雅思阅读 192: The Brain That Keeps the Pain（持续感知疼痛的大脑）

改编由 Stanford Report / Molecular Pain / PMC reviews。雅思阅读 Section 3 难度，约 1050 词。 素材来源：https://news.stanford.edu/stories/2026/04/chronic-acute-pain-circuits-systems-research-treatments

Reading Passage

A. Acute pain is useful. It is the alarm that pulls your hand from the flame, that tells you not to walk on a sprained ankle. It begins in specialised nerve endings called nociceptors, which detect heat, pressure or chemical damage and send signals up the spinal cord to the brain. Chronic pain is something else entirely. It persists for months or years after the original injury has healed, sometimes for no identifiable reason at all. It is not simply acute pain that lasts too long; it is a different biological state. Roughly 60 million Americans live with chronic pain, and the condition is one of the leading reasons patients seek medical care, consume opioid medication and lose days of work. It is also a leading driver of the opioid crisis, because the drugs that dull acute pain do not reliably touch the chronic kind. Patients are left with a choice between unhelpful medication and unrelieved suffering. For decades, doctors treated it as a symptom of an underlying injury — fix the injury and the pain should stop. When that logic fails, as it so often does, the medical system has had little to offer.

B. The central concept that has reshaped the field is central sensitization. After an injury, the pain-signalling neurons in the spinal cord and brain do not simply return to their resting state. Their excitability rises and stays raised. Nerves that should only respond to strong, damaging stimuli begin to fire at light touch; areas around the injury become tender; even normally harmless sensations can hurt. The International Association for the Study of Pain defines central sensitization as an increased responsiveness of pain-signalling neurons to normal or weak input. The mechanism resembles long-term potentiation, the strengthening of synapses that underlies learning and memory in the hippocampus. In effect, the nervous system "learns" the pain and then cannot unlearn it. This is why chronic pain is not just a sensory event but a learned, persistent state, and why opioids — which block nociceptor signals at the periphery — often fail to help. The pain signal is no longer coming from the tissue; it is being generated by the nervous system itself.

C. Recent work has begun to map the specific brain circuits that maintain this state. A 2026 Stanford study made a striking finding: chronic pain and acute pain, long assumed to share a single pathway, appear to run through largely separate circuits. Researchers identified a specific neural loop that stays active during chronic pain in mice, and demonstrated that silencing it relieved the chronic pain without impairing the animals' normal acute-pain reflexes — they still pulled their paws away from heat. The implication is profound. If chronic pain uses its own circuit, it can in principle be targeted without dulling the protective acute-pain response that keeps people safe. The same study pointed to a circuit involving areas of the prefrontal cortex that are associated with emotion and decision-making, suggesting that chronic pain is as much a product of brain-wide rewiring as of local nerve injury. This is why patients often describe chronic pain as something that colours their entire life, not just the injured body part. The pain follows them into work, sleep and conversation, reshaping daily choices long after the original wound has healed. Depression, sleep disturbance and social withdrawal frequently accompany it, not because the patient is weak but because the nervous system has been rewired. Treating those consequences is now as much a neuroscience problem as a pain problem, and progress in one feeds the other.

D. The cells that maintain this rewiring are not only neurons. Glial cells — once dismissed as passive "glue" holding neurons in place — have emerged as active participants. Astrocytes in the brain and spinal cord release inflammatory signals that keep pain neurons sensitised long after the original injury has resolved. Brain-derived neurotrophic factor (BDNF), a molecule best known for supporting learning and memory, is also released by activated glia and drives the strengthening of pain synapses. Sex differences are now recognised as central rather than incidental: chronic pain disproportionately affects women, and recent reviews have documented distinct cellular and molecular signatures in male and female nervous systems. This matters because most preclinical pain research was historically conducted in male animals, reflecting a now-discredited assumption that male and female biology was interchangeable. A drug that works in a male mouse may not work in a female patient.

E. The clinical implications are only beginning to be worked out. Drugs that target glial activation, BDNF signalling or the specific prefrontal circuit are in early development, but none is yet a routine treatment. What has changed is the conceptual framework. Chronic pain is no longer understood as a symptom of something broken in the body that must be fixed; it is a disease of the nervous system in its own right, with its own circuits, its own molecular mediators and its own natural history. This explains why pain can persist after surgery heals, why it runs in families and why it responds poorly to analgesics designed for acute injuries. It also points toward treatments that target the brain's plasticity rather than the body's damage — including psychological approaches, exercise and, one day, drugs that silence the specific circuit without turning off the alarm that keeps a hand away from the flame. The goal is not to eliminate pain but to unlearn it. For patients who have lived with chronic pain for a decade, the idea that their nervous system has learned a bad habit is not a dismissal; it is, perhaps for the first time, a diagnosis that points somewhere. It points away from endless surgery and toward retraining the nervous system itself.

Questions 1-4

Choose the correct heading for paragraphs B, C, D and E from the list of headings below.

List of Headings i. The difference between acute and chronic pain ii. Central sensitization: when the nervous system learns the pain iii. Chronic pain runs through its own brain circuit iv. Beyond neurons: glial cells, BDNF and sex differences v. From symptom to disease: new treatments on the horizon vi. How opioids are manufactured vii. Why acute pain is dangerous

1. Paragraph B: ____
2. Paragraph C: ____
3. Paragraph D: ____
4. Paragraph E: ____

Questions 5-8

Choose the correct letter, A, B, C or D.

5. According to the passage, how is chronic pain different from acute pain? A. It is simply acute pain that lasts longer. B. It is a distinct biological state involving rewired nervous systems. C. It only affects the hands. D. It is always caused by a visible injury.

6. What is central sensitization? A. A decrease in pain signalling over time. B. Increased responsiveness of pain neurons to normal or weak input. C. A surgical procedure to reduce pain. D. A type of headache.

7. What did the 2026 Stanford study show? A. Chronic and acute pain use identical circuits. B. Silencing a specific chronic-pain circuit relieved chronic pain without affecting acute pain. C. Mice do not feel chronic pain. D. Opioids cured chronic pain completely.

8. Why is the historical focus on male animals a problem? A. Male animals are harder to study. B. Chronic pain has distinct cellular signatures in males and females, and women are more affected. C. Female animals never feel pain. D. Male animals cannot be bred in laboratories.

Questions 9-13

Do the following statements agree with the claims of the writer?

Write:

• TRUE if the statement agrees with the information
• FALSE if the statement contradicts the information
• NOT GIVEN if there is no information on this

9. Roughly 60 million Americans live with chronic pain.
10. Central sensitization works through a mechanism similar to long-term potentiation.
11. Opioids are always effective at treating chronic pain.
12. Glial cells were once considered passive support cells.
13. A drug that silences the chronic-pain circuit is already widely prescribed.

Questions 14-15

Complete the summary below using NO MORE THAN TWO WORDS from the passage.

After injury, pain neurons stay sensitised through a process resembling long-term potentiation; astrocytes release inflammatory signals, and (14) __________ drives the strengthening of pain (15) __________.

答案与解析

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