Lateralized microstructural changes in early-stage Parkinson's disease in anterior olfactory structures, but not in substantia nigra.

Parkinson's disease (PD) is a progressive neurological disorder characterized by motor symptoms as well as severe deficits in olfactory function and microstructural changes in olfactory brain regions. Because of the evidence of asymmetric neuropathological features in early-stage PD, we examined whether lateralized microstructural changes occur in olfactory brain regions and the substantia nigra in a group of early-stage PD patients. Using diffusion tensor imaging (DTI) and the University of Pennsylvania Smell Identification Test (UPSIT), we assessed 24 early-stage PD patients (Hoehn and Yahr stage 1 or 2) and 26 healthy controls (HC). We used DTI and a region of interest (ROI) approach to study the microstructure of the left and right anterior olfactory structures (AOS; comprising the olfactory bulbs and anterior end of the olfactory tracts) and the substantia nigra (SN). PD patients had reduced UPSIT scores relative to HC and showed increased mean diffusivity (MD) in the SN, with no lateralized differences. Significant group differences in fractional anisotropy (FA) and MD were seen in the AOS, but these differences were restricted to the right side and were not associated with the primary side of motor symptoms amongst PD patients. No associations were observed between lateralized motor impairment and lateralized microstructural changes in AOS. Impaired olfaction and microstructural changes in AOS are useful for early identification of PD but asymmetries in AOS microstructure seem unrelated to the laterality of PD motor symptoms.

Olfactory deficits in patients with schizophrenia and severe polydipsia.

BACKGROUND: The present study was designed to assess olfactory function in severely polydipsic/hyponatremic patients with schizophrenia who also had intermittent water intoxication. METHODS: The University of Pennsylvania Smell Identification Test and an olfactory acuity battery were administered to three groups of male subjects: 9 patients with schizophrenia and severe polydipsia/hyponatremia, 9 control nonpolydipsic/normonatremic patients with schizophrenia, and 9 normal controls. RESULTS: Male patients with severe polydipsia/hyponatremia and intermittent water intoxication had marked olfactory acuity and identification deficits when compared to the patient control group of similar age and age at illness onset, and to normal controls. CONCLUSIONS: The finding of deficient acuity (detection threshold) in the polydipsic/hyponatremic group but not the nonpolydipsic, normonatremic group suggests that for this subgroup, abnormalities of olfactory sensory function may occur in a pattern previously reported for other brain disorders such as Alzheimer's disease.

Impaired olfactory identification in relatives of patients with familial schizophrenia.

OBJECTIVE: Impaired olfactory identification ability has previously been demonstrated in patients with schizophrenia. This study assessed olfactory function in psychotic and nonpsychotic members of multigenerational families with familial schizophrenia to determine whether deficits were present in both groups. METHOD: The University of Pennsylvania Smell Identification Test was administered birhinally to three groups of subjects aged less than 65 years: 19 psychotic and 27 nonpsychotic members of families with familial schizophrenia and 43 age- and sex-matched healthy volunteers. RESULTS: Nonpsychotic family members had significantly higher mean University of Pennsylvania Smell Identification Test scores than psychotic family members but were impaired relative to the healthy volunteer group. These group differences could not be accounted for by age, sex, or smoking habit. Fifty-eight percent of the psychotic and 34% of the nonpsychotic family members performed in the microsmic (impaired) range, compared to 9% of the healthy volunteers. CONCLUSIONS: Impaired olfactory deficits may aggregate in families with schizophrenia and may be indicative of a genetic predisposition to psychosis.

Olfactory function in monozygotic twins discordant for schizophrenia.

OBJECTIVE: Abnormalities of olfactory identification ability have been proposed as a marker of cerebral dysfunction in schizophrenia. The authors studied the potential role of genetic factors in olfactory dysfunction by assessing monozygotic twins discordant for schizophrenia and matched comparison subjects. METHOD: The subjects were 12 pairs of monozygotic twins discordant for schizophrenia and 12 healthy subjects matched for sex and age. Each subject completed the University of Pennsylvania Smell Identification Test. RESULTS: The combined twin group scored significantly lower on smell identification than did the comparison group. The affected and unaffected twin groups did not differ from each other. CONCLUSIONS: Genetic factors may contribute to cerebral dysfunction as assessed by olfactory identification ability.

Olfactory hallucinations and olfactory identification ability in patients with schizophrenia and other psychiatric disorders.

Olfactory identification ability and the prevalence of olfactory hallucinations were examined in 183 hospitalized patients from three diagnostic groups. One hundred and thirty-one patients with schizophrenia, 21 patients with major depression, 31 women with eating disorders along with 77 normal control subjects were examined using the University of Pennsylvania Smell Identification Test (UPSIT) and were questioned regarding the presence of olfactory hallucinations. Olfactory identification deficits were observed only in patients with schizophrenia. In contrast, olfactory hallucinations were reported by members of all psychiatric diagnostic categories (34.6% of patients with schizophrenia; 19% of depressed patients and 29% of eating disorders patients). For patients with schizophrenia, women were more likely to report olfactory hallucinations and had higher UPSIT scores than men.

Left nostril olfactory identification impairment in a subgroup of male patients with schizophrenia.

Abnormal structural brain asymmetries have been reported in schizophrenia in brain areas which overlap with olfactory processing regions, with abnormalities more often described within the left hemisphere. We attempted to determine whether the olfactory agnosia observed in some male patients with schizophrenia was more likely left-hemisphere based. We assessed unirhinal (single nostril) olfactory identification and detection threshold in 65 male patients who met DSM-IV criteria for the diagnosis of schizophrenia and 59 healthy male control subjects. A two-way, mixed-design ANCOVA with diagnosis as the between-group factor, nostril as the within-subject factor and age as covariate was used to compare olfactory identification ability. This analysis demonstrated that patients with schizophrenia performed more poorly than the healthy controls across nostrils, but no differences were observed in either group between nostrils. However, when patients were classified according to unirhinal olfactory status (impaired left < right, impaired right < left, normosmic left < right, normosmic right < left), impaired patients were more than twice as likely to be classified as having a left nostril disadvantage than right nostril disadvantage. In contrast, within the normosmic group of patients, this pattern was reversed. Moreover, when those patients whose unirhinal olfactory scores differed by less than two points were removed from the analysis, a 2:1 ratio of left < right versus right < left was observed in the impaired patients. These results suggest that for impaired male patients with schizophrenia, olfactory identification deficits are more likely found for the left nostril, perhaps indicative of abnormalities in olfactory processing within the left hemisphere.

Improvement in cognitive functioning in patients with first-episode psychosis during treatment with quetiapine: an interim analysis.

BACKGROUND: The efficacies of second-generation antipsychotic medications in reducing symptoms are reasonably well-documented, but their effects on cognition are less clearly understood. AIMS: To under take an interim analysis of an open label, 2-year study examining the effects of quetiapine on cognition in patients with a first episode of schizophrenia and related disorders. METHOD: Cognitive testing was performed before quetiapine was initiated and repeated after 3, 6 and 12 months of treatment. To date, 13 patients have been fully assessed (mean dose 517.9 mg/day; s.d. = 225.8). RESULTS: Statistically significant improvement was noted on measures of attention (Continuous Performance Test; CPT), verbal productivity (Verbal Fluency Test) and executive function (Object Alternation Test) after 6 and 12 months of treatment. For the CPT, improvement was also noted after 3 months of treatment. CONCLUSIONS: During treatment for 1 year with quetiapine, cognitive performance was improved in young patients with psychosis. Continued controlled investigations of the effects of quetiapine on cognition are desirable.

Toxicity of the systemic insecticide, imidacloprid, to forest stream insects and microbial communities.

Imidacloprid was added to laboratory aquatic microcosms at concentrations of 12, 24, 48 and 96 microg/L to determine effects on leaf-shredding aquatic insect survival and feeding rates, and on aquatic microbial decomposition of leaf material. Survival of the stonefly, Pteronarcys dorsata, was significantly reduced at 48 and 96 microg/L. There was no significant mortality of the cranefly, Tipula sp., but most surviving tipulids were very sluggish and non-responsive to prodding at 48 and 96 microg/L. Leaf decomposition by these leaf-shredding insects was significantly reduced at all test concentrations. There were no significant adverse effects on microbial decomposition of leaf material.

Olfactory identification ability in patients with panic disorder.

Deficits in olfactory identification ability have been reported in some groups of psychiatric patients, but not others. Our study examined olfactory identification ability in patients with panic disorder. Results indicate that this ability is intact in this population and, further, that psychotropic medications appear not to interfere with olfaction.

Extrapyramidal signs and clinical symptoms in first-episode schizophrenia: response to low-dose risperidone.

The purpose of this study was to determine the prevalence of extrapyramidal signs or symptoms (EPS) and clinical symptoms in first-episode schizophrenia, before any treatment, during and after treatment with a novel antipsychotic, risperidone. Twenty-two (17 men; 5 women) patients were examined using the Extrapyramidal Symptom Rating Scale, Positive and Negative Syndrome Scale (PANSS), Clinical Global Impressions-Severity of Illness and Improvement, and Global Assessment of Functioning. Three patients (14%) had distinct EPS at baseline, whereas all were free of EPS after treatment with risperidone. On the maximum dose of risperidone (5-8 mg), 32% of the total sample developed mild akathisia or parkinsonism, both of which diminished with dosage reduction. No clinically significant EPS were observed in patients receiving 2 to 4 mg of risperidone. Analysis of symptom response of the lower (2-4 mg) versus the higher (5-8 mg) doses of risperidone resulted in superior outcome in the 2- to 4-mg group for all three symptom clusters of the PANSS. In addition, 91% of the low-dose group achieved a 20% or greater reduction in total PANSS score compared with 27% for the high-dose group. These findings have clinical relevance directed at the early and longer-term treatment of schizophrenia.

Clinical features of schizophrenia in a woman with hyperandrogenism.

Ample evidence supports sex differences in the clinical features of schizophrenia. In this regard, estrogen may contribute to later onset and less severe course of illness in women. Direct investigation of hormonal status in schizophrenia is extremely difficult. The present report documents the clinical features of schizophrenia in a young woman with long-standing hyperandrogenism related to polycystic ovarian disease. We postulate that hyperandrogenism contributed to a relatively early onset, olfactory dysfunction, and other clinical features of schizophrenia more commonly associated with men. Additionally, acute estrogen depletion following cessation of oral contraceptives may have precipitated psychosis, while recommencement of oral contraceptives could have contributed to subsequent improvement in symptoms.