|Year : 2016 | Volume
| Issue : 2 | Page : 30-35
Paryakula drishti of Unmada: Deficits of smooth pursuit eye movements and anti-saccades in schizophrenia
Kshama Gupta, Prasad Mamidi
Department of Kaya Chikitsa, Parul Institute of Ayurveda, Parul University, Vadodara, Gujarat, India
|Date of Web Publication||1-Nov-2017|
Department of Kaya Chikitsa, Parul Institute of Ayurveda, Parul University, Vadodara, Gujarat
Source of Support: None, Conflict of Interest: None
Bhuta vidya (Ayurvedic psychiatry) is one of the eight specialties of Ayurveda. Unmada is a broad term which includes various psychiatric disorders described in modern psychiatry. The classification, etiology, pathogenesis, signs and symptoms, prognosis, and treatment of Unmada are available in all Ayurvedic classical texts. Abnormal eye movements such as “Paryakula drishti” (abnormal eye movements which denotes excitement or confusion or agitation)/“Chakshusho aakulata” (abnormal eye movements denotes confusion or perplexity)/“Chakshusho aswasthatvam” (abnormal eye movements) and “Chakshushoscha apasarpanam” (abnormal tracking) are mentioned among various signs and symptoms of Unmada. In Ayurveda, till date, no studies have been conducted, and no focus has been given on these abnormal eye movements of Unmada. The present study aims at understanding of these abnormal eye movements mentioned in Unmada with the help of modern research and literature. Abnormal smooth pursuit eye movements, decreased pursuit gain, increased saccadic frequency, increased anticipatory saccades, and anti-saccade errors are well-documented in schizophrenia patients. It seems that ancient Indian Ayurvedic sages had tremendous observational and clinical skills by which they were able to detect abnormal eye movements in the patients suffering from various psychiatric disorders thousands of years before. Various abnormal eye movements such as smooth pursuit eye movements deficits, abnormal saccadic eye movements, and other abnormal eye movements in schizophrenia resembles with “Paryakula drishti/Chakshusho aakulata/Chakshusho apasarpanam” of Unmada. Currently available research based on abnormal eye movements in schizophrenia supports the Ayurvedic view.
Keywords: Anti-saccades, Ayurveda, Paryakula drishti, Unmada, schizophrenia, smooth pursuit eye movements
|How to cite this article:|
Gupta K, Mamidi P. Paryakula drishti of Unmada: Deficits of smooth pursuit eye movements and anti-saccades in schizophrenia. Int J Yoga - Philosop Psychol Parapsychol 2016;4:30-5
|How to cite this URL:|
Gupta K, Mamidi P. Paryakula drishti of Unmada: Deficits of smooth pursuit eye movements and anti-saccades in schizophrenia. Int J Yoga - Philosop Psychol Parapsychol [serial online] 2016 [cited 2021 Sep 19];4:30-5. Available from: https://www.ijoyppp.org/text.asp?2016/4/2/30/217478
| Introduction|| |
Unmada is a broad term which includes various psychiatric diseases. Unmada means, “a state of disturbed mental functions.” According to Acharya Charka, deviation of manas (mind), buddhi (decision), smriti (memory), sangya gyanam (orientation and responsiveness), bhakti (desire), sheela (habit), cheshta (activity), and achaara (conduct) like eight factors (either all together or some of them) is the characteristic pathological feature of Unmada. Abnormal eye movements like “Paryakula drishti” (abnormal eye movements which denotes excitement or confusion or agitation)/“Chakshusho aakulata” (abnormal eye movements denotes confusion or perplexity)/“Chakshusho aswasthatvam” (abnormal eye movements/vision) and “Chakshushoscha apasarpanam” (abnormal tracking) are mentioned among various signs and symptoms of Unmada.,,,,, In Ayurveda, till date, no works have been conducted on abnormal eye movements of Unmada. The present study aims at understanding of these abnormal eye movements mentioned in Unmada with the help of modern research and literature.
| Abnormal Eye Movements Mentioned in Unmada|| |
The classification, etiology, pathogenesis, signs and symptoms, prognosis, and treatment of Unmada are available in all Ayurvedic classical texts. Acharya Charaka has mentioned, “Chakshusho aakulata” and “Chakshushoscha apasarpanam” in Unmada poorva roopa (prodromal signs and symptoms of Unmada). “Paryakula drishti” is one of the signs of Unmada according to Acharya Charaka. In “Ashtanga samgraha” (written by Vriddha vagbhata), “Chakshusho aswasthatvam” and “Chakshushoscha apasarpanam” are mentioned in Unmada poorva roopa. In “Madhava nidaana”, “Paryakula drishti” is mentioned as one of the sign of Unmada. In “Sushruta Samhita” and “Ashtanga hridaya,” no references are available regarding abnormal eye movements in Unmada context.,
The meaning of the word, “Paryakula” is “excited” or “agitated” or “confused” or “bewildered” or “disordered” or “affected” or “perturbed” and “Aakulata” denote either “confusion” or “perplexity.” The word “Apasarpanam” means “zoom out” or “going back” or “retreating.”Paryakula drishti or Chakshusho aakulata or Chakshusho apasarpanam denotes an abnormal gaze or abnormal eye movements or unstable gaze in general.
| Eye Movements|| |
Eye movements are defined as any shift of the eye position in its orbit. They are important for vision, attention, memory and they also determine what we see, attend to and remember about our surroundings. Eye movements are thus central to various executive functions. A better understanding of eye movements provides a valuable window into executive functions. Eye movements are useful to stabilize images on the retina and to keep objects of interest on the fovea (the retinal area which has the greatest visual acuity and the greatest representation in visual cortices). There are four basic types of eye movements: saccades, smooth pursuit eye movements, vergence movements, and vestibule-ocular movements.
Smooth pursuit eye movements
Smooth pursuit eye movements (SPEMs) are voluntary tracking eye movements that allow us to keep the retinal image of a moving target within the foveal area. Whenever the retinal image moves out of the foveal area visual acuity decreases, and it is either because of motion of the visual object or head movements. SPEMs compensate for such retinal image dislocations. The smooth pursuit system generates eye movements that track slowly moving targets. Smooth pursuit movements are conjugate eye movements (in which both the eyes move in the same direction). SPEMs are generally much slower than saccades. Smooth pursuit is a voluntary task which requires both motivation and attention. SPEMs are the result of a complex transformation from visual motion signals at the fovea to an oculomotor signal. The cortical input to the smooth eye movement generation centers in the brain stem is required to enable smooth tracking motion.
Saccades are rapid, ballistic movements of the eyes which abruptly change the point of fixation. They range in amplitude from the small movement made while reading to the much larger movements made while gazing around a room. Saccades serve to rapidly shift gaze to bring a new object of interest to the fovea. Saccades are further subdivided into two sub classes: reflexive and voluntary. Reflex saccades are elicited in response to a sudden movement, flash or change in the environment. The latency (onset of movement) of a reflexive saccade to a visual target is typically around 200–-250 ms (but it can be as short as 70–80 ms). Voluntary saccades are more complex, and they involve executive functions which are thought to critically involve frontal cortex, and they have latencies as long as 400 ms.
Vergence movements are disconjugate (disjunctive) type of eye movements and they involve a convergence or a divergence.
Vestibulo-ocular movements stabilize the eyes relative to the external world, thus compensating for head movements. During locomotion (self-motion) or during head movements, images of the visual world would blur up and slip across the retina with each movement in the absence of compensatory eye movements. Two classes of eye movements evolved to stabilize images on the retina during head and body movements. They are: vestibulo-ocular and optokinetic reflexes. In vestibulo-ocular reflex, when the head moves to the left, “vestibular” sensors in the inner ear are triggered and signal nuclei in the horizontal and vertical gaze centers of the brain stem to create an equal and opposite eye velocity signal. The result is that the vestibule-ocular reflex initiates a rapid eye movement to the right (with in 15 ms) to compensate for the head movement, keeping the retina stable with respect to the external world. The optokinetic reflex complements the first by full-field “visual” information about self movement to compensate for the perturbation of the visual world on the retina. That is, as a result of self-motion to the left, the entire visual image will move across the retina in a right ward direction. The speed of the image triggers nuclei in the brainstem to create an equal right ward eye velocity signal. The result is the optokinetic reflex, an eye movement in the same direction as the retinal slip to keep the retina stable with respect to the external world.
| Abnormal Eye Movements in Schizophrenia|| |
Schizophrenia is the most prevalent psychiatric illness in the world, occurring in about 1% of the population. It is also considered the most costly and debilitating psychiatric disorder and is among the top causes of disability in developing countries. Schizophrenia is usually characterized by hallucinations, delusions, blunted affect, alogia (i.e., poverty of speech), and avolition. Numerous cognitive functions such as executive control, working memory, and attention are disturbed in schizophrenic patients. Schizophrenia is probably a heterogeneous disorder with uncertain phenotypic expressions.
Eye movement tasks have been shown to be a more reliable and sensitive measures to investigate the deficits in schizophrenia patients. The study of eye movements is an important research tool that will shed light on both executive functions and also debilitating human disorders like schizophrenia. Eye movements provide invaluable information about various executive functions and provide an efficient, noninvasive way to study the role of abnormal brain processes in a variety of human disorders. Eye movements are also used for investigating the cognitive and neurological processes involved in the pathophysiology of schizophrenia.
Smooth pursuit eye movement deficits in schizophrenia
Among various biochemical and psychophysiological characteristics studied as the genetic marker of schizophrenia the status of SPEM dysfunction as a genetic marker has been most consistently supported by previous studies. The smooth pursuit system generates eye movements which track slowly moving targets. The function of pursuit system is to maintain the image of the target on the fovea. Many studies have reported impaired smooth pursuit in patients with acute and chronic schizophrenia. In 65%–80% of the patients with chronic schizophrenia defective pursuits were observed. Some studies claimed that increased distractibility or an information overload might be the causes for these deficits. A genetic contribution to smooth pursuit may be a trait associated with vulnerability to schizophrenia. Abnormal pursuit has been previously described in patients with schizoaffective disorders and manic-depressive psychosis also.
There are at least two possible causes of abnormal SPEMs found in schizophrenic patients: an impaired smooth pursuit tracking system associated with low gain and increased numbers of compensatory or catch-up saccades and saccadic disinhibition which associated with increased numbers of noncompensatory saccades or saccadic intrusions. Impairment in frontal function has been proposed as a pathophysiological explanation for abnormality in SPEMs of schizophrenic patients, impairments in attention, motivation, and also affect. The prefrontal cortex, specifically, the frontal eye fields are involved in the generation of SPEMs. Schizophrenic patients with abnormal SPEM show a deficit on a task of voluntary orienting, as represented in a study by the anti-saccade task. Abnormal SPEMs in patients with schizophrenia are often considered as a consequence of impaired motion perception. Characteristics of smooth pursuit deficits in schizophrenia are predictive pursuit, global decrease in pursuit smoothness, and accuracy which may be caused by impairment in low-level motion processing, and/or higher-level predictive mechanisms such as an inability to generate or use efference copy information.
Abnormal SPEMs are one of the most reproducible findings in schizophrenia research. Schizophrenia patients have decreased pursuit gain when compared to healthy individuals. SPEM deficits are not specific to schizophrenia only they have been observed in multiple neurological and psychiatric disorders such as Parkinson's disease, Alzheimer's disease, and in affective disorders also. Evidence of prefrontal cortex abnormalities being associated with SPEM deficits in schizophrenic patients was found in a structural magnetic resonance imaging study showing that lower smooth pursuit gain was associated with decreased gray matter integrity in the right prefrontal cortex in schizophrenia patients. Abnormal SPEM performance in schizophrenia to some extent is related to attention deficits. Visual fixation errors also found increased in schizophrenia patients compared to control subjects.
Abnormalities of SPEMs in schizophrenia patients and their first-degree relatives have been well documented. First-degree relatives of affected probands showed higher prevalence than members of unaffected families. Several studies have also demonstrated deficits in SPEM in bipolar disorders patients. Patients with unipolar depression also showed pursuit deficits. An association of eye tracking disorder and deficit syndrome in schizophrenia patients has been reported. These deficits might serve as a phenotypic marker for the genetic liability for schizophrenia.
Deficits in anti-saccade tasks in schizophrenia
In the anti-saccade task a participant is required to refrain from looking at a target appearing unpredictably in the left or right peripheral location, and instead, make rapid voluntary eye movements (saccades) to the opposite peripheral location. Generation of a reflexive saccade in direction of the peripheral target is considered an error. Anti-saccade performance is sensitive to the function of several cognitive processes and the task has become an important research tool in the field of psychology and psychiatry for investigating cognitive deficits. The anti-saccade task has been evolved as a promising endophenotype in studies of schizophrenia. There is an evidence of increased anti-saccade errors in individuals with schizotypal traits and in patients with prodromal symptoms of psychosis which indicates that anti-saccade deficits precede the appearance of schizophrenia. Several studies have shown reduced spatial accuracy of correct anti-saccades in the patients of schizophrenia.
Anti-saccade deficits are not specific to schizophrenia they are also found in several other psychiatric and neurological disorders. There is an evidence for the involvement of several cognitive processes in anti-saccade performance such as inhibitory processes, attention, working memory, error monitoring, and learning. Anti-saccade errors in schizophrenia patients are often interrupted due to failures in inhibitory processes. Impaired attention may contribute to anti saccade deficits in schizophrenia. Schizophrenic patients were less able to suppress irrelevant stimuli during the anti-saccade task. Working memory refers to the ability to temporally store and manipulate task relevant information while performing a goal directed task. Significant correlation found in schizophrenia patients between spatial working memory and anti-saccade performance. Worse spatial working memory has been associated with worse anti-saccade performance in patients of schizophrenia. Schizophrenia patients have shown that anti-saccade deficits are significantly associated with working memory deficits.
The abnormal patterns of eye movements found in schizophrenic patients are saccadic intrusions and saccadic smooth pursuit. Abnormally high velocity of saccades during pursuit tracking in schizophrenic patients was found. An increased prevalence of dysmetric saccades has also been reported in schizophrenics. Schizophrenia patients have an excessive number of fast, jerky eye movements, which are called saccades, during a task requiring a SPEM response. Increased saccadic frequency and increased anticipatory saccades were found in patients with schizophrenia.
Impairments in the performance of the smooth pursuit, the saccades and the anti-saccades were found in schizophrenia patients. Previous studies of anti-saccade performance have reported that schizophrenic patients show significantly higher error rates and longer latencies than normal subjects. Higher error rates and longer latencies suggest that schizophrenic patients have difficulty in suppressing reflective saccades to the target and correctly initiating voluntary saccades to the opposite side. Both anti-saccade difficulty and impaired eye tracking in schizophrenic patients are consistent with a prefrontal dysfunction hypothesis.
In an anti-saccade task, a peripheral target is presented and the correct response is to look to the opposite side of the screen, away from the target. The anti-saccade task requires a person to inhibit the reflexive inclination to look at the target and also to generate a voluntary saccade to the correct location opposite to the target. Abnormal responses in the anti-saccade task include increased latency and directional errors (looking toward the target). Schizophrenic subjects have showed two basic deficits in SPEMs: reduced gain of smooth pursuit and increased saccadic events. One measure of accuracy in SPEM paradigms is pursuit gain (the ration between eye velocity and target velocity). Errors in gain can be amended with catch-up saccades (when smooth pursuit lags behind the target) and back up saccades (when tracking ahead of the target). Intrusive saccades, which interrupt smooth pursuit tracking and they denote inhibitory failures or inappropriate activations. People with schizophrenia show reduced gain that is, their eyes do not keep up with the target, and they fall behind due to this schizophrenic patients often exhibit increased saccadic activity (catch-up saccades) during smooth pursuit. Numerous studies have shown deficits in various voluntary saccade tasks such as delayed, remembered, or predictive saccades. Schizophrenic patients with smooth pursuit deficits make significantly more errors on the anti-saccade task.
Deficits in prosaccades in schizophrenia
Prosaccades are rapid eye movements toward suddenly appearing visual stimuli. Prolonged latency and reduced accuracy of prosaccades in schizophrenia patients is well-documented. A prosaccade task is generally used to elicit reflexive saccade in which the participant fixates a center spot, a visual target appears to the left or right of center, and the participant is instructed to look at the target. Voluntary saccades can be elicited by many different eye movement paradigms.
Other deficits in schizophrenia
Numerous studies have proved that various deficits in voluntary saccade tasks including delayed, remembered, or predictive saccades. In a delayed saccade task, person is required to make an eye movement to the target. However, the person is also instructed to wait until a “go” signal is given. Therefore, the person should inhibit the reflexive tendency to look at the target immediately and generate voluntary, saccade when the “go” signal is presented. In a memory guided saccade task, the target is removed from the screen during the delay period. Now the person should inhibit the eye movement until the “go” signal and also remember where the target was presented. This task demands working memory.
Acute and chronic schizophrenia patients have showed a number of abnormalities of extra ocular movement including staring, abnormal blink rate, absent glabellar reflex, and increase in horizontal eye movements. The disturbances in eye movements shown by schizophrenic patients are usually attributed to the heightened state of fear or arousal associated with the acute psychosis. Abnormal SPEMs performance in schizophrenia to some extent is related to attention deficits. Visual fixation errors increased in schizophrenia patients compared to control subjects. Eye movement disturbances in visual exploration have been reported in patients with schizophrenia, and visual scan path abnormalities have been proposed to serve as a trait marker for the disorder. Reduced visual scan paths on photographs of faces, complex scenes, geometric shapes, Rorschach stimuli, photographs of landscapes, fractals, and meaningless patterns was detected in Schizophrenia patients.
Attention (focusing on relevant information and ignoring distracters), working memory (maintaining information until execution) and motor planning (goal-directed motor planning and programming) are generally considered to be key executive functions. Various abnormalities in executive functions (complex, higher order processes moderated primarily by the frontal lobe, specifically by the prefrontal cortex) are documented in schizophrenia patients.
| Conclusion|| |
Various abnormal eye movements like SPEM deficits, abnormal saccadic eye movements, and other abnormal eye movements in schizophrenia resembles with “Paryakula drishti/Chakshusho aakulata/Chakshusho apasarpanam” of Unmada. It seems that ancient Indian Ayurvedic sages had great observational and clinical skills by which they were able to detect abnormal eye movements in patients suffering with various psychiatric disorders, thousands of years before. Currently available research based on abnormal eye movements in schizophrenia supports the Ayurvedic view.
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| References|| |
Gupta K, Mamidi P. Kaphaja unmada: Myxedema psychosis? Int J Yoga Philosop Psychol Parapsychol 2015;3:31-9.
Vaidya Jadavji Trikamji Acharya, editors. Agnivesha, Elaborated by Charaka and Dridhabala Commentary by Chakrapani. Charaka Samhita, Nidaana Sthana, Unmada Nidaana Adhyaya, 7/6 & 7. Varanasi: Chaukhamba Surbharati Prakashan; 2008. p. 223-4.
Vaidya Jadavji Trikamji Acharya, editors. Agnivesha, Elaborated by Charaka and Dridhabala Commentary by Chakrapani. Charaka Samhita, Chikitsa Sthana, Unmada Chikitsa Adhyaya, 9/6. Varanasi: Chaukhamba Surbharati Prakashan; 2008. p. 468.
Vaidya Jadavji Trikamji Acharya, Narayana Ram Acharya, editors. Sushruta. Sushruta Samhita, Commentary by Dalhana. Uttara Tantra, Unmada Pratishedha Adhyaya, 62/1-35. Varanasi: Chaukhamba Orientalia; 2009. p. 803-5.
Sharma S, editor. Vriddha Vagbhata. Ashtanga Sangraha, Commentary by Indu. Uttara Tantra, Unmada Pratishedha Adhyaya, 9/5. 3rd
ed. Varanasi: Chowkhamba Sanskrit Series Office; 2012. p. 676.
Bhishagacharya Harishastri Paradkara Vaidya, editor. Vagbhata. Ashtanga Hridaya, Commentary by Arunadatta and Hemadri. Uttara Tantra, Unmada Pratishedha Adhyaya, 6/1 – 60. 9th
ed. Varanasi: Chowkhamba Sanskrit Series Office; 2005. p. 797-801.
Tripathi B, editor. Madhavakara. Rogavinischaya/Madhava Nidana, Unmada Nidana, 20/6, Commentary 'Madhukosha' by Vijayarakshita & Shrikanthadatta. 1st
ed. Varanasi: Chaukhamba Surbharati Prakashan; 2012. p. 480.
Sereno AB, Babin SL, Hood AJ, Jeter CB. Executive functions: Eye movements and neuropsychiatric disorders. Encyclopedia Neurosci2009;4:117-22.
Kathmann N, Hochrein A, Uwer R, Bondy B. Deficits in gain of smooth pursuit eye movements in schizophrenia and affective disorder patients and their unaffected relatives. Am J Psychiatry 2003;160:696-702.
Yee RD, Baloh RW, Marder SR, Levy DL, Sakala SM, Honrubia V, et al.
Eye movements in schizophrenia. Invest Ophthalmol Vis Sci 1987;28:366-74.
Sharan R, Chaterjee S, Janakiramaiah N, Gangadhar BN. Eye movements and schizophrenia. Indian J Psychiatry 1990;32:72-6.
] [Full text]
Sereno AB, Holzman PS. Antisaccades and smooth pursuit eye movements in schizophrenia. Biol Psychiatry 1995;37:394-401.
Chen Y, Levy DL, Nakayama K, Matthysse S, Palafox G, Holzman PS, et al.
Dependence of impaired eye tracking on deficient velocity discrimination in schizophrenia. Arch Gen Psychiatry 1999;56:155-61.
Spering M, Dias EC, Sanchez JL, Schütz AC, Javitt DC. Efference copy failure during smooth pursuit eye movements in schizophrenia. J Neurosci 2013;33:11779-87.
Stark L. Abnormal patterns of normal eye movements in schizophrenia. Schizophr Bull 1983;9:55-72.
Boudet C, Bocca ML, Chabot B, Delamillieure P, Brazo P, Denise P, et al.
Are eye movement abnormalities indicators of genetic vulnerability to schizophrenia? Eur Psychiatry 2005;20:339-45.
Stevens JR. Disturbances of ocular movements and blinking in schizophrenia. J Neurol Neurosurg Psychiatry 1978;41:1024-30.
Delerue C, Hayhoe M, Boucart M. Eye movements during natural actions in patients with schizophrenia. J Psychiatry Neurosci 2013;38:317-24.