Other Tools of Significant Diagnostic Value
In HSE, Launes et al. reported an increased uptake of technetium-99m-hexamethyl oxime (99mTc-HMPAO) in the affected temporal lobes. The subsequent study by Nara et al. demonstrated that the degree of uptake of radioactivity correlates to the prognosis of the patient. The study employing SPECT is now regarded as a sensitive method for detecting brain lesions caused by viral infections. At this point, we should make a comment on the report by Rieck et al., where they demonstrated discordant results using another tracer, 99m-Tc-ethyl cysteinate dimer (99mTc-ECD) from those by 99mTc-HMPAO on four patients with HSE. Signal hyperintensity in the lesions where T2-W MR images showed hyperintensity is congruent with increased uptake of 99mTc-HMPAO and decreased uptake of 99mTc-ECD. This finding strongly suggested that uptake of the tracers in SPECT examination is not always increased, and that it depends on the pathological conditions of the lesions. Disturbed membrane and intracellular metabolism might also change tracer kinetics and lead to discordant uptake of both agents. Nevertheless, brain SPECT is a sensitive method for detecting infectious lesions of HSE in typical cases. Therefore, we should include this method for detecting and following up HSE infection (Table 1).
Encephalitis or Encephalopathy Caused by HIV
In spite of the enormous efforts made in the development of combination antiretroviral therapy, damage to the CNS by HIV still remains a significant problem. After HIV infection, infected monocytes activate microglia leading to diffuse white-matter injury and neurodegeneration in patients with advanced immunosuppression. These processes finally result in cognitive alterations and involuntary movements in most cases of HIV-associated encephalitis. The persistent viral infection of the brain by HIV causes structural alterations that can be detected by MRI. Earlier studies have demonstrated the loss of brain parenchyma in HIV-infected patients (an increase in cerebrospinal fluid volume, decrease in striatal gray matter volume, and decrease in cerebral white-matter volume). These progressive striatal and white-matter volume losses are already recognized even at the medically asymptomatic stage, and are accelerated in the more advanced stages of the illness. Previous MR imaging studies have revealed an association between cognitive decline and the overall degree of cerebral atrophy, especially with atrophy of the caudate region. Moreover, Aylward et al. demonstrated that the degree of cognitive impairment, even in nondemented patients, was significantly correlated with loss of striatal volume, reduced volume of posterior cortex and reduced cerebral white-matter volume.
HIV Vasculopathy or Vasculitis
Brain stroke is now a rising cause of mortality in HIV-infected and AIDS populations. At present, however, the etiology of stroke remains to be elucidated. HIV can cause vasculitis in humans just as VZV does, and it is postulated that the occurrence of stroke might be due to vasculitis or vasculopathy caused by HIV infection. A previous study suggested that HIV vasculopathy appeared to be associated with large, cortical, hemispheric stroke, while VZV vasculitis seemed to be present more often with deep-seated, small, subcortical ischemic infarcts, although our case of HIV vasculopathy showed small, deep-seated white matter infarctions (Table 1 & Figure 3).
MRI of 61-year-old male patient with HIV encephalopathy who presented cognitive impairment and Parkinsonism.
(A) Axial T2-weighted image 1-year before onset of symptoms. (B) Axial fluid-attenuated inversion recovery pulse image before onset of symptoms. (C) Axial T2-weighted image after onset of symptoms showed ventricular expansion and volume loss of caudate nuclei. (D) Axial fluid-attenuated inversion recovery image after onset of symptoms showed multiple ischemic lesions (arrows) caused by HIV vasculopathy. Arrows indicate the lesions caused by vasculopathy.
Future Virology. 2012;7(9):901-909. © 2012 Future Medicine Ltd.