How we can help you
We specialize in providing help in areas that other foundations often miss or leave unaddressed. When a family member is diagnosed with Parkinson’s Disease, a cascade of questions and concerns materialize that can easily overwhelm a family. Most often, the issues of on-going therapy and education on how family members can become effective caregivers will need to be addressed.
Beyond the issues of therapy and caregiver education there are other adjustments that need to be considered. Specific concerns, that most often arise in a progression of unanswered questions, can have an overwhelming impact on a family’s sense of security and self-worth.
- Why is this happening? What caused this? How difficult is this going to be? How is this going to impact my family? Who can I turn to when I start to feel overwhelmed? How do I deal with all of the emotions I’m feeling? (Mental Health & Well-Being Services).
- How will I be able to provide for my family in the future? (Financial Planning & Retirement Services).
- How can I protect my assets so that they will be available as a resource for my family when I am unable to do so? (Legal Assistance & Estate Planning Services).
- If our family needs to relocate to receive better care or to reduce expenses who can I turn to for help? (Housing, Relocation & Real Estate Services).
- Will I be able to help with my children’s education expenses in the future? (Education Planning & Tuition Assistance).
- When will they find a cure? What health steps can we take in the meantime? (Medical Research & Information Services).
When an impacted individual or family is faced with making these decisions on their own and without help from qualified individuals familiar with the impact of neurological diseases, the task list can be overwhelming. Why make things more difficult by going it alone when you can contact an experienced Find Neuro Help representative and allow them to assist you? Our services are free of charge. The consultation costs you nothing and should you choose a service we offer, the cost, if any, is subsidized by the donations we receive.
Parkinson’s disease (PD) is one of the most common neurodegenerative diseases. Parkinson’s disease (PD) is as synucleinopathy (or) (neurodegenerative) disease. That is represented by an unusually large accumulation of alpha-syncline proteins in the body’s neurons, nerve fibers and glial cells.
P.D is most common in men above 70 years old. About 4% of the world’s population beyond age 80 have Parkinson’s. Only 4% of those living with PD contract the disease prior to age 50. The youngest known male to be diagnosed with the disease was 14 years old, the youngest female was 15 years of age. Our understanding of the pathogenesis of P.D has been improved over the past decade, with several key gene mutations revealing various mechanisms of pathogenesis in various cases of PD.
The primary pathological standard is dopamine-producing cell loss within the substantia nigra region of the brain. At the passing of most Parkinson’s patients, 50–70% of the individual’s dopamine-producing cells are dead. The earliest recorded pathological changes in PD. (Ref. 3) was observed in the medulla oblongata/pontine tegmentum and olfactory bulb. In the early stages of the disease (Stage 1 & 2) individuals are pre-symptomatic. As the disease advances to Braak stages 3 and 4—the substantia nigra, midbrain, and basal forebrain become involved. Finally, the disease progresses to the neocortex.
The speed of this progression is based on the distribution of Lewy bodies (The Hallmark of P.D). Lewy bodies are α-synuclein-immune-reactive inclusions that consist of an elevated number of neuro-filament proteins. These Lewy bodies include ubiquitin, (a heat shock protein) that targets other proteins for the breakdown. Mutations in the α-synuclein gene have been linked to forms of PD. Lewy bodies exist as a hallmark of PD and Dementia but are not found as consistently or pathologically in any other known neurodegenerative diseases.
The ubiquitin-proteasome system (UPS) is a potential cause in the development of cell death. (5) UPS is important for intracellular processes that maintain cell viability. It accomplishes this by removing undesirable proteins that are no longer useful to cell function. When UPS stops functioning, proteins accumulate including α-syncline, a major component of Lewy bodies. The Olfactory Bulb is one of the first sites of LB deposits. The Olfactory bulb is responsible for smell and taste, therefore a disturbance in these two senses is often a result of LB buildup. This early buildup could be a pathway that eventually leads to neuronal dysfunction and eventual death.
PD is classified as a sporadic disease, however there have been a growing number of single gene mutations identified. At least 10 genes have been Identified that map linkage with six genes. These are: Ubiquitin C-terminal Hydrolase like 1 (UCH-L1), parkin (PRKN), LRRK 2, PINK 1, DJ-1 genes and o-syncline (SNCA).
These single gene defects, with the exception of LRRK 2, are responsible for only a small number of patients with PD. SNCA gene mutation is the catalyst for early onset of PD.
The LRRK 2 gene the common cause of familial or sporadic PD. Genetics appear to play an insignificant role in contracting (P.D). When one family member tests positive with P.D, there is only a 5% chance of other family members contracting the disease.
The LRRK2 gene encodes itself for a protein named Dardarin (The Basque word for tremor) Symptoms at onset are typical of idiopathic PD, namely unilateral bradykinesia rigidity and tremor in some cases.
There has been extensive research into mitochondrial genetics and function in PD. Abnormalities in the oxidative phosphorylation enzyme pathway has consistently been detected in PD brains, blood platelets and skeletal muscle. Defects in other complexes have also been reported.
Mitochondrial DNA studies have been unable to identify a consistent gene mutation to explain the oxidative phosphorylation defects in PD.
Environmental factors may possibly uncover a predispose to P.D, yet to date findings are inconclusive. Those individuals that live in a rural environment seem to have an increased risk of PD. Epidemiological studies have shown some evidence that exposure to pesticide use and wood preservatives may be a causal factor. It’s possible that mitochondrial dysfunction in PD could be triggered by one or more environmental toxins.
The characteristic features of PD include bradykinesia, rigidity, and resting tremor. Postural instability is often the result of Parkinson’s progression.
It is noteworthy that an alternative diagnosis in up to a quarter of patients with PD diagnosed by general neurologists. Misdiagnosis is far less prevalent in patients diagnosed in expert movement disorder clinics. This supports the argument supporting the argument for early referral of patients to specialist experts in movement disorders.
Accurately diagnosing epilepsy is challenging because clinicians rarely have the opportunity to observe seizures and there are many types of seizures and epilepsy syndromes with differing presentations. A clinician typically diagnoses epilepsy based on the patient’s self-report or a family member’s report of seizures and the patient’s medical history. This is complicated by the fact that a number of medical conditions that are not epilepsy can look like seizures. Diagnostic tests can provide relevant information, usually starting with the electroencephalogram (EEG). However, because the typical duration of an EEG is only 20 to 45 minutes, it is unlikely to coincide with an actual seizure. Further, the initial EEG may not show evidence of seizures in approximately half of people with epilepsy. Continuous video-EEG monitoring, which can last from hours to days and is usually conducted in a hospital setting, is often the only way to definitively diagnose the type of seizure and affected areas of the brain.
Advances in technology permit family members and other caregivers to record seizures as they occur. A 2007 case study described where the mother of a teenager with epilepsy was able to capture his seizure on a cell phone camera, which a doctor had not been able to diagnose due to seizure infrequency. Similarly, the improved visualization of seizures through digital cameras with video capabilities and video monitoring in home settings may be particularly beneficial for individuals with infrequent seizures or with more than one type of seizure and for those who do not have easy access to epileptologists and epilepsy monitoring units. Also, the recording of seizures using web-based tracking systems, diaries, or journals can help people with epilepsy and their families maintain records of seizure activity and evaluate patterns with their health care provider. The observation of seizure patterns can help identify a target for medication and lifestyle interventions to improve seizure management.
Additional tests that doctors most commonly use to determine whether a person has a form of epilepsy and, if so, what kind of seizures the person has include:
Your doctor will take samples of your blood to test for possible infections or other conditions that might explain your symptoms. The test results might also identify potential causes for epilepsy.
As with any doctor’s office visit, your doctor will want to complete a full health history. They will want to understand when your symptoms began and what you have experienced. This information can help your doctor determine what tests are needed and what types of treatments may help once a cause is found.
A computed tomography (CT) scan takes cross-sectional pictures of your brain. This allows doctors to see into each layer of your brain and find possible causes of seizures, including cysts, tumors, and bleeding.
Magnetic resonance imaging (MRI) takes a detailed picture of your brain. Doctors can use the images created by an MRI to study very detailed areas of your brain and possibly find abnormalities that may be contributing to your seizures.
A functional MRI (fMRI) lets your doctors see your brain in very close detail. An fMRI allows doctors to see how blood flows through your brain. This may help them understand what areas of the brain are involved during a seizure.
A positron emission tomography (PET) scan uses small amounts of low-dose radioactive material to help doctors see your brain’s electrical activity. The material is injected into a vein and a machine can then take pictures of the material once it has made its way to your brain.
In addition to the symptoms previously mentioned, there are other signs that support proper diagnosis; these include:
- A change of handwriting
- Reduced facial expression.
- Facial Flaking
- A loss of arm swing on one side.
- A reduced sense of smell.
- Reduced Swallowing
- Impaired Reflexes
- Impaired Vision (Less Blinking Occurs, Eyes Dry Out)
- Depression (40% of P.D patients)
- Head or voice tremor
Although P.D Diagnosis is clinical, conventional brain imaging with MRI or CT is sometimes used when hydrocephalus or vascular parkinsonism is suspected
Single-photon emission computerized tomography (or) (SPECT) imaging uses a dopamine transporter (DAT) to distinguish PD from other conditions with similar symptoms such as; Essential Tremor and Dystonic Tremor, Neuroleptic-Induced Parkinsonism, and Psychogenic Parkinsonism.
After several years of sustained response to levodopa therapy, individuals find fluctuation in motor performance. Levodopa’s effectiveness begins to wane. Periods of immobility unrelated to levodopa dosage begin to take effect.
Levodopa-induced dyskinesia usually occurs following prolonged therapy with 50% of patients developing motor fluctuations and dyskinesia around 5 to 10 years following treatment with levodopa and 20 to 30% developing dyskinesia after 2 years.
In younger patients, the progression is worse, with almost every patient beginning treatment prior to age 40 developing motor complications within 6 years of introduction of levodopa. Treatment of levodopa-induced dyskinesia has drawbacks. Reducing the daily dose often renders patients rigid and immobile.
Peak-dose dyskinesia is related to high-plasma concentrations of levodopa. This condition can be managed by fractionating levodopa dosage. Amantidine has also been effective in reducing peak-dose dyskinesia.
Biphasic dyskinesia occurs when plasma levodopa levels rise or fall. This can affect the lower extremities and is difficult to control.
Off-period dystonia can be caused by periods of inadequate mobility. An understanding of the pathophysiology of motor complications while using levodopa therapy is only is only partially understood.
Several treatments have been used to reduce motor complications. It appears that pramipexole and ropinirole have benefit over bromocriptine by reducing ‘off’ time. Amantadine, an anti-viral agent, was discovered by chance to have a positive influence on reduction of motor complications. Evidence supports that amantadine reduces the frequency of motor complications, including freezing, Amantadine has shown some side effects in elderly patients including; confusion, hallucinations, ankle swelling and livedo reticularis.
Entacapone is a peripheral catechol-O-methyltransferase COMT (In layman terms it’s an enzyme that degrades neurotransmitters, thereby lengthening the effectiveness of Levadopa by 45 to 50%). Entacapone compliments the action of amino acid de-carboxylase (AADC) inhibitors. When entacapone or tolcapone are added to levodopa therapy, they create a more sustained plasma and central nervous system level of dopamine, more than levodopa alone. In essence these two enzymes improve motor function.
Surgery as a means of treating PD dates back more than 50 years. In those days patients with severe tremor would receive ablative surgery on the contralateral thalamus. Levodopa, replaced surgical treatment and ironically regained its popularity as levodopa-induced complications prompted surgeons to revisit surgical intervention. The initial focus was on lesion surgery in the form of pallidotomy
The next chapter in P.D surgery came by way of stimulators. The surgery involved placement of high-frequency deep brain stimulators (DBS) in discrete areas referred to as the basal ganglia of the brain. The operation although technically difficult, is rather low risk in experienced hands, but the infrastructure and support team required limits the availability of this form of treatment. The procedure has its psychiatric side effects, in particularly depression is common following DBS.
Patients having cognitive impairment and significant depression are generally speaking not suitable for the procedure. STN DBS is most often performed in patients under the age of 75, who are free of substantial systemic co-morbidity and without structural abnormality on MR imaging.
Patients should be responsive to levodopa treatment and disabled while off levodopa and independent while on it. Patients will usually have had P.D for at least 5 years to allow for atypical causes of parkinsonism to become evident.
Age appears less critical in DBS performed for disabling tremor. Recent studies show evidence that DBS surgery may be beneficial in improving axial stability. Assessment of whether an individual is a patient for DBS requires assessment by a well experienced multi-disciplinary team.
There are several non-motor complications in PD. They are mostly unrelated to dopaminergic pathways and can be manifest by individuals before the onset of general P.D symptoms appears.
Sleep disorders include both disturbed nocturnal sleep and excessive daytime somnolence. Nocturnal sleep disturbance is experienced in 60–98% of individuals and correlates with disease severity and levodopa dosages. Rem Behavioral Disturbance (RBD) is increasingly recognized in individuals with neurodegenerative disease, there is evidence that the rate of progression can predict cognitive impairment in PD patients without dementia. A small dosage of clonazepam at night may prove helpful.
Daytime sleep events are more prevalent in individuals with P.D. In extreme cases, the individual may experience sudden irresistible sleep attacks without warning. These episodes are more frequent with the use of dopamine agonists, particularly ropinirole and pramipexole.
Patients should be counseled to stop driving and avoid operating machinery should this condition develop. The condition subsides as the offending drug is withdrawn.
Cognitive involvement in PD is common. Many individuals with PD develop dementia, within 10 years or more following the onset of motor symptoms. On average 40% of all P.D patients will experience dementia. Dementia in individuals impacted by PD can be related to several different pathologies. However, Lewy bodies and/or Alzheimer pathology are most relevant. Cholinesterase inhibitors such as rivastigmine, donepezil, and galantamine have shown a modest benefit in cognitive function.
Mood disturbance and PD
Depression is the primary mood disturbance in PD with a prevalence of 50% and can occur at any stage of the illness. Depression can be treated with antidepressants including tricyclics and serotonin uptake inhibitors (SSRIs). Pramipexole has a significant antidepressant action.
Psychosis and confusion in PD
Psychosis has been found in up to 30% of PD patients. It is often manifest by hallucinations, delusions, and sometimes aggression. Patients may become paranoid toward partners and other family members.
The newer ‘atypical’ antipsychotic agents such as quetiapine and clozapine are better tolerated and often effective.
PD is one of the more prevalent neurodegenerative diseases. The causes of P.D are unclear, although genetics and environmental factors may play a role in the individual contracting the disease, each circumstance varies. The diagnosis remains clinical at best. There are many agents and a few surgical interventions to treat P.D complications. Future PD treatments will likely focus on disease-modifying drugs that offer neuroprotection.
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