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Sickness behaviour — MRCPsych Paper A MCQ

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HardNeuroimaging, neuroendocrinology and psychoneuroimmunologySickness behaviourMRCPsych Paper A

During an acute, laboratory-confirmed influenza infection, an adult with no previous psychiatric disorder develops reduced food intake, increased sleep, fatigue and withdrawal from social interaction. These changes begin with the systemic inflammatory symptoms and remit as the infection resolves. Which mechanism most directly organises this coordinated behavioural response?

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Correct answer: B — Peripheral pro-inflammatory cytokine signalling activating central immune-neural pathways

The correct answer is B. During infection, pro-inflammatory cytokines such as IL-1, IL-6 and TNF communicate with the brain through humoral and neural pathways, including vagal afferents. This produces a coordinated motivational state—sickness behaviour—characterised by reduced appetite, increased sleep, fatigue and social withdrawal. Its close temporal relationship to infection and subsequent resolution distinguish it from primary negative symptoms of schizophrenia. Classical conditioning may modify later responses but does not alone explain the innate acute syndrome. Hippocampal kindling models progressive seizure susceptibility rather than infection-related behavioural change. Dopamine-transporter blockade increases extracellular dopamine and is associated with psychostimulant effects, not this coordinated inflammatory response.

Reference: Dantzer R, Kelley KW. Twenty years of research on cytokine-induced sickness behavior. Brain, Behavior, and Immunity. 2007;21(2):153–160. https://pubmed.ncbi.nlm.nih.gov/17088043/