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95 Cards in this Set
- Front
- Back
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5 nuclei of the BG
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Caudate
Putamen GP Subthalamic nucleus Substantia niagra (parts reticulate and pars compacta) |
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What makes up the striatum?
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Caudate and putamen
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What makes up the output nuclei? Output goes where?
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GPI
Substantia Niagra pars reticulate To motor thalamus and PPN |
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Where is dopamine made? Where is it sent?
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Substantia nigra compacta - provides it the striatum (caudate and putamen)
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Where does the caudate receive input from? putamen?
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Caudate: Frontal (executive fxt), prefrontal (premotor), limbic (emotion)
Putamen: same as above but also Sensorimotor cortex |
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Activity of the output nuclei (GPI and SNR) without dopamine?
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Tonically active, which inhibits the VLT and PPN = inhibits movt
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Describe the "normal" direct pathway and compare it to the Parkinson's direct pathway
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NORMAL: SNC sends dopamine to putamen (excitatory)
Putamen sends inhibitory impulses to output Nu This inhibits output nuclei, which allows the VLT to be facilitory to the motor cortex PARKINSON's: Lack of dopamine to putamen Causes less inhibitory impulses to be sent to output nuclei Output nuclei is excited, and it sends inhibitory impulses to VLT = dec excitation of motor cortex |
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Describe the "normal" indirect pathway and compare it to the Parkinson's indirect pathway
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NORMAL: SNC sends dopamine to putamen (inhibitory)
Putamen inhibits GPE GPE inhibits subthalamic Nu Desite this, subthalamic Nu is still tonically active and is facillatory to output nu. Inc excitement of output nu. inhibits VLT and results in dec excitatory impulses to motor cortex PARKINSON's: Less dopamine means that putamen and GPE can't be AS INHIBITORY as normal, which results in less inhibition of subthalamic nu Less inhibition of subthalamic nu = increased excitatory to output nuclei = inc inhibitory to VLT |
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How does the BG affect medial AND lateral tracts?
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Output nuclei go to VLT which goes to motor cortex to affect lateral tracts
Output nuclei go to PPN, which go to RST and VST = LMNs to postural mm (medial) |
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How does direct pathway cause disinhibition?
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Output nuclei are tonically active usally, which inhibit VLT
Putamen inhibits the output nuclei, whcih results in disinhibition of VLT and it can be facilitory to motor cortex |
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How may the direct and indirect pathway "brake one another"
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If direct is overactive = extraneous movt. If indirect is overactive = akinesia
ie. too much dopamine |
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What descending systems does the BG affect?
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Lateral tracts via thalamocortical activation
RST and VST via PPN activation |
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What occus with the PPN normally? In parkinson's?
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NORMAL: output nuclei inhibit PPN, which inhibits VST and RST (but still tonically active)
PARKINSON'S: PPN cells die = dec inhibition from PPN and VST and RST become overactive to postural mm |
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Functions of the BG
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1. Preparation for movt: postural set/readines
2. Senesory integrative fxt 3. Approp amt of contraction 4. Regulates mm tone 5. Striatum = automatic, repetitive, rhythmical, overlearned skills 6. Shifting attention 7. Recogizing interpersonal space 8. Visuoperceptual role; vision to guide movts |
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Give an example of how the BG is involved in preparation of movt
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Neutral pelvis prior to reaching
Contraction of core mm prior to standing |
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Explain the BG's role in senesory integrative fxt
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Uses sensory info to determine what mo. patterns to use. Sets the environmental context for movt
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What is the stratum specifically involved with? Why is ths important?
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Automatic, repetitive, rhythmical, overlearned patterns
Walking, chewing, swallowing Turns movts on nd off o that we can move in any directionwe want |
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Afferent Nu vs. Efferent Nu of BG
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Afferent: Caudate and putamen. Receive from cortex (visual and frontal), thalamus, and SNC.
Efferent: GPE and SNR to thalamus and PPN |
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What is the "brains" of the BG?
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The putamen and caudate, b/c these receive info from the cortex, thalamus, SNC and adjust the "gain" of movt and other shit
They then send it to the output Nu (SNR and GPI), which relay it back to cortex and PPN to affect movt |
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Clincal triad of Parkinson's
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Resting tremor
Bradykinesia Rigidity |
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What parts of movement does a Parkinson's pt have trouble with?
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Initiation, alteration, or stopping a motion
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3 types of Parkinson's
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1. Idiopathic: PIGD; tremor predominant
2. Young adult onset >40 yo 3. Juvenile onset >21 yo |
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Explain the idiopathic form of Parkinson's
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Largest category, we don't know why SNC stops producing dopamine (60-80% loss of dopamine)
Tremor predominant with postural instability and gait disorders |
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Explain the characteristics of Young Adult Onset Parkinson's (<40 yo)
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Tremor predominant
Autosommal dominant with family hx and problem with chromosome 4 on alpha synucelin Freezing, dementia, balance problems |
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Explain the characteristics of Juvenile Onset (<21 yo) Parkinson's
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Chromosome 6 on Parkin2 gene
Primary complaint is dystonia (high mm contraction that is painful). C/o achiness, cramping, N/T, and feeling cold |
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Describe Hoehn and Yahr Stage 1 Parkinson's
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Mild, unilateral, inconvienent s/s (not even close to disabling)
Tremor of one limb Friends may have noticed changes in posture, locomotion, facial expression |
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Describe Hoehn and Yahr Stage 1.5 Parkinson's
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Unilateral s/s plus trunk involvement
Rotations at trunk decrease and a little difficulty with gait |
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Describe Hoehn and Yahr Stage 2 Parkinson's
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Bilateral and trunk s/s with minimal disability
No balance impairment (modified) |
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Describe Hoehn and Yahr Stage 2.5 Parkinson's
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Bilateral and trunk s/s
Recovery on pull test with ankle/hip strategy BALANCE starts to be impaired |
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Describe Hoehn and Yahr Stage 3 Parkinson's
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Significant slowing of body movts (bradykinesia apparent)
Impairment of equilibrium on standing/walking (small, shuffling steps) Generalized dysfunction that is moderatley severe, but still INDEPENDENT with everything |
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Describe Stage 4 Hoehn and Yahr Parkinson's
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Severe s/s - can walk to a limited extent (AD)
Rigidity and brdaykinesia DISABLED - no longer able to live alone Tremor may be LESS than earlier stages |
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Describe Stage 5 Hoehn and Yahr Parkinson's
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Cachectic stage - mm wasting b/c difficult to eat and lack of mobility
Cannot stand or walk Pulmonary complications due to bed rest Constant nursing req'd |
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What is the UPDRS? How is it rated?
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Unified Parkinson's Dx Rating Scale
Measures: 1. Mentation, behavior, mood 2. ADL 3. Motor sections Done by interview and rated from 0-199 with 0 = no disability |
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What type of "Thought Disorder" may a Parkinson's pt have
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Difficulty sleeping and dreaming - some meds make this worse
Can become hallucinations, delusions, psychosis |
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Why is depression common with Parkinson's pts?
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Possibly due to limbic system involvement
B/c they're old and have a disabling dx |
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Why may a Parkinson's pt have difficulty with salivation?
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Maybe postural (flexed) or muscle related (weak mouth/tounge)
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What type of speech problems may you see in a Parkinson's pt?
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Loss of expression or volume
Monotome Dysarthria |
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How can you distinguish Tremor from Dyskinesia?
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Tremor = rhythmical and occurs at rest ie. pill rolilng 4-7 bmp
Dyskinesia: Abnomral posturing, like circular hand movt when walking |
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2 types of rigidity of Parkinson's pt
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1. Lead pipe: can't move in either direction
2. Cogwheel rigidity: Tested at wrist and ankle; take wrist into extension and move it in a circular pattern. It will "ratchet." Not smooth. thought to be caused by rigidity disturbed by tremor |
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What is the Schwab and England Activities of Daily Living scale?
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Rating scale assessed by rater or patient. Pretty much just put themselves in a category from independent to dependent in 10% increments
Pretty much asks how independently they can do chores and how long it takes them (ie. "more dependent". Needs help with 1/2 of chores - 50%) |
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9 s/s of Parkinson's
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1. Bradykinesia/Akinesia
2. Freezing 3. Rigidity 4. Tremor - resting and postural 5. Postural instability 6. Gait festination 7. Attentional/cognitive deficits 8. Micrographia (small handwriting) 9. Microphonia (low voice) |
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Secondary problems arising from bradykinesia?
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Can affect balance b/c postural corrections are too slow
Can cause disuse atrophy/weakness |
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What is freezing and why does it happen?
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Motion stops, even mid-stride. COG will continue to shift forward and may result in a fall
Don't know what it is caused by, but appears to be a deficit in the visuoperceptive field: pt has defecits using vision to guide movts |
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What causes postural instability?
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Rigidity and stiffness. Trunk tremor can cause this
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What is Gait Festination
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Idea pt is chasing his COG, possibly due to flexed posture and instability
Anteropulsion or retropulsion festination Short, shuffling steps - looks like walking on toes Hesitation with stepping |
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What type of attention and cognitive problems does a Parkinson's pt have?
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Loss of dual attention and short attention span
Cognitive = memory, problem solving, procedural learning (repetitive learning not helpful) Declarative learning is preserved |
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Difference between bradykinesia/akinesia and hypokinesia
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Bradykinesia = dec in motion and akinesia = lack of motion
Hypokinesia is a lack of automatic movement; dec step length, Parkinson's (Festination) gait is characterized by hypoknesia |
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List 4 options for Dopamine Replacement drugs
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Levodopa (precursor of dopamine)
Sinemet (Levodopa plus Carbidopa) Senemet CR Stalevo: Sinemet plus Entacapone |
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Why is a Parkinson's pt at high risk for falls?
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Ineffective sensory processing - proprioceptive defecits
Lack of anticpatory postural rxts (hypokinesia) Interaction a akinesia, bradykinesia, rigidity |
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Why use Sinemet instead of just plain Levodopa for dopamine replacement therapy?
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Sinement has Levodopa PLUS Carbidopa. Carbidopa is decarboylase inhibitor that inhibits decarboxylase.
Without it, decarboxylase would convert Levodopa to dopamine outside the CNS and it would not be able to cross the BBB |
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What is Stalevo?
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Sinemet (Carbidopa/Levodopa) plus Entacapone, which is a COMT inhibitor that prevents COMT from coverting L dopa to an inactive metabolite in the periphery
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Cons of Dopamine replacement therapy?
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On-off phenomenon
Dyskinesia after 3-5 years (not part of Parkinson's) usually in UE, but can be LE (balance) |
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Benefit of Stalevo over other dopamine replacement drugs?
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Blocks 2 enzymes (decarboxylase and COMT) from preventing the drug reaching the target tissue
Helpful for the on/off effect BUT... may inc dyskinesia |
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Side effects of Dopamie replacements
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Drowsiness, dry mouth, dizziness, nausea
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How do dopamine agonists work? Side effects?
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Bind to dopamine receptors and exert their effcts
Drowsiness, dry mouth, dizziness, nausea, Hypotension and Confusion BUT.. do not cause dyskinesia |
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List 5 Dopamine Agonists
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BP ruined Proud America
Bromocriptine (Parlodel) Pergolide (Permax) - pulled Ropinirole (Requip) Pramipexole (Marpex) Apomorphine (Apokyn) |
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What is Apomorphine (Apokyn)? When used?
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Dopamine agonist... we think, not sure
Used as a 'rescue medication' for on/off phenomenon |
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What enzyme do Neuroprotetive agents inhibit? Name the drugs
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Suck Cock Russ
Selegiline (Deprenyl, Eldpryl, Atapryl) Coenzyme Q-10 Rasagaline Monoamine oxidase (MOA): enzyme that breaks down dopamine AT CNS SYNAPSES |
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What is Selegiline (Deprenyl, Eldepryl, Atapryl)? When may it be prescribed?
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Neuroprotectie agent: Monoamine oxidase (MOA) inhibior during ealy stages to prolong the effect of endogenous dopamine (b/c drug works to prevent breakdown of dopamine at CNS synapses)
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What s/s of Parkinson's do anticholinergic's treat? MOA?
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Block ACh receptors in BG that seem to be overactive
Tremors and rigidity |
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3 types of Anticholinergics that TO is making us memorize. Adverse effects?
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Trihexaphenadryl (Artane)
Procyclidine (Kemadrin) Benzotropine Mesylate (Cogentin) Dry mouth, blured bision, nervousness and confusion, sedation |
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2 examples of COMT inhibitors? How do they work? Adverse effect?
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Tolcapone (Tasmar)
Entacapone (Comtan) Prevent COMT enzyme from breaking down dopamine in periphery Liver toxicity - last resort; need blood tests frequently |
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2 types of 'miscellaneous drugs' for Parkinson's?
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Amantadine (Symmetrel): dopamine agonist, dystonia and maybe fatigue
Rivastigmine for dementia |
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5 types of drugs used to treat Parkinson's
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Dopamine replacement
Dopamine agonist Nueroprotective (MOA inhibitors) COMT inhibitors Anticholingergics |
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List as many secondary impairments as you can
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Dyskinesias
On/off phenomenon Kyphsis Osteoporosis Cardipulm Muscle atrophy/weakness Contractures/loss of flexibility Venous pooling Decbiti Malnutrition/weight loss Decreased speech production Drooling Pain Fatigue |
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2 common secondary impairments caused by medication
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Dyskinesias
On/off phenomena |
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Is kyphosis rigid in Parkinson's? Consequences?
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No, when on meds can sit up right
EXTs get stretched and weak Can become rigid |
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Cardiopulm problems assiociated with Parkinson's
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OH and ex induced OH
CV drugs can cause arrhthmias, especially in off phase Responses to ex may be blunted due to dysautnomia PULMONARY: PE, flex'd posture = dec rib excursion and shallow breaths = reduced VC |
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What mm get especially weak with Parkinson's?
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Quads, PFs, Glutes
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Why is weight loss and malnutrition a problem with Parkinsons?
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Dec appetitie
Dysphagia (slow, difficult eating) |
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What type of Autonomic problems may a Parkinson's pt have?
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Thermoregulation - very cold or warm
Dec pupillary response to light (very sensitive to light/glare) Dec motility GI tract Dec appetite |
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2 types of pain experienced by Parkinson's pt?
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Postural stress: Flex'd posture with mm being stressedin cervicothoracic region
Dystonia: painful camping ie. gastroc/foot |
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4 surgical tx for Parkinson's
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Pallidotomy
Deep brain stim Fetal tissue transplant Gene therapy |
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Explain the Pallidotomy procedure
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Pt awake, burr hole into skull and use heat probe to destroy GPI
Pt needs to be awake to tell them adverse effects b/c close to internal capsule = motor Destroy GPI (output nu. b/c it is tonically active, inhibiting VLT) |
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What is improved after a Pallidotomy? How long does it last?
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Done unilaterally, but bilateral effects (disabling cognitive if done bilatera)
Bradykinesia/akinesia, rigidity and AMB very improved Motivation and mov initiation improved Balance and freezing not effected much |
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Areas for deep brain stim in BG?
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Thalamus for tremor
GPI or subthalamic Nu - bradykinesia, akinesia, rigidity |
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What is the idea behind Fetal Tissue Transplant?
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Stem cells to SNC to increas dopamine producing cells. Not successful
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What is the idea behind Gene Therapy?
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Deliver genes via viral vector
Glutamic acid decarboxylase to subthalmaic n, which is a precursor to GABA (inhibitory to thalamus) |
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Overall goals of tx for Parkinsons?
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Decrease rigidity
Improve postural control Inc movt. intiation (ext cues) Faciliate normal gait Correct postural defecits Improve respiration Improve swallowing,chewing, facial expression Educate pt and caregivers |
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How can we treat rigidity?
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PROM, A/AROM
"Rocking", "rotation", "counter-rotation" btw trunk ad LEs to dec tone Stress reduction - yoga, deep breathing, meditation |
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How can we treat postural control in early stages of dx?
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Balance ex: Initially really challenge pt: dif surfaces, sppeds, obstacle, perturbatoins, LOS
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How do we tx postural control in the latter stages of Parkinson's?
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Conc on 1 activity at a time
Teach to break things down into steps Don't multitask External cues: music, yardsticks, laser pointers Emphasize LARGE movts at extremes of movt t/o FROM |
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How can we improve pts movt initiation and facilitate normal gait?
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External cues: slap thighs, self talk "step big", laser, yard sticks
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Respiratory exercises for Parkinson's pt?
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D2 patterns
Deep breathig Diaphragmatic breathing Chest breathing |
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What type of equipment may we need to order for the pt?
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AD, cammode, tub bench, hospital bed, RW, W/C
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When should we teach functional activities?
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Early on AND t/o dx
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Why is AMB so hard for Parkinson's pt?
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It is not automatic anymore
Very cortically driven and they must think about it |
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What type of learning can a pt do early in the dx process?
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Procedural - dif speeds, surfaces, lengths, and change quickly
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How can you train balance early in the dx process?
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Perturbations, LOS, Surfaces, BOS
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Should we encourage multitasking with pts?
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Early on yes, but not later
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How should we teach pts to do turns?
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Normal early in dx process
Wide, long turns later in dx process |
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How can we teach pt to AMB?
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Long strides, think big, step out
With or without muscial beat to motivate performance Visual and auditory cues |
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How should we teach pt to stand and AMB late in dx process?
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Stand. Scan. Plan.
Break down the movt Still want them to pick up feet and encourage proper step length |
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How can we teach pt to overcome freezing?
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Sensory cues, sticky notes , self talk
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What does PT aim at doing in moderate stages of dx?
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Inc movt speed and AMP
Optimize postural alignment Maintain postural stability |
