PD pathology results from a degenerative process which reduces the function of dopaminergic substantia nigra (SN) neurons below a certain threshold until it manifests as clinical symptoms17. It should be noted that degeneration of the SN is not the sole location of degeneration – regions such as the locus coeruleus, raphe nuclei, basal forebrain, and frontal cortex undergo a similar process17. The pathology is still not fully understood, but the degenerative process has been found to stem from the glossopharyngeal, vagal, and olfactory cranial nerve nuclei and then ascend upwards through the brainstem18. The degeneration of these origin structures have been theorized to be responsible for the non-motor symptoms presented in PD18. Regions of interest: A majority of DBS studies have focused on the motor dysfunction seen in PD focusing therapies targeted towards the STN and GPi. Because these studies are well-covered and various literature reviews are already published, we will focus on other anatomical structures of interest. However, after one study conducted a three year follow-up on patients after DBS of the GPi and STN in advanced (also referred to as late-stage, or LSPD) PD, it was discovered that PD patients with STN DBS exhibited better off-phase motor improvement than GPi DBS patients4. Peduculopontine Nucleus: Another study was attracted to the pedunculopontine nucleus (PPN) because of its reciprocal connections with the GPi and basal ganglia, structures commonly
Simply because the imaging methods used such as CCT or an MRI are structural neuroimaging methods that cannot provide characteristics that are generally featured in PD, both which are commonly tools used by physicians. However, it is possible for the physician to use functional neuroimaging methods such as PET and SPECT, which are definitive and more accurate in diagnosing patient’s first sign of parkinsonism. This form of early diagnosis does come with a hefty price that many cannot afford along with the fact that it is not broadly available in many clinics or imaging centers. With that said a new method, the TCS is more reliable in effectively diagnosing early symptoms of PD. It was concluded that with the use of the TCS “up to 90%” of patients have shown an enlarged echogenic size (hyperechogenicity) of the substantia nigra (SN). An enlarged echogenic of the SN leads to a diminishment of the nerves in the SN, that is seen in PD. The nerve cells in SN are responsible for control of movements and coordination by sending out signals to tissues on both sides of the brain. A 37-month study led by multiple researchers have determined that an enlarged SN was correlated with a higher risk for PD. TCS has also been known to precisely diagnosis the severity and differentiation of PD patients, distinguishing how sensitive and the specificity of individual patients.
Parkinson disease (PD) is one of the most common neurologic disorders. and it affects approximately 1% of individuals older than 60 years old. Parkinson’s disease is a condition that progresses slowly by treatment. In addition, loss of pigmented dopaminergic neurons of the substantianigra pars compacta and the presence of Lewy bodies and Lewyneurites are the two major neuropathologic findings in Parkinson disease (Hauser, 2016).
Parkinson 's disease is a progressive neurologic degenerative disease of the Central Nervous system. The brain produces Dopamine and Norepinephrine, which are chemicals needed for smooth muscle movement and coordination, heart rate, and blood pressure. Dopamine and Norepinephrine are released by basal ganglions that are produced in a bundle of nerve cells in the brainstem called substantia nigra. In Parkinson 's patients, the substantia nigra are destroyed and neither of the chemicals can be released into the body. (3) The decrease in Norepinephrine causes heart arrhythmia and low blood pressure, causing the person to get dizzy upon standing or tire easily. The lack of Dopamine, the smooth muscle movement and coordination controller is now gone, or significantly decreased, resulting in the first signs of Parkinson’s disease, pill-rolling, a one handed tremor and a decreased appetite. (2)
Mr. A. is a 56-year-old man who was diagnosed with PD 8 months ago. He reports slowness with walking, a tendency to drag his left leg, and limited swinging of his left arm when he’s walking. His neurologist started him on 1 mg daily of Azilect, a drug that helps relieve tremors early in the course of the disease. Mr. A. works full time and does not currently exercise. He heard that exercise may be helpful for people with PD but doesn’t know which exercises are best for him and how much he should exercise.
The occipital lobe is in a posterior position and the function of the occipital lobe is vision including perception and colour and movement (Stannard Gromisch, 2012). Atrophy is described as a process of tissue wastage or cell death (Lippincott Williams & Wilkins, 2006). According to (Jones & Gaillard, 2005-2013) the pathology of PCA includes Neuritic plagues and neurofibrillary tangles which are found in the parieto-occipital and temporo-occipital areas, as well as occasionally in the primary visual cortex. It is thought that PCA is a version of AD, with very little difference in the pathology. “Neuritic plagues or senile plagues are extracellular and composed of a central core of beta-amyloid peptides aggregated together with fibrils of beta-amyloid, dystrophic neurites, reactive astrocytes, phagocytic cells, and other proteins and protein fragments derived from degenerating cells or liberated from neurons” (Weerakkody & Gaillard, 2005-2013).
Some dopaminergic (i.e., dopamine-releasing) neurons run from the substantia nigra to the corpus striatum; their loss gives rise to the clinical manifestations of Parkinson's Disease (Korczyn 1994); others, involved in the rewarding effects of drugs and natural stimuli, run from the mesencephalon to the nucleunucleus accumbens.
neurons in the substantia nigra in case of Parkinson’s disease, motor neurons in the motor
Though it is believed that the loss of dopaminergic innervation is the cardinal neurotransmitter system involving in PD, other systems of innervation such as serotonergic, cholinergic and glutamatergic innervations are also involved in the pathogenesis of PD16. The serotonergic transmission is thought to be heavily affected due to the non-physiological administration of L-DOPA during the treatment of PD17.After exogenous administration of L-DOPA, it is meant to be converted by the nigrostriatal dopaminergic neurons that contain a large amount of DA converting decarboxylase enzyme. However, as dopaminergic neurons are heavilydenervatedin PD, 5-HT neurons are then primarily responsible for the conversion and the release of DA after the exogenously
Parkinson’s disease is affected by the degeneration of dopaminergic neurons which is responsible to produce dopamine. Dopaminergic neurons have their cell bodies in substantia nigra pars compacta (SNpc) in basal ganglia (O’Sullivan and Schmitz, 2007). Basal ganglia are a collection of interconnected gray matter nuclear masses deep within the brain”. These gray matter masses are caudate, putamen, globus pallidus, subthalamic nucleus and the substantia nigra. Basal ganglia receive its input through striatum (O’Sullivan and Schmitz, 2007).
PD is increasingly recognized as an extensive multi-system disease with widespread neurological impairment, affecting a variety of brain regions not directly involved in motor control. The extranigral pathology includes the olfactory bulb, the dorsal motor nucleus of the glossopharyngeal and vagal nerves, the intermediate reticular zone, subnuclei of the reticular formation and the raphe system, the locus coeruleus (LC), regions of the basal forebrain, many subnuclei of the thalamus and amygdala, and, in severe cases, the neocortex [64-67]. In 2003, Heiko Braak and colleagues [68] traced the course of the pathology in incidental PD cases and developed a staging procedure based on the location of α-synuclein-containing inclusion bodies, also
As previously discussed, the basal ganglia circuit is an important aspect of the pathophysiology of PD. There are five dopamine receptors that are found in the basal ganglia. They are categorized from D1 to D5. D1 and D2 are most significant with relation to the pathophysiology of PD. They are found primarily within motor stratum. These receptors have denervation hypersensitivity due to dopaminergic neuron deficiency. The dopamine producing neurons decrease significantly as the disease process advances, resulting in the depletion of dopamine in the nigrostriatal pathway and the substantia nigra. The subthalamic nucleus is not inhibited due to this hypersensitivity. his can lead to heightened inhibition in the thalamus, causing instability of
It has been known that PD is a disorder affecting the basal ganglia. The term basal ganglia is generally applied to a collection of nuclei situated deep within the cerebral hemispheres, lying laterally to the thalamus (Gazzeniga, George, and Mangun, 2008). The basal ganglia are important subcortical structures. They are composed of five nuclei: caudate, putamen, globus pallidus, subthalamic nucleus, and substantia nigra. These nuclei are not thought of a single anatomical entity; rather, they form a functional unity whose contribution is greatly to motor control. Interestingly, this system does not influence movement through spinal cord pathways, but rather acts as part of a feedback loop to all areas of the cerebral cortex, with primary input into motor areas (Aird, 2000). A number of excitatory and inhibitory neurotransmitters are what control this whole process, and a balance of both is required to ensure that smooth, purposeful movement takes place. In order to understand the pathways of which the basal ganglia take part in, it is essential to know the input and output connections of the basal ganglia. The input
Due to years of research for Parkinson’s, a current theory known as Braak’s Hypothesis, discusses that the beginning signs for the disease is found in the nervous system, medulla, and olfactory bulb. According to Braak and his colleagues they have found that, “The Braak hypothesis not only proposes that lower brainstem pathology is a necessary pre-condition for the occurrence of PD, but also that it is sufficient. In other words, there is such a compelling liklihood that Stage 1 or Stage 2 synuclein pathology will evolve to Stages 3 or 4, and, more importantly, evolve to manifest clinical parkinsonism that this pathology can be considered to represent “early PD”, as has been claimed. (NCBI)” This hypothesis
Introduction: A long-term degenerative neurological condition (LTDNC) is a term used to describe diseases that affect the nervous system leading to its degeneration. Conditions such as Parkinson’s disease, amyotrophic lateral sclerosis, multiple sclerosis etc. are all categorized by impairment in brain, nerve and spinal cord pathway cells (Canadian Institute for Health Information, 2007). Due to such disruptions, the nerve signals between the brain and the body are affected which result in problems with walking, controlling movement, balance, full or partial paralysis, breathing and talking problems, occurrence of seizures, lack of bladder and bowel control at later stages, and even problems with the heart (Canadian Institute for Health Information, 2007). In 2011, the Canadian Institute for Health Information reported that Canada has one of the highest incidences of multiple sclerosis (MS) in the world, where approximately 93,500 individuals are currently affected. Despite the prevalence of the disease, there is still much that remains unknown. According to the 2012 statistics from the ALS Society of Canada, the number of new diagnoses per year is
Functional neuroimaging study using PET or blood oxygen level-dependent functional MRI frequently demonstrated increased activation in the cerebellum in patients with PD during performance of various upper limb movements (Rascol et al., 1997; Catalan et al., 1999; Wu and Hallett, 2005; Yu et