Module 13 Flashcards
1
Q
Nervous system review
A
- 2 anatomical divisions
1) Central Nervous System
2) Peripheral Nervous System - 2 different cell types
1) Neurons
2) Glial cells - Neurons
1) Myelinated Unmyelinated
2
Q
Multiple Sclerosis
A
- 20-50 yrs old
- Chronic demyelination of CNS that results
in scarring - 4 different types
1) remitting-relapsing
2) primary progressive
3) secondary-progressive
4) progressive-relapsing - Causes
1) Autoimmune - prior virus infection, genetic, environment-away from equator
2) FHx? 15% of MS pts have a family member with MS
Identical twins - 30% chance of getting MS
3) F>M - Signs and Symptoms – vary due to which nerves are affected
1) Need 2 separate episodes at different locations to help diagnose
2) Visual changes – unilateral acute, due to cranial nerve demyelination- Optic neuritis
3) Balance, memory, weakness, fatigue, spasticity, bladder dysfunction
4) Tremor, lack of coordination or unsteady gait
- Optic neuritis
- 4 different types which really means four different ways the disease can progress
- Know these causes
- Correlation with prior virus not causation
- Tightest correlation is family history
- Females statistically get it more than guys
- Two separate episodes at two different locations in the body in order to have MS
3
Q
Multiple Sclerosis nerves
A
The nerves that branch off the central nervous system (CNS) provide messages to the muscles and organs for normal function. When there is CNS damage, the function of these organs and tissues may be compromised. In multiple sclerosis, the demyelination of nerve cells may lead to bowel incontinence, bladder problems and/or sexual dysfunction.
4
Q
Multiple Sclerosis testing
A
- Testing – hard to diagnosis-process of elimination
- MRI
- Demyelinating lesions in white matter - sclerotic plaques (gliosis) are diagnostic
- Lumbar puncture – specific pattern of antibodies
- Oligoclonal bands (IgG) – 90% of MS pts
- Evoked Potential tests
- Nerve conduction speed
- Can sometimes see demylination on the MRI
- Oligo means having few, not a lot of
5
Q
Multiple Sclerosis testing
A
- Each of the two to five oligoclonal bands seen by protein electrophoresis represent proteins (or protein fragments) secreted byplasma cells into the CSF, although why exactly these bands are present, and whichproteinsthese bands represent, has not yet been elucidated. Approximately 79%-90% of all patients with multiple sclerosis have permanently observable oligoclonal bands.
- IgG oligoclonal bands (OCBs) represent IgG unique to the cerebrospinal fluid (CSF), that is, without corresponding IgG in the serum. They are commonly used as part of the diagnostic workup for multiple sclerosis (MS) but are not essential to make the diagnosis. OCBs are not unique to MS; rather they provide evidence of IgG synthesis thought to reflect the compartmentalized central nervous system (CNS) humoral immune activation present in MS. OCBs are found in other inflammatory and infectious diseases affecting the CNS, although these can be differentiated from MS using additional CSF and/or clinical findings.
- The bands tend to disappear from the cerebrospinal fluid as a person recovers from the neurological disease.
- Not diagnostic but can help lead to proper diagnosis
6
Q
Multiple Sclerosis main points
A
- Autoimmune
- Usually females
- family history
- Tinnitus
- Decrease hearing
- Nystagmus
- Diplopia
- Blurred vision
- Dysarthria
- Dysphagia
- Onset 20’s to 40’s
- Urinary retention
- Spastic bladder
- constipation
- Weakness may progress to paralysis
- Muscles spasticity
- Ataxia
- Vertigo
7
Q
Upper vs. Lower Motor Neuron Review
A
- Review these: understand what can happen to a individual if they become damaged
- Upper motor neuron the neuron cell body originates in the brain. The axon exits the brain and can continue down to neck or all the way down
- Lower motor neuron the neuron cell body begins in spinal cord and axon exits spinal cord and often goes to muscle
- Lesion is bad, it could lead to death, cancerous growth
- Upper motor neuron lesion in their brain what happens
- Anytime you have spinal cord damage can have either upper or lower motor neuron damage because the axon of the neuron in the brain passes through the spinal cord
- Stroke is the biggest cause of upper motor damage
- Upper motor neurons cross at the brain stem at the medulla
8
Q
ALS - Amyotrophic Lateral Sclerosis
A
- Atrophy of upper AND lower motor neurons
- Lou Gehrig disease
- Causes
- Idiopathic, M>F, 40-60
- Genetic > possibly multifactorial
- Possibly excess glutamate
- Signs and Symptoms
- Diminished muscle strength progresses to atrophy
- Weakness and spasms, difficulty speech, fatigue
- Spastic & flaccid paralysis (depending on severity of UMN/LMN lesion)
- Respiratory infections
- No intellectual or sensory impact
- Testing
- MRI
- Nerve and muscle conduction tests
- Increased GLUTAMATE (neurotransmitter that is usually quickly cleared)
- Has a toxic effect on nerve cells
- Tx - riluzole (Rilutek) – extends time. No cure (average 3 – 5 years post Dx)
- Riluzole is a neuroprotective drug that blocks glutamatergic neurotransmission in the CNS. Riluzole inhibits the release of glutamic acid from cultured neurons, from brain slices, and from corticostriatal neurons in vivo. Riluzole also blocks some of the postsynaptic receptors for glutamic acid.
- Damage to both upper and lower motor neurons (brain and spinal cord)
- Idiopathic (just don’t know)
- Upper and lower motor neuron signs
- They think just fine
- Only treatment on the market is riluzole (rilutek) blocks release and binding to post synaptic
9
Q
ALS - Amyotrophic Lateral Sclerosis
A
- Could be in brain stem or spinal nerves
- Cranial nerves are lower motor neurons
- Possible cause too much glutamade
10
Q
Myasthenia Gravis
A
- Loss of acetylcholine receptors at NMJ
of voluntary muscles - Causes
1) Chronic autoimmune disease
2) F 60 - Signs and Symptoms
- Muscle weakness/fatigability >
- eyes first; ptosis, diploplia
- Progressive muscle weakness with activity
- Worse with stress, heat, or physical exercise
- 10-25% have thymus tumors
- Muscle weakness/fatigability >
- Testing
- Edrophonium (Tensolin) test: (+ if muscles regain strength for a period)
- EMG
- Repetitive nerve stimulation test – shows rate of fatigue
- Tx – No cure, Tx focuses on symptoms
- Patients can lead normal or near normal lives with meds
- Anticholinergic medication (anti-acetlycholinesterase)
- Thymus removal
- Nicotinic receptors for MG
- Note: Muscarinic is on smooth and cardiac
- Cranial nerves 3,4, 6
- Gets worse when a person exerts themselves
11
Q
Myasthenia Gravis occurs when?
A
Myasthenia gravis occurs when the immune system makes antibodies that damage or block many of the muscle’s acetylcholine (ACh) receptors on the surface of muscle cells. This prevents ACh from binding to the damaged receptors and acting on the muscle, which reduces muscle contractions, leading to weakness and fatigue.
12
Q
Myasthenia Gravis
A
- Tensilon (Edrophonium) Chloride Test
- Edrophonium- an effective, reversible, acetylcholinesterase inhibitor- will reduce the muscle weakness by blocking the enzymatic effect of acetylcholinesterase enzymes, prolonging the presence of acetylcholine in the synaptic cleft
13
Q
Ptosis - Drooping eyelids and weakness of muscles of eye movement
A
Myasthenia Gravis
14
Q
Bell’s Palsy
A
- Weakness and paralysis of one side of the face
- Causes
- greater than 15 and less than 60
- Which Nerve?
Viral URI, herpes simplex, EBV
Signs and Symptoms
Sudden onset, paralysis, pain, HA
Can lead to corneal damage – lack of lubrication
Testing
CT to R/O stroke
Treatment:
Often short-lived
Anti-inflammatories, acyclovir (anti-viral)
Prognosis:
Most people have full or nearly full recovery within weeks or months
Some do not recover full function
15
Q
The 7th cranial nerve exits the skull at the?
A
Stylomastoid foramen, passes through the parotid gland, and subdivides into 5 branches that supply the facial muscles. Paralysis of the nerve may occur without any known cause. Bells palsy is thought to be caused by swelling of the nerve within the facial (fallopian) canal.
