This case is about a headmaster, Mr Boddy, who was simply experiencing a number of issues that increased in severeness and had an ever-increasing effect on his life. The symptoms were becoming more and more clear to both Mr Boddy and his children which lead to him heading to see his GP who referenced him to an expert. The specialist started out him on the course of medicine but made a decision to change it within less than a year. From the symptoms described in the event, it is apparent that Mr Boddy has Parkinson's Disease. The problems presented in this case were discussed and learning goals were produced which will be explored in this essay.
Anatomy and function of the basal ganglia
The basal ganglia are a group of deep nuclei that can be found at the base of the forebrain and are linked to the thalamus. The deep nuclei that make up the basal ganglia are the caudate nucleus, the putamen, the globus pallidus, the substantia nigra and the subthalamic nucleus. (Michael-Titus, et al. , 2010)The primary function of the basal ganglia is to start and maintain electric motor actions plus they play a essential role in the decision-making functions in the mind by control cognitive and emotional information from the environment. They also talk to the supplementary motor unit cortex to organise the right excitation of the principal motor unit cortex as well as scaling the strength of the response. Another function is that they change movement on one minute by tiny basis by communicating with the cerebellum. (Buot & Yelnik, 2012)
The nuclei of the basal ganglia can be categorized as either input nuclei or output nuclei. The input nuclei are made up of the caudate and the putamen and as they are functionally similar they are known together as the striatum. They could be seen in Number 1 where they are simply coloured purple. Most of its input comes from the cerebral cortex, nonetheless it also gets some suggestions from the other basal ganglia nuclei. (Rolls, 1994) The end result nuclei will be the globus pallidus, substantia nigra and subthalamic nuclei. They can even be seen in Shape 1 and are in very close proximity to the striatum. The substantia nigra is split into two parts, the pars compacta(SNpc) and the pars reticulata (SNpr). The SNpc will be the cells that produce dopamine and are broken in parkinsons which is what occurred to Mr Boddy. The SNpr receives source from the striatum and delivers it to the ventral anterior, ventral lateral, and mediodorsal thalamic nuclei to control head and eyeball motions as well as perform other functions. The globus pallidus is split into the internal (GPi) and external (GPe). The function of inner part of the nucleus is to send outputs to the thalamus. However, the function of the exterior portion of the nucleus is not fully understood but it appears to modify and target activity in the rest of the basal ganglia. (Hanna, et al. , 2011) Damage to the basal ganglia is exactly what induced Mr Boddy's Parkinsons disease.
Neurological pathway of dopamine and neurotransmitters involved in basal ganglia pathway
One of the main effects of Parkinson's is on movement and this holds true with Mr Boddy as he developed a great deal of motion problems. Thus, there should be a challenge with the basal ganglia's modulation of movement. The standard modulation of motion can be discussed in terms of any "brake theory". Essentially, to start one motion the brakes must be employed to other activities. So harm to the basal ganglia will lead to an inability to avoid current moves as well as difficulty initiating movement. (Rhoades & Bell, 2009)
The initiation of any motor program and the maintenance of the motor programme are respectively controlled by the dopaminergic immediate and indirect pathways. Whether a electric motor programme is certainly going to get started on or be preserved depends upon the discussion of both pathways. So damage to the substantia nigra pars reticulata which produces dopamine has undesireable effects on both of these pathways and alters their function thus modifying their combined impact which manifests as the symptoms of Parkinsons. The immediate pathway is excitatory and the indirect pathway is inhibitory. (Lenglet, et al. , 2012)
The immediate pathway is turned on via excitatory glutamatergic neurones from the cortex. This combined with the dopamine being released from the substantia nigra pars compacta causes inhibition, via GABAergic neurones, of the inner globus pallidus which in turn causes the web reduced amount of the inhibition, via GABAergic neurones, of the thalamus. This finally brings about the increased excitation of the cortex via glutamatergic neurones which in turn triggers increased excitatory output from the cortex to the muscle fibres via the lateral corticospinal tract. The excitatory immediate pathway is seen in Physique 2. The indirect pathway is nearly the same as the direct pathway. Once stimulated by the cortex, the neurones from the striatum task onto the external globus pallidus nuclei which causes inhibition. This inhibition leads to the net decrease in the inhibition of the subthalamic nucleus. This ends in the subthalamic nucleus' projection of excitatory, glutamatergic, inputs into the internal globus pallidus which causes inhibition of the thalamus and this decreases excitement of the motor unit cortex. Which in turn ends up with reduced muscle activity. Much like the direct pathway, the indirect pathway is illustrated in Amount 2. The key reason why dopamine released from the substantia nigra can have both excitatory and inhibitory impacts is as a result of dopamine receptors. The dopamine receptors D1 and D5 are found in the inner globus pallidus and are excitatory. The dopamine receptors D2-D4 are found in the external globus pallidus and are inhibitory. (Lenglet, et al. , 2012)
In Parkinson's disease substantia nigra pars compacta have degenerated and therefore are producing less dopamine. This affects the D1-D5 receptors which results in less excitement of the immediate pathway and release of the inhibition of the indirect pathway. This means that the indirect pathway becomes the dominant one that inhibits the thalamus and so will reduce motor activity in the engine cortex. This ends in the quality symptoms of parkinsons. A diagram of the changes can be seen in Figure 3. These changes are what triggered the problems that Mr Boddy was experiencing and the increasing intensity of his symptoms was probably triggered by the continuing degeneration of his substantia nigra pars compacta skin cells. (Wu, et al. , 2012)
Symptoms of Parkinson's
The symptoms that Mr Boddy experienced are mainly brought on by the lack of dopamine resulting in the dominance of the indirect pathway. The first sign that he developed was sleeping problems which was most probably caused because the body has trouble initiating a sleeping pattern. So once he wakes up in the middle of the night to go to the toilet for example, then he'll not have the ability to get back to sleep as a result of under activity of the direct pathway. The loss of the sense of humour and the tremors are also triggered by Mr Boddy becoming trapped in a motor unit programme. The pill-rolling tremor is quality of Parkinson's. The clumsiness and slipping over occur because the basal ganglia harm means so it cannot connect normally with the cerebellum.
There are also a number of other symptoms that within patients with parkinsons disease. Even though everyone presents with Parkinson's in a different way, there are a variety of symptoms that can be found in everyone. They can be listed in Desk 1.
Diagnosis of Parkinson's
Diagnosis of Parkinson's is manufactured out of a medical history and neurological examinations by themselves. This is because the one test for Parkinson's at the present time can only be performed during a post mortem. After the neurological exams and the history have been taken the NICE recommendations (Desk 2) need to be applied to the finding. In Mr Boddy's circumstance, he previously two of the three criteria in Step one 1 as well as four of the conditions that had to be met in Step 3 3 to produce a definite analysis.
Lewy bodies can be found during a post-mortem of an individual with Parkinson's. They seem as spherical public which contain irregular alpha synuclein health proteins deposits and are found on the brainstem. A good example of a Lewy body is seen in Shape 4.
Treatment of Parkinson's
There are lots of treatments for Parkinson's disease, each with the own side results which means that their use must be totally controlled and checked.
The most effective class of drug at elevating the symptoms of Parkinson's is L- dopa. L-dopa is the precursor for dopamine and it can cross the bloodstream brain barrier where it is changed into dopamine by dopa decarboxylase to revive the dopamine levels in the mind to a standard level. Dopamine itself cannot be given as it cannot mix the bloodstream brain barrier. However, if L-dopa is given on its own it will breakdown in the body and activate the vomiting centre in the brain and cause vomiting. In like manner counteract this issue, it is given with a dopa decarboxylase inhibitor which can stop the change to dopamine in the body. Since it cannot cross the blood brain hurdle dopamine can still be produced in the brain. The main side-effect is the fact after an extended period of use side effects known as "on-off sensation" develop. Which can be where there are durations of activity (on) accompanied by a state of being immobile (off). The individual can suddenly change between both of these states. Another side effect is dyskinesia. (Goetz, 2007)
To avoid the finish of dose part ramifications of L-dopa other drugs that are less effective are given first to extend enough time before L-dopa must be given and the "on-off result" starts happening. One type is a dopamine agonist. They work by binding to the post-synaptic receptors in the brain and also have similar results to L-dopa. However possible part results include nausea, throwing up and fatigue. A good example is bromocriptine or rotigotine. Another school of drug that is utilized is Monoamine oxidase inhibitors. They work by avoiding the breakdown of dopamine. Their side effects include; frustration, joint pain and unhappiness. Catechol-O-methyl transferase (COMT) inhibitor functions by preventing the break down of L-Dopa and the undesireable effects are nausea, throwing up, diahorrea and abs pain. A good example of a COMT inhibitor is entacapone. Mr Boddy was given Rasagiline to begin with which is a monoamine oxidase inhibitor. And he was turned to L-Dopa which possessed a marked impact. (Longmore, 2007)
Deep brain activation is another option for the treating Parkinsons. It cannot remedy Parkinson's but by firing high consistency impulses in to the brain it can reduce the symptoms of Parkinson's as well as lowering the adverse effects of the drugs which enhances the patients standard of living. Maybe it's recommended to Mr Boddy that he attempts this program when the "on-off effects" start happening. (Rodriguez-Oroz, et al. , 2005)
Prognosis of Parkinson's
If Parkinson's isn't treated then patients will be bedridden after a decade of starting point of the condition. The symptoms will enhance rapidly. In people taking drugs the time taken for the condition to reach a level where these are foundation ridden is more than 15 years. (Poewe, 2006) However, the span of the disease is different in every person with the disease development being faster in folks who are elderly. (Obeso, et al. , 2010) Disability is linked to motor symptoms in the beginning of the disease but as it advances they may be linked to motor symptoms that don't react to medicine. Life expectancy for folks with PD is also reduced. (Poewe, 2006) The advice that can be given to Mr Boddy is that there is no chance of knowing for certain how Parkinson's will affect his future. However, the best case scenario is the fact he can keep on as normal for another 7 to 10 years before his symptoms greatly have an impact on his job and family life.
In conclusion, this was an extremely interesting subject to look into and it made me understand how complex the condition is and how much of a direct effect it is wearing someone's life. If I had more time I would like to look further into the hereditary links behind Parkinson's as well as looking into new methods of examination that are being developed as I didn't have the time to do so.
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