Diagnostic workup

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Making a diagnosis of HIVE requires a synopsis of clinical information and the results of laboratory tests. No laboratory test result on its own warrants the diagnosis of HIVE. Rather, the diagnosis requires the exclusion of other conditions (Table

Clinically, the cognitive and psychological signs and symptoms are invariably accompanied by motor signs, although these may be subtle (Table 2). The HIV dementia scale (Power 1995) is an easy-to-use bedside instrument for the detection and quantification of the cognitive impairment of HIVE.

Laboratory tests are mainly employed to exclude differential diagnoses. MRI should be performed in preference to CT, and often shows patchy, diffuse, hyper-intense and relatively symmetrical lesions in the white matter. These changes indicate leukoencephalopathy. In addition, atrophy with enlargement of the ventricles and the extraventricular CSF spaces may be seen. However, none of these findings are specific for HIVE, and the disease may be present with a normal MRI. Unlike progressive multifocal leukoencephalopathy (PML), the white matter lesions do not affect the cortical U-fibers, i.e. they don't reach the cortical ribbon. Edema, space occupying lesions and contrast enhancement are not typical of HIVE and should raise suspicion of other conditions.

TABLE 3: Differential diagnoses of HIV encephalopathy and diagnostic work-up

Condition

Adequate diagnostic step (commentary)

Neurosyphilis

Antibody testing and CSF analysis (pleocytosis >45/3) (serological findings may be atypical for active neurosyphilis)

CMV encephalitis

Toxoplasmosis

Primary CNS lymphoma

VZV encephalitis

Cryptococcal meningitis

Tuberculous meningitis and other bacterial infections

CSF (pleocytosis, potentially granulocytic; decreased glucose, elevated total protein)

PCR for CMV in CSF, CMV antigen (pp65) in blood

Antibody testing in blood and CSF (IgG and antibody index may be increased)

MRI (potentially sub-ependymal hyperintensity and contrast enhancement)

Occurs mostly in association with manifestation of other organs (retinitis, colitis, pneumonitis, esophagitis)

CT / MRI (single or multiple lesions found most frequently in basal ganglia or thalamus, space occupying effect, edema, frequently with contrast enhancement (patchy or ring-shaped))

Presence of toxoplasma-specific IgG in blood and CSF (rarely total seronegativity)

(may rarely pass as diffuse microglial nodule encephalitis)

CT / MRI (single or multiple lesions most frequently adjacent to ventricles, space occupying effect, edema, almost invariably intense contrast enhancement (patchy more than ring-shaped))

CSF cytology

EBV PCR in CSF (HIV-associated CNS lymphomas EBV-induced)

PET or SPECT (tracer enhancement in lesion)

CSF (marked inflammatory signs)

VZV specific IgG in blood and CSF (IgM may be absent)

VZV PCR in CSF

Mostly antecedent or accompanying cutaneous zoster lesions

CSF (opening pressure frequently elevated, cell count and protein may be normal), India ink stain

Cryptococcal antigen in blood and CSF, fungal culture

CSF, culture, PCR for mycobacteria appropriate tests

Progressive multifocal leukoencephalopathy (PML)

MRI (single or multiple lesions of white matter, no space occupying effect, no edema, no contrast enhancement)

PCR for JC virus in CSF

Intoxication

Determination of drug levels / screening for illicit drugs

Metabolic encepha-lopathy and impaired general physical condition

Determination of electrolytes, renal and hepatic markers, hormones (thyroid, cortisol), blood count

Hypoxemia? (blood gas analysis)

Reduced physical state? (bed ridden, wasting, pyrexia)

Depression with "pseudo dementia"

Psychiatric examination

Other "subcortical" dementia forms

Normal pressure hydrocephalus, Parkinsonian syndromes, other neurodegenerative conditions, subcortical arteriosclerotic en-cephalopathy

CSF analysis shows a normal or even decreased white cell count. In contrast, total protein and albumin concentrations may be slightly elevated (blood-brain-barrier disruption). Oligoclonal bands and an increased IgG index indicate autochthonous immunoglobulin production within the CNS. However, these findings are unspe-cific and are frequently present in the asymptomatic stages of HIV infection. Although there is a statistically significant correlation of a higher CSF viral load with HIVE, this association is of little value in the context of an individual patient. The electroencephalogram (EEG) shows no or only mild signs of generalized slowing. Moderate or severe slowing or focal arrhythmic delta activity are atypical for HIVE.

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