Imaging 14:48-59 (2002)
© 2002 The British Institute of Radiology
Imaging of the central nervous system in HIV infection
N A Sibtain, MRCP and
R J S Chinn, MRCP, FRCR
Department of Radiology, Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH, UK
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Summary
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- Neurological disease is common in HIV infection.
- There are four main categories of disease: primary effects of HIV; opportunistic infections; neoplasia; and vascular diseases.
- MRI remains the technique of choice for evaluation of these patients.
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Introduction
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Human immunodeficiency virus (HIV) is neurotropic and crosses the blood–brain barrier at anearly stage in the disease. Thus, the central nervous system (CNS) is a major target of HIV, with approximately two-thirds of patients developing CNS involvement during the course of their disease.
The spectrum of CNS disease in acquired immune deficiency syndrome (AIDS) is wide and can be broadly categorized into primary effects of HIV, opportunistic infections, neoplasms and vascular disease.
Clinical findings are non-specific, and are often unhelpful in distinguishing between the vast array of neurological disease processes in AIDS. They may range from mild cognitive impairment to frank neurological deficit and, in extreme cases, coma. Since clinical presentation can be surprisingly subtle, there has to be a low threshold for further investigation, and this generally takes the form of cerebrospinal fluid (CSF) analysis combined with cross-sectional imaging. Although recent advances in polymerase chain reaction (PCR) CSF analysis have increased the ability to make a specific diagnosis, a large part of the diagnostic process still relies on radiological interpretation. MRI is the modality of choice owing to its higher sensitivity of lesion detection and superior contrast resolution compared with CT. Nevertheless, the ready availability of CT allows it to remain a first line investigation, typically in the form of a screening tool prior to lumbar puncture.
There is a considerable overlap of imaging features between the various disease subtypes; therefore, a systematic approach to interpretation is essential. Since MRI is the mainstay of investigation of the CNS in AIDS, this review concentrates on the MRI appearances. It aims to simplify the process of radiological analysis by categorizing the various patterns of disease and highlighting the main differential diagnoses for each pattern.
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Diffuse white matter disease
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HIV encephalopathy
The most common cause of neurological disease in AIDS is from direct involvement of the CNS by HIV itself. HIV encephalopathy (HIVE) presents with a progressive dementia characterized by cognitive impairment and is later accompanied by motor symptoms such as gait disturbance and tremor. Collectively, the clinical syndrome is known as AIDS dementia complex [1]. Pathology reveals a subacute encephalitis; cerebral atrophy and demyelination ensue later [2].
Most affected patients develop cerebral atrophy, which may be the sole CT abnormality. Progression of disease results in the classical appearance of confluent, bilateral and symmetrical white matter lesions seen as diffuse white matter change in the periventricular regions and centrum semiovale, with relative sparing of the subcortical white matter and posterior fossa structures. They are hypodense on CT. MRI is more sensitive and shows the lesions to be of high T2 signal intensity and of isointense signal on T1 weighted (T1W) images. There is no enhancement or mass effect (Figure 1
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Figure 1. (a) Coronal T1 weighted and (b) axial T2 weighted images of a patient with HIV encephalopathy. The images demonstrate diffuse cerebral atrophy. In addition, confluent high T2 signal change is seen in the periventricular white matter of the frontal and parieto-occipital regions.
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Diffuse cytomegalovirus encephalitis
Cytomegalovirus (CMV) is a subtype of herpes virus that remains latent in most adults and may reactivate with AIDS. It is the most common opportunistic viral infection in these patients. Despite being a frequent finding at autopsy [3], ante-mortem diagnosis of diffuse CMV encephalitis is difficult, with both clinical and imaging findings mimicking those of HIVE. Patients with CMV have usually had a longer duration of AIDS, with lower CD4 counts (less than 200 cells mm-3), and have a more rapidly advancing dementia than is observed with HIVE. Survival times are significantly shorter, with death in 5–8 weeks [4]. The MRI characteristics of diffuse CMV encephalitis are identical to that of HIVE, i.e. diffuse high T2 signal white matter lesions without enhancement or mass effect. CT is also often normal or shows only atrophy. CMV takes other forms on imaging, and these are described below.
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Patchy white matter disease
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HIVE
A patchy distribution of white matter lesions can also occur, with the same signal characteristics as the diffuse form. Less common findings are basal ganglia lesions and small white matter lesions. FLAIR (fluid attenuated inversion recovery) sequences are useful for detecting the latter [5] and for distinguishing them from non-specific T2 hyperintensities predominantly caused by prominent perivascular spaces.
Progressive multifocal leucoencephalopathy
Progressive multifocal leucoencephalopathy (PML) is a rapidly progressive AIDS-defining disease of the CNS caused by the JC papovavirus. Up to 80% of the population have latent infection, and reactivation of the virus occurs when cell mediated immunity becomes impaired. The virus has selective tropism for oligodendrocytes, resulting in a progressive demyelinating disease. It affects approximately 8% of AIDS patients [6], usually leading to death within 6–9 months. Prior to the introduction of highly active anti-retroviral therapy (HAART), there were only a few reports of patients surviving longer than 1year [7]. However, recent studies have shown that HAART significantly prolongs the survival of patients with PML [8].
Typical imaging findings are of patchy areas of low T1 signal and high T2 signal in the subcortical white matter. Lesions are often bilateral and asymmetrical although despite the name of the condition it may be unifocal. The lesions exert no mass effect. A scalloped appearance occurs owing to involvement of arcuate fibres, which are the white matter fibres directly beneath the cortical grey matter that follow the gyral pattern. There is a parietal predominance; less common sites include the posterior fossa, basal ganglia and thalamus. Involvement of these central structures is due to contiguous spread along the white matter fibres that traverse them [6] (Figure 2).
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Figure 2. (a) Axial T2 weighted and (b) coronal T1 weighted images in a patient with progressive multifocal leucoencephalopathy. There is high T2 and low T1 signal white matter abnormality in the right frontal region that extends along the gyral core, with preservation of the grey matter. (c) Coronal T1 weighted image of the same patient shows the low T1 signal to extend along the white matter tracts, through theright internal capsule to the cerebral peduncle. Incidental note is made of agenesis of the corpus callosum.
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HIVE vs PML
Differentiation between HIVE and PML is important owing to the difference in prognosis between the two conditions. PCR assays that detect JC virus DNA in the CSF are highly sensitive and specific [9], and this has relieved the burden on radiologists somewhat. Nevertheless, a distinction based on MRI can be achieved in most cases; Table 1 highlights the key differences. A few studies have investigated the use of other imaging modalities, proton magnetic resonance spectroscopy (MRS) in particular. MRS provides an in vivo assessment of the metabolite content of a focal intracranial lesion. Differences in metabolite profiles between various lesions may permit a specific diagnosis to be made based on spectral analysis. HIVE characteristically shows high levels of myoinositol, a glial marker, and choline, a cell membrane marker, whilst N-acetyl-L-aspartate (NAA), a marker for neuronal integrity and quantity, is reduced [10, 11]. In PML, higher levels of choline and more variable levels of myoinositol in comparison with HIVE have been shown to occur [12], but studies on this subject are limited. A more substantial finding is that reduced levels of NAA occur early in HIVE before conventional MRI abnormalities have occurred, suggesting that MRS may be used forthe early detection of HIV-induced brain damage [13].
Herpes viral encephalitides
Herpes simplex virus produces a necrotizing encephalitis in the immunocompromised host that is more diffuse than the classic type, which has a predilection for the medial temporal and inferior frontal lobes. Poorly defined areas of oedema with scattered foci of haemorrhagic signal are seen on imaging. Varicella-zoster virus (VZV) also causes a multifocal encephalitis that predominantly affects the white matter. An enhancing margin may be seen at the edge of the lesion. Rapidly progressive cranial nerve palsies and retinitis are also features [14].
Non-specific white matter T2 hyperintensities
These small (sub 5 mm) foci of increased signal on T2 weighted (T2W) imaging may number up to five as an incidental finding, and there is no difference in incidence or number of foci between seropositive and seronegative groups. These lesions are thought to represent pathological partial demyelination, increased perivascularfluid and mild gliosis. Possible causes include prior inflammation/vasculitis, small congenital brain cysts, ventricular diverticula, drug abuse and arteriosclerosis as seen in elderly patients [14].
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Focal mass with enhancement
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Toxoplasmosis
Toxoplasmosis is the most frequent CNS infection in the AIDS population, occurring at CD4 counts below 100 cells mm-3. It is due to theobligate intracellular protozoan Toxoplasma gondii and it produces a benign or subclinical infection in the immunocompetent patient and a reactivation illness in the immunocompromised. CSF findings are non-specific and detection of T.gondii DNA by PCR has only moderate sensitivity [15]. CT and MRI typically reveal multiple enhancing lesions with perifocal oedema and mass effect in the basal ganglia and grey–white matter interface of the cerebral hemispheres (Figure 3). However, any part of the brain can be affected, and lesions are solitary in approximately 14% of cases. The lesions are hypodense or isodense on CT, and show ring or solid enhancement. MRI is more sensitive, and on T1W images lesions are hypointense. On T2W images, lesions may be isointense or hypointense to brain parenchyma, with surrounding hyperintense oedema, or may have a hyperintense centre with an isointense rim that enhances.
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Figure 3. Coronal T1 weighted enhanced images. (a) Ring enhancement in two lesions in the grey–white matter junction of the right cerebral hemisphere, and in a third in the region of the right basal ganglia. Each lesion shows associated local oedema with mass effect. (b) 3 weeks after anti-toxoplasma therapy, there has been resolution of the local mass effect. One lesion has disappeared. The lesion in the basal ganglia has shrunk and there is only a small residual focus of enhancement in the insular cortex.
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Lymphoma
Primary central nervous system lymphoma (PCNSL) is the second most common cause of an intracranial mass after toxoplasmosis, occurring in up to 6% of all AIDS patients. Histologically it is of the non-Hodgkin's B-cell type and it has a high mitotic rate: tumour volume may double in less than 14 days [16]. Epstein-Barr virus (EBV) expression is present in the majority of tumours, suggesting that this virus is implicated in the tumorigenesis [17]. CSF cytology is unhelpful; conversely, EBV in the DNA has a high sensitivity and specificity [15]. PCNSL is typically a solitary hyperdense mass on CT, reflecting its high cellular density. Multifocal lesions are seen in 50% of cases [18]. On MRI it is of hypointensity or isointensity on both T1W and T2W imaging, with additional high signal central areas of necrosis on T2W images. Enhancement patterns are variable and may be homogeneous, heterogeneous or ring-like (Figure 4). Haemorrhage or calcification is rarely encountered. Typical sites include the periventricular white matter, basal ganglia, corpus callosum and thalami. Periventricular spread of tumour that encases the ventricles is highly characteristic (Figure 5). Uncommon locations of PCNSL are more common in AIDS patients than in non-AIDS patients; the brain stem, cranial nerves, pineal gland and cavernous sinus are such examples.
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Figure 4. Coronal T1 weighted (a) pre-contrast and (b) post-contrast images of a patient with lymphoma. There is a solitary large mass in the left parietal region that abuts the meningeal surface, with associated nodular rim enhancement, mass effect and oedema.
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Figure 5. Coronal T1 weighted enhanced image demonstrating a subependymal lesion with an enhancing rim, partially effacing the frontal horn of the left lateral ventricle. There are further smaller foci of enhancement in the right head of caudate and left lentiform nucleus. The subependymal nature is very typical for lymphoma, which need not be solitary.
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Lymphoma vs toxoplasmosis
These are the two most common focallyenhancing intracranial masses. Distinguishing between them often poses a diagnostic challenge to the radiologist owing to their varied and similar appearances. However, a rapid and definitive diagnosis is essential since the untreated mean survival of PCNSL is only 3–4 months [19]. To compound the issue, treatment regimens for the two conditions are extreme: radiotherapy and steroids may improve survival in lymphoma, and life-long maintenance therapy is required in patients with toxoplasmosis to prevent relapse. The high sensitivity and specificity of PCR detection of EBV DNA in CSF has been highlighted; however, contraindication to lumbar puncture in such patients commonly precludes the use of this test. Thus, imaging plays a crucial role, and knowledge of the key differentiating features on MRI is essential in providing an accurate, albeit not definitive, diagnosis (see Table 2).
At most centres, the current clinical policy for AIDS patients with intracranial mass lesions is anempirical trial of anti-toxoplasmosis therapy, followed by repeat imaging in 14 days to assess for "imaging response". This is defined as a decrease in all the previously identified lesions. If lesions remain stable or increase in size, then brain biopsy is indicated [21]. There are, however, drawbacks to this approach. Addition of steroids to the treatment regimen in patients who deteriorate during the 2 weeks of trial therapy will render interpretation of follow-up images futile. Furthermore, brain biopsy is associated with significant morbidity and mortality [9], and sampling errors may occur [22]. Thus, there is a demand for alternative imaging modalities to help solve this dilemma, and these involve functional imaging techniques, i.e. SPECT (single photon emission CT), PET (positron emission tomography) and MRS.
There have been encouraging reports of the ability of thallium-201 (201Tl) SPECT to distinguish between toxoplasmosis and PCNSL [23]. 201Tl is a cyclotron-produced radionuclide with ahalf-life of 73 h that behaves as a potassium analogue in its distribution. The presence of a sodium–potassium analogue ATPase system in PCNSL therefore results in avid 201Tl uptake by the tumour. On the contrary, 201Tl concentration in infections and inflammatory foci is relatively low. This differentiating pattern of uptake becomes more marked on delayed scans (at 3–4 h). One study advocates the use of additional gallium scanning, which is an indicator of white cell activity in thallium-negative lesions. This maydifferentiate infections from other thallium-negative lesions such as PML and infarcts [24].
PET exploits the fact that lymphomas are more metabolically active than infections, and it has been shown to be accurate in differentiating between the two. However, O'Doherty et al [25] have highlighted the importance of performing the scan afterseveral days on anti-toxoplasmosis therapy toavoid false positive uptake in acute inflammatory toxoplasma lesions. The use of PET is further hindered by its cost and lack of availability.
Studies using MRS have shown that a diagnosis can be made on the basis of the different metabolite profiles of lymphoma and toxoplasmosis [26]. In lymphoma the choline peak is relatively elevated, whereas the NAA level is low. In abscesses, including toxoplasmosis, there is marked elevation of lipid and lactate, a marker for anaerobic metabolism, whilst both choline and NAA levels are low. However, there are pitfalls in that necrosis or haemorrhage within lymphomatous lesions will alter its spectral characteristics and thus resemble toxoplasmosis. Voxel malpositioning and lengthy scanning times are further problems that contribute to the relative underusage of this technique [27].
Cryptococcomas
Cryptococcus neoformans is the third most common infectious organism to involve the CNS, occurring in 5% of AIDS patients [28]. The fungus is acquired through inhalation and spreads haematogenously to the CNS. It initially colonizes the CSF and meninges, and subsequently forms gelatinous pseudocysts owing to the production of abundant mucoid material within the perivascular Virchow–Robin spaces. If the disease is allowed to fulminate, there is an eventual disruption of the blood–brain barrier and an intraparenchymal collection of inflammatory cells and organisms forms, the so-called crytococcoma [29]. This is seen as a solid or ring-enhancing parenchymal mass with variable surrounding oedema, located in close relation to the perivascular space. They may also arise within the choroid plexus [30], a feature that can lead to an obstructive hydrocephalus.
Mycobacterial infections
Tuberculosis (TB) can occur in the early stages of HIV disease and may be the first AIDS-defining illness. CNS involvement is seen in 10% of all patients with AIDS-related TB compared with 2–5% of all patients with TB [31]. Reactivation of latent disease is the major mechanism. Achest radiograph may provide significant supportive evidence if CNS TB is suspected on the basis of a neuroimaging study, since approximately two-thirds of patients with AIDS-related TB will have an abnormal chest radiograph [32]. Typical CSF findings do not always occur [33], and cultures for TB take up to 6–8 weeks. Therefore imaging plays an important role in diagnosis and the appearances take a variety of forms. Intraparenchymal tuberculomas (tuberculous granulomas) are seen as multiple lesions less than 1 cm that predominate at the grey–white matter interface and periventricular regions. They have little mass effect or oedema [34]. CT demonstrates the lesions poorly; ring-enhancing lesions may be seen. The target sign, although not pathognomic, is suggestive, and refers to central calcification or punctate enhancement surrounded by a region of hypodensity with rim enhancement [35]. On T1W images the lesions are isointense to grey matter and may have a hyperintense rim. On T2W images the appearances correlate with the evolutive phase of the granuloma. Early non-caseating granulomas show T2 hyperintensity and nodular enhancement with subsequent caseastion resulting in T2 hypointensity and rim enhancement. An additional central hyperintensity may occur owing to more central liquefactive necrosis [36]. Healed tuberculomas may calcify or may progress to focal areas of encephalomalacia. Tuberculous abscesses are larger, with appearances similar to that of bacterial abscesses. They are solitary loculated masses with mass effect and oedema, and show ring enhancement that is usually thin and uniform. They are hypodense on CT and of high T2 signal on MRI.
There are isolated reports in the literature of atypical mycobacteria involving the CNS in AIDS patients, but these reports have not concentrated on the radiographic features. Autopsy studies have revealed small aggregates of cells containing the organism in a perivascular location. Granuloma formation is poorly formed or absent [37, 38]. In a case of microbiologically proven Mycobacterium avium intracellulare (MAI) infection of the brain from our institution, MRI showed multiple nodular or rim enhancing lesions with signal characterisics not dissimilar to that of tuberculomas. More pathological correlates are required to establish whether well formed granulomata do occur with CNS MAI infection.
Cytomegalovirus
CMV encephalitis can rarely give rise to a lesion with central mass and ring enhancment, which may be difficult to differentiate from lymphoma [39].
Neurosyphilis
HIV-induced cell mediated immunity causes a rapid progression and wider degree of dissemination of this spirochete infection compared with that seen in immunocompetent patients. CNS involvement is encountered in the secondary andtertiary stages and takes several forms. This includes the presence of durally based, well circumscribed masses or gummas that extend into the cortex with variable oedema. They are hypodense on CT, hypointense to isointense on T1W MRI and hyperintense on T2W sequences, usually with uniform enhancement. However, gummas are relatively rare and diffuse meningeal disease is a more frequent manifestation [40].
Bacterial and other fungal abscesses
Preservation of humoral immunity in AIDS accounts for the paucity of pyogenic CNS infections in these patients. Whilst they are rare in immunocompetent patients, and moderately rare in HIV-positive patients, they become significant when the more common pathogens are excluded, as they have the potential to be treated with routine antibiotics. Imaging features of bacterial abscesses are not unusual, but the organisms that cause them are. These include Nocardia, Rhodococcus equi and Bartonella henselae [41].
Aside from Cryptococcus, fungal infections such as Aspergillus are relatively rare, but may be an unusual cause of a focally enhancing mass.
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Focal mass without enhancement
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Pseudocysts and cryptococcomas
The cryptococcal organism produces abundant mucoid material within the subarachnoid space. Extension of this material alongside the perforating arteries causes enlargement of the perivascular Virchow–Robin spaces, giving rise to gelatinous pseudocysts or "soap bubbles". They are seen as low density foci on CT. They are less than 3 mm in size and follow the expected location of the Virchow–Robin spaces. This includes the basal ganglia, thalami, substantia nigra and periventricular regions. They are more easily visualized on MRI, where their signal intensity is similar to that of CSF, although it is slightly higher on T1W images owing to its proteinaceous content [42]. They have mass effect, but associated oedema is rare, and the lesions do not enhance because the blood–brain barrier is not disrupted (Figure 6). It should be noted that generalized atrophy could give an identical appearance of dilated perivascular spaces; thus, the diagnosis of cryptococcosis in such cases should be made with caution [43]. Finally, the larger intraparenchymal cryptococcomas do not always enhance.
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Figure 6. (a) Axial T2 weighted and (b) coronal T1 weighted enhanced images of a patient with cryptococcosis. The images demonstrate enlargement of the perivascular spaces in the basal ganglia. These are expanded by jelly-like hyphal material and do not enhance.
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Toxoplasmosis and atypical PCNSL
Enhancement and rim formation of toxoplasma lesions may be thinner, subtle or absent in patients with severely depressed cell mediated immunity. Similarly, in PCNSL, enhancement of lesions may be variable or absent. Of particular concern is the follow-up study, since administration of corticosteroid therapy may recover the integrity of the blood–brain barrier. This can falsely lead to the impression that a lesion has responded to anti-toxoplasma therapy.
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Focal lesion: no mass with enhancement
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Toxoplasmosis
The appearance of a discrete toxoplasma cerebritis may occur before an abscess wall is poorly formed owing to poor host responses.
Cerebral infarction
Gyral enhancement due to luxury perfusion can give rise to these appearances. Cerebrovascular disease is discussed in detail below.
Viral encephalitides
Gyral enhancement can occur in poorly defined regions of oedema.
Bacterial cerebritis
The initial manifestation of bacterial infection is of a cerebritis, seen as an area of oedema with poorly defined contrast enhancement. A wall eventually forms to produce an abscess. In clinical practice, however, it is extremely rare to demonstrate the disease process at this early stage.
PML
Lack of contrast enhancement is the rule, although there are an increasing number of reports describing faint peripheral enhancement of these white matter lesions. This may represent an immune reconstitution response to the JC virus[44].
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Focal lesion: no mass without enhancement
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In this context, unifocal PML and a diffuse infiltrative form of PCNSL both need to be considered. In the former, a lower T1 signal will be seen with absolutely no mass effect. In the latter, careful scrutiny is likely to identify some subtle effacement of the sulci, or minor ventricular compression.
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Meningitis/meningeal disease
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HIV meningoencephalitis
In pathological terms a meningoencephalitis may occur at seroconversion as well as at the later stages of HIV infection. This may be one of themost common CNS features of HIV infection represented clinically by a mild headache. Imaging reveals no meningeal abnormality and the diagnosis is made from CSF analysis.
Cryptococcosis
The fungus initially colonizes the CSF and meninges, producing a granulomatous meningitis. However, imaging rarely reveals any meningeal abnormality [45] (Figure 7).
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Figure 7. Coronal T1 weighted enhanced image demonstrating widespread meningeal enhancement in a patient with cryptococcal meningitis.
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Mycobacterial infection
A basal meningitis is the most frequent form of infection and is seen as leptomeningeal thickening and enhancement predominantly involving the basal cisterns, prepontine and ambient cisterns and suprasellar areas [46]. Communicating hydrocephalus is a common sequela and is due to associated convexity involvement.
Neurosyphilis
Diffuse or focal meningeal enhancement may be seen, but commonly there is no abnormality.
Metastatic systemic lymphoma
Meningeal involvement is typical of metastatic non-Hodgkin's lymphoma, resulting in leptomeningeal thickening and enhancement (Figure 8).
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Figure 8. Coronal T1 weighted enhanced image demonstrating an enhancing meningeal plaque and multiple meningeal nodules of secondary CNS lymphoma.
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Ventriculitis
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CMV and other herpes viruses
A necrotizing ventriculoencephalitis occurs in CMV infection, and MRI may reveal irregular T2 hyperintense periventricular bands that are of low T1 signal, with associated subependymal enhancement [4]. These features are also seen in advanced herpes zoster, and less commonly with the other herpes viruses [47].
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Cerebrovasular disease
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Several factors contribute to the increased frequency of cerebrovascular events in HIV patients compared with age- and sex-matched controls. Autopsy studies have shown that much of the disease is clinically silent [48]. Although infarction is not a common component of infection, it is well known to occur with TB or cryptococcal meningitis or neurosyphilis. In TB meningitis, cerebral infarcts occur from arteritis, vasospasm and thrombosis of the small perforating arteries that have origins at the base of the brain and course through the gelatinous leptomeningeal exudates. Neurosyphilis results in large and small vessel vasculitis, and cerebral vasculitis also occurs with toxoplasmosis, CMV and VZV infection. The increased prevalence of cocaine and intravenous drug abuse in this patient cohort is also contributory, resulting in vasospasm, vasculitis and endocarditis. In addition, there is increasing evidence of a primary HIV vasculopathy occurring in patients without concomitant opportunistic infection or drug abuse [49].
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Diseases of the spine
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There is a relative paucity of radiological literature on this topic, since imaging is relatively insensitive to the disease processes found. The incidence of myelopathy may be as high as 20% according to autopsy series [50]. Abnormalities may be due to infection by HIV itself, resulting in a vacuolar myelopathy or a myelitis. The former resembles subacute combined degeneration of the cord and appears as symmetrical and diffuse increased T2 signal of the white matter tracts. A myelitis may cause grey matter abnormalities that are focal and asymmetrical, and is associated with HIVE [51]. CMV produces a necrotizing myelitis and subacute polyradiculitis, presenting clinically with radicular pain, paraparesis and urinary retention. Other opportunistic infections are rarely reported and include TB, herpes viruses, neurosyphilis and toxoplasmosis. Lymphoma can metastasize to the epidural spaces, infiltrate the leptomeningeal spaces and nerve roots, and spread secondarily to the spinal cord.
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Conclusion
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The variety of neuroimaging abnormalities encountered in AIDS is complex. The coexistence of multiple pathologies that have been described to occur in up to 30% of autopsy cases [52, 53] complicates matters further. In addition, whilst there is a tendency to assume that abnormal MRI brain findings are solely attributed to the patient's immunocompromised state, one should not overlook the fact that the incidence of primary and secondary neoplastic disease is the same as that of the age-matched population. Thus, there is a constant demand for novel imaging strategies, and it is likely that the functional imaging modalities will play an increasingly important role as their availability increases.
The introduction of HAART has transformed the prognosis of HIV infection [54], and the incidence of both PCNSL [55] and opportunistic infections [54] has been falling since its introduction in 1996. Furthermore, patients with HIVE and PML have shown evidence of disease regression [8, 56]. However, despite anti-retroviral therapy, diseases of the CNS remain a dominant cause of morbidity and mortality in AIDS patients.
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Summary
Introduction
