Visada Depression Ayurveda and Modern View

Visada Depression

• Visada Vi + Sad + Ghan = Visada 1) Vi – Visesena Siyante Asminanena 2) Visaddhyate Anena va’

The term Visada has been derived from the Samskrta root “Sad” by applying the prefix “Vi”. Its literal meanings are stupor, depression, and despondency.

• “Citta Dehayon Glani” (Dal on Su.Su -15/9) that means depression is a stale in which retardation of bodily and mind functions seen i.e. psychomotor retardation Cakrapani has explained the term as incapability of mind as well as the body to work (Ca.Ci.-3/36)

Visada Depression Ayurveda and Modern View

• Vak Kaya Cittavasado Visadaha. Dalhan on Su.Ka.- 3/21 i.e. cannot think or guess properly or inability to respond properly by mind. body and speech.
• Caraka mentions Visada as one of the Nanatmaja Vikara (disorder) of Vata (Ca.Su. -20/11)
• it is one of the symptom of Vataja Javara (Ca.Ni-1/ 21)
• it is a symptom of Hina Sattva (Ca.Vi- 8/119)
• In Susruta Samhita Visada has been described as a Manasa Vyadhi (Su.Su -1/23).
• In Su.Sha- 1/25 it is included in one of the characteristics of Tamasa Prakriti
• while mythological the Visada is developed from the anger (Krodha)of Brahma (Su.Ka.-3/21)
• while in Astanga Samgraha it is explained Visada as the causative factor of vitiation of Vyana Vayu (A.S.Ni.- 16/24-25),
• it is a symptom of Visadagdhena viddhasya (A.S.Utt- 40/104-107)
• while in Astanga Hrdaya–Visada as a symptom of Garbhabhava originated by Tamo Guna (As. Hr. Sa- 3/8),
• in (A.H.Ni-2/17) it is mentioned as a symptom of Vataja Jvara, it is also a symptom of Visadagdha arrow injured person (A.H.Utt.- 35/40-44) in (A.H.Ni-16/23) it is mentioned as an etiological factor of Unmada as well as vitiation of Vyana.
• Visada is found as symptom in diminution of Sukra (Ca.Su-17/69)
• Sadak Pitta is essential for the desired (Abhipretartha Sadhana).
• Udana is related with function of mind, Prana support all Indriyas Vyana defiles due to Visada (A. S. Ni – 16/24).
• Thus, we can say that derangement in the function of Prana, Udana and Kshina sadhak Pitta and impaired Dhatus like Rasa, Sukra, and Ojas lead to Visada.
• Symptom of Visada is also found in Pittavrita Udana, The symptoms like fainting, exhausation, deterioration of Ojas and malaise are the symptom of Udana covered by Pitta
• Depression is also a frequent finding in patient Parkinson’s disease (Taylor et.al (1986b) in several prospective studies the frequency of the depression reported to be around 40% (Celesia and Wanamaker (1977) Mindham et al (1976) Mayeux et at (1984), Gotham et al (1986).
• In recent prospective study of a consecutive series of 105 patients with Parkinson’s disease they found that 21% met DSM III (American Psychiatric association 1980), for major depression while 20% met DSM III criteria for dysthymic minor depression (S.E. Starkstein, T. J. Preziosi, P. L. Bolduc and R. a. Robinson’s- Unpublished reports).
• Mayeux et al (1984b) measure serotonin in metabolites in depressed and non depressed Parkinson’s disease patient and suggested that altered serotonin metabolism, in conjunction with predisposing personality characterististies may be responsible for depression in a high proportion of patients However such measure cannot establish that altered serotonin metabolism or catabolism is a causative factor in such patient
• Now recently some data support the view that depression of Parkinson’s disease is associated specifically with decreased CNS serotonin level Biochemically the cereprospinal fluid (CSF) of Parkinson’s disease depressives has been reported to reflect hypofunction of the dopaminergic, serotonergic, adrenergic and cholinergic system, and all those neurotransmitter have been implicated in the cause of mood syndrome.
• Dopaminergic and serotonergic abnormalities have been the most consistently demonstrable.
• The neurodestructive process that devastates the dopamine neuron in nigra and accounts for the motoric manifestation of Parkinson’s disease may also affect the ascending serotonergic neurons originating in the dorsal raphe.
• Alternatively, destruction of the ascending mesocortical dopamine neurons (projecting from the ventral tegmental area to the orbital frontal and prefrontal cortex) may cause metabolic hypofrontality and secondary serotonergic dysfunction by disrupting the descending cortical projection to dorsal raphe.
• The report those monoamine oxidase inhibitors are able to restore CSF serotonin but not dopamine to normal level supports the suggestion that the dopamine deficit is structural and that the serotonin abnormality is secondary.

Some clinical symptoms of depression

• in-patient Parkinson’s disease find out are as follow.
• – Persistent sad, anxious or empty mood; sleeping too much or too little, middle of night or early morning walking.
• – Reduced appetite and weight loss, or increased appetite and weight gain.
• – Loss of pleasure and interest in activities. Once, enjoyed included sex, Difficulty in concentrating, remembering or making decision.
• – Fatigue or loss of energy feeling guilty, hopeless or worthless thoughts of deaths or suicide tendency are found.

• The on–off syndrome in which patients experience severe fluctuation in mobility ranging from normal movement to a frozen state has been associated with change in mood.
• Many studies have reported change in mood coincident with change in motor function, namely subjective and objective dysphoria in the off period and less frequently abnormal elation and euphoria on period.
• Some study found that, patient with major depression had significantly greater intellectual impairment as evidenced by low – mini – mental state score (MMSE) than patient with minor depression or nondepression patient.
• Similar finding have been reported previously by Mayeux et al (1981) using modified MMSE.