Consciousness and Cognition: Delirium, Dementia and Brain Imaging | Part 1 | 意識認知 | OET Music

Dr Allison Lu · Pip & Barnaby · Medical English

本頁提供本曲完整英文歌詞與影片搭配的繁中醫學提示。歌詞保留原演唱文字;遇到過度簡化或舊門檻,請搭配下方提示與原始資料閱讀。這是概念學習材料,不替代個別醫療評估。

Lyrics · 完整歌詞

An acute change in attention
or cognition in an older person warrants prompt assessment for delirium
and its underlying cause.
Delirium is acute and fluctuating, and its core deficit is inattention;
consciousness drifts between drowsiness and agitation and worsens at night.
It almost always has a precipitant: infection, electrolyte disturbance, hypoxia,
drugs or alcohol withdrawal.
Dementia, by contrast, is chronic and steadily progressive,
with attention relatively spared until late.
The first task is therefore to search for the cause,
not to label.
Once a chronic course is established,
the single boundary between mild cognitive impairment
and dementia is impairment of daily activities;
language and executive scores cannot draw it.

Each dementia is a misfolded protein in a particular place.
Alzheimer disease deposits extracellular amyloid-beta plaques and intracellular hyperphosphorylated tau tangles,
so cerebrospinal fluid amyloid-beta 42 falls while phosphorylated tau rises.
Dementia with Lewy bodies combines fluctuating cognition, visual hallucinations,
spontaneous parkinsonism and REM sleep behaviour disorder.
Its striatal dopamine receptors are fragile,
so haloperidol provokes severe parkinsonism or a neuroleptic malignant-like state
and is contraindicated;
low-dose levodopa and cholinesterase inhibitors are used instead.
Normal pressure hydrocephalus impairs gait first, then continence, then cognition,
because the leg fibres beside the ventricles are compressed earliest.
Removing 30 to 50 millilitres of cerebrospinal fluid predicts shunt response.

Every new dementia is screened for B12 deficiency, hypothyroidism and syphilis,
the treatable causes.

An acute change in attention
or cognition in an older person warrants prompt assessment for delirium
and its underlying cause.


Seizure and syncope are separated by their prologue and epilogue.
Syncope follows an autonomic warning and ends in rapid, complete recovery;
a seizure bites the lateral tongue and leaves post-ictal confusion.
Absence seizures show three-hertz spike-and-wave discharges without a post-ictal phase,
and myoclonic jerks usually spare consciousness.
Temporal lobe epilepsy arises from the hippocampus and amygdala,
and bilateral hippocampal resection is forbidden because it abolishes new memory.
Status epilepticus is declared at five minutes.
A benzodiazepine, lorazepam 0.1 mg/kg intravenously or midazolam 10 mg intramuscularly,
comes first because it increases GABA-A channel opening.
Repeating it endlessly fails through respiratory depression and receptor desensitisation, so levetiracetam,
valproate or fosphenytoin follows, and anaesthesia with intubation is the third step.

Images keep their own timetable.
Diffusion-weighted imaging shows cytotoxic oedema within minutes of ischaemia,
whereas FLAIR needs six to twelve hours.
Gradient echo and susceptibility sequences detect microbleeds
and haemosiderin more sensitively than CT.
Raised intracranial pressure declares itself through the Cushing reflex of hypertension,
bradycardia and irregular breathing.
An empty delta sign after contrast marks venous sinus thrombosis in a young woman
on the pill
or in the puerperium.

Under the microscope, proteins name the disease:
alpha-synuclein for Parkinson and Lewy body disease,
TDP-43 and SOD1 rather than tau for amyotrophic lateral sclerosis,
prion protein for spongiform change.
Hypertensive haemorrhage arises deep, from Charcot-Bouchard microaneurysms of the perforating arteries,
whereas amyloid angiopathy deposits amyloid-beta in cortical vessels and bleeds lobar.
Herpes simplex encephalitis shows Cowdry type A inclusions
and haemorrhagic necrosis of the medial temporal lobes,
reached along the trigeminal and olfactory routes.

An acute change in attention
or cognition in an older person warrants prompt assessment for delirium
and its underlying cause.

Medical Notes · 醫學學習提示

  1. 急性注意力改變是需要立即評估的警訊
  2. 長者突然認知改變,須評估譫妄
  3. 同時尋找感染、缺氧、藥物等誘因
  4. 譫妄常急性起病且波動,核心是注意力障礙
  5. 可能躁動或嗜睡;低活動型也不能漏掉
  6. 常有一個或多個誘因:感染、代謝異常、缺氧
  7. 也要檢視藥物、酒精或鎮靜藥戒斷
  8. 失智多呈慢性病程,但不一定持續線性惡化
  9. 注意力是否保留依失智類型而異;兩者可並存
  10. 先評估生理狀況、用藥與可處理的原因
  11. 不可僅貼上失智或精神疾病標籤
  12. 慢性認知下降須結合病史、功能與認知檢查
  13. 輕度認知障礙通常仍能維持生活獨立
  14. 失智的認知缺損會妨礙日常獨立功能
  15. 分數不是唯一標準,須考量原有能力與其他病因
  16. 失智並非全是單一蛋白疾病,亦有血管與混合病因
  17. 阿茲海默病典型病理:細胞外 Aβ、細胞內 tau
  18. CSF Aβ42 或其比值下降、p-tau 上升可支持診斷
  19. 路易氏體失智可有認知波動與反覆視幻覺
  20. 另有自發性巴金森症與 REM 睡眠行為障礙
  21. 對多巴胺阻斷藥可能高度敏感;非字面上的受體脆弱
  22. haloperidol 可引發嚴重動作惡化或惡性反應
  23. 路易氏體失智與巴金森病應避免 haloperidol
  24. 認知與動作症狀用藥須分別評估,非直接替代鎮靜藥
  25. 正常壓力水腦常以步態障礙突出,三症順序不固定
  26. 涉及腦室周邊網絡功能;不能只歸因於腿部纖維壓迫
  27. 放液 30–50 mL 後評估改善;陰性不排除分流受益
  28. 常查 B12 與甲狀腺功能;梅毒檢查依風險與情境
  29. 可治療因素可能共存,不代表失智一定可逆
  30. 暈厥與癲癇須整合發作前後及目擊者描述
  31. 反射性暈厥常有前兆;心因性暈厥可能沒有
  32. 側舌咬傷與發作後混亂支持癲癇,但不是每次都有
  33. 典型失神可見約 3 Hz 棘慢波,通常無明顯發作後混亂
  34. 肌陣攣意識可保留,仍須判斷病因與發作類型
  35. 內側顳葉癲癇常涉及海馬;非所有顳葉發作皆源於此
  36. 雙側海馬嚴重損傷可造成新記憶形成障礙
  37. 持續抽搐達 5 分鐘,或反覆且未恢復,須啟動急救
  38. IV lorazepam 0.1 mg/kg,每次上限 4 mg;IM midazolam 10 mg 限 >40 kg
  39. benzodiazepine 增強 GABA-A 抑制;同步監測呼吸與循環
  40. 依流程有限次重複後,迅速加入第二線抗癲癇藥
  41. 第二線可用 levetiracetam 等;難治者需加護監測與麻醉
  42. 影像表現隨時間與病灶而變化,不能當作精準時鐘
  43. 急性缺血 DWI 可早期異常;須合併 ADC 與臨床判讀
  44. FLAIR 可能數小時內轉陽,並非固定 6–12 小時
  45. GRE/SWI 對微出血及磁敏感效應較敏感
  46. 含鐵血黃素沉積可呈低訊號;圖非診斷影像
  47. Cushing 反應可能提示嚴重顱壓升高
  48. 高血壓、心搏過慢、呼吸異常是晚期警訊;不可等齊才處理
  49. 增強影像空三角徵可提示靜脈竇血栓,但並非必見
  50. 雌激素避孕藥是風險因素之一,非限定族群
  51. 產褥期亦有較高風險;需靜脈影像確認
  52. 病理蛋白有助分類,但不能一蛋白對應所有病例
  53. α-synuclein 與巴金森病、路易氏體病相關
  54. ALS 常見 TDP-43;SOD1 等基因型有不同病理
  55. 異常 prion 蛋白與海綿狀腦病變相關
  56. 高血壓相關腦出血常在深部,涉及小穿通動脈病變
  57. 腦類澱粉血管病常涉及皮質血管並造成腦葉出血
  58. HSV 腦炎可見核內包涵體;不能只靠病理等候診斷
  59. 常侵犯內側顳葉,可有出血性壞死
  60. 傳播機制涉及神經路徑;疑似 HSV 腦炎須緊急處理

References