Chronic mania and persistent euphoric states

Can a human be happy all the time?

Let me clarify; I don’t mean “happiness” in any kind of complex sense. I don’t mean wellbeing or eudaimonia or life satisfaction or anything like that. I mean being in a good mood – better than good, “high”, bubbly, enthusiastic.

In the psychiatry literature they call this state “euphoria” or “elation.” It can be produced by recreational drugs, or by placing electrodes in some locations in the brain, or by some brain injuries, or by neurological or psychiatric disorders. It is common in manic and hypomanic episodes. And, of course, it is a normal mood that healthy sober people can enter as well.

But most euphoric states are transient, and most ways to deliberately induce euphoria don’t work. Morphine, for instance, can produce euphoria, but not continuously for months at a time; you develop tolerance for the drug until the euphoria-producing dose and the fatal dose intersect. And people who have a stroke of good fortune like winning the lottery don’t stay euphoric forever – they initially feel great but then adapt to their changed circumstances.

So, you might ask, is there some kind of negative feedback loop in the brain such that euphoria is always temporary? Is it literally impossible to feel awesome all the time, for months or years at a stretch?

Turns out the answer is no.

There is something called chronic mania, which is just what it sounds like: a manic state, including euphoria/elation, which lasts for over 6 months, sometimes forever.

The nineteenth-century psychiatrist Emil Kraepelin was the first to give a clinical description of chronic mania, though some modern neurologists think that today those patients would be diagnosed with frontotemporal dementia[1], and in his day, chronic mania was the second most common reason for a patient to be committed to a mental hospital.[2]

Apart from the length of their episodes, chronic mania patients differ from bipolar patients in a few systematic ways. Chronic mania generally doesn’t alternate with depression, and is more likely than bipolar mania to come with an “elated mood.” Chronic mania, compared to bipolar mania, is more likely to come with delusions, especially delusions of grandeur, while bipolar mania is more likely to come with symptoms of psychomotor agitation like tension, pressured speech, loss of sleep, and elevated sex drive.[2] Chronic mania is more likely to begin after age 40.[3]

The typical pattern, from case studies, seems to be of a person who may have had transient manic episodes in the past, “settling into” a chronic manic state where they are generally euphoric but out of touch with reality, engaging in reckless, inappropriate, or obnoxious behavior, until they come to the attention of psychiatrists when neighbors or relatives bring them to the hospital.

Case Studies

Kraepelin commented on the behavioral disinhibition and poor impulse control of chronic mania patients:

“Only the coarser enjoyments, eating, drinking, smoking, snuffing, still arouse in them vivid feelings, further the satisfaction of their personal wishes and wants…[they] talk more than their share, swagger, try to gain for themselves all possible little advantage.”[1]

He also notes that they engage in hoarding behavior:

“They collect all possible rubbish in their pockets, make a mess with it all round about, rub and wipe things, adorn themselves with rags and scraps of ribbon.”[1]

Frederic Wertham, a psychiatrist writing in 1929, described cases of chronic mania that fit the overall pattern.[4] In all seven cases, the chronic mania began after age 30 (later than the typical onset of bipolar disorder), and in all cases it lasted several years. In several cases, the patients had previously had briefer manic episodes.

Wertham describes traits such as “pressure of activity, great sociability, lack of fatigue, good humor”, “noisiness and talkativeness”, “buoyant” and “elated” moods, “wild schemes” and delusions (of unrealistic business deals, religious revelations, million-dollar inheritances), “joviality and playfulness with jokes and laughing”, “vulgar and profane” language and sexual advances towards nurses.

Like Kraepelin’s patients, one of Wertham’s patients collects useless items and decorates herself – she “wore flowers in her hair and bits of colored wool tied to her buttons…continued decorating herself with little objects.”

Wertham notes some patterns: chronic mania patients tend to be middle-aged at onset, tend to have highly sociable and active personalities even before their illness, have no sign of cognitive decline (as you’d expect in dementia), and tend to be heavyset.

Similar features show up in more recent case studies of chronic mania: older age, hoarding, delusions, disinhibited behavior.

One 68-year-old woman[5] had been in an “elevated mood” state for 30 years, during which she increasingly hoarded objects and lived in increasing squalor, refusing all help. She had no sign of dementia or memory loss when tested, and no history of drug abuse. Prior to her illness she had had one depressive episode after the death of her husband, and before that she had been a “rather jovial schoolmistress” – like Wertham’s patients, her baseline personality was cheerful. She recovered after treatment with lithium.

A 65-year-old Indian man had been manic for 48 years,[6] with the onset beginning after a fever at age 12. He was “cheerful, optimistic, talkative, outgoing, and overly confident,” and became involved in politics with some success. But he also engaged in reckless behavior, traveling by train across India without paying his fare, stealing objects and giving them away to the poor. He “would often describe himself as a messenger of God with special powers, stating God had created him for the welfare of poor people”. He couldn’t hold down a job and he was divorced twice, but his mood was “persistently cheerful or irritable.” He was eventually hospitalized due to complaints by neighbors and relatives, and recovered after a temporary course of treatment with antipsychotics.

A 33-year-old woman who had been manic for 17 years[7] “expressed grandiose beliefs and evidenced a euphoric mood”, and had been unable to keep a job due to her “over-familiar” behavior. She had never abused drugs. “Her parents described her premorbid personality as generally affable, co-operative and creative but occasionally forceful and stubborn.”

Chronic Mania and Brain Damage

A variety of case studies of chronic mania identified a neurological cause.

One young woman who had mania-like symptoms since childhood (behavior problems, restlessness, talkativeness, labile and disinhibited mood, sexually provocative behavior starting at adolescence) was found upon radiological examination to have severe degeneration of the cerebellum.[8]

Another patient, a young man who had been electrocuted by getting entangled with a wire two years previously, developed manic symptoms of grandiose and persecutory delusions, hallucinations, poor judgment, and increased appetite.[9]

A 55-year-old man who had become irritable, extremely sociable, and extravagant with money was found to have an oligodendroglioma, a large brain tumor in the left temporoparietal lobe, and his symptoms improved after surgery.[10]

An eight-year-old child who had been ill with polioencephalomyelitis had a marked personality change – “he started talking excessively, singing songs and dancing. The symptoms became worse once he came home. He started talking with relatives, neighbours and strangers, content of talk was how he would act in a movie, how he would build a big house, that he would marry a beautiful lady, etc. He was singing film songs, was going out of the house and it used to be very difficult to locate and bring him back. His appetite was increased, sleep was disturbed. Majority of the time, he was very happy and cheerful.”[11]

A patient with a stroke damaging the periventricular zone of the hypothalamus was reported to have developed “persistent euphoria”, while in another case of brain surgery on the hypothalamus, “every time the surgeon gently wiped coagulated blood from the ventricle floor the patient burst out laughing, whistled, made jokes, and uttered obscene remarks.”[12]

An 81-year-old woman with a stroke in the right thalamus “became increasingly euphoric and talkative, and had grandiose delusions…believed that her health was better than ever and joked inappropriately. She also reported a decreased need for sleep.” After treatment with a temporary course of antipsychotics, she recovered but was still “mildly euthymic.”[13]

Out of 66 consecutive patients treated for head trauma, 6 (9%) developed mania[14]. The only lesion location significantly associated with mania was the temporal pole (p = 0.0005), which is also one of the first areas damaged in frontotemporal dementia and Alzheimer’s disease.

Compared to patients who developed bipolar disorder after brain injury, patients who developed only mania after brain injury were significantly more likely to have cortical lesions (esp. the orbitofrontal cortex and the right basotemporal cortex.)[15]

Another study found that mania after brain injury was “was associated primarily with orbitofrontal, thatamic, caudate, and basotemporal lesions in the right hemisphere.”[16]

The most common locations of lesions for patients with post-stroke mania (out of 74 cases) are the right frontal lobe and basal ganglia. Out of 16 patients who developed mania after a brain tumor, the tumor was in the frontal lobe, temporal lobe, or subcortical limbic structure in 13 patients, and two patients (12.5%) had chronic mania. [17]

One of the symptoms of multiple sclerosis is reported to be euphoria, or “euphoria sclerotica”, an unusual cheerfulness, optimism, and lack of awareness of their physical disability.

In a study of 44 MS patients and 22 healthy controls, 13% of MS patients had euphoria and 13% had disinhibition while no control subjects had either. There was a significant (p < 0.01) correlation between the degree of euphoria in the MS patients and the severity of frontotemporal degeneration observable on an MRI. [18]

Charcot’s original definition of multiple sclerosis in 1873 described “foolish laughter without cause” as one of the symptoms; Brown and Davis, in their survey of 100 cases in 1926, reported 63% of patients were euphoric. In an 1986 study of 76 MS patients, 48% were found to be euphoric, and the euphoric patients were more likely than the non-euphoric ones to have a progressive course of disease, to have brain involvement, and to have more severe physical & functional disability.[19]

Brain damage can cause mania, including chronic mania, in patients with no psychiatric history, particularly damage to the frontal and temporal lobes. Damage to other locations such as the cerebellum, thalamus, and hypothalamus can also cause mania. There also seems to be a tendency for mania to be more common as a result of damage to the right brain hemisphere.

The frontal and temporal lobes are involved in self-restraint and appropriate behavior, so it’s not surprising that damage to them should cause some of the disinhibitory and compulsive aspects of mania. Apparently, brain damage can also cause persistently euphoric states.

Conclusions

I think we can safely say that it is possible for humans to remain in a euphoric state, continuously for months or years on end. (Often in these case studies the euphoria is punctuated by irritability, but not sadness or depressed mood.)

Now, most of the examples we know of these prolonged euphoric states are undesirable. They often come with reckless or harmful behavior, delusions, and cognitive impairment.

They’re also unpredictable – some but not all people who get strokes, tumors, or injuries to these brain areas will become manic or otherwise euphoric.

But the existence of persistent euphoric states suggests that it could be in principle possible to deliberately induce a long-lasting elevated mood without some of the problematic side effects.

It’s a common finding that deep brain stimulation of the nucleus accumbens or subthalamic nucleus can cause transient feelings of euphoria, and sometimes outright manic episodes.[21][22][23][24][25][26][27][28] However, there is a tolerance effect here – with continuous stimulation for a year, the same stimulus that initially caused euphoria produced no perceivable effect at 12 months.[29] It’s not impossible that some variant on this type of electrical stimulation could produce long-term euphoria, though, at a deliberately tuned dose (since higher voltages cause stronger mood effects). So I’m intrigued by the prospects of developing a form of “wireheading done right.”

References

[1]Gambogi, Leandro Boson, et al. “Kraepelin’s description of chronic mania: a clinical picture that meets the behavioral variant frontotemporal dementia phenotype.” Arquivos de neuro-psiquiatria 74.9 (2016): 775-777.

[2]Perugi, Giulio, et al. “Chronic mania.” The British journal of psychiatry 173.6 (1998): 514-518.

[3]Cameron, Kenneth. “Chronic mania.” Journal of Mental Science 82.340 (1936): 592-594.

[4]Wertham, F. I. “A group of benign chronic psychoses: prolonged manic excitements: with a statistical study of age, duration and frequency in 2000 manic attacks.” American Journal of Psychiatry 86.1 (1929): 17-78.

[5]Fond, G., F. Jollant, and M. Abbar. “The need to consider mood disorders, and especially chronic mania, in cases of Diogenes syndrome (squalor syndrome).” International psychogeriatrics 23.3 (2011): 505.

[6]Mendhekar, D. N., et al. “Chronic but not resistant mania: a case report.” Acta Psychiatrica Scandinavica 109.2 (2004): 147-149.

[7]Malhi, G. S., P. B. Mitchell, and G. B. Parker. “Rediscovering chronic mania.” Acta Psychiatrica Scandinavica 104.2 (2001): 153-156.

[8]Cutting, J. C. “Chronic mania in childhood: case report of a possible association with a radiological picture of cerebellar disease.” Psychological medicine 6.4 (1977): 635-642.

[9]Ameen, Shahul, Siddhartha Dutta, and Vinod Kumar Sinha. “Electroencephalogram changes and its improvement with sodium valproate in a patient with electrocution-induced chronic mania.” Bipolar disorders 5.3 (2003): 228-229.

[10]Rahul, S. A. H. A., and Kiran Jakhar. “Oligodendroglioma presenting as chronic mania.” Shanghai archives of psychiatry 27.3 (2015): 183.

[11]Subrahmanya, B., and Shivaprakash HS Narayana. “CHRONIC MANIA FOLLOWING POLIOENCEPHALOMYELITIS—A CASE REPORT.” Indian journal of psychiatry 23.3 (1981): 266.

[12]Barbosa, Daniel AN, et al. “The hypothalamus at the crossroads of psychopathology and neurosurgery.” Neurosurgical focus 43.3 (2017): E15.

[13]Kulisevsky, Jaime, Marcelo L. Berthier, and Jesús Pujol. “Hemiballismus and secondary mania following a right thalamic infarction.” Neurology 43.7 (1993): 1422-1422.

[14]Jorge, Ricardo E., et al. “Secondary mania following traumatic brain injury.” American Journal of Psychiatry 150 (1993): 916-916.

[15]Starkstein, Sergio E., et al. “Manic-depressive and pure manic states after brain lesions.” Biological Psychiatry 29.2 (1991): 149-158.

[16]Robinson, Robert G., et al. “Comparison of mania and depression after brain injury: causal factors.” Am J Psychiatry 145.2 (1988): 172-178.

[17]Satzer, David, and David J. Bond. “Mania secondary to focal brain lesions: implications for understanding the functional neuroanatomy of bipolar disorder.” Bipolar Disorders 18.3 (2016): 205-220.

[18]Diaz-Olavarrieta, Claudia, et al. “Neuropsychiatric manifestations of multiple sclerosis.” The Journal of neuropsychiatry and clinical neurosciences 11.1 (1999): 51-57.

[19]Rabins, PETER V. “Euphoria in multiple sclerosis.” Neurobehavioral aspects of multiple sclerosis (1990): 180-185.

[20]Mosley, Philip E., et al. “Persistence of mania after cessation of stimulation following subthalamic deep brain stimulation.” The Journal of neuropsychiatry and clinical neurosciences 30.3 (2018): 246-249.

[21]Synofzik, Matthis, Thomas E. Schlaepfer, and Joseph J. Fins. “How happy is too happy? Euphoria, neuroethics, and deep brain stimulation of the nucleus accumbens.” AJOB Neuroscience 3.1 (2012): 30-36

[22]Haq, Ihtsham U., et al. “Smile and laughter induction and intraoperative predictors of response to deep brain stimulation for obsessive-compulsive disorder.” Neuroimage 54 (2011): S247-S255.

[23]Anderson, Karen E., and Jake Mullins. “Behavioral changes associated with deep brain stimulation surgery for Parkinson’s disease.” Current neurology and neuroscience reports 3.4 (2003): 306-313.

[24]Greenberg, Benjamin D., et al. “Three-year outcomes in deep brain stimulation for highly resistant obsessive–compulsive disorder.” Neuropsychopharmacology 31.11 (2006): 2384-239

[25]Kuhn, Jens, et al. “Transient Manic‐like Episode Following Bilateral Deep Brain Stimulation of the Nucleus Accumbens and the Internal Capsule in a Patient With Tourette Syndrome.” Neuromodulation: Technology at the Neural Interface 11.2 (2008): 128-131.

[26]Mosley, Philip E., et al. “Persistence of mania after cessation of stimulation following subthalamic deep brain stimulation.” _The Journal of neuropsychiatry and clinical neurosciences _30.3

[27]Chopra, Amit, et al. “Voltage-dependent mania after subthalamic nucleus deep brain stimulation in Parkinson’s disease: a case report.” Biological psychiatry 70.2 (2011): e5-e7.

[28]Tsai, Hsin-Chi, et al. “Hypomania following bilateral ventral capsule stimulation in a patient with refractory obsessive-compulsive disorder.” Biological psychiatry 68.2 (2010): e7-e8.

[29]Springer, Utaka S., et al. “Long-term habituation of the smile response with deep brain stimulation.” Neurocase 12.3 (2006): 191-196.

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