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Q1=Understand how sensory modulation occurs within the dorsal horn.
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Q2=Describe visceral sensory information flow into and out of the cord.
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Q3=Know the longitudinal organization of nuclear groups within the cord gray matter.
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Q4=Be able to locate and label the major nuclei and fiber tracts located within the: cervical cord (C2); cervical enlargement (C7); thoracic cord (T4); and lumbar cord (L2).
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Q5=Describe the blood supply to the spinal cord and its areas of greatest vulnerability.
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Q6=Be able to locate a lesion within the spinal cord given a set of clinical signs.
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Q7=Be able to list the clinical signs that would result from a specific spinal cord lesion.
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Q8=Identify and understand the pertinent anatomy of the skeletal spinal column, intervertebral discs, spinal cord, and spinal nerves.
A8=* Skeletal spinal column ^o 7 cervical vertebra ^o 12 thoracic vertebra ^o 5 lumbar vertebra ^o 5 sacral vertebra ^* Nerve roots ^o 8 cervical - exit above ^o 12 thoracic - exit below ^o 5 lumbar - exit below ^o 5 sacral - exit below
Q9=Recognize the clinical characteristics of spinal cord lesions and spinal root lesions.
A9=* Spinal cord lesions ^o Typically not painful ^o Increased tone ^o Hyper-reflexia (except within one week of injury; acute spinal cord shock) ^o Level of lesion indicated by highest level of disturbance ^o Weakness precedes sensory loss ^* Spinal root lesions ^o Lower motor neurons ^o Mixed nerves ^o Radicular pain (pain radiates rapidly down limb in distribution of specific nerve root; usually precedes sensory loss or loss of function) ^o Loss of reflex ^o Less often weakness and numbness
Q10=Be able to clinically determine the level and distribution of spinal cord injury.
A10=* Spine plain films - essential initial radiologic evaluation ^* Myelogram - for examining subarachnoid space ^* CT scan - excellent for evaluating bony anatomy (can combine with myelogram) ^* MRI - superior visualization of neural tissue (diagnostic tool of choice)
Q11=Understand and delineate the specific cervical and lumbar root syndromes.
A11=* C5 - C4-5; shoulder; (no reflex); deltoid muscle ^* C6 - C5-6; radial arm & thumb; bicep reflex; biceps muscles ^* C7 - C6-7; mid-hand, index & middle fingers; tricep reflex; triceps muscles ^* C8 - C7-T1; ulnar arm, hand, ring & little fingers; (no reflex); ADQ and hand intrinsic muscles ^* L4 - L3-4; anterior thigh and knee; patellar reflex; quadriceps muscles ^* L5 - L4-5; dorsal/plantar foot & first toe; (no reflex); EHL, anterior tibial muscles ^* S1 - L5-S1; lateral foot and little toe; Achilles reflex; gastroc muscles ^* Spinal cord injury ^o Complete - total loss of motor and sensory function below lesion ^o Incomplete ^* Anterior cord syndrome ^* HALLMARK = preservation of vibration and proprioception ^* Loss of motor function below level of injury ^* Loss of pain and temperature sensation below injury ^* Central cord syndrome ^* HALLMARK	= motor impairment greater in arms than legs ^* Esp. following hyperextension injury in patients with cervical spondylosis ^* Variable sensory loss ^* Some recovery is common; legs and bladder before upper extremities; hand weakness least likely to resolve ^* Brown-Sequard syndrome ^* HALLMARK = ipsilateral motor loss below level of lesion ^* Ipsilateral loss of vibration and proprioception ^* Occurs with hemi-section or hemi-injury of cord ^* Contralateral loss of pain and temperature below lesion
Q12=Understand the components and goals of rehabilitation after spinal cord injury.
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Q13=What are important features of nerve root compression?
A13=o Especially in lumbar or cervical spinal canal (rarely thoracic) ^o Herniated discs - usually acute onset of signs and symptoms ^o Degenerative spurs - slow, chronic onset ^o Neurological findings may be identical with both herniated discs and degenerative spurs
Q14=What are the traditional dermatomes?
A14=o Nipples = T4 ^o Umbilicus = T10 ^o Knee cap = L4
Q15=What are the different types of spinal cord tumors?
A15=o Intramedullary - within spinal cord ^o Intradural extramedullary - within dural sac, but outside the spinal cord ^* 60-70% of intradural tumors ^o Extradural - within spinal canal but outside the dura ^* Primary bone tumor or metastesis ^* Metastatic compression paraplegia usually preceded by at least one to two weeks of local back pain ^o Cauda equina ^* Tumors below L2 compress cauda equina and not spinal cord ^* Typically lower motor neuron signs
Q16=Become familiar with the major theories and perspectives on development, including: temperament; attachment; cognition; moral development; social learning theory and other behaviorist perspectives; and emotional development.
A16=* Temperament (Chess/Thomas) ^o Easy temperament = positive mood, regular biological rhythms, adaptability, low intensity, and positive approach to novelty ^o Difficult temperament = negative mood, irregular biological rhythms, slowness to adapt, intense reactions, and negative responses to novelty ^o Slow to warm up = mild intensity, gradual adaptation, negative responses to novelty, moderate risk for future behavior problems ^o NOTE: only extremes of temperament appear to be accurate predictors of future personality and behavior ^* Attachment (Ainsworth) ^o Strange situation test ^* Testing situations when caregiver leaves and returns, interspersed with non-caregiver entering and leaving ^* Securely attached - protests with separation; jubilant upon return; outcome = cooperative, popular, resilient, and resourceful ^* Insecurely attached - shows avoidance upon return; outcome = emotionally insulated, hostile, and antisocial ^* Insecurely resistant - passive or angry behavior periodically present on return; outcome = tense, impulsive, easily frustrated, passive, and helpless ^* Insecurely disorganized - inconsistency, confusion, or incoherence ^o Development ^* Undiscriminating social responsiveness = birth-3 mo's; favorable response to attention from any adult ^* Discriminating social responsiveness = 3-8 mo's; differential responses to different people ^* Active initiative in seeking proximity and contact = 7 mo's ^* Goal-directed partnership = 3 yrs; recognizes caretaker's goals may be different and adapts ^* Cognition (Piaget) ^o Schema = the mental representation of a pattern of a behavioral response to an environmental stimulus ^o Assimilation = process of altering schemata based on impact of behavior ^o Accommodation = process of altering schemata based on characteristics of new stimuli ^o Development ^* Stages = sensorimotor stage, preoperational stage, concrete operations, formal operations ^* Sensorimotor stage - birth-18 mo's; instinct is driving force; no logical reasoning ^* Primary circular reactions = birth-4 mo's; sensory changes based on interaction with own body ^* Secondary circular reactions = 4-10 mo's; connection made between actions and surrounding environment ^* Object permanence = 8-11 mo's; understands that things not in view may still exist ^* Preoperational stage - 2-7 yrs; incorporation of abstract thought (use of symbols) ^* Egocentric = child assumes others think what the child thinks ^* Concrete = based on reference to child's own experience ^* Transductive = cause and effect are inferred based on proximity in time or space ^* Magical thinking = events are assumed to be caused by child's own thoughts or wishes ^* Concrete operations - begins at 7 yrs ^* No longer bound by immediate perceptions ^* Can account for more than one variable at a time ^* Conservation is mastered (e.g. conservation of volume between different sizes of vessels) ^* Formal operations - 12 - 14 yrs ^* May not be reached by all ^* Capacity to manipulate abstract ideas without reference to concrete objects ^* NOTE: contrary to Piaget's belief, formal operations may be taught ^* Emotional development ^o Freud ^* Oral ^* Anal ^* Oedipal ^* Latency ^* Adolescence ^o Greenspan's expansions ^* Self-regulation = early neonate, infancy ^* Interest in world = 2-7 mo's ^* Falling in love = social smile, mutual interest ^* Develop intentional communication = beginning to play, use behavior to demonstrate desires ^* Emergence of organized sense of self = do an action to get a response, realize they can affect world ^* Creating emotional ideas = child will begin to develop feelings; parents should guide emotions
Q17=Become familiar with the chronology of major developmental landmarks in the first six years of life, and with the concepts of "developmental quotient" and "intelligence quotient."
A17=* 2 mo's = responsive social smile ^* 3 mo's = support head; primitive vocalizations ^* 5 mo's = sit with assistance; vocalizations of increasing complexity (vowels before consonants) ^* 6-8 mo's = sit ^* 10-12 mo's = stand; scribble; first words; responds to name ^* 14 mo's = walk ^* 18 mo's = 10 meaningful words ^* 2 yrs = runs well; three-word sentences; refers to self by name ^* 3 yrs = relatively fluent language; parallel play; copies circle ^* 4 yrs = copies cross; cooperative play ^* 5 yrs = sphincter control; draws person; counts ten objects; names primary colors
Q18=Understand the meaning of italicized words in the syllabus (infancy, toddler, preschooler, school age, adolescence, psychosexual, psychosocial, de rigeur, attachment behavior, cognitive development, language development, moral development, perception and memory development, temperament, noble savages, tabula rasa, stages of development, intelligence tests, Wechsler Primary and Preschool Scale of Intelligence, Wechsler Intelligence Sclae for Children, intelligence quotient, developmental age, developmental quotient, standard scores, developmental milestones, gross motor milestones, fine motor/adaptive milestones, language milestones, personal social milestones, nine dimensions, goodness of fit, attachment, bonding, strange situation, securely attached, insecure attachment, schema, assimilation, accommodation, primary and secondary circular reactions, object permanence, preoperational stage, formal operations, Kohlberg, Piaget, Pavlov, classical conditioning, operant conditioning, and social learning).
A18=* Infancy = birth-1+ yrs; prior to acquiring symbolic language skills ^* Toddler = 1-3 yrs; rudimentary locomotor skills ^* Preschooler = 3-6 yrs; pre-school social skills ^* School age = 6-puberty (12 yrs); ends with onset of puberty ^* Adolescence = 12-18 (21) yrs; ends with early adulthood ^* Attachment behavior = actions which promote proximity between the infant and the caregiver ^* Bonding = primarily refers to the parental side of attachment, but may also be used to imply the mutual attachment of parent and child
Q19=Become familiar with characteristics of children's behavior and thinking at different stages of development.
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Q20=What is goodness of fit
A20=ability of parent and child to adapt to one another and develop a close and unambivalent bond
Q21=Know long hierarchical vs. single-source divergent systems and neurotransmitters predominant in those systems.
A21=* Long hierarchical = very fast; point to point; brain to spinal cord; glutamate and aspartate ^* Single-source divergent = cell bodies in midbrain or brainstem; project into brain with many targets per cell body; ACh, monoamines, and neuropeptides ^* Local circuit = GABA, glycine, glutamate, ACh, and neuropeptides
Q22=Know which neurotransmitters have ionotropic receptors and which have metabotropic receptors and the ion selectivities of the ionotropic receptors.
A22=* Ionotropic = glutamate, aspartate, glycine, GABA, ACh (nicotinic); coupled to ion channels; fast transmission ^o Excitatory = glutamate, aspartate, ACh; inc Na, Ca; dec K ^o Inhibitory = GABA and glycine; inc Cl (GABA also can inc Ca influx) ^* Metabotropic = glutamate, GABA, ACh (muscarinic), norepinephrine, serotonin, dopamine; slow transmission; coupled to G-proteins which affect second messengers
Q23=Know the primary mechanism of inactivation of each neurotransmitter.
A23=* GABA - reuptake  (metabolized to glutamate) ^* Monoamines - reuptake ^* Glutamate - reuptake ^* ACh - metabolism (AChE) ^* Neuropeptides - metabolism ^* Diffusion is not a main mechanism, but does occur
Q24=Know key anatomical locations of the neurotransmitters, especially the monoamines and opiate peptides.
A24=* Glutamate - cell bodies in cerebral cortex, projecting to striatum and spinal cord ^* GABA - inhibitory interneurons in local circuits and projection neurons in circuits of basal ganglia and cerebellum ^* ACh - medial septal nucleus to habenula; nucleus basalis to neocortex (TEST), motor neurons in brainstem and spinal cord, preganglionic autonomic neurons in brainstem, spinal cord, and striatum; IMPORTANT: main cell body for ACh is nucleus basalis ^* Dopamine - nigrostriatal pathway (TEST); mesocortical and mesolimbic system; tuberoinfundibular ^* NE - cell bodies in locus ceruleus and lateral tegmental system ^* HT (seretonin) - cell bodies in raphe nuclei (TEST), project rostrally to forebrain and caudally to brainstem and pinal cord ^* Opioids - hypothalamus ^o Beta-endorphin - arcuate nucleus of hypothalamus and solitary tract of medulla ^o Enkephalin - local circuits an wide projections, esp. globus pallidus ^o Dynorphins - posterior pituitary and hypothalamus
Q25=Know key functions of the neurotransmitters.
A25=* Glutamate - synaptic plasticity; learning and memory ^* GABA - local feedforward and feedback circuits, important for spatial and temporal restriction; serial GABAergic inhibitory synapses are the basis of synaptic disinhibition ^* ACh - basal forebrain: cortical activation and memory processing; thalamus: arousal and REM sleep; striatum: posture and movement; transmitter of all brainstem and spinal cord motor neurons, preganglionic autonomic neurons, and postganglionic parasympathetic pathways ^* DA - nigrostriatal: motor planning and execution; mesolimbic-mesocortical: complex target-oriented behavior, emotion-related behavior, sensory and motor processing, psychosis and drug abuse (TEST); neuroendocrine: tonic inhibition of prolactin release (TEST), increase in growth hormone release ^* NE/Epi - locus ceruleus neurons important in arousal and attention, autonomic and neuroendocrine regulation, sympathetic junctions in heart, blood vessels, and viscera; drug abuse also important ^* Serotonin - pain regulation ^o HT1 - cerebral vasoconstriction; sleep, feeding, thermoregulation, anxiety, locomotion ^o HT2 - platelet aggregation, smooth muscle contraction, vasoconstriction, vasodilation ^o HT3 - emesis behaviors, anxiety ^o HT4 - GI motility ^* Histamine - arousal mechanisms, neuroendocrine control, food and water intake, thermoregulation
Q26=Know important drugs associated with the neurotransmitters. 
A26=* GABA - alcohol, general anesthetics, benzodiazepines, barbiturates ^* ACh - nerve gases (SLUD = salivation, lacrimation, urination, diarrhea), neuromuscular blockers, nicotine, tacrine (Alzheimer's) ^* NE/Epi - amphetamines, cocaine, reserpine ^* Serotonin - tricyclic antidepressants (amitriptolene), SSRI (prozac, zoloft), fenfluramine ^o HT1 - sumatripan (agonist = anti-migraine) ^o HT2 - LSD (CNS agonist); LSD (peripheral antagonis), clozapine (antagonist) ^o HT3 - metoclopramide (antagonist = anti-emetic) ^o HT4 - metoclopramide (agonist = pro-motility agent)
Q27=Know important diseases associated with the neurotransmitters.
A27=* Glutamate - convulsive disorders and excitotoxicity; Parkinsons, Huntington's chorea, amyolaterotropic sclerosis, seizures, stroke, epilepsy ^* GABA - convulsions ^* ACh - Alzheimer's (loss of cholinergic neurons in nucleus basalis), myasthenia gravis (autoimmune vs. AChR) ^* DA - emesis and nausea as side-effect of some drugs; Parkinson's (treatments inc synaptic DA); schizophrenia; psychosis (treatments block DA receptors), addiction, hyperkinetic movements (Chorea) ^* NE - affective disorders, somnolences, depression, hypotension ^* Serotonin - affective behavior, appetite, migraine headaches, anxiety
Q28=Understand the basic structure of the peripheral nerve.
A28=* Motor unit = muscle-axon-neuron ^* Node of Ranvier = created by gaps between Schwann cell sheaths; high concentration of sodium channels; necessary for rapid, saltatory conduction ^* Peripheral nerve = contains fascicle with multiple myelinated axons; axons of different sizes travel together ^* Large axons = motor fibers or vibration and proprioception ^* Smaller axons = pain fibers; may not have myelin ^* ACh released at motor end plate ^* Classification ^o Aalpha = large; fastest; motor, some sensory ^o Adelta = moderate size; moderate speed; cold ^o C = smallest; slowest; heat
Q29=Understand the physiology of peripheral neuropathy.
A29=* Normal axon repair = transection of an axon => formation of myelin balls along axon => regeneration of the axon if endoneurium is preserved
Q30=Understand the pathology of peripheral neuropathy, including Wallerian degeneration, axonal atrophy, and segmental demyelination.
A30=* Small collateral branches may grow out from the regenerating axon, leading to complete remyelination, but with internodes being smaller than they were originally ^* Wallerian degeneration is anterograde degeneration characterized by the disappearance of axons and myelin sheaths and the secondary proliferation of Schwann cells ^* Axonal atrophy - problem is in the axon itself; secondary demyelination (i.e. secondary to axonal atrophy); common in chronic axonal injury; clusters along region of axon ^* Segmental demyelination - immune/inflammation or infilatration; loss of internodes is random; seen in acquired demyelinating neuropathies ^* Diffuse demyelination - uniform or diffuse demyelination along nerve; inherited demyelinating neuropathies
Q31=Know the essential symptoms and clinical findings of neuropathy.
A31=* Weakness ^* Reflex loss ^* Sensory loss
Q32=Understand the pathological and clinical differences between motor neuron disease and sensory or sensory/motor neuropathies.
A32=* Motor - weakness, usually distal >> proximal; if motor roots are affected, may see weakness of hip flexors ^* Sensory - peripheral sensory loss, distal > proximal, legs > arms; begins in feet ... shins ... knees & fingers ... thigh & hands; usually affects all types of fibers, but may be selective if due to drug or toxin; decreased reflexes
Q33=Understand the pathological and clinical differences between demyelinating and axonal neuropathies.
A33=* Axonal ^o Hereditary motor sensory neuropathy type II (HMSNII) - axonal or demyelinating; clinical appearance is similar, but otherwise very different; patients have pes cavux (arching of the foot), hammering of the toes; chronic, gradual weakness (esp. ankles), loss of reflexes ^o Heavy metals - arsenic (poisoning; pain followed by weakness; Mee's lines), mercury, thallium, gold (arthritis treatment; motor and sensory) ^o Metabolic causes - diabetes, hypothyroidism (carpal tunnel syndrome), acromegaly (carpal tunnel or diabetes-like peripheral neuropathy); liver/renal disease (toxin (urea) build-up; sensory loss) ^o Toxins - alcohol (progressive painful sensory neuropathy; parethesias in feet); acrylamide (sensory before motor); organophosphates (acute = AChE inhibition; chronic = progressive sensory loss); hexacarbons (glue sniffing; dose-related effects); other (carbon monoxide, carbon disulfide, ethylene oxide) ^o Medications - phenytoin (epilepsy; mild sensory); nitrofurantoin (mild sensory); dapsone (mild sensory or motor); nitrous oxide (peripheral neuropathy in dentists); colchicines (gout; cross-linking of tubulin) ^o Infectious causes - varicella zoster (dermatomal; very painful; may develop sever motor weakness); HIV (very common; mild sensory, inflammatory demyelinating, or myelopathy); Lyme disease (cranial nerve involvement, esp. VII; listen for history of tick bite, bullous target lesion, rheumatologic symptoms) ^o Inflammatory/infiltrative - important, because treatments exist; polyarteritis nodosa, systemic lupus erythematosis, rheumatoid arthritis, scleroderma, and isolated vasculitis (treat with steroids and immunosuppression, can affect multiple different nerves, may develop severe asymmetric weakness); sarcoidosis (infiltrative neuropathy; granulomas damage axons); amyloidosis (infiltrative neuropathy; possibly caused by neoplasm (multiple myeloma), chronic disease, or familial) ^o Nutritional deficiencies - thiamine and folate (non-specific sensory); post-gastrectomy syndrome and B12 deficiency (dorsal columns, and corticospinal tract, and PNS are affected; IMPORTANT: with a combination of upper and lower motor neuron findings, think B12 deficiency) ^o Neoplastic - multiple myeloma (amyloidosis, Ab depositing in PNS leading to axonal or myelin damage); paraneoplastic disease (Ab against cancer also attacks PNS; loss of proprioception and vibratory sense) ^* Demyelinating ^o Acquired inflammatory demyelinating neuropathy (AIDP; aka Guillain-Barre syndrome) - history of severe flu-like symptoms two weeks ago; abnormal CSF (high protein without cells); severe weakness distally and proximally (rapid progression from legs to arms), loss of reflexes, possibly sensory loss; treatment with steroids, IV Ig, or plasma exchange ^o Chronic inflammatory demyelinating neuropathy (CIDP) - gradual onset over 4 weeks; symmetric pattern, affect large fibers (motor and large sensory); distal and proximal weakness with a loss of relfexes ^o Inherited neuropathies (e.g. HMSNI) - thin legs, pes cavus; myelin more severely damaged than with axonal form; rapid progression
Q34=Understand the principles of distinguishing between specific types of neuropathy.
A34= 
Q35=What are the neurological features of polio?
A35=degeneration of lower motor units (nerves and anterior horn cells); decreased weakness in limbs; possible fasciculations
Q36=What are the neurological features of amyotrophic lateral sclerosis
A36=(ALS; aka Lou Gehrig's disease) anterior horn cells and corticospinal tract damage; upper and lower motor neurons are affected; brain rarely involved; cognition and sensory exam normal; increased reflexes
Q37=Understand common symptoms and signs of myopathy.
A37=* Weakness that is symmetric and proximal ^* Painless or only mild tenderness (exception is metabolic myopathy, which has exertional pain) ^* Bulk and sensation normal ^* Reflexes normal or only mildly decreased
Q38=Understand classic findings in congenital, inflammatory, metabolic, toxic, and mitochondrial myopathies, myotonic dystrophy, and muscular dystrophy, as well as the differences between these disorders.
A38=* Congenital - static, benign to severe, possibly dysmorphic ^* Myotonic dystrophy - NOTE: most common adult muscular dystrophy; myotonia present on EMG, but doesn't interfere with activity; may also have cataracts, diabetes, cardiac conduction abnormalities, testicular atrophy; UTR trinucleotide repeat ^* Inflammatory - polymyositis (autoimmune, lymphocytes invade muscle, steroid responsive); dermatomyositis (similar to polymyositis, with vascular involvement, skin changes, steroid responsive, possible malignancy association); inclusion body myositis (inclusions seen on biopsy, weakness is distinct {quadriceps, wrist flexors, finger flexors}, IMPORTANT: not steroid responsive and is most common; cause unknown) ^* Metabolic myopathy - defective glycogen and lipid metabolism; IMPORTANT: presents with muscle pain, which is uncommon ^* Mitochondrial myopathy - energy crisis; maternal inheritance; associated with opthalmoplegia, encephalopathy, cardiac conduction defects, and retinopathy
Q39=Know the defect in Duchene muscular dystrophy and Becker muscular dystrophy.
A39=* Duchene - X-linked, absence of dystrophin ^* Becker - X-linked, reduction in dystrophin
Q40=Know the classic histologic findings of mitochondrial myopathy.
A40=* Clumped mitochondria or abnormal inclusions on biopsy ^* Ragged red fibers = clumped mitochondria ^* Fat build-up in muscle
Q41=Understand the utility of EMG testing to confirm or exclude the diagnosis of myopathy.
A41=* Spontaneous firing - disruption of neuromuscular junction; damage to inflammation (separates nerve from muscle) or damage to nerve or muscle ^* Lower electrical signal - muscle fiber atrophy ^* Constant electrical activity - myotonic dystrophy ^* Abnormal electrical activity with contraction ^o Smaller, shorter signal - fewer normal muscle fibers ^o Increased number of signals - more electrical activity required because each damaged muscle fiber produces less energy
Q42=Know appropriate initial evaluation of suspected myopathy.
A42=* EMG ^* CK - looks for systemic illness ^* Biopsy ^* Exercise testing ^* Urine myoglobin ^* Genetic testing
Q43=Understand currently available, commonly used symptomatic and disease-modifying treatments.
A43=* Inflammatory myopathy - steroids or other immune modulators ^* Myotonia - channel-active meds to improve relaxation ^* Muscle weakness - supportive braces or assistive devices ^* Metabolic myopathies - vitamins, cofactors (e.g. carnitine) ^* Myoglobinuria - forced diuresis to reduce kidney damage ^* Myopathy associated with hypo/hyper-thyroidism, hypercortisolism, or toxin - fix underlying problem
Q44=Recognize common associated conditions/illnesses.
A44=* Rhabdomyolysis - can be caused by medications, crush, over-activity, ischemia; check urine for myoglobin; forced diuresis, alkalinize urine
Q45=Recognize important differences in the inflammatory myopathies.
A45=* Polymyositis - steroid responsive; autoimmune; lymphocytes invade muscle ^* Dermatomyositis - steroid responsive; autoimmune; lymphocytes invade muscle; assoc with malignancy, skin changes, vascular involvement ^* Inclusion body myositis - not steroid responsive; distinct weakness pattern affecting quadriceps, wrist and finger flexors
Q46=Identify the general anatomy of the neuromuscular junction: presynaptic nerve terminal, synaptic cleft, and post-synaptic termination of nerve branches on single muscle fibers.
A46= 
Q47=Describe the neurophysiology of neuromuscular transmission: spontantious release of acetylcholine (ACh); miniature end-plate potentials (MEPPs); synchronous release of ACh triggered by the nerve action potential; generation of the end-plate potential (EPP); interaction of ACh with acetylcholine receptors (AChRs) on the muscle fiber; and resultant muscle fiber action potential when EPP exceeds threshold.
A47=* Spontaneous release of single quanta of ACh triggers miniature end-plate potentials when the ACh reaches the muscle postsynaptic membrane ^* Nerve action potential triggers a calcium-dependent synchronous release of ACh ^* ACh diffuses across the synaptic cleft and binds to the AChR on the muscle fiber, increasing the permeability of the membrane to Na+ and K+ ^* Na currents produce a graded end-plate potential (EPP) ^* When an EPP is produced above threshold, there is a muscle fiber action potential (MFAP), resulting in muscle contraction
Q48=Recognize symptoms, signs, and physiologic abnormalities of well-known neuromuscular disorders:  myasthenia gravis (MG) and Lambert-Eaton myasthenic syndrome (LEMS).
A48=* Myasthenia gravis - Ab against AChR lead to AChR degredation on the muscle fiber and "flattens" the junctional folds, thereby allowing ACh to diffuse away; ineffective AChR lead to decreased EPP's; end result is lack of ACh signaling and weakness; repetitive stimulation in MG leads to progressive decline in response; no MEPPs, because no receptors to detect ACh ^* Lambert-Eaton myasthenic syndrome (LEMS) - Ab to calcium channels impair ACh release; decreased ACh release decreases the EPP; ACh release improved with continued calcium-dependent release of ACh
Q49=What are important features of myasthenia gravis?
A49=o Predilection for cranial (esp. ocular and bulbar) and proximal limb muscles ^o Varying severity; remission possible ^o AChE inhibitors reverse weakness ^o No evidence for denervation (e.g. no decrease in reflexes) ^o Treat by removing thymus, therapeutic plasma exchange, and immunosuppression ^o Associated with thymoma
Q50=What are important features of Lambert-Eaton myasthenic syndrome?
A50=o Associated with small cell carcinoma ^o Affects large proximal muscles ^o Typically male and over 40 ^o Impotence ^o Distal paresthesias ^o Treat by removing small cell carcinoma, therapeutic plasma exchange, and immunosuppression
Q51=Identify the structural components of peripheral nerves and know their roles in nerve regeneration and repair.
A51=* Connective tissue - 20-60% of nerve; strength and resilience; important for regeneration ^* Endoneurium - little structural support; surrounds individual nerve fibers (i.e. axon and Schwann cell); forms basal lamina for Schwann cell; few layers of collagen; IMPORTANT: director of axonal regeneration ^* Perineurium - surrounds bundles of nerve fibers (fascicles; 4-10 fascicles/nerve); site of blood-nerve barrier; several layers of collagen, fibroblasts, capillaries (tight junctions); fascicles branch extensively within nerve - intraneural plexus; proximal, fascicle contents are heterogeneous, while distal fascicles contain closely related fibers ^* Epineurium - peripheral (outer; thick, superficial collagen layer; primary structural element of nerve) and interfascicular (inner; packing material; contains blood vessels; preferred site of suturing); provides structural support ^* Mesoneurium - loose connective tissue surrounding nerve; contains arcades of blood vessels; nerve not dependent on blood vessels entering nerve perpendicularly, because of vessels in intraneural plexus ^* Blood supply - arcades in mesoneurium; longitudinal vessels in epineurium; capillaries within fascicles
Q52=Discuss the three grades of nerve injury.
A52=* Neurapraxia - mildest; loss of function without loss of continuity; no physical change to axon or connective tissue; possible focal demyelination or membrane changes leading to conduction blockade; complete and rapid recovery within 3-4 months; motor loss more severe than sensory loss ^* Axonotmesis - continuity lost; myelin sheath damaged; endoneurial sheath preserved, therefore regeneration possible; distal axonal degeneration = Wallerian degeneration; regeneration proceeds down endoneurial guide tube to original terminus; recovery occurs proximally to distally ^* Neurotmesis - stretching is most common civilian injury; complete loss of nerve continuity by division or internal disruption; complete, permanent loss of function; surgical repair required for recovery
Q53=Understand the processes of nerve injury and repair, including Wallerian degeneration, axonal sprouting, and axon growth.
A53=* Degeneration and regeneration occur simultaneously ^* Wallerian degeneration - active process, not just cell death; occurs distal to injury and requires axonal death; axon and myelin sheath break down; particles ingested by Schwann cells and macrophages; degeneration takes 3-5 days, nerve stimulable until then; at 8 weeks, endoneurial tube only filled with Schwann cells ^* Central cell response - the nucleus immediately moves to the cell periphery; Nissl's substance decreases; in 2-3 weeks, see and increased production of RNA, proteins, lipids and decreased neurotransmitter production; increased transport ^* Proximal axon - degenerates back 2-3 mm; axons develop sprouts; Schwann cells proliferate; axons advance 1 mm/day or 1 inch/month
Q54=Identify the factors enhancing and directing axonal growth.
A54=* Most influenced by condition of endoneurial sheath ^* Axon sprouts have many filopodia (growth cones) which adhere selectively to the basal lamina of Schwann cells (fibronectin and laminin), which enables contact guidance to pull the growth cone forward
Q55=Discuss the pathophysiology of chronic nerve entrapment and identify some common entrapment syndromes.
A55=* Occurs when the endoneurial sheath is disrupted ^* Axonal confusion - motor axon to sensory target or sensory nerve to motor target ^* Lateral neuromas - axons get tangled on the side of a nerve ^* End bulb neuroma - axons get tangled on the end of a nerve
Q56=Discuss the evaluation and treatment of a nerve injury, from either laceration or stretch.
A56=* Evaluation - test motor and sensory functions; each nerve innervates a specific group of muscles or a specific sensory area; rule out nerve injury by testing most distal muscle supplied by nerve ^* Emergency exploration - worsening neurological deficit; should be worst at time of presentation and get better or stabilize with most injuries; example = false aneurysm, AV fistula, hematomas ^* Treatment ^o Localize lesion ^o Open or closed ^* Open and sharp - early repair ^* Open and jagged - wait for demarcation ^* Missile wounds - treat as closed; nerve usually intact ^* Closed - typically stretch or compression, most often at brachial plexus; may spontaneously recover or be a severe internal injury; wait three months to rule out neurapraxia; look at muscle innervated distal to site of injury; without recovery at 3-4 months, explore nerve ^* Exploration - physical appearance of little use; use nerve stimulator to assess nerve action potential
Q57=What are prognostic factors when dealing with nerve damage?
A57=age, location, nerve type (pure better prognosis than mixed)
Q58=Why is an 18 month limit important when dealing with nerve damage patients?
A58=Without recovery at 12-18 months, too much atrophy to regain use
Q59=How many axons are required for recovery in nerve damage?
A59=Require a minimum of 5,000 axons for recovery
Q60=Why is recovery with the radial nerve better than with most nerves?
A60=* Radial nerve is almost pure motor
Q61=Which nerve is used for grafting?
A61=Sural nerve used for grafting
Q62=Know histology and fiber types of the skeletal muscle.
A62=* Sarcoplasm with myofibrils, sarcomeres, actin and myosin, Z bands, T-tubules; (Z-actin-myosin-myosin-actin-Z) ^* Each motor unit (lower motor neuron in anterior horn of spinal cord, axon of that neuron, and muscle fibers it innervates) contains fibers of the same type ^* Endomysium (smallest), perimysium, epimysium ^* Fiber types ^o Type I - governed by type I neurons; sustained activities; deltoid and soleus; more mitochondria (consequently stain more darkly) ^o Type II - govered by type II neurons; quick, short activities; lots in eyelids; less mitochondria (consequently stain more lightly)
Q63=Know and understand the difference between the pathology of the myopathic and neurogenic process.
A63=* Myopathic reactions ^o Segmental necrosis, myophagocytosis ^o Regeneration ^o Vacuolization ^o Hypertrophy, fiber splitting ^o "myopathic" atrophy; type II atrophy ^o Variation of fiber shape - round, not polygonal
Q64=Understand the concept and know general features of major categories of muscle disorders, such as inflammatory myopathies, muscular dystrophies, denervation atrophy, congenital myopathies, and metabolic disorders.
A64=* Denervation atrophy - ALS, spinal muscle atrophy; nuclei are pyknotic and shrunken ^* Muscular dystrophy ^o X-linked - Duchenne's (absence of dystrophin; increased amounts of connective tissue; pseudohypertrophy of gastroc), Becker's (low levels of dystrophin; less severe; later onset) ^o Autosomal - myotonic (internalized nuclei); named by muscle groups affected (e.g. occulopharyngeal, facioscapulohumeral, limb-girdle); most have atrophy and hypertrophy of affected muscle fibers with fat and connective tissue replacing muscle ^* Congenital myopathies ^o Central core disease - large central cores in type I fibers; predisposed to malignant hyperthermia ^o Nemaline rod myopathy - red rod inclusions with trichrome; "wood chips" are alpha-actinin clumps interrupting muscle fibers ^o Centronuclear myopathy - only one diagnosed by EMG; small diameter muscle fibers with centrally located nuclei ^* Metabolic myopathies - vacuoles may replace muscle fibers; vacuoles contain storage material ^* Mitochondrial myopathies - ragged red myopathies; large, irregularly shaped mitochondria stain red; parking lot inclusions by EM; can be seen in any cell with mitochondria ^* Drug-induced myopathies - also produce vacuoles, but vacuoles are empty ^* Inflammatory myopathies - polymyositis (invading inflammatory cells; treat with steroids); dermatomyositis (little inflammation in muscle; a lot of necrosis in capillaries, which leads to muscle ischemia; occult malignancy in adults); inclusion body myositis (IMPORTANT: not treated with steroids, because they could cause a steroid myopathy; only seen on frozen section; vacuoles are present with inclusions)
Q65=Understand the concept of end-stage muscle condition.
A65=* No muscle fibers left; replaced with fat ^* Any disorder can proceed to this stage ^* No point in biopsy, little information obtained and not worth pain
Q66=Recognize features of major pathologic changes in peripheral nerve such as axonal degeneration/regeneration and demyelination/remyelination.
A66= 
Q67=Understand the value of various special methods in interpretation of nerve and muscle biopsies.
A67=* Plastic sections are much better for assessing myelination, Wallerian degeneration, can classify as "likely demyelinating" or "likely remyelinating" ^* EM - allows visualization of unmyelinated axons and determine condition of Schwann cells (myelinated axon = 1 Schwann cell/axon; unmyelinated axon = many axons/Schwann cell) ^* Sural nerve can be easily biopsied, but it is only a sensory nerve ^* Frozen section necessary to visualize inclusion bodies in inclusion body myositis
Q68=Know general pathologic features of most frequent peripheral neuropathies.
A68=* Axonal degeneration - Wallerian ^* Axonal regeneration ^* Segmental demyelination ^* Inflammatory ^o AIDP or Guillian-Barre syndrome; mononuclear inflammation, segmental demyelination, axonal damage, and remyelination ^o CIDP - onion bulbs form (Schwann cell cytoplasm and collagen); occurs with repeated bouts of demyelination/remyelination ^o Vasculitis - rule out with any peripheral neuropathy, because can be treated; PAN (systemic or isolated, traumatic neuroma, rarely regenerates) ^* Hereditary neuropathies - HMSN I, II, III; can be purely myelin or purely axonal ^* Metabolic neuropathies - amyloidosis (amyloid within nerve fascicle; liver transplant by 45); diabetes type I (20 year old nerve almost devoid of axons); diabetes type II affects neurons less than type I ^* Toxic neuropathies - arsenic, mercury, gold, thallium
Q69=Name the four components common to all levels of the brainstem.
A69= 
Q70=Know the general principles related to the cranial nerves and their connections.
A70= 
Q71=Describe the longitudinal organization of the cranial nerve nuclei and know the name, functional component, and connections of the nuclei associated with cranial nerves XII, XI, X, VII, VI, and III.
A71= 
Q72=Diagram and label the important nuclear groups and fiber tracts found within the four cross sectional levels of the brainstem discusses in class.
A72= 
Q73=Describe the blood supply to the medulla, pons, and midbrain.
A73= 
Q74=Be able to locate a brainstem lesion given a set of clinical signs.
A74= 
Q75=Be able to list the clinical signs that would result from a specific brain lesion.
A75= 
Q76=Describe Freud's topographical model of the mind and structural model of the psychic apparatus.
A76=* Conscious - thoughts and feelings within awareness ^* Preconscious - thoughts, feelings, and memories available to consciousness when attention is focused on them ^* Unconscious - instinctual drives and wishes seeking fulfillment
Q77=Compare Freud's stages of psychosexual development with Erikson's psychosocial stages of the life cycle.
A77=* Frued (psychosexual stages) ^o Oral - birth-18 mo's; individual seeks love and nurturing; develops trust ^o Anal - 18 mo's-3 yrs; autonomy and self-control ^o Phallic - 3-5 yrs; sexual identity foundation is laid; superego and internal resources for drive regulation are formed ^o Latency - 5-11 yrs; strengthen gender identity ^o Genital - 11 yrs-adulthood; intense sex drive; reworking of prior conflicts; development of mature sense of personal identity and acceptance of adult roles ^* Erikson (psychosocial stages) ^* Comparison ^o Trust vs mistrust <=> oral ^o Autonomy vs. shame and doubt <=> anal ^o Initiative vs. guilt <=> phallic ^o Industry vs. inferiority <=> latency ^o Identity vs. role diffusion <=> genital
Q78=Describe the key concept of, and major contributors to each of the major psychodynamic theories.
A78=* Analytical psychology - Carl Jung (collective consciousness; archetypes = concepts brain is preprogrammed to use) ^* Object relations - Melanie Klein (mother-object), John Bowlby (parent-child relationships; attachment and separation) ^* Interpersonal therapy - Harry Stack Sullivan (interpersonal forces; continue to adulthood) ^* Self psychology - Heinz Kohut (sense of self through empathic interactions; failure leads to narcissisitic disorders) ^* Humanistic psychology - Carl Rogers (self-actualization; therapists should maintain unconditional positive regard) ^* Psychosocial development - Erik Erikson (psychological development continued throughout life in a series of predictable life crises)
Q79=Define defense mechanism and describe the common defense mechanisms and identify examples of each.
A79=* Defense mechanisms = Unconscious psychological process that protects the individual against awareness of internal drives or conflicts, and external stressors or dangers ^* Highly adaptive (mature) defenses ^o Altruism - gratification through vicarious experience (e.g. grieving parent forms support group) ^o Humor - unpleasant feelings enter consciousness and are expressed in a way to minimize discomfort (e.g. anxious speaker begins talk with a joke) ^o Sublimation - drives are channeled into socially-acceptable acts (e.g. aggressive person plays football) ^o Suppression - conscious decision to postpone or avoid unpleasant subjects (e.g. enjoy spring break and ignore upcoming exams) ^* Less adaptive defenses ("neurotic" no longer used) ^o Displacement - unacceptable impulses transferred to a safer object (e.g. a resident who was humiliated by an attending criticizes a medical student) ^o Intellectualization - unpleasant feelings are avoided by taking refuge in a conscious thought process (e.g. a doctor gets a bad lab results and then analyses procedure to determine if it is accurate) ^o Isolation of affect - distressing feelings are removed from thoughts of an unpleasant event or impulse (separates thoughts from feelings; rarely works; post-traumatic stress syndrome; e.g. a bland description of combat by a soldier) ^o Rationalization - rational explanations are given for unacceptable motives or behaviors (e.g. ruthless tycoon explains that greed is good for the economy) ^o Reaction formation - unacceptable thought or impulse is transformed into its opposite (e.g. adulterous minister preaches vehemently against infidelity) ^o Repression - unpleasant memories are removed from consciousness (e.g. overworked medical resident recalls medical school as relaxing and stress-free) ^* Primitive (immature) defenses ^o Acting out - impulsive action based on an unconscious wish or drive (e.g. young woman cuts her wrists immediately after a fight with her boyfriend) ^o Denial - an unconscious decision to remove current unpleasant material from awareness (e.g. cardiac patient repeatedly forgets to take medication; "I never thought of that", "I keep forgetting" ^o Projection - unacceptable impulses or drives toward another person are attributed to that person (e.g. married business manager is convinced that an subordinate has a crush on her) ^o Splitting - other people are split into "all good" and "all bad" categories (e.g. after becoming involved with "the most wonderful man in the world", a woman decides he is a "total creep.")
Q80=Define and describe the significance of transference and countertransference.
A80=* Transference - feelings of the patient toward the therapist, especially important previous relationships (occurs in all relationships, but is used therapeutically in psychodynamic psychotherapy) ^* Countertransference - feelings of the therapist toward the patient (occurs in all relationships) ^* Interpretation - therapist identifies feelings, drives, and defenses in action ^* Therapist tends to be more passive; longer term therapy
Q81=Define and contrast the major schools of psychotherapy: psychodynamic, cognitive/behavioral, and supportive.
A81=* Psychodynamic psychotherapy - goal is to uncover, identify, and modify drives and defenses; develop and work through transference and countertransference ^* Cognitive and behavioral - based on learning theory; thoughts and actions are focus of treatment; time-limited; good for depression and anxiety; behavior modification and exposure therapy ^* Supportive - enhance and support existing defenses and adaptive behaviors
Q82=Distinguish "psychosomatic" from "hypocondriasis."
A82=* Psychosomatic - unity of mind and body ^* Hypochondriasis - delusion that one is suffering from a disease
Q83=Understand the concept of stress as it has evolved.
A83=* Initially defined as a reponse to uncontrolled adversity have physiological consequences of enlarged adrenal glands, atrophied lymphatic organs, and stomach and duodenal ulcers. ^* Subsequently defined as an event that increases cortisol secretion, activates the sympathetic nervous system, and increases the production of adrenal epinephrine.
Q84=Be able to explain to a layperson the basic features of stress-response.
A84=* The body produces a hormone when stressed to prepare for fight or flight.  The production of this hormone leads to heightened senses, but also leads to long term consequences in the chronic state. 
Q85=Understand the practical, neurobiological differences between acute and chronic forms of stress.
A85=* Acute - increases in cortisol releasing hormone leads to an increase in cortisol and norepinephrine ^* Chronic - cortisol and norepinephrine are high due to sensitization and feedback resistance, so adaptation to chronic stress may occur (body can't shut off cortisol and catecholamines)
Q86=Be able to apply knowledge about the interplay between the HPA axis and various forms of stress to common situations.
A86=* Psychological stress responses activate the hypothalamus-pituitary-adrenal (HPA) axis, resulting in enhanced peripheral release of ACTH and corticosterone ^* Adrenalectomy and sympatholytic drugs can minimize the damaging effects of chronic stress ^* The HPA stress response pathway can be stimulated by infusion of glucocorticoids ^* Chronic stress can lead to atrophy of the hippocampus, which is important in memory, anxiety, learning, stress control, and cognition
Q87=Be able to answer:  Does stress damage the brain?
A87=* Stress can lead to decreased expression of serotonin receptors, increased amounts of acetylcholine esterase, and decreased dendritic spine branching.
Q88=Be able to answer:  Is clinical depression a risk factor for death?
A88=* Depression has a relative risk for death of 1.2-2.7.  So, depression is a risk factor for death, especially for coronary disease.
Q89=Be able to answer:  Does stress "cause" the common cold and/or ulcers?
A89=* Stress does not cause the common cold, but it can contribute to the body succumbing to it.  Stress can cause ulcers by stimulating the increased secretion of hormones.
Q90=Know the general role the cerebellum plays in motor activity and its suggested roles in cognitive functions.
A90=* Coordinate goad-directed and spontaneous movements ^* Regulate posture and vestibular function ^* Involved in learning complex motor skills ^* Suggested role in learning verbal tasks
Q91=Know the gross anatomy of the cerebellum and relate the anatomical subdivisions to the functional subdivisions.
A91=* Anterior lobe ^* Posterior lobe ^* Floculonodular lobe - vestibulocerebellum ^* Vermis (midline) - part of spinocerebellum ^* Hemispheres (lateral; medial and lateral zones) - medial forms part of spinocerebellum ^* Vestibulocerebellum (floculonodular lobe) ^o inputs = afferent fibers from vestibular nuclei and nerves; enter through inferior cerebellar peduncles ^o outputs = Purkinje cell axons exit through inferior cerebellar peduncles and synapse onto neurons in the vestibular nuclei ^o function = regulates balance and posture and is involved in the control of eye movements; oldest part of cerebellum ^* Spinocerebellum (vermis and adjacent intermediate/medial zone) ^o inputs = spinal cord ^* Dorsal spinocerebellar tract = nucleus dorsalis of Clarke at C8-L2; enters cerebellum through the inferior peduncle ^* Cuneocerebellar tract = accessory cuneate nucleus at C7 and above; enters cerebellum through the inferior peduncle ^* Ventral spinocerebellar tract = lateral ventral horn region of lumbar spinal cord; enters cerebellum through superior peduncle ^o Outputs ^* Vermis = Purkinje cells within vermis synapse in the ipsilateral fastigial nucleus, sending axons bilaterally to the vestibular nuclei and brainstem reticular formation ^* Intermediate/medial zone = Purkinje cells in medial zone synapse in ipsilateral interposed nucleus, sending axons through the superior peduncle to synapse primarily in the contralateral red nucleus, with a minor component entering the contralateral ventrolateral complex of the thalamus.  Axons leaving the red nucleus, cross the midline, and form the descending rubrospinal tract ^o Function = proprioceptive inputs; regulation of axial musculature via vermis and fastigial nuclear connections and proximal limb musculature via the intermediate/medial zone and interposed nuclear connections ^* Cerebrocerebellum (lateral zone) ^o Inputs = axons from deep pontine nuclei of brainstem cross the midline and enter the contralateral cerebellar hemisphere through the midcerebellar peduncles ^o Outputs = Purkinje cells in the lateral zone project to the ipsilateral dentate nucleus, which sends axons through the superior peduncle, across the midline (caudal midbrain level) in the decussation of the superior cerebellar peduncle, to synapse in the contralateral ventrolateral complex of the thalamus.  Axons leaving the thalamus synapse in the motor and pre-motor coretex, which is the origin of the pontocerebellar pathway ^o Function = motor planning, regulation of fine movements of distal limb musculature originating at the level of the cortex
Q92=Know the names of the three, paired cerebellar peduncles, and the source and modality of the fibers contained therein.
A92=* Peduncles attach cerebellum to pons ^* Peduncles are paired across the midline ^* Inferior cerebellar peduncle - transmits axons from fastigial deep cerebellar nucleus ^* Middle cerebellar peduncle ^* Superior cerebellar peduncle - transmits axons from interposed and dentate deep cerebellar nuclei
Q93=Know the essential circuitry of the cerebellar cortex.
A93=* Granule cells - small; axonal fiber parallel to surface synapse with Purkinje cell dendrites in molecular layer ^* Purkinje cells - large; sole output of cerebellar cortex ^* Three types of interneurons ^o Stellate cells ^o Basket cells ^o Golgi cells
Q94=Know how the cerebellar cortex relates to the deep cerebellar white matter and the deep cerebellar nuclei.
A94=* Cortex - three layers: molecular, Purkinje cell, and granule cell (superficial to deep) ^* White matter - axons ^* Deep cerebellar nuclei - fastigial, interposed, and dentate (medial to lateral); receive inputs from Purkinje cells and send axons out of the cerebellum through the inferior cerebellar peduncle (fastigial nucleus) or superior cerebellar peduncle (interposed and dentate nuclei)
Q95=Know the afferent and efferent connections of the cerebellum.
A95=* Mossy fibers - widely distributed origins in CNS; synapse with granule cells ^* Climbing fibers - origin in inferior olivary nucleus; synapse with Purkinje cells
Q96=Know the neurotransmitter used by the major fiber inputs and outputs of the cerebellum
A96=* Input - generally excitatory ^* Output - Purkinje, inhibitory = GABA
Q97=Know the role of the cerebellum in motor learning.
A97=* Ability to modify function in relation to experience is called motor plasticity or motor learning ^* Motor acts involved progress from being conscious to unconscious
Q98=Know the source of blood supply to the cerebellum.
A98=* Anterior and posterior inferior cerebellar arteries ^* Superior cerebellar artery
Q99=Know the signs of a lesion in the cerebellum.
A99=* Unlike cerebrum, cerebellar motor and sensory representations are located ipsilateral ^* Cerebellar lesions result in errors in the direction, force, speed, and amplitude of movements ^* Loss of the ability to perform rapid alternating movements
Q100=How do the spinocerebellum and cerebrocerebellum combine their functions?
A100=They cooperate to compare the motor plan (intention) with motor performance (what was achieved) and act to adjust the motor plan
Q101=Be familiar with the major components of the cerebellum.
A101= 
Q102=Understand the principles of localization of cerebellar disorders.
A102= 
Q103=Know the major connections of the cerebellar cortex with the deep cerebellar nuclei and brainstem.
A103= 
Q104=Understand the afferent and efferent connections of the cerebellum with the spinal cord, thalamus, and cerebral cortex.
A104= 
Q105=Comprehend the clinical significance of the anatomical connections of the cerebellum to the spinal cord, brainstem, thalamus, and cerebral cortex.
A105= 
Q106=Know the major neuronal structures within the medulla, pons, and mesencephalon, including nuclear groups, long ascending pathways, and long descending pathways.
A106= 
Q107=Understand the clinical effects of lesions localized to the major components of the brainstem.
A107= 
Q108=List the anatomical limits of the diencephalon and name its major components.
A108= 
Q109=Understand the diencephalon and the cerebral hemispheres in relationship to the development of the corpus callosum, the roof of the third ventricle, and its choroid plexus and the transverse cerebral fissure.
A109= 
Q110=Describe the blood supply to the diencephalon.
A110= 
Q111=Describe the anatomical organization of the dorsal thalamus.
A111= 
Q112=Describe the connections of the dorsal thalamus and the principles they reflect.
A112= 
Q113=Describe the organization of thalamic projections within the internal capsule.
A113= #