Sahel Medical Journal

: 2021  |  Volume : 24  |  Issue : 2  |  Page : 65--69

Computerized tomographic brain findings of CNS manifestations in HIV/AIDS patients receiving HAARTS treatment

Philip Oluleke Ibinaiye1, Sefiya Adebanke Olarinoye-Akorede1, Suleiman T Sa'ad2, Nasiru M Tahir2, Aminu U Usman2, Abubakar Ali-Gombe3, Sani Garko2, Dahiru M Yunsa4, Timothy Y Umoru2, Bello O Usman1, Abdulaziz Umar1,  
1 Department of Radiology, Ahmadu Bello University Teaching Hospital, Zaria, Nigeria
2 Department of Radiology, Federal Teaching Hospital, 2Department of Medicine, Federal Teaching Hospital, Gombe, Nigeria
3 Department of Medicine, Federal Teaching Hospital, Gombe, Nigeria
4 Department of Radiology, Federal Medical Centre Yola, Lamido Zubairu Road, Yola, Nigeria

Correspondence Address:
Dr. Sefiya Adebanke Olarinoye-Akorede
Department of Radiology, Ahmadu Bello University Teaching Hospital, Zaria


Background: Despite current availability of highly active antiretroviral therapy (HAART) in our hospital, neurologic complications of HIV are common. Aim: The aim of this study was to document brain computed tomography (CT) findings in HIV patients receiving HAART who developed neurological complications and to examine the relationship of these findings with CD4 cell counts. Materials and Methods: Twenty patients with central nervous system symptoms out of 200 HIV/AIDS patients receiving HAART at the HIV Clinic of Federal Teaching Hospital, Gombe, were retrospectively studied. The findings were reviewed alongside their clinical features, CD4 + count, and HAART history. Results: CT findings were positive in 12 (60%) of the patients, while no abnormality was seen in 8 (40%). The most common brain abnormality was atrophy (35%). Two out of five patients (40%) with CD4 counts >200 had abnormal CT findings compared with 9 out of 14 patients (64%) with CD4 counts <200 cells who had CT abnormalities. This finding was statistically significant (R = 0.864, P = 0.00). Conclusion: There is high incidence of neurological complications and positive brain CT scan among the patients who defaulted from HAART treatment and with CD4 cell counts of <200 cells/microliter.

How to cite this article:
Ibinaiye PO, Olarinoye-Akorede SA, Sa'ad ST, Tahir NM, Usman AU, Ali-Gombe A, Garko S, Yunsa DM, Umoru TY, Usman BO, Umar A. Computerized tomographic brain findings of CNS manifestations in HIV/AIDS patients receiving HAARTS treatment.Sahel Med J 2021;24:65-69

How to cite this URL:
Ibinaiye PO, Olarinoye-Akorede SA, Sa'ad ST, Tahir NM, Usman AU, Ali-Gombe A, Garko S, Yunsa DM, Umoru TY, Usman BO, Umar A. Computerized tomographic brain findings of CNS manifestations in HIV/AIDS patients receiving HAARTS treatment. Sahel Med J [serial online] 2021 [cited 2021 Jul 24 ];24:65-69
Available from:

Full Text


The pathologic basis of the central nervous system (CNS) manifestations seen in HIV/AIDS patients has been attributable directly to the virus as well as indirectly from reduction in immune status, allowing for opportunistic infections and neoplasms to become manifest.[1] There is no body system that is exempted from the infection; however, the brain is said to be involved as an initial manifestation in about a quarter of HIV-positive patients.[1] While more than half of the patients will have neurologic disease in the course of the disease, findings at autopsy show neurologic abnormality in almost 90%.[2] The syndrome complex of neuro-HIV includes acute fulminant encephalopathy, neurologic immune reconstruction inflammatory syndrome, HIV-associated neurocognitive disorders (HANDs), CNS opportunistic infections (CNS-OIs), CNS lymphoma (PCNSL), progressive multifocal neuroencephalopathy, stroke, vascular myelopathy, and distal sensory polyneuropathy.[3],[4],[5],[6],[7],[8],[9],[10]

The introduction of antiretroviral agents has changed the face of HIV infection and its complications worldwide. Despite a general decline in environments where treatment is optimal, there is still increased incidence of some CNS manifestations such as HAND, distal symmetrical polyneuropathy, and cerebrovascular accidents due to improved survival of patients.[11],[12] In most parts of Sub-Saharan Africa, however, the overall burden still persists due to factors such as availability and affordability[13] or poor compliance and comorbidities where the drugs are available.

Most treatment algorithms begin with brain imaging (computed tomography [CT]/magnetic resonance imaging [MRI]) even before cerebrospinal fluid analysis (to rule out raised intracranial pressure). Due to its protean manifestation, there is no characteristic imaging feature that is pathognomonic for HIV.[14] However, imaging findings could be characterized in appropriate clinical setting and absence of co-founders could help make a confident diagnosis, rule out important differentials, and detect complications. Brain imaging is also an invaluable noninvasive tool for planning treatment, some of which could simply be medical. Only few studies in Nigeria have corroborated brain CT findings with CD4 counts in HIV-positive patients with neurologic complications. Our study is aimed at filling this gap and to compare our current findings with previous ones available in the literature.

 Materials and Methods

This was a retrospective review of 20 patients with CNS symptoms out of 200 HIV-positive patients who received treatment at HIV Clinic of Federal Teaching Hospital, Gombe, and later developed neurological symptoms. The study spanned from January 2012 to August 2015. These patients were referred to the radiology department for brain CT examination. The examination was carried out using a multi-slice CT machine (Phillips Brilliance 16-slice CT scanner, manufactured by Royal Phillips Amstelplein 2, 1070 MX Amsterdam, Netherlands), at 5 mm slice thickness, employing our standard brain protocol for pre- and postcontrast studies. Postcontrast studies were carried only after the initial noncontrast study scan had been reviewed to rule out acute hemorrhage. The images were reported by a consultant radiologist with 12 years experienced in Neuroradiology.

The patients' biodata and clinical, immunological, and drug history were extracted from their hospital case notes. Data were analyzed using SPSS (version 17 Chicago Illinois); relevant correlations were carried out such as CD4 cell counts versus CT findings and CD4 cell counts versus duration of HIV to test for statistical level of significance. The level of statistical significance was set at P < 0.05.

No autopsy or histology was performed.


The patients' age ranged from 12 to 57 years; mean age was 34.4 ± 10.3 years. The mean age for males was 34.3 ± 10.3 years, while that of females was 33.4 ± 8.3 years. The duration of HIV infection in males and females patients, respectively, was 2.1 ± 1.6 years and 4.0 ± 3.4 years, while the mean onset of CNS complaints from diagnosis of HIV infection was 2.4 ± 1.2 years [Table 1].{Table 1}

Only 5 patients were compliant on treatment, while 15 were either noncompliant or defaulted [Table 2].{Table 2}

[Table 3] shows the nature and frequency of clinical presentation among the patients. The most common presentation was hemiparesis in 10 (50% of the patients) followed by headache 9 (45% of patients).{Table 3}

Eight (40%) of the patients had normal CT findings, while twelve (60%) had abnormal findings on CT scan. The distribution of lesions in the brain was as follows: cerebellum 1, cerebral cortex 4, lentiform nucleus 2, thalamus 2, periventricular white matter 3, and external capsule 1.

The most common CT findings were cerebral atrophy in seven patients (35%) and ex vacuo ventricular dilatation in five patients (25%) and periventricular white matter changes in five patients (25%). Cerebral infarcts occurred in four patients (20%), out of which one was hypertensive. Intracranial masses were demonstrated in two (10%) of the patients, the two cases were males and later defaulted from treatment (CD4 counts <100 cells). One of the masses was in the basal ganglia and showed ring enhancement, while the other was solitary and in the frontal lobe. Three cases (15%) also demonstrated extensive fingerlike nonenhancing hypodense lesions in the temporal and parietal lobes [Figure 1], [Figure 2], [Figure 3], [Figure 4].{Figure 1}{Figure 2}{Figure 3}{Figure 4}

Information on CD4 count was absent in one patient and therefore CD4 results of only 19 patients were analyzed in [Table 4]. Two out of five patients (40%) with CD4 counts >200 had abnormal CT findings compared with 9 out of 14 patients (64%) with CD4 counts <200 cells who had CT abnormalities. This finding was statistically significant (R = 0.864, P = 0.00).{Table 4}

Patients with CD4 count <200 are 2.7 times more likely to have positive CT findings compared to those with a CD4 count of >200, but the finding was not statistically significant (P = 0.67).

The CD4 count versus duration of HIV showed a negative and nonsignificant correlation (R = 0.048, P = 0.84).

The overall prevalence of neurologic disease in HIV-positive patients in our study was 10%. While the prevalence was 3.2% among those who are actively compliant with highly active antiretroviral therapy (HAART).


CNS can be involved at any stage of the disease and not necessarily at the late stage; hence early diagnosis is key especially as neuroimaging techniques such as CT and MRI are becoming increasingly available in our environment. From our study, the average onset of neurologic symptoms from the duration of HIV infection was about 2 years.

The overall prevalence of neurologic disease in HIV-positive patients in our study was 10%. While the prevalence was only 3.2% among those who are actively compliant with their treatment (HAART). This is significantly lower than previous reports. Oshinaike[15] reported that a third of their patients on HAART had clinically evident neurologic disease while another African study[16] showed that 44.6% also had neurologic complications of HIV disease. Both authors agreed that neurologic involvement was associated with patients who had a more advanced disease, i.e., lower CD4 counts than patients without neurologic manifestation. The finding that the frequency of neurologic complications increases with severity of immune depression (low CD4count) was corroborated in our study.

This study shows a 60% prevalence of abnormal CT finding in HIV-positive patients with neurologic symptoms. Males were twice as likely to have positive CT findings (80%) when compared with females (40%), the likely reason being that female patients attend their clinic appointment regularly and are more compliant with drugs regimen than their males' counterpart. Graham et al.[17] also stated high prevalence of CT abnormalities in HIV patients presenting with uncomplicated headache and low CD4 counts. For patients with CD4 counts >200, MRI was suggested. We also advocate MRI scan for early detection of subtle brain changes. In our series, we noted five patients with advanced disease (CD4 <200) and focal neurologic signs with negative CT findings; perhaps further MRI studies would have revealed subtle abnormalities that were missed on CT. Furthermore, early MRI findings cannot be ruled out in patients with CD4 counts >200 cells even if CT finding is normal.

The predominant CT findings in our study were cerebral atrophy (35%) and ex vacuo ventricular dilatation (25%), periventricular white matter changes (25%), cerebral infarcts (20%), and cerebral masses with mass effects (10%). In HIV infection, CNS disease has diverse and overlapping features. Atrophy plus ex vacuo ventricular dilatation is the most common finding in HIV encephalitis.[17] CT is similar to MRI in depicting cortical atrophy but CT is superior to MRI in showing meningeal disease.[17]

The differential diagnoses of the intracranial masses associated with this study were toxoplasmosis, cerebral abscess, and lymphoma. Neuro-toxoplasmosis and primary CNSPCNSL have similar imaging features; however, multiple ring-enhancing lesions, located in the basal ganglia and thalamus in the presence of cerebral atrophy, would be highly suggestive of toxoplasmosis, while solitary lesions would suggest lymphoma. Tuberculous abscess can be differentiated from bacterial abscess as the former is associated with enhancement of basal meninges.

We also made an imaging diagnosis of progressive multifocal leukoencaphalitis in 3 (15%) patients who had extensive, fingerlike nonenhancing lesions involving the white matter of the temporal and parietal lobes. This can be differentiated from PCNSL which is enhancing and also demonstrate the mass effect. These imaging features can inform the early institution of medical therapy.

The use of effective HAART reduces the incidence of HIV infection and its complications. In Nigeria, there has been an overall reduction in incidence by 21% since its peak in 1997,[18] and this has been attributed to effective therapy. This big picture is not reflected in every center. Apart from cost and availability being leading factors where the burden still lingers, a major contributor in our center was noncompliance. Only 6 (30%) of the patients with CNS complications in our study were compliant with therapy. The statistics from our study shows a strong and significant correlation between CD4 count and HAART status. All defaulters showed CD4 counts <200, out of which 64% had abnormal CT scans.

Hemiparesis was the commonest presentation in this study, and it occurred majorly in patients <40 years of age who did not have previous comorbidities such as hypertension. CT brain in this group of patients revealed atrophy and infarcts. Stroke is not an unusual finding in HIV patients, and it occurs as part of the syndrome complex or as a complication of treatment.[16]

Headache was the next frequent in our study, occurring in 45% of the patients. It was the commonest presentation (60%–90%) in previous studies.[16],[19],[20] Headache in HIV-positive patients should be considered exhaustively as it could be the sole presentation of a sinister CNS disease. It is reported to be the only complaint in 97.3% of patients with Cryptococcus meningitis by Namme Luma et al.[16]


There is high incidence of neurological complications and positive brain CT scan findings among the patients who defaulted from HAART treatment and with CD4 cell counts of <200 cells/microliter. We recommended that further MRI studies should be carried out on HIV patients with neurological symptoms, but normal CT finding as this may reveal subtle abnormalities that are missed on CT.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Adeolu AA, Malomo AO, Shokunbi MT, Shokunbi WA, Obajimi MO, Komolafe EO, et al. Cranial computed tomographic (CT) findings in HIV-positive Nigerian patients presenting for neurosurgical evaluation. West Afr J Med 2006;25:69-74.
2de Gans J, Portegies P. Neurological complications of infection with human immunodeficiency virus type 1. A review of literature and 241 cases. Clin Neurol Neurosurg 1989;91:199-219.
3Newsome SD, Johnson E, Pardo C, McArthur JC, Nath A. Fulminant encephalopathy with basal ganglia hyperintensities in HIV-infected drug users. Neurology 2011;76:787-94.
4McCombe JA, Auer RN, Maingat FG, Houston S, Gill MJ, Power C, et al. Neurologic immune reconstitution inflammatory syndrome in HIV/AIDS: Outcome and epidemiology. Neurology 2009;72:835-41.
5McArthur JC, Haughey N, Gartner S, Conant K, Pardo C, Nath A, et al. Human immunodeficiency virus-associated dementia: An evolving disease. J Neurovirol 2003;9:205-21.
6Luft BJ, Remington JS. Toxoplasmic encephalitis in AIDS. Clin Infect Dis 1992;15:211-22.
7Bibas M, Antinori A. EBV and HIV-related lymphoma. Mediterr J Hematol Infect Dis 2009;1:e2009032.
8Ovbiagele B, Nath A. Increasing incidence of ischemic stroke in patients with HIV infection. Neurology 2011;76:444-50.
9Ogun SA, Adelowo OO, Familoni OB, Adefuye OB, Alebiosu C, Jaiyesimi AE, et al. Spectrum and outcome of clinical diseases in adults living with AIDS at the Ogun state university teaching hospital. East Afr Med J 2003;80:513-7.
10Lehmann HC, Chen W, Borzan J, Mankowski JL, Höke A. Mitochondrial dysfunction in distal axons contributes to human immunodeficiency virus sensory neuropathy. Ann Neurol 2011;69:100-10.
11Gonzalez-Duarte A, Cikurel K, Simpson DM. Selected neurologic. Complications of HIV and antiretroviral therapy. Prn Noteb 2006;11:60-5.
12Sacktor N. The epidemiology of human immunodeficiency virus-associated neurological disease in the era of highly active antiretroviral therapy. J Neurovirol 2002;8 Suppl 2:115-21.
13Alkali NH, Bwala SA, Nyandaiti YW, Danesi MA. NeuroAIDS in Sub-Saharan Africa: A clinical review. Ann Afr Med 2013;12:1-0.
14Post MJ, Tate LG, Quencer RM, Hensley GT, Berger JR, Sheremata WA, et al. CT, MR, and pathology in HIV encephalitis and meningitis. AJR Am J Roentgenol 1988;151:373-80.
15Oshinaike O, Akinsegun A, Njideka O, Oluwadamilola O, Olaitan O, Adedoyin D, et al. New-onset seizures in HIV patients on antiretroviral therapy at a tertiary centre in South-West, Nigeria. World J AIDS 2013;3:67-70.
16Luma HN, Tchaleu BCN, Temfack E Doualla MS, Ndenga DPM, Mapoure YM,et al, HIV-associated central nervous system disease in patients admitted at the Douala General Hospital between 2004 and 2009: a retrospective study. AIDS Res Treat. 2013.
17Graham CB 3rd, Wippold FJ 2nd, Pilgram TK, Fisher EJ, Smoker WR. Screening CT of the brain determined by CD4 count in HIV-positive patients presenting with headache. AJNR Am J Neuroradiol 2000;21:451-4.
18International Statistics on HIV/AIDS. NACA 18th November; 2015. Available from: [Last accessed on 2018 Apr 11].
19Bolokadze N1, Gabunia P, Ezugbaia M, Gatserelia L, Khechiashvili G. Neurological complications in patients with HIV/AIDS. Georgian Med News. 2008;165:34-8.
20Berhe T, Melkamu Y, Amare A. The pattern and predictors of mortality of HIV/AIDS patients with neurologic manifestation in Ethiopia: A retrospective study. AIDS Res Ther 2012;9:11.