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REVIEW ARTICLE
Year : 2018  |  Volume : 11  |  Issue : 6  |  Page : 466-470  

Maukirana grahonmada – Psychiatric manifestations of Graves' hyperthyroidism and ophthalmopathy?


Department of Kaya Chikitsa, Abhilashi Ayurvedic College and Research Institute Abhilashi University, Mandi, Himachal Pradesh, India

Date of Submission06-May-2018
Date of Acceptance24-Jul-2018
Date of Web Publication15-Nov-2018

Correspondence Address:
Prasad Mamidi
Department of Kaya Chikitsa, Abhilashi Ayurvedic College and Research Institute, Abhilashi University, Mandi, Himachal Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mjdrdypu.mjdrdypu_75_18

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  Abstract 


Bhuta vidya (Ayurvedic psychiatry) is one of the eight specialties of Ayurveda. It deals with various psychiatric conditions caused by the affliction of evil spirits. Unmada (a broad term which consists various psychiatric problems) is a major psychiatric condition described in Ayurvedic and it is characterized by deranged mental functions. “Bhutonmada” (psychiatric conditions of idiopathic nature) is a type of unmada caused by the affliction of “bhoota”/“graha” (evil spirits or supernatural powers). Maukirana grahonmada (MG) is one among 18 types (deva, asura, rushi, guru, vruddha, siddha, pitru, gandharva, yaksha, rakshasa, sarpa, brahma rakshasa, pishacha, kushmanda, nishada, preta, maukirana, and vetala) of bhutonmada. Till date, there were no studies available on MG and the present study aims at better understanding along with clinical applicability of MG. MG is characterized by Ugravaadinam (agitation/aggression/verbal abuse), Rakta, trasta netram (reddish and tired eyes), Yaachantam annam (begging food), and Yaachantam udakarm (begging water). It is very difficult to understand MG based on these few lakshana's (signs and symptoms). Graves' disease (GD) (hyperthyroidism) with ophthalmopathy has shown similarity with MG. GD associated with hyperthyroidism and ophthalmopathy has shown marked similarity with MG. MG is having similarity with GD and Graves' ophthalmopathy.

Keywords: Ayurveda, Graves' disease, hyperthyroidism, Maukirana grahonmada, ophthalmopathy, psychiatry


How to cite this article:
Mamidi P, Gupta K. Maukirana grahonmada – Psychiatric manifestations of Graves' hyperthyroidism and ophthalmopathy?. Med J DY Patil Vidyapeeth 2018;11:466-70

How to cite this URL:
Mamidi P, Gupta K. Maukirana grahonmada – Psychiatric manifestations of Graves' hyperthyroidism and ophthalmopathy?. Med J DY Patil Vidyapeeth [serial online] 2018 [cited 2018 Dec 19];11:466-70. Available from: http://www.mjdrdypv.org/text.asp?2018/11/6/466/245436




  Introduction Top


“Bhuta vidya” (Ayurvedic psychiatry) is one of the eight specialties of Ayurveda. It deals with the mode of exorcising, evil spirits, and making offerings to various demons for the cure of diseases originating from their malignant influence. The word “bhuta” denotes “supernatural power”/“demon”/“extraterrestrial force”/“paranormal force” or a popular “mythological personality.” Bhutonmaada is a psychiatric condition characterized by abnormal behavior and psychomotor activity seen in a person with sudden onset and without known etiopathology (idiopathic).[1]Unmada (a broad term which includes various psychiatric problems under one roof) is a major psychiatric illness described in all Ayurvedic classics and is characterized by deranged mental functions. Etymological meaning of Unmada is, “a state of deranged mental functions.” Deviation of manas (mind), buddhi (decision), smriti (memory), sangya gyanam (orientation and responsiveness), bhakti (desire), sheela (habit), cheshta (activity), and achaara (conduct) (either all of them or some) is the characteristic pathological feature of Unmada.[2] There are 18 types of bhutonmada (deva, asura, rushi, guru, vruddha, siddha, pitru, gandharva, yaksha, rakshasa, sarpa, brahma rakshasa, pishacha, kushmanda, nishada, preta, maukirana, and vetaala) and Maukirana grahonmada (MG) is one among them.[3]

There is no description available regarding MG in Charaka samhita,[4]Sushruta samhita,[5] and Madhava nidana.[6] Only lakshana's (signs and symptoms) of MG are explained in Ashtanga samgraha[7] and Ashtanga hridaya.[8] The description of MG is similar in both texts (Ashtanga samgraha and Ashtanga hridaya). MG is characterized by the features such as Ugravaadinam (agitation/aggression/verbal abuse), Rakta, trasta netram (reddish and tired eyes), Yaachantam annam (begging food), and Yaachantam udakarm (begging water).[7],[8] Till date, there were no studies available on MG and it is an underexplored concept of Ayurveda. The present study is focused at better understanding of MG along with its clinical applicability. The various features of MG have shown similarity with “Hyperthyroidism, especially seen in “Graves' disease” (GD) and “Graves' ophthalmopathy.” The similarity between MG and GD has been explored in the following sections.


  Review Methodology Top


Ayurvedic material related to “Maurkirana grahonmada”/“Grahonmada”/“Bhutonmada” was collected from major Ayurvedic texts, that is, Charaka samhita, Sushruta samhita, Ashtanga sangraha, Ashtanga hridaya, and Madhava nidana. Materials pertaining to “Graves disease” (relevant) were collected from electronic databases “Google Scholar search” and “Google search” published/appeared from 1967 to December 2016. The key words used for search were, “Graves disease,” “Graves hyperthyroidism,” “Graves ophthalmopathy,” “Thyrotoxicosis,” “Hyperthyroidism,” “Hypoglycemia in hyperthyroidism,” “Excessive thirst in hyperthyroidism”, “Goitre,” “Chemosis in hyperthyroidism,” “Bhutonmada,” and “Grahonmada.” Abstracts and full-text articles published in “English” language only were considered.


  Graves' Disease Top


GD was first recognized in the 19th century as a syndrome comprising an overactive thyroid gland, an accelerated heart rate, and ocular abnormalities. Critical understanding of this disease was the discovery of its autoimmune basis, which results from complex interactions between genetic and environmental factors. GD has adverse effects on quality of life, as a consequence of somatic and psychiatric symptoms and an inability to work. Many characteristic signs and symptoms of GD result from elevated thyroid hormone levels. Symptoms and signs result from hyperthyroidism are a consequence of underlying autoimmunity. Weight loss, fatigue, heat intolerance, tremors, and palpitations are the most common symptoms.[9] Graves' ophthalmopathy is an organ-specific autoimmune process strongly linked to Graves' hyperthyroidism. Although the hyperthyroidism can be successfully treated, it is often the ophthalmopathy that produces the greatest long-term disability in patients with this disease. Eyelid retraction, proptosis, periorbital edema, chemosis, and disturbances of ocular motility can lead to both cosmetic and functional sequelae.[10] GD is a syndrome characterized by hyperthyroidism, a particular ophthalmopathy, and pretibial myxedema. Usually, thyroid enlargement, goiter, and excessive thyroid hormone action are the features of the illness, but the presence of all or any individual component fits a patient within the syndrome. GD typically includes two major categories of phenomena. Those specific to GD, and caused by the autoimmunity per se, include the exophthalmos, thyroid enlargement and thyroid stimulation, and the dermal changes. The second set of problems is caused by the excess thyroid hormone. This thyrotoxicosis or hyperthyroidism does not differ from that induced by any other cause of excess thyroid hormone.[11]


  Etiology, Pathogenesis, Course, and Prognosis of Maukirana Grahonmada and Graves' Disease Top


In bhutonmada, causative factors are not traceable. Pragyaparaadha (intellectual blasphemy) or karma (idiopathic) plays an important role in the pathogenesis of bhutonmada. Actions of the past life (daiva) are linked to diseases and acts as precipitating factors for the manifestation of various diseases (especially bhutonmada). The onset of bhutonmada is sudden or instantaneous without significantly affecting the body physiology. The signs and symptoms of bhutonmada are also infinite. The course of bhutonmada is unpredictable. The prognosis of bhutonmada is also unpredictable.[3] There is no special description regarding etiology, pathogenesis, course, and prognosis of MG available in Ayurvedic texts. The common etiology, course, and prognosis mentioned for bhutonmada are applicable for MG also. Like other bhutonmada's, in MG also the etiopathology, course, and prognosis are idiopathic and unpredictable in nature.[4],[5],[6],[7],[8]

GD is a disease of autoimmunity, but the final cause of autoimmunity remains unclear. Since GD is accepted as a syndrome induced by autoimmunity to the thyroid, the question of cause resolves into why autoimmunity to the thyroid is present. It is not clear that any other “cause” of GD is present, other than disordered immunity. There is, for example, no evidence that the thyroid or its protein antigens are initially abnormal. The ultimate cause (s) remain uncertain for GD.[11] GD also affects the eyes (Graves' ophthalmopathy) and the skin (localized dermopathy or myxedema), but the causes of these less common components of the disease are not known. The course of Graves' ophthalmopathy is largely independent of thyroid status, although it tends to be more severe in patients in whom hyperthyroidism is poorly controlled. Typically, there is a period of worsening over 12–18 months, followed by a period of stabilization. However, unpredictable and sudden worsening of ophthalmopathy can occur at any time.[12] The ocular changes associated with thyroid dysfunction have been recognized for >150 years, yet controversy still remains regarding the pathogenesis.[10] It seems that the etiopathology, course, and prognosis of GD are still not understood completely. Various features such as variable clinical presentation, unpredictable prognosis, unknown underlying pathological processes and idiopathic nature (not in all but in some cases) of GD shows similarity with the etiopathology, course, and prognosis, etc., explained for grahonmada/bhutonmada.


  Similarity of Clinical Picture in between Maukirana Grahonmadaand Graves' Disease Top


Various lakshana's of MG such as Ugravaadinam, Rakta, trasta netram, Yaachantam annam, and Yaachantam udakarm, etc., features resembles with various features of GD associated with ophthalmopathy. The similarity in between the signs and symptoms of these two conditions (MG and GD with ophthalmopathy) is as follows:

Ugravaadinam (agitation/aggression/verbal abuse)

The word “Ugravaadinam” denotes verbal abuse or threatening or aggressiveness or agitation or irritability. It has been recognized that thyroid disease can cause psychiatric disorders. Hyperthyroidism can cause anxiety, dysphoria, emotional lability, and mania. Thyrotoxicosis commonly presents with anxiety, dysphoria, emotional lability, intellectual dysfunction, and mania. Even after restoration of biochemical euthyroidism, many patients with hyperthyroidism have persistent residual neuropsychiatric symptoms. Subclinical hyperthyroidism patients show nervousness, irritability, and anxiety in comparison with controls. Mania may also be observed in hyperthyroidism. Severe hyperthyroidism can result in thyroid storm, a condition that ranges in neuropsychiatric presentation from hyperirritability, anxiety, and confusion. According to a study, both euthyroid and hyperthyroid women with a history of treated hyperthyroidism and ophthalmopathy caused by GD had significantly more anxiety disorders including panic disorder, social anxiety, and generalized anxiety, than a control group with no history of thyroid disease. Patients with remitted hyperthyroidism had significantly shown more anxiety, hostility, mania, and sleep disturbances compared with controls. Subclinical hyperthyroidism may be associated with nervousness and irritability even mild thyroid dysfunction has been associated with changes in mood.[13]

Subtle neuropsychological symptoms such as anxiety, irritability, tremor, and insomnia are not uncommon in severe thyrotoxicosis, regardless of the cause. Excessive irritability, insomnia, aggressive behavior, irrational talking, physical and verbal abusiveness are found in a patient of GD with thyrotoxicosis. Since Von Basedow described the fist case of manic psychosis in a patient with exophthalmic goiter over a century ago, a few cases have been reported, including major depressive, manic, paranoid, and schizophreniform disorders. Thyrotoxicosis is now a recognized cause of organic psychosis.[14] Aggressiveness and worsening hyperactivity are commonly found during the initial hyperthyroid phase in chronic autoimmune thyroiditis.[15] The patient complains of nervousness or irritability and appears to be restless and fidgety in thyrotoxicosis. It sometimes seems impossible for the thyrotoxic patient to remain still for an instant. Some patients become hyperirritable and combative, and this can precipitate accidents or even assaultive behavior. In some patients, the emotional pattern is that of hypomania, and in others, hyperactivity seems to produce a state of exhaustion.[11] By considering these facts, it can be assumed that “Ugravaadinam” of MG denotes hyperirritability/nervousness/anxiety/aggressive behavior/hypomania or mania-like symptoms caused by hyperthyroidism/thyrotoxicosis in GD.

Rakta, trasta netram (reddish and tired eyes)

Rakta and trasta netram” denotes reddish and tired eyes. The ophthalmological problem and pretibial myxedema are unique to GD. GD displays an array of possible clinical patterns extending from that of goiter and thyrotoxicosis but without ophthalmopathy, to that of ophthalmopathy without goiter or thyrotoxicosis. The eye signs characteristic of GD often constitutes the most striking feature. Prominence of the eyes with wild or staring expression is often observed. Lag of the lids behind the globes on downward rotation and lag of the globes behind the lids in upward rotation, infrequent blinking, failure to wrinkle the forehead on looking upward, swelling of the lids, and decreased ability to converge are also cardinal manifestations. The bulbar conjunctiva may be edematous (chemosis). The insertions of the medial and lateral rectus muscles are often enlarged, inflamed, and quite obvious. The eye symptoms are extremely distressing. Diplopia is common. More frequent are symptoms due to conjunctival or corneal irritation. These symptoms include burning, photophobia, tearing, pain, and a gritty or sandy sensation.[11]

“Graves” ophthalmopathy' is characterized by edema and inflammation of the extraocular muscles. The inflammation is due to infiltration of the extraocular muscles and orbital connective tissue by lymphocytes and macrophages. Clinically evident ophthalmopathy occurs in about 50% of patients, in 75% of whom the eye signs appear within a year before or after the diagnosis of hyperthyroidism. Clinicians can estimate the activity of the eye disease by giving a point for each of the following signs: Retrobulbar pain, pain on eye movement, eyelid erythema, conjunctival injection, chemosis, swelling of the caruncle, and eyelid edema.[12] Some patients have dry eye, increased tearing, and ocular discomfort early in the active phase. This is followed by an inactive phase in which the ocular manifestations become stable.[9] Graves' ophthalmopathy is an organ-specific autoimmune process strongly linked to Graves' hyperthyroidism. Eyelid retraction, proptosis, periorbital edema, chemosis, and disturbances of ocular motility can lead to both cosmetic and functional sequelae. The ocular changes associated with thyroid dysfunction have been recognized for >150 years.[10] It seems that “Rakta trasta netram” of MG denotes “Graves' ophthalmopathy.”

Yaachantam annam (begging food)

The word “Yaachantam annam” denotes increased appetite and excessive food intake. Hypermetabolic rate is one of the features of hyperthyroidism in GD.[14] Increased appetite associated with weight loss is found in thyrotoxicosis. The appetite is characteristically increased. The effect of this increase is to offset, in part (sometimes completely), the loss of weight that might be expected from the increased catabolism. Indeed, the pattern of weight loss with increased appetite is nearly pathognomonic of thyrotoxicosis. Occasionally, glycosuria is seen in uncomplicated thyrotoxicosis. Glycosuria may reflect accelerated absorption of sugar from the intestine and glucose intolerance. Absorption of carbohydrate from the intestine is accelerated, as is its removal from the plasma. After a standard oral glucose load is given, the thyrotoxic patient characteristically has an early and rapid rise in blood glucose concentration in 30–60 min (possibly to >200 mg/dl) and a rapid fall, so that by 2 h the concentration is normal. The early peak may be associated with glycosuria. Thyrotoxicosis increases the demand for insulin, perhaps by accelerating its metabolism. In addition, resistance to the action of insulin is present. Type I diabetes mellitus cooccurs with increased frequency in autoimmune thyroid disease. Postpartum thyroid dysfunction is especially common in patients with diabetes.[11] Excessive hunger and loss of weight are found in patients of GD (Locke W). The increased appetite (may be due to excessive catabolism or hyperactivity or impaired carbohydrate metabolism in hyperthyroidism) found in thyrotoxicosis/hyperthyroidism in GD resembles with “Yaachantam annam” of MG.

Yaachantam udakarm (begging water)

The word “Yaachantam udakam” denotes dehydration or excessive thirst. Increased perspiration is one of the features of thyrotoxicosis. Increased thirst, profuse sweating, hyperdefecation, sensitivity to heat, hypermetabolic rate, and increased activity commonly found in a patient of thyrotoxicosis or GD can cause dehydration or electrolyte imbalance which in turn causes excessive thirst. Marked flushing is often noted. A drawn or sunken appearance may result from emaciation or dehydration. A change in reaction to external temperature is a very classic symptom of hyperthyroidism. The development of a preference for cold weather, of a desire for less clothing and less bed covering, and of decreased ability to tolerate hot weather is highly suggestive of hyperthyroidism. Cutaneous manifestations are nearly always present when hypermetabolism is significant. Active sweating occurs under circumstances that would provoke no response in normal persons. The hand of the thyrotoxic person is erythematous, hot, and moist (sometimes actually dripping wet), in a state of hot hyperhidrosis. The vasomotor system is overactive. Many of these cutaneous manifestations may be considered expressions of or incidental to increased heat elimination in hyperthyroidism patient.[11]

Hot, smooth sweating skin, frequent bowel movements, and intolerance to heat are some of the features of GD.[16] Thyrotoxicosis due to GD is an uncommon albeit known cause of polyuria. This was associated with excessive thirst and loss of weight of 6 kg with normal appetite in a patient of GD. The mechanism of polyuria in GD is not clear. Excessive water intake along with increased solute excretion was also noted in thyrotoxic rats. Polyuria should be recognized as a presenting feature of thyrotoxicosis after ruling out commoner causes such as hyperglycemia, diuretics, and diabetes insipidus.[17] Polyuria, glycosuria, frequent bowel movements, excessive sweating, and metabolism in a hyperthyroidism/thyrotoxicosis patient may cause dehydration or electrolyte imbalance and leads to excessive thirst. This resembles with the “Yaachantam udakam” of MG.


  Conclusion Top


“Maukirana grahonmada” is one among 18 types of bhutonmada. The signs and symptoms of MG have shown similarity with GD with Graves' ophthalmopathy. Signs and symptoms of MG such as Ugravaadinam; Rakta, trasta netram; Yaachantam annam; and Yaachantam udakarm, etc., resembles with the features such as hyperirritability/agitation/verbal abuse/restlessness/anxiety, chemosis, increased appetite, and increased thirst (various features of hyperthyroidism in GD and Graves' ophthalmopathy). MG has shown similarity with GD with Graves' ophthalmopathy.

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  References Top

1.
Mamidi P, Gupta K. Guru, vriddha, rishi and siddha grahonmaada: Geschwind syndrome? Int J Yoga Philosop Psychol Parapsychol 2015;3:40-5.  Back to cited text no. 1
    
2.
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4.
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5.
Vaidya Jadavji Trikamji Acharya, Narayana Ram Acharya, editor. Sushruta. Sushruta Samhita, Commentary by Dalhana. Uttara Tantra, Amanusha Upasarga Pratishedha Adhyaya, 60/7-16. Varanasi: Chaukhamba Orientalia; 2009. p. 794-5.  Back to cited text no. 5
    
6.
Dr. Brahmananda Tripathi, editor. Madhavakara. Rogavinischaya/Madhava Nidana, Unmada Nidana, 20/18-25, Commentary ‘Madhukosha’ by Vijayarakshita and Shrikanthadatta, 1st ed. Varanasi: Chaukhamba Surbharati Prakashan; 2012. p. 487-92.  Back to cited text no. 6
    
7.
Dr. Shivprasad Sharma, editor. Vriddha Vagbhata. Ashtanga Sangraha, Commentary by Indu, Uttara Tantra, Bhoota Vigyaneeyam Adhyaya, 7/22. 3rd ed. Varanasi: Chowkhamba Sanskrit Series Office; 2012. p. 670.  Back to cited text no. 7
    
8.
Bhishagacharya Harishastri Paradkara Vaidya, editor. Vagbhata. Ashtanga Hridaya, Commentary by Arunadatta and Hemadri, Uttara Tantra, Bhoota Vigyaneeyam Adhyaya, 4/39. 9th ed. Varanasi: Chowkhamba Sanskrit Series Office; 2005. p. 792.  Back to cited text no. 8
    
9.
Smith TJ, Hegedüs L. Graves' disease. N Engl J Med 2016;375:1552-65.  Back to cited text no. 9
    
10.
Chan W, Wong GW, Fan DS, Cheng AC, Lam DS, Ng JS, et al. Ophthalmopathy in childhood graves' disease. Br J Ophthalmol 2002;86:740-2.  Back to cited text no. 10
    
11.
DeGroot LJ, Larsen PR, Hennemann G. Graves' Disease and the Manifestations of Thyrotoxicosis. The Thyroid and its Diseases. New York: Churchill Livingstone; 1996. p. 371. Available from: http://www.thyroidmanager.org/wp-content/uploads/chapters/graves-disease-and-the-manifestations-of-thyrotoxicosis.pdf. [Last accessed on 2017 Sep 19].  Back to cited text no. 11
    
12.
Weetman AP. Graves' disease. N Engl J Med 2000;343:1236-48.  Back to cited text no. 12
    
13.
Feldman AZ, Shrestha RT, Hennessey JV. Neuropsychiatric manifestations of thyroid disease. Endocrinol Metab Clin North Am 2013;42:453-76.  Back to cited text no. 13
    
14.
Ugwu ET, Maluze J, Onyebueke GC. Graves' thyrotoxicosis presenting as schizophreniform psychosis: A Case report and literature review. Int J Endocrinol Metab 2017;15:e41977.  Back to cited text no. 14
    
15.
Dunne C, De Luca F. Long term follow up of a child with autoimmune thyroiditis and recurrent hyperthyroidism in the absence of TSH receptor antibodies. Case Rep Endocrinol 2014; 2014: 1-4. Available from: https://www.hindawi.com/journals/crie/2014/749576/cta/. [Last accessed on 2018 Aug 06].  Back to cited text no. 15
    
16.
Locke W. Unusual manifestations of graves's disease. Med Clin North Am 1967;51:915-24.  Back to cited text no. 16
    
17.
Muthukrishnan J, Saurabh D. An unusual cause of polyuria. Indian J Endocrinol Metab 2012;16:1051-2.  Back to cited text no. 17
    




 

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