Aphasia

Aphasia is a disorder caused by damage to the parts of the brain that control language. Aphasia may occur secondary to brain injury or degeneration and involves the left cerebral hemisphere to a greater extent than the right. Language function lateralizes to the left hemisphere in 96-99% of right-handed people and 60% of left-handed people. Aphasia syndromes have been described based on patterns of abnormal language expression, repetition, and comprehension. The neuroanatomic substrate of language comprehension and production is complex, including auditory input and language decoding in the superior temporal lobe, analysis in the parietal lobe, and expression in the frontal lobe, descending via the corticobulbar tracts to the internal capsule and brainstem, with modulatory effects of the basal ganglia and the cerebellum. Some people recover from aphasia without treatment. Most, however, need language therapy as soon as possible.

Wernickes aphasia

Causes Aphasia is a symptom and not a disease; it can be caused due to

Stroke Brain tumors, Head injuries, infections and Degenerative diseases Dementia (Some dementias, such as frontotemporal dementia, primary progressive aphasia, or Pick disease, have aphasic syndromes that closely resemble the aphasic stroke syndromes except that they begin gradually and progressively worsen. If aphasia is the sole deficit over a 2-year period,it is termed as primary progressive aphasia) A rare cause of aphasia in children is the Landau-Kleffner syndrome, a syndrome of acquired epileptic aphasia. A rare but important condition not to overlook is herpes simplex encephalitis. The aphasia in herpes simplex encephalitis may mimic Wernicke aphasia mimicking a stroke deficit, but often with associated confusion.

Aphasia is diagnosed based on language examination and the localization of a lesion in the left hemisphere.

Physical findings of aphasias Broca aphasia Broca's aphasia, also called motor aphasia, results from damage to the front portion or frontal lobe of the language-dominant area of the brain. Broca's aphasia characterizes

patients as people who have loss the production of complete sentence structures in speech and writing. Phrases are short and may be telegraphic or agrammatic, including major nouns and verbs but no functor words (articles, adjectives, adverbs, or conjunctions). Patients have telegraphic speech, also called agrammatism. Naming of actions is typically worse than naming of objects. Thus, patients with Broca's aphasia is characterized as "non-fluent aphasia". Hearing comprehension is usually not affected, so they are able to understand other people's speech and conversation and can follow commands. Reading ability is impaired, and they may have difficulty finding the right word when speaking. A writing deficit usually parallels the phonologic deficit. Depression is extremely frequent because patients are typically aware of their deficits

Wernicke aphasia Verbal output is either normal or increased. Speech production demands little or no effort and articulation is normal. Sentences are of normal length with normal prosody. However sentences are devoid of meaningful words so that almost no information is conveyed, an output that can be called empty speech; paraphasia is common. Words are also substituted by meaningless, nonsense words (neologisms). Jargon aphasia is a severe form of Wernickes aphasia with rapid verbal output, abundant paraphasic substitutions and incomprehensible verbalization. Comprehension of spoken language is disturbed in aphasia. The severity of the comprehension deficit is variable. Comprehension ability may decrease with testing, a phenomenon called fatigue or jamming. Two varieties of comprehension defect are described.

In one variety (Predominantly word deaf)

another variety, (Predominantly word blind)

Classic Wernickes aphasia features a combination of the two. Repetition of spoken language is invariably normal. Writing is also abnormal in Wernickes aphasia.

Conduction aphasia The defining feature of conduction aphasia the repetition difficulty. Conduction aphasia may be Wernicke like or Broca like.
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When of the former variety, verbal output is fluent and paraphasic, but the amount of output is less than in Wernickes aphasia. In the latter, articulation is excellent and comprehension of spoken language is intact; however fluency may be diminished. The ability to write is invariably disturbed to some extent. Most often syllables and letters are substituted or misspelled or misplaced. Often conduction aphasia is not diagnosed at the onset but develops in the recovery phase from Wernickes aphasia.

Global aphasia In this type of aphasia, the patient has deficits in all aspects of language: - spontaneous speech, - naming, - repetition, - auditory comprehension, - reading, and writing The deficits need not be total. Global aphasia is commonly seen in patients with large infarctions of the left cerebral hemisphere, typically involving the occlusion of the internal carotid or middle cerebral artery and resulting in a large, wedge-shaped infarction of the frontal, temporal, parietal, and deep portions of the middle cerebral artery territory.

Pure word deafness Patients with pure word deafness cannot comprehend spoken language, but they are not deaf. Their verbal output and reading comprehension are said to be intact. The condition can occur because of damage to the superior temporal gyrus bilaterally, but cases have been described with unilateral, left temporal lesions.

Can he hear? No Deaf

Yes Does he understand?

No

Fluent speech

Yes Yes Can he repeat?

No

Global aphasia

No Yes Wernickes aphasia

Proper use of words

Transcortical sensory aphasia No Can he repeat? No Yes Transcortical motor aphasia Brocas aphasia

Yes

Can he repeat? No Yes Can he name objects? Yes Conductive aphasia

No Nominal aphasia

Normal speech

Transcortical motor aphasias Transcortical motor aphasia involves a deficit in the initiation of speech, reduced phrase length, and abnormal grammar. Mutism may be present initially. Repetition may be relatively unimpaired, distinguishing these patients from those with Broca aphasia who cannot repeat fluently. Transcortical sensory aphasias In transcortical sensory aphasia, patients can produce fluent speech, but it is often empty and paraphasic.. In general, they act much like patients with Wernicke aphasia, except they can repeat. This type of aphasia is typically seen in advancing Alzheimer disease and other progressive dementias, but it is also seen occasionally in patients with stroke, typically those with bilateral lesions in the parieto-occipital cortex or a lesion in the left temporo-occipital cortex. Mixed transcortical aphasia Mixed transcortical aphasia, also called the syndrome of isolation of the speech area, involves ability to repeat but not to produce spontaneous speech or comprehend language. Patients may repeat in an echolalic fashion, and they may complete common phrases begun by the examiner. This syndrome resembles global aphasia, except for the preserved repetition. Anomic aphasia Patients with anomic aphasia present with fluent speech, intact or mostly intact repetition, intact auditory comprehension, reading, and writing, but an inability to name objects and body parts. Anomic aphasia may follow recovery from another type of aphasia. Pure alexia without agraphia In patients with this syndrome, the patient can write but cannot read his or her own written output. If the letters of a word are read aloud, the patient can often put them together so that the word can be deciphered. The patient often has verbal alexia which refers to an inability to read words. (word blindness). Patients with this syndrome do not lose the ability to see verbal stimuli, but visual information has lost access to the language area. Many patients have disturbed color naming as well as a mild degree of anomia.

Alexia with agraphia This disorder often overlaps with Wernickes aphasia. In htose cases the patients often have a paraphasic output, impaired naming and pure repetition as well as disturbed written comprehension (word blindness) more than auditory comprehension (word deafness). Diagnosis

Bedside and neuropsychologic testing Brain imaging Verbal interaction can typically identify gross aphasias.

Testing to identify specific deficits should include assessment of the following:

Spontaneous speech: Speech is assessed for fluency, number of words spoken, ability to initiate speech, presence of spontaneous errors, word-finding pauses, hesitations, and prosody. Naming: Patients are asked to name objects. Those who have difficulty naming often use circumlocutions (eg, what you use to tell time for clock). Repetition: Patients are asked to repeat grammatically complex phrases (eg, no ifs, ands, or buts). Comprehension: Patients are asked to point to objects named by the clinician, carry out one-step and multistep commands, and answer simple and complex yes-or-no questions. Reading and writing: Patients are asked to write spontaneously and to read aloud. Reading comprehension, spelling, and writing in response to dictation are assessed.

Brain imaging (eg, CT, MRI) is required to characterize the lesion (eg, infarct, hemorrhage, mass). In Ayurvedic perspective

By understanding the above details, this conditions can be co-related to disorder of VAK ioned in Ayurvedic classics. Even though the word VAK denotes verbal symbols (which is being influenced by Vakbuddhi) is mainly taken into consideration.The disease VAKSANGA mentioned in Nanatmaja vatavyadhi by Charaka and Vagabhata bears some similarity with Aphasia.Vaksanga in a limited sense conveys only a disorder of expression.But the expression depends on comprehension of verbal and written symbols.In Aphasia speech,comprehension,naming ,repetition or all may be affected.Upto some extent APHASIA resembles the features of Buddhi Bramsha.We should not forget that speech is a higher mental (cortical) function.In may patients of dementia,speech may be affected.There may be poverty of speech in some, and in others vocabulary may be affected .But paraphasia hardly occurs.Naming the objects will be accurate.Aphasia can co-exist with dementia if the language 7

area is involved.But the author has restricted Aphasia to VAKSANGA,eventhough ir would not cover all the cardinal features of the disease because comparison with Buddhi Bramsha may produce an unwanted thought or confusion about this condition to some psychiatric problem.It should be remembered that the features of higher mental dya-function (Buddhi Bramsham) will also be associated with VAKSANGAM.

VAKSANGA AND PAKSHAGHATA Vaksanga and pakshaghata are mentioned as separate diseases in Aseethi vatavikaras by charaka and vaghbhata.While describing Pakshaghata,vaksanga is mentioned as a feature only by charka.Others did not mention,disorder of speech with paralysis.Speech disorder is mentioned as a feature along with Arditham.(cha/ch:28/vag.v.v.nid).Arditha can be interpreted as facial paralysis alone or the facial paralysis associated with hemiplegia.(As such speech will be affected in Facial palasy).There may be slurring of speech as facial muscles become weak.Language will be affected in hemiplegia if dominant hemisphere is affected.The arditha mentioned by Charaka and Vagbhata is characterized by hemiplegia with Aphasia.As many authors talks ardita as facial palsy alone the author has restricted Aphasia.

PRANA & UDANA IN SPEECH The Pranavayu is located in Shiras and it is attributed to functions of cognition ,thought process and understanding.It is vital among the five and the normalcy of other vayus depends on it .Udana,the counter part of prana is mainly dominant in Uras,Nasika and Nabi.It is attributed to endeavor ,strength,wisdom,courage ,memoy and VAKPRAVRUTHI (As.Sam.Sut20). Susrutha stresses udana, for the act of articulation and singing (Su.Ni I) from this descrition we can understand that normal functioning of vayu (prana and udana) are essential for speech.We can say that PRANA helps in maintaining Indriya Buddhi, and comprehensive part of the language and UDANA is responsible for articulation (ie.expression of thoughts in to sentences).

MODE OF EXISTENCE AND VITIATION 8

The normalcy of vayu is inevitable for optimum health and vitality. The normalcy of other elements in the body depends on the normalcy of vayu.Anulomana or Avyahathagati(M.N.Vathavyadhi) of vayu denotes its normalcy .In this state vayu will be unobstructed ,so its moves normally uninfluenced by other doshas.The vitiation of vayu takes place either by Dhathukshaya or Avarana.(M.N-V.V) Dhatukshaya denotes chronicity and Avarana denotes acute phase.Avarana is the state in which Anuloamana is affected .In this state the movement or the existence of vayu will be masked or encapsulated and gives an entirely different clinical picture.Chatkrapani explains that Avarana can occur in three ways .ie,obstruction (sanga) amalgamation (samsarga) and vimargagamana (deviation).The path of vayu can be obstructed in the srotas by another dosha or it takes a different path or it can mingle with other doshas.That is why in many Avarana vyadhis, the cardinal signs of the illness are not clearly seen.The clear features manifest after the active phase is over.Moreover each from of vayu can be mutually amalgamated or masked(Anyonyavarana) and produce pathology.

VAKSANGA:AN OUT PUT OF AVARANA

Vaksanga is mentioned as a feature of Avarana vyadhi .The details and thereferences are narrated below.
Aurutha Dosha Samana Udana Auarana Dosha Prana Kapha Signs produced Mookatwa,Gadgadatwa,. Vaivarnya,Vakgraha Swaragraha (cha.chi 28)

Vyana

Kapha

Vakgraha,A.H-47,48 (Vatharaktanidana)

SAMPRAPTHI GHATAKAS Dosha Dushyam -Prana,Udana and Vyanavayu -Snayu,Sira,Sandhi

Rogamargam -Madhyamam Doshagathi Rogadhishtanam -Tiryak -Siras,Vak Indriyam,Ardhakayam.

POORVA ROOPAM In vatha vyadhi the prodromal signs will be unclear, and masked.

RUPAM The normal functions of vayu including Cheshta and VAKPRAVRUTHI will be affected .No specific description about Vaksanga is mentioned as we get descriptions about other vatha vyashis .But in Aphasia(Vaksanga) there will be loss of ability to formulate to express or to understand spoken words.There may be difficulty in reading (dyslexia) writing (dysgraphia) and failure to understand gestures,signs and music.

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DIFFERENTIAL DIAGNOSIS Aphasia (vaksanga) should be differentiated from other diseases in which speech is involved. They are: 1.Jihwa sthambam 2.Swara bheda 3Gadgadatwa 4.Mookatwa 5.Minminatwa 6.Vakgraha in Badhirya 7.Vakgraha in Apasmara 8.Vakgraha in Smriti Bhramsa.

JIHWA STHAMBAM Is the disease mentioned under vatavyadhi which is characterized by spasticity or rigidity of the tongue associated with difficulty in articulation (dysarthria) and sysphonia and dysphagia (of solids and liquids) (Vagbhata/15/31,M.N Vathavyadhi)

From this description we can understand that, it is a disease in which,basically the movement of tongue is affected,(Jihwa Sthambham) and there is difficulty in swallowing.

Tongue is concerned with the articulation of speech (peripheral mechanism).It is not directly related to the language.Hypoglossal nerve,the 12th cranial nerve,which is primarily a

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motor nerve originates in medulla passes through hypoglossal canal and supplies the muscles of the tongue .It helps in movement of tongue during speech and swallowing.Let us analyse some of the disorders of the tongue which resemble Jijwasthambha. a)Bulbar Palsy:

Which results from the paralysis of the muscles which are supplied by the motor nuclei (the medulla or bulb).It clinically manifests as the triad of symptoms dysphagia,dysarthria and nasal regurgitation .This syndrome may result from various causes.Acute bulbar palsy may be seen in brainstem infracts involving the medulla,but more commonly in acute infective poly neuropathy (Guillain-Barre syndrome) and myasthenia gravis during a crisis.Rarely it is seen in bulbar poliomyelitis,Ev 70 disease,and diptheric neuropathy.The chronic form of progressive bulbar palsy is usuallyone of the manifestations of motor neuron disease. b)Progessive bulbar palsy: A progressive disorder involving the motor nuclei of the medulla resulting in paralysis of tongue,palate and pharynx.It usually starts in 6th decade of life and may be the first involvement of MND or may follow the involvement of spinal cord in ALS.

Features: This disease frewuently starts in hypoglossal nuclei and manifests as bilateral wasting and paralytical tongue with fibrillations.With the progression of the disease the patient is unable to protrude the tongue and it eventually gets shriveled and lies functionless in the floor of the mouth.Some patients develop dysarthira due to involvement of soft palate, larynx,and tounge.The speech becomes thick with a nasal quality and pronounciation of linguals ,labinals and palatal consonants become difficult.Nasal regurgitation is common and aspiration pneumonia may occur.The patients becomes aphonic with total inability to swallow.

C)Pseudobulbar palsy:

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The symptoms of pseudobulbar palsy are similar to bulbar palsy.The clinical differentiation between them is easy.The tongue is not wasted and movements are poor.The cough and gag-reflex are brisk and the patients give a history of choking as swallowing liquids early in the course of the disease .The disease is due to involvement of supra nuclear

pathways to bulbar nuclei(ie: Bilateral corticobulbar tract lesions).

The commonest cause is multiple lacunar infarcts involving the centrum semi-ovale and internal capsules.It is also seen in MND brainstem glimas and advanced stages of multiple sclerosis,rarely it may be transiently seen in stem encephalitis and central pontine myelinolysis.

Features: There is spastic ,slurred dysarthria and dysphagia with choking on swallowing liquids and food as the palatal and pharyngeal reflexes are preserved .The tongue is not wasted,movements poor, become immobile in the floor in advanced stages.The masticatory and facial muscles are spastic with exaggerated jaw jerk and brisk facial reflexes. Although there is a lack of facial expression,the patient losses emotional control with increasing frequency and bursts into spontaneous bouts of crying and laughing.

So all the 3 diseases mentioned ablve have the feature of Jihwasthambam.So Jihwa sthamba can be anyone of the diseases mentioned earlier, in which the tongue is being affected, and not the language area in the cortex.Hence it is the disease dysarthria,not Aphasia.

II.Swara bhedam

This condition has been mentioned as a separate entity and one among the cardinal features pf Rajayakshma.Susrutha says that two blood vessles are concerned with Bhasha and Ghosha (language and for phonation). In this condition, the swara vaha-srothas are being 13

affected.Due to excess talking poison,injury etc vathadi dosha will increase and affect the swara vaha srothas.Susrutha says,injury to Neela and Manya vessels will produce hoarseness of voice ,dumbness and anorexia.It is classified as Doshaja,Kshayaja, and Medoja.

Swarabedha is a disorder of phonation.Phonation is the production of sound resulting from the passage of air through larynx.The strength ,tone ,and pitch of the voice depends on the structure and neuro muscular control of the laryngeal and respiratory system.With normal articulation various types of phonemes are pronounced not only with the action of articulatory ,muscles but also due to the alteration in the airstream.The phonemes are thus given a correct from by movements of lips,tongue and palate and any abnormality of the system produces dysarthria,hyper-hyponasility or change in intonation.

So Swarabedha is only dysphonia or hoarseness of voice due to any lesion interfering with the laryngeal mechanism which governs voice production.Ther are a variety of nonneurologicl causes,the commonest one is a sore throat with inflammation of larynx.Hysteria is also a wellknown cause of dysphonia,commonly seen in females.They can cough normally and sudden recovery may take place.Patients with tracheostomy are aphonic as the tube in the trachea prevents the expired air from reaching the larynx.Tumour and local lesions in the larynx also cause dysphonia, and the voice tends to become deep and husky in the patients with hypothyroidism.

The neuromuscular causes of dysphonia The mechanism of phonation is dependent on the muscles of the vocal cord supplied by Vagus.The adductors and the tensors contract on phonation and abductors on inspiration. In some cases of myasthenia gravis the fatigueness of laryngeal muscles causes dysphonia.Disorders of LMN (polio,MND,SM,poly neuritis and CN damage) can produce dysphonia.

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A untilateral recurrent laryngeal nerve lesion causes paralysis of vocal cord.Total bilateral paralysis of the vocal cord causes dysphonia, so that the patients can only whisper.The LMN disorders invoving the nuclei of the Vagus in medualla can produce dysphonia.Dysphonia is a feature of bulbar and pseudo bulbar palsy.Dysphonia can occur in extra pyramidal lesions. Susruthas view:

Susrutha says about a congential dysphonia called KAKASWARA (S.Uth 53/M.N.),for which the cause may be varied.He says another condition called SWARAGNA (S.U 16/61) which is characterized by dysphonia,hoarseness of voice and paralysis of throat.

Charakas view: Swarabheda is mentioned as sonithadushti vikara (ch.su.24) Charaka describes the signs of prognosis of death in VARNASWAREEYAM INDRIYAM in relation to SWARA/voice .He syas that the normal human voice resembles the voice of swan,crane,wheel,drums,sparrow ,crow and dove.The voice of patients resembles goat,which is feeble,inaudible

indistinct,choked,hoarse are the signs of death.So Swarabhedha is only a peripheral mechanism ,and not a central one.

III.Gadgadatwam This condition is classified by Acharya Madhava in Vatha vyadhi prakarana.This can be co-related with stammering which is characterised by stoppages and disruption in the fluency that interrupt, the flow of speec;stoppages may take the form of repetition of sounds and syllables of words or may be due to the prolongation of sounds and can involve silent blocking of air during speech.

Persons who stammer have diiculty in controlling their speech flow and demonstrate highly individual variability in fluency,which can be related to mixed situation fatigue and various other individual factors.They are aware of the situation,embarrassed by it and find speaking 15

takes extra physical and mental effort.This effort to speak will frequently result in concomitant physical movements and facial grimaces.Some authors use stuttering as synonym.There are quarter a million stammerers in the country and 15 million stammerers through out the world.The prevalence is more in children and in boys.Stammering has got multifactorial etiology which includes constitutional predisposition,incomplete cerebal dominance and a group of psychological factors.(M.N.V.V). IV.Mookatwa: This is mentioned by Madhava.Susrutha,says injury to Nila and MAnya marmas produce mukatwa.This is called Muteness or dumbness,where there is absense of power to speak completely.This can be due to mental deficiency or due to deafness in childhood.In severe motor Aphasia this can be seen.A kinetic mutism is seen in lesions of

diencephalons(M.N.V.V)(Su.Nis-1)

V.Minminatwa: This is also told by Acharya Madhava.As described earlier the phonemes get correct form by movements of lips,tongue and palate.Any abnormality of this system produces change in intonation causing hypo or hyper nasality.This nasality is calledminminatwa(M.N-Vstsvyadhi).

Speech defects in other diseases.

VI.Bahyayama:This condition is characterised by bending of the patient dorsally like a bow, leading to fixed eyes,lockjaw,vomiting,stiffness, and Vakgraha.This resembles a convulsive neurological disorder and not Aphasia.(c.ch.28/45)

VII.Hanusramsam:This resembles TRISMUS, and there may be dysarthira and dysphonia,due to dislocated jaw.(A.H.N-15).

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VIII.Badhirya:The development of normal speech lagely depends on the ability to hear.Deafness,if congential or acquired in infancy will delay or prevent normal speech development .In any speech disorder it is essential to assertain whether or not there is any hearing deficit.

IX.Balagraha:We get some references about speech defects along with disorders of Graha.Grahas are supposed to be super human agencies that may invade an unhygienic person with or without any wound or who transgress the limits of proper behaviour inorder to enjoy themselves or even to extract veneration.(S.U.60/5).Speech defect is mentioned as one of the features of SkandaGraha which is characterised by hemiplegia ,facial palsy.and speech defects.There may be spasticity with axcess salivation.This condition resembles infantile paralysis with Aphasia.Vaksanga is also mentioned in Meshagraha (A.H-U 3/6-8/12-14).

X.Swaragraha in Apasmara:Incoherent speech is mentioned as a eature of Vathika Apasmara.(Ch.Ni8-8).In petitmal attacks the normal flow of speech may be affected.The child may loose conversation during the transient perios of loss of awareness.In partial may have an epileptic aura with an epileptogenic lesion in any part of the speech area,the attack itself may consists of transcient Apasia or there may be an Aphasic aura preceding grandmal seizure.Aphasia or hemiplegia discovered for the first time after an epileptic attack may be the result of an epileptogenic lesion,but such sighs occurring postically doesnot have the same lacalizing significance as aura,as they may be due to an inhibitory effect Paralysis).Recovery From this usually take place within few days. XI.Yoshapasmara:This condition is mentioned in Bhaishajyaratanavali. this can be co-related to Hysteria which is the condition charactersied by psycho or somatic symptoms without any organic basis.This doesnot have any anatomical significance.This can produce psychological,visceral,sensory and motar symptoms which includes of fit(Todds

hemiplegia/Aphasia.

XII.SMRITHI BHRAMSA

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Is the deterioration of memeoryie,the recording,retending and recollecting the events.In any patients with dementia whatever the cause-speech may be affected.Usually there is poverty of speech.In some vocabulary becones limited earlyin others it may be preserved until quite late in the illness.There is difficulty in relating series but unlike aphasic patients a

paraphasia,neologism and portmanteaux words do not occur.Names for objects are often completely accurate although they have a close association.Interjections are rarely used although speech may be exclainmatory.Speech is simplified consisting of

statements,descriptions or requests,often of no importance ,and in severe cases ther is failure to communicate.

It has been found that the ratio between the number of verbs and adjectives used varies as in neurotics, and there is also variation in length of sentences and punctions.The frequency of the pronoun I is also of interest:used in 5% of words over telephone by a normal person,it is used in 0.01% in technical speech.Both in dementia and aphasia,sentences are started and not finished (Aposiopesis) and there is filling with unnecessary additions (paralogisms) preservation is extremely common.Words are used normally but then reiterated and this also occurs in writing(echographia).Aphasia may co-exist with dementia if the language area is involved.In picks and Alzheimers disease speech is slow and ther may be interpolation of the s and t sounds and the voice also tends to become higher pitched.

A demented patient has difficulty in understanding quick or noisy speech.Gesture,mine may be impaired,possibly in part due to slowness of movements(akinesia).The term alogia has been used for impoverishment of speech in dementia.This differs from the purely communicative defects of aphasia,which is due to a local lession of the specific area of brain concerned to PRAJNA and Apasmara is a disease in which SMRITI is affected along with there may be SWARA/VAK VAIGUNYA also.Smrithi Brashsha is mentioned as a lakshana in Mada and other graharogas.

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