Neurological involvement is frequent in HIV patients and may be the first manifestation of the disease.
The etiology of these clinical manifestations is very varied:
-Own action of the virus.
-Due to the treatment against the virus.
Regarding imaging techniques,
we have CT (with greater availability,
although its negative results are not exclusive for pathology) and MRI (with greater sensitivity and specificity when detecting alterations).
Own action of the virus: HIV encephalopathy or dementia-AIDS complex.
-Progressive multifocal leukoencephalopathy (PML)
Aspergillus and Candida
Neoplasms: Mainly lymphoma.
Effects of antiretroviral treatment
DEMENTIA-AIDS COMPLEX (Fig.1)
It is a neurodegenerative syndrome that occurs due to the intrinsic action of HIV in the central nervous system,
which causes progressive demyelination and gliosis phenomena.
Clinically patients (those who are in an advanced state) have a cognitive and progressive motor deterioration.
There are several recognized risk factors for the onset of this syndrome: A value of CD4<200 cells/μl,
the time it takes HIV infection,
a seroconversion at an old age and also the level of virus present in the cerebrospinal fluid.
Diffuse and symmetric atrophy.
Gliosis and demyelination in periventricular and deep white matter,
without associated mass effects.
The sequences with intravenous contrast are not very useful since the enhancements are not usually noticeable.
hypodensities of symmetric distribution in the deep and periventricular white matter can be observed.
a prolongation of the T1 and T2 times (Hypointensity in the T1-weighted sequences and hyperintensity in T2-weighted sequences) will be evidenced.
Juxtacortical "U" fibers will not be affected.
Spectroscopy: decrease in NAA together with an increase in Cho and mI.
PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY (Fig.2)
Progressive demyelinating disease due to the reactivation of JC virus in a situation of immunosuppression (CD4 <100).
Destruction of oligodendrocytes.
Non-specific clinical presentation.
It may be indistinguishable from HIV encephalopathy.
Multiple and asymmetric demyelinating lesions,
with involvement of subcortical white matterand periventricular,
also including an affectation of the fibers in "U".
CT imaging:Hypodense and asymmetric focal lesions in the white matter.No mass effects or pathological enhancements are observed after contrast administrationintravenous.
Prolongation of times T1 and T2.
Affectation of "U" fibers.
Greater affectation and more frequently in the parieto-occipital region,
the corpus callosum andthe cerebellum.
Occasionally you can see a tenuous peripheral enhancement,
indicative of a better prognosis.
On diffusion sequences,
a restriction of the same with a peripheral ring pattern will be appreciated.
Spectroscopy: Decrease NAA,
Increase Cho and lactate.
TOXOPLASMOSIS (Figures 9-18)
Toxoplasmosis is caused by Toxoplasma gondii,
a protozoan that is activated in situations of established immunosuppression.
It is the most common cause of opportunistic infection in patients with HIV,
as well as being the first cause of space-occupying lesion in these patients.Its anatomopathological substrate is a necrotizing encephalitis.
-It affects the cortico-subcortical junctions,
basal ganglia and thalami,
although it can also affect the brainstem.
-They tend to be multiple,
although they can be presented alone.
Single or multiple hypodense lesions with peripheral ring enhancement will be visualized.
Iso-hypointense lesions in T1-weighted sequences.Very rarely they can be hyperintense due to hemorrhagic phenomena or coagulative necrosis; however,
in cases of doubts between toxoplasmosis and lymphoma,
this is strongly in favor of toxoplasmosis,
since in lymphomas there are usually no hemorrhages before treatment.
DWI: no diffusion restriction.
This is important if we are dealing with a case in which we suspect pyogenic abscesses or lymphoma.
Perfusion MRI: In cerebral toxoplasmosis there is no increase in rCBV,
unlike what occurs in lymphomas.
Spectroscopy: In the lymphomas there will be an increase of Cho.
We must also pay attention to the treatment that the patient is taking,
because steroids can alter the peaks of NAA and Cho.
CRYPTOCOCCOSIS (Figures 3-8)
Cryptococcus Neoformans is the most frequent cause of CNS fungal infection.
It can occur by reactivation of latent infection or hematogenously from a pulmonary focus.
Patients usually present CD4 levels <100 cells / μl and presents with symptoms of meningitis or meningoencephalitis.
- Gelatinous pseudocysts: represent the perivascular spaces of Virchow-Robin dilated,
and are usually multiple and diffuse,
with a predilection for the basal ganglia,
the thalami and the cortico-spinal junctions.
- The CT is not really useful in this entity,
and we can only intuit lesions with a variable densitometry.-
- On MRI there will be an extension of both T1 and T2 times,
as well as an enhancement after the administration of contrast that will depend on the degree of immunosuppression.
DWI is usually normal (unlike pyogenic abscess,
in which there is usually restriction to it).
- If meningoencephalitis exists,
we will observe a meningeal enhancement; this is a distinctive feature that can differentiate it from bacterial TB or meningoencephalitis,
in which the enhancement may not be so leptomeningeal and tends to converge.-
- Cryptococomas are presented as nodes located in basal ganglia,
thalami and cerebellum,
which associate surrounding edema of vasogenic type and also peripheral enhancement.
In addition to the cryptococomas,
there are also have granulomas,
which can appear in both parenchyma,
nerve roots etc.
LYMPHOMA (Figures 19-22)
In the case of primary lymphoma of the central nervous system,
immunosuppression is the main risk factor.
Using imaging methods it can be difficult to differentiate a case of lymphoma from a toxoplasmosis.
-It is usually a single lesion most of the time,
although it can also be multiple.
-It may be supratentorial or infratentorial,
although it is more common to have a supratentorial location,
with frequent involvement of basal ganglia and corpus callosum.
- There may be a dissemination of the process through the cerebral perivascular spaces.
When there are periventricular lesions,
there is frequent invasion of the adjacent ependyma.
-CT: it is not very useful,
but it usually appears as a hyperdense mass or at least slightly hyperdense.
-MRI: With sequences with intravenous contrast,
there may be a ring enhancement as in the cases of toxoplasma lesions,
but in the case of lymphoma,
the enhancement tends to be rather not well-defined edges; if there is a well-defined enhancement,
the option of toxoplasmosis should be considered.
being a tumor with a fairly high cell density,
has diffusion restriction.
IMMUNE RECONSTITUTION INFLAMMATORY SYNDROME (IRIS)
The restoration of immunity in some cases worsens the disease.
The exact etiology is unknown.
It presents deterioration despite increased CD4 and decreased viral load.
It can cause death.It happens in the first months of therapy.
The treatment is to continue with the therapy.