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523 Cards in this Set
- Front
- Back
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Patient presents with decreased pain and temperature sensation over
the lateral aspects of both arms.a |
Syringomyelia.
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Penlight in patient’s right eyeiproduces bilateral pupillary
constriction. When moved to the left eye, there is paradoxical dilatation. |
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. |
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 |
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. |
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. |
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 |
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 |
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. |
Prolactinoma.
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43-year-old man experiences
dizziness and tinnitus. CT shows enlarged internal acoustic meatus.z |
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. |
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). |
Absence seizures.
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Man on several medications,
including antidepressants and his symptoms? antihypertensives, has mydriasis What is the cause |
TCA.
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Woman on MAO inhibitor
has hypertensive crisis after a meal. |
Tyramine (wine or cheese).
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Astrocyte
marker: |
GFAP.
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Astrocytes
what they do |
physical support, repair, K+ metabolism;
help maintain blood-brain barrier. |
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CNS/PNS Support Cells
role of Ependymal cells |
–inner lining of ventricles.
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CNS/PNS Support Cells
role of Microglia |
phagocytosis.
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CNS/PNS Support Cells
role of Oligodendroglia |
central myelin production
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CNS/PNS Support Cells
role of Schwann cells– |
peripheral myelin production.s
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These cells are destroyed in
multiple sclerosis. |
Oligodendroglia
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Acoustic neuroma is an
example of |
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. |
Microglia
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HIV-infected ????? fuse to
form multinucleated giant cells in the CNS. |
microglia
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HIV-infected microglia fuse to
form ??? |
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 |
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 |
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 |
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. |
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. |
Pacinian
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Cup-shaped nerve endings (tactile disks) in dermis
of fingertips, hair follicles, hard palate. Involved in light, crude touch. |
Merkel’s
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Inner ear
makeup of peri vs endo lymph |
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 |
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). |
Hair cells
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Semicircular canals contain
????? which detect |
Ampullae
Angular acceleration. |
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Utricle and saccule contain
????? which detect . |
maculae–
linear acceleration. |
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?????? contain
maculae––detect linear acceleration. |
Utricle and saccule
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???????? contain
Ampullae––detect Angular acceleration. |
Semicircular canals
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cochlea
???????? picks up high- frequency sound. ?????? picks up low-frequency sound. |
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 |
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 |
The hypothalamus wears TAN
HATS. Thirst Adenohypophysis Neruohypophysis Hunger Autonomic regulation Temp regulation Sexual urges |
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Hypothalamus
Location involved in Thirst |
Thirst and water balance (supraoptic nucleus).
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Hypothalamus
Location involved in Neurohypophysis |
Neurohypophysis and median eminence release
hormones synthesized in hypothalamic nuclei. |
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Hypothalamus
Location involved in Hunger ans satiety |
Hunger (lateral ucleus; damage → anorexia/starvation
Satiety (ventromedial nucleus; damage → hyperphagia and obesity). |
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Hypothalamus
Location involved in Autonomic regulation |
anterior hypothalamus
regulates parasympathetic; posterior hypothalamus regulates sympathetic circadian rhythms (suprachiasmatic nucleus). |
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Hypothalamus
Location involved in Temperature regulation |
(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 |
(Septal nucleus––
destruction → rage). |
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Hypothalamus
mnemonic Hunger |
If you zap your ventromedial
nucleus, you grow ventrally and medially. |
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Hypothalamus
mnemonic Temp |
If you zap your Posterior
hypothalamus, you become a Poikilotherm (cold-blooded snake). A/C = anterior cooling. |
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Posterior pituitary
aka |
neurohypophysis
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neurohypophysis
aka |
Posterior pituitary
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neurohypophysis
where axonal projections come from |
Receives hypothalamic axonal projections from
-supraoptic (ADH) -paraventricular (oxytocin) nuclei. |
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Derivation of the word
Oxytocin |
oxys = quick;
tocos = birth. |
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Major relay for ascending sensory information
that ultimately reaches the cortex. |
Thalamus
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Thalamus
Function of the LGN |
Lateral geniculate nucleus (LGN)––visual.
Lateral for Light. Medial for Music. |
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Thalamus
Function of the MGN |
Medial geniculate nucleus (MGN)––auditory.
Lateral for Light. Medial for Music. |
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Thalamus
Function of the VPL |
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 |
Ventral posterior nucleus, medial part (VPM)
––facial sensation (via CN V). |
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Thalamus
Function of the VA |
Ventral anterior/lateral (VA/VL) nuclei
––motor. |
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Thalamus
Function of the VL |
Ventral anterior/lateral (VA/VL) nuclei
––motor. |
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Thalamus
which nucleus Visual |
Lateral geniculate nucleus (LGN)––visual.
Lateral for Light. Medial for Music. |
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Thalamus
which nucleus auditory. |
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). |
Ventral posterior nucleus, lateral part (VPL)
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Thalamus
which nucleus facial sensation (via CN V). |
Ventral posterior nucleus, medial part (VPM)
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Thalamus
which nucleus motor. |
Ventral anterior/lateral (VA/VL) nuclei
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Limbic system is
Responsible for |
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 ??????? |
substantia nigra
direct pathway indirect pathway). |
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Frontal lobe
functions |
“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. |
Anterior communicating artery––
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supplies medial surface of the brain, leg-foot area of motor and
sensory cortices. |
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. |
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; |
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). |
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 |
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 |
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 |
Needle in
subarachnoid space |
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lumbar puncture
what is not pierced |
Pia is not pierced.
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lumbar puncture
where to go in |
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 |
(ascending pressure,
vibration, touch, and proprioceptive sensation) |
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Spinal tract anatomy and functions
Tract and function Spinothalamic tract |
(ascending pain and
temperature sensation) |
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Spinal tract anatomy and functions
Tract and function Lateral corticospinal tract |
(descending
voluntary movement of contralateral limbs) |
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Which Tract
(ascending pressure, vibration, touch, and proprioceptive sensation) |
Dorsal column-medial
lemniscal pathway |
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Which Tract
(ascending pain and temperature sensation) |
Spinothalamic tract
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Which Tract
(descending voluntary movement of contralateral limbs) |
Lateral corticospinal
tract |
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Dorsal column-medial
lemniscal pathway 1st-order neuron |
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 |
Nucleus cuneatus or gracilis
(medulla) |
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Dorsal column-medial
lemniscal pathway 2nd-order neuron |
Decussates in medulla → ascends contralaterally in medial lemniscus
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Dorsal column-medial
lemniscal pathway Synapse 2 |
VPL of
thalamus |
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Dorsal column-medial
lemniscal pathway 3rd-order neuron |
Sensory cortex
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Spinothalamic tract
1st-order neuron |
Sensory nerve ending (A-delta and C fibers) → enters spinal cord
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Spinothalamic tract
Synapse 1 |
Ipsilateral gray matter (spinal cord)
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Spinothalamic tract
2nd-order neuron |
Decussates at anterior white commissure → ascends contralaterally
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Spinothalamic tract
Synapse 2 |
VPL of
thalamus |
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Spinothalamic tract
3rd-order neuron |
Sensory cortex
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Lateral corticospinal tract
1st-order neuron |
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 |
Cell body of anterior horn
(spinal cord) |
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Lateral corticospinal tract
2nd-order neuron |
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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None
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Fasciculus gracilis =
Fasciculus cuneatus = |
Legs
Arms |
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Dorsal column
organization mnemonic |
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 |
subclavius muscle.
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Upper extremity nerve injury
Site of injury and motor deficit Radial |
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 |
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 |
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 |
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 |
Loss of function of coracobrachialis, biceps, and
brachialis muscles (biceps reflex). |
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Upper extremity nerve injury
Deficit in sensation/course Radial |
Posterior brachial cutaneous.
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Upper extremity nerve injury
Deficit in sensation/course Median |
Posterior antebrachial
cutaneous. Passes through supinator. |
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Upper extremity nerve injury
Deficit in sensation/course Ulnar |
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 |
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 |
Passes through coracobrachialis.
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Erb-Duchenne
palsy cause |
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 |
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). |
Erb-Duchenne
palsy findings |
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“Waiter’s tip” owing to
appearance of arm. |
Erb-Duchenne
palsy |
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Thoracic outlet syndrome
aka |
Klumpke’s palsy
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Klumpke’s palsy
aka |
Thoracic outlet syndrome
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Klumpke’s palsy
cause |
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 |
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 |
Thoracic outlet syndrome
aka (Klumpke’spalsy) |
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Lower extremity nerve injury
motor deficit Common peroneal |
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 |
Loss of plantar flexion. Tibial nerve innervates
posterior compartment. |
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Lower extremity nerve injury
motor deficit Femoral |
Loss of knee extension/knee jerk.
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Lower extremity nerve injury
motor deficit Obturator |
Loss of hip adduction.
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foot nerve mnemonic
|
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). |
Common peroneal
(L4–S2) |
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Which nerve is damaged and give spinal nerves
Loss of plantar flexion. |
Tibial nerve (L4-S3)
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Which nerve is damaged and give spinal nerves
Loss of knee extension/knee jerk. |
Femoral (L2–L4)
|
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Which nerve is damaged and give spinal nerves
Loss of hip adduction. |
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 |
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 |
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 |
Ulnar C7-T1
|
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Which nerve is damaged and give spinal nerves
loss of deltoid action. |
Axillary C5-C6
|
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Which nerve is damaged and give spinal nerves
Loss of function of coracobrachialis, biceps, and brachialis muscles |
Musculocutaneous C5-C7
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Radial nerve
mnemonic |
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. |
Radial nerve
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Thenar-hypothenar
muscles |
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 |
––ischial spine.
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Clinically important
landmarks Appendix Lumbar puncture––iliac crest. |
––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 |
––iliac crest.
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Landmark
dermatomes cervical |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
CNS stimulates γ motor neuron →contracts intrafusal fiber → increased sensitivity of reflex arc.
|
|
|
4 Primitive reflexes
|
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 |
|
|
Primitive reflexes when do they go and when do they return
|
Normally disappear within 1st
year. May reemerge following frontal lobe lesion. |
|
|
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. |
|
|
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. |
|
|
Cranial nerve function
I |
Smell
|
|
|
Cranial nerve function
II |
Sight
|
|
|
Cranial nerve function
III |
Eye motion, Pupil constriction, accommodation, eyelid opening
|
|
|
Cranial nerve function
IV |
Eye movement
|
|
|
Cranial nerve function
V |
Mastication, facial sensation
|
|
|
Cranial nerve function
VI |
Eye movement
|
|
|
Cranial nerve function
VII |
Facial movement, taste from anterior 2/3 of tongue, lacrimation, salivation (submaxillary and sublingual glands), eyelid closing
|
|
|
Cranial nerve function
VIII |
Hearing, balance
|
|
|
Cranial nerve function
IX |
Taste from posterior 1/3 of tongue, swallowing, salivation (parotid gland), monitoring carotid body and sinus chemo- and baroreceptors
|
|
|
Cranial nerve function
X |
Taste from epiglottic region, swallowing, palate elevation, talking, thoracoabdominal viscera, monitoring aortic arch chemo- and baroreceptors
|
|
|
Cranial nerve function
XI |
Head turning, shoulder shrugging
|
|
|
Cranial nerve function
XII |
Tongue movement
|
|
|
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. |
|
|
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. |
|
|
Vagal nuclei
name them |
Nucleus Solitarius
Nucleus aMbiguus Dorsal motor nucleus |
|
|
what does it do
Nucleus Solitarius |
Visceral Sensory information (e.g., taste,
baroreceptors, gut distention). VII, IX, X. |
|
|
what does it do
Dorsal motor nucleus |
Sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI.
|
|
|
what does it do
Nucleus ambiguus |
Nucleus aMbiguus IX, X, XI.
Motor innervation of pharynx, larynx, and upper esophagus (e.g., swallowing, palate elevation). |
|
|
Which nucleus
Visceral Sensory information (e.g., taste, baroreceptors, gut distention). |
Nucleus Solitarius
|
|
|
Which nucleus
Sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI. |
Dorsal motor nucleus
|
|
|
Which nucleus
Motor innervation of pharynx, larynx, and upper esophagus (e.g., swallowing, palate elevation). |
Nucleus ambiguus
|
|
|
What nerve/vessel passes through
Cribriform plate |
CN I
|
|
|
What nerve/vessel passes through
Middle cranial fossa |
(CN II–VI)––through sphenoid bone
|
|
|
What nerve/vessel passes through
Optic canal |
CN II, ophthalmic artery, central
retinal vein) |
|
|
What nerve/vessel passes through
Superior orbital fissure |
(CN III, IV, V1, VI,
ophthalmic vein) |
|
|
What nerve/vessel passes through
Foramen Rotundum |
(CN V2)
|
|
|
What nerve/vessel passes through
Foramen Ovale |
(CN V3)
|
|
|
What nerve/vessel passes through
Foramen spinosum |
(middle meningeal
artery) |
|
|
What nerve/vessel passes through
Posterior cranial fossa |
(CN VII–XII)––through
temporal or occipital bone: |
|
|
What nerve/vessel passes through
Internal auditory meatus |
(CN VII, VIII)
|
|
|
What nerve/vessel passes through
Jugular foramen |
(CN IX, X, XI, jugular vein)
|
|
|
What nerve/vessel passes through
Hypoglossal canal (CN XII) |
(CN XII)
|
|
|
What nerve/vessel passes through
Foramen magnum |
spinal roots of CN XI,
brain stem, vertebral arteries) |
|
|
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) |
|
|
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) |
|
|
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. |
|
|
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). |
|
|
Mastication
muscles/nerves mnemonic |
M’s Munch.
Lateral Lowers (when speaking of pterygoids wrt jaw motion). |
|
|
Muscles with
glossus innervation |
All muscles with root glossus in their names (except
palatoglossus, innervated by vagus nerve) are innervated by hypoglossal nerve. |
|
|
Muscles with
glossus/palat mnemonic |
Glossus: hypoglossal nerve.
Palat: vagus nerve (except TENSor, who was too TENSE). |
|
|
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) |
|
|
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). |
|
|
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
|
|
|
Primary brain tumors in Kids
Characteristic perivascular pseudorosettes. Rod-shaped blepharoplasts (basal ciliary bodies) found near nucleus. |
Ependymoma
|
|
|
Primary brain tumors in Kids
Most often cerebellar; associated with von Hippel-Lindau |
Hemangioblastoma
|
|
|
Primary brain tumors in Kids
Can produce EPO →2° polycythemia. |
Hemangioblastoma
|
|
|
Primary brain tumors in Kids
Rosenthal fibers—eosinophilic, corkscrew fibers. |
Pilocytic astrocytoma
(low-grade) |
|
|
Primary brain tumors in Kids
Foamy cells and high vascularity are characteristic. |
Hemangioblastoma
|
|
|
Primary brain tumors in Kids
Derived from remnants of Rathke’s pouch. |
Craniopharyngioma
|
|
|
Primary brain tumors in Kids
Calcification is common. |
Craniopharyngioma
|
|
|
Primary brain tumors in Kids
Most common childhood supratentorial tumor. |
Craniopharyngioma
|
|
|
Primary brain tumors in Kids
confused with pituitary adenoma (can also cause bitemporal hemianopia). |
Craniopharyngioma
|
|
|
Primary brain tumors in Kids
order of incidence |
F. Pilocytic astrocytoma
(low-grade) G. Medulloblastoma H. Ependymoma I. Hemangioblastoma J. Craniopharyngioma |
|
|
Primary brain tumors in Adults
order of incidence |
A. Glioblastoma multiforme
(grade IV astrocytoma) B. Meningioma C. Schwannoma D. Oligodendroglioma E. Pituitary adenoma |
|
|
Given the Spinal cord lesion
give the Conditions and the clinical findings lower motor neuron lesions only, due to destruction of anterior horns |
Poliomyelitis and Werdnig-
Hoffmann disease: flaccid paralysis |
|
|
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; |
Multiple sclerosis:
scanning speech, intention tremor, nystagmus |
|
|
Given the Spinal cord lesion
give the Conditions and the clinical findings degeneration of dorsal roots and dorsal columns; |
Tabes dorsalis (3° syphilis):
Impaired proprioception, ocomotor ataxia |
|
|
Given the Spinal cord lesion
give the Conditions and the clinical findings fibers of spinothalamic tract damaged |
Syringomyelia:
bilateral loss of pain and temperature sensation |
|
|
Given the Spinal cord lesion
give the Conditions and the clinical findings demyelination of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts; |
Vitamin B12 neuropathy and
Friedreich´s ataxia: ataxic gait, hyperreflexia, impaired position and vibration sense |
|
|
Given the Spinal cord lesion
give the Conditions and the clinical findings spares dorsal columns and tract of Lissauer |
Complete occlusion of
ventral artery; |
|
|
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 |
ALS:
|
|
|
What is Syringomyelia
what is damaged and how does it present |
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 |
|
|
derivation of
Syringomyelia |
Syrinx (Greek) = tube, as in
syringe. |
|
|
Syringomyelia
association |
Often presents in patients with
Arnold-Chiari malformation. |
|
|
Syringomyelia
location |
Most common at C8–T1.
|
|
|
What is Tabes dorsales and what are the clinical findings
|
Degeneration of dorsal columns and dorsal roots due to 3° syphilis, resulting in impaired
proprioception and locomotor ataxia. |
|
|
Tabes dorsalis
what other symptoms are associated with it |
Charcot’s joints,
shooting Lightning) pain, Argyll Robertson pupils (accommodation but not reactive to light), absence of DTRs. |
|
|
Charcot’s joints
|
progressive degeneration of a weight-bearing joint leading to deformity
|
|
|
Hemisection of spinal cord.
aka |
Brown-Séquard syndrome
|
|
|
Brown-Séquard syndrome
aka |
Hemisection of spinal cord.
|
|
|
Brown-Séquard syndrome
findings |
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 |
|
|
Brown-Séquard syndrome above T1
|
If lesion occurs above T1, presents with Horner’s syndrome.
|
|
|
Horner’s syndrome aka
|
Sympathectomy of face
|
|
|
Sympathectomy of face
aka |
Horner’s syndrome
|
|
|
Horner’s syndrome
clinical findings |
1. Ptosis (slight drooping of eyelid)
2. Anhidrosis (absence of sweating) and flushing (rubor) of affected side of face 3. Miosis (pupil constriction) |
|
|
Horner’s syndrome
assiciations |
Associated with lesion of spinal cord above T1
(e.g., Pancoast’s tumor, hemisection, late-stage syringomyelia). |
|
|
The 3-neuron oculosympathetic pathway projects from
|
the hypothalamus to the
intermediolateral column of the spinal cord, then to the superior cervical (sympathetic) ganglion, and finally to the pupil, the smooth muscle of the eyelids, and the sweat glands of the forehead and face. |
|
|
findings of CN and cerebellar lesions
CN XII lesion (LMN) |
tongue deviates toward side of lesion (lick your wounds).
|
|
|
findings of CN and cerebellar lesions
CN V motor lesion |
jaw deviates toward side of lesion.
|
|
|
findings of CN and cerebellar lesions
Unilateral lesion of cerebellum |
patient tends to fall toward side of lesion.
|
|
|
findings of CN and cerebellar lesions
CN X lesion |
uvula deviates away from side of lesion.
|
|
|
findings of CN and cerebellar lesions
CN XI lesion |
weakness turning head to contralateral side of (away from)lesion.
Shoulder droop on side of lesion. |
|
|
CN VII lesions
associations |
BLASTeD
Bell's palsy seen in -Lyme -AIDS -Sarcoid -Tumors -Diabetes |
|
|
CN VII lesions
UMN vs LMN |
Contralateral paralysis of lower face only.
Ipsilateral paralysis of upper and lower face. |
|
|
Brain herniation syndromes
name them and what they herniate through |
1. Cingulate herniation
under falx cerebri 2. Downward transtentorial (central) herniation 3. Uncal herniation 4. Cerebellar tonsillar herniation into the foramen magnum |
|
|
Brain herniation syndromes
complications |
Can compress anterior cerebral artery.
Coma and death result when these herniations compress the brain stem. |
|
|
What is the Uncus
|
medial temporal lobe.
|
|
|
in Uncal herniation
what causes Ipsilateral dilated pupil/ptosis |
Stretching of CN III
|
|
|
in Uncal herniation
what causes Contralateral homonymous hemianopia |
Compression of ipsilateral posterior cerebral artery
|
|
|
in Uncal herniation
what causes Ipsilateral paresis |
Compression of contralateral crus cerebri (Kernohan’s notch)
|
|
|
in Uncal herniation
what causes Duret hemorrhages/ paramedian artery rupture |
Caudal displacement of brain stem
|
|
|
In Uncal Herniation what does
Stretching of CN III lead to? |
Ipsilateral dilated
pupil/ptosis |
|
|
In Uncal Herniation what does
Compression of ipsilateral posterior cerebral artery lead to? |
Contralateral homonymous
hemianopia |
|
|
In Uncal Herniation what does
Compression of contralateral crus cerebri (Kernohan’s notch) lead to? |
Ipsilateral paresis
|
|
|
In Uncal Herniation what does
Caudal displacement of brain stem lead to? |
Duret hemorrhages––
paramedian artery rupture |
|
|
Parkinson’s disease drugs
name 4 strategies |
-Agonize dopamine
receptors -Increase dopamine -Prevent dopamine breakdown -Curb excess cholinergic activity |
|
|
Parkinson’s disease drugs
Name the ones that Agonize dopamine receptors And give mechanisms |
Bromocriptine (ergot alkaloid and partial dopamine agonist), pramipexole, ropinirole
|
|
|
Parkinson’s disease drugs
Name the ones that Increase dopamine And give mechanisms |
Amantadine (may ↑ dopamine release)
L-dopa/carbidopa (converted to dopamine in CNS) |
|
|
Parkinson’s disease drugs
Name the ones that Prevent dopamine breakdown And give mechanisms |
Selegiline (selective MAO type B inhibitor)
; entacapone, tolcapone (COMT inhibitors) |
|
|
Parkinson’s disease drugs
Name the ones that Curb excess cholinergic activity And give mechanisms |
Benztropine (Antimuscarinic; improves tremor
and rigidity but has little effect on bradykinesia) |
|
|
Parkinson’s disease
drugs improves tremor and rigidity but has little effect on bradykinesia |
Benztropine
|
|
|
Parkinson’s disease
drugs mnemonic |
BALSA:
Bromocriptine Amantadine Levodopa (with carbidopa) Selegiline (and COMT inhibitors) Antimuscarinics |
|
|
Parkinsonism is due to loss ?????
|
loss of dopaminergic neurons and excess cholinergic activity.
|
|
|
L-dopa (levodopa)
Mechanism |
↑ 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. |
|
|
L-dopa (levodopa)
Clinical use |
Parkinsonism.
|
|
|
L-dopa (levodopa)
Toxicity |
Arrhythmias from peripheral conversion to dopamine. Carbidopa minimizes this
|
|
|
L-dopa (levodopa)
wrt long term use |
Long-term use can →
dyskinesia following administration, akinesia between doses. |
|
|
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. |
|
|
Selegiline
mech |
Selectively inhibits MAO-B, thereby ↑ the availability of dopamine.
|
|
|
Selegiline
Clinical use |
Adjunctive agent to L-dopa in treatment of Parkinson’s disease.
|
|
|
Selegiline
Toxicity |
May enhance adverse effects of L-dopa.
|
|
|
Sumatriptan
Mechanism |
5-HT agonist. Causes vasoconstriction. Half-life < 2 hours.
|
|
|
Sumatriptan
Clinical use |
Acute migraine,
cluster headache attacks. |
|
|
Sumatriptan
Toxicity |
Coronary vasospasm, mild tingling
(contraindicated in patients with CAD or Prinzmetal’s angina). |
|
|
contraindicated in patients with CAD or Prinzmetal’s angina)
Coronary vasospasm, mild tingling |
Sumatriptan
|
|
|
Which epilepsy drugs can be used for partial seziures
|
All except
-Ethosuximide -Benzodiazepines (diazepam or lorazepam) |
|
|
Epilepsy drugs
1st line for Tonic-Clonic |
Phenytoin
Carbamazapine Valproic acid |
|
|
Epilepsy drugs
1st line for trigeminal neuralgia |
Carbamazepine
|
|
|
Epilepsy drugs
1st line for Absence |
Ethosuximide
|
|
|
Epilepsy drugs
1st line for prophylaxis of Status |
Phenytoin
|
|
|
Epilepsy drugs
1st line for acute Status |
Benzodiazapines (diazapam or lorazapam)
|
|
|
Epilepsy drugs
1st line for Pregnant women or children |
Phenobarbital
|
|
|
Epilepsy drugs
which one is Also used for peripheral neuropathy |
Gabapentin
|
|
|
Epilepsy drugs
which one is Also used for acute seizures of eclampsia |
Benzodiazepines (diazepam or
lorazepam) |
|
|
Epilepsy drugs
which one is Also used for myoclonic seizures |
Valproic acid
|
|
|
Epilepsy drugs
1st line for prevent seizures of eclampsia |
MgSO4
|
|
|
Epilepsy drugs mech
Phenytoin |
↑ Na+ channel inactivation
|
|
|
Epilepsy drugs mech
Carbamazepine |
↑ Na+ channel inactivation
|
|
|
Epilepsy drugs mech
Lamotrigine |
Blocks voltage-gated Na+
channels |
|
|
Epilepsy drugs mech
Gabapentin |
↑ GABA release
|
|
|
Epilepsy drugs mech
Topiramate |
BlocksNa+ channels,
↑ GABA action |
|
|
Epilepsy drugs mech
Phenobarbital |
↑ GABAA action
|
|
|
Epilepsy drugs mech
Valproic acid |
↑ Na+ channel inactivation,
↑ GABA concentration |
|
|
Epilepsy drugs mech
Ethosuximide |
Blocks thalamic T-type Ca2+
channels |
|
|
Epilepsy drugs mech
Benzodiazepines (diazepam or lorazepam) |
↑ GABAA action
|
|
|
Epilepsy drug toxicities
Benzodiazepines |
Sedation, tolerance, dependence.
|
|
|
Epilepsy drug toxicities
Carbamazepine |
dyscrasias (agranulocytosis, aplastic anemia),
liver toxicity, teratogenesis, induction of cytochrome P-450. |
|
|
Epilepsy drug toxicities
Ethosuximide |
GI distress,
urticaria, Stevens-Johnson syndrome. |
|
|
Epilepsy drug toxicities
Phenobarbital |
Sedation, tolerance, dependence, induction of cytochrome P-450.
|
|
|
Epilepsy drug toxicities
Phenytoin |
Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, megaloblastic
anemia, teratogenesis, SLE-like syndrome, induction of cytochrome P-450. |
|
|
Epilepsy drug toxicities
Valproic acid |
GI distress,
rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain. |
|
|
Epilepsy drug toxicities
Lamotrigine |
Stevens-Johnson syndrome.
|
|
|
Epilepsy drug toxicities
Gabapentin |
Sedation, ataxia.
|
|
|
Epilepsy drug toxicities
Topiramate |
Sedation, mental dulling, kidney stones, weight loss.
|
|
|
How to treat an overdose of
Barbiturates |
Treat overdose with symptom management (assist
respiration, ↑ BP). |
|
|
How to treat an overdose of
Benzodiazepines |
Treat overdose with flumazenil (competitive antagonist
at GABA receptor). |
|
|
Epilepsy drug toxicities
Contraindicated in porphyria. |
Barbiturates
|
|
|
Clinical use for
Phenytoin |
Tonic-clonic seizures. Also a class IB antiarrhythmic
|
|
|
Clinical use for
Barbiturates |
Sedative for anxiety, seizures, insomnia, induction
of anesthesia (thiopental). |
|
|
Clinical use for
Benzodiazepines |
Anxiety, spasticity, status epilepticus (lorazepam and
diazepam), detoxification (especially alcohol withdrawal–DTs), night terrors, sleepwalking. |
|
|
short acting Benzo's
|
Short acting = TOM Thumb =
Triazolam, Oxazepam, Midazolam. |
|
|
Benzodiazepines
Mechanism Mnemonic |
FREnzodiazepines (increased
FREquency). Facilitate GABAA action by ↑ frequency of Cl− channel opening. |
|
|
Barbiturates
Mechanism mnemonic |
BarbiDURATe (increased
DURATion). Facilitate GABAA action by ↑ duration of Cl− channel opening, thus ↓ neuron firing. |
|
|
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 |
|
|
Anesthetics—
general principles required characteristic |
CNS drugs must be lipid soluble (cross the blood-brain barrier) or be actively transported.
|
|
|
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. |
|
|
Name the
Inhaled anesthetics |
Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane,
nitrous oxide. |
|
|
Mech of
Inhaled anesthetics |
unknown.
|
|
|
effects of
Inhaled anesthetics |
Myocardial depression, respiratory depression, nausea/emesis, ↑ cerebral blood flow
(↓ cerebral metabolic demand). |
|
|
toxicity of
Inhaled anesthetics |
Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane),
malignant hyperthermia (rare). |
|
|
Name the
Intravenous anesthetics |
B. B. King on OPIATES
PROPOses FOOLishly. Barbiturates Benzodiazepines Arylcyclohexamines (Ketamine) Opiates Propofol |
|
|
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. |
|
|
Intravenous anesthetics
Barbiturates how terminated |
Effect terminated by
redistribution from brain. ↓ cerebral blood flow. |
|
|
Intravenous anesthetics
Benzodiazepines which one, uses |
Midazolam most common drug used for endoscopy; used adjunctively with gaseous anesthetics and
narcotics. |
|
|
Intravenous anesthetics
Benzodiazepines adverse reactions and Tx |
May cause severe postoperative
respiratory depression, ↓ BP (treat with flumazenil), and amnesia. |
|
|
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. |
|
|
Intravenous anesthetics
Opiates |
Morphine, fentanyl used with other CNS depressants
during general anesthesia. |
|
|
Intravenous anesthetics
Propofol |
Used for rapid anesthesia induction and short
procedures. |
|
|
Intravenous anesthetics
nausea and propofol |
Less postoperative nausea than
thiopental. |
|
|
Local anesthetics which are
Esters vs Amides |
Esters––procaine, cocaine, tetracaine;
amides––lIdocaIne, mepIvacaIne, bupIvacaIne (amIdes have 2 I’s in name). |
|
|
Local anesthetics
mech |
Block Na+ channels by binding to specific receptors on inner portion of channel.
|
|
|
Local anesthetics
mech specifically for 3° amine |
3° amine local anesthetics penetrate membrane in uncharged form, then bind to ion
channels as charged form. |
|
|
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. |
|
|
Local anesthetics
considerations WRT order of nerve blockade (structure of nerve) |
small unmyelinated pain fibers > small myelinated autonomic fibers > large myelinated
autonomic fibers. |
|
|
Local anesthetics
considerations WRT order of nerve blockade (function of nerve) |
pain (lose first) > temperature > touch > pressure (lose
last). |
|
|
Local anesthetics
clinical use |
Minor surgical procedures, spinal anesthesia
|
|
|
Local anesthetics
and allergies |
If allergic to esters (more likely), give amides.
|
|
|
Local anesthetics
Toxicities |
-CNS excitation,
-severe cardiovascular toxicity (bupivacaine), -hypertension, hypotension, -arrhythmias (cocaine). |
|
|
Which
Local anesthetic can cause severe cardiovascular toxicity |
(bupivacaine)
|
|
|
Which
Local anesthetic can cause arrhythmias |
(cocaine)
|
|
|
Neuromuscular blocking drugs
uses |
Used for muscle paralysis in surgery or mechanical ventilation
|
|
|
Neuromuscular blocking drugs
wrt selectivity |
Selective for motor
(vs. autonomic) nicotinic receptor. |
|
|
Neuromuscular blocking drugs
name the depolarizing ones |
Succinylcholine
|
|
|
Neuromuscular blocking drugs
name the nondepolarizing ones |
Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rapacuronium.
|
|
|
Succinylcholine.
mech |
Neuromuscular blocking drugs
Depolarizing |
|
|
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). |
|
|
Mech of Nondepolarizing Neuromuscular blocking drugs
|
Competitive––compete with ACh for receptors
|
|
|
Nondepolarizing Neuromuscular blocking drugs
reversal of blockade |
Reversal of blockade––neostigmine, edrophonium, and other cholinesterase inhibitors.
|
|
|
Dantrolene
uses |
treatment of malignant hyperthermia,
and neuroleptic malignant syndrome |
|
|
Causes of Malignant Hyperthermia
|
the concomitant
use of inhalation anesthetics (except N2O) and succinylcholine. |
|
|
Malignant Hyperthermia
Tx |
Dantrolene
|
|
|
causes of neuroleptic malignant syndrome
|
(a toxicity of antipsychotic drugs).
|
|
|
neuroleptic malignant syndrome
Tx |
Dantrolene
|
|
|
Dantrolene
Mech |
prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.
|
|
|
Brain Locations of Synthesis of neurotransmitters
NE |
Locus Ceruleus
|
|
|
Brain Locations of Synthesis of neurotransmitters
Dopamine |
Ventral tegmentum and SNc
|
|
|
Brain Locations of Synthesis of neurotransmitters
5-HT |
Raphe Nucleus
|
|
|
Brain Locations of Synthesis of neurotransmitters
ACh |
Basal nucleus of Mynert
|
|
|
Sensory corpuscles
which ones are in all skin |
Free nerve endings (C, A-delta fibers)
|
|
|
Sensory corpuscles
Free nerve endings (C, A-delta fibers) where and what |
all skin and some viscera
Pain and Temp |
