Printer Friendly

Neuroimaging of CNS involvement in HIV.


Central nervous system (CNS) involvement in HIV infection has a significant associated morbidity and mortality if not recognised early. One-third of AIDS-defining illnesses involve the CNS and 40% of patients with HIV suffer from neurological symptoms [1]. Neuroimaging is crucial in these patients, where characteristic imaging features not only enable detection, diagnosis and initiation of treatment but are also used to verify treatment response and to guide brain biopsy.

Since the introduction of highly active antiretroviral therapy (HAART), HIV/AIDS has become a chronic disorder with marked reductions in mortality and morbidity, not only from the virus itself but also from opportunistic infections and tumours. However, HAART has led to a number of complications not previously seen in HIV medicine, and including immune reconstitution syndrome (IRIS) [2].

In this review we describe the major imaging findings of CNS involvement in HIV-infected patients. For the purposes of the review, conditions of the CNS in HIV-positive patients are subdivided into the following categories:

* Direct effects of HIV;

* Opportunistic infections in the immunocompromised host;

* CNS tumours;

* Cerebrovascular complications;

* Effects of treatment with HAART.

There are often multiple coexisting pathologies (or layers) in the CNS [3] where treatment may not produce the expected clinical benefit. In addition, unmasking of a subclinical condition by a new insult is often seen. For example, subclinical HIV encephalopathy may be unmasked by cryptococcal infection such that the patient develops symptoms of HIV encephalopathy rather than cryptococcal symptoms [3].

Direct effects of HIV

At seroconversion, up to 70% of HIV-infected individuals can have a symptomatic glandular fever-like syndrome, which in 10% of these cases is associated with neurological symptoms and signs such as aseptic meningitis, encephalitis, acute disseminated encephalomyelitis, transverse myelitis, polymyositis, brachial neuritis or a cauda equine syndrome [4].

HIV encephalopathy is part of the acute HIV syndrome during seroconversion whereas AIDS dementia complex, also known as HIV-associated dementia complex, is characterised by cognitive, motor and behavioural features in advanced AIDS when the CD4 lymphocyte count falls below 200 cells/[mm.sup.3]. In the post-HAART era, the incidence of HIV dementia has fallen from 21 cases per 1000 person-years to 10.5 cases per 1000 person-years in the USA and a less severe dysfunction, minor cognitive motor disorder, has become more common [5].

The virus can affect all cell types in the brain, causing glial and neuronal degeneration, and is found most commonly in the white matter, especially the deep white matter of the centrum semiovale [6], followed by the subcortical grey matter and much less commonly in the cortical grey matter.

Imaging studies can support the diagnosis of AIDS dementia complex and can exclude other neurological opportunistic infections or neoplasms. The most common finding is diffuse cortical atrophy, often occurring before there are clinical symptoms [7]. However, even in severe HIV infection, atrophy is often not seen [8,9]. T2-weighted magnetic resonance sequences demonstrate hyperintense white matter lesions in a periventricular distribution with particular involvement of the centrum semiovale (Figure 1) [8]. In the early stages, the lesions tend to be patchy and can be very subtle with ill-defined borders. As the disease progresses they become more diffuse and can involve large areas of the cerebral white matter, thereby mimicking advanced stages of multiple sclerosis or small vessel ischaemic disease [10]. Infection of the brain with cytomegalovirus (CMV) can produce a pattern indistinguishable from the above.

Recent advances in neuroimaging techniques have enabled detection of selective patterns of brain deficits in HIV-infected patients with cognitive impairment. Diffusion abnormalities in the splenium of the corpus callosum in patients infected with HIV correlate with dementia severity and deficits in motor speed [11]. High-resolution imaging has revealed decreased cortical grey matter thickness of 15% in primary sensory,motor and premotor cortices in patients with AIDS [12], which in another study correlated with cognitive impairment and the CD4 T-lymphocyte depletion [13]. Recently, decreases in caudate blood flow and volume have been shown to be significantly associated with increasing HIV-associated neurocognitive impairment [14].

Opportunistic infections in the immunocompromised host


Toxoplasmosis is the most common opportunistic central nervous system (CNS) infection and the most common cause of a space-occupying lesion in AIDS patients [15]. Approximately 30% of HIV-positive people will develop toxoplasmosis encephalitis at some point in the illness [16], usually from reactivation of latent infection.

Toxoplasmosis produces necrotising encephalitis. Lesions are usually multiple and bilateral but may be solitary. They are found within the brain parenchyma, spreading to the meninges, but widespread meningitis is rare. Lesions are typically supratentorial, mainly at the corticomedullary junction (as a result of haematogenous spread), the basal ganglia or the thalamus. Infratentorial (especially cerebellar) lesions are also seen [17].

Non-enhanced CT demonstrates rounded masses that are isodense to grey matter with oedema and mass effect. Occasionally these masses are hyperdense due to haemorrhagic necrosis [1]. The lesions may show nodular homogeneous enhancement or ring enhancement, unless the patient has a very low cellular immunity in which case there may be no enhancement (CD4 cell count <50 cells/[mm.sup.3]) [3]. Treated toxoplasmosis results in encephalomalacia or calcified glial scars [18].



MRI is more sensitive than CT in detecting toxoplasmosis lesions. On T1-weighted sequences the lesions are hypo- or isointense to grey matter and on T2-weighted sequences they are hyper- or isointense to grey matter (Figure 2a). Early in therapy the lesions tend to be hyperintense in T2-weighted sequences due to necrosis, becoming isointense after many weeks of treatment. Contrast enhancement is seen in the majority (Figure 2b) although ring enhancement may be minimal and ill defined if the CD4 cell count is low. It is very rare to detect no abnormality on MRI. There is usually surrounding vasogenic oedema and satellite lesions may also be present [1].

Ventricular enlargement is often associated with CNS toxoplasmosis and this may be due either to atrophy or hydrocephalus (communicating or non-communicating) [6]. Rare manifestations include toxoplasmosis myelitis but there are usually coexistent brain lesions. The spinal cord demonstrates homogeneous contrast enhancement [19,20].

The main differential of toxoplasmosis is primary CNS lymphoma (PCNSL), which is more likely if the lesions are located in the basal ganglia or if there is subependymal spread of periventricular lesions. PCNSL may show variable enhancement (especially ring enhancement) and microhaemorrhage [6].

Magnetic resonance spectroscopy can aid in the diagnosis, with toxoplasmosis demonstrating an increase in the lipid and lactate peaks and a decrease in other metabolites. PCNSL demonstrates a marked increase in the choline peak as it is the more cellular of the two [21]. Diffusion-weighted imaging (DWI) may also help in the differential diagnosis of cerebral toxoplasmosis: there is more restriction of water diffusion in the core of a pyogenic abscess than in a toxoplasmosis lesion [22] and there are significantly higher apparent diffusion coefficient values in toxoplasmosis lesions than in PCNSL [23]. In spite of all these imaging differences, assessment of response to empiric therapy may be the only way to diagnose a toxoplasmosis lesion definitively.

Thallium single-photon emission computed tomography (SPECT) and 2-fluoro-deoxy-D-glucose positron emission tomography (FDG-PET) may also aid in differentiating the two conditions: more uptake of tracer is seen in lymphoma as this is a more metabolically active condition than toxoplasmosis [24].

Tuberculosis (TB)

Ten percent of patients with AIDS-related TB have CNS involvement, a much higher rate than is seen in the immunocompetent host [25]. CNS TB involvement may be due to reactivation of previous infection or primary infection, and may be the initial presenting feature of HIV infection; it has a high mortality of 79% [26]. Haematogenous spread occurs to the brain parenchyma or leptomeninges and can result in meningitis, abscess or granuloma formation and infarction [27].

TB meningitis

Thick leptomeningeal exudates form, especially in the basal portions of the brain, obliterating the basal cisterns and leading to marked communicating hydrocephalus. The thick gelatinous exudate may cause an arteritis of the vessels in the basal subarachnoid space causing infarctions of the basal ganglia and inferior frontal lobes [28,29].

On contrast-enhanced CT there is diffuse enhancement of the basal subarachnoid cisterns and occasionally of the tentorium and sylvian fissures, but contrast-enhanced MRI is more sensitive in detecting leptomeningeal enhancement [28]. One of the important differentials for this nodular pattern of enhancement is neurosarcoidosis [30].


Tuberculomas tend not to be isolated findings but rather to be associated with TB meningitis. They are found at the corticomedullary junction and in periventricular and pericisternal distributions, predominantly in the supratentorium. They may also be found in the subarachnoid, subdural and epidural space [27]. Tuberculomas may be solitary or multiple but are generally smaller than 1 cm in diameter with little mass effect or oedema.

Nodular enhancement is seen on CT. Early tuberculomas are hypodense on CT and show little enhancement. On MRI, early lesions are hypo- or isointense on T1-weighted sequences and on T2-weighted sequences have a hypointense rim (fibrin) with a hyperintense centre (liquefaction). MRI signal characteristics alone may not differentiate tuberculomas from pyogenic abscesses [26] although significant oedema/mass effect favours the latter. Treated lesions are calcified on CT.

TB abscesses

TB abscesses are much more common in HIV-positive patients than in HIV-negative patients. Solid caseation, as seen in tuberculomas, is not a feature but semi-liquid pus packed with bacilli is typical. TB abscesses are larger (commonly more than 3 cm in diameter) and have a more accelerated clinical course than tuberculomas. They may be multilocular and tend to be solitary. Mass effect and ring enhancement are common and imaging features are very similar to those of a pyogenic abscess (Figure 3a, b) [26].

Cerebral infarction/vasculitis

This results from spasm and thrombosis of the perforating vessels as they course through the gelatinous exudates in the basal cisterns to supply the basal ganglia. Large vessel territories such as the middle cerebral artery territory may also be affected. Imaging findings are those of acute infarction.

TB of the spine

This may result in epidural or paraspinal abscess formation, intra- or extramedullary tuberculomas, spondylitis or arachnoiditis [31]. MRI findings include destruction of the anterior aspect of one or more vertebral bodies, with narrowed intervertebral disc spaces. T2-weighted hyperintensity in the bone marrow, intervertebral discs and paraspinal soft tissue is seen as are leptomeningeal, nerve root and ring enhancement [32,33].

Differential diagnosis

Radiological differentials include syphilis, toxoplasmosis and necrotic lymphoma. An important differential diagnosis of meningeal disease and infarction is syphilis, but it is usually possible to differentiate the two by taking into account chest X-ray findings as well as serum and cerebrospinal fluid studies. Toxoplasmosis lesions do not tend to be multilocular and although necrotic PCNSL can be multilocular and show meningeal enhancement, communicating hydrocephalus and basal ganglia infarction are not usually features.


Cryptococcus is the most common fungal intracranial infection in AIDS. Overall survival has significantly improved in the era of HAART [34]. Cryptococcal infection may result in basal meningitis or in the formation of cryptococcomas (gelatinous pseudocysts) that are located in the perivascular spaces. They appear as non-enhancing small perivascular hypodensities on CT and as hyperintense foci on T2-weighted magnetic resonance sequences [35]. Direct fungal invasion of the brain results in cryptococcomas that are associated with a granulomatous reaction. Cryptococcomas have the appearance of small nodular or ring-enhancing parenchymal lesions, indistinguishable from other granulomatous infections. A recent multicentre study of cryptococcal meningoencephalitis found MRI to be abnormal in 92% of cases, whereas CT was positive in only 53%. The commonest MRI findings were dilated perivascular spaces; other findings included pseudocysts, parenchymal mass lesions and meningeal enhancement (Figure 4a). The latter is relatively rare, as cryptococcal infections do not evoke much of an inflammatory meningeal response. Meningeal enhancement may, however, occur in the context of IRIS (Figure 4b) [36]. An arachnoiditis may occur in the spine and is usually found with coexisting cranial meningitis.


Cytomegalovirus (CMV)

CNS CMV results from reactivation of latent infection. It infects endothelial cells and spreads haematogenously. It may present with encephalitis, meningitis, ventriculitis and small infarcts. Rarely, a necrotising ventriculoencephalitis may be seen. It may also present with myelitis or an inflammatory polyradiculitis of the spinal nerve roots or cranial nerves [37].

Toxoplasmosis or cryptococcosis frequently coexists with CMV infection [38]. It is difficult to diagnose on CT with poor correlation between autopsy histology findings and imaging findings. Findings include diffuse white matter hypodensity, subependymal contrast enhancement and focal enhancing lesions (ring or nodule) [38].

On MRI, CMV lesions are hyperintense on T2-weighted imaging. On T1-weighted gadolinium-enhanced images, ependymal and subependymal contrast enhancement is seen in CMV ventriculitis. FLAIR MR images may demonstrate a very striking high signal intensity rim outlining the ventricles, giving the appearance of owl's eyes [39]. Diffuse enhancement of the spinal cord parenchyma, nerve roots and meninges may also be seen [40].

Progressive multifocal leukoencephalopathy (PML)

PML results from reactivation of Jamestown Canyon virus (JC virus, JCV), infecting oligodendrocytes causing demyelination and gliosis [41]. Eighty-five percent of cases now occur in HIV-positive individuals [42]. In the post-HAART era, although the incidence of most neurological complications has declined, it is not clear whether the same is true for PML and in a number of patients it is temporally associated with immune reconstitution [43,44].

The white matter lesions are initially predominantly in the occipital, parietal and frontal lobes, later spreading to the deep white matter. The cortical grey matter, however, is usually spared [45]. The lesions are usually supratentorial but in 10% of cases may be infratentorial [46].


There may be large confluent areas of white matter demyelination with direct extension into the adjacent grey matter in advanced cases. PML may be distinguished from toxoplasmosis and PCNSL due to the lack of mass effect with the patients experiencing no symptoms or signs of raised intracranial pressure. Very rarely PML may be seen in the spinal cord [46].

Magnetic resonance is much more sensitive than CT in detecting PML. Large single or multiple lesions involving the white matter are normally seen, with the parieto-occipital and frontal white matter most commonly affected. The lesions are hypointense to white matter on T1-weighted sequences, and are hyperintense to the surrounding white matter on T2-weighted and FLAIR sequences (Figure 5). There may be focal areas of haemorrhage with T1 shortening and T2 prolongation. Scalloping may be seen at the grey--white matter interface due to involvement of arcuate fibres. No contrast enhancement or mass effect are usually seen [47].

HIV encephalitis is a differential of PML: the abnormalities are less symmetric and more discrete in PML. Furthermore, on T1 sequences, the low signal lesions of PML are much more obvious than the HIV encephalitis lesions [42]. Contrast enhancement or mass effect are normally absent in PML but may occur in the context of an immune reaction following treatment with HAART [48]. Otherwise, mass effect and enhancement in a patient with known PML should alert to a coexistent process such as toxoplasmosis [49].

DWI has recently proved very helpful in characterising PML lesions. Henderson et al. first described the appearance of a high signal intensity 'leading edge', and low signal centre on the diffusion-weighted images (Figure 5b) [50]. Histopathological correlation showed enlarged extracellular spaces with sparse oligodendrocytes and macrophages in the lesion centre and loss of myelin, numerous macrophages, and oligodendrocytes with intramuscular inclusions at the lesion periphery.

In a recent report, Kuker et al. investigated DWI and MR contrast enhancement to assess response of PML to therapy. They found that areas of restricted diffusion correlated with disease progression. Contrast enhancement was found to herald clinical remission with virus elimination from the cerebrospinal fluid indicating an inflammatory response and immunological virus elimination [51]. In another report, PML lesions on DWI were characterised by a central core of DWI low signal and increased mean diffusivity, surrounded by a rim of DWI hyperintensity and decreased mean diffusivity [52]. A larger central core component correlated with worsened clinical status and longer disease duration. In addition, high b value DWI provides superior definition of the leading edge of the lesion with additional information on the integrity of the white matter tracts [53].


Treponema pallidum results mainly in a small vessel endarteritis but can also affect the medium and large arteries. The perforator vessels are typically affected, resulting in basal ganglia or brainstem infarcts. Gummas are rarely found in the cortical grey matter: these are isodense to grey matter on NECT and enhance avidly post contrast. Similarly, they are isointense on T1-weighted sequences, showing avid contrast enhancement and are hyperintense on T2-weighted sequences. Cranial nerve involvement may also be seen [4].


Other viral and bacterial infections

HIV-positive patients may develop any of the viral or bacterial infections to which the immunocompetent individuals are susceptible, including HSV and staphylococcal and streptococcal infections with identical imaging appearances [4].

CNS tumours

Primary CNS lymphoma is the commonest neoplasm in HIV/AIDS but neoplasms of glial or metastatic origin have to be considered in the differential diagnosis of a cerebral mass lesion.

Primary CNS Lymphoma (PCNSL)

PCNSL is the second most common cause of CNS space-occupying lesions in HIV after toxoplasmosis, and is also the main differential for toxoplasmosis as discussed earlier [54]. Primary CNS lymphoma is much more common than secondary CNS lymphoma in the HIV-positive population and tends to be of the non-Hodgkin's B-cell type [55].

PCNSL in HIV-positive patients tends to occur in a younger age group. It is more likely to be multifocal and more commonly shows central necrosis. It occurs mainly in the periventricular white matter, basal ganglia, corpus callosum and cortex, and is occasionally subependymal or even wholly intraventricular [56]. Ring enhancement is more common in HIV-positive patients,whereas homogeneous enhancement is more common in HIV-negative patients.

MRI demonstrates lesions that are hypointense on T1-weighted sequences and hyperintense on T2-weighted sequences with typical ring enhancement (Figure 6), although it may also be homogeneous. Subependymal spread, periventricular location, extension across the corpus callosum and size over 4 cm are more typical of PCNSL than toxoplasmosis. Lack of grey matter involvement also favours lymphoma. Multiple lesions, basal ganglia location and haemorrhage favour toxoplasmosis [6, 57].

If lymphomas are found in the spine, this is more likely to be the result of spread from an extra-CNS site [58] and may occur in any of the compartments of the spine and vertebral column, especially in the bone marrow from where it may extend into the epidural space. Lymphomatous meningitis may also occur in the spine. Spinal lymphoma is of low or intermediate signal intensity on T2-weighted images [59] and has similar T1 signal and enhancement patterns to intracranial lymphoma [6].

Glial tumours

Non-lymphomatous brain tumours are not AIDS-defining diseases, but there is increasing evidence that HIV might have an oncogenic influence on glial cells [60, 61]. The incidence of glial neoplasm in a biopsy series of AIDS patients with cerebral mass lesions has been reported to be as high as 6%, with an approximately equal split between high- and low-grade glial tumours (Figure 7) [60].


It is important to also consider metastatic deposits in the differential diagnosis of a CNS space-occupying lesion, particularly from Kaposi's sarcoma.

Cerebrovascular complications

Cerebral infarction in patients with HIV infection can be frequent, affecting up to 18% of patients (Figure 8) [62]. The pathogenesis is multifactorial with concomitant cerebral infections, cocaine use and intravenous drug abuse all contributing. Inflammatory vasculopathies can occur as a result of the HIV infection itself or due to concomitant infection with varicella zoster virus (VZV). Although VZV infection in HIV is typically manifested by encephalitis, myelitis and meningitis [63], cerebral angiopathy with aneurysm formation on a background of lymphocytic meningitis may be seen [64]. Contrast-enhanced T1-weighted imaging of the affected vessel may show aneurysmal dilatation with thickening and contrast enhancement of the vessel wall [65] and cerebral angiography may demonstrate focal stenoses and aneurysmal dilatation. Rarely, an occlusive vasculopathy similar to moyamoya disease may occur [66].

Effects of treatment with HAART

The effects of HAART in reducing opportunistic infections in HIV-positive patients are well known. HAART also prolongs the survival of HIV-positive individuals affected by PML. A recent study demonstrated a favourable clinical outcome in patients with stable or improved MRI findings within 6 months [67]. Diffusion-weighted imaging may show reversal of white matter tract disruption by PML after HAART [53].





IRIS, the paradoxical deterioration in health as immune function improves with treatment, is linked with a rapid rise in CD4 cell count, and patients who are antiretroviral treatment-naive are more at risk of developing the syndrome. The immune system may react to different antigens present in the brain, and clinical manifestations vary. Symptoms may improve following steroid treatment and modification of antiretroviral therapy. IRIS has been reported as deterioration of cryptococcal infections (Figure 4b) and PML following commencement on HAART (Figure 9) [36, 68].

IRIS may also be responsible for a progressive demyelinating leukoencephalopathy in patients on HAART, frequently associated with cognitive decline [36]. MRI shows non-enhancing areas and often confluent regions of T2 hyperintensity that progress. This diagnosis should be considered, particularly in patients in whom JC virus in the cerebrospinal fluid is negative. The diagnosis, radiological manifestations and treatment of IRIS are certainly a major challenge in the HAART era.


A wide range of central nervous system pathologies can be seen in HIV-positive patients. Neuroimaging is essential in accurate diagnosis and in treatment follow-up. Imaging techniques may range from basic CT to functional MR and nuclear medicine techniques.


[1.] Offiah CE, Turnbull IW. The imaging appearances of intracranial CNS infections in adult HIV and AIDS patients. Clin Radiol, 2006, 61, 393-401.

[2.] Dhasmana DJ, Dheda K, Ravn P et al. Immune reconstitution inflammatory syndrome in HIV-infected patients receiving antiretroviral therapy: pathogenesis, clinical manifestations and management. Drugs, 2008, 78, 191-208.

[3.] Brew BJ. HIV Neurology. Contemporary Neurology series. Oxford: Oxford University Press, 2001.

[4.] Manji H, Miller R. The neurology of HIV infection. J Neurol Neurosurg Psychiatr, 2004, 75, 29-35.

[5.] Dore GJ, McDonald A, Li Y et al. Marked improvement in survival

following AIDS dementia complex in the era of highly active retroviral therapy. AIDS, 2003, 17, 1539-1545.

[6.] Provenzale JM, Jinkins JR. Brain and spine imaging findings in AIDS patients. Radiol Clin North Am, 1997, 35, 1127-1166.

[7.] Korbo L, Praestholm J, Skot J. Early brain atrophy in HIV infection: a radiological-stereological study. Neuroradiology, 2002, 44, 308-313.

[8.] Chrysikopolous HS, Press GA, Grafe MR et al. Encephalitis caused by human immunodeficiency virus: CT and MR imaging manifestations with clinical and pathological correlation. Radiology, 1990, 175, 185-191.

[9.] Grafe MR, Pres GA, Berthothy DP et al. Abnormalities of the brain in AIDS patients: correlation of post mortem MR findings with neuropathology. Am J Neuroradiol, 1990, 11, 905-911.

[10.] Levy RM, Rothholtz V. HIV-1 related neurologic disorders. Neuroimaging Clin N Am, 1997, 7, 527-559.

[11.] Wu Y, Storey P, Cohen BA et al. Diffusion alterations in corpus callosum of patients with HIV. Am J Neuroradiol, 2006, 27, 656-660.

[12.] Thompson PM, Dutton RA, Hayashi KM et al. Thinning of the cerebral cortex visualized in HIV/AIDS reflects CD4+ T lymphocyte decline. Proc Natl Acad Sci U S A, 2005, 102, 15647-15652.

[13.] Chiang MC, Dutton RA, Hayashi KM et al. 3D pattern of brain atrophy in HIV/AIDS visualized using tensor-based morphometry. Neuroimage, 2007, 34, 44-60.

[14.] Ances BM, Roc AC, Wang J et al. Caudate blood flow and volume are reduced in HIV+ neurocognitively impaired patients. Neurology, 2006, 66, 862-866.

[15.] Levy RM, Pons VG, Rosenblum ML. Central nervous system mass lesions in acquired immunodeficiency syndrome. J Neurosurg, 1984, 61, 9-16.

[16.] Grant IH, Gold JWM, Roseblum et al. Toxoplasma gondii serology in HIV-infected patients: the development of central nervous system toxoplasmosis in AIDS. AIDS, 1990, 4, 519-521.

[17.] Dina TS. Primary central nervous system lymphoma vs toxoplasmosis in AIDS. Radiology, 1991, 179, 823-828.

[18.] Moeller AA, Backmund HC. HIV-Infektion und Nervensystem. Stuttgart, Thieme, 1991.

[19.] Resnick DK, Comey CH, Welch WC et al. Isolated toxoplasmosis of the thoracic spinal cord in a patient with acquired immunodeficiency syndrome. J Neurosurg, 1995, 82, 493-496.

[20.] Vyas R, Ebright JR. Toxoplasmosis of the spinal cord in a patient with AIDS: case report and review. Clin Infect Dis, 1996, 23, 1061-1065.

[21.] Kastrup O, Wanke I, Maschkle M. Neuroimaging of infections. Neurorx, 2005, 2, 324-332.

[22.] Chong-Han CH, Cortez SC, Tung GA. Diffusion-weighted MRI of cerebral toxoplasmosis abscess. Am J Roentgenol, 2003, 18, 1711-1714.

[23.] Camacho DL, Smith JK, Castillo M. Differentiation of toxoplasmosis and lymphoma in AIDS patients using apparent diffusion coefficients. Am J Neuroradiol, 2003, 24, 633-637.

[24.] Ruiz A, Ganz WI, Post MJ et al. Use of thallium-201 brain SPECT to differentiate cerebral lymphoma from toxoplasma encephalitis in AIDS patients. Am J Neuroradiol, 1994, 15, 1885-1894.

[25.] Berenguer J, Moreno S, Laguna F et al. Tuberculous meningitis in patients infected with the human immunodeficiency virus. N Engl J Med, 1992, 326, 668-672.

[26.] Whiteman M, Espinoza L, Post MJD et al. Central nervous system tuberculosis in HIV-infected patients: clinical and radiographic findings. Am J Neuroradiol, 1995, 16, 1319-1327.

[27.] Villoria MF, de la Torre J, Fortea F et al. Intracranial tuberculosis in AIDS: CT and MRI findings. Neuroradiology, 1992, 34, 11-14.

[28.] Villoria MF, Fortea F, Moreno S et al. MR imaging and CT of central nervous system tuberculosis in patients with AIDS. Radiol Clin North Am, 1995, 4, 805-820.

[29.] Bernaerts A, Vanhoenacker FM, Parizel PM et al. Tuberculosis of the central nervous system: overview of neuroradiological findings. Eur Radiol, 2003, 13, 1876-1890.

[30.] Cortez K, Kottilil S, Mermel LA. Intracerebral tuberculoma misdiagnosed as neurosarcoidosis. South Med J, 2003, 96, 494-496.

[31.] Shanley DJ. Tuberculosis of the spine: imaging features. Am J Roentgenol, 1995, 164, 659-664.

[32.] De Backer AI, Mortele KJ, Vanschoubroeck JJ et al. Tuberculosis of the spine: CT and MR imaging features. JBR-BTR, 2005, 88, 92-97.

[33.] Chang KH, Man MH, Choi YW et al. Tuberculous arachnoiditis of the spine: findings on myelography, CT and MR imaging. Am J Neuroradiol, 1989, 10, 1255-1262.

[34.] Lotholarly O, Poizat G, Zeller V et al. Longterm outcome of AIDS associated cryptococcosis in the era of combination antiretroviral therapy. AIDS, 2006, 20, 2183-2191.

[35.] Miszkiel KA, Hall-Craggs MA, Miller RF et al. The spectrum of MRI findings in CNS cryptococcosis in AIDS. Clin Radiol, 1996, 51, 842-850.

[36.] Venkataramana A, Pardo CA, McArthur JC et al. Immune reconstitution inflammatory syndrome in the CNS of HIV-infected patients. Neurology, 2006, 67, 383-388.

[37.] Whiteman MLH, Dandapani BK, Sherbert RT et al. MRI of AIDS related polyradiculomyelitis. J Comput Assist Tomogr, 1994, 18, 7-11.

[38.] Post MJD, Chan JC, Hensley GT et al. Toxoplasma encephalitis in Haitian adults with acquired immunodeficiency syndrome: a clinicopathological CT correlation. Am J Neuroradiol, 1983, 4, 155-162.

[39.] Rubin DI. NeuroImages. 'Owl's eyes' of CMV ventriculitis. Neurology, 2000, 54, 2217.

[40.] Talpos D, Tien RD, Hesselink JR et al,Magnetic resonance imaging of AIDS related polyradiculopathy. Neurology, 1991, 41, 1996-1997.

[41.] Padgett BL, Walker DL, ZuRhein G et al. Cultivation of papovalike virus from human brain with progressive multifocal leukoencephalopathy. Lancet, 1971, i, 1257-1260.

[42.] Manji H, Miller R. Progressive multifocal leucoencephalopathy: progress in the AIDS era. J Neurol Neurosurg Psychiatr, 2000, 69, 569-571.

[43.] Cinque P, Pierotti C, Vigano MG et al. The good and evil of HAART in HIV-related progressive multifocal leukoencephalopathy. J Neurovirol, 2001, 7, 358-363.

[44.] Cinque P, Bossolasco S, Brambilia AM et al. The effect of highly active antiretroviral therapy-induced immune reconstitution on development and outcome of progressive multifocal leukoencephalopathy: study of 43 cases with review of the literature. J Neurovirol, 2003, 9 suppl 1, 73-80.

[45.] Koralnik IJ. New insights into progressive multifocal leukoencephalopathy. Curr Opin Neurol, 2004, 17, 365-370.

[46.] Bauer W, Chamberlin W, Horenstein S. Spinal demyelination in progressive multifocal leucoencephalopathy. Neurology, 1969, 19, 287-288.

[47.] Whiteman ML, Post MJ, Berger JR. Progressive multifocal leucoencephalopathy in 47 HIV seropositive patients: neuroimaging with clinical and pathological correlation. Radiology, 1993, 187, 233-240.

[48.] Thurnher MM, Post MJ, Rieger A et al. Initial and follow-up MR imaging findings in AIDS-related progressive multifocal leukoencephalopathy treated with highly active antiretroviral therapy. Am J Neuroradiol, 2001, 22, 977-984.

[49.] De Gans J, Portegies P. Neurological complications of infection with human immunodeficiency virus type 1: a review of the literature and 241 cases. Clin Neurol Neurosurg, 1989, 91, 199-219.

[50.] Henderson RD, Smith MG, Mowat P et al. Progressive multifocal leukoencephalopathy. Neurology, 2002, 58, 1825.

[51.] Kuker W, Mader I, Nagele T et al. Progressive multifocal leukoencephalopathy: value of diffusion-weighted and contrast-enhanced magnetic resonance imaging for diagnosis and treatment control. Eur J Neurol, 2006, 13, 819-826.

[52.] Cosottini M, Taravelli C, Del Bono L et al. Diffusion-weighted imaging in patients with progressive multifocal leukoencephalopathy. Eur Radiol, 2008, 18, 1024-1030.

[53.] Usiskin SI, Bainbridge A, Miller RF, Jager HR. Progressive multifocal leukoencephalopathy: serial high-b-value diffusion-weighted MR imaging and apparent diffusion coefficient measurements to assess response to highly active antiretroviral therapy. Am J Neuroradiol, 2007, 28, 285-286.

[54.] Levy RM, Mills CM, Posin JP et al. The efficacy and clinical impact on brain imaging in neurologically symptomatic AIDS patients: a prospective CT/MRI study. J Acquir Immune Defic Syndr, 1990, 3, 461-471.

[55.] Poon TP, Mataso I, Thertkoff V et al. CT features of primary cerebral lymphoma in AIDS and non-AIDS patients. J Comput Assist Tomogr, 1989, 13, 6-9.

[56.] Lee YY, Bruner JM, Van Tassel P et al. Primary central nervous system lymphoma: CT and pathologic correlation. Am J Neuroradiol, 1986, 7, 599-604.

[57.] Johnson BA, Fram EK, Johnson PC, Jacobowitz R. The variable MR appearance of primary lymphoma of the central nervous system: comparison with histopathologic features. Am J Neuroradiol, 1997, 18, 563-572.

[58.] Henin D, Smith TW, De Girolami U et al. Neuropathology of the spinal cord in the immunodeficiency syndrome. Hum Pathol, 1992, 23, 1106-1114.

[59.] Safai B, Diaz B, Schartz J. Malignant neoplasms associated with human immunodeficiency virus infection. CA Cancer J Clin, 1992, 42, 74-95.

[60.] Vannemreddy PS, Fowler M, Polin RS et al. Glioblastoma multiforme in a case of acquired immunodeficiency syndrome: investigation of a possible oncogenic influence of human immunodeficiency virus on glial cells. Case report and review of the literature. J Neurosurg, 2000, 93, 156-157.

[61.] Gildenberg PL. Acquired immunodeficiency syndrome and central nervous system tumors. J Neurosurg, 2000, 92, 161-164.

[62.] Gillams AR, Allen E, Hrieb K et al. Cerebral infarction in patients with AIDS. Am J Neuroradiol, 1997, 18, 1581-1585.

[63.] De La Blanchardiere A, Rozenberg F, Caumes E et al. Neurological complications of varicella-zoster virus infection in adults with human immunodeficiency virus infection. Scand J Infect Dis, 2000, 32, 263-269.

[64.] De Broucker T, Verollet D, Schoindre Y et al. Cerebral vasculitis with aneurysms caused by varicella-zoster virus infection during AIDS: a new clinicoangiographical syndrome. Rev Neurol, 2008, 164, 61-71.

[65.] Berkefeld J, Enzensberger W, Lanfermann H. MRI in human immunodeficiency virus-associated cerebral vasculitis. Neuroradiology, 2000, 42, 526-528.

[66.] Sharfstein SR, Ahmed S, Islam MQ et al. Case of moyamoya disease in a patient with advanced acquired immunodeficiency syndrome. J Stroke Cerebrovasc Dis, 2007, 16, 268-272.

[67.] Giancola ML, Rizzi EB, Lorenzini P et al. Progressive multifocal leukoencephalopathy in HIV-infected patients in the era of HAART: radiological features at diagnosis and follow-up and correlation with clinical variables. AIDS Res Hum Retroviruses, 2008, 24, 155-162.

[68.] Charlier C, Dromer F, Leveque C et al. French Cryptococcosis Study Group. Cryptococcal neuroradiological lesions correlate with severity during cryptococcal meningoencephalitis in HIV-positive patients in the HAART era. PLoS ONE, 2008, 3, e1950.

Correspondence to: HR Jager, Lyshom Department of Neuroradiology, The National Hospital for Neurology and Neurosurgery, 8-11 Queen Square, London WC1N 3BG, UK Email:
COPYRIGHT 2008 Mediscript Ltd.
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2008 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:LEADING ARTICLE; central nervous system
Author:Descamps, M.J.L.; Hyare, H.; Zerizer, I.; Jager, H.R.
Publication:Journal of HIV Therapy
Article Type:Report
Geographic Code:4EUUK
Date:Sep 1, 2008
Previous Article:Radiological imaging in the context of HIV infection: size of the lesion is not everything.
Next Article:Magnetic resonance imaging and spectroscopy of the brain in HIV disease.

Terms of use | Privacy policy | Copyright © 2022 Farlex, Inc. | Feedback | For webmasters |