Parkinsmism involved in basal ganglia circuit
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Parkinsmism involved in basal ganglia circuit
- 1. Parkinsonism Approach by Basal Ganglia circuit aspect Neural Science MS / PhD Integrated Student Jongmin Yu(jmyu@gist.ac.kr) Applied Computing Laboratory Gwangju Institute of Science and Technology 1
- 2. 1 Introduction 2 The Pathology 3 Approach to Basal Ganglia circuit aspect 4 Reference, Q&A
- 3. 본Neural Science 과제의 기본 정보 Introduction Def) Parkinsonism a neurological syndrome characterized by tremor, hypokinesia, rigidity, and postural instability. There are both Motor and Non-Motor aspects Generally considered to affect the older population Symptom Motor - Tremor , Stiffness, Slowness, Stooped, posture, Unsteady gait Non-Motor(often more distressing) – Constipation, Depression, Sleep disturbance, anxiety Type Idiopathic PD(Parkinson’s Disease) –Most common Multiple System Atrophy(MAS) Progressive Supranuclear Palsy(PSP) Cortico Basal Degeneration(CBD) ETC – Vascular parkinsonism, Drug-induced parkinsonism, Juvenile Parkinson’s 3
- 4. 본Neural Science 과제의 기본 정보 The pathology of Parkinsonism Etiology : Unclear (dopamine neurons degenerate ) Progressive loss of dopamine brain cells(from the substantia nigra : midbrain) → Reduced amount of dopamine in the Basal Ganglia(corpus striatum) less dopamine is transported to the striatum, the area of the brain that co-ordinates movement. symptoms begin when the loss of dopamine reaches a critical point, 4
- 5. 본Neural Science 과제의 기본 정보 Approach to Basal Ganglia circuit aspect(1) Basal ganglia circuitry in normal conditions 5
- 6. 본Neural Science 과제의 기본 정보 Approach to Basal Ganglia circuit aspect(2) Basal ganglia circuitry in Parkinson’s disease 6
- 7. References 본 과제의 기본 정보 ReferencNeural Science es Cambridge University Press ISSN 1462-3994 (Disclaimer and copyright) Weyhenmeyer, James A.; Gallman, Eve. A. (2007). Rapid Review of Neuroscience. Mosby Elsevier. p. 102. ISBN 0-323-02261-8. Soltanzadeh, Akbar (2004). Neurologic Disorders. Tehran: Jafari. ISBN 964-6088-03-1 http://www.parkinsoninfo.org/ (Parkinson’s Research foundation) 7
- 8. Q&A
Notas do Editor
- Good morning every one in Neural Science class.I’m Jongmin Yu, announcer of this presentation, presentation topic is ‘Declarative memory’ another case is HM case.
- Declarative memory’s presentation element is this, First I will explain Background in this topic,And second I will give you that more detail academic knowledge and following example.And last session is summary which I explained, and may be I hope giving Q&A session. Then let’s begin.
- Definition : itfirst documented by James Parkinson and the 2nd common chronic neurodegenerative disease (first : Alzheimer)Idiopathic Parkinson’s disease (PD) was first documented by James Parkinson in 1817, and he wrote an essay on it known as “The Shaking Palsy”. It is the 2nd common chronic neurodegenerative disease after Alzheimer's disease, and it is progressive and disabling in its development. There is no cure.People with Parkinson’s don’t have enough of the chemical dopamine because the nerve cells in the brain that make it have died. Dopamine-producing nerve cells are found in the basal ganglia, a section located deep in the lower region of the brain. Dopamine is thought to be responsible for movement, mood, motivation and thinking. Symptoms of Parkinson’s will start to appear when between 60% and 80% of the dopamine-producing nerve cells have already been lost.Type : Idiopathic PD is the most common form of Parkinsonism, accounting for 75%. The other types of Parkinsonism’s include Multiple System Atrophy (MSA), Progressive Supranuclear Palsy (PSP) and Cortico Basal Degeneration (CBD), plus the genetic forms, medication induced and following severe head trauma (eg.Boxing)Symptom : Some quick supportive features of Parkinson's:¨Always asymmetrical- predominantly one side of the body¨Slow insidious progression¨May firstly complain of clumsiness, stiffness, fatigue, depression, constipation, pain or a tremor in one hand or finger.How someone's Parkinson's symptoms affect them can change from day to day, and even hour to hour. This can be either caused by the persons Parkinson’s or the medication used to treat it. Because of this, re-assessment of the needs of your patient should be carried out regularly. Symptoms will get worse when someone’s Parkinson’s drugs are Wearing Off and should improve again after Parkinson’s drugs are taken. Print of a Wearing Off diary page HEREType:Idiopathic pds the most common type of parkinsonism. Unlike some other forms which have specific causes it is not known why idiopathic Parkinson's occurs.The main symptoms of idiopatic Parkinson's are tremor, rigidity and slowness of movement.Symptoms and the rate at which the condition progresses vary from person to person. This can make diagnosis difficult.An early diagnosis means that treatment for Parkinson's can begin sooner, which may be more effective.One of the ways doctors diagnose idiopathic Parkinson's is by seeing if there is a response to Parkinson's medication.If there is no change then the symptoms may point to another form of parkinsonism.When this happens, the term 'atypical parkinsonism' is often used.The term early onset Parkinson's is used when people are diagnosed under the age of 40.- See more at: http://www.parkinsons.org.uk/content/types-parkinsons-and-parkinsonism#sthash.BQTcwVTO.dpufMAS : Multiple system atrophy (MSA) is a progressive neurological disorder that affects adult men and women. It is caused by degeneration or atrophy of nerve cells in several (or multiple) areas of the brain which can result in problems with movement, balance and automatic functions of the body such as bladder and blood pressure control.The Multiple System Atrophy Trust is the UK’s support and information service for people with multiple system atrophy, their families and carers. It also funds research into the treatment and causes of MSA.PSP: PSP is caused by the progressive death of nerve cells in the brain, leading to difficulty with balance, movement, vision, speech and swallowing. It is so called because it’s:Progressive – it gets steadily worse over timeSupranuclear – it damages parts of the brain above the pea-sized ‘nuclei’ that control eye movementsa Palsy – it causes weaknessPSP is associated with an over-production of a protein called tau in certain areas of the brain. In PSP, it forms into clumps – or neurofibrillary tangles – which are believed to damage nerve cells.There is nothing to suggest that the disease is inherited but research indicates that some people may have a genetic susceptibility that puts them more at risk of developing the condition than others.PSP is a rare condition. Research into the prevalence of the disease suggests that there are around 4,000 people in the UK living with the condition at any one time, though neurologists believe the figure could be as high as 10,000.CBD : A Brief Guide to CBDCortico Basal Degeneration (CBD) is a degenerative brain disease, affecting people from the age of 40 onwards. Although there are biological similarities to PSP, with similar nerve cell damage and build up of tau protein in the brain, the classical clinical picture is quite distinct.Cortico - affecting the brain cortexBasal - also affecting other parts of the brain such as the basal gangliaDegeneration - death of nerve cells in the brainAs yet, there has been no research into the prevalence of CBD but we do know that it is much less common than PSP. People are often initially misdiagnosed as having Parkinson’s disease or a stroke.At the moment there is no treatment to stop or slow the progression of CBD. However, many symptoms can be treated and are usually managed in a similar way to those for PSP.Signs and SymptomsCBD often starts with progressive numbness and loss of use of one hand. There can also be jerking of the fingers, slowness and awkwardness and the feeling of having an ‘alien limb’ – with complex unintentional movements of one limb causing problems with normal motor tasks.Gradually the arm and/or leg on one side is affected and then the arm and/or leg on the other. People with CBD often have trouble controlling one hand when doing everyday things such as writing or tying shoelaces – tasks that involve individual muscle movements we take for granted. Eye movements can also be disturbed but these are normally less debilitating than in PSP.
- Dopamine Responsible for movement, Mood, Motivation, ThinkingUnder the influence of dopamine, signals from the striatum regulate all forms of movement.Despite intense research efforts around the world, the molecular causes of Parkinson’s disease are still unclear. What doctors and scientists do know is that PD is caused by the progressive loss of dopamine brain cells (neurons) in a part of the brain called the substantianigra, which produces the chemical dopamine. As the cells die, less dopamine is produced and transported to the striatum, the area of the brain that co-ordinates movement. Under the influence of dopamine, signals from the striatum regulate all forms of movement. Parkinson’s disease symptoms begin when the loss of dopamine reaches a critical point, typically when 50 to 80 percent of dopamine neurons have died. Because there is such a dramatic loss of dopamine neurons by the time the disease is diagnosed, it extremely difficult for doctors and scientists to research PD at its earliest stages. Thus, much of the research done on PD uses animal models that most closely mirror the onset of PD in humans.The question of why dopamine neurons degenerate is being intensely investigated by scientists in our labs, and all over the world. In recent years, great strides have been made in solving this mystery. While there is still no definitive answer, it is now widely accepted that there is no single “cause” that triggers the disease. Instead, Parkinson’s disease likely results from a confluence of inherited (genetic / familial) and environmental factors that interact in complex ways to set disease processes in motion. Around 5 percent of cases are hereditary in the classic sense that if one or both parents have it, their children are at higher risk. But in the vast majority of cases, no obvious familial link is present. Instead, it is believed that there are a variety of triggers, including exposure to toxins and severe head injuries. Also, individuals may inherit a degree of susceptibility to the disease, which only causes Parkinson’s disease when other factors are present.Symptoms of Parkinson’s will start to appear when between 60% and 80% of the dopamine-producing nerve cells have already been lost.Substantianigra:Although the substantianigra appears as a continuous band in brain sections, anatomical studies have found that it actually consists of two parts with very different connections and functions: the pars compacta and pars reticulata. The pars compacta serves mainly as an input to the basal ganglia circuit, supplying the striatum with dopamine. The pars reticulata, on the other hand, serves mainly as an output, conveying signals from the basal ganglia to numerous other brain structures.Under the influence of dopamine, signals from the striatum regulate all forms of movement. Parkinson’s disease symptoms begin when the loss of dopamine reaches a critical point, typically when 50 to 80 percent of dopamine neurons have died. Because there is such a dramatic loss of dopamine neurons by the time the disease is diagnosed, it extremely difficult for doctors and scientists to research PD at its earliest stages. Thus, much of the research done on PD uses animal models that most closely mirror the onset of PD in humans.The question of why dopamine neurons degenerate is being intensely investigated by scientists in our labs, and all over the world. In recent years, great strides have been made in solving this mystery. While there is still no definitive answer, it is now widely accepted that there is no single “cause” that triggers the disease. Instead, Parkinson’s disease likely results from a confluence of inherited (genetic / familial) and environmental factors that interact in complex ways to set disease processes in motion. Around 5 percent of cases are hereditary in the classic sense that if one or both parents have it, their children are at higher risk. But in the vast majority of cases, no obvious familial link is present. Instead, it is believed that there are a variety of triggers, including exposure to toxins and severe head injuries. Also, individuals may inherit a degree of susceptibility to the disease, which only causes Parkinson’s disease when other factors are present.
- Figure 2. Basal ganglia circuitry in normal conditions. In normal brain, parallel neuronal networks of the striatum connect and integrate functions between the basal ganglia nuclei, various regions of the cerebral cortex and the thalamus. In the motor circuit, shown here, areas of the motor cortex project in a somatotopic pattern to the posterolateral putamen, where they synapse through excitatory glutamatergic neurons onto the medium spiny striatal neurons. These striatal neurons use gamma-aminobutyric acid (GABA) as their primary neurotransmitter and substance P (SP) or enkephalin (Enk) as co-transmitters, and are organised into two pathways: the ‘direct’ and the ‘indirect’ pathway. The direct pathway connects the striatum to the internal segment of the globuspallidus (GPi) and the substantianigra pars reticulata (SNr). The GPi and SNr are the output nuclei of the basal ganglia (GPi/SNr) and project to the brainstem and the thalamus and from the latter to the cortex. The influence of the GPi and SNr on the thalamus is inhibitory, whereas the thalamic projection to the cortex is excitatory. The indirect pathway also connects the striatum to the output nuclei of the basal ganglia but these fibres first pass through synaptic connections in the external segment of the globuspallidus (GPe) and then the subthalamic nucleus (STN). Output from the STN to the GPi/SNr is excitatory. Excitatory projections are shown in blue; inhibitory connections are shown in black. Abbreviation: PPN, pedunculopontine nucleus (fig002rbc).
- Figure 3. Basal ganglia circuitry in Parkinson’s disease. In Parkinson’s disease (PD), the natural balance of the circuit shown in Figure 2 is lost owing to the depletion of dopamine in the striatum. Both the direct and indirect pathways operate through the GPi/SNr output nuclei and their influence is inhibitory on the thalamus. Thus, increased activity in the output nuclei leads to increased inhibition on the glutamatergic excitation of the motor cortex and a subsequent reduction in movement, observed in patients as bradykinesia. In addition, other structures such as the pedunculopontine nucleus (PPN) receive an abnormal input from the basal ganglia, which contribute to some of the clinical signs, such as gait disturbance. These changes in the PD brain are shown here by the differing thickness of arrows, which represents the relative degree of activation in each projection. Abbreviations: Enk, enkephalin; GABA, gamma-aminobutyric acid; GPe, globuspallidus, external segment; GPi, globuspallidus, internal segment; SNc, substantianigra pars compacta; SNr, substantianigra pars reticulata; SP, substance P; STN, subthalamic nucleus (fig003rbc).