Pediatr Radiol (1994) 24:611-612

Pediatric
Radiology
9 Springer-Verlag 1994

Cerebral infarction in pediatric
acquired immunodeficiency syndrome
D.M. Moriarty 1, J. O. Hailer t, J. P. Loh 1, S. Fikrig 2
1 Department of Radiology, SUNY/Health Science Center at Brooklyn, 450 Clarkson Avenue, Brooklyn, NY 11203, USA
2 Department of Pediatrics, SUNY/Health Science Center at Brooklyn, 450 Clarkson Avenue, Brooklyn, NY 11203, USA
Received: 21 January 1994/Accepted: 2 March 1994

Abstract. C e r e b r a l i n f a r c t i o n is a n
u n c o m m o n c o m p l i c a t i o n o f A I D S in
pediatric patients. We have seen
three HIV-infected children who dev e l o p e d a c u t e n e u r o l o g i c a l deficits
d u e to s t r o k e . C e r e b r a l i n f a r c t i o n
m u s t b e c o n s i d e r e d in t h e w o r k - u p
o f a child w i t h A I D S w h o p r e s e n t s
w i t h f o c a l n e u r o l o g i c a l deficit, seiz u r e o r m e n t a l status c h a n g e .
S t r o k e is a c o m p l i c a t i o n o f H I V inf e c t i o n t h a t o c c u r s in a p p r o x i m a t e l y
1 % o f a f f e c t e d c h i l d r e n [1]. A t autopsy, e v i d e n c e of c e r e b r a l infarct i o n was d o c u m e n t e d in 1 0 - 3 0 % o f
c h i l d r e n w i t h H I V i n f e c t i o n [2]. W e
h a v e s e e n t h r e e c h i l d r e n w i t h focal
infarction who are HIV positive.

Case reports
Case 1
An 8-year-old HIV-positive boy presented
with sudden onset of right hemiparesis and
a right facial palsy.
Past medical history included multiple
hospitalizations for recurrent oral and esophageal candidiasis. Laboratory work-up
revealed spinal fluid which was negative
for organisms or infection. Platelets, prothrombin, and partial thromboplastin time
were normal. On physical examination, the
patient was afebrile and alert with a right facial palsy and a right hemiparesis. There
were brisk deep tendon reflexes and an upgoing right toe.
Initial non-enhanced axial computed tomography (CT) of the head revealed evolving low-attenuation lesions of the left basal
Correspondence to: J. O. Haller

Fig.la-c. Case 1. a CT shows low-attenuation lesions in the left basal ganglia, b, c MRA
demonstrates absence of signal within the branches of the left middle cerebral artery on
both the source image and the coronal reconstructed image
ganglia (Fig. I a). A magnetic resonance angiogram (MRA) of the head revealed absence of signal within the sylvian branches
of the left middle cerebral artery on both
the source images (Fig. l b ) and the coronal
reconstructed images (Fig. 1 c). These findings correlated with the CT findings demonstrating an evolving left middle cerebral artery stroke.

Case 2
A 14-year-old HIV-positive girl presented
with progressive neurological signs and
ataxia.
Laboratory and clinical work-up revealed no evidence of acute infection. A
magnetic resonance imaging (MRI) scan
demonstrated a left cerebellar hemisphere
high T2-weighted signal lesion in the distribution of the left posterior inferior cerebellar artery. These findings are consistent
with a left cerebellar infarction (Fig. 2).

612
tion the patient was afebrile with a right
hemiparesis and a right facial palsy.
The post-contrast CT demonstrated a
vague area of patchy gyriform enhancement in the left parietal lobe (Fig.3). A
study 4 days prior to this, in retrospect, demonstrated a vague loss of gray/white discrimination in this region. These findings
are most typical of an evolving cerebrovascular accident in the left parietal lobe.

Discussion

Fig.2. Case 2. MRI shows a left cerebellar
hemispheral lesion with high T2-weighted
signal intensity, consistent with an infarction
Fig.3. Post-contrast CT shows an area of
patchy gyriform enhancement in the left parietal lobe

Case 3
A 2-year-old HIV-positive boy presented
with a right hemiparesis and lethargy.
Past medical history included numerous
hospital admissions for pneumocystis pneumonia and otitis media. Laboratory workup revealed spinal fluid which was negative
for organisms, and toxoplasmosis titers
were also negative. On physical examina-

Patients with A I D S are at an increased risk of strokes [3]. The
cause of these strokes is often unknown, however, vasculopathies of
various etiologies have been implicated in many cases [2, 3]. Opportunistic infection may lead to vasculop a t h y and subsequent stroke in patients with A I D S [1]. Pathogens
such as Candida albicans and cytomegalovirus are known to cause vascular invasion and secondary thrombosis of cerebral vessels in the immunocompromised host. However, in
children, in contrast to adults, infection of the CNS with opportunistic
organisms is u n c o m m o n [4].
L y m p h o m a is a known neoplastic
cause of vasculopathy in the immunocompromised host. This tumor
can be focally invasive of blood vessel walls resulting in direct vascular
injury, invasion of the lumen and focal thrombosis [1].
The vasculopathy in patients with
A I D S also may be due to primary infection by the human immunodeficiency virus itself. In addition, H I V
may indirectly mediate vascular injury by the reaction of elastases from
repeated infections. This may injure
the elastic lamina of vessels [5].
These strokes at the site of vasculopathy are thought to be thrombotic
rather than embolic vascular occlusions [2].
Hemorrhagic infarcts also have
been reported in children with
A I D S although these are reported

to occur less frequently than nonhemorrhagic infarcts. In one report
of four patients with hemorrhagic infarcts, all had immune thrombocytopenia.
The three patients presented had
clinical evidence of stroke with
abrupt onset of neurological deficits.
Imaging studies confirmed clinical
suspicions revealing characteristic
lesions that corresponded to the
area of focal deficit. Clinically and
radiologically there was no evidence
of infection or lymphoma in these
patients. CNS lymphoma and opportunistic infections are distinctly unusual in children with AIDS, in contrast to adults. Therefore, we believe
that cerebral infarction in these patients was due to primary infection
by the H I V virus itself. These children are alive and undergoing continued medical therapy for AIDS at
this time. Cerebral infarction secondary to H I V vasculopathy should
be a consideration in pediatric
A I D S patients.

References
1. Kieburtz KD, Eskin TA (1993) Opportunistic cerebral vasculopathy and stroke
in patients with the acquired immunodeficiency syndrome. Arch Neurol 50: 430432
2. Park YD, Belman AL (1990) Stroke in
pediatric acquired immunodeficiency
syndrome. Arch Neurol 28:303-311
3. Engstrom J, Lowenstein DH (1988) Cerebral infarctions and transient neurologic
deficits associated with AIDS. Neurology 38:241
4. Behman AL, Diamond G, Dickson D
(1988) Pediatric acquired immunodeficiency syndrome, neurologic syndromes.
Am J Dis Child 142:29-35
5. Joshi VV, Power B (1987) Arteriopathy in
children with acquired immune deficiency syndrome. Pediatr Patho1261-275