Apathy is a condition characterized by a lack of motivation that manifests in emotional, behavioral, and cognitive domains. Although previous studies have indicated that apathy is associated with frontal lesions, few studies have focused on the different subdomains of apathy, and no in vivo human biochemical data have been obtained to examine the neurochemical changes related to apathy in patients with Alzheimer's disease (AD). Thus, we investigated the frontal neurochemical alterations related to apathy among patients with AD using proton magnetic resonance spectroscopy (1H MRS).

Apathy was assessed through the Apathy Evaluation Scale (AES). 1H MRS was performed to measure neurochemical metabolite levels in the anterior cingulate region and right orbitofrontal region. Associations between neurochemical metabolites and the total score and subscores of each domain of the AES were analyzed.

Altogether, 36 patients completed the study. Patients with lower N-acetylaspartate/creatine ratios (NAA/Cr) in the anterior cingulate region demonstrated higher total apathy scores (β = −0.56, p = 0.003) with adjustments for age, gender, educational level, dementia severity, and depression severity. In a further analysis, a lower NAA/Cr in the anterior cingulate region was associated with all subdomains of apathy, including cognition (β = −0.43, p = 0.028), behavior (β = −0.55, p = 0.002), and emotion (β = −0.50, p = 0.005). No statistically significant associations were discovered in the right orbitofrontal region.

Our results suggest that apathy, in each of its cognitive, behavioral, or emotional subdomains is associated with brain neurochemical alterations in the anterior cingulate region. Abnormal neuronal integrity over the anterior cingulate cortex may exhibit a central role in causing all aspects of apathy in patients with AD.

Theories regarding how spontaneous panic and agoraphobia relate are based mostly on cross-sectional and/or clinic data.

To determine how spontaneous panic and agoraphobia relate longitudinally, and to estimate the incidence rate of and other possible risk factors for first-onset agoraphobia, using a general population cohort.

A sample of 1920 adults in east Baltimore were assessed in 1981 -1982 and the mid-1990s with the Diagnostic Interview Schedule (DIS). Psychiatristdiagnoses were made in a subset of the sample at follow-up (n=816).

Forty-one new cases of DIS/DSM–III–R agoraphobia were identified (about 2 per 1000 person-years at risk). As expected, baseline DIS/DSM-III panic disorder predicted first incidence of agoraphobia (OR=12, 95% CI 3.2-45), as did younger age, female gender and other phobias. Importantly, baseline agoraphobia without spontaneous panic attacks also predicted first incidence of panic disorder (OR=3.9, 95% CI 1.8-8.4). Longitudinal relationships between panic disorder and psychiatrist-confirmed agoraphobia were strong (panic before agoraphobia OR=20, 95% CI 2.3–180; agoraphobia before panic OR=16, 95% CI 3.2–78).

The implied one-way causal relationship between spontaneous panic attacks and agoraphobia in DSM–IV appears incorrect.

The objective is to estimate parameters of the natural history of panic disorder, including its prodrome, incidence, recovery and recurrence.

In 1981 the Baltimore Epidemiologic Catchment Area Study interviewed 3481 individuals probabilistically selected from the household population. During 1993–1996, 1920 of these individuals (73% of survivors) were interviewed again. Baseline and follow-up interviews included the National Institute of Mental Health Diagnostic Interview Schedule. During the follow-up, a subsample was assessed by psychiatrists using the World Health Organization Schedules for Clinical Assessment in Neuropsychiatry (SCAN).

There were 35 new cases of panic disorder in 24 475 person years of exposure, yielding an annual incidence of 1.43 per 1000 per year. Data from the SCAN assessments suggest the incidence estimate is conservative. Incidence is greater in females and declines with age. About one-third of the new cases arise without agoraphobia, but about half have anxiety of some sort present for many years prior to meeting criteria for diagnosis. People with agoraphobia have less intense onsets but slower recoveries than those without agoraphobia.

Panic is heterogeneous in its pattern of onset and recovery. Some of the heterogeneity is associated with the presence of other anxiety over a long period of the life.