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NEUROPSYCHIATRIC

MANIFESTATIONS OF HIV/AIDS
GROUP 1
DDU DEPARTMENT OF PSYCHIATRY

January 26, 2024 GROUP 1 1


OUTLINE

• INTRODUCTION OF HIV/AIDS
• ETIOLOGY
• SEROLOGIC TEST OR LABORATORY INVESTIGATION
• COURSE
• CLINICAL FEATURES
• DIFFERENTIAL DIAGNOSIS
• TREATMENT

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ACQUIRED IMMUNODEFICIENCY
SYNDROME(AIDS)
• AIDS is a clinical syndromes that is chronic potentially
life threatening condition cause by human
immunodeficiency virus ( HIV)
• AIDS may affect the nervous system in a variety of ways.
• Cerebral involvement may manifest with an early
mononucleosis-like syndrome, and later, with dementia
or seizures; there may also be a myelopathy with Para
paresis and a peripheral sensorimotor polyneuropathy.
• Fatigue and depression are also common, and rarely,
mania may be seen.

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ETIOLOGY
 AIDS is caused by infection with HIV. This RNA virus is
found in blood, semen, vaginal fluid, breast milk, and
colostrum, and may be spread via all these fluids.

 Although the virus is also found in saliva, urine, and


tears ,there is a yet no convincing evidence that it can
be spread by these.

 HIV gains attachment to cell such as lymphocytes,


monocytes, and macrophages by virtue of the CD4+
molecule founds on the cell membrane.

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 Once inside the cell, the enzyme reverse transcriptase
catalyze the reverse transcription of the genomic viral
RNA into DNA, which eventually becomes inserted into
chromosomes of the host cells.
 With cell activation, this inserted DNA is copied, which
is eventually followed by the production of the mature
HIV virus particles.
 Subsequent to infection there is an intense viremia
followed by a vigous cellular and humoral immune
response, such that, in most cases, the viremia is
substantially contained within about 3 months. The
virus, however, is not eradicated but rather continues
to reproduce within lymphoid tissue.
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 Tragically, the cell the cell most likely to be infected is
the CD4+ T-lymphocyte with the result that, over many
years, there is gradual loss of these ‘’helper’’
lymphocytes and the bodies defenses are subverted to
the point at which a significant viremia again occurs.

 In addition, with the loss of these CD4+ helper


lymphocytes, opportunistic infections begin to appear.

 It is not entirely clear how HIV gains entry into the CNS.

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o Once inside the CNS HIV is found primarily in
monocytes, macrophage, and microglia although
astrocytes and neurons may also be infected, this is far
less prominent.

o In AIDS dementia, the primary pathologic change


include diffuse myelin pallor, scattered microglial
nodules and multi nucleated giant cells: there may
also be a relatively minor degree of neuronal loss
within the cerebral cortex.

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CLINICAL FEATURES
Although nervous system involvement , such as AIDS
dementia, may rarely be the presenting symptoms of
AIDS, in most cases patients already have other evidences
of the illness, such as
 Generalized lymphadenopathy
 Constitutional symptoms
 Thrush
 Diarrhea
 Shingles
 Cytopenia (including thrombocytopenia)
 Kaposi’s sarcoma and pneumocystis pneumonia
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 Early on in the infection, often concurrent with
serotoconversion, patients may develop a
mononucleosis Like syndrome, which may be
accompanied by an aseptic meningitis.
 Cranial nerve palsies, particularly affecting the fifth,
seventh, and eighth nerves may accompany the
meningitis and there may rarely also be nan
encephalitis with delirium.
 Prevalence of hiv dementia in infected adult is
reported to be 15%
 AIDS dementia typically appears about 10 years after
the initial infection ; generally only when CD4+ count
has fallen below 200 cells/mm3.
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 The dementia is of sub acute or gradual onset and is
characterized by apathy, poor concentration and
forgetfulness; in some cases there may be agitation,
delusions, and visual hallucinations, and accompanying
the dementia one often sees dysarthria, ataxia, and
long tract signs, such as hyperreflexia, and Babinski
signs; in one case, the dementia was accompanied by
chorea.
 With progression, there may be muteness, confusion,
seizures, and myoclonus.

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Seizures occur in a small minority of patients, and these
may be due to HIV infection itself or to opportunistic
Infections e.g. Toxoplasmosis or metabolic abnormalities
E.g. hypomagnesaemia or hypocalcaemia.
 Although grand mal seizures are most common both
simple partial and complex partial seizures may also
occur.

 the spinal cord may be affected by a vacuolar


myelopathy, with Para paresis and sensory ataxia;
with in the peripheral nervous system there may be a
sensorimotor polyneuropathy which may be quite
painful.
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 Delirium is state of global derangement of cerebral
function which prevalence is reported to be between
43-65%
 The clinical presentation in HIV patient is same as
those in non HIV infected individual like reduced
clarity of environment, a change in cognition memory
(deficit disorientation and other )
 Minor gognitive motor disorder is a less severe
neurcognitive disorder emergrnt in earler hiv infection
 it Prevalence are variable, often up to 60 % by late
stage AIDS.
 The disorder is confirmed when mild impairment are
in at least tow of the following domains
verbal/language, attention memory, abstractio, and
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motor skill
 The disorder is confirmed when mild impairment are
in at least tow of the following domains
verbal/language, attention memory, abstraction, and
motor skill

 Depression is like wise common; however it is unclear


whether this syndrome occurs as a direct effect of CNS
involvement or rather reflect other factors.
 Lifetime prevalence in HIV infected patient is 22-45%
 Fatigue is common in AIDS and may be debilitating.
 Mania although rare in AIDS, may be contrast occur
directly as which associated with late stage HIV
infection
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 Mania although rare in AIDS, may be contrast occur
directly as which associated with late stage HIV
infection

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Course
In natural course of events, AIDS dementia is relentlessly
Progressive, and death usually occurs within 3-6 months.

Serologic testing
Generally the virus becomes positive with in 2-12weaks of
the initial infection and inevitably positive by 6 months ; thus
in patients with AIDS dementia, the scan shows both patchy
and confluent areas of increased signal intensity in the
Centrum semiovale of a patient with AIDS.

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 Magnetic resonance imaging (MRI) in AIDS dementia
generally reveals a degree of cortical atrophy and
ventricular dilation, and there may also be multiple
areas, some confluent, of increased signal intensity in
the centrum semiovale on T2 weighted scans.

 Enzyme linked immune sorbent assay (ELISA) test will


be positive, as well as the confirmatory western blot
test.

 The CSF in AIDS dementia generally displays a


mononuclear pleocytosis, a mildly elevated total
protein level, an increased IgG index, and oligoclonal
bands.
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HIV associated neurocognitive deficiency: the
Frascati criteria.
1) Asymptomatic neurocognitive impairment-doesn’t
interfere with every day functioning, doesn’t meet the
criteria for delirium or dementia and there is no evidence
of another pre existing cause for it.
2) Mild neurocognitive disorder-mild interference with
every day functioning, does not meet the criteria for
delirium and dementia and no evidence of another pre
existing cause for it.
3) Dementia –marked interference with day to day
functioning and no evidence of another pre existing cause
for it.
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Differential diagnosis
 Opportunistic CNS infections are very common and
may cause dementia, delirium, focal signs or seizures.
 These include toxoplasmosis, cytomegalovirus,
encephalitis, progressive multi focal, mycosis, TB,
leukoencephalopathy, varicella zoster encephalitis or
vasculopathy, herpes simplex encephalitis and
neurosyphilis.

 primary CNS lymphoma and rarely, Kaposi sarcoma


may also appears as space- occupying lesions.

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 For unclear reasons, vitamin B12 deficiency is not
uncommon in patients with AIDS and as it may produce
a dementia or a spinal cord syndromes. Similar to
vacuolar myelopathy it should always be checked for
concurrent drug addiction (e.g. cocaine) and alcoholism
are also common.

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Treatment
 If possible, is directed at the underlying conditions.
cognitive stimulating activities.
 Prosthetic devices.
 Rigorous internal medical follow up.
 In addition to implementing treatment, where possible,
of the underlying cause of dementia, consideration may
also be given to symptomatic treatment of various
clinical features such as agitation, delusion,
hallucination, depression, and insomnia.

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In addition to these anti dementia drugs such as; Selegiline
may improve cognitive performance a dose no longer than
10mg should be used to avoid the risk of a hypertension
crisis.

 Cholinesterase inhibitors; donepezil, rivastigmine and


galantamine and NMDA receptor blocker memantine.

o Painful peripheral neuropathy may respond to GABA


pentine lamotrigine, smoked cannabis, but amitriptyline
does not appear to be effective.
o Fatigue may respond to treatment with
methylphenidate; however this should not be given to
patients
January 26, 2024 who might abuseGROUP
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 HAART
 Antiepileptic drugs
 Antidepressants
 Antipsychotic
 Mood stabilizers
 Zolpidem
 Psychological therapy
 Exercise
 Psychosocial intervention and social support

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Reference

• Text book of clinical neuropsychiatry second edition


(David P Moore MD PHD)
• Text book of neuropsychiatry article in American
journal of psychiatry-April 2003
• Neuropsychiatric manifestations of HIV infection and
AIDS chapter 90(by Dwight L. Evans Karen I .
Manson Jane Leserman Russell Bauter John Jetitto)
• HIV infection and its psychiatric manifestations: A
clinical overview article in advances in psychiatric
treatment- July 2017
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Thank you

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Group members
• Amina Ziyad------------------------1204111
• Abdulahi saed---------------------1104224
• Ahmed Dahir-----------------------120440
• Abdikani Hassan------------------1204443
• Alamudin Mohammed----------1206020

January 26, 2024 GROUP 1 25

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