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Fig. 45.5A,B. Intracranial calcifications in congenital toxoplasmosis. (A) Posterior-anterior and (B) lateral views of the skull showing scattered bilateral calcific flecks, nodules and linear streaks in frontal and parietal lobes of an infected infant.

Fig. 45.6A,B. Congenital toxoplasmosis with intracranial hyrocephalus. The grossly dilated lateral ventricles are outlined with air on (A) AP and (B) lateral radiographs after pneumoencephalography. There is spreading of the cranial sutures due to increased intracranial pressure. There is extensive calcification lining the walls of the dilated lateral ventricles, mimicking exactly the intracranial calcifications seen in cytomegaloviral infections. AFIP 220250.


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Imaging Diagnosis

Toxoplasmosis is probably the commonest cause of scattered intracranial calcifications in the neonate. Only infections acquired in utero will lead to intracranial calcification in the child.

Human toxoplasmosis was initially described as a cause of encephalomyelitis in 1937. Some five years later, radiographic findings were described in ten patients. In nine of these patients, there was diffuse intracerebral calcification, usually occurring as tiny 2-mm foci within the cortex or as linear streaks, particularly in the basal ganglia or thalamus. There may also be increased intracranial pressure and hydrocephalus. In a series of patients reported by Feldman, the incidence of intracranial complications in patients with clinical and serological evidence of toxoplasmosis was 59%. Intracranial calcifications were found in 32% of another series of patients reported by Couvreur and Desmonts in 1962, many of whom had milder and subclinical disease. Eighty-seven percent of cases had intracranial calcifications in a further series reported by Francois and De Witte.
The timing of intracranial calcification in toxoplasmosis is variable. It may occur early and be seen on the initial computed tomography (CT) scan, or alternatively it may first be detected subsequent to treatment.

There is also considerable variation in the type of calcification. Most calcifications are bilateral; they may be small 1 to 2-mm punctate flecks, slightly larger 3 to 4-mm nodules, curvilinear streaks, or plaques (Fig. 45.5). In general, meningeal calcifications are plaque-like and bilateral, whereas those in the cerebral cortex tend to be punctate deposits or nodules. Those in the basal ganglia or thalamus are more often striated or curvilinear. The calcifications may be randomly scattered through the brain parenchyma; most often they are present in the parietal region, but they also may be found in specific cerebral structures such as the choroid plexus, the ependyma, the meninges or the caudate nucleus and thalamus. Calcification within the caudate nucleus usually involves the head of the nucleus and is always bilateral and often symmetrical. The frontal lobes are often involved but temporal and occipital calcifications are less common. Calcifications which can be seen on imaging are extremely rare in the infratentorial region, although the cerebellum, fourth ventricle, and aqueduct are frequently involved histopathologically. Calcifications which are ependymal or subependymal along the dilated lateral ventricles mimic the calcifications seen in cytomegalovirus disease (Fig. 45.6).
Cerebral calcifications do not always remain unchanged. In a series of 32 children with toxoplasmic intracranial calcifications studied by Müssbichler in 1968, two of six children examined with serial radiographs showed no change in the size of the calcification, but two children showed an increase in the size of almost all of the calcifications; in another child additional calcifications appeared after the first examination.

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