Module 11 - Parkinson's, Seizures, & MS Flashcards
(166 cards)
1
Q
Nerve Cell Hillock
A
location where the axon leaves the cell body
2
Q
What causes the signals generated in neurons?
A
The sum of the inputs that are excitatory or inhibitory at the axon hillock
3
Q
Nerve signals are what kind of phenomenon
A
all or nothing
4
Q
When the cell gets to threshold…
A
propagation occurs and the signal can go to another nerve cell or to a motor end plate
5
Q
The more myelin…
A
the faster the conduction
6
Q
__ is needed to make myelin
A
Fat
7
Q
Nodes of Ranvier
A
areas of ion flow where the action potential jumps from node to node
Clustering or NaK channels allow for saltatory conduction in one direction as channels close behind them
8
Q
Saltatory Conduction
A
pattern of myelinated axons allowing increased speed of conduction of action potentials
9
Q
In Multiple sclerosis we are worried about what
A
demyelination of central nerves and loss of saltatory conduction in certain areas
10
Q
Parkinson’s Disease
A
A progressive degenerative disorder of dopamine secreting neurons that control muscle movement
Incurable
11
Q
What causes Parkinsons Disease
A
depletion of dopamine and excess of acetylcholine
12
Q
Excitatory Inputs are made with what Neurotransmitter
A
Acetylcholine
13
Q
Inhibitory Inputs are made with what Neurotransmitter
A
Dopamine
14
Q
Is Parkinson’s Fatal?
A
no, but death may occur from complications
15
Q
Forms of Parkinsons Disease
A
Primary Idiopathic PD
Secondary Parkinsonianism
16
Q
Primary Idiopathic Parkinson Disease
A
PD without a known cause
17
Q
Secondary Parkinsonianism
A
Parkinson’s disease caused by some other event like trauma, infection, tumor, atherosclerosis, toxins
18
Q
What kind of genetically inherited forms of Parkinsons Disease are there
A
- A rare autosomal dominant form
2. An early onset autosomal recessive form
19
Q
Parkinson’s could be from an interaction of what things? Or a result of what?
A
Interaction between genetics and environment
Or it could be a side effect of anti psychotic medicines that block dopamine receptors
20
Q
___ is not effected until later in Parkinson’s Disease
A
Cognition
21
Q
What usually kills in Parkinsons Disease
A
the complications from immobility not the disease itself
22
Q
The majority of Parkinson’s Disease patients are what age when diagnosed
A
60s to 70s
23
Q
How is Parkinson’s Disease diagnosed?
A
Diagnosis is CLINICAL - there are no lab tests for it
However, diagnostic tests can be done to rule out other things such as CT or MRI to rule out stroke or tumor
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Q
Area Affected in Parkinson’s
A
Dopamine secreting neurons deep in the basal ganglia (Extrapyramidal brain nuclei)
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What does the impact on dopamine secreting neurons in the basal ganglia have on a Parkinsons Patient
Influences initiation modulation and completion of movement
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For fine motor movements what must be balanced?
Acetylcholine (Excitatory) and Dopamine (Inhibitory) release balance
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Degeneration of dopaminergic neurons leads to...
Deficiency of dopamine and relative excess of acetylcholine at the synapse --> this causes rigidity tremors and bradykinesia
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Dopamine deficiency prevents...
affected brain cells from performing their normal inhibitory function in the CNS
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Extrapyramidal System
Neural network of motor systems that control involuntary reflexes and movement
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Pyramidal System
the motor cortex and voluntary movements
The nerves leaves the motor cortex and axons cross at the medulla oblongata
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__ __ cannot occur without dopamine
Smooth Coordination
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Normally, what is the dopamine:acetylcholine ratio
1:1
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Classic Manifestations of Parkinson's
Resting Tremor
Bradykinesia
Rigidity
Postural Dysfunction
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What is the Resting Tremor like in Parkinson's Disease
Asymmetric, rhythmic, low amplitude (not spastic
Usually unilateral in hands and feet
Pill Rolling
Disappears during sleep but worsens with stress
Intermittent --> progressively worsens
35
What is the Bradykinesia in Parkinson's Disease like
slowness of voluntary movement
generalized slowness of movement
failure of antagonistic muscles to relax
loss of ability to walk, blink, or swallow saliva
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What is the Rigidity like in Parkinson's Disease
involuntary contractions of striated muscle
Stiffness of limbs
resistance to ROM
Uniform --> lad pipe rigidity or jerky --> cogwheel rigidity NOT spasticity
You have to work against it to get moving and it will become bilateral with progression
Once they start moving, hard to initiate and modulate stopping and turning - take fast short steps
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What is the Postural Dysfunction like in Parkinson's Disease
Shuffling gait and balance problems
Loss of postural reflexes causing high fall risk
Stooped posture - leans to one site when seated
Festinating Gait
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Festinating (Parkinsonian) Gait
short, accelerating steps
hard to initiate and hard to modulate in order to stop and turn
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What is not affected in Parkinson's Disease
Intellect - so they are aware of symptoms and deficits and cannot control what the body does -- therefore it is disturbing to them
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What are some other Parkinson's Disease Manifestation
Fine Motor deficits (fingers and hand) are slow and difficult
Micrographia
Hypomimia
Dysarthria and Monotone, high pitch low voice volume
Freezing
Slight foot drag
Turns are hesitant and En Block
Dandruff, oily skin, and seborrhea
Less blinking
Drooling and dysphagia leading to swallowing issues
Autonomic dysfunction - urine retention, diaphoresis, orthostatic hypotension, constipation
Depression and Anxiety
Dementia in late stages
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Micrographia
Small Cramped Handwriting
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Hypomimia
Decrease in facial expression
masklike faces
less blinking
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What is the voice like in Parkinson's disease
low volume hoarse and breathy
high pitch and monotone
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Parkinson's Disease patients have a very high __ risk
fall
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Why are UTI rates high in Parkinson's disease?
They cannot control autonomic functions like relaxing and contracting the bladder easily
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Complications from Parkinson's Disease
Disability to varying degrees
Difficulty performing ADLs
SE from medications
Late - Dementia
Injury from Falls
Aspiration
UTI
Pressure Ulcers
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What is usually less affected in Parkinson's Disease
Intelligence and Lifespan
*Can have a full life and not die early but you know what is happening to you - you are aware
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What is the goal of Parkinson's treatment
There is NO CURE at this time --> so the goal is to relieve symptoms and maintain function through pharmacologic, surgical, and PT means
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What sort of drugs may be given to Parkinson's pts?
Dopaminergic (Levodopa-Carbidopa)
Anticholinergic (Artane, Cogentin)
Other (Eldpryl, Tasmar, Symmetrel)
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Levodopa-Carbidopa
A dopaminergic drug given to PD patients
Levidopa is an inactive dopamine form that can cross the blood brain barrier and convert to dopamine in the brain - but there are enzymes in the periphery that do this do so we use Carbidopa to inhibit periphery conversion before crossing since active dopamine cannot cross
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What are anticholinergics good for in Parkinson's Disease patients but can cause what?
Good for stopping drooling, but they cause dry mouth and cause more drinking with risk for aspiration of fluids
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What sort of surgeries may be done on Parkinson's patients
Pallidotomy by Stereotactic Neurosurgery
Fetal tissue Transplants
Deep Brain Stimulation
*these are not used as much*
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What is the mainstay treatment for Parkinson's
Levodopa-Carbidopa Drugs
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Pallidotomy by Stereotactic Neurosurgery
obliteration of ventrolateral nucleus of the thalamus and Globus pallidus which prevents involuntary movement
For PD
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Fetal Tissue Transplants
For PD
transplanting cells from the basal ganglia or adrenal medulla of fetuses into the caudate
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Deep Brain Stimulation
Pacemaker like brain implants that decrease tremors and is controlled by the patient via a magnet
for PD
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When are surgical measures sued for Parkinson's?
When they are not responding to medication management.
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Why is PT so important in Parkinson's?
PROM, walking, bathing, speech therapy, massages are all important to maintain independent function which we want to promote as long as possible safely
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Nursing Care measures for Parkinson's
Education
Referral to support groups
Exercise program – maintain mobility and safety
Assess: Chewing, swallowing, depression, nutrition (as it may be hard to chew and swallow or get food)
Speech therapy for dysarthria
Home safety (bars, etc anything to make the home safer)
Clothing choices: Non-skid Velcro shoes, shirts without buttons, slacks with elastic waistbands,
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Epilepsy
Seizure Disorder
Condition of the brain characterized by susceptibility to recurrent seizures
These are not just a febrile seizure when they were kids, its seizures every once in a while
It is from Paroxysmal events associated with abnormal electrical discharges of neurons in the brain
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Epileptogenic Focus
area of the cerebral cortex causing the seizures - where the brain is making the electric storm
Neurons in the brain depolarize or become hypoexcitable --> fires more readily than normal when stimulated as a result
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Types of Epilepsy
Primary
Secondary
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Primary Epilepsy/Seizure Disorder
Idiopathic - no apparent structural brain changes occur
We do not know what is causing it
The brain cells fire and reset and electrical discharges keep going throughout the brain causing varying symptoms depending on location
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Secondary Epilepsy/Seizure Disorder
Structural changes or metabolic alterations in the brain leading to increased automaticity
Could be something like a brain tumor, atherosclerosis, or a metabolic disorder
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What is the prevalence of epilepsy
1-2% --> 2 million people
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When is the occurrence/diagnosis of Epilepsy most commonly seen?
Highest in childhood and with old age
even babies can get it though, anyone can
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What is Epilepsy's prognosis with treatment?
Very good
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Anytime pH is ___ a baby will have a seizure
<7
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Anoxia
Brain starved of oxygen
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The majority of epilepsy is ___
idiopathic (50%)
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Potential causes for a Seizure Disorder
Idiopathic ( ~ 50%)
Birth trauma
Perinatal infection
Anoxia
Infection
Toxins
Brain Tumors
PKU or TB
Head injury/trauma
Metabolic disorders
CVA
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What is diagnosis of Seizure Disorders primarily based on?
Based on occurrence of one or more seizures - not just one
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What is the diagnostic test for choice for seizures? What is the catch?
EEG - the catch is it may have normal findings if they are not actively having a seizure
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What may a CT or MRI or Skull X Ray show for seizure disorders?
structural brain abnormalities or assessments for bony structures
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What can serum chemistries do for seizure disorder diagnosis?
It can allow evaluation of metabolic conditions (BUN, CBC, Ketones, Uric Acid etc)
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What does an EEG show with a tonic clonic seizure
high fast voltage spikes in all leads
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What does an EEG show if there is no seizures?
Rounded spike wave complexes
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What is the pathophysiology of a Seizure Disorder
Neurons in the brain depolarize and become hyperexcitable by lowering the threshold --> this causes firing more readily than normal in this epileptogenic focus area
The resting membrane potential is less negative or inhibitory connections are missing d/t GABA activity or electrolyte shifts (lower threshold to fire)
Once the epileptogenic focus fires electric currents spread out to surrounding cells firing with greater amplitude and cause impulse cascades around the brain
This increased firing increases metabolic demand and can lead to brain damage
Eventually inhibitory neurons should stop this firing
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Where can impulse cascades of epileptogenic fire occur?
Partial Seizure - One side of the brain
Generalized Seizure - both sides of the brain
Cortical, subcortical, and brain stem areas
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What happens to metabolic demand in seizuires?
demand for O2 and nutrients increase by 200% and if they are not met then brain damage will occur
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What happens if inhibitory neurons cannot stop a seizure?
Status Epilepticus occurs and without treatment fatal anoxia will occur
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Why is the resting membrane potential lower/ less negative for seizures?
Either:
a. Inhibitory connections are missing because of GABA
or
b. Electrolyte shifts like hyponatremia, hyperkalemia, and hypocalcemia occur
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GABA
gamma aminobutyric acid
chief inhibitory NT in the CNS
without it seizure can occur from a lowered threshold
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What are the 3 major manifestations of a Seizure Disorder
1. Characterization by recurrent seizures
2. Aura in the Prodrome phase
3. Postictal State after generalized seizure
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Aura
a sensory sign indicating an imminent seizure in the prodromal phase of epilepsy
could be anything depending on area of brain impacted like visual, auditory, kinesthetic, olfactory, etc
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Prodrome
something that comes right before another event
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Postictal State
In generalized seizure, consciousness is loss and once returned they must reorient slowly
May cause loss of bowel and bladder
Can be embarrassing
HA, Confusion, Fatigue, Combativeness, Lethargy, and a Slow Return to consciousness occurs
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Partial Seizure
come from a local area and cause focal problems
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2 Kinds of Partial seizures
Simple Partial (Jacksonian)
Complex Partial
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Simple Partial (Jacksonian) Seizure
Begins locally and does NOT cause alteration in consciousness
Sensory sx (flashing lights, smells, hallucinations), Autonomic Sx (sweating, flushing), and Psychic sx (dream states, anger, fear) occur
S.A.P.
Since they are conscious, they know they're having a seizure
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Complex Partial Seizure
Partial seizure that DOES alter consciousness
Amnesia for events that occur during and immediately after the seizure occurs
During, the patient may still follow simple commands
Lasts 1-3 minutes
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Generalized Seizure
Most commonly thought of seizure
A generalized electrical abnormality within the brain
can be convulsive (tonic clonic) or non convulsive ( no movement)
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Tonic Clonic
a convulsive seizure with movement
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4 Types of Generalized Seizures
Absence (Petit Mal)
Myoclonic
Grand Mal
Atonic
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Absence Seizure (Petit Mal)
Brief generalized seizure with change in LOC lasting 1-10 seconds
Look like they are daydreaming and not paying attention
Blank out and teachers may notice
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Myoclonic Seizures
Bilateral massive epileptic myoclonus generalized seizures
May be rhythmic
Brief involuntary muscular jerks of body or extremities occurs - not normal to happen in an entire side of the body though
Consciousness usually NOT affected
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Generalized Tonic Clonic (Grand Mal) Seizure
Generalized seizure
Classic seizure
Rhythmic movements: quiet period, movement, quiet period etc
Begins with a loud cry --> Loss of Consciousness --> Body falls --> body spasms (tonic phase) and relaxes (clonic phase)
Usually 2-5 minutes long
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Atonic Seizure
Generalized seizure
Loss of postural tone and temporary loss of consciousness
"Drop Attacks"
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Status Epilepticus
A medical emergency
Continuous seizure state that can occur in ALL seizure types
It is accompanied by resp distress followed by hypoxia or anoxia
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What may Status Epilepticus be due to
Abrupt withdrawal of anticonvulsant medications
hypoxic encephalopathy
acute head trauma
metabolic encephalopathy
septicemia d/t encephalitis or meningitis
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What is the most life threatening form of status epilepticus?
Grand Mal / Generalized Tonic Clonic Status Epilepticus (huge metabolic demand)
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Status epilepticus can occur in what seizure types?
ALL of them
More common in grand mal, simple partial, and complex partial though
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Unclassified Seizures
seizures that do not fit characteristics of partial or generalized seizures or status epilepticus
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Complications from Seizure Disorders
Hypoxic brain damage and mental deficiencies as a result
Depression and Anxiety
Social Isolation (do not want embarrassment, danger from driving, triggers)
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Treatment for Seizure Disorders
Identify type of seizure – note time & activity (can help allow for better treatment)
Reverse cause of disorder if possible
Pharmacologic - Based on seizure type
Surgery (last line treatment)
Vagal nerve stimulators – reduce frequency of seizures in some patients
Counseling
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What sort of surgeries may be done for seizure disorders?
1. Resective surgery to excise the epileptogenic focus
2. Corpus collostomy --> remove connections between hemispheres to limit activity - but this can affect all aspects of life
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Note what things about a seizure?
Type and Activity like what they did did they yell first, etc
note time brain potentially went without oxygen
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Nursing Care During a Seizure
Protect from injury
Place on ground in side lying position
Maintain airway
Apply O2 and Monitor responses
Do NOT put anything in their mouth as they can chew through things and hurt themselves or others
Note auras and triggers
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Nursing Care After a Seizure
Administer anticonvulsants per order
Monitor therapeutic levels of meds
Education about factors that precipitate
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Tips for Things to do During a Seizure
Cushion Head
Loosen Neckware
Turn on Side
Nothing in Mouth
Look for ID
DO NOT HOLD DOWN
As seizure ends, offer help
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Pediatric Febrile Seizures
Typically occur between 3mo and 6 y/o age
lasts a few seconds to a few minutes - rarely goes beyond 15 minutes
Hypothesized as arising from fever affecting the developing brain
Can be grand mal to causing baby needing to reorient when waking up, becoming diaphoretic, or wetting themselves
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What fevers usually cause pediatric febrile seizures
greater than 100.4 F
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When is the peak for pediatric febrile seizures?
between 12-18 months - 1 to 1.5 years
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Most pediatric febrile seizures are outgrown...
most often by age 3 but almost all by age 5
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What should a caregiver do if a pediatric do if a child has a febrile seizure lasting more than 15 minutes?
Call 911 if longer than 15 minutes or sooner if they show signs of breathing issues
If its the first febrile seizure, the pediatrician will need to be seen soon after
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Multiple Sclerosis
Demyelination of the white matter of the brain and spinal cord (CENTRAL NERVOUS SYSTEM) - damage to nerve fibers and their targets occur
Characterized by exacerbations and remissions
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How does Gullain Barre syndrome differ from MS
GB is demyelination of peripheral nerves while MS is demyelination of CNS
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The major cause of chronic disability in young adults is...
multiple sclerosis
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When do s/s of MS begin to occur
between ages 20-40 with an average age of 27
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When do most MS diagnoses occur
between 55-64 years of age
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What is the ratio for Parkinson's between Sexes?
Female:Male is 1:1
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What is the ratio for MS between Sexes?
Female:Male is 3.1:1
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What areas tend to have more MS incidence
Northern Areas rather than southern ones
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Where is gray and white matter in the brain? in the spinal cord?
Brain: Gray matter is cell bodies outside the brain with white matter inside
Spinal Cord: The white matter is outside with gray matter insides
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MS is thought to be caused by what?
An autoimmune disease allowing you to destroy your white matter
A virus may initiative this with a protein similar to proteins in the myelin sheath and this confuses the immune system which then attacks the white matter
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MS Syndromes
Corticospinal
brain Stem
cerebellar
cerebral
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Corticospinal MS
Symmetric muscular weakness and stiffness
spastic paralysis
bowel and bladder incontinence
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Brain Stem MS
Dysfunction of CN 3 through 12
leads to::
Ophthalmoplegia
Nystagmus
Dysarthria
facial and muscle weakness
Paresthesia
Ptosis
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Cerebellar MS
spastic gait
ataxia
intention tremors (a symptom not always means MS)
hypotonia
130
Cerebral MS
optic neuritis
impaired vision
intellectual and emotional deterioration
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Ophthalmoplegia
double vision
132
Ptosis
Droopy eyelid
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Nystagmus
involuntary eye movement horizontally or vertically
more of a central problem if vertical
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Optic Neuritis
visual clouding, loss of vision, and visual field pain when eye is moving
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Types of MS
relapsing
Primary progressive
secondary progressive
progressive relapsing
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Relapsing MS
remitting MS (25% of pop)
clear relapses (acute attacks or exacerbations) with full/partial recovery and lasting disability
disease does not worsen between attacks
There is initial events with remission back at baseline functioning with some more minor flares between events
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Primary progressive MS
uncommon - 15% of pop
steady progression from the onset with minor recovery or plateaus
Line steadily increases with some plateauing - never returns to baseline
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Secondary Progressive MS
40% of pop
Begins with clear relapses and recovery and lasting disability steadily progressive and worsens between attacks
Line will act much like relapsing with flares and remissions at baseline until eventually the flares do not return to baseline and continuously get worse and increase
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Progressive Relapsing MS
rare
steadily progressive from the onset, but has clear acute attacks
140
Causes for MS
- Unknown cause but autoimmune - antibodies will attack self and destroy CNS neurons
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What are some current theory on the cause of MS
1. Slow acting or latent viral infection stimulating autoimmune response
2. Environmental and genetic factors
3. Trauma toxins and nutritional deficiencies
* perhaps also familial*
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What is needed to make an MS diagnosis
evidence of 2 or more neurologic attacks
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How is diagnosis undergone for MS
Get evidence of 2 or more attacks with periodic testing and close observation
MRI will show multifocal white matter lesions that look dark when they should be white
EEG will show abnormalities in a third of patients
Lumbar punctures will have normal CSF proteins but increased CSF IgG
CSF Electrophoresis will show evidence of kappa light chains
Evoked Potentials will show slowed nerve impulse conduction
144
What kind of nerves are affected in MS?
Central nervous system nerve, peripheral nerves are unaffected
145
Pathophysiology of MS
sporadic patches of axon demyelination and nerve fiber loss throughout CNS --> widely disseminated and varied neuro dysfunction
Slowed neural impulses leads to alterations in movement, reflexes, and mental status
Swelling and edema occur causing further injury to neurons and development of scar tissue plaques on myelin
146
What is causing the presence or absence of function in MS?
It is the presence or absence of axons determining function NOT loss of myelin.
This can either be autoimmune destruction of axon with subsequent myelin attacks OR autoimmune attacks against myelin that slow conduction
147
Plaques
lesions of MS
Phase 1 Plaques - small inflammatory lesions develop
Phase 2 Plaques - lesions extend and consolidate to form scar tissue
These inhibit and slow nerve conduction
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What do manifestations of MS depend on
extent and location of myelin destruction, extent of remyelination, and adequacy of restored synaptic transmissions
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What are some manifestations of MS
Ocular disturbances
sensory impairment
muscle dysfunction
urinary disturbances
bowel disturbances
fatigue
speech problems
150
Ocular Disturbances in MS
Optic Neuritis (from demyelination of optic nerve)
Diplopia
Ophthalmoplegia (large pupil)
Ptosis
Blurred Vision
Nystagmus
Scotoma
151
Sensory Impairment in MS
burning (like electric signals burning body)
Pins and Needles
Electrical sensations (sometimes these symptoms occur with electrical storms like lightening)
152
Muscle Dysfunction in MS
weakness
paralysis (monoplegia to quadriplegia)
spasticity
hyperreflexia
intention tremor
gait ataxia
153
Urinary Disturbances in MS
incontinence
frequency
urgency
frequent infections
154
Bowel Disturbances in MS
involuntary evacuation OR constipation
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Speech Problems in MS
poor articulation and dysphagia occur
156
What is often the most debilitating s/s of MS
Fatigue
157
Scotoma
blind spot in otherwise normal visual field
158
S/S of MS are precipitated by what?
Stress and sometimes heat
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The key to MS Manifestations is knowing...
demyelination causes slowed nerve impulses, BUT axon destruction from plaques and scar tissues removes the function of the nerve
160
Secondary complications of MS
injuries from falls
UTI
Constipation
joint contractures
pressure ulcers
rectal distention
pneumonia (have trouble coughing)
insomnia
161
Tertiary complications of MS
depression from role changes and loss of independence
Loss of social support - social isolation
family/spousal stress - divorce
financial problems from unemployment
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Goals of MS Treatment
Treat acute exacerbations
treat disease process
treat related s/s
163
Treatment of M mostly revolves around...
good treatments for s/s and complications that are controllable as there are not many treatments for the MS itself
164
Pharmacologic treatments in MS are doing what...
treating what is happening, and are not a cure
165
What is pharmacologic treatment like in MS
Immunosuppressant therapy - at disease onset and with any exacerbation
Antiviral drugs - to try and slow disease
SQ immune substance interferon beta - to decrease number and severity of exacerbations
Innovative therapies - to foster antigenic self tolerance
166
Education to give MS Patients
bladder training
sexual functioning
avoidance of complications
avoidance of fatigue and stress
