Step 1 First Aid – Neurology

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CNS/PNS origins: Neuroectoderm (gives rise to what?)
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CNS neurons Ependymal cells (inner lining of ventricles, make CSF) Oligodendrocytes Astrocytes
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CNS/PNS origins: Neural Crest (gives rise to what?)
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Schwann cells PNS neurons
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CNS/PNS origins: Mesoderm (gives rise to what?)
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M icroglia, like M acrophages, originate from M esoderm
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Neurons
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Comprise nervous system. Permanent cells — do not divide in adulthood. Large cells w/ prominent nucleoli.
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Nissl substance
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RER found in cell body and dendrites, but not axon of neurons.
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Astrocytes
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Physical support, repair, K+ metabolism, removal of excess NT. Maintenance of BBB. Reactive gliosis in response to injury.
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Astrocyte marker?
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GFAP
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Microglia
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CNS phagocytes. Mesodermal origin. Not readily discernible in Nissle stains. Have small, irregular nuclei and relatively little cytoplasm.
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What happens to microglia in the presence of tissue damage?
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Microglia –(tissue damage)–< large ameboid phagocytic cells
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What happens to HIV-infected microglia?
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HIV-infected microglia fuse to form multinucleated giant cells in the CNS
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Oligodendria
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Each oligodendrocyte myelinates multiple CNS axons (up to 30 each). In Nissle stains, they appear as small nuclei with dark chromatin and little cytoplasm.
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What is the predominant type of glial cell in white matter?
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Oligodendrocytes.
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What cells are destroyed in multiple sclerosis?
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Oligodendrocytes.
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What do oligodendrocytes look like on H&E?
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“Fried Eggs”
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Schwann cells
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Each Schwann cell myelinates only 1 PNS axon. Also promote axonal regeneration. Derived from neural crest.
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What are the cells that are destroyed in Guillain-Barré syndrome?
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Schwann cells.
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An acoustic neuroma is a type of…? Where is it located?
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Acoustic neuroma is a type of Schwannoma. It is typically located in internal acoustic meatus (CN VIII)
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Sensory receptors/corpuscles: Free nerve endings (C, A-delta fibers) Location? Senses?
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In all skin, epidermis, some viscera. Senses pain and temperature.
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Sensory receptors/corpuscles (location and senses): In all skin, epidermis, some viscera. Senses pain and temperature. Which is this?
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Free nerve endings (C, A-delta fibers)
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Sensory receptors/corpuscles: Meissner’s corpuscles Location? Senses?
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In glabrous (hairless) skin. Senses dynamic fine touch (e.g., manipulation), adapt quickly.
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Sensory receptors/corpuscles (location and senses): In glabrous (hairless) skin. Senses dynamic fine touch (e.g., manipulation), adapt quickly. Which is this?
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Meissner’s corpuscles
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Sensory receptors/corpuscles: Pacinian corpuscles Location? Senses?
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In deep skin layers, ligaments, and joints. Sense vibration, pressure.
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Sensory receptors/corpuscles (location and senses): In deep skin layers, ligaments, and joints. Sense vibration, pressure. Which is this?
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Pacinian corpuscles
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Sensory receptors/corpuscles: Merkel’s disks Location? Senses?
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(cup-shaped, unencapsulated) In hair follicles. Sense static touch (e.g., shapes, edges, textures), adapt slowly.
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Sensory receptors/corpuscles (location and senses): (cup-shaped, unencapsulated) In hair follicles. Sense static touch (e.g., shapes, edges, textures), adapt slowly. Which is this?
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Merkel’s disks
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Peripheral nerve layers: Endoneurium
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Invests a single nerve fiber (Endo = inner)
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Peripheral nerve layers: Perineurium
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(P erineurium is the P ermeability barrier) Surrounds a fascicle of nerve fibers. (Peri = around) Must be rejoined in microsurgery for limb reattachment.
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Peripheral nerve layers: Epineurium
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Dense connective tissue that surrounds entire nerve (fasicles and blood vessels) (Epi = outer)
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Neurotransmitters: NE Change in dz? Location of synthesis?
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Increased in anxiety, decreased in depression. Made in the locus ceruleus.
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Increased in anxiety, decreased in depression. Made in the locus ceruleus. What NT is this?
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NE
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Neurotransmitters: Dopamine Change in dz? Location of synthesis?
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Increased in schizophrenia, decreased in Parkinson’s. Made in the ventral tegmentum and SNc
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Increased in schizophrenia, decreased in Parkinson’s. Made in the ventral tegmentum and SNc What NT is this?
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Dopamine
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Neurotransmitters: 5-HT Change in dz? Location of synthesis?
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Decreased in anxiety, depression. Made in the raphe nucleus
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Decreased in anxiety, depression. Made in the raphe nucleus What NT is this?
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5-HT
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Neurotransmitters: ACh Change in dz? Location of synthesis?
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Decreased in Alzheimer’s, Huntington’s. Made in the basal nucleus of Meynert.
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Decreased in Alzheimer’s, Huntington’s. Made in the basal nucleus of Meynert. What NT is this?
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ACh
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What 3 structures form the blood-brain barrier (BBB)?
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1.) Tight junctions btw nonfenestrated capillary endothelial cells 2.) Basement membrane 3.) Astrocyte processes
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Besides the BBB, what are 2 similar barriers?
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1.) Blood-testis barrier 2.) Maternal-fetal blood barrier of placenta
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What happens at the BBB w/ infarction?
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Infarction destroys endothelial cell tight junctions, leading to vasogenic edema
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Glucose and amino acids at the BBB
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Cross slowly by carrier-mediated transport mechanism.
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Nonpolar/lipid-soluble substances at the BBB
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Cross rapidly via diffusion.
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Specialized brain regions w/ fenestrated capillaries and no BBB
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Allow molecules in the blood to affect brain function (e.g., area postrema – vomiting center after chemo, OVLT – osmotic sensing) or neurosecretory products to enter circulation (e.g., neurohypophysis – ADH release)
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Hypothalamus functions
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The hypothalamus wears TAN HATS : T hirst and water balance A denohypophysis control N eurohypophysis releases hormones from hypothalamus H unger A utonomic regulation T emperature regulation S exual urges
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Inputs to the hypothalamus
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OVLT (senses change in osmolarity) Area postrema (responds to emetics)
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Supraoptic nucleus of the hypothalamus
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Area that makes ADH.
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Area that makes ADH.
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Supraoptic nucleus of the hypothalamus
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Paraventricular nucleus of the hypothalamus
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Area that makes oxytocin.
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Area that makes oxytocin.
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Paraventricular nucleus of the hypothalamus
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Lateral area of the hypothalamus
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Controls hunger: destruction leads to anorexia. (“If you zap the lateral nucleus, you shrink laterally “) Inhibited by leptin.
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Ventromedial area of the hypothalamus
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Controls satiety: destruction leads to hyperphagia. (“If you zap your ventromedial nucleus, you grow ventrally and medially .”) Stimulated by leptin.
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Anterior hypothalamus
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Cooling (Anterior = cooling, or A/C). A nterior is pA rasympathetic.
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Posterior hypothalamus
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Heating (posterior = get fired up / heating). Sympathetic. If you zap your P osterior hypothalamus, you become a P oikilotherm (cold-blooded, like a snake)
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Septal nucleus of the hypothalamus
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area responsible for sexual urges
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area responsible for sexual urges
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Septal nucleus of the hypothalamus
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Suprachiasmatic nucleus of the hypothalamus
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Circadian rhythm. (“You need to sleep to be charismatic [chiasmatic]”).
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Posterior pituitary (neurohypophysis)
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Receives hypothalamic axonal projections from supraoptic (ADH) and paraventricular (oxytocin) nuclei. Oxytocin: oxys = quick; tocos = birth.
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Anterior pituitary aka…?
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A nterior pituitary = A denohypophysis
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Thalamus
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Major relay for ascending sensory information that ultimately reaches the cortex.
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Blood supply to the thalamus
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posterior communicating, posterior cerebral, and anterior choroidal arteries.
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Lateral geniculate nucleus (LGN) of thalamus
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(hint: “L ateral for L ight”) area of thalamus for visual information.
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area of thalamus for visual information.
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Lateral geniculate nucleus (LGN) of thalamus (hint: “L ateral for L ight”)
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Medial geniculate nucleus (MGN) of the thalamus
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(hint: M edial for M usic) Area of the thalamus responsible for auditory information
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Area of the thalamus responsible for auditory information
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Medial geniculate nucleus (MGN) of the thalamus (hint: M edial for M usic)
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Ventral posterior nucleus, lateral part (VPL) — of thalamus
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part of the thalamus responsible for body sensation (proprioception, pressure, pain, touch, vibration via dorsal columns, spinothalamic tract).
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part of the thalamus responsible for body sensation (proprioception, pressure, pain, touch, vibration via dorsal columns, spinothalamic tract).
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Ventral posterior nucleus, lateral part (VPL) — of thalamus
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Ventral posterior nucleus, medial part (VPM) — of the thalamus
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(hint: you put M akeup on your face, and sensory info is relayed through the VPM ) Area of thalamus responsible for facial sensation (via CN V)
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Area of thalamus responsible for facial sensation (via CN V)
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Ventral posterior nucleus, medial part (VPM) — of the thalamus (hint: you put M akeup on your face, and sensory info is relayed through the VPM )
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Motor and sensory locations in the thalamus
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Motor is anterior to sensation in the thalamus, just like the cortex.
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Limbic system: Includes what? Responsible for what?
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Includes cingulate gyrus, hippocampus, fornix, and mammillary bodies. Responsible for F eeding, F leeing, F ighting, F eeling, and sex (….) (The famous 5 F’s )
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Input to the cerebellum
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Receives contralateral cortical input via middle cerebellar peduncle and ipsilateral proprioceptive information via inferior cerebellar peduncle. Input nerves = climbing and mossy fibers.
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Output from the cerebellum
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Provides stimulatory feedback to contralateral cortex to modulate movement. Output nerves = Purkinje fibers output deep to nuclei of cerebellum, which in turn output to cortex via superior cerebellar peduncle.
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Deep nuclei of the cerebellum
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Lateral to medial: D entate, E mboliform, G lobose, F astigial (“D on’t E at G reasy F oods”)
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Lateral cerebellum
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area of the cerebellum responsible for voluntary movement of extremities
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area of the cerebellum responsible for voluntary movement of extremities
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Lateral cerebellum
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Medial cerebellum
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Area of cerebellum responsible for balance, truncal coordination.
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Area of cerebellum responsible for balance, truncal coordination.
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Medial cerebellum
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Basal ganglia (overall function)
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Important in voluntary movements and making postural adjustments. Receives cortical input, provides negative feedback to cortex to modulate movement.
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Important in voluntary movements and making postural adjustments. Receives cortical input, provides negative feedback to cortex to modulate movement.
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Basal ganglia (overall function)
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Excitatory pathway of the basal ganglia
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Substantia Nigra pars compacta’s (SNc’s) dopamine binds to D1 receptros in the excitatory pathway, stimulating the excitatory pathway (incr motion). Therefore, loss of dopamine in Parkinson’s inhibits the excitatory pathway (decr motion). Key: Grey = stimulatory || Black = inhibitory SNc = Substantia nigra pars compacta GPe = Globus pallidus externus GPi = Globus pallidus internus STN = Subthalamaic nucleus D1 = Dopamine D1 receptor (excitatory) D2 = Dopamine D2 receptor (inhibitory)
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Inhibitory pathway of the basal ganglia
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SNc’s dopamine binds to D2 receptros in the inhibitory pathway, inhibiting the inhibitory pathway (incr motion). Therefore, loss of dopamine in Parkinson’s dz excites (i.e., disinhibits) the inhibitory pathway (decr motion). Key: Grey = stimulatory || Black = inhibitory SNc = Substantia nigra pars compacta GPe = Globus pallidus externus GPi = Globus pallidus internus STN = Subthalamaic nucleus D1 = Dopamine D1 receptor (excitatory) D2 = Dopamine D2 receptor (inhibitory)
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Parkinson’s disease
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Degenerative disorder of CNS associated w/ Lewy bodies (composed of alpha-synuclein) and depigmentation of the substantia nigra pars compacta (loss of dopaminergic neurons). Rare cases have been linked to exposure to MPTP, a contaminant in illicit street drugs. (“TRaP = T remor (at rest), cogwheel R igidity, a nd P ostural instability. You are TRaP ped inside your body.”)
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Degenerative disorder of CNS associated w/ Lewy bodies (composed of alpha-synuclein) and depigmentation of the substantia nigra pars compacta (loss of dopaminergic neurons). Rare cases have been linked to exposure to MPTP, a contaminant in illicit street drugs. (“TRaP = T remor (at rest), cogwheel R igidity, a nd P ostural instability. You are TRaP ped inside your body.”)
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Parkinson’s disease
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Hemiballismus
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Sudden, wild flailing of 1 arm. Characteristic of contralateral subthalamic nucleus lesion. Loss of inhibition of thalamus through globus pallidus. (“Hemiballismus = Half ballistic — like throwing a baseball”)
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Huntington’s dz
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Autosomal-dominant trinucleotide repeat d/o. Chromosome 4. Atrophy of caudate nucleus (loss of GABAergic neurons) leads to enlarged lateral ventricles on CT. Chorea, depression, progressive dementia. Sx manifest in affeccted indvls btw ages 20-50. (Expansion of CAG repeats: “C audate loses A Ch and G ABA”)
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Autosomal-dominant trinucleotide repeat d/o. Chromosome 4. Atrophy of caudate nucleus (loss of GABAergic neurons) leads to enlarged lateral ventricles on CT. Chorea, depression, progressive dementia. Sx manifest in affeccted indvls btw ages 20-50. (Expansion of CAG repeats: “C audate loses A Ch and G ABA”)
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Huntington’s dz
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Chorea
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Sudden, jerky, purposeless movements. Characteristic of basal ganglia lesion (e.g., Huntington’s disease) (Chorea = dancing (Greek). Think choral dancing or choreography)
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Athetosis
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Slow, writhing movements, especially if fiingers. Characteristic of basal ganglia lesion (e.g., Huntington’s dz) (Athetos = not fixed (Greek). Think snakelike.)
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Essential/postural tremor
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Action tremor, autosomal dominant. Essential tremor pts often self-medicate w/ alcohol, which decreases the tremor. Tx: beta-blockers.
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Resting tremor
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Not noticeable distally. Seen in Parkinson’s (“pill-rolling” tremor)
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Intention tremor
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Slow, zigzag motion when pointing twd a target; associated w/ cerebellar dysfunction.
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Cerebral cortex: where are the Sylvian fissure vs. Central sulcus?
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A: Sylvian fissure is above temporal lobe; central sulcus divides frontal and parietal lobes.
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Cerebral cortex: What is the arcuate fasciculus?
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Connection between Associative auditory cortex (Wernicke’s area; dominant hemisphere) and Motor speech area (Broca’s area; dominant hemisphere)
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Cerebral cortex: Where is the primary auditory cortex (Heschel’s gyrus)? The primary motor area? The primary sensory area? The premotor area (part of extrapyramidal circuit)?
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Frontal lobe functions
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“Executive functions” Planning, inhibition, concentration, orientation, language, abstraction, judgment, motor regulation, mood. Lack of social judgment is most notable in frontal lobe lesion. (“D amage = D isinhibition” – e.g., Phineas Gage)
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Homonculus: What is it? What is it used for? What reaches into the Sylvian fissure? The longitudinal fissure?
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Topographical representation of sensory and motor areas in the cerebral cortex. Used to localize lesion (e.g., in blood supply) leading to specific defects. For example, lower extremity deficit in sensation or movement indicates involvement of anterior cerebral artery.
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Brain lesion in: Broca’s area
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(hint: BRO ca’s is BRO ken speech.) Consequence: Motor (nonfluent/expressive) aphasia w/ good comprehension.
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Motor (nonfluent/expressive) aphasia w/ good comprehension. Where is the lesion?
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Broca’s area (hint: BRO ca’s is BRO ken speech.)
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Brain lesion in: Wernicke’s area
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(hint: W ernicke’s is W ordy but makes no sense.) Consequence: Sensory (fluent/receptive) aphasia w/ poor comprehension, neologisms.
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Sensory (fluent/receptive) aphasia w/ poor comprehension, neologisms. Where is the lesion?
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Wernicke’s area (hint: W ernicke’s is W ordy but makes no sense.)
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Brain lesion in: Arcuate fasciculus (connects Wernicke’s to Broca’s area)
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Consequence: Conduction aphasia; good comprehension, fluent speech, but poor repitition.
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Conduction aphasia; good comprehension, fluent speech, but poor repitition. Where is the lesion?
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Arcuate fasciculus (connects Wernicke’s to Broca’s area)
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Brain lesion in: Amygdala (bilateral)
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Consequence: Kluver-Bucy syndrome (hyperorality, hypersexuality, disinhibited behavior)
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Kluver-Bucy syndrome (hyperorality, hypersexuality, disinhibited behavior) Where is the lesion?
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Amygdala (bilateral)
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Brain lesion in: Frontal lobe
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Consequence: Personality changes and deficits in concentration, orientation, and judgment; may havve reemergence of primitive reflexes.
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Personality changes and deficits in concentration, orientation, and judgment; may havve reemergence of primitive reflexes. Where is the lesion?
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Frontal lobe
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Brain lesion in: Right parietal lobe
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Consequence: Spatial neglect syndrome (agnosia of the contralateral side of the world)
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Spatial neglect syndrome (agnosia of the contralateral side of the world) Where is the lesion?
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Right parietal lobe
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Brain lesion in: Reticular activating system (midbrain)
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Consequence: Reduced levels of arousal and wakefulness (e.g., coma)
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Reduced levels of arousal and wakefulness (e.g., coma) Where is the lesion?
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Reticular activating system (midbrain)
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Brain lesion in: Mammillary bodies (bilateral)
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Consequence: Wernicke-Korsakoff syndrome (confusion, confabulation, ophthalmoplegia, ataxia)
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Wernicke-Korsakoff syndrome (confusion, confabulation, ophthalmoplegia, ataxia) Where is the lesion?
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Mammillary bodies (bilateral)
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Brain lesion in: Basal ganglia
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Consequence: May result in tremor at rest, chorea, or athetosis
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May result in tremor at rest, chorea, or athetosis Where is the lesion?
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Basal ganglia
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Brain lesion in: Cerebellar hemisphere
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(hint: cerebellar hemispheres are laterally located, so they affect the lateral limbs) Consequence: Intention tremor, limb ataxia; Damage to the cerebellum results in ipsilateral deficits; Fall toward side of lesion
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Intention tremor, limb ataxia; Damage to the cerebellum results in ipsilateral deficits; Fall toward side of lesion Where is the lesion?
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Cerebellar hemisphere (hint: cerebellar hemispheres are laterally located, so they affect the lateral limbs)
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Brain lesion in: Cerebellar vermis
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(hint: vermis is centrally located, so it affects the central body) Consequence: Truncal ataxia, dysarthria.
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Truncal ataxia, dysarthria. Where is the lesion?
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Cerebellar vermis (hint: vermis is centrally located, so it affects the central body)
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Brain lesion in: Subthalamic nucleus
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Consequence: Contralateral hemiballismus
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Contralateral hemiballismus Where is the lesion?
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Subthalamic nucleus
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Brain lesion in: Hippocampus
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Consequence: Anterograde amnesia — inability to make new memories
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Anterograde amnesia — inability to make new memories Where is the lesion?
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Hippocampus
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Brain lesion in: Paramedian pontine reticular formation (PPRF)
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Consequence: Eyes look away from side of lesion
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Eyes look away from side of lesion Where is the lesion?
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Paramedian pontine reticular formation (PPRF)
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Brain lesion in: Frontal eye fields
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Consequence: Eyes look toward lesion.
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Eyes look toward lesion. Where is the lesion?
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Frontal eye fields
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Aphasia (definition) vs. Dysarthria (definition)
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Aphasia is a higher-order inability to speak. vs. Dysarthria is a motor inability to speak.
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Broca’s aphasia
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Nonfluent aphasia w/ intact comprehension. Broca’s area — inferior frontal gyrus. (“Bro ca’s Bro ken Boca ” [boca = mouth in Spanish])
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Wernicke’s aphasia
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Fluent aphasia with impaired comprehension. Wernicke’s area — superior temporal gyrus. (“W ernicke’s is W ordy but makes no sense.” or “W ernicke’s = W hat?”)
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Global aphasia
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Nonfluent aphasia w/ impaired comprehension. Both Broca’s and Wernicke’s areas affected.
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Conduction aphasia
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Poor repitition but fluent speech, intact comprehension. Arcuate fasciculus — connects Broca’s and Wernicke’s areas.
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Anterior cerebral artery: what areas of cortex does it supply?
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Supplies anteromedial surface of brain [darkest grey]
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Middle cerebral artery: what areas of cortex does it supply?
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Supplies lateral surface of brain [White areas below]
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Posterior cerebral artery: what areas of cortex does it supply?
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Supplies posterior and inferior surfaces [medium grey areas below]
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Anterior cerebral artery: Where is it? What does it supply?
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[Right anterior cerebral artery is labeled below — top/left] Supplies medial surface of the brain, leg-foot area of motor and sensory cortices.
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Middle cerebral artery: Where is it? What does it supply?
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[Labeled below at top/left, just beneath right anterior cerebral art.] Supplies lateral aspect of brain, trunk-arm-face area of motor and sensory cortices, Broca’s and Wernicke’s speech areas (on dominant hemisphere), optic radiations.
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What deficit occurs w/ problems in the middle cerebral artery?
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Contralateral face and arm paralysis and sensory loss, aphasia (dominant sphere), left-sided neglect.
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Posterior cerebral artery: Where is it? What does it supply?
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[labeled below along middle/right] Supplies the visual cortex.
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What deficit is associated with problems in the posterior cerebral artery?
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Contralateral homonymous hemianopia with macular sparing.
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Anterior communicating artery: Where is it? What is associated with this artery?
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[labeled below along top/right] Most common site of circle of Willis aneurysm; lesions may cause visual field defects.
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Posterior communicating artery: Where is it? What is associated with this artery?
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[labeled below along middle/left] Common area of aneurysm; Causes CN III palsy.
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Lateral striate: Where are they? What do they supply?
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[labeled below along middle/right] Divisions of the middle cerebral artery that supply the internal capsule, caudate, putamen, and globus pallidus.
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What deficit is associated with the lateral striate?
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“Arteries of stroke”; infarct of internal capsule causes pure motor hemiparesis.
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Watershed zones of the circle of Willis
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Between anterior cerebral/middle cerebral, posterior cerebral/middle cerebral arteries. Damaged in severe hypotension –< upper leg/upper arm weakness, defects in higher-order visual processing.
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Posterior Inferior Cerebellar Artery (PICA): Where is it? What deficits are associated with an infarct here?
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[labled below at bottom/right] Infarcts cause Wallenberg’s syndrome (aka lateral medullary syndrome) (nystagmus, ipsilateral ataxia, nausea, vomiting, Horner’s syndrome)
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Basilar artery: Where is it? What would an infarct here cause?
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[labeled below along middle/left] Infarct causes locked-in syndrome.
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In general, strokes of the anterior circle of Willis vs. the posterior circle of Willis
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stroke of the anterior circle : General sensory and motor dysfunction, aphasia. stroke of the posterior circle : Cranial nerve deficits (vertigo, visual deficits), coma, cerebellar deficits (ataxia)
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Anterior spinal artery: Where is it? What defects are associated?
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[at bottom of picture, below] Medial medullary syndrome: contralateral hemiparesis (lower extremities), medial lemniscus (decr proprioception), ipsilateral paralysis of hypoglossal nerve
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Anterior Inferior Cerebellar Artery (AICA) Where is it located? What deficits are associated?
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[labeled below in lower right] Lateral inferior pontine syndrome: ipsilateral facial paralysis, ipsilateral cochlear nucleus, vestibular (nystagmus), ipsilateral facial pain and temperature, ipsilateral dystaxia (MCP, ICP)
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Berry aneurysms: Where do they occur? What is the most common complication?
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Occur at the bifurcations in the circle of Willis. Most common site is bifurcation of the anterior communicating artery. Rupture (most common complication) leads to hemorrhagic stroke/subarachnoid hemorrhage.
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Berry aneurysms: associated with? other risk factors?
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Associated with: Adult polycystic kidney dz Ehlers-Danlos syndrome Marfan’s syndome Risk factors: Advanced age HTN Smoking Race (higher risk in blacks)
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Charcot-Bouchard microaneurysms: Associated with? What do they affect?
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Associated with chronic HTN Affects small vessels (e.g., in basal ganglia, thalamus)
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Epidural hematoma
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Rupture of middle meningeal artery (branch of maxillary artery), often secondary to fracture of temporal bone. Lucid interval. CT shows “biconvex disk” not crossing suture lines. Can cross falx, tentorium.
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Subdural hematoma
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Rupture of bridging veins. Venous bleeding (less pressure) with delayed onset of Sx’s. Seen in elderly individuals, alcoholics, blunt trauma, shaken baby. Crescent-shaped hemorrhage that crosses suture lines. Cannot cross falx, tentorium.
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Factors predisposing to a subdural hematoma
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Brain atrophy Shaking Whiplash
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Subarachnoid hemorrhage
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Rupture of aneurysm (usually berry aneurysm) or an AVM. Pts complain of “worst headache of my life.” Bloody or yellow (xanthochromic) spinal tap. 2-3 days afterward, there is a risk of vasospasm (Tx w/ Ca2+ channel blockers).
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Parenchymal hematoma
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Caused by HTN, amyloid angiopathy [see below], DM, and tumor. Typically occurs in basal ganglia and internal capsule.
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Hemorrhagic stroke
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Intracerebral bleeding, often due to aneurysm rupture. May be secondary to ischemic stroke following reperfusion (incr vessel fragility)
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Ischemic stroke
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Emboli block large vessels; etiologies include: atrial fibrillation, carotid dissection, patent foramen ovale, endocarditis. Lacunar strokes block small vessels, are secondary to HTN. Tx: tPA w/in 3 hours.
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Transient Ischemic Attack (TIA)
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Brief, reversible episode of neurologic dysfunction due to focal ischemia. Typically, Sx’s last >24 hours.
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Stroke imaging
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Bright on diffusion-weighted MRI in 3-30 minutes [below/left], dark on CT in ~24 hours [below/right] [Images are of a right MCA stroke; diffusion MRI and CT]
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Dural venous sinuses: Where do they run? What is the sequence?
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Venous sinuses run in the dura mater where its meningeal and periosteal layers separate. Cerebral veins –< venous sinuses –< internal jugular vein
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Where is the supereior sagittal sinus? The confluence of the sinuses? The Occipital sinus? The Transverse and sigmoid sinuses?
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The superior sagittal sinus (main location of CSF return via arachnoid granulations) is along the superior/median border of the brain. The confluence of the sinuses is posterior, bringing together the occipital sinus (inferiorly), sagittal sinus (superiorly), transverse sinuses (laterally), and straight sinus (ventrally)
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Where is the inferior sagittal sinus? The Great cerebral vein (of Galen)? The Straight sinus?
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The inferior sagittal sinus runs deep to the superior sagittal sinus in the median line. The great cerebral vein runs inferior to that, and the two sinuses meet at the straight sinus, which feeds into the confluence of the sinuses posteriorly.
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What is one vein that feeds into the dural venous sinuses?
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The Superior ophthalmic vein feeds into the cavernous sinus, which reaches the sup. sagittal sinus and the transverse sinus by way of the Sphenoparietal sinus.
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Where is CSF made? Where is reabsorbed?
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CSF is made by ependymal cells lining the ventricles; it is reabsorbed by venous sinus arachnoid granulations.
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What connects the lateral to the 3rd ventricle?
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The foramen of Munro.
question

What connects the 3rd and 4th ventricles?
answer

The cerebral aqueduct
question

What connects the 4th ventricle and the subarachnoid space?
answer

Foramina of L ushka = L ateral Foramen of M agendie = M edial
question

Hydrocephalus
answer

Accumulation of excess CSF in ventricular system –< increased intracranial pressure; ventricular dilation –< clinical triad of dementia, gait problems, urinary incontenincence. ("Wet, wobbly, and wacky")
question

Normal pressure (communicating) hydrocephalus
answer

Caused by impaired absorption of CSF by arachnoid granulations (e.g., arachnoid adhesions post-meningitis)
question

Obstructive (non-communicating) hydrocephalus
answer

Caused by structual blockage of CSF circulation w/in the ventricular system (e.g., stenosis of the aqueduct of Sylvius)
question

Hydrocephalus ex vacuo
answer

Appearance of increased CSF in atrophy. Intracranial pressure normal, triad not seen.
question

Total # of spinal nerves? Per section?
answer

There are 31 spinal nerves. (“31 like the 31 flavors at Baskin-Robbins”) 8 Cervical 12 Thoracic 5 Lumbar 5 Sacral 1 Coccygeal
question

Numbering of cervical spinal nerves
answer

Nerves C1-C7 exit via intervertebral foramina above the corresponding vertebra. All other nerves exit below .
question

Where does vertebral disk herniation usually occur?
answer

Vertebral disk herniation (nucleus pulposus hernaites through annulus fibrosus) usually occurs btw L5 and S1.
question

How far does the spinal cord extend in adults? The subarachnoid space? Where do you perform a lumbar puncture?
answer

In adults, the spinal cord extends to the loweer border of L1-L2; subarachnoid space extends to lower border of S2. Lumbar puncture is usually performed in L3-L4 or L4-L5 interspaces, at the level of the cauda equina. (“To keep the cord alive , keep the spinal needle btw L3 and L5 “)
question

Where do you get CSF from in a lumbar puncture?
answer

CSF is obtained from lumbar subarachnoid space btw L4 and L5 (at the level of iliac crests)
question

Structures pierced in a lumbar puncture (in order)
answer

1.) Skin/superficial fascia 2.) Ligaments (supraspinous, interspinous, ligamentum flavum) 3.) Epidural space 4.) Dura mater 5.) Subdural space 6.) Arachnoid 7.) Subarachnoid space – CSF (Pia is not pie rced)
question

What do the dorsal columns of the spinal cord relay?
answer

Pressure, vibration, touch, proprioception.
question

How are the dorsal columns of the spinal cord organized?
answer

Medially: fasciculus gracilis (lower body, extremities) Laterally: fasciculus cuneatus (upper body, extremities) (“Dorsal column is organized as you are, with hands at sides. Arms outside, legs inside.”)
question

What do the lateral corticospinal tract and spinothalamic tract relay? Where are they located? How are they organized?
answer

Lateral corticospinal tract relays voluntary motor information, is located in the lateral spinal cord. Spinothalamic tract relays pain and temperature, is located antero-laterally. (“L egs are L ateral in L ateral corticospinal, spinothalamic tracts”)
question

What arteries follow the spinal cord?
answer

2 Posterior spinal arteries, 1 anterior spinal artery
question

Where are the intermediate horn sympathetics found?
answer

The lateral gray matter of the thoracic [only] spinal cord
question

Ascending spinal tracts and synapsing
answer

They synapse then cross.
question

Spinal tract: Dorsal column — medial lemniscal pathway
answer

function? Ascending pressure, vibration, touch, and proprioceptive sensation
question

Ascending pressure, vibration, touch, and proprioceptive sensation what spinal tract is this?
answer

Dorsal column — medial lemniscal pathway
question

Spinal tract: Spinothalamic tract
answer

function? Ascending pain and temperature sensation
question

Ascending pain and temperature sensation what spinal tract is this?
answer

Spinothalamic tract
question

Spinal tract: Lateral corticospinal tract
answer

function? Descending vvoluntary movement of contralateral limbs
question

Descending vvoluntary movement of contralateral limbs what spinal tract is this?
answer

Lateral corticospinal tract
question

Spinal tract: Dorsal column — medial lemniscal pathway
answer

What is the 1st order neuron? Sensory nerve ending –< cell body in dorsal root ganglion –< enters spinal cord, ascends ipsilaterally in dorsal column
question

Sensory nerve ending –< cell body in dorsal root ganglion –< enters spinal cord, ascends ipsilaterally in dorsal column This is the 1st order neuron in which spinal tract?
answer

Dorsal column — medial lemniscal pathway
question

Spinal tract: Spinothalamic tract
answer

What is the 1st order neuron? Sensory nerve ending (A-delta and C fibers) (cell body in dorsal root ganglion) –< enters spinal cord
question

Sensory nerve ending (A-delta and C fibers) (cell body in dorsal root ganglion) –< enters spinal cord This is the 1st order neuron in which spinal tract?
answer

Spinothalamic tract
question

Spinal tract: Lateral corticospinal tract
answer

What is the 1st order neuron? Upper motor neuron: cell body in primary motor cortex | Descends ipsilaterally (thru internal capsule) until decussating at caudal medulla (pyramidal decussation) | Descends contralaterally
question

Upper motor neuron: cell body in primary motor cortex | Descends ipsilaterally (thru internal capsule) until decussating at caudal medulla (pyramidal decussation) | Descends contralaterally This is the 1st order neuron in which spinal tract?
answer

Lateral corticospinal tract
question

Spinal tract: Dorsal column — medial lemniscal pathway
answer

What is the 1st synapse? Ipsilateral nucleus cuneatus or gracilis (medulla)
question

Ipsilateral nucleus cuneatus or gracilis (medulla) This is the 1st synapse in which spinal tract?
answer

Dorsal column — medial lemniscal pathway
question

Spinal tract: Spinothalamic tract
answer

What is the 1st synapse? Ipsilateral gray matter (spinal cord)
question

Ipsilateral gray matter (spinal cord) This is the 1st synapse in which spinal tract?
answer

Spinothalamic tract
question

Spinal tract: Lateral corticospinal tract
answer

What is the 1st synapse? Cell body of anterior horn (spinal cord)
question

Cell body of anterior horn (spinal cord) This is the 1st synapse in which spinal tract?
answer

Lateral corticospinal tract
question

Spinal tract: Dorsal column — medial lemniscal pathway
answer

What is the 2nd order neuron? Decussates in medulla –< ascends contralaterally in medial lemniscus
question

Decussates in medulla –< ascends contralaterally in medial lemniscus This is the 2nd order neuron in which spinal tract?
answer

Dorsal column — medial lemniscal pathway
question

Spinal tract: Spinothalamic tract
answer

What is the 2nd order neuron? Decussates at anterior white commissure –< ascends contralaterally
question

Decussates at anterior white commissure –< ascends contralaterally This is the 2nd order neuron in which spinal tract?
answer

Spinothalamic tract
question

Spinal tract: Lateral corticospinal tract
answer

What is the 2nd order neuron? Lower motor neuron : leaves spinal cord
question

Lower motor neuron : leaves spinal cord This is the 2nd order neuron in which spinal tract?
answer

Lateral corticospinal tract
question

Spinal tract: Dorsal column — medial lemniscal pathway OR Spinothalamic tract
answer

What is the 2nd synapse? VPL of thalamus
question

VPL of thalamus This is the 2nd synapse in which spinal tract?
answer

Dorsal column — medial lemniscal pathway OR Spinothalamic tract
question

Spinal tract: Lateral corticospinal tract
answer

What is the 2nd synapse? Neuromuscular junction
question

Neuromuscular junction This is the 2nd synapse in which spinal tract?
answer

Lateral corticospinal tract
question

Spinal tract: Dorsal colum — medial lemniscal pathway OR Spinothalamic tract
answer

What is the 3rd order neuron? Sensory cortex
question

Sensory cortex This is the 3rd order neuron in which spinal tract?
answer

Dorsal colum — medial lemniscal pathway OR Spinothalamic tract
question

Spinal tract: Lateral corticospinal tract
answer

What is the 3rd order neuron? N/A (no 3rd-order neuron)
question

N/A (no 3rd-order neuron) This is the 3rd order neuron in which spinal tract?
answer

Lateral corticospinal tract
question

Lower vs. Upper motor neuron lesion
answer

Lower MN lesion = everything lowered (less muscle mass, decr muscle tone, decr reflexes, downgoing toes) Upper MN = everythinig up (tone, DTRs, toes)
question

Spinal tract: UMN vs. LMN lesion: Weakness
answer

What is the 3rd order neuron? Both
question

Both
answer

This is the 3rd order neuron in which spinal tract? UMN vs. LMN lesion: Weakness
question

Spinal tract: UMN vs. LMN lesion: Atrophy
answer

What is the 3rd order neuron? (-) UMN (+) LMN
question

(-) UMN (+) LMN This is the 3rd order neuron in which spinal tract?
answer

UMN vs. LMN lesion: Atrophy
question

Spinal tract: UMN vs. LMN lesion: Fasciculations (muscle twitching)
answer

What is the 3rd order neuron? (-) UMN (+) LMN
question

(-) UMN (+) LMN This is the 3rd order neuron in which spinal tract?
answer

UMN vs. LMN lesion: Fasciculations (muscle twitching)
question

Spinal tract: UMN vs. LMN lesion: Reflexes
answer

What is the 3rd order neuron? Increased in UMN Decreaseed in LMN
question

Increased in UMN Decreaseed in LMN This is the 3rd order neuron in which spinal tract?
answer

UMN vs. LMN lesion: Reflexes
question

Spinal tract: UMN vs. LMN lesion: Tone
answer

What is the 3rd order neuron? Increased in UMN, decreased in LMN
question

Increased in UMN, decreased in LMN This is the 3rd order neuron in which spinal tract?
answer

UMN vs. LMN lesion: Tone
question

Spinal tract: UMN vs. LMN lesion: Babinski sign (upgoing toes — normal in infants)
answer

What is the 3rd order neuron? (+) in UMN, (-) in LMN
question

(+) in UMN, (-) in LMN This is the 3rd order neuron in which spinal tract?
answer

UMN vs. LMN lesion: Babinski sign (upgoing toes — normal in infants)
question

Spinal tract: UMN vs. LMN lesion: Spastic paralysis
answer

What is the 3rd order neuron? (+) in UMN (-) in LMN
question

(+) in UMN (-) in LMN This is the 3rd order neuron in which spinal tract?
answer

UMN vs. LMN lesion: Spastic paralysis
question

Spinal cord lesions: Poliomyelitis and Werdnig-Hoffmann disease What areas are affected? What are the Sx?
answer

Lower motor neuron lesion only, due to destruction of anterior horns; flaccid paralysis
question

Lower motor neuron lesion only, due to destruction of anterior horns; flaccid paralysis What spinal cord lesion is this?
answer

Poliomyelitis and Werdnig-Hoffmann disease
question

Spinal cord lesions: Multiple sclerosis What areas are affected? What are the Sx?
answer

Mostly white matter of cervical region; random and asymmetric lesions, due to demyelination; scanning speech, intention tremor, nystagmus
question

Mostly white matter of cervical region; random and asymmetric lesions, due to demyelination; scanning speech, intention tremor, nystagmus What spinal cord lesion is this?
answer

Multiple sclerosis
question

Spinal cord lesions: ALS What areas are affected? What are the Sx?
answer

Combined upper and lower motor neuron deficits with no sensory deficit; both upper and lower motor neuron signs.
question

Combined upper and lower motor neuron deficits with no sensory deficit; both upper and lower motor neuron signs. What spinal cord lesion is this?
answer

ALS
question

Spinal cord lesions: Complete occlusion of the anterior spinal artery What areas are affected? What are the Sx?
answer

Spares dorsal columns and tract of Lissauer; upper throacicc ASA territory is a watershed area, as artery of Adamkiewicz supplies ASA below ~T8
question

Spares dorsal columns and tract of Lissauer; upper throacicc ASA territory is a watershed area, as artery of Adamkiewicz supplies ASA below ~T8 What spinal cord lesion is this?
answer

Complete occlusion of the anterior spinal artery
question

Spinal cord lesions: Tabes dorsalis (tertiary syphilis) What areas are affected? What are the Sx?
answer

Degeneration of dorsal roots and dorsal columns; impaired proprioception, locomotor ataxia
question

Degeneration of dorsal roots and dorsal columns; impaired proprioception, locomotor ataxia What spinal cord lesion is this?
answer

Tabes dorsalis (tertiary syphilis)
question

Spinal cord lesions: Syringomyelia What areas are affected? What are the Sx?
answer

Crossing fibers of spinothalamic tract damaged; bilateral loss of pain and temperature sensation.
question

Crossing fibers of spinothalamic tract damaged; bilateral loss of pain and temperature sensation. What spinal cord lesion is this?
answer

Syringomyelia
question

Spinal cord lesions: Vitamin B12 neuropathy and Friedrich’s ataxia What areas are affected? What are the Sx?
answer

Demyelination of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts; ataxic gait, hyperreflexia, impaired position and vibration sense.
question

Demyelination of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts; ataxic gait, hyperreflexia, impaired position and vibration sense. What spinal cord lesion is this?
answer

Vitamin B12 neuropathy and Friedrich’s ataxia
question

Poliomyelitis: Cause? Transmission? Replication? Pathogenesis?
answer

Caused by poliovirus, which is transmitted by fecal/oral route. Replciates in the oropharynx and small intestine before spreading through the bloodstream to the CNS, where it leads to destruction of cells in the anterior horn of the spinal cord, leading in turn to LMN destruction.
question

Poliomyelitis: Sx?
answer

Malaise, hedache, fever, nausea, abdominal pain, sore throat. Signs of LMN lesions — muscle weakness and atrohphy, fasciculations, fibrillation, and hyporeflexia.
question

Poliomyelitis: Findings?
answer

CSF w/ lymphocytic pleocytosis w/ slight elevation of protein (w/ no change in CSF glucose). Virus recovered from stool or throat.
question

Werdnig-Hoffman dz (aka infantile spinal muscular atrophy)
answer

Autosomal-recessive inheritance; presents at birth as a “floppy baby,” tongue fasciculations; median age of death 7 months. Associated w/ degenration of anterior horns. LMN involvement only.
question

Amyotrophic lateral sclerosis (commonly known as Lou Gehrig’s dz)
answer

Associated w/ both LMN and UMN signs; no sensory, cognitive, or oculomotor deficits. Can be caused by defect in superoxide dismutase 1 (SOD1), betel nut ingestion.
question

Tabes dorsalis
answer

Degeneration of dorsal columns and dorsal roots due to tertiary syphilis, resulting in impaired proprioception and locomotor ataxia.
question

Associated with Tabes dorsalis
answer

Charcot’s joints Shooting (lightning) pain Argyll Robertson pupils (aka “prostitute’s pupils” – accomodate, but do not react) Absence of DTRs
question

Friedrich’s ataxia: Inheritance? Etiology? Sx? Onset?
answer

Autosomal-recessive trinucleotide repeat disorder (GAA; frataxin gene). Leads to impairment in mitochondrial functioning. Staggering gait, frequent falling, nystagmus, dysarthria, hypertrophic cardiomyopathy. Presents in childhood w/ kyphoscoliosis.
question

Brown-SĂ©quard Syndrome: What is it?
answer

Heisection of the spinal cord
question

Brown-SĂ©quard Syndrome: Findings?
answer

1.) Ipsilateral UMN signs (corticospinal tract) below lesion 2.) Ipsilateral loss of tactile, vibration, proprioception sense (dorsal column) below lesion 3.) Contralateral pain and temperature loss (spinothalamic tract) below lesion 4.) Ipsilateral loss of all sensation at level of lesion 5.) LMN signs (e.g., flaccid paralysis) at level of lesion If lesion occurs above T1, presents w/ Horner’s syndrome
question

Horner’s syndrome
answer

Sympathectomy of face: 1.) P tosis (slight drooping of eyelid) 2.) A nhidrosis (absence of sweating) and flushing (rubor) of affected side of face 3.) M iosis (pupil constriction) (“PAM is horny [Horner’s]) Associated w/ lesion of spinal cord above T1 (e.g., Pancoast’s tumor, Brown-SĂ©quard syndrome [cord hemisection], late-stage syringomyelia)
question

3 Neuron pathway involved in Horner’s syndrome
answer

The 3-neuron oculosympathetic pathway projects from the hypothalamus to the intermediolateral column of the spinal cord, then to the superior cervical (sympathetic) ganglion, and finally to the pupil, the smooth muscle of the eyelids, and the sweat glands of the forehead and face. Interruption of any of these pathways results in Horner’s syndrome.
question

Clinically important landmarks for a pudendal nerve block (to relieve pain of pregnancy)
answer

Ischial spine
question

Clinically important landmarks for Appendix
answer

2/3 of the way from the umbilicus to the anterior superior iliac spine (McBurney’s point)
question

Clinically important landmarks for lumbar puncture
answer

Iliac crest.
question

Landmark dermatomes: C2
answer

Posterior half of a skull “cap”
question

Landmark dermatomes: C3
answer

High turtleneck shirt
question

Landmark dermatomes: C4
answer

Low-collar shirt
question

Landmark dermatomes: T4
answer

At the nipple. (T4 at the teat pore )
question

Landmark dermatomes: T7
answer

Xiphoid process
question

Landmark dermatomes: T10
answer

At the umbilicus (important for early appendicitis pain referral) (T10 at the belly butTEN )
question

Landmark dermatomes: L1
answer

At the inguinal ligament (“L1 is IL [I nguinal L igament])
question

Landmark dermatomes: L4
answer

Includes kneecaps
question

Landmark dermatomes: S2, S3, S4
answer

Erection and sensation of penile and anal zones (“S2, 3, 4, keep the penis off the floor”)
question

Muscle spindles vs. Golgi tendon organs
answer

Muscle spindles monitor muscle length (help you pick up a heavy suitcase when you didnt know how heavy it was). Golgi T endon organs monitor muscle T ension (make you drop a heavy suitcase you’ve been holding too long).
question

Muscle spindle: pathway?
answer

In parallel with muscle fibers. Muscle stretch –< intrafusal stretch –< stimulates Ia afferent –< stimulate alpha motor neuron –< reflex muscle (extrafusal) contraction
question

Spindle muscle control: the Gamma loop
answer

CNS stimulates gamma motor neuron –< contracts intrafusal fiber –< increased sensitivity of reflex arc
question

Clinical reflexes and their respective nerve roots: Achilles? Patella? Biceps? Triceps?
answer

Achilles = S1 nerve root Patella = L4 nerve root Biceps = C5 nerve root Triceps = C7 nerve root * Note that they count up in order: S1,2 L3,4 C5,6 C7,8
question

Babinski sign
answer

Dorsiflexion of the big toe and fanning of other toes; sign of UMN lesion, but normal reflex in 1st year of life.
question

Primitive reflexes
answer

Normally disappear within 1st year of life. May reemerge following frontal lobe lesion. Include: Moro reflex, rooting reflex, suckling reflex, Palmar and plantar reflexes, Babinski reflex
question

Moro reflex
answer

Extension of limbs when started
question

Rooting reflex
answer

Movement of head toward one side if cheek or mouth is stroked (nipple seeking)
question

Sucking reflex
answer

Sucking response when roof of mouth is touched
question

Palmar and palantar reflexes
answer

Curling of fingers/toes if palms of hands/feet are stroked
question

Cranial nerves that lie medially at the brainstem
answer

III, VI, XII Remember: 3 (x2) = 6 (x2) = 12
question

Brain stem: could you label these structures?
answer

question

Which cranial nerve arises dorsally and emerges ventrally?
answer

CN IV [see below, CN IV is along left in the middle]
question

Dorsal brainstem structures: Pineal gland
answer

Melatonin secretion, circadian rhythms.
question

Dorsal brainstem structures: superior colliculi
answer

Conjugate vertical gaze center. (“you have your eyes above your ears, and the superior colliculus (visual) is above the inferior colliculus (auditory).”)
question

Dorsal brainstem structures: inferior colliculi
answer

Auditory (“you have your eyes above your ears, and the superior colliculus (visual) is above the inferior colliculus (auditory).”)
question

Parinaud syndrome
answer

Paralysis of conjugate verticle gaze due to lesion in superior colliculi (e.g., pinealoma)
question

Cranial nerves: Olfactory (CN I) function? type? mnemonic?
answer

Smell (only CN w/o thalamic relay to cortex) S ensory; “S ome” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
question

Which cranial nerve is this? (Function, type, mnemonic) Smell (only CN w/o thalamic relay to cortex) S ensory; “S ome” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
answer

Olfactory (CN I)
question

Cranial nerves: Optic (CN II) function? type? mnemonic?
answer

Sight. S ensory; “S ay” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
question

Which cranial nerve is this? (Function, type, mnemonic) Sight. S ensory; “S ay” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
answer

Optic (CN II)
question

Cranial nerves: Oculomotor (CN III) function? type? mnemonic?
answer

Eye movement (SR, IR, MR, IO), pupillary constriction, accommodation, eyelid opening (levator palpebrae) M otor; “M oney” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
question

Which cranial nerve is this? (Function, type, mnemonic) Eye movement (SR, IR, MR, IO), pupillary constriction, accommodation, eyelid opening (levator palpebrae) M otor; “M oney” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
answer

Oculomotor (CN III)
question

Cranial nerves: Trochlear (CN IV) function? type? mnemonic?
answer

Eye movement (SO) M otor; “M oney” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
question

Which cranial nerve is this? (Function, type, mnemonic) Eye movement (SO) M otor; “M oney” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
answer

Trochlear (CN IV)
question

Cranial nerves: Trigeminal (CN V) function? type? mnemonic?
answer

Mastication, facial sensation. B oth, “B ut” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
question

Which cranial nerve is this? (Function, type, mnemonic) Mastication, facial sensation.
answer

B oth, “B ut” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”] Trigeminal (CN V)
question

Cranial nerves: Abducens (CN VI) function? type? mnemonic?
answer

Eye movement (LR) M otor; “M y” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
question

Which cranial nerve is this? (Function, type, mnemonic) Eye movement (LR) M otor; “M y” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
answer

Abducens (CN VI)
question

Cranial nerves: Facial (CN VII) function? type? mnemonic?
answer

Facial movement, taste from anterior 2/3rds of tongue, lacrimation, salivation (submandibular and sublingual glands), eyelid closing (orbicularis oculi), stapedius muscle in ear B oth; “B rother” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
question

Which cranial nerve is this? (Function, type, mnemonic) Facial movement, taste from anterior 2/3rds of tongue, lacrimation, salivation (submandibular and sublingual glands), eyelid closing (orbicularis oculi), stapedius muscle in ear B oth; “B rother” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
answer

Facial (CN VII)
question

Cranial nerves: Vestibulocochlear (CN VIII) function? type? mnemonic?
answer

Hearing, balance. S ensory; “S ays” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
question

Which cranial nerve is this? (Function, type, mnemonic) Hearing, balance. S ensory; “S ays” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
answer

Vestibulocochlear (CN VIII)
question

Cranial nerves: Glossopharyngeal (CN IX) function? type? mnemonic?
answer

Taste from posterior 1/3rd of tongue, swallowing, salivation (parotid gland), monitoring carotid body and sinus chemo- and baroreceptors, and stylopharyngeus (elevates pharynx, larynx) B oth; “B ig” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
question

Which cranial nerve is this? (Function, type, mnemonic) Taste from posterior 1/3rd of tongue, swallowing, salivation (parotid gland), monitoring carotid body and sinus chemo- and baroreceptors, and stylopharyngeus (elevates pharynx, larynx) B oth; “B ig” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
answer

Glossopharyngeal (CN IX)
question

Cranial nerves: Vagus (CN X) function? type? mnemonic?
answer

Taste from epiglottic region, swallowing, palate elevation, talking, coughing, thoracoabdominal viscera, monitoring aortic arch chemo- and baroreceptors. B oth; “B rains” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
question

Which cranial nerve is this? (Function, type, mnemonic) Taste from epiglottic region, swallowing, palate elevation, talking, coughing, thoracoabdominal viscera, monitoring aortic arch chemo- and baroreceptors. B oth; “B rains” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
answer

Vagus (CN X)
question

Cranial nerves: Accessory (CN XI) function? type? mnemonic?
answer

Head turning, shoulder shrugging M otor; “M atter” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
question

Which cranial nerve is this? (Function, type, mnemonic) Head turning, shoulder shrugging M otor; “M atter” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
answer

Accessory (CN XI)
question

Cranial nerves: Hypoglossal (CN XII) function? type? mnemonic?
answer

Tongue movement M otor; “M ore” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
question

Which cranial nerve is this? (Function, type, mnemonic) Tongue movement M otor; “M ore” [Mnemonic for type of information carried by CN’s: “Some Say Marry Money, But My Brother Says Big Brains Matter Most.”]
answer

Hypoglossal (CN XII)
question

Cranial nerve nuclei: Where are they located, generally?
answer

Located in tegmentum portion of brainstem (btw dorsal and ventral portions). Lateral nuclei = sensory M edial nuclei = M otor
question

Cranial nerve nuclei located in the midbrain
answer

Nuclei of CN III and IV
question

Cranial nerve nuclei located in the pons
answer

Nuclei of CN V, VI, VII, and VIII
question

Cranial nerve nuclei located in the medulla
answer

Nuclei of CN IX, X, XI, and XII
question

CN reflexes: Corneal OR Lacrimation (use the same nerves) Afferent? Efferent?
answer

Afferent = V-1 Efferent = VII
question

Afferent = V-1 Efferent = VII What CN reflex is this?
answer

Corneal OR Lacrimation (use the same nerves)
question

CN reflexes: Jaw jerk Afferent? Efferent?
answer

Afferent = V-3 (sensory) Efferent = V-3 (motor)
question

Afferent = V-3 (sensory) Efferent = V-3 (motor) What CN reflex is this?
answer

Jaw jerk
question

CN reflexes: Pupillary Afferent? Efferent?
answer

Afferent = II Efferent = III
question

Afferent = II Efferent = III What CN reflex is this?
answer

Pupillary
question

CN reflexes: Gag Afferent? Efferent?
answer

Afferent = IX Efferent = IX and X
question

Afferent = IX Efferent = IX and X What CN reflex is this?
answer

Gag
question

Vagal nuclei: Nucleus Solitarious
answer

Visceral S ensory information (e.g., taste, baroreceptors, gut distension) CN VII, IX, X (“S olitarius = viS ceral S ensory”)
question

Vagal nuclei: Nucleus ambiguous
answer

M otor innervation of pharynx, larynx, and upper esophagus (e.g., swallowing, palate elevation) CN’s IX, X, XI (“aM biguous = M otor”)
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Vagal nuclei: Dorsal motor nucleus
answer

Sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI.
question

Cranial nerve and vessel pathways: What exits via the cribiform plate?
answer

CN I
question

Cranial nerve and vessel pathways: What exits via the middle cranial fossa?
answer

CN II-VI, thru the sphenoid bone: 1.) Optic canal : CN II, ophthalmic artery, central retinal vein 2.) S uperior orbital fissure : CN III, IV, V-1, VI, ophthalmic vein 3.) Foramen R otundum : CN V-2 4.) Foramen O vale : CN V-3 5.) Foramen spinosum : middle meningeal artery (“Divisions of CN-V exit owing to S tanding R oom O nly”)
question

Cranial nerve and vessel pathways: What exits via the Posterior cranial fossa?
answer

CN VII-XII, thru the temporal and occipital bone: 1.) Internal auditory meatus : CN VII, VIII 2.) Jugular foramen : CN IX, X, XI, jugular vein 3.) Hypoglossal canal : CN XII 4.) Foramen magnum : Spinal roots of CN XI, brain stem, vertebral arteries
question

What/where is the cavernous sinus? What is the route of blood thru it?
answer

A collection of venous sinuses on either side of the pituitary. Blood from eye and superficial cortex | Cavernous sinus | Internal jugular vein
question

What nerves pass through the cavernous sinus?
answer

CN II, IV, V-1, V-2, VI, and postganglionic sympathetic fibers en route to the orbit all pass thru the cavernous sinus. Only CN VI is “free-floating”. Cavernous portion of internal carotid artery is also here.
question

What is cavernous sinus syndrome?
answer

Nerves that control extraocular muscles (plus V-1 and V-2) pass thru the cavernous sinus. Therefore, cavernous sinus syndrome (e.g., due to mass effect): ophthalmoplegia, ophthalmic and maxillary sensory loss.
question

CN XII lesion (LMN) What is the defect?
answer

Tongue deviates toward the side of the lesion (“lick your wounds”)
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CN V motor lesion What is the defect?
answer

Jaw deviates toward the side of lesion
question

CN X lesion what is the defect?
answer

Uvula deviates away from side of lesion
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CN XI lesion what is the defect?
answer

Weakness turning head to contralateral side of lesion. Shoulder droop on side of lesion.
question

Facial lesions: UMN lesion
answer

Lesion of motor cortex or connection btw cortex and facial nucleus. Contralateral paralysis of lower face only, since upper face recives bilateral UMN innervation.
question

Facial lesions: LMN lesion
answer

Ipsilateral paralysis of upper and lower face.
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Facial lesions: Bell’s palsy
answer

Complete destruction of the facial nucleus itself or its branchial efferent fibers (facial nerve proper) Peripheral ipsilateral facial paralysis w/ inability to close eye on involved side. Can occur idiopathically; gradual recovery in most cases.
question

In what dz’s/disorders is Bell’s palsy seen as a complication?
answer

A IDS L yme dz H erpes zoster S arcoidosis T umors D iabetes (“AL exander graH am Bell with STD “)
question

KLM sounds (kuh, la, mi)
answer

Say it aloud. “Kuh-kuh-kuh” tests palate elevation (CN X – vagus) “La-la-la” tests tongue (CN XII – hypoglossal) “Mi-mi-mi” tests lips (CN VII – facial) (“It would be a K aL aM ity to lose CN X, XII, and VII”)
question

Muscles of mastication
answer

3 Muscles close jaw: M asseter, teM poralis, and M edial pterygoid (“M ‘s M unch”) 1 Muscle opens jaw: Lateral pterygoid (“Lateral Lowers” — [lateral pterygoid]) All above are innervated by the trigeminal nerve (V-3)
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Muscles with glossus
answer

All muscles with the root glossus in their names (except palatoglossus, innervated by vagus nerve) are innervated by the hypoglossal nerve. Palat : vagus nerve Glossus : hypoglossal nerve
question

Muscles with palat
answer

All muscles with the root palat in their names (except tensor veli palatini , innervated by mandibular branch of CN V) are innervated by vagus nerve. Palat : vagus nerve (except TENS or, who was too TENSE )
question

Inner ear as a “series of tubes”
answer

A series of tubes in the temporal bone (bony labrynth) filled with perilymph (Na+ rich, similar to ECF) that includes cochlea, vestibule, and semicircular canals. W/in the bony labyrinth is a 2nd series of tubes (membranous labyrinth) filled w/ endolymph (K+ risch, similar to ICF) that includes cochlear duct (w/in the cochlea), utricle and saccule (w/in the vestibule), and semicircular canals. *peri = think outside of the cell (Na+), vs. Endo = think inside the cell (K+)
question

Where is the endolymph (of the inner ear) made?
answer

Made by the stria vascularis.
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What do the utricle and saccule contain? What do they detect?
answer

Contain maculae – detect linear acceleration.
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What do the semicircular canals contain? What do they detect?
answer

Contain A mpullae, detect A ngular acceleration.
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Hair cells (of the inner ear): Where are they? What do they do?
answer

Located w/in the organ of Corti. Are the sensory elements in both vestibular apparatus (spatial orientation) and cochlea (hearing).
question

How can you remember where frequencies are sensed along the cochlear membrane?
answer

The cochlear membrane = scuba flipper: narrow/stiff at the base (high frequency), and wide/flexible at the apex (low frequency).
question

Conductive hearing loss
answer

Bone conduction < air conduction on Rinne; Weber localizes to the affected ear.
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Sensorineural hearing loss
answer

Air conduction < Bone conduction on Rinne; Weber localizes to normal ear.
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Hearing loss in the elderly
answer

High frequency –< low frequency
question

Could you label this picture?
answer

Answers
question

What are the muscles that make up the iris? What receptors do they have, and what are their effects?
answer

Dilator/radial muscle (alpha1 –< myd riasis [pupillary d ilation]) Sphincter/circular/constrictor muscle (M3 –< miosis [pupillary constriction])
question

Where are the ciliary muscles? What receptors do they have, and what effect?
answer

Shown below/right. M3 –< accomodation
question

Where is aqueous humor made? Where is it reabsorbed? [give the whole pathway]
answer

Aqueous humor is made by ciliary process | Travels past lens to posterior Chamber | Anterior chamber | Trabecular meshwork (absorbs aqueous humor | Canal of Schlemm (collects aqueous humor from trabecular meshwork)
question

Glaucoma (general pathogenesis)
answer

Impaired flow of aqueous humor | Increased intraocular pressure | Optic disk atrophy w/ cupping
question

Open angle glaucoma
answer

Obstructed outflow (e.g., canal of Schlemm); associated w/ myopia, advanced age, African-American race. More common, “silent,” painless.
question

Closed angle glaucoma
answer

Obstruction of flow btw iris, lens –< pressure builds up behind iris. Painful, impaired vision. Do NOT give epinephrine.
question

Cataract
answer

Painless, bilateral opacification of lens, leading to decrease in vision. Risk factors: age, smoking, EtOH, sunlight, DM, trauma, infxn.
question

Papilledema
answer

Increased intracranial pressure –< elevated optic disk with blurred margins, bigger blind spot.
question

Innervation of the extraocular muscles?
answer

CN VI innervates the L ateral R ectus CN IV innervates the S uperior O blique CN III innervates the R est Thus, the “chemical formula”: LR6 SO4 R3
question

What are the 3 actions of the superior oblique?
answer

It abducts, intorts, and depresses.
question

CN III damage
answer

Eye looks down and out; ptosis, pupillary dilation, loss of accomodation.
question

CN IV damage
answer

Diplopia w/ defective downward gaze
question

CN VI damage
answer

Medially directed eye.
question

Testing extraocular muscles
answer

To test fxn of each muscle, have te pt look in the following directions: [*note that the oblique muscles are tested by looking medially and opposite to what you would expect from “superior” and “inferior”] “IOU : to test I nferior O blique, have pt look U p.”
question

Strabismus vs. Amblyopia
answer

Strabismus is misalignment of eyes. Multiple etiologies. Amblyopia is a reduction of vision from disuse in critical period. May be secondary to strabismus, deprivation, unequal refractive errors.
question

What controls pupillary constriction (miosis)
answer

P upillary sphincter muscle, P arasympathetic innervation. Innervation — CN III from Edinger-Westphal nucleus –< ciliary ganglion.
question

What controls pupillary D ilation (myD riasis)?
answer

RaD ial muscle (aka pupillary D ilator muscle), sympathetic. Innervation — T1 preganglionic sympathetic –< superior cervical ganglion –< postganglionic sympathetic –< long ciliary nerve.
question

Pupillary light reflex
answer

Light in either retina sends a signal via CN II to pretectal nuclei (dashed lines, below) in midbrain that activate bilateral Edinger-Westphal nuclei; pupils constrict bilaterally (consensual reflex). Result: illumination of 1 eye results in bilateral pupillary constriction.
question

Marcus Gunn pupil
answer

Afferent pupillary defect (e.g., due to optic nerve damage or retinal detachment). Decreased bilateral pupillary constriction when light is shone in affected eye.
question

CN III in cross-section
answer

Center carries output to ocular muscles, affected primarily by vascular disease (e.g., DM) Outside carries parasympathetic output, affected 1st by compression (e.g., PCA berry aneurysm, uncal herniation); use pupillary light reflex in assessment, “blown pupil”
question

Retinal detachment
answer

Separation of neurosensory layer of retina from pigment epithelium | Degeneration of photoreceptors | Vision loss May be secondary to trauma, diabetes.
question

Age-related macular degeneration (ARMD)
answer

Degeneration of macula (central area of retina). Causes loss of central vision (scotomas). “Dry”/atrophic ARMD is slow, causes gradual decrease in vision “Wet” ARMD is rapid, due to neovascularization.
question

Visual field defects: Right anopia What would this look like in the visual field? Where is the lesion?
answer

#1, below
question

#1, below What is this visual field defect called?
answer

Right anopia
question

Visual field defects: Bitemporal hemianopia What would this look like in the visual field? Where is the lesion?
answer

#2, below
question

#2, below What is this visual field defect called?
answer

Bitemporal hemianopia
question

Visual field defects: Left homonymous hemianopia What would this look like in the visual field? Where is the lesion?
answer

#3, below
question

#3, below What is this visual field defect called?
answer

Left homonymous hemianopia
question

Visual field defects: Left upper quadrantic anopia (right temporal lesion) What would this look like in the visual field? Where is the lesion?
answer

#4, below
question

#4, below What is this visual field defect called?
answer

Left upper quadrantic anopia (right temporal lesion)
question

Visual field defects: Left lower quadrantic anopia (right parietal lesion) What would this look like in the visual field? Where is the lesion?
answer

#5, below
question

#5, below What is this visual field defect called?
answer

Left lower quadrantic anopia (right parietal lesion)
question

Visual field defects: Left hemianopia w/ macular sparing What would this look like in the visual field? Where is the lesion?
answer

#6, below
question

#6, below What is this visual field defect called?
answer

Left hemianopia w/ macular sparing
question

Visual field defects: Central scotoma (macular degeneration) What would this look like in the visual field? Where is the lesion?
answer

#7, below
question

#7, below What is this visual field defect called?
answer

Central scotoma (macular degeneration)
question

Internuclear ophthalmoplegia (MLF syndrome)
answer

Lesion in the medial longitudinal fasciculus (MLF) –< medial rectus palsy on attempted lateral gaze. Nystagmus in abducting eye. Convergence normal. Syndrome is seen in many pts w/ multiple sclerosis ("M LF = M S") When looking left, the left nucleus of CN VI fires, which contracts the lateral rectus and stimulates the contralateral (right) nucleus of CN III via the right MLF to contract the right medial rectus.
question

Dementia (defined)
answer

Decreased cognitive ability, memory, fxn, with intact consciousness.
question

Alzheimer’s dz: Epidemiology? Groups at increased risk?
answer

Most common cause of dementia in the elderly. Down syndrome pts are at increased risk of developing AD.
question

Alzheimer’s dz: genetics?
answer

Familial form (10%) assocaited w/ genes on chromosomes 1, 14, 19 (APOE4 allele; autosomal dominant), and 21 (p-App ) gene.
question

Alzheimer’s dz: pathogenesis?
answer

Widespread, accelerated cortical atrophy with decreased ACh. Associated w/ senile plaques (extracellular, beta-amyloid core) and neurofibrillary tangles (intracellular, abnormally phosphorylated tau protein; tangles correlate w/ degree of dementia). May cause amyloid angiopathy –< intracranial hemorrhage.
question

Pick’s dz (frontotemporal dementia)
answer

Dementia, aphasia, parkinsonian aspects; Associated w/ Pick bodies (intracellular, aggregated tau protein), frontotemporal lobe atrophy. Spares parietal lobe and posterior 2/3rds of superior temporal gyrus.
question

Lewy body dementia
answer

Parkinsonism with dementia and hallucinations. Caused by alpha-synuclein defect.
question

Creutzfeldt-Jakob dz (CJD)
answer

Rapidly progressive (wks-mos) dementia w/ myoclonus, spongiform cortex; associated w/ prions.
question

“Other” causes of dementia
answer

Multi-infarct (2nd most common cause of dementia in the elderly) Syphilis HIV Vitamin B12 deficiency Wilson’s dz
question

Multiple sclerosis: What is it?
answer

Autoimmune inflammation and demyelination of CNS (brain and spinal cord).
question

Multiple sclerosis: How do pts present? What is the course of the dz?
answer

Pts can present with: optic neuritis (sudden loss of vision) MLF syndrome (internuclear ophthalmoplegia) Hemiparesis Hemisensory Sx’s Bowel/bladder incontinence. Relapsing and remitting course.
question

Multiple sclerosis: Who is affected?
answer

Most often affects women in their 20s and 30s; more common in whites.
question

Findings in multiple sclerosis
answer

Elevated protein (IgG) in CSF. Periventricular plaques (areas of oligodendrocyte loss and reactive gliosis) w/ preservation of axons.
question

Charcot’s triad of MS
answer

Charcot’s traid of MS is a SIN : S canning speech I ntention tremor (+I ncontinence, I nternuclear ophthalmoplegia) N ystagmus
question

Tx for multiple sclerosis
answer

Beta-interferon or immunosuppressant therapy. Symptomatic Tx for neurogenic bladder, spasticity, and pain.
question

Guillan-Barre syndrome (acute inflammatory demyelinating polyradiculopathy) What is it/what are the main Sx?
answer

Inflammation and demyelination of peripheral nerves and motor fibers of ventral roots (sensory effect less severe than motor), causing symmetric ascending muscle weakness beginning in distal lower extremities. Facial paralysis in 50% of cases. Autonomic fxn may be severely affected (e.g., cardiac irregularities, HTN, or hypotension).
question

Guillan-Barre syndrome (acute inflammatory demyelinating polyradiculopathy) What is the prognosis?
answer

Almost all pts survive; the majority recover completely after wks to months.
question

Guillan-Barre syndrome (acute inflammatory demyelinating polyradiculopathy): Findings?
answer

Elevated CSF protein w/ normal cell count (albuminocytologic dissociation). Elevated protein –< papilledema.
question

Guillan-Barre syndrome (acute inflammatory demyelinating polyradiculopathy): is associated with…?
answer

Associated with infxns –< autoimmune attack of peripheral myelin due to molecular mimicry (e.g., Campylobacter jejuni or herpesvirus infxn), inoculations, and stress, but no definitive link to pathogens.
question

Guillan-Barre syndrome (acute inflammatory demyelinating polyradiculopathy): Management/Tx?
answer

Respiratory support is critical until recovery. Additional Tx: plasmapheresis, IV immune globulins.
question

Progressive multifocal leukoencephalopathy (PML)
answer

Demyelination of CNS due to destruction of oligodendrocytes. Associated w/ JC virus and seen in 2-4% of AIDS pts (reactivation of latent viral infxn). Rapidly progressive, usually fatal.
question

Acute disseminated (postinfectious) encephalomyelitis
answer

Multifocal perivenular inflammation and demyelination after infxn (e.g., chickenpox, measles) or certain vaccinations (e.g., rabies, smallpox)
question

Metachromatic leukodystrophy
answer

Autosomal-recessive lysosomal storage dz, most commonly due to arylsulfatase A deficiency. Builup of sulfatides leads to impaired production of myelin sheath.
question

Charcot-Marie Tooth disease (aka hereditary motor and sensory neuropathy HMSN)
answer

Group of progressive hereditary nerve d/o’s related to defective production of proteins involved in the structure and fxn onf peripheral nerves or the myelin sheath.
question

Seizure
answer

Characterized by synchronized, high-frequency neuronal firing. Variety of forms.
question

Partial seizures
answer

1 area of brain. Most commonly originates in the mesial temporal lobe. Often preceded by seizure aura; can secondarily generalize.
question

2 types of partial seizures
answer

1.) Simple partial (consciousness intact): motor, sensory, autonomic, psychic 2.) Complex partial (impaired consciousness)
question

Generalized seizures
answer

Diffuse.
question

5 Types of generalized seizures
answer

1.) Absence (petit mal) – blank stare 2.) Myoclonic – quick, repetitive jerks 3.) Tonic-clonic (grand mal) – alternating stiffening and movement 4.) Tonic – stiffening 5.) Atonic – “drop” seizures (falls to floor); commonly mistaken for fainting
question

Epilepsy
answer

A d/o of recurrent seizures (febrile seizures are not epilsepsy)
question

Causes of seizures by age: Children?
answer

Genetic Infxn (febrile) Trauma Congenital Metabolic
question

Causes of seizures by age: Adults?
answer

Tumors Trauma Stroke Infxn
question

Causes of seizures by age: Elderly?
answer

Stroke Tumor Trauma Metabolic Infxn
question

Headache (definition)
answer

Pain due to irritation of structures such as dura, cranial nerves, or extracranial structures, not brain parenchyma itself.
question

Migrain headache
answer

4-72 hours of unilateral pulsating pain w/ nausea, photophobia, or phonophobia. +/- “aura” of neurologic Sx before HA, including visual dsensory, speech disturbances. Due to irritation of CN V and release of substance P, CGRP, vasoactive peptides.
question

Tension headache
answer

< 30 minutes of bilateral steady pain. Not aggravated by light or noise; no aura.
question

Cluster headache
answer

Repetitive brief headaches characterized by unilateral periorbital pain associated w/ ipsilateral lacrimation, rhinorrhea, Horner’s syndrome. Much more common in males.
question

“Other” causes of headache
answer

Subarachnoid hemorrhage (“worst headache of my life”) Meningitis Hydrocephalus Neoplasia Arteritis
question

Vertigo (definition)
answer

Illusion of movement, not to be confused w/ dizziness or lightheadedness.
question

Peripheral vertigo
answer

More common type. Inner ear etiology (e.g., semicircular canal debris, vestibular nerve infxn, Meniere’s dz). Positional testing –< delayed horizontal nystagmus.
question

Central vertigo
answer

Brain stem or cerebellar lesion (e.g., vestibular nuclei, posterior fossa tumor). Positional testing –< immediate nystagmus in any direction; may change directions.
question

Neurocutaneous disorders: Sturge-Weber syndrome
answer

Congenital d/o w/ port-wine stains and ipsilateral leptomeningeal angioma. Can cause glaucoma, seizures, hemiparesis, and mental retardation. Occurs sporadically.
question

Neurocutaneous disorders: Tuberous sclerosis
answer

Hamartomas in CNS, skin, organs; cardiac rhabdomyoma, renal agiomyolipoma, subependymal giant cell astrocytoma, MR, seizures, hypopigmented “ash leaf spots,” sebaceous adenoma, shagreen patch. Autosomal dominant.
question

Neurocutaneous disorders: Neurofibromatosis type I (von Recklinghausen’s disease)
answer

Café-au-lait spots Lisch nodules (pigmented iris hamartomas) Neurofibromas in skin. Autosomal dominant
question

Neurocutaneous disorders: von Hippel-Lindau dz
answer

Cavernous hemangiomas in skin, mucosa, organs; renal cell carcinoma hemangioblastoa in retina, brain stem, cerebellum. Autosomal dominant.
question

Primary brain tumors
answer

Clinical presentation due to mass effects (e.g., seizures, demential, focal lesions); Primary tumors rarely undergo metastasis. The majority of adult primary tumors are supratentorial, while the majority of childhood primary tumors are infratentorial. Note: half of adult brain tumors are metastases (well circumscribed; usually present at the gray-white junction).
question

Adult peak incidence tumors: Glioblastoma multiforme (grade IV astrocytoma)
answer

Most common primary brain tumor. Prognosis grave; > 1yr life expectancy. Found in cerebral hemispheres. Can cross corpus callosum (“butterfly glioma” [below]) Stain astrocytes for GFAP. “Pseudopalisading” pleomorphic tumor cells — border central areas of necrosis and hemorrhage [above/right]
question

Most common primary brain tumor. Prognosis grave; > 1yr life expectancy. Found in cerebral hemispheres. Can cross corpus callosum (“butterfly glioma” [below]) Stain astrocytes for GFAP. “Pseudopalisading” pleomorphic tumor cells — border central areas of necrosis and hemorrhage [above/right] What tumor does this describe?
answer

Glioblastoma multiforme (grade IV astrocytoma)
question

Adult peak incidence tumors: Meningioma
answer

2nd most common primary brain tumor. Most often occurs in convexities of hemispheres and parasagittal region. Arises from arachnoid cells external to brain. Resectable. Spindle cells concentrically arranged in a whorled pattern; psammoma bodies (laminated calcifications).
question

2nd most common primary brain tumor. Most often occurs in convexities of hemispheres and parasagittal region. Arises from arachnoid cells external to brain. Resectable. Spindle cells concentrically arranged in a whorled pattern; psammoma bodies (laminated calcifications). What tumor does this describe?
answer

Meningioma
question

Adult peak incidence tumors: Schwannoma
answer

3rd most common primary brain tumor. Schwann cell origin; often localized to CN VIII –< acoustic schwannoma. Resectable. Bilateral schwannoma found in neurofibromatosis type II.
question

Adult peak incidence tumors: Oligodendroma
answer

Relatively rare, slow groing. Most often in frontal lobes. Chicken-wire capillary pattern. ‘ Oligodendrocytes = “fried egg” cells — round nuclei w/ clear cytoplasm. Often calcified in oligodendroglioma.
question

Adult peak incidence tumors: Pituitary adenoma
answer

Most commonly prolactinoma. Bitemporal hemianopia (due to pressure on optic chiasm) and hyper- or hypopituitarism are sequelae. Rathke’s pouch.
question

Childhood peak incidence tumors: Pilocytic (low-grade) astocytoma
answer

Usually well circumscribed. In children, most often found in posterior fossa. May be supratentorial. GFAP positive. Benign; good prognosis. Rosenthal fibers — eosinophilic, corkscrew fibers.
question

Usually well circumscribed. In children, most often found in posterior fossa. May be supratentorial. GFAP positive. Benign; good prognosis. Rosenthal fibers — eosinophilic, corkscrew fibers. What tumor does this describe?
answer

Pilocytic (low-grade) astocytoma
question

Childhood peak incidence tumors: Medullo-blastoma
answer

Highly malignant cerebellar tumor. A form of primitive neuroectodermal tumor (PNET). Can compress 4th ventricle, causing hydrocephalus. Rosettes or perivascular pseudorosette pattern cells. Radiosensitive.
question

Highly malignant cerebellar tumor. A form of primitive neuroectodermal tumor (PNET). Can compress 4th ventricle, causing hydrocephalus. Rosettes or perivascular pseudorosette pattern cells. Radiosensitive. What tumor does this describe?
answer

Medullo-blastoma
question

Childhood peak incidence tumors: Ependymoma
answer

Ependymal cell tumors most commonly found in 4th ventricle. Can cause hydrocephalus. Poor prognosis. Characteristic perivascular pseudorosettes. Rod-shaped blepharoplasts (basal ciliary bodies) found near nucleus.
question

Ependymal cell tumors most commonly found in 4th ventricle. Can cause hydrocephalus. Poor prognosis. Characteristic perivascular pseudorosettes. Rod-shaped blepharoplasts (basal ciliary bodies) found near nucleus. What tumor does this describe?
answer

Ependymoma
question

Childhood peak incidence tumors: Hemangioblastoma
answer

Most often cerebellar; associated w/ von Hippel-Lindau syndrome when found w/ retinal angiomas. Can produce EPO –< secondary polycythemia. Foamy cells and high vascularity are characteristic.
question

Most often cerebellar; associated w/ von Hippel-Lindau syndrome when found w/ retinal angiomas. Can produce EPO –< secondary polycythemia. Foamy cells and high vascularity are characteristic. What tumor does this describe?
answer

Hemangioblastoma
question

Childhood peak incidence tumors: Craniopharyngioma
answer

Benign childood tumor, confused w/ pituitary adenoma (can also cause bitemporal hemianopia). Most common childhood supratentorial tumor. Derived from remnants of Rathke’s pouch. Calcification is common (tooth enamel-like).
question

Benign childood tumor, confused w/ pituitary adenoma (can also cause bitemporal hemianopia). Most common childhood supratentorial tumor. Derived from remnants of Rathke’s pouch. Calcification is common (tooth enamel-like). What tumor does this describe?
answer

Craniopharyngioma
question

Herniation syndromes: Cingulate (subfalcine) herniation under falx cerebri
answer

Can compress anterior cerebral artery. #1 below:
question

Can compress anterior cerebral artery. #1 below: What herniation syndrome is this?
answer

Cingulate (subfalcine) herniation under falx cerebri
question

Herniation syndromes: Downward transtentorial (central) herniation
answer

#2 below
question

#2 below What herniation syndrome is this?
answer

Downward transtentorial (central) herniation
question

Herniation syndromes: Uncal herniation
answer

(hint: Uncus = medial temporal lobe) #3 below:
question

#3 below: What herniation syndrome is this?
answer

Uncal herniation (hint: Uncus = medial temporal lobe)
question

Herniation syndromes: Cerebellar tonsillar herniation into the foramen magnum
answer

#4 below:
question

#4 below: What herniation syndrome is this?
answer

Cerebellar tonsillar herniation into the foramen magnum
question

Hernation syndromes: what is the biggest danger?
answer

Coma and death result when these hernations compress the brain stem.
question

Clinical signs of uncal herniation: Ipsilateral dilated pupil/pstosis
answer

Stretching of CN III (innervates levator palpebrae)
question

Clinical signs of uncal herniation: Contralateral homonymous hemianopia
answer

Compression of ipsilateral posterior cerebral artery
question

Clinical signs of uncal herniation: Ipsilateral paresis
answer

Compression of contralateral crus cerebri (Kernohan’s notch)
question

Clinical signs of uncal herniation: Duret hemorrhages — paramedian artery rupture
answer

Caudal displacement of brain stem.
question

Epinephrine Class of drug? Mechanism? SE’s?
answer

alpha-agonist. Decreases aqueous humor synthesis due to vasoconstriction. SE: mydriasis, stinging; do not use in closed-angle glaucoma.
question

Brimonide Class of drug? Mechanism? SE’s?
answer

alpha-agonist. Decreased aqueous humor synthesis. SE: no pupillary or vision changes.
question

Timolol, betaxolol, carteolol Class of drug? Mechanism? SE’s?
answer

beta-blockers. Decrease aqueous humor secretion SE: no pupillary or vision changes.
question

Acetazolamide Class of drug? Mechanism? SE’s?
answer

Diuretic. Decrease aqueous humor secretion due to decreased HCO3- (via inhibition of carbonic anhydrase) SE: no pupillary or vision changes.
question

Pilocarpine, carbachol, physostigmine, echothiophate Class of drug? Mechanism? SE’s?
answer

Cholinomimetics Increase outflow of aqueous humor; contract ciliary muscle and open trabecular meshwork; use pilocarpine in emergencies; very effective at opening canal of Schlemm. SE: Miosis, cyclospasm.
question

Latanoprost (PGF-2alpha) Class of drug? Mechanism? SE’s?
answer

Prostaglandin. Increases outflow of aqueous humor. SE: darkens color of iris (browning).
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Opioid analgesics (list)
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Morphine Fentanyl Codeine Heroin Methadone Meperidine Dextromethorphan
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Mechanism of opioid analgesics
answer

Act as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission — open K+ channels, close Ca2+ channels, leading to decrease in synaptic transmission.
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Clinical toxicity of opioid analgesics
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Pain cough suppression (dextromethorphan) diarrhea (loperamide and diphenoxylate) acute pulmonary edema maintenance programs for addicts (methadone)
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Toxicity of opioid analgesics
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Addiction Respiratory depression Constipation Miosis (pinpoint pupils ) Additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated w/ naloxone or naltrexone (opioid receptor antagonist).
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Mechanism of butorphanol
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Partial agonist at opioid mu receptors, agonst at kappa receptors.
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Clinical use of butorphanol
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Pain; causes less respiratory depression than full agonists.
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Toxicity of butorphanol
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Causes withdrawal if on full agonist.
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Mechanism of tramadol
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Very weak opioid agonist; also inhibits serotonin and NE reuptake (works on multiple neurotransmitters — “tram it all ” in).
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Clinical use of tramadol
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Chronic pain.
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Toxicity of tramadol
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Similar to opioids. Decreases seizure threshold.
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Epilepsy drugs: Phenytoin Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?
answer

Used in partial seizures (simple and complex). 1st line drug for Tonic-clonic seizures. 1st line drug for prophylaxis of status seizures. Mechanism: increased Na+ channel inactivation.
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Used in partial seizures (simple and complex). 1st line drug for Tonic-clonic seizures. 1st line drug for prophylaxis of status seizures. Mechanism: increased Na+ channel inactivation. What epilepsy drug does this describe?
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Phenytoin
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Epilepsy drugs: Carbamezepine Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?
answer

Used for partial seizures (simple and complex). 1st line drug for tonic-clonic seizures. Mechanism: increases Na+ channel inactivation. *Also 1st line drug for trigemnial neuralgia.
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Used for partial seizures (simple and complex). 1st line drug for tonic-clonic seizures. Mechanism: increases Na+ channel inactivation. *Also 1st line drug for trigemnial neuralgia. What epilepsy drug does this describe?
answer

Carbamezepine
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Epilepsy drugs: Lamotrigine Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?
answer

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: blocks VG-Na+ channels.
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Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: blocks VG-Na+ channels. What epilepsy drug does this describe?
answer

Lamotrigine
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Epilepsy drugs: Gabapentin Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?
answer

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: increases GABA release. *Also used for peripheral neuropathy.
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Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: increases GABA release. *Also used for peripheral neuropathy. What epilepsy drug does this describe?
answer

Gabapentin
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Epilepsy drugs: Topiramate Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?
answer

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: blocks Na+ channels, increases GABA action
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Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: blocks Na+ channels, increases GABA action What epilepsy drug does this describe?
answer

Topiramate
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Epilepsy drugs: Phenobarbital Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?
answer

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: increases GABA-A action. *1st line in pregnant women, children.
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Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: increases GABA-A action. *1st line in pregnant women, children. What epilepsy drug does this describe?
answer

Phenobarbital
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Epilepsy drugs: Valproic acid Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?
answer

Used for partial seizures (simple and complex). 1st line drug for tonic-clonic seizures. May also be used in absence seizures. Mechanism: increases Na+ channel inactivation, increases GABA concentration. *Also used for myoclonic seizures.
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Used for partial seizures (simple and complex). 1st line drug for tonic-clonic seizures. May also be used in absence seizures. Mechanism: increases Na+ channel inactivation, increases GABA concentration. *Also used for myoclonic seizures. What epilepsy drug does this describe?
answer

Valproic acid
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Epilepsy drugs: Ethosuximide Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?
answer

1st line drug for absence seizures. Mechanism: blocks thalamic T-type Ca2+ channels.
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1st line drug for absence seizures. Mechanism: blocks thalamic T-type Ca2+ channels. What epilepsy drug does this describe?
answer

Ethosuximide
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Epilepsy drugs: Benzodiazepines (diazepam or lorazepam) Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?
answer

1st line for acute status seizures. Mechanism: increase GABA-A action. *Also used for seizures of eclampsia (1st line to prevent seizures of eclampsi is MgSO4)
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1st line for acute status seizures. Mechanism: increase GABA-A action. *Also used for seizures of eclampsia (1st line to prevent seizures of eclampsi is MgSO4) What epilepsy drug does this describe?
answer

Benzodiazepines (diazepam or lorazepam)
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toxicity of epilepsy drugs: Toxicity of Benzodiazepines
answer

Sedation Tolerance Dependence
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toxicity of epilepsy drugs: Toxicity of Carbamazepine
answer

Diplopia Ataxia Blood dyscrasias (agranulocytosis, aplastic anemia) Liver toxicity Teratogenesis Induction of cytochrome P-450
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toxicity of epilepsy drugs: Toxicity of ethosuximide
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GI distress Fatigue Headache Urticaria Stevens-Johnson syndrome (“EFGH = E thosuximide, F atigue, G I, H eadache”)
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toxicity of epilepsy drugs: Stevens-Johnson syndrome
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prodrome of malaise and fever followed by rapid onset of erythematous/purpuric macules (oral, ocular, genital). Skin lesions progress to epidermal necrosis and sloughing.
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toxicity of epilepsy drugs: Toxicity of phenobarbital
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Sedation Tolerance Dependence Induction of cytochrome P-450
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toxicity of epilepsy drugs: Toxicity of phenytoin
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Nystagmus Diplopia Ataxia Sedation Gingival hypreplasia Hirsutism Megaloblastic anemia Teratogenesis SLE-like syndrome Induction of cytochrome P-450
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toxicity of epilepsy drugs: Toxicity of valproic acid
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GI distress rare but fatal hepatotoxicity (measure LFTs) Neural tube defects in fetus (spina bifida) Tremor Weight gain. Contraindicated in pregnancy.
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toxicity of epilepsy drugs: Toxicity of lamotrigine
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Stevens-Johnson syndrome
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toxicity of epilepsy drugs: Toxicity of Gabapentin
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Sedation Ataxia
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toxicity of epilepsy drugs: Toxicity of Topiramate
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Sedation Mental dulling Kidney stones Weight loss
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Mechanism of phenytoin
answer

Use-dependent blockade of Na+ channels; inhibition of glutamate release from excitatory presynaptic neuron.
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Clinical use of phenytoin
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Tonic-clonic seizures. Also a class IB antiarrhythmic.
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Toxicity of phenytoin
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Nystagmus, ataxia, diplopia, sedation, SLE-like syndrome, induction of cytochrome P-450. Chronic use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia (decreased folate absorption). Teratogenic (fetal hydantoin syndrome).
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Mechanism of barbiturates (phenobarbital, pentobarbital, thiopental, secobarbital)
answer

Facilitate GABA-A action by increasing duration of Cl- channel opening, thus decreasing neuron firing. (“BarbiDURAT e [increased DURAT ion]”)
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Clinical use of barbiturates (phenobarbital, pentobarbital, thiopental, secobarbital)
answer

Sedative for anxiety, seizures, insomnia, induction of anestheisa (thiopental)
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Toxicity of of barbiturates (phenobarbital, pentobarbital, thiopental, secobarbital)
answer

Dependence, additive CNS depression effects w/ EtOH, respiratory or CV depression (can lead to death), drug interactions owing to induction of liver microsomal enzymes (cytochrome P-450). Tx overdose w/ Sx managment (assist respiration, increase BP) Contraindicated in pregnancy.
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Mechanism of benzodiazepines (diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam)
answer

Facilitate GABA-A action by increasing frequency of Cl- channel opening. Decreases REM sleep. Most have long half-lives and active metabolites. (“FRE enzodiazepines [increased FRE quency]”)
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Short acting benzodiazepines
answer

TOM thumb T riazolam O xazepam M idazolam. Highest addictive potential.
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Clinical use of benzodiazepines (diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam)
answer

Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially EtOH withdrawal – DTs), night terrors, sleep walking.
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Toxicity of benzodiazepines (diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam)
answer

Dependence, additive CNS depression effects w/ EtOH. Less risk of respiratory depression and coma than w/ barbiturates. Tx overdose w/ flumazenil (competitive antagonist at GABA receptor)
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General principles of anesthetics: CNS drugs must be…?
answer

CNS drugs must be lipid soluble (cross the BBB) or be actively transported.
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General principles of anesthetics: Solubility and drug effect?
answer

Drugs with low solubility in blood = rapid induction and recovery times. Drugs with high solubility in lipids = high potency = 1 / MAC (where MAC = Minimum Alveolar Concentration at which 50% of the population is anesthetized. Decreases w/ age). e.g., N2O has low blood and lipid solubility, and thus fast induction and low potency. Halothane, in contrast, has high lipid and blood solubility, and thus high potency and slow induction.
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Inhaled anesthetics (list)
answer

Halothane Enflurane Isoflurane Sevoflurane Methoxyflurane Nitrous oxide
question

Mechanism of inhaled anesthetics
answer

Unknown!
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Effects of inhaled anesthetics
answer

Myocardial depression Respiratory depression Nausea/emesis Increased cerebral blood flow (decreased cerebral metabolic demand)
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Toxicity of inhaled anesthetics
answer

Hepatoxicity (halothane) Nephrotoxicity (methoxyflurane) Proconvulsant (enflurane) Malignant hyperthermia (rare) Expansion of trapped gas (nitrous oxide)
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IV anesthetics (list)
answer

B arbiturates B enzodiazepines Arylcyclohexylamins (K etamine) Opiates Propofol (“BB K ing on OPIATES POPO ses FOOL ishly”)
question

Barbiturates (as IV anesthetics)
answer

Thiopental — high potency, high lipid solubility, rapid entry into brain. Used for induction of anesthesia and short surgical procedures. Effect terminated by redistribution from brain. Decreased cerebral blood flow.
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Benzodiazepines (as IV anesthetics)
answer

Midazolam most common drug used for endoscopy; used adjuctively w/ gaseous anesthetics and narcotics. May cause severe postoperative respiratory depression, decr BP (Tx overdose w/ flumazenil), and amnesia.
question

Arylcyclohexamines (Ketamine) — as IV anesthetics
answer

PCP analogs that act as dissociative anesthetics. Block NMDA receptors. Cardiovascular stimulants. Cause disorientation, hallucination, and bad dreams. Increase cerebral blood flow.
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Opiates (as IV anesthetics)
answer

Morphine, fentanyl used w/ other CNS depressants during general anesthesia.
question

Propofol (as an IV anesthetic)
answer

Used for rapid anesthesia induction and short procedures. Less postoperative nausea than thiopental. Potentiates GABA-A.
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Local anesthetics (list)
answer

Esters Procaine, cocaine, tetracain Amides lI docaI ne, mepI vacaI ne, bupI vacaI ne (“amI des have 2 I ‘s in their names)
question

Mechanism of local anesthetics
answer

Block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effecctive in rapidly firing neurons. Tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels in charged form.
question

3 principles of local anesthetics
answer

1.) In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively. More anesthetic is needed in these cases. 2.) Order of nerve blockade: Small-diameter fibers < large diameter. Myelinated fibers < unmyelinated fibers. Overall, size factor predominates over myelination such that: small myelinated fibers < small unmyelinated fibers < large myelinated fibers < large unmyelinated fibers. Order of loss: pain (lose first) < temperature < touch < pressure (lost last). 3.) Except for cocain, given w/ vasoconstrictors (usually epinephrine) to enhance local action: decreased bleeding, increased anesthesia by decreasing systemic concentration.
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Clinical use of local anesthetics
answer

Minor surgical procedures, spinal anesthesia. If allergic to esters, give amides.
question

Toxicity of local anesthetics
answer

CNS excitation, severe cardiovascular toxicity (bupivacaine), HTN, hypotension, and arrhytmias (cocaine)
question

Neuromuscular blocking drugs (generally)
answer

Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.
question

Depolarizing neuromuscular blocking drugs
answer

Succinylcholine (complications include hypercalcemia and hyperkalemia) Reversal of blockade: Phase I (prolonged depolarization) — no antidote. Block potentiated by cholinesterase inhibitors. Phase II (repolarized but blocked) — antidote consists of cholinesterase inhibitors (e.g., neostigmine)
question

Nondepolarizing neuromuscular blocking drugs
answer

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium. Competitive: compete w/ ACh for receptors. Reversal of blockade: neostigmine, edrophonium, and other cholinesterase inhibitors.
question

Uses of dantrolene
answer

Used in Tx of malignant hyperthermia, which is caused by the concomitant use of inhalation anesthetics (except N2O) and succinylcholine. Also used to Tx neuroleptic malignant syndrome (a toxicity of antipsychotic drugs)
question

Mechanism of dantrolene
answer

Prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.
question

What is Parkinson’s dz due to (that is addressed by anti-PD drugs)? What agents are used?
answer

Parkinsonism is due to loss of dopaminergic neurons and excess cholinergic activity. “BALSA” B romocriptine A mantadine L evodopa (with carbidopa) S elegiline (and COMT inhibitors) A ntimuscarinics
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Parkinson’s dz drugs, strategy: Agonize dopamine receptors Agents?
answer

Bromocriptine (ergot alkaloid and partial dopamine agonist) Pramipexole Ropinirole
question

Parkinson’s dz drugs, strategy: Increase dopamine Agents?
answer

Amantadine (may increase dopamine release); also used as an antiviral against influenza A and rubella; toxicity = ataxia. L-dopa/carbidopa (converted to dopamine in the CNS)
question

Parkinson’s dz drugs, strategy: Prevent dopamine breakdown Agents?
answer

Selegiline (selective MAO type B inhibitor); Entacapone, Tolcapone (COMT inhibitors)
question

Parkinson’s dz drugs, strategy: Curb excess cholinergic activity Agents?
answer

Benz tropine (A ntimuscarinic; improves tremor and rigidity but has little effect on bradykinesia). (“Tx your tremor before you drive your Mercedes-BENZ “)
question

For Tx of essential familly tremors?
answer

Use beta-blocker.
question

Mechanism of L-dopa (levodopa)/carbidopa
answer

Increase level of dopamine in brain. Unlinke dopamine, L-dopa can cross BBB and is converted by dop decarboxylase in the CNS to dopamine.
question

Clinical use of L-dopa (levodopa)/carbidopa
answer

Parkinsonism
question

Toxicity of L-dopa (levodopa)/carbidopa
answer

Arrhythmias from peripheral conversion to dopamine. Long-term use can –< dyskinesia following administration, akinesia btw doses. Carbidopa, a peripheral decarboxylase inhibitor, is given w/ L-dopa in order to increase the bioavailability of L-dopa in the brain and to limit peripheral SE's.
question

Mechanism of selegiline
answer

Selectively inhibits MAO-B, thereby increasing the availability of dopamine.
question

Clinical use of selegiline
answer

Adjunctive agent to L-dopa in Tx of Parkinson’s dz.
question

Toxicity of selegiline
answer

May enhance adverse effects of L-dopa.
question

Mechanism of Sumatriptan
answer

5-HT[1B/1D]* agonist. Causes vasoconstriction, inhibition of trigeminal activation and vasoactive peptide release. Half-life is > 2 hours. [*the “1B/1D” in brackets is subscript]
question

Clinical use of sumatriptan
answer

Acute migraine, cluster HA attacks.
question

Toxicity of Sumatriptan
answer

Coronary vasospasm (contraindicated in pts w/ CAD or Prinzmetal’s angina) Mild tingling.
question

Alzheimer’s drugs: Memantine mechanism?
answer

NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+)
question

Alzheimer’s drugs: Memantine Toxicity?
answer

Dizziness, confusion, hallucinations.
question

Alzheimer’s drugs: Donepezil mechanism?
answer

Acetylcholinesterrase inhibitor
question

Alzheimer’s drugs: Donepezil Toxicity?
answer

Nausea, dizziness, insomnia.

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