mkdir -p /tmp/workspace/neuro-exam && ls /tmp/workspace/

cat << 'PYEOF' > /tmp/workspace/neuro-exam/generate_pdf.py from reportlab.lib.pagesizes import A4 from reportlab.lib.styles import getSampleStyleSheet, ParagraphStyle from reportlab.lib.units import cm from reportlab.lib import colors from reportlab.platypus import (SimpleDocTemplate, Paragraph, Spacer, Table, TableStyle, PageBreak, HRFlowable) from reportlab.lib.enums import TA_LEFT, TA_CENTER, TA_JUSTIFY # ── Data ──────────────────────────────────────────────────────────────────── questions = [ # ═══════════════════════════════════════════════════════════════════════════ # SECTION 1 – MUST KNOW (Q1-15) # ═══════════════════════════════════════════════════════════════════════════ { "section": "SECTION 1: MUST KNOW", "q": 1, "case": "Neurocysticercosis (CT)", "stem": "A 28-year-old male presents with new-onset seizures. CT brain shows multiple small hyperdense nodular lesions with surrounding oedema and a 'hole-with-dot' appearance. What is the MOST likely diagnosis?", "opts": ["A. Brain metastases", "B. Neurocysticercosis", "C. Cerebral toxoplasmosis", "D. Tuberculoma"], "ans": "B", "exp": "The 'hole-with-dot' (scolex) sign on CT — a small hyperdense dot (scolex) within a hypodense cyst — is pathognomonic of neurocysticercosis (NCC), caused by Taenia solium larval cysts. It is the most common cause of adult-onset epilepsy in endemic regions." }, { "section": None, "q": 2, "case": "Neurocysticercosis (CT)", "stem": "On CT, the calcified stage of neurocysticercosis appears as:", "opts": ["A. Ring-enhancing lesion with oedema", "B. Small hypodense cyst with central dot", "C. Small punctate hyperdense calcification without oedema", "D. Heterogeneous mass with mass effect"], "ans": "C", "exp": "In the calcified/nodular-calcified stage, the larvae are dead and the cysts calcify. CT shows small, dense calcifications with NO surrounding oedema and no enhancement — the 'burnt-out' lesion. This stage is non-active and often an incidental finding." }, { "section": None, "q": 3, "case": "Glioma (CT)", "stem": "CT of a 45-year-old shows an ill-defined, infiltrating hypodense mass in the right frontal lobe crossing the corpus callosum to the left hemisphere. Which glioma type classically shows this 'butterfly' pattern?", "opts": ["A. Pilocytic astrocytoma", "B. Glioblastoma multiforme (GBM)", "C. Oligodendroglioma", "D. Ependymoma"], "ans": "B", "exp": "GBM (WHO grade IV) is the most common primary malignant brain tumour in adults. Its hallmark is the 'butterfly glioma' — crossing midline via the corpus callosum. CT shows irregular hypodense mass with central necrosis, ring enhancement, and surrounding oedema." }, { "section": None, "q": 4, "case": "Cerebral Atrophy (CT)", "stem": "CT brain of a 70-year-old with progressive memory decline shows widened sulci, enlarged ventricles, and reduced cortical volume. The MOST likely radiological diagnosis is:", "opts": ["A. Normal pressure hydrocephalus", "B. Cerebral atrophy", "C. Communicating hydrocephalus", "D. Subdural hygroma"], "ans": "B", "exp": "Cerebral atrophy on CT is characterised by cortical volume loss (widened sulci/Sylvian fissures), enlarged ventricles (ex vacuo dilatation), and widened interhemispheric fissure. It reflects neuronal loss and is seen in dementia, ageing, and chronic neurological disease." }, { "section": None, "q": 5, "case": "NAD (CT)", "stem": "A psychiatry resident reports a CT brain as 'NAD'. In neuroimaging reporting, NAD stands for:", "opts": ["A. No Acute Disease", "B. No Abnormality Detected", "C. Normal Anatomical Definition", "D. No Active Degeneration"], "ans": "B", "exp": "NAD = 'No Abnormality Detected'. It means the CT is within normal limits with no structural lesions, no oedema, no midline shift, normal grey-white differentiation, and no hemorrhage. It is NOT the same as ruling out all pathology (e.g. early ischaemia or epilepsy may not show on CT)." }, { "section": None, "q": 6, "case": "Infarct/Gliosis with Atrophy (MRI)", "stem": "On MRI, an old cerebral infarct appears as:", "opts": ["A. Hypointense on T1, hyperintense on T2/FLAIR with volume loss", "B. Hyperintense on T1, hypointense on T2", "C. Diffusion restriction on DWI", "D. Ring-enhancing on T1 post-contrast"], "ans": "A", "exp": "An old (chronic) infarct undergoes cystic encephalomalacia and gliosis. MRI shows: T1 hypointense (CSF-like cavity), T2/FLAIR hyperintense (gliosis rim), volume loss (ipsilateral sulcal widening, ex vacuo dilatation). No diffusion restriction (DWI restriction is seen only in ACUTE infarct, <24-72 hrs)." }, { "section": None, "q": 7, "case": "Old infarct in right temporo-parieto-occipital region and left caudate region (CT)", "stem": "A CT shows a hypodense area in the right temporo-parieto-occipital region conforming to a vascular territory. This pattern is most consistent with occlusion of which vessel?", "opts": ["A. Anterior cerebral artery (ACA)", "B. Middle cerebral artery (MCA) + posterior cerebral artery (PCA) territory", "C. Posterior cerebral artery (PCA) and MCA territory", "D. Basilar artery"], "ans": "C", "exp": "The temporo-parieto-occipital region is supplied by the MCA (temporal and parietal) and PCA (occipital). A large hypodense area here suggests MCA+PCA territory infarction or a large MCA territory infarct extending posteriorly. The left caudate is supplied by the lenticulostriate arteries (from MCA), so caudate infarct = small vessel/lenticulostriate territory." }, { "section": None, "q": 8, "case": "Normal (MRI)", "stem": "On a normal MRI brain, grey matter appears compared to white matter on T1-weighted images as:", "opts": ["A. Isointense", "B. Hyperintense (brighter)", "C. Hypointense (darker)", "D. Signal void"], "ans": "C", "exp": "On T1-WI: White matter = hyperintense (bright) due to myelin lipid content. Grey matter = hypointense (darker than white matter). CSF = very hypointense (dark). On T2-WI the reverse applies — grey matter is brighter than white matter, and CSF is brightest." }, { "section": None, "q": 9, "case": "Low-grade Glioma / Ganglioglioma (MRI)", "stem": "MRI shows a cortically-based, well-circumscribed lesion in the temporal lobe of a 20-year-old with longstanding partial seizures. It is T2 hyperintense, T1 hypointense, with a cystic component and a mural nodule. The MOST likely diagnosis is:", "opts": ["A. GBM", "B. DNET", "C. Ganglioglioma", "D. Meningioma"], "ans": "C", "exp": "Ganglioglioma is the most common brain tumour causing chronic temporal lobe epilepsy in young patients. Classic MRI: cortical/temporal location, well-defined, cyst with enhancing mural nodule, T2 hyperintense, may calcify. It is a WHO grade I-II tumour with excellent prognosis post-resection." }, { "section": None, "q": 10, "case": "Cerebral Atrophy (CT)", "stem": "The MOST common cause of cerebral atrophy seen on neuroimaging in a psychiatric patient would be:", "opts": ["A. Normal ageing", "B. Chronic alcohol use disorder", "C. Schizophrenia", "D. Major depressive disorder"], "ans": "B", "exp": "Chronic alcohol use disorder is the most common REVERSIBLE cause of cerebral atrophy in psychiatric patients, causing prominent cortical atrophy and cerebellar vermis atrophy. Normal ageing also causes atrophy, but in the psychiatric context, alcohol is the most common identifiable cause. Schizophrenia shows subtle atrophy, but not as pronounced." }, { "section": None, "q": 11, "case": "Neurocysticercosis (CT)", "stem": "The FIRST-LINE antiepileptic drug used in neurocysticercosis-associated seizures is:", "opts": ["A. Carbamazepine", "B. Phenytoin", "C. Sodium valproate", "D. Levetiracetam"], "ans": "A,C", "exp": "Both carbamazepine and sodium valproate are acceptable first-line AEDs for seizures due to NCC (focal and generalised, respectively). Carbamazepine is preferred for focal/partial seizures. Antiparasitic therapy (albendazole ± praziquantel) is combined with corticosteroids (dexamethasone) to reduce oedema. NOTE: If options force single answer, carbamazepine is most commonly stated for NCC focal seizures." }, { "section": None, "q": 12, "case": "Glioma (CT)", "stem": "Which CT feature BEST differentiates high-grade glioma from low-grade glioma?", "opts": ["A. Presence of calcification", "B. Ring enhancement with central necrosis", "C. Temporal lobe location", "D. Hypodensity on CT"], "ans": "B", "exp": "Ring enhancement with central necrosis and significant peritumoral oedema on CT/MRI is the hallmark of HIGH-grade glioma (GBM, WHO grade IV). Low-grade gliomas (WHO grade II) are typically non-enhancing, homogeneous, hypodense on CT, without necrosis. Calcification is more common in oligodendroglioma (low grade)." }, { "section": None, "q": 13, "case": "Infarct/Gliosis with Atrophy (MRI)", "stem": "Gliosis on MRI FLAIR sequence appears as:", "opts": ["A. Hypointense", "B. Hyperintense", "C. Isointense with brain parenchyma", "D. Signal void"], "ans": "B", "exp": "Gliosis (reactive astrocyte proliferation post-injury) appears HYPERINTENSE on T2 and FLAIR sequences due to increased water content and disrupted myelin. FLAIR suppresses free CSF (so CSF appears dark) but does NOT suppress gliotic tissue — making periventricular and subcortical gliosis distinctly bright on FLAIR." }, { "section": None, "q": 14, "case": "Old infarct – left caudate (CT)", "stem": "A psychiatric patient with a history of stroke has an old infarct in the left caudate nucleus. The MOST characteristic neuropsychiatric sequela of caudate infarction is:", "opts": ["A. Wernicke aphasia", "B. Depression and apathy / subcortical dementia", "C. Visual hallucinations", "D. Alien hand syndrome"], "ans": "B", "exp": "The caudate nucleus is part of the striato-thalamo-cortical circuit. Left caudate infarcts are associated with depression, apathy, abulia, and subcortical cognitive dysfunction (subcortical dementia). Larger left caudate lesions may also cause transcortical motor aphasia or psychosis. Wernicke aphasia = posterior temporal (not caudate)." }, { "section": None, "q": 15, "case": "Normal MRI", "stem": "A patient referred for first episode psychosis has a normal MRI brain report. The CORRECT interpretation for a clinician is:", "opts": ["A. Definitively rules out all organic causes of psychosis", "B. No structural lesion to explain the presentation, but functional/metabolic causes not excluded", "C. The psychosis is entirely functional", "D. No further investigations needed"], "ans": "B", "exp": "A normal structural MRI rules out space-occupying lesions, infarcts, demyelination, and gross atrophy, but does NOT exclude metabolic encephalopathies, autoimmune encephalitis (anti-NMDA receptor, etc.), EEG abnormalities, or early neurodegenerative disease. Further workup (CSF, EEG, autoimmune antibodies, metabolic panel) may still be needed." }, # ═══════════════════════════════════════════════════════════════════════════ # SECTION 2 – GOOD FOR PASSING (Q16-30) # ═══════════════════════════════════════════════════════════════════════════ { "section": "SECTION 2: GOOD FOR PASSING", "q": 16, "case": "Neurocysticercosis (CT)", "stem": "The lifecycle stage of Taenia solium responsible for neurocysticercosis in humans is:", "opts": ["A. Adult tapeworm", "B. Egg ingested → oncosphere → cysticercus (larval stage)", "C. Free-swimming cercaria", "D. Proglottid"], "ans": "B", "exp": "Humans become intermediate hosts when they ingest T. solium eggs (from contaminated food/water or auto-infection in intestinal taeniasis). Oncospheres hatch, penetrate gut wall, enter bloodstream, and lodge in CNS forming cysticerci. The adult tapeworm in gut (from undercooked pork) does NOT cause NCC." }, { "section": None, "q": 17, "case": "Neurocysticercosis (CT)", "stem": "Racemose neurocysticercosis differs from parenchymal NCC in that it:", "opts": ["A. Shows the scolex dot sign on CT", "B. Is located in the subarachnoid space/cisterns and lacks a scolex", "C. Calcifies rapidly", "D. Responds better to antiparasitic therapy"], "ans": "B", "exp": "Racemose NCC is a rare, severe form where cysts grow in the basal cisterns/subarachnoid space in grape-like clusters. There is NO scolex (it degenerates). CT/MRI shows lobulated CSF-intensity masses in cisterns. It causes obstructive hydrocephalus, is harder to treat, and has a worse prognosis than parenchymal NCC." }, { "section": None, "q": 18, "case": "Glioma (CT)", "stem": "WHO 2021 classification of CNS tumours now incorporates which molecular marker as ESSENTIAL for grading gliomas?", "opts": ["A. EGFR amplification", "B. IDH mutation status (IDH1/IDH2)", "C. MGMT methylation", "D. 1p/19q co-deletion alone"], "ans": "B", "exp": "The WHO 2021 CNS classification made IDH mutation status integral to glioma diagnosis. IDH-mutant gliomas (grades 2-4) have better prognosis than IDH-wildtype. IDH-wildtype diffuse astrocytoma is essentially GBM behaviour. MGMT methylation predicts response to temozolomide. 1p/19q co-deletion + IDH mutation = oligodendroglioma." }, { "section": None, "q": 19, "case": "Cerebral Atrophy (CT)", "stem": "Cerebral atrophy predominantly affecting the FRONTAL lobes with personality change and disinhibition in a 58-year-old is MOST consistent with:", "opts": ["A. Alzheimer's disease", "B. Frontotemporal dementia (FTD)", "C. Lewy body dementia", "D. Vascular dementia"], "ans": "B", "exp": "Frontotemporal dementia (Pick's disease spectrum) shows frontal and anterior temporal lobe atrophy — the 'knife-blade atrophy' of gyri on CT/MRI. It presents with personality change, disinhibition, and executive dysfunction before memory problems (unlike Alzheimer's, which shows hippocampal/parietal atrophy and early memory loss)." }, { "section": None, "q": 20, "case": "Cerebral Atrophy (CT)", "stem": "In normal pressure hydrocephalus (NPH), which CT finding DISTINGUISHES it from cerebral atrophy?", "opts": ["A. Enlarged ventricles", "B. Dilated ventricles DISPROPORTIONATE to sulcal widening (tight sulci)", "C. Widened sulci", "D. Periventricular hypodensity"], "ans": "B", "exp": "In NPH, ventricular enlargement is disproportionately greater than sulcal widening — sulci appear normal or tight (Evans index >0.3). In cerebral atrophy, both ventricles and sulci enlarge proportionately (ex vacuo dilatation). NPH triad = wet (incontinence), wobbly (gait), wacky (cognitive decline). This distinction is clinically critical." }, { "section": None, "q": 21, "case": "Infarct / Gliosis with Atrophy (MRI)", "stem": "Wallerian degeneration following a cortical infarct appears on MRI as:", "opts": ["A. T2 hyperintensity along the ipsilateral corticospinal tract", "B. T1 hyperintensity in the contralateral hemisphere", "C. Diffusion restriction in the brainstem", "D. Enhancement along cranial nerves"], "ans": "A", "exp": "Wallerian degeneration is anterograde axonal degeneration distal to the site of injury. After a hemispheric infarct, the ipsilateral corticospinal tract (internal capsule → cerebral peduncle → brainstem) shows T2/FLAIR hyperintensity due to myelin breakdown and axonal loss — appearing weeks to months after the infarct." }, { "section": None, "q": 22, "case": "Old infarct – right temporo-parieto-occipital (CT)", "stem": "A patient with an old right temporo-parieto-occipital infarct presents with inability to recognise faces. This is termed:", "opts": ["A. Prosopagnosia", "B. Anosognosia", "C. Simultanagnosia", "D. Alexia without agraphia"], "ans": "A", "exp": "Prosopagnosia (face blindness) results from damage to the fusiform face area in the right (or bilateral) temporo-occipital cortex. The right hemisphere is dominant for facial recognition. This is a classic neuropsychiatric consequence of right posterior cortical strokes." }, { "section": None, "q": 23, "case": "Old infarct – right temporo-parieto-occipital (CT)", "stem": "Left-sided hemispatial neglect is a classic manifestation of infarction in which region?", "opts": ["A. Left parietal lobe", "B. Right parietal lobe (inferior parietal lobule)", "C. Left frontal lobe", "D. Right occipital lobe"], "ans": "B", "exp": "Hemispatial neglect (hemineglect) is the failure to attend to stimuli on the side contralateral to the lesion. Right inferior parietal lobule (IPL) damage (typically MCA territory) causes LEFT-sided neglect. Right hemisphere neglect is more common and more severe than left hemisphere neglect due to the right hemisphere's role in bilateral spatial attention." }, { "section": None, "q": 24, "case": "Low-grade Glioma / Ganglioglioma (MRI)", "stem": "Low-grade gliomas (WHO grade II) on MRI most characteristically show:", "opts": ["A. Ring enhancement and necrosis", "B. Homogeneous T2 hyperintensity without enhancement", "C. Heterogeneous signal with haemorrhage", "D. Dural tail sign"], "ans": "B", "exp": "Low-grade gliomas (diffuse astrocytoma, oligodendroglioma — WHO grade II) are classically homogeneously T2/FLAIR hyperintense, T1 hypointense, with minimal or NO contrast enhancement. Absence of enhancement is a hallmark. Enhancement signals dedifferentiation to higher grade. Calcification (especially 'fried egg' oligodendroglioma) may be present." }, { "section": None, "q": 25, "case": "Ganglioglioma (MRI)", "stem": "Ganglioglioma is composed of which two cell types?", "opts": ["A. Oligodendrocytes and neurons", "B. Dysplastic ganglion cells (neurons) and neoplastic glial cells", "C. Ependymal cells and astrocytes", "D. Schwann cells and fibroblasts"], "ans": "B", "exp": "Ganglioglioma is a mixed glioneuronal tumour composed of dysplastic/neoplastic ganglion cells (neurons) and neoplastic glial cells (usually astrocytic). It is WHO grade I (low grade). It is the most common tumour in chronic temporal lobe epilepsy and has an excellent prognosis after surgical resection." }, { "section": None, "q": 26, "case": "Normal MRI", "stem": "Which MRI sequence is MOST sensitive for detecting cortical dysplasia and epileptogenic lesions?", "opts": ["A. T1 MPRAGE", "B. FLAIR (Fluid Attenuated Inversion Recovery)", "C. T2 TSE", "D. SWI (Susceptibility Weighted Imaging)"], "ans": "B", "exp": "FLAIR is the most sensitive routine sequence for epileptogenic lesions including focal cortical dysplasia, gliosis, DNET, and cortical tubers (TSC). By suppressing CSF signal, FLAIR makes subtle cortical signal abnormalities conspicuous. High-resolution FLAIR and post-processing (voxel-based morphometry) further improve detection of subtle dysplasia." }, { "section": None, "q": 27, "case": "Cerebral Atrophy (CT)", "stem": "In Alzheimer's disease, the EARLIEST and MOST characteristic site of atrophy on MRI is:", "opts": ["A. Frontal lobe", "B. Medial temporal lobe / hippocampus", "C. Occipital lobe", "D. Cerebellum"], "ans": "B", "exp": "Alzheimer's disease shows earliest and most prominent atrophy of the medial temporal lobe — entorhinal cortex, hippocampus, and parahippocampal gyrus. This is quantified by the Medial Temporal Atrophy (MTA) scale (Scheltens scale) on coronal MRI. Later, parietal and posterior cingulate atrophy develops. Frontal is FTD." }, { "section": None, "q": 28, "case": "Infarct/Gliosis (MRI)", "stem": "The BEST MRI sequence to detect an ACUTE infarct within the first 6 hours is:", "opts": ["A. T2-weighted imaging", "B. FLAIR", "C. Diffusion-weighted imaging (DWI)", "D. T1 post-contrast"], "ans": "C", "exp": "DWI detects cytotoxic oedema (restricted diffusion) within minutes to hours of ischaemic stroke — far earlier than T2 or FLAIR (which become positive at 6-12 hrs). DWI shows the infarcted area as BRIGHT (restricted), confirmed by ADC map showing corresponding DARK (low ADC). DWI is the gold standard for hyperacute stroke imaging." }, { "section": None, "q": 29, "case": "NAD (CT)", "stem": "A CT brain reported as NAD does NOT exclude which of the following conditions?", "opts": ["A. Large meningioma", "B. Cerebral oedema from tumour", "C. Autoimmune encephalitis (e.g. anti-NMDAR encephalitis)", "D. Subdural haematoma (acute)"], "ans": "C", "exp": "Autoimmune encephalitis (anti-NMDAR, anti-LGI1, etc.) classically presents with psychiatric symptoms, seizures, and cognitive decline — but CT brain is NORMAL in the majority of cases. MRI may show subtle FLAIR changes in hippocampus/medial temporal. CSF analysis and specific antibody panels are required for diagnosis. CT cannot detect autoimmune inflammation." }, { "section": None, "q": 30, "case": "Old infarct – left caudate (CT)", "stem": "Post-stroke depression occurs in approximately what percentage of stroke survivors and is MOST associated with lesions in which region?", "opts": ["A. 5-10%, parietal lobe", "B. 30-40%, left anterior (frontal/caudate) lesions", "C. 60-70%, brainstem", "D. 10-15%, occipital lobe"], "ans": "B", "exp": "Post-stroke depression (PSD) affects ~30-40% of stroke survivors. Left hemisphere lesions — particularly left frontal and left caudate/basal ganglia — have the strongest association with PSD (Robinson's hypothesis). The proximity of the lesion to the frontal pole and disruption of monoaminergic pathways (dopamine/serotonin) is the proposed mechanism." }, # ═══════════════════════════════════════════════════════════════════════════ # SECTION 3 – GOOD ENOUGH (Q31-45) # ═══════════════════════════════════════════════════════════════════════════ { "section": "SECTION 3: GOOD ENOUGH", "q": 31, "case": "Neurocysticercosis (CT)", "stem": "The recommended antiparasitic regimen for active parenchymal NCC with 1-2 viable cysts is:", "opts": ["A. Albendazole alone", "B. Praziquantel alone", "C. Albendazole + praziquantel combined", "D. No antiparasitic; AEDs only"], "ans": "C", "exp": "Current evidence (NEJM 2014; Garcia et al.) shows that combined albendazole (15 mg/kg/day) + praziquantel (50 mg/kg/day) for 10 days is MORE effective than either drug alone in resolving viable parenchymal cysts and reducing seizure recurrence. Both drugs should be given with corticosteroids (dexamethasone) to reduce inflammatory reaction." }, { "section": None, "q": 32, "case": "Glioma (CT)", "stem": "Oligodendroglioma classically shows which CT finding not typically seen in astrocytoma?", "opts": ["A. Homogeneous hypodensity", "B. Calcification (often 'gyriform' or 'ribbon-like')", "C. Ring enhancement", "D. Haemorrhage"], "ans": "B", "exp": "Oligodendroglioma has a high propensity for calcification (70-90% of cases), often in a gyriform, ribbon-like, or 'fried egg' pattern on CT. It is typically located in the frontal lobe cortex and subcortex. On MRI, it may show T2 heterogeneity due to calcification (susceptibility artefact on SWI/GRE). IDH mutation + 1p/19q co-deletion confirms the diagnosis." }, { "section": None, "q": 33, "case": "Cerebral Atrophy (CT)", "stem": "The Evans index is used to quantify ventricular size on CT. It is calculated as:", "opts": ["A. Maximum width of lateral ventricles / maximum inner skull diameter", "B. Bifrontal horn width / inner biparietal diameter", "C. Third ventricle width / skull diameter", "D. Total CSF volume / total brain volume"], "ans": "B", "exp": "Evans index = maximum width of the frontal horns of lateral ventricles / maximum inner biparietal (skull) diameter on axial CT. Values >0.3 indicate ventriculomegaly. It is used to assess ventricular enlargement in NPH, hydrocephalus, and atrophy. Note: Evans index does not distinguish NPH from atrophy; clinical correlation is essential." }, { "section": None, "q": 34, "case": "Cerebral Atrophy (CT)", "stem": "Cerebellar vermis atrophy on CT is classically associated with which psychiatric/neurological condition?", "opts": ["A. Alzheimer's disease", "B. Chronic alcohol use disorder", "C. Schizophrenia", "D. Bipolar disorder"], "ans": "B", "exp": "Chronic alcohol use causes selective cerebellar vermis atrophy (anterior superior vermis) due to direct neurotoxicity and thiamine deficiency. CT shows widening of the superior vermian fissures and reduced vermian volume. This is often accompanied by cortical atrophy and white matter changes. It is the most recognisable CT brain signature of chronic alcoholism." }, { "section": None, "q": 35, "case": "Low-grade Glioma / Ganglioglioma (MRI)", "stem": "DNET (Dysembryoplastic Neuroepithelial Tumour) is radiologically differentiated from ganglioglioma mainly by:", "opts": ["A. T2 hypointensity", "B. 'Bubbly' or multicystic appearance with cortical location and no peritumoral oedema", "C. Presence of a mural nodule", "D. Ring enhancement"], "ans": "B", "exp": "DNET classically shows a 'bubbly'/multicystic 'soap bubble' appearance on T2/FLAIR — multiple small cystic spaces — with a cortical or juxtacortical location, NO peritumoral oedema, and NO or minimal enhancement. Ganglioglioma typically has a single large cyst with a mural nodule that may enhance. Both cause chronic epilepsy in young patients." }, { "section": None, "q": 36, "case": "Infarct/Gliosis with Atrophy (MRI)", "stem": "Secondary atrophy (atrophy remote from the primary lesion) after a large cortical infarct is due to:", "opts": ["A. Oedema resolution", "B. Trans-neuronal/Wallerian degeneration causing loss of connected neurons", "C. CSF pressure changes", "D. Medication effects"], "ans": "B", "exp": "After a large cortical infarct, trans-neuronal degeneration and Wallerian degeneration cause atrophy of connected structures remote from the primary lesion. Classic examples: ipsilateral thalamus, contralateral cerebellar hemisphere (crossed cerebellar diaschisis), and ipsilateral caudate. This represents anterograde and retrograde axonal degeneration." }, { "section": None, "q": 37, "case": "Old infarct – right temporo-parieto-occipital (CT)", "stem": "A patient with right temporo-occipital infarct develops formed visual hallucinations of people and animals. This is MOST likely:", "opts": ["A. Schizophrenia", "B. Charles Bonnet syndrome", "C. Delirium", "D. Dementia with Lewy bodies"], "ans": "B", "exp": "Charles Bonnet syndrome is characterised by complex, formed visual hallucinations in a person with visual impairment (due to eye disease or occipital/visual pathway lesions) WITHOUT psychiatric disorder. The patient has insight that the hallucinations are not real. It is important to distinguish from psychotic disorders — especially in elderly stroke patients with occipital infarcts." }, { "section": None, "q": 38, "case": "Old infarct – left caudate (CT)", "stem": "Hemiballismus (flinging movements of the limbs) is classically associated with lesion of which basal ganglia structure?", "opts": ["A. Caudate nucleus", "B. Subthalamic nucleus (STN)", "C. Globus pallidus interna", "D. Substantia nigra"], "ans": "B", "exp": "Hemiballismus is the classic result of CONTRALATERAL subthalamic nucleus (STN) lesion — most commonly due to small infarct (lacunar) in the STN. The STN normally inhibits the globus pallidus interna. When lost, involuntary, violent flinging movements occur. Caudate lesions cause more subtle chorea or neuropsychiatric symptoms." }, { "section": None, "q": 39, "case": "NAD (CT)", "stem": "A 25-year-old presents with acute psychosis and a CT brain reported as NAD. Which investigation should be PRIORITISED next to exclude organic psychosis?", "opts": ["A. EEG only", "B. MRI brain + CSF for autoimmune encephalitis antibodies + metabolic panel", "C. Repeat CT with contrast", "D. PET scan"], "ans": "B", "exp": "In first-episode psychosis with normal CT, a structured organic workup is mandatory: MRI brain (better sensitivity for encephalitis, lesions), CSF examination (protein, cells, autoimmune antibodies including anti-NMDAR, anti-LGI1, anti-CASPR2), metabolic panel (thyroid, electrolytes, LFTs, glucose, B12), urine drug screen, and EEG. Anti-NMDAR encephalitis is a common missed mimicker of psychosis." }, { "section": None, "q": 40, "case": "Normal MRI", "stem": "Which psychiatric disorder has the most consistently reported structural MRI abnormalities (though subtle)?", "opts": ["A. Generalized anxiety disorder", "B. Schizophrenia", "C. Phobia", "D. Adjustment disorder"], "ans": "B", "exp": "Schizophrenia has the most replicated structural MRI findings: lateral ventricular enlargement, reduced total brain volume (2-3%), reduced grey matter in prefrontal cortex, temporal lobe (superior temporal gyrus), hippocampus, and thalamus. These are GROUP-LEVEL findings and not diagnostic at the individual patient level — hence MRI in a schizophrenia patient may be reported as 'normal'." }, { "section": None, "q": 41, "case": "Glioma (CT)", "stem": "Temozolomide chemotherapy in GBM is MOST effective in patients with:", "opts": ["A. EGFR amplification", "B. MGMT promoter methylation", "C. IDH-wildtype status", "D. 1p/19q co-deletion"], "ans": "B", "exp": "MGMT (O6-methylguanine-DNA methyltransferase) is a DNA repair enzyme. MGMT promoter methylation SILENCES this gene, preventing tumour cells from repairing temozolomide-induced DNA damage. MGMT-methylated GBM patients show significantly better response to temozolomide + radiotherapy (Stupp protocol) and improved survival." }, { "section": None, "q": 42, "case": "Infarct/Gliosis (MRI)", "stem": "The penumbra in acute ischaemic stroke refers to:", "opts": ["A. The infarcted core of dead tissue", "B. The ischaemic but potentially salvageable tissue surrounding the infarct core", "C. The area of haemorrhagic transformation", "D. The contralateral healthy brain"], "ans": "B", "exp": "The ischaemic penumbra is the zone of tissue surrounding the infarct core that is severely hypoperfused but not yet irreversibly damaged — neurons are electrically silent but still metabolically viable. It is the TARGET of thrombolysis and thrombectomy. On perfusion imaging: core = DWI bright (dead), penumbra = perfusion deficit > DWI lesion (mismatch)." }, { "section": None, "q": 43, "case": "Ganglioglioma (MRI)", "stem": "The WHO grade of most gangliogliomas and its clinical significance is:", "opts": ["A. Grade IV; poor prognosis", "B. Grade I; excellent prognosis with surgical resection", "C. Grade III; requires chemoradiation", "D. Grade II; requires surveillance imaging only"], "ans": "B", "exp": "Most gangliogliomas are WHO grade I (benign). Complete surgical resection is often curative, with excellent long-term seizure control and survival. Anaplastic ganglioglioma (WHO grade III) is rare. The low grade and resectability make ganglioglioma the most 'curable' tumour-associated epilepsy syndrome in young adults." }, { "section": None, "q": 44, "case": "Neurocysticercosis (CT)", "stem": "NCC is the MOST common cause of acquired epilepsy in:", "opts": ["A. High-income countries", "B. Latin America, Sub-Saharan Africa, South and Southeast Asia (endemic regions)", "C. East Asia only", "D. Paediatric age group worldwide"], "ans": "B", "exp": "NCC is the leading cause of acquired (symptomatic) epilepsy worldwide, especially in Latin America (Mexico, Peru, Brazil), Sub-Saharan Africa, India, and Southeast Asia — where pig husbandry and poor sanitation allow T. solium transmission. It accounts for up to 30% of epilepsy cases in endemic regions. It is increasingly seen in immigrant populations in non-endemic countries." }, { "section": None, "q": 45, "case": "Cerebral Atrophy (CT)", "stem": "Cortical atrophy disproportionately affecting the posterior regions (posterior cortical atrophy) on MRI is most associated with:", "opts": ["A. Frontotemporal dementia", "B. Atypical Alzheimer's disease / posterior cortical atrophy syndrome", "C. Vascular dementia", "D. Creutzfeldt-Jakob disease"], "ans": "B", "exp": "Posterior cortical atrophy (PCA) is an atypical variant of AD characterised by progressive visual-spatial and visual-perceptual deficits. MRI shows disproportionate parieto-occipital and posterior temporal atrophy with relative frontal and hippocampal sparing. Pathologically, it is usually AD (amyloid plaques and neurofibrillary tangles predominate posteriorly)." }, # ═══════════════════════════════════════════════════════════════════════════ # SECTION 4 – DISTINCTION (Q46-60) # ═══════════════════════════════════════════════════════════════════════════ { "section": "SECTION 4: DISTINCTION", "q": 46, "case": "Neurocysticercosis (CT)", "stem": "Del Brutto diagnostic criteria for NCC include absolute, major, minor, and epidemiological criteria. An ABSOLUTE criterion is:", "opts": ["A. Positive serology (ELISA) for cysticercosis", "B. Histological demonstration of the parasite from biopsy", "C. CT showing calcified lesion", "D. Patient from endemic region"], "ans": "B", "exp": "Del Brutto criteria (2017 revised) Absolute criteria include: (1) histological demonstration of the parasite on biopsy, (2) visualization of subretinal parasite by fundoscopy, (3) neuroimaging showing cystic lesion with scolex ('hole-with-dot'). Serology and epidemiology are only supportive (major/minor/epidemiological levels). Absolute criteria alone = definitive diagnosis." }, { "section": None, "q": 47, "case": "Glioma (CT)", "stem": "The Stupp protocol for GBM involves:", "opts": ["A. Surgery alone", "B. RT (60 Gy/30 fractions) + concurrent temozolomide → adjuvant temozolomide x 6 cycles", "C. Temozolomide alone for 12 months", "D. Bevacizumab + lomustine"], "ans": "B", "exp": "The Stupp protocol (NEJM 2005) is the standard of care for GBM: maximal safe surgical resection → concurrent radiotherapy (60 Gy in 30 fractions over 6 weeks) + temozolomide (75 mg/m²/day) → 4-week break → adjuvant temozolomide (150-200 mg/m²/day, 5 days/28-day cycle, 6 cycles). Median survival improved from ~12 to ~14.6 months. MGMT-methylated patients benefit most." }, { "section": None, "q": 48, "case": "Cerebral Atrophy (CT)", "stem": "Hypometabolism on FDG-PET in the posterior cingulate cortex and precuneus is an EARLY marker of:", "opts": ["A. Frontotemporal dementia", "B. Alzheimer's disease", "C. Lewy body dementia", "D. Vascular dementia"], "ans": "B", "exp": "Posterior cingulate cortex (PCC) and precuneus hypometabolism on FDG-PET is the earliest and most consistent metabolic signature of Alzheimer's disease — even before structural atrophy is visible on MRI. The PCC is a default mode network hub and is highly vulnerable early in AD pathology. This is a key biomarker in research and is increasingly used clinically." }, { "section": None, "q": 49, "case": "Old infarct – right temporo-parieto-occipital (CT)", "stem": "Balint's syndrome results from bilateral parieto-occipital infarcts and consists of which TRIAD?", "opts": ["A. Apraxia, agnosia, aphasia", "B. Simultanagnosia, optic ataxia, oculomotor apraxia", "C. Hemianopia, neglect, anosognosia", "D. Prosopagnosia, achromatopsia, alexia"], "ans": "B", "exp": "Balint's syndrome (bilateral dorsal stream / parieto-occipital damage): (1) Simultanagnosia – inability to perceive more than one object at a time; (2) Optic ataxia – inability to accurately reach/point under visual guidance; (3) Oculomotor apraxia – inability to voluntarily direct gaze to a new target. Caused by bilateral watershed infarcts or posterior cortical atrophy (AD)." }, { "section": None, "q": 50, "case": "Low-grade Glioma / Ganglioglioma (MRI)", "stem": "The MOLECULAR signature that definitively distinguishes oligodendroglioma from diffuse astrocytoma under WHO 2021 classification is:", "opts": ["A. IDH mutation alone", "B. IDH mutation + 1p/19q co-deletion", "C. ATRX loss + IDH mutation", "D. TERT promoter mutation alone"], "ans": "B", "exp": "WHO 2021: Oligodendroglioma is defined by IDH mutation AND 1p/19q co-deletion (whole arm co-deletion due to translocation). Diffuse astrocytoma = IDH mutation + ATRX loss/TP53 mutation WITHOUT 1p/19q co-deletion. This molecular classification supersedes histological appearance alone. 1p/19q co-deletion is the sine qua non of oligodendroglioma." }, { "section": None, "q": 51, "case": "Infarct/Gliosis with Atrophy (MRI)", "stem": "Crossed cerebellar diaschisis (CCD) on functional imaging after a hemispheric infarct refers to:", "opts": ["A. Ipsilateral cerebellar hypermetabolism", "B. Contralateral cerebellar hypometabolism/hypoperfusion due to disruption of corticopontocerebellar pathway", "C. Ipsilateral brainstem infarct", "D. Bilateral cerebellar atrophy"], "ans": "B", "exp": "CCD = reduction in blood flow and metabolism in the CONTRALATERAL cerebellar hemisphere after a supratentorial lesion (infarct, tumour, haemorrhage). It occurs because the corticopontocerebellar pathway (frontoparietal cortex → ipsilateral pons → contralateral cerebellum) is interrupted, deafferenting the contralateral cerebellar cortex. Seen on FDG-PET/SPECT. May partially recover with rehabilitation." }, { "section": None, "q": 52, "case": "Old infarct – left caudate (CT)", "stem": "Striatal dopamine transporter (DaT) imaging (DaTscan) would be ABNORMAL in which of the following conditions that can mimic each other clinically?", "opts": ["A. Drug-induced parkinsonism", "B. Parkinson's disease / DLB / MSA", "C. Essential tremor", "D. Vascular parkinsonism from small vessel disease"], "ans": "B", "exp": "DaTscan (123I-Ioflupane SPECT) images presynaptic dopamine transporters in the striatum. It is abnormal (reduced uptake, 'comma' → 'period' pattern) in Parkinson's disease, DLB, and MSA — which have true dopaminergic neurodegeneration. It is NORMAL in drug-induced parkinsonism (receptor blockade, not loss), essential tremor, and psychogenic tremor — helping distinguish these clinically." }, { "section": None, "q": 53, "case": "Neurocysticercosis (CT)", "stem": "The inflammatory 'perilesional oedema' around NCC cysts on CT/MRI is triggered by:", "opts": ["A. Bacterial superinfection", "B. Host immune response to degenerating larva releasing antigenic material", "C. Haemorrhage into the cyst", "D. Chemical meningitis from CSF"], "ans": "B", "exp": "When the Taenia solium cysticercus begins to degenerate (colloidal/granular-nodular stage), it releases antigenic proteins that trigger a vigorous host inflammatory response: T-cell activation, eosinophilia, and oedema. This peri-lesional oedema is responsible for many acute symptoms (seizures, focal deficits). Corticosteroids are given with antiparasitic drugs to dampen this reaction." }, { "section": None, "q": 54, "case": "Glioma (CT)", "stem": "H3 K27M mutation in diffuse midline glioma is associated with:", "opts": ["A. Excellent prognosis and responds to temozolomide", "B. Aggressive behaviour, WHO grade 4 designation, and poor prognosis regardless of histology", "C. Low grade and curable with surgery", "D. Oligodendroglial differentiation"], "ans": "B", "exp": "H3 K27M-mutant diffuse midline glioma (affecting thalamus, brainstem, spinal cord) was reclassified as WHO grade 4 in the 2021 update due to invariably aggressive behaviour and dismal prognosis (median survival 9-15 months), regardless of histological grade. Radiotherapy is palliative. ONC201 (a DRD2 antagonist) has shown early promise in H3K27M-mutant gliomas." }, { "section": None, "q": 55, "case": "Normal MRI", "stem": "Magnetic resonance spectroscopy (MRS) in schizophrenia consistently shows reduced levels of which metabolite in the prefrontal cortex and temporal lobe?", "opts": ["A. Creatine (Cr)", "B. N-acetylaspartate (NAA)", "C. Choline (Cho)", "D. Myoinositol"], "ans": "B", "exp": "N-acetylaspartate (NAA) is a marker of neuronal/axonal integrity and density. MRS studies in schizophrenia consistently show REDUCED NAA in the prefrontal cortex (DLPFC), anterior cingulate, hippocampus, and thalamus — reflecting reduced neuropil and neuronal density. This correlates with cognitive impairment. NAA reduction is seen even in first-episode, drug-naive patients, confirming it is a disease feature not a medication effect." }, { "section": None, "q": 56, "case": "Cerebral Atrophy (CT)", "stem": "In frontotemporal dementia, which CSF biomarker pattern is typically seen compared to Alzheimer's disease?", "opts": ["A. Low Abeta42, high total-tau and p-tau (same as AD)", "B. Normal or mildly elevated total-tau with NORMAL Abeta42 and normal p-tau", "C. Elevated 14-3-3 protein", "D. Low NFL (neurofilament light chain)"], "ans": "B", "exp": "AD CSF pattern: low Abeta42 (deposited in plaques), high total-tau and phospho-tau (neurodegeneration). FTD pattern: Abeta42 is NORMAL (no amyloid pathology), total-tau may be mildly elevated, p-tau is typically normal. Elevated 14-3-3 = CJD. Elevated NFL is non-specific (seen in many neurodegenerative diseases including FTD and AD). This CSF distinction helps differentiate AD from FTD." }, { "section": None, "q": 57, "case": "Low-grade Glioma / Ganglioglioma (MRI)", "stem": "BRAF V600E mutation is found in a high proportion of which paediatric/young adult brain tumour?", "opts": ["A. Diffuse astrocytoma", "B. Ganglioglioma (and pilocytic astrocytoma via BRAF fusion)", "C. GBM", "D. Ependymoma"], "ans": "B", "exp": "BRAF V600E mutation is present in ~50-60% of gangliogliomas and is also common in pleomorphic xanthoastrocytoma (PXA). Pilocytic astrocytoma characteristically shows BRAF-KIAA1549 fusion (not V600E). BRAF V600E mutations are targetable with vemurafenib/dabrafenib — opening a potential therapeutic window for recurrent BRAF-mutant ganglioglioma." }, { "section": None, "q": 58, "case": "Infarct/Gliosis with Atrophy (MRI)", "stem": "Superficial siderosis on MRI (hypointense rim on T2*/SWI around the brain surface) after repeated subarachnoid haemorrhage is due to:", "opts": ["A. Calcium deposition along the meninges", "B. Haemosiderin deposition from chronic repeated haemorrhage into CSF/subarachnoid space", "C. Gadolinium deposition from repeated MRI contrast studies", "D. Iron deposition from haematological disease"], "ans": "B", "exp": "Superficial siderosis results from chronic or repeated haemorrhage into the subarachnoid space (CSF). Haemoglobin breakdown products (haemosiderin and ferritin) are phagocytosed by leptomeningeal cells and deposited along the brain/spinal cord surface. On SWI/GRE: characteristic hypointense (black) rim coating the brain convexities, cerebellar folia, and brainstem. Clinically: SNHL + cerebellar ataxia + myelopathy." }, { "section": None, "q": 59, "case": "Old infarct – right temporo-parieto-occipital (CT)", "stem": "The phenomenon of cerebral diaschisis is best described as:", "opts": ["A. Spread of infarction to adjacent territory", "B. Remote metabolic/functional depression in areas connected to but anatomically distant from the primary lesion", "C. Bilateral mirror infarctions", "D. Secondary haemorrhagic transformation of the infarct"], "ans": "B", "exp": "Diaschisis (Von Monakow, 1914) describes functional depression in brain regions that are anatomically intact but disconnected from a damaged area. It is due to loss of excitatory inputs. Examples: crossed cerebellar diaschisis (contralateral cerebellum after hemispheric stroke), thalamic diaschisis (ipsilateral thalamus after frontal infarct). Diaschisis may partially recover with neuroplasticity and rehabilitation." }, { "section": None, "q": 60, "case": "NAD (CT) + Normal (MRI)", "stem": "A 30-year-old with new-onset psychosis and seizures has a normal CT and normal MRI. CSF shows mild lymphocytic pleocytosis. Anti-NMDAR antibodies are positive. The PATHOPHYSIOLOGY of psychosis in this condition is:", "opts": ["A. Loss of GABAergic interneurons causing dopamine excess", "B. Antibody-mediated internalization/downregulation of synaptic NMDA receptors on GABAergic interneurons, leading to disinhibition of glutamate and secondary dopamine dysregulation", "C. Direct neuronal destruction by complement activation", "D. Serotonin receptor blockade by the antibody"], "ans": "B", "exp": "Anti-NMDAR encephalitis: Anti-GluN1 (NR1) subunit IgG antibodies bind and cause internalization (not destruction) of NMDAR complexes. NMDAR hypofunction on GABAergic interneurons is most severe, disinhibiting glutamate release and increasing striatal dopamine — producing a clinical picture resembling phencyclidine (PCP) psychosis. This explains why the condition mimics schizophrenia and responds to immunotherapy, not antipsychotics alone." }, ] # ── PDF Generation ───────────────────────────────────────────────────────── doc = SimpleDocTemplate( "/tmp/workspace/neuro-exam/MD_Psychiatry_Neuroimaging_60Q.pdf", pagesize=A4, rightMargin=2*cm, leftMargin=2*cm, topMargin=2*cm, bottomMargin=2*cm ) styles = getSampleStyleSheet() # Custom styles title_style = ParagraphStyle('Title2', parent=styles['Title'], fontSize=18, spaceAfter=6, textColor=colors.HexColor('#1a237e'), alignment=TA_CENTER) subtitle_style = ParagraphStyle('Sub', parent=styles['Normal'], fontSize=11, spaceAfter=20, textColor=colors.HexColor('#455a64'), alignment=TA_CENTER) section_style = ParagraphStyle('Section', parent=styles['Heading1'], fontSize=13, spaceBefore=18, spaceAfter=8, textColor=colors.white, backColor=colors.HexColor('#1a237e'), leftIndent=-0.5*cm, rightIndent=-0.5*cm, borderPadding=(6, 10, 6, 10)) qnum_style = ParagraphStyle('QNum', parent=styles['Normal'], fontSize=10, textColor=colors.HexColor('#b71c1c'), spaceBefore=12, spaceAfter=2, fontName='Helvetica-Bold') case_style = ParagraphStyle('Case', parent=styles['Normal'], fontSize=9, textColor=colors.HexColor('#37474f'), spaceAfter=3, fontName='Helvetica-Oblique') stem_style = ParagraphStyle('Stem', parent=styles['Normal'], fontSize=10.5, spaceAfter=4, leading=15, alignment=TA_JUSTIFY) opt_style = ParagraphStyle('Opt', parent=styles['Normal'], fontSize=10, spaceAfter=2, leftIndent=10) ans_label = ParagraphStyle('AnsLbl', parent=styles['Normal'], fontSize=10, textColor=colors.HexColor('#1b5e20'), fontName='Helvetica-Bold', spaceBefore=6) exp_style = ParagraphStyle('Exp', parent=styles['Normal'], fontSize=9.5, leading=14, textColor=colors.HexColor('#212121'), leftIndent=10, spaceAfter=8, alignment=TA_JUSTIFY) divider_style = ParagraphStyle('Div', parent=styles['Normal'], spaceAfter=0, spaceBefore=0) story = [] # Cover story.append(Spacer(1, 1.5*cm)) story.append(Paragraph("MD Psychiatry Exam", title_style)) story.append(Paragraph("Neuroimaging Case Questions", subtitle_style)) story.append(HRFlowable(width="100%", thickness=2, color=colors.HexColor('#1a237e'))) story.append(Spacer(1, 0.4*cm)) info_data = [ ["Total Questions:", "60"], ["Sections:", "4 (Must Know | Good for Passing | Good Enough | Distinction)"], ["Cases Covered:", "9 neuroimaging cases (CT and MRI)"], ["Format:", "Single Best Answer MCQ with detailed explanations"], ["Date:", "July 2026"], ] info_table = Table(info_data, colWidths=[5*cm, 12*cm]) info_table.setStyle(TableStyle([ ('FONTNAME', (0,0), (0,-1), 'Helvetica-Bold'), ('FONTSIZE', (0,0), (-1,-1), 10), ('TEXTCOLOR', (0,0), (0,-1), colors.HexColor('#1a237e')), ('ROWBACKGROUNDS', (0,0), (-1,-1), [colors.HexColor('#e8eaf6'), colors.white]), ('LEFTPADDING', (0,0), (-1,-1), 6), ('RIGHTPADDING', (0,0), (-1,-1), 6), ('TOPPADDING', (0,0), (-1,-1), 4), ('BOTTOMPADDING', (0,0), (-1,-1), 4), ])) story.append(info_table) story.append(Spacer(1, 0.6*cm)) # Case list story.append(Paragraph("<b>Cases Included:</b>", styles['Normal'])) case_list = [ "1. Neurocysticercosis (CT)", "2. Glioma (CT)", "3. Cerebral Atrophy (CT)", "4. NAD (CT)", "5. Infarct/Gliosis with Atrophy (MRI)", "6. Normal (MRI)", "7. Low-grade Glioma / Ganglioglioma (MRI)", "8. Old infarct in right temporo-parieto-occipital region (CT)", "9. Old infarct in left caudate region (CT)" ] for c in case_list: story.append(Paragraph(f"&nbsp;&nbsp;&nbsp;{c}", styles['Normal'])) story.append(PageBreak()) # Questions section_colors = { "SECTION 1: MUST KNOW": colors.HexColor('#1a237e'), "SECTION 2: GOOD FOR PASSING": colors.HexColor('#004d40'), "SECTION 3: GOOD ENOUGH": colors.HexColor('#bf360c'), "SECTION 4: DISTINCTION": colors.HexColor('#4a148c'), } section_subtitles = { "SECTION 1: MUST KNOW": "Questions 1-15 | Core concepts every psychiatry resident must know", "SECTION 2: GOOD FOR PASSING": "Questions 16-30 | Detailed knowledge for a comfortable pass", "SECTION 3: GOOD ENOUGH": "Questions 31-45 | Advanced clinical and radiological knowledge", "SECTION 4: DISTINCTION": "Questions 46-60 | Molecular, advanced, and research-level knowledge", } for item in questions: # Section header if item["section"]: sec = item["section"] col = section_colors.get(sec, colors.HexColor('#1a237e')) sec_style = ParagraphStyle('SecH', parent=styles['Heading1'], fontSize=13, spaceBefore=10, spaceAfter=4, textColor=colors.white, backColor=col, borderPadding=(7, 10, 7, 10)) story.append(Paragraph(sec, sec_style)) story.append(Paragraph(section_subtitles.get(sec, ""), subtitle_style)) # Q number + case story.append(Paragraph(f"Q{item['q']}.", qnum_style)) story.append(Paragraph(f"[Case: {item['case']}]", case_style)) story.append(Paragraph(item['stem'], stem_style)) for opt in item['opts']: story.append(Paragraph(opt, opt_style)) story.append(Spacer(1, 0.15*cm)) story.append(Paragraph(f"Answer: {item['ans']}", ans_label)) story.append(Paragraph(f"<i>Explanation:</i> {item['exp']}", exp_style)) story.append(HRFlowable(width="100%", thickness=0.5, color=colors.HexColor('#cfd8dc'))) story.append(Spacer(1, 1*cm)) story.append(Paragraph("— End of Question Bank —", subtitle_style)) doc.build(story) print("PDF generated successfully!") PYEOF python3 /tmp/workspace/neuro-exam/generate_pdf.py

mkdir -p /tmp/workspace/neuro-exam && echo "dir ready"

~/neuro-exam/generate_pdf.py

python3 /tmp/workspace/neuro-exam/generate_pdf.py

ls -lh /tmp/workspace/neuro-exam/