Parkinsons – Paralysis Agitans

Parkinson’s or as it’s less commonly known Paralysis Agitans is the second most common neurodegenerative disease within the UK following Alzheimer’s. It affects 6.3 million people worldwide and is most definitely age related (Hoa Huu Phuc Nguyen M. Angela Cenci, 2015). Parkinson’s originates in the Cortico-basal nuclei within the Brain. The Cortico-basal Nuclei connects the cerebral cortex with neural systems, this connection effects an individuals over all behaviour. Within the behavioural effector systems there is a structure called the thalamic nuclei. This structure sends messages to the frontal cortical areas; this is where the brain sends messages to other nerves around the body to carry out movement (Gerfen and Bolam.2010). The progressive degeneration changes within the cortico-basal nuclei mostly in the substania nigra mean that these messages become interrupted. A lesser amount of dopamine is secreted meaning that there is an imbalance in the cortico-basal nuclei. When this small structure is damaged progressively, the over stimulation affects movement and posture which are two of the most obvious symptoms this is due to an increase in muscle tone and involuntary or voluntary activity, this eventually does result in muscle tremors and muscular ridgity. The limited knowledge in the public eye means that most people associate Parkinson’s with Dementia; however dementia is only a symptom that 20% of patients with this condition experience, usually occurring in the final stages of the degenerative condition. Dementia and Parkinson’s do have similarities for example both have a reduced number of cortical neurons. However these conditions do come hand in hand (Gould and Dyer 2011).
Mrs Smyth presented with muscle tremors, short shuffling steps, a stooped posture and increasing anxiety. These symptoms are caused by the degeneration of a group of nuclei found at the base of the forebrain. The basal ganglia are responsible for smooth movement. The increase of dopamine in the striatum, a subcortical part of the brain. (Thomas Wichmann, 2011) causes the motor symptoms of this condition. Overtime this means that the impulse originating in the motor cortex passing through the medulla is not able to travel to the peripheral nerves needed to carry out normal movement. Dopaminergic neuron loss is also a cause for Parkinson’s disease, they are found in several locations in the vertebrate brain (Pasterkamp 2009). Of these neurons, the ones required for movement, the Substantia nigra dopaminergic neurons, a midbrain neuron, works together with glutamate, an amino acid and have long projections in the striatum that are paramount for movement. The Olfactory bulb neurons, another dopamine producing neuron, are short axonal projections that are required for processing sensory information. The vast majority of these cells are tiny periglomerular interneurons that are roughly between 5 and 10urn in diameter although some can differ to between 10 and 15urn. Both of these neurons are continuously generated throughout an adult’s lifespan and are the major dopamine producing systems within the Brain,(Lindvall 2012) It is a chemical messenger that aids signals in the brain to travel to other parts of the body. Also both of these neurons are distributed mostly on the glomerular layer. These neurons receive region specific messages for movement from the axon terminals of the olfactory receptor nerve fibres. The loss of these neurons is the hallmark cause of Parkinson’s disease. This is due to the elevated volume of Dopamine that is produced which causes these neurons to fail and not repair. This in turn means that not enough dopamine is produced. Dopamine is a catcholaminergic transmitter; this transmitter has the capacity to become neurotoxic in high concentrations or in an oxidative environment which is commonly found in those suffering with Parkinson’s disease. The increase of this neurotransmitter causes the degeneration of the dopaminergic neurons needed for movement and sensory development, usually due to oxidative stress. However normal aging can also cause this because of an elevated release of dopamine from the synaptic vesicles (Gille, 2005). It is also thought that the mitochondria contributes to Parkinson’s. The mitochondria are the powerhouse within the cell. It produces the energy needed for as little as cell survival. The mitochondria also contains a component called free radicals; this component can damage membranes, proteins and DNA and in turn cause oxidative stress (Reeve 2012). Lewy bodies can also be a feature of Parkinson’s disease. Lewy bodies are abnormal aggregates of protein, alpha-synuclein, they can develop within the nerve cells that are associated with Parkinson’s disease. They are made up of a dense core and surrounding fibrils, however in Parkinson’s disease these structures become swollen and displace other components within the cells. It is not yet known exactly how Lewy bodies contribute to Parkinson’s disease. It is thought that the clusters of protein cause interruptions within the cells stopping it from functioning normally; however, there is also research that suggests that they may help by keeping harmful proteins separate from the cell (Sharp 2013). As previously stated not all patients diagnosed with Parkinson’s disease will develop these Lewy bodies which can develop in end stage Parkinson’s surfacing as dementia.

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