The Effects of HIV-Associated Dementia to Neurological Brain Functions

The Effects of HIV-Associated Dementia to Neurological Brain Functions


Present day research programmes have reported a significant increase in the life expectancy of individuals living with HIV. The increased life expectancy is due to the advent of antiretroviral therapy that was introduced by researchers not so long ago. Even though life expectancy has gone up, medical practitioners have had several encounters with the neuropsychiatric presentation of HIV.  The HIV- triggered neurotoxin cascades located in the central nervous system (CNS) has presented various individuals exhibiting cognitive deficits. The illness presents patients having depression in the early stages as well as in the critical full-blown stages whose pathogenesis has not been able to be clearly stated. The various Psychological disorders among patients can result in severe conditions that may predispose the patient to insanity and even death. It is therefore essential to have a better understanding and awareness of these neuropsychiatric manifestations even as the quality of life becomes advanced when it comes to managing the chronic disease.

Keywords: HIV, Antiretroviral, Neurocognitive, Central Nervous System (CNS), Minor cognitive and minor dysfunctions (MCMD)





Researchers round the globe have found and estimation of about forty million people infected with HIV. HIV type 1 virus is the most commonly known virus type (De Almeida, Kamat, Cherner, Umlauf, Ribeiro, De Pereira, and Ellis, 2017). This report is one that was given by the Joint United Nations Program. Approximately five hundred and forty thousand adult and one million children in North America are said to be living with the disease (De Almeida et al., 2017).  The number of women infected with the virus across the world has also rapidly increased over the past few years. As a result of the rapid increase, women have accounted for half of the world’s population living with the disease. Life expectancy has improved; however after the introduction and advancements in treating the illness. Despite these improvements, medics are still having a problem of dealing with the presentation of the disease in the patient’s neurons. Minor cognitive and motor disorder (MCMD) and HIV- associated dementia (HAD) are the most prevalent forms of neurological manifestations. Clinicians should practice appropriate intervention such as early diagnosis on seropositive patients exhibiting these syndromes. In this article, we will present a report on the neuropsychiatric manifestations of HIV as well as treatment methods and determination.

Etiology of the disease

In 1981, researchers reported the first cases of HIV. Two years later, there was an identification of the virus and reported. However, in the pre-dominant disease stage, various neurological conditions were detected. Research revealed that HIV can cross into the blood-brain barrier. The crossing over is because HIV can be secluded from the cerebrospinal fluid (CSF) and can also exist in tissues of the brain. HIV-associated dementia incidences were reported to be approximately twenty cases per a thousand person-years. With the invasion of the antiretroviral therapy that is highly active (HAART) in the late 1990S, the cases dropped to around ten per a thousand person-years.  A significant reduction in opportunistic diseases in the central nervous system (CNS) was also detected by the clinicians (Woods et al., 2016). Other qualified researchers also noticed a reduction in the spread of opportunistic nervous infections.  The HIV prevalence, however, was detected after an autopsy report to have increased after the invasion of the antiretroviral therapy. This increase clearly shows that there was a continuous infiltration of HIV in the central nervous system despite the improvement in therapeutic alternatives. HIV moves over the blood-brain barrier by a mode of a mechanism known as the Trojan –horse. After finding its way to the brain, the virus moves to the glial cells, secreting neurotoxins that bring about damages in the neurons and even death. The clinical neurological deficits determine the extent to which the neurons have suffered damage (Woods et al., 2016). Autopsy reports on HIV positive patients have reported on the existence of the virus in cortical structures and subcortical structures. The structures are namely the frontal lobes,  the subcortical white matter, and the basal ganglia. Other studies believe that the main areas for the initial manifestation of the HIV infection are the caudate nucleus together with the basal ganglia

Individuals suffering from extreme cases of neurocognitive deficits or HIV-associated dementia have been found to exhibit the viral load of HIV and higher plasma levels. HIV viral loads in the plasma are many at times similar to those present in serum. Even though HIV may remain inactive inside the central nervous system, its existence results in a significant reduction in cognitive operations. These deficits fail to show in some other groups of patients, and eventually, many researchers would tend to suggest that there might be involvement in external triggers (Woods et al., 2016).  For the determination of which group of people is more susceptible to neurological conditions, extensive research should be carried out. Indirect as well as direct adversities of HIV present in the CNS lead to neurocognitive deficits. For asymptomatic patients, there is evidence that is conflicting on whether there happens to be an actual existence of similar deficits. Some researchers have found neuropsychological deficits in asymptomatic individuals while others have detected almost the same levels of neurocognitive impairment in the seropositive and negative patients (Woods et al., 2016). Research, however, reveals that, when there is a presence of deficits in patients who are asymptomatic, they are reduced to lesser cognitive domains. Psychomotor retardation due to depressive symptoms results in deficits in verbal and memory.

On the other hand, the absence of depressive symptoms results in deficits in verbal and non-verbal cognitive domains. The progression of HIV results in the impairment of additional cognitive domains. The existence of HIV in the frunto- subcortical system as well as its harmful impact on functioning memory suggests that the official function is also impaired. Mind together with learning are also altered by the process. Psychomotor retardation or slowness is the most common as well as the most prominent neurocognitive deficit (De Almeida et al., 2017). It is possible to see the cognitive with or without normal functioning of the motor. It is therefore essential to assess the HIV-seropositive patients for these neurocognitive impairment types. This assessment should, therefore, be conducted in existence or behavioral indications. Several criteria for the diagnosis of HIV associated dementia (HAD)  together with the MCMD have been put forth by the Neurology American Academy. MCMD is perceived to be a much lesser type of HAD while HAD on itself is considered to represent neural death. MCMD represents neural dysfunction. The pathology of the central nervous system must be banned because both HAD and MCMD are exclusion diagnoses.

There is a need to examine tumors, pathogens affecting the CNS together with encephalopathy causes. Researchers and clinicians should conduct this examination before attributing the motor deficits and cognitive deficits to HIV infection. Progressive multifocal leukoencephalopathy, as well as toxoplasmosis, are the most common CNS infections. They are mainly caused by papovavirus. The ruling out of opportunistic infections brings about two neurocognitive deficits potential therapeutic options: Removal of the viral effects on the CNS through advanced and effective viral load control methods or development of protective neuron agents to protect the CNS against coming into contact with HIV-induced low virotoxins (López et al., 2017). Antiretrovirals are not always guaranteed to cross over the blood-brain- barrier. However, by the reduction of HAD after the introduction of the antiretroviral therapy (HAART) excellent results have been achieved.

Symptoms and cause

HIV infection brings about various psychiatric conditions. The recognition of the mental states may, however, be complicated. The complexity is as a result of social and psychological circumstances linked with the disease (Lopez et al., 2017). Psychiatric symptoms may go unnoticed and hence untreated. HIV patients may develop certain conditions that end up interfering with the CNS. Depression being one of the mental disorders may be as a result of the increased mortality rate amongst the seropositive women and women living with HIV as well as the gradual and continuous spread of the disease in seropositive men. Conditions such as psychosis and mood imbalance disorders are more likely to generate and bring about the presentation of this condition.

Depression again is brought about when the individual suffering from HIV refuses to accept the condition at hand. Stigmatization of patients living with HIV in society makes them feel sidelined among other people living in the given community. The feeling of being sidelined may force individuals to develop self-hatred and disgust and may end up developing suicidal thoughts (López et al., 2017). A lot of individuals tend to associate HIV with death and immorality and carelessness. Therefore the person who has just received a diagnosis of the disease is more likely to fall into a depression as a result of mental conflicts. Depression remains undiagnosed and uncontrolled in the HIV- infected group. When it comes to HIV, depressive diagnosis disorders can be severe.  This challenge is as a result of vegetative symptoms like insomnia, Alzheimer’s, amnesia and fatigue in most of the HIV patients even in the absence of depression (Marin-Webb, V, Jessen, Kopp, Jessen, and Hahn, 2016). These symptoms, however, relate with more of mental disorder than with clinical correlations of the disease. It is therefore essential for clinical detections on the depressive symptoms to be set up. The treatment of depressive signs and symptoms has been found by researchers to enhance the psychological functioning as well as life expectancy and quality of the infected individuals.

Mania is another psychological disorder linked with infection of HIV in other patients. The increase in mania cases relates to cognitive changes or dementia. Mania or insanity is considered a secondary HIV syndrome that has dangerous attacks on the vital CNS. In other terms, mania is commonly referred by clinicians as AIDS mania and is a phenomenologically different condition from the well known  and original manic syndrome. Clinicians associate a typical manic syndrome with bipolar disorder in its severity as well as symptom profile.

Psychosis is yet another disorder related to HIV-dementia in the CNS. Antiretroviral may at times precipitate psychosis, but it is an occasionally rare phenomenon. Psychosis was predominantly detected in patients having neurocognitive impairments related to AIDS (Marin-Webb et al., 2016). Navia and price used chart reviews to find out that 15% of a possible 46 patients with HIV-associated dementia experienced symptoms of psychosis (Price, Bartlett and Bloom, 2016). Psychosis can have detrimental results on the patients as it may cause them to lose themselves and their sanity.

Treatment options

The Psychiatric existence and presentation of HIV infection can be controlled and treated by clinicians. Trycyclin antidepressants (TCA) should be administered to HIV-seropositive patients (Woods et al., 2016). The FDA has provided positive reports on  the safety and efficacy of the tricyclic antidepressants. Imipramine being one of the TCA has been found very useful in depression treatment. Clinicians are also advised to provide HIV patients with mood stabilizers as the FDA has also accepted them for efficacy (Price et al., 2016). The knowledge on the influence of various agents on the general metabolism of the drug is essential even as medical practitioners administer the mood-stabilizing medicines to HIV patients. Carbamazepine being a mood-stabilizing drug may react with antiretroviral. The use of antipsychotic agents may as well be used to treat neurological disorders resulting from HIV. The method of these antipsychotic agents is not well studied and further research ought to be conducted to establish a familiar ground. The healing process also depends on how the patients choose to cope with the disease (Marin-Webb et al., 2016). Psychological therapies and counselling play an important role in a situation like the one stated. The patients should be educated and assured that they can as well live with the disease without necessarily letting the whole thought of death go into their subconscious.




In conclusion, patients living with HIV infection are more privileged in matters of life expectancy and mortality than it was the case in the olden days. The recent advancement in the antiretroviral has made things better for them. The relations in the immune system the neuropsychiatric symptoms and the neuroendocrine symptoms remain undefined, neuropsychiatric emergence complications in HIV can have detrimental consequences if not correctly identified. Careful diagnosis should be carried out on the patients to avoid complications. Patients diagnosed with HIV should accept their situations and deal with them. Psychologists should conduct thorough counselling on the patients just for the sake of their sanity. HIV is not necessarily a death penalty as many would like to consider it.  It can be addressed and managed to ensure a prolonged life expectancy as well as a sound sense of judgment amongst the people living with it.



De Almeida, S. M., Kamat, R., Cherner, M., Umlauf, A., Ribeiro, C. E., de Pereira, A. P., … & Ellis, R. J. (2017). Improving detection of HIV-associated cognitive impairment: comparison of the International HIV Dementia Scale and a Brief Screening Battery. Journal of acquired immune deficiency syndromes (1999), 74(3), 332.

López, E., Steiner, A. J., Smith, K., Thaler, N. S., Hardy, D. J., Levine, A. J., … & Goodkin, K. (2017). Diagnostic utility of the HIV dementia scale and the international HIV dementia scale in screening for HIV-associated neurocognitive disorders Applied Neuropsychology: Adult, 24(6), 512-521.

Marin-Webb, V., Jessen, H., Kopp, U., Jessen, A. B., & Hahn, K. (2016). Validation of the international HIV dementia scale as a screening tool for HIV-associated neurocognitive disorders in a German-speaking HIV outpatient clinic. PloS one, 11(12), e0168225.

Price, R., Bartlett, J., & Bloom, A. (2016). HIV-associated neurocognitive disorders: epidemiology, clinical manifestations, and diagnosis. UpToDate Web site https://www. uptodate. com/contents/HIV-associated-neurocognitive-disorders-epidemiology-clinical-manifestations-and-diagnosis.

Woods, S. P., Iudicello, J. E., Morgan, E. E., Cameron, M. V., Doyle, K. L., Smith, T. V., … & Ellis, R. J. (2016). Health-related everyday functioning in the internet age: HIV-associated neurocognitive disorders disrupt online pharmacy and health chart navigation skills. Archives of Clinical Neuropsychology, 31(2), 176-185.

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