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Central diabetes insipidus

A 28-year-old man is recovering from a severe head injury. He is passing more than 8 litres of dilute urine a day and is constantly thirsty. Serum sodium is 152 mEq/L, serum osmolality 310 mOsm/kg and urine osmolality 90 mOsm/kg. Blood glucose is normal. Damage to which pair of hypothalamic nuclei best explains this?

Explanation

Key fact
Vasopressin is made in the supraoptic and paraventricular nuclei and merely stored in the posterior pituitary - so hypothalamic damage causes central diabetes insipidus.

Supraoptic and paraventricular. These are the magnocellular nuclei that synthesise vasopressin, and losing them gives dilute urine with concentrated blood.

How it happens

  1. Dilute urine with hypernatraemia means water is being lost against need.
  2. Normal glucose excludes an osmotic diuresis.
  3. Urine osmolality of 90 against a serum of 310 means the collecting duct is not reabsorbing water.
  4. That points to absent vasopressin action.
  5. Vasopressin is synthesised in the supraoptic and paraventricular nuclei.
  6. Their axons run down the pituitary stalk, which trauma commonly shears.

Made above, stored below

Supraoptic and paraventricular cell bodies sit in the hypothalamus with axons running down a sheared stalk to granule-filled terminals in the posterior lobe, while the anterior lobe has its own separate portal vessels

Why not the others

Remember
SON and PVN make it; the posterior pituitary only stores it. That is why a stalk or hypothalamic injury, not a pituitary adenoma, causes diabetes insipidus.

Go deeper

Desmopressin separates the two forms: urine concentrates in central diabetes insipidus and does not in the nephrogenic type.

Post-traumatic diabetes insipidus is often triphasic - an initial polyuria, a transient antidiuretic phase as stored hormone leaks out, then permanent deficiency.

Ganong's Review of Medical Physiology, 27th ed. (McGraw Hill, 2025); Harrison's Principles of Internal Medicine, 22nd ed. (McGraw Hill, 2025).

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