Chronic pain is linked to changes in cognitive function. However, little is known about its influence on number sense, despite the fact that intact numerical-spatial processing is a prerequisite for valid scale-based pain assessments. This study aimed to elucidate whether number sense is changed in chronic pain (CP), to determine if changes have an impact on pain assessments using pain rating scales and what patient factors might contribute.
N=42 chronic pain patients and n=42 matched controls were analyzed (age range: 33-68 years). Numerical-spatial abilities were investigated by using number line tasks, where participants either estimated the position of a given number (position marking) or the value of a predefined mark (number naming). Pain intensity was assessed using numerical rating (NRS), verbal rating (VRS) and visual analogue scales (VAS). Additional measures included attention and working memory, verbal intelligence, medication and depression. Results revealed that in number naming, patients deviated more from expected responses than controls, and that VAS scores were significantly higher than both NRS and VRS and correlated with deviations in position making. Changes in number naming were predicted by pain intensity, sex and IQ but not by attention, memory or opioid medication.
This article presents new insight on which cognitive mechanisms are influenced by chronic pain with the focus on numerical spatial abilities. It could therefore provide useful knowledge in developing new pain assessment tools specifically for patients suffering from chronic pain.
Speech impairment is a frequent and often serious symptom of Parkinson's disease (PD), characterized by a disorder of phonation, articulation and prosody. While research on the pathogenesis of the prominent limb motor symptoms has made considerable progress in recent years, the pathophysiology of PD speech impairment is still incompletely understood. To investigate the neural correlates of speech production in PD, EEG was recorded in 14 non-demented patients with idiopathic PD and preserved verbal fluency on regular dopaminergic medication (8 women; mean age ± SD: 69.5 ± 8.0 years). The control group consisted of 15 healthy age-matched individuals (7 women; age: 69.7 ± 7.0 years). All participants performed a visually-cued, overt speech production task; required utterances were papapa and pataka. During the preparatory phase of speech production, in a time window of 200-400 ms after presentation of the visual cue, β-power was significantly increased in PD patients compared to healthy controls. Previous research has shown that the physiological decrease of β-power preceding limb movement onset is delayed and smaller in PD patients off medication and normalizes under dopaminergic treatment. By contrast, our study demonstrates that β-power during preparation for speech production is higher in patients on dopaminergic therapy than controls. Thus, our results suggest that the mechanisms that regulate β-activity preceding limb movement and speech production differ in PD. The pathophysiological role of this increase in β-power during speech preparation needs to be determined.
Speech impairment is a frequent and often serious symptom of Parkinson's disease (PD), characterized by a disorder of phonation, articulation and prosody. While research on the pathogenesis of the prominent limb motor symptoms has made considerable progress in recent years, the pathophysiology of PD speech impairment is still incompletely understood. To investigate the neural correlates of speech production in PD, EEG was recorded in 14 non-demented patients with idiopathic PD and preserved verbal fluency on regular dopaminergic medication (8 women; mean age ± SD: 69.5 ± 8.0 years). The control group consisted of 15 healthy age-matched individuals (7 women; age: 69.7 ± 7.0 years). All participants performed a visually-cued, overt speech production task; required utterances were papapa and pataka. During the preparatory phase of speech production, in a time window of 200-400 ms after presentation of the visual cue, β-power was significantly increased in PD patients compared to healthy controls. Previous research has shown that the physiological decrease of β-power preceding limb movement onset is delayed and smaller in PD patients off medication and normalizes under dopaminergic treatment. By contrast, our study demonstrates that β-power during preparation for speech production is higher in patients on dopaminergic therapy than controls. Thus, our results suggest that the mechanisms that regulate β-activity preceding limb movement and speech production differ in PD. The pathophysiological role of this increase in β-power during speech preparation needs to be determined.
Front Hum Neurosci. 2017 Jul 24;11:371. doi: 10.3389/fnhum.2017.00371. eCollection 2017.
Speech impairment is a frequent and often serious symptom of Parkinson's disease (PD), characterized by a disorder of phonation, articulation and prosody. While research on the pathogenesis of the prominent limb motor symptoms has made considerable progress in recent years, the pathophysiology of PD speech impairment is still incompletely understood. To investigate the neural correlates of speech production in PD, EEG was recorded in 14 non-demented patients with idiopathic PD and preserved verbal fluency on regular dopaminergic medication (8 women; mean age ± SD: 69.5 ± 8.0 years). The control group consisted of 15 healthy age-matched individuals (7 women; age: 69.7 ± 7.0 years). All participants performed a visually-cued, overt speech production task; required utterances were papapa and pataka. During the preparatory phase of speech production, in a time window of 200-400 ms after presentation of the visual cue, β-power was significantly increased in PD patients compared to healthy controls. Previous research has shown that the physiological decrease of β-power preceding limb movement onset is delayed and smaller in PD patients off medication and normalizes under dopaminergic treatment. By contrast, our study demonstrates that β-power during preparation for speech production is higher in patients on dopaminergic therapy than controls. Thus, our results suggest that the mechanisms that regulate β-activity preceding limb movement and speech production differ in PD. The pathophysiological role of this increase in β-power during speech preparation needs to be determined.
It is widely believed that most stroke recovery occurs within 6 mo, with little benefit of physiotherapy or other modalities beyond 1 yr. We report a remarkable case of stroke recovery beginning 23 yr after a severe stroke due to embolization from the innominate artery and subclavian artery, resulting from compression of the right subclavian artery by a cervical rib. The patient had a large right frontoparietal infarction with severe left hemiparesis and a totally nonfunctional spastic left hand. He experienced some recovery of hand function that began 23 yr after the stroke, 1 yr after he took up regular swimming. As a result, intensive physiotherapy was initiated, with repetitive large muscle movement and a spring-loaded mechanical orthosis that provides resistance to finger flexors and supports finger extensors. Within 2 yr, he could pick up coins with the previously useless left hand. Functional MRI studies document widespread distribution of the recovery in both hemispheres. This case provides impetus not only to more intensive and prolonged physiotherapy, but also to treatment with emerging modalities such as stem cell therapy and exosome and microRNA therapies.NEW & NOTEWORTHY Widespread bilateral activation of both sides of the cerebrum and cerebellum are demonstrated on functional MRI after motor recovery of a completely nonfunctional left hand that began 23 yr after a severe stroke. This suggests that the generally accepted window of recovery beyond which further therapy is not indicated should be entirely reconsidered. Physiotherapy and new modalities in development might be indicated long after a stroke.