Emotional reactivity and emotion recognition in frontotemporal lobar degeneration.

BACKGROUND: Frontotemporal lobar degeneration (FTLD) is associated with a profound decline in social and emotional behavior; however, current understanding regarding the specific aspects of emotional functioning that are preserved and disrupted is limited. OBJECTIVE: To assess preservation of function and deficits in two aspects of emotional processing (emotional reactivity and emotion recognition) in FTLD. METHODS: Twenty-eight FTLD patients were compared with 16 controls in emotional reactivity (self-reported emotional experience, emotional facial behavior, and autonomic nervous system response to film stimuli) and emotion recognition (ability to identify a target emotion of fear, happy, or sad experienced by film characters). Additionally, the neural correlates of emotional reactivity and emotion recognition were investigated. RESULTS: FTLD patients were comparable to controls in 1) emotional reactivity to the fear, happy, and sad film clips and 2) emotion recognition for the happy film clip. However, FTLD patients were significantly impaired compared with controls in emotion recognition for the fear and sad film clips. Volumetric analyses revealed that deficits in emotion recognition were associated with decreased lobar volumes in the frontal and temporal lobes. CONCLUSIONS: The socioemotional decline typically seen in frontotemporal lobar degeneration patients may result more from an inability to process certain emotions in other people than from deficits in emotional reactivity.

Brain calcification in severely stressed neonates receiving parenteral calcium.

Morphologic evidence for calcium salts within the brains of severely stressed neonates at autopsy correlated to the mean daily parenteral dose of calcium gluconate (P less than 0.01). Survival analysis indicated that parenteral administration of calcium contributed a negative effect to predicted survival (P less than 0.05).

Multimodal assessment of human brain calcification with respect to parenteral calcium gluconate in stressed neonates.

Parenteral calcium may augment the degree of calcification within brains of human neonates (p less than 0.01). This observation is supported by histochemistry, atomic absorption of ashed brain, selected area diffraction, and energy dispersive microanalysis. Survival analysis indicates that a standard replacement dose may have an adverse effect of severely stressed neonates (p less than 0.01). Nuclei within the optic-tract, circumferential pons and temporal lobe showed calcium salt deposits before other cytologic evidence of necrosis was discernible. Most calcification occurred in regions of ongoing necrosis primarily in the neuropil. But Purkinje cell and supraoptic neurons and apparent neurons from the fascia dentata, Ammon's Horn, were densely calcified in several brains. In those infants surviving longer periods both the neuropil and nuclei of glial scar stained for calcium salts.

Calcium-induced spongiform and necrotizing myelopathy.

Selective axonal calcification has been consistently observed in experimental spinal cord trauma in laboratory animals as well as in human spinal cord injury. A hypothesis of calcium influx resulting in activation of proteolytic and/or lipolytic enzymes has been proposed as a major mechanism of nerve fiber degeneration. The current study was undertaken to determine the effects of calcium influx into nontraumatized spinal cord tissue, utilizing 10 per cent calcium chloride at a pH of 7.4 slowly dripped onto the dorsal surface of the surgically exposed spinal cord of adult male Sprague-Dawley rats. Controls consisted of animals similarly treated with solutions of sodium chloride, magnesium chloride, and potassium chloride at the same pH and osmolarity. Sham-operated and normal animals were also observed. The experimental animals that received calcium chloride consistently developed paraplegia that was evident within 24 hours after treatment. The initial spinal cord lesion consisted of discrete areas of spongiosis in posterior and lateral columns in the segment beneath the application of calcium. The spongiosis progressed in severity and was accompanied or followed by necrosis. The gray matter was relatively spared; however, the posterior horns became consistently necrotic. Calcium was observed histochemically in the areas of spongiosis/necrosis but not in spared areas. Although the topography of the calcium-induced myelopathy differs from that of spinal cord injury, the progression of the clinical and pathologic changes is consistent with the calcium-mediated hypothesis of necrosis in the latter.