Finanzierung Unterstützung der Motor Neuron Disease Research Institute of Australia (MNDRIA), Sylvia und Charles Viertel Charitable Foundation Clinical Investigator Grant, Ramaciotti Foundation und National Health and Medical Research Council of Australia (Projektförderung Nummer APP1024915) wird dankbar anerkannt.

1. Patientenvorbereitung <ol><li> Rekrutieren Patienten prospektiv und konsekutiv. Hinweis: Das folgende Protokoll wird von den Sydney West Area Health Service Human Research Ethics Committees genehmigt. Einverständniserklärung wurde von allen Patienten zur Verfügung gestellt. Die Patienten wurden prospektiv und fortlaufend von der ALS / neuromuskuläre Klinik Westmead Krankenhaus rekrutiert. </li><li> Bestimmen die Eignung von ALS-Patienten für den Test. Patienten, die nicht mit ALS oder eine neuromuskuläre Erkrankung diagnostiziert werden, ausschließen. </li><li> Patienten mit einer koexistierenden fokalen Neuropathie, Median Neuropathie am Handgelenk oder am Ellenbogen ulnaren Neuropathie ausschließen. </li><li> Patienten mit einer generalisierten Neuropathie, wie diabetische Polyneuropathie auszuschließen. </li><li> Ausführlich untersucht und klinisch Follow-up-Patienten die Diagnose ALS oder neuromuskulären Erkrankungen imitieren bestätigen. </li><li> Stellen Sie sicher, dass die informierte Zustimmung wird von allen Patienten zur Verfügung gestellt, einschließlich ALS und neuromuskuläre Erkrankung, Mimik Patienten, für all die neurophysiologischen Verfahren. </li></ol> 2. Klinische Bewertung <ol><li> Bestimmen Sie die klinische Staging aller ALS-Patienten mit Hilfe der Amyotrophe Lateralsklerose Functional Rating Scale-Revised (ALS-FRS-R) 18 punkten. </li><li> Bestimmen Sie die Rate der Krankheitsprogression in allen ALS-Patienten nach der Formel bereits berichtet; (48-ALSFRS-R) / Dauer der Symptome) 19. </li><li> Bestimmen Sie die Muskelkraft bei allen Patienten mit Bewertung der Medical Research Council (MRC) Maßstab 20. Entwickeln Sie eine Gesamt MRC-Score, die obere Extremität (Schulter Entführung; Ellbogenflexion; Ellenbogenstreckung; Handgelenk Dorsalflexion, Finger Entführung; Daumen Entführung, Gesamtpunktzahl 60) und der unteren Extremitäten (Hüfte gebeugt, Knie gestreckt; Knöcheldorsalflexion, Gesamtpunktzahl 30) Muskelgruppen . Die Gesamt MRC-Score sollte 90 sein, wenn die Muskelkraft ist normal. </li><li> Bestimmen Sie den Ort der Krankheitsbeginn, definiert als bulbäre oder Leben, in allen ALSPatienten. </li></ol> 3. Neurophysiologische Bewertung <ol><li> Verpflichten motorischen Nervenleitungsstudien auf der von der Entführer aufgenommen Median und ulnaren Nerven mit der Verbindung Muskelaktionspotential (CMAP) Antworten pollicis brevis (APB), erste Rücken interossea (FDI) und Entführer stellige minimi (ADM) Muskeln. </li><li> Bereiten Sie die anregende Stellen am Handgelenk, durch die Reinigung der Hautoberfläche mit einem Schleifmittel-Gel auf den Hautwiderstand zu verringern, gefolgt von der Anwendung von einem Alkoholtupfer. Stellen Sie den Reizstrom zu 20% über der erforderlich ist, um eine maximale CMAP Antwort (supra Strom) erzeugen Intensität. </li><li> Stellen Sie sicher, dass die ausgewählte Stimulationsstelle weist die niedrigste Schwelle für Stimulation, so dass Volumen Leitung vermieden. </li><li> Bereiten Sie die Aufnahme vor Ort über jeden Muskel durch die Reinigung der Hautoberfläche mit einem Schleifmittel-Gel auf den Hautwiderstand zu verringern, gefolgt von der Anwendung von einem Alkoholtupfer. </li><li> Notieren Sie die Größe der Verbindung Motor aktiviertauf Potential (CMAP) von den APB, ADM, und ausländische Direktinvestitionen Muskeln. Antworten zu 10 mm Goldscheibenelektroden in einem Bauch Sehne Anordnung über jede Muskel positioniert aufgezeichnet werden. Insbesondere, positionieren Sie den aktiven Elektrode über dem Mittelpunkt der jeweiligen Muskel Sicherstellung einer negativen take-off der CMAP Antwort, während die Referenzelektrode über die Basis der Daumen (APB und FDI CMAP Aufnahmen) und die Basis der Ziffer 5 positioniert werden (ADM CMAP Aufnahmen). </li><li> Stellen Sie den Abstand zwischen Kathode und der stimulierenden Elektrode für aktive APB und ADM Motor Verbindung Aktionspotential Antworten auf 5 cm und der Abstand zu der FDI bei 8 cm. </li><li> Positionieren Sie die elektro neutral Erdplatte auf der dorsalen Aspekt der seits zwischen anregend und G1-Elektrode, mit leitfähigen Gel Artefakt zu reduzieren. Vor der Anwendung des neutralen Erde bereiten die Website durch die Reinigung der Hautoberfläche mit einem Schleifmittel-Gel auf den Hautwiderstand zu verringern, gefolgt von der Anwendung von einem Alkoholtupfer. </li><li>Sicherstellen, dass die Filtereinstellungen liegen zwischen 3 Hz (Niederfrequenz-Filter) und 10 kHz (Hochfrequenz-Filter). </li><li> Stellen Sie sicher, dass die Laufgeschwindigkeit auf 20 ms oder 2 ms / Teilung eingestellt. </li><li> Stellen Sie sicher, dass die Empfindlichkeit für die Aufnahme CMAP Antworten auf 5 mV eingestellt. </li><li> Überwachung der Temperatur am Ort der Stimulation während der Studie und zu gewährleisten, dass der Schenkel Temperatur wird auf 32 ° C gehalten wird </li></ol> 4. Analyse und Interpretation <ol><li> Messen Baseline-to-Peak-Amplituden CMAP (mV) über die APB, ausländischen Direktinvestitionen und ADM Muskeln bei ALS-Patienten und die neuromuskuläre Erkrankung Mimik Kontrollen. </li><li> Berechnen Sie die Split-Hand-Index (Abbildung 1) durch Multiplikation der CMAP Amplitude über den APB und FDI Muskeln aufgezeichnet, geteilt durch das Produkt CMAP Amplitude über die ADM Muskel aufgezeichnet, wie folgt: SI = APB CMAP * FDI CMAP _________________________ &amp; #160; ADM CMAP </li><li> Bestimmen Sie das Diagnoseprogramm des Split-Hand-Index durch den Vergleich der SI-Werte zwischen ALS-Patienten und neuromuskuläre Erkrankung, Mimik pathologische Kontrollen nach den Standards für die Berichterstattung über die diagnostische Genauigkeit (STARD) Kriterien. </li><li> Bestimmen Sie die optimale Diagnose Cutoff-Werte für die Split-Hand-Index mithilfe der receiver operating characteristic (ROC) Kurven. Ableiten ROC-Kurve durch Auftragen der Empfindlichkeit (y-Achse) und 1-Spezifität (x-Achse) für die SI-Werte von ALS und neuromuskuläre Erkrankung Patienten abgeleitet. </li></ol>

<ol>
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J. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=The+&#8220;split+hand+syndrome&#8220;.">The &#8220;split hand syndrome&#8220;.</a> Muscle Nerve. 23, 138 (2000).</li><li>Kuwabara, S., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Dissociated+small+hand+muscle+atrophy+in+amyotrophic+lateral+sclerosis:+frequency,+extent,+and+specificity.">Dissociated small hand muscle atrophy in amyotrophic lateral sclerosis: frequency, extent, and specificity.</a> Muscle Nerve. 37, 426-430 (2008).</li><li>Kuwabara, S., Mizobuchi, K., Ogawara, K., Hattori, T. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Dissociated+small+hand+muscle+involvement+in+amyotrophic+lateral+sclerosis+detected+by+motor+unit+number+estimates.">Dissociated small hand muscle involvement in amyotrophic lateral sclerosis detected by motor unit number estimates.</a> Muscle Nerve. 22, 870-873 (1999).</li><li>Menon, P., Kiernan, M. C., Vucic, S. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Appearance,+phenomenology+and+diagnostic+utility+of+the+split+hand+in+amyotrophic+lateral+sclerosis.">Appearance, phenomenology and diagnostic utility of the split hand in amyotrophic lateral sclerosis.</a> Neurodegener. Dis. Manag. 1, 457-462 (2011).</li><li>Brooks, B. R., Miller, R. G., Swash, M., Munsat, T. 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Neurophysiol. 119, 497-503 (2008).</li><li>de Carvalho, M., Swash, M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Awaji+diagnostic+algorithm+increases+sensitivity+of+El+Escorial+criteria+for+ALS+diagnosis.">Awaji diagnostic algorithm increases sensitivity of El Escorial criteria for ALS diagnosis.</a> Amyotroph Lateral Scler. 10, 53-57 (2009).</li><li>Boekestein, W. A., Kleine, B. U., Hageman, G., Schelhaas, H. J., Zwarts, M. 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Psychiatr. 81, 646-649 (2010).</li><li>Noto, Y. I., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Awaji+ALS+criteria+increase+the+diagnostic+sensitivity+in+patients+with+bulbar+onset.">Awaji ALS criteria increase the diagnostic sensitivity in patients with bulbar onset.</a> Clin. Neurophysiol. 123, 382-385 (2012).</li><li>Schrooten, M., Smetcoren, C., Robberecht, W., Van Damme, P. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Benefit+of+the+Awaji+diagnostic+algorithm+for+amyotrophic+lateral+sclerosis:+A+prospective+study.">Benefit of the Awaji diagnostic algorithm for amyotrophic lateral sclerosis: A prospective study.</a> Ann. 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Die Autoren haben nichts zu offenbaren.

Die vorliegende Studie berichtet über das Diagnoseprogramm des Split-Hand-Index in ALS, einer neuartigen neurophysiologischen diagnostischen Biomarker. Die SI zuverlässig unterschieden ALS von neuromuskulären Erkrankungen, mit einer optimalen Diagnose-Cut-off-Wert von 5,2. Die Verringerung der SI war in Gliedmaßen-onset ALS-Patienten prominentesten. Wichtig ist, dass ein wesentlicher Anteil der ALS-Patienten, die in der diagnostischen Kategorie &quot;möglich&quot; nach den kürzlich entwickelten Diagnosekriterien <...

Die geteilte Seite bezieht sich auf Vorzugs Atrophie der Daumenballen komplexe Gruppe von intrinsischen Handmuskeln [abductor pollicis brevis (APB) und erste Rücken interossea (FDI)], mit relativer Erhaltung der Kleinfingermuskulatur und ist eine spezifische und frühe klinische Merkmal der amyotrophen lateraler Sklerose (ALS) 1-4. Die Erkenntnis, dass die Split-Hand-Zeichen ist spezifisch für ALS, schlägt vor, eine mögliche Rolle für die Split-Hand-Zeichen als Biomarker in Diagnose ALS 3. Quantifizierung des geteilten Handzeichen, durch die Entwicklung eines neuartigen neurophysiologischen Biomarker können Beihilfen in ALS-Diagnose zu fördern. Insbesondere wird die Split-Hand-Index (SI), die die Split-Hand-Phänomen quantifiziert, indem die Verbindung Muskelaktionspotential (CMAP) abgeleitet Amplitude über die Handballen komplexe Muskeln (APB-und FDI) aufgezeichnet, geteilt durch das Produkt CMAP Amplitude über die hyp aufgezeichnetothenar Muskeln (nämlich die abductor digiti minimi, ADM) 5. Die Diagnose der ALS beruht weitgehend auf der Grundlage klinischer Kriterien umfasst eine Kombination von oberen und unteren motorischen Neurons 6 unterzeichnet. Diese Kriterien wurden jedoch vor allem im Sinne einer Diagnose von ALS in den frühen Stadien des Krankheitsprozesses 7-10 als unempfindlich. Eine aktuelle Änderung der Diagnosekriterien wurden entwickelt, 11, und obwohl diese Kriterien erscheinen, um die diagnostische Sensitivität zu erhöhen 12-16, scheint der Anstieg Empfindlichkeit bulbären ALS-Patienten-onset 15 beschränkt. In Abwesenheit einer Test pathognomonisches kann die Diagnose von ALS signifikant verzögert 8 werden. Letztlich kann die Institution der neuroprotektiven Therapien und Rekrutierung in klinischen Studien verzögert werden, vielleicht über den kritischen therapeutische Zeitfenster 9, 17. Folglich wird dieDiagnoseprogramm der SI wurde prospektiv in sporadischen ALS-Patienten beurteilt.

<table border="0" cellpadding="0" cellspacing="0">
	<colgroup>
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	<tbody>
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			<td height="20" style="height:20px;width:125px;"></td>
			<td style="width:120px;"></td>
			<td style="width:136px;"></td>
			<td style="width:203px;"></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;">Abrasive gel (Nu Prep)</td>
			<td>Weaver and Company</td>
			<td>N-TA\/P\H-3 ENG</td>
			<td>Skin preperation</td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td colspan="2">(www.doweaver.com)</td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td></td>
			<td></td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;">Alcohol wipe</td>
			<td>Triad Disposables</td>
			<td>103101</td>
			<td>Skin preperation</td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td colspan="2">(www.triad-group.net)</td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td></td>
			<td></td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;">Recording gel (Ten20 Conductive gel)</td>
			<td>Weaver and Company</td>
			<td>N-TA\/P\H-3 ENG</td>
			<td>Recording motor responses</td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td colspan="2">(www.doweaver.com)</td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td></td>
			<td></td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;">Amyotrophic lateral sclerosis rating scale-revised questionnaire</td>
			<td>Publication&#160;</td>
			<td>Experimental builder</td>
			<td>Stage disease</td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td colspan="2">(see Methods and References)</td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td></td>
			<td></td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;">Medical Research Council muscle strength scale</td>
			<td>Medical Research Council-UK</td>
			<td>Experimental builder</td>
			<td>Stage disease</td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td colspan="2">(see Methods and References)</td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td></td>
			<td></td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td></td>
			<td></td>
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			<td></td>
			<td></td>
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			<td colspan="2" height="20" style="height:20px;">Table of equipment used</td>
			<td></td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;">Name of the equipment used</td>
			<td>Company</td>
			<td>Catalog number</td>
			<td>Comments</td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td></td>
			<td></td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;">Nerve conduction machine (Synergy/Nicolet EDX)</td>
			<td>CareFusion (www.carefusion.com/medical-products/neurology)</td>
			<td>SA110106M</td>
			<td>To measure split hand index</td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td></td>
			<td></td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;">Synergy software</td>
			<td>CareFusion</td>
			<td>765654679</td>
			<td>To measure split hand index</td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td colspan="3">(www.carefusion.com/medical-products/neurology)</td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td></td>
			<td></td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;">Tem millimeter gold cup disc electrodes</td>
			<td>Grass Technologies</td>
			<td>F-E5GH-60</td>
			<td>To record motor responses</td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td colspan="2">(www.grasstechnologies.com)</td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td></td>
			<td></td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;">Neural earth plate</td>
			<td>Westmead Hospital</td>
			<td>Experimental builder</td>
			<td>To record limb temperature</td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;"></td>
			<td></td>
			<td></td>
			<td></td>
		</tr>
		<tr height="20">
			<td height="20" style="height:20px;">Thermometer</td>
			<td>Westmead Hospital</td>
			<td>Experimental builder</td>
			<td>To record limb temperature</td>
		</tr>
	</tbody>
</table>

utility of dissociated intrinsic hand muscle atrophy in the diagnosis of amyotrophic lateral sclerosis

Die Split-Hand-Phänomen bezieht sich auf vorherrschende Verschwendung von Thenarmuskeln und ist eine frühe und spezifische Merkmal der amyotrophen Lateralsklerose (ALS). Eine neuartige Split-Hand-Index (SI) wurde entwickelt, um die Split-Hand-Phänomen zu quantifizieren und ihre Diagnoseprogramm wurde bei ALS-Patienten beurteilt. Die Split-Hand-Index wurde berechnet, indem das Produkt der Verbindung Muskelaktionspotential (CMAP) abgeleitet Amplitude über die abductor pollicis brevis und erste Rückenmuskulatur durch die interossea CMAP Amplitude über die abductor digiti minimi Muskel aufgezeichnet. Um das Diagnoseprogramm des Split-Hand-Index zu ermitteln, wurden ALS-Patienten prospektiv untersucht und ihre Ergebnisse wurden auf neuromuskuläre Erkrankung Patienten verglichen. Die Split-Hand-Index wurde bei ALS deutlich reduziert im Vergleich zu neuromuskuläre Erkrankung Patienten (P &lt;0,0001). Limb-onset ALS-Patienten zeigte die größte Reduktion der Split-Hand-Index und Wertvon 5,2 oder weniger zuverlässig differenziert ALS aus anderen neuromuskulären Erkrankungen. Folglich erscheint die Split-Hand-Index, um eine neue diagnostische Biomarker für ALS, vielleicht erleichtert eine frühere Diagnose.

Klinische Phänotyp Insgesamt wurden 44 ALS-Patienten untersucht, von denen 76% (N = 33) wurden als definitive oder wahrscheinliche und 24% (N = 11) wie möglich ALS klassifiziert nach den Kriterien Awaji 11. Die Diagnose der ALS wurde in der &quot;möglichen&quot; Kohorte bestätigt nach umfangreichen Untersuchungen und klinische Follow-up von bis zu 3 Jahren und 53% in diesem Zeitraum starben. Bulbäre einsetzende Erkrankung zeigte sich in 41%, während die Gliedmaßen-Au...

Watch this Scientific Journal Video about Utility of Dissociated Intrinsic Hand Muscle Atrophy in the Diagnosis of Amyotrophic Lateral Sclerosis at JoVE.com

Utility of Dissociated Intrinsic Hand Muscle Atrophy in the Diagnosis of Amyotrophic Lateral Sclerosis

Dissoziierte Atrophie der intrinsischen Handmuskeln, der sogenannten Split-Hand, scheint eine Besonderheit der amyotrophen Lateralsklerose (ALS) sein. Folglich wurde eine neue neurodiagnostische Test, der sogenannten Split-Hand-Index wurde entwickelt, um die klinische Phänomen der geteilten Hand, die Mimik von ALS-Erkrankungen differenziert zu quantifizieren.

Nutzen der Dissoziierte Eigen Hand Muskelatrophie in der Diagnose von Amyotrophe Lateralsklerose

The split hand phenomenon refers to predominant wasting of thenar muscles and is an early and specific feature of amyotrophic lateral sclerosis (ALS). A ...

utility-dissociated-intrinsic-hand-muscle-atrophy-diagnosis

Research

JoVE Journal

Medicine

31.2K Aufrufe.  Westmead Hospital.  Dissoziierte Atrophie der intrinsischen Handmuskeln, der sogenannten Split-Hand, scheint eine Besonderheit der amyotrophen Lateralsklerose (ALS) sein. Folglich wurde eine neue neurodiagnostische Test, der sogenannten Split-Hand-Index wurde entwickelt, um die klinische Phänomen der geteilten Hand, die Mimik von ALS-Erkrankungen differenziert zu quantifizieren. 

Serie: Utility of Dissociated Intrinsic Hand Muscle Atrophy in the Diagnosis of Amyotrophic Lateral Sclerosis

A Protocol for Comprehensive Assessment of Bulbar Dysfunction in Amyotrophic Lateral Sclerosis (ALS)

Improved methods for assessing bulbar impairment are necessary for expediting diagnosis of bulbar dysfunction in ALS, for predicting disease progression across speech subsystems, and for addressing the critical need for sensitive outcome measures for ongoing experimental treatment trials. To address this need, we are obtaining longitudinal profiles of bulbar impairment in 100 individuals based on a comprehensive instrumentation-based assessment that yield objective measures. Using instrumental approaches to quantify speech-related behaviors is very important in a field that has primarily relied on subjective, auditory-perceptual forms of speech assessment1. Our assessment protocol measures performance across all of the speech subsystems, which include respiratory, phonatory (laryngeal), resonatory (velopharyngeal), and articulatory. The articulatory subsystem is divided into the facial components (jaw and lip), and the tongue. Prior research has suggested that each speech subsystem responds differently to neurological diseases such as ALS. The current protocol is designed to test the performance of each speech subsystem as independently from other subsystems as possible. The speech subsystems are evaluated in the context of more global changes to speech performance. These speech system level variables include speaking rate and intelligibility of speech.
The protocol requires specialized instrumentation, and commercial and custom software. The respiratory, phonatory, and resonatory subsystems are evaluated using pressure-flow (aerodynamic) and acoustic methods. The articulatory subsystem is assessed using 3D motion tracking techniques. The objective measures that are used to quantify bulbar impairment have been well established in the speech literature and show sensitivity to changes in bulbar function with disease progression. The result of the assessment is a comprehensive, across-subsystem performance profile for each participant. The profile, when compared to the same measures obtained from healthy controls, is used for diagnostic purposes. Currently, we are testing the sensitivity and specificity of these measures for diagnosis of ALS and for predicting the rate of disease progression. In the long term, the more refined endophenotype of bulbar ALS derived from this work is expected to strengthen future efforts to identify the genetic loci of ALS and improve diagnostic and treatment specificity of the disease as a whole. The objective assessment that is demonstrated in this video may be used to assess a broad range of speech motor impairments, including those related to stroke, traumatic brain injury, multiple sclerosis, and Parkinson disease.

A Protocol for Comprehensive Assessment of Bulbar Dysfunction in Amyotrophic Lateral Sclerosis ALS

Objective assessments of the physiological mechanisms that support speech are needed to monitor disease onset and progression in persons with ALS and to quantify treatment effects in clinical trials. In this video, we present a comprehensive, instrumentation-based protocol for quantifying speech motor performance in clinical populations.

Ein Protokoll für eine umfassende Beurteilung der bulbären Dysfunction in Amyotrophe Lateralsklerose (ALS)

Improved methods for assessing bulbar impairment are necessary for expediting diagnosis of bulbar dysfunction in ALS, for predicting disease progression ...

Forschung

Medizin

Intraspinal Cell Transplantation for Targeting Cervical Ventral Horn in Amyotrophic Lateral Sclerosis and Traumatic Spinal Cord Injury

Respiratory compromise due to phrenic motor neuron loss is a debilitating consequence of a large proportion of human traumatic spinal cord injury (SCI) cases 1 and is the ultimate cause of death in patients with the motor neuron disorder, amyotrophic laterals sclerosis (ALS) 2.
ALS is a devastating neurological disorder that is characterized by relatively rapid degeneration of upper and lower motor neurons. Patients ultimately succumb to the disease on average 2-5 years following diagnosis because of respiratory paralysis due to loss of phrenic motor neuron innnervation of the diaphragm 3. The vast majority of cases are sporadic, while 10% are of the familial form. Approximately twenty percent of familial cases are linked to various point mutations in the Cu/Zn superoxide dismutase 1 (SOD1) gene on chromosome 21 4. Transgenic mice 4,5 and rats 6 carrying mutant human SOD1 genes (G93A, G37R, G86R, G85R) have been generated, and, despite the existence of other animal models of motor neuron loss, are currently the most highly used models of the disease.
Spinal cord injury (SCI) is a heterogeneous set of conditions resulting from physical trauma to the spinal cord, with functional outcome varying according to the type, location and severity of the injury 7. Nevertheless, approximately half of human SCI cases affect cervical regions, resulting in debilitating respiratory dysfunction due to phrenic motor neuron loss and injury to descending bulbospinal respiratory axons 1. A number of animal models of SCI have been developed, with the most commonly used and clinically-relevant being the contusion 8.
Transplantation of various classes of neural precursor cells (NPCs) is a promising therapeutic strategy for treatment of traumatic CNS injuries and neurodegeneration, including ALS and SCI, because of the ability to replace lost or dysfunctional CNS cell types, provide neuroprotection, and deliver gene factors of interest 9.
Animal models of both ALS and SCI can model many clinically-relevant aspects of these diseases, including phrenic motor neuron loss and consequent respiratory compromise 10,11. In order to evaluate the efficacy of NPC-based strategies on respiratory function in these animal models of ALS and SCI, cellular interventions must be specifically directed to regions containing therapeutically relevant targets such as phrenic motor neurons. We provide a detailed protocol for multi-segmental, intraspinal transplantation of NPCs into the cervical spinal cord ventral gray matter of neurodegenerative models such as SOD1G93A mice and rats, as well as spinal cord injured rats and mice 11.

Neural precursor transplantation is a promising strategy for protecting and/or replacing lost/dysfunctional cervical phrenic motor neurons in spinal cord injury (SCI) and the motor neuron disorder, amyotrophic laterals sclerosis (ALS). We provide a protocol for cell delivery to cervical spinal cord ventral horn in rodent models of ALS and SCI.

Intraspinale Cell Transplantation für Targeting Cervical Vorderhorn in Amyotrophe Lateralsklerose und traumatische Rückenmarksverletzungen

Respiratory compromise due to phrenic motor neuron loss is a debilitating consequence of a large proportion of human traumatic spinal cord injury (SCI) ...

Clinical Testing and Spinal Cord Removal in a Mouse Model for Amyotrophic Lateral Sclerosis (ALS)

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder resulting in progressive degeneration of motoneurons. Peak of onset is around 60 years for the sporadic disease and around 50 years for the familial disease. Due to its progressive course, 50% of the patients die within 30 months of symptom onset. In order to evaluate novel treatment options for this disease, genetic mouse models of ALS have been generated based on human familial mutations in the SOD gene, such as the SOD1 (G93A) mutation. Most important aspects that have to be evaluated in the model are overall survival, clinical course and motor function. Here, we demonstrate the clinical evaluation, show the conduction of two behavioural motor tests and provide quantitative scoring systems for all parameters. Because an in depth analysis of the ALS mouse model usually requires an immunohistochemical examination of the spinal cord, we demonstrate its preparation in detail applying the dorsal laminectomy method. Exemplary histological findings are demonstrated. The comprehensive application of the depicted examination methods in studies on the mouse model of ALS will enable the researcher to reliably test future therapeutic options which can provide a basis for later human clinical trials.

Clinical Testing and Spinal Cord Removal in a Mouse Model for Amyotrophic Lateral Sclerosis ALS

A mouse model for amyotrophic lateral sclerosis (ALS) is examined clinically and behaviorally. As a prerequisite for an accompanying immunohistological analysis the preparation of the spinal cord is depicted in detail.

Klinische Tests und Rückenmark Removal in einem Mausmodell für Amyotrophe Lateralsklerose (ALS)

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder resulting in progressive degeneration of motoneurons. Peak of onset is around 60 ...

Real-time Digital Imaging of Leukocyte-endothelial Interaction in Ischemia-reperfusion Injury (IRI) of the Rat Cremaster Muscle

Ischemia-reperfusion injury (IRI) has been implicated in a large array of pathological conditions such as cerebral stroke, myocardial infarction, intestinal ischemia as well as following transplant and cardiovascular surgery.1 Reperfusion of previously ischemic tissue, while essential for the prevention of irreversible tissue injury, elicits excessive inflammation of the affected tissue. Adjacent to the production of reactive oxygen species, activation of the complement system and increased microvascular permeability, the activation of leukocytes is one of the principle actors in the pathological cascade of inflammatory tissue damage during reperfusion.2, 3 Leukocyte activation is a multistep process consisting of rolling, firm adhesion and transmigration and is mediated by a complex interaction between adhesion molecules in response to chemoattractants such as complement factors, chemokines, or platelet-activating factor.4
While leukocyte rolling in postcapillary venules is predominantly mediated by the interaction of selectins5 with their counter ligands, firm adhesion of leukocytes to the endothelium is selectin-controlled via binding to intercellular adhesion molecules (ICAM) and vascular cellular adhesion molecules (VCAM).6, 7 
Gold standard for the in vivo observation of leukocyte-endothelial interaction is the technique of intravital microscopy, first described in 1968.8
Though various models of IRI (ischemia-reperfusion injury) have been described for various organs, 9-12 only few are suitable for direct visualization of leukocyte recruitment in the microvascular bed on a high level of image quality.8 
We here promote the digital intravital epifluorescence microscopy of the postcapillary venule in the cremasteric microcirculation of the rat 13 as a convenient method to qualitatively and quantitatively analyze leukocyte recruitment for IRI-research in striated muscle tissue and provide a detailed manual for accomplishing the technique. We further illustrate common pitfalls and provide useful tips which should enable the reader to truly appreciate, and safely perform the method.
In a step by step protocol we depict how to get started with respiration controlled anesthesia under sufficient monitoring to keep the animal firmly anesthetized for longer periods of time. We then describe the cremasteric preparation as a thin flat sheet for outstanding optical resolution and provide a protocol for leukocyte imaging in IRI that has been well established in our laboratories.

Real-time Digital Imaging of Leukocyte-endothelial Interaction in Ischemia-reperfusion Injury IRI of the Rat Cremaster Muscle

Digital intravital epifluorescence microscopy of postcapillary venules in the cremasteric microcirculation is a convenient method to gain insights into leukocyte-endothelial interaction in vivo in ischemia-reperfusion injury (IRI) of striated muscle tissue. We here provide a detailed protocol to safely perform the technique and discuss its applications and limitations.

Real-time Digital Imaging von Leukozyten-Endothel-Interaktion in der Ischämie-Reperfusionsschaden (IRI) der Ratte Cremastermuskel

Ischemia-reperfusion injury (IRI) has been implicated in a large array of pathological conditions such as cerebral stroke, myocardial infarction, ...

Tibial Nerve Transection - A Standardized Model for Denervation-induced Skeletal Muscle Atrophy in Mice

The tibial nerve transection model is a well-tolerated, validated, and reproducible model of denervation-induced skeletal muscle atrophy in rodents. Although originally developed and used extensively in the rat due to its larger size, the tibial nerve in mice is big enough that it can be easily manipulated with either crush or transection, leaving the peroneal and sural nerve branches of the sciatic nerve intact and thereby preserving their target muscles. Thus, this model offers the advantages of inducing less morbidity and impediment of ambulation than the sciatic nerve transection model and also allows investigators to study the physiologic, cellular and molecular biologic mechanisms regulating the process of muscle atrophy in genetically engineered mice. The tibial nerve supplies the gastrocnemius, soleus and plantaris muscles, so its transection permits the study of denervated skeletal muscle composed of fast twitch type II fibers and/or slow twitch type I fibers. Here we demonstrate the tibial nerve transection model in the C57Black6 mouse. We assess the atrophy of the gastrocnemius muscle, as a representative muscle, at 1, 2, and 4 weeks post-denervation by measuring muscle weights and fiber type specific cross-sectional area on paraffin-embedded histologic sections immunostained for fast twitch myosin.

The tibial nerve transection model is a well-tolerated, validated, and reproducible model of skeletal muscle atrophy. The model surgical protocol is described and demonstrated in C57Black6 mice. &#160;

Tibialisnerv Durchtrennung - ein standardisiertes Modell für Denervation-induzierte Skelettmuskelatrophie in Mice

The tibial nerve transection model is a well-tolerated, validated, and reproducible model of denervation-induced skeletal muscle atrophy in rodents. ...

High-throughput Flow Cytometry Cell-based Assay to Detect Antibodies to N-Methyl-D-aspartate Receptor or Dopamine-2 Receptor in Human Serum

Over the recent years, antibodies against surface and conformational proteins involved in neurotransmission have been detected in autoimmune CNS diseases in children and adults. These antibodies have been used to guide diagnosis and treatment. Cell-based assays have improved the detection of antibodies in patient serum. They are based on the surface expression of brain antigens on eukaryotic cells, which are then incubated with diluted patient sera followed by fluorochrome-conjugated secondary antibodies. After washing, secondary antibody binding is then analyzed by flow cytometry. Our group has developed a high-throughput flow cytometry live cell-based assay to reliably detect antibodies against specific neurotransmitter receptors. This flow cytometry method is straight forward, quantitative, efficient, and the use of a high-throughput sampler system allows for large patient cohorts to be easily assayed in a short space of time. Additionally, this cell-based assay can be easily adapted to detect antibodies to many different antigenic targets, both from the central nervous system and periphery. Discovering additional novel antibody biomarkers will enable prompt and accurate diagnosis and improve treatment of immune-mediated disorders.

Over the recent years, live cell-based assays have been used successfully to detect antibodies against surface and conformational antigens. Here, we describe a method using high-throughput flow cytometry enabling the analysis of large cohorts of patients. Detection of novel antibodies will improve diagnosis and treatment of immune-mediated disorders.

Hochdurchsatz-Durchflusszytometrie zellbasierten Assay auf Antikörper gegen N-Methyl-D-Aspartat-Rezeptor oder Dopamin-2-Rezeptor im menschlichen Serum Detect

Over the recent years, antibodies against surface and conformational proteins involved in neurotransmission have been detected in autoimmune CNS diseases ...

Ischemic Tissue Injury in the Dorsal Skinfold Chamber of the Mouse: A Skin Flap Model to Investigate Acute Persistent Ischemia

Despite profound expertise and advanced surgical techniques, ischemia-induced complications ranging from wound breakdown to extensive tissue necrosis are still occurring, particularly in reconstructive flap surgery. Multiple experimental flap models have been developed to analyze underlying causes and mechanisms and to investigate treatment strategies to prevent ischemic complications. The limiting factor of most models is the lacking possibility to directly and repetitively visualize microvascular architecture and hemodynamics. The goal of the protocol was to present a well-established mouse model affiliating these before mentioned lacking elements. Harder et al. have developed a model of a musculocutaneous flap with a random perfusion pattern that undergoes acute persistent ischemia and results in ~50% necrosis after 10 days if kept untreated. With the aid of intravital epi-fluorescence microscopy, this chamber model allows repetitive visualization of morphology and hemodynamics in different regions of interest over time. Associated processes such as apoptosis, inflammation, microvascular leakage and angiogenesis can be investigated and correlated to immunohistochemical and molecular protein assays. To date, the model has proven feasibility and reproducibility in several published experimental studies investigating the effect of pre-, peri- and postconditioning of ischemically challenged tissue.

The window of the murine dorsal skinfold chamber presented visualizes a zone of acute persistent ischemia of a musculocutaneous flap. Intravital epi-fluorescence microscopy permits for direct and repetitive assessment of the microvasculature and quantification of hemodynamics. Morphologic and hemodynamic results can further be correlated with histological and molecular analyses.

Ischämischen Gewebeschädigung des Rückenhautkammer der Maus: Ein Hautlappen Modell zu Akute Persistent Ischämie Untersuchen

Despite profound expertise and advanced surgical techniques, ischemia-induced complications ranging from wound breakdown to extensive tissue necrosis are ...

Single-stage Dynamic Reanimation of the Smile in Irreversible Facial Paralysis by Free Functional Muscle Transfer

Unilateral facial paralysis is a common disease that is associated with significant functional, aesthetic and psychological issues. Though idiopathic facial paralysis (Bell&#8217;s palsy) is the most common diagnosis, patients can also present with a history of physical trauma, infectious disease, tumor, or iatrogenic facial paralysis. Early repair within one year of injury can be achieved by direct nerve repair, cross-face nerve grafting or regional nerve transfer. It is due to muscle atrophy that in long lasting facial paralysis complex reconstructive methods have to be applied. Instead of one single procedure, different surgical approaches have to be considered to alleviate the various components of the paralysis.
The reconstruction of a spontaneous dynamic smile with a symmetric resting tone is a crucial factor to overcome the functional deficits and the social handicap that are associated with facial paralysis. Although numerous surgical techniques have been described, a two-stage approach with an initial cross-facial nerve grafting followed by a free functional muscle transfer is most frequently applied. In selected patients however, a single-stage reconstruction using the motor nerve to the masseter as donor nerve is superior to a two-stage repair. The gracilis muscle is most commonly used for reconstruction, as it presents with a constant anatomy, a simple dissection and minimal donor site morbidity.
Here we demonstrate the pre-operative work-up, the post-operative management, and precisely describe the surgical procedure of single-stage microsurgical reconstruction of the smile by free functional gracilis muscle transfer in a step by step protocol. We further illustrate common pitfalls and provide useful tips which should enable the reader to truly comprehend the procedure. We further discuss indications and limitations of the technique and demonstrate representative results.

The use of the masseteric nerve as donor nerve represents a single-stage alternative to the criterion standard two-stage procedure of cross-facial nerve grafting and free muscle transfer in facial paralysis. We provide a detailed description to safely perform this technique with a gracilis muscle transfer and discuss indications and limitations.

Einstufige Dynamische Reanimation des Lächelns in Irreversible Fazialisparese von Free Funktionsmuskelüber

Unilateral facial paralysis is a common disease that is associated with significant functional, aesthetic and psychological issues. Though idiopathic ...

A Method of Trigonometric Modelling of Seasonal Variation Demonstrated with Multiple Sclerosis Relapse Data

This report describes a novel Stata-based application of trigonometric regression modelling to 55 years of multiple sclerosis relapse data from 46 clinical centers across 20 countries located in both hemispheres. Central to the success of this method was the strategic use of plot analysis to guide and corroborate the statistical regression modelling. Initial plot analysis was necessary for establishing realistic hypotheses regarding the presence and structural form of seasonal and latitudinal influences on relapse probability and then testing the performance of the resultant models. Trigonometric regression was then necessary to quantify these relationships, adjust for important confounders and provide a measure of certainty as to how plausible these associations were. Synchronization of graphing techniques with regression modelling permitted a systematic refinement of models until best-fit convergence was achieved, enabling novel inferences to be made regarding the independent influence of both season and latitude in predicting relapse onset timing in MS. These methods have the potential for application across other complex disease and epidemiological phenomena suspected or known to vary systematically with season and/or geographic location.

Combining plot analysis with trigonometric regression is a robust method for exploring complex, cyclical phenomena such as relapse onset timing in multiple sclerosis (MS). This method enabled unbiased characterisation of seasonal trends in relapse onset permitting novel inferences around the influence of seasonal variation, ultraviolet radiation (UVR) and latitude.

Eine Methode der trigonometrischen Modellierung der saisonalen Schwankungen mit Multipler Sklerose Relapse Daten zeigten,

This report describes a novel Stata-based application of trigonometric regression modelling to  55 years of multiple sclerosis relapse data from 46 ...

Design, Fabrication, and Administration of the Hand Active Sensation Test (HASTe)

The concept of personalizing neurologic rehabilitation, based on individual impairments, has experienced a recent surge. In parallel, the number of outcome measures of upper extremity motor performance has grown. However, clinicians and researchers lack practical, quantitative measures of the hand&#8217;s natural role as a receptor of the environment. The Hand Active Sensation Test (HASTe), developed by Williams and colleagues in 2006, is a valid and reliable measure of haptic performance. Though not available commercially, the HASTe can be fabricated from inexpensive materials, and it has been used successfully to identify impairments in haptic touch in individuals with stroke. (Williams, 2006). This paper presents the methods of design and fabrication of the HASTe testing kit, as well as a visual screen to be used during administration, and instructions for the tests administration and scoring.

Design, Fabrication, and Administration of the Hand Active Sensation Test HASTe

The Hand Active Sensation Test (HASTe) is a valid and reliable measure of haptic performance, which has been used successfully to identify impaired haptic touch in individuals with stroke. The purpose of this paper is to describe the design, fabrication and administration of the HASTe.

Konstruktion, Fertigung und Verwaltung der Hand Aktive Sensation Test (Eile)

The concept of personalizing neurologic rehabilitation, based on individual impairments, has experienced a recent surge. In parallel, the number of ...