- Email: [email protected]
11. Microelectrode recordings in the framework of neuromodulation
e112
Society Proceedings / Clinical Neurophysiology 123 (2012) e101–e114
T2 (NT2) lesions and CEL at months 3, 6, 9 and 12 vs baseline (BL). Analyses are based on the intention to treat population. Results: Nineteen patients were included (NAT n = 10; IFNB-1b n = 9) having comparable baseline characteristics. Time to first on study relapse showed a trend favouring NAT without reaching significance (p = 0.125, log-rank test). Among secondary clinical and radiological outcomes, the majority showed a trend favouring NAT without reaching significance except for number of NT2 lesions at month 6 being significantly higher in the IFNB-1b group (p = 0.043, U-Mann Whitney). Adverse events were within the expected range. Conclusions: Our results suggest no pronounced inflammatory activity after de-escalation of NAT to IFNB-1b and indicate that the concept should be evaluated further.
rendered the highest sensitivity (80%) and, principally, specificity rate (88%), followed by MRI (71.4% and 50%), PET (62.9% and 37.5%) and SPECT (54.3% but a higher specificity as compared to MRI and PET of 62.5%). The sensitivity of ESI was high in both temporal and extratemporal lobe epilepsy (91% and 75%, resp). The chance to become seizure-free if the focus source maximum is resected is 97%. Conclusion: From a clinical point of view, ESI is a very attractive non-invasive technique with a high localization yield which provides superior temporal resolution in the millisecond range, as compared to methods based on changes in metabolic or vascular correlates of neural activity. From a practical perspective, this type of examination does not require sedation, it can be performed at patient’s bedside and it is suitable in the pediatric population and cognitively impaired patients. doi:10.1016/j.clinph.2012.03.073
Disclosures C. Zecca has received personal compensation from Teva, Merck Serono, Biogen Idec, Bayer Schering, Novartis. D. Meier has nothing to disclose. U. Candrian has nothing to disclose. F. Cotton has nothing to disclose. C.R.G. Gutmann has received personal compensation from Tibotec/Johnson and Johnson and was the recipient of a research grant from Teva Neuroscience. M. Sintzel or her agency has received consulting fees and/or honoraria from Bayer HealthCare Pharmaceuticals, Fresenius Medical Care, UCB, Ospedale Regionale di Lugano and ETH Zurich. C. Gobbi has received personal compensation from Teva, Merck Serono, Biogen Idec, Bayer Schering, Novartis. doi:10.1016/j.clinph.2012.03.072
9. Clinical yield of electric source imaging in epilepsy—Agustina M. Lascano a, Verena Brodbeck a, Laurent Spinelli a, Michael Wissmeier b, Maria Isabel Vargas b, Serge Vulliemoz a, Claudio Pollo c, Karl Schaller d, Christoph M. Michel e, Margitta Seeck a (a Epilepsy Unit, Neurology Clinic, University Hospital and University of Geneva, Switzerland, b Department of Radiology, University Hospital of Geneva, Geneva, Switzerland, c Department of Neurosurgery, University Hospital (CHUV), Lausanne, Switzerland, d Department of Neurosurgery, University Hospital of Geneva, Geneva, Switzerland, e Functional Brain Mapping Laboratory, Neurology Clinic and Department of Fundamental Neuroscience, University Hospital and University Medical Centre, University of Geneva, Switzerland) Objective: In patients with drug-resistant epilepsy who are candidate for surgery, non-invasive functional imaging methods are helpful in guiding surgical resections. Our main aim was to determine localisation precision of the epileptogenic focus with electric source imaging (ESI) and to compare it to other well-established imaging tools. Methods: One hundred fifty-two pharmaco-resistant epileptic patients with more than 1 year post-operative follow-up were included. Sensitivity (defined as % of seizure free patients with focus localization within the resected zone) and specificity (defined as % of patients with focus localization outside the operated area) of different techniques was assessed: ESI, magnetic resonance imaging (MRI), positron emission tomography (PET) and single-photon emission-computed tomography (SPECT). Results: A total of 43 patients underwent all examinations. Highresolution ESI (>64 electrodes) using individual MRI as a head model
10. In vivo cortical spreading depression in epilepsy patients is not limited to clinically significant trauma—S. Biethahn a, A. Brandt b, A. Schulze-Bonhage b (a Kantonsspital Aarau, Aarau, Switzerland, b Universitätsklinikum, Freiburg, Germany) Introduction: Cortical spreading depression (CSD) – initially considered a correlate for migraine auras – has also been related to other neurologic diseases in vitro. In vivo it has been shown in stroke and trauma patients and was considered to be a sign of poor outcome (Strong, 2002; Fabricius 2006; Dreier et al., 2012). The aim of our study was to investigate CSD in epilepsy patients undergoing invasive presurgical video-EEG-monitoring, allowing to collect CSDdata in patients without severe brain damage. Methods: Data of 18 patients with pharmacoresistant epilepsy undergoing invasive video-EEG-monitoring with 44 up to 106 subdural electrodes and with a high pass filter of 0,02 Hz filter settings were evaluated. CSD was defined as a slow wave in the range of 1– 5 mm/min with suppression of the normal EEG-activity. Data were related to the extent of periprocedural hemorrhage, the origin and number of seizures and histopathologic findings. Results: In 7/18 patients we could detect CSD. Two of them developed a clinically symptomatic subdural hematoma (SDH), paralleled by an increase of CSD-frequency; in 4/7 subclinical hemorrhage or minor lesions could be demonstrated on MRI, while one patient showed no abnormality on MRI. In comparison, minor hemorrhage was documented in 5/11 patients without CSD. There was no obvious spatial or temporal relation of CSD to seizure onset. The main histopathological finding both in patients with and without CSD was focal cortical dysplasia. Conclusion: Our data show CSD for the first time in vivo in patients without major brain trauma in patients with epilepsy. The main finding was that CSD is not limited to major brain damage but might also appear after mild trauma without clinical relevance or even without detectable trauma. Out data did not show a temporal or spatial correlation of CSD to seizure onset or histopathological findings. However, larger numbers and a longer follow-up are necessary to draw conclusions about the clinical relevance of CSD in epilepsy patients. doi:10.1016/j.clinph.2012.03.074
11. Microelectrode recordings in the framework of neuromodulation—R. Tyrand, S. Momjian, A. Bartoli, B. Jenny, K. Schaller, P. Pollak, M. Seeck, C. Boëx (HUG, Geneva, Switzerland)
Society Proceedings / Clinical Neurophysiology 123 (2012) e101–e114
Introduction: Microelectrode recordings (MER) in humans offer a fascinating modality to study neuropathophysiology and neurosciences. While MER is conducted during surgeries for deep brain stimulation (DBS) in patients with movement disorders, our principal goal was here to exploit MER to optimize and better understand effects of cerebral electrical stimulation. In this framework, we established a platform to record and analyse MER in humans, not only in patients with movement disorders but also in patients with epilepsy. We present here the evaluation of different electrodes and first analyses of MER, recorded simultaneously or not to DBS. Methods: Different types of microelectrodes (lE) have been evaluated for cortical or depth recordings in 8 patients. Fast ripples were automatically detected by online algorithm. Neuronal spikes are extracted from multi-unit recordings with homemade software, for clustering and auto-correlation. Multi-unit activities were recorded simultaneously to 1 Hz stimulation in patients with epilepsy (biphasic pulses, 450 ls or 60 ls/ph, 500 lA for macrostimulation; 25 lA and 60 ls/ph for microstimulation, 3 minute). Results: Eight patients with epilepsy participated in the study (3 subdural, 7 depth electrodes). The MER of the 3 patients with cortical lE and two patients with lE on depth electrodes (Ad-TechÒ) did not show any spikes, probably because of unsuitable length of contacts. In 5/7 patients with lE at the distal end of depth electrodes, spikes could be recorded for 4–10 days. Different pattern recorded from the hippocampus or from cortical dysplasia were compared to those recorded in the subthalamic nucleus or to the substantia nigra. High frequency oscillations (up to 700 Hz) were detected at the epileptic focus in 2 patients. Preliminary MER recorded during 1 Hz macrostimulation did not show increase of firing in all 5 patients who participated to DBS, while microstimulation (1 Hz), conducted in one patient with cortical dysplasia, induced significant increase in spike firings (p < 0.03). Conclusions: A platform to record lE is now established, offering MER in patients with epilepsy, in addition to patients with movement disorders undergoing DBS surgery. For the first time in humans, we showed that the microstimulation showed an excitatory effect at 1 Hz stimulation. Microstimulation appears here as valuable complementary tool to better understand the effects of DBS. doi:10.1016/j.clinph.2012.03.075
12. Diagnostic value of contact heat evoked potentials in spinal cord disorders—A. Ulrich, J. Haefeli, J. Blum, A. Curt (Balgrist University Hospital, Spinal Cord Injury Centre, Zürich, Switzerland) Introduction: The segmental electrophysiological assessment of sensory pathways in spinal cord disorders (SCD) with dermatomal somatosensory (dSSEPs) and contact heat evoked potentials (dCHEPs) has gained increasing interest over the recent years. DSSEPs are a reliable and sensitive method to track dorsal column pathways from single dermatomes. However, in distinct lesion patterns, like the central or anterior cord syndrome, the dorsal column remains intact. DCHEPs potentially provide significant diagnostic information about the integrity of central and ventral (i.e. spinothalamic) pathways which are frequently involved in incomplete SCD. The objective of this study was to evaluate the diagnostic value of dCHEPs compared to dSSEPs in the assessment of SCD. Methods: In a retrospective cohort study dCHEPs and dSSEPs were analysed in patients with SCD of varying degrees (i.e. neurological completeness) and causes (i.e. traumatic and non-traumatic). Myelopathy was evident in spinal MRI of all subjects included. Spinal cord damage was distinguished into three categories according to clinical completeness and MRI pattern: (a) complete, (b) incom-
e113
plete-diffuse and (c) central or anterior cord damage. CHEPs and SSEPs were applied at dermatomal key sensory points above, at and below the level of lesion according to MRI. Results: Seventy-five patients were included (complete n = 7, incomplete-diffuse n = 33, central/anterior cord damage n = 35). In total 319 dermatomes were tested with both dCHEPs and dSSEPs (57 dermatomes above, 262 at/below lesion level). In complete and incomplete-diffuse cord damage both dCHEPs and dSSEPs were comparably sensitive to detect segmental sensory impairment with a sensitivity of 100% for dCHEPs and 90.9% for dSSEPs in complete cord damage (p = 1.0, chi-square test) while slightly reduced in incomplete-diffuse cord damage (91.7% for dCHEPs and 86.1% for dSSEPs, p = 0.71). In central/anterior cord damage dCHEPs showed a significantly higher sensitivity compared to dSSEPs (94.3% compared to 25.7%, p < 0.001) and compared to clinical pinprick testing (68.75%, p < 0.001). Conclusions: The assessment of spinothalamic pathways with dCHEPs is of high sensitivity in SCD. In central and anterior cord damage dCHEPs are significantly distinct from dSSEPs. DCHEPs complement the clinical and conventional electrophysiological assessment in SCD and allow objectifying the affection of nociceptive pathways that might be missed or underestimated by clinical means. doi:10.1016/j.clinph.2012.03.076
13. Displaying the motor components of the MSFC as an interval score on a iPhone app with SAGAS 20/10—C. Vaney a, S. Vaney a, M. Zeiter a, S. Bayard a, C. Kuonen a, S. Rapillard b, T. Rapillard b (a Berner Klinik Montana, Crans Montana, Switzerland, b STR ing S + T Rapillard, Vétroz, Switzerland) Background: The restrictive emphasis on ambulation and the limited sensitivity to changes figure among the shortcomings of the Expanded Disability Status Scale (EDSS). The MS Functional Composite (MSFC) proposed as an alternative, does not assess the hands separately, depends on the stratification of a reference population and the clinical significance of the Z-score change is poorly defined. Objectives: Hence the need for an assessment tool based on the motor components of the MSFC that would consider hand function separately and that could be expressed using a clearly defined, clinically relevant interval scoring system. Methods: The Short and Graphic Ability Score (SaGAS 20/10) is composed by 3 measures: the 25 feet timed walk at fast speed (T25FW) and the nine-hole peg test (9-HPT) of each hand separately. The timed performances (t) of these 3 measures expressed as a logarithmic function of time in three (sS) subscores that are constructed in such a way that any interval of 1.0 unit corresponds to a change of 20%, considered as clinically meaningful. (T25FWsS) T25FW subscore = 20–11.474 x log (4/t); a walking time of 4 s corresponding to a maximum T25FWsS of 20. (9HPTsS) 9HPT subscore = 10– 11.474 x log (20/t); a 9HPT of 20 s corresponding to a maximum NHPTsS of 10. The SaGAS 20/10 is computed: (T25FWsS + NHPTsS right hand + NHPTsS left hand)/2. The 3 subscores can be displayed graphically as a Vitruvian Man on an IPhone app. 148 consecutive patients (mean age 56.5; Mean EDSS 6.1 ± 1.1) with definitive MS were assessed at the beginning and at the end of their rehabilitation stay. Results: The SaGAS 20/10 at admission in our population was 11.6 (±2.5). Range 0.0–19.4. The correlation coefficients between SaGAS 20/10 and the EDSS (r = 0.62) and the Rivermead Mobility Index (r = 0.82) were all statistically significant (p < 0.001). The SaGAS 20/10 was more sensitive than the EDSS for the clinically relevant changes (>1 point on SaGAS 20/10) occurring during the rehabilitation stay (32.3% vs. 8.1%; p < 0.001).
Society Proceedings / Clinical Neurophysiology 123 (2012) e101–e114
T2 (NT2) lesions and CEL at months 3, 6, 9 and 12 vs baseline (BL). Analyses are based on the intention to treat population. Results: Nineteen patients were included (NAT n = 10; IFNB-1b n = 9) having comparable baseline characteristics. Time to first on study relapse showed a trend favouring NAT without reaching significance (p = 0.125, log-rank test). Among secondary clinical and radiological outcomes, the majority showed a trend favouring NAT without reaching significance except for number of NT2 lesions at month 6 being significantly higher in the IFNB-1b group (p = 0.043, U-Mann Whitney). Adverse events were within the expected range. Conclusions: Our results suggest no pronounced inflammatory activity after de-escalation of NAT to IFNB-1b and indicate that the concept should be evaluated further.
rendered the highest sensitivity (80%) and, principally, specificity rate (88%), followed by MRI (71.4% and 50%), PET (62.9% and 37.5%) and SPECT (54.3% but a higher specificity as compared to MRI and PET of 62.5%). The sensitivity of ESI was high in both temporal and extratemporal lobe epilepsy (91% and 75%, resp). The chance to become seizure-free if the focus source maximum is resected is 97%. Conclusion: From a clinical point of view, ESI is a very attractive non-invasive technique with a high localization yield which provides superior temporal resolution in the millisecond range, as compared to methods based on changes in metabolic or vascular correlates of neural activity. From a practical perspective, this type of examination does not require sedation, it can be performed at patient’s bedside and it is suitable in the pediatric population and cognitively impaired patients. doi:10.1016/j.clinph.2012.03.073
Disclosures C. Zecca has received personal compensation from Teva, Merck Serono, Biogen Idec, Bayer Schering, Novartis. D. Meier has nothing to disclose. U. Candrian has nothing to disclose. F. Cotton has nothing to disclose. C.R.G. Gutmann has received personal compensation from Tibotec/Johnson and Johnson and was the recipient of a research grant from Teva Neuroscience. M. Sintzel or her agency has received consulting fees and/or honoraria from Bayer HealthCare Pharmaceuticals, Fresenius Medical Care, UCB, Ospedale Regionale di Lugano and ETH Zurich. C. Gobbi has received personal compensation from Teva, Merck Serono, Biogen Idec, Bayer Schering, Novartis. doi:10.1016/j.clinph.2012.03.072
9. Clinical yield of electric source imaging in epilepsy—Agustina M. Lascano a, Verena Brodbeck a, Laurent Spinelli a, Michael Wissmeier b, Maria Isabel Vargas b, Serge Vulliemoz a, Claudio Pollo c, Karl Schaller d, Christoph M. Michel e, Margitta Seeck a (a Epilepsy Unit, Neurology Clinic, University Hospital and University of Geneva, Switzerland, b Department of Radiology, University Hospital of Geneva, Geneva, Switzerland, c Department of Neurosurgery, University Hospital (CHUV), Lausanne, Switzerland, d Department of Neurosurgery, University Hospital of Geneva, Geneva, Switzerland, e Functional Brain Mapping Laboratory, Neurology Clinic and Department of Fundamental Neuroscience, University Hospital and University Medical Centre, University of Geneva, Switzerland) Objective: In patients with drug-resistant epilepsy who are candidate for surgery, non-invasive functional imaging methods are helpful in guiding surgical resections. Our main aim was to determine localisation precision of the epileptogenic focus with electric source imaging (ESI) and to compare it to other well-established imaging tools. Methods: One hundred fifty-two pharmaco-resistant epileptic patients with more than 1 year post-operative follow-up were included. Sensitivity (defined as % of seizure free patients with focus localization within the resected zone) and specificity (defined as % of patients with focus localization outside the operated area) of different techniques was assessed: ESI, magnetic resonance imaging (MRI), positron emission tomography (PET) and single-photon emission-computed tomography (SPECT). Results: A total of 43 patients underwent all examinations. Highresolution ESI (>64 electrodes) using individual MRI as a head model
10. In vivo cortical spreading depression in epilepsy patients is not limited to clinically significant trauma—S. Biethahn a, A. Brandt b, A. Schulze-Bonhage b (a Kantonsspital Aarau, Aarau, Switzerland, b Universitätsklinikum, Freiburg, Germany) Introduction: Cortical spreading depression (CSD) – initially considered a correlate for migraine auras – has also been related to other neurologic diseases in vitro. In vivo it has been shown in stroke and trauma patients and was considered to be a sign of poor outcome (Strong, 2002; Fabricius 2006; Dreier et al., 2012). The aim of our study was to investigate CSD in epilepsy patients undergoing invasive presurgical video-EEG-monitoring, allowing to collect CSDdata in patients without severe brain damage. Methods: Data of 18 patients with pharmacoresistant epilepsy undergoing invasive video-EEG-monitoring with 44 up to 106 subdural electrodes and with a high pass filter of 0,02 Hz filter settings were evaluated. CSD was defined as a slow wave in the range of 1– 5 mm/min with suppression of the normal EEG-activity. Data were related to the extent of periprocedural hemorrhage, the origin and number of seizures and histopathologic findings. Results: In 7/18 patients we could detect CSD. Two of them developed a clinically symptomatic subdural hematoma (SDH), paralleled by an increase of CSD-frequency; in 4/7 subclinical hemorrhage or minor lesions could be demonstrated on MRI, while one patient showed no abnormality on MRI. In comparison, minor hemorrhage was documented in 5/11 patients without CSD. There was no obvious spatial or temporal relation of CSD to seizure onset. The main histopathological finding both in patients with and without CSD was focal cortical dysplasia. Conclusion: Our data show CSD for the first time in vivo in patients without major brain trauma in patients with epilepsy. The main finding was that CSD is not limited to major brain damage but might also appear after mild trauma without clinical relevance or even without detectable trauma. Out data did not show a temporal or spatial correlation of CSD to seizure onset or histopathological findings. However, larger numbers and a longer follow-up are necessary to draw conclusions about the clinical relevance of CSD in epilepsy patients. doi:10.1016/j.clinph.2012.03.074
11. Microelectrode recordings in the framework of neuromodulation—R. Tyrand, S. Momjian, A. Bartoli, B. Jenny, K. Schaller, P. Pollak, M. Seeck, C. Boëx (HUG, Geneva, Switzerland)
Society Proceedings / Clinical Neurophysiology 123 (2012) e101–e114
Introduction: Microelectrode recordings (MER) in humans offer a fascinating modality to study neuropathophysiology and neurosciences. While MER is conducted during surgeries for deep brain stimulation (DBS) in patients with movement disorders, our principal goal was here to exploit MER to optimize and better understand effects of cerebral electrical stimulation. In this framework, we established a platform to record and analyse MER in humans, not only in patients with movement disorders but also in patients with epilepsy. We present here the evaluation of different electrodes and first analyses of MER, recorded simultaneously or not to DBS. Methods: Different types of microelectrodes (lE) have been evaluated for cortical or depth recordings in 8 patients. Fast ripples were automatically detected by online algorithm. Neuronal spikes are extracted from multi-unit recordings with homemade software, for clustering and auto-correlation. Multi-unit activities were recorded simultaneously to 1 Hz stimulation in patients with epilepsy (biphasic pulses, 450 ls or 60 ls/ph, 500 lA for macrostimulation; 25 lA and 60 ls/ph for microstimulation, 3 minute). Results: Eight patients with epilepsy participated in the study (3 subdural, 7 depth electrodes). The MER of the 3 patients with cortical lE and two patients with lE on depth electrodes (Ad-TechÒ) did not show any spikes, probably because of unsuitable length of contacts. In 5/7 patients with lE at the distal end of depth electrodes, spikes could be recorded for 4–10 days. Different pattern recorded from the hippocampus or from cortical dysplasia were compared to those recorded in the subthalamic nucleus or to the substantia nigra. High frequency oscillations (up to 700 Hz) were detected at the epileptic focus in 2 patients. Preliminary MER recorded during 1 Hz macrostimulation did not show increase of firing in all 5 patients who participated to DBS, while microstimulation (1 Hz), conducted in one patient with cortical dysplasia, induced significant increase in spike firings (p < 0.03). Conclusions: A platform to record lE is now established, offering MER in patients with epilepsy, in addition to patients with movement disorders undergoing DBS surgery. For the first time in humans, we showed that the microstimulation showed an excitatory effect at 1 Hz stimulation. Microstimulation appears here as valuable complementary tool to better understand the effects of DBS. doi:10.1016/j.clinph.2012.03.075
12. Diagnostic value of contact heat evoked potentials in spinal cord disorders—A. Ulrich, J. Haefeli, J. Blum, A. Curt (Balgrist University Hospital, Spinal Cord Injury Centre, Zürich, Switzerland) Introduction: The segmental electrophysiological assessment of sensory pathways in spinal cord disorders (SCD) with dermatomal somatosensory (dSSEPs) and contact heat evoked potentials (dCHEPs) has gained increasing interest over the recent years. DSSEPs are a reliable and sensitive method to track dorsal column pathways from single dermatomes. However, in distinct lesion patterns, like the central or anterior cord syndrome, the dorsal column remains intact. DCHEPs potentially provide significant diagnostic information about the integrity of central and ventral (i.e. spinothalamic) pathways which are frequently involved in incomplete SCD. The objective of this study was to evaluate the diagnostic value of dCHEPs compared to dSSEPs in the assessment of SCD. Methods: In a retrospective cohort study dCHEPs and dSSEPs were analysed in patients with SCD of varying degrees (i.e. neurological completeness) and causes (i.e. traumatic and non-traumatic). Myelopathy was evident in spinal MRI of all subjects included. Spinal cord damage was distinguished into three categories according to clinical completeness and MRI pattern: (a) complete, (b) incom-
e113
plete-diffuse and (c) central or anterior cord damage. CHEPs and SSEPs were applied at dermatomal key sensory points above, at and below the level of lesion according to MRI. Results: Seventy-five patients were included (complete n = 7, incomplete-diffuse n = 33, central/anterior cord damage n = 35). In total 319 dermatomes were tested with both dCHEPs and dSSEPs (57 dermatomes above, 262 at/below lesion level). In complete and incomplete-diffuse cord damage both dCHEPs and dSSEPs were comparably sensitive to detect segmental sensory impairment with a sensitivity of 100% for dCHEPs and 90.9% for dSSEPs in complete cord damage (p = 1.0, chi-square test) while slightly reduced in incomplete-diffuse cord damage (91.7% for dCHEPs and 86.1% for dSSEPs, p = 0.71). In central/anterior cord damage dCHEPs showed a significantly higher sensitivity compared to dSSEPs (94.3% compared to 25.7%, p < 0.001) and compared to clinical pinprick testing (68.75%, p < 0.001). Conclusions: The assessment of spinothalamic pathways with dCHEPs is of high sensitivity in SCD. In central and anterior cord damage dCHEPs are significantly distinct from dSSEPs. DCHEPs complement the clinical and conventional electrophysiological assessment in SCD and allow objectifying the affection of nociceptive pathways that might be missed or underestimated by clinical means. doi:10.1016/j.clinph.2012.03.076
13. Displaying the motor components of the MSFC as an interval score on a iPhone app with SAGAS 20/10—C. Vaney a, S. Vaney a, M. Zeiter a, S. Bayard a, C. Kuonen a, S. Rapillard b, T. Rapillard b (a Berner Klinik Montana, Crans Montana, Switzerland, b STR ing S + T Rapillard, Vétroz, Switzerland) Background: The restrictive emphasis on ambulation and the limited sensitivity to changes figure among the shortcomings of the Expanded Disability Status Scale (EDSS). The MS Functional Composite (MSFC) proposed as an alternative, does not assess the hands separately, depends on the stratification of a reference population and the clinical significance of the Z-score change is poorly defined. Objectives: Hence the need for an assessment tool based on the motor components of the MSFC that would consider hand function separately and that could be expressed using a clearly defined, clinically relevant interval scoring system. Methods: The Short and Graphic Ability Score (SaGAS 20/10) is composed by 3 measures: the 25 feet timed walk at fast speed (T25FW) and the nine-hole peg test (9-HPT) of each hand separately. The timed performances (t) of these 3 measures expressed as a logarithmic function of time in three (sS) subscores that are constructed in such a way that any interval of 1.0 unit corresponds to a change of 20%, considered as clinically meaningful. (T25FWsS) T25FW subscore = 20–11.474 x log (4/t); a walking time of 4 s corresponding to a maximum T25FWsS of 20. (9HPTsS) 9HPT subscore = 10– 11.474 x log (20/t); a 9HPT of 20 s corresponding to a maximum NHPTsS of 10. The SaGAS 20/10 is computed: (T25FWsS + NHPTsS right hand + NHPTsS left hand)/2. The 3 subscores can be displayed graphically as a Vitruvian Man on an IPhone app. 148 consecutive patients (mean age 56.5; Mean EDSS 6.1 ± 1.1) with definitive MS were assessed at the beginning and at the end of their rehabilitation stay. Results: The SaGAS 20/10 at admission in our population was 11.6 (±2.5). Range 0.0–19.4. The correlation coefficients between SaGAS 20/10 and the EDSS (r = 0.62) and the Rivermead Mobility Index (r = 0.82) were all statistically significant (p < 0.001). The SaGAS 20/10 was more sensitive than the EDSS for the clinically relevant changes (>1 point on SaGAS 20/10) occurring during the rehabilitation stay (32.3% vs. 8.1%; p < 0.001).