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SY4.1 Pathophysiology and Measurement of Spasticity
S6 saccule. This click induced cervical response became more consistent and reliable by revision recording procedures, i.e., putting the electrodes on the SCM muscle and high quality EMG recording technique by Colebatch, Halmagyi and Skuse (1994). This sound induced sacculo-collic reflex is termed as Vestibular evoked myogenic potentials (VEMP) since they are muscular responses induced by vestibular stimulation. VEMP is an inhibitory response recorded during tonic contraction of SCM muscle. Parameters of VEMP test include latency, amplitude and threshold of the biphasic (p13n23) waveform. Several modifications (electrode location, sound characteristics, monoaural vs binaural, etc) had been studied and many alternative protocols, such as tapping, galvanic stimuation, also has been introduced. Since amplitude parameter is determined by the intensity of the sound stimulus and the level of tonic contraction of the neck, several methods were compared to maintain consistent muscle contraction, i.e., rectifed VEMP using simultaneous EMG recording or use of prestimulus rectification of muscle contraction and visual feedback of the rectified EMG level or BP manometer. But, latency and VEMP threshold were relatively consistent parameters compared to amplitude parameters regardless of stimulus condition. VEMP testing may provide a useful, non-invasive method to assess the saccular function and functional integrity of the inferior vestibular nerve. Comprehensive assessment of vestibular function including VEMP is an important process to understand the extent of lesion and the course of disease in the evaluation of dizzy patients. SY3.2 Clinical Application of Vestibular Evoked Myogenic Potentials in Peripheral Vestibular Disorders James G. Colebatch * UNSW Clinical School, POW Medical Research Institute and Dept. of Neurology, Prince of Wales Hospital, Australia E-mail address: [email protected] The vestibular evoked myogenic potential (VEMP) has become a widely used method of vestibular assessment. The response has similarities to evoked potentials but also important differences due to its origin from modulation of EMG. Technical aspects relating to the stimulus and recording conditions need to be adhered to. Air conducted sound (eg clicks) are the most commonly used stimuli but other types of stimulation can also be used. It is not a replacement for more traditional forms of vestibular assessment such as the caloric test but has a different origin and therefore adds further information regarding vestibular function. Interpetation of VEMP findings in most cases is improved by knowing the findings with other forms of vestibular testing. VEMPs are of value in making diagnoses of and assessing a variety of peripheral vestibular disorders, including superior canal dehiscence (SCD), M´ eni` ere’s disease, vestibular neuritis, vestibular schwannomas and vestibular failure. SY3.3 Clinical Application of Vestibular Evoked Myogenic Potential in Central Vestibular Disorders Ji Soo Kim * Dept. of Neurology, College of Medicine, Seoul National University, Seoul National University Bundang Hospital, Korea E-mail address: [email protected] Vestibular-evoked myogenic potential (VEMP) is generated via a rapidly conducting disynaptic pathway, originating in the saccule and proceeding along the vestibular afferent fibers to the vestibular nuclei, and then through rapidly conducting projections that synapse with sternocleidomastoid (SCM) nuclei. In primates, the saccular projections reach the superior and inferior vestibular nuclei, and proceed bilaterally to the spinal cord. In cats, the sacculocollic reflex shows a bilaterally symmetrical innervation pattern with excitatory connections to both neck extensor motoneuron pools and inhibitory connections to both neck flexor motoneuron pools. The sacculocollic inhibitory signal may travel down from the inferior vestibular nucleus mostly along the medial vestibulospinal tract to the ipsilateral SCM muscle, since the medial vestibulospinal tract (VST) contains inhibitory fibers while the lateral VST is excitatory. The medial VST originates in the medial, inferior, and lateral nuclei, and descends in the medial longitudinal fasciculus (MLF) bilaterally while the lateral vestibulospinal tract originates in the lateral nucleus and descends in the ipsilateral ventral funiculus of the spinal
Invited Speakers: Symposia cord. However, the characteristics and the diagnostic values of VEMP have rarely been studied in central vestibulopathies. In patients with Wallenberg syndrome, lateral medullary lesion may affect VEMP by damaging the vestibular fascicles, the vestibular nuclei, or descending fibers from the vestibular nuclei to the neck muscles. VEMP may be also abnormal in patients with medial medullary infarction (MMI) by interrupting descending fibers in MLF. In our study, 6 of the 10 patients with MMI showed absence (n = 2) or decreased amplitude (n = 3) of the ipsilesional VEMP, and the remaining one exhibited delayed p13/n23 latencies. In patients with abnormal VEMP, the lesions extended to the dorsal tegmentum while those with normal VEMP showed restricted anteromedial lesions involving the pyramids. The cerebellum harbors the nodulus and ventral uvula that receive heavy projections from both primary and secondary vestibular afferents and inhibit the vestibular system. However, VEMP is mostly normal in patients with cerebellar lesions. Absence or delayed formation of VEMP has also been reported in patients with multiple sclerosis, even in those with normal MRI. VEMP is a valuable tool to investigate otolithic dysfunction in central as well as peripheral vestibular disorders. Scrutinized evaluation of VEMP in patients with circumscribed central lesions may extend our understandings of the central vestibular pathways subserving the saccular function. Reference(s) Chen CH, Young YH. Vestibular evoked myogenic potentials in brainstem stroke. Laryngoscope 2003; 113: 990 993. Colebatch JG, Halmagyi GM. Vestibular evoked potentials in human neck muscles before and after unilateral vestibular deafferentation. Neurology 1992; 42: 1635 1636. Kushiro K, Zakir M, Ogawa Y, Sato H, Uchino Y. Saccular and utricular inputs to sternocleidomastoid motoneurons of decerebrate cats. Exp Brain Res 1999;126:410 416. Newlands SD, Vrabec JT, Purcell IM, Stewart CM, Zimmerman BE, Perachio AA. Central projections of the saccular and utricular nerves in macaques. J Comp Neurol 2003; 466: 31 47. Pollak L, Kushnir M, Stryjer R. Diagnostic value of vestibular evoked myogenic potential in cerebellar and lower-brainstem strokes. Neurophysiol Clin 2006;36:227 233. Versino M, Colnaghi S, Callieco R, Bergamaschi R, Romani A, Cosi V. Vestibular evoked myogenic potentials in multiple sclerosis patients. Clin Neurophysiol 2002;113:1464 1469. Welgampola MS, Colebatch JG. Characteristics and clinical applications of vestibular-evoked myogenic potentials. Neurology 2005; 64: 1682 1688. Symposium 4. Clinical Evaluation and Management of Spasticity SY4.1 Pathophysiology and Measurement of Spasticity Lawrence K.S. Wong * Chinese University of Hong Kong, Hong Kong E-mail address: [email protected] Spasticity has been defined as an increase in muscle tone due to hyperexcitability of the stretch reflex. It is characterized by a velocitydependent increase in tonic stretch reflexes. Spasticity is usually accompanied by other signs of upper motor neuron signs such as weakness and hyperreflexia. The pathophysiologic basis of spasticity is not completely clear. Imbalance of the descending excitatory and inhibitory control may play an essential role. There are many measurement of spasticity available, some are for clinical use and some for research use. H-reflex, Ashworth scale, Wartenburg pendulum, hand-held dynamometer and various disability scales all have their strength and weakness. More recent development of new methods will also be discussed. SY4.2 Comprehensive Management of Spasticity Moon Suk Bang * Dept. of Rehabilitation Medicine, Seoul National University College of Medicine, Korea E-mail address: [email protected] Widely accepted definition of spasticity is “a motor disorder characterized by a velocity dependent increase in tonic stretch reflexes (muscle
Invited Speakers: Symposia cord. However, the characteristics and the diagnostic values of VEMP have rarely been studied in central vestibulopathies. In patients with Wallenberg syndrome, lateral medullary lesion may affect VEMP by damaging the vestibular fascicles, the vestibular nuclei, or descending fibers from the vestibular nuclei to the neck muscles. VEMP may be also abnormal in patients with medial medullary infarction (MMI) by interrupting descending fibers in MLF. In our study, 6 of the 10 patients with MMI showed absence (n = 2) or decreased amplitude (n = 3) of the ipsilesional VEMP, and the remaining one exhibited delayed p13/n23 latencies. In patients with abnormal VEMP, the lesions extended to the dorsal tegmentum while those with normal VEMP showed restricted anteromedial lesions involving the pyramids. The cerebellum harbors the nodulus and ventral uvula that receive heavy projections from both primary and secondary vestibular afferents and inhibit the vestibular system. However, VEMP is mostly normal in patients with cerebellar lesions. Absence or delayed formation of VEMP has also been reported in patients with multiple sclerosis, even in those with normal MRI. VEMP is a valuable tool to investigate otolithic dysfunction in central as well as peripheral vestibular disorders. Scrutinized evaluation of VEMP in patients with circumscribed central lesions may extend our understandings of the central vestibular pathways subserving the saccular function. Reference(s) Chen CH, Young YH. Vestibular evoked myogenic potentials in brainstem stroke. Laryngoscope 2003; 113: 990 993. Colebatch JG, Halmagyi GM. Vestibular evoked potentials in human neck muscles before and after unilateral vestibular deafferentation. Neurology 1992; 42: 1635 1636. Kushiro K, Zakir M, Ogawa Y, Sato H, Uchino Y. Saccular and utricular inputs to sternocleidomastoid motoneurons of decerebrate cats. Exp Brain Res 1999;126:410 416. Newlands SD, Vrabec JT, Purcell IM, Stewart CM, Zimmerman BE, Perachio AA. Central projections of the saccular and utricular nerves in macaques. J Comp Neurol 2003; 466: 31 47. Pollak L, Kushnir M, Stryjer R. Diagnostic value of vestibular evoked myogenic potential in cerebellar and lower-brainstem strokes. Neurophysiol Clin 2006;36:227 233. Versino M, Colnaghi S, Callieco R, Bergamaschi R, Romani A, Cosi V. Vestibular evoked myogenic potentials in multiple sclerosis patients. Clin Neurophysiol 2002;113:1464 1469. Welgampola MS, Colebatch JG. Characteristics and clinical applications of vestibular-evoked myogenic potentials. Neurology 2005; 64: 1682 1688. Symposium 4. Clinical Evaluation and Management of Spasticity SY4.1 Pathophysiology and Measurement of Spasticity Lawrence K.S. Wong * Chinese University of Hong Kong, Hong Kong E-mail address: [email protected] Spasticity has been defined as an increase in muscle tone due to hyperexcitability of the stretch reflex. It is characterized by a velocitydependent increase in tonic stretch reflexes. Spasticity is usually accompanied by other signs of upper motor neuron signs such as weakness and hyperreflexia. The pathophysiologic basis of spasticity is not completely clear. Imbalance of the descending excitatory and inhibitory control may play an essential role. There are many measurement of spasticity available, some are for clinical use and some for research use. H-reflex, Ashworth scale, Wartenburg pendulum, hand-held dynamometer and various disability scales all have their strength and weakness. More recent development of new methods will also be discussed. SY4.2 Comprehensive Management of Spasticity Moon Suk Bang * Dept. of Rehabilitation Medicine, Seoul National University College of Medicine, Korea E-mail address: [email protected] Widely accepted definition of spasticity is “a motor disorder characterized by a velocity dependent increase in tonic stretch reflexes (muscle