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68 Cards in this Set
- Front
- Back
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Define: Parkinsons
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Extrapyramidal neurodegenerative disorder characterized by resting tremor, rigidity and bradykinesia.
Degeneration of substantia nigra dopaminergic neurons |
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Parkinson's: Epidemiology
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High relation to family history, especially if positive father history
subsequent generations develop disease earlier slightly more often seen in males |
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Parksinon's: PRIMARY PREVENTION
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Etiology remains unknown >75% of cases
Some studies suggest a correlation with environmental toxins: CO, Carbon disulfide, Maganese, chronic psychotropic ingestion, or chronic use of GI drugs e.g. reglan, compazine |
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Parkinson's: SECONDARY PREVENTION
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NONE
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Parkinson's: Symptomatology and assessment
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-Bradykinesis
-Cogwheel rigidity of limbs -Mask-like facial immobility -Slow shuffling gait, turns slow, accelerate uncontrollably as disease progresses -Posture: body stopped forward, flexed knees, arms close to body, with pill rolling hands -Rhythmic resting tremors which typically begin in one hand, progress to ipsilateral foot, then progress bilaterally tremors are absent during sleep, increased with stress and fatigue voice monotonous and hypotonic handwriting microscopic especially at end of sentence seborrhea, blepharospasm, hyperthermia anorexia, diaphoresis, urinary symptoms constipation, visual defects spatial relationship difficulties cognitive defects, depression, anxiety |
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Parkinson's: tremors
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-Rhythmic resting tremors which typically begin in one hand, progress to ipsilateral foot, then progress bilaterally
tremors are absent during sleep, increased with stress and fatigue |
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What is a common cause of death in patients with parkinson's
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urosepsis
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Differential diagnosis for Parkinson's
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Benign essential tremor
Progressive supranuclear palsy Depression (often presents with mast like face) Dementia Drug induced parkinsonism Multiple neurological disorders including: olivopontocerebellar atrophy, striatonigral degeneration, cortica-based ganlionic degeneration, Huntington's disease |
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***PARKINSON'S IS A DIAGNOSIS OF ________
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EXCLUSION
NOT TEST UNTIL AUTOPSY |
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What is the mainstay of Parkinson's treatment
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dopamine replacement therapy with CARBIDOPA, LEVODOPA, DOPAMINE AGONISTS, MONOAMINE OXIDASE TYPE B INHIBITORS, CATECHOL-O-METHYLTRANSFERASE INHIBITORS AND AMANTADINE
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Parkinson's disorder and quality of life
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Nonmotor features such as cognitive impairment, mood disorders, autonomic dysfunction, gastrointestinal and genitourinary dysfunction have a SUBSTANTIAL IMPACT ON PARKINSON'S DISEASE PATIENTS AND THEIR QUALITY OF LIFE
NEEDS TO BE ADDRESSED |
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Parkinson's disease: when to refer to neurologist
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ALL patients with parkinsons disease should be referred to neurologist
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What are diagnostic tests used to exclude differentials for parkinsons disease
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CT or MRI
Beck's or similar depression inventory LABS -CBC - Chem profile - TSH (hyperthyroid may have tremors) - Others depending on symptom presentation |
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Parkinson's disease: Medications: MAO B Inhibitor
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SELEGLINE (ELDEPRYL)
Selective B inhibitor- no dietary restriction For early therapy for those without disability or as adjunctive therapy in advanced stages usually with some improvement for approximately 1 year The main use of selegiline is in the treatment of Parkinson's disease. It can be used on its own or in a combination with another agent, most often L-DOPA.[3] For the newly diagnosed Parkinson's patients, some claim that selegiline slows the progression of the disease, although this claim has not been widely accepted and the methodology has been rejected by the Food and Drug Administration (FDA).[4] It delays the time point when the L-DOPA (levodopa) treatment becomes necessary from 10-12 to 18 months,[5] which is beneficial despite not being definitive evidence of neuroprotection. The idea behind adding selegiline to levodopa is to decrease the dose of levodopa and thus reduce the motor complications of levodopa therapy.[6] Comparisons of patients on levodopa + placebo vs levodopa + selegiline showed that selegiline allowed reduction of the levodopa dose by about 40%. Selegiline + levodopa also extended the time until the levodopa dose had to be increased from 2.6 to 4.9 years.[5] As a result there were fewer motor complications in selegiline groups.[6] In one trial, selegiline + levodopa completely halted the progress of Parkinson's disease over 14 months, while in the placebo + levodopa group the deterioration of the patients' condition continued. However, the interpretation of this trial as proving neuroprotective action of selegiline has been questioned |
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Parkinson's disease: Medications: LEVODOPA-CARBIDOPA (SINEMET SR 50/200)
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L-dopa converted to dopamine in CNS
Levodopa has maximum effectiveness for only 5 years titrate medication upwards as tolerated every 2 days until 1000 mg L-dopa Add dopamine agonist if dyskinesia occurs or >600 mg L-dopa ***DIFFICULTY WITH THIS DRUG IS WEAR OFF EFFECT AND RETURN OF SYMPTOMS (ESP IF OCCURS WITHIN 4 HOURS OF ADMINISTRATION) Carbidopa-levodopa is a combination of two drugs, levodopa and carbidopa. Carbidopa-levodopa is used in the treatment of Parkinson's disease. Parkinson's disease is believed to be caused by low levels of dopamine in certain parts of the brain. When levodopa is taken orally, it crosses into the brain through the "blood- brain barrier." Once it crosses, it is converted to dopamine. The resulting increase in brain dopamine concentrations is believed to improve nerve conduction and assist the movement disorders in Parkinson disease. Carbidopa does not cross the blood-brain barrier. Carbidopa is added to the levodopa to prevent the breakdown of levodopa before it crosses into the brain. The addition of carbidopa allows lower doses of levodopa to be used. This reduces the risk of side effects from levodopa such as nausea and vomiting When a patient is treated with carbidopa/levodopa over time, symptoms may reemerge before the next scheduled dose. This is called symptom reemergence due to "wearing-off |
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LEVODOPA CARBIDOPA IMPORTANT CONSIDERATION
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***DIFFICULTY WITH THIS DRUG IS WEAR OFF EFFECT AND RETURN OF SYMPTOMS (ESP IF OCCURS WITHIN 4 HOURS OF ADMINISTRATION)
When a patient is treated with carbidopa/levodopa over time, symptoms may reemerge before the next scheduled dose. This is called symptom reemergence due to "wearing-off If you take carbidopa/levodopa for Parkinson's disease (PD), you may find that your symptoms begin to come back before the next scheduled dose of carbidopa/levodopa. This change is called "wearing-off." Inform your health care professional (HCP) if you notice symptom reemergence. This is due to medication "wearing-off," and it may mean it's time to adjust or change your medication. Consult your HCP before making any change to your medication regimen. Consistent communication with HCPs is essential for managing your symptoms as they surface. |
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STALEVO
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Parkinson's medication
to replace immediate release CARBIDOPA-LEVODOPA therapy (without entacapone-comtan) when patients experience the signs and symptoms of end-of-dose "Wearing off" (only for patients taking a total daily dose of levodopa of 600 mg or less and not experiencing dyskinesias) Stalevo was approved by the FDA in June 2003 to treat adult patients with idiopathic Parkinson’s disease in two scenarios. First, to substitute with equivalent strength of each of the three components for immediate-release carbidopa/levodopa and entacapone previously administered as individual products. Second, to replace immediate-release carbidopa/levodopa therapy (without entacapone) when patients experience the signs and symptoms of end-of-dose "wearing-off" but only for patients taking a total daily dose of levodopa of 600 mg or less and not experiencing dyskinesias. |
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DOPAMINE AGONIST MAY _______
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decrease L-dopa use (+SE)
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Parkinsons: Medication management: DOPAMINE AGONISTS
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Titrate meds as tolerated to response or maximum dose
Bromocriptine (Parlodel) Pergolide (Permax) more potent and long acting Pramipexole (Mirapex) better tolerated than Parlodel Ropinorole (Requip) Last two may be given as monotherapy in eary stage anticholinergics Some medical drugs act as dopamine agonists and can treat hypodopaminergic (low dopamine) conditions; they are typically used for treating Parkinson's disease and certain pituitary tumors (prolactinoma), and may be useful for restless legs syndrome (RLS). Both Requip (Ropinirole) and Mirapex (Pramipexole) are FDA-approved for the treatment of RLS. There is also an ongoing clinical trial to test the effectiveness of the dopamine agonist Requip (ropinirole) in reversing the symptoms of SSRI-induced sexual dysfunction and Post-SSRI sexual dysfunction (PSSD).[1] Additionally, a systematic review and meta-analysis concluded that prophylactic treatment with cabergoline reduces the incidence, but not the severity, of ovarian hyperstimulation syndrome (OHSS), without compromising pregnancy outcomes, in females undergoing stimulated cycles of in vitro fertilization (IVF).[2] Agonists of dopaminergic receptors can also be used as an antidote for overdose of antipsychotic drugs such as haloperidol or risperidone. |
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Parkinsons: Medication Management: Anticholinergics
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Cogentin for tremor
Anticholinergic medicines block nerve impulses (cholinergic nerve impulses) that help control the muscles of the arms, legs, and body. They also restrict the action of acetylcholine, an important chemical messenger in the brain (like dopamine) that helps regulate muscle movement, sweat gland function, and intestinal function. For normal motor or muscle control, the effects of acetylcholine and dopamine need to be carefully balanced. When dopamine levels are low (as they are in people who have Parkinson's disease), a chemical imbalance results, causing symptoms such as tremor and rigid muscles. Anticholinergic medicines decrease levels of acetylcholine to achieve a closer balance with dopamine levels. |
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Parkinsons: Medication Management: Catechol-O-methyltranserfase inhibitors (COMT inhibitors)
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prolong effects of L-dopa
TOLCAPONE (TASMAR) ENTACAPONE (COMTAN) Levodopa, a precursor of catecholamines, is an important substrate of COMT. COMT inhibitors, like entacapone, save levodopa from COMT and prolong the action of levodopa. Entacapone is a widely used adjunct drug of levodopa therapy. When given with an inhibitor of dopa decarboxylase (carbidopa or benserazide), levodopa is optimally saved. This "triple therapy" is becoming a standard in the treatment of Parkinson's disease. |
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pharmacological notes for parkinsons: addition of any medication to regimen may allow for ______ in parkinson's medication dosage
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addition of any medication to regimen may allow for DECREASE in parkinson's medication dosage
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Parkinsons: sequella
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Many sequella of Parkinson's disease are associated with medication side effects: falls, infections, GI disorders such as constipation, anorexia, nausea
complications of falls is the leading cause of death in individuals with parkinson's--25% of patients have orthostatic hypotension Bronchopneumonia and urinary infections account for the 2nd leading cause of death |
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what is the leading cause of death for patients with parkinsons's
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complications of falls is the leading cause of death in individuals with parkinson's--25% of patients have orthostatic hypotension
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what is the 2nd leading cause of death for patients with parkinsons?
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Bronchopneumonia and urinary tract infections
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Nonpharmacological treatment
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High Bulk, adequate diet
Bowel/bladder/sexual function monitoring for early interventions sitting upright to diminish risk for aspiration slowly rise from sitting or supine elastic stockings (<stasis) Physical activity/stimulating supportive environment counseling |
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Traumatic Brain Injury: Definition
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dynamic processes with initial bleeding with secondary injury from edema and continued intracranial bleeding
there is an initial bleed and then secondary issues similar with MI or stroke- initial injury and then continued injury |
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What is the number one cause of Traumatic Brain Injury
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Falls
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What is the number two cause of Traumatic Brain Injury
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MVA
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What is the principle cause of death and disability in young adults
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Traumatic Brain Injury
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What is the number one priority for primary prevention for Traumatic Brain injury
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CAR SAFETY
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PRIMARY PREVENTION: TRAUMATIC BRAIN INJURY
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1) Car safety (number one priority)
2) Seatbelts 3) Bike and motorcycle helmets 4) Sport protective head gear 5) Instructions to avoid voluntary head collisions (e.g. football player to another player, soccer players with ball). |
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What is a health policy that affects prevention of traumatic brain injury
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Seatbeat use (mandated by life)
Sport protective head gear |
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Whenever you see traumatic brain injury...
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Consider abuse
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SECONDARY PREVENTION: TRAUMATIC BRAIN INJURY
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NO SECONDARY PREVENTION
(screening before its symptomatic-pt will present with symptoms) |
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Concussion: pathology
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unknown
A concussion is the results of an impact to the brain, often causing bruising and maybe some mild swelling. This bruising/swelling interrupts/slows the pathways for thought processes. As the bruising heals, everything goes back to normal. |
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Concussion: Time Course
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Immediate loss of consciousness or stun with rapid return of consciousness.
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Epidural Hematoma: Pathology
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Mass effect with herniation
buildup of blood occurs between the dura mater (the tough outer membrane of the central nervous system) and the skull. The dura mater also covers the spine, so epidural bleeds may also occur in the spinal column. Often due to trauma, the condition is potentially deadly because the buildup of blood may increase pressure in the intracranial space, compress delicate brain tissue, and cause brain shift. |
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Epidural Hematoma: Time Course
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Immediate loss of consciousness, lucid interval then delayed loss of consciousness.
Epidural hematomas may present with a lucid period immediately following the trauma and a delay before symptoms become evident. After the epidural hematoma begins collecting, it starts to compress intracranial structures which may impinge on the CN III. This can be seen in the physical exam as a fixed and dilated pupil on the side of the injury. The eye will be positioned down and out, due to unopposed CN IV and CN VI innervation |
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Cerebral contusion: Pathology
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Diffuse axonal injury (DAI), contusion
is a bruise of the brain tissue. Like bruises in other tissues, cerebral contusion can be associated with multiple microhemorrhages, small blood vessel leaks into brain tissue. |
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Cerebral Contusion: Time Course
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Immediate deficit, variable later deterioration
The symptoms of a cerebral contusion (bruising on the brain) depend on the severity of the injury, ranging from minor to severe. Individuals may experience a headache; confusion; sleepiness; dizziness; loss of consciousness; nausea and vomiting; seizures; and difficulty with coordination and movement. They may also have difficulty with memory, vision, speech, hearing, managing emotions, and thinking. Signs depend on the contusion's location in the brain |
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Acute Subdural Hematoma: Pathology
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Diffuse axonal injury (DAI), contusion, mass effect
Blood gathers within the outermost meningeal layer, between the dura mater, which adheres to the skull, and the arachnoid mater, which envelops the brain. Usually resulting from tears in bridging veins which cross the subdural space, subdural hemorrhages may cause an increase in intracranial pressure (ICP), which can cause compression of and damage to delicate brain tissue. Subdural hematomas are often life-threatening when acute. In contrast, epidural hematomas are usually caused by tears in arteries, resulting in a build-up of blood between the dura mater and skull. |
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Acute Subdural Hematoma: Time Course
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Immediate loss of consciousness with progressive deterioration
Symptoms of subdural hemorrhage have a slower onset than those of epidural hemorrhages because the lower pressure veins bleed more slowly than arteries. Therefore, signs and symptoms may show up in minutes, if not immediately but can be delayed as much as 2 weeks. If the bleeds are large enough to put pressure on the brain, signs of increased ICP or damage to part of the brain will be present. |
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Chronic Subdural Hematoma: Pathology
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Diffuse mass effect
A chronic subdural hematoma is an "old" collection of blood and blood breakdown products between the surface of the brain and its outermost covering (the dura). The chronic phase of a subdural hematoma begins several weeks after the first bleeding. A subdural hematoma develops when the tiny veins that run between the dura and surface of the brain (bridging veins) tear and leak blood. This is usually the result of a mild head injury. A collection of blood then forms over the surface of the brain. In a chronic subdural collection, blood leaks from the veins slowly over time, or a fast hemorrhage is left to clear up on its own. A subdural hematoma is more common in the elderly because of normal brain shrinkage that occurs with aging. This shrinkage stretches and weakens the bridging veins. These veins are more likely to break in the elderly, even after a minor head injury. You or your family may not remember any injury that could explain it. |
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Chronic Subdural Hematoma: Time Course
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very delayed deficit
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What is a DIFFUSE AXONAL INJURY
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Closed head injury
Most common traumatic brain injury Normally result of rapid deceleration of head Results from shearing after rapid deceleration BRUISING, SMALL PETTICHAL HEMORRHAGE OR LACERATION OF BRAIN CAN OCCUR Unlike brain trauma that occurs due to direct impact and deformation of the brain, DAI is the result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated, as may occur in auto accidents, falls, and assaults.[8] It usually results from rotational forces or severe deceleration.[9][10] Vehicle accidents are the most frequent cause of DAI; it can also occur as the result of child abuse[11] such as in shaken baby syndrome.[12] The major cause of damage in DAI is the disruption of axons, the neural processes that allow one neuron to communicate with another. Tracts of axons, which appear white due to myelination, are referred to as white matter. Acceleration causes shearing injury, which refers to damage inflicted as tissue slides over other tissue. When the brain is accelerated, parts of differing densities and distances from the axis of rotation slide over one another, stretching axons that traverse junctions between areas of different density, especially at junctions between white and grey matter.[2] Two thirds of DAI lesions occur in areas where grey and white matter meet |
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Loss of consciousness cause
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loss of consciousness is no longer believed to be related to damage to reitcular activating system of brainstem, rather of the "loading" force of brain against skull and resultant turbulent impacts.
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DIFFUSE AXONAL INJURY: MILD
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Usually no loss of consciousness of amnesia
No focal findings May have 1-2 episodes of emesis May have HA 14-15 GCS Continuous alert and oriented |
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DIFFUSE AXONAL INJURY: MODERATE
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No focal findings on exam (no paresthesia, etc)
May have transient loss of consciousness May have amnesia HA 8-13 GCS EVIDENCE OF BASILAR FRACTURE -CSF Rhinorrhea - Hemotypanium (VERY red tympanic membrane) - Battle sign (late) - Raccoon eyes (late) |
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EVIDENCE OF BASILAR SKULL FRACTURE
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-CSF Rhinorrhea
- Hemotypanium (VERY red tympanic membrane) - Battle sign (late) - Raccoon eyes (late) |
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DIFFUSE AXONAL INJURY: SEVERE
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Recurrent or continuous loss of consciousness
focal exam findings decreased level of consciousness <8 GCS |
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Differential diagnosis: Diffuse Axonal Injury
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Simple concussion
Cerebral contusion/laceration Acute epidural hemorrhage Acute, subacute, chronic subdural hematoma Cerebral hemorrhage CVA with mild head trauma (e.g. CVA immediately preceding MVA) ***all patients with GCS of <15 should be evaluated with a CT scan |
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*****All patient with a GCS < _____ should be evaluated with a CT Scan
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All patient with a GCS < 15 should be evaluated with a CT Scan
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What medical imaging is considered to be a more reliable indicator of diffuse axonal injury?
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DIFFUSION TENSOR MAGNETIC RESONANCE IMAGING (DTI)
The integrity of the white matter fiber tracts can be determined non-invasely with DTI interactive tractography successfully enabled inspection of white matter structures that were in proximity to lesions, critical structures, and functional cortical areas, allowing the surgeon to explore the relationships between them. CTs are helpful, and MRIs add some information but cannot predict the severity of injury or outcome. |
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CARE FOR SEVERE DIFFUSE AXONAL INJURY
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***ABC's REMAIN PRIORITY
CONTINUE C-spine immobilization Comprehensive and recurrent neurological exams CT Trauma or neurosurgical consult Seizure prophylaxis Positioning Intubation for airway maintenance and breathing -hyperventilation is supported in literature Consider ICP monitor ICP reduction - Mannitol therapy for raised ICP may have a beneficial effect on mortalitiy when compared to pentobarbital treatment - but Mannitol may have a detrimental effect on mortality when compared to hypertonic saline. |
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Do you use steroids for traumatic brain injurys
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NO
BRAIN BAR STEROIDS increases morbidity and mortality |
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Traumatic brain injury and hyperbaric oxygen treatment
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while hyperbaric oxygen therapy is related to an increased survivorship after TBI, there is no data to support decreased morbidity in large scale meta-analysis by Cochrane data base
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Define: Spinal cord injury
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Disruption caused by compression, angular deformity, or transection of the cord
supraspinal control of sensory, autonomic, and motor functions inferior to lesions can be lost extreme hypotension after injury can lead to cord infarction. |
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SPINAL CORD INJURY: PRIMARY PREVENTION
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Similar to traumatic brain injury
Seatbelts Bicycle and motorcycle helmets Safety Equipment with sports Education regarding safe diving, safety from falls |
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SPINAL CORD INJURY: SECONDARY PREVENTION
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NONE
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What is the cause for about half of spinal cord injuries?
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motor vehicle accident
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Spinal cord injury: epidemiology
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due to fracture, dislocation, or both
usually due to hyperflexion, though in cervical spine, hyperextension may be causative |
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Spinal cord injury: Progression
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Pericapillary hemorrhage
Infarction of gray matter and early white matter edema present within 4 hours of injury global infarction of injured level with necrosis of white matter and paralysis below lesion becomes "permanent" |
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Spinal cord injury: Symptomatology: Early
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Back pain possible
Loss of reflexes at and below injury Positive Babinskis sign (DOWN-POSITIVE-opposite of what you would normally get) Weakness and flaccidity of body below injury Sensory loss Loss of sphincter control- "anal wink" Often urinary and fecal retention. |
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SPINAL CORD INJURY: TERTIARY PREVENTION: EMS TREATMENT
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EMS treatment
-ABCDE- anoxia early though late risk - Airway - Intubation (without movement of spine) as needed - Breathing - Circulation - Disability - D- disability: immobilization of spine! KEY - Exposure - E- exposure for evaluation of additional injuries |
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SPINAL CORD INJURY: TERTIARY PREVENTION: ED CARE
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Continuation of ABC measures
Complete neurological exam Exclude surgically remediable and potentially reversible cord compression due to dislocation of a vertebral body Myleography use is controversial MRI less risky than myelogram Referral to specialized center for neurosurgical/trauma surgical care and recovery. |
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What is the treatment for spinal cord injuries
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METHOPREDNISOLONE IS THE ONLY EFFECTIVE TREATMENT SO FAR IN STUDIES.
Unlike TBI, high doses steroid have been found to improve outcomes in SCI-specifically with motor functioning |
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What is the benefit of giving steroids with spinal cord injuries?
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Unlike TBI, high doses steroid have been found to improve outcomes in SCI-specifically with motor functioning
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