Ardita – अर्दित – चरकोक्त ( च.चि.28 ) – the neuroscience ;
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 TIA and 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.
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.
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.
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.
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.
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.
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.
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].
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.
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.
Anomia – deficit of naming
Paraphasia – Name the object with wrong word or fail to come up with appropriate word, may provide a circum-locutious description of the object.
Semantic paraphasia – If patient offers an incorrect but legitimate word (pen for pencil) the naming error is semantic paraphasia.
Phoenemic paraphasia – word approximates correct answer but is phonetically inaccurate (plentil for pencil).
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]
Alexia describes an inability to either read aloud or comprehend single words and simple sentences
Prof. Dr. Satyendra Narayan Ojha ,
MD (KC), Ph.D.
Director , Yashawant ayurveda college , Post graduate teaching and research center ,
Kodoli ,Panhala , Kolhapur