Postradiation reactions in the CNS are well described and catalogued in the conventional radiotherapy literature; acute, subacute and late CNS reactions are recognized. Tumours predispose to these normal tissue reactions by the oedema and pressure epiphenomena that occur in their environs, and probably by other mechanisms associated with tissue breakdown. That late normal tissue reactions (particularly permanent late sequelae--universally referred to as 'necrosis') occur in the normal nervous system is in the complication list of every radiosurgery centre. This article, for the first time, places postradiosurgery observations within or without the existing classification of reactions, and draws attention to the fact that previous 'radiosurgery risk factor' papers in the literature may be wrong to pool different 'reactions' in the formulation of risk formulae for normal brain damage following single shot radiotherapy. Acute reactions occur in the same manner as described for conventional radiotherapy, being a transient swelling phenomenon that occurs 12-48 h after therapy; they are fully reversible and do not usually augur late problems; routine administration of short duration steroids around the time of radiosurgery may prevent or delay the clinical signs. Subacute reactions occur 3-10 months later (a later time than the subacute reactions following conventionally fractionated radiotherapy), and may prove fully or partially reversible, or progress to permanent sequelae; the difference between these and late sequelae (which tend to be permanent themselves) then becomes blurred. That tumour swelling occurs in the subacute phase and is associated with oedema in the surrounding normal brain is an interesting observation (occurring in extra- and intra axial slow-growing tumours); it denotes tumour damage and has not been encountered in the conventionally-fractionated radiotherapy literature. Tumour shrinkage occurs later, with subsidence of the surrounding oedema, and this phenomenon may therefore be regarded (paradoxically) as a good prognostic sign, a point about which the referring clinician should be made aware. Similarly, contrast enhancement in the tumour perimeter at this time reflects a host reactive response and not tumour activity. Persistent clinical neurological signs and MRI changes (best seen on the T2 weighted sequences) beyond 2 years, indicate late damage or reaction. Usually, this represents scarring or coagulative necrosis without mass effect, but if there is a low signal area with mass effect and considerable surrounding oedema, liquefactive necrosis has occurred and (as in the brachytherapy literature) surgical decompression is very occasionally needed.