Phenomenological comparison of poststroke depression and functional depression

The authors used structured clinical interviews to compare depressive symptoms in 43 patients with poststroke major depression and 43 patients with major depression without a known medical cause. The depressive syndrome profiles in the two patient groups were highly similar.     

Late-life depression: the differences between early- and late-onset illness in a community-based sample

BACKGROUND: Several studies have described etiological and clinical differences between elderly depressed patients with early onset of their illness compared to late onset. While most studies have been carried out in clinical samples it is unclear whether the findings can be generalized to the elderly population as a whole. The aim of this study was to compare early-onset (EOD) and late-onset (LOD) depressive illness in a community-based sample. METHODS: Large (n = 3107) representative sample of older persons (55-85 years) in the Netherlands. Two-stage screen procedure to identify elderly with MDD. The Center for Epidemiologic Studies Depression scale (CES-D) was used as a screen and the Diagnostic Interview Schedule (DIS) to diagnose MDD. Data on 90 older persons with early-onset depression and 39 with late-onset depression were available. RESULTS: Those with LOD were older, and more often widowed. Family psychiatric history, vascular pathology, and stressful early and late life events did not differ between groups. EOD subjects had more often double depression and more anxiety. CONCLUSIONS: In a community-based sample we did not detect clear differences in etiology and phenomenology between EOD and LOD. This discrepancy with reports from clinical samples could be due to selection bias in clinical studies. Consequently, all patients with late-life depression deserve a diagnostic work-up of both psychosocial and somatic risk factors and treatment interventions should be focused accordingly.     

Distinction of early- and late-onset depression in the elderly by their lifetime symptomatology

OBJECTIVE. It has been proposed that early-onset depression (EOD) and late-onset depression (LOD) differ etiologically and phenomenologically. To validate the phenomenological distinction, the affective symptoms of elderly subjects with EOD and LOD were compared. METHODS. Seventy-one patients with age-at-onset of depression below 60 years (EOD) and 67 age-matched patients with age-at-onset above 60 years (LOD) were consecutively recruited from the Departments of Psychiatry of the University of Mainz and the University of Bonn. To reduce the effect of interepisode variance of symptoms, we focused on the lifetime prevalence of different affective symptoms which were evaluated using the Composite International Diagnostic Interview (CIDI). Logistic regression analysis was performed to identify particular depressive symptoms which might discriminate EOD and LOD, and to account for possible sociodemographic differences between the two groups. RESULTS AND CONCLUSION. Low spirits and feelings of worthlessness were more frequently found in EOD, they were sufficient discriminators to distinguish elderly subjects with EOD and LOD. This study provides further evidence for a phenomenological distinction between early- and late-onset depression in the elderly.     

Early-onset versus late-onset bipolar II chronic depression

Age at onset is an important dimension in the classification of mood disorders. Recent findings on early-onset (EO) versus late-onset (LO) unipolar chronic depressions support this subtyping. The aim of the present study was to determine clinical differences between EO and LO bipolar II chronic depression and to support this subtyping also in bipolar II. Eighty-seven consecutive bipolar II chronic depression outpatients were interviewed with the Structured Clinical Interview for DSM-IV, the Montgomery Asberg Depression Rating Scale, and the Global Assessment of Functioning scale. EO cut-offs were 21 and 23 years of age. Variables, studied with linear and logistic regression, were age, gender, age at onset, illness duration, recurrences, atypical, melancholic, and psychotic features, axis I comorbidity, and severity. Lower age at onset was significantly associated with lower age, longer illness duration, less psychosis, less severity, more atypical features, and more axis I comorbidity. Results support the subtyping of bipolar II chronic depression in EO and LO on the basis of different clinical features.     

A family study of Alzheimer disease and early- and late-onset depression in elderly patients

BACKGROUND: The substantial symptomatic overlap between depression and dementia in old age may be explained by common genetic vulnerability factors. METHODS: We investigated this idea by comparing the occurrence of both disorders in first-degree relatives of 78 patients with Alzheimer disease (AD), of 74 with late-onset depression (onset age of > or = 60 years), of 78 with early-onset depression, of 53 with comorbid lifetime diagnoses of AD/depression, and of 162 population control subjects. Diagnostic information on their 3002 relatives was obtained from structured direct assessments and from family history interviews. RESULTS: The 90-year lifetime incidence of primary progressive dementia was significantly higher in relatives of patients with AD (30%) and comorbid AD/depression (27%) than in relatives of patients with early-onset (21%) or late-onset (26%) depression, or of controls (22%) (P =.01). Lifetime incidence of depression was significantly higher in relatives of patients with early-onset depression (13%) than in relatives of patients with AD (10%) or controls (9.0%) (P =.006). Lifetime incidence of depression was similar in control relatives and in relatives of those patients with comorbid AD/depression (8.6%). Relatives of patients with late-onset depression also showed similar occurrence of depression until the age of 80 years, but the figure increased sharply thereafter to 19.1% by the age of 90 years. CONCLUSIONS: Primary progressive dementia and early-onset depression represent clinical entities with distinct inheritance. Late-onset depression does not share substantial inheritance in common with dementia or with early-onset depression, but does show modest familial clustering.     

Comparison of spontaneously recovered versus nonrecovered patients with poststroke depression

We followed 16 patients who developed depression immediately after a stroke for 6 months. By that time, six patients showed no depression (recovered group), while 10 patients were still depressed (nonrecovered group). There were no significant differences in demographic variables and social functioning between the groups, but the nonrecovered group showed less improvement in cognitive function and more physical impairments. Patients in the nonrecovered group had mainly cortical lesions, while those in the recovered group had mainly subcortical and posterior circulation strokes.     

Methodological characteristics in establishing rat models of poststroke depression

BACKGROUND: Ideal model of poststroke depression (PSD) may be induced in rats guided by the theoretical evidence that "primary endogenous mechanism" and "reactivity mechanism" theories for PSD in human being. OBJECTIVE: To investigate the feasibility of comprehensive methods to induce PSD models in rats. DESIGN: A randomized controlled animal trial. SETTING: Department of Neurology, Affiliated Hospital of Chengdu University of Traditional Chinese Medicine. MATERIALS: Male SD rats of SPF degree, weighing 350-500 g, were provided by the experimental animal center of Chengdu University of Traditional Chinese Medicine. The rats were raised for 1 week adaptively, then screened behaviorally by open-field test and passive avoidance test. Forty-five rats with close scores were randomly divided into normal control group (n =10), simple stroke group (n =10), stress group (n =10) and PSD group (n =15). METHODS: The experiments were carried out in the laboratory of Chengdu University of Traditional Chinese Medicine from July 2002 to February 2003. ① Rat models of focal cerebral ischemia were induced by thread embolization, then treated with separate raising and unpredictable stress to induce PSD models. ②The neurologic deficit was evaluated by Longa 5-grade standard (the higher the score, the severer the neurologic deficit) and horizontal round rod test (normal rat could stay on it for at least 3 minutes). ③ The behavioral changes of PSD rats were evaluated by the saccharin water test, open-field text and passive avoidance test, including the changes of interest, spontaneous and exploratory activities, etc. ④ The levels of monoamine neurotransmitters, including norepinephrine (NE), serotonin (5-HT) and dopamine, in brain were determined using fluorospectrophotometry. MAIN OUTCOME MEASURES: ① Score of Longa 5-grade standard; Stayed time in the horizontal round rod test; ② Amount of saccharin water consumption; Open-field text: time stayed in the central square, times wondering among squares, times for upright grooming; Passive avoidance test: total number of shocks, duration of being shocked; ③ Contents of NE, 5-HT and dopamine in brain. RESULTS: Six rats died and 3 rats failed in the model establishment, and finally 36 rats were involved in the analysis of results. ① 22 stroke rats were evaluated by the Longa 5-grade standard (including 9 in the stroke group and 13 in the PSD group), the scores at 4, 8 and 24 hours after consciousness were 2.58±0.69, 2.32±0.58 and 1.37±0.60, respectively. ② 20 stroke rats were evaluated by the horizontal round rod test (including 8 in the stroke group and 12 in the PSD group), and the time stayed on the rod at 1, 3 and 5 days after stroke were (110.94±31.40), (149.53±16.56) and (169.88±8.44) s, respectively. ③ The body masses at 7 and 14 days after stroke were significantly lower in the PSD group than the normal control group [(348.8±47.7), (390.9±22.9) g, P < 0.05; (321.7±43.8), (392.6±23.5) g, P < 0.01]. ④ The amount of saccharin-water consumption was significantly lower in the PSD group than the normal control group [(8.48±1.15), (113.0±11.8) mL/kg, P < 0.01]. ⑤ The PSD rats had reduced activities in the open-field test and passive avoidance deficits, which were obviously different from those in the normal control group (P < 0.05). ⑥ The NE and 5-HT contents in bilateral frontoparietal cortexes and brain stem in the PSD group were significantly decreased as compared with those in the normal control group (P < 0.05); The contents of dopamine in left frontoparietal cortex and brain stem were also obviously lower than those in the normal control group (P < 0.05). CONCLUSION: It is correct and feasible to induce PSD rat model by giving separating raising and stress to rat models of focal cerebral ischemia established by thread embolization of internal carotid artery.     

Familial aggregation of early- and late-onset Parkinson's disease

The role of heredity in early- versus late-onset Parkinson's disease (PD) is controversial. We estimated the degree of increased risk of PD in first-degree relatives of 221 PD probands with age of onset 50 years or younger and 266 PD probands with age of onset older than 50 years compared with the first-degree relatives of 409 control probands. Risk of PD was similar among first-degree relatives of early-onset PD probands (risk ratio [RR], 2.9; 95% confidence interval [CI], 1.6-5.0; p = 0.0002) and late-onset PD probands (RR, 2.7; 95% CI, 1.6-4.4; p = 0.0002) when each was compared with first-degree relatives of controls. However, siblings of early-onset PD probands were at markedly increased risk of PD compared with siblings of controls (RR, 7.9; 95% CI, 2.5-25.5; p = 0.0005), whereas parents of early-onset PD probands were not at significantly increased risk compared with parents of controls (RR, 1.7; 95% CI, 0.9-3.3; p = 0.2). In late-onset families, both siblings (RR, 3.6; 95% CI, 1.3-10.3; p = 0.02) and parents (RR, 2.5; 95% CI, 1.4-4.6; p = 0.003) were at increased risk compared with control relatives. This pattern is consistent with an autosomal recessive contribution to the inheritance of early but not late-onset PD. Genetic factors are important in both early- and late-onset PD, but specific genes and mode of inheritance may differ between the two groups.     

Neuropsychologic features of early- and late-onset Alzheimer's disease

Forty-one patients with clinically diagnosed Alzheimer's disease were divided into two groups for comparison of neuropsychologic features in those with early- and late-onset disease. Handedness was also assessed in all patients. Twenty-three patients with onset before age 65 had significantly more language impairment, whereas 18 patients with onset at age 65 or older had more difficulty with visuoconstructional function. Memory was severely impaired in all patients. Only one patient in each group was left-handed, and the same results were obtained when these were excluded. These observations support the notion of left hemisphere vulnerability in early-onset Alzheimer's disease and can be interpreted as demonstrating the clinical variability of the illness rather than the necessity of dividing it into two distinct entities.     

Monocular horizontal OKN in observers with early- and late-onset strabismus.

Several reports on monocular optokinetic nystagmus (OKN) in observers with strabismus have found that asymmetry of OKN tends to occur in both eyes of observers with an early onset of strabismus but only in the deviating eye of those with a later onset of strabismus. Our objective was to quantify and compare the magnitude of the OKN asymmetry in each eye as a function of observer's age at onset of strabismus. We studied monocular OKN in ten observers with early-onset (up to 24 months of age), seven observers with late-onset (after 24 months of age) unilateral strabismus, and 12 normally sighted control observers. In the deviating eye, observers with early-onset strabismus showed large OKN asymmetries in favour of nasalward motion while observers with late-onset strabismus showed smaller OKN asymmetries in that eye. The majority of early- and late-onset observers showed near normal OKN in the non-deviating eye although the early-onset observers showed bilateral asymmetries more often. These findings may be due to both age at onset of strabismus and chronological age and are discussed in terms of the issue of plasticity or recovery of function.     

Rapsyn mutations in hereditary myasthenia: distinct early- and late-onset phenotypes

Rapsyn mutations in 16 unrelated patients with a congenital/hereditary myasthenic syndrome were identified, and a mutation (N88K) common to each of them was found. Two distinct phenotypes were noted: early and late onset. The former is frequently associated with arthrogryposis multiplex congenita and life-threatening crises. The late-onset phenotype developed in adolescence or adulthood and was initially mistaken for seronegative myasthenia gravis. Recognition of this late-onset phenotype should prevent inappropriate immunotherapy.     

Parental alcohol use and brain volumes in early- and late-onset alcoholics.

BACKGROUND: Studies have shown that alcoholics have smaller brain volumes than non-alcoholic cohorts, but an effect of family history (FH) of heavy drinking on brain volume has not been demonstrated. We examined the relationship between an FH of heavy drinking and both brain shrinkage as measured by the ratio of brain volumes to intracranial volume (ICV) as well as maximal brain growth as measured by ICV in early-onset and late-onset alcoholics. METHODS: With T1-weighted resonance imaging, we measured ICV, brain volume, and white and gray matter volume in adult treatment-seeking late-onset and early-onset alcoholics with either a positive or a negative FH of heavy alcohol use, and in healthy control subjects. We also calculated brain shrinkage using a ratio of soft tissue volumes to ICV. RESULTS: The FH positive alcoholic patients had significantly smaller ICVs than FH negative patients, suggesting smaller premorbid brain growth. Brain shrinkage did not correlate with FH. Late-onset alcoholics showed a greater difference in ICV between FH positive and FH negative patients than early-onset alcoholics. Late-onset FH positive patients also had significantly lower IQ scores than late-onset FH negative patients, and IQ scores were correlated with ICV. CONCLUSIONS: These data provide evidence that parental alcohol use might increase risk for alcoholism in offspring in part by a genetic and/or environmental effect that might be related to reduced brain growth.     

Treatment of poststroke generalized anxiety disorder comorbid with poststroke depression: merged analysis of nortriptyline trials.

OBJECTIVE: The existence of anxiety disorders plays an important role in the prognosis and associated impairment among patients with poststroke depression. The authors examined the efficacy of nortriptyline treatment for patients with comorbid generalized anxiety disorder (GAD) and depression after stroke. METHODS: Data from three studies were merged to provide 27 patients with comorbid GAD and depression, who participated in double-blind treatment studies comparing nortriptyline (N=13) and placebo (N=14). Severity of anxiety was measured with the Hamilton Rating Scale for Anxiety (Ham-A), and severity of depression was measured with the Hamilton Rating Scale for Depression (Ham-D). Activities of daily living were assessed by use of the Johns Hopkins Functioning Inventory (JHFI). RESULTS: There were no significant differences between the nortriptyline and placebo groups in demographic characteristics, stroke type, and neurological findings. Patients receiving nortriptyline treatment showed significantly greater improvement on the Ham-A, Ham-D, and JHFI than patients receiving placebo. The anxiety symptoms showed earlier improvement than depressive symptoms in patients treated with nortriptyline. CONCLUSIONS: These findings suggest that poststroke GAD comorbid with poststroke depression may be effectively treated with nortriptyline, and data indicate the need for a trial specifically designed to examine treatment of anxiety disorder.     

Vascular depression: a new view of late-onset depression

We have suggested that cerebrovascular disease may predispose, precipitate, or perpetuate some late-life depressive syndromes. The mechanisms of "vascular depression" include disruption of cortico-striato-pallido-thalamo-cortical (CSPTC) pathways or their modulating systems. This view is supported by the presentation of vascular depression, which consists of depressive symptoms, cognitive abnormalities, as well as neuroimaging findings that may result from CSPTC impairment. Moreover, clinical and electrophysiological evidence of CSPTC impairment, an abnormality frequently found in patients with vascular depression, appears to be associated with poor response to antidepressant treatment and early relapse and recurrence. The vascular depression hypothesis provides the conceptual background for studies that may have clinical and theoretical impact. Agents influencing dopamine, acetylcholine, and opioid neurotransmitters may be studied in vascular depression, since these are essential neurotransmitters of the frontostriatal circuitry. Drugs used for prevention and treatment of cerebrovascular disease may be shown to reduce the risk for vascular depression or improve its outcomes. The choice of antidepressants in vascular depression may depend on their effect on neurological recovery from ischemic lesions. Finally, identification of specific relationships between specific symptoms, cognitive deficits, and disability may lead to interventions that target the patients' deficits as well as their interactions with psychosocial factors known to contribute to depression. Research can clarify the pathways to vascular depression by focusing on the site of lesion, the resultant brain dysfunction, the presentation of depression and time of onset, and the contribution of nonbiological factors.     

The assessment of poststroke depression

Poststroke depression (PSD) is a common clinical consequence of stroke. PSD is associated with poor functional and social outcomes, reduced quality of life, the presence of cognitive impairment, and increased mortality. Despite the potential benefit associated with the identification and treatment of PSD, it often remains unrecognized and undertreated. The present study provides a critical review and synthesis of measurement properties for 10 instruments used in the assessment of depression following stroke. Assessment considerations specific to PSD are addressed, and tools are reviewed within the context of stroke. To facilitate the timely detection, diagnosis, and initiation of treatment for PSD, a two-step assessment process is recommended, thereby taking strategic advantage of the strengths and limitations associated with self-report and observer-rating assessment tools.     

Personality disorder comorbidity in early-onset versus late-onset major depression in Japan

This study explored the comorbidity of DSM-III-R personality disorders in early-onset versus late-onset major depression in Japan. The subjects were 117 consecutive outpatients with major depression, with 26 classified as having an early onset (first depressive episode at age 22 or earlier) and 91 classified as having a late onset (first depressive episode at age 23 or later). Personality disorders were assessed using the Structured Clinical Interview for DSM-III-R Personality Disorders after a 2-month antidepressant treatment. The results indicated that early-onset major depression was characterized by greater personality disorder comorbidity than late-onset major depression in Japan. Subjects with any one cluster A or B personality disorder were more prevalent in the early-onset group. In terms of each personality disorder, histrionic, narcissistic, and borderline patients were more prevalent, and the number of criteria met for schizotypal and cluster B personality disorders was significantly larger in early-onset major depression after corrections for age and gender. The results suggested that the higher prevalence of personality pathologies in early-onset major depression may reflect a higher likelihood to convert into bipolar disorders or a stronger impact of having experienced depressive episodes in young individuals. The possibility that the predisposing personality pathology may be different in early-onset and late-onset major depression is also discussed.     

Familial risk of early- and late-onset multiple sclerosis: a Swedish nationwide study

Journal of Neurology - Persons who develop multiple sclerosis (MS) at a young age may bear a higher genetic risk load than persons who develop MS later in life; however, the contribution of...