Major depressive disorders
Dysthmic disorder
Depressive disorders not otherwise specified
Bipolar 1 disorder
Bipolar II disorder
Cyclothymic disorder
Bipolar disorder not otherwise specified
Mood disorder due to a medical condition
Substance induced mood disorder
Mood disorder not otherwise specified
Each of these disorders may involve a depressive episode, manic episode, mixed episode, hypomanic episode or a combination of any two different episodes. Thus a Bipolar I disorder is characterized by one or more manic or mixed episodes usually accompanied by a depressive episode while a Bipolar II disorder is characterized by one or more Major depressive episodes accompanied by at least one hypomanic episode.
Further classification could involve determining whether the cause is primary or secondary and from here the terms primary mania or secondary mania evolve [11]. One can differentiate mania based on the cause by dividing it into primary or idiopathic mania and secondary mania (where there is an identifiable cause.) This classification of primary and secondary mania was first suggested by Robins and Guze in 1972 [12] and improved by Klerman and Barret and later Krauthemmer in 1978 [13]. However the distinction of primary versus secondary disorders was first muted by Alistair Munro.
Initially secondary mania was described by Robins and Guze as mania occurring in patients who had no previous or concurrent psychiatric illness. Klermman and Barret later described it as an illness following past history of medical, traumatic or pharmacological complaints and use. Krauthemmer took the concept further to describe secondary mania as mania that can occur in association with organic dysfunction – medical and pharmacological toxic – in patients with no history of affective disorder. He was also the first to describe the clinical characteristics of secondary mania being different from primary mania where he noticed that patients of secondary mania were older with no family history of mania. The concept of secondary mania is that a patient can present with symptoms that are similar to the diagnostic criteria for primary mania but with an identifiable cause. In some cases the clinical characteristics are different. Thus HIV secondary mania became to be recognized as a disorder of HIV infective brain degeneration.
Secondary Mania of HIV/AIDS
Over the last 10 years research done in Africa and Uganda in particular has shown that mental health issues in HIV are not just psychological reactions to having the disease but rather a consequence of the HIV virus attacking brain tissue [2]. Dementia, major depression, psychosis, and mania are some of the mental health conditions that have been studied quite extensively by Ugandan researchers and have been shown to be different entities from the same conditions in HIV negative populations [2, 3, 14–19]. Mental health disorders in HIV/AIDS seem to be a sequalae of the neuropathogenesis of the virus itself which leads to presentations of some mental health conditions to be different between HIV positive and HIV negative groups.
In the case of mania this has led to the development of the term secondary mania of HIV/AIDS also referred to as HIV mania which was well described by Nakimuli-Mpungu et al. [18]. They described secondary mania of HIV/AIDS as a distinct syndrome with different clinical presentation from patients with primary mania without HIV and bipolar mania in HIV. This differing clinical presentation impacts on treatment modalities prognosis and in low resource settings investigations and as such clinicians need to be aware of this syndrome.
Etiology
In primary mania there have been various studies on the different aetiologies of mania. It should be noted that they are usually multifactorial and as such a biopsychosocial model is usually adopted to define the different causes of primary mania. The main theories of mania include increased neurotransmitter function especially dopamine and serotonin; genetics proved through family and twin studies and psychodynamic factors as described by Abraham, Lewin and Klein [20]. From the late 1970s Krauthemmer suggested organic causes of mania. He noted that drugs metabolic disturbances and infections were all associated with developing manic episodes. Since then a large number of organic substances have been associated with development of manic symptoms (see Table 19.2).
Table 19.2
Causes of secondary mania
Drugs of abuse |
Alcohol abuse |
Amphetamine abuse |
Cocaine abuse |
Hallucinogen abuse |
Opiate abuse |
Collagen vascular disease |
Systemic Lupus Erythematosus |
Infectious disease |
Neurosyphilis |
Herpes Encephalitis |
Influenza |
St. Louis Encephalitis |
HIV/AIDS |
Endocrine disease |
Hyperthyroidism |
Hypothyroidism |
Neurologic disease |
Multiple Sclerosis |
Huntington’s Chorea |
Wilson disease |
Head trauma |
Complex partial seizures |
Cerebrovascular accidents |
Migraine headache |
Neoplasms (esp. diencephalic or third ventricle) |
Medications |
Neuropsychiatric |
Monoamine oxidase inhibitors |
Heterocyclic antidepressants, SSRI |
Methylphenidate |
Disulfiram |
Levodopa |
Cardiovascular |
Captopril |
Hydralazine |
Endocrine |
Bromocriptine |
Steroids |
Miscellaneous |
Baclofen |
Bromide |
Procarbazine |
Yohimbine |
Cimetidine |
Isoniazid |
Vitamin deficiency |
Vitamin B12 deficiency |
Folate deficiency |
Niacin deficiency |
Thiamine deficiency |
Pathogenesis
As is the case for many psychiatric conditions that are co morbid with HIV, the pathogenesis is not entirely understood. Five main theories have been postulated to determine how HIV causes mania in particular. These include the following:
i.
Direct effects of the virus on the central nervous system.
ii.
Opportunistic infections and the metabolic effects associated with them.
iii.
Drugs used in the treatment of HIV/AIDS like HAART especially the non nucleoside reverse transcriptase inhibitor Efavirenz and steroids.
iv.
Psychological challenges associated with having HIV/AIDS.
v.
HIV associated neuro cognitive disorders (HAND) causing brain degenerations
vi.
HIV associated CNS neoplasms.
Previous studies have tried to determine the pathogenesis of HIV-related mania. HIV preferentially affects sub cortical gray matter such as the caudate nuclei and cortical white matter, both of which are important in the regulation of mood, thus manic symptoms indicating CNS HIV infection. HIV-related mania may be caused by accumulation of intracellular free calcium, which has been implicated in the pathogenesis of bipolar disorder [21] and has similarly been shown to be increased in HIV infected neurones [22, 23]. On the other hand, El-Mallakh suggested that mania or hypomania appeared to be related to immunosuppression and progression of HIV disease.
Clinical Features
Making a diagnosis of mania ideally entails following the set criteria as laid out in the DSM IV TR. In summary the classification states that the symptoms should last for at least 1 week (or less if hospitalization is required); should not involve a mixed episode, not be due to the effects of a substance and should affect social occupational functioning.
A patient with HIV mania usually meets the criteria set out for a manic episode. Primary mania is highly hereditary but in the case of HIV mania the patient usually does not have previous history of this illness or family history of the disease [16–19]. Patients with secondary mania of HIV/AIDS however present with irritability more than euphoria; are more over talkative with decreased need for sleep. They are more cognitively impaired with more perceptual disturbances [16–18, 24]. The DSM classification of a manic episode does not report any cognitive or perceptual disturbances.
![](https://freepngimg.com/download/social_media/63059-media-icons-telegram-twitter-blog-computer-social.png)
Stay updated, free articles. Join our Telegram channel
![](https://clinicalpub.com/wp-content/uploads/2023/09/256.png)
Full access? Get Clinical Tree
![](https://videdental.com/wp-content/uploads/2023/09/appstore.png)
![](https://videdental.com/wp-content/uploads/2023/09/google-play.png)