Saturday, 21 January 2012
AbstractRecent advances in mobile phone technology have placed an impressive array of sensing and communication equipment at the hands of an ever-growing number of people. One of the areas which can potentially be transformed by the availability of what is essentially a cheap, ubiquitous networked sensor, is that of remote diagnosis of movement disorders, such as Parkinson's disease. This work describes a smartphone-based method for detecting and quantifying the hand tremor associated with movement disorders using signals from the accelerometer and gyroscope embedded in the patient's phone. Our approach is web-based and user-friendly, requiring minimal user interaction. In clinical experiments with twenty subjects, we found that by combining both accelerometer and gyroscope signals, we were able to correctly identify those with hand tremor, using very simple signal metrics.
OBJECTIVE:To describe the phenotype of levodopa-induced "on" freezing of gait (FOG) in Parkinson disease (PD).
METHODS:We present a diagnostic approach to separate "on" FOG (deterioration during the "on state") from other FOG forms. Four patients with PD with suspected "on" FOG were examined in the "off state" (>12 hours after last medication intake), "on state" (peak effect of usual medication), and "supra-on" state (after intake of at least twice the usual dose).
RESULTS:Patients showed clear "on" FOG, which worsened in a dose-dependent fashion from the "on" to the "supra-on" state. Two patients also demonstrated FOG during the "off state," of lesser magnitude than during "on." In addition, levodopa produced motor blocks in hand and feet movements, while other parkinsonian features improved. None of the patients had cognitive impairment or a predating "off" FOG.
CONCLUSIONS:True "on" FOG exists as a rare phenotype in PD, unassociated with cognitive impairment or a predating "off" FOG. Distinguishing the different FOG subtypes requires a comprehensive motor assessment in at least 3 medication states.
Thursday, 19 January 2012
J Neurol. 2012 Jan 17. doi: 10.1111/j.1468-1331.2011.03643.x. [Epub ahead of print]
Nielsen HH, Qiu J, Friis S, Wermuth L, Ritz B.
Background and purpose: It has been speculated that gastrointestinal infection with Helicobacter pylori (HP) contributes to the development of Parkinson's disease (PD). We used nationwide Danish registers to investigate this hypothesis. Methods: We identified 4484 patients with a first time PD diagnosis between 2001 and 2008 from the Danish National Patient Register (DNPR) and 22 416 population controls from the Danish Civil Registration System (CRS). Information on drug use was obtained from the National Prescription Registry (NPR). We used logistic regression to compute odds ratios (OR) for the association between treatment for HP and risk of PD. Results: Prescriptions for HP-eradication drugs and proton pump inhibitors (PPI) 5 or more years prior to the diagnosis of PD were associated with a 45% and 23% increase in PD risk, respectively. Hospitalizations and outpatient visits for gastritis and peptic/duodenal ulcers, however, were not associated with PD. Conclusions: Our population-based study suggests that chronic HP infections and/or gastritis contribute to PD or that these are PD-related pathologies that precede motor symptoms.
Wednesday, 18 January 2012
Gallagher D, Schrag A
Neurobiol. Dis. 2012 Jan 3. [Epub ahead of print]
Psychiatric symptoms are important non-motor features in PD, which occur at high frequency and have significant impact on health related quality of life. This review concentrates on the prevalence, pathophysiology, diagnosis and treatment of depression, anxiety, apathy and psychosis. The pathophysiology of these disorders is complex, reflecting the widespread brainstem and cortical pathology in PD, with involvement of several neurotransmitters, including dopaminergic, serotonergic, noradrenergic and cholinergic systems. The diagnosis of psychiatric conditions, in particular affective disorders, is challenging because of the overlap of somatic features of psychiatric disorders and underlying movement disorder. The pathogenesis is likely to differ considerably from non-PD patients, and treatments used in general psychiatry services may not be as effective in PD and will require clearer clarification in well-designed clinical studies. Management strategies include adjustment of dopaminergic medication, use of psychotropic treatments and behavioural and psychological approaches. However, the future challenge will be to develop treatments developed specifically for the pathogenesis of PD.
Friday, 13 January 2012
Xia R, Mao ZH.
AbstractParkinson's disease (PD) is a chronic progressive neurodegenerative disease that is clinically manifested by a triad of cardinal motor symptoms - rigidity, bradykinesia and tremor - due to loss of dopaminergic neurons. The motor symptoms of PD become progressively worse as the disease advances. PD is also a heterogeneous disease since rigidity and bradykinesia are the major complaints in some patients whereas tremor is predominant in others. In recent years, many studies have investigated the progression of the hallmark symptoms over time, and the cardinal motor symptoms have different rates of progression, with the disease usually progressing faster in patients with rigidity and bradykinesia than in those with predominant tremor. The current treatment regime of dopamine-replacement therapy improves motor symptoms and alleviates disability. Increasing the dosage of dopaminergic medication is commonly used to combat the worsening symptoms. However, the drug-induced involuntary body movements and motor complications can significantly contribute to overall disability. Further, none of the currently-available therapies can slow or halt the disease progression. Significant research efforts have been directed towards developing neuroprotective or disease-modifying agents that are intended to slow the progression. In this article, the most recent clinical studies investigating disease progression and current progress on the development of disease-modifying drug trials are reviewed.
Tuesday, 10 January 2012
ST. PAUL, Minn. – Using a nicotine patch may help improve mild memory loss in older adults, according to a study published in the January 10, 2012, print issue of Neurology®, the medical journal of the American Academy of Neurology.
Nicotine has been shown to improve cognitive performance in smokers who have stopped smoking and previous short-term studies with nicotine have shown attention and memory improvement in people with Alzheimer’s disease. This study looked at nicotine in people with mild cognitive impairment, which is the stage between normal aging and dementia when people have mild memory or thinking problems but no significant disability.
The study involved 74 people with an average age of 76 who had mild cognitive impairment and were not smokers. Half of the participants received a nicotine patch of 15 mg per day for six months and half received a placebo. The participants took several tests of memory and thinking skills at the start of the study and again after three and six months.
After six months of treatment, the nicotine-treated group regained 46 percent of normal performance for age on long-term memory, whereas the placebo group worsened by 26 percent over the same time period.
“People with mild memory loss should not start smoking or using nicotine patches by themselves, because there are harmful effects of smoking and a medication such as nicotine should only be used with a doctor's supervision,” said study author Paul Newhouse, MD, of Vanderbilt University School of Medicine in Nashville. “But this study provides strong justification for further research into the use of nicotine for people with early signs of memory loss. We do not know whether benefits persist over long periods of time and provide meaningful improvement.”
There were no serious side effects for the people receiving the nicotine patch.
Nicotine stimulates receptors in the brain that are important for thinking and memory skills. People with Alzheimer’s disease lose some of these receptors.
The study was supported by the National Institute on Aging and the National Institute of General Medical Sciences. Pfizer Inc. provided the transdermal nicotine patches.