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| | === ''Vidhi Vimarsha'' === | | === ''Vidhi Vimarsha'' === |
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| | + | === Reference === |
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| − | Further diets that are rich in saturated fats and sugar decrease levels of Brain derived neurotrophic factor [BDNF]. BDNF is a neurotrophin considered generally beneficial for maintaining neuronal function and for promoting recovery after neurologic insult. Reduced BDNF leads to poorer neuronal performance. Results of a study have shown that rats fed on a diet high in saturated fats and refined sugars (similar in content to the “junk food” that has become popular in western society) for a period of 1 -2 months performed significantly worse on the spatial learning water maze test. Even more alarming is that the high fat diet consumption exacerbated the effects of experimental brain injury. The effects of this high caloric diet seem to be related to elevated levels of oxidative stress and reduced synaptic plasticity which can reversed by antioxidant treatment or exercise. High caloric intake also is perceived as risk factor for Alzheimer’s disease. Concept of atibhojana, snigdha etc. leads to āma utpatti, a cause for Vātavyādhi. Research results show that noninvasive approaches such as diet and exercise can have profound consequences for increasing resilience of the CNS to injuries and for maintaining cognitive abilities. Diet and exercise are 2 very important parts of lifestyle and daily routine each can influence the capability of the brain to fight disease and to react to challenges. Physical activity can benefit neuronal function and plasticity by enhancing synaptic plasticity and reducing oxidative stress. Physical exercise can have direct effects on the brain and spinal cord by supporting the maintenance of the synaptic structure, axonal elongation and neurogenesis in the adult brain whereas excessive exertion (ativyāyāma) is hold to cause degenerative changes.
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| − | Stress is unpleasant, even when it is transient. A stressful situation–whether something environmental or psychological can trigger a cascade of stress hormones that produce well orchestrated physiological changes. Fight and flee are the 2 response which the body is accustomed too. Repeated stress leads to hormonal and neuro-adaptive changes which may be the cause for damage. All krodha (fight response) and bhaya (flight response) described by Ācharyas explain the similar effects on the body.
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| − | Śītā guna- Prolonged exposure to the cold causes the body to slow blood circulation to the periphery. The reduced blood flow can intensify neuropathy symptoms and potentially cause further damage to already affected peripheral nerves.
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| − | Research is essential to rule out effects of śītā guna on cryoglobulinemia; a condition of cold antibody in blood which cause vasculitis and neuropathy as well. Increase cryoglobulinemia increases viscosity leading to reduced blood flow thereby causing neuropathy.
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| − | Ativyavāya – Donald L Hilton and others in their research paper on pornography addiction: A neuroscience perspective, were of the opinion that compulsive sexuality can indeed be addictive. It concludes for the first time that a sexual compulsion can cause physical, anatomic change in the brain, the hallmark of brain addiction. A preliminary study showed frontal dysfunction specifically in patients unable to control their sexual behavior. The study used diffusion MRI to evaluate function of nerve transmission through white matter. It demonstrated abnormality in the superior frontal region, an area associated with compulsivity. Hormonal changes similar to overeating induced obesity were also observed.
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| − | Ati plavana, atiadva, ati vyāyāma, ati vichesta: Normal exercise has a good neurobiological impact. It increases the secretion of positive hormones and also helps in neurogenesis whereas over exercising can lead to an increased resting heart rate, a cause for increased cardiac output leading to hypertension, risk factor for stroke. Unexplained weight loss and decreased appetite is another factor. Further decreased of essential elements leads to neurological deficits as discussed before.
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| − | Further cortisol and stress hormones levels tend to increase with decrease in testosterone levels.
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| − | Emotions are intimately linked with organic life. They either result is an, “abnormal excitation of the nervous network, which induces changes in heart rate and secretions, or interrupts the normal relationship between the peripheral nervous system and brain.” Cerebral activity is focused on the source of emotions; voluntary muscles may become paralyzed and sensory perceptions may be altered including the feeling of physical pain. The idea of emotions involves specific areas of brain and activation of these areas is associated with increase blood supply.
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| − | VERSE 19-20
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| − | In all disorders of Vāta dōṣa the purvarupa may not be registered separately. For example the textual presentation of Ardita (Vegavāna) may be a purvarupa of pakṣāghāta just like Transient Ischemic Attack are considered as warning signs of stroke. In abrupt onsets, purvarupa cannot be distinguished from rupa as in the case of manyasthambha in Apatanaka. Acute convulsive disorders manifest abruptly without any premonitory symptoms. In diseases of very insidious onset also premonitory signs are not appreciated sepertely. In most of the mayopathies this happens.
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| − | VERSE -24-38
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| − | Various gatavāta are seen in general practice. Pakvāśaya gatavāta is a syndromic presentation in which habitual constipation is associated with obstructive uropathy symptoms, LBA, inguinal hernia etc symptoms.
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| − | Āmāshaya gatavāta is GERD like presentations with features of lax esophageal sphincter, hiatus hernia or simply non ulcer dyspepsia.
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| − | Tvakgatavāta is icthyosis of various presentations.
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| − | In raktagata vāta, rakta dhātu gets vitiated by vāta dōṣa leading to shoshan of rakta dhātu; thus raktadhātu is unable to carry-out its normal function of jeevana, varnaprasādana, mānsa poshan etc. Vaivarnya is caused due to loss of varnaprasādana karma, due to depletion of mānsa poshana, krishata and tivra ruja (Ischaemic pain) is observed. CREST syndrome can also be understood on the basis of rakta gatavāta.
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| − | Mānsa meda dhātu have similar characteristic both being snigdha, guru, sthira guna pradhan which gets vitiated by rūkṣa, laghu and cala guna of vāta leading to disorder called mānsamedogata vāta. Various myopathies can be included under mānsamedogata vāta specially Carnitine palmitoyltransferase deficiency in which severe pain with fatigueness is seen. Myasthenia gravis can also be considered in mānsamedogata vāta.
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| − | Asthigata vāta is multiple clinical conditions in which osteoporosity are a marked feature and majjāgata vāta is the same associated with marked synovitis. Due to external injury or due to pressure the asthi and majjā dhātu gets deranged leading to pain mainly at asthi parva or at the level of joints. The pain is continuous and it may later on show periarticular muscular atrophy as its late complication. It can be collectively understood under osteoarthritis where in focal loss of articular hyaline cartilage is seen with simultaneous proliferation of new bone with remodelling of joint contour (sclerosis).
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| − | Śukragata vāta may be either premature ejaculation, anejaculation os seminal abnormalities. In śukragata vāta, śukra are formed but either the count is less or there is some anomaly with its structure. Hence along with early ejaculation there is also abnormality in the foetus. Anomalies caused by extra sex chromosomes or less sex chromosomes can be included under this group (Aneploidy or polyploidy).
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| − | In śukragata vāta sperms are formed but the count may be reduced as in Viral Orchitis, Tuberculosis, Sexually Transmitted Diseases, Chemotherapy, Ionizing radiation and drugs in which testosterone levels remain normal. It may cause premature or delayed ejaculations and also may cause abnormality in the foetus.
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| − | Snāyugata vāta is characterized with radiculopathy (Sciatica), convulsions (Hemifacial spasm) or deformities (Torticolism). Sandhigatavāta is classical osteoarthritis.
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| − | In Sirāgata vāta, Ācharya have used two words mahati sirā and tanu sirā which resembles the two conditions related to vessels viz. aneurysm and narrowing of vessels. Aneurysms are a result of a weakened blood vessel wall. The repeated trauma of blood flowing through the vessel may contribute to degeneration of the vessel wall. Bleeding through the aneurysym may cause edema (śōpha). Pulsation (spandate) may be felt.
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| − | Narrowing of vessels mainly in the periphery is to be considered. Peripheral artery disease wherein there is no pulsation (suptā iti nispandā) and pain is observed. Intermittant Claudication, rest pain is the symptoms observed. Further due to reduced blood supply tissue loss (susyati) is also seen. Muscular atrophy manifests as sequel of Peripheral Arterial Disease.
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| − | VERSE 38-42
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| − | Ardita may be understood as many clinical conditions. Normally it is diagnosed as Bell’s palsy. The facial paralysis may be either of Upper Motor Neuron (UMN) or Lower Motor Neuron (LMN) origin. The etiological factors explained in Ashtanga Hridaya like bearing weight over head, over exertion activities to temporomandibular joint etc may lead to local causes to form LMN pathology. Here as Ardita is explained as vegavān disease clinical conditions like Transient Ischaemic Attack (TIA) and Reversible Ischaemic Neurological Disease (RIND) etc also may be understood in terms of Ardita. Further Hemifacial spasm, synkynesis etc has an after effect of poor managed or unresolved facial palsy is aso understood as ardita.
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| − | Caraka from shlok no. 38 onwards has classified the disease on basis of presenting symptoms. Since even in modern classification one may find neurological deficits become difficult to classify on basis of disease because for example facial presentation may be due to Trigeminal nerve, facial nerve, infective as in herpes, tumour like brain lesion, infarct or hemorrhagic in origin. Irrelevant of aetiological factors one needs give importance to the symptoms.
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| − | In context of facial palsy may be / may not be associated with involvement of other parts of the body. A complete interruption of the facial nerve at the stylo-mastoid foramen paralyzes all muscles of facial expression. The corner of mouth droops, the creases and skin-fold are effaced, the forehead is unfurrowed and the eyelids will not closed [stabdhaṁ nētraṁ]. Upon attempted closure of the lids, the eye on the paralyzed side rolls upward (Bells phenomenon), food collects between the teeth and lips and saliva may dribble from the corner of the mouth [vakraṁ vrajatyāsyē bhōjanaṁ]. If the nerve to the stapedius is interrupted, there is hyperacusis (sensitivity to loud sounds). Lesions in the internal auditory meatus may affect the adjacent auditory and vestibular nerves, causing deafness, tinnitus or dizziness (bādhyētē śravaṇau). Chakrapāni has explained it to be prabhav but today after complete anatomical study above explanation for hearing deficit may be proved.
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| − | If the peripheral facial paralysis has existed for some time and recovery of motor function is incomplete, a continuous diffuse contraction of facial muscles may appear.
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| − | Further other than Bells palsy facial palsy may be seen unilaterally or bilaterally in Lymes Disease. The Ramsay Hunt Syndrome caused by reactivation of Herpes zoster in the geniculate ganglion. Facial palsy that is often bilateral occurs in sarcoidosis and in Guillain Barre Syndrome, Leprosy, Diabetes mellitus, connective tissue diseases including Sjogren’s syndrome and Amyloidosis. The rare Melkersson Rossential Syndrome consists of recurrent facial paralysis and tumors of temporal bone.
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| − | In supranauclear lesion there may be a dissociation of emotional and voluntary facial movements and often some degree of paralysis of arm or leg or aphasia.
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| − | Further in corticobular involvement, weakness is usually observed only in the lower face and tongue; extra ocular, upper facial pharyngeal and few muscles are almost always spared. With bilateral corticobulbar lesions, pseudobulbar palsy often develops: dysarthria, dysphagia, dysphonia and emotional labiality accompany bilateral facial weakness and a brisk jaw jerk. A “pure motor” hemiparesis of the face, arm or leg is often due to a small, discrete lesion in the posterior limb of the internal capsule, cerebral peduncle or upper pons. Some brainstem lesion produces “crossed paralysis” consisting of ipsilateral cranial nerve signs and contralateral hemiparesis.
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| − | From above discussion one can understand various presentation of facial palsy which may / may not be associated with involvement of other parts of the body. Misdirection of food, resulting in nasal regurgitation and laryngeal and pulmonary aspiration during swallowing is characteristic of oropharyngeal dysphagia [bhōjanaṁ vakranāsikam].
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| − | Vakraṁ vrajatyāsyē, Chakrapāni comments, nā samam mukhena khādati kintu vakra ekadeshena explains the weakness of oral muscle due to which patient is unable to chew and swallow equally from both the sides.
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| − | Dinā jihya samutkshipta kalā sajjati ca āsya vāka explains the language disturbances (aphasia) seen in such patients. Aphasia should be diagnosed only when there are deficits in the formal aspects of language such as naming, word choice, comprehension, spelling and syntax. The neural substrate of language is composed of a distributed network centered in the perisylvian region of the left hemisphere. The posterior pole located at temporoparietal junctior and includes region known as Wernicke’s area and the anterior pole of language network is known as Broca’s area. Both this area are interconnected with each other with additional perisylvian, temporal, prefrontal and posterior parietal regions making up a neural network sub serving the various aspects of language function.
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| − | Anomia – deficit of naming
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| − | Paraphasia – Name the object with wrong word or fail to come up with appropriate word, may provide a circum-locutious description of the object.
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| − | Semantic paraphasia – If patient offers an incorrect but legitimate word (pen for pencil) the naming error is semantic paraphasia.
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| − | Phoenemic paraphasia – word approximates correct answer but is phonetically inaccurate (plentil for pencil).
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| − | Spontaneous speech [samutshipta atitvarita] is described as “fluent” if it maintains appropriate output volume, phrase length and melody or as “non fluent” if it is sparse, halting and overage utterance length below four words [kaleti avyaktā]
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| − | Alexia describes an inability to either read aloud or comprehend single words and simple sentences.
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| − | VERSE 43-51
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| − | Emprosthotonus and opisthotonus are two grave situations. These are also vegavāna – episodic in nature. These come generally considered under Ākshepaka vikāra (convulsions). Ākshepaka may be sārvadehika (generalized) or sthānika (local). These are caused when upadhātu like sirā, snāyu and kandarā are involved. Convulsions have two phases called tonic and clonic. If the patient posses tonic spasms without convulsive movements it is known as Dandaka. It can be compared with Botulism. These ākshepaka vyādhi is found to be very difficult to cure. So Ācharya advice here that, in diseases starting from ardita etc to consider these as pratyākhyeya or vivarjya as they possess frequent paroxyms. But it seems that, the description and treatment of Hanugraha does not fit to this category since it is a reducible orthopedic condition. In Ashtanga Hridaya other than these explained ākshepaka vikāra there are vranāyāma (tetanus), garbapata samutpanna ākshepaka (eclampsia?) etc are also explained. Antarāyama and bahirāyama are state of severe hyperflexion and hyperextension respectively alongwith spasticity in which an individual’s head, neck and spinal column enter into a complete bridging or arching position.
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| − | Bahirāyāma also known as opisthotonus the abnormal posturing is an extra- pyramidal effect and is caused by spasm of the axial muscles along the spinal column. It is seen in some cases of severe cerebral palsy and traumatic brain injury or as a result of the severe muscular spasm associated with tetanus. It can be feature of severe acute hydrocephalus. In neonate it may be symptom of meningitis, tetanus and severe kernicterus or the rare Maple Syrup Urine Disease. This marked extensor tone can cause infants to “rear backwards” and stiffen out as the mother or nurse attempts to hold or feed them.
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| − | It is sometimes seen in lithium intoxication, strychnine poisoning. Involvement of sirā is seen in bahirāyama and antarāyama. Chakrapāni explains it to be sirāgata vāta. Depending on nerve impulse agonist and antagonist muscle both either extend or flexed.
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| − | Locked jaw (hanustambha), teeth biting (dantanām dashana), salivation (lālā srāva), jrumbā (yawning) are common ‘symptoms for bahirāyama and antarāyama.’
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| − | Manyāstambha can be compared with spasmodic torticolis which is an extremely painful chronic neurological movement disorder is causing the neck to involuntarily turn into left, right, upward and / or downward. The condition is also referred as cervical dystonia. Other symptoms include muscle hypertrophy, neck pain, dysarthria and tremor. It may be secondary too cerebrovascular diseases, peripheral or central trauma, toxins, metabolic, drug induced, paraneoplastic syndromes, CNS tumour, kernicterus etc.
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| − | Hanustambha or Trismus or lock jaw refers to reduced opening of the jaws caused by spasm of the muscles of mastication, or may generally refer to all causes of limited mouth opening. Historically and commonly, the term lock jaw was sometimes used as a synonym for both trismus and tetanus.
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| − | Common Causes
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| − | – Pericoronitis – inflammation of soft tissue around impacted third molar.
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| − | – Inflammation of muscles of mastication. It is frequent sequel to surgical removal of mandibular third molar (lower wisdom tooth).
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| − | – Peritonsillar abscess
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| − | – Temporomandibular joint dysfunction
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| − | – Submucous fibrosis
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| − | – Fracture of the zygomatic arch
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| − | Other Causes
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| − | – Acute osteomyelitis
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| − | – Ankylosis of Temporomandibular joint
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| − | – Mumps
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| − | – Seizure
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| − | – Stroke
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| − | – Malignant hyperthermia
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| − | – Malignant otitis externa
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| − | – Local anesthesia
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| − | – Needle prick to medial pterygoid muscle.
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| − | Verse 50
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| − | The explanation given in shlok 50 resembles some of the hyperkinetic movement disorders; they are characterized by the presence of a variety of different involuntary movements.
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| − | Athetosis – slow, distal, writhing, involuntary movements with prosperity to affect the arms and hands.
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| − | Chorea – Rapid, semi purposeful, graceful, dancelike, nonpaterned involuntary movements involving distal or proximal muscle groups.
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| − | Dystonia – Involuntary patterned sustained or repeated muscle contraction, often leading to twisting movements and abnormal posture.
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| − | Myoclonus – Sudden, brief (<100ms), shocklike, arrhythmic muscle twitches
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| − | Tics – Brief, repeated, stereotyped muscle contractions that are often suppressible. Can be simple and involve a single muscle group or complex and affect a range of motor activities.
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| − | Tremor – Rhythmic oscillation of a body part due to intermittent muscle contractions
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| − | Focal Dystonias – There are most common forms of dystonia. They typically present in the fourth to sixth decades and affect women more than men. The major types are:
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| − | 1) Blepharospasm – Dystonic contractions of eyelids with increased blinking that can interfere with reading, watching TV and driving.
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| − | 2) Oromandibular Dystonia (OMD) – contractions of muscles of the lower face lips, tongue and jaw (opening or closing)
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| − | 3) Cervical Dystonia – Dystonic contraction of neck muscle.
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| − | 4) Limb Dystonia – these can be present in either arms or legs and are often brought out by task specific activities such as handwriting playing a musical instrument
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| − | Ca.Si.9/12-15 explains apatānaka and apatantraka vyādhi. It is in continuation of marmagata vyādhi. This is symptoms of typical meningeal irritation caused after trauma, subarachnoid hemorrhage or inactive encephalitis. Non epileptic convulsions are to be considered in these cases. Aseptic meningitis, encephalitis (herpes simplex, arboviruses, rabies) post infectious encephalomyelitis may also be considered.
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| − | Verse 51
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| − | The explanation given for dandaka resembles self limiting acute paralysis as seen in Guillian Barre syndrome.
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| − | VERSE 53-55
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| − | In these verses Ācharya Caraka explains three paralytic disorders namely monoplegia (ekāngarōga), hemiplegia (pakṣavadha) and quadriplegia (sarvāngarōga). In Ashtanga Hridaya ekāngarōga and pakṣavadha are explained as synonyms. According to Caraka ekāngarōga is monoplegia which is associated with toda and shoola which seems to be peripheral radiculopathy with motor deficit or focal brain lesions. In pakṣavadha paralysis, aphasia and sensory symptoms may co exist. Paralysis is loss of muscle function for one or more muscles. It may be accompanied by a sensory loss.
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| − | Causes
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| − | – Stroke – a) Hemorrhagic b) Ischemic
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| − | – Trauma with nerve injury
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| − | – Cerebral palsy
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| − | – Poliomyelitis
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| − | – Cerebral palsy
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| − | – Peripheral neuropathy
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| − | – Parkinson’s disease
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| − | – Spina bifida
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| − | – Multiple sclerosis
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| − | – Amyotrophic Lateral Sclerosis
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| − | – Botulism
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| − | – Guillain Barre Syndrome
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| − | Hatvaikaṁ: – explains loss of voluntary movement either in one part /or whole body. It usually refers to the limbs either mono i.e. one leg or one arm [ekāngarōga] or para i.e. both legs, hemi i.e. one arm and one leg on either side of the body [dakṣiṇaṁ vāmam ēva vā] and quadri i.e. all four limbs (sarvāṅga rōga].
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| − | Cēṣṭā nivr̥ttiṁ is seen due to loss of muscle power and tone.
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| − | Rujā /pain are due to reduced venous return leading to increase lactic acid within the muscle causing the pain. Thus physiotherapy helps to reduce pain.
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| − | Sirāḥ Snāyūrviśōṣya – explains atrophy i.e. partial or complete wasting of a part of the body. Poor nourishment, poor circulation, loss of nerve supply and disuse or lack of exercise is the cause.
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| − | Pādaṁ saṅkōcayatyēkaṁ hastaṁ vā: Damage to the pyramidal tract and its accompanying para pyramidal (cortico-reticulospinal) fibers give rise to UMN syndrome including positive and negative features. Impaired ability of damaged motor neurons to regulate descending pathways gives rise to disordered spinal reflexes, increased excitability of muscle spindles and decreased synaptic inhibition. This results in increased muscle tone of symptomatic muscle. The increased muscle tone may further lead to contractures.
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| − | Stroke symptoms typically start suddenly, over seconds to minute and in most cases do not progress further. The more extensive area of brain affected, more functions are likely to be lost.
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| − | Symptoms as per affected area:
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| − | A) CNS pathways – Spinothalamic tract, corticospinal tract and dorsal column
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| − | – Hemiplegia and muscle weakness of face
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| − | – Numbness
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| − | – Reduction in sensory or vibratory sensation
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| − | – Initial flaccidity (reduced muscle tone), replaced by spasticity (increased muscle tone), excessive reflexes and obligatory synergy.
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| − | B) If Brainstem which gives rise to cranial nerve gets involved, than
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| − | – altered smell, taste, hearing or vision
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| − | – drooping of eyelid (ptosis) and weakness of ocular muscle
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| − | – decreased reflexes: gag, swallow, pupil reactivity to light
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| − | – decreased sensation and muscle weakness of the face
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| − | – balance problems and nystagmus
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| − | – altered breathing and heart rate
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| − | – weakness in sternocleidomastoid muscle with inability to turn head on one side
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| − | – weakness in tongue
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| − | C) Cerebral cortex
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| − | – aphasia
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| − | – dysarthria
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| − | – apraxia
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| − | – visual field defect
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| − | – memory deficit
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| − | – disorganized thinking, confusion, hypersexual gestures (frontal lobe)
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| − | D) Cerebellum
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| − | – altered walking gait
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| − | – altered movement coordination
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| − | – vertigo and or disequlibrium
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| − | VERSE 56-57
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| − | Gr̥dhrasī can be correlated to Lumbo sacral radiculopathy, especially sciatica. There are opinions that the term pr̥ṣṭha used just after kati and prior to uru is misinterpreted as spinal column. The meaning as “posterior aspect” seems to be more apropriate in this context. But Chakrapāni specifically clarifies that Gr̥dhrasī manifest initially as catch in the gluteal region associated with spasm, ache and pain followed with catch spreading to hip, spine, thigh etc. The two types of gr̥dhrasī can be roughly correlated to Lumbar Degenerative Disc Disease as Vātika which is more prevalent in older age group and Intervertebral Disc Herniation as Vātakapha which is more prevalent in younger age group. The previous one is manifested as dehydrated disc and the later as bulged nucleus pulposus. The radiographic findings cannot be considered as ultimate for treatment strategies, which is specifically designed according to symptomatology and upashaya.
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| − | Gr̥dhrasī / sciatica is a set of symptoms including pain caused by general compression or irritation of one of five spinal nerve roots of each sciatic nerve. Sciatica is a relatively common form of lower back and leg pain. Sciatica is a set of symptoms rather than diagnosis; its cause being irritation at the root of nerve; in other words radiculopathy similarly Ācharya has mentioned khalli disease which is again a type of radiculopathy when brachial and lumbo sacral radiculopathy coexist. Radix means root; thus as set of conditions in which one or more nerves roots are affected shortly after exit from spinal cord. It may be secondary to degenerative disease, osteoarthritis, facet joint degeneration, ligamentous hypertrophy and spondylolisthesis. More rare cause may include radiation, diabetes mellitus, neoplastic disease or any meningeal based disease process. Depending on dermatome of the nerve supply pains are seen. Therefore Caraka mentions symptoms of upper & lower extremity. Khalli can also be considered as limb dystonia such as writer’s cramp, musician cramps.
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| − | VERSE 58-61
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| − | Samsarga dōṣa should be identified in all above discussed presentations. For example in case of pakṣāghāta, pitta anubanda features are very commonly seen in certain Thalamic infarctions. Eventhough swedana is a primary line of treatment in pakṣāghāta, it is not useful in thalamic infarctions which is otherwise called as sensory stroke. Further it responds to śītā sthambana treatments like takradhara.
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| − | VERSE 61-71
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| − | In case of Pitta āvr̥ta vāta due to intake of pittakara hetu quantitative vridhi of pitta takes place. It starts accumulating and now opposes the gati of vāta which is unable to get rid off the pitta dōṣa so pitta vridhi lakshana are observed. Symptoms like dāha etc are observed. The symptoms can be compared with heat stroke where the failure of heat regulating mechanism takes place. Giddiness, syncope may be observed, heat cramps may occur due to loss of sodium, potassium, chlorides in the blood. Hyperthermia reduces blood flow to brain causing giddiness.
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| − | In case of Kaphāvr̥ta vāta effect of cold stress should be considered. Muscular weakness is observed along with hypothermia. Symptoms may also arise in morning hours of cold seasons and rainy season. Working in air-conditioned rooms for longer hours can also create such symptoms. Even in common cold without pyrexia such symptoms may be produced.
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| − | Raktāvr̥ta vāta are near to some connective tissue disorders manifested with myalgia, insidious arthralgia, talengectacia and soft tissue inflammations.
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| − | Hetu explained in vidhishonitiya adhyaya are responsible for quantitative increase of rakta dhātu which impedes the gati of vāta dōṣa hence normal parivahana is hampered and stagnation takes place leading to sanga this is the reason why in rakta āvr̥ta vāta, rāga yukta śōtha, mandala, local dāha and vedāna have been explained. It can be compared with urticaria or vasculitis wherein there are rashes, burning sensation, pain, wheel and flare like presentation.
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| − | Mānsa dhātu is formed when vāyu, ambu, teja and rakta usma together bring sthirata to the mānsaposakansa. Sthira, kathina are the guna of mānsa while lepana is the karma of mānsa dhātu. Such mānsa when opposes the gati of vāta, kathina pidakā and śōtha is formed. Nodules and tumours are defined as the solid, raised and firm growth. Mānsāvr̥ta vāta looks like thrombophlebitis, deep vein thrombosis or lymphangitis etc with acute inflammatory symptoms.
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| − | Medasāvr̥ta vāta is otherwise called as ādyavāta or urusthamba. When ambu, snigdha guna along with the dhātusma acts on poshakansa a soft, snigdha meda dhātu is formed. When such medadhātu will obstruct the gati of vāta dōṣa it leads to origin of snigdha, mridu, ambulatory śōtha. Lipoma bullae can also be understood in context of medasāvr̥ta vāta.
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| − | Mānsa meda āvr̥ta vāta may also be a complication of prameha since mānsa and meda are the āvaraka along with kapha and pitta to develop āvr̥ta vāta in basti and in turn leading to madhumeha as explained in Ca.Su.17. It indicates when mānsa and meda become more vitiated and cause more kleda genesis or become kledānvita; they lead to different micro and macro angiopathy related complication. Meda-āvr̥ta vāta can be compared with Diabetic nephropathy.
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| − | Pipīlikānāṁ ca sañcāra are the abnormal sensory positive phenomenon or it may be the late complication of microangiopathy.
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| − | In asthyāvr̥ta vāta a relative asthi vriddhi in the form of osteophytes is observed (compensatory to decrease bone density) increasing the symptoms of pain along with chances of fracture. Eka sthāna vridhi and anya sthāna kṣaya is another principle which explain the concept of osteophytes. Osteophytes may compress the nerves root causing tingling or suchivāta vedana (entrapment or compressive neuropathy). In Asthyāvr̥ta vāta asthi is vitiated and leading to āvarana of vātasya mārga. When osteophytes are formed in osteoarthritis, spondylosis, it compresses underlying nerve fibres and manifest severe pain while joint movement in osteoarthritis and compressive neuropathy in spondylosis. Posterior incroachment can lead to spinal cord compression and related features like pseudo intermittent claudication.
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| − | In majjāvr̥ta vāta the majja dhātu impedes the gati of vāta (nerve conduction) leading to the symptoms like vināma; pain etc. Diffuse bulging of cord may be considered as well spinal canal stenosis.
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| − | In śukrāvr̥ta vāta immature sperms are formed which lose their forward movement activity. Ciliary dyskinesia (Kartagener Syndrome) can be included in this group. Since motility is reduced it leads to infertility. Y chromosomes microdeletions and POLG variants are increasingly recognised as a cause of azoospermia or oligospermia. Primary gonadal deficiency with low-testesterone and decreased spermatogenesis are the reason for infertility.
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| − | Patients with normal hormonal levels and low sperm count may be found in obstructive anomaly of vas deferens and epididymus.
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| − | Annāvr̥ta Vāta: Āhar when taken in excess the prokinetic movement is reduced and the āhar is not propelled forward leading to strech reflex. The pain of obstruction of hollow abdominal viscera is classically described as intermittent food related abdominal pain followed by remission.
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| − | Mūtra-āvr̥ta vāta: These symptoms are seen in mūtravega dharan. Normal urine formation takes place but the patient does not evacuate it timely leads to the avarodha of vāta gati. Vāta is unable to contract the detrusor muscle thus there is mūtra apravriti and inturn bladder distension. This condition may also arise in neurogenic bladder.
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| − | Atonic bladder – Micturition reflex contraction cannot occur if the sensory nerve fibres from the bladder to the spinal cord are destroyed, thereby preventing transmission of strech signals from the bladder. When this happens, a person loses bladder control, despite intact efferent fibers from the cord to the bladder and despite intact neurogenic connections within the brain. Instead of emptying periodically the bladder fills to capacity and overflows a few drops at a time through the urethra. This is called overflow incontinence. Crush injury is the common cause.
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| − | Purishāvr̥ta Vāta: Dietary fibres adsorb water and this increases the bulk of stools and helps reducing the tendency to constipation by encouraging bowel propulsive movements. Diet low in fibres content reduces the healthy bowel movements. Stools are formed but due to slow transit there is hard and pelty stool formation which finds it difficult to pass out.
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| − | Malavega dharan may also cause the above symptoms. In Diabetes mellitus whenever there is neurogenic involvement, peristalsis are reduced creating the above symptom. Spastic colon may also be considered.
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| − | VERSE 72-74
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| − | The different symptoms or clinical presentations explained in these verses suggestive of involvement of CNS as well as chronic degenerative nature. These disease presentations manifest in madhyama rōga mārga. If the diseases are diagnosed earlier the prognostic factors are good. In chronic conditions even after cure, chances of permanent deficits / deformities exist. Vātarōga with complications like hr̥drōga, vidradhi etc also should be seriously considered.
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| − | VERSE 75-82
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| − | The line of treatment of absolute vāta vitiation is explained here. It excludes all possible association of other dōṣa. Majority of such clinical conditions are degenerative in nature. It is further charecterised with tissue depletion. Supportive measures are more important than eliminative procedures. Snēhana is the primary line of treatment explained. Various types of articles and medications are highlighted here. All of them are falling under the category of phospholipids. Lipid metabolism and involvement of neural membrane phospholipids in neurodegeneration of human brain etc are found to be recently as significant. Breakdown of cellular membranes is a characteristic feature of neuronal degeneration in acute (stroke) and chronic (senile dementia) neurological disorders. A review by J Klein summarizes recent experimental and clinical work which concentrated on changes of choline-containing phospholipids as indicators of neuronal membrane breakdown. Experimental studies identified glutamate release, calcium influx, and activation of cellular phospholipase A2 (PLA2) as important steps initiating membrane breakdown in cultured neurons or brain slices under hypoxic or ischemic conditions. Proton NMR studies have shown an elevation of choline-containing compounds in the brain of Alzheimer patients while neurochemical studies in post mortem-brain demonstrated increase of the catabolic metabolite, glycerophosphocholine, an indicator of PLA2 activation. In contrast, studies of cerebrospinal fluid, phosphorus NMR studies, and measurements of phospholipases in post mortem Alzheimer brain gave ambiguous results which may be explained by methodical limitations. The finding that, in experimental studies, choline was a rate-limiting factor for phospholipid biosynthesis has stimulated clinical studies aimed at counteracting phospholipid breakdown, e.g. by combinations of choline and cytidine. Future experimental approaches should clarify whether loss of membrane phospholipids is cause or consequence of the neurodegenerative disease process.[21]
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| − | Probably loss of memebrane phospholipids is cause or consequence of the neurodegenerative disease process. Ayurveda advocates usage of various Snēhana in perview of the statement ‘Snēhasāro āyām purusah prānasca Snēhabhuyishta”.
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| − | Swedana is also very important in management of vāta rōga. It is ideally indicated in Vāta and vāta kapha conditions. On continuous application of snigdha property, gradually there exists an association of kapha. Sweda effectively eliminate stiffness, pain and coldness and imparts better flexibility, improvement in peripheral circulation and relieves oedema.
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| − | VERSE 83-88
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| − | Here the term ‘sā dōṣatva’ is of some controversy. It is generally understood as having associated dōṣa. But the specific treatment explained here is for vāta alone. So it is argued that there is no chance for a newer associated dōṣa. Chakrapāni clarifies that ‘sā dōṣatvam’ should be understood in relation to different karma done already. If any procedural fault is there it should be corrected with shodana karma to be explained here. But it can also be understood in a different way. ‘Sā dōṣatvam’ happens in singular vātaj diseases as the initial treatment procedures are going on. For example continuous Snēhana therapy may lead to association āma and kapha which is to be managed by deepana and pācana as explained. The same way continuous administration of swedana may impart involvement pitta prakopa which should be managed with mridu virēcana like eraṇḍataila with milk. ‘Sā dōṣatva’ can also be interpreted as residual dōṣa which normally not amenable to Snēha and sweda alone or together. In such conditions mridu samsodana is explained. In all these circumstances bala should be considered as in vāta prakopa alone. Bala of the patient is normally reduced and further gets compromised by continuous treatment.
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| − | VERSE 96
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| − | Aortic stenosis (AS) [Hridaya pradesh sthān dusti]
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| − | Constant production of pressure required to
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| − | Overcome the pressure gradient caused by AS
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| − |
| |
| − | Left Ventricular hypertrophy
| |
| − | Thickened muscular layer but the arteries that-
| |
| − | Supply muscles do not get significantly longer or bigger
| |
| − |
| |
| − | Blood supply to meet oxygen demand
| |
| − |
| |
| − | Ischaemia [Apatarpan]
| |
| − |
| |
| − | Dhātukṣaya
| |
| − |
| |
| − | Vātaprakopa
| |
| − |
| |
| − | Angina Hrudayagata Vāta
| |
| − | Study done by Kurin G A & oths [www.ndoi.n&m.nih.gov./pubmed 18380926) showed that Desmodium gangeticum posses the ability to scavange the free radicals generated during ischaemia and ischaemia reperfusion and thereby preserves the mitochondrial respiratory enzymes that eventually lead to cardioprotection.
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| − | Bahusirsa gata vāta is the clinical condition resembling frozen shoulder.
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| − | VERSE 99-103
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| − | The line of treatment of Ardita is explained here. It focuses disease above cervical seventh vertebra (urdhwajatru). As per modern science facial paralysis is almost a disease of auto recovery still some residual paralysis remains on the affected side. A well executed timely ayurvedic treatment make absolute cure without any evidence of facial deviation. In Ashtanga Hridaya vamana and raktamokshana are also explained in the treatment strategy of ardita. Vamana is useful in certain middle ear associated facial nerve symptoms (for eg. hyperacusis) seen along with recurrent upper or and lower respiratory tract infections. The same way raktamokshana is indicated in facial herpes infection.
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| − | Virēcana is the direct line of treatment for pakṣaghata. Virēcana was considered as an excellent option to relieve intracranial oedema. Further it ignites majjadhatwagni and boost intellect. It is worthy to observe that virēcana is the pratiloma sodhana in urdhwaga raktapitta and cerebrovascular accidents may be understood as concealed urdhwaga raktapitta.
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| − | Gr̥dhrasī is practically better controlled by parasurgical procedures explained in Ayurveda. Classical Basti practice also yield good outcome.
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| − | Verse 134
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| − | Vitex nigunto has good anti-inflammatory and analgesic activity. Leaf extracts have shown to reduce oxidative stress. Roots extracts have enzyme inhibitory activity.
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| − | VERSE 184
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| − | In Pittāvr̥tē vāta a balance of śītā and uṣṇā cikitsā has to be followed because extensive śītā cikitsā reduce pitta but increases vāta therefore a balance has to be maintained therefore the word ‘vyatyāsāt kārayēt’. Even in heat stroke management, the goal of treatment is to reduce temperature by at least 0.20c/min to approximately 390C. Active external cooling generally is halted at 390C to prevent overshooting, which can result in iatrogenic hypothermia. Ice water immersing is generally followed but the disadvantage it causes subcutaneous vasoconstriction, preventing the transfer of heat via conduction. Ice water may also increases shivering, which inturn increases heat production. Therefore śītā uṣṇā cikitsā has been mentioned.
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| − | Sēcanam of takra, ghrita and kshira has been mentioned. Yamaka Snēha of ghr̥ta and taila helps to balance pitta and vāta further kshira sēcana also improves bala of patient by process of dermal absorption.
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| − | VERSE 189
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| − | ‘Sthānam jayet purvam’ is a basic cikitsā sutra. Āmāshaya is among the main seat of kapha and if kapha is associated with āmāshaya gata vāta then first treat kapha by administrating vaman. Vaman helps in removing excessive mucus in stomach lining. Further, symptoms such as visucika etc explain āmavisha present in āmāshaya which can be removed by vaman.
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| − | Verse 197
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| − | Study on rat shows, the omega 3 deficient rats had significantly reduced DHA content in both brain regions. In the hippocampus, DHA deficient rats had 72% higher acetylcholine. Thus study is necessary if Snēha virēcana has omega 3 fatty acids. Further role of laxation and its anticholinergic effect should be studied.
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| − | Verse 202- 206
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| − | Prāna Āvr̥ta Vyāna
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| − | Prāna vāyu acts like a controller. It is responsible for the ādāna karma. Gyanendriya perceive their objects with the help of prāna vāyu.
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| − | Vyāna vāyu is responsible for gati or conduction. Hence vyāna vāyu plays a significant role in rasa vikshepan. Conduction is not only related to cardiac cycle but all types of neural conduction should be considered.
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| − | Whenever the controller prāna will restrict the gati of conducting vyāna vāyu the indriya will not be able to perceive its subject (vishaya). It may happen in one indriya (homonymous) or in all indriya (heteronymous) together. If it happens in all indriya it can be compared with the vegetative stage or deep coma.
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| − | Rasarakta vikshepan is karma of vyāna vāyu. In case of eye; vascular disease related to retina / optic disc causes visual loss.
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| − | Alzheimers Disease may also be considered. Macroscopically, the brain is atrophic, particularly the cerebral cortex and hippocampus. Many different neurotransmitter abnormalities have been described; particularly impairment of cholinergic transmission through noradrenaline, 5 H-T, glutamate and substance P is also involved. Inability to retrieve information (smriti kṣaya) is the symptom. Later apraxia, visuo spatial impairment and aphasia are seen.
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| − | Vyāna Āvr̥ta Prāna
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| − | Sweda sravan is normal function of vyāna vāyu thus whenever vyāna gets vitiated it causes sweda atipravriti. It explains sympathetic overactivity or cholinergic effect. Sweat glands secrete large quantities of sweat when sympathetic nerves get stimulated. Visha is one of the hetu of vyāna prakopa.
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| − | Perception is the function of prāna vāyu when it gets āvr̥ta its perception function is reduced. It is negative sensory feeling caused in disorders like diabetes mellitus.
| |
| − | Excessive sweating may cause tvak vikār due to dehydration.
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| − | Treatment
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| − | Snēha yuktaṁ virēcanam:
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| − | Snēha helps to reduce vyāna and virēcana helps in bringing anuloma gati to prāna vāyu.
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| − | Prāna Āvr̥ta Samāna
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| − | Pānini has explained that ātmā alongwith budhi activates the mana with the help of prāna. Mana stimulates the kāyāgni with the help of samāna vāyu and gives prerna to vāyu in upward direction which depending on ashta sthān produces various sounds. Thus vitiation of prāna or samāna leads to symptoms like gadgada and mūkatā.
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| − | Dysarthria, Mutism is associated with perisylvian region of left hemisphere. Posterior pole being Wernickes area and anterior pole of language is known as Brocas area. An essential function of this area is to transform neural word representation into their articulatory sequences so that words can be uttered in the form of spoken language. Both the poles are interconnected with each other and with additional perisylvian, temporal, prefrontal & posterior parietal regions making up a neural network subserving the various aspects of language function. Damage to any one of these components or to their interconnections can give rise to language disturbances (aphasia).
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| − | Treatment
| |
| − | Catuṣprayōgā snēhā – gives bala to samāna
| |
| − | Yāpana – gives bala to prāna.
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| − | Verse 204
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| − | Omega 3 fatty acids play a crucial role in brain function, as well as normal growth and development. Snēha is similar to meda and asthigata meda is majjā. Therefore Snēha helps in bruhan of majjā and also does regularization of vāta.
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| − | Verse 205
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| − | Samāna Āvr̥ta Apāna
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| − | Samāna vāyu helps in agni sandukshan also it has role in anna dharan, pacāna, virecana and taking kitta downward. Samāna vāyu is agni-samipasta vāta prakār. Grahani avayava helps in apakwa āhār dharan and pakwa āhār is pushed forward in pārshwabhag. In Samāna āvr̥ta Apāna, vridha Samāna does not help in dharan of apakwa āhār. Grahani vyādhi is so called because grahani is unable to do dharan of āhār. As apakwa āhār moves forward parshwa shool begins. Due to vitiated Samāna the number of intermediate metabolites increases and it obstruct gati of āpāna causing ischemia causing hr̥drōga.
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| − | Treatment
| |
| − | Agnideepaka ghrita
| |
| − | Deepan sarpi is to be administered in Samāna āvr̥ta apāna. Deepan karma helps to improve the enzymatic effect reducing the intermediate metabolites. Further Snēha regularizes vāta and thereby obstruction of āpāna is removed.
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| − | Omega 3 fatty acids supplementation greater than one gram daily for at least one year may be protective against cardiac death, sudden death and myocardial infarction in people. Omega 3 fatty acids reduce blood triglyceride levels. It also has anti-inflammatory effect.
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| − | Deepan sarpi helps in agnivardhan and does anuloman. It helps in āma pācana and reduces inflammation and has healing effect therefore useful in grahani.
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| − | VERSE 206-217
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| − | Prāna Āvr̥ta Udāna
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| − | Role of udāna vāyu is to give urjā, bala, increase prayatna, srotas preenan etc. They get hampered when prāna does āvarana over udāna vāyu. The prāna vāyu has adhogati while udāna vāyu has urdhwagati does mismatching takes place leading to sangraha of niḥśvās and ucchvāsa. Failure of control over the immune system leads to autoimmune disorder. The above condition can be seen in rheumatic heart disease and also in allergic rhinitis.
| |
| − | Treatment
| |
| − | Urdhvabhāgikaṁ karma means Snēha, nasya etc. Nasya has its local effect on nose improving the local immune response as well as on respiratory centre. Nasya has good effect on allergic rhinitis. Role of vaman needed to be studied.
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| − | Āśvāsan cikitsā can be related to maintenance of patient. Because it is also seen clinically that most of patients of allergic situations can be maintained but not cured. Similarly patient who have developed stenosis of mitral valve are too maintained. Modern science opts for operative in late cases.
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| − | Udāna Āvr̥ta Prāna
| |
| − | Bala, varna, oja, prayatna depend on Udāna vāyu while controller and assimilator is prāna vāyu.
| |
| − | In udāna āvr̥ta prāna the prāna gati is restricted does perceiverance and control is lost while udāna vāyu being prakopita oja, varna, bala nāśa is seen.
| |
| − | The above symptoms are seen in terminally ill patient in which fatigueness and weakness is commonly seen associated with psychological symptoms like hopelessness, meaninglessness, confusion, delirium which are similar to oja nāśa.
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| − | Underlying various disorders reduce the energy store. It occurs due to disease induced factors such as TNF, cytokines and from secondary factors such as cachexia, dehydration, anemia, infection hypothyroidism and Diabetic Ketoacidosis (DKA). Changes in muscle enzymes also play an important role. RAS system may get involve later on causing semicoma followed by coma and lastly death.
| |
| − | Treatment
| |
| − | Āśvāsan cikitsā over here again means maintaining the patient. As discussed in symptoms it is underlying process in various dangerous diseases. Even modern science in emergencies maintains the basic criteria i.e. BP, Heart rate, Urine output, electrolyte balance etc.
| |
| − | Sukhaṁ caivōpapādayēt i.e. no shodhan or karshan should be done. Ācharya have cautioned by explaining that emergency caused due to shodhan cikitsā are more dangerous than bruhan cikitsā. In Udāna āvr̥ta prāna there is oja nāśa therefore avoid karshan in any form. Sinchet śītavāriṇā explain that rugna prabodhan should be done repeatedly.
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| − | Udāna Āvr̥ta Apāna
| |
| − | In above condition one needs to emphasize on gati of vāta prakār. Udāna has its urdhwagati while apāna vāyu has anuloma gati. In udāna āvr̥ta apāna; the later changes its gati and now becomes udāna bhava āpana as commented by Chakrapāni ‘Urdhwagati swabhava āpana’. Thus urdhwagati is increased causing symptoms like chardi, shwas etc.
| |
| − | Cigarette smoking often results in mucous gland enlargement and goblet cell hyperplasia. Goblet cells increase in number but in extent through the bronchial tree. Bronchi undergoes squamous metaplasia which disrrupts mucociliary clearence leading to COPD.
| |
| − | Antiperistalsis means peristalsis up the digestive tract rather than downward. This may begin as far down in the intestinal tract as the ileum. It can push the contents upto duodenum and stomach leading to their over distention which becomes the exciting factor that initiates the actual vomiting act.
| |
| − | Basti and anuloman cikitsā helps in regularizing the peristalsis. The reverse movement of prostration is diverted downward. Due to anuloman, urdhwa gati of udāna is also pacified and regularized, further over distention of abdomen is reduced.
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| − | Apāna Āvr̥ta Udāna
| |
| − | Apāna has adogati and is responsible for kitta utsarjan while udāna vāyu is responsible for urja and has urdhwagati.
| |
| − | Apāna when resist udāna the udāna vāyu becomes apāna bhava āpāna. As udāna vāyu gets āvr̥ta, urja or agni is reduced causing agnimāndya. The increase kitta and reduced urja gives rise to moha and alpāgni.
| |
| − | Uraemia may be understood in the above condition where the concentration of blood urea (kitta bhag) increases in blood.
| |
| − | Treatment
| |
| − | As understood in Raktapitta cikitsā ‘Pratimargam ca haret’ is the cikitsā siddhant; vaman should be administered if there is excessive atisār. Vaman has urdhwagati which gives bala to udāna vāyu. Deepan karma which will give bala to agni and inturn bala to udāna. Grāhi aushada reduces the hyperperistalsis seen in apāna vridhi and also helps in absorption of electrolytes fluid thereby reduces quantity and frequency of stool.
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| − | Vyāna Āvr̥ta Apāna
| |
| − | Apāna vāyu has its own anuloma gati and its role is to eliminate the faecal matter, urine etc. In this āvarana, vyāna opposes the gati of apāna thus anuloman does not take place. Features resemble adhovāta vegadharan vyādhi like ādmān, udawarta, gulma and vedana. When the person stresses while passing motions the hard stools cause painful condition called the fissure.
| |
| − | Gastro-Intestine has its own intrinsic set of nerves known as intramural plexus or the intestinal enteric nervous system located on the walls of gut. Both parasympathetic and sympathetic stimulation originating in the brain can affect gastro intestinal activity mainly by increasing or decreasing specific actions in the gastrointestinal intramural plexuses. Strong sympathetic stimulation inhibits peristalsis and increases the tone of sphinctures. Net results in slow propulsion of food through tract sometimes decrease the secretion as well even to the extent of constipation. As the peristalsis is reduced the food remains in stomach or early part of small intestine which send the strech impulse to vomiting centre causing the vomiting.
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| − | Anuloman gives bala to apāna vāyu reducing the ādmān. Snigdha anuloman gives softness the stools thereby reducing pain and fissure. Snigdha anuloman is cikitsā for udavarta and Gulma.
| |
| − | Apāna Āvr̥ta Vyāna
| |
| − | Function of apāna vāyu is excretion of fecal matter, urine, menstrual blood and sperm at a specific interval. Apāna when gets vridha and restricts the gati of vyāna the utsarga vriti of āvaraka is seen. Thus atipravriti of purisha, mūtra and retasa is seen.
| |
| − | There is interplay between gati of apāna with gati of vyāna. The srijan karma and gati karma of apāna vāyu vitiates vyāna vāyu which becomes āvr̥ta and thus rasa vikshepan karma is reduced.
| |
| − | Diarrhoea causes dehydration leading to reduced ventricular filling pressure. Modulation comes into play causing increase heart rate and peripheral vasoconstriction but if the dehydration continues the cardiac output is reduced thus leading to reduced rasa vikshepan causing hypovolaemic shock.
| |
| − | Symptoms explain apāna ati pravritti therefore sangrahan cikitsā has been mentioned. Sangrahan drugs are jaliyansa shoshaka by their usna guna except for some drugs like musta which are grahi although śītā gunatmak.
| |
| − | Sangrahan maintains the fluid volume thereby maintaining the cardiac output and electrolyte imbalance.
| |
| − | Sangrahan karma reduces the utsarjan karma of apāna and improves the dharan karma of
| |
| − | apāna.
| |
| − | Samāna Āvr̥ta Vyāna
| |
| − | Many systemic metabolic abnormalities cause altered sensorium by interrupting the delivery of energy substrates. Almost all instance of diminished alertness can be traced to widespread abnormalities of the cerebral hemisphere or to reduced activity of a special thalamocortical alerting system termed the reticular activating system (RAS). Suppression of RAS and cerebral function can take place incase of metabolic derangement such as hypoglycaemia or hepatic failure leading to stage of reduced comprehension, coherence and capacity to reason. Irrelevant talk, lack of appreciation of spatial relation of self or external environment (agnosia) may also occur.
| |
| − | Exercise improves the vyāna bala and vyāna activates Samāna to stimulate the agni uttejaka bhava. Whereas laghu bhojan prevents the excessive load on agni thereby reducing the intermediate metabolites. Activity of agni uttejaka bhava (Samāna vāyu) is reduced. Thereby pacifying Samāna vāyu and giving bala to vyāna.
| |
| − | Udāna Āvr̥ta Vyāna
| |
| − | Vyāna vāyu is responsible for gati, vikshepan, sweda sravan, nimesha, unmesha etc. but whenever it gets āvr̥ta swa karma hāni occurs and if it gets āvr̥ta by udāna the one responsible for bala, prayatna, urjā causes symptoms like stabdhata, alpāgni, asweda, chestahāni and nirmilan.
| |
| − | Continuous generalized electrical discharges of the cortex are associated with coma even in the absence of epileptic motor activity. The self limited coma that follows seizures termed the postictal state may be due to exhaustion of energy resources or effects of locally toxic molecules that are byproduct of seizures.
| |
| − | Alpa, mita and laghu bhojan helps to empowerise agni. Laghu āhār gets easily digested and absorbed and comes into circulation. This gives bala to vyāna which provides nutrition by its rasa vikshepa karma thereby pacifying the udāna.
| |
| − | ANUKTA ĀVARANA
| |
| − | Vyāna Āvr̥ta Udāna
| |
| − | Vyāna is associated with gati and prakshepan while udāna is associated with bala prayatna and urjā. Vikrut vyāna has impaired gati which when impedes udāna will reduce the bala, prayatna ādi karma of udāna.
| |
| − | Sympathetic fibres originate in the hypothalamus, pass down the brain stem and cervical spinal cord to emerge at T1 level, return back up to the eye in association with the internal carotid artery and supply the dilator pupillae. Lesion in the sympathetic pathway cause Horner’s syndrome. The reason may be central (at the level of Hypothalamus / brain stem) or at the periphery (at the level of lung apex, carotid artery) or may be idiopathic.
| |
| − | Vyāna āvr̥ta udāna can also be considered in paroxysmal tachycardia. Abnormalities in different portions of the heart including the atria, the Purkinje system, or the ventricles, can occasionally cause rapid rhythmical discharge of impulses that spread in directions throughout the heart. This is believed to be caused most frequently by re-entrant circus movement feedback pathways that set up local repeated self re-excitation. The above process occurs unless considerable ischemic damage and may lead to ventricular fibrillation. Thus there is never a coordinate contraction of all the ventricular muscle at once which is required for cardiac pumping. Patient may complaint of palpitation or symptoms such as dizziness, dyspnoea, fatiguebility i.e. bala, prayatna are reduced.
| |
| − | Apāna Āvr̥ta Samāna
| |
| − | Apāna is responsible for srijan karma. Vikrita Apāna increases the nishkraman prakriya. Increase Hustration reflex causes excessive propulsion movement. Excess motility causes reduced absorption. The body in unable to reabsorb bicarbonate ions i.e. Samāna karma is reduced. Loss of bicarbonate causes rise of H+. Body compensates the process by increased ventilation. The PaCO2 is reduced secondarily by hyperventilation which mitigates the rise in H+ leading to metabolic acidosis.
| |
| − | Diarrhea associated with passage of more than 200g of stool with urgency of defaecation and faecal incontinence. This may lead to malabsorption leading to hypoalbuminaemia, hypocalcaemia and vitamin D deficiency, hypomagnesaemia, phosphate, zinc and weight loss.
| |
| − | Prāna Āvr̥ta Apāna
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| − | Prāna vāyu function is associated with controlling system of the body, as said by Nyāyachandrikākār. Prāna vāyu helps in assimilation and maintain homeostasis.
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| − | Apāna is responsible for elimination. Considering pakvāshaya it may be compared with srijan of purisa mūtra etc. and at cellular level function of apāna is removal of cellular products within the cell. In this particular condition of prāna āvr̥ta apāna the vikrita prāna obstructs the gati of apāna and it is unable to release the cellular products. This can be understood in condition of Brainstem lesion where in the control over CO2 expiration is lost. Depletion of CO2 expiration leads to increase in concentration of CO2 in blood resulting in respiratory failure of Type II origin i.e. severe respiratory acidosis. A simple sleep apnoea / hypopnoea syndrome may also be considered.
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| − | Udāna Āvr̥ta Samāna
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| − | In this particular condition as udāna vikriti takes place anabolism increase reducing the catabolism. This is observed in Hypothyroidism where in weight gain is seen with decreased appetite.
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| − | Leptin is secreted by adipose cells and acts primarily through the Hypothalamus. Its level of production provides an index of adipose energy stores. High leptin levels decrease food intake and increase energy expenditure. The OB gene is present in humans and expressed in fats. The obesity in these individuals begins shortly after birth, is severe and is accompainied by neuroendocrine abnormalities. Role of central hypothyroidism has been understood in mouse model.
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| − | Leptin Leptin Receptor Signal Proopiomelanocortin
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| − | (POMC) Expression
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| − | Alpha MSH
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| − | Melanocortin & Receptor Signal
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| − | Appetite
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| − | Another condition may be considered where increased acetylcholine stimulates increased ATP (-urjā) which further increases excessive secretion of fluids and electrolytes in addition to normal viscid alkaline mucus which further increases gastrointestinal activity causing reduced absorption (annasoshan, vivechan karma) leading to malabsorption diarrhea.
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| − | Vyāna Āvr̥ta Samāna
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| − | There is interplay between gati of vyāna with gati of Samāna. Therefore when rasa vikshepan karma of vyāna related to Samāna vāyu is vitiated, the later becomes āvr̥ta and in turn annapācana, vivechan and munchan karma of Samāna are inhibited or decreased.
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| − | Sympathetic nerves have dual action in some cases; it increases secretion but if parasympathetic is already causing copious secretion than sympathetic usually reduces the secretion mainly by vasoconstriction reducing the blood supply.
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| − | Although Enteric Nervous System (ENS) can function autonomously; Autonomic Nervous System (ANS) connects ENS centrally. When ANS activity is increased it has its impact on gastrointestinal tract. Sympathetic overstimulation causes vasoconstriction which reduces secretion of gastric juices and pancreas exocrine secretion. Their insufficiency can cause malabsorption syndrome in which predominant feature is steatorrhoea, deficiency of fat soluble vitamins, protein and carbohydrate deficiency related features.
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| − | As compensatory mechanism vasodilatation in skin leads to excessive sweating and skin related features.
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| − | Samāna Āvr̥ta Prāna
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| − | Role of Samāna along with agnideepan is to help in pācana and sāra kitta vibhajan. Thus along with pitta, Samāna plays its major role in metabolism. If Samāna gets vitiated then sāra kitta vibhajan does not takes place properly and kitta bhaga gets upashoshit along with sāra bhaga. Thus kitta munchan prakriyā does not take place. This condition may be noted in metabolic acidosis, hypercalcemia and uraemia. The kitta bhaga now alters the gati of prāna or in other words neuronal excitability. It may show symptoms like confusion seizures, coma and death. It may also depress the respiratory centre causing hyperventilation or Kussmaul breathing.
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| − | Samāna Āvr̥ta Udāna
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| − | The same kitta bhāg depending on sthān obstructs the gati of udāna. The bala, prayatna, urjā ādi karma are reduced.
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| − | Conditions can be observed in hepatic coma where in increase levels of ammonia (kitta bhāg) interfere with cerebral energy metabolism and with Na+, K+, ATPase pump. Number and size of astrocytes are increased. They alter the nerve cell function and causes symptoms of fatiguebility, altered sensorium and coma. (prayatna nāśa).
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| − | Similarly Hyperthyroidism may also be considered. Samāna is said to be agnibala pradha, it leads to increase in catabolism. Energy gets exhausted with increase catabolism reducing the bala prayatna which is the role of udāna vāyu as seen in thyrotoxicosis.
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| − | Apāna Āvr̥ta Prāna
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| − | Interplay exists between apāna the eliminator and prāna the controller of the body system. Mismatching between apāna and prāna karma leads to various disorders. If the srijan karma and gati of apāna related to ādān karma of prāna gets vitiated the prāna vāyu gets āvr̥ta and in turn causing difficulty in breathing, confusion, coma and death.
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| − | Loss of Na+, Cl-, H+ and extra cellular fluid depletion occurs in excessive administration of diuretics or in congenital chlorodiarrhoea. It leads to increase concentration of plasma HCO3 which leads to condition such as apathy, confusion and drowsiness.
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| − | In anxiety induced hyperventilation excessive loss of CO2 takes place. PaCO2 andH+ falls. The low PaCO2 results in reduced renal Na+/H+ exchange due to which patient feels short of oxygen.
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| − | VERSE 221
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| − | Pitta Āvr̥ta Prāna
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| − | Prāna vāyu is said to be controller, it helps in assimilation of āhār etc. In pittāvr̥ta prāna there is quantitative increase of pitta and it opposes the gati of prāna, hence ingested food is vomitted out and since the āhār is not completely digested it comes out in the vidagda form, as pitta has increased there are symptoms of dāha, vidāha, murchha, bhrama and śītā kamana
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| − | Whenever food is ingested it stimulates the pharyngeal sensory receptors which send the impulse to the swallowing centre from where the motor impulses are sent with the help of 5th, 9th, 10th, 12th, cranial nerves to the pharynx and upper esophagus similarly sensory signals that initiate vomitting originate mainly from the pharynx, esophagus, stomach and upper portion of small intestine. The impulse traverses by both vagal and sympathetic afferent nerve fibres to the vomitting centre from where motor impulse that cause vomitting are transmitted by way of 5th, 7th, 9th, 10th & 12th cranial nerves to the upper GIT causing vomitting. Thus vomitting may be initiated by nervous signals arising in the brain. Stimulation of the floor of 4th ventricle called chemoreceptor trigger zone with the help of administration of certain drugs initiate vomitting. If the gastric contents are incompletely digested are vomited out with a burning sensation associated with abdominal pain, vertigo, etc. Viral encephalitis may also be considered which is associated with high grade fever, focal neurological signs and seizures. These emergencies are difficult to treat so as said by Caraka that pitta and kapha āvr̥ta prāna are difficult to treat.
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| − | Kapha Āvr̥ta Prāna
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| − | Vridha kapha opposes the gati of controller prāna hence inspiration and expiration functions are hampered at the same time chardi, ṣṭhīvana and kṣavathū symptom increases in frequency. Depression of respiratory centre in the medulla should be considered. Abnormal ventilation may be considered as in case of COPD where in mucus plugs prevent the gases exchange. The mucus accumulated in nasal and throat cavity obstructs the gati of prāna causing irritation, the afferent impulses passes to the medulla where the reflex of kṣavathū and ṣṭhīvana is triggered the same impulse also stimulates the vomitting centre causing chardi.
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| − | Pitta Āvr̥ta Udāna
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| − | Karma of udāna vāyu is to generate urjā, it is vāka pravriti mulak, prayatna bala, varna, kārak along with srotas prinan, dhi dhriti smriti mano bodhana are the karma of udāna.
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| − | The pitta which has increased quantitatively along with its tiksna, uṣṇā etc guna is responsible for āvarana of udāna vāyu. Thus prayatna, bala, varna nāśa take place similar to the ojo bhransa explained by Sushruta, body gets fatigue as there is reduced energy and burning sensation between nābhi and ura along with murchha, dāha bhrama ādi vridha pitta lakshana.
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| − | As ATP production is hampered (Urjā hāni) metabolism gets hampered leading to GERD (Gastro Eosophageal Reflux Disease) causing heart burn and associated symptoms like fatigueness vertigo etc.
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| − | Kapha Āvr̥ta Udāna
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| − | Śītā, guru, manda guna yukta vridha kapha has qualities opposite of vāta. Especially when vitiated kapha impedes udāna vāyu, vāka pravriti, bala, varna, utsāha are loss thus creating the above symptoms. Pānini has explained swarotpatti in which he says ātmā and budhi come together and they give prerana to the mana which further stimulates vāyu and it moves upward through the thorax cavity and with the help of astasthān helps in shabdhotpati.
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| − | Vāyu prakār which is moving in thorax cavity in upward direction should be understood as udāna. Kapha obstructs this particular gati causing vākswargraha, thus muscular movement in larynx mouth and respiratory system does not occur in succession causing dysarthria.
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| − | As ATP is unable to generate energy, daurbalya and guru gātratā symptoms are enhanced.
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| − | Pitta āvr̥ta Samāna
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| − | Pitta gives āshraya for agni while Samāna is said to be agni uttejaka bhava. When āvarana of Samāna takes place abhāva of agni uttejana occurs but it takes with the help of pitta hence there are generalised symptoms of pittavridhi with usma upaghāt. Hence excessive sweating leading to trishna associated with dāha murcha aruchi which are pittavridhi samānya lakshana.
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| − | Zollinger Ellison Syndrome may be understood in this case wherein gastrinoma secretes large amount of gastrin which stimulate the parietal cells of stomach to secrete acid to their maximal capacity.
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| − | Increase aldosteronism may also be considered under pitta āvr̥ta samāna.
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| − | Kapha āvr̥ta Samāna
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| − | In Kapha āvr̥ta Samāna the śītā , manda guru guna obstructs gati of Samāna. Thus agni uttejaka abhavta is seen leading to agnimandya. Difference between the pitta and kapha āvr̥ta samāna is the excessive drava gunatmaka vridhi which prevents agnivridhi in case of pittāvr̥ta samāna while incase of kaphāvr̥ta samāna the enzymes are absent and there is no conversion of ATP.
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| − | Pitta āvr̥ta vyāna
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| − | Vyāna vāyu is responsible for all gati, prasarana, ākuncana, utshepa, avakshepa, nimesha unmesha ādi kriya.
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| − | Whenever āvarana of vyāna vāyu takes place sanga or restriction of sarvānga gātra takes place and dāha, santāpa are the sāmānya lakshana of vridha pitta.
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| − | Inflammatory myopathies may be considered under pitta āvr̥ta vyāna. Systemic features like fever and fatigue are common. Other systemic autoimmune disease such as SLE (Systemic lupas erythomatosis) or vasculitis can also cause myositis. Polymyalgia rheumatica may also be considered where in muscular pain and stiffness is present. There is no true vasculitis but there is close association with giant cell arteritis, fatigueness, fever and depression.
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| − | Kapha āvr̥ta vyāna
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| − | In case of kapha āvr̥ta vyāna gurutā ādi are samānya lakshana of vridha kapha. Fibromyalgia may be considered in kapha āvr̥ta vyāna. In this disorder there is no structural, inflammatory or endocrine abnormality. Marked fatigability, pain along with signs of osteoarthritis is observed.
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| − | Pitta āvr̥ta apāna
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| − | The quantitatively increased pitta offers resistance to the gati of apāna. Role of apāna is dharana of the sharir. Mala bhāg is excreted out with the help of apāna vāyu, raja pravartan, garbha nishkraman are also functions of apāna.
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| − | The vridha pitta imparts its haridra peeta varna to mūtra and purisa. Due to its usna and tikshna guna santāpa is felt at guda or medra sthāna. Pitta is mala bhāg of rakta and rakta helps in poshan of raja dhātu. Both pitta and raja have samāna gunadharma hence pitta vridhi also leads to raja vridhi causing raja atidarshan.
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| − | This condition may be compared with infective inflammatory changes in urethra, anorectum and vagina. HSV (Herpes simplex virus) increases vaginal discharge along with vulval pain and dysuria. In trichomoniasis infection there is vulva and vaginal inflammation along with froathy yellow / green discharge. HSV and trichomoniasis may also be responsible for proctitis and urethritis.
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| − | Kapha āvr̥ta apāna
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| − | The snigdha, guru, pichchhila, drava guna yukta kapha has its resemblance similar to meda and kleda does the bahudrava kapha when gets basti prabhava and along with meda and kleda reach the mūtravaha srotas and get settle at glomerulus (āsādya pratirudyate gatwā awatistate) leading to utpatti of kaphaj prameha.
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| − | This condition can be compared with alimentary glycosuria, a rapid but transitory rise of blood glucose following a meal. The concentration exceeds the normal renal threshold; during this time glucose will be present in the urine.
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| − | Vridha kapha by its snigdha, pichchhil, āma swaroop, guna changes the consistency and physical appearance of the mala converting it into bhinna, āma, kapha sansrista guru varca.
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| − | Prognosis of Pitta and Kapha Āvr̥ta vāta Prakār
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| − | - Ācharyas beleive āvarana of prāna and udāna vāyu by both kapha, pitta are a serious condition.
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| − | - Anabhisyandhi, snigdha and sroto shodhak dravya should be selected.
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| − | - Yāpana basti with madhur rasa pradhan dravya.
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| − | - Anuvāsan basti
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| − | - If patient is balwan mrudu anuloman is useful
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| − | - Rasāyana cikitsā to be followed
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| − | - Shilajeet and guggulu should be administered along with milk.
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| − | - Use of Lasuna, guggulu, shilajeeta rasāyana are mentioned here specificaly, shows their importance in breaking mārgasya āvarana/avarodha.
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| − | - Chyavanprasa and Abhayaamalaki rasayan should be given.
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| − | - If apāna vāyu does the āvarana then deepana, grāhi, vāta anulomaka and pakvashaya shodhana dravya should be selected.
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| − | - In āvarana due to pitta, therapy which alleviates pitta but does not work against vāyu should be given.
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| − | - If kapha does the āvarana then therapies which reduce kapha and which do anuloma of vāta should be selected.
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| − | Reference
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| | 1. Sushruta. Sushrutasamhita with Nibandhasamgraha Commentary, Nidanasthānam 1/8; Vd. Yadavji Trikmji Ācharya (eds),Reprint, Choukhamba Krishnadas Academy, 2004 | | 1. Sushruta. Sushrutasamhita with Nibandhasamgraha Commentary, Nidanasthānam 1/8; Vd. Yadavji Trikmji Ācharya (eds),Reprint, Choukhamba Krishnadas Academy, 2004 |
| | 2. B C Joshy, Neurology in Ancient India – some evidences, Indian journal of History of science, 19(4):366-396(1984) | | 2. B C Joshy, Neurology in Ancient India – some evidences, Indian journal of History of science, 19(4):366-396(1984) |