Temporal adaptation of sensory attenuation for self-touch.

The sensory consequences of our actions appear attenuated to us. This effect has been reported for external sensations that are evoked by auditory or visual events and for body-related sensations which are produced by self-touch. In the present study, we investigated the effects of prolonged exposure to a delay between an action and the generated sensation on sensory attenuation for self-touch. Previously, it has been shown that after being presented to a systematic exposure delay, artificially delayed touch can feel more intense and non-delayed touches can appear less intense. Here, we investigated the temporal spread of the temporal recalibration effect. Specifically, we wondered whether this temporal recalibration effect would affect only the delay that was used during exposure trials or if it would also modulate longer test delays. In the first two experiments, we tested three test delays (0, 100 and 400 ms) either in randomized or in blocked order. We found sensory attenuation in all three test intervals but no effect of the exposure delay. In Experiment 3, we replicated the experiment by Kilteni et al. (ELife 8:e42888, 2019. https://doi.org/10.7554/eLife.42888 ) and found evidence for temporal recalibration by exposure delay. Our data show that the temporal selectivity of sensory attenuation of self-touch depends on presenting a singular test delay only. Presenting multiple test delays leads to a temporally broad spread of sensory attenuation.

Motor variability modulates calibration of precisely timed movements.

Interacting with the environment often requires precisely timed movements, challenging the brain to minimize the detrimental impact of neural noise. Recent research demonstrates that the brain exploits the variability of its temporal estimates and recalibrates perception accordingly. Time-critical movements, however, contain a sensory measurement and a motor stage. The brain must have knowledge of both in order to avoid maladapted behavior. By manipulating sensory and motor variability, we show that the sensorimotor system recalibrates sensory and motor uncertainty separately. Serial dependencies between observed interval durations in the previous and motor reproductions in the current trial were weighted by the variability of movements. These serial dependencies generalized across different effectors, but not to a visual discrimination task. Our results suggest that the brain has accurate knowledge about contributions of motor uncertainty to errors in temporal movements. This knowledge about motor uncertainty seems to be processed separately from knowledge about sensory uncertainty.

Tactile motor attention induces sensory attenuation for sounds.

Sensory events appear reduced in intensity when we actively produce them. Here, we investigated sensory attenuation in a virtual reality setup that allowed us to manipulate the time of tactile feedback when pressing a virtual button. We asked whether tactile motor attention might shift to the tactile location that makes contact with the button. In experiment one, we found that a tactile impulse was perceived as more intense when button pressing. In a second experiment, participants pushed a button and estimated the intensity of sounds. We found sensory attenuation for sounds only when tactile feedback was provided at the time the movement goal was reached. These data indicate that attentional prioritization for the tactile modality during a goal-directed hand movement might lead to a transient reduction in sensitivity in other modalities, resulting in sensory attenuation for sounds.

[Familial partial lipodystrophy type 1. A rare or underdiagnosed syndrome?]. / Lipodistrofia parcial familiar tipo 1. ¿Un síndrome subdiagnosticado o raro?

Familial partial lipodystrophy (FPL) type 1 is a syndrome characterized by loss of subcutaneous fat in arms and legs and an excess of body fat in face, neck, and torso. This rare syndrome is usually diagnosed when patients present cardiovascular complications or pancreatitis due to the severe metabolic abnormalities. Here we present the case of a 45 year old diabetic female without any pathological family history, a poor glycemic control (HbA1c 11.7%), hypertriglideridemia (3000 mg/dl), a body mass index (BMI) of 38, thin limbs, subcutaneous fat loss in gluteal area and ledge of fat above them, prominent veins in lower extremities, moon face, and acanthosis nigricans; as well as hypertension (150/100 mmHg) and subcutaneous folds measuring less than average were observed. Hypercortisolism was discarded and leptin levels were measured (16.8 mg/ml, VR: BMI > 30: 50 mg/ml). Due to these clinical and biochemical manifestations, and low leptin levels (16.8 mg/ml), Kobberling syndrome was suspected; however, LMNA mutation analysis was negative. Changes in lifestyle and treatment with fenofibrate, biphasic insulin 50/50, and enalapril were initiated showing a a significant metabolic improvement: HbA1c (7.8%) and TG (243 mg/dl). FPL type 1 is a familial disease, although there are spontaneous cases. No specific mutation is responsible for this syndrome. Due to its clinical manifestations, Cushing syndrome must be discarded.

Lipodistrofia parcial familiar tipo 1: ¿Un síndrome subdiagnosticado o raro?

La lipodistrofia parcial familiar de tipo1 (LPF 1) es un síndrome caracterizado por la pérdida parcial de grasa subcutánea en extremidades con distribución incrementada de la misma en rostro, cuello y tronco. Es una identidad familiar aunque hay casos espontáneos. Hasta ahora no se conoce mutación responsable. Se debe realizar diagnóstico diferencial con el síndrome de Cushing. Es un síndrome poco frecuente y en oportunidades se llega al diagnóstico cuando los pacientes presentan complicaciones cardiovasculares o afectación pancreática como consecuencia de una grave alteración metabólica. Se presenta el caso de una paciente de 45 años con diabetes mellitus desde los 20 años de edad, mal control glucémico (HbA1c: 11.7%) e hipertrigliceridemia (TG: 3000 mg/dl), índice de masa corporal (IMC): 38, extremidades adelgazadas, pérdida de grasa subcutánea en glúteos, sobreelevación de pliegue por encima de los mismos, venas prominentes en miembros inferiores, cara de luna llena y marcada acantosis nigricans, hipertensión (TA: 150/100 mm Hg) y medidas de pliegues subcutáneos disminuidos. El dosaje de leptina fue 16.8 mg/ml. El estudio genético para gen LMNA fue negativo. Se instauraron medidas de cambio de estilo de vida, tratamiento con fenofibrato, insulina premezcla 50/50 y enalapril, obteniéndose una franca mejoría clínica, de la HbA1c (7.8%) y de los TG (243 mg/dl).

Familial partial lipodystrophy (FPL) type 1 is a syndrome characterized by loss of subcutaneous fat in arms and legs and an excess of body fat in face, neck, and torso. This rare syndrome is usually diagnosed when patients present cardiovascular complications or pancreatitis due to the severe metabolic abnormalities. Here we present the case of a 45 year old diabetic female without any pathological family history, a poor glycemic control (HbA1c 11.7%), hypertriglideridemia (3000 mg/dl), a body mass index (BMI) of 38, thin limbs, subcutaneous fat loss in gluteal area and ledge of fat above them, prominent veins in lower extremities, moon face, and acanthosis nigricans; as well as hypertension (150/100 mmHg) and subcutaneous folds measuring less than average were observed. Hypercortisolism was discarded and leptin levels were measured (16.8 mg/ml, VR: BMI > 30: 50 mg/ml). Due to these clinical and biochemical manifestations, and low leptin levels (16.8 mg/ml), Kobberling syndrome was suspected; however, LMNA mutation analysis was negative. Changes in lifestyle and treatment with fenofibrate, biphasic insulin 50/50, and enalapril were initiated showing a a significant metabolic improvement: HbA1c (7.8%) and TG (243 mg/dl). FPL type 1 is a familial disease, although there are spontaneous cases. No specific mutation is responsible for this syndrome. Due to its clinical manifestations, Cushing syndrome must be discarded.

Lipodistrofia parcial familiar tipo 1: ¿Un síndrome subdiagnosticado o raro?

La lipodistrofia parcial familiar de tipo1 (LPF 1) es un síndrome caracterizado por la pérdida parcial de grasa subcutánea en extremidades con distribución incrementada de la misma en rostro, cuello y tronco. Es una identidad familiar aunque hay casos espontáneos. Hasta ahora no se conoce mutación responsable. Se debe realizar diagnóstico diferencial con el síndrome de Cushing. Es un síndrome poco frecuente y en oportunidades se llega al diagnóstico cuando los pacientes presentan complicaciones cardiovasculares o afectación pancreática como consecuencia de una grave alteración metabólica. Se presenta el caso de una paciente de 45 años con diabetes mellitus desde los 20 años de edad, mal control glucémico (HbA1c: 11.7%) e hipertrigliceridemia (TG: 3000 mg/dl), índice de masa corporal (IMC): 38, extremidades adelgazadas, pérdida de grasa subcutánea en glúteos, sobreelevación de pliegue por encima de los mismos, venas prominentes en miembros inferiores, cara de luna llena y marcada acantosis nigricans, hipertensión (TA: 150/100 mm Hg) y medidas de pliegues subcutáneos disminuidos. El dosaje de leptina fue 16.8 mg/ml. El estudio genético para gen LMNA fue negativo. Se instauraron medidas de cambio de estilo de vida, tratamiento con fenofibrato, insulina premezcla 50/50 y enalapril, obteniéndose una franca mejoría clínica, de la HbA1c (7.8%) y de los TG (243 mg/dl).(AU)

Familial partial lipodystrophy (FPL) type 1 is a syndrome characterized by loss of subcutaneous fat in arms and legs and an excess of body fat in face, neck, and torso. This rare syndrome is usually diagnosed when patients present cardiovascular complications or pancreatitis due to the severe metabolic abnormalities. Here we present the case of a 45 year old diabetic female without any pathological family history, a poor glycemic control (HbA1c 11.7%), hypertriglideridemia (3000 mg/dl), a body mass index (BMI) of 38, thin limbs, subcutaneous fat loss in gluteal area and ledge of fat above them, prominent veins in lower extremities, moon face, and acanthosis nigricans; as well as hypertension (150/100 mmHg) and subcutaneous folds measuring less than average were observed. Hypercortisolism was discarded and leptin levels were measured (16.8 mg/ml, VR: BMI > 30: 50 mg/ml). Due to these clinical and biochemical manifestations, and low leptin levels (16.8 mg/ml), Kobberling syndrome was suspected; however, LMNA mutation analysis was negative. Changes in lifestyle and treatment with fenofibrate, biphasic insulin 50/50, and enalapril were initiated showing a a significant metabolic improvement: HbA1c (7.8%) and TG (243 mg/dl). FPL type 1 is a familial disease, although there are spontaneous cases. No specific mutation is responsible for this syndrome. Due to its clinical manifestations, Cushing syndrome must be discarded.(AU)

Lipodistrofia parcial familiar tipo 1. ¿Un síndrome subdiagnosticado o raro? / [Familial partial lipodystrophy type 1. A rare or underdiagnosed syndrome?].

Familial partial lipodystrophy (FPL) type 1 is a syndrome characterized by loss of subcutaneous fat in arms and legs and an excess of body fat in face, neck, and torso. This rare syndrome is usually diagnosed when patients present cardiovascular complications or pancreatitis due to the severe metabolic abnormalities. Here we present the case of a 45 year old diabetic female without any pathological family history, a poor glycemic control (HbA1c 11.7

), hypertriglideridemia (3000 mg/dl), a body mass index (BMI) of 38, thin limbs, subcutaneous fat loss in gluteal area and ledge of fat above them, prominent veins in lower extremities, moon face, and acanthosis nigricans; as well as hypertension (150/100 mmHg) and subcutaneous folds measuring less than average were observed. Hypercortisolism was discarded and leptin levels were measured (16.8 mg/ml, VR: BMI > 30: 50 mg/ml). Due to these clinical and biochemical manifestations, and low leptin levels (16.8 mg/ml), Kobberling syndrome was suspected; however, LMNA mutation analysis was negative. Changes in lifestyle and treatment with fenofibrate, biphasic insulin 50/50, and enalapril were initiated showing a a significant metabolic improvement: HbA1c (7.8

) and TG (243 mg/dl). FPL type 1 is a familial disease, although there are spontaneous cases. No specific mutation is responsible for this syndrome. Due to its clinical manifestations, Cushing syndrome must be discarded.