Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
133 Cards in this Set
- Front
- Back
|
Cell types:
|
neurons, glia, vascular cells, ependymal cells)
|
|
|
Basicall Cell biology parts
symmetrical? |
dendrites, cell body (soma), axon, growth cone, presynaptic terminal
polarized |
|
|
Major forms of glial cells and their fxns
|
-astrocytes (multiple neural support functions), -oligodendrocytes (myelinate CNS axons)
- schwann cells (myelinate PNS axons) - microglia |
|
|
Neurons transmit?
|
electricla signals via AP
|
|
|
The firing of neurons involve?
an influx of____ which ___ the membrane potential away from the ____ Later ___ channels open causing ____ of membrane potentioanl Other channels which play a role in modulating neurla activity Neurons are uniform and the same? |
-Na, depolarizes, resting potential
-K+ hyperpolarizination -Cl- and Ca++ -no, diverse in their morphologies and fxns with distinct firing patterns |
|
|
Gross Divisions of the nervous system
|
Central - brain, spinal cord
- NEURAL TUBE DERIVED Peripheral - spinal & cranial nerves outside of brain & spinal cord, schwann cells - enteric nervous system, autonomic nervous system - NEURAL CREST DERIVED |
|
|
Development of the nervous system
|
neural plate folds up to form the neural tube
•neurons and glia form from neural stem cells that lie along the ventricle and migrate out laterally to form the neuropil •inside-out development of the cerebral cortex (and other regions of the CNS) |
|
|
Gross divisions of the central nervous system (CNS)
|
Spinal cord, medulla, pons, cerebellum, midbrain, diencephalon, cerebral cortex
•Ventricles •3-vesicle stage, 5-vesicle stage and subsequent derivatives |
|
|
how do developmental defects effects flow of CSF?
|
-Hydrocephalus: obstruction to foramen and pathways between ventricles can lead to accumulation and lack of flow of CSF
|
|
|
Embryonic Brain, Adult brain, ventricular space
|
-Prosencephalon
-Telencephalon[lateral ventricles] -cerebral cortex -Hippocampus, olfactory bulb, basal ganglia, basal foramen -Diencephalon[3rd ventricles] -Hypothalamus -Dorsal thalamus Mesencephalon[Cerebral Aqueducts) -midbrain Rhombencephalon[4th ventricle] -Metencephalon -pons -cerebellum -Myelencephalon -medulla oblongota Spinal Cord -spinal cord -central canal |
|
|
Key differences between electrical & chemical synapses (for your future reference):
|
Electrical synapses can be bidirectional
-An electrical synapse can be inhibitory AND excitatory -Electrical synapses are usually formed dendrite to dendrite or soma to soma; chemical synapses are usually formed axon terminal to dendrite |
|
|
Criteria for a neurotransmitter:
|
Present in presynaptic cell
2. Released by depolarization 3. Acts on receptors on postsynaptic cell |
|
|
Excitation: generally leads
|
to influx of Na+ Inhibition: generally leads to influx of Cl-
|
|
|
Glutamate:
Acetylcholine: GABA Glycine Biogenic Amines ATP and Purines Neuroactive peptide Nitric Oxide |
Glutamate: major excitatory neurotransmitter in the CNS
Acetylcholine: excitatory neurotransmitter in the neuromuscular junction GABA: major inhibitiry neurotransmitter Glycine: another inhibitory neurotransmitter Biogenic amines: dopamine, serotonin, norepinhrine, epinephrine, histamine: mostly excitatory ATP and purines: excitatory Neuroactive peptide: endorphins, enkephalon, substance P, etc.: modulate activities Nitric oxide: excitatory and inhibitory |
|
|
Peptide Transmitters are made?
proccesed to from? Transported to? Other NTs are made in? and stored in? |
Peptide transmitters are made in the cell soma, processed to form active portions, transported to axon terminals, and stored in large, dense vesicles
Other neurotransmitters (amino acid-based, ACh, etc.) are synthesized in the axon terminal and stored in smaller, clear vesicles |
|
|
Neurotransmission at chemical synapses
|
1. Transmitter synthesis, uptake & storage in vesicles
2. Action potential invades axonal ending 3. Opening of Ca2+ channels 4. Influx of Ca2+ 5. Vesicle fusion with presynaptic membrane 6. Transmitter release 7 & 8. Transmitter acts at postsynaptic receptors 9. Change in cell excitability 10. Recycling of vesicle |
|
|
Glial Cells
-Ratio? Oligodendrocytes fxns,ratio Schwann cells: derived from, fxn? ratio? -Mylenination increases? -astrocytes: diversity? fxns? -microglia: derived from? fxn? -radial glia: similar to? fxn? |
-Outnumber neurons 5-10:1
-Oligodendrocytes-myelinate CNS axons, multiple oligodendrocytes per axon -Schwann cells- Neural crest derived, myelinate PNS axons, one Schwann cell per axon -Myelination increases nerve conductance -Astrocytes- many different types, play complex roles- surround and modify synapses, trophic support for neurons, capillary blood pressure regulation, nutrient support, injury response -microglia- not CNS derived, but rather from blood system (macrophage), act to keep the nervous system clear, are activated and more are recruited into the nervous system in injury response -radial glia-astrocyte-like, provide scaffold for migrating neurons in the cortex and other places, often serve another function as neural stem cells |
|
|
Loss of myelination leads to?
|
-Loss of myelination is the underlying cause of several diseases including multiple sclerosis- leads to decreased nerve conductance and eventually loss of neurons
|
|
|
Astrocyte/oligodendrocytes respond to?
effect on axon regrowth? |
-astrocyte/oligodendrocyte response to injury can impede axon regrowth;
but Schwann cell response seem to facilitate axon regrowth (hence peripheral nerves regenerate much better than central nerves) |
|
|
the speed of conductance is?
|
proprotional to the diameter of the nerves and extend of myelination
|
|
|
Astrocyte fxns(7)
|
Structural support (glia =’glue’)
(CNS has no extracellular matrix - astrocytes provide support) (2) ‘Maintain’ extracellular environment K+ uptake Glutamate uptake (3) Provide energy metabolites essential for neuronal function (4) Interact with synapses: influence synaptic activity, plasticity and synapse number (5) Regulate blood flow through cerebral vessels (6) Blood-brain barrier (induction and repair) (7) React to injury |
|
|
Astrocyte processes intermingle among axon terminals and dendrites
may also? |
envelope synapses
take up K+ take up glutamate (specific transporters) participate in regulation of synapse number |
|
|
Astrocytes play important roles in___ and ____
effect on blood vessels? |
Astrocytes play important roles in synaptic transmission
and provide nutrient support to neurons Astrocytes contact with blood vessels also regulates capillary blood pressure and can also affect the formation/function of the blood-brain barrier (which at this level comes from endothelial cells) |
|
|
white matter gets greater as you?
|
move up towards the brainstem
|
|
|
|
|
|
Muscle Spindles:
located in? regulates? reflex? ascending? |
-intrafusal muscle
-Position/movement(velocity) -stretch reflex: 1. stretch muscle spindle-->Ia afferent--> alpha-MNs-->contract same muscle + inhibit antagonistic muscle -DRG-->dorsal lateral column-->ascend-->synapse at VPL/VPM-->medial lescussiate-->hypothalamus |
|
|
How to maintain spindle input if already stretched?
|
gamme neurons regulate tension/stretch in intrafusal muscle,
w/o this, muscle spindles would not be able to fire when muscle is not stretched/is contracting |
|
|
GTO
location? -respond to? reflex? fibers? |
-located in tendons
-respond to tension not length -tension reflex -Ib which inhibit alpha MN and activate antagonist muscles |
|
|
Pacinian
|
-touch and vibration
|
|
|
Muscle Spindles:
located in? regulates? reflex? ascending? |
-intrafusal muscle
-Position/movement(velocity) -stretch reflex: 1. stretch muscle spindle-->Ia afferent--> alpha-MNs-->contract same muscle + inhibit antagonistic muscle -DRG-->dorsal lateral column-->ascend-->synapse at VPL/VPM-->medial lescussiate-->hypothalamus |
|
|
How to maintain spindle input if already stretched?
|
gamme neurons regulate tension/stretch in intrafusal muscle,
w/o this, muscle spindles would not be able to fire when muscle is not stretched/is contracting |
|
|
GTO
location? -respond to? reflex? fibers? |
-located in tendons
-respond to tension not length -tension reflex -Ib which inhibit alpha MN and activate antagonist muscles |
|
|
Pacinian
|
-touch and vibration
-ascends up the dorsal column, decussates at the medulla |
|
|
Encapsulated ending
|
--Meissner
-light touch -fast -synapse in ventral horn, decussates, ascends up spinothalamic |
|
|
Free Nerve ending
|
-slow
-synapses within dorsal horn -decussates -ascends via spinothalamic |
|
|
jaw closing reflex
|
-primary sensory-->1a afferent-->ventral horn-->alpha motor neuron-->same muscle
|
|
|
reciprocal inhibition
|
-primary ending-->!a afferent-->inhibitory interneuron-->inhibit antagonistic muscle
|
|
|
Reflex Overall
|
-Homonynous & synergisitc muscles stimulated, antagonistic muscles inhibited
|
|
|
Myotatic Reflex
|
stretch-->muscle spindle(intrafusal)-->1a afferent-->ventral horn-->alpha motor-->extrafusal muscle
gamma motor-->intrafusal muscle |
|
|
Inverse Myotatic Reflex
fxn? |
-tension-->GTO-->1B neuron-->inhibited-->interneuron-->alpha motor
protects tendon and muscle from excessive tension |
|
|
Flexor Reflex
used to? uses? maintains? pathways: |
-protective reflex
-multisynapses: maintains posture -Reciprocal innervation: -on side of ipsilateral to the stimulus: flexors excited, extensors inhibited Double reciprocal innervation: produces oppose pattern of muscle activation on contralateral side; flexors inhibited, extensor excited |
|
|
Paresis-->Paralysis:
sequalaue of? characterized by? fibrillation and fasciulations? |
Sequelae of the Lower MN Syndrome (damage to ventral horn or cranial motoneurons).
Characterized by: Paralysis (loss of movement) Paresis (weakness) Areflexia (loss of reflexes) Loss of muscle tone & atrophy of muscle mass Fibrillations & fasciculations (spontaeous twitches) of denervated muscle fibers (fibrillation) & motor units (fasciculations). Altered excitability of muscle fibers – fibrillation Abnormal activity of injured α-MN - fasciculation |
|
|
Spasticity
sequelae of? characterized by? caused by? ameliorated by? |
One of a number sequelae of the Upper MN Syndrome (damage to descending motor pathways).
Characterized by: increased muscle tone hyperactive stretch reflex clonus (an oscillatory motor response to muscle stretching) Caused by removal of inhibitory descending influences exerted by the cortex and postural centers (vestibular nuclei & reticular formation). Ameliorated by lesions to vestibular nuclei (animal models) and deafferentation (removal of DRG) in animal & human subjects. Suggesting that spasticity represents an abnormal increase in afferent gain |
|
|
Meissner
Pacinian ruffinis Merkels Free nerve |
- skin motion, slip
-high frequency vibration -cutaneous stretch -shape, force texture -pain |
|
|
Superficial receptors vs. deep deceptors
|
-superfical more precise, small recpetive firleds
-deep receptors have broad receptive fields |
|
|
What dictates AP speed?
Fiber types and speeds |
-myleination and diameter
- Aa>Ab>Ad>C Aa: primary muscle spindle, golgi tendon organ Ab: skin mechanoreceptors, seconadry muscle spindle Ad: coarse touch, temperature and pain C: coarse touch, temp and pain |
|
|
Aa Ab Fibers
Myleintion, diameter, sense, thermal threshold? Ad Myleintion, diameter, sense, thermal threshold? C Myleintion, diameter, sense, thermal threshold? |
-myleinated
-large -proprioception, light touch -none Ad -lightly -medium -nociception(mechanical, thermal, chemical) -type I 53 C -Type II 43 C -unmylen -small -innocous temp, itch, nociception(mechanical, thermal, chemical) -43 degrees Ad |
|
|
Dorsal Column-Medial Lemniscus
|
Cutaneous Mechanoreceptors (tactile)
4 classes of mechanoreceptors 4 associated afferents Proprioception & Kinesthesia (position) Muscle spindles, golgi tendon organs & joint receptors The path to cortex Locations & projections of 1st, 2nd & 3rd order neurons Where decussation occurs Differences between DRG inputs & Vth nerve inputs Basic arrangement of topography throughout the system The organization of somatosensory cortex 4 areas Basic arrangement of topography |
|
|
Mechanosensory info(proprioception)
|
-1st order(DRG, !a and 1b, II, AB)
-ascend up dorsal column: cuneate tract, gracile tract -2nd order neuron(medulla) -deccusate medial lemnicus -3rd order: VPL of thalamus -ascend to somatosensory cortex |
|
|
Pain and Temperature Sensory info(nociception)
|
-1st order: DRG, Adelta, C fibers)
-2nd order -dorsal horn of spinal cord -decussates -ascends via anterolateral tract 3rd order: -VPL of thalamus -ascends to somatosensory cortex *visceral pain: ascends via dorsal columns |
|
|
Dorsal colum-Medial Lemniscus-FACE mechanosensory
Topographic representation in theface |
-mechanosensory:psuedo-unipolar neurons cell bodies in trigeminal ganglion and ganglia assoicated with 7, 9, 10 nerves
2nd order neurons: -prinicpal(sensory) nucleus of the trigeminal complex in mid pons -decussate -ascend via the trigeminothalamic tract *some neurons do not decussate but join the ipsilateral trigeminothalamic tract 3rd. Order -VPM -primary somatic sensory cortex -Dorsal-->ventral -V3, V2, V1-->think upside down face - |
|
|
Central Pain Pathways
Sensory Discriminative component |
-pain/temp from face: pseudo-unipolar neuron cell bodies in trigeminal ganglion and other ganglia(VII, IX, X)
-descend to middle medulla/caudal medulla via the spinal trigeminal tract -decussate -ascend trigeminal tract 3rd order: VPM ascend to primary somatic sensory |
|
|
VII, IX, X pain
|
Level 5: pain and temp from ear psuedounipolar geniculate ganglion,
-descend ipsilateral trigeminal tract to level 1 2nd order neuron: -spinal nucleus V -decussate -ascend trigeminathalamic tract to VPM Level 3: Pain and temp from ear, post 1/3 tongue, upper pharynx eustachian tube-->superior ganglion 9 -descends trigeminal tract to level 1 -synapses at spinal nucleus -decussates and ascends via trigeminal tract to VPM -Pain,temp from ear, lower pharynx, larynx, upper esophagus-->superior ganglion 10 -descends via trigeminal tract -synpase at spinal nucleus 5 -decussates and ascendings trigeminothalamic tract to VPM |
|
|
Central Pain Pathways
Affective motivational component: |
-Information from upper(cervical) or lower(lumbar)
-synapse in dorsal horn area -decussate -ascend the anteriorlateral system -synapse: -mid pons: parabrachial nucleus -thalamus: intralmainar nuclei of thalamus -Medulla: parabrachial nucleus) -Peri-Aqueductal grey |
|
|
Dorsal column Medial lemniscus:
VP complex Post Central Gyrus |
-VPM, VPL
- Post central gyrus = somatic snesory cortex |
|
|
Motor Homunculus
|
-Medial = toes/feet
-lateral= throat, jaw, tonue |
|
|
I
|
Olfactory
Sensory Smell |
|
|
II
|
Optic
Sensory Vision |
|
|
III
|
-Oculomotor
-Motor -Eye movements; papillay constriction and accomodation, muscles of the eyelid |
|
|
IV
|
-Trochleaer
-Motor -eye movements |
|
|
V
|
-Trigemnial Nerve
-sensory/Motor -somatic sensation from face, mouth, cornea, muscles of mastication |
|
|
VI
|
-Abducens
-Motor - eye movements |
|
|
VII
|
-facial nerve
-sensory and motor -controls the muscles of facial expression -taste anterior tongue -lacrimal and salivary glands |
|
|
VIII
|
-auditory/vestibular nerve
-sensory -hearing sense of balance |
|
|
IX
|
Glossopharyngeal
-sensory and motor -sensation from pharynx; taste from posterior tongue, carotid baroreceptors |
|
|
X
|
-Vagus nerve
-sensory and motor -autonomic fxns of gut, sensation from pharynx, muscles of vocal cords, swallowing |
|
|
XI
|
-Accessory nerve
-motor -shoulder and neck muscles |
|
|
XII
|
-hypoglossal nerve
-motor -movements of tongue |
|
|
Cranial Nerve Tests
|
-1: Test sense of smell with standard odor
2: measure acuity and integrity of visual field 3: test eye movements(patient can't look up, down or medial if nerve involded), look for ptosis, pupillary dilation 4: can't look downward when aducted 5: test sensation on face palpate masseter/temporal muscle 6: can't look laterally 7: test facial expresion plus taste on anterior tongue 8: audtion with tuning forc, vestibular fxn with caloric test 9: test swallowing: pharyngeal gag reflex 10: swallowing + hoarsenss 11: SCM and trapezius muscles 12: deviation of tongue during protrsuion, points to side of lesion |
|
|
Branchial Arch 1
|
-Cranial Nerve 5
-V3 -Masster and temporalis |
|
|
Branchial Arch 2
|
-CN 7
-facial expression muscle |
|
|
Brnachial Arch 3
|
-CN9
-stylopharyngeus |
|
|
Brnachial arch 4
|
-CN10
-pharynx/larynx |
|
|
Branchial arch 6
|
-CN 11
- trapezius -SCM |
|
|
|
|
|
Mid-Brain
|
-Somatic Motor
-Oculomotor III -Trochlear nucleusIV -Visceral motor -edinger-westpah nucleus III -General Sensory -trigeminal sensory: mesencephalic nucleus, 5,7,9,10 |
|
|
Pons
|
-Somatic Motor
Abduscens nucleus 6 -Branchial Motor trigeminal motor nucleus 5 facial nucleus 7 -Visceral motor: -superior salivatory nucleus 7 -inferior salivatory nucleus 9 -General sensory -trigeminal sensory: principal nucleus: 5, 7, 9, 10 Speical Sensory: vestibular nuclei 8, cochlear nuclei 8 |
|
|
Medulla
|
Somatic Motor:
-hypoglossal nucleus 12 branchial Motor: -nucleus ambiguus 9,10 spinal accessory nucleus 9 Visceral motor Dorsal motor nucleus of vagus 10 Genreal sensory: Trigeminal snesory: spinal nucleus 5,7,9,10 Special sensory: vesitbular(8), cochlear(8) |
|
|
Developmental organization of fxnal columns in brainstem
|
-Dorsal/Lateral = sensory
-ventral/medial = motor -vsiceral: middle near sulcus limitans -Afferent = incoming; efferent = outgoing |
|
|
Damage to cranial nerve 4th
|
-super olique muscle failure
-patient attempting to look straight but with 9th nerve inaction-->uncompensated offset by other muscles -eye looks kind of down to right patients right |
|
|
Damage to CN 6
|
-subject attempting to look straight ahead but no lateral rectus action to offset action of other muscles
-cross eyed ish |
|
|
5th cranial nerve component
divisions? |
-GSA: sensory component
-3 divisons V1, V2, V3 -motor off V3 V1: top of head to nose V2: nose to mouth V3: mouth to chin |
|
|
Distribution 7:
-motor for? nerve of branchial arch? components? |
-motor for muscles of facial expression
-branchail arch 2 -SVE |
|
|
damage to 7th nerve-->
sx? |
-bell palsy
-unilateral -no eye closure -inability to wrinkle forhead on affected side -no mouth retraction and drooling -droopy eyelid -hyperacusis(failure to dampen loud noises) |
|
|
cannot smile voluntarily on the left side
CN? why not bells? lesion where? |
-none, voluntary right motor cortex
-cannot voluntarily smile -can non-volunatrily smile--> shows integrity of 7th crnail nerve -facial muscles get innervation from more than one nerve-->ability to smile involuntarily -upper right motor cortex |
|
|
What happens with hypoglossal (CNXII) nerve damage?
What is the test for damage? What direction will the tongue point? Why does the tongue shrivel? Is this an upper or a lower motor neuron lesion? |
What happens with hypoglossal (CNXII) nerve damage? Defective tongue innervation
What is the test for damage? Tongue extension What direction will the tongue point? Towards the lesioned side Why does the tongue shrivel? Lack of muscle control on one side Is this an upper or a lower motor neuron lesion? Lower |
|
|
Cranial Nerves with contralateral
|
CN12
CN7 lower |
|
|
Innervation of tongue
|
V: genreal sensory
VII: taste to anterior 2/3 IX: taste to poster 1/3 and genreal sensory X: taste(epiglottis) also GVA |
|
|
T/F
Individual reaction and tolerance to pain varies. Patients who are in pain always have observable signs. Pain response is influenced by emotional state, religious beliefs, and strong feelings. Obvious pathology, test results, and/or type of surgery determine the existence and the intensity of pain. Anxiety, fear, apprehension intensifies pain response. Patients should wait as long as possible before taking analgesics. This abstinence teaches a better tolerance for |
T
F T F T F |
|
|
Pain Facts:
Unrelieved pain after surgery/traumma has? Patients have right to treatment which...? Pain in dentistry |
Unrelieved pain after surgery or trauma has negative physical and psychological consequences.
Patients have a right to treatment that includes prevention of pain and adequate relief of pain. Although pain is a common occurrence in dental procedures, it is generally manageable and often avoidable. Accurate assessment, methodical prevention, and aggressive treatment are the tools required to minimize pain. |
|
|
Nociceptive Pain
|
Mechanical, thermal, or chemical activation of nociceptors
Somatic vs. visceral: Visceral: poorly localized, refered to somatic representation -chemical, heat, trauma, cold |
|
|
Inflammatory pain:
treatment |
-damaged tissue, immunocompetent tumor cells release chemicals that activate/sensitize nociceptors which in turn results in sensitization of CNS neurons
common factors: histamine, prostalganddins, serotonin, bradykinin, H+, TNF alpha, interleukins, endothelins, nerve growth factor cox 2 inhibitors, opiods |
|
|
Peripheral Sensitization:
5 |
Characteristic of nociceptors
Increased number of impulses elicited by successive stimuli Reduced threshold Initiation of or increase in ongoing activity Involvement of arachidonic acid metabolites (e.g. prostaglandins, leukotrienes) |
|
|
Central Sensitization:
early vs. late |
-Early: involve neuropeptides
-Late: involve prostaglandins |
|
|
Neuropathic Pain
involves, caused by? leads to? treatment |
- Lesions or disorders of the nervous system
Multiple etiologies (e.g. diabetes, cancer, peripheral nerve crush or constriction) Abnormal input and processing tricyclic antidepressants anticonvulsants Na channel blockers NMDA receptor antagonist Opioids |
|
|
Altered sensory processing in neuropathic pain
|
-Changes in synaptic connectivity
ex. sprouting, non-nocicpetive afferent(AB) directly links to pain neuron skipping excitatory interneuron Loss of inhibition of pain transmission neuron |
|
|
Causes of Orofacial Pain(7)
|
Dental – tooth/gum
TMJ TemporoMandibular Joint Muscle Nerve Intracranial Extracranial Neurovascular |
|
|
Non Painful Clicking (TMD)
treatment? |
• Does not require treatment if it is not painful. (30% of the population have joint noises).
• May require treatment if “jamming” is occurring with increasing frequency. |
|
|
Intermittent Locking and/or Painful Clicking
|
May require intervention with anterior advancement splint until joint inflammation subsides and joint adapts to the mechanical dysfunction
|
|
|
Treating the Painful Episodic Locking Joint(4)
|
• Home Care Protocol
• Tomograms • NSAID’s for inflammation • Repositioning Splint Therapy (pushes jaw bones forward to allow disc to regain normal position) |
|
|
Treating the Anterior Displacement w/o
Reduction (Closed Lock) |
Manipulation-get the disc to move back on or out of the way (under anesthesia)
• Physical Therapy • Arthrocentesis • Arthroscopic Surgery (rare) |
|
|
what is reduction?
|
+ able to pop disc back into place
- not able to pop disc back into place |
|
|
arthritides
- what is it? sx?(7) |
• Tender to palpation and manipulation
• Pain with chewing. • Swelling • Posterior teeth may not touch. • Crepitus (late sign)-crinkling sounds • Reduced joint space-due to collapse of the joint which also leads to jaw alignment problems) • Loss of subcortical bone or sclerosis |
|
|
TMJ osteoarhritis:
|
Pain in Joint
Osteolysis Loss of Joint space Loss of subcondral bone. -teeth fall, back teeth cotnact, anterior don't |
|
|
Diagnosis of Arthritis
(5) |
• Joint pain
• Crepitation • Pain with joint loading/chewing • Tomograms • ANA, CBC, Platelet, Diff, Sed rate (Westergren)-autoimmune measurements |
|
|
Treatment of Arthritis
|
Home Care Protocol
• Hinge Axis movement exercises • NSAID’s ( e.g. Relafen 500mg b.i.d.) for 2 weeks. • Corticosteroids (e.g. Medrol Dose Pack) for 1 to2 weeks. • Joint Injection with Steroids (preferred) • Joint Injection with Hyaluronic Acid (joint lubricant |
|
|
Definition of Myofascial Pain
|
A regional muscle pain syndrome that is characterized by painful triggerpoints that refer to sites remote from the triggerpoint site (such as the teeth).- often diagnosed by pressing on the muscles which are often in spasm and associated with teeth clenching
|
|
|
Treatment of Myofascial Pain
|
Eliminate the provoking factors
• Correct posture • Myofascial Protocol Teach Muscle Stretching-”N” position with mouth open and tongue up Instruct in use of moist heat and ice Decrease muscle load Teach Spray and Stretch • Manage stress • Trigger point injections-can act by stretching the muscle fibers |
|
|
Neuropathic
sx? caused by? leads to(3)? some causes of it...? |
Dysesthesia: unpleasant, abnormal sensation
• Allodynia: painful response to non-painful stimuli • Paresthesia: abnormal sensation (numbness, tingling) Some causes include Varicella Zoster virus (Shingles) and Herpes Zoster |
|
|
Trigeminal neuralgia
sx? common? sides? pattern of occurence? causes? diagnosis? test for what in younger patients |
• “stabbing, electrical shock”
• unilateral, intermittant • Cycles, remissions. • Causes unclear- possible that blood vessel (superior cerebellar artery may compresses trigeminal nerve on pons. • MRI brain required on every patient! • In younger patients, must test for multiple sclerosis (2-4%). |
|
|
trigeminal neuralgia
treatment(5)? |
Medications (primarily anti-seizure and anti-depression drugs)
Surgery – microvascular decompression-put cushion between artery and nerve. Radiofrequency rhizotomy. Glycerol injection. Gamma knife radiation. |
|
|
Intracranial Causes of Pain:
3 |
• In the brain.
• Stroke. • Tumor. |
|
|
Extracranial Causes of Pain:
2 |
• Sinusitis
• Parotitis (parotid/salivary) |
|
|
Neurovascular Causes of Pain:
|
• Migraine.
• Tension-type headache. • Temporal arteritis. • Cluster headache. |
|
|
Tension-Type Headache:
common? diagnosis? |
Most prevalent HA disorder – affects almost everyone.
Diagnostic Criteria: A) At least 10 previous HA episodes fulfilling criteria B to D. B) Headache lasting from 30min – 7 days C) At least 2 of the following pain characteristics: - Pressing/tightening - Mild or moderate severity - Bilateral location - No aggravation by routine physical activity. D) No vomiting |
|
|
Tension Type Headache treatment
|
Acute episodes – NSAIDS, muscle relaxants, acetaminophen, ASA.
Prophylaxis – amitriptyline is drug of choice. Physical therapy, posture, relaxation, exercise |
|
|
Migraine Headache (with or without aura):
Diagnostic criteria: time period? 2 of the following? 1 of the following how many attacks? health history? |
Diagnostic criteria:
A) Headache attacks last 4 to 72 hours B) Headache has at least two of the following characteristics: - Unilateral location (most common presentation) - Pulsating quality - Moderate or severe intensity - Aggravation by routine physical activity C) During headache at least one of the following occurs: - Nausea and/or vomiting - Photophobia and phonophobia D) At least five attacks occur fulfilling the above criteria E) History, physical examination, and neurologic examination do not suggest any underlying organic disease |
|
|
Migrane headache treatment?
|
Treatment:
• Mild to moderate – ASA, NSAIDS, acetaminophen. • Moderate to severe – triptans, ergotamines, opiates. • Meds to treat associated nausea/vomiting. • Preventative meds – tricyclics, B blockers, Ca channel blockers, valproate, topiramate, NSAIDS. |
|
|
Other causes of headache:
Menstrual Migraine Cluster Headache Subarachnoid Hemorrhage Basilar Migraine Medication Overuse- Trigeminal Neuralgia Venous Sinus Thrombosis Paroxysmal Hemicrania Sexual Activity- Low CSF Pressure Temporal Arteritis with Polymyalgia Rheumatica Tolosa-Hunt Syndrome |
Menstrual Migraine (estrogen withdrawal)
Cluster Headache (autonomic dysfunction) Subarachnoid Hemorrhage (headache is the red herring) Basilar Migraine (presents with mulitple brainstem dysfunctions) Medication Overuse Trigeminal Neuralgia (electrical-like, excruciating pain radiating to teeth) Venous Sinus Thrombosis (severe symptoms, consider risk factors) Paroxysmal Hemicrania (cluster-like) Sexual Activity Low CSF Pressure (associated with position-dependent symptoms) Temporal Arteritis with Polymyalgia Rheumatica (one sided headache seen mostly in elderly) Tolosa-Hunt Syndrome (cavernous sinus thrombosis affects multiple nerves) |
|
|
|
|
|
Precepts in the use of oral analgesics for treating acute dental pain
asprin/acetaminophen opioid combo? newer nsaids? |
Aspirin or acetaminophen provides more pain relief than conventional doses of oral opioids for dental pain
An opioid in combination with aspirin or acetaminophen can provide additive pain relief- they act at different levels Newer NSAIDs produce analgesia at least comparable to standard acetaminophen-opioid combinations |
|
|
Oral surgery pain model (3rd molar extraction)
used because? subjects/tissues? findings: |
Probably best overall model for oral analgesics
Reliable stimulus for moderate-severe pain Healthy young subjects Healthy preoperative tissues Strongly validated -Aspring 650mg + Codeine 60mg > Aspring 650mg>codein60mg> placebo |
|
|
Non-steroidal anti-inflammatory drugs (NSAIDs)
Mechanism of action |
Inhibition of the cyclooxygenase (COX-1 and COX-2) enzyme system in the periphery and centrally.
Other less well-defined spinal and brainstem mechanisms may also be involved. |
|
|
Non-steroidal anti-inflammatory drugs (NSAIDs)
Chemical classification |
Salicylic acid derivatives
Aniline derivatives(acetaminophen) Propionic acid derivatives Anthranilic acid derivatives Selective COX-2 inhibitors |
|
|
Asparin/Salicylates:
Analgesic effect Antipyretic effect Antiinflammatory effect Adverse effect(7) |
- peripheral and central actions
- no tolerance or addiction - ceiling effect 650-1000 mg, therapeutic dose: 325-650 every 4 h Antipyretic effect - inhibition of prostaglandin synthesis in the brain Antiinflammatory effect - inhibition of prostaglandin synthesis in the brain and periphery Cardiovascular effect - no major effects Adverse effects Salicylism (acute overdose: tinnitus, nausea, vomiting, hyperthermia, hyperventilation) Excessive bleeding (inhibits platelet aggregation) GI ulceration Renal toxicity Hepatic toxicity Anaphylactoid reactions (asthma) Reye’s syndrome |
|
|
Analine Derivatives (Acetominophen)
analgesic antipyretic antiinflammatory cardiovascular blood adverse effects? |
-peripheral and central actions
antipyretic: prevention of prostaglandin syn. in brain antiinflammatory: less potent that aspirin cardiovascular: no major effects blood: doesn't inhibit platelet aggregation adverse: -hepatoxicity -nephrotoxicitiy -allergy -blood dyscrasias |
|
|
NSAIDs
Phenylropionic acid derivatives(5) |
ibuprofen (Motrin, Advil, Nuprin, Rufin)
fenoprofen (Nalfon) flurbiprofen (Ansaid) ketoprofen (Orudis) naproxen (Naprosyn, Anaprox, Aleve) |
|
|
NSAIDS
Cyclooxygenase-2 Inhibitors (Celebrex) advantage/disadvantages |
Advantage: More selective
Potentially reduced toxicity Better for people with history of gastric or duodenal ulcers and bleeding problems Potential concerns: Renal function Cardiovascular function (this killed the use of Vioxx) |
|
|
Opioids
Therapeutic uses 6 Side Effetcs 5 |
Analgesia
Sedation Antidiarrheal Antitussive Anesthesia Relief of pulmonary edema Nausea & vomiting Constipation Orthostatic hypotension Respiratory depression Miosis |
|
|
Opioids: Contraindications and cautions
|
Allergy
Compromised respiration Head injuries Myxedema and multiple sclerosis Mother prior to delivery Asthmatic attack |
|
|
Opioid receptor antagonists
|
-naloxone
-not effective orally -short duration of action 1-4hrs Naltrexone -effective orally -long duration of action 48-72 hrs Mixed agonist-antagonist: pentazocine, butophanol, nalbuphine |
|
|
Opiods receptors inovlved in:
|
-area with pain:
transmission: -pain -synapse in dorsal horn -secondary neuron decussates ascends -synpase in ventral caudal thalamus -3rd neuron moves to diencephalon -or 2nd neuron branches off and synapses in medulla -acends to ventral caudal thalamus and synapses -3rd neuron transmits to cortex Modulation: -cortex--> PAG in midgrain -PAG-->Medullar Roststral ventral medulla -Rostral ventral medulla--> dorsal root of gray matter -decussates Modulation |
|
|
Opiod fxns?
|
-decrease gCa in SP/Glu c-fiber neuron(outside spinal cord)
-decrease synpatic potential by decreasing transmitter rlease -hyperpolairze dorsal horn neurons(interneuron Enk |
