Tuesday, December 10, 2019
Clinical Psychology and Gerontology Parkinson Disease
Question: Discuss about the Clinical Psychology and Gerontology for Parkinson Disease. Answer: Parkinson Disease and Effect on Speech: Parkinsons disease is the chronic degenerative disorder of the central nervous system. This disease specifically affects motor system of the person. Symptoms of this disease appear in gradual manner. In initial phase of this disease symptoms like shaking, rigidity, slow movement and inability in walking appear. Other than these physical symptoms psychological symptoms also appear like thinking problem, dementia, depression and anxiety. Sleep related problems and emotional problems also appear in Parkinsons disease patients. Genetic and environmental factors are responsible for the occurrence of this disease. People with exposure to pesticides and head injuries are at greater risk of Parkinsons disease (Pfeiffer et al., 2012). Motor symptoms of the disease mainly occur due to the death substantia nigra cells. This substantia nigra is the region of the midbrain. As a result, dopamine deficiency occurs in the substantia nigra of the brain. Death of cells mainly occurs due to the formati on of lewy bodies in the neurons. Alzheimer's disease, multiple cerebral infarction and drugs also can cause Parkinsons disease. There is no specific technique is available for the diagnosis of Parkinsons disease. Physician generally diagnose Parkinsons disease based on the past medical history, symptoms, and neurological examination. Neuroimaging can be used to rule out other neurological diseases. Susceptibility weighted imaging of magnetic resonance imaging (MRI) can be used to differentiate Parkinsons disease form other neurological disease. Diffusion MRI can be used differentiate between typical and atypical Parkinsons disease. Basal ganglia can be evaluated for dopaminergic activity using positron emission tomography (PET) and single-photon emission computed tomography (SPECT) radioactive tracers (Verstreken, 2016). Treatments used for Parkinsons disease are levodopa, dopamine agonists and monoamine oxidase B (MAO-B) inhibitors (Yorkston, 1996). Rehabilitation can be provided through physical therapy and occupational therapy. Speech impairment in Parkinsons disease is a very common problem. However attention towards speech impairment is neglected as compared to the movement impairments like gait and upper limb control. Few studies studied speech aspects like frequency and co-occurrence of voice, articulation and fluency impairment. Speech impairment mainly occurs in Parkinsons disease patient due to altered amplitude of response. In Parkinsons disease patients this amplitude is at lower level as compared to the normal level. This lowering of amplitude mainly occurs due to the dysfunction of the basal ganglion. Trouble in gait like hesitation, festination and motor block are generally proportional to the difficulty in fluency of Parkinsons disease persons speech. Reduced volume is most common fe ature of speech impairment in PD persons followed by fluency deficit. Basal ganglion also performs function of provision of internal cues (Desmurget et al., 2004). These internal cues can be used to perform smooth functioning in order initiate sub-movements in the motor activity. Defect in these internal cues lead to the motor instability. In motor instability, there is decrease in amplitude as compared to the duration of motor sequence. This cue deficit leads to the articulation impairment in the PD person. Articulation impairment is proportional to the upper and lower limb demonstration of cue. These two phenomenons such as motor set disturbance and motor instability are generally superimposed because in most of the patients, there is co-occurrence of voice and articulation impairment. Pathophysiological changes in the speech impairment are almost similar to the limb motor deficit. Speech deficit is PD patients is also associated with other factors of PD like cognitive impairment, deficit in working memory and executive function (Miller et al., 2006). In few studies, it has been indicated that speech impairment is associated with depression in PD patients. However, it has been observed that there no difference in speech impairment in minor and major depression. Speech impairment can occur at any stage of the disease and it gets worsen with the progression of the disease. Medical and Surgical Treatment: Although dopamine therapy is useful in the movement aspects of the PD like rigidity, akinesia, bradykinesia and tremor, it doesnt exhibited satisfactory long term outcome for improvement in speech in PD patients (Goberman, 2005; Trail et al., 2005). Few studies indicated that dopamine therapy is useful in the specific aspects of speech like improvement in speech motor function better laryngeal control of voice onset and vocal fold closure during speech, better speech intelligibility, greater prosodic voice fundamental frequency inflection, greater vocSPL, better voice quality, enhanced lip function during speech and nonspeech tasks, and less voice tremor. However, most of the studies failed to demonstrate clinical improvement in the speech impairment. From this it can conclude that speech impairment in PD patients is not related to the dopamine (Goberman et al., 2002; Sanabria et al. 2001). Clonazepam exhibited improvement in some aspects of speech like inaccurate consonants, small r ushes of speech and improper silences of PD person (Biary, et al., 1988). Neurological technique like deep brain stimulation (DBS) of the thalamus, pallidum or subthalamic nucleus (STN), ablative surgeries (pallidotomy and thalamotomy) and fetal cell implantation exhibited inconsistent results in improvement in speech in PD patients. Thalamic stimulation improved few motor aspects of the speech, however it demonstrated negative effects on the perceptual assessment and electrophysiological measurements after the completion of the surgery (Krack et al., 2003). Pallidal stimulation also exhibited positive and negative effects on the perceptual assessment of speech after the completion of surgery. Few patients exhibited prominent improvement in the speech, however remaining patients didnt exhibited improvement in speech. DBS-STN exhibited improvement in the lip movement however, it exhibited worsening effect on speech intelligibility. DBS-STN generally improve levodopa responsive symptoms in PD patients, hence, this procedure may not be useful in speech in PD patients (Witt et al., 2004). This is because there was no improvement in speech impairment after treatment with levodopa. However, it can argue that position of the stimulator and tuning of placement plays important role in the improvement in the speech. In the studies it has been proved that voltage reach to the inside part of capsule can produce hesitations and face muscle tightness. In the same way, spread of the voltage to the cerebello-thalamic fibers can produce slurred articulation and stuttering (Tornqvist et al., 2005). Hence, further research should be done in this direction to get maximum benefits out of this method. Behavioural Therapy: Multiple factors are responsible for the impairment in the speech of PD patients. Hence, along with neuropharmacological and neurosurgical approaches, behavioral approaches also studied for the treatment of speech in PD patients. This behavioral speech therapy was also applied in patients with neurological surgeries. Literature suggests that these behavioral therapies were not useful 1) in the prevention of PD progression, 2) alone for treatment in any of the symptoms of PD, 3) as adjuvant therapy to neuropharmacological and neurosurgery, 4) in the prevention of complications due to motor impairment and nonmotor complications in PD. In behavioral therapy conclusive results were not obtained because of flaws in study methodology and incorporation of less number of participants (Suchowersky et al., 2006). Neuroimaging prior to and after completion of speech therapy would have given exact idea of effect of behavioral therapy in PD patients. These therapies incorporate speaker oriented therapies and communication oriented therapies. Speaker oriented therapies require PD patient to learn implementation of varied behavioral strategies to improve precision (Ramig et al., 1996). Learner should be self motivated to acquire newer aspects of speaking and practice it on regular basis. Integration of these behavioral therapies with instrumental or technical aspects, proved to be more beneficial as compared to the behavioral treatment alone. Instruments such as Visivox, Visipitch and a sound level meter can be integrated with behavioral therapies. These prosodically based treatments exhibited beneficial outcome in the supralaryngeal and phonatory deficits in PD and improving intelligibility and speech naturalness (Dromey, 2003; Bunton et al., 2001; Tjaden et al., 2001). Communication oriented strategies can be used as alone and also can be used as supplementary treatment for speaker oriented strategies. Communication oriented strategies include 1) preparation of communication partner, monitoring comprehension and implementation of active listening, 2) identification of subject and application of grammar to improve understanding of message, 3) gesture and 4) resolving communication breakdown (DInnocenzo et al., 2006). Low-tech AAC is mostly appropriate to PD patients who use speech to some extent as part of their communication and those to whom speech is completely dysfunctional. Alphabet cues can be used to improve speech and communication in Low-tech AAC treatment. Portable typing devices and communication books and boards can be used in Low-tech AAC treatment (Hustad and Weismer, 2007). Respiration Treatment: Respiratory studies in PD patients revealed impairment in vital capacity, volume of air spend at the time of maximal phonation task, intraoral air pressure at the time of consonant or vowel pronunciation, chest wall movement and activation of respiratory muscle. Electromyographic evaluation revealed decrease in the neural drive to laryngeal muscles and activation of laryngeal and respiratory muscle (Huber et al., 2003). Respiration treatment can achieve improvements like maximum duration sustained phonation, sound improvement and paused duration. These outcomes of the respiration treatment are consistent with the goals of the treatment. Respiration treatment also produce improved post treatment duration in speech and magnitude of speech as compared to previously established treatments. Kinematic, spirometric, acoustic, and pressure data are used to evaluate effectiveness of respiratory speech therapy. Specific data used to evaluate respiratory speech therapy are breathing rate, minut e ventilation, rib cage to lung volume, duration of inspirations, and oral pressure (Bunton, 2005). Lee Silverman Voice Treatment (LSVT): LSVT is the most advanced treatment option for speech in PD patients. Working procedure for the LSVT is basically based on the features responsible for the speech disorder in PD patients. These features comprises of 1) lowering of the amplitude of the neural drive to muscles of speech, which lead to soft voice, 2) impairment in sensory perception which lead to the loss of control over vocal output monitoring, and 3) inability of the PD patient to generate sufficient number of internal cues which lead to inability to produce optimum loudness in the voice. As LSVT is based on the basic mechanisms behind speech impairment, this treatment option emerged as most successful treatment option (Fox et al., 2002; Fox et al., 2006). All the components related to the speech in PD are considered in LSVT. These components include aspects related to neurology, physiology, motor learning, muscle training, and neuropsychology. Important concepts considered in the LSVT are 1) focus on voice by increas ing amplitude or vocal loudness, 2) increasing sensory perception, 3) administration of treatment with highest efforts, 4) increasing intensity of treatment and 5) measurement of outcome of the treatment. LSVT works on target basis. This therapy mainly focused on increasing vocal loudness by increasing amplitude of movement. Focus on this target acts as activator to increase efforts and to bring coordination of other systems (Pinto et al., 2004). In LSVT, there is the provision for sensory awareness training with motor actions. By virtue of this, LSVT assist in accepting increased loudness and improve the capability to self monitor vocal loudness. LSVT helps PD patients to maintain treatment effects for longer duration. This LSVT also addresses basic problems in PD patients. These problems comprises of deficit in speed, memory and execution in PD patients. LSVT also promotes over learning and acquisition of vocal efforts necessary for normal loudness. Systematic teaching, homework and carryover tasks are incorporated in the LSVT. This helps in daily living situations. Studies indicated that improvement in the vocal loudness obtained through LSVT can last for longer duration as compared to the any other treatment in PD patients. In the evaluation of the outcome of the LSVT, modern techniques are incorporated. In LSVT, vocal fold closure can be measured by few of these modern techniques like videostroboscopy as well as electrog lottography, subglottal air pressure, and maximumflowdeclination rate (MFDR) (Fisher and Yip, 2005). In other treatment methods these techniques are not incorporated. Hence, data obtained through LSVT treatment is valid data and it has scientific basis. In LSVT treatment group increased vocal effort lead to the improved vocal fold valving and consequently increased speech production. Moreover, there is no vocal hyperfunction in LSVT treatment. Vocal hyperfunction includes unnecessary strain and disproportionate vocal fold closure. LSVT treatment also gives information about the mechanisms involved in the speech and speech abnormalities in PD. LSVT also gives information about changes occurred due to the treatment effect. In the literature, it has been mentioned that LSVT treatment also brings positive alterations in the articulation, swallowing and facial expression. Positron Emission Tomography (PET) revealed that there is correlation between the improvement in speech and improvement in the neural functioning in LSVT treatment group (Liotti et al., 2006). LSVT treatment proved effective in most of the cases. However, in few patients with severe depression, severe dementia and people with surgery; LSVT doesnt exhibited beneficial outcome. Further research should be done on the PD patients to understand different mechanisms of speech. In recent studies, LSVT treatment was used to generate data to improve swallowing, articulation, gesture required for communication, facial expression and neural functioning. Recent LSVT studies were planned to evaluate voice and articulation separately. For this purpose two different studies were planned like voice LSVT and articulation LSVT. By providing these specific interventions, outcome in both voice and articulation can be obtained effectively. In recent studies implementation of the external clues in LSVT proved to be beneficial in improving vocal loudness in PD patients. Conclusion: PD is the degenerative disease of the central nervous system. In PD mostly impairment of the motor activities occurs. Most of the focus for the treatment of PD is gait and movement of extremities. Most of the PD patients develop speech impairment at some point of time. As a result, there is adverse effect on the quality of life. However, speech impairment got less attention from the researchers. As a result very less people received treatment for speech therapy in PD. Medical and surgical treatments for speech impairment in PD patients doesnt provide beneficial outcome. Results obtained from these approaches are variable. Future studies should be planned to reduce this variability. In current scenario, LSVT appears to be most successful therapy for speech impairment in PD patients. LSVT therapy is based on the processes involved in the speech. LSVT therapy is designed to act on these processes. As a result LSVT therapy is more beneficial as compared to the other therapies. Implementa tion of these processes in other therapies would be helpful in improving outcome of these studies. Plenty of opportunities are available for the improvement in theses studies. Moreover, ongoing and future directions of research for speech therapy have potential to understand mechanisms underlying speech impairment. This would be helpful in developing effective speech therapy for PD patients. References: Biary N, Pimental PA, Langenberg PW. (1988). A double-blind trial of clonazepan in the treatment of parkinsonian dysarthria. Neurology, 38(2), 255258. Bunton K, Kent RD, Kent JF, and Duffy JR. (2001). The effects of flattening fundamental frequency contours on sentence intelligibility in speakers with dysarthria. Clinical Linguistics Phonetics, 15(3), 181193. Bunton K. (2005). Patterns of lung volume use during an extemporaneous speech task in persons with Parkinson disease. Journal of Communication Disorders, 38, 331348 DInnocenzo J, Tjaden K, and Greenman G. (2006). Intelligibility in dysarthria: Effect of listener familiarity and speaking condition. Clinical Linguistics and Phonetics, 20(9), 659675. Dromey C. (2003). Spectral measures and perceptual ratings of hypokinetic dysarthria. Journal of Medical Speech-Language Pathology, 11, 8594. Fisher B, and Yip J. (2005). Physical therapy for individuals with Parkinsons disease: a paradigm shift. Parkinson Report, XVI(2), 1013. Fox CM, Morrison CE, Ramig LO, and Sapir S. (2002). Current perspectives on the Lee Silverman Voice Treatment (LSVT) for people with idiopathic Parkinsons disease. American Journal of Speech-Language Pathology, 11, 111123. Fox C, Ramig L, Ciucci M, Sapir S, McFarland D, and Farley B. (2006). The science and practice of LSVT/LOUD: neural plasticityprincipled approach to treating individuals with Parkinson disease and other neurological disorders. Seminars in Speech and Language, 27(4), 283299. Goberman A, Coelho C, and Robb M. (2002). Phonatory characteristics of parkinsonian speech before and after morning medication: the ON and OFF states. Journal of Communication Disorders, 35, 217239. Goberman A. (2005). Correlation between acoustic speech characteristics and non-speech motor performance in Parkinson disease. Medical Science Monitor, 11, CR109CR116 Huber JE, Stathopoulos ET, Ramig LO, and Lancaster SL. (2003). Respiratory function and variability in individuals with Parkinsons disease: Pre- and post- Lee Silverman Voice Treatment. Journal of Medical Speech-Language Pathology, 11(4), 185201. Hustad KC, and Weismer G. (2007). Interventions to improve intelligibility and communicative success for speakers with dysarthria. In: Weismer G, editor. Motor Speech Disorders. San Diego, CA: Plural Publishing Inc. Krack P, Batir A, VanBiercom N et al. (2003). Five-year follow-up of bilateral stimulation of the subthalamic nucleus in advanced Parkinsons disease. New England Journal of Medicine, 20, 19251934. Liotti M, Ramig LO, Vogel D et al. (2003). Hypophonia in Parkinsons disease. Neural correlates of voice treatment revealed by PET. Neurology, 60, 432440. Miller N, Noble E, Jones D, and Burn D. (2006). Life with communication changes in Parkinsons disease. Age Ageing, 35(3), 235239. Pfeiffer RF, Wszolek ZK, and Ebadi, M. (2012). Parkinson's Disease. CRC Press. Pinto S, Ozsancak C, Tripoliti E, Thobois S, Limousin-Dowsey P, and Auzou P. (2004). Treatments for dysarthria in Parkinsons disease. Lancet Neurology, 3, 547556. Ramig LO, Countryman S, OBrien C, Hoehn M, and Thompson L. (1996). Intensive speech treatment for people with Parkinsons disease: short and long term comparison of two techniques. Neurology, 47, 14961504. Sanabria J, Ruiz PG, Gutierrez R et al. (2001). The effect of levodopa on vocal function in Parkinsons disease. Clinical Neuropharmacology, 24, 99102. Suchowersky O, Gronseth G, Perlmutter J, Reich S, Zesiewicz T, and Weiner WJ. (2006). Practice parameter: neuroprotective strategies and alternative therapies for Parkinson disease. Neurology, 66, 976982. Tjaden K, and Wilding GE. (2004). Rate and loudness manipulations in dysarthria: acoustic and perceptual findings. Journal of Speech, Language, and Hearing Research, 47(4), 766-83. Tornqvist AL, Schaln L, and Rehncrona S. (2005). Effects of different electrical parameter settings on the intelligibility of speech in patients with Parkinsons disease treated with subthalamic deep brain stimulation. Movement Disorders, 20, 416423. Trail M, Fox C, Ramig O, Sapir, S, Howard J, and Lai EC. (2005). Speech treatment for Parkinsons disease. Neuro Rehabilitation, 20, 205-221. Verstreken P. (2016). Parkinson's Disease: Molecular Mechanisms Underlying Pathology. Academic Press. Witt K, Pulkowski U, Herzog J et al. (2004). Deep brain stimulation of the subthalamic nucleus improves cognitive flexibility but impairs response inhibition in Parkinson disease. Archives of Neurology, 61, 697700. Yorkston KM. (1996). Treatment efficacy: dysarthria. Journal of Speech Language and Hearing Research, 39, S46S57.
Subscribe to:
Post Comments (Atom)
No comments:
Post a Comment
Note: Only a member of this blog may post a comment.