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Transcript of Parkinson's Disease
By: Shannon Massine & Samantha Flaherty 2nd most common involuntary movement disorder
Considered the "prototypical" illness of involuntary movement disorders
Parkinson's Disease is a subcortical demetia
Parkinson's is a neurodegenerative disease Features of Parkinson's Disease Paucity of trunk and limb movement
Patients with akinesia and rigidity can’t rapidly flex spine, hips, or knees (rock slowly)
Patients sit motionless with legs uncrossed and feet flat, arms on chair or in lap (rarely reposition themselves, don’t shift weight, no unnecessary movements)
Loss of reflexes in combination of akinesia and rigidity that results in festinating gait (tend to lean forward and have accelerated pace)
Shuffling gait (turning example)
Video Signs & Symptoms Masked face
Blink less, fewer facial expressions, move head less often, "stare" or have an emotionless expression
Handwriting deteriorates (gets smaller and tremulous)- micrographia
Ex: Can tell onset of the illness based on signatures on checks
Voice loses volume and fluctuation
Speech becomes hypophonic and monotonous (weak and whisper)
Development of sleep disturbances Symptoms Continued Pathology Common Attributes 3 Cardinal Features Tremor
Most conspicuous feature, least debilitating symptom and least associated with dementia and depression
Primarily in the hands
Resting Tremor (vs. intention tremor)
Pill rolling tremor (absent during sleep)
Asymmetric or unilateral pattern (hemiparkinsonism)
Rigidity: inflexibility or stiffness- cogwheel rigidity
Bradykinesia: slow or absence of movement Neurological Exam: The neurologist will ask the patient to sit, stand, walk and extend arms
Normal person sways or takes one or two steps backward
Patient with Parkinson's has to take many steps backward (impaired postural reflexes)
In pronounced cases, patients will fall back into the physician's arms (unable to correct posture)
PET with fluorodopa shows decreased dopamine activity in the basal ganglia Testing for Parkinson's Disease Normal Dopamine production Phenylalanine Phenylalanine hydroxylase Tyrosine Tyrosine hydroxylase DOPA DOPA decarboxylase Dopamine Risk Factors Age
Most are 60 or older
Caucasian more than any other race
More in men than women
Play a significant role only if the onset occurs at 50 years or younger.
Can occur in individuals younger than 21 but early onset is rare
Mutations in the parkin gene and alpha synuclein gene Herbicides and Insecticides
Cyanide Toxins Risk Factors Continued Parkinson Like Diseases Parkinsonism Clinical features of Parkinson’s disease in the absence of the illness
L-dopa doesn’t reverse Parkinsonism Parkinson-Plus Diseases A group of related neurodegenerative illnesses that share many of the same signs as Parkinson’s Disease and are subcortical dementias
They follow a more rapid course and respond less well to dopaminergic medications Diseases Comorbid With Parkinon's Depression Affect 30% of all Parkinson’s patients
First occurs to obvious reasons (reduced income, loss of independence, etc.) and gets worse as the disease progresses
Antidepressants, psychological support Dementia Affects 20% of all Parkinson’s patients older than 70
Occurs as Parkinson’s progresses and as patient ages
Differs from Alzheimer dementia and is distinguished by
Slowed thinking Comorbid Dieases Continued Psychosis Affects 20-40% of Parkinson’s patients
High levels of antiparkinson medication
Visual hallucinations are the most common
When a patient starts showing psychosis they have to be put in a nursing home and they usually die within 2 years
Taper or discontinue antiparkinson medication
Don’t give medicine at night Treatment L-DOPA Dopamine-Preserving Medication Medications preserve dopamine by inhibiting enzymes that metabolize it
Does not slow the progression of Parkinson’s but improves the patients symptoms
Can’t cross the blood brain barrier so they don’t interfere with normal nigrostriatal conversion of L-Dopa to dopamine
Dopamine Agonists Maintains normal dopamine activity by enhancing dopamine synthesis
Bypasses tyrosine hydroxylase deficiency
L-dopa to dopamine
Alleviates motor symptoms for many years
Does not reverse neurodegeneration
Remains affective until all the nigro-striatal tract neurons have degenerated (around 5 years) Stimulate postsynaptic dopamine receptors
Have ability to bypass degenerated presynaptic neurons and act directly on DA receptors
Relieve immobility but may cause hypertension, nausea, and vomiting
Bromocriptine, pergolide, pramipexole Surgery Ablative Procedures Minute lesions in the thalamus or GPi
Risks: serious potential complications (cerebral hemorrhage or unintended lesions) Transplantation Graft dopamine producing tissue into the basal ganglia
Cells have to grow and survive and they usually survive for less than 6 months
Risky because the brain can reject it Deep Brain Stimulation (DBS) Place tiny electrodes in the subthalamic nucleus or GPi.
They connect the electrodes to a pacemaker-like device implanted in the chest
Allows for greater mobility and reduce dyskinesia
Successful in moderate to severe cases
Smaller lesions, fewer complications (verbal fluency and dysarthria worsen)
Video of a patient before and after
DBS Other Therapies Biopsychosocial Model Video
Who does it affect?
What can be done and for whom? Physical Therapy
Music Therapy http://www.youtube.com/watch?v=WYDoHmg9ECI Imaging Imaging Dopamine Synthesis References Images from: www.google.com/Parkinson's/Disease
Aarsland D, Anderson K, Larsen JP, et al: The rate of cognitive decline in Parkinson’s disease. Arch Neurol 61:1906-1911, 2004.
Factor AS, Feustel PJ, Friedman JH, et al: Hallucinations in Parkinson’s disease patients with psychosis. Neurology 60:1756-1761, 2003.
Goetz CG, Poewe W, Rascol O, et al: Evidence-based medical review update: Pharmacological and surgical treatments of Parkinson’s disease: 2001 to 2004. Mov Disord 20:523-539, 2005.
Haahr, A., Kirkevold, M., Hall, E. C., & Østergaard, K. (2011). Living with advanced Parkinson’s disease: A constant struggle with unpredictability. Journal Of Advanced Nursing, 67(2), 408-417. doi:10.1111/j.1365-2648.2010.05459.x.
Kaufman DM, Clinical neurology for psychiatrists. 6th ed. Philadelphia: Saunders, 2007. Print.
Löhle, M., & Reichmann, H. (2011). Controversies in neurology: Why monoamine oxidase B inhibitors could be a good choice for the initial treatment of Parkinson’s disease. BMC Neurology, 11
Marconi, R., Landi, A., & Valzania, F. (2008). Subthalamic nucleus stimulation in Parkinson’s disease. Neurological Sciences, 29(Suppl5), S389-S391. doi:10.1007/s10072-008-1055-6.
Nutt JG, Wooten GF: Diagnosis and initial management of Parkinson’s disease. N Engl J Med 353:1021-1027, 2005.
Piacentini, S. S., Versaci, R. R., Romito, L. L., Ferré, F. F., & Albanese, A. A. (2011). Behavioral and personality features in patients with lateralized Parkinson’s disease. European Journal Of Neurology, 18(5), 772-777. doi:10.1111/j.1468-1331.2010.03279.x.
Surendran, S., & Rajasankar, S. (2010). Parkinson’s disease: Oxidative stress and therapeutic approaches. Neurological Sciences, 31(5), 531-540. doi:10.1007/s10072-010-0245-1.
Troster AI, Stalp LD, Paolo AM, et al: Neuropsychological impairment in Parkinson’s disease with and without depression. Arch Neirol 52:1164-1169, 1995.
Witjas T, Baunez C, Henry JM, et al: Addiction in Parkinson’s disease: Impact of subthalamic nucleus deep crain stimulation. Mov Disord 20:1052-1054, 2005.
Zahodne, L. B., Marsiske, M., Okun, M. S., Rodriguez, R. L., Malaty, I., & Bowers, D. (2012). Mood and motor trajectories in Parkinson's disease: Multivariate latent growth curve modeling. Neuropsychology, 26(1), 71-80. doi:10.1037/a0025119. Oxidative Stress Plays a key role in motor abnormalities and neurodegeneration
Defective mitochondria can’t detoxify hazardous oxidants
Herbal medicines can improve motor function
Substances that have a “protective effect” Cigarette Smoking
Coffee In Parkinson's Disease, nigrostriatal neurons slowly degenerate and lose their tyrosine hydroxylase
Video of Normal vs. Parkinson’s dopamine Synthesis