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58 Cards in this Set
- Front
- Back
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Central nervous system |
•CNS – made up of brain and spinal cord |
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Peripheral nervous system |
•PNS – made up of afferent and efferent nerves |
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Brain |
•Cerebrum •Cerebellum •Brainstem |
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Cerebrum |
Frontal lobe Parietal lobe Temporal lobe Occipital lobe |
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Frontal Lobe |
-motor, behavior, emotions, higher intellect |
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Parietal Lobe |
- sensory function |
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Temporal Lobe |
-hearing, smelling |
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Occipital Lobe |
-visual center |
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Cerebellum |
•balance and coordination |
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Brainstem |
-Midbrain -Pons -Medulla oblongata |
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Spinal Cord |
Cervical nerve roots Thoracic nerve roots Sacral nerve roots |
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Cervical Nerve Root |
• control upper extremity function |
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Thoracic Nerve Root |
•control trunk |
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Sacral Nerve Root |
control lower extremity function |
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Upper Motor Neurons |
•A motor neuron (interneuron) found completely within the CNS, thatsynapses with or regulates the actions of lower motor neurons in the spinalcord and cranial nerves •Lesions produce spastic paralysis in the muscles they innervate |
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Lower Motor Neuron |
•A peripheral motor neuron that originates in the ventral horns of thegray matter of the spinal cord and terminate in skeletal muscles •Lesions of these neurons produce flaccid paralysis of the muscles theyinnervate •Also known as efferent fibers |
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Nerve Fibers |
•Axon isconcerned with transmission of impulses •Form the major portion of the white matter of the brain and spinal cord •Most fibers in PNS are myelinated •Myelin sheath is layer of Schwann cell membranes wrapped around theaxon |
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Meninges |
Dura Mater Subdural Space Arachnoid Mater Subarachnoid Space Pia Mater |
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Dura Mater |
•outer layer – tough, fibrous, double-layered membrane |
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Subdural Space |
•lies beneath the dura and is a potential area to fill with bloodfollowing an injury |
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Arachnoid Mater |
•a loose, web-like covering |
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Subarachnoid Space |
•contains CSF and cerebral arteries and veins |
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Pia Mater |
•delicate connective tissue that adheres closely to all convolutions onthe surface of the brain and contains many small blood vessels –participates inblood brain barrier |
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Cerebrospinal Fluid |
•CSF provides a cushion for the brain •CSF should be maintained as a constant (pressure, electrolyteconcentration, volume, etc) within the CNS •Changes in the characteristics of CSF can be used as a diagnostic tool •Increases in amount can increaseintracranial pressure causing neurological problems |
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Meningitis |
•An inflammation of the meninges, usually but not always caused by aninfectious illness •Can be due to anything that activates the inflammatory process |
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Bacterial Meningitis 1 of 3 |
•Most common causes are Streptococcus pneumonia, Neisseria meningitides,and Haemophilus influenzae (not as common in US since vaccine introduced in1990’s) •Almost all bacterial infections enter the nervous system afterhaving invaded and infected another region |
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Bacterial Meningitis 2 of 3 |
•Typically begins with sudden onset of severe headache, back pain,photophobia, fever and chills, and nuchal rigidity (hyperextended, stiff neck) •Clinical signs of meningeal irritation include Kernig’s sign (resistance to leg extension with supine hip flexion) and Brudzinski’s sign (neck flexion causes hip and knee flexion) •An increase in ICP cancause vomiting, irritability and lethargy progressing to stupor and seizures |
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Bacterial Meningitis 3 of 3 |
•Diagnosed by lumbar puncture where CSF is examined •CSF pressure will be elevated with increased number of leukocytes •Causative organism in CSF or blood must be identified to treateffectively |
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Treatment of Bacterial Meningitis |
•Antibiotic •Rest •Maintenance of fluid and electrolyte balance•Avoidance or control of convulsions with anti-convulsant medications |
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Viral Meningitis |
•Also called aseptic meningitis •Often follow infection with mumps or measles•Symptoms are mild including fever, headache, and stiff neck •Disease is self-limiting (get so bad then body takes over) •Treatment is supportive care (keeping them comfortable, givingsomething for HA if they have HA) |
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Encephalitis |
•Inflammation of the gray and white matter of the brain •Almost always associated with meningitis •Most common causes are viruses |
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Symptoms of Encephalitis |
•Vary depending on the infected region of the brain, but include: –Seizures –Fever –Cranial nerve paralysis –Abnormal reflexes –Muscle weakness –Confusion/delirium –Coma |
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Treatment of Encephalitis |
•Mostly supportive care: –Control of fever –Maintenance of fluid and electrolyte balance –Maintenance of respiratory and urinary function –Anticonvulsants –Glucocorticoids to decrease cerebral edema –Sedatives for restlessness –Analgesics for headache and fever |
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Patient Care for Encephalitis |
•Continuous neurological assessment (mental status, motor function, etc) •Slight head elevation to prevent increase in ICP•ROM exercises as long as they do not increase ICP•Quiet environment •Rehab usually necessary for treatment of neurological deficits |
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Poliomyelitis 1 of 2 |
•Inflammation of the gray matter of the spinal cord •An acute viral disease characterized by fever, sore throat, headache,vomiting, and often stiffness of the neck and back •Attacks the CNS injuring or destroying the nerve cells •Late consequences include atrophy of groups of muscles ending inpermanent deformity •Preventable with standard vaccines given to children |
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Poliomyelitis 2 of 2 |
•Poliovirus is found in the throat for the first few days and in theintestines for as long as 17 weeks •Disease spreads by droplets of moisture from an infected person’sthroat or by their feces•Incubation period (interval from exposure to infection and theappearance of symptoms) is 1-2 weeks |
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Symptoms of Polio |
•Dependent on type, but include: –Fever –Headache –Vomiting –Sore throat –Pain –Stiffness in back and neck in nonparalytic polio –Weakness/flaccid paralysis in paralytic polio –Difficulty in swallowing, speaking, and breathing in bulbar polio |
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Treatment of Polio |
•No cure and must be allowed to runs its course•Supportive care for symptoms•ROM exercises to prevent deformities |
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Prevention of Polio |
•First, safe, effective vaccine developed by Jonas Salk and referred toas Salk vaccine •Was a dead polio virus •Later replaced by live vaccine developed by Sabin•American Academy of Pediatrics recommends infants be given TOPV dropsat 2, 4, 6, and 18 months •Additional doses may be recommended prior to school entry and every 5years until age 18 |
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Post-Polio Syndrome 1 of 2 |
•The development of motor and respiratory muscle weakness, muscleatrophy, fatigue, and diminished endurance occurring 15-35 years after aninitial bout of polio •Results from progressive motor denervation and may be due to overuse ofspared motor neurons •Considered an autoimmune response |
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Post-Polio Syndrome 2 of 2 |
•Weakness may occur in muscle previously affected or in ones notaffected •Patients may need mobility aids,modifications of home and work places, planned rest periods, and orthoses tomaintain optimal function |
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Parkinson’s Disease 1 of 3 |
•A progressive degenerative disease of the CNS that produces movementdisorders and changes in cognition and mood •Affects motor function and movement control through extrapyramidal tracts due to changes in the basal ganglia |
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Parkinsonism |
•Some conditions affect the basal ganglia and result in similar symptomsto Parkinson’s disease |
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Parkinson’s Disease 2 of 3 |
•A decreased number of neurons secrete dopamine (inhibitory neurotransmitter) causing over stimulation in this area •Over stimulation increases muscle tone and activity leading to tremors(at rest or when stressed), muscular rigidity, muscle atrophy, difficultyinitiating movement, postural instability, abnormallydiminished motor function (hypokinesia) (Chasingtheir center of gravity)or slowed movement (bradykinesia) |
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Parkinson’s Disease 3 of 3 |
•Affects ~1% of people over the age of 50 in the US •Affects men more than women•Underlying cause is not known (Idiopathic)•Often occurs in clusters in families, but unknown if it is due togenetics or to exposure to common precipitating agents (viruses, toxins, etc.) •Usually begins unilaterally in UE before progressing throughout trunkand other extremities |
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Early Signs of Parkinson’s |
•Fatigue •Muscle weakness •Muscle aching •Decreased flexibility •Less spontaneous change in facial expression |
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Hallmarks of Parkinson’s 1 of 2 |
•Pill-rolling tremor in hands that later progress to feet, face, tongue,and lips •Muscular rigidity – cogwheel, (consistent jerky movement only seen withrigidity. Normal in these patients) lead-pipe (same motion as clasp-knife, just know itis named this in rigidity) • Difficulties initiating movements •Slow movements (bradykinesia) or no movement (akinesia) •Gait disturbances –Shuffling gait (change in surface could cause themto fall) –Festination (short, accelerated gait) chase their center of gravity, end upbeing toe walkers and lose that heel to toe gate, end up with posture that is kyphotic) –Freezing (kyphotic posture but stand in one spot andshuffle their feet (running in place. Something has changed for them, open area to door, surface change, turna corner.) –Decreased arm swing due to rigidity (more at risk for falling) –Flat-foot or toe-heel gait |
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Hallmarks of Parkinson’s 2 of 2 |
•Masklike facial expression (later on they develop this whichcauses them to have a flat expression) •Cognitive impairments•Breathing difficulties (because they are in that kyphotic position and its hard to take a deepbreath) •Speech and swallowing problems (speech becomes deminished because they are in the kyphotic position and they can not forcefullygive enough breath to be louder in that position, swallowing is also a problembecause they can choke very easy, can end up on a diet with thickening liquidsbecause of this) |
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Posture in the Parkinson’s Patient |
•Forward head •Kyphosis ofthoracic spine with possible scoliosis secondary to unequal rigidity in trunk •Flexion and adduction of hips and shoulders because they are sitting a lot, but thatis not where their tone is, they are higher tone in extensors than at flexors,they are not at equal, more tone in extensors because of antigravity muscles.) •Flexion of knees and elbows •Plantarflexed ankles •Results in COG being pulled forward |
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Causes of Balance Impairment |
•Loss of postural reflexes •Visiospatial deficits •Start hesitation •Freezing •Festinating gait •Orthostatic hypotension •Vertigo •Retropulsion (leaning backward during gait) |
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Other Signs of Parkinson’s |
•Difficulties with sit ↔ stand (when the go to sit they plop,extensors are over riding flexors and so they don’t’ have very good control.) •; bed mobility (the rotation of getting out of bedwill give them trouble.) Micrographia – handwriting becomes smaller and more cramped •Voice becomes quiet and monotone with some dysarthria •Difficulties with chewing/swallowing •Difficulties with blinking causing a blank stare |
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Later Stages of Parkinson’s |
•Autonomic changes causing orthostatic hypotension, urinary retention,constipation•UTIs and respiratory infections are common complications withrespiratory infections being common cause of death (pneumonia most common cause of death in parkinsons patients.)•Dementia occurs in ~20% of affected persons (too little dophamine) |
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Stages of Parkinson’s |
Stage I Stage II Stage III Stage IV Stage V |
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Stage I of Parkinson's |
•symptoms are mild, unilateral, and include tremors and shaking in oneextremity; may inconvenience the day-to-day tasks |
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Stage II of Parkinson's |
•symptoms are bilateral and may cause gait or balance disturbances andability to complete normal physical tasks becomes more apparent |
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Stage III of Parkinson's |
•symptoms can be moderately severe; may include inability to walkstraight or to stand with a noticeable slowing of physical movements |
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Stage IV of Parkinson's |
•severe symptoms with limited ambulation, rigidity, and bradykinesia;patients may be unable to complete day-to-day tasks and cannot live on theirown; tremors may disappear |
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Stage V of Parkinson's |
•severe symptoms with limited ambulation, rigidity, and bradykinesia;patients may be unable to complete day-to-day tasks and cannot live on theirown; tremors may disappear |
