Dementia is associated with insulin resistance in patients with Parkinson's disease.

BACKGROUND: Parkinson's disease is a neurodegenerative disorder involving the basal ganglia. Type-2 Diabetes Mellitus is an important risk factor for Alzheimer disease and vascular dementia. However, the association between Parkinson's disease and Diabetes Mellitus is controversial. OBJECTIVE: To investigate glucose metabolism abnormalities in 110 Parkinson's disease patients with and without dementia. SUBJECTS AND METHODS: We evaluated Insulin Resistance, glucose and insulin levels after a 2-h-oral-glucose-tolerance-test in 53 Parkinson's disease with dementia and 57 with Parkinson's disease without dementia, with normal fasting glucose. RESULTS: BMI, waist circumference, fasting glucose and insulin values, HbA1c, triglycerides, blood lipid profile, depression rating, educational levels, levodopa-dosage and antipsychotic use were similar in both groups. Disease duration and motor impairment were higher in patients with Parkinson's disease and dementia group. After 2-h-oral-glucose-tolerance-test, the prevalence of glucose metabolism abnormalities was significantly higher in group with Parkinson's disease and dementia group (p=0.03). The insulin resistance was present in 62% patients with Parkinson's disease with dementia, of whom 30% had also impaired glucose tolerance, 5,6% newly diagnosed Diabetes Mellitus and 26% only Insulin Resistance. These percentages were significantly higher in group with Parkinson's disease and dementia, also after adjustment for disease duration and motor disability. CONCLUSIONS: Our study suggests that PD patients with dementia are two times more likely to have insulin resistance than patients with PD.

Effects of insulinic therapy on cognitive impairment in patients with Alzheimer disease and diabetes mellitus type-2.

BACKGROUND: Type-2 Diabetes Mellitus (DM-2) is an important risk factor for Alzheimer disease (AD) and vascular dementia (VD). The role of insulinic therapy on cognitive decline is controversial. OBJECTIVE: To evaluate cognitive impairment in patients with AD and DM-2 treated with either oral antidiabetic drugs or combination of insulin with other diabetes medications. METHODS: 104 patients with mild-to-moderate AD and DM-2 were divided into two groups, according to antidiabetic pharmacotherapy: group A, patients treated with oral antidiabetic drugs and group B, patients treated with insulin combined with other oral antidiabetic medications. Cognitive functions were assessed by the Mini Mental State Examination (MMSE) and the Clinician's Global Impression (CGI), with a follow-up of 12 months. RESULTS: At the end of the study, the MMSE scores showed a significant worsening in 56.5% patients of group A and in 23.2% patients of group B, compared to baseline MMSE scores (P=.001). Also CGI-C scores showed a significant worsening for all domains after 12 months in group A vs group B (P=.001). The two groups were matched for body mass index, serum lipids, triglycerides, Apo epsilon4 allele and smoke habit. Conversely, ischemic heart disease and hypertension were significantly higher in group B (P=.002). After adjustment for this risk variables, our results remained significant (P=.001). CONCLUSIONS: Our study suggests that insulinic therapy could be effective in slowing cognitive decline in patients with AD.

Acute hemifacial dystonia possibly induced by clebopride.

Dystonic reactions produce twisting and repetitive movements or abnormal posturing. Severe dystonic reactions have been shown to occur in concert with numerous medications. This report details the case of a patient who developed hemifacial dystonia as acute side reaction from administration of clebopride for dyspeptic prophylaxis. When the drug was immediately stopped, the dystonic posture disappeared completely within 2 weeks. The use of clebopride may be associated with not only a reversible or persistent parkinsonism syndrome but also hemifacial dystonia; therefore, attention must be drawn to this possible side effect.

Glucose metabolism in the idiopathic blepharoptosis: utility of the Oral Glucose Tolerance Test (OGTT) and of the Insulin Resistance Index.

BACKGROUND: Diabetes mellitus (DM), neuromuscular, hereditary or immunological disorders are the most common identified causes of blepharoptosis. However, in about 15-25% they remained uncertain. OBJECTIVE: To determined the role of glucose metabolism abnormality in idiopathic blepharoptosis. METHODS: We identified 162 patients with unilateral idiopathic blepharoptosis and 128 control subjects. In all we evaluated a glucose and insulin levels at fasting and after 2 h-OGTT. In addition we determined insulin resistance (IR), by HOMA-index. RESULTS: Following a 2 h-OGTT the prevalence of undiagnosed glucose metabolism abnormality was significantly higher in blepharoptosis patients vs. control group (P<.001). The IR was documented in 129 patients (78%), of whom 55 (34%) had Impaired Glucose Tolerance (IGT), 36 (22%) newly diagnosed DM (NDDM) and 38 (30%) only IR. The Body Mass Index, blood pressure, serum lipids, triglycerides and smoking were not associated with an increased risk of developing ptosis. Conversely, waist circumference were significantly increased in blepharoptosis patients (P=.003). CONCLUSIONS: In this study we focused on emerging evidence that prediabetic status may represent a risk factor for developing blepharoptosis. We propose that 2 h-OGTT and mainly HOMA-index should be determined as a rule in all patients with idiopathic blepharoptosis.

SUNCT and high nocturnal prolactin levels: some new unusual characteristics.

SUNCT is a rare condition characterised by a short-lasting periorbital pain associated with autonomic symptoms and is usually unresponsive to pharmacological treatment. We report a case of SUNCT syndrome linked to a pituitary micro-adenoma, with only nocturnal attacks. The nocturnal levels of prolactin (PRL) were increased, while other hormonal, haematological, serological and biochemical investigations and levels of PRL did not reveal abnormal findings during the day-time. PRL serum secretion after thyrotropin-releasing hormone test was lower than nocturnal secretion, but not enough to induce severe attacks. We suggest that in our patient the rise of nocturnal levels of PRL could have a direct role in the worsening of this headache, perhaps secondarily to an altered regulation of the hypothalamic-hypophysial axis, however the actual influence of sleep and the interaction between all neurotransmitters and hormones needs to be clarified further.