1

NEUROGENIC STUTTERING - Diagnosis and Treatment

NEUROGENIC STUTTERING Introduction:

Stuttering is most often developmental phenomenon that is one that appears as a child learns to produce language. Stuttering can be mainly differentiated into two that is acquired stuttering and developmental stuttering. Acquired stuttering is relatively uncommon phenomenon having sudden onset in adulthood.

According to VanRiper (1971) there are three categories of acquired adult onset of dysfluency. 1. The dysfluency may be a form of occult stuttering (sudden appearance of stuttering). 2. Psychogenic stuttering (Sudden onset, and is temporarily linked to some of psychological trauma). 3. Neurogenic stuttering that linked to demonstrable neurological insult/neurological damage.

Neurogenic stuttering is a type of fluency disorder in which a person has difficulty in producing speech in a normal, smooth fashion. Individuals with fluency disorders may have speech that

2 sounds fragmented or halting, with frequent interruptions and difficulty producing words without effort or struggle. Neurogenic stuttering typically appears following some sort of injury or disease to the central nervous system i.e. the brain and spinal cord, including cortex, subcortex, cerebellar, and even the neural pathway regions. It may be transient or persistent. The lesion may occur in conjunction with bilateral/unilateral brain damage, focal or diffuse lesions (left or right hemispheres), cortical or semi cortical damage. In the majority of cases, the injury or disease that caused the stuttering can be identified. In a small number of cases, however, the individual may only show evidence of some form of speech disruption without any clear evidence of neurological damage. Moreover, neurogenic stuttering in patients may be an early diagnostic sign of a neurological problem.

Definitions:
Neurogenic stuttering is a type of fluency disorder in which a person has difficulty in producing speech in a normal, smooth fashion resulted from inability to coordinate all of the muscles involved in producing speech. (Helm & Butcher 80)

Canter (1971) defines neurogenic stuttering as a stutter like disruption subsequent to nervous system damage. This does not seem to be associated with any particular lesion site. It may occur in conjunction with bilateral or unilateral damage with focal or diffuse lesions with cortical/sub cortical damage to the CNS. Helm Estabrooks (1999) suggested a definition and included a new term stuttering associated with neurological disorder (SAAND) is an acquired or required disorder of fluency characterized by notable involuntary repetitions or prolongations of speech that are not the result of language formulation or psychiatric problem.

3 Disorders of rhythm of speech in which the individual knows precisely what he wishes to say about that time is unable to say it because of an involuntary repetitions, prolongations or cessation of a sound (manual of international statistical classification of diseases, injuries and causes of death (WHO) )

Who is at risk for neurogenic stuttering? Generally individuals experiencing neurogenic stuttering have had a history of normal speech production prior to the injury or disease. In a few cases, neurogenic stuttering may occur in individuals who experienced developmental stuttering in childhood but had apparently recovered. Neurogenic stuttering can occur at any age; however, it appears more often in adulthood, and the highest incidence is in the geriatric population. This profile is quite different from developmental stuttering which is not typically seen as a result of brain damage and which most commonly appears in early childhood in children between 2 and 5 years of age.

Etiological factors:
Neurogenic stuttering can have multiple etiologies Market etal (1990) conducted a survey and reported an association with TBI (traumatic brain injury) 88 % stroke in 37% drugs in 6% and neurosurgery in 4%. Among these TBI is the most common cause of neurogenic stuttering some of the etiological factors are summarized here 1. Stroke 2. Head trauma 3. Progressive diseases 4. Parkinsons diseases 5. Supranuclear palsy 6. Brain tumour 7. Alzheimers disease 8. Dialysis dementia 9. Drug usage

4 10. Cerebrovascular accident (stroke), with or without aphasia 11. Ischemic attacks (temporary obstruction of blood flow in the Brain) 12. Other diseases, such as meningitis, Guillain-Barr Syndrome, and AIDS

Catherine Theys, Astrid van Wieringen, Luc F. De Nil ( 2 0 0 8 ) o f 5 8 D utch -s pea ki n g follo w i n g rep o rte d ca use by of that p atie nts with

in

a sur ve y

ne ur o ge n i c neur o l o g i cal

st utteri n g inj uries p re vale nt f oll o w e d

vari o us str o k e in

w as th e i r b rai n

the

m o st

st u tteri n g tra u m ati c diseases,

patie n t s, inju r y, ca uses

n e ur o d e ge n erati ve

an d

ot h er

(surgery, encephalitis, epilepsy, medication, and an unspecified cause) .

The rare causes include dialysis dementia, seizure disorders, bilateral thalamotomy, and thalamic stimulation (Duffy, 2005). According to Helm Estabrooks (1983) brain anoxia during open heart surgery, adolescent seizures, surgery of thalamus can also cause SAAND.

In the majority of cases, the injury or disease that caused the stuttering can be identified. In a small number of cases, however, the individual may only show evidence of some form of speech disruption without any clear evidence of neurological damage.

Site of lesion:
Various types of neurogenic stuttering have been associated with temporary progressive and non progressive neurological conditions including damage to areas such as low and high brain stem, basal ganglia, cerebellum, left and right cortical hemispheres, white matter tracts, cerebellar motor

systems and has also been seem to occur after frontal, parietal and temporal lobe lesions with in the left hemispheres.

5 The survey study by Market et al (90) reported that 88% of neurogenic stuttering cases had left hemisphere damage (LHD), 9% had right hemisphere damage (RHD), 11% had subcortical lesions and 10% had bilateral lesions, and lesions were not identified in 32% of the cases.

This predominance of LHD in neurogenic stuttering is consistent with the finding of Yairi, Ginalautas and Aven who documented three times as many dysfluencies during spontaneous speech in a group with Brocas aphasia and LHD than in non brain injured control group and a group of people with RHD. The control group and RHD did not differ significantly in the frequencies of dysfluencies. It is not worthy; however that neurogenic stuttering has been reported in several cases with RH lesions with out evidence of aphasia or AOS (apraxia of speech).

The frontal, temporal, and parietal lobes may be involved in people with neurogenic stuttering. This is consistent with cortical stimulation studies that have elicited sound and word repetitions from all cortical areas except the occipital lobes. Ludlow etal (1986) reported that cortical speech regions such as Brocas area and primary motor area were involved in 80% of neurogenic stuttering patients, but that the frequency of such lesions was not significantly greater than that for non stuttering individuals. Single lesion seems less likely to produce lasting neurogenic stuttering than multifocal or diffuse lesions. Helm, Butcher and Benson found that multifocal lesions were most common in their group of 10 neurogenic stuttering patients. The role of basal ganglia in stuttering was first found through evidence from cases of acquired stuttering due to basal ganglia damage. As early as 1934, Suman suggested that is result of disturbed basal ganglia function. Basal ganglia stroke with subsequent stuttering and the association of neurogenic stuttering and the parkinsonian syndromes also implicate the basal ganglia control circuit damage in this disorder.

Kono I, Hirano T, Ueda Y, Nakajima K(1998)reported acquired stuttering resulting from a striatocapsular infarction. Brain CTs and MRI revealed a striatocapsular infarction extending from the putamen to the caudate nucleus in the left hemisphere. From the previous reports of stuttering derived from parkinsonism and lesions in the supplementary motor area and thalamus, the authors

6 proposed that the stuttering arose from a collapse of basal ganglia circuits that connect the cerebral cortex and basal ganglia, including the extrapyramidal tract system.

Anthony M Ciabarra, Mitchell S Elkind,James K Roberts, Randolph S Marshall (2000) studied three patients with subcortical lesions resulted in stuttering - pontine infarct and left basal ganglionic infarct. Subcortical mechanisms of speech control and timing may contribute to the pathophysiology of acquired stuttering.

Dysfluencies have also been associated with the lesions in the supplementary motor area (SMA), thalamus, midbrain and pons and in response to mechanical perturbation of the thalamus during surgery suggesting that interruption of a cortico thalamic feedback circuit might cause dysfluency. Not infrequently, neurogenic stuttering may develop in individuals with out identifiable lesions as in certain degenerative diseases, closed head injury and drug toxicity.

Characteristics:
Canter (1970) listed seven such characteristics as follows:

1. Repetition and prolongation are not restricted to initial syllables. - The neurogenic stutterers are likely to emit repetitions of the word final syllable as in Aluminium num-num repetitions and prolongations are not restricted to initial syllables. However Rosenberg etal (1978) found no stuttering on the word final sound syllable but found repetitions of the medial syllable of the words.

2. The phonemic loci of the dysfluencies differ from that of developmental stuttering.

3. There is no specific relationship between dysfluencies and the grammatical function of words. --A word which is content or functional whether it occurs in the initial or final position of a sentence is likely to be stuttered with equal probability by neurogenic stutterers.

7 4. Dysfluency is not necessarily on formulated speech, self- formulated speech may be easier than the automatic speech tasks.

5. There is no observable adaptation effect (i.e. improved fluency with repeated reading of a passage).

6. The speaker may be annoyed but not necessarily anxious about his stuttering.

7. There may be no secondary symptoms such as facial grimacing or fist clenching.

Other characteristics include; Absence of specific word or sound fears.

A greater consistency in the errors or error patterns.

Absence of delay or postponement in attempt to say.

Absence of situational or individual variability complaints

Do not show any change in the stuttering under certain fluency inducing situations like singing, shadowing or choral reading, imposed rhythm and certain conditions affecting auditory reception like masking, delayed auditory feedback etc.

Frequency of stuttering may not increase under anxiety provoking situations. Absence of spontaneous recovery Spontaneous recovery doesnt occur with neurogenic stutterers particularly that which is due to bilateral damage (Helm butcher and Benson, 1978) while that associated with unilateral lesion may recover.

Neuropsychological characteristics of SAAND:

8 Difficulty in drawing 3-D figure as a cube, both upon command and to copy. Difficulty in copying block design. Difficulty in reproducing and sustaining alternating, sequential hand positions Difficulty in singing melodies. Difficulty in reproducing rhythmic tapping patterns again

These characteristics are not unique to all SAAND patients, that may be depending upon the extend and site of damage to the various system.

Nancy A. Helm, Russell B. Butler and D. Frank Benson (1978) examined the speech characteristics, neuropsychologic deficits of 10 patients with acquired stuttering. The speech characteristics which differentiate acquired stuttering include: absence of adaptation effect; occurrence of stuttering on any syllable with in a word, and stuttering on both grammatical and substantive words. The neurobehavioral deficits correlated with acquired stuttering include: impaired ability to draw or copy three-dimensional figures or reproduce block designs, and difficulty in reproducing and sustaining sequential motor tasks, melodies, and rhythmic tapping patterns.

Types of neurogenic stuttering:

Canter (1971) has identified three general types of dysarthric, dyspraxic and dysnomic and provides several subtypes of dysarthic stuttering.

Dysarthric stuttering:
Dysarthria refers to a group of motor speech disorders resulting from damage to the central or peripheral nervous system (Darley, Aronson and Brown 1975). A number of conditions such as Parkinsons disease, stroke, multiple sclerosis, and myasthenia gravis can affect the nervous system and cause a dysarthria. Dysarthria people sound different from each other depending on what portions of their nervous system have been affected. Dysarthric stuttering appears to emerge from the same lack of muscle control as the primary dysarthric disorder, which is seen, for example, in individuals who have Parkinsons disease or have a cerebellar lesion.

9 Canter has apparently identified several subtypes of neurogenic dysarthric stutterers. The dysarthria associated with Parkinsons disease is called hypokinetic dysarthria. According to Canter, the hypokinetic dysarthric speech may be characterized by one or three stuttering patterns.

- Frequent prolongations with a consequent disruption of flow of speech, which he equates with Articulatory freezing. - Rapid syllable, word and phrase repetition, which he further describes as being effortless and - Long silent blocks associated with a transient inability to initiate any kind of motor activity. Damage to the cerebellum can result in what is usually called an ataxic dysarthria, and the ataxic speaker may also stutter, (Canter) calls that stuttering perhaps the most severe and dramatic of the variables of dysarthric stuttering. Symptomatic of these condition are violent prolongations. He also mentions accelerating repetitions that may end in silent or audible prolongations due to proxysmal spasm of vocal tract musculature triggered muscle tension.

Apraxic stuttering:
Apraxia of speech is usually described as deficit of motor programming. Apraxic stuttering may arise from a basic problem in motor planning. Silent blocks and repetitions occur as the speaker struggles to sequence the appropriate speech movements. The sound repetitions and prolongations are reflections of the speakers attempt to correct articulation or movement errors. Multiple repetitions of the correct initial sound or syllable suggests that the speaker was not trying to self correct. These repetitions, like prolongations of a correct sound, may result from their impairment in voluntarily triggering the motor speech mechanism and may properly be called as apraxic neurogenic stuttering (Canter, 1971).

10 Trost (1971) said the prolongations and repetition behaviors in apraxic adults showed noteworthy similarities with those behaviors observed in non organic stutterers. Schuell, Jenkins and Jimenex Pabon (1964) observed that every speaker with apraxia (they called it sensorimotor involvement) passes through a period of stuttering during recovery and some authors are so convinced of the co-occurrence of speech apraxia and stuttering that they argue stuttering is an apraxia (Shtremel,1963).

Dysnomic stuttering:

Dysnomia refers to difficulty in recalling words. It results typically from damage to the left dominant hemisphere and is part of the more general syndrome of aphasia in which reading, writing, and understanding and even gesturing are impaired. Dysnomic stuttering sometimes accompanies aphasia. Stuttering symptoms occur as an individual searches for the word he is having trouble retrieving. Canter (1971) offers this description of dysnomic stuttering sometimes these words lapses are marked by pauses and articulatory groupings. In other cases, the patient repeats the preceding word or phrase or fills in the impending silence with prosodic grunts or interjections.

Numerous other authors have described stuttering among the symptoms of aphasia (Schiller 1947, Arend, Hendzel and Weiss 1962, Former 1975). Arend & Handzu describe one of their cases speech deficit as stuttering. It does not diminish their observation that stuttering can coexist with aphasia following dominant (usually left) hemisphere damage. Farmer, tried to measure the stuttering associated with aphasia, she studied Stuttering of repetitions in the speech of a group of non aphasia brain damaged adults and in three patients with wernickes aphasia, two with conduction aphasia, four with brocas aphasia and three with anomic aphasia. The wernickes aphasic people had the most disfluencies, the conductions were next, the brocas were third and the anomic were fourth. Statistically however the only significant differences were between wernickes and brocas aphasics and between wernickes and anomic aphasics. Farmer concluded that lesions to the left hemisphere resulting in inefficient language performance may reflect temporal disorganization in the form of stuttering repetitions.

11 Stuttering is not the manifestation of the language deficit, although it may certainly accompany one or language deficit is a necessary prerequisite to neurogenic stuttering. Stuttering also appears in the absence of any language deficits. Helm and Canter (1980) make his point best. They say, Little support was found to either the notion that acquired stuttering is invariably an inherent part of some aphasic syndrome.

Classification based on Etiologies:

1. Stuttering associated with stroke: Stuttering has been described as a symptom of stroke in both the dominant and nondominant hemispheres, and in all lobes except the occipital. . Catherine Theys, Astrid van Wieringen, Luc F. De Nil (2008) have reported neurogenic stuttering within the first week after the stroke, for 20 of the 29 stroke patients. Stroke patients often repeat syllables and words, while prolongations and blocks are not that frequently reported. S a h i n t w o patie n ts str o k e wit h w h o et al. ( 2 0 0 5 ) disc usse d an o n

stu tte ri n g b ot h

follo w i n g o nl y of

isc he m i c initial

st uttere d an d o n e

so u n ds

an d

s ylla bles

them

s h o w e d se c o n d a r y st utteri n g c h a ra c teristi cs.

D y s f l ue n cies p h o n e m es, re petitio n, p ara gra p hs, a da ptatio n carr yi n g f or m a

m a y

be

hear d

o n or

initial an d fu n c tio n se q u e n c es,

m e d ial w o r ds, ro t e

substa nti v e auto m atize d si n g i n g effe ct. tu n e , a n d

tap p e d

speec h. N o in

Re d u ce d

perf o r m a n ce b l o c k

tap p i n g sti c k

rh yt h m s,

desi g ns m e m o r y,

m o d el,

d esi g ns

fro m

se q ue ntial ha n d

p ositi o n s.

Arthur C. Grant; Valerie Biousse; Albert A. Cook; Nancy J. Newman, (1999) studied four patients who developed stuttering speech in association with an acute ischemic stroke (with infarctions in left middle cerebral artery, left temporal lobe, right parietal Lt handed, left

12 occipital) and concluded that the clinical presentation of stroke-associated stuttering is variable, as are the locations of the implicated infarctions.

Jokel et al. (2007) have reported that the nature of disfluencies in stroke patients may differ depending on the complexity of the speech sample, with more complex language material triggering more word repetitions and other disfluencies, characteristic of more language-based disfluencies, while stuttering-like disfluencies are observed more readily in less complex speech tasks.

B o r sel, a 38

V a n

Der

M a d e,

Sa nte ns( 2 0 0 3 ) ne ur o ge n ic lesio n speec h st u t t e r i n g of an d

re p o rted st utte ri n g the le ft

year

o l d a n N o

case

wi th

f oll o w i n g thala m u s. p r o b le m s.

isc h aem i c histor y o f of

lan g u a g e in

Fre q ue n c y speec h

in c rease d

p r o p ositio n al c o n f r o ntatio n F re q u e n c y

(co n v ersatio n, w o r d in

m o n o l o g u e , retri e v a l ) .

na m i n g, decreased

no n - pr o p ositi o n al repetitio n, rea di n g

speec h(a ut o m a tic alo u d )

speec h,

Depending up on the nature of the brain damage, the patient with neurogenic stuttering may be more or less likely to have aphasia or other disruptions of higher cortical functions. It is not always true that neurogenic stuttering has to be associated or co-exists with aphasia. However stuttering or stuttering like behaviors have been described in association with amnestic aphasia (Arend, Handzel, Weiss 1962), Brocas aphasia (Trost 1977), Apraxia of speech (Canter 1971), Conduction aphasia (Farmer 1975) etc Neurogenic stuttering without aphasia is seen in cases of circumscribed subcortical infarction in the right hemisphere (in right-handed individuals) and striatocapsular infarction (Soroker N, BarIsrael Y, Schechter I, Solzi P, 1990; Kono I, Hirano T, Ueda Y, Nakajima K, 1998; Fleet WS, Heilman KM ,1985).

13 Farmer (1975), Ackermann (1994), Mazzucchi et al.(1981) noticed stuttering with aphasia in their patient with a cortical lesion in the left hemisphere. A lesion in the left hemisphere is likely to impair the regions implicated in the production of speech and language, and thus it is not surprising that Farmer came to the conclusion that: ...lesions to the left hemisphere resulting in inefficient language performance may reflect temporal disorganisation in the form of stuttering repetitions . Anthony M Ciabarra, Mitchell S Elkind, James K Roberts, Randolph S Marshall (2000)reported acquired stuttering in a patient with a left subcortical infarct and a mild aphasia. In case of patients with severe aphasia the stuttering component may be of no concern. But for patients with milder aphasia the stuttering may be frustrating as it inhibits verbal expression as a result of more concern. 2. Stuttering associated with head trauma:

The most common variety of head injury associated with neurogenic stuttering is CHI (closed head injury) resulting from motor vehicle accidents. In CHI the brain may suffer focal damage due to the compression of the skull, skull fractures with depressed bone fragments or traumatic hemorrhages. In addition CHI may cause diffuse, microscopic damage to the white matter pathways throughout the brain. CHI patients may develop prolonged coma, seizures or dementia. These reasons may lead to the memory problems, personality disturbances and dramatic changes in cognitive style with loss in ability to think abstractly.

M a r k et, ( 1 9 9 0 ) o n

M o nta g ue, a sur ve y re p orte d lesio ns of

B u f fal o, 81 th a t the

an d

Dr u m m o n d w ith ac q uire d and ca use w ere of

patie nts hea d m ost

st utteri n g isc he m i c o f the

tra u m a fre q ue nt sites

were

st utte r i n g left

(7 5 % )

an d

lesio n F or the

o fte n the

lateralize d the

(38 % ).

m aj orit y

patie nts

foll o w in g were

differential

speech

c haracteristics p r ol o n gatio ns an d

prese nt: w ere n ot

re p et iti o n s, restr i c t e d to

blo c k s

14 initial s m all syllab les (8 0 % ); st u t t e r i n g as o c c u rre d well as o n on gram m a tical (79 % ); not an xi o u s w o r ds the

su bsta nti ves a n n o y e d speec h ( 6 8 % ). b u t

spea ker and

see m e d sec o n d ar y prese n t was

(6 7 % ); were

c h aracteristics A bse n ce 4 6 % of an

rarel y

ada ptatio n

effe ct

re p orte d f or

o f t h e p atie nts.

3. Stuttering associated with extrapyramidal lesions:

This form is thought to be the result of a faulty motor execution that gives rise to slurred speech and sound prolongation, repetition and blocks associated with articulatory freezing. SAAND is most commonly seen in Parkinsons disease where stuttering was the first symptom being reported (including Wilsons disease) Canter (1971). K o l l e r si x patie nts m ostl y wit h (1 9 8 3 ) descri be d disease speec h

ex t ra p y r a m i d al sel f - f o r m u l at e d

st uttere d a n d

d uri n g

prese nte d

w i t h a p o siti v e a d a ptati o n e f f e ct.

4. Stuttering associated with drug usage:

Stuttering can be caused due to intake of various pharmacological agents. Quader(1977)describes that amyetryptyline a tricyclic, antidepressant results in stuttered speech and also theophyline, a broncho dialator for asthma that developed severe stuttering.

The literature on stuttering as a side effect of pharmacological agents were identified by means of a computer assisted search. A diversity of drugs has been reported to induce stuttering in susceptible persons, including some agents that improve the speech of some stutterers. In all instances normal speech returned shortly after the offending was discontinued. Multiple interacting neurotransmitter systems seems to be involved (Brody, John Paul ; 1998)

McClean, M. D., & McLean, A., Jr. (1985) reported a case of stuttering acquired in association with phenytoin use for post-head-injury seizures. The extent and nature of dysfluencies and the

15 motor performance of speech and nonspeech muscle systems were evaluated over an extended period during which changes in anticonvulsant medication were made. Reductions in dysfluency levels and improved motor performance were observed following a medication change from phenytoin to carbamazepine. Performance on tests assessing nonmotor functions, such as memory and attention, was equivalent before and after the medication change. The apparent association between dysfluency levels, motor performance deficits, and phenytoin suggest that in the present case stuttering resulted in part from a general impairment in motor control.

5. SAAND associated with dementia:

In patients undergoing dialysis for kidney diseases, stuttering appeared with early signs of dementia and confusion. Later stuttering is replaced by mutism.

6. SAAND associated with tumors and penetrating missile wounds:

Stuttering has been reported after a penetrating missile wounds (Schiller 1947). There have also been reports of remission of stuttering after removal of tumor (Luchisinger, 1965).

Catherine Theys, Astrid van Wieringen, Luc F. De Nil ( 2 0 0 8 ) o f 5 8 D utch -s pea ki n g rep o rte d p atie nts with st utteri n g

in

a sur ve y

ne ur o ge n i c

t h a t t he lesions were left lateralized in more than half

of the stroke patients group and other-(surgery, encephalitis, epilepsy, medication, and an unspecified cause) group, while they were mostly bilateral in the neurodegenerative group and frequently either bilateral or left lateralized in the trauma group. These results indicate that left hemisphere involvement is frequently present in neurogenic stuttering. For stroke patients in general, a left cerebral hemisphere injury is also reported more frequently than a right cerebral hemisphere injury.

The speech disfluencies reported for the patients across all four etiological groups in the survey consisted predominantly of repetitions of sounds and syllables. While word repetitions were reported in almost 90% of the patients with a neurodegenerative disease, this type of speech disfluency was mostly absent in the other etiology groups. Speech blocks seemed

16 characteristic for the stroke as well as for the trauma patients but not for the other two etiology groups. repetitions of sounds and syllables were equally likely to be observed for the stroke patients as were articulatory blocks. Word repetitions and prolongations, on the other hand, occurred to a lesser extent in the stroke group.

In addition, reports that patients with a neurodegenerative disease often freeze, block or prolong sounds during their speech do not appear to be consistent with the findings in the survey, repetitions were the predominantly dysfluency type in these patients. Finally, the frequent repetitions, prolongations and blocks of the head injury patients in the survey were comparable to the disfluency types of the TBI patients reported in the literature.

Stuttering was not restricted to initial syllables in more than half of the patients for whom this information was reported. This result is similar to that reported in the literature, with 61% reported by Stewart and Rowley (1996), 80% by Market et al. (1990), and 75% by Ringo and Dietrich (1995). For the four etiology groups, medial disfluencies were more frequently reported than disfluencies on final word segments which occurred rather infrequently.

Some of the differential characteristics for stroke-induced stuttering, trauma-induced stuttering, and stuttering following extrapyramidal disease seen are: stuttering always present on initial phonemes in all the etiology groups, possible presence of aphasia in stroke and TBI patients, and low frequency of adaptation in TBI patients.

The results from the survey showed that aphasic, dysarthric and specific word finding problems were the most likely concomitant communication problems.

Differential diagnosis:
Differential diagnosis between neurogenic stuttering and developmental stuttering

Characteristics Neurological lesion Onset of stuttering

Neurogenic stuttering Present Sudden

Developmental Absent Gradual

stuttering

17 Situational, individual Not observed Present variability in stuttering Position of sound syllable Not specific on which stuttering occurs Loci of stuttering Adaptation effect Avoidance Reduced rate of speech Stuttering under Not specific Absent Absent No change More on initial position and stressed words More on certain words Present Present Reduced stuttering Decreases

fluency No change

inducing conditions Anxiety situations Spontaneous recovery Less likely Observed provoking No change Increased stuttering

H e l m - E sta b r o o ks f oll o w i n g b et w e e n si x neurogenic occ ur as be

(1 9 9 9 )

has

sug g este d stuttering :

the (1)

dif fere ntial stuttering o n on and

characteristics

developmental

d isfl ue n cies as fre q ue ntly m a y

gra m m atical w o r d s substa nti ve but w o r ds; does not

nearly (2) the

spea ker a n xi o us; b l o c ks w o r ds suc h

an n o y e d,

ap pear an d of

(3 ) not

repetitio ns, occ ur o nly ( 4) o n

prol o n g ati o ns initial s ylla bles

d o an d

uttera n ces;

sec o n d a r y e ye

sy m p t o m s or fist o f and

as

facial are

gri m a cin g, not

blin k i n g, w it h

cle n c hi n g

ass o c iate d is n o

m o m e nts effect;

d isfl ue n c y; ( 5) there ( 6) st utte rin g vari o us

ada ptatio n

occ urs ty pes of

relati v e l y speec h th a t

co nsiste ntl y Ri n g o and

acr oss

tas k s. of

D i etric h

(1 9 9 5 )

fo u n d

fi ve for

the

rep orte d of

c haracteristics st utteri n g acr oss

(e x ce pt vari o u s

co n siste n c y of sp e e c h

ty pes

tas ks)

18 in cl u d e d ( 1 9 7 1 ) re p orte d re vie w e d. in and in a the criteria pro p ose d by Ca nter w ere the y H el m - E s tabr o o ks maj o rity of the (1 9 9 3 ) cases

A o r b y

n u m b e r all

of

case st u d i e s see m

to

co n f ir m

so m e

of the b e ha vi o ral patie nt n o

ch ara cteristics su g g este d Le der (19 9 6 ) has Par k i ns o ns w o r d Disease no n o o n

H el m - E s tabr o o ks a

(19 9 9 ). wi th

d escri be d w h o

sh o w e d

specific

fears,

sec o n d ar y a da ptatio n all ty pes

st u t t e r i n g effect o f a an d w h o

c hara cteristics, stuttere d et eq uall y al.

speec h. patie nt speec h

Peri n o

(2 0 0 0 ) d urin g ha d an d no n o

d escri be d

st utte r e d oral read i n g,

c o n v ersatio n al sec o n d ar y specific

a n d

st utteri n g f ears.

c haracteristics

w o r d

I n

c o n t r a st,

ot her that not m a y

case all

st u d i e s patie nts to all

hav e w ith of the

d e m o n strated n e ur o ge nic su g geste d a n d

st utteri n g d if fere ntial (20 0 1 )

co n f o r m

chara cteris tics. o n a

M o w r er w h o tha n an d read

Y o u nts

repo rte d o n

p atie nt w o r ds speec h w h e n he

st uttere d o n

m o re

fre q ue ntl y w o r ds an d di d V a n w h o

co ntent w h ose occ ur

f u n cti o n

la n g u a ge alo u d.

pro b le m s

n ot

Si m ilarl y, a patie nt

B orsel w as

et

al.

(2 0 0 3 ) m o r e

d escri be d

relati vel y

d isfl ue nt d u ri n g

pr o p ositio nal speech.

U n u s u al a n

p h o n e m i c

loci

of

st u tt e r i n g

e ve nts

and

in verse

re l ati o n s h i p

b et w e e n

pr o p ositi o n ality

19 a n d disfl u e n c y of the w ere onl y repo rte d st u d i e s. that of in a m i n o rit y rece nt re view e d see m to w h o be case M o r e the these the

repo rts o f

su g g e st sh o w m o st

p erce nta ge

patie nts m a y

c haracteristics b e ha vi o ral st utteri n g

e ven

lo w e r, of m o r e tha n

and

that

characteristics m a y in deed be

neur o g e n i c si m i l ar to

d e vel o p m e n tal su g geste d, state m e nt that at

st utte ri n g ti m e s is the

pre vi o usly p. 10 9 ) of

c o n f ir m i n g

L e b r u ns

(19 9 7,

sy m p t o m a t ol o g y

a d ult-o nset

st utteri n g

un distin g u i sha ble

fro m

t h a t o f d e v e l o p m e n t a l stu tt e r i n g.

M o r e also

rece ntl y, ha ve

V a n

B o r sel th a t

an d

Taillie u ca n n ot

(2 0 0 1 ) reliab l y and

ar g u e d

one the the

d if fere ntiate d e vel o p m e n tal b ase d n ot in solely

bet w e e n for m the of

acq u ire d flue n c y

disor der or

o n and or

ver bal

o ut p ut.

W h et her

ac q uire d the sa m e

d e v e l o p m e n t a l st utteri n g speec h an d

result

differe nt is f u rt h e r

no n -speec h b y o n the fact

c haracteristics that m ost

co m p licated are based

o bser vatio n s

sin gle

c li n i c a l case st u d ies.

20

Assessment:
Helm-Estabrooks(1999) and Ringo and Dietrich(1995) provide a framework for assessing neurogenic stuttering and distinguishing it from other disorders. These authors suggested that the following procedures are important for evaluating individual cases.

A detailed case history reflecting: Onset of stuttering (age at onset, time period between the first diagnosis of the neurological condition and the first occurrence of stuttering, suddenness of onset) and its association with other neurological or psychological signs. changes in stuttering since onset

-- If a client began to stutter or if previous stuttering recurred or worsened in association with the occurrence of neurological problems, neurogenic stuttering should be suspected. On the other hand, stuttering that appeared in conjunction with the onset of psychological problems may be of psychogenic origin. the clients level of concern, anxiety, or fear about his stuttering extent to which stuttering interferes with communication the clients history and family history of speech, language, or learning problems the clients and relatives handedness -- data on the clients and relatives handedness and history of speech, language, or

21 learning problems are primarily used to determine if a client might have a predisposition for stuttering. Left-handedness or ambidexterity, as well as history of speech or language problems in a family, may predispose an individual to stuttering. neurological and psychological health history

This information can be gathered initially through a case history and then supplemented during the interview. Direct assessment of speech: SSI-3 should be administered, and speech should be video taped during conversation and reading samples. Stuttering in speech samples should be analyzed for: # Proportion of stuttering on function (grammatical) words versus content (substantive) words # Presence of stuttering on noninitial syllables, such as in the words exciteme-me-ment, canister-er-er and cow-b-b-b-oy # Absence of secondary (i.e., escape and avoidance) behaviors, such as eye blinks, head nods, and use of um to get a word started Repeating the same short passage (Rainbow passage and grandfather passage) reading aloud to determine if stuttering is reduced progressively through six readings (adaptation effect). Speaking in a variety of fluency inducing conditions, especially speaking in a rhythm while swinging an arm, speaking while listening to loud masking noise, and speaking slowly under delayed auditory feedback set at 250-msec delay.

Other assessment batteries:

22 Helm-Estabrooks (1999) recommended using the Aphasia Diagnostic Profiles (ADP; Helm-Estabrook, 1992) to exclude the possibility that the stuttering actually reflects language formulation problems.

= There are many standardized tests that can be used to determine the presence or absence of aphasia or word finding problems. Aphasia Diagnostic Profile (ADP) and the Boston Naming Test (BNT) have norms for aphasic and non aphasic individuals, by comparing the results clinician can determine whether the speech dysfluencies displayed are likely the result of word finding problems or of a motor speech function. Samples of narrative and expository speech and oral repetition can be obtained by using the ADP or from subtests of other clinical examination such as the Boston Diagnostic Aphasic Examination (BDAE).

= Individuals with SAAND are more likely to produce dysfluencies when performing automatized speech tasks than are those with developmental stuttering and also person with SAAND also show less variability across the tasks than will those with developmental stuttering. Counting 1 to 30, reciting months of year, the lord prayer etc. are used to determine produces dysfluencies on these tasks.

Other tests:
=To examine co-occurring problems other than stuttering in neurological disorders such as memory problems seen in stroke and head trauma, The Arizona battery for communication disorders in dementia, Brief test of head injury etc. are used. Helm-Estabrooks (1999) also recommended that, if other neurological problems might be present that may interfere with treatment, other neuropsychological tests might be important to asses the clients capabilities. In addition reports of neuropsychological and neurological examinations may be crucial for selecting patients for treatment for SAAND and for choosing appropriate management techniques.

Neurological tests:

23 The neurological tests which can be done to identify the site of lesion includes, EEG (electroencephalography) PET (positrone emission tomography) MRI (magnetic resonance imaging) CT SCAN (computerized tomography) EEG lateralization studies have strongly suggested abnormal hemispheric dominance in stutterers. In fluent speakers, the left language dominant hemisphere is most active during speech and language tasks.

PET study (Fox et. al, 1996) reported increased activation in the right hemisphere in language tasks in developmental stutterers. Using PET Brown et. al found that activity in the left hemisphere was more active during the production of stuttered speech, where as activation of the right hemisphere was more correlated with fluent speech. Thus the author concluded that the primary dysfunction is located in the left hemisphere and that the hyper activation of the right hemisphere might not be the cause of stuttering but rather compensatory processes. A similar compensatory processes was been observed after stroke and aphasia, where an intact right hemisphere can at least partially compensate for a loss of function (Weiller et. al 1995). Right hemisphere hyper activation during fluent speech has been more recently confirmed with fMRI (Neumann, 2003). fMRI have revealed two important facts: 1) In stutterers the right hemisphere is seems to be hyper active, 2) A timing problem seems to exist between left frontal and left central cortex.

Moore, Hayens (1980) studied stutterers using PET and fMRI and concluded that it is possible to visualize brain activity of stutterers and compare these patterns to fluent controls. Turgut N, Utku U, Balci K(2002) reported a case of 61-year-old right-handed man with sudden onset of right hemiparesia and stuttering without aphasia. There was a circumscribed cortical infarction in the left parietal cortex on computerized tomography (CT) and magnetic resonance imaging (MRI) showed a recent infarct. Single photon emission computed tomography (SPECT) images evidenced perfusion abnormalities in the same region.

24

Clinical management of neurogenic stuttering

Candidacy for SAAND therapeutic intervention:
Based on the information gathered from the assessment, decision can be made as to whether a particular patient is a candidate for therapeutic intervention and if so what specific approach is likely to produce positive results.

The first question to be asked in selecting SAAND patients for therapeutic intervention is

Does the stuttering represent a communication handicap? In some cases the dysfluencies are so mild, although noticeable, that do not appreciably interfere with communication. But in other cases, stuttering is part of a larger communication problem (such as aphasia) that must be taken precedence in the rehabilitation program. Does the patient have a rapidly progressing neurological disorder?

If so, even severe stuttering may represent a minor problem in overall scheme of life. For ex: patients undergoing extensive dialysis therapy for kidney disease may have a chance of developing stuttering along with early signs of confusion and dementia. As disease progresses, the condition of the patient worsens. Because of the severe and progressive nature of the disease these patients probably were not candidates for speech therapy.

Is the individual is motivated to work on the problem? Some patients may be somewhat annoyed, but not highly anxious about the stuttering. Depending on neuropathology of their disorder, each patient may show total indifference to the dysfluencies. Such individuals are poor candidate for any therapeutic program that involves behavior modification.

Sometimes patients will be candidates for drug therapy, which requires interdisciplinary cooperation between a speech language pathologist and a neurologist. Baartaz and Mesulam

25 (1919) described a 40 year old woman who developed seizures and began to stutter following a closed head injury. When her seizures were brought under control with phenytoin her speech dysfluencies diminished.

Thus selection of SAAND patients for various therapeutic interventions will depend on the overall health status of each individual as well as etiology of the stuttering, its neuropathological correlates, and any concomitant behavioral disorders.

Treatment goals:
Goals for the therapy will be determined in part according to each individuals life style, work status, age, general health etc for ex: sales person with relatively mild degree of nonfluency may consider stuttering to be a significant handicap. In contrast, a bedridden person who can communicate basic needs may not consider himself or herself significantly handicapped by the stuttering. In some cases however memory and some cognitive deficits may prevent the patient from participating in the goal setting process. In such cases family members, caretakers and the clinician will determine the extend to which stuttering interferes with communicative needs of the individual and formulate the goals for treatment.

Treatment procedures:
Because individuals with neurogenic stuttering do not usually have the cognitive and emotional involvement that characterize developmental stuttering in adults, treatment is often entirely behavioral. An exception is when the neurological etiology of the stuttering is known and can be treated by surgery or drugs.

Behavioral treatments:
It has been suggested that neurogenic stuttering can be differentiated from developmental stuttering by the finding that neurogenic stutterers do not become more fluent with rhythmic speech, masking, or speaking slowly. Paradoxically, these very conditions may be therapeutically useful for some patients.

Pacing:

26 Developed by Helm (1979) for patients with palilalia but has been used for neurogenic stuttering. This is essentially a technique of speaking one syllable at a time, so that each syllable is spoken separately, without the usual co-articulation across syllables. As a result, speech is produced more slowly and with a regular, staccato rhythm. Often however patients do not respond to instructions for producing slower paced speech because of an underlying neurological drive to speak at faster rates. This appears true of individuals with Parkinson disease. For such patients pacing devices may be required.

The pacing device, first described in 1979, has six multicolored squares with raised dividers. The patient was encouraged to tap his or her forefinger from square to square while speaking in a syllable by syllable manner. Rentschler, Driver, & Callaway(1984) described another small device that fits over the patients forefinger. Holes are punched in kay splint material in a molded form that fits over the finger. With either of these devices the patient moves a finger from place to place, timing each syllable with a finger movement. Both a large board and a more portable pocket size board for those patients who can mange finer finger movements are now available. Helm-Estabrooks (1999) suggested that pacing could begin with a device and progress to simply tapping rhythmically on the thigh to produce fluent speech.

Aphasia, word finding problems associated with stroke, memory problems in head trauma will interfere in learning new strategy for speaking and initiation difficulties may result in failure to implement the use of communication aids especially pacing.

Delayed auditory feedback and masking:

In 1984 Rentschler and colleagues described a 41yr old man who developed stuttering following drug overdose with chlorazepate dipotassium. Binaural white noise masking at 95db resulted in fluent speech and with reduced levels of noise intensity stuttering returned. Marhshall and Starach used DAF to successfully treat a 22 year old man who developed SAAND after a closed head injury. The DAF procedure was introduced 4yrs after the injury occurred. Marshall, R.C. / Neuburger, S.I. (1987) examined the effects of Delayed Auditory Feedback (DAF) with three cases of acquired stuttering following head injury. To determine the effects of

27 DAF on stuttering behavior a multiple baseline design across three speaking tasks was employed. All subjects reduced stuttering with application of DAF. Stuttering behavior on untreated tasks continuing in baseline was not affected by DAF. When treatment was applied to the untreated tasks, stuttering events decreased for all three subjects. Results indicate DAF has potential as a treatment procedure with cases of acquired stuttering in a way similar to cases of developmental stuttering.

Venu

Balasubramanian,

Ludo

Max,

John

Van

Borsel,

Kathleen

O.

Rayca,

DonaldRichardson (2003) reported the experimental data consist of stuttering frequency measures under various conditions that are well known to enhance fluency in most individuals with developmental stuttering i.e. adaptation, unison reading, delayed auditory feedback (DAF), and frequency altered feedback (FAF) in a 57-year-old male following ischemic lesion to the orbital surface of the right frontal lobe and the pons. The patient read six 200-word texts under different conditions: Six solo readings (Text 1), five unison readings followed by five solo readings (Text 2), five readings with non-altered auditory feedback (Text 3), five readings with 50 ms delayed auditory feedback (Text 4), five readings with increased FAF (Text 5), and five readings with decreased FAF (Text 6). Results indicate that, unlike the typical situation for developmental stuttering, this individual with acquired neurogenic stuttering did not show increased fluency during an adaptation paradigm or under unison, DAF, and FAF conditions. Slow rate and easy onset:

According to a survey conducted by Market etal (1990), clinicians most commonly use slow speech rate techniques, easy voice onset approaches or a combination of two for treatments of SAAND. Although 82.2% reported positive results no specific descriptions of the therapy protocols were provided.

Stuttering modification:
Only a modest percentage of clinicians surveyed by Market et. al (1990) reported that they had used such stuttering modification tools as light contacts, preparatory sets, cancellations, and pullouts.

28 Bio feedback and relaxation:

Biofeedback techniques similar to those employed with developmental stuttering have been used for treatment of SAAND. A stroke patient with stuttering, with no evidence of oral apraxia was treated using Biofeedback technique. Using an electromyographic biofeedback unit an integrated baseline of masseter tension level was obtained for five minutes of conversation, followed by five minutes of relaxation techniques. He then was asked to maintain a lower tension level by observing and responding to biofeedback for five minutes of conversation. After a four month twice weekly course of this biofeedback/ relaxation therapy and home relaxation exercises, he has discharged with only mild stuttering. Similarly, Helm-Estabrooks (1986) and Rubow and Collegues(1986) used biofeedback and relaxation training to successfully treat SAAND following stroke.

Other approaches: C at heri ne De Nil ( 2 0 0 8 ) p atie nts T h e ys, in a Astri d sur ve y va n of W ieri n g e n, 58 L u c F.

D utc h -s pea ki n g re p orte d that

with

ne ur o ge nic

st utteri n g

a large majority of the patients in the survey received speech and language therapy. If specific stuttering therapy was provided, a combination of multiple therapy techniques was usually reported. F r e q u e n t l y slo w i n g c o g n iti ve spea ki n g use d thera p y ap pr o ac hes were:

sp e e c h thera p y, lou d er.

rate,

breathin g

thera p y, and

fl ue n c y

sha pi n g,

Many clinicians start with traditional fluency therapy and

complement or replace it with other techniques if necessary. Approximately half of the patients were reported to improve during the therapy, which supports the positive outcome measures found by Market et al. (1990) and Stewart and Rowley (1996), although it is not clear to what extent these improvements were therapy-specific or, in some patients, may have reflected natural neurological recovery.

Surgical intervention:
Neurosurgery:

29 Sometimes when a neurological problem requires surgical intervention, the surgery resolves or improves stuttering. Cases reported by Donnan (1979) & Jones (1966) suggested that, for whatever reason, surgery that resolves a neurological problem may also resolve stuttering. In 1979 Donnan described a 65 year old woman who developed stuttering concurrently with an episode of cerebral ischemia. Donnan described her stuttering as rapid easy repetition of the initial sound syllable of every word. He reported that the woman displayed no sound blocks or facial grimacing, agnosia or apraxia. A carotid angiogram showed left carotid stenosis with elevated plaques due to hemorrhage beneath the plaques. An endarterectomy was done and upon recovering from the anesthesia the woman was found to be completely free from stuttering. The post surgical angiogram showed uninterrupted left carotid blood flow. In such cases the role of the speech clinician is limited to documenting the nature and severity of stuttering associated with carotid artery disease and its treatment. Thalamic stimulation:

Bhatnagar and Andy (1938) described a 61 year old man with stuttering associated with a long history of trigeminal pain. Over an 18 year period he was treated with various medications and bilateral trigeminal ganglion blocks. Methysergide maleate (sansert) was the only drug which reduced speech disfluencies but it had adverse function on kidney function. There were no cooccurring aphasia or memory problems and the patient showed no adaptation effect, anxiety or secondary characteristics. A surgical procedure was used to implant a chronic stimulation electrode in the left centromedian thalamic nucleus for relief of chronic pain. A battery operated stimulator was used to stimulate the electrode three or four times a day for 20 minute period. This resulted in remarkable improvement in speech fluency as well considerable pain reduction.

Orlando J. Andy, Subhash C. Bhatnagar (1992) observed four neurosurgical subjects with acquired stuttering subsequent to subcortical pathology of mesothalamus. The patients suffered from chronic pain, seizures, and somatosensory disorders. They also exhibited unpredictable and uncontrollable speech, spasmodic blocks which were devoid of accessory features, and adaptation effect. Therapeutic mesothalamic stimulation, used as a treatment of last resort to relieve the pain and associated symptoms, also had an ameliorating effect on the stuttering. Spontaneously occurring focal abnormal EEG discharges were anatomically delineated and used as a guide for

30 therapeutic stimulation electrode placement. Attenuation of the abnormal discharges was followed by alleviation of symptoms.

This investigation suggested an electropathologic basis for their mesothalamic-generated speech dysfluencies. The cooccurrence of pain, seizures, somatosensory disorders, and stuttering, and their concurrent amelioration, suggests that both chronic pain and stuttering may be implicated by similar or related reticular electropathologic generators, couched in overlapping reticular networks extending from the brain stem to the thalamus, and that the acquired stuttering may be recruited as one component of a larger syndrome complex.

Transcutaneous nerve stimulation:

An electronic device is vibrated against skin (usually hand) during moments of stuttering. TNS unit originally developed for pain control was also successful in reducing this patients speech dysfluencies. Butler (1977) reported a case of 68year old woman who experienced a series of minor stroke to both cerebral hemispheres. Severe stuttering occurred after fifth stroke, which also produced a transient hemiparesis. The woman was left handed but had been converted to use right hand for writing. Her language skills remained essentially intact but she had mild dysarthric and marked by dysfluent speech with severe blocking or prolongations of initial and medial syllables especially consonant blends. Trials with a speech pacing board increased her dysfluency as she tried to speak in a deliberate syllable by syllable manner. But when an electro larynx is vibrated against her left hand, moments of stuttering during an oral reading task decreased from 38 to 8.

Pharmacological treatment:
There is evidence to suggest that the drugs may have either a negative or positive effect on speech fluency. Case studies have reported that drugs for seizure disorders, schizophrenia, depression, anxiety, Parkinsons disease, and asthma can precipitate stuttering in individuals who

31 have not stuttered previously. In most of these cases, stuttering is reduced or eliminated when drug dosage is adjusted or an alternative drug is used.

Baratz and Mesulam (1981) reported a case in which stuttering associated with head injury and seizures diminished when the seizures were brought under control with phenytoin. Mcclean and Mcclean (1985) reported that their patients with post head injury seizures stuttered when treated with phenytoin but reduced his dysfluency levels when switched to carbamazeptine.

Stuttering has also been associated with dopamine receptor blocking drugs like phenothiazine. Nunberg and Greenwald (1981) described two patients with chronic schizophrenia who developed severe stuttering when severe phenothiazine levels were high enough to eliminate psychosis. These investigators then had to find a dosage that would mange both psychosis and stuttering at acceptable levels of daily living.

Quader (1977) described two patients in whom stuttering was associated with administration of amitriphyline, tricyclic antidepressant. In both cases speech returned to normal when the drug was discontinued. Similarly Elliot and Thomas (1937) reported onset of stuttering in a 22 year old woman who was treated with alprazolam for anxiety and depression.

Expected outcomes:

Given the many approaches to the treatment of SAAND one might expect that there is an effective form of therapy for each individuals with stuttering associated acquired neurological disorders. But SAAND is not unitary disorder nor it is typically undimensional. It is therefore difficult to predict how well a specific patient will respond to therapeutic intervention. Sometimes clinician and patients must make compromises as in cases where certain drug is best for alleviating neurological or psychiatric symptom but also result in some speech dysfluency. Parkinsons patients with SAAND seem to respond well to a variety of techniques whereas stroke patients with SAAND seem harder to treat. Control of epilepsy also may result in control of the stuttering. Patients with rapidly progressing disorders such as tumors will probably not be candidates for formal treatment although supportive counseling may be required. Thus we cannot

32 make a blank statement about the expected outcomes of SAAND patients and their responds to treatment. Instead one should consider each patient individually beginning with the case history, progressing through the clinical evaluation, and finally choosing what appears to be the best approach to the management and treatment.

Conclusion:
SAAND is one of the most interesting, puzzling and challenging speech problem seen in a wide range of neurological disorders from Parkinsons disease to closed head injury. There is mounting evidence that a variety of transient static and progressive neuorological conditions which may result in dysfluent speech patterns is labeled as stuttering by clinicians, family members and patients themselves. In fact evidence is so compelling, clinician should also consider adult onset of stuttering as a symptom of possible neurological dysfunction. S o is i m p o rta n t to ta k e all the rele v a nt o nset c o n cer ni n g n e ur ol o gical a n d speec h the p a t i e n ts an d histor y, of it

fact ors the site into

disease a n d

st utteri n g,

lesi o n

n o n -sp eec h m a k i n g a

characteristics

acc o u nt

befo re

dia g n o sis.

The early diagnosis is

important as it may lead to successful treatment of a neurological disorder causing the stuttering or to successful treatment of the communication disorder itself.

REFERENCES
Anthony M Ciabarra, Mitchell S Elkind, James K Roberts, Randolph S Marshall(2000) Subcortical infarction resulting in acquired stuttering .Neurol Neurosurg Psychiatry; 69:546-549 Curlee F. Richard (1993): Stuttering and related disorders of fluency, Thieme medical publishers, Newyork Duffy, J. R. (1995). Motor speech disorders: substrates, differential diagnosis and management. St. Louis: Mosby John Van Borsel, Caroline Taillieu (2001) Neurogenic stuttering versus developmental stuttering: An observer judgement study. Journal of Communication Disorders, Volume 34, 385-395 John Van Borsel, Sandie Van Der Made, Patrick Santens (2003)Thalamic stuttering: A distinct clinical entity?.Brain and Language, 85, 185-189 Manning H Walter(2001):Clinical decision making in fluency disorders:Singular publishing group.

33
Marshall, R.C., Neuburger, S.I,(1987) Effects of delayed auditory feedback on acquired stuttering following head injury. Journal of Fluency Disorders, 12 (5), p.355-365 Nancy A. Helm, Russell B. Butler and D. Frank Benson(1978). Acquired stuttering. NEUROLOGY;28:1159 Nass R, Schreter B, Heier L(1994) Acquired stuttering after a second stroke in a two-year-old. Dev Med Child Neurol. Jan;36(1):73-8. Onslow , Mark (1996):Behavioral management of stuttering, Singular publishing group. Orlando J. Andy, Subhash C. Bhatnagar.(1992) Stuttering acquired from subcortical pathologies and its alleviation from thalamic perturbation. Brain and Language,42, 385-401 Silverman F.H (1992): Stuttering and other fluency disorders, Allyn and Bacon. Soroker N, Bar-Israel Y, Schechter I, Solzi P(1990). Stuttering as a manifestation of righthemispheric subcortical stroke. European journal of Neurology;30(5):268-70. Theys, C, van Wieringen, A, De Nil, L.F (2008)A clinician survey of speech and non-speech characteristics of neurogenic stuttering. Journal of Fluency Disorders, 33 (1),1-23 Venu Balasubramanian, Ludo Max, John Van Borsel, Kathleen O. Rayca, DonaldRichardson (2003).Acquired stuttering following right frontal and bilateral pontine lesion: A case study. Brain and Cognition,53,185-189