DISCUSSION To evaluate how successful our experimentation was in showing H reflex, only comparisons with numeric values and trends in data within literature are applicable. The results which were shown in figure 1 for the CMAPs where the amplitude of the CMAPs increased as the perceived tension increased were to be expected. Because in order for a greater force to be applied there must be increased force of contraction, which the amplitude demonstrates, through electrical activation intensity. Also frequency of contraction may be increased aswell, as more muscle fibres are recruited when an increased effort is exerted, however in the figure it is hard to determine whether there has been a change in the frequency of action potentials. Though …show more content…
This was due to the axonal, rather than synaptic stimulation of the alpha motoneurons causing collision of action potentials in the motoneurons between the axonal origins and the sensory response potentials (Knikou 2008). The greater the intensity of stimulation got the more the action potentials cancelled, leading to the H wave diminishing and eventually becoming …show more content…
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The purpose of this paper was to describe the differences in neural activity in the motor circuit on animal subjects with hypo and hyperkinetic disorders. Hyperkinetic disorders are disorders that cause problems with movement initiation and reduce voluntary movements. While hyperkinetic disorders cause too much involuntary movements. There have been many primate models of Parkinson's disease but the one caused by MPTP is the one that is most alike to Parkinson's disease found in humans. Animals that are treated with MPTP develop symptoms that are similar to people with Parkinson's disease such as Akinesia, Bradykinesia, flexed posture, muscle rigidity, and postural tremor. Not all monkeys develop the tremor characteristic but the African
Parkinson's Disease is a literally crippling neurodegenerative disorder, manifested in about 1% of the aged population. People who have Parkinson's Disease gradually lose control of their movements; specific symptoms include, "tremor, slowness of movement, stiffness, difficulty in walking, and loss of balance." (1) Evidence strongly suggests that Parkinson's Disease is the result of severe cell loss in the substantia nigra. This brain structure is principally involved in the production of dopamine. (2) Dopamine, among other functions, is the neurotransmitter involved in initiation of movement. Hence, the link between dopaminergic cell loss and cessation of voluntary movement, as manifested
Andics, A., Gabor, A., Gacsi, M., Farago, T., Szabo, D., & Mikloski, A. (2016). Neural
Parkinson disease is a neurodegenerative disorder affecting primarily the patient’s motor function. The disease is characterized by rigidity, tremor at rest, bradykinesis, and decreased postural reflexes (Bollinger, Cowan, LaFontaine, Ronai, 2012). Parkinson disease was largely documented and brought to the forefront by James Parkinson, who published an article discussing the condition in 1817 (Lees, 2007). While great strides in understanding and treatment have been made, Parkinson disease is still considered an idiopathic disease (Lau & Breteler, 2006). Many areas of the disease process have been noted, but no one has been marked as the primary causative process, as well as little has been solidified in diagnostic procedures
Potential is recorded when the muscle becomes active but not wWhen the muscle is at rest, no action is potential recorded; however, as soon as the muscle becomes active, potentials are recorded. The potential recorded during activity is attributed as a result of to the asynchronous discharge of motoneurons [Remark 4] in the vicinity of the electrodes. During minimal voluntary activity, only a few number of motor units discharges, and as the voluntary effort increases, the more number of units is activated. This is called known as recruitment of motor units.
The speed of a nerve impulse is an important aspect of the human nervous system and can be altered by different stimulants. In 1850, Hermann von Helmholtz succeeded in measuring the speed of the nerve impulse. He found it to be much slower than the previously believed speed of 50 to 100 meters per second. This finding was then followed by intensive investigation of the nervous system within the framework of the physical and biological sciences. However modern measurements range from 6 to 122 meters per second, depending on the type of nerve fibre (Jonides, Rozin and Gleitman, 1983).
Pinnington, N., Elliott, A., Sciences, F. of L., Manchester and Kingdom, U. (2007) Proceedings of the physiological society. Available at: http://www.physoc.org/proceedings/abstract/Proc%20Physiol%20Soc%208PC39 (Accessed: 3 March 2016).
The author believes that deep brain stimulation is not an effective treatment for Parkinson’s disease and that it still requires further investigation and examination. In this paper, the author discusses three main issues of deep brain stimulation in the treatment of Parkinson’s disease. Firstly, deep brain stimulation may lead to negative effects on patients’ cognition, emotion and behavior. Secondly, implanted hardware devices increase the risks of surgical complications of deep brain stimulation operations. Thirdly, long-term effects of deep brain stimulation are still unclear and controversial.
Parkinson’s Disease (from hereon PD) is an extrapyramidal disorder characterized primarily by massive idiopathic degeneration of dopaminergic neurons in the substantia nigra, resulting in greatly decreased levels of dopamine in the striatum. The diagnosis, which is essentially a clinical judgment due to the lack, thus far of a simple diagnostic test, has historically been on the basis of the presence of at least two of the three main features of PD: bradykinesia (or akinesia or hypokinesia), rigidity, and resting tremor. In addition to these symptoms, most PD patients also show postural disturbances, impaired righting reflexes, and abnormal ocular movements. The extent of the disease and its symptoms can be quantified by one of a few
In 1817, James Parkinson published his famous treatise: "An Essay on the Shaking Palsy," describing the symptoms which now collectively bear his name. Although many scientists before his time had described various aspects of motor dysfunction (ataxia, paralysis, tremor) Parkinson was the first to collect them into a common syndrome; one which he believed formed a distinctive condition. His sixty-six page essay contained five chapters describing symptoms, differential diagnoses, causality, possible treatments, and prospects for future study. What is most intriguing concerning Parkinson’s analysis (besides its consistent accuracy) is the fact that his clinical observations and inferences were made by watching the
Question 1: A person with Parkinson’s disease (PD) demonstrates physical, cognitive and behavioural difficulties. These difficulties are based on the evidence of years of research about PD and the characteristics that are associated with this neurodegenerative disorder. Jankovic (2008) describes cardinal features of PD; tremor at rest, rigidity, bradykinesia, and postural instability which will be discussed in terms of their key aspects. Tremor tends to not interfere with daily activities as the tremor decreases with voluntary movement (Dauer, & Przedbors, 2003). Rest tremor disappear with action or during sleep, and usually involve the hands and may involve the lips, chin, jaw and legs; however, rarely involve the neck, head or voice (Jankovic,
Patients diagnosed with Parkinson’s disease have been identified as the population. The intervention chosen is deep brain stimulation in comparison to traditional Parkinson’s oral medications. The outcome chosen was to see if one treatment option may be more effective than the other in terms of relieving motor and nonmotor symptoms. If one method is more effective, that treatment could serve as evidence based practice in the hospital setting and can improve the quality of life of many
Parkinson’s disease is a chronic brain disorder that limits mobility in patients that are diagnosed with it. Information about the disease was first published in Western medicine in 175 AD, although evidence of it it has been seen since earlier ancient times. Since then, much has been learned about the disease. In the 1960s, the differences in chemicals in the brains of Parkinson’s disease patients were first identified. Researchers now believe that Parkinson’s is caused by the gradual breakdown of nerve cells in the brain. The degeneration of these cells leads to a lack of dopamine in the brain, which makes nerve functioning more difficult as it is harder for the brain to coordinate muscle movement. The gradual breakdown of neurons causes the symptoms of Parkinson’s to worsen as the patient gets older. Since the 1960s, research on Parkinson’s has been ongoing but not yet conclusive.
There are two types of cortical neurons being considered in the model, excitatory neurons and inhibitory neurons.
To obtain a valid diagnosis of Parkinson’s disease, clinicians should examine some motor and non-motor features. The motor features of Parkinson’s disease are characterized by resting tremors, muscular rigidity, bradykinesia, and postural and gait impairment. According to Samii, Nutt, and Ransom, “A resting tremor with a frequency of 3-5 Hz is the first symptom in 70% of Parkinson’s disease patients” (1783). Most people, if they have tremors, do not have this range of frequency. Hand tremors are more common in patients as a presenting sign than foot tremors, and they usually get worse with anxiety and walking. Rigidity is another sign of Parkinson’s disease, which is more prevalent in the tremulous limb. Rigidity is the inability