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524 Cards in this Set
- Front
- Back
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Question
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Answer
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Patient presents with decreased pain and temperature sensation over the lateral aspects of both arms.a
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Syringomyelia.
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Penlight in patient’s right eyeiproduces bilateral pupillary constriction. When moved to the left eye, there is paradoxical dilatation.
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Atrophy of the left optic nerve.
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Patient describes decreaed prick sensation on the lateral aspect of her leg and foot.
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Dorsiflexion and eversion of foot (common peroneal nerve).
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Elderly woman presents with arthritis and tingling over the lateral digits of her right hand.
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Carpal tunnel syndrome, median nerve compression.
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20-year-old dancer reports decreased plantar flexion and sensation over the back of her thigh, calf, and lateral half of her foot.n
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Tibial (L4–S3). injury
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Woman involved in a motor vehicle accident cannot turn her head to the left and has and right shoulder droop.
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Right CN XI (runs through jugular foramen with CN IX X), innervating sternocleidomastoid and trapezius muscles.n
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Man presents with one wild, flailing arm.
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lesion of Contralateral subthalamic nucleus (hemiballismus).s
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Patient with cortical lesion does not know that he has a disease.
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lesion of Right parietal lobe.
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Patient cannot protrude tongue toward left side and has a right-sided spastic paralysis
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lesion in Left medulla, CN XII.
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Teen falls while rollerblading and hurts his elbow. He can’t feel the medial part of his palm.l
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Ulnar nerve due to broken medial condyle.
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Field hockey player presents to the ER after falling on her arm during practice. with midshaft humerous break. complications
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Radial nerve and deep brachial artery, which run together.
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patient can't blink on right side and can't seal lips
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bells' palsy CN VII
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patient complains of pain numbness and tingling and has wasting of thenar eminence
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carpal tunnel syndrome; median nerve
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stage of sleep with variable BP,penile tumescence, and variable EEG.
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REM sleep.
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Woman presents with headache, visual disturbance, galactorrhea, and amenorrhea.
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Prolactinoma.
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43-year-old man experiences dizziness and tinnitus. CT shows enlarged internal acoustic meatus.z
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Schwannoma.
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25-year-old female presents with sudden uniocular vision loss and slightly slurred speech. She has a history of weakness and paresthesias that have resolved.
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Multiple sclerosis.
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10-year-old child “spaces out” in class (e.g., stops talking midsentence and then continues as if nothing had happened).
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Absence seizures.
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Man on several medications, including antidepressants and his symptoms? antihypertensives, has mydriasis What is the cause
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TCA.
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Woman on MAO inhibitor has hypertensive crisis after a meal.
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Tyramine (wine or cheese).
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Astrocyte marker:
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GFAP.
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Astrocytes what they do
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physical support, repair, K+ metabolism; help maintain blood-brain barrier.
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CNS/PNS Support Cells role of Ependymal cells
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–inner lining of ventricles.
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CNS/PNS Support Cells role of Microglia
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phagocytosis.
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CNS/PNS Support Cells role of Oligodendroglia
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central myelin production
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CNS/PNS Support Cells role of Schwann cells–
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peripheral myelin production.s
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These cells are destroyed in multiple sclerosis.
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Oligodendroglia
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Acoustic neuroma is an example of
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schwannoma.
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Permeability barrier; must be rejoined in microsurgery for limb reattachment.
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Perineurium–
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Acoustic neuroma Location
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commonly associated with internal acoustic meatus (CN VII, VIII).
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Predominant type of glial cell in white matter.
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Oligodendroglia
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Mesodermal origin. Not readily discernible in Nissl stains. Have small irregular nuclei and relatively little cytoplasm.
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Microglia
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HIV-infected ????? fuse to form multinucleated giant cells in the CNS.
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microglia
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HIV-infected microglia fuse to form ???
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multinucleated giant cells in the CNS.
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Derivation of All CNS/PNS support cells
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Microglia, like macrophages, originate from mesoderm. All other CNS/PNS supportive cells originate from ectoderm.
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Sensory corpuscles Meissner’s where and what
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small in dermis of palms, soles, and digits of skin. glabrous (hairless) skin. light discriminatory touch of
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Sensory corpuscles Pacinian where and what
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Large found in deeper layers of skin at ligaments, joint capsules, serous membranes, mesenteries. Involved in pressure, coarse touch, vibration, and tension.
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Sensory corpuscles Merkel’s where and what
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Cup-shaped nerve endings (tactile disks) in dermis of fingertips, hair follicles, hard palate. Involved in light, crude touch.
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Small, encapsulated nerve endings found in dermis of palms, soles, and digits of skin. Involved in light discriminatory touch of glabrous (hairless) skin.
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Meissner’s
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Large, encapsulated nerve endings found in deeper layers of skin at ligaments, joint capsules, serous membranes, mesenteries. Involved in pressure, coarse touch, vibration, and tension.
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Pacinian
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Cup-shaped nerve endings (tactile disks) in dermis of fingertips, hair follicles, hard palate. Involved in light, crude touch.
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Merkel’s
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Inner ear makeup of peri vs endo lymph
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Peri––think outside of cell (Na+). ECF like Endo––think inside of cell (K+). ICF like
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Inner ear location of of peri vs endo lymph
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Peri––(bony labyrinth) Endo––(membranous labyrinth)
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Hair cells are the sensory elements in
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both vestibular apparatus (spatial orientation) and cochlea (hearing).
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the sensory elements in both vestibular apparatus (spatial orientation) and cochlea (hearing).
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Hair cells
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Semicircular canals contain ????? which detect
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Ampullae Angular acceleration.
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Utricle and saccule contain ????? which detect .
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maculae– linear acceleration.
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?????? contain maculae––detect linear acceleration.
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Utricle and saccule
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???????? contain Ampullae––detect Angular acceleration.
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Semicircular canals
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cochlea ???????? picks up high- frequency sound. ?????? picks up low-frequency sound.
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Base of the cochlea Apex of the cochlea
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Hearing loss in the elderly––what pitch
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high frequency → low frequency.
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what forms the BBB
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. Tight junctions between nonfenestrated capillary endothelial cells . Basement membrane . Astrocyte processes
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Other barriers include: not BBB
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1. Blood-testis barrier 2. Maternal-fetal blood barrier of placenta
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BBB transport wrt Glucose, proteins and lipids
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Glucose and amino acids cross by carrier-mediated transport mechanism. Nonpolar/lipid-soluble substances cross more readily than do
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Parts of brain w/o BBB
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(e.g., area postrema––vomiting after chemo) or neurosecretory products to enter circulation (e.g., neurohypophysis––ADH release). e
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infarction and BBB
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Infarction destroys endothelial cell tight junctions → vasogenic edema.
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Hypothalamus functions
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The hypothalamus wears TAN HATS. Thirst Adenohypophysis Neruohypophysis Hunger Autonomic regulation Temp regulation Sexual urges
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Hypothalamus Location involved in Thirst
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Thirst and water balance (supraoptic nucleus).
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Hypothalamus Location involved in Neurohypophysis
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Neurohypophysis and median eminence release hormones synthesized in hypothalamic nuclei.
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Hypothalamus Location involved in Hunger ans satiety
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Hunger (lateral ucleus; damage → anorexia/starvation Satiety (ventromedial nucleus; damage → hyperphagia and obesity).
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Hypothalamus Location involved in Autonomic regulation
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anterior hypothalamus regulates parasympathetic; posterior hypothalamus regulates sympathetic circadian rhythms (suprachiasmatic nucleus).
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Hypothalamus Location involved in Temperature regulation
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(posterior hypothalamus regulates heat conservation and production when cold; Anterior hypothalamus coordinates Cooling when hot).
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Hypothalamus Location involved in Sexual urges and emotions
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(Septal nucleus–– destruction → rage).
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Hypothalamus mnemonic Hunger
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If you zap your ventromedial nucleus, you grow ventrally and medially.
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Hypothalamus mnemonic Temp
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If you zap your Posterior hypothalamus, you become a Poikilotherm (cold-blooded snake). A/C = anterior cooling.
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Posterior pituitary aka
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neurohypophysis
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neurohypophysis aka
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Posterior pituitary
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neurohypophysis where axonal projections come from
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Receives hypothalamic axonal projections from -supraoptic (ADH) -paraventricular (oxytocin) nuclei.
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Derivation of the word Oxytocin
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oxys = quick; tocos = birth.
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Major relay for ascending sensory information that ultimately reaches the cortex.
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Thalamus
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Thalamus Function of the LGN
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Lateral geniculate nucleus (LGN)––visual. Lateral for Light. Medial for Music.
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Thalamus Function of the MGN
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Medial geniculate nucleus (MGN)––auditory. Lateral for Light. Medial for Music.
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Thalamus Function of the VPL
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Ventral posterior nucleus, lateral part (VPL) ––body sensation (proprioception, pressure,pain, touch, vibration via dorsal columns, spinothalamic tract).
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Thalamus Function of the VPM
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Ventral posterior nucleus, medial part (VPM) ––facial sensation (via CN V).
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Thalamus Function of the VA
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Ventral anterior/lateral (VA/VL) nuclei ––motor.
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Thalamus Function of the VL
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Ventral anterior/lateral (VA/VL) nuclei ––motor.
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Thalamus which nucleus Visual
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Lateral geniculate nucleus (LGN)––visual. Lateral for Light. Medial for Music.
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Thalamus which nucleus auditory.
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Medial geniculate nucleus (MGN)–– Lateral for Light. Medial for Music.
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Thalamus which nucleus ––body sensation (proprioception, pressure pain, touch, vibration via dorsal columns, spinothalamic tract).
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Ventral posterior nucleus, lateral part (VPL)
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Thalamus which nucleus facial sensation (via CN V).
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Ventral posterior nucleus, medial part (VPM)
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Thalamus which nucleus motor.
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Ventral anterior/lateral (VA/VL) nuclei
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Limbic system is Responsible for
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The famous 5 F’s. Feeding, Fighting, Feeling, Flight, and sex (use your imagination).
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Important in voluntary movements and making postural adjustments.
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Basal ganglia
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Parkinson’s disease symptoms due to ↓ input from the ??????(leading to ↓ stimulation of the ?????and ↓ inhibition of the ???????
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substantia nigra direct pathway indirect pathway).
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Frontal lobe functions
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“Executive functions”––planning, inhibition, concentration, orientation, language, abstraction, judgment, motor regulation, mood.
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most notable in frontal lobe lesion.
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Lack of social judgment
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Anterior cerebral artery––supplies
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medial surface of the brain, leg-foot area of motor and sensory cortices.
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Middle cerebral artery––supplies
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lateral aspect of brain, trunk-arm-face area of motor and sensory cortices, Broca’s and Wernicke’s speech areas.
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most common site of circle of Willis aneurysm; lesion may cause visual-field defects.
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Anterior communicating artery––
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supplies medial surface of the brain, leg-foot area of motor and sensory cortices.
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Anterior cerebral artery––
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–supplies lateral aspect of brain, trunk-arm-face area of motor and sensory cortices, Broca’s and Wernicke’s speech areas.
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Middle cerebral artery–
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common area of aneurysm; causes CN III palsy.
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Posterior communicating artery––
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“arteries of stroke”; supply internal capsule, caudate, putamen, globus pallidus.
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Lateral striate––
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divisions of middle cerebral artery
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Lateral striate––
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In general, stroke of anterior circle →
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general sensory and motor dysfunction, aphasia;
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stroke of posterior circle →
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cranial nerve deficits (vertigo, visual deficits), coma, cerebellar deficits (ataxia).
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General location of a stroke that leads to general sensory and motor dysfunction, aphasia;
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In general, stroke of anterior circle
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General location of a stroke that leads to cranial nerve deficits (vertigo, visual deficits), coma, cerebellar deficits (ataxia).
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stroke of posterior circle
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Venous sinuses run in the ?
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dura mater where its meningeal and periosteal layers separate
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Cerebral veins → ? → ?
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venous sinuses → internal jugular vein.
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Lateral ventricle → 3rd ventricle via
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foramen of Monro.
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3rd ventricle → 4th ventricle via
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aqueduct of Sylvius.
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4th ventricle → subarachnoid space via:
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Foramina of Luschka = lateral. Foramen of Magendie = medial.
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Spinal nerves number of each
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There are 31 spinal nerves altogether: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal. 31, just like 31 flavors!
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Vertebral disk herniation usually occurs where
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between L5 and S1.
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lumbar puncture order of Structures pierced
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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
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lumbar puncture where does needle end up
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Needle in subarachnoid space
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lumbar puncture what is not pierced
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Pia is not pierced.
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lumbar puncture where to go in
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between L4 and L5 (at the level of iliac crests).
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Spinal tract anatomy and functions Tract and function Dorsal column-medial lemniscal pathway
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(ascending pressure, vibration, touch, and proprioceptive sensation)
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Spinal tract anatomy and functions Tract and function Spinothalamic tract
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(ascending pain and temperature sensation)
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Spinal tract anatomy and functions Tract and function Lateral corticospinal tract
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(descending voluntary movement of contralateral limbs)
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Which Tract (ascending pressure, vibration, touch, and proprioceptive sensation)
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Dorsal column-medial lemniscal pathway
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Which Tract (ascending pain and temperature sensation)
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Spinothalamic tract
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Which Tract (descending voluntary movement of contralateral limbs)
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Lateral corticospinal tract
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Dorsal column-medial lemniscal pathway 1st-order neuron
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Sensory nerve ending → dorsal root ganglion → enters spinal cord, ascends ipsilaterally in dorsal column
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Dorsal column-medial lemniscal pathway Synapse 1
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Nucleus cuneatus or gracilis (medulla)
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Dorsal column-medial lemniscal pathway 2nd-order neuron
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Decussates in medulla → ascends contralaterally in medial lemniscus
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Dorsal column-medial lemniscal pathway Synapse 2
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VPL of thalamus
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Dorsal column-medial lemniscal pathway 3rd-order neuron
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Sensory cortex
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Spinothalamic tract 1st-order neuron
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Sensory nerve ending (A-delta and C fibers) → enters spinal cord
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Spinothalamic tract Synapse 1
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Ipsilateral gray matter (spinal cord)
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Spinothalamic tract 2nd-order neuron
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Decussates at anterior white commissure → ascends contralaterally
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Spinothalamic tract Synapse 2
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VPL of thalamus
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Spinothalamic tract 3rd-order neuron
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Sensory cortex
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Lateral corticospinal tract 1st-order neuron
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Upper motor neuron: 1° motor cortex → descends ipsilaterally until decussating at caudal medulla (pyramidal decussation)→ descends contralaterally
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Lateral corticospinal tract Synapse 1
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Cell body of anterior horn (spinal cord)
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Lateral corticospinal tract 2nd-order neuron
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Lower motor neuron: Leaves spinal cord
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Lateral corticospinal tract Synapse 2
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Neuromuscular junction
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Lateral corticospinal tract 3rd-order neuron
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Fasciculus gracilis = Fasciculus cuneatus =
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Legs Arms
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Dorsal column organization mnemonic
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Fasciculus gracilis = legs. Fasciculus cuneatus = arms. Dorsal column is organized as you are, with hands at sides––arms outside and legs inside.
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Clavicle fracture is relatively common––brachial plexus is protected from injury by
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subclavius muscle.
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Upper extremity nerve injury Site of injury and motor deficit Radial
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Shaft of humerus loss of triceps brachii (triceps reflex), brachioradialis (brachioradialis reflex), and extensor carpi radialis longus (→ wrist drop).
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Upper extremity nerve injury Site of injury and motor deficit Median
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Supracondyle of humerus no loss of power in any of the arm muscles; loss of forearm pronati wrist flexion, finger flexion, and several thumb movements; eventually, thenar atrophy.
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Upper extremity nerve injury Site of injury and motor deficit Ulnar
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Medial epicondyle–– impaired wrist flexion and adduction, and impaired adduction of thumb and the ulnar 2 fingers (→ claw hand).
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Upper extremity nerve injury Site of injury and motor deficit Axillary
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Surgical neck of humerus or anterior shoulder dislocation loss of deltoid action.
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Upper extremity nerve injury Site of injury and motor deficit Musculocutaneous
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Loss of function of coracobrachialis, biceps, and brachialis muscles (biceps reflex).
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Upper extremity nerve injury Deficit in sensation/course Radial
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Posterior brachial cutaneous.
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Upper extremity nerve injury Deficit in sensation/course Median
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Posterior antebrachial cutaneous. Passes through supinator.
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Upper extremity nerve injury Deficit in sensation/course Ulnar
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Loss of sensation over the lateral palm and thumb and the radial 2 and 1/2 fingers. Passes through pronator teres.
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Upper extremity nerve injury Deficit in sensation/course Axillary
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Loss of sensation over the medial palm and ulnar 11/2 fingers. Passes through flexor carpi ulnaris.
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Upper extremity nerve injury Deficit in sensation/course Musculocutaneous
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Passes through coracobrachialis.
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Erb-Duchenne palsy cause
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Traction or tear of the upper trunk of the brachial plexus (C5 and C6 roots); follows blow to shoulder or trauma during delivery.
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Erb-Duchenne palsy findings
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Findings: limb hangs by side (paralysis of abductors), medially rotated (paralysis of lateral rotators), forearm is pronated (loss of biceps).
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Findings: limb hangs by side (paralysis of abductors), medially rotated (paralysis of lateral rotators), forearm is pronated (loss of biceps).
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Erb-Duchenne palsy findings
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“Waiter’s tip” owing to appearance of arm.
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Erb-Duchenne palsy
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Thoracic outlet syndrome aka
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Klumpke’s palsy
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Klumpke’s palsy aka
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Thoracic outlet syndrome
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Klumpke’s palsy cause
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An embryologic defect; can compress subclavian artery and inferior trunk of brachial plexus (C8, T1), resulting in thoracic outlet syndrome:
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Klumpke’s palsy findings
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1. Atrophy of the thenar and hypothenar eminences 2. Atrophy of the interosseous muscles 3. Sensory deficits on the medial side of the forearm and hand 4. Disappearance of the radial pulse upon moving the head toward the opposite side
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1. Atrophy of the thenar and hypothenar eminences 2. Atrophy of the interosseous muscles 3. Sensory deficits on the medial side of the forearm and hand 4. Disappearance of the radial pulse upon moving the head toward the opposite side
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Thoracic outlet syndrome aka (Klumpke’spalsy)
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Lower extremity nerve injury motor deficit Common peroneal
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Loss of dorsiflexion (→ foot drop). Deep peroneal nerve innervates anterior compartment; superficial peroneal nerve innervates lateral compartment.
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Lower extremity nerve injury motor deficit Tibial
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Loss of plantar flexion. Tibial nerve innervates posterior compartment.
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Lower extremity nerve injury motor deficit Femoral
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Loss of knee extension/knee jerk.
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Lower extremity nerve injury motor deficit Obturator
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Loss of hip adduction.
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foot nerve mnemonic
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PED = Peroneal Everts and Dorsiflexes; if injured, foot dropPED. TIP = Tibial Inverts and Plantarflexes; if injured, can’t stand on TIPtoes.
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Which nerve is damaged and give spinal nerves Loss of dorsiflexion (→ foot drop).
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Common peroneal (L4–S2)
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Which nerve is damaged and give spinal nerves Loss of plantar flexion.
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Tibial nerve (L4-S3)
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Which nerve is damaged and give spinal nerves Loss of knee extension/knee jerk.
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Femoral (L2–L4)
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Which nerve is damaged and give spinal nerves Loss of hip adduction.
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Obturator (L2–L4)
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Which nerve is damaged and give spinal nerves loss of triceps brachii brachioradialis and extensor carpi radialis longus
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Radial C5-T1
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Which nerve is damaged and give spinal nerves Supracondyle of humerus––no loss of forearm pronation wrist flexion, finger flexion, and several thumb movements
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Median C6-T1
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Which nerve is damaged and give spinal nerves impaired wrist flexion and adduction, and impaired adduction of thumb and the ulnar 2 fingers
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Ulnar C7-T1
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Which nerve is damaged and give spinal nerves loss of deltoid action.
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Axillary C5-C6
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Which nerve is damaged and give spinal nerves Loss of function of coracobrachialis, biceps, and brachialis muscles
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Musculocutaneous C5-C7
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Radial nerve mnemonic
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Radial nerve innervates the BEST! Known as the “great extensor nerve.” Provides innervation of the Brachioradialis, Extensors of the wrist and fingers, Supinator, and Triceps.
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Known as the “great extensor nerve.” Provides innervation of the Brachioradialis, Extensors of the wrist and fingers, Supinator, and Triceps.
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Radial nerve
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Thenar-hypothenar muscles
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Thenar––Opponens pollicis, Abductor pollicis brevis, Flexor pollicis brevis. Hypothenar––Opponens digiti minimi, Abductor digiti minimi, Flexor digiti minimi.
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Clinically important landmarks Pudendal nerve block
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––ischial spine.
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Clinically important landmarks Appendix Lumbar puncture––iliac crest.
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––2/3 of the way from the umbilicus to the anterior superior iliac spine (McBurney’s point).
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Clinically important landmarks Lumbar puncture
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––iliac crest.
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Landmark dermatomes cervical
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C2 is the posterior half of a skull “cap.” C3 is a high turtleneck shirt. C4 is a low-collar shirt.
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Landmark dermatomes Thoracic
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T4 (at the Teat pore) at the nipple. T7 is at the xiphoid process. T10 (belly butTEN) is at the umbilicus (important for early appendicitis pain referral).
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Landmark dermatomes Lumbar and Sacral
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L1 is at the IL inguinal ligament. L4 (down on al 4's)includes the kneecaps. S2, S3, S4 (keep the penis off the floor)erection and sensation of penile and anal zones.
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Landmark dermatomes wrt appendix
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T10 (belly butTEN) is at the umbilicus (important for early appendicitis pain referral).
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Spindle muscle control what they monitor Muscle spindle
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Muscle spindles monitor muscle length (help you pick up a heavy suitcase when you didn’t know how heavy it was).
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Spindle muscle control what they monitor Golgi tendon
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Golgi tendon organs monitor muscle tension (make you drop a heavy suitcase you’ve been holding too long).
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Muscle spindle path
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In parallel with muscle bers. Muscle stretch → intrafusal stretch → stimulates Ia afferent → stimulates α motor neuron → reflex muscle (extrafusal) contraction.
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Gamma loop path
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CNS stimulates γ motor neuron →contracts intrafusal fiber → increased sensitivity of reflex arc.
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4 Primitive reflexes
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1. Moro reflex––extension of limbs when startled 2. Rooting reflex––nipple seeking 3. Palmar reflex––grasps objects in palm 4. Babinski reflex––large toe dorsiflexes with plantar stimulation
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Primitive reflexes when do they go and when do they return
|
Normally disappear within 1st year. May reemerge following frontal lobe lesion.
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Clinical reflexes what nerve roots are tested with the hammer
|
Biceps = C5 nerve root. Triceps = C7 nerve root. Patella = L4 nerve root. Achilles = S1 nerve root.
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Clinical reflexes what does babinski test
|
Babinski––dorsiflexion of the big toe and fanning of other toes; sign of UMN lesion, but normal reflex in 1st year of life.
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Cranial nerve function I
|
Smell
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Cranial nerve function II
|
Sight
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Cranial nerve function III
|
Eye motion, Pupil constriction, accommodation, eyelid opening
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Cranial nerve function IV
|
Eye movement
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Cranial nerve function V
|
Mastication, facial sensation
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Cranial nerve function VI
|
Eye movement
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Cranial nerve function VII
|
Facial movement, taste from anterior 2/3 of tongue, lacrimation, salivation (submaxillary and sublingual glands), eyelid closing
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Cranial nerve function VIII
|
Hearing, balance
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|
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Cranial nerve function IX
|
Taste from posterior 1/3 of tongue, swallowing, salivation (parotid gland), monitoring carotid body and sinus chemo- and baroreceptors
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Cranial nerve function X
|
Taste from epiglottic region, swallowing, palate elevation, talking, thoracoabdominal viscera, monitoring aortic arch chemo- and baroreceptors
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Cranial nerve function XI
|
Head turning, shoulder shrugging
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Cranial nerve function XII
|
Tongue movement
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Cranial nerve nuclei in general where are they located
|
Located in tegmentum portion of brain stem (between dorsal and ventral portions). Lateral nuclei = sensory. Medial nuclei = Motor.
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Cranial nerve nuclei locations/levels of each
|
1. Midbrain––nuclei of CN III, IV. 2. Pons––nuclei of CN V, VI, VII, VIII. 3. Medulla––nuclei of CN IX, X, XI, XII.
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Vagal nuclei name them
|
Nucleus Solitarius Nucleus aMbiguus Dorsal motor nucleus
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what does it do Nucleus Solitarius
|
Visceral Sensory information (e.g., taste, baroreceptors, gut distention). VII, IX, X.
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what does it do Dorsal motor nucleus
|
Sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI.
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what does it do Nucleus ambiguus
|
Nucleus aMbiguus IX, X, XI. Motor innervation of pharynx, larynx, and upper esophagus (e.g., swallowing, palate elevation).
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Which nucleus Visceral Sensory information (e.g., taste, baroreceptors, gut distention).
|
Nucleus Solitarius
|
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Which nucleus Sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI.
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Dorsal motor nucleus
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Which nucleus Motor innervation of pharynx, larynx, and upper esophagus (e.g., swallowing, palate elevation).
|
Nucleus ambiguus
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What nerve/vessel passes through Cribriform plate
|
CN I
|
|
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What nerve/vessel passes through Middle cranial fossa
|
(CN II–VI)––through sphenoid bone
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What nerve/vessel passes through Optic canal
|
CN II, ophthalmic artery, central retinal vein)
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What nerve/vessel passes through Superior orbital fissure
|
(CN III, IV, V1, VI, ophthalmic vein)
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What nerve/vessel passes through Foramen Rotundum
|
(CN V2)
|
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What nerve/vessel passes through Foramen Ovale
|
(CN V3)
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What nerve/vessel passes through Foramen spinosum
|
(middle meningeal artery)
|
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What nerve/vessel passes through Posterior cranial fossa
|
(CN VII–XII)––through temporal or occipital bone:
|
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What nerve/vessel passes through Internal auditory meatus
|
(CN VII, VIII)
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What nerve/vessel passes through Jugular foramen
|
(CN IX, X, XI, jugular vein)
|
|
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What nerve/vessel passes through Hypoglossal canal (CN XII)
|
(CN XII)
|
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What nerve/vessel passes through Foramen magnum
|
spinal roots of CN XI, brain stem, vertebral arteries)
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|
name the Middle cranial fossa and give the structures that pass through them
|
Middle cranial fossa (CN II–VI)––through sphenoid bone: 1. Optic canal (CN II, ophthalmic artery, central retinal vein) 2. Superior orbital fissure (CN III, IV, V1, VI, ophthalmic vein) 3. Foramen Rotundum (CN V2) 4. Foramen Ovale (CN V3) 5. Foramen spinosum (middle meningeal artery)
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name the Posterior cranial fossa and give the structures that pass through them
|
Posterior cranial fossa (CN VII–XII)––through temporal or 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)
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Divisions of CN V exit owing
|
Divisions of CN V exit owing to Standing Room Only. Superior orbital fissure CN V1 Foramen Rotundum (CN V2) Foramen Ovale (CN V )
|
|
|
Blood from eye and superficial cortex →
|
cavernous sinus → internal jugular vein.
|
|
|
CN ?????? and ????? fibers en route to ???? all pass through the cavernous sinus. Only ?????? is “free-floating.” Cavernous portion of ?????? is also here.
|
III, IV, V1, V2, and VI postganglionic sympathetic the orbit CN VI internal carotid artery
|
|
|
The nerves??????pass through the cavernous sinus.
|
that control extraocular muscles (plus V1 and V2)
|
|
|
Cavernous sinus syndrome Cause and findings
|
due to mass effect ophthalmoplegia, ophthalmic and maxillary sensory loss.
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|
|
due to mass effect ophthalmoplegia, ophthalmic and maxillary sensory loss.
|
Cavernous sinus syndrome
|
|
|
Mastication muscles/nerves and what each does
|
3 muscles close jaw: Masseter, teMporalis, Medial pterygoid. 1 opens: lateral pterygoid. All are innervated by the trigeminal nerve (V3).
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|
|
Mastication muscles/nerves mnemonic
|
M’s Munch. Lateral Lowers (when speaking of pterygoids wrt jaw motion).
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|
|
Muscles with glossus innervation
|
All muscles with root glossus in their names (except palatoglossus, innervated by vagus nerve) are innervated by hypoglossal nerve.
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|
Muscles with glossus/palat mnemonic
|
Glossus: hypoglossal nerve. Palat: vagus nerve (except TENSor, who was too TENSE).
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|
Muscles with palat innervation
|
All muscles with root palat in their names are innervated by vagus nerve. (except tensor veli palatini, innervated by mandibular branch of CN V)
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|
Extraocular muscles and nerves
|
CN VI innervates the Lateral Rectus. CN IV innervates the Superior Oblique.(trochlear) CN III innervates the Rest. The “chemical formula” LR6SO4R3.
|
|
|
actions of the The superior oblique
|
abducts, introverts, depresses.
|
|
|
Pupillary light reflex pathway
|
CN II to pretectal nuclei in midbrain that activate bilateral Edinger-Westphal nuclei; pupils contract bilaterally (consensual reflex).
|
|
|
Internuclear ophthalmoplegia aka
|
MLF syndrome
|
|
|
MLF syndrome aka
|
Internuclear ophthalmoplegia
|
|
|
Internuclear ophthalmoplegia mech and who gets
|
Lesion in the medial longitudinal fasciculus (MLF). Results in medial rectus palsy on attempted lateral gaze. Nystagmus in abducting eye. Convergence is normal. MLF =multiple sclerosis.
|
|
|
Internuclear ophthalmoplegia mnemonic
|
MLF =MS.
|
|
|
Normal MLF function when looking left
|
When looking left, the left nucleus of CN VI fires, which contracts the left lateral rectus and stimulates the contralateral(right) nucleus of CN III via the right MLF to contract the right medial rectus.
|
|
|
Verbal CN testin
|
KLM sounds 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).
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|
|
Neural tube defects cause and test
|
Associated with low folic acid intake during pregnancy. Elevated α-fetoprotein in amniotic fluid and maternal serum.
|
|
|
Spina bifida occulta mech and description
|
––failure of bony spinal canal to close, but no structural herniation. Usually seen at lower vertebral levels.
|
|
|
Meningocele
|
––meninges herniate through spinal canal defect.
|
|
|
Meningomyelocele
|
–meninges and spinal cord herniate through spinal canal defect.
|
|
|
consequences of Brain lesions at Broca’s area
|
Motor (nonfluent/expressive) aphasia with good comprehension
|
|
|
consequences of Brain lesions at Wernicke’s area
|
Sensory (fluent/receptive) aphasia with poor comprehension
|
|
|
consequences of Brain lesions at Arcuate fasciculus
|
Conduction aphasia; poor repetition with good comprehension, fluent speech
|
|
|
consequences of Brain lesions at Amygdala (bilateral)
|
Klüver-Bucy syndrome (hyperorality, hypersexuality, disinhibited behavior)
|
|
|
consequences of Brain lesions at Frontal lobe
|
Personality changes and deficits in concentration, orientation, and judgment; may have reemergence of primitive reflexes
|
|
|
consequences of Brain lesions at Right parietal lobe
|
Spatial neglect syndrome (agnosia of the contralateral side of the world)
|
|
|
consequences of Brain lesions at Reticular activating system
|
Coma
|
|
|
consequences of Brain lesions at Mammillary bodies (bilateral)
|
Wernicke-Korsakoff syndrome
|
|
|
consequences of Brain lesions at Basal ganglia
|
May result in tremor at rest, chorea, or athetosis
|
|
|
consequences of Brain lesions at Cerebellar hemisphere
|
Intention tremor, limb ataxia
|
|
|
consequences of Brain lesions at Cerebellar vermis
|
Truncal ataxia, dysarthria
|
|
|
consequences of Brain lesions at Subthalamic nucleus
|
Contralateral hemiballismus
|
|
|
Where is the lesion with the following findings Motor (nonfluent/expressive) aphasia with good comprehension
|
Broca’s area
|
|
|
Where is the lesion with the following findings Sensory (fluent/receptive) aphasia with poor comprehension
|
Wernicke’s area
|
|
|
Where is the lesion with the following findings Conduction aphasia; poor repetition with good comprehension, fluent speech
|
Arcuate fasciculus
|
|
|
Where is the lesion with the following findings hyperorality, hypersexuality, disinhibited behavior
|
Amygdala (bilateral)
|
|
|
Where is the lesion with the following findings Personality changes and deficits in concentration, orientation, and judgment; may have reemergence of primitive reflexes
|
Frontal lobe
|
|
|
Where is the lesion with the following findings Spatial neglect syndrome (agnosia of the contralateral side of the world)
|
Right parietal lobe
|
|
|
Where is the lesion with the following findings Coma
|
Reticular activating system
|
|
|
Where is the lesion with the following findings Wernicke-Korsakoff syndrome
|
Mammillary bodies (bilateral)
|
|
|
Where is the lesion with the following findings tremor at rest, chorea, or athetosis
|
Basal ganglia
|
|
|
Where is the lesion with the following findings Intention tremor, limb ataxia
|
Cerebellar hemisphere
|
|
|
Where is the lesion with the following findings Truncal ataxia, dysarthria
|
Cerebellar vermis
|
|
|
Where is the lesion with the following findings Contralateral hemiballismus
|
Subthalamic nucleus
|
|
|
cerebellar lesion mnemonic
|
Hemispheres are laterally located––affect lateral limbs. Vermis is centrally located––affects central body.
|
|
|
Connects Wernicke’s to Broca’s area.
|
Arcuate fasciculus
|
|
|
what does the Arcuate fasciculus do
|
Connects Wernicke’s to Broca’s area.
|
|
|
mnemonic for speech problems and brain lesions
|
BROca’s is BROken speech. Wernicke’s is Wordy but makes no sense.
|
|
|
word derivation Chorea
|
dancing (Greek). Think choral dancing or choreography.
|
|
|
description Chorea
|
Sudden, jerky, purposeless movements.
|
|
|
Chorea what disease process
|
Characteristic of basal ganglia lesion (e.g., Huntington’s disease).
|
|
|
word derivation Athetosis
|
Athetos = not fixed (Greek). Think snakelike.
|
|
|
description Athetosis
|
Slow, writhing movements, especially of fingers.
|
|
|
Athetosis what disease process
|
Characteristic of basal ganglia lesion.
|
|
|
description Hemiballismus
|
Sudden, wild flailing of 1 arm.
|
|
|
Hemiballismus what disease process
|
Characteristic of contralateral subthalamic nucleu lesion. Loss of inhibition of thalamus through globus pallidus.
|
|
|
most common cause of dementia in the elderly.
|
Alzheimer’s disease
|
|
|
Associated with senile plaques (extracellular, β-amyloid core) and neurofibrillary tangles (intracellular, abnormally phosphorylated tau protein).
|
Alzheimer’s disease
|
|
|
Familial form (10% associated with genes on chromosomes 1, 14, 19 (APOE4 allele), and 21 (p-App gene
|
Alzheimer’s disease
|
|
|
Alzheimer’s disease what are the plaques and tangles made of and where are they
|
plaques (extracellular, β-amyloid core) neurofibrillary tangles (intracellular, abnormally phosphorylated tau protein).
|
|
|
Alzheimer’s disease what genes/chromosomes are involved
|
Familial form (10% associated with genes on chromosomes 1, 14, 19 (APOE4 allele), and 21 (p-App gene)
|
|
|
2nd most common cause of dementia in the elderly.
|
Multi-infarct dementia
|
|
|
Multi-infarct dementia may cause
|
May cause amyloid angiopathy →intracranial hemorrhage.
|
|
|
Pick’s disease what and where
|
dementia, aphasia, arkinsonian aspects; and is specific for the frontal and temporal lobes.
|
|
|
Pick bodies
|
(intracellular, aggregated tau protein)
|
|
|
Name Degenerative diseases of the Cerebral cortex
|
Alzheimer’s disease Pick’s disease
|
|
|
Name Degenerative diseases of the Basal ganglia and brain stem
|
Huntington's Parkinson's
|
|
|
Name Degenerative diseases of the Spinocerebellar Motor neuron
|
Olivopontocerebellar atrophy; Friedreich’s ataxia. Amyotrophic lateral sclerosis (ALS) Werdnig-Hoffmann Polio–
|
|
|
Huntington’s disease who mech findings
|
autosomal-dominant Atrophy of caudate nucleus (loss of GABAergic neurons). chorea, dementia.
|
|
|
Huntington’s disease genetic location with mnemonic
|
Chromosome 4––expansion of CAG repeats. CAG––Caudate loses ACh and GABA.
|
|
|
Parkinson’s disease major association
|
Lewy bodies and depigmentation of the substantia nigra pars compacta (loss of dopaminergic neurons)
|
|
|
Parkinson’s disease rare association
|
. Rare cases have been linked to exposure to MPTP, a contaminant in illicit street drugs.
|
|
|
Parkinson’s disease findings
|
TRAP = Tremor (at rest), cogwheel Rigidity, Akinesia, Postural instability (you are TRAPped in your body).
|
|
|
Olivopontocerebellar atrophy
|
Friedreich’s ataxia.
|
|
|
Amyotrophic lateral sclerosis (ALS)– findings and <cause/marker>
|
with both LMN and UMN signs; no sensory deficit. Can be caused by defect in SOD1.
|
|
|
Can be caused by defect in SOD1.
|
Amyotrophic lateral sclerosis (ALS)–
|
|
|
Commonly known as Lou Gehrig’s disease.
|
Amyotrophic lateral sclerosis (ALS)
|
|
|
Werdnig-Hoffmann disease who findings mech
|
autosomal-recessive presents at birth as a “floppy baby,” tongue fasciculations; median age of death 7 months. Associated with degeneration of anterior horns.
|
|
|
Poliomyelitis clinical findings
|
Malaise, headache, fever, nausea, abdominal pain, sore throat. Signs of LMN lesions–– muscle weakness and atrophy, fasciculations, fibrillation, and hyporeflexia.
|
|
|
Poliomyelitis how acquired/virus steps
|
Caused by poliovirus, which is transmitted by the fecal-oral route. Replicates in the oropharynx and small intestine before spreading through the bloodstream to the CNS,where it leads to the destruction of cells in the anterior horn of the spinal cord, leading in turn to LMN destruction.
|
|
|
Poliomyelitis lab findings
|
CSF with lymphocytic pleocytosis with slight elevation of protein. Virus recovered from stool or throat.
|
|
|
Classic triad of MS
|
Classic triad of MS is a SIN: Scanning speech Intention tremor Nystagmus
|
|
|
MS Epidemiology
|
Most often affects women in their 20s and 30s; more common in whites. ↑ prevalence with ↑ distance from the equator
|
|
|
MS What are the plaques and subsequent lab values
|
plaques (areas of oligodendrocyte loss and reactive gliosis) with preservation of axons; ↑ protein (IgG) in CSF.
|
|
|
MS course
|
relapsing-remitting course
|
|
|
MS clinical findings
|
optic neuritis (sudden loss of vision), MLF syndrome (internuclear ophthalmoplegia), hemiparesis, hemisensory symptoms, bladder/ bowel incontinence
|
|
|
PML what is it caused by who gets it
|
Progressive multifocal leukoencephalopathy associated with JC virus 2–4% of AIDS patients (reactivation of latent viral infection).
|
|
|
name the Demyelinating and dysmyelinating diseases
|
MS PML Acute disseminated postinfectious) encephalomyelitis. Metachromatic leukodystrophy Guillain-Barré syndrome
|
|
|
Metachromatic leukodystrophy what type of disease is it
|
Demyelinating lysosomal storage disease
|
|
|
MS Tx
|
β-interferon or immunosuppressant therapy.
|
|
|
Guillain-Barré syndrome aka
|
acute idiopathic polyneuritis
|
|
|
acute idiopathic polyneuritis aka
|
Guillain-Barré syndrome
|
|
|
Guillain-Barré mech
|
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.
|
|
|
Guillain-Barré clinical findings
|
rapid ascending paralysis lower extremities. Facial diplegia in 50% of cas Autonomic function may be severely affected (e.g., cardiac irregularities, hypertension, or hypotension).
|
|
|
Guillain-Barré mortality and course
|
Almost all patients survive; majority recover completely after weeks to months.
|
|
|
Guillain-Barré associations
|
Associated with infections → immune attack of peripheral myelin (e.g., herpesvirus or Campylobacter jejuni infection), inoculations, and stress, but no definitive link to pathogens.
|
|
|
Guillain-Barré Tx
|
Respiratory support is critical until recovery. Additional treatment: plasmapheresis, IV immune globulins.
|
|
|
Guillain-Barré lab findings
|
Findings: elevated CSF protein with normal cell count (“albuminocytologic dissociation”). Elevated protein → papilledema.
|
|
|
Partial seizures location and types
|
1 area of the brain. 1. Simple partial (consciousness intact)–– motor, sensory, autonomic, psychic 2. Complex partial (impaired consciousness)
|
|
|
Generalized seizures location and types/descriptions
|
diffuse, more than one area. 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
|
|
|
What is Epilepsy
|
Epilepsy is a disorder of recurrent seizures (febrile seizures are not epilepsy).
|
|
|
What can happen to partial seizures
|
can secondarily generalize
|
|
|
Causes of seizures by age:
|
Children––genetic, infection, trauma, congenital, metabolic. Adults––tumors, trauma, stroke, infection. Elderly––stroke, tumor, trauma, metabolic, infection.
|
|
|
CT shows “biconvex disk” not crossing suture lines.
|
Epidural hematoma
|
|
|
Crescent-shaped hemorrhage that crosses suture lines.
|
Subdural hematoma
|
|
|
Epidural hematoma cause
|
Rupture of middle meningeal artery, 2° to fracture of temporal bone.
|
|
|
Subdural hematoma cause
|
Rupture of bridging veins.
|
|
|
Subdural hematoma course
|
Venous bleeding (less pressure) with delayed onset of symptoms.
|
|
|
Subdural hematoma who
|
Seen in elderly individuals, alcoholics, blunt trauma, shaken baby
|
|
|
Subdural hematoma predisposing factors
|
––brain atrophy shaking, whiplash
|
|
|
Subarachnoid hemorrhage cause
|
Rupture of an aneurysm (usually berry aneurysm) or an AVM. Bloody or xanthochromic spinal tap.
|
|
|
“worst headache of my life.”
|
Subarachnoid hemorrhage
|
|
|
Subarachnoid hemorrhage lab findings
|
Patients complain of Bloody or xanthochromic spinal tap.
|
|
|
Subarachnoid hemorrhage clinical findings
|
“worst headache of my life.”
|
|
|
Parenchymal hematoma cause
|
hypertension, amyloid angiopathy, diabetes mellitus, and tumor.
|
|
|
Berry aneurysms where
|
Berry aneurysms occur at the bifurcations in the circle of Willis. Most common site is bifurcation of the anterior communicating artery.
|
|
|
Berry aneurysms most common complication
|
Rupture
|
|
|
Berry aneurysms Rupture leads to
|
hemorrhagic stroke/subarachnoid hemorrhage
|
|
|
Berry aneurysms who specific conditions
|
adult polycystic kidney disease, Ehlers-Danlos syndrome, Marfan’s syndrome. factors:
|
|
|
Berry aneurysms risk factors (not APCKD, Marfan's,...)
|
advanced age, hypertension, smoking, race (higher risk in blacks)
|
|
|
Brain tumor locations The majority of adult 1° tumors are ? the majority of childhood 1° tumors are ?
|
supratentorial, infratentorial.
|
|
|
Adult Primary brain tumors most common
|
GBM Glioblastoma multiforme (grade IV astrocytoma)
|
|
|
Adult Primary brain tumors Prognosis grave; < 1- year life expectancy. Found in cerebral hemispheres. Can cross corpus callosum
|
GBM Glioblastoma multiforme (grade IV astrocytoma)
|
|
|
Adult Primary brain tumors Stain astrocytes with GFAP.
|
GBM Glioblastoma multiforme (grade IV astrocytoma)
|
|
|
Adult Primary brain tumors “Pseudopalisading” tumor cells––border central areas of necrosis and hemorrhage.
|
GBM Glioblastoma multiforme (grade IV astrocytoma)
|
|
|
Adult Primary brain tumors 2nd most common
|
Meningioma
|
|
|
Adult Primary brain tumors Most often occurs in convexities of hemispheres and parasagittal region.
|
Meningioma
|
|
|
Adult Primary brain tumors Arises from arachnoid cells external to brain. Resectable.
|
Meningioma
|
|
|
Adult Primary brain tumors Spindle cells concentrically arranged in a whorled pattern;
|
Meningioma
|
|
|
Adult Primary brain tumors often localized to 8th nerve →acoustic. Resectable.
|
C. Schwannoma
|
|
|
Adult Primary brain tumors Bilateral schwannoma found in?
|
neurofibromatosis type 2.
|
|
|
Adult Primary brain tumors Relatively rare, slow growing. Most often in frontal lobes
|
Oligodendro- glioma
|
|
|
Adult Primary brain tumors psammoma bodies (laminated calcifications).
|
Meningioma
|
|
|
Adult Primary brain tumors Prolactin secreting is most common form.
|
Pituitary adenoma
|
|
|
Adult Primary brain tumors Bitemporal hemianopia and hyper- or hypopituitarism are sequelae.
|
Pituitary adenoma
|
|
|
Pituitary adenoma most common form
|
Prolactin secreting
|
|
|
Primary brain tumors Adult Rathke's pouch
|
Pituitary adenoma
|
|
|
Primary brain tumors in adult round nuclei with clear cytoplasm.
|
Oligodendroglioma “fried egg”
|
|
|
Primary brain tumors in Kids Diffusely infiltrating glioma. most often found in posterior fossa. Benign; good prognosis.
|
Pilocytic astrocytoma (low-grade)
|
|
|
Primary brain tumors in Kids Highly malignant cerebellar tumor. A form of primitive neuroectodermal tumor (PNET).
|
Medulloblastoma
|
|
|
Primary brain tumors in Kids compress 4th ventricle, causing hydrocephalus.
|
Medulloblastoma or Ependymoma
|
|
|
Primary brain tumors in Kids Rosettes or perivascular pseudorosette pattern of cells.
|
Medulloblastoma
|
|
|
Primary brain tumors in Kids tumors most commonly found in 4th ventricle. Can cause hydrocephalus. Poor prognosis.
|
Ependymoma
|
|
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Primary brain tumors in Kids Characteristic perivascular pseudorosettes. Rod-shaped blepharoplasts (basal ciliary bodies) found near nucleus.
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Ependymoma
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Primary brain tumors in Kids Most often cerebellar; associated with von Hippel-Lindau
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Hemangioblastoma
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Primary brain tumors in Kids Can produce EPO →2° polycythemia.
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Hemangioblastoma
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Primary brain tumors in Kids Rosenthal fibers—eosinophilic, corkscrew fibers.
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Pilocytic astrocytoma (low-grade)
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Primary brain tumors in Kids Foamy cells and high vascularity are characteristic.
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Hemangioblastoma
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Primary brain tumors in Kids Derived from remnants of Rathke’s pouch.
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Craniopharyngioma
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Primary brain tumors in Kids Calcification is common.
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Craniopharyngioma
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Primary brain tumors in Kids Most common childhood supratentorial tumor.
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Craniopharyngioma
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Primary brain tumors in Kids confused with pituitary adenoma (can also cause bitemporal hemianopia).
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Craniopharyngioma
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Primary brain tumors in Kids order of incidence
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F. Pilocytic astrocytoma (low-grade) G. Medulloblastoma H. Ependymoma I. Hemangioblastoma J. Craniopharyngioma
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Primary brain tumors in Adults order of incidence
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A. Glioblastoma multiforme (grade IV astrocytoma) B. Meningioma C. Schwannoma D. Oligodendroglioma E. Pituitary adenoma
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Given the Spinal cord lesion give the Conditions and the clinical findings lower motor neuron lesions only, due to destruction of anterior horns
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Poliomyelitis and Werdnig- Hoffmann disease: flaccid paralysis
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Given the Spinal cord lesion give the Conditions and the clinical findings mostly white matter of cervical region; random and asymmetric lesions, due to demyelination;
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Multiple sclerosis: scanning speech, intention tremor, nystagmus
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Given the Spinal cord lesion give the Conditions and the clinical findings degeneration of dorsal roots and dorsal columns;
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Tabes dorsalis (3° syphilis): Impaired proprioception, ocomotor ataxia
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Given the Spinal cord lesion give the Conditions and the clinical findings fibers of spinothalamic tract damaged
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Syringomyelia: bilateral loss of pain and temperature sensation
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Given the Spinal cord lesion give the Conditions and the clinical findings demyelination of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts;
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Vitamin B12 neuropathy and Friedreich´s ataxia: ataxic gait, hyperreflexia, impaired position and vibration sense
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Given the Spinal cord lesion give the Conditions and the clinical findings spares dorsal columns and tract of Lissauer
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Complete occlusion of ventral artery;
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Given the Spinal cord lesion give the Conditions and the clinical findings combined upper and lower motor neuron deficits with no sensory deficit; both upper and lower motor neuron signs
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ALS:
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What is Syringomyelia what is damaged and how does it present
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Enlargement of the central canal of spinal cord. Crossing fibers of spinothalamic tract are damaged. Bilateral loss of pain and temperature sensation in upper extremities with preservation of touch sensation. tion
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derivation of Syringomyelia
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Syrinx (Greek) = tube, as in syringe.
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Syringomyelia association
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Often presents in patients with Arnold-Chiari malformation.
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Syringomyelia location
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Most common at C8–T1.
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What is Tabes dorsales and what are the clinical findings
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Degeneration of dorsal columns and dorsal roots due to 3° syphilis, resulting in impaired proprioception and locomotor ataxia.
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Tabes dorsalis what other symptoms are associated with it
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Charcot’s joints, shooting Lightning) pain, Argyll Robertson pupils (accommodation but not reactive to light), absence of DTRs.
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Charcot’s joints
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progressive degeneration of a weight-bearing joint leading to deformity
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Hemisection of spinal cord. aka
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Brown-Séquard syndrome
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Brown-Séquard syndrome aka
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Hemisection of spinal cord.
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Brown-Séquard syndrome findings
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1. Ipsilateral UMN signs (corticospinal tract) below lesion––not shown 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 at level of lesion
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Brown-Séquard syndrome above T1
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If lesion occurs above T1, presents with Horner’s syndrome.
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Horner’s syndrome aka
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Sympathectomy of face
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Sympathectomy of face aka
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Horner’s syndrome
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Horner’s syndrome clinical findings
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1. Ptosis (slight drooping of eyelid) 2. Anhidrosis (absence of sweating) and flushing (rubor) of affected side of face 3. Miosis (pupil constriction)
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Horner’s syndrome assiciations
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Associated with lesion of spinal cord above T1 (e.g., Pancoast’s tumor, hemisection, late-stage syringomyelia).
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The 3-neuron oculosympathetic pathway projects from
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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.
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findings of CN and cerebellar lesions CN XII lesion (LMN)
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tongue deviates toward side of lesion (lick your wounds).
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findings of CN and cerebellar lesions CN V motor lesion
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jaw deviates toward side of lesion.
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findings of CN and cerebellar lesions Unilateral lesion of cerebellum
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patient tends to fall toward side of lesion.
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findings of CN and cerebellar lesions CN X lesion
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uvula deviates away from side of lesion.
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findings of CN and cerebellar lesions CN XI lesion
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weakness turning head to contralateral side of (away from)lesion. Shoulder droop on side of lesion.
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CN VII lesions associations
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BLASTeD Bell's palsy seen in -Lyme -AIDS -Sarcoid -Tumors -Diabetes
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CN VII lesions UMN vs LMN
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Contralateral paralysis of lower face only. Ipsilateral paralysis of upper and lower face.
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Brain herniation syndromes name them and what they herniate through
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1. Cingulate herniation under falx cerebri 2. Downward transtentorial (central) herniation 3. Uncal herniation 4. Cerebellar tonsillar herniation into the foramen magnum
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Brain herniation syndromes complications
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Can compress anterior cerebral artery. Coma and death result when these herniations compress the brain stem.
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What is the Uncus
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medial temporal lobe.
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in Uncal herniation what causes Ipsilateral dilated pupil/ptosis
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Stretching of CN III
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in Uncal herniation what causes Contralateral homonymous hemianopia
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Compression of ipsilateral posterior cerebral artery
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in Uncal herniation what causes Ipsilateral paresis
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Compression of contralateral crus cerebri (Kernohan’s notch)
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in Uncal herniation what causes Duret hemorrhages/ paramedian artery rupture
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Caudal displacement of brain stem
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In Uncal Herniation what does Stretching of CN III lead to?
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Ipsilateral dilated pupil/ptosis
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In Uncal Herniation what does Compression of ipsilateral posterior cerebral artery lead to?
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Contralateral homonymous hemianopia
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In Uncal Herniation what does Compression of contralateral crus cerebri (Kernohan’s notch) lead to?
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Ipsilateral paresis
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In Uncal Herniation what does Caudal displacement of brain stem lead to?
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Duret hemorrhages–– paramedian artery rupture
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Parkinson’s disease drugs name 4 strategies
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-Agonize dopamine receptors -Increase dopamine -Prevent dopamine breakdown -Curb excess cholinergic activity
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Parkinson’s disease drugs Name the ones that Agonize dopamine receptors And give mechanisms
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Bromocriptine (ergot alkaloid and partial dopamine agonist), pramipexole, ropinirole
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Parkinson’s disease drugs Name the ones that Increase dopamine And give mechanisms
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Amantadine (may ↑ dopamine release) L-dopa/carbidopa (converted to dopamine in CNS)
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Parkinson’s disease drugs Name the ones that Prevent dopamine breakdown And give mechanisms
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Selegiline (selective MAO type B inhibitor) ; entacapone, tolcapone (COMT inhibitors)
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Parkinson’s disease drugs Name the ones that Curb excess cholinergic activity And give mechanisms
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Benztropine (Antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia)
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Parkinson’s disease drugs improves tremor and rigidity but has little effect on bradykinesia
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Benztropine
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Parkinson’s disease drugs mnemonic
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BALSA: Bromocriptine Amantadine Levodopa (with carbidopa) Selegiline (and COMT inhibitors) Antimuscarinics
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Parkinsonism is due to loss ?????
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loss of dopaminergic neurons and excess cholinergic activity.
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L-dopa (levodopa) Mechanism
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↑ level of dopamine in brain. Unlike dopamine, L-dopa can cross blood-brain barrier and is converted by dopa decarboxylase in the CNS to dopamine.
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L-dopa (levodopa) Clinical use
|
Parkinsonism.
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L-dopa (levodopa) Toxicity
|
Arrhythmias from peripheral conversion to dopamine. Carbidopa minimizes this
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L-dopa (levodopa) wrt long term use
|
Long-term use can → dyskinesia following administration, akinesia between doses.
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Carbidopa mech and uses
|
a peripheral decarboxylase inhibitor, is given with L-dopa in order to ↑ the bioavailability of L-dopa in the brain and to limit peripheral side effects.
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Selegiline mech
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Selectively inhibits MAO-B, thereby ↑ the availability of dopamine.
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Selegiline Clinical use
|
Adjunctive agent to L-dopa in treatment of Parkinson’s disease.
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Selegiline Toxicity
|
May enhance adverse effects of L-dopa.
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Sumatriptan Mechanism
|
5-HT agonist. Causes vasoconstriction. Half-life < 2 hours.
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Sumatriptan Clinical use
|
Acute migraine, cluster headache attacks.
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Sumatriptan Toxicity
|
Coronary vasospasm, mild tingling (contraindicated in patients with CAD or Prinzmetal’s angina).
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contraindicated in patients with CAD or Prinzmetal’s angina) Coronary vasospasm, mild tingling
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Sumatriptan
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Which epilepsy drugs can be used for partial seziures
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All except -Ethosuximide -Benzodiazepines (diazepam or lorazepam)
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Epilepsy drugs 1st line for Tonic-Clonic
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Phenytoin Carbamazapine Valproic acid
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Epilepsy drugs 1st line for trigeminal neuralgia
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Carbamazepine
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Epilepsy drugs 1st line for Absence
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Ethosuximide
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Epilepsy drugs 1st line for prophylaxis of Status
|
Phenytoin
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Epilepsy drugs 1st line for acute Status
|
Benzodiazapines (diazapam or lorazapam)
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Epilepsy drugs 1st line for Pregnant women or children
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Phenobarbital
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Epilepsy drugs which one is Also used for peripheral neuropathy
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Gabapentin
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Epilepsy drugs which one is Also used for acute seizures of eclampsia
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Benzodiazepines (diazepam or lorazepam)
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Epilepsy drugs which one is Also used for myoclonic seizures
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Valproic acid
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Epilepsy drugs 1st line for prevent seizures of eclampsia
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MgSO4
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Epilepsy drugs mech Phenytoin
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↑ Na+ channel inactivation
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Epilepsy drugs mech Carbamazepine
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↑ Na+ channel inactivation
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Epilepsy drugs mech Lamotrigine
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Blocks voltage-gated Na+ channels
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Epilepsy drugs mech Gabapentin
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↑ GABA release
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Epilepsy drugs mech Topiramate
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BlocksNa+ channels, ↑ GABA action
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Epilepsy drugs mech Phenobarbital
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↑ GABAA action
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Epilepsy drugs mech Valproic acid
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↑ Na+ channel inactivation, ↑ GABA concentration
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Epilepsy drugs mech Ethosuximide
|
Blocks thalamic T-type Ca2+ channels
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Epilepsy drugs mech Benzodiazepines (diazepam or lorazepam)
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↑ GABAA action
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Epilepsy drug toxicities Benzodiazepines
|
Sedation, tolerance, dependence.
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Epilepsy drug toxicities Carbamazepine
|
dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome P-450.
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Epilepsy drug toxicities Ethosuximide
|
GI distress, urticaria, Stevens-Johnson syndrome.
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Epilepsy drug toxicities Phenobarbital
|
Sedation, tolerance, dependence, induction of cytochrome P-450.
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Epilepsy drug toxicities Phenytoin
|
Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, megaloblastic anemia, teratogenesis, SLE-like syndrome, induction of cytochrome P-450.
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Epilepsy drug toxicities Valproic acid
|
GI distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain.
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Epilepsy drug toxicities Lamotrigine
|
Stevens-Johnson syndrome.
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Epilepsy drug toxicities Gabapentin
|
Sedation, ataxia.
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Epilepsy drug toxicities Topiramate
|
Sedation, mental dulling, kidney stones, weight loss.
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How to treat an overdose of Barbiturates
|
Treat overdose with symptom management (assist respiration, ↑ BP).
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How to treat an overdose of Benzodiazepines
|
Treat overdose with flumazenil (competitive antagonist at GABA receptor).
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Epilepsy drug toxicities Contraindicated in porphyria.
|
Barbiturates
|
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Clinical use for Phenytoin
|
Tonic-clonic seizures. Also a class IB antiarrhythmic
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Clinical use for Barbiturates
|
Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental).
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Clinical use for Benzodiazepines
|
Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal–DTs), night terrors, sleepwalking.
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|
short acting Benzo's
|
Short acting = TOM Thumb = Triazolam, Oxazepam, Midazolam.
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Benzodiazepines Mechanism Mnemonic
|
FREnzodiazepines (increased FREquency). Facilitate GABAA action by ↑ frequency of Cl− channel opening.
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Barbiturates Mechanism mnemonic
|
BarbiDURATe (increased DURATion). Facilitate GABAA action by ↑ duration of Cl− channel opening, thus ↓ neuron firing.
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Anesthetics— general principles blood and lipid soubility
|
Drugs with ↓ solubility in blood = rapid induction and recovery times. Drugs with ↑ solubility in lipids =↑ potency =1/MAC
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Anesthetics— general principles required characteristic
|
CNS drugs must be lipid soluble (cross the blood-brain barrier) or be actively transported.
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Anesthetics— general principles N2O vs Halothane
|
N2O has low blood and lipid solubility, and thus fast induction and low potency. Halothane, in contrast, has ↑ lipid and blood solubility, and thus high potency and slow induction.
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Name the Inhaled anesthetics
|
Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide.
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Mech of Inhaled anesthetics
|
unknown.
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effects of Inhaled anesthetics
|
Myocardial depression, respiratory depression, nausea/emesis, ↑ cerebral blood flow (↓ cerebral metabolic demand).
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toxicity of Inhaled anesthetics
|
Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), malignant hyperthermia (rare).
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Name the Intravenous anesthetics
|
B. B. King on OPIATES PROPOses FOOLishly. Barbiturates Benzodiazepines Arylcyclohexamines (Ketamine) Opiates Propofol
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Intravenous anesthetics Barbiturates which one, potency and uses
|
Thiopental––high potency, high lipid solubility, rapid entry into brain. Used for induction of anesthesia and short surgical procedures.
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Intravenous anesthetics Barbiturates how terminated
|
Effect terminated by redistribution from brain. ↓ cerebral blood flow.
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Intravenous anesthetics Benzodiazepines which one, uses
|
Midazolam most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics.
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Intravenous anesthetics Benzodiazepines adverse reactions and Tx
|
May cause severe postoperative respiratory depression, ↓ BP (treat with flumazenil), and amnesia.
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Intravenous anesthetics Arylcyclohexamines name, use, adverse reactions
|
(Ketamine) PCP analogs that act as dissociative anesthetics. Cardiovascular stimulants. Cause disorientation, hallucination, and bad dreams. ↑ cerebral blood flow.
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Intravenous anesthetics Opiates
|
Morphine, fentanyl used with other CNS depressants during general anesthesia.
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Intravenous anesthetics Propofol
|
Used for rapid anesthesia induction and short procedures.
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Intravenous anesthetics nausea and propofol
|
Less postoperative nausea than thiopental.
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Local anesthetics which are Esters vs Amides
|
Esters––procaine, cocaine, tetracaine; amides––lIdocaIne, mepIvacaIne, bupIvacaIne (amIdes have 2 I’s in name).
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Local anesthetics mech
|
Block Na+ channels by binding to specific receptors on inner portion of channel.
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Local anesthetics mech specifically for 3° amine
|
3° amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form.
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Local anesthetics considerations WRT infection
|
In infected (acidic) tissue, anesthetics are charged and cannot penetrate membrane effectively. Therefore, more anesthetic is needed in these cases.
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Local anesthetics considerations WRT order of nerve blockade (structure of nerve)
|
small unmyelinated pain fibers > small myelinated autonomic fibers > large myelinated autonomic fibers.
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Local anesthetics considerations WRT order of nerve blockade (function of nerve)
|
pain (lose first) > temperature > touch > pressure (lose last).
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Local anesthetics clinical use
|
Minor surgical procedures, spinal anesthesia
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Local anesthetics and allergies
|
If allergic to esters (more likely), give amides.
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Local anesthetics Toxicities
|
-CNS excitation, -severe cardiovascular toxicity (bupivacaine), -hypertension, hypotension, -arrhythmias (cocaine).
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Which Local anesthetic can cause severe cardiovascular toxicity
|
(bupivacaine)
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Which Local anesthetic can cause arrhythmias
|
(cocaine)
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Neuromuscular blocking drugs uses
|
Used for muscle paralysis in surgery or mechanical ventilation
|
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Neuromuscular blocking drugs wrt selectivity
|
Selective for motor (vs. autonomic) nicotinic receptor.
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Neuromuscular blocking drugs name the depolarizing ones
|
Succinylcholine
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Neuromuscular blocking drugs name the nondepolarizing ones
|
Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rapacuronium.
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Succinylcholine. mech
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Neuromuscular blocking drugs Depolarizing
|
|
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Depolarizing Neuromuscular blocking drugs 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).
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Mech of Nondepolarizing Neuromuscular blocking drugs
|
Competitive––compete with ACh for receptors
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Nondepolarizing Neuromuscular blocking drugs reversal of blockade
|
Reversal of blockade––neostigmine, edrophonium, and other cholinesterase inhibitors.
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Dantrolene uses
|
treatment of malignant hyperthermia, and neuroleptic malignant syndrome
|
|
|
Causes of Malignant Hyperthermia
|
the concomitant use of inhalation anesthetics (except N2O) and succinylcholine.
|
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Malignant Hyperthermia Tx
|
Dantrolene
|
|
|
causes of neuroleptic malignant syndrome
|
(a toxicity of antipsychotic drugs).
|
|
|
neuroleptic malignant syndrome Tx
|
Dantrolene
|
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|
Dantrolene Mech
|
prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.
|
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|
Brain Locations of Synthesis of neurotransmitters NE
|
Locus Ceruleus
|
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|
Brain Locations of Synthesis of neurotransmitters Dopamine
|
Ventral tegmentum and SNc
|
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|
Brain Locations of Synthesis of neurotransmitters 5-HT
|
Raphe Nucleus
|
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|
Brain Locations of Synthesis of neurotransmitters ACh
|
Basal nucleus of Mynert
|
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|
Sensory corpuscles which ones are in all skin
|
Free nerve endings (C, A-delta fibers)
|
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|
Sensory corpuscles Free nerve endings (C, A-delta fibers) where and what
|
all skin and some viscera Pain and Temp
|
