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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
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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.
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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. Parkinson‟s diseases
5. Supranuclear palsy
6. Brain tumour
7. Alzheimer‟s disease
8. Dialysis dementia
9. Drug usage
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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-Barré Syndrome, and AIDS
Catherine Theys, Astrid van Wieringen, Luc F. De Nil ( 2 0 0 8 ) i n a s u r v e y
o f 5 8 D u t c h - s p e a k i n g p a t i e n t s w i t h n e u r o g e n i c
s t u t t e r i n g f o l l o w i n g v a r i o u s n e u r o l o g i c a l
i n j u r i e s r e p o r t e d t h a t s t r o k e w a s t h e m o s t
p r e v a l e n t c a u s e o f s t u t t e r i n g i n t h e i r p a t i e n t s ,
f o l l o w e d b y t r a u m a t i c b r a i n i n j u r y ,
n e u r o d e g e n e r a t i v e d i s e a s e s , a n d o t h e r c a u s e s
(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.
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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 Broca‟s 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 Broca‟s 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
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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.
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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 doesn‟t 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:
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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
Parkinson‟s 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 Parkinson‟s disease or have a cerebellar lesion.
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Canter has apparently identified several subtypes of neurogenic dysarthric stutterers. The
dysarthria associated with Parkinson‟s 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 speaker‟s 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).
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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 case‟s
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
wernicke‟s aphasia, two with conduction aphasia, four with brocas aphasia and three with anomic
aphasia. The wernicke‟s 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 wernicke‟s and brocas aphasics and between wernicke‟s 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.
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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 e t a l . ( 2 0 0 5 ) d i s c u s s e d
t w o p a t i e n t s w i t h s t u t t e r i n g f o l l o w i n g a n
i s c h e m i c s t r o k e w h o b o t h s t u t t e r e d o n l y o n
i n i t i a l s o u n d s a n d s y l l a b l e s a n d o n e o f t h e m
s h o w e d s e c o n d a r y s t u t t e r i n g c h a r a c t e r i s t i c s .
D y s f l u e n c i e s m a y b e h e a r d o n i n i t i a l a n d m e d i a l
p h o n e m e s , s u b s t a n t i v e o r f u n c t i o n w o r d s ,
r e p e t i t i o n , a u t o m a t i z e d s e q u e n c e s , r o t e
p a r a g r a p h s , s i n g i n g a n d t a p p e d s p e e c h . N o
a d a p t a t i o n e f f e c t . R e d u c e d p e r f o r m a n c e i n
c a r r y i n g a t u n e , t a p p i n g r h y t h m s , b l o c k d e s i g n s
f o r m m o d e l , s t i c k d e s i g n s f r o m m e m o r y ,
s e q u e n t i a l h a n d p o s i t i 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
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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 s e l , V a n D e r M a d e , S a n t e n s ( 2 0 0 3 ) r e p o r t e d
a 3 8 y e a r o l d c a s e w i t h n e u r o g e n i c s t u t t e r i n g
f o l l o w i n g a n i s c h a e m i c l e s i o n o f t h e l e f t
t h a l a m u s . N o h i s t o r y o f s p e e c h a n d l a n g u a g e
p r o b l e m s . F r e q u e n c y o f s t u t t e r i n g i n c r e a s e d i n
p r o p o s i t i o n a l s p e e c h ( c o n v e r s a t i o n , m o n o l o g u e ,
c o n f r o n t a t i o n n a m i n g , w o r d r e t r i e v a l ) .
F r e q u e n c y d e c r e a s e d i n n o n - p r o p o s i t i o n a l
s p e e c h ( a u t o m a t i c s p e e c h , r e p e t i t i o n , r e a d i n g
a l o u d )
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), Broca‟s 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, Bar-
Israel Y, Schechter I, Solzi P, 1990; Kono I, Hirano T, Ueda Y, Nakajima K, 1998; Fleet WS,
Heilman KM ,1985).
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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 e t , M o n t a g u e , B u f f a l o , a n d D r u m m o n d
( 1 9 9 0 ) o n a s u r v e y o f 8 1 p a t i e n t s w i t h a c q u i r e d
s t u t t e r i n g r e p o r t e d t h a t h e a d t r a u m a a n d
i s c h e m i c l e s i o n s w e r e t h e m o s t f r e q u e n t c a u s e
o f t h e s t u t t e r i n g ( 7 5 % ) a n d l e s i o n s i t e s w e r e
o f t e n l e f t l a t e r a l i z e d ( 3 8 % ) . F o r t h e m a j o r i t y o f
t h e p a t i e n t s t h e f o l l o w i n g d i f f e r e n t i a l s p e e c h
c h a r a c t e r i s t i c s w e r e p r e s e n t : r e p e t i t i o n s ,
p r o l o n g a t i o n s a n d b l o c k s w e r e n o t r e s t r i c t e d t o
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i n i t i a l s y l l a b l e s ( 8 0 % ) ; s t u t t e r i n g o c c u r r e d o n
s m a l l g r a m m a t i c a l w o r d s a s w e l l a s o n
s u b s t a n t i v e s ( 7 9 % ) ; t h e s p e a k e r s e e m e d
a n n o y e d b u t n o t a n x i o u s ( 6 7 % ) ; a n d s e c o n d a r y
s p e e c h c h a r a c t e r i s t i c s w e r e r a r e l y p r e s e n t
( 6 8 % ) . A b s e n c e o f a n a d a p t a t i o n e f f e c t w a s
r e p o r t e d f o r 4 6 % o f t h e p a t i e n t s .
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 Parkinson‟s disease where stuttering was the first symptom being reported
(including Wilson‟s disease) Canter (1971). K o l l e r ( 1 9 8 3 ) d e s c r i b e d
s i x p a t i e n t s w i t h e x t r a p y r a m i d a l d i s e a s e
s t u t t e r e d m o s t l y d u r i n g s e l f - f o r m u l a t e d s p e e c h
a n d p r e s e n t e d w i t h a p o s i t i v e a d a p t a t i o n e f f e c t .
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
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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 ) i n a s u r v e y
o f 5 8 D u t c h - s p e a k i n g p a t i e n t s w i t h n e u r o g e n i c
s t u t t e r i n g r e p o r t e d 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
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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 Neurogenic stuttering Developmental stuttering
Neurological lesion Present Absent
Onset of stuttering Sudden Gradual
17
Situational, individual
variability in stuttering
Not observed Present
Position of sound syllable
on which stuttering occurs
Not specific More on initial position and
stressed words
Loci of stuttering Not specific More on certain words
Adaptation effect Absent Present
Avoidance Absent Present
Reduced rate of speech No change Reduced stuttering
Stuttering under fluency
inducing conditions
No change Decreases
Anxiety provoking
situations
No change Increased stuttering
Spontaneous recovery Less likely Observed
H e l m - E s t a b r o o k s ( 1 9 9 9 ) h a s s u g g e s t e d t h e
f o l l o w i n g s i x d i f f e r e n t i a l c h a r a c t e r i s t i c s
b e t w e e n neurogenic stuttering and developmental stuttering : ( 1 )
d i s f l u e n c i e s o c c u r o n g r a m m a t i c a l w o r d s n e a r l y
a s f r e q u e n t l y a s o n s u b s t a n t i v e w o r d s ; ( 2 ) t h e
s p e a k e r m a y b e a n n o y e d , b u t d o e s n o t a p p e a r
a n x i o u s ; ( 3 ) r e p e t i t i o n s , p r o l o n g a t i o n s a n d
b l o c k s d o n o t o c c u r o n l y o n i n i t i a l s y l l a b l e s o f
w o r d s a n d u t t e r a n c e s ; ( 4 ) s e c o n d a r y s y m p t o m s
s u c h a s f a c i a l g r i m a c i n g , e y e b l i n k i n g , o r f i s t
c l e n c h i n g a r e n o t a s s o c i a t e d w i t h m o m e n t s o f
d i s f l u e n c y ; ( 5 ) t h e r e i s n o a d a p t a t i o n e f f e c t ; a n d
( 6 ) s t u t t e r i n g o c c u r s r e l a t i v e l y c o n s i s t e n t l y
a c r o s s v a r i o u s t y p e s o f s p e e c h t a s k s . R i n g o a n d
D i e t r i c h ( 1 9 9 5 ) f o u n d t h a t f i v e o f t h e r e p o r t e d
c h a r a c t e r i s t i c s ( e x c e p t f o r c o n s i s t e n c y o f
s t u t t e r i n g a c r o s s v a r i o u s t y p e s o f s p e e c h t a s k s )
18
i n c l u d e d i n t h e c r i t e r i a p r o p o s e d b y C a n t e r
( 1 9 7 1 ) a n d H e l m - E s t a b r o o k s ( 1 9 9 3 ) w e r e
r e p o r t e d i n a m a j o r i t y o f t h e c a s e s t h e y
r e v i e w e d .
A n u m b e r o f c a s e s t u d i e s s e e m t o c o n f i r m s o m e
o r a l l o f t h e b e h a v i o r a l c h a r a c t e r i s t i c s s u g g e s t e d
b y H e l m - E s t a b r o o k s ( 1 9 9 9 ) . L e d e r ( 1 9 9 6 ) h a s
d e s c r i b e d a p a t i e n t w i t h P a r k i n s o n ’ s D i s e a s e
w h o s h o w e d n o s p e c i f i c w o r d f e a r s , n o
s e c o n d a r y s t u t t e r i n g c h a r a c t e r i s t i c s , n o
a d a p t a t i o n e f f e c t a n d w h o s t u t t e r e d e q u a l l y o n
a l l t y p e s o f s p e e c h . P e r i n o e t a l . ( 2 0 0 0 )
d e s c r i b e d a p a t i e n t s t u t t e r e d d u r i n g
c o n v e r s a t i o n a l s p e e c h a n d o r a l r e a d i n g , h a d n o
s e c o n d a r y s t u t t e r i n g c h a r a c t e r i s t i c s a n d n o
s p e c i f i c w o r d f e a r s .
I n c o n t r a s t , o t h e r c a s e s t u d i e s h a v e
d e m o n s t r a t e d t h a t n o t a l l p a t i e n t s w i t h
n e u r o g e n i c s t u t t e r i n g m a y c o n f o r m t o a l l o f t h e
s u g g e s t e d d i f f e r e n t i a l c h a r a c t e r i s t i c s . M o w r e r
a n d Y o u n t s ( 2 0 0 1 ) r e p o r t e d o n a p a t i e n t w h o
s t u t t e r e d m o r e f r e q u e n t l y o n c o n t e n t w o r d s t h a n
o n f u n c t i o n w o r d s a n d w h o s e s p e e c h a n d
l a n g u a g e p r o b l e m s d i d n o t o c c u r w h e n h e r e a d
a l o u d . S i m i l a r l y , V a n B o r s e l e t a l . ( 2 0 0 3 )
d e s c r i b e d a p a t i e n t w h o w a s r e l a t i v e l y m o r e
d i s f l u e n t d u r i n g p r o p o s i t i o n a l s p e e c h .
U n u s u a l p h o n e m i c l o c i o f s t u t t e r i n g e v e n t s a n d
a n i n v e r s e r e l a t i o n s h i p b e t w e e n p r o p o s i t i o n a l i t y
19
a n d d i s f l u e n c y w e r e o n l y r e p o r t e d i n a
m i n o r i t y o f t h e r e v i e w e d c a s e s t u d i e s . M o r e
r e c e n t r e p o r t s s e e m t o s u g g e s t t h a t t h e
p e r c e n t a g e o f p a t i e n t s w h o s h o w m o s t o f t h e s e
c h a r a c t e r i s t i c s m a y e v e n b e l o w e r , a n d t h a t t h e
b e h a v i o r a l c h a r a c t e r i s t i c s o f n e u r o g e n i c
s t u t t e r i n g m a y i n d e e d b e m o r e s i m i l a r t o
d e v e l o p m e n t a l s t u t t e r i n g t h a n p r e v i o u s l y
s u g g e s t e d , c o n f i r m i n g L e b r u n ’ s ( 1 9 9 7 , p . 1 0 9 )
s t a t e m e n t t h a t “ a t t i m e s t h e s y m p t o m a t o l o g y o f
a d u l t - o n s e t s t u t t e r i n g i s u n d i s t i n g u i s h a b l e f r o m
t h a t o f d e v e l o p m e n t a l s t u t t e r i n g ” .
M o r e r e c e n t l y , V a n B o r s e l a n d T a i l l i e u ( 2 0 0 1 )
a l s o h a v e a r g u e d t h a t o n e c a n n o t r e l i a b l y
d i f f e r e n t i a t e b e t w e e n t h e a c q u i r e d a n d
d e v e l o p m e n t a l f o r m o f t h e f l u e n c y d i s o r d e r
b a s e d s o l e l y o n t h e v e r b a l o u t p u t . W h e t h e r o r
n o t a c q u i r e d a n d d e v e l o p m e n t a l s t u t t e r i n g r e s u l t
i n t h e s a m e o r d i f f e r e n t s p e e c h a n d n o n - s p e e c h
c h a r a c t e r i s t i c s i s f u r t h e r c o m p l i c a t e d b y t h e f a c t
t h a t m o s t o b s e r v a t i o n s a r e b a s e d o n s i n g l e
c l i n i c a l c a s e s t u d i e s .
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 client‟s level of concern, anxiety, or fear about his stuttering
extent to which stuttering interferes with communication
the client‟s history and family history of speech, language, or learning problems
the client‟s and relatives‟ handedness
-- data on the client‟s 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 client‟s 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, it‟s neuropathological
correlates, and any concomitant behavioral disorders.
Treatment goals:
Goals for the therapy will be determined in part according to each individual‟s 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 patient‟s 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 pull-
outs.
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 a t h e r i n e T h e y s , A s t r i d v a n W i e r i n g e n , L u c F .
De Nil ( 2 0 0 8 ) i n a s u r v e y o f 5 8 D u t c h - s p e a k i n g
p a t i e n t s w i t h n e u r o g e n i c s t u t t e r i n g r e p o r t e d t h a t
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 u s e d t h e r a p y a p p r o a c h e s w e r e :
s l o w i n g s p e e c h r a t e , b r e a t h i n g t h e r a p y ,
c o g n i t i v e t h e r a p y , f l u e n c y s h a p i n g , a n d
s p e a k i n g l o u d e r . 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 co-
occurring 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, Parkinson‟s 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.
Parkinson‟s 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 Parkinson‟s 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 i t
i s i m p o r t a n t t o t a k e a l l t h e r e l e v a n t f a c t o r s
c o n c e r n i n g t h e p a t i e n t ’ s h i s t o r y , o n s e t o f t h e
n e u r o l o g i c a l d i s e a s e a n d s t u t t e r i n g , l e s i o n s i t e
a n d s p e e c h a n d n o n - s p e e c h c h a r a c t e r i s t i c s i n t o
a c c o u n t b e f o r e m a k i n g a d i a g n o s i s . 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.
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