From the Guidelines
Intracranial calcifications are a common finding in both toxoplasmosis and cytomegalovirus (CMV) infections, particularly in congenital cases or in immunocompromised individuals, with toxoplasmosis typically presenting as multiple small, scattered lesions in the basal ganglia and periventricular regions, and CMV presenting with periventricular calcifications in a linear pattern following the ventricular outline 1.
Key Features of Toxoplasmosis and CMV Infections
- Toxoplasmosis:
- Caused by the parasite Toxoplasma gondii
- Typically presents with multiple small, scattered lesions in the basal ganglia and periventricular regions
- Can cause hydrocephalus and calcifications in congenital cases
- Treatment usually includes pyrimethamine, sulfadiazine, and folinic acid
- CMV Infections:
- Caused by the cytomegalovirus
- Typically presents with periventricular calcifications in a linear pattern following the ventricular outline
- Can cause necrotizing ventriculoencephalitis
- Treatment usually includes ganciclovir or valganciclovir
Diagnosis and Treatment
- Diagnosis typically involves serological testing for antibodies, PCR for viral or parasitic DNA, and neuroimaging
- Treatment should be individualized based on the specific infection and patient factors
- For toxoplasmosis, treatment with pyrimethamine, sulfadiazine, and folinic acid is recommended, while for CMV, treatment with ganciclovir or valganciclovir is recommended 1.
Clinical Considerations
- Both infections are particularly concerning during pregnancy as they can cross the placenta and affect the developing fetal brain
- The presence of intracranial calcifications often indicates chronic or resolved infection, and the pattern and distribution of these calcifications can help differentiate between these two pathogens during radiological assessment
- A combination of clinical, radiological, and laboratory findings is necessary for accurate diagnosis and treatment of these infections 1.
From the Research
Association between Intracranial Calcification and Infections
The association between intracranial calcification and infections such as Toxoplasmosis (Toxoplasma gondii) and Cytomegalovirus (CMV) is a significant area of study. Key points to consider include:
- Intracranial calcification can be a consequence of congenital toxoplasmosis, which may result in severe neurological or ocular disease, including blindness, as well as cardiac and cerebral anomalies 2, 3.
- The severity of the infection depends on the gestational age at which the infection occurs, with early infections having a lower transmission rate but higher severity if the fetus is infected 3.
- Diagnosis of congenital toxoplasmosis can be done through serological screening of anti-Toxoplasma antibodies (IgM and IgG), while PCR of the amniotic fluid or placenta is the confirmatory test 3, 4.
- Intracranial calcification can also be associated with other infections, including CMV, which is part of the TORCH infections (toxoplasmosis, other, rubella, CMV, and herpes) 5, 6.
- The differential diagnosis of intracranial calcification should consider the age at presentation, location of the calcification, and associated neuroimaging findings, as well as clinical and familial information 5, 6.
Causes of Intracranial Calcification
Intracranial calcification can be caused by various factors, including:
- Infectious causes, such as toxoplasmosis, CMV, and other TORCH infections 2, 3, 5, 6.
- Congenital causes, such as congenital toxoplasmosis and other genetic disorders 3, 5, 6.
- Endocrine/metabolic causes, such as parathyroid and thyroid dysfunction, and inborn errors of metabolism 5.
- Vascular causes, such as cavernous malformations, arteriovenous malformations, and chronic venous hypertension 5.
- Neoplastic causes, such as pediatric brain tumors 5.
Diagnosis and Management
Diagnosis and management of intracranial calcification due to infections such as toxoplasmosis and CMV involve:
- Serological screening and PCR testing for diagnosis 2, 3, 4.
- Treatment with spiramycin to prevent congenital transmission, and pyrimethamine, sulfadiazine, and folinic acid to treat infected fetuses 2, 3.
- Consideration of the patient's immune status and potential for reactivation of latent infections 4.