Download - Neuropsychiatric Aspects of HIV and AIDS
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Case Summary
42 years old Vietnamese man, who is a known case ofAIDS for 3 years, currently on HAART treatment,presented with a 2 months history of worsening memory,keep forgetting things associated with motor dysfunction(unable to carry out daily routine activities). Patient alsohas been feeling depressed for the past 2monthsassociated with lose of appetite and insomnia. He is
unable to concentrate and becomes tired easily. Past medical history of Pneumocystic carinni infection
and is a substance abuser.
No other significant history
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Physical examination nothing significant
MSE Appearance : dress appropriately, good eye contact, co-
operative with some degree of psychomotor retardation
Speech : rate was slow, normal quantity.
Mood & Affect : Depressed, affect was restricted.
Thought & Perception: No obsession or delusion. Feelingworthless/guilt. Suicidal ideation. No hallucination.
Cognition: MMSE score 13 (unable to draw the clock, nogood concentration with impaired short and long termmemory)
Judgement & Insight : Poor judgement and partial insight.
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Investigation
FBC
U&E
Urine FEME and Urine toxicology
LFT
LP CXR
CT and MRI of brain
Blood Culture
Tests for herpes simplex, CMV, cryptococcal and VDRL
HIV viral load and CD4 count
Results : everything was normal, except very high viral load and CD4 was
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Diagnosis
HIV associated Dementia / AIDS dementia complex
Major Depressive Disorder?
To rule out other general medical conditions due toAIDS.
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NEUROPSYCHIATRICASPECTS OF HIV & AIDS
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Introduction
HIV epidemic was identified in the 1980s, and
neurologists described several HIV related CNS
syndromes within the first several years of the
epidemic.
These include acquired immunodeficiency syndrome
(AIDS) dementia, the associated AIDS mania,
increased rates of depression, and psychiatricconsequences of CNS injuries
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HIV transmission
HIV is a retrovirus. HIV-1 is the primary causative agent for most HIV
related disorders
HIV is present in blood, semen, cervical and vaginal
secretions, and, to a lesser extent, saliva, tears, breastmilk, and the cerebrospinal fluid of those who areinfected.
Modes of transmission include Heterosexual and homosexual intercourse
Needles Blood products
Vertical transmission
The risk for transmission is higher with higher viral loadsand with the coexistence of sexually transmitteddiseases that compromise skin or mucosal integrity.
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AIDS develops 8 11 years after infection
The virus binds to the CD4 receptor on T4
lymphocytes
The virus injects ribonucleic acid (RNA) into the
lymphocyte
HIV pathophysiological mechanisms gradually
disable all T4 lymphocytes and destroy cellmediated immunity, and opportunistic infections
develop
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Epidemiology
Estimated 33 million people have been infected withHIV worldwide
More than 12 million deaths as result
The chance of becoming infected after a singleexposure to an HIV infected person is relatively low:
0.8 3.2% for unprotected receptive anal intercourse
0.05 0.15% with unprotected vaginal sex
0.32% after puncture with an HIV contaminated needle
0.67% after using a contaminated needle to inject
drugs
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Classification
The Center of Disease Control (CDC) classifies AIDS
based on CD4+ counts and the presence or
absence of HIV associated clinical conditions
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Clinical manifestation About 30% of person infected with HIV experience a flulikesyndrome 3 6 weeks after becoming infected
Most never notice any symptoms immediately or shortly aftertheir infection
The flulike symdrome include Fever Myalgia
Headaches
Fatigue
Gastrointestinal symptoms
Rash Splenomegaly
Lymphadenopathy
The two most common coinfections in person infected with HIVwho have AIDS are Pneumocystis carinii pneumonia andKaposis sarcoma
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Investigations
Serum testing
Enzyme linked immunosorbent assay (ELISA)
Western blot The ELISA is the initial screen. The western blot is more
specific and is used to confirm positive ELISA results
Seroconversion is the change after HIV infection
from a negative HIV antibody test result to apositive HIV antibody test result
Usually occurs 6 12 weeks after infection but maytake 6 12 months
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HIV In Psychiatric
Primary HIV neurocognitive disorders: Asympomatic neurocognitive impairment
HIV mild neurocognitive disorder
HIV associated dementia
Other primary HIV neurobiological complications: Meningitis
Vacuolar myelopathy
Neuropathies and myopathy
Secondary neurobiological complications: Infections Neoplasia
CVS
Drugs/nutritional/metabolic
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HIV In Psychiatric
Presentations:
Delirium
Dementia
Minor cognitive motor disorder
Major Depressive Disorder
Anxiety Disorders
Sleep Disorders
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HIV Associated Dementia / AIDS
Dementia Complex
The cumulative prevalence of HIV dementia in the
lifetime of an infected adult has been reported to be
near 15 percent, although the incidence has decreased
by about 50 percent since the introduction of HAART. HIV-associated dementia is generally seen in late stages
of HIV illness, usually in patients who have had a CD4+
count under 200 cells per microliter.
Furthermore, certain risk factors have been associated
with eventual development of HIV dementia, namely,
higher HIV RNA viral load, lower educational level,
older age, anemia, illicit drug use, and female sex.
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Clinically, the dementia presents with the typicaltriad of symptoms seen in other subcorticaldementias
memory and psychomotor speed impairments,
depressive symptoms,
movement disorders.
Initially, patients may notice slight problems withreading, comprehension, memory, and mathematicalskills, but since these symptoms are subtle, they maybe overlooked or discounted as fatigue and illness.
Later, patients develop more global dementia, withmarked impairments in naming, language, andpraxis.
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Motor symptoms are also often subtle in early
stages, including
occasional stumbling while walking or running slowing of fine repetitive movements
slight tremor.
In late stages, motor symptoms may be quite severe,
with marked difficulty in smooth limb movements,
especially in the lower extremities.
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Apathy is a common early symptom of HIV-associated dementia
A frank depressive syndrome also commonly
develops, typically with irritable mood andanhedonia instead of sadness and crying spells
Sleep disturbances are common, as is weight loss
Psychosis develops in a significant number of
patients, typically with paranoid ideas
Overall, HIV-associated dementia is rapidly
progressive, usually ending in death within two
years.
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Criteria (Grants & Atkinson)
HIV-1 associated Dementia
Marked acquired impairment in cognitive functioning,
involving at least 2 ability domains (memory, attention).
The impairment produces marked interference with dayto day functioning.
Has been present for at least 1 month.
Pattern of cognitive impairment does not meet criteria
for delirium.
There is no evidence of another cause that could
explain the dementia.
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HIV-1 associated Mild Neurocognitive Disorder (MND)
acquired impairment in cognitive functioning, involving atleast 2 ability domains (memory, attention), at least 1.0standard deviation below the mean for age and educationappropriate norms using neuropsychological tests.
The impairment produces at least mild interference in dailyfunctioning at least one of these: self report, observation byothers.
Present for at least 1 month. Does not meet criteria for dementia or delirium
No evidence of another preexisting cause.
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Major depression is a risk factor for HIV infectionby virtue of its impact on behavior, intensification of
substance abuse, exacerbation of self-destructivebehaviors, and promotion of poor partner choice inrelationships.
Depression can be seen as a vector of HIV
transmission. So, HIV is a causal factor in depression and that
depression is a causal factor in HIV transmission andits morbidity.
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Conclusion
Important role for mental
health care in HIV treatmentand prevention
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