Subject(s)
Meningeal Neoplasms/diagnosis , Meningioma/diagnosis , Adolescent , Contrast Media , Diagnosis, Differential , Humans , Image Enhancement/methods , Magnetic Resonance Imaging/methods , Male , Meningeal Neoplasms/complications , Meningeal Neoplasms/surgery , Meningioma/surgery , Seizures/etiology , Temporal Lobe/diagnostic imaging , Temporal Lobe/pathology , Temporal Lobe/surgery , Tomography, X-Ray Computed/methodsABSTRACT
BACKGROUND: There is growing evidence from case-control and from cohort studies that smoking is inversely related to the risk of developing Parkinson's disease (PD). However, it is still controversial if PD starts at an older age in ever-smoking patients compared to never-smoking ones. PATIENTS AND METHODS: The present retrospective study compares in a large series of 512 out-patients, collected over the last 24 years, the age of onset of the complaints, the age at which PD was diagnosed and the start of levodopa treatment between ever- and never-smokers. Also, the occurrence of long-term side-effects of the drug was evaluated. 184 PD patients with a history of smoking were compared with 328 who had never smoked. The subgroups with and without a family history of PD were analysed separately. RESULTS: In the overall ever-smoking group, as well as in the subgroup without a family history, the onset of the disease and the time of the diagnosis of PD and the time at which levodopa was started occurred at an older age than in the never-smoking group. This difference could not be demonstrated in the patients with a family history, due to the low number of cases and the lack of statistical power. Although the follow-up period was the same in both study groups, motor fluctuations and dyskinesia were more frequent and appeared earlier after levodopa treatment in the non-smoking compared to the ever-smoking PD patients. Only for cognitive impairment there was a non-significant trend in the smoking group. CONCLUSION: The present study confirms the protective action of smoking on PD and also suggests some modulating effect of smoking on the dopaminergic system.
Subject(s)
Age of Onset , Movement Disorders/epidemiology , Movement Disorders/physiopathology , Parkinson Disease/epidemiology , Parkinson Disease/physiopathology , Smoking , Aged , Antiparkinson Agents/therapeutic use , Case-Control Studies , Cognition Disorders/drug therapy , Cognition Disorders/physiopathology , Cohort Studies , Dyskinesia, Drug-Induced/physiopathology , Female , Human Development , Humans , Levodopa/therapeutic use , Male , Middle Aged , Movement Disorders/drug therapy , Parkinson Disease/drug therapy , Smoking/adverse effects , Time FactorsABSTRACT
BACKGROUND: Despite extensive research, it still remains controversial as to what the precise location of the critical lesions underlying amnesia actually is. The amnesic syndrome is believed to be heterogeneous and due to several distinct functional deficits. PATIENTS AND METHODS: Two patients, a 45-year-old woman and a 56-year-old man, with sudden cardiopulmonary arrest and successful resuscitation, were left with a clear amnesic syndrome as main neurological sequela. During their revalidation period, they underwent a positron emission tomographic (PET) examination, utilizing the (13)NH(3) bolus technique at rest and after intravenous acetazolamide administration. RESULTS: Both PET studies showed more or less similar features with a decrease in regional cerebral blood flow (rCBF) in the frontal, temporal and parietal lobes. In addition, the rCBF was increased in both thalami of the 45-year-old woman and in the striata of the 56-year-old man. Acetazolamide vasoreactivity was most lost in the frontal lobes. CONCLUSIONS: In the present PET study, we demonstrated that destruction of the inhibitory pathways to the thalamus and basal ganglia by ischaemic-hypoxic frontal lesions could be one of the mechanisms leading to amnesia.
