Dementia With Lewy Bodies And Parkinson Disease Dementia
, MD, PhD, Department of Neurology, University of Mississippi Medical Center
Dementia with Lewy bodiesParkinson disease dementia
Dementia is chronic, global, usually irreversible deterioration of cognition.
Dementia with Lewy bodies is the 3rd most common dementia. Age of onset is typically > 60.
Lewy bodies are spherical, eosinophilic, neuronal cytoplasmic inclusions composed of aggregates of alpha-synuclein, a synaptic protein. They occur in the cortex of some patients who have dementia with Lewy bodies. Neurotransmitter levels and neuronal pathways between the striatum and the neocortex are abnormal.
Lewy bodies also occur in the substantia nigra of patients with Parkinson disease Parkinson Disease Parkinson disease is a slowly progressive, degenerative disorder characterized by resting tremor, stiffness , slow and decreased movement , and eventually gait and/or… read more , and dementia may develop late in the disease. About 40% of patients with Parkinson disease develop Parkinson disease dementia, usually after age 70 and about 10 to 15 years after Parkinson disease has been diagnosed.
Both dementia with Lewy bodies and Parkinson disease dementia have a progressive course with a poor prognosis.
How Does Parkinsons Disease Develop
As the disease progresses people who have Parkinsons are increasingly likely to have a tremor, shaking, slowness of movement and rigidity. It can also cause problems with balance, sleep, swallowing, speech and increase the risk of falls. This can cause embarrassment, distress, discomfort and social isolation.
Research has indicated that in Parkinsons disease the persons cognitive processes can also be affected and these may get progressively worse over the years, with some people going onto develop dementia in the later stages of Parkinsons. The cognitive changes could include:
- a reduction in reasoning, judgement, planning and decision-making abilities
- difficulty learning new things
The person may also show signs of depression or anxiety.
What Are The Symptoms Of These Diseases
The main symptoms of Parkinson’s disease involve motor control, such as tremor , slowness of movement, stiffness of the limbs and trunk as well as postural instability. Many patients develop a decline in thinking and reasoning known as Parkinsons disease dementia if it occurs more than one year after the initial diagnosis of Parkinsons disease. Common symptoms for PDD include decline in memory, concentration and judgment, visual hallucinations, depression, irritability, and anxiety.
The central feature of Lewy body dementia is progressive cognitive decline, combined with pronounced fluctuations in alertness and attention, complex visual hallucinations, and motor symptoms such as rigidity and the loss of spontaneous movement. It can easily be mistaken for Alzheimers disease or for Parkinsons disease dementia .
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Memory And Thinking Problems
You may experience forgetfulness, slowed thinking and difficulty concentrating. You might find it harder to follow conversations, and remember some words and names. This can make communication difficult.
You may also find it increasingly difficult to make decisions, plan activities and solve problems. This can make everyday activities harder.
Dysfunction Of The Nucleus Basalis Of Meynert Cholinergic Network Impairs Encoding Of Memories
Aside from its role in orienting of attention, the NBM cholinergic network has also been implicated in memory encoding. The release of acetylcholine from its end terminals has been shown to induce plastic reorganization of cortical receptive field maps, representing the putative encoding of a physiological memory . Simultaneously, as described above, this transmitter release directly desynchronizes the neocortical EEG by inducing fast gamma, beta and theta oscillations , and evidence suggests that phase-coupling of these oscillations between cortical and MTL regions is necessary for memory encoding in humans . Conversely NBM lesions in animals have been shown to block this electrocortical activation , and cause impairments of learning and memory , as well as impairments in orienting of attention .
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Dysfunction In The Fronto
Volitional shifts of attention are thought to depend on top-down signals within a fronto-parietal network comprising prefrontal cortical areas and posterior parietal cortices , wherein prefrontal regions modulate activity in the network according to task demands .
The major cortical neural networks affected in PDD. Areas of cortical atrophy associated with visuospatial and visuoperceptual deficits in PDD are based on the data presented in . Areas of cortical atrophy specifically associated with the presence of visual hallucinations in PDD are based on the data presented in . Functional cortical regions comprising the fronto-parietal attention network are based on the data presented in . Cortical regions are identified according to the Allen Brain Atlas for the human brain, and manually drawn onto the corresponding 3D brain image. In this representation the same cortical regions are affected symmetrically in both hemispheres, however in the original studies above the extent of atrophy in these regions was not symmetrical between hemispheres, and varied between individual patients. In the inferior view of the cortex the cerebellum has been removed to expose the fusiform gyri more clearly. DLPFC = dorsolateral prefrontal cortex PPC = posterior parietal cortex VLPFC = ventrolateral prefrontal cortex.
Pd Dementia And Safety Concerns
Safety issues should be considered and monitored from the time of diagnosis. As PDD progresses, ensure that your loved one is not left alone and try to:
- Evaluate driving privileges before safety is a concern. Your doctor can make a driving evaluation referral.
- Work out legal and financial issues and safeguard finances. People with dementia are at greater risk of falling victim to scams and fraud.
- Minimize prescription risks. Confirm with the doctor the medication names and doses of the person with PD. If the person is in dementias early stages and capable, fill up their weekly pill box together and monitor use.
- Look into medical alert systems. These systems can be critical in the event of a fall or if your loved one wanders outside of the home. Many types of systems are available, from bracelets and pendants to smartwatches with fall detection and one-button connections to 911.
- Evaluate gun safety. If your loved one owns a firearm or has one in the home, consider bringing it up with their doctor and taking additional safety precautions.
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Atrophy Within The Medial Temporal Lobe Network Correlates With Progression To Parkinsons Disease Dementia
Medial temporal lobe structures are involved in memory storage and retrieval , and patients with Parkinsons disease demonstrate hypoactivation of these structures during visual memory tasks from the point of diagnosis . However, previous volumetric MRI studies have provided conflicting results as to whether significant MTL atrophy occurs in PDD . These discrepancies are likely due to the differing criteria for dementia used, and the fact that results were not co-varied by motor scores to determine atrophy specific to cognitive decline. To address these issues, a recent study used the MDS Task Force Criteria for PDD and recent criteria for PD-MCI to select representative patient groups for voxel-based morphometry MRI analysis . Having adjusted results by individual UPDRS motor scores they showed that cognitive progression from Parkinsons disease to PD-MCI to PDD specifically correlated with increasing grey matter atrophy in MTL structures including the hippocampi, parahippocampi and amygdalae. A recent meta-analysis of six voxel-based morphometry MRI studies involving a total of 105 patients with PDD and 131 control subjects confirms this .
What Is Aggressive Parkinsons Disease
As written above, Parkinsons dementia aggression is that form of Parkinsons which makes the patient exhibit aggressive behavior. They vent out their aggression either verbally or physically, in the various forms that have been written above. Besides verbal and physical outbursts, PD Dementia patients are also prone to hallucinating caused by the medication administered. Hallucinations in PD Dementia patients primarily occur because of the effects of dopaminergic agents for motor symptoms.
Loss of dopamine neurons in the ventral tegmental area is one of the likeliest of all neuropathological causes as changes in serotonin and norepinephrine systems are not. For the uninitiated, the ventral tegmental area is the origin of the mesolimbic dopaminergic projection. Plenty of studies have gone into analyzing the cause behind the aggression in PD Dementia patients. Depression in PD Dementia patients has been identified due to changes in the medial frontal cortex and the anterior cingulate. Akinetic-rigid variants have been found in patients showing signs of major depression.
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Management Of Parkinsons Disease Dementia
The relative importance of cholinergic network dysfunction in PDD is reflected in current treatment strategies, which focus on the use of AChEIs, such as rivastigmine, donepezil and galantamine, to boost cholinergic function. Two large placebo-controlled trials have shown that rivastigmine significantly improves deficits in orienting of attention, vigilance and cognitive fluctuation in patients with PDD , and indeed patients with more severe attentional deficits appear to respond best . These results serve to reinforce the cholinergic basis of attention deficits in PDD according to the neural network model. Benefits from AChEIs have also been demonstrated for executive deficits visuospatial tasks and hallucinations . Whether these improvements are due to amelioration of the cholinergic network deficits underlying these cognitive processes, or are secondary to an overall improvement in attention assisting other overlapping cognitive functions, or a combination of both, is unknown.
Independent Dysfunction In Posterior Visual Processing Networks Underlies Visual Hallucinations
The mechanism underlying the generation of visual hallucinations in PDD is more complex and likely represents interacting dysfunction between several different brain networks. Since the presence of hallucinations is closely correlated with visuospatial and visuoperceptual deficits in PDD , dysfunction in associative visual cortices within the dorsal and ventral processing streams has long been implicated in their generation. This is supported by neuropathological studies which have demonstrated strong correlations between Lewy body burden in parietal and temporal lobes and the presence of hallucinations in PDD . Nevertheless, MRI studies comparing brain atrophy patterns between patients with Parkinsons disease with and without visual hallucinations have not consistently supported these pathological associations, differentially implicating medial temporal , insular , pedunculopontine nucleus and frontal atrophy . All may play a part in generation of hallucinations however, the degree of cognitive impairment between patients with and without hallucinations was not controlled for in these studies, meaning that atrophy patterns may have related to cognitive differences rather than the presence of hallucinations per se. In addition, the use of differing classification criteria for PDD further complicates interpretation of these results.
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How Is Parkinsons Disease Dementia Diagnosed
No single test can diagnose Parkinsons disease dementia. Instead, doctors rely on a series or combination of tests and indicators.
Your neurologist will likely diagnose you with Parkinsons and then track your progression. They may monitor you for signs of dementia. As you get older, your risk for Parkinsons dementia increases.
Your doctor is more likely to conduct regular testing to monitor your cognitive functions, memory recall, and mental health.
Future Directions And Treatment Strategies
As this review has shown, the dysfunctional neural networks underlying the cognitive symptoms of PDD are diverse and distributed throughout the brain. There is overlap between network functions, each of which depend on differing primary neurotransmitters. In addition, evidence suggests that neurotransmitters can modulate the functional effects of one another , and thereby damage to one network during the pathogenesis of PDD may in turn influence dysfunction in another . Furthermore, as discussed in detail above, the cellular-level pathology causing damage to these networks in PDD is heterogeneous, while the effects of different genes on the pathophysiology of the disorder is only now being slowly unravelled.
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How Can We Support The Sleep/wake Cycle Of Pdd
For people with PDD who are confused about the day-night cycle, some daily strategies can be helpful. At night, starting a lights out routine that happens at the same hour every day, where all curtains are closed and lights are turned off, can help the person understand that it is sleep time. During the day, opening the curtains, allowing the person with PDD to spend as much time in the daylight as possible, avoiding naps, and organizing stimulating activities, can be helpful. Having lots of calendars and clocks in every room might also help a person with PDD be less confused about the time of day.
Behaviors Seen In Parkinsons Disease Dementia
As dementia progresses, managing disorientation, confusion, agitation, and impulsivity can be a key component of care.
Some patients experience hallucinations or delusions as a complication of Parkinsons disease. These may be frightening and debilitating. Approximately 50 percent of those with the disease may experience them.
The best thing to do when giving care to someone experiencing hallucinations or delusions from Parkinsons disease dementia is to keep them calm and reduce their stress.
Take note of their symptoms and what they were doing before they exhibited signs of hallucinating and then let their doctor know.
This element of the disease can be particularly challenging for caregivers. Patients may become unable to care for themselves or be left alone.
Some ways to make caregiving easier include:
- sticking to a normal routine whenever possible
- being extra comforting after any medical procedures
- limiting distractions
- using curtains, nightlights, and clocks to help stick to a regular sleep schedule
- remembering that the behaviors are a factor of the disease and not the person
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Diagnosis: Parkinson’s Dementia Or Dementia With Lewy Bodies
During assessment, a specialist may look at when the dementia symptoms first appeared before reaching a diagnosis of Parkinson’s dementia or dementia with Lewy bodies.
If there have been motor symptoms for at least one year before dementia symptoms occur, specialists will often give a diagnosis of Parkinson’s dementia.
If dementia symptoms occur before or at the same time as motor symptoms, specialists will usually give a diagnosis of dementia with Lewy bodies.
However, it should be noted that in some cases of dementia with Lewy bodies, no motor symptoms develop at all.
Theres no single test – diagnosis is made through several different assessments, usually starting with an appointment with your GP or Parkinson’s nurse.
Some people find it helps to go to the appointment with someone who knows them well, who can give the GP or Parkinson’s nurse information about changes they’ve noticed.
Your GP can discuss your symptoms with you and carry out a physical examination, including blood and urine tests, to rule out other potential causes of the symptoms .
Your GP may also review your medication, in case your symptoms are side effects.
If your GP thinks you have dementia, they can refer you to a specialist, such as a neurologist, psychiatrist or geriatrician.
You might be referred to a memory clinic or memory service. In some areas of the country, you can refer yourself to these services.
But if you feel you need to see the specialist again, you can ask to be referred back.
Describing The Genes Associated With The Sixth Sense
by Anke Brodmerkel, Max Delbrück Center for Molecular Medicine
To perform coordinated movements, we rely on special sensory neurons in our muscles and joints. Without them, the brain wouldn’t know what the rest of our body was doing. A team led by Niccolò Zampieri has studied their molecular markers to better understand how they work and describes the results in Nature Communications.
Sight, hearing, smell, taste, touch: We’re all familiar with the five senses that allow us to experience our surroundings.
Equally important but much less well known is the sixth sense: “Its job is to collect information from the muscles and joints about our movements, our posture and our position in space, and then pass that on to our central nervous system,” says Dr. Niccolò Zampieri, head of the Development and Function of Neural Circuits Lab at the Max Delbrück Center in Berlin. “This sense, known as proprioception, is what allows the central nervous system to send the right signals through motor neurons to muscles so that we can perform a specific movement.”
This sixth sensewhich, unlike the other five, is entirely unconsciousis what stops us from falling over in the dark, and what allows us to raise a cup of coffee to our mouth with our eyes shut in the morning.
Precise connections are crucial
Guidance for nascent nerve fibers
One aim is better neuroprostheses
Altered muscle tension causes a crooked spine
More information:Nature Communications
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Prognostic Factors For Development Of Parkinsons Disease Dementia
In the clinic the diagnosis of PDD is based upon the Movement Disorders Society Task Force criteria , which incorporates detection of the cognitive features described above. However, it is recognized that early identification of patients at risk of developing PDD is useful in order to monitor them more closely so that therapeutic and supportive strategies can be implemented at a stage of the disease when they are likely to have greatest efficacy. Detailed neuropsychological testing, although able to detect early subclinical deficits, is not widely available, and therefore identification of clinical features with high predictive value for PDD has pragmatic value for clinicians. Large longitudinal cohort studies have demonstrated that inability to copy the intersecting pentagons figure on the MMSE, impairments of semantic verbal fluency and recognition memory, and development of a postural instability and gait difficulty motor phenotype are significant predictors for PDD . Errors on the Pill Questionnaire and presence of REM sleep behavioural disorder are also associated with later development of PDD, although their positive predictive values are lower .
Dysfunction In Cholinergic And Noradrenergic Networks Impairs Bottom
One view of automatic orienting of attention considers it to be mediated by bottom-up or stimulus-driven signals from the NBM in the basal forebrain . This nucleus consists of 90% cholinergic neurons and its widespread projection axons provide the main cholinergic innervation to the entire cortical mantle . Selective activation of the nucleus basalis of Meynert network causes an increase in acetylcholine levels in the cortical target field, which boosts the signal-to-noise ratio for salient stimuli, thereby enhancing the strength of their neural representations . In facilitating this process the NBM effectively amplifies detection of salient stimuli by posterior regions of the fronto-parietal network and ensures their attentional significance . Animal experiments have shown that this NBM-driven cortical signal enhancement is responsible for generating event-related potentials on the EEG . These can be measured on the human EEG as negative deflections occurring 80100 ms after an unpredictable stimulus , and have long been regarded as the electrophysiological correlate of orienting of attention .
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