A patient has presented to hospital with anorexia-like symptoms (very lean, loss of appetite, almost no adipose tissue). An MRI scan of the patient’s brain has found that a region of the hypothalamus has been lesioned by a tumour. Which nucleus or nuclei could it be?Single choice
A
Ventromedial hypothalamus
B
Lateral Hypothalamus
C
Arcuate nucleus of the hypothalamus
D
Median eminence

Question

A patient has presented to hospital with anorexia-like symptoms (very lean, loss of appetite, almost no adipose tissue). An MRI scan of the patient’s brain has found that a region of the hypothalamus has been lesioned by a tumour. Which nucleus or nuclei could it be?Single choice

A

Ventromedial hypothalamus

B

Lateral Hypothalamus

C

Arcuate nucleus of the hypothalamus

D

Median eminence

BlackTom AI · Accepted Answer

The lateral hypothalamus (LH) contains key orexigenic neurons (orexin and melanin-concentrating hormone–producing cells) that promote feeding behavior; damage to the LH leads to profound anorexia (aphagia) and weight loss.

Relevant knowledge points and concepts:
- Hypothalamic nuclei regulate feeding: LH is commonly called the “hunger center” (stimulation → eating; lesion → refusal to eat). 
- The ventromedial hypothalamus (VMH) is the classic “satiety center” (lesion → hyperphagia, obesity). 
- The arcuate nucleus contains both orexigenic (NPY/AgRP) and anorexigenic (POMC/CART) neurons and integrates peripheral signals (leptin, ghrelin); its damage produces complex dysregulation rather than the classic aphagia. 
- Paraventricular nucleus (PVN) modulates autonomic/endocrine responses and contributes to satiety signaling but is not the primary locus whose lesion causes aphagia.

Step-by-step reasoning:
1. Patient presentation: severe anorexia-like symptoms, very lean, loss of appetite, almost no adipose tissue → implies chronic lack of feeding/energy intake. 
2. Identify which hypothalamic lesion produces failure to eat: historical animal lesion studies show that LH lesions produce aphagia and weight loss; animals with LH destruction stop eating and starve. 
3. Contrast with VMH lesion: VMH lesions produce overeating and obesity, the opposite of this patient’s phenotype, so VMH is unlikely. 
4. Arcuate nucleus lesions disrupt integrated appetite signaling; complete destruction can reduce or alter appetite but typically do not produce the classic severe aphagia seen with LH lesions. PVN lesions produce autonomic/endocrine changes and altered satiety but not the prototypical near-total appetite loss and loss of adipose tissue.

Why the correct answer is correct:
Lesion of the lateral hypothalamus removes the primary neural drive to initiate feeding (orexin/MCH pathways), causing profound anorexia and severe weight loss—exactly matching the clinical picture.

Why other options are incorrect:
- VMH lesion → hyperphagia/obesity (opposite). 
- Arcuate lesion → complex, not the classic aphagia pattern. 
- PVN lesion → endocrine/autonomic disturbances, not primary aphagia.

Conclusion: The lesion is in the Lateral Hypothalamus, which matches the provided correct answer: Lateral Hypothalamus.

A patient has presented to hospital with anorexia-like symptoms (very lean, loss of appetite, almost no adipose tissue). An MRI scan of the patient’s brain has found that a region of the hypothalamus has been lesioned by a tumour. Which nucleus or nuclei could it be?Single choice

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