Patients characteristics and laboratory findings at the time of diagnosis of CSF escape or HIV-encephalitis are reported in Table 1.
Patients clinical symptoms and signs are graphically reported in Table 2.
Neurological presentation consisted of memory and cognitive impairment (HIV-E=10; CSF escape=10),
agitation/psychosis/delusions (HIV-E=4; CSF escape=0),
alteration of consciousness (HIV-E=3; CSF escape=4),
cerebellar signs (HIV-E=3; CSF escape=11),
focal deficits (HIV-E=2; CSF escape=8).
MRI findings are graphically reported in Table 3.
In classical HIV-E,
MRI showed diffuse bilateral periventricular white matter hyperintensity (Fig 1),
most frequently symmetrical involving frontal lobes,
in 11/16 cases (69%) and cortical and/or subcortical atrophy in 14/16 cases (82%) (Fig 2 and Fig 3).
In CSF escape,
MRI showed areas of white matter hyperintensity either involving the periventricular (Fig 4 and Fig 5) or other brain or cerebellum regions in 16/19 cases (84%),
corpus callosum can also be involved,
edema with compression on the lateral ventricular and sulcal effacement in 10/19 cases (53%) [7-8],
and no abnormalities in 3 cases.
In CSF escape,
apparent diffusion coefficient (ADC) (Fig 6) confirmed that white matter abnormalities were sustained by vasogenic edema [9].
Neurological and MRI picture improved or regressed following cART optimization,
with edema resolution disclosing a residual cortical and/or subcortical atrophy.
Fig 7 shows a typical evolution in a patient with CSF escape.
Patient "CP": HIV patient in therapy.
History of malaise,
asthenia,
pyrexia,
occipital-temporo-parietal pulsating headache in the previous weeks,
on 11/12/2010 tonic-clonic crisis and fever and progressive degeneration of consciousness to coma GCS 3.
13/12/2010 MRI showed diffuse bilateral T2 signal alteration of deep white matter associated to a sort of brain swelling with apparent compression on the wall of lateral ventricle,
effacement of sulci.
Proteins were present in CSF at lumbar puncture (LP). 22/12/2010 LP: HIV-RNA 24190 cp/mL,
JCV neg,
Parvovirus B19 neg,
standard culture examinations neg. 27/12/2010 ART optimization: AZT/3TC + DRV/r,
MVC,
Desametasone 12mg with subsequence decalage at 8mg until 11/02.
Slow neurological recovery with consensual improvement of electroencephalographic controls,
non fever, new MRI on 3/1/2011 (only 7 days after the introduction of therapy),
showed a progression of the "intensity" of signal alteration and compression due to vasogenic edema.
PL confirm detectable CSF HIV-RNA while undetectable in plasma,
or CSF HIV- RNA >2-fold than plasma levels.
This pattern changed during resolution of the escape (LP of 24/1/2011 no viral load detectable) with reduction of all components of WM swallowing/vasogenic (extracellular) edema until a complete disappearance of signal alteration going progressively with correction of therapy during follow up.
This evolution can reach the complete resolution of the findings (MRI of 24/1/2011).
Typically,
underlying atrophy may re-emerge (MRI of 30/3/2011).
To be observed is that at the moment of the beginning of clinical stabilization starts the improvement of signal alteration.
This goes in a progressive way but more slowly than the clinical resolution with a sort of mismatch of clinical-radiological features.