Speech-Language Pathology And Dysphagia In Multiple Sclerosis
Merson RM, Rolnick MI
Phys Med Rehabil Clin N Am 1998 Aug;9(3):631-41
William Beaumont Hospital, Dept of Speech-Language Pathology, Royal Oak, Michigan, USA
PMID# 9894114; UI# 99109680
Dysarthria occurs in approximately 40% of all patients with MS, when Speech and Voice Disturbances do occur, they usually present as a Spastic-Ataxic Dysarthria with Disorders of Voice Intensity, Voice Quality, Articulation, and Intonation.
While language disturbances such as Aphasia, Auditory Agnosia, Anomia, Dysgraphia, and Dyslexia are very rare in MS, Cognitive Deficits and Swallowing Disorders are common.
Treating Dysarthria, Dysphagia, and Cognitive Deficits in MS patients is effective for reestablishing functional daily activities.
The types, severity, and rates of deterioration in MS are highly variable; complete restoration to normal functioning is therefore not always expected.
For these reasons, careful documentation of clinical-treatment outcomes and the factors influencing these outcomes should be regularly collected and reported.
Lip And Tongue Function In Multiple Sclerosis: A Physiological Analysis
Murdoch BE, Spencer TJ, Theodoros DG, Thompson EC
Motor Control 1998 Apr;2(2):148-60
The Univ of Queensland, Motor Speech Research Unit, Dept of Speech Pathology & Audiology, Brisbane, 4072, Australia
PMID# 9644286; UI# 99097211
A physiological analysis of the articulatory function of 16 adults with Multiple Sclerosis (MS) was performed using lip and tongue transduction systems.
Sixteen NonNeurologically impaired adults, matched for age, gender, and education, served as controls.
The MS speakers demonstrated patterns of tongue function that were significantly different from those of the control speakers. Specifically, the MS speakers were found to have significantly reduced tongue strength, endurance, and rate of repetitive movements.
In addition, preclinical signs of Lingual Dysfunction were evident in NonDysarthric MS speakers on endurance and rate tasks when compared to control subjects.
These physiological findings could account for the perceptual findings of impaired articulation and reduced intelligibility. No lip dysfunction was found on either the physiological or perceptual assessments.
A Case Of Adult Type AdrenoLeukoDystrophy With An Acute Onset And Repeated Episodes Of Ataxic Dysarthria
Ochi H, Yamashita Y
Rinsho Shinkeigaku 1996 Nov;36(11):1229-33
Matsuyama Red Cross HospitalDept of Neurology, Japan
PMID# 9046854; UI# 97198838
We report a 30-year-old man with adult type AdrenoLeukoDystrophy (ALD) who manifested an acute onset and repeated episodes of Ataxic Dysarthria.
He noticed a moderate Dysarthria after a high grade fever in February of 1995; however, two weeks later his symptom disappeared completely. Three months later, he noticed the Dysarthria again and he was referred to our hospital for further examination.
General physical findings on admission revealed a dark skin color, pigmentation of Gingivae and reduced body hair. Neurologically he was normal except for a moderate Ataxic Dysarthria.
Cranial T2-weighted MRI showed multiple high intensity lesions in the SubCortical White Matter of Frontal Lobe, bilateral PeriTrigonal White Matter, Splenium of the Corpus Callosum and bilateral Cerebellar White Matter.
Only Cerebellar lesions responsible for his symptom were enhanced on MRI after Gadolinium administration.
Initially we diagnosed him with Multiple Sclerosis (MS) based upon the clinical course and MRI findings, and then started CorticoSteroid treatment.
His Dysarthria was slightly improved after the treatment and bilateral Gadolinium-enhanced lesions of Cerebellar White Matter on MRI disappeared.
Multimodality Evoked Potentials such as short latency SomatoSensory Evoked Potentials, BrainStem Auditory Evoked Potentials and pattern-reversal Visual Evoked Potentials, disclosed a Prolonged Central Conduction Time associated with bilaterally symmetric individual interpeak latencies.
These findings, which supported diffuse and bilateral subclinical DeMyelinating Lesions in the Central Nervous System, were unusual for MS; therefore his Plasma Very-Long-Chain Fatty Acids (VLCFA) were assayed for ALD.
Finally, he was diagnosed with adult type ALD because of the high ratio of C26: 0/C22: 0 (0.075; normal 0.033). It is very difficult to clinically distinguish the early stage of adult type ALD especially in patients like this from MS.
Therefore it is useful and important to evaluate not only the level of Plasma VLCFA, but also to evaluate multimodality Evoked Potentials.