From acute to long-term alterations in pain processing and modulation after spinal cord injury: mechanisms related to chronification of central neuropathic pain.

A severe and debilitating consequence of a spinal cord injury (SCI) is central neuropathic pain (CNP). Our aim was to investigate the processes leading to CNP emergence and chronification by analyzing causal relationship over time between spinothalamic function, pain excitability, and pain inhibition after SCI. This longitudinal follow-up study included 53 patients with acute SCI and 20 healthy controls.

Biomarkers for predicting central neuropathic pain occurrence and severity after spinal cord injury: results of a long-term longitudinal study.

Central neuropathic pain (CNP) after spinal cord injury (SCI) is debilitating and immensely impacts the individual. Central neuropathic pain is relatively resistant to treatment administered after it develops, perhaps owing to irreversible pathological processes. Although preemptive treatment may overcome this shortcoming, its administration necessitates screening patients with clinically relevant biomarkers that could predict CNP early post-SCI.

Increased psychological distress among individuals with spinal cord injury is associated with central neuropathic pain rather than the injury characteristics.

Study Design: Cross-sectional study.

Objectives: Central neuropathic pain (CNP) is common after spinal cord injury (SCI). The psychological impact of CNP is not clear.

Differential pain modulation properties in central neuropathic pain after spinal cord injury.

It seems that central neuropathic pain (CNP) is associated with altered abilities to modulate pain; whereas dysfunction in descending pain inhibition is associated with the extent of chronic pain distribution, enhanced pain excitation is associated with the intensity of chronic pain. We investigated the hypothesis that CNP is associated with decreased descending pain inhibition along with increased neuronal excitability and that both traits are associated with spinothalamic tract (STT) damage. Chronic spinal cord injury subjects with CNP (n = 27) and without CNP (n = 23) and healthy controls (n = 20) underwent the measurement of pain adaptation, conditioned pain modulation (CPM), tonic suprathreshold pain (TSP), and spatial summation of pain above injury level.

A rare recessive distal hereditary motor neuropathy with HSJ1 chaperone mutation.

Objective: Distal hereditary motor neuropathies (dHMN) form a clinically and genetically heterogeneous group of disorders, characterized by muscle weakness and atrophy predominating at the distal part of the limbs, due to the progressive degeneration of motor neurons in the spinal cord. We report here a novel rare variant of dHMN with autosomal recessive inheritance in a large Jewish family originating from Morocco. The disease is characterized by a predominance of paralysis at the lower limbs and an early adulthood onset.

Heterotopic ossification in Guillain-Barré syndrome: incidence and effects on functional outcome with long-term follow-up.

Objective: To define the incidence, effects on functional abilities, and possible causation of heterotopic ossification (HO) in Guillain-Barré syndrome (GBS) patients admitted for inpatient rehabilitation.

Design: Long-term prospective study on neurologic and functional outcome of GBS patients admitted for rehabilitation.

Setting: Rehabilitation department, inpatient and outpatient, within a university-affiliated medical center.

From the philosophy auditorium to the neurophysiology laboratory and back: from Bergson to Damasio.

Henri Bergson (1859-1941) was probably the most influential French philosopher at the turn of the twentieth century. In 1927 he was awarded the Nobel Prize for literature. Far beyond the restricted academic philosophical milieu, the impact of his thinking reached personalities as diverse as Claude Debussy, Marcel Proust, George Bemard Shaw, and the impressionists.

Sensory determinants of thermal pain.

It is still unclear whether the quality of painful thermal sensation is determined only by conduction in specific, dedicated nociceptive channels (i.e. C or Adelta nociceptors) or whether it is a result of integrated activity in both nociceptive and non-nociceptive systems.