CASE REPORT Dystrophic calcifi- cation in an old cerebral infarction Ian C Duncan FFRad(D) SA Basil J Sher FC Rad(D) SA Sunninghi/l Hospita/ Sandton Case report A 61-year-old female patient pre- sented with severe mitral regurgita- tion and left ventricular outflow obstruction, treated by mitral valve replacement and cardiac myomecto- my respectively. The immediate post- operative period was complicated by multiorgan failure and a right -sided frontal lobe cerebral infarct probably on a cardia embolic basis (Fig. I). She made a good recovery from all of these post operative complications. Eighteen months later she presented again with transient bilateral recur- rent visual field defects, headache and vertigo with nausea and vomiting. As part of the neurological imaging work-up an unenhanced computed tomographic (CT) scan of the brain was performed which showed no evi- dence of any recent haemorrhage or recurrent infarction, but which show~d the uncommon finding of dystrophic calcification within the old right frontal infarct (Fig. 2). Fig. 1. Unenhanced axial CT scan showing a non- haemormagic infarct in the right fronta//obe. Fig. 2. Unenhanced axial CT scan done 18 months later showing areas of dystrophic calcifi- cation foJ/owing a gyriform pattern. 48 SA JOURNAL OF RADIOLOGY • June 2003 Discussion Dystrophic calcification within cerebral infarcts is an uncommon phenomenon. The first reported cases in the radiological literature date back to 19841 and 19852 where a total of six cases were identified by means of CT scanning. Calcification within the infarcted territories was found on CT scans performed between 9 months and 5 years after the initial ictus. In none of these six cases was the serum calcium level elevated although in two cases a low serum cal- cium had been recorded on several occasions. In 1988, Parisi et al:' described a 60-year-old man who pre- sented with a large left frontoparietal infarction. A follow-up CT scan done 18 days after the initial presentation showed areas of hyperintensity within the infarct thought initially to repre- sent haemorrhagic transformation. As a result the anticoagulation therapy was stopped whereafter the patient continued to deteriorate and eventu- ally died 4 days later. Autopsy of the brain showed no evidence of recent haemorrhage but did demonstrate the presence of calcium salts throughout the infarcted area, particularly within the grey matter at the margins of the infarct. Again no significantly elevat- ed serum calcium levels were ever found during the period of hospitali- sation. The importance of this partic- ular case was the rapidity of onset of the CT hypertensity and the initial mistaken diagnosis of haemorrhagic transformation of the infarct although such haemorrhagic trans- formation must still represent the commonest cause of a change within any recently infarcted area to a hyper- intense appearance on CT scans, par- ticularly in a patient on anticoagula- CASE REPORT Table I. Causes of intracranial calcification Physiological Pineal gland Habenular commissure Choroid plexus Dural, cerebral falx Idiopathic basal ganglia calcification Ligamentous calcification Pathological • Arteriosclerosis • Cerebral aneurysm • Intracranial vascular malformation • Previous haematoma including subdural haematoma • Tumour: craniopharyngioma, oligodendroglioma, chordoma, meningioma, choroid plexus papilloma, dermoid, ependymoma, astrocytoma, lipoma of the corpus callosum, pituitary adenoma, medulloblastoma, metastases • Infections: tuberculoma, cysticercosis, toxoplasmosis, cytomegalovirus, rubella, herpes, HIV, healed abcess • Fahr syndrome • Sturge- Weber syndrome • Tuberous sclerosis, Down's syndrome, MELAS, Cockayne syndrome, neurofi- bromatosis • Hypercalcaemia: Parathyroid disease, renal failiure • Hypoparathyroidism, pseudohypoparathyroidism • Carbon monoxide, lead poisoning • Systemic lupus erythematosus • Post cerebral irradiation or methotrexate therapy tion therapy. The exact pathophysiologic mech- anism by which this dystrophic calci- fication occurs remains unknown. Hypercalcaemia does not appear to play any role in its development. CT is far more sensitive than plain film imaging in detecting calcification and many more calcified areas or lesions can thus be identified with CT imag- ing. Other known causes of cerebral calcification are listed in Table I. To date no reports concerning the magnetic resonance imaging (MR!) appearance of dystrophic calcification in cerebral infarcts have appeared. Again given the Tl hyperintense sig- nal of so-called 'wet calcium' within a tissue or the T2 hypointense signal sometimes seen in areas of calcifica- tion, the MR appearance could also be confused with subacute or chronic haemorrhage within an infarct. In conclusion, this case represents an example of rare dystrophic calcifi- cation within a cerebral infarct. As shown in the literature the onset of such calcification can occur within days of presentation and must be dif- ferentiated from haemorrhagic trans- formation in this setting. References I. Kapila A. Calcification of cerebral infarction. Radiology 1984; 153: 685-687. 2. Kuzuhara S, Naito Y, Namura Y, Takahashi R, Chiba K. CT demonstration of calcification within old cerebral infarcts. J Comput Assist Tomagr 1985; 9: 268-271. 3. Parisi J, Place J, Nag S. Calcification in a recent cerebral infarct - Radiologic and pathologic correlation. Call J Neurol Sci J 988; 15: 152-1SS. 49 SA JOURNAL OF RADIOLOGY. June 2003