Acute demyelinizating encephalomyelitis (ADEM) as initial presentation of primary HIV infection

Mogensen, Trine H.; Marinovskij, Edvard; Larsen, Carsten Schade

doi:10.1080/00365540601137379

Cited by 22 publications

(22 citation statements)

References 9 publications

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“…Neither CD8 ϩ naïve nor central memory cells were related to NAA [23][24][25] A handful of case studies during PHI have described profound neurologic changes that can occur with HIV seroconversion including transient encephalopathy, frank meningoencephalitis, and demyelinating disease. 20,21,25 However, it is generally believed this early infection in non-rapid disease animals and humans is typically transient and productive infection is not thought to occur again until the development of AIDS. 24,26 The early HIV subjects were enrolled in this study within months of their seroconversion, during an early stage of infection, and did not report severe neurologic problems or have significant structural changes observed by MRI.…”

Section: Correlations Of 1 H Magnetic Resonance Spectroscopymentioning

confidence: 99%

“…10,11 Little is known about the brain during PHI and all early HIV-infected individuals were recruited based on the presentation of symptoms of acute viral ailment and not the occurrence of neurologic deficits, although studies have suggested the presence of brain abnormalities during this time. [20][21][22] Previous magnetic resonance studies have indicated that the frontal cortex shows signs of damage and dysfunction during the asymptomatic stage of infection, long before onset of AIDS or related dementia. Significant reductions in NAA/Cr were observed in the frontal gray matter tissue of relatively healthy, cognitively asymptomatic (or even with ADC score 0.5), chronically HIV-infected subjects.…”

Section: Figurementioning

confidence: 99%

“…Sagittal T1, axial T2, and fluid-attenuated inversion recovery images did not indicate significant structural changes indicative of encephalopathy, meningoencephalitis, or demyelinating disease in this early setting of HIV infection, as reported in a handful of case reports in the setting of PHI. [20][21][22] Spectroscopy indicated NAA and Glx concentrations, involved with the neuronal component of the brain, were reduced in frontal cortical gray matter ( figure 1A and table 3). Metabolites contributing more to the glial component (MI, Cr, and Cho) were not found to be different between the cohorts.…”

Section: Statistical Analysis Differences In Metabolism and T Cellmentioning

confidence: 99%

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Changes in MRS neuronal markers and T cell phenotypes observed during early HIV infection

Lentz¹,

Kim²,

Lee³

et al. 2009

Neurology

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Objective: To determine if changes in brain metabolites are observed during early HIV infection and correlate these changes with immunologic alterations.Methods: Eight subjects with early HIV infection, 9 HIV-seronegative controls, and 10 chronically HIV-infected subjects without neurologic impairment underwent 1 H magnetic resonance spectroscopy. Subjects with early stage infection were identified near the time of HIV seroconversion and imaged within 60 days of an evolving Western blot, while still having detectable plasma virus. Subjects had blood drawn for viral RNA and T cell quantification.Results: Both N-acetylaspartate (NAA) and Glx (glutamate ϩ glutamine) were decreased in the frontal cortical gray matter of seropositive subjects. NAA levels were found to be decreased in the centrum semiovale white matter of chronically HIV-infected subjects, but not in those with early infection. Both HIV-infected cohorts demonstrated a lower number of CD4 ϩ T lymphocytes and a higher number of CD8 ϩ T lymphocytes in their blood. Lower NAA levels in the frontal cortex of subjects with early infection were associated with an expansion of CD8 ϩ T cells, especially effector CD8 ϩ T cells. Conclusions: These results verify metabolism changes occurring in the brain early during HIVinfection. Lower NAA and Glx levels in the cortical gray matter suggests that HIV causes neuronal dysfunction soon after infection, which correlates to the expansion of CD8 ϩ T cells, specifically to an activated phenotype. Utilizing magnetic resonance spectroscopy to track NAA levels may provide important information on brain metabolic health while allowing better understanding of the virus-host interactions involved in CNS functional deficits. Neurology ® 2009;72:1465-1472 GLOSSARY APC ϭ allophycocyanin; Cho ϭ choline; Cr ϭ creatine; CTL ϭ cytotoxic T lymphocyte; Cy5.5 ϭ cyanin 5.5; FITC ϭ fluorescein isothiocyanate; FOV ϭ field of view; Glx ϭ glutamate ϩ glutamine; MI ϭ myoinositol; MRS ϭ magnetic resonance spectroscopy; NAA ϭ N-acetylaspartate; NRTI ϭ nucleoside reverse transcriptase inhibitors; PE ϭ phycoerythrin; PerCP ϭ peridinium chlorophyll protein; PHI ϭ primary HIV infection; SIV ϭ simian immunodeficiency virus; TE ϭ echo time; TI ϭ inversion time; TR ϭ repetition time.

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Section: Correlations Of 1 H Magnetic Resonance Spectroscopymentioning

confidence: 99%

Section: Figurementioning

confidence: 99%

Section: Statistical Analysis Differences In Metabolism and T Cellmentioning

confidence: 99%

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Changes in MRS neuronal markers and T cell phenotypes observed during early HIV infection

Lentz¹,

Kim²,

Lee³

et al. 2009

Neurology

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“…have reported a 45-year-old bisexual male with clinical symptoms (cognitive dysfunction and right hemiparesis), MRI, and CSF examination findings suggestive of acute demyelinating encephalomyelitis as the initial presentation of primary HIV-infection. [10] Allen et al . had reported a 32-year-old homosexual male presenting with behavioral changes and diagnosed as acute demyelinating encephalomyelitis with a 5 year-old history of HIV-infection.…”

Section: Discussionmentioning

confidence: 99%

Acute disseminated encephalomyelitis: Extremely rare presentation of pediatric human immunodeficiency virus infection

2014

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Acquired human immunodeficiency virus (HIV) infection in a 10-year-old child, presenting with monoparesis, progressing to triplegia over 4 weeks is an extremely rare feature. The child had left upper motor neurone facial palsy with left hemiplegia, paralyzed right lower limb, grade zero power, exaggerated deep tendon reflexes and bilateral extensor plantars. Child tested positive for HIV by ELISA. CD3+ absolute count was 431. CD3+ CD4 count was 28, and CD45 absolute count was 478. Magnetic resonance imaging of brain and spine showed multiple ill-defined foci of hyperintensity in white matter suggestive of ADEM. Acute demyelinating encephalomyelitis (ADEM) is an extremely rare presenting feature of perinatally acquired HIV infection in paediatrics. Clinically child remained same even with methylprednisolone, intravenous immunoglobulin, antituberculosis therapy, trimethoprim-sulfamethoxazole prophylaxis and supportive therapy. Child had sudden clinical deterioration and death before antiretroviral therapy could be initiated. This case emphasizes that pediatricians and neurophysicians should suspect HIV as an etiology of ADEM in cases with atypical clinical presentation and social risk factors, in spite of its very rare occurrence.

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“…Of almost 4,000 papers considered, we selected 13 articles respecting criteria of acute onset, unknown aetiology and disagreement with diagnostic criteria for MS (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19). In one paper, published in 1985 (16), the virus responsible for the immunodeficiency is named HTLV-III instead of HIV, but it is known that the two definitions corresponded at that time.…”

Section: Resultsmentioning

confidence: 99%

HIV-Related Acute Inflammatory Leukoencephalopathy of Undetermined Origin: Review of the Literature

Bargiggia

Pichiecchio²,

Delbue

et al. 2010

Int J Immunopathol Pharmacol

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HIV-related acute inflammatory leukoencephalopathy of undetermined origin (AIL) has been anecdotally described in literature as being responsible for cognitive and motor deficits. We carried out a review of all the cases of AIL published in literature. Articles were selected according to 2 criteria: acute onset of symptoms; undetermined aetiology and non-fulfilment of multiple sclerosis diagnostic criteria. They were then analyzed in terms of clinical, biological and instrumental features, therapy, diagnostic classification and prognosis. Although rare (21 patients out of about 4,000 publications), AIL is of particular interest, as the comprehension of its mechanisms could give some insight into the direct and immune-mediated actions of HIV within the brain. All the reported patients share several clinical, histopathological, radiological and CSF features, leading to hypothesize a similar aetiopathogenetic mechanism. Conversely, we observed a high heterogeneity of treatment and diagnostic classification, which could have conditioned the broad prognostic variability. The absence of a defined aetiology leads to consider these forms as a particular subgroup of “not determined leucoencephalopathies” (NDLE), with both MRI and histological pattern dominated by inflammation as distinctive feature.

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Acute demyelinizating encephalomyelitis (ADEM) as initial presentation of primary HIV infection

Cited by 22 publications

References 9 publications

Changes in MRS neuronal markers and T cell phenotypes observed during early HIV infection

Changes in MRS neuronal markers and T cell phenotypes observed during early HIV infection

Acute disseminated encephalomyelitis: Extremely rare presentation of pediatric human immunodeficiency virus infection

HIV-Related Acute Inflammatory Leukoencephalopathy of Undetermined Origin: Review of the Literature

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