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    Capítulo 8 - Disartria Hipocinética

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    M_LX

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    CHAPTER 8 Hypokinetic Dysarthria AA. Definitions of Hypokinetio Dysarthria 'B. Neurological Basis of Hypokinetic Dysarthria 1. Characteristics of Parkinsonism 2. Etiology of Parkinsonism 3, Pharmacologic Treatments for Parkinsonism C. Etiologies of Hypokinetic Dysarthria 1. Idiopathic Parkinson's Disease 2. Neuroleptic-Induced Parkinsonism 3. Postencephalitic Parkinsonism 4, Traumatic Head Injury 5, Toxic Metal Poisoning 6. Stroke D, Speech Characteristics of Hypokinetic Dysarthria 1. Prosody 2, Articulation 3, Phonation . Koy Evaluation Tasks for Hypokineti Dysartivia (continued) 200" MOTOR SPEECH DISORDERS F. Treatment of Hypokinetic Dysarthria 1, Articulation 2. Phonation 8. Resiration 4, Prosody G. Summary of Hypokinetic Dysarthria H, Study Questions DEFINITIONS OF HYPOKINETIC DYSARTHRIA Most definitions of hypokinetic dysarthria mention that individuals with this disorder have reduced vocal loudness, a harsh or breathy vocal quality, and abnormal speaking rates. Although these are not all of the characteristics of hypokinetic dysarthria, they are among the most com- mon ones. It is interesting to note that many individuals with this dysarthria have slow speaking rates, but in some there can be an abnor ‘mally increased rate of speech. The following two definitions encompass much of the most important aspects of hypokinetic dysarthria. Hypokinetic dysarthria is a perceptually distinguishable motor speech disorder associated with basal ganglia control circuit patholo- gy: It may be manifest in any or all of the respizatory, phonatory, res- onatory, and articulatory level of speech, but its characteristics are ‘most evident in voice, articulation, and prosody. Is deviant speech characteristics reflect the effects of rigidity, reduced force and range of movement, and slow but sometimes fast repetitive movements on speech. (Duty, 1995, p. 166) ‘Hypokinetic dysarthria [is] characterized by reduced vocal loudness with concomitant harsh-hoarse quality, slow speaking rate with intermittent bursts of rapid fire articulation, excessive and overly long pauses, prolonged syllables, monoloudness, and reduced phonation time. (Dworkin, 1991, p.9) NEUROLOGICAL BASIS OF HYPOKINETIC DYSARTHRIA It is the only which increased rate of speech may be one of the symp: In several ways, hypokinetic dysarthria is. unig dysarth HYPOKINETIC DYSARTHRIA 201 toms. It also is the only dysarthria in which the vast majority of cases share the same etiological factor (parkinsonism). Because it accounts for so much of the hypokinetic dysarthria seen in clinical caseloads, parkinsonism is considered the de facto cause of this dysarthria ‘throughout most of this chapter. The reader should keep in mind, how- ever, that parkinsonism is not the only cause of hypokinetic dysarthria. A few other disorders can lead to this dysarthria, and they are dis- cussed in the etiology section of this chapter. Hypokinetic dysarthria occurs when the symptoms of parkinson- {sm affect the muscles of speech production. The parkinsonian symp- toms that have the greatest effect on speech are muscle rigidity, reduced range of motion, and slowed movement. In nearly every instance, these symptoms are caused by dysfunction in the basal gan- glia or by damage to the basal ganglia's neural connections to other parts of the CNS. The term iypokinetic may be misleading to readers encountering, it for the first time. Initially, it may be confused with hypotonia, which is decreased muscle tone. A beginning clinician may consequently assume that an individual with parkinsonism will have ‘weak and floppy muscles. This assumption would be quite wrong, however. Literally, hypokinetic means “less motion,” not decreased ‘muscle tone. In fact, individuals with parkinsonism usually demon- strate increased muscle tone. When applied to individuals with parkin- sonism, the term hypokinetic describes their decreased range and fre- quency of movement, For example, individuals with parkinsonism usually demonstrate a shuffling, “baby step” type of walking known as, festinating gait, and their ability to express emotion through their facial expressions will be greatly diminished, a phenomenon known as masked facies. In addition, they may blink their eyes infrequently and. have difficulty starting or stopping movements. The reasons for these behaviors are discussed in the following paragraphs. Characteristics of Parkinsonism ‘The characteristics of parkinsonism are a unique collection of symp- toms, One of the most prevalent symptoms is tremor. Parkinsonian tremors are seen most commonly in the fingers and hands, but they also can involve the limbs and face. These tremors have a frequency of ibout 4 to 6 oscillations per second. They are called resting tremors, because they are most noticeable while the body is not moving, tingly, the tremors may become less pronounced or disappear ly when the boxly is completely relaxed or when an affected 202 MOTOR SPEECH DISORDERS body part is being moved voluntarily. During moments of agitation or nervousness, however, the tremors may become significantly worse. Bradykinesia is the slow and reduced range of movement seen in. individuals with parkinsonism. It is a very common symptom of parkinsonism. The shuffling walk and the lack of facial expression ‘mentioned previously are good examples of bradykinesia. Limb, trunk, and neck movements also are affected frequently by bradykinesia ‘Typically, the movements of affected body parts are slow, labored, and very limited in their range. In addition to the difficulties of walking and facial expression, bradykinesia also can affect speech, finger move- ‘ments, writing, and many other voluntary movements. It is important tonote, however, that the slowness and reduced range of movement of bradykinesia is not the result of muscle weakness. Individuals with parkinsonism usually demonstrate nearly normal muscle strength. AS ‘with all the symptoms of parkinsonism, bradykinesia is caused by dys- function in the basal ganglia, “Muscular rigidity is the result of increased muscle tone. The mus cles of individuals with this condition are always in a greater than not- ‘mal state of contraction, both at rest and during movement. Rigidity _most typically affects the neck, trunk, and limbs. The effects of rigidity can usually be observed casily. For instance, when an affected body partis pulled to an extended position, there will be constant resistance to the movement. This is sometimes described as “lead pipe resis- tance,” because it feels to the person who is doing the pulling that a piece of soft motal is being bent. In some joints, however, there may be fa sublle, rhythmic alteration in the rigidity as a body part is being, ‘moved. This intermittent change in rigidity is described as “cogwheel resistance” because of its step-by-step, ratchetlike motion. Although rigidity and bradykinesia are separate symptoms of parkinsonism, figidity can exacerbate the slowed and restricted movements of bradykinesia, Itshould be noted that there are differences between rigidity and spasticity, although they are both the result of increased muscle tone. One of the clearest distinctions between them is how they react to pas- sive movement. In spasticity, there will be an increasing resistance to the passive movement, followed by an abrupt relaxation of the mus being tested. The increase in resistance is especially evident when the passive movement is rapid. In contrast, patients with rigidity lemon- strate a more or less constant resistance t0 the passive movement, no matter how quickly the examiner moves the affected body part (Wiederholt, 1995). Akinesia is a delay in the initiation of movements and is yet another common characteristic of parkinsonian, Examples of akines HYPOKINETIC DYSARTHRIA = 203 can be seen in many of the movements of individuals with parkinson- ism, For instance, when an individual with parkinsonism is asked to verbally answer a question, there may be a noticeable pause before any ‘words are spoken. This delayed initiation of speech may last only afew seconds, but sometimes it is much longer. Occasionally, someone with severe akinesia may become “stuck” in a certain posture and be com pletely unable to move. Strangely, when an individual is stuck in one ‘of these frozen positions, a brief touch from another person is some~ ‘times all that is needed to initiate or continue a movement. In addition to this difficulty in initiating movements, many individuals with parkinsonism can have trouble stopping a movement once itis started. For instance, while reaching for a glass of water, they may knock itover because they were unable to stop reaching once the movement was ini- tiated, Not surprisingly, itis often reported that individuals with aki- nesia are reluctant to actively move about their home or other sur- roundings, because they are afraid of being injured when they do so. Disturbances of postural reflexes also are seen in individuals with parkinsonism. Such disturbances are especially evident when these individuals are doing relatively automatic tasks. For example, they may have difficulty maintaining their balance while walking, In addition, the normal walking arm swing will be absent; their arms will hhang stiffly at their sides. If pushed lightly while standing, they are likely to fall, because they cannot quickly shift their center of balance. ‘They may be unable to rise from a chair, because they do not naturally shift their trunk forward as they attempt to stand. Normally, the basal ganglia help regulate these postural reflexes through neural connec tions with the extrapyramidal system. However, when the basal gan- glia are not functioning properly, these postural problems of balance and movement can become obvious. Although tremor, bradykinesia, rigidity, akinesia, and disturbed postural veffexes are the primary symptoms of parkinsonism, chere are humerous other symptoms that may appear in individuals with this, disorder. These include depression, swallowing difficulties, dementia, and, of course, hypokinetic dysarthria, Although these additional symptoms do not appear in all individuals with parkinsonism, they can be common features of this disorder nevertheless. Etiology of Parkinsonism ‘As already mentioned, parkinsonism is caused by dysfunction in the 4, The basal ganglia are that play an importa basal ga 204 = _ MOTOR SPEECH DISORDERS Basal Ganglia > Thalamus Figure 8-1. Decreased dopamine in the basal ganglia is associated with most ‘causes of parkinsonism. (Adapted from Neuroscience of Communication, by D. Webster, 1999. p. 176. San Diego: Singular Publishing Group, inc. Copyright 1999 by Singular Publishing Group, Ine. Adapted with permission) (Figure 8-1). The individual members of the basal ganglia are the catt- date nucleus, the globus pallidus, and the putamen. Because the cau- date nucleus and the putamen are made of many of the same type of neurons and are functionally related, they are known together as the striatum. The basal ganglia are located deep in the brain and are quite ‘complex in their interconnections with each other and with other parts. of the CNS. One of the most important neural pathways of the basal ganglia is the looped control circuit that connects it to the cerebral cor- tex (Figure 8-2). The first part of this control circuit is composed of neural fibers that descend from the cortex. Through these fibers, the cortex tranemits information about planned upcoming movements to the basal ganglia. The basal ganglia, in turn, smooth and refine these planned movements, especially movements that are going to be slow and continuous, Once this refinement is completed, the basal ganglia sends the refined neural impulses for the planned movements up to the ‘motor cortex, where they are then transmitted through the pyramidal system to the lower motor neurons and out to the muscles, ‘To function properly, the basal ganglia depends on the balanced interaction of several neurotransmitters. Two of the most important are dopamine and acetylcholine. Dopamine is largely an inhibitory neuro transmitter and tends to slow neural activity within the striatum, The dopamine used by the striatum is produced by special neurons in the HYPOKINETIC DYSARTHRIA = 205 The Basal Ganglia Control Circuit ‘Association cortex "The primary motor makes a rough cortex sends the plan of a refined movement movement to the muscles ‘The basal ganglia ‘The thalamus, smooths and makes ——> refines further that movement refinements igure 0-2. A schematic diagram of the basal ganglia control circuit. substantia nigra, which isa collection of gray matter cells located near the basal ganglia. Acetylcholine also affects the function of the basal ‘ganglia, but unlike dopamine, it has an excitatory effect on these areas Of the brain. It tends to facilitate neural firing. In general, parkinsonism is caused by a reduction of dopamine in the striatum. The loss of dopamine has a profound effect on the work- ings of the striatum, because it is placed in a state of neurochemical imbalanee, When this imbalance occurs, there is relatively too much pumitter (acetylcholine) acting on the neurons of the 206 = _ MOTOR SPEECH DISORDERS striatum compared to the available amount of inhibitory neurotrans- ‘iter (dopamine). The higher levels of this excitatory neurotransmit- ter in the striatum are thereby thought to be the primary cause of the rigidity, bradykinesia, and other symptoms of parkinsonism. ‘The causes of reduced dopamine in the striatum are varied. In most cases, such as idiopathic Parkinsons disease, the etiology is not understood. In this disease, the dopamine-producing neurons in the substantia nigra slowly begin to degenerate for unknown reasons. As they degenerate, they produce less and less dopamine for use in the striatum, which then is unable to function properly, There are numer- cous other ways in which these dopamine-producing neurons can be damaged, including the effects of drugs and toxic poisoning, damage from infections, tumors, head injury, cerebral anoxia, and cerebtovas- cular disease Pharmacological Treatments for Parkinsonism ‘There are several pharmacological treatments for hypokinetic move- ‘ment disorders. One treatment approach is to replace dopamine in the striatum. However, direct dosages of dopamine are not effective because they cannot pass the blood-brain barrier and, consequently, will not reach the striatum. (The blood-brain barrier is the body's mechanism that controls the flow of matter ftom the blood stream to the extracellular fluid in the brain, Part of this barrier’s effectiveness is the tight arrangement of the cells in the walls of the cerebral capillar- ies.) Because of the blood-brain barrier, dopamine replacement treat- ‘ments use a precursor of dopamine known as I-dopa, a chemical that can reach the striatum and then is converted into dopamine by the brain, Once in the striatum, this drug compensates for the dopamine that is not being produced by the substantia nigra. Another treatment approach attempts to correct the neurotrans- mitter imbalance in the basal ganglia by decreasing the amount of acetylcholine activity in the striatum. Anticholinergic drugs act to either deplete acetylcholine in the basal ganglia or to interfere with its effect on these brain structures. In some individuals with parkinson- ism, the best treatment results occur when I-dopa combined with cer {ain anticholinergic drugs. ‘The effectiveness of these treatm ablishe can significantly reduce tremor, bradykinesia, akinesia, and rig many hypokinetic movement disorders, In addition, ledopa tr ‘ean profong, the life of an individual fit started early eno dopa HYPOKINETIC DYSARTHRIA 207 course of some disorders. Although I-dopa is effective on many symp- toms of hypokinetic disorders, Wiederholt (1995) reported that the speech disturbances associated with these disorders are least helped by this drug. In addition, the side effects of I-dopa can range from minor to quite serious. The minor problems include gastrointestinal distur- bance, poor control of blood pressure, insomnia, and agitation. The ‘more serious side effects usually appear after a prolonged course of ‘treatment and include such significant psychiatric symptoms as hallu-

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