ABSTRACT
Studies of clinically depressed patients have documented left frontal lobe hypoactivity. Smokers also show an increased prevalence of depression and evidence that nicotine normalizes qEEG indices of left frontal lobe activity. Tryptophan depletion (TD) has been shown to increase negative mood in smokers, particularly those with recurrent depression. Thus, in smokers, we expected that increased depression during TD would be associated with decreased cerebral blood flow, specifically in the left frontal lobe. Hamilton depression scores and relative regional cerebral blood flow (rCBF) were measured with SPECT using (99m)Tc-hexamethylpropyleneamineoxime in seven smokers after TD and after a control procedure. Decreased bilateral cerebral blood flow to the inferior frontal (IF) lobe following TD relative to placebo was associated with increased depressed mood (r= -.653, P<.05). Among smokers, a decrease in brain serotonin is associated with increased depressed mood and with focal bilateral decreases in IF activity. Chronic nicotine exposure appears to be associated with cortical responses suggestive of depressive vulnerability.
Subject(s)
Cerebrovascular Circulation/physiology , Depressive Disorder/physiopathology , Frontal Lobe/blood supply , Smoking/physiopathology , Tryptophan/deficiency , Adult , Analysis of Variance , Cerebral Cortex/blood supply , Depressive Disorder/psychology , Double-Blind Method , Humans , Middle Aged , Smoking/psychology , Tomography, Emission-Computed, Single-Photon/methodsABSTRACT
Frontotemporal dementia is an underdiagnosed illness with predominant behavioral and executive manifestations. Historically, diagnosis has been based on a combination of clinical history, neuropsychological testing, and brain imaging. No effective treatment currently exists for this disorder. A case is presented using quantitative EEG with methylphenidate challenge correlated with SPECT. The patient underwent neuropsychological testing, a SPECT brain study, and a quantitative EEG, which was repeated after methylphenidate administration. SPECT was significant for hypoperfusion to the bilateral frontotemporal regions, with left-sided hypoperfusion greater than homologous right as demonstrated by LORETA analysis. QEEG correlated with SPECT, and demonstrated profound left greater than right bi-frontotemporal slowing, which normalized partially after methylphenidate administration. The patient has remained on methylphenidate as an outpatient, and has had significant behavioral improvement. Quantitative EEG may provide both diagnostic and therapeutic data with regard to frontotemporal dementia. Further studies of methylphenidate in this population are needed to confirm these data.
Subject(s)
Brain Mapping/methods , Dementia/diagnosis , Dementia/drug therapy , Electroencephalography/methods , Methylphenidate/therapeutic use , Aged , Central Nervous System Stimulants/therapeutic use , Dementia/diagnostic imaging , Electroencephalography/drug effects , Humans , Male , Tomography, Emission-Computed, Single-Photon/methodsSubject(s)
Arthritis, Infectious/diagnostic imaging , Bone Neoplasms/diagnostic imaging , Bone Neoplasms/secondary , Rotator Cuff Injuries , Shoulder Joint/diagnostic imaging , Aged , Bone and Bones/diagnostic imaging , Diagnosis, Differential , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Radionuclide ImagingABSTRACT
Seven clinically healthy, nondiabetic (ND) and four Type II diabetic (D) men were assessed for circadian rhythms in oxidative "stress markers." Blood samples were collected at 3h intervals for approximately 27 h beginning at 19:00h. Urine samples were collected every 3 h beginning with the 16:00h-19:00h sample. The dark (sleep) phase of the light-dark cycle extended from 22:30h to 06:30h, with brief awakening for sampling at 01:00h and 04:00h. Subjects were offered general hospital meals at 16:30h, 07:30h, and 13:30h (2400 cal in total/24h). Serum samples were analyzed for uric acid (UA) and nitrite (NO) concentrations, and urine samples were assayed for 8-hydroxydeoxyguanosine (8-OHdG), malondialdehyde (MDA), and 8-isoprostane (ISP). Data were analyzed statistically both by the population multiple-components method and by the analysis of variance (ANOVA). The 24h mean level of UA and NO was greater in D than in ND subjects (424 vs. 338 micromol/L and 39.2 vs. 12.7 microM, respectively). A significant circadian rhythm in UA (p = 0.001) and NO (p = 0.048) was evident in ND but not in D (p = 0.214 and 0.065). A circadian rhythm (p = 0.004, amplitude = 8.6 pmol/kgbw/3h urine vol.) was also evident in urine 8-OHdG of ND but not of D. The 24h mean levels of ND and D were comparable (76.8 vs. 65.7 pmol/kgbw/3h urine vol.). No circadian rhythm by population multiple-components was evident in MDA and ISP levels of ND subjects, or in 8-OHdG, MDA, and ISP in D. However, a significant time-effect was demonstrated by ANOVA in all variables and groups. The 24h mean of MDA and ISP in D was significantly greater than in ND (214 vs. 119 nmol/3h urine vol. and 622 vs. 465 ng/3h urine vol.). The peak concentrations of the three oxidative "stress markers" in urine, like those of serum NO, occurred early in the evening in both groups of men. This observation suggests a correlation between increased oxidative damage and increased rate of anabolic-catabolic events as evidenced by similarities in the timing of peak NO production and in parameters relevant to metabolic functions.
