right hemianopia", GREEN],
    ["Lesion", "Post. superior temporal gyrus (BA 22) + inf. parietal", DARK],
    ["Vascular", "Left MCA inferior division — temporal branches", DARK],
    ["Behaviour", "Often UNAWARE; paranoid; unconcerned (anosognosia)", PURPLE],
  ];
  rows.forEach((r, i) => {
    const y = 1.1 + i * 0.41;
    box(s, 0.3, y, 1.9, 0.38, LGRAY, MGRAY, r[0], DARK, 10, true);
    box(s, 2.2, y, 4.1, 0.38, WHITE, MGRAY, r[1], r[2], 10, false);
  });
}

// ============================================================
// SLIDE 18 — WERNICKE MRI LESION OVERLAP
// ============================================================
{
  const s = slide();
  header(s, "Wernicke's Aphasia — MRI Lesion Overlap Map", "12-patient lesion overlap: posterior superior temporal — angular gyrus", ORANGE);
  footer(s, "Diagnostic neuroimaging — PMC Clinical VQA database");
  if (img("wernicke_overlap")) {
    s.addImage({ data: img("wernicke_overlap"), x:1.0, y:1.0, w:8.0, h:4.0, sizing:{type:"contain",w:8.0,h:4.0} });
  }
  s.addText("Lesion overlap from 12 Wernicke's aphasia patients. Maximal overlap (red/orange) concentrated in posterior superior temporal lobe, extending to angular gyrus and temporoparietal junction — classic Wernicke territory. Left MCA inferior division.", {
    x:0.3, y:5.0, w:9.4, h:0.35, fontSize:9, color:GRAY, fontFace:"Calibri", italic:true });
}

// ============================================================
// SLIDE 19 — GLOBAL APHASIA
// ============================================================
{
  const s = slide();
  header(s, "Global Aphasia — Most Severe Form", "All language modalities severely impaired — large left MCA territory");
  footer(s);
  if (img("global_aphasia_mri")) {
    s.addImage({ data: img("global_aphasia_mri"), x:5.7, y:0.95, w:4.1, h:3.0, sizing:{type:"contain",w:4.1,h:3.0} });
    s.addText("MRI DWI/FLAIR: Large left MCA territory infarction. Hyperintense lesion involving both frontal (Broca) and temporal (Wernicke) regions. Causing global aphasia.", { x:5.7, y:3.95, w:4.1, h:0.5, fontSize:8.5, color:GRAY, fontFace:"Calibri", italic:true, align:"center" });
  }
  const features = [
    ["Fluency", "NON-FLUENT or MUTE; stereotypic utterances only", RED],
    ["Comprehension", "SEVERELY IMPAIRED", RED],
    ["Repetition", "SEVERELY IMPAIRED", RED],
    ["Naming", "Severely impaired", RED],
    ["Reading/Writing", "Both severely impaired", RED],
    ["Motor signs", "RIGHT HEMIPLEGIA + hemisensory loss + hemianopia", RED],
    ["Lesion", "Large left hemisphere — both Broca + Wernicke territory", DARK],
    ["Prognosis", "POOR — worst outcome of all aphasia types", DRED],
  ];
  features.forEach((r, i) => {
    const y = 1.1 + i * 0.47;
    box(s, 0.3, y, 1.9, 0.43, LGRAY, MGRAY, r[0], DARK, 10, true);
    box(s, 2.2, y, 3.3, 0.43, WHITE, MGRAY, r[1], r[2], 10, false);
  });
}

// ============================================================
// SLIDE 20 — CONDUCTION APHASIA
// ============================================================
{
  const s = slide();
  header(s, "Conduction Aphasia — Arcuate Fasciculus Lesion", "Wernicke (1874) & Geschwind (disconnection hypothesis)", PURPLE);
  footer(s);
  box(s, 0.3, 1.02, 9.4, 0.75, MPURP, PURPLE,
    "DEFINITION: Fluent speech + relatively intact comprehension + SEVERELY impaired repetition. Caused by disconnection of Wernicke's area from Broca's area via the arcuate fasciculus. The key feature is repetition impaired out of proportion to other deficits.",
    DARK, 10.5, false);
  const rows = [
    ["Fluency", "FLUENT; phonemic paraphasias", GREEN],
    ["Comprehension", "Relatively INTACT", GREEN],
    ["Repetition", "SEVERELY IMPAIRED — disproportionate", RED],
    ["Naming", "Impaired — phonemic paraphasias", ORANGE],
    ["Motor signs", "Usually absent; mild right arm weakness", GREEN],
    ["Lesion", "Arcuate fasciculus / Supramarginal gyrus (BA 40)", DARK],
    ["Vascular", "Left MCA — parietal branches, post. Sylvian", DARK],
    ["Key behaviour", "Conduit d'approche: repeated self-correction toward target", PURPLE],
  ];
  rows.forEach((r, i) => {
    const y = 1.85 + i * 0.42;
    box(s, 0.3, y, 1.9, 0.39, LGRAY, MGRAY, r[0], DARK, 10, true);
    box(s, 2.2, y, 7.2, 0.39, WHITE, MGRAY, r[1], r[2], 10, false);
  });
  if (img("arcuate_dti_single")) {
    s.addImage({ data: img("arcuate_dti_single"), x:7.5, y:1.85, w:2.3, h:2.0, sizing:{type:"contain",w:2.3,h:2.0} });
    s.addText("DTI: Arcuate fasciculus — lesion here → conduction aphasia", { x:7.5, y:3.85, w:2.3, h:0.35, fontSize:7.5, color:GRAY, fontFace:"Calibri", italic:true, align:"center" });
  }
}

// ============================================================
// SLIDE 21 — TRANSCORTICAL APHASIA (MOTOR + SENSORY)
// ============================================================
{
  const s = slide();
  header(s, "Transcortical Aphasias — Intact Repetition", "Watershed territory lesions — INTACT repetition is the hallmark", AMBER);
  footer(s, "Lichtheim (1885)  |  Bradley & Daroff's Neurology");
  s.addText("KEY RULE: INTACT REPETITION = Transcortical Aphasia (watershed ischaemia — hypotension, cardiac arrest)", {
    x:0.3, y:0.88, w:9.4, h:0.3, fontSize:11, bold:true, color:RED, fontFace:"Calibri", align:"center" });
  const tcs = [
    {
      name:"TRANSCORTICAL MOTOR (TCM)", color:RED,
      rows:[
        ["Fluency", "NON-FLUENT; reduced initiation; latency"],
        ["Comprehension", "INTACT"],
        ["Repetition", "INTACT ✓ — hallmark"],
        ["Lesion", "Ant/sup to Broca; SMA; ACA watershed"],
        ["Cause", "ACA infarct; hypotension; cardiac arrest"],
        ["Behaviour", "Apathy, abulia — frontal lobe syndrome"],
      ]
    },
    {
      name:"TRANSCORTICAL SENSORY (TCS)", color:PURPLE,
      rows:[
        ["Fluency", "FLUENT; echolalic; semantic paraphasias"],
        ["Comprehension", "IMPAIRED"],
        ["Repetition", "INTACT ✓ — with pronounced ECHOLALIA"],
        ["Lesion", "Post. watershed: temporal-parietal-occipital jct"],
        ["Cause", "MCA–PCA watershed ischaemia"],
        ["Behaviour", "Echolalia, unaware, repeats examiner verbatim"],
      ]
    }
  ];
  tcs.forEach((t, i) => {
    const x = i === 0 ? 0.3 : 5.2;
    box(s, x, 1.22, 4.5, 0.42, t.color, t.color, t.name, WHITE, 11, true);
    t.rows.forEach((r, ri) => {
      const y = 1.64 + ri * 0.56;
      box(s, x, y, 1.5, 0.53, LGRAY, MGRAY, r[0], DARK, 10, true);
      box(s, x+1.5, y, 3.0, 0.53, WHITE, MGRAY, r[1],
        r[1].includes("INTACT") || r[1].includes("✓") ? GREEN : r[1].includes("IMPAIRED") || r[1].includes("NON-FLUENT") ? RED : DARK, 10, false);
    });
  });
}

// ============================================================
// SLIDE 22 — ANOMIC APHASIA + SUBCORTICAL
// ============================================================
{
  const s = slide();
  header(s, "Anomic & Subcortical Aphasia", "Most common residual + basal ganglia/thalamic aphasia");
  footer(s);
  const two = [
    {
      name:"ANOMIC APHASIA (Amnesic)", color:GREEN, x:0.3,
      def:"Most BENIGN aphasia; often residual from recovery of any type. Isolated word-finding difficulty with otherwise preserved language.",
      rows:[
        ["Fluency", "Fluent — circumlocutory"],
        ["Comprehension", "INTACT"],
        ["Repetition", "INTACT"],
        ["Naming", "IMPAIRED — hallmark; anomia"],
        ["Motor signs", "Usually absent"],
        ["Lesion", "Angular gyrus (BA 39) or variable temporal"],
      ]
    },
    {
      name:"SUBCORTICAL APHASIA", color:AMBER, x:5.2,
      def:"Thalamic or striatal lesions causing aphasia not fitting classic cortical patterns. Hypophonic, fluctuating, prominent anomia.",
      rows:[
        ["Fluency", "Variable — often hypophonic"],
        ["Comprehension", "Variably impaired"],
        ["Repetition", "Variable"],
        ["Naming", "IMPAIRED — anomia prominent"],
        ["Motor signs", "Right hemiparesis (capsular)"],
        ["Lesion", "Thalamus, caudate, putamen, internal capsule"],
      ]
    }
  ];
  two.forEach(t => {
    box(s, t.x, 1.05, 4.5, 0.42, t.color, t.color, t.name, WHITE, 11, true);
    s.addText(t.def, { x:t.x+0.1, y:1.5, w:4.3, h:0.58, fontSize:10, color:GRAY, fontFace:"Calibri", italic:true, valign:"middle" });
    t.rows.forEach((r, ri) => {
      const y = 2.1 + ri * 0.5;
      box(s, t.x, y, 1.4, 0.46, LGRAY, MGRAY, r[0], DARK, 10, true);
      box(s, t.x+1.4, y, 3.1, 0.46, WHITE, MGRAY, r[1],
        r[1].includes("INTACT") ? GREEN : r[1].includes("IMPAIRED") ? RED : DARK, 10, false);
    });
  });
}

// ============================================================
// SLIDE 23 — MASTER COMPARISON TABLE
// ============================================================
{
  const s = slide();
  header(s, "Aphasia Syndromes — Master Comparison Table", "The 4 key diagnostic domains: Fluency · Comprehension · Repetition · Lesion");
  footer(s);
  const cols = ["Syndrome", "Fluency", "Comprehension", "Repetition", "Key Feature", "Lesion"];
  const colW = [1.55, 0.95, 1.4, 1.1, 2.3, 2.5];
  const colX = [0.2, 1.75, 2.7, 4.1, 5.2, 7.5];
  const rows = [
    ["BROCA",        "Non-fluent",  "Intact*",    "Impaired",  "Agrammatism; R hemiparesis",  "Inf. frontal (BA 44/45)"],
    ["WERNICKE",     "Fluent",      "IMPAIRED",   "Impaired",  "Jargon; unaware; paraphasias","Post. sup. temporal (BA 22)"],
    ["GLOBAL",       "Non-fluent",  "IMPAIRED",   "Impaired",  "All modalities severe; mute", "Large left MCA territory"],
    ["CONDUCTION",   "Fluent",      "Intact",     "SEVERELY↓", "Conduit d'approche; phonemic","Arcuate fasciculus/supraMarg"],
    ["TCM",          "Non-fluent",  "Intact",     "INTACT ✓",  "Apathy; abulia; echolalia±",  "Ant/sup Broca; SMA; ACA wsh"],
    ["TCS",          "Fluent",      "IMPAIRED",   "INTACT ✓",  "Echolalia; unaware",          "Post. watershed TPC jct"],
    ["ANOMIC",       "Fluent",      "Intact",     "Intact",    "Circumlocution; tip-of-tongue","Angular gyrus / variable"],
    ["SUBCORTICAL",  "Hypophonic",  "Variable",   "Variable",  "Fluctuating; hypophonia",     "Thalamus/striatum/capsule"],
  ];
  const hY = 1.08;
  cols.forEach((c, ci) => {
    box(s, colX[ci], hY, colW[ci], 0.4, RED, RED, c, WHITE, 9.5, true);
  });
  rows.forEach((row, ri) => {
    const rowY = 1.48 + ri * 0.47;
    const fill = ri % 2 === 0 ? WHITE : LGRAY;
    row.forEach((cell, ci) => {
      s.addShape(pres.ShapeType.rect, { x:colX[ci], y:rowY, w:colW[ci], h:0.44, fill:{color:fill}, line:{color:MGRAY, pt:0.5} });
      const clr = cell.includes("INTACT") || cell.includes("✓") ? GREEN
                : cell.includes("IMPAIRED") || cell.includes("Non-fluent") || cell.includes("SEVERELY") ? RED
                : cell.includes("Variable") ? AMBER : ci===0 ? RED : DARK;
      s.addText(cell, { x:colX[ci]+0.04, y:rowY+0.03, w:colW[ci]-0.08, h:0.38, fontSize:ci===0?10:9, bold:ci===0, color:clr, fontFace:"Calibri", valign:"middle" });
    });
  });
}

// ============================================================
// SLIDE 24 — SECTION: SPEECH DISORDERS
// ============================================================
{
  const s = slide();
  sectionDivider(s, "SECTION 5\nSpeech Disorders", "Dysarthria · Dysphonia · Apraxia of Speech", ORANGE);
}

// ============================================================
// SLIDE 25 — DYSARTHRIA TYPES TABLE
// ============================================================
{
  const s = slide();
  header(s, "Dysarthria — Classification & Localization", "Motor speech disorder: language content INTACT, motor output impaired", ORANGE);
  footer(s, "Bradley & Daroff's Neurology in Clinical Practice  |  Harrison's 22E");
  const head = ["Type", "Lesion Site", "Speech Quality", "Clinical Cause", "Associated Signs"];
  const rows = [
    ["FLACCID",     "LMN / Brainstem / cranial nerves",  "Nasal, breathy, hypophonic, weak",        "Bulbar palsy, GBS, MG, ALS (LMN)",  "Fasciculations, wasting, nasal regurg"],
    ["SPASTIC",     "Bilateral UMN / corticobulbar",     "Strained, strangled, slow, harsh",         "Pseudobulbar palsy, bilateral strokes","Brisk jaw jerk, emotional lability"],
    ["ATAXIC",      "Cerebellum",                        "Scanning, irregular rhythm, explosive",    "MS, cerebellar ataxia, alcohol",      "Ataxia, nystagmus, intention tremor"],
    ["HYPOKINETIC", "Basal ganglia (Substantia nigra)",  "Rapid (festinant), monotone, hypophonic",  "Parkinson's disease",                 "Rigidity, tremor, mask facies"],
    ["HYPERKINETIC","Basal ganglia / extrapyramidal",    "Variable rate/volume, involuntary outbursts","Huntington's, dystonia, Sydenham's", "Chorea, dystonia, tics"],
    ["MIXED",       "Multiple levels (UMN + LMN)",       "Combined features (nasal + strained)",     "ALS / Motor Neuron Disease",          "Both UMN and LMN signs together"],
  ];
  const colW2 = [1.3, 2.1, 2.1, 1.95, 2.3];
  const colX2 = [0.2, 1.5, 3.6, 5.7, 7.65];
  head.forEach((h, ci) => {
    box(s, colX2[ci], 1.08, colW2[ci], 0.42, ORANGE, ORANGE, h, WHITE, 9.5, true);
  });
  rows.forEach((row, ri) => {
    const ry = 1.5 + ri * 0.62;
    const fill = ri % 2 === 0 ? WHITE : LGRAY;
    row.forEach((cell, ci) => {
      s.addShape(pres.ShapeType.rect, { x:colX2[ci], y:ry, w:colW2[ci], h:0.59, fill:{color:fill}, line:{color:MGRAY, pt:0.5} });
      s.addText(cell, { x:colX2[ci]+0.04, y:ry+0.04, w:colW2[ci]-0.08, h:0.51, fontSize:ci===0?10:9, bold:ci===0, color:ci===0?RED:DARK, fontFace:"Calibri", valign:"middle" });
    });
  });
}

// ============================================================
// SLIDE 26 — SECTION: LITERACY DISORDERS
// ============================================================
{
  const s = slide();
  sectionDivider(s, "SECTION 6\nLiteracy Disorders", "Alexia & Agraphia — Dejerine's Syndromes (1891 & 1892)", PURPLE);
}

// ============================================================
// SLIDE 27 — DEJERINE SYNDROMES (ALEXIA) + PCA IMAGE
// ============================================================
{
  const s = slide();
  header(s, "Alexia — Dejerine's Literacy Syndromes", "Pure Alexia without Agraphia (1892) vs Alexia with Agraphia (1891)", PURPLE);
  footer(s, "Dejerine J (1891, 1892)  |  Bradley & Daroff's Neurology in Clinical Practice");
  if (img("pca_mri_flair")) {
    s.addImage({ data: img("pca_mri_flair"), x:7.0, y:1.05, w:2.8, h:2.5, sizing:{type:"contain",w:2.8,h:2.5} });
    s.addText("Left PCA territory infarction: thalamus + medial occipital cortex — pure alexia without agraphia", { x:7.0, y:3.55, w:2.8, h:0.5, fontSize:8, color:GRAY, fontFace:"Calibri", italic:true, align:"center" });
  }
  const dej = [
    {
      title:"PURE ALEXIA WITHOUT AGRAPHIA", year:"Dejerine 1892", color:RED,
      items:[
        "CAN write normally — CANNOT read own writing",
        "'Linguistic blindfolding' — letters look like random symbols",
        "Oral language (speech + comprehension) INTACT",
        "Letter-by-letter reading in recovery phase",
        "RIGHT HOMONYMOUS HEMIANOPIA — virtually always present",
        "COLOUR ANOMIA — cannot name colours",
        "LESION: Left medial occipital + splenium of corpus callosum",
        "VASCULAR: Left posterior cerebral artery (PCA) territory",
        "MECHANISM: Geschwind disconnection — right visual cortex\n  cannot transfer info to left hemisphere language areas",
      ]
    },
    {
      title:"ALEXIA WITH AGRAPHIA", year:"Dejerine 1891", color:PURPLE,
      items:[
        "CANNOT read AND cannot write — 'acquired illiteracy'",
        "Oral language relatively preserved",
        "Often mild fluent paraphasic speech",
        "No hemiparesis typically",
        "GERSTMANN SYNDROME common:",
        "  • Finger agnosia  • Acalculia",
        "  • Left-right disorientation  • Agraphia",
        "LESION: Angular gyrus (BA 39), left inferior parietal lobule",
        "VASCULAR: Left MCA inferior parietal branches",
      ]
    }
  ];
  dej.forEach((d, i) => {
    const x = i === 0 ? 0.3 : 3.7;
    box(s, x, 1.05, 3.2, 0.42, d.color, d.color, `${d.title}\n${d.year}`, WHITE, 9.5, true);
    bullet(s, d.items, x+0.1, 1.5, 3.05, 3.85, DARK, 9.5);
  });
}

// ============================================================
// SLIDE 28 — CLINICAL APPROACH FLOWCHART
// ============================================================
{
  const s = slide();
  header(s, "Clinical Approach to Language & Speech Disorder", "Bedside algorithm — Flowchart");
  footer(s);

  function fBox(x, y, w, h, text, fill, border, tc, fs) {
    s.addShape(pres.ShapeType.rect, { x, y, w, h, fill:{color:fill||LGRAY}, line:{color:border||MGRAY, pt:1} });
    s.addText(text, { x:x+0.05, y:y+0.04, w:w-0.1, h:h-0.08, fontSize:fs||10, bold:true, color:tc||BLACK, fontFace:"Calibri", align:"center", valign:"middle" });
  }
  function arrow(x, y1, y2) {
    s.addShape(pres.ShapeType.line, { x, y:y1, w:0, h:y2-y1, line:{color:RED, pt:1.5} });
    s.addText("▼", { x:x-0.1, y:y2-0.15, w:0.22, h:0.18, fontSize:8, color:RED, fontFace:"Calibri" });
  }
  function hArrow(x1, y, x2) {
    s.addShape(pres.ShapeType.line, { x:x1, y, w:x2-x1, h:0, line:{color:RED, pt:1.2} });
    s.addText(x2>x1?"►":"◄", { x:x2>x1?x2-0.15:x2, y:y-0.1, w:0.18, h:0.18, fontSize:8, color:RED, fontFace:"Calibri" });
  }

  fBox(3.4, 1.0, 3.2, 0.42, "Communication Difficulty", LGRAY, RED, RED, 11);
  arrow(5.0, 1.42, 1.78);
  fBox(3.4, 1.78, 3.2, 0.42, "Language content abnormal?", LGRAY, RED, DARK, 10);
  s.addText("NO →", { x:6.65, y:1.88, w:0.6, h:0.22, fontSize:9, bold:true, color:RED, fontFace:"Calibri" });
  hArrow(6.65, 1.99, 7.5);
  fBox(7.5, 1.78, 2.3, 0.42, "SPEECH DISORDER\n(Dysarthria / Dysphonia)", MORAN, ORANGE, ORANGE, 9);
  s.addText("YES", { x:5.05, y:2.24, w:0.5, h:0.18, fontSize:9, bold:true, color:GREEN, fontFace:"Calibri" });
  arrow(5.0, 2.2, 2.55);
  fBox(3.4, 2.55, 3.2, 0.42, "Is speech FLUENT?", LGRAY, RED, DARK, 10);
  // Non-fluent left
  s.addText("NON-FLUENT", { x:1.0, y:2.65, w:1.4, h:0.22, fontSize:8.5, bold:true, color:RED, fontFace:"Calibri" });
  hArrow(3.4, 2.76, 2.2);
  s.addShape(pres.ShapeType.line, { x:2.2, y:2.76, w:0, h:0.37, line:{color:RED, pt:1.2} });
  fBox(0.3, 3.13, 3.8, 0.42, "Repetition intact?", LGRAY, ORANGE, DARK, 10);
  fBox(0.3, 3.68, 1.8, 0.38, "YES → TCM", MORAN, ORANGE, ORANGE, 9);
  fBox(2.2, 3.68, 1.9, 0.38, "NO → BROCA / GLOBAL", MRED, RED, RED, 9);
  // Fluent right
  s.addText("FLUENT", { x:6.7, y:2.65, w:0.8, h:0.22, fontSize:8.5, bold:true, color:GREEN, fontFace:"Calibri" });
  hArrow(6.6, 2.76, 7.5);
  s.addShape(pres.ShapeType.line, { x:7.5, y:2.76, w:0, h:0.37, line:{color:RED, pt:1.2} });
  fBox(5.9, 3.13, 3.8, 0.42, "Comprehension intact?", LGRAY, PURPLE, DARK, 10);
  fBox(5.9, 3.68, 1.8, 0.38, "YES: check repetition", LGRAY, GREEN, GREEN, 9);
  fBox(7.8, 3.68, 1.9, 0.38, "NO → WERNICKE / TCS", MPURP, PURPLE, PURPLE, 9);
  // Bottom legend
  fBox(0.3, 4.2, 2.1, 0.38, "Fluent + Intact + ↓↓↓ Rep\n= CONDUCTION", MRED, RED, RED, 8.5);
  fBox(2.55, 4.2, 2.1, 0.38, "Fluent + Intact + Intact Rep\n= ANOMIC", MGREEN, GREEN, GREEN, 8.5);
  fBox(4.8, 4.2, 2.1, 0.38, "Non-fluent + Intact + Intact\n= TRANSCORTICAL MOTOR", MORAN, ORANGE, ORANGE, 8.5);
  fBox(7.05, 4.2, 2.65, 0.38, "All 3 impaired + Non-fluent\n= GLOBAL APHASIA", MRED, DRED, DRED, 8.5);
}

// ============================================================
// SLIDE 29 — REHABILITATION & MANAGEMENT
// ============================================================
{
  const s = slide();
  header(s, "Rehabilitation & Management of Aphasia", "Acute, sub-acute and chronic phase management");
  footer(s, "Harrison's Principles of Internal Medicine 22E (2025)  |  Bradley & Daroff's Neurology");
  const phases = [
    {
      phase:"ACUTE PHASE", color:RED,
      items:[
        "Treat underlying cause: stroke thrombolysis/thrombectomy, tumour, abscess",
        "CT/MRI brain: define lesion, establish aetiology",
        "Multidisciplinary team: neurology + speech & language therapy (SLT)",
        "Communication aids: writing board, picture cards, AAC devices",
        "Nil by mouth assessment if dysphagia present (SALT assessment)",
      ]
    },
    {
      phase:"SPECIFIC THERAPY", color:ORANGE,
      items:[
        "Speech & Language Therapy (SLT): cornerstone of aphasia rehabilitation",
        "Melodic Intonation Therapy (MIT): for Broca's aphasia — uses melody/rhythm",
        "Constraint-Induced Language Therapy (CILT): intensive practice",
        "Semantic Feature Analysis (SFA): for anomic aphasia",
        "Technology: tablet-based apps, AAC devices for severe global aphasia",
      ]
    },
    {
      phase:"ADJUNCT TREATMENTS", color:PURPLE,
      items:[
        "Transcranial Direct Current Stimulation (tDCS): emerging evidence",
        "Repetitive TMS (rTMS): inhibit right hemisphere suppressing left recovery",
        "Pharmacotherapy: memantine, donepezil (limited evidence)",
        "Psychological support: depression is common in Broca's aphasia",
        "Family/carer training: communication strategies at home",
      ]
    }
  ];
  phases.forEach((p, i) => {
    const y = 1.06 + i * 1.42;
    box(s, 0.3, y, 2.0, 1.28, p.color, p.color, p.phase, WHITE, 11, true);
    bullet(s, p.items, 2.4, y+0.04, 7.4, 1.2, DARK, 10.5);
    s.addShape(pres.ShapeType.rect, { x:0.3, y:y+1.28, w:9.4, h:0.04, fill:{color:MGRAY}, line:{color:MGRAY} });
  });
}

// ============================================================
// SLIDE 30 — REFERENCES
// ============================================================
{
  const s = slide();
  s.addShape(pres.ShapeType.rect, { x:0, y:0, w:10, h:0.75, fill:{color:RED}, line:{color:RED} });
  s.addText("REFERENCES", { x:0.3, y:0.06, w:9.4, h:0.63, fontSize:24, bold:true, color:WHITE, fontFace:"Calibri", valign:"middle" });
  s.addShape(pres.ShapeType.rect, { x:0, y:0.75, w:10, h:0.05, fill:{color:AMBER}, line:{color:AMBER} });
  const refs = [
    "1.  Longo DL, Fauci AS, et al. Harrison's Principles of Internal Medicine, 22nd Edition (2025). Chapter on Language Disorders. McGraw Hill Medical.",
    "2.  Bradley WG, Daroff RB, et al. Bradley and Daroff's Neurology in Clinical Practice, 8th Edition (2022). Chapter 13: Aphasia and Related Disorders. Elsevier.",
    "3.  Broca P. Remarques sur le siège de la faculté du langage articulé. Bulletin de la Société Anatomique de Paris. 1861;6:330–357.",
    "4.  Wernicke C. Der Aphasische Symptomencomplex: Eine Psychologische Studie auf Anatomischer Basis. Breslau: Cohn & Weigert; 1874.",
    "5.  Dejerine J. Sur un cas de cécité verbale avec agraphie, suivi d'autopsie. Comptes Rendus de la Société de Biologie. 1891.",
    "6.  Dejerine J. Contribution à l'étude anatomoclinique et clinique des différentes variétés de cécité verbale. Comptes Rendus de la Société de Biologie. 1892.",
    "7.  Geschwind N. Disconnexion syndromes in animals and man. Brain. 1965;88:237–294.",
    "8.  Lichtheim L. On aphasia. Brain. 1885;7:433–484.",
    "9.  Kreisler A, et al. The anatomy of aphasia revisited. Neurology. 2000;54:1117–1123.",
    "10. Radiological images: PMC Clinical VQA dataset (Hugging Face). MedPix-VQA database. Used for educational purposes.",
  ];
  refs.forEach((r, i) => {
    const isBold = i < 2;
    s.addText(r, { x:0.3, y:0.9+i*0.46, w:9.4, h:0.43, fontSize:10.5, bold:isBold, color:i<2?BLACK:GRAY, fontFace:"Calibri", valign:"middle" });
  });
}

// ── Write ─────────────────────────────────────────────────────────────────
console.log("Writing file...");
pres.writeFile({ fileName: "/tmp/Lang_Speech_30Slides.pptx" })
  .then(() => {
    execSync("cp /tmp/Lang_Speech_30Slides.pptx /home/daytona/workspace/speech-language-ppt/Lang_Speech_30Slides.pptx");
    console.log("DONE — /home/daytona/workspace/speech-language-ppt/Lang_Speech_30Slides.pptx");
  }).catch(e => console.error("PPT error:", e));

Running Command

cd /home/daytona/workspace/speech-language-ppt && node build_30slides.js 2>&1

Running Command

ls -lh /home/daytona/workspace/speech-language-ppt/Lang_Speech_30Slides.pptx

Your 30-slide presentation is ready — 1.5 MB with embedded radiological images.

📥
Lang Speech 30Slides
Presentation · PPTX

Complete slide breakdown (30 slides, white background, red/orange/purple accent palette):

#	Slide	Content
1	Title Slide	Full title, references, brain lobes image
2	Contents	All 9 sections with colour labels
3	Section divider	Neuroanatomy
4	Cerebral Lobes & Language Areas	Brain lobe diagram with functional roles
5	Broca's & Wernicke's Areas	Classical language map diagram with arcuate fasciculus
6	fMRI Language Network	resting-state fMRI showing L hemisphere lateralisation
7	Brodmann Areas — MUC Model	BA 44/45, 22, 39, 40, 6, 17–19 with functions
8	Section divider	White Matter Tracts
9	Arcuate Fasciculus — DTI	DTI tractography image + key facts
10	All Language Tracts	AF, SLF, IFOF, ILF, Uncinate — DTI atlas
11	Section divider	Classification
12	Language vs Speech Classification	Side-by-side table
13	Definition of Aphasia	4 domains + bedside tests
14	Section divider	Aphasia Syndromes
15	Broca's Aphasia	Clinical features + T2 MRI sagittal
16	Broca's — CT & FLAIR	CT chronic infarct + MRI FLAIR/DWI
17	Wernicke's Aphasia	Clinical features + CT haemorrhage
18	Wernicke's — Lesion Overlap MRI	12-patient MRI overlap map
19	Global Aphasia	Clinical features + MRI DWI/FLAIR
20	Conduction Aphasia	Features + DTI arcuate fasciculus
21	Transcortical Aphasias (TCM + TCS)	Side-by-side comparison
22	Anomic & Subcortical Aphasia	Side-by-side comparison
23	Master Comparison Table	All 8 syndromes × 6 features
24	Section divider	Speech Disorders
25	Dysarthria — 6 types table	Flaccid/Spastic/Ataxic/Hypokinetic/Hyperkinetic/Mixed
26	Section divider	Literacy Disorders
27	Dejerine Syndromes — Alexia	Pure Alexia vs Alexia+Agraphia + left PCA MRI
28	Clinical Flowchart	Step-by-step diagnostic algorithm
29	Rehabilitation & Management	Acute, SLT, tDCS/TMS, pharmacotherapy
30	References	Harrison's 22E, Bradley & Daroff, Broca, Wernicke, Dejerine, Geschwind

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