The authors' study supports the use of a syndrome approach for neuropsychiatric evaluation in patients with AD. Individual neuropsychiatric symptoms can be reclassified into five distinct psychiatric syndromes. Clinicians should incorporate a thorough psychiatric and neurologic examination of patients with AD and consider therapeutic strategies that focus on psychiatric syndromes, rather than specific individual symptoms.
We measured, by RIA methods, ictal and interictal levels of substance P (SP), calcitonin-gene related peptide (CGRP) and neurokinin A (NKA) in the plasma of 30 young migraine patients with aura (MPA) and 45 migraine patients without aura (MWA), and compared the results with those of 30 age-matched controls. There were no significant differences between the levels of these vasoactive peptides in the control group and the levels in both migraine groups studied in headache-free periods. An elevation of CGRP levels in plasma was found during attacks in MPA and, to a lesser extent, in MWA (p < 0.03 and p < 0.05, respectively). A significant increase in NKA levels was also demonstrated in the MPA and MWA groups (p < 0.02 and p < 0.04, respectively). These data suggest, although indirectly, that CGRP and NKA could be involved in the pathogenesis of migraine attacks in juvenile migraine patients.
We determined the plasma levels of ET1, both interictally and ictally, in 50 migraine patients, 20 with aura (MPA) and 30 without aura (MPWA), comparing them with the levels of 40 age‐matched tension‐type headache patients (20 episodic and 20 chronic) (ETTHP and CTTHP) and the levels of a group of 20 healthy control subjects (CS). No statistically significant difference was evident between the mean ET1 plasma levels of MPA and those of MPWA, assessed in headache‐free periods. The mean ET1 plasma levels of MPA and MPWA, assessed interictally, were significantly higher than those of CS. However, the values of plasma ET1 in ETTP and in CTTHP did not differ statistically from those of CS. MPA and MPWA ET1 plasma levels increased significantly within 2 h from the onset of attacks (p<0.0001) and remained significantly higher between 4 and 6 h from the onset. The ET1 plasma levels of ETTHP and CTTHP assessed during attacks did not differ statistically from those of the same patients assessed in the headache‐free periods. The increase in ET1 levels in MPA and MPWA patients when assessed ictally, suggests that this peptide is involved in the haemodynamic changes and vascular tone modifications observed during migraine attacks, particularly in the first phase of the ictal period.
Characteristics associated with life expectancy in Alzheimer's disease (AD) are still far from known. Here we aimed at examining the ability of baseline/longitudinal clinical variables to predict time to death. One-hundred fifty AD outpatients underwent diagnostic, neuropsychiatric, and functional assessment at baseline (when ApoE ɛ4 was also investigated) and at each subsequent annual visit. A random effects joint modeling approach was used to simultaneously model the baseline and longitudinal trajectory of each factor and predict the time to death, adjusting for demographic covariates. An ancillary analysis of ApoE ɛ4 status as a predictor was also conducted. Kaplan-Meier survival curves were constructed to elucidate the relationship between each factor and the estimated probability of death over time. Shorter survival was associated with male gender, higher education, older age, lower cognition, and worse functioning in daily life, but not ApoE ɛ4 status. Longitudinal trajectories increased predictive power over using just baseline levels highlighting apathy, and secondarily aberrant motor behaviors and sleep disorders, as a highly reliable predictor for mortality. Apathy was the strongest neuropsychiatric predictor of time to death, which supports its role in the pathogenesis of the disorder. An increased knowledge of factors modulating survival in AD is a strategic prerequisite to plan therapeutic interventions.
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