‘The soul, fortunately, has an interpreter . . . the eye’. Charlotte Bronte
Eye changes are commonly distinctive in those with a bipolar disorder during manic/hypomanic and depressive states. This is not a new observation, with Scottish psychiatrist Sir Alexander Morison (1840) providing illustrative pictorial plates of many patients, including one with puerperal mania whose ‘. . . eyes had a wild glistening appearance and wandered rapidly from one object to another’ (p. 23) and another whose eyes were ‘brilliant’ (p. 79).
In the first author’s clinical experience, if there are eye changes during manic/hypomanic episodes, the most commonly observed ones are (1) ‘sparkling eyes’ – where the eyes are bright and there may be a shimmering quality (i.e. shining with or without wavering) and (2) dilated pupils. Very rarely a colour change may be observed – most commonly involving those with blue eyes having them turn from blue to brown, but the eyes can also blacken (anecdotally described as more common in dysphoric manic/hypomanic states but also observed by the first author in several patients when they developed a mixed state). For the clinical psychiatrist managing a patient with a bipolar disorder, observing the patient as unusually bright-eyed may be a key marker identifying a manic/hypomanic state.
For those with a bipolar disorder, episodes of depression are most commonly melancholic in type, with psychom*otor disturbance being its most prototypic feature. In such states, there is commonly decreased facial reactivity and less ‘light in the eyes’, often creating a vacant or inert impression. Sufferers may also report perceptual dimming (e.g. that ‘life has lost its colours’). The eye changes in Morison’s bipolar patients during manic and depressive episodes well capture the respective sparkling and vacant phases despite the book’s black and white plates.
The question contemplated here is to speculate on possible determinants of such bipolar eye changes (particularly in the manic/hypomanic phase)?
Those in a manic/hypomanic state are generally happy, euphoric, or even elated. As it is normal for those without any clinical mood disorder to also be bright-eyed when happy or excited, is this simply the explanation? In addition, those in a manic/hypomanic state may dress in bright clothes. Make up chosen in such states is often bright and radiant, with many eye liners designed to create brighter and more ‘brilliant’ eyes. Such artefactual explanations may be in play but are unlikely to be fully explanatory.
Eye gaze is central to social communication and which may advance essential social information being both communicated and ascertained. Since the human eye has a large, white scleral area surrounding the coloured iris and great motility, a drastic change from ‘poker faced, gaze-camouflaging’ eyes to ‘gaze-signalling’ eyes engineered the remarkable difference between humans and other primates in the ability to communicate using gaze signals. Anecdotally, we observe that those with a bipolar disorder evidence more direct eye gaze during manic/hypomanic states and less direct gaze during depressive states.
Eye glint – specular reflection of light by the cornea – has been identified as a potential cue to gaze direction. Gaze-signal enhancement is also thought to enhance the communication required for increased cooperative and mutualistic behaviours. It is commonly increased during hypo/manic states and reduced in bipolar depressive phases. Such changes may be correlates of, or contribute to, improved performance commonly observed in hypo/manic states and compromised performance in bipolar depressive states.
Turning to underpinning factors, from a neurobiological perspective and expressed simplistically, mania is commonly positioned as a hyperdopaminergic state while levels of noradrenalin are also increased (Kurita, 2016). Increased norepinephrine levels in manic/hypomanic states causing sympathetic discharge would result in pupillary dilation, causing the eyes to dilate. The dilatation would result in increased contrast with the white sclera and make the eyes appear darker. For someone with blue irises, the blue would then be pushed to the periphery so that the blue eyes would then be less obvious.
Perception is commonly enhanced during manic/hypomanic phases. In one descriptive paper (Parker, 2014), some patients with a bipolar disorder observed that their vision sharpened during manic/hypomanic states, with objects often more vivid or brighter (causing some patients to wear sunglasses) or observed with greater clarity. Furthermore, some noticed their vision becoming more focused (wishing only to observe one thing at a time), or that colours were amplified, or that their visual periphery expanded so that they were more likely to see things out of the corner of their eye, or noted an inability to filter things (like a scratch on a table) out of their vision.
Depressive episodes in those with a bipolar disorder are most commonly melancholic in type, with psychom*otor retardation being a key sign and symptom. The concomitant decreased facial reactivity (here around the eyes) generates less luminosity, while any eye lag or hooded eyelids at such times may seemingly darken the appearance of the eyes.
In an earlier paper (Hyett and Parker, 2013), we overviewed potentially salient neurobiological changes in visual cortical processing regions and the retina during (unipolar and bipolar) melancholic states. As in Parkinson’s disease, there can be lowered visual ‘contrast sensitivity’ whereby distinguishing differing levels of contrast in an image or scene is reduced, and which presumably reflects compromised dopaminergic functioning.
Pupillary size is controlled by parasympathetic and sympathetic divisions of the autonomic nervous system. Pupil constriction tends to occur more rapidly in response to light in melancholic patients, and likely reflecting norepinephrine hypoactivation. It may then be that the ‘loss of light in the eyes’ in the melancholic phase reflects constricted pupils in part as well as ocular dryness-associated loss of ‘sparkle’. Since the iris and lacrimal system are both sympathetically and parasympathetically innervated, and there is sympathetic innervation of Müller’s muscle, pupil diameter, and palpebral width, eye ‘sparkle’ may be affected by autonomic neural tone, significantly modulating ocular appearance.
In addition to changes in the visual cortex, several studies have suggested changes in the retina as well, and with the retina having dopamine as well as multiple other neurotransmitters. For example, Mehraban et al. (2016) quantified reduction in retinal nerve fibre layer thickness in a sample of patients with a bipolar disorder, with such structural changes allowing that the retina is a site for functional changes as well.
We have suggested that those with a bipolar disorder may, during manic/hypomanic states, evidence sparkling eyes, have dilated pupils and, albeit rarely, evidence iris colour changes – especially blackening. Conversely, during depressive episodes, they may have ‘less light in the eyes’ and report or experience perceptual dimming. Such changes may have an atavistic base. Possible determinants remain quite speculative and are likely to involve multiple mechanistic processes.
The observations can have distinct clinical relevance. Eye changes in those with a known bipolar disorder can inform the clinician and family members as to whether the patient is in a manic/hypomanic or depressive phase. This paper seeks to highlight such clinical signals and briefly and clearly speculatively overview several candidate determinants of such striking changes.
Footnotes
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding: The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was supported by the Australian National Health and Medical Research Council (NHMRC; grant no. GNT1176689). The contents of the published material are solely the responsibility of the individual authors and do not reflect the views of the NHMRC.
ORCID iDs: Gordon Parker https://orcid.org/0000-0003-3424-5519
Michael J Spoelma https://orcid.org/0000-0003-2844-0748
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