Pruritus:

The pathophysiology of pruritus is poorly understood but is due to peripheral mechanisms (e.g. skin disease), central or neuropathic mechanisms (e.g. multiple sclerosis), neurogenic (e.g. cholestasis/μ-opioid receptor stimulation, p. 386) or psychogenic mechanisms (e.g. parasitophobia). Evidence suggests that low stimulation of unmyelinated C-fibres in the skin is associated with the sensation of itch (high stimulation produces pain). Histamine, tachykinins (e.g. substance P) and cytokines (e.g. interleukin-2) may also play a role peripherally in the skin. The major nerve pathways for itch and the influence of the central nervous system are not well characterized but opioid μ-receptor-dependent processes can regulate the perception and intensity of itch.
Pruritus (see lichen simplex, nodular prurigo/neurodermatitis) in the absence of a demonstrable rash can be caused by a number of different medical problems

Medical conditions associated with pruritus
Iron deficiency anaemia
Internal malignancy (especially lymphoma)
Diabetes mellitus
Chronic renal failure
Chronic liver disease (especially primary biliary cirrhosis)
Thyroid disease
HIV infection
Polycythaemia vera

Asteatotic eczema and cholinergic urticaria are common causes of pruritus where the rash is often missed. The term idiopathic pruritus or 'senile' pruritus probably overlaps with asteatotic eczema and this is common in the elderly.
Treatment involves avoiding soaps and using symptomatic measures (as for asteatotic eczema). Phototherapy may help intractable cases. Oral opiate antagonists, which act centrally, are under assessment. Underlying medical problems should be treated.