JIACM 2008; 9(3): 212-3
AIDS Dementia Complex
Sujeet Raina*, Rashmi Kaul**, Mahesh DM***, SS Kaushal****, Dalip Gupta*****
A thirty-year-old driver, a right handed man, was admitted
in our medical ward with three months history of
progressive neurological symptoms in the form of
difficulty in concentrating while driving his truck, and
progressive decline of memory for recent as well as past
events as narrated by his attendants. In addition he had
history of unsteadiness of gait for the last one month.
There was history of behavioural abnormalities in the form
of apathy, social withdrawal, and episodic agitation. There
was no history of fever, headache, vomiting, seizures, bowel
or bladder involvement. No past history of any psychiatric
illness was present. On central nervous system
examination, our patient was conscious with the evidence
of impaired attention, judgement, and memory with the
minimental status examination score of 20/30.
Examination of cranial nerves including fundus was
normal. Speech, motor, and sensory examination was
normal. No meningeal signs were present and review of
other systems was also normal. Laboratory investigations
showed normal haemogram and biochemistry. CSF
analysis revealed normal biochemistry and cytology. CSF
was VDRL nonreactive, negative for cryptococcal infection,
and negative for tubercular antigen by polymerase chain
reaction. CT head (plain and contrast) revealed diffuse
cortical atrophy with prominent lateral and third
ventricles. There was hypodensity of periventricular white
Fig. 1: Cranial CT plain (right) and contrast through lateral
ventricles showing prominent lateral ventricle and cerebral
sulci.
* Senior Resident, *** PG Student, **** Professor and Head, ***** Associate Professor, Department of Medicine,
** Senior Resident, Department of Pathology, Indira Gandhi Medical College, Shimla - 171 001, Himachal Pradesh.
Fig. 2: Cranial CT plain (right) and contrast through third
ventricle showing prominent third ventricle horns with non-
enhancing white matter hypodensities in frontoparietal
region.
matter bilaterally more prominent in the frontoparietal
region without any contrast enhancement (Fig. 1 and 2).
Since the patient was a driver and a frequent traveller, he
was tested for HIV infection and was found to be HIV
positive. CD4 count was 31/mm3. In view of these clinical
features and investigations, our patient was diagnosed to
have AIDS dementia complex or HIV encephalopathy. The
patient was started on HAART (Lamivudine,Stavudine and
Nevirapine) and co-trimoxazole with Azithromycin as
prophylaxis. Haloperidol with promethazine was used in
the situation of agitation under proper psychiatric
consultation and care.
Comment
AIDS dementia complex term was used when progressive
dementia was noted with motor and behavioural
dysfunction in patients with acquired immune deficiency
syndrome1.HIV encephalopathy is the initial AIDS-defining
illness in 3% of patients with HIV infection. Clinically,
significant encephalopathy eventually develops in one-
fourth of patients with AIDS2.AIDS dementia complex is
most commonly seen in patients with known diagnosis
of AIDS, but it can be the presenting AIDS-defining illness
as in this case. This syndrome is to be differentiated from
other diseases that affect the CNS of HIV infected patients
on the basis of clinical findings and appropriate
investigations as no specific criteria for diagnosis of HIV
encephalopathy are present.
Toxoplasmosis and CNS lymphoma present as focal
neurological deficits with ring-enhancing lesions seen on
CT/MRI, while cryptococcal meningitis and CNS tuberculosis
present as meningitis and diagnostic CSF studies.
Progressive multifocal leucoencephalopathy also presents
with focal neurological deficits and CT/MRI reveals non-
enhancing subcortical white matter lesions without cortical
atrophy3. Potent antiretroviral regimens, usually consisting
of three or more antiretrovirals, are considered standard
of care. The optimal HAART regimen for treatment of HIV-
Dhasnotbeenestablished.Initially,itwasanticipated,based
on pharmacokinetic properties that particular regimens
would have better CNS penetration and efficacy. However,
from the MACS cohort, it was demonstrated that
neurocognitive improvement with HAART was
independent of theoretical CNS penetration. Most AIDS
Journal, Indian Academy of Clinical Medicine z Vol. 9, No. 3
dementia complex patients treated with HAART remain
neurologically stable for years after starting HAART, or may
show some partial reversal of neurological deficits. From
uncontrolledstudies,itisclearthatasubstantialproportion
of individuals with AIDS dementia complex actually show
partial reversal of neuropsychological deficits with HAART4.
Symptomatic treatment with neuroleptic drugs is
associated with increased risk of extrapyramidal side-effects
in these patients; therefore careful monitoring is required2.
References
1. Navia B, Jordan B, Price R. The AIDS dementia complex I.
Clinical Features. Ann Neurol 1986; 19: 517-24.
2. Fauci SA, Clifford LH. HIV disease: AIDS and related disorders.
In: Kasper DL, Braunwald E, Fauci SA, Hauser SL, Longo DL,
Jameson JL, eds. Harrisons Principles of Internal Medicine.
16th ed. New York. McGraw-Hill.2005; 1115-6.
3. Raina S, Kaushal SS, Gupta D et al. Progressive Multifocal
Leucoencephalopathy - as a presenting manifestation of
AIDS. JAPI 2007; 55: 797-801.
4. McArthur JC. HIV dementia: an evolving disease. J
Neuroimmunology 2004; 157: 3-10.
z July-September, 2008 213