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Concept
Primary polydipsia
Summary
Primary polydipsia and psychogenic polydipsia are forms of polydipsia characterised by excessive fluid intake in the absence of physiological stimuli to drink. Psychogenic polydipsia which is caused by psychiatric disorders, often schizophrenia, is often accompanied by the sensation of dry mouth. Some forms of polydipsia are explicitly non-psychogenic. Primary polydipsia is a diagnosis of exclusion.
Signs and symptoms of psychogenic polydipsia include:
Excessive thirst and xerostomia, leading to overconsumption of water
Hyponatraemia, causing headache, muscular weakness, twitching, confusion, vomiting, irritability etc., although this is only seen in 20–30% of cases.
Hypervolemia, leading to oedema, hypertension and weight gain (due to the kidneys being unable to filter the excess blood) in extreme episodes
Tonic-clonic seizure
Behavioural changes, including fluid-seeking behaviour; patients have been known to seek fluids from any available source, such as toilets and shower rooms.
The most common presenting symptom is tonic-clonic seizure, found in 80% of patients. Psychogenic polydipsia should be considered a life-threatening condition, since it has been known to cause severe hyponatraemia, leading to cardiac arrest, coma and cerebral oedema.
Psychogenic polydipsia in individuals with schizophrenia is associated with differences seen in neuroimaging. MRI scans may be used to help with differentiating between PPD and diabetes insipidus, such as by examining the signal of the posterior pituitary (weakened or absent in central DI). Some patients, most often with a history of mental illness, show a shrunken cortex and enlarged ventricles on an MRI scan, which makes differentiation between psychogenic and physiological cause difficult. However, these changes will likely only develop after chronic PPD associated with severe mental illness, as opposed to less severe forms of the disorder as seen in those with anxiety and affective disorders. PPD is also linked with significant reductions in insular cortex volume, although this may be caused by the secondary hyponatraemia.
Official source
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