Term
Pain, crude, touch, cross point
Name pathway, direction of AP, and location of decussation. |
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Definition
| Anterolateral pathway, ascending, within the spinal cord. |
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Term
Motor information system, direction, cross point
Name pathway, direction of AP, and location of decussation. |
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Definition
| Corticospinal tract, descending, pyramidal decussation. |
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Term
Light touch, vibration, proprioception
Name pathway, direction of AP, and location of decussation. |
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Definition
| Posterior column-medial lemniscal pathway, ascending, nucleus cunneatus and nucleus gracilis (caudal medulla) decussation. |
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Term
| Decussation occurs at which neuron? |
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Definition
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Term
| What are the primary motor cortex and the primary somatosensory cortex responsible for? |
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Definition
Primary motor cortex:
Controlling voluntary movements.
Primary somatosensory cortex:
Receives the incoming information from the body and coordinates with the primary motor cortex. |
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Term
| What is the relationship of the primary motor cortex and the primary somatosensory cortex to each other (in terms of physical location and communication)? |
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Definition
Primary motor cortex is ventral to the primary somatosensory cortex.
Areas of either align for particular regions of the body. |
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Term
| Lateral portions of the primary motor cortex are associated with? Media portions? |
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Definition
Lateral:
Arm and face
Medial:
-Lower extremity |
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Term
| What is somatotopy? Give the order of neuron destination from lateral to medial. |
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Definition
Somatotopy is the correspondence of receptors in regions or parts of the body via respective nerve fibers to specific functional areas of the cerebral cortex.
Neck, arm, trunk, leg. |
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Term
Chemical messenger responsible for diffuse pain.
(why?) |
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Definition
Neuropeptides:
-Substance P in particular
Why:
-receptors not as good
-reduced re-uptake and control
Substance P is dark staining. |
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Term
What are central pattern generators?
What do they do?
How did we get them? |
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Definition
Group of neurons which control rythmic motor patterns such as walking and breathing.
neurons work together to create coordinated movement
-Some neurons inhibitory some excitatory.
-order of firing coordinates this activity.
Pre-programmed in development
-Fine tunned overtime and practice. |
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Term
What is spinal shock and how long does it last?
Recovery is characterized by? |
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Definition
Significant depression of spinal reflexes post spinal cord injury.
Spinal shock lasts a minimum of 2 weeks in humans.
Recovery is characterized by hyperactivity (caused by denervation sensitivity, increased receptors, or post-synaptic membrane sprouting). |
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Term
What are glucocorticoids used for?
How long is their use indicated? |
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Definition
Anti-inflammatory effects post spinal injury. Limits the extent of damage.
Acute use only. |
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Term
| In a case of an HNP, what are the other factors which can cause pain besides direct nerve compression? |
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Definition
Inflammation and cytokines
Pain fibers growing into damaged disc areas
Pathologic nerve degeneration/demyelination |
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Term
What distinguished neurogenic claudication from vascular claudication pain?
What distinguished these pain types from degenerative disc disease. |
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Definition
Neurogenic claudication can be induced by standing.
The claudications are alleviated by sitting. Lumbar disc disease is not.
Vascular claudication needs a period of movement. |
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Term
| What factors present in muscle spasm produce the associated pain? |
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Definition
| Ischemia and metabolic factors. |
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Term
What i referred pain?
Is it affected by posture? |
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Definition
Pain from viscera in abdomen or pelvis which is interpreted as back pain.
No. |
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Term
| A lesion on the ______ can lead to a patient having an emotional response that is not necessarily appropriate to the pain signal that is being produced within the body |
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Definition
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Term
| _____ is the neurotransmitter for the nociceptor afferent fiber, Alpha-delta fiber, and C fibers. This neurotransmitter works in conjunction with neuropeptides to regulate firing. |
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Definition
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Term
| What is the percentage of LBP that resolves on it own? |
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Definition
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Term
| What is the lifetime prevalence of LBP? |
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Definition
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Term
| How long will it take for the vast majority of LBP cases to resolve? |
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Definition
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Term
| Give 3 examples of mechanical LBP? |
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Definition
| Strains, Sprains, DJD, Osteoarthritis, Congenital anomalies, HNP. |
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Term
| At what level does the Caudal Equina extend from the Conus Medularus |
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Definition
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Term
| A patient presents to the ER with intermittent back pain which repetitively becomes severe quickly, briefly remits, and becomes severe quickly again without changes in position. What is the major differential which this case points to? |
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Definition
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Term
| A 17 year old male presents to the clinic with a history of back pain. He reports no history of trauma. What is the major differential for this age group and sex which this presentation could indicate? |
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Definition
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Term
| A 75 year old male presents to the clinic with a history of back pain. He reports no history of trauma. Urine contains Bence-Jones proteins and plasma cells were found in his bone marrow. What is the likely pathology for this age group which this presentation could indicate? |
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Definition
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Term
What tests are indicated if a tumor is suspect in a LBP case?
Name 4 of the 8 red flags which warrant imaging. |
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Definition
CBC, ESR, and imaging.
50 or over, history of malignancy, systemic symptoms (elevated ESR), trauma, motor defect, litigation/compensation, steroid use, IV drug abuse. |
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Term
If LBP exists with no red flags is imaging warranted immediately?
What are we likely to see in most all imaging studies of an individual over 60 years of age? |
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Definition
No. Watchful waiting. Most cases will resolve on their own within 4-6 weeks.
Image if no improvement after 3-4 weeks.
Likely to see degenerative changes in up to 90% of spines 60 and older.
These changes may not be problematic. |
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Term
Identify the red flag with its associated pathology.
Pain with valsalva, cough, or sitting.
Pain radiating below the knee.
Incontinence or saddle anesthesia.
Severe/rapidly progressive neurologic defecit. |
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Definition
Pain with valsalva, cough, or sitting.
HNP
Pain radiating below the knee.
HNP below L3
Incontinence or saddle anesthesia.
Caudal equina syndrome, spinal cord compression.
Severe/rapidly progressive neurologic defecit.
Caudal equina syndrome, spinal cord compression. |
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Term
| What is stenosis? What are the types of stenosis which could induce back pain and radiculitis? |
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Definition
Central stenosis:
Narrowing of the vertebral canal.
Intervertebral stenosis:
Narrowing of the intervertebral foramen. |
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Term
Osteophytes are? They indicate?
If osteophytes are located anteriorly should we worry about them as a cause of radicular pain? |
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Definition
Bony overgrowths from the vertebra. Indication of osteoarthritis. Theoretically initiated by the body to increase stability of one level on another.
No. |
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Term
What is a seronegative spinal arthropathy?
When do they tend to occur?
What is a key player in these disease?
Name a few. |
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Definition
Seronegative arthropathies are negative for RF.
Tends to occur in young individuals.
HLA B 27
Psoriatic arthritis, ankylosing spondylitis, juvenile arthritis. |
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Term
| Patient presents to the clinic with LBP which is painful to percussion and has an elevated temperature. The patient reports being an IV drug user, on dialysis, recently undergoing surgery, and has had a recent skin infection. What is the likely cause of this patient's back pain? |
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Definition
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Term
| Name 4 of the 8 Red Flags for Low Back Pain (M.I.L.D. S.T.A.N.)? |
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Definition
| Malignancy history, Infection (fever, night chills, elevated ESR), Litigation, Drug abuse, Steroid use, Trauma, Age > 50, Neurological (motor defect). |
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Term
| When do we refer cases of low back pain to surgery? |
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Definition
| Caudal equina syndrome, severe or progressive neurological deficits are present. |
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Term
This drug is used in the treatment of malignant hypothermia?
What is its mechanism of action? |
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Definition
Dantrolene
Dissociates excitation-contraction coupling. (Presumably by interferring with the release of Ca2+ from the SR). |
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Term
Dantrolene is used in the treatment of what conditions.
What form for each condition? |
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Definition
IV: Malignant hypothermia
Oral: Spasm due to cerebral palsy, spinal cord injury, and multiple sclerosis. |
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Term
| Depolarizing neuromuscular blocking agent, high affinity for nicotinic receptors, two acetylcholine molecules linked together. |
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Definition
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Term
What is medication is used to facilitate intubation?
What are the major factor that make this a good choice? |
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Definition
Succinylcholine
Rapid onset (~1 min) and short duration of effect (5-10 mins).
Brief period of excitation followed by flaccid paralysis. |
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Term
| What is acetylcholinesterase? What are its affects? Succinylchloride effects? |
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Definition
Acetylcholinesterases are the primary agent which limits acetylcholine concentration and time of action in the synaptic cleft.
This limits excitation of nicotinic receptors.
Succinylchloride is resistant to acetylcholinesterase activity. |
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Term
| Succinylchloride can cause what toxicities? |
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Definition
| Arythmias, hyperkalemia, transient intraabdominal and intraoccular pressure,and post operative muscle pain. |
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Term
| What are non-depolarizing neuromuscular blockers? How can their activity be reversed? |
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Definition
Non-depolarizing neuromuscular blockers bind and block nicotinic receptors on the motor end plate preventing AP transmission.
These non-depolarizing neuromuscular blockers are competitive and their activity is overcome by increased concentrations of acetylcholine. |
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Term
Is succinylchloride a non-depolarizing neuromuscular blocker?
Name the non-depolarizing neuromuscular blockers and give their effective time range overall. |
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Definition
No. Succinylchloride is a depolarizing agent.
Non-depolarizing neuromuscular blockers include:
Atracurium
Cisatracurium
Rocuromium
Vecuronium
(Above are intermediate acting ~20-60 minutes).
Pancuronium is long acting ~60-100 minutes. |
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Term
What is an indirect mechanism to increase acetylcholine concentration and acting time in the synaptic cleft?
What are the drugs that do this? |
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Definition
Inhibit acetylcholinesterase activity (Indirect way of increasing acetylcholine).
Neostigmine |
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Term
| What is neostigmine used for? |
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Definition
| Acetylcholinesterase inhibitor used to overcome the effects of non-depolarizing neuromuscular blockers particularly Rocuronium. |
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Term
| What are the indications for non-depolarizing neuromuscular blockers? |
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Definition
Muscle paralysis during mechanical breathing and surgery.
Prevent shivering from therapeutically induced hypothermia. |
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Term
| Where do non-depolarizing neuromuscular blockers act? |
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Definition
| These drugs work at the spinal cord or at the higher levels of the CNS. |
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Term
| What is the evidence for the effectiveness of skeletal muscle relaxants in cases of back pain? |
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Definition
Many of these drugs have been around for long periods.
Research has been poorly designed.
Not exactly known method of action.
Not shown to have greater effects than NSAIDs or acetominophen.
No skeletal muscle relaxant has been shown to be better than another. |
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Term
What is GABA? What does it do?
What drugs are GABA agonists? |
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Definition
GABA is the major inhibitory neurotransmitter of the mammalian CNS.
Baclofen and Benzodiazepines and GABA agonists. |
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Term
What neurons use GABA primarily and where are they located?
What is the primary excitatory neurotransmitter of the CNS? |
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Definition
Inhibitory interneurons in the CNS.
Glutamate is the excitatory neurotransmitter of the CNS. |
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Term
| What is Tizanidine and what does it do? |
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Definition
-Acts on a2 receptors on the pre-synaptic neuron.
-Prevents the release of Glutamate (excitatory neurotransmitter). |
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Term
| What is Balofen and what does it do? |
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Definition
-Acts on GABA-b receptors on both the presynaptic and post synaptic neurons.
-Pre-synaptic:
-Prevent the release of the neurotransmitter Glutamate (excitatory neurotransmitter).
-Post-synaptic (motor neuron):
-Opens GABA-b receptors on post-synaptic cell body resulting in hyperpolarization and inhibition of depolarization. |
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Term
| What are benzodiazeprines and what do they do? |
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Definition
-Act on GABA-a receptors on the motor neuron cell body.
-Inhibit depolarization.
-Open GABA-a receptors allowing influx of Cl- ions which hyperpolarize the motor neuron cell body to inhibit depolarization. |
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Term
| What are the risks associated with skeletal muscle relaxant usage? |
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Definition
Many CNS side effects of skeletal muscle relaxants.
Sedation, drowsiness, fatigue, dizziness. |
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Term
| Carisoprodol is more commonly known as? |
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Definition
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Term
| What is the trade name of cyclobenzaprine? What is its basic structure? What are its effects? |
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Definition
Flexeril
Tricyclic compound similar to older anti-depressants.
Strong anti-cholinergic effects.
Inhibition of muscle stretch reflex which is poorly understood.
Reduces muscle hyperactive reflexes. |
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Term
| What are anti-cholinergic drug side effects? Which muscle relaxants should we be concerned about these with? |
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Definition
Dry mouth, confusion/memory, constipation, blurred vision, and urinary retention.
Cyclobenzaprine. |
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Term
| What is Dazepam? What drug class is it a part of? What does it do? |
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Definition
Diazepam increases interneuron inhibition of afferent motor units.
Diazepam is a benzodiazeprine. |
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Term
| What drugs are primarily used for muscle spasm? |
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Definition
| Cyclobenziprine, chlorphenesin, methocarbomol, orphenadrine. |
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Term
| What drugs are used primarily for muscle spasticity due to stroke etc.? |
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Definition
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Term
| What drug can be used for both muscle spasm or spasticity due to stroke etc.? |
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Definition
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Term
| What muscle relaxant drug has an intracellular mechanism of action? |
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Definition
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Term
| What muscle relaxants act at the Neuromuscular Junction as paralyzing agents? |
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Definition
| Succinylcholine (Depolarizing), Nonpolarizing = Cisatracurium, Rocurium, Atracurium, Pancuronium, Vecuronium |
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Term
| What drugs are muscle relaxants acting at the Spinal Cord or higher levels of CNS? Which are best for palsy, stroke or spinal cord injury? An acute back injury? |
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Definition
| GABA (Palsy, stroke, SCI)- Baclofen, Tizanidine, Diazepam; Acute Back Injury- Cyclobenzaprine |
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Term
A forty year old female presents to the clinic with pain along the entire spinal column which has been present for the last 7 months. She has multiple tender points and complains of fatigue and extreme sensitivity to touch. She reports no other joint pain.
What is the most likely diagnosis?
What are you going to do to treat this person? |
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Definition
Fibromyalgia.
Blood tests to rule out RA and Systemic Lupus Erathematosis.
Treat somatic dysfunction. |
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Term
| What is a key tool in the evaluation and treatment of Fibromyalgia? |
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Definition
Fingers (OMT).
Tender points are characteristic. |
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Term
| What differentiates Myofascial Pain Syndrome from Fibromyalgia? |
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Definition
Myofascial Pain Syndrome:
-Males eqaul to females
-No sleep disturbances
-Regional pain
-Trigger points
Fibromyalgia:
-Tender points
-Females predominantly
-Sleep disturbances
-Widespread |
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Term
| Name the associated symptoms of Chronic Fatigue Syndrome? |
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Definition
Chronic Fatigue Syndrome
-Preceded by viral infection
-Pain localized
-Reduced number of (less than 11 of the 18) tender points.
4 of these:
-Decreased memory
-Sore Throat
-Tender Lymph Nodes
-Multi-joint pain
-Headache
-Malaise
-Muscle Pain |
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Term
| What portion of the sleep cycle is most commonly disturbed in Fibromyalgia? |
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Definition
Non-REM sleep.
Less third and fourth stage sleep. |
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Term
| Are genetics and environmental factors possibly associated with Fibromyalgia? |
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Definition
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Term
| What are the current theories on fibromyalgia? |
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Definition
Abnormal processing of nociceptor input.
-Skeletal muscle
Dysfunction of hypothalamic pituitary adrenal axis
-Dopaminergic changes |
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Term
| What are the treatment recommendations for fibromyalgia? |
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Definition
-Patient education
-Aerobic exercise
-Low dose antidepressants
-Cognitive therapy
-Osteopathic Manipulative Treatment |
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Term
| Is strength training indicated with fibromyalgia? |
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Definition
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Term
|
Definition
Defensive state.
-Enhanced neuroendocrine and Immunologic response.
Increased norepinephrine, adrenal corticosteroid, and cytokine release. |
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Term
| What are the OMT treatment goals for fibromyalgia? |
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Definition
Balancing of sympathetic and parasympathetic nervous system tone.
-Done by treating somatic dysfunction
Lymph flow. |
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Term
| What treatment is best used for tender points? |
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Definition
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