Neuropsychiatric Symptoms And Dementia
Visual hallucinations and illusions are common in PD and reportedly occur in a third to 40% of patients . Although virtually all anti-parkinsonian medications have been reported to induce hallucinations and psychosis, visual hallucinations have also been reported to occur prior to drug treatment . Neuropathological changes in the amygdala and hippocampus caused by the disease process seem to be implicated in the aetiology . Frequently, images of people, small animals or objects are conceived or the hallucinations may have multiple content. The images may be familiar or not. They last from seconds to minutes, and may recur over the day . Usually, non-demented patients retain insight and the hallucinations are usually not threatening. Less commonly, the hallucinations are olfactory , auditory and tactile . One study showed that visual component was lacking in 10% of cases . Minor visual phenomena such as sense of presence and visual illusions affect 17â72% of patients and delusions about 5% . Higher load of dopaminergic treatment may be related to the hallucinations, but disease severity, cognitive impairment, depression, older age and worse visual acuity may also be important .
Drug Delivery Systems For Neurotrophic Factor Therapy
Besides GDNF, other neurotrophic factor such as basic fibroblast growth factor have been evaluated. One example involves gelatin nanostructured lipid carriers encapsulating bFGF that can be targeted to the brain via nasal administration . Overall, the nanoformulation stimulated dopaminergic function in surviving synapses and played a neuroprotective role in 6-OHDA hemiparkinsonian rats. A very recent study took advantage of the neuroprotective properties of Activin B, which was administered in a parkinsonian mice using a thermosensitive injectable HG . The biomaterial allowed a sustained protein release over 5 weeks and contributed to substantial cellular protection and behavioral improvement.
Inpatient Management Of Parkinson’s Disease
Patients with PD are often admitted to hospital for other reasons, but the unique challenges of the condition mean that outcomes related to PD are often suboptimal. Many hospitals have an alert system to inform members of the PD team of admission to allow proactive in-reach consultations. It is essential that antiparkinsonian medications are given on time and in correct dosage, as sudden reduction or withdrawal of medication can lead to severe morbidity or even mortality due to parkinsonismhyperpyrexia syndrome. Dopamine blocking drugs must not be given. When patients with PD cannot take their usual oral medications, we recommend that an equivalent dosage be given via nasogastric tube. If this is not possible, or enteral medication is contraindicated, cautious use of rotigotine patch can be helpful.
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Medical Cannabis Convening Findings: Top Takeaways And Guidance
Medical cannabis remains a hot topic in the PD community. However, little is known about medical cannabis and how it effects PD symptoms or potential side effects. To address this, we published a statement to help guide the PD community in making informed decisions about using cannabis for Parkinsons. READ NOW
Lifestyle And Other Protective Factors
Cigarette smoking and caffeine consumption are the two most consistent protective factors associated with a reduced risk of PD. Other reported associations include higher serum urate, ibuprofen use and exercise, among others. The negative association between cigarette smoking and PD is most intriguing. This inverse relationship is not easily explained, but some have suggested that PD-related cautious personality predisposes some individuals to quitting neuroprotective smoking as the biological mechanism involved in PD. The other hypothesis links nicotine to dopaminergic neuronal protection since it has been shown to stimulate the release of dopamine in the striatum and preserve dopaminergic function in experimental models. It is also possible that there are other unidentified neuroprotective components in cigarette smoke.
The relative risk reduction of PD among caffeine drinkers is between 0.5 and 0.8 and, similar to smoking, a dose-dependent effect has been consistently demonstrated in most studies. Caffeine, an antagonist of adenosine A2a receptor, has been postulated to exert neuroprotective role by blocking this receptor. In addition to caffeine, it is possible that antioxidants present in some beverages may contribute to a protective effect among black tea drinkers, independent of caffeine.
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Altered Regional Homogeneity And Functional Connectivity During Microlesion Period After Deep Brain Stimulation In Parkinsons Disease
Background. Patients with Parkinsons disease undergoing deep brain electrode implantation experience a temporary improvement in motor symptoms before the electrical stimulation begins. We usually call this the microlesion effect , but the mechanism behind it is not clear. Purpose. This study aimed to assess the alterations in brain functions at the regional and whole-brain levels, using regional homogeneity and functional connectivity , during the postoperative microlesion period after deep brain stimulation in PD patients. Method. Resting-state functional MRI data were collected from 27 PD patients before and after the first day of DBS and 12 healthy controls in this study. The ReHo in combination with FC analysis was used to investigate the alterations of regional brain activity in all the subjects. Results. There were increased ReHo in the basal ganglia-thalamocortical circuit , whereas decreased ReHo in the default mode network , prefrontal cortex , and the cerebello-thalamocortical circuit after DBS. In addition, we also found abnormal FC in the lingual gyrus, cerebellum, and DMN. . Microlesion of the thalamus caused by electrode implantation can alter the activity of the basal ganglia-thalamocortical circuit, prefrontal cortex, DMN, and CTC circuit and induce abnormal FC in the lingual gyrus, cerebellum, prefrontal cortex, and DMN among PD patients. The findings of this study contribute to the understanding of the mechanism of MLE.
Progression Of Parkinson’s Disease
The disease progression of PD from diagnosis has been conceptualised into four stages . It is also important to recognise a prodromal phase in which non-motor symptoms, such as anosmia, constipation and rapid-eye-movement sleep behaviour disorder may predict the development of motor PD. Motor complications are more common as PD progresses, and typify transition to the complex phase. Many so-called axial symptoms of later stage PD, such as dysphagia, gait disturbance and falls, do not respond to levodopa, but may be helped by multidisciplinary team input. Dementia occurs in up to 80% of people with PD after 20 years disease duration. The rate of PD progression is heterogeneous and is generally more rapid in those with older age and more severe motor impairment at onset.
Stages of Parkinson’s disease. RBD = rapid eye movement sleep behaviour disorder.
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General Approach To Management
The primary goal in the management of PD is to treat the symptomatic motor and nonmotor features of the disorder, with the objective of improving the patients overall quality of life. Appropriate management requires an initial evaluation and diagnosis by a multidisciplinary team consisting of neurologists, primary care practitioners, nurses, physical therapists, social workers, and pharmacists., It is also important that the patient and his or her family have input into management decisions.
Effective management should include a combination of nonpharmacological and pharmacological strategies to maximize clinical outcomes. To date, therapies that slow the progression of PD or provide a neuroprotective effect have not been identified., Current research has focused on identifying biomarkers that may be useful in the diagnosis of early disease and on developing future disease-modifying interventions.,
The Impact Of Living With Parkinsons Disease: Balancing Within A Web Of Needs And Demands
Catharina Sjödahl Hammarlund
1The PRO-CARE Group, Faculty of Health Science, Kristianstad University, Kristianstad, Sweden
2Department of Health Sciences, Lund University, Lund, Sweden
3The Research Platform for Collaboration for Health, Faculty of Health Science, Kristianstad University, Kristianstad, Sweden
Abstract
1. Introduction
Parkinsons disease is a progressive, neurological disease involving motor and nonmotor symptoms . Its symptom profile and progression differ between individuals. The core pathology believed to cause the main motor symptoms is a striatal dopamine deficit due to progressive loss of nigrostriatal dopaminergic neurons . Symptomatic dopaminergic therapy is initially successful, but a fluctuating drug response and dyskinesias often develop after some years. With the occurrence and progression of both motor and nonmotor symptoms, often in complex and fluctuating patterns , the disease is typically perceived as unpredictable and difficult to control .
2. Materials and Methods
2.1. Participants and Recruitment
2.2. Data Collection
2.3. Data Analysis
3. Results
The impact of living with PD can be understood as Changed prerequisites for managing day-to-day demands, Loss of identity and dignity, Compromised social participation, and The use of practical and psychological strategies with internal variations seen as subcategories .
3.1. Changed Prerequisites for Managing Day-to-Day Demands
3.2. Loss of Identity and Dignity
4. Discussion
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The Clinical Symptoms Of Parkinson’s Disease
Department of Neurology, Broomfield Hospital, Chelmsford, Essex, CM1 7ET UK
Queen Mary School of Medicine and Dentistry, University of London, London, UK
Department of Neurology, Broomfield Hospital, Chelmsford, Essex, CM1 7ET UK
Queen Mary School of Medicine and Dentistry, University of London, London, UK
How Is The Diagnosis Made
Currently, diagnosis of Parkinson disease is based on clinical features from history and examination, and over time based on the response to dopamine agents and the development of motor fluctuations. Motor manifestations of the disorder begin asymmetrically, and commonly include a resting tremor, a soft voice , masked facies , small handwriting , stiffness , slowness of movements , shuffling steps and difficulties with balance. A classic symptom is resting tremor, usually affecting one upper limb, although 20% of patients do not have it 30% may first present with tremor in a lower extremity, and there may also be a lip, jaw or even tongue tremor at rest., Head and voice tremors are uncommon, and one should consider essential tremor in the differential diagnosis in such cases. Of all the major features, bradykinesia has the strongest correlation with the extent of dopamine deficiency. Diagnosis has been formalized by the criteria of the UK Parkinsons Disease Society Brain Bank, with diagnostic accuracy of up to 90% .
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Surgical Therapies With Transplantation And Gene Therapy
Cell transplantation is regarded as a potential future PD treatment. There have been trials using autologous and non-autologous cells. Human embryonic stem cells and induced pluripotent stem cells are few of the cells that have been included in these transplantation studies. One of the concerns with cell transplantation using stem cells is the ethical bounds that must be considered.
Since the first clinical trial in 1987 involving the transplantation of dopaminergic- neuron-rich human fetal mesencephalic tissue into PD patients striatums, more research has aimed to explore whether the grafted dopaminergic neurons will live and form connections in the brain, if the patients brain can harmonize and make use of the grafted neurons, and if the grafts can generate significant clinical improvement. Clinical trials with cell therapy intend to discover if there are long-lasting improvements following restoration of striatal DA transmission by grafted dopaminergic neurons. Experimental data from rodents and nonhuman primates show that fetal ventral mesencephalon intrastriatal grafted DA neurons demonstrate many morphological and functional characteristics of normal DA neurons. Significant improvements of PD-like symptoms in animal models have been demonstrated after successful reinnervation by the grafts. Dopaminergic grafts can reinnervate the striatum in the brain, restore regulated release of DA in the striatum, and can become functionally integrated into neural circuitries.
Diagnosis And Treatment Of Parkinson Disease: Molecules To Medicine
1Institute for Cell Engineering, 2Department of Neurology, 3Department of Neuroscience, and 4Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Address correspondence to: Ted M. Dawson, Institute for Cell Engineering, Department of Neurology and Neuroscience, Johns Hopkins University School of Medicine, 733 North Broadway, BRB Suite 731, Baltimore, Maryland 21205, USA. Phone: 614-3359 Fax: 614-9568 E-mail: .
Find articles bySavitt, J.in: |PubMed |
1Institute for Cell Engineering, 2Department of Neurology, 3Department of Neuroscience, and 4Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Address correspondence to: Ted M. Dawson, Institute for Cell Engineering, Department of Neurology and Neuroscience, Johns Hopkins University School of Medicine, 733 North Broadway, BRB Suite 731, Baltimore, Maryland 21205, USA. Phone: 614-3359 Fax: 614-9568 E-mail: .
Find articles byDawson, V.in: |PubMed |
1Institute for Cell Engineering, 2Department of Neurology, 3Department of Neuroscience, and 4Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Address correspondence to: Ted M. Dawson, Institute for Cell Engineering, Department of Neurology and Neuroscience, Johns Hopkins University School of Medicine, 733 North Broadway, BRB Suite 731, Baltimore, Maryland 21205, USA. Phone: 614-3359 Fax: 614-9568 E-mail: .
J Clin Invest.
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Most Popular Parkinsons Articles Of 2020
What Parkinsons disease topics were most popular among our community in 2020? While the year was unprecedented, the Parkinsons Foundation remained dedicated to covering the topics you found most critical on our Parkinsons Today blog. Thanks to our supporters, we are able to provide new, year-round resources from our PD Library and podcast to Parkinson.org and Expert Briefing webinars to our community, all at no cost.
These are the 10 most-read blogs of 2020:
Article Of The Year 2020
Update on the Management of Parkinsons Disease for General Neurologists
Journal profile
Parkinsons Disease publishes research related to the epidemiology, etiology, pathogenesis, genetics, cellular, molecular and neurophysiology, as well as the diagnosis and treatment of Parkinsons disease.
Editor spotlight
Parkinson’s Disease maintains an Editorial Board of practicing researchers from around the world, to ensure manuscripts are handled by editors who are experts in the field of study.
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How Is Parkinson Disease Treated
Dopaminergic medications are the mainstay of symptomatic therapy for motor symptoms in Parkinson disease. The mechanisms of action, starting and target doses and adverse effects of medications are summarized in Appendix 2, available at www.cmaj.ca/lookup/suppl/doi:10.1503/cmaj.151179/-/DC1. Discovered in the 1960s, levodopa was the first symptomatic treatment for Parkinson disease, followed by the availability of dopamine agonists and monoamine oxidase B inhibitors. Until recently, the decision regarding which treatment to initiate has been debated. There is no one medication that is recommended for treatment initiation currently, but factors such as symptom severity, embarrassment, ability to perform activities, cost and patient preference should be taken into account. If symptoms are very mild, the patient may choose not to begin therapy.,
Because patients with early-onset disease are more likely to develop levodopa-induced abnormal movements , dopamine agonists are often introduced as initial treatment however, this early advantage of dopamine agonists over levodopa diminishes over time . There is also some controversial evidence for neuroprotection with the monoamine oxidase B inhibitor rasagiline at the 1 mg daily dose however, its cost is not covered in most provinces and may require application to the exceptional access program, as is done in Ontario.
Canonical Role Of Pink1 In Mitophagy
Proteolytic processing of PINK1. PINK1 gene encodes a 581 amino acid protein with an N-terminal mitochondrial targeting motif that contains a transmembrane domain , an un-conserved region, a kinase domain with three insertions in the N lobe, and a conserved C-terminal region . IMM-localized mitochondrial processing peptidases putatively cleave PINK1 at aa 34 and 35 to form a 60 kDa intermediate cleavage product. PARL and/or m-AAA cleave the intermediate 60 kDa intermediate product in between Ala103 and Phe104 to generate 52/48 kDa processed forms of PINK1.
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Who Gets Parkinson Disease
The exact cause of Parkinson disease is unknown, but it is assumed to be the result of a combination of environmental influences superimposed on genetic predisposition or susceptibility . There is increasing evidence that the genetic and environmental insults leading to Parkinson disease commonly lead to abnormal forms of a normal protein, -synuclein, which seems to contribute to cell death., The onset of Parkinson disease can be categorized as juvenile , early onset and late onset ., The juvenile form is rare, is often familial , is most frequently associated with a parkin gene mutation and has an atypical presentation., Of patients with Parkinson disease, 10%16% have an affected first- or second-degree relative first-degree relatives may have double the risk of Parkinson disease compared with the general population. In early- and late-onset Parkinson disease, the frequency of a positive family history is not statistically different.
Symptomatic Treatment Of Levodopa
Levodopa-resistant symptoms
There are many levodopa-resistant motor symptoms such as dysarthria and dysphagia, freezing of gait, postural instability and dysautonomia. Freezing, sudden immobility of the feet when attempting to walk, often associated with falls, may be seen in either the off or the on period. Although off-period freezing may improve with optimisation of medications, on-period freezing is usually resistant to pharmacologic treatment.
Physical therapy, including strategies that utilise sensory cues, such as stepping over a horizontal laser beam, may be helpful. Dysarthria and dysphagia are often treated by speech and voice therapists. Injection of botulinum toxin has been found to be effective in controlling high-amplitude rest and postural hand tremor which may be resistant to levodopa. Botulinum toxin may be also beneficial in the treatment of a variety of other non-levodopa responsive parkinsonian symptoms such as blepharospasm, apraxia of eyelid opening, anterocollis, camptocormia, bruxism, sialorrhea, seborrhea, hyperhidrosis, overactive bladder and constipation.
Non-motor symptoms
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Neuro Talk: Myths And Realities Of Parkinsons Disease
Does Parkinsons only affect movement? Can doctors predict its progression? Can stem cells cure Parkinsons? In this Neuro Talk, our Chief Scientific Officer, James Beck, PhD, debunks seven common myths about Parkinson’s disease. WATCH NOW
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Neuropathology Of Parkinsons Disease
Macroscopically, the brain in idiopathic PD is often unremarkable with mild atrophy of the frontal cortex and ventricular dilation in some cases. The main distinctive morphological change in the PD brain is observed in transverse sections of the brainstem, where almost all cases present with loss of the darkly pigmented area in the substantia nigra pars compacta and locus coeruleus. This pigmentation loss directly correlates with the death of dopaminergic neuromelanin-containing neurons in the SNpc and noradrenergic neurons in the locus coeruleus . Cell death in the SNpc is mostly restricted to a specific group of neuromelanin-containing dopaminergic neurons, namely the A9 neurons, while other neuronal and glial cell types are largely spared .
Coronal section at the level of the substantia nigra pars compacta in a control and a PD brain stained by hematoxylin and eosin. In both sections, the dark brown cells are the neuromelanin-containing dopaminergic neurons.
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