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Spastic
Dysarthria
As
noted above, spastic dysarthria results from damage to the
pyramidal tract. Recall that most pyramidal tract cells
originate in the cortex of the precentral gyrus of the
frontal lobe which is also known as the motor strip. The
pyramidal tract fibers that carry messages to the spinal
nerves are called the corticospinal tract. The part of the
pyramidal tract that sends information to the cranial nerves
involved in speech and swallowing is called the
corticobulbar tract. According to Dworkin (1991, p.188),
spastic dysarthria is characterized by "Generalized
hypertonicity, weakness, immobility, abnormal force
physiology, and exaggerated reflexes of virtually all
muscles of the speech mechanism produce obvious dysfunction
of the articulation subsystem. Speech is slow-labored, and
imprecise articulatory efforts, compounded by disturbances
of respiration; resonation, and phonation often render
speech unintelligible."
The spinal nerves
receive only contralateral innervation from the
corticospinal tract. This means that spinal nerves on the
left side of the body receive input only from the motor
strip of the right hemisphere while those on the right side
of the body are innervated by the half of the motor strip
located in the left hemisphere. Therefore, unilateral
lesions of the pyramidal tract can cause paralysis of the
muscles innervated by the spinal nerves on the opposite side
of the body. For example, damage to the left half of the
corticospinal tract could result in paralysis of the right
side of the body.
On the other hand,
almost all of the cranial nerves receive bilateral
innervation from the fibers of the corticobulbar tract. This
means that both the left and right members of most pairs of
cranial nerves are innervated by the motor strips of the
right and left hemispheres of the brain. This redundancy is
a safety mechanism. If there is a unilateral lesion of the
pyramidal tract, both sides of body areas connected to the
cranial nerves will continue to receive messages about
voluntary motor movement from the cortex. These messages may
not be quite as strong as they were previously, but
paralysis will not occur. This means that the muscles
involved in speech would continue to function adequately in
spite of damage to one side of the pyramidal tract.
Therefore, only bilateral lesions of the pyramidal tract
will cause a serious, spastic dysarthria. When such
bilateral lesions occur, they produce a condition known as
pseudo-bulbar palsy. This name is derived from the term
bulbar palsy which is used to describe the symptoms of brain
stem lesions.
(The two
exceptions to the innervation scheme described above are the
portion of CN XII that controls tongue protrusion and the
part of CN VII that innervates the lower face. Like spinal
nerves these two cranial nerve nuclei receive only
contralateral innervation from the pyramidal tract. Thus, a
unilateral pyramidal tract lesion could cause drooping of
the lower part of the face or problems with tongue
protrusion on the opposite side of the body. However,
neither a unilateral weakness of the facial muscles nor the
inability to protrude one half of the tongue are likely to
cause a significant speech impairment. For this reason it
can still be said that only bilateral pyramidal tract
lesions seriously affect speech.)
It should be noted
that although speech will not be much impaired by unilateral
pyramidal tract damage, swallowing may be compromised by
this type of lesion. Unilateral lesions are unlikely to
cause a serious dysphagia, but they may produce
abnormalities that require treatment. Remember that
swallowing requires great precision as does speech and is
therefore easily impaired by neurological damage. Many of my
dysphagia patients over the years had been diagnosed with
unilateral upper motor neuron lesions. Swallowing is less
forgiving than speech of neurological damage.
The Extrapyramidal
Tract
This
system is involved in automatic motor movements, and in
gross rather than fine motor movement. It works with the
autonomic nervous system to help with posture and muscle
tone and has more influence over midline structures than
over those in the periphery. It regulates reflexes and
maintains posture and tone (Duffy, 1995). Facial expression
is one important communicative behavior that is mediated by
the extrapyramidal tract. In contrast to the pyramidal
tract, the extrapyramidal tract is an indirect,
multisynaptic tract that is primarily inhibitory.
Components of the
extrapyramidal tract include the basal
ganglia, the red nucleus, the substantia
nigra, the reticular
formation, and the cerebellum. All of these structures
send information to the lower motor neurons in an indirect,
multi-synaptic fashion.
The basal ganglia
acts to inhibit the release
phenomenon, or the rapid firing of motor
neurons. It is aided in this function by the substantia
nigra of the midbrain. The muscles most often affected by
this inhibitory function are those controlling the head, the
hands, and the fingers.
The
neurotransmitters involved in the inhibitory function of the
basal ganglia include dopamine, which is produced by the
substancia nigra, acetylcholine, and GABA, which is a glutamate.
Dopamine is an especially powerful inhibitor.
Extrapyramidal
Projections to Lower Motor Neurons
The
rubrospinal tract passes through the red nucleus. The
cerebellum sends messages to the spinal nerves along this
tract. Information flows from the superior cerebellar
peduncle to the red nucleus and finally to the spinal
nerves. This information is very important for somatic
motor, or skeletal muscle control and the regulation of
muscle tone, smoothness of movement and for posture.
The
reticulospinal
tract
runs from the reticular nuclei of the pons and medulla to
the spinal nerves. It is involved in somatic motor control
like the rubrospinal tract and also plays an important role
in the control of autonomic functions.
The tectospinal
tract
has points of origin throughout the brain stem, but
especially in the midbrain area, and ends in the spinal
nerves. It is involved in the control of neck muscles and
also in visual and auditory reflexes. So, when you jump
after hearing a noise or duck when you see something coming
toward you, this tract helps to mediate these reactions.
The
vestibulospinal
tract
runs from the vestibular nuclei located in the lower pons
and medulla to the spinal nerves. It is involved in balance.
(Note that all of
these tracts receive input from the cerebellum.)
Extra Pyramidal
Diseases and Syndromes Affecting
Communication/Swallowing
Lesions in the extrapyramidal tract
cause various types of diskinesias or disorders of
involuntary movement.
The problems
mostly common anomalies affecting the extrapyramidal tract
include degenerative
diseases, metabolic encephalopathy, encephalitis, and tumors.
Parkinson's
Disease, which is a degenerative disease, is
probably the most frequently occurring illness that results
from extrapyramidal tract lesions. It occurs when the
dopaminergic neurons of the substantia nigra are destroyed.
Its symptoms include:
Tremor
Festinating
movements, especially a festinating gait, but
these movements can also affect speech. (Festinating
movements are movements which become increasingly rapid and
uncontrolled).
Hypokinetic
dysarthria
Slow
movements
Tremor
Postural
instability
Altered
gait
Weak
Voice
Mask-like
facial expression
Freezing
This will be
discussed in greater detail a little later.
Diseases
associated specifically with lesions of the basal ganglia
include Huntington's Chorea and Sydenham's
Chorea.
The word "chorea" comes from the Greek "khoros" which means
to dance. Both of these diseases are associated with jerky,
uncontrolled movements of the limbs. Sydenham's chorea was
probably the cause of the malady that was known as St.
Vitus' Dance during the middle ages. Huntington's Chorea is
an inherited degenerative disease. These will be discussed
further a little later.
Essential Tremor
Syndrome, which is associated with spastic dysphonia may
also be the result of basal ganglia lesions.
Lesions of the
basal ganglia will also cause hyperkinetic
dysarthria.
Note that not only
is the definition of the extrapyramidal system
controversial, but also many sources say that it is very
difficult to make functional distinctions between the
extrapyramidal and pyramidal systems. When upper motor
neuron lesions occur, it is often difficult to determine
which tract has been damaged.
Hyperkinetic
Dysarthria
Hyperkinetic dysarthria results from
damage to the extrapyramidal tract. It specifically results
from lesions of the basal ganglia. The extrapyramidal system
is involved in automatic motor movements and works with the
autonomic nervous system to control posture and muscle tone.
Components of the extrapyramidal system include the basal
ganglia (caudate and lenticular nuclei), the red nucleus,
the substantia nigra, the reticular formation and the
cerebellum. Also included are the rubro spinal, reticulo
spinal, and vestibulo spinal tracts. The latter runs from
the vestibular nucleus in the pons to the spinal cord. The
vestibular nucleus also connects to the semicircular canals
in the ear and to the cerebellum for balance and orientation
in space. Again, hyperkinetic dysarthria most often results
from damage to the basal ganglia specifically. Dworkin
(1991) describes hyperkinetic movements as quick, jerky and
unsustained as with Huntington's chorea, or slow, writhing
and sustained as observed in people with athetosis and
dystonia. He describes those with essential tremor and
myoclonus as having tremorous movements. As you can see
there are several different types of speech movement
abnormalities in people with hyperkinetic dysarthria.
Dworkin's 1991 text is exclusively on remediation of motor
speech disorders. While being mindful that there is a good
deal of diversity among patients, Dworkin (1991, p.189),
generally recommends the following type of sub-system
exercises for hyperkinetic dysarthria: "1. Lingual, labial,
and mandibular force physiology training. 2. Phonetic
stimulation in various contexts." He also feels that this
treatment in general can also apply to ataxic patients after
they receive treatment of the respiratory and phonation
sub-systems.
Conditions that
may cause hyperkinetic dysarthria include essential tremor
syndrome, chorea, athetosis, and dystonia and tardive
dyskinsia. All result in the suprimposition of automatic
movements upon volitional movements.
1. Essential
tremor syndrome is also known as heredofamilial
tremor. Usually, various parts of the body, including the
jaw, head and hands are affected, displaying oscillatory
movements superimposed upon voluntary and involuntary
movements. When only the laryngeal musculature is
affected, the condition is called organic voice tremor.
In this case, phonation is abnormal but resonance and
articulation are not impaired. The voice disorder
resulting from organic voice tremor may involve
alternations of pitch and loudness at regular intervals.
It may also involve irregular, complete stoppage of
voicing. When the later symptom occurs, organic voice
tremor may resemble spastic dysphonia. However, there is
no strong concensus as to whether the two disorders are
actually related.
2.
Chorea
is a "disorder characterized by irregular, spasmodic,
involuntary movements of the limbs or facial muscles"
(Love & Webb, 1992, p. 289). "Choreic movements are
rapid and coordinated but purposeless." These "fidgets"
can cause dysarthria by impairing the coordination of
respiration with speech and interrupting the movements of
the articulators during speech (Love & Webb, 1992, p.
149). There are two types of chorea, Sydenham's
Chorea
and Huntington's
Chorea.
3.
Sydenham's chorea is a non-hereditary form of the
disorder that occurs during childhood following
infections like strep throat, rheumatic fever or scarlet
fever. The symptoms of this disorder will resolve
spontaneously within six months of onset. (It is believed
that this is the disease that was known as St. Vitus'
Dance during the Middle Ages.)
4.
According to Fitz Gerald (1996),
Huntington's
chorea is transmitted genetically
(chromosome 4 ). Because the disorder is transmitted by a
single, dominant gene, a patient's children have a fifty
percent chance of developing it themselves. This form of
chorea is progressive and fatal, causing the loss of
neurons in the cortex as well as in the caudate nucleus
and globus pallidus. The onset of Huntington's chorea
typically occurs in the 50's although it may begin much
earlier, even in childhood.
5. Athetosis is a disorder that
causes slow writhing movements of the entire body but
especially of the arms, face and tongue. These movements
can affect speech by interrupting the action of the
articulators and of the respiratory system. Athetosis
most often results from lesions of the putamen. The
caudate nucleus may also be involved. It is a rare
disorder that usually occurs as a form of cerebral palsy
brought on by perinatal anoxia. An especially rare form
of athetosis begins during adolescence and follows a
progressive course. According to Fitz Gerald (1996),
spontaneous movements are considered an escape phenomenon
caused by damage to the striatum and/or subthalamic
nuclei. This silences the globus pallidus permitting the
ventral lateral (VA) nucleus of the thalamus to fire
spontaneously.
6.
Dystonia causes slow jerky movements which
are most likely to occur in the trunk, neck and proximal
parts of the limbs. These may be exacerbated by voluntary
movements, like those involved in speech (Love &
Webb, 1992). Rosenfeld (1991) feels that it results from
a combination of dopaminegric and cholinergic
overactivity in the basal ganglia. When oralfacial
muscles are involved the condition is called focal mouth
dystonia (Duffy, 1995).
Some have speculated that spastic and spasmodic
dysphonia, a condition "characterized by effortful,
strained voice quality with voice arrests" (Love &
Webb, 1992), may be a localized form of dystonia. Not
much evidence supports this view, however. Although it
has been believed that the intermittent aphonia seen in
cases of spastic dysphonia is the result of
hyperadduction or spasm of the vocal folds. Indirect
laryngoscopy generally shows that the folds continue to
move normally during these episodes (Love & Webb,
1992). It should also be noted that some cases of spastic
dysphonia appear to be psychogenic in origin and are thus
not related to any hyperkinetic movement disorder.
As its etiology has not yet been identified, the
treatment of spastic dysphonia remains controversial. In
the past, the recurrent laryngeal nerve was cut to
ameliorate symptoms. While this operation improves voice
for a time, symptoms generally reappear. At this time,
injections of botulinum-A toxin
(Botox)
seem to be the most promising treatment for spastic
dysphonia.
7.
Tardive Dyskinesia is a condition which
results from longterm use of anti-psychotic drugs called
phenothiazines. These drugs are sometimes used to treat
schizophrenia. This movement disorder causes
"choreiform.and peculiar rythmical movement" (Love &
Webb, 1992), note that these are especially likely to
affect the tongue and lips. Involuntary movements of the
tongue in and out of the mouth, which are known as
fly-catcher's
movements, are characteristic of tardive
dyskinesia. It should be noted that the symptoms of this
form of hyperkinesia do not always resolve when the use
of phenothiazines is discontinued.
Hypokinetic
Dysarthria
Hypokinetic dysarthria is usually the
result of Parkinson's Disease (discussed earlier). The
disorder causes the degeneration of the substantia nigra,
which is one component of the extrapyramidal system. The
substantia nigra supplies dopamine to the cells of the basal
ganglia, allowing it to inhibit the release phenomenon or
the rapid firing of motor neurons. Thus, involuntary
movements occur as a result of the shortage of dopamine
caused when the substantia nigra is damaged. Dworkin (1991)
recommends the same type and sequence of sub-system
exercises as for hyperkinetic dysarthria described above.
According to Dworkin (1991) "widespread rigidity and
associated pareisis of virtually all muscles of the speech
mechanism justify treatments to improve resonance,
phonation, articulation, and indeed prosody." It is
currently believed that Parkinson's Disease results from
genetically based abnormalities of the mitochondria, passed
on through the female. This trait appears to be X-linked.
According to Fitzgerald (1996), the disease affects about 1%
of people over fifty years of age.
Parkinsonism, or
Parkinson's-like symptoms, can also cause hypokinetic
dysarthria. Parkinsonism can result from carbon monoxide
poisoning, arteriosclerosis, the use of tranquilizers like
Haldol, or from repeated blows to the head. (Mohammad Ali
has developed Parkinsonism due to injuries he received
during his career as a boxer). Another Parkinson-like
symptom , tardive dyskinesia (fly catcher syndrome) often
occurs as a side effect of psychoactive medication.
Parkinson's
Disease and Parkinsonism are often treated with L-dopa.
Levadopa is metabolized to dopamine, a neurotransmitter,
during passage through the blood-brain barrier (Fitz Gerald,
1996).
The symptoms of
Parkinson's disease include:
1. Pill-rolling
tremor
- patients move their thumbs and forefingers together as
if rolling a small pill between them. This movement
occurs at rest, but subsides during voluntary movement
and sleep.
2. Masked
facies
- Parkinson's patients usually display little facial
expression, so their faces are described as
"mask-like."
3.
Festinating movements - Movements become more rapid and
less coordinated over time. Festinations may affect both
gait and speech. For example, a Parkinson's patient may
begin to walk successfully but, as he continues, his
steps will become faster and increasingly uncontrolled.
As a patient continues to talk, his speech will become
increasingly unintelligible.
4.
Rigidity - If the limbs of a Parkinson's
patient are moved passively, the muscles will often
contract involuntarily, causing rigidity. This rigidity
may be constant or intermittent. Intermittent rigidity is
called cogwheel rigidity.
5.
Bradykinesia - This is the "reduced speed of
movement of a muscle through its range" (Love & Webb,
1992, p. 146). Not to be confused with tardive dyskenesia
that can occur as a side effect of psychoactive
drugs.
6.
Hypokinesia - This is "the reduced amplitude
of muscle movement" (Love & Webb, 1992, p.
146).
7.
Micrographia - Is the "tendency for
handwriting to be very small in the height of the letters
and to get progressively smaller as the person continues
to write" (Love and Webb, 1992, p. 146).
8.
Dementia - Between 30 and 40 percent of
Parkinson's patients suffer from dementia.
Ataxic
Dysarthria
Ataxic
dysarthria results from cerebellar lesions. Such damage could
be caused by stroke, trauma or by neurological disorders
like muscular sclerosis. The cerebellum plays an important
role in the coordination of motor movement due to its
integration of sensory and motor information. Due to its
connections with the vestibular system, it also affects
equilibrium. Therefore, cerebellar lesions result in
incoordination and the disruption of smooth movements
(tremor) as well as problems with gait and balance. After
cerebellar damage, patients are slow to initiate movements.
Their movements often under or overshoot targets. For
example, if an ataxic patient is trying to pick up a glass
of water, she may either fail to move far enough toward the
glass or may reach beyond it.
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