{"id":36409,"date":"2026-03-31T21:47:28","date_gmt":"2026-03-31T16:17:28","guid":{"rendered":"https:\/\/atsixty.com\/?p=36409"},"modified":"2026-04-07T00:52:34","modified_gmt":"2026-04-06T19:22:34","slug":"cns-pathology","status":"publish","type":"post","link":"https:\/\/atsixty.com\/index.php\/2026\/03\/31\/cns-pathology\/","title":{"rendered":"CNS Pathology"},"content":{"rendered":"\n<div id=\"atsixty-nsp2-quiz\">\n<style>\n#atsixty-nsp2-quiz {\n  --terra: #C0603A;\n  --terra-light: #d4795a;\n  --terra-pale: #fdf3ef;\n  --teal: #2A7A6F;\n  --teal-light: #3a9688;\n  --teal-pale: #eef6f5;\n  --ink: #1e1e1e;\n  --muted: #6b6b6b;\n  --rule: #e2d8d4;\n  --correct-bg: #e8f5e9;\n  --correct-border: #43a047;\n  --wrong-bg: #fdecea;\n  --wrong-border: #e53935;\n  --white: #fff;\n  --shadow: 0 2px 16px rgba(192,96,58,0.08);\n  font-family: Georgia, 'Times New Roman', serif;\n  color: var(--ink);\n  margin: 1rem 0 2rem;\n}\n#atsixty-nsp2-quiz * { box-sizing: border-box; margin: 0; padding: 0; }\n\n#atsixty-nsp2-quiz .quiz-shell {\n  background: #f7f2ee;\n  border: 1px solid #eee3dd;\n  border-radius: 12px;\n}\n#atsixty-nsp2-quiz .quiz-sentinel { height: 1px; 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They are activated in virtually all CNS insults \u2014 infection, trauma, ischaemia, neurodegeneration. Activated microglia form <em>microglial nodules<\/em> (viral encephalitis) and <em>rod cells<\/em> (neurosyphilis). <em>Astrocytes<\/em> respond with gliosis; oligodendrocytes produce myelin; ependymal cells line ventricles.\",\n      difficulty: \"easy\"\n    },\n    {\n      q: \"Gliosis \u2014 the CNS equivalent of fibrosis \u2014 is characterised by proliferation and hypertrophy of which cell type?\",\n      correctAnswer: \"Astrocytes, forming a dense gliofibrillary scar (GFAP-positive)\",\n      opts: [\n        \"Astrocytes, forming a dense gliofibrillary scar (GFAP-positive)\",\n        \"Microglia, forming granulomas around necrotic foci\",\n        \"Schwann cells, remyelinating damaged axons\",\n        \"Oligodendrocytes, replacing lost neurons\"\n      ],\n      exp: \"<strong>Reactive gliosis<\/strong>: astrocytes upregulate GFAP, enlarge, and proliferate \u2192 dense glial scar that walls off damaged tissue but <em>inhibits<\/em> axonal regeneration. Unlike hepatic fibrosis (collagen), the CNS scar is cellular\/glial. GFAP immunostaining is used to identify astrocytic tumours (gliomas). Schwann cells remyelinate PNS, not CNS.\",\n      difficulty: \"easy\"\n    },\n    {\n      q: \"In multiple sclerosis, the primary pathological target is:\",\n      correctAnswer: \"Myelin sheaths of CNS axons, with relative axonal sparing early in disease\",\n      opts: [\n        \"Neuronal cell bodies in the cerebral cortex, causing irreversible atrophy from onset\",\n        \"Myelin sheaths of CNS axons, with relative axonal sparing early in disease\",\n        \"Peripheral nerve myelin produced by Schwann cells\",\n        \"The blood\u2013brain barrier endothelium, causing diffuse vasogenic oedema\"\n      ],\n      exp: \"<strong>MS<\/strong>: autoimmune demyelination targeting <em>CNS<\/em> myelin (oligodendrocyte-derived). Plaques (periventricular, optic nerves, spinal cord, brainstem) show myelin loss with relative axon preservation early \u2014 hence clinical remission is possible. Axonal loss accumulates with repeated attacks \u2192 permanent deficit. PNS myelin (Schwann cell) is unaffected \u2014 distinguishes MS from Guillain-Barr\u00e9 syndrome.\",\n      difficulty: \"easy\"\n    },\n    {\n      q: \"The WHO grading of CNS tumours is primarily based on:\",\n      correctAnswer: \"Histological features including cellularity, mitoses, necrosis, and microvascular proliferation, now integrated with molecular markers\",\n      opts: [\n        \"Tumour size on MRI and degree of mass effect\",\n        \"Patient age and performance status at time of diagnosis\",\n        \"Histological features including cellularity, mitoses, necrosis, and microvascular proliferation, now integrated with molecular markers\",\n        \"Response to corticosteroid therapy in the first 72 hours\"\n      ],\n      exp: \"WHO CNS tumour grading (2021 classification) integrates <strong>histology + molecular markers<\/strong>. Grade 1\u20134 reflects mitotic activity, cellularity, necrosis, and microvascular proliferation. Key molecular markers: <em>IDH1\/2 mutation<\/em> (better prognosis in gliomas), <em>1p\/19q codeletion<\/em> (oligodendroglioma), <em>MGMT methylation<\/em> (chemotherapy response), <em>EGFR amplification<\/em> (GBM). Tumour size and steroid response are clinical, not grading criteria.\",\n      difficulty: \"medium\"\n    },\n    {\n      q: \"Which of the following intracellular inclusions is correctly matched with its disease?\",\n      correctAnswer: \"Lewy bodies (\u03b1-synuclein) \u2014 Parkinson disease\",\n      opts: [\n        \"Neurofibrillary tangles (tau) \u2014 Lewy body dementia\",\n        \"Lewy bodies (\u03b1-synuclein) \u2014 Parkinson disease\",\n        \"Hirano bodies (actin) \u2014 Huntington disease\",\n        \"Negri bodies (viral protein) \u2014 Creutzfeldt-Jakob disease\"\n      ],\n      exp: \"<strong>Lewy bodies<\/strong>: eosinophilic cytoplasmic inclusions of <em>\u03b1-synuclein<\/em> in substantia nigra dopaminergic neurons \u2014 hallmark of <strong>Parkinson disease<\/strong>. <em>Neurofibrillary tangles<\/em> (hyperphosphorylated tau) = Alzheimer disease. <em>Negri bodies<\/em> = rabies (not CJD \u2014 CJD shows spongiform change + PrP deposits). <em>Huntington<\/em>: intranuclear huntingtin inclusions in striatum.\",\n      difficulty: \"medium\"\n    },\n    {\n      q: \"A 70-year-old hypertensive man suddenly develops slurred speech and right-sided weakness. CT brain at 2 hours is normal. MRI DWI shows restricted diffusion in the left MCA territory. Which type of stroke is this, and what is the most likely vessel pathology?\",\n      correctAnswer: \"Ischaemic infarct; atherosclerosis of large cerebral vessels or small vessel lipohyalinosis (lacunar)\",\n      opts: [\n        \"Haemorrhagic infarct; ruptured Charcot-Bouchard microaneurysm\",\n        \"Ischaemic infarct; atherosclerosis of large cerebral vessels or small vessel lipohyalinosis (lacunar)\",\n        \"Venous sinus thrombosis; hypercoagulable state\",\n        \"Hypertensive encephalopathy; diffuse blood\u2013brain barrier breakdown\"\n      ],\n      exp: \"Early CT is normal in <strong>ischaemic stroke<\/strong> (haemorrhage is immediately visible). MRI DWI detects ischaemia within minutes. The <strong>left MCA territory<\/strong> causes contralateral weakness + speech involvement. In a hypertensive elderly patient, aetiology is <em>atherosclerosis<\/em> (large vessel) or <em>lipohyalinosis<\/em> (small vessel \u2192 lacunar infarct). Charcot-Bouchard microaneurysms cause <em>intracerebral haemorrhage<\/em>, not ischaemic infarct.\",\n      difficulty: \"easy\"\n    },\n    {\n      q: \"A 55-year-old woman presents with sudden-onset 'worst headache of her life,' vomiting, and neck stiffness. CT shows blood in the basal cisterns. The most likely source is:\",\n      correctAnswer: \"Ruptured saccular (berry) aneurysm at the circle of Willis\",\n      opts: [\n        \"Hypertensive bleed into the putamen\",\n        \"Rupture of an arteriovenous malformation in the cerebral hemisphere\",\n        \"Ruptured saccular (berry) aneurysm at the circle of Willis\",\n        \"Cortical vein thrombosis with haemorrhagic venous infarction\"\n      ],\n      exp: \"<strong>Subarachnoid haemorrhage (SAH)<\/strong>: thunderclap headache + meningism + blood in <em>basal cisterns<\/em> on CT = ruptured <strong>berry aneurysm<\/strong> until proven otherwise. Most common sites: anterior communicating artery, posterior communicating artery, MCA bifurcation. Associated with ADPKD, Marfan, Ehlers-Danlos. Hypertensive bleeds (A) occur in basal ganglia\/thalamus\/pons \u2014 not subarachnoid. AVM bleeds (B) are typically lobar in younger patients.\",\n      difficulty: \"easy\"\n    },\n    {\n      q: \"A 25-year-old returns from sub-Saharan Africa with fever, severe headache, and confusion. LP shows: opening pressure elevated, CSF turbid, glucose 1.2 mmol\/L (serum 5.0), protein 2.8 g\/L, neutrophils 3000\/mm\u00b3. Gram stain shows gram-positive diplococci. Most likely diagnosis and causative organism?\",\n      correctAnswer: \"Bacterial meningitis \u2014 Streptococcus pneumoniae\",\n      opts: [\n        \"Tuberculous meningitis \u2014 Mycobacterium tuberculosis\",\n        \"Viral (aseptic) meningitis \u2014 Enterovirus\",\n        \"Cryptococcal meningitis \u2014 Cryptococcus neoformans\",\n        \"Bacterial meningitis \u2014 Streptococcus pneumoniae\"\n      ],\n      exp: \"<strong>Bacterial meningitis<\/strong>: high neutrophils, very low glucose (&lt;50% serum), high protein, turbid CSF. Gram-positive diplococci = <em>S. pneumoniae<\/em> (most common in adults). TB meningitis: lymphocytes, very low glucose, very high protein, subacute course. Viral: lymphocytes, normal glucose, mildly elevated protein, clear CSF. Cryptococcal: India ink positivity, mucicarmine-positive capsule; immunocompromised patients.\",\n      difficulty: \"medium\"\n    },\n    {\n      q: \"A 35-year-old HIV-positive patient (CD4 count 45 cells\/\u00b5L) presents with headache, fever, and a ring-enhancing lesion in the basal ganglia on MRI. Toxoplasma IgG is positive. The most appropriate next step is:\",\n      correctAnswer: \"Empirical anti-toxoplasma therapy (pyrimethamine + sulfadiazine); reassess at 2 weeks\",\n      opts: [\n        \"Empirical anti-toxoplasma therapy (pyrimethamine + sulfadiazine); reassess at 2 weeks\",\n        \"Immediate stereotactic biopsy of the lesion for histology\",\n        \"Lumbar puncture for CSF cytology to exclude CNS lymphoma\",\n        \"Start empirical antituberculous therapy as TB is most common in HIV\"\n      ],\n      exp: \"Ring-enhancing basal ganglia lesion + CD4 &lt;100 + positive Toxoplasma IgG = <strong>cerebral toxoplasmosis<\/strong> until proven otherwise. Standard approach: <em>empirical treatment first<\/em> \u2014 clinical and radiological response at 2 weeks confirms diagnosis, avoiding biopsy risk. If no response \u2192 biopsy to exclude <strong>primary CNS lymphoma<\/strong> (also ring-enhancing, EBV-driven in AIDS). LP is relatively contraindicated with mass lesion (herniation risk).\",\n      difficulty: \"hard\"\n    },\n    {\n      q: \"A 62-year-old presents with 6 weeks of progressive right arm weakness and headache. MRI shows a ring-enhancing mass with surrounding oedema in the left frontal lobe. Biopsy shows pleomorphic tumour cells, microvascular proliferation, and central necrosis. IDH wild-type. Diagnosis?\",\n      correctAnswer: \"Glioblastoma (WHO Grade 4, IDH wild-type)\",\n      opts: [\n        \"Metastatic carcinoma \u2014 lung primary most likely\",\n        \"Primary CNS lymphoma \u2014 diffuse large B-cell type\",\n        \"Glioblastoma (WHO Grade 4, IDH wild-type)\",\n        \"Anaplastic astrocytoma (WHO Grade 3, IDH mutant)\"\n      ],\n      exp: \"<strong>Glioblastoma (GBM)<\/strong>: most common primary malignant brain tumour in adults. Ring-enhancing, oedema, mass effect. Histology hallmarks: <strong>pseudopalisading necrosis<\/strong> + <strong>microvascular proliferation<\/strong> (glomeruloid tufts). <em>IDH wild-type<\/em> = worse prognosis (IDH mutant = secondary GBM from lower-grade precursor, better survival). Metastases (A) are typically multiple, at grey-white junction; lymphoma (B) is periventricular, homogeneously enhancing, in immunocompromised.\",\n      difficulty: \"hard\"\n    },\n    {\n      q: \"A 45-year-old presents with new-onset seizures. MRI shows a well-circumscribed, slow-growing frontal lobe mass with calcification. Biopsy: uniform round cells with 'fried-egg' cytoplasm in a chicken-wire capillary network. Molecular testing: IDH mutant, 1p\/19q co-deleted. Diagnosis?\",\n      correctAnswer: \"Oligodendroglioma (WHO Grade 2)\",\n      opts: [\n        \"Diffuse astrocytoma (IDH mutant, WHO Grade 2)\",\n        \"Pilocytic astrocytoma (WHO Grade 1)\",\n        \"Ependymoma (WHO Grade 2)\",\n        \"Oligodendroglioma (WHO Grade 2)\"\n      ],\n      exp: \"<strong>Oligodendroglioma<\/strong>: classic 'fried-egg' cells (clear perinuclear halo \u2014 artefact) + chicken-wire vasculature + calcification. Molecularly defined: <strong>IDH mutation + 1p\/19q codeletion<\/strong> (required for diagnosis per WHO 2021). Frontal lobe, seizures in middle-aged adults. Better prognosis than astrocytoma; responds to PCV chemotherapy. Pilocytic astrocytoma (B) = WHO Grade 1, cerebellar, children, Rosenthal fibres, IDH wild-type.\",\n      difficulty: \"hard\"\n    },\n    {\n      q: \"A 28-year-old woman presents with a second episode of neurological symptoms: now right leg weakness and bladder dysfunction, 8 months after an episode of transient visual loss in her right eye. MRI shows periventricular white matter lesions disseminated in space and time. CSF: oligoclonal IgG bands. Diagnosis?\",\n      correctAnswer: \"Multiple sclerosis (relapsing-remitting)\",\n      opts: [\n        \"Multiple sclerosis (relapsing-remitting)\",\n        \"Neuromyelitis optica spectrum disorder (NMOSD \u2014 anti-AQP4)\",\n        \"Acute disseminated encephalomyelitis (ADEM)\",\n        \"Cerebral vasculitis with ischaemic white matter lesions\"\n      ],\n      exp: \"<strong>RRMS<\/strong>: young woman, relapsing neurological episodes with recovery, periventricular lesions disseminated in <em>space and time<\/em> (McDonald criteria), oligoclonal bands in CSF. Previous optic neuritis (visual loss) is a classic first presentation. <em>NMOSD<\/em> (B): targets optic nerves + long spinal cord segments (\u22653 vertebrae), AQP4-IgG positive, more severe attacks. <em>ADEM<\/em> (C): monophasic, post-infectious\/vaccination, children, encephalopathic.\",\n      difficulty: \"medium\"\n    },\n    {\n      q: \"A 78-year-old man presents with a 3-year history of progressive memory loss, confusion, and visuospatial difficulties. His wife reports he sometimes sees 'small animals' in the room. He has a mild resting tremor but no rigidity. Which diagnosis best fits, and what is the expected pathological finding?\",\n      correctAnswer: \"Lewy body dementia \u2014 cortical and limbic Lewy bodies (\u03b1-synuclein) with neuronal loss\",\n      opts: [\n        \"Alzheimer disease \u2014 amyloid plaques and neurofibrillary tangles (tau) in hippocampus and cortex\",\n        \"Lewy body dementia \u2014 cortical and limbic Lewy bodies (\u03b1-synuclein) with neuronal loss\",\n        \"Vascular dementia \u2014 multiple cortical and subcortical infarcts on imaging\",\n        \"Frontotemporal dementia \u2014 TDP-43 or tau inclusions with frontal lobe atrophy\"\n      ],\n      exp: \"<strong>Lewy body dementia (LBD)<\/strong>: progressive dementia + <em>visual hallucinations<\/em> (well-formed, recurrent) + mild Parkinsonism. Key: dementia precedes or coincides with motor features (cf. Parkinson disease dementia: motor symptoms > 1 year before cognitive decline). Pathology: <strong>cortical + limbic Lewy bodies (\u03b1-synuclein)<\/strong>. Fluctuating cognition and REM sleep disorder are additional features. Cholinesterase inhibitors help.\",\n      difficulty: \"hard\"\n    },\n    {\n      q: \"An 82-year-old woman with a 7-year history of Alzheimer disease dies. At autopsy, her brain weighs 950 g (normal ~1350 g). Which regions show the most severe atrophy in Alzheimer disease?\",\n      correctAnswer: \"Hippocampus and entorhinal cortex, with relative sparing of primary motor and sensory cortex\",\n      opts: [\n        \"Basal ganglia (caudate and putamen) with ventricular dilatation\",\n        \"Cerebellum and brainstem with Purkinje cell loss\",\n        \"Hippocampus and entorhinal cortex, with relative sparing of primary motor and sensory cortex\",\n        \"Frontal and temporal poles with knife-blade gyri and severe Pick cell inclusions\"\n      ],\n      exp: \"<strong>Alzheimer disease<\/strong>: diffuse cortical atrophy (widened sulci, narrow gyri) predominantly in <strong>hippocampus, entorhinal cortex, temporal and parietal association areas<\/strong>. Primary motor\/sensory cortex is relatively spared \u2014 explains why motor symptoms are late. Histology: <em>amyloid (senile) plaques<\/em> (A\u03b2, extracellular) + <em>neurofibrillary tangles<\/em> (tau, intranuclear). Option D (knife-blade gyri + Pick cells) = frontotemporal dementia.\",\n      difficulty: \"medium\"\n    },\n    {\n      q: \"A 19-year-old is brought unconscious after a road accident. He briefly regained consciousness at the scene, then deteriorated. CT shows a biconvex (lens-shaped) hyperdense extra-axial collection over the right temporal region. The most likely diagnosis and vessel involved is:\",\n      correctAnswer: \"Extradural haematoma \u2014 rupture of the middle meningeal artery (temporal bone fracture)\",\n      opts: [\n        \"Extradural haematoma \u2014 rupture of the middle meningeal artery (temporal bone fracture)\",\n        \"Acute subdural haematoma \u2014 tearing of bridging veins between cortex and dural sinuses\",\n        \"Subarachnoid haemorrhage \u2014 ruptured berry aneurysm at the Circle of Willis\",\n        \"Contrecoup cerebral contusion \u2014 contre-coup injury to the contralateral temporal lobe\"\n      ],\n      exp: \"<strong>Extradural (epidural) haematoma<\/strong>: biconvex hyperdensity on CT, temporal location, classic <em>lucid interval<\/em> (brief recovery, then rapid deterioration as haematoma expands). Caused by <strong>middle meningeal artery<\/strong> rupture \u2014 typically from temporal bone fracture at the pterion (thinnest skull point). Surgical emergency. <em>Subdural haematoma<\/em> (B): crescent-shaped, bridging vein tear, often elderly\/alcoholics after minor trauma \u2014 no lucid interval typically.\",\n      difficulty: \"medium\"\n    }\n  ];\n\n  function shuffle(arr) {\n    const a = [...arr];\n    for (let i = a.length - 1; i > 0; i--) {\n      const j = Math.floor(Math.random() * (i + 1));\n      [a[i], a[j]] = [a[j], a[i]];\n    }\n    return a;\n  }\n\n  let session = [], answered = [], total = 0;\n\n  function prepareSession() {\n    session = shuffle(BANK).map(q => {\n      const opts = shuffle(q.opts);\n      return { ...q, opts, ansIdx: opts.indexOf(q.correctAnswer) };\n    });\n    answered = new Array(session.length).fill(null);\n    total = 0;\n    Q.sn.textContent = '0';\n    Q.sm.textContent = session.length * 4;\n  }\n\n  function diffBadge(d) {\n    return d ? `<span class=\"diff diff-${d}\">${d}<\/span>` : '';\n  }\n\n  function buildQuiz() {\n    Q.container.innerHTML = '';\n    Q.sr.textContent = session.length;\n\n    session.forEach((q, i) => {\n      const card = document.createElement('div');\n      card.className = 'q-card';\n\n      const letters = ['A','B','C','D'];\n      const optsHTML = q.opts.map((opt, j) => `\n        <div class=\"opt\" id=\"nsp2-o-${i}-${j}\">\n          <span class=\"opt-letter\">${letters[j]}<\/span>\n          <span>${opt}<\/span>\n        <\/div>`).join('');\n\n      card.innerHTML = `\n        <div class=\"q-head\">\n          <div class=\"q-num\" id=\"nsp2-n-${i}\">${i + 1}<\/div>\n          <div class=\"q-text\">${q.q}<\/div>\n        <\/div>\n        <div class=\"options\">${optsHTML}<\/div>\n        <div class=\"explanation\" id=\"nsp2-e-${i}\">\n          <div class=\"exp-label\">Explanation ${diffBadge(q.difficulty)}<\/div>\n          ${q.exp}\n        <\/div>`;\n\n      Q.container.appendChild(card);\n      q.opts.forEach((_, j) => {\n        document.getElementById(`nsp2-o-${i}-${j}`)\n          .addEventListener('click', () => answer(i, j));\n      });\n    });\n\n    Q.submit.classList.remove('visible');\n  }\n\n  function answer(qi, oi) {\n    if (answered[qi] !== null) return;\n    const q = session[qi];\n    const ok = oi === q.ansIdx;\n    answered[qi] = ok ? 'correct' : 'wrong';\n    total++;\n\n    q.opts.forEach((_, j) => {\n      const el = document.getElementById(`nsp2-o-${qi}-${j}`);\n      if (j === q.ansIdx)       el.classList.add('correct');\n      else if (j === oi && !ok) el.classList.add('wrong');\n      else                      el.classList.add('dimmed');\n    });\n\n    document.getElementById(`nsp2-e-${qi}`).classList.add('show');\n    document.getElementById(`nsp2-n-${qi}`).classList.add(ok ? 'answered-c' : 'answered-w');\n\n    updateStats();\n    updateProgress();\n    if (total === session.length) Q.submit.classList.add('visible');\n  }\n\n  function updateStats() {\n    const c = answered.filter(a => a === 'correct').length;\n    const w = answered.filter(a => a === 'wrong').length;\n    const r = answered.filter(a => a === null).length;\n    const n = (c * 4) - w;\n    Q.sc.textContent = c;\n    Q.sw.textContent = w;\n    Q.sr.textContent = r;\n    Q.sn.textContent = n >= 0 ? '+' + n : n;\n    Q.sm.textContent = session.length * 4;\n  }\n\n  function updateProgress() {\n    Q.progress.style.width = (total \/ session.length * 100) + '%';\n  }\n\n  function showScore() {\n    const c  = answered.filter(a => a === 'correct').length;\n    const w  = answered.filter(a => a === 'wrong').length;\n    const sk = answered.filter(a => a === null).length;\n    const mx = session.length * 4;\n    const ns = (c * 4) - w;\n    const pc = Math.round((ns \/ mx) * 100);\n    const bw = Math.max(0, Math.min(100, pc));\n    const msg = pc >= 85 ? 'Outstanding! Strong command of neuropathology.' :\n                pc >= 65 ? 'Good foundation \u2014 revisit the explanations for gaps.' :\n                pc >= 50 ? 'Passing, but targeted revision is recommended.' :\n                pc >= 0  ? 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