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Introduction.

In 1817, James Parkinson’s described Parkinson’s disease asa ‘shaking palsy’. Parkinson’s disease is a very complex disease and is termedas a progressive neurodegenerative disease. The term fits appropriate as adegeneration of the cells in the basal ganglia (substania nigra) takes placeand gradually worsens as time progresses.

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Within the UK, 1 in 500 people arediagnosed with the disease and although Parkinson’s may affect people of allages and genders, the mean onset for the development of the disease is 55 yearsold. Additionally, for reasons yet unknown to researchers, men are more likelyto develop the disease than women. Individuals diagnosed with Parkinson’s areunable to produce the inhibitory neurotransmitter dopamine which is responsiblefor motor control. However the reasons for the death and loss of thedopaminergic cells remain unknown to researchers therefore meaning that the ultimatepathogenesis of Parkinson’s remains unknown. Due to dopamine being aninhibitory neurotransmitter, the loss of it causes an imbalance betweenexcitation and inhibition therefore leading to the symptoms of Parkinson’s(tremor, bradykinesia, rigidity).  Main body The basal ganglia located in the brain deep beneath thecerebral cortex is a group of nucleic and ‘anatomically are involved in theprocessing of motor, limbic , sensory and associative information’    (J Reynolds, L Brownlie ,2015) .

Thesestructures include the lentiform nucleus, caudate nucleus, subthalamic nucleusand substania nigra. The putamen and globus pallidus collectively make up thelentiform nucleus in the basal ganglia.  The caudate nucleus plays a significant rolein the learning of the brain specifically in the storing and processing ofmemories. Its work as a feedback processor means ‘it usesinformation from past experiences to influence future actions and decisions'(healthline medical team 2015). This means that it most valuable function comeswith the development of communication skills. In the basal ganglia, the subthalamic nucleus represents the soleexcitatory structure and plays the crucial role of the processing that iscarried out by the basal ganglia.

In terms of Parkinson’s disease, the sectionof the basal ganglia that is in heavy focus is the substania nigra. Initially recognised by Vicq d’Azir in 1786, ‘as a large cell mass located dorsalto the cerebral peduncle at the basis of the mesencephalon’. Located in the midbrain, it is the region responsiblefor the vital role of reward and movement.

Often mistaken for one structure, itis made up of two anatomically and functionally distinct parts the substanianigra pars compacta and substania nigra pars reticulata. Its name is areflection of its dark appearance as substania nigra means ‘black substance’ inLatin. Located in the substania nigra isthe dopaminergic neurones. These neurones are responsible for the secretion ofthe neurotransmitter dopamine. The pathophysiology of Parkinson’s is criticallydependant on these dopaminergic neurones. When a destruction of these dopaminergicneurone occurs in a healthy human being, consequently there becomes a depletionof dopamine stores therefore causing a degeneration of the dopaminergicnigrostriatal pathway. Furthermore, in the corpus striatum, an imbalance ofexcitatory (acetylcholine) and inhibitory (dopamine) neurotransmittersoccurs.  The deficiency of dopamine(neurotransmitter involved in motor function) therefore leads to the complexsymptoms of Parkinsonism ‘compromising slowness of movement, difficulty ininitiating and ending movement, tremor and rigidity (S Mera, 1996).

  There are clear differences in the dopaminestores in those of healthy individuals in comparison to those who havedeveloped Parkinson’s disease as demonstrated by figure2.  Parkinson’s disease contains very distinctive symptoms andits most noticeable feature is in the form of an uncontrollable resting tremorwhich is usually presented in the arm and hand of the patient. The tremorresembles a rotary action and therefore often referred to as ‘pinrolling’.  The tremor is present whilstthe patient is at rest and increases in rhythmic movement and harder to controlwhen the patient is in an emotional or a stressed state. The tremor oftendiminishes whilst in movement and in sleep. Although not all patients develop aresting tremor, it is the most common and prevalent symptom of Parkinson’s as70% of all patients diagnosed with the disease do eventually develop a restingtremor.  Bradykinesia (a slowing ofmovement) describes the slowness of conscious movement due to the increase indifficulty for the patient to initiate or terminate a particular movement forexample getting out of chairs or walking. An extensive deal of concentration isrequired for the patient to start and stop movement such as walking thereforewhen in motion it occurs in a shuffling movement with very small steps.

Thislater leads to frustration as the patient is ‘aware of what to do but isphysically unable to do it’ (S, Mera, 1996). This can consequently lead toakinesia – the disability for an individual to initiate movement. Another common symptom of Parkinson’s disease is ‘cogwheel’rigidity. This is muscle stiffness that can occur in any part of the bodycausing stiffness and pain therefore limiting movement.  It is usually caused by an increase in muscletone due to the muscles being in constant state of slight contraction. As thesymptom develops in later stages, it may begin to affect to tongue thereforeleading to drooling.

There are secondary list of symptoms that may also occuras a result of Parkinson’s disease such as depression. According to the mentalhealth foundation, ‘Depression is different from feeling down or sad.Unhappiness is something which everyone feels at one time or another, usuallydue to a particular cause. A person experiencing depression will experienceintense emotions of anxiety, hopelessness, negativity and helplessness’. Thisis common with individuals with Parkinson’s disease due to frustration obtainedfrom the inability to perform physical movements as well as chemical imbalancesin the brain as the depletion of dopamine is also heavily linked to thedevelopment of depression.  Anothersecondary symptom of Parkinson’s disease is constipation.   ‘Constipationis a common condition that affects people of all ages. It can mean that you’renot passing stools regularly or you’re unable to completely empty your bowel'(NHS choices 2015).

  Due to poorperistalsis, sluggish bowel moment and the anticholinergic drugs used intreatment of Parkinson’s patients do often suffer from constipation as a side effect.Speech and memory difficulties are also evident in most patients suffering fromParkinson’s. Although the aetiology of Parkinson disease remains unknown,researchers have outlined possible environmental and genetics links thatpotentially lead to an increased chance of an individual to develop thedisease.

For example studies show that people living in an industrial area orworking in industrial areas such as welders are more likely to developParkinson’s due to exposure to heavy metals such as manganese lead, copper etc.As mentioned previously, the disease is more common with individuals above theages of 60 and more common in males rather than females (reason unknown). Genetically,Parkinson’s disease phenotype has been found on the long arm of chromosome 4and although most cases of Parkinson’s are sporadic, in 10-15% of cases thereis a family hereditary history of the disease henceforth promoting a geneticcomponent to the disease however this may also just simply mean that somefamily members are exposed to the same environmental agents.   There is currently no cure available for Parkinson’sdisease however there are various treatments available that can help improvethe quality of life on an individual living with Parkinson’s.  The most popular and common treatment for thesymptoms of Parkinson’s is in form of the drug levodopa (L-dopa).

The idea isto replenish the depleted dopamine stores inside the brain however dopamineitself cannot cross the blood brain barrier due to in being too polar thereforeL-dopa a precursor of dopamine is used. L-dopa is able to successfully crossthe blood brain barrier and can then be converted into dopamine inside thebrain. However  the prescription ofdecarboxylase inhibitor is required alongside L-dopa with the significantreason of inhibiting the conversion of L-dopa into dopamine in the livermaximising the amount of drug available for activity inside the brain where thedopamine would be extremely beneficial toward the symptoms of Parkinson’s. The prescriptionof decarboxylase also lowers the dosage of L-dopa required to generateeffectiveness.  Although the use of L-dopa is initially extremelybeneficial, it does carry its specific side effects such as wearing off due tolong term use making it almost effective less over a long period of time. Itcan also potentially lead to movement disorders such as dyskinesia anddystonia.  It can also be responsible forside effects such as aggression and altered sleep.

Another disadvantage ofL-dopa is although it does increase the life expectancy and alleviatessymptoms, it does not prevent the continued degeneration of the neuroneshenceforth only produces symptomatic relief. Another drug that can be used forthe symptoms of Parkinson’s disease is amantadine and although it is less potentthan L-dopa, it has lesser side effects. It is thought to be involved in thestimulation of dopamine from its granular stores though its precise mechanismis unclear.  Monoamine oxidase Binhibitors (MAO-B inhibitor) can also be prescribed for example selegiline canextend the duration of symptom improvement if given in conjunction with L-dopa.More specifically selegiline acts as a neuroprotective agents and thereforeslows down the progression of the disease.     A different approach to drug treatment is the use of celltransplantation.

Cell Transplantation is the surgical process of replacing thedopaminergic neurones lost in Parkinson’s disease which began in the late 1980’s. It is still in in experimental phase dueto encountering postoperative complications such as high mortality rates.  The process works by using grafted foetalcells and according to neuroscience studies, “the adrenal medulla producesdopamine normally and auto transplantation ensures that there will be norejection problems”. Post mortem studies of the individuals who have died showthat only a few of the grafted foetal cells survive. The process has also beenhit with many ethical issues where many people thought and felt that foetalrights were being violated and that the use of foetal cells may encourageabortions.    Many people also depend onthe use of therapies to help deal with the symptoms such as taking part inregular exercise and taking advantage of physiotherapy can improve symptomssuch as bradykinesia.  The benefits of exercisecan also help with a lot of the secondary Parkinsonism symptoms such asdepressions as it can be a form of stress relief deviating patients fromdepression.   Conclusion Although idiopathic Parkinson’s does not have a preventivemethod nor a cure, there are medical improvements that have had positiveimpacts towards living with the disease.

Treatment such as gene therapy which focuseson preventing the progressive degeneration of the neurones and also thereplenishing of the dopaminergic neurones. In my opinion I believe with thepower of science and dedication of doctors, the future of Parkinson’s isgetting much closer to a method much suitable for the cure rather than theprevention and even although the romans have stated ‘prevention is better thanthe cure’ I believe it will be much harder to prevent the degeneration of the neuronesleading to Parkinson’s than curing and replacing the neurones via different scientificprocedures. Furthermore, I believe the most important thing today is to focuson the ways on maximising the quality of life for an individual with Parkinson’sand helping them manage the disease as best as they possibly can. 

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