Speech disorders of Parkinsonism: a review

E M Critchley, E M Critchley

Abstract

Study of the speech disorders of Parkinsonism provides a paradigm of the integration of phonation, articulation and language in the production of speech. The initial defect in the untreated patient is a failure to control respiration for the purpose of speech and there follows a forward progression of articulatory symptoms involving larynx, pharynx, tongue and finally lips. There is evidence that the integration of speech production is organised asymmetrically at thalamic level. Experimental or therapeutic lesions in the region of the inferior medial portion of ventro-lateral thalamus may influence the initiation, respiratory control, rate and prosody of speech. Higher language functions may also be involved in thalamic integration: different forms of anomia are reported with pulvinar and ventrolateral thalamic lesions and transient aphasia may follow stereotaxis. The results of treatment with levodopa indicates that neurotransmitter substances enhance the clarity, volume and persistence of phonation and the latency and smoothness of articulation. The improvement of speech performance is not necessarily in phase with locomotor changes. The dose-related dyskinetic effects of levodopa, which appear to have a physiological basis in observations previously made in post-encephalitic Parkinsonism, not only influence the prosody of speech with near-mutism, hesitancy and dysfluency but may affect work-finding ability and in instances of excitement (erethism) even involve the association of long-term memory with speech. In future, neurologists will need to examine more closely the role of neurotransmitters in speech production and formulation.

References

    1. J Neurosurg. 1971 Aug;35(2):203-10
    1. Lancet. 1976 Mar 6;1(7958):544
    1. Brain. 1971;94(4):669-80
    1. Science. 1953 Aug 14;118(3059):193
    1. Neurology. 1973 Oct;23(10):1117-25
    1. Am Rev Tuberc. 1958 Nov;78(5):682-91
    1. Brain Lang. 1975 Jan;2(1):45-64
    1. Brain Lang. 1975 Jan;2(1):65-9
    1. Lancet. 1970 Feb 28;1(7644):464
    1. Lancet. 1970 Nov 21;2(7682):1082-3
    1. J Am Geriatr Soc. 1956 Dec;4(12):1280-4
    1. J Speech Hear Disord. 1978 Feb;43(1):47-57
    1. Lancet. 1971 Feb 20;1(7695):395
    1. Neurology. 1973 Aug;23(8):865-70
    1. Lancet. 1962 Jul 7;2(7245):1-6 contd
    1. Br Med J. 1971 Jan 2;1(5739):7-13
    1. J Speech Hear Res. 1969 Sep;12(3):462-96
    1. Brain Lang. 1975 Jan;2(1):101-20
    1. Br Med J. 1964 Sep 12;2(5410):656-9
    1. Int J Neurol. 1971;8(2):300-20
    1. Neurology. 1980 Dec;30(12):1273-9
    1. Lancet. 1976 Jun 26;1(7974):1394-5
    1. Brain. 1961 Sep;84:363-79
    1. Confin Neurol. 1966;27(1):197-207
    1. Folia Phoniatr (Basel). 1967;19(2):105-8
    1. Neuropsychologia. 1978;16(4):497-9
    1. J Speech Hear Res. 1969 Jun;12(2):246-69
    1. Brain Lang. 1975 Jan;2(1):70-7
    1. Can Med Assoc J. 1969 Dec 27;101(13):59-68
    1. Brain. 1968;91(4):619-38
    1. Q J Med. 1980;49(195):283-93
    1. J R Coll Physicians Lond. 1970 Oct;5(1):87-98
    1. J Speech Disord. 1950 Sep;15(3):252-65
    1. Brain. 1968 Mar;91(1):99-116
    1. Brain Lang. 1975 Jan;2(1):31-44
    1. Lancet. 1976 Feb 7;1(7954):292-6

Source: PubMed

3
Abonner