Systems 3 review.txt

• Ependymal cells
• Choroid cells
• Brain, spinal cord

• Pia and arachnoid mater
• Choroid stroma
• PNS(spinal&cranial nerves outside brain & SC, schwann cells, ENS ANS)

Dura mater

• Frontal: higher cognitive
• Parietal: spatial and navigation
• Temporal: Auditory, speech and memory
• Occipital: Vision

• 1. Blood brain barrier
• 2. Choroid Cell barrier
• 3. Arachnoid barrier: tight junctions
• 4. Perineurial barrier (
• What is the sulcus limitans?
• Separates developing gray matter into basal(motor,ventral, interneurons) and alar(sensory,dorsal, 2o) plates along spinal cord through mesencephalon.
• Primary 1o sensory neurons come from neural crest
• In brainstem, Separates cranial nerve motor nuclei(medial) from sensorty nuclei(lateral)

• 1. 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: 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 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

• 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
• -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 is the underlying cause of several diseases including multiple sclerosis- leads to decreased nerve conductance and eventually loss of neurons
• -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)

Diameter, myelination

• (1) 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

Greater

• Medial to Lateral:
• Fasciculus(dorsal column): Gracile (sacral, lumbar), Cuneate (thoracic, cervical)
• Lateral Corticospinal Tract(lateral column): cervical, thoracic, lumbar
• Spinothalmic tracts(ventral column): cervical, thoracic, lumbar sacral

Rexed’s Laminae goes from I to IX dorsal to ventral and X forms the central canal connects VII

• Lower Motoneuron
• Typically an -motoneuron whose axon innervates skeletal muscle:
• - soma in CNS, but axon leaves CNS & enters the PNS.
• Upper Motoneuron
• A motoneuron with the soma and axon entirely within CNS (i.e. descending fibers)
• - directly or indirectly innervates lower motoneurons

• All muscles innervated by at least 1 alpha-motorneuron (most 1)
• Vary in size
• Muscle fiber type in a unit is constant (slow, fast-fatigue resistant, fast fatigable)

• I-alpha afferent senses stretch enters dorsal and synapses with alpha-motor(stimulate extensor) and interneuron(inhibit flexor via gamma motor neuron)
• Homonymous & synergistic muscles stimulated
• Antagonistic muscles inhibited (via interneuron)

• Protects tendon and muscle from injury due to excessive tension
• GTO afferent via Ib neuron
• Interneuron->alpha-motor neuron

• Protective reflex using multisynaptic relays to maintain posture.
• Stimulus conveyed via A-delta nociceptor
• Reciprocal innervation: Ipsilateral (stimulus side)= flexors excited, extensors inhibited
• Double reciprocal innervation: Conralateral flexors inhibited, extensors excited
• Net effect: stimulus limb flexed, opposite side extended
• Interneurons used for inhibition

• Damage to ventral horn or cranial motorneurons
• Symptoms: paralysis, paresis(weakness), areflexia, loss of muscle tone & atrophy
• Fibrillations: spontaneous twitches(altered excitability) of denerved muscle fibers
• Fasciculations: spontaneous twitches of motor units, abnormal injured alpha MN

• Damage to descending motor pathways
• Symptoms: increased muscle tone, hyperactive stretch reflex, clonus
• Clonus: oscillatory motor response to muscle stretching)
• Causes of symptoms: removal of inhibitory descending influenced exerted by the cortex and postural centers (vestibular nuclei & reticular formation)
• Ameliorated by lesions to vestibular nuclei and deafferentation (removal of DRG)
• Therefore spasticity represents an abnormal increase in afferent gain.

• Meissner corpuscle: skin motion, slip
• Pacinian corpuscle: high-freq vibration
• Ruffini’s corpuscles: cutaneous stretch
• Merkel’s disks: shape, force and textures
• Free nerve endings: pain
• Superficial: precise, small field
• Deep: broad

Loss of sphincter pupillae: eyes dilated at rest, no light reflex

• Rest: eye is elevated and extorted
• Adducted: inability to depress.

Lateral rectus abducts eye, therefore when looking straight ahead eye is adducted(crossed)

V3, mastication (masseter, temporalis, lateral & medial pterygoid, anterior digastric, mylohyoid, tensor veli palatine and tensor tympani

• CN VII: Loss of facial expression and hyperacusis: loss of muscle to stapedius function
• Also loss of anterior 2/3 taste

• Upper lesion in the contralateral side of not smiling
• Stroke injury to descending influences of voluntary RIGHT motor cortex. (left side not smiling)

• Defective tongue innervation
• During Extension tongue deviates to damaged or lesioned side and shrivels on that side.
• Lower motor neuron lesion

• Accurate assessment
• Methodical prevention
• Aggressive treatment

• Nociceptors: increased impulses elicited by successive stimuli
• Reduced threshold
• Initiation or increase of ongoing activity
• Arachidoniic acid metabolites: prostaglandins, leukotrienes

• Early: neuropetides
• Late: prostaglandins via IL-1 Interleukin 1

• G-protein coupling decreases adenylyl cyclase, cAMP, PKA, CA2+influx channels and increase K+ efflux
• 1. Decrease Ca2+ flux->dec neurotransmitter rls
• 2. Decrease synaptic transmitter activity
• 3. Hyperpolarize dorsal horn neurons

• Nausea, constipation, orthostatic hypotension, RESPIRATORY DEPRESSION, miosis(pupil constriction, may mask head injury symptoms)
• May suppress immune system

• Inhibit immune function
• Enhance tumor growth

• Naloxone: short, non-oral
• Naltrexone: long, oral

• Tolerance:decreased pharm effect from improper administration
• Dependence: adaptation to reset homeostasis from repeated drugs

Short-acting->long acting->dilution

• Further CNS depression.
• MAO inhibitors, phenothiazines, tricyclic antidepressants, local anesthetics

Ibuprofen 800mg x3 x 3 days and PPI

• Anterior Disk Displacement w/Reduction: non-painful=no treatment
• Anterior Disk Displacement w/o reduction(close lock): MANIPULATION, PT, arthrocentesis, surgery
• May need splint(NSAIDSs) to stop inflammation
• Splint may alter bite

40-60mm

• Achy joint, tender, pain, swelling, malocclusion, crepitus(creaking), reduced joint space, loss of subcortical bone or sclerosis
• Diagnosis: pain, crepitation, pain w/chewing, tomograms, Westergren autoimmune measurements
• Treatment: home care, hinge axis exercise, NSAIDs, corticosteroids, JOINT INJECTED STEROIDS or lube

• Masseter to molars
• Splenius: top of head
• Temporalis: temple, orbit, anterior teeth

• Identify triggerpoints (injections), elimate provoking factors, correct posture
• N stretching
• Moist heat and ice
• Decrease muscle load
• Spray and stretch
• Manage stress

• Sharp, shooting, electric, burning, tingling
• Intermittent
• Dysesthesia: abnormal sensatioin
• Allodynia: pain from non-painful stimuli
• Parasthesia: abnormal numbing sensation

• Peripheral: static mechanical allodynia (A-delta and C damage)
• Central: dynamic mechanical allodynia (brain, neurotransmission w/o stimuli)

• Stabbing, electrical shock
• Unilateral intermittent, cyclic
• May be due to superior cerebellar artery compression
• MRI REQUIRED
• Rule out MS
• Treatment: anti-seizure(gabapentin), anti-depressants, surgery (cushion artery & nerve), rhizotomy, glycerol, gamma knife

Stroke, tumor

Sinusitis, parotitis

• Migraine
• Tension-type
• Temporal arteritis
• Cluster

• Most prevalent
• Pressing/tightening, mild
• BILATERAL
• No physical aggravation or vomiting.
• Treatment: NSAIDs, muscle relaxors, Tylenol, ASA, relaxation
• Amitriptyline:prophylaxis

• UNILATERAL, PULSATING, MODERATE TO SEVERE
• Nausea, vomiting, photo or phonophobia
• Treatment: ASA NSAIDS,Tylenol
• Moderate: triptans, ergotamines, opiates, antiemetics
• Preventative: tricyclics, B blockers, Ca blockers, valproate, topiramate

• Menstrual Migraine (estrogen withdrawal) use single phase estrogen
• Cluster Headache (autonomic dysfunction)ORBITAL
• Subarachnoid Hemorrhage (headache is the red herring) spinal consequences
• 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, unilateral numbness weakness)
• Paroxysmal Hemicrania (cluster-like, gout med indomethacin)
• Sexual Activity
• Low CSF Pressure (associated with position-dependent symptoms chiari malformation)
• Temporal Arteritis with Polymyalgia Rheumatica
• (one sided headache seen mostly in elderly, generalized achiness)
• Tolosa-Hunt Syndrome (cavernous sinus thrombosis affects multiple nerves, especially of orbit)

Visual symptoms, sensory symptoms, dysphasic speech disturbance.

• Analgesic: peripheral & central, no tolerance/addiction
• Antipyretic: inhibits PG synth in brain
• Antiinflammatory: inhibits PG in brain and periphery
• CV: none
• Adverse: salicylism, bleeding (inhibits platelet aggregation), GI ulcer, renal/hepatic toxicity, asthma, Reye’s

• Acetominophen
• Analgesic: peripheral & centeral
• Antipyretic: prevent PG in brain
• Antiinflammatory: not much
• CV: none
• Blood: no inhibition of platelet aggregation
• Adverse: Hepato/nephron toxicity, allergy, blood dyscrasias