Somatosensory Evoked Responses in Down Syndrome

Straumanis, John J.

doi:10.1001/archpsyc.1973.04200040086014

Cited by 36 publications

(11 citation statements)

References 16 publications

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“…Striking deficits in sensory functioning, measured more conventionally, are not apparent in DS (Knights et af. 1967), although somatosensory evoked potentials show slightly prolonged initial latencies (Straumanis et al 1973) which are consistent with reduced median-nerve conduction velocities (Stimson et af. 1969).…”

Section: Discussionmentioning

confidence: 76%

Deficits Forces the Production of Grip Down Syndrome

Cole

Abbs

Turner

1988

Develop Med Child Neuro

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Summary Down syndrome (DS) and control individuals were examined as to their ability to adapt grip forces to changes in the properties of lifted objects. The DS group generated substantially greater grip forces than the controls in all tests and failed to adapt normally to changes in the frictional properties of the objects. Their greater grip forces were not due to greater slipperiness of the skin of their fingers. These results are consistent with other findings of subtle deficits in DS individuals' use of somatosensory information for controlling movement and posture. RÉSUMÉ Déficit dam I'effet d'agrippement chez le mongolien Des mongoliens (DS) et des contrbles ont été examinés pour leur capacitéà adapter des forces d'agrippement aux modification de propriété des objets soulevés. Le groupe DS générait des forces d'agrippement significativement plus élevées que les contrôles pour toutes les épreuves et échouaient à une adaptation normale aux modifications de propriétés de frottement des objets. Leur plus grande force d'agrippement n'était pas dûe au caractère plus glissant de leur doigts. Ces résultats coíncident avec d'autres données de déficits minimes dans I'utilisation par les mongoliens des informations sensorielles somatiques pour contrôler le mouvement et la posture. ZUSAMMENFASSUNG Störung der Greiffnktion bei Kindern mit Down Syndrom Kinder mit Down Syndrom (DS) und Kontrollkinder wurden hinsichtlich ihrer Fähigkeit untersucht, die Kraft beim Zugreifen der Lageveränderung von Gegenständen anzupassen. Die DS Gruppe hat bei allen Tests deutlich starkere Greifkräfte entwickelt als die Kontrollgruppe und konnte nicht normal auf Lageveränderungen von Gegenständen reagieren. Die stärkere Kraft des Zugreifens war nicht durch größere Schlüpfrigkeit der Haut ihrer Fingern bedingt. Die Ergebnisse stimmen mit anderen Befunden subtiler Störgungen bei der Verarbeitung somato‐sensorischer Information zur Bewegungs‐ und Haltungskontrolle bei DS Kindern überein. RESUMEN DCéficits en la produccion de fuerzas de prensión en individuos con sindrome de Down Se examinaron individuos con sindrome de Down (SD) y controles acerca de su habilidad para adaptar la fuerza de prensión a las propiedades de los objectos levantados. El grupo con SD producían de forma substancial unas mayores fuerzas de prensión que los controles en todas las pruebas y fallaron en la adaptación normal a los cambios de las propiedades de fricción de los objectos. Sus mayores fuerzas de prensión no se debian a un mayor deslizamiento de la piel de sus dedos. Estos resultados estan de acuerdo con otros hallazgos de deficits sutiles en individuos con SD en al uso de la informacion somárica para el control del movimiento y la postura.

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Section: Discussionmentioning

confidence: 76%

Deficits Forces the Production of Grip Down Syndrome

Cole

Abbs

Turner

1988

Develop Med Child Neuro

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“…Analogous mechanisms could also be operating in our patients. Indeed, in trisomy 21 patients, neurophysiologic studies have shown an increased amplitude of sensory evoked potentials that were attributed to a central deficit of inhibition of different stimuli (Bigum et al., 1970; Barnet et al., 1971; Straumanis et al., 1973; Ferri et al., 1994). Reduction of central inhibitory control in trisomy 21 might result from a combination of structural brain abnormalities typical of this chromosomal disorder, including reduction of neuronal density, decreased density and size of synapses, reduction of dendritic spines of pyramidal neurons, atrophy, and lack of growth of dendritic trees (Guerrini et al., 1990).…”

Section: Discussionmentioning

confidence: 99%

Lennox‐Gastaut syndrome with late‐onset and prominent reflex seizures in trisomy 21 patients

et al. 2009

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Summary Purpose: Lennox‐Gastaut syndrome (LGS) is a severe epileptic condition characterized by multiple seizure types including tonic seizures, slow spike‐and‐wave discharges on electroencephalography (EEG), and cognitive impairment. LGS can occur in apparently healthy subjects or in patients with preexisting brain damage. The onset peaks between 3 and 5 years of age and the prognosis is usually poor. Herein we report 13 subjects with trisomy 21 who developed LGS. Methods: We retrospectively reviewed the clinical and EEG data of consecutive patients with LGS and trisomy 21 referred to five epilepsy centers over the last 30 years. Results: Data for 13 patients (8 male, 5 female) were collected. The mean age at onset was 9.1 years (range 5–16). The mean age at last follow‐up was 23.5 years (range 11–43 years). Seizure onset was after age 8 years in eight (62%) patients and between age 5 and 8 in the other five. In none of the cases did a West syndrome precede the onset of LGS. Nine of 13 patients (69%) had unambiguous reflex seizures, mostly precipitated by sudden unexpected sensory stimulations, usually preceding or accompanying the onset of a full‐blown LGS picture. Interictal and ictal EEG findings were typical for LGS. All patients were drug‐resistant. Discussion: Patients with trisomy 21 may present a peculiar LGS, characterized by late onset and high occurrence of reflex seizures. Mechanisms underlying this particular presentation of LGS may include dendritic rarefaction and decreased interneurons, as well as functional abnormalities leading to overall decreased brain inhibition in these patients.

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“…In the present study, we found a prolonged central conduction time (interpeak latencies of N 13 ‐N 20 ) and N 20 peak latency but normal conduction velocity of the peripheral nerve in DS infants. Straumanis et al reported that N 20 peak latency was delayed in adult patients with DS [18]. The body height of patients with DS is generally subnormal and it was considered that this might have affected the latencies of the somatosensory evoked potentials.…”

Section: Discussionmentioning

confidence: 99%