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Day 4 > Neurology and Special Senses - First Aid > Flashcards

Neurology and Special Senses - First Aid Flashcards

1
Q

Regional Specification of Developing Brain

A
  • Telencephalon is the 1st part.
  • Diencephalon is the 2nd part.
  • The rest are arranged alphabetically:
    • Mesencephalon
    • Metencephalon
    • Myelencephalon
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2
Q

Central and Peripheral Nervous Systems Origins:

  • CNS Neurons
  • Ependymal Cells
    • inner lining of ventricles
    • make CSF
  • Oligodendrocytes
  • Astrocytes
A

Neuroepithelia in Neural Tube

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3
Q

Central and Peripheral Nervous Systems Origins:

  • PNS Neurons
  • Schwann Cells
A

Neural Crest

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4
Q

Central and Peripheral Nervous Systems Origins:

Microglia (like macrophages)

A

Mesoderm

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5
Q

Neural Tube Defects

A
  • Neuropores fail to fuse (4th week) → persistent connection between amniotic cavity and spinal canal.
  • Associated with maternal diabetes as well as low folic acid intake before conception and during pregnancy.
  • ↑ α-fetoprotein (AFP) in amniotic fluid and maternal serum (except spina bifida occulta = normal AFP).
  • ↑ acetylcholinesterase (AChE) in amniotic fluid is a helpful confirmatory test.
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6
Q

Neural Tube Defects:

  • failure of caudal neuropore to close, but no herniation
  • usually seen at lower vertebral levels
  • dura is intact
  • associated with tuft of hair or skin dimple at level of bony defect
A

Spina Bifida Occulta

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7
Q

Neural Tube Defects:

  • meninges (but no neural tissue) herniate through bony defect
  • associated with spina bifida cystica
A

Meningocele

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8
Q

Neural Tube Defects:

meninges and neural tissue (eg. cauda equina) herniate through bony defect

A

Meningomyelocele

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9
Q

Neural Tube Defects:

  • also known as rachischisis
  • exposed unfused neural tissue without skin/meningeal covering
A

Myeloschisis

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10
Q

Neural Tube Defects:

  • failure of rostral neuropore to close → no forebrain, open calvarium
  • Clinical Findings: polyhydramnios (no swallowing center in brain)
A

Anencephaly

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11
Q

Neurologic Defects:

  • failure of left and right hemispheres to separate
  • usually occurs during weeks 5–6
  • may be related to mutations in sonic hedgehog signaling pathway
  • moderate form has cleft lip/palate, most severe form results in cyclopia
  • seen in trisomy 13 and fetal alcohol syndrome
  • MRI reveals monoventricle and fusion of basal ganglia
A

Holoprosencephaly

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12
Q

Posterior Fossa Malformations:

  • ectopia of cerebellar tonsils (1 structure)
  • congenital
  • usually asymptomatic in childhood
  • manifests in adulthood with headaches and cerebellar symptoms
  • associated with spinal cavitations (eg. syringomyelia)
A

Chiari I Malformation

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13
Q

Posterior Fossa Malformations:

  • herniation of low-lying cerebellar vermis and tonsils (2 structures) through foramen magnum with aqueductal stenosis → hydrocephalus
  • usually associated with lumbosacral meningomyelocele (may present as paralysis/sensory loss at and below the level of the lesion)
A

Chiari II malformation

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14
Q

Posterior Fossa Malformations:

  • agenesis of cerebellar vermis leads to cystic enlargement of 4th ventricle that fills the enlarged posterior fossa
  • associated with noncommunicating hydrocephalus, spina bifida
A

Dandy-Walker Syndrome

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15
Q

Neurologic Defects:

  • cystic cavity (syrinx) within central canal of spinal cord
  • fibers crossing in anterior white commissure (spinothalamic tract) are typically damaged first
  • results in a “cape-like,” bilateral symmetrical loss of pain and temperature sensation in upper extremities (fine touch sensation is preserved)
  • associated with Chiari malformations and other congenital malformations
  • acquired causes include trauma and tumors
  • most common at C8–T1
A

Syringomyelia

syrinx = tube, as in syringe

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16
Q

Tongue Development

A
  • 1st and 2nd branchial arches form anterior 2/3 (thus sensation via CN V3, taste via CN VII).
  • 3rd and 4th branchial arches form posterior 1/3 (thus sensation and taste mainly via CN IX, extreme posterior via CN X).
  • Motor innervation is via CN XII to hyoglossus (retracts and depresses tongue), genioglossus (protrudes tongue, “the genie sticks out his tongue”), and styloglossus (draws sides of tongue upward to create a trough for swallowing).
  • Motor innervation is via CN X to palatoglossus (elevates posterior tongue during swallowing).
  • Taste—CN VII, IX, X (solitary nucleus)
  • Pain—CN V3, IX, X
  • Motor—CN X, XII
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17
Q

Neuroanatomy:

  • signal-transmitting cells of the nervous system
  • permanent cells—do not divide in adulthood
  • signal-relaying cells with dendrites (receive input), cell bodies, and axons (send output)
  • cell bodies and dendrites can be seen on Nissl staining (stains RER)
  • RER is not present in the axon
  • injury to axon → Wallerian degeneration—degeneration of axon distal to site of injury and axonal retraction proximally; allows for potential regeneration of axon (if in PNS)
  • macrophages remove debris and myelin
A

Neurons

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18
Q

Neuroanatomy:

  • most common glial cell type in CNS
  • physical support, repair, extracellular K+ buffer, removal of excess neurotransmitter, component of blood-brain barrier, glycogen fuel reserve buffer
  • reactive gliosis in response to neural injury
  • derived from neuroectoderm
  • GFAP—marker
A

Astrocytes

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19
Q

Neuroanatomy:

  • phagocytic scavenger cells of CNS (mesodermal, mononuclear origin)
  • activated in response to tissue damage
  • not readily discernible by Nissl stain
  • HIV-infected cells fuse to form multinucleated giant cells in CNS
A

Microglia

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20
Q

Neuroanatomy:

  • glial cells with a ciliated simple columnar form that line the ventricles and central canal of spinal cord
  • apical surfaces are covered in cilia (which circulate CSF) and microvilli (which help in CSF absorption)
A

Ependymal Cells

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21
Q

Neuroanatomy:

  • ↑ conduction velocity of signals transmitted down axons → saltatory conduction of action potential at the nodes of Ranvier, where there are high concentrations of Na+ channels
  • synthesized by oligodendrocytes in CNS (including CN I and II) and Schwann cells in PNS (including CN III-XII)
  • wraps and insulates axons: ↑ space constant and ↑ conduction velocity
A

Myelin

COPS:

  • CNS = Oligodendrocytes
  • PNS = Schwann cells
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22
Q

Neuroanatomy:

  • myelinates only 1 PNS axon
  • also promote axonal regeneration
  • derived from neural crest
  • injured in Guillain-Barré syndrome
A

Schwann Cells

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23
Q

Neuroanatomy:

  • myelinates axons of neurons in CNS
  • can myelinate many axons (∼ 30)
  • predominant type of glial cell in white matter
  • derived from neuroectoderm
  • “fried egg” appearance histologically
  • injured in multiple sclerosis, progressive multifocal leukoencephalopathy (PML), and leukodystrophies
A

Oligodendrocytes

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24
Q

Sensory Receptors:

  • C—slow, unmyelinated fibers
  • Aδ—fAst, myelinated fibers
  • all skin, epidermis, some viscera
  • pain, temperature
A

Free Nerve Endings

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25
Q

Sensory Receptors:

  • large, myelinated fibers
  • adapt quickly
  • glabrous (hairless) skin
  • dynamic, fine/light touch, position sense
A

Meissner Corpuscles

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26
Q

Sensory Receptors:

  • large, myelinated fibers
  • adapt quickly
  • deep skin layers, ligaments, joints
  • vibration, pressure
A

Pacinian Corpuscles

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27
Q

Sensory Receptors:

  • large, myelinated fibers
  • adapt slowly
  • finger tips, superficial skin
  • pressure, deep static touch (eg. shapes, edges), position sense
A

Merkel Discs

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28
Q

Sensory Receptors:

  • dendritic endings with capsule
  • adapt slowly
  • finger tips, joints
  • pressure, slippage of objects along surface of skin, joint angle change
A

Ruffini Corpuscles

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29
Q

Peripheral Nerve

A
  • Endoneurium
    • invests single nerve fiber layers (inflammatory infiltrate in Guillain-Barré syndrome)
  • Perineurium
    • blood-nerve permeability barrier
    • surrounds a fascicle of nerve fibers
    • must be rejoined in microsurgery for limb reattachment
  • Epineurium
    • dense connective tissue that surrounds entire nerve (fascicles and blood vessels)
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30
Q

Neuropathology:

  • reaction of neuronal cell body to axonal injury
  • changes reflect ↑ protein synthesis in effort to repair the damaged axon
  • characterized by:
    • round cellular swelling
    • displacement of the nucleus to the periphery
    • dispersion of Nissl substance throughout cytoplasm
  • concurrent with Wallerian degeneration
A

Chromatolysis

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31
Q

Neurotransmitter Changes with Disease

A
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32
Q

Meninges

A
  • Three membranes that surround and protect the brain and spinal cord:
    • Dura Mater
      • thick outer layer closest to skull
      • derived from mesoderm
    • Arachnoid Mater
      • middle layer
      • contains web-like connections
      • derived from neural crest
    • Pia Mater
      • thin, fibrous inner layer that firmly adheres to brain and spinal cord
      • derived from neural crest
  • CSF flows in the subarachnoid space, located between arachnoid and pia mater
  • Epidural Space—a potential space between the dura mater and skull containing fat and blood vessels
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33
Q

Blood-Brain Barrier

A
  • Prevents circulating blood substances (eg. bacteria, drugs) from reaching the CSF/CNS.
  • Formed by 3 structures:
    • Tight Junctions between nonfenestrated capillary endothelial cells
    • Basement Membrane
    • Astrocyte Foot Processes
  • Glucose and amino acids cross slowly by carrier-mediated transport mechanisms.
  • Nonpolar/lipid-soluble substances cross rapidly via diffusion.
  • A few specialized brain regions with fenestrated capillaries and no blood-brain barrier allow molecules in blood to affect brain function (eg. area postrema—vomiting after chemo; OVLT [organum vasculosum lamina terminalis]—osmotic sensing) or neurosecretory products to enter circulation (eg. neurohypophysis—ADH release).
  • Infarction and/or neoplasm destroys endothelial cell tight junctions → vasogenic edema.
  • Other notable barriers include:
    • Blood-Testis Barrier
    • Maternal-Fetal Bood Barrier of Placenta
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34
Q

Neuroanatomy:

  • Maintains homeostasis by:
    • regulating yhirst and water balance
    • controlling Adenohypophysis (anterior pituitary) and Neurohypophysis (posterior pituitary) release of hormones produced in the hypothalamus
    • regulating hunger, Autonomic nervous system, temperature, and sexual urges
  • areas not protected by blood-brain barrier:
    • OVLT (senses change in osmolarity)
    • Area Postrema (found in medulla, responds to emetics)
A

Hypothalamus

TAN HATS:

  • Thirst and water balance
  • Adenohypophysis
  • Neurohypophysis
  • Hunger
  • Autonomic nervous system
  • Temperature
  • Sexual urges
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35
Q

Hypothalamus:

  • hunger
  • destruction → anorexia, failure to thrive (infants)
  • stimulated by Ghrelin
  • inhibited by Leptin
A

Lateral Nucleus

Lateral injury makes you Lean.

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36
Q

Hypothalamus:

  • satiety
  • destruction (eg. craniopharyngioma) → hyperphagia
  • stimulated by Leptin
A

Ventromedial Nucleus

VentroMedial injury makes you Very Massive.

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37
Q

Hypothalamus:

  • cooling
  • parasympathetic
A

Anterior Nucleus

A/C = Anterior Cooling

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38
Q

Hypothalamus:

  • heating
  • sympathetic
A

Posterior Nucleus

  • Heating controlled by Posterior hypothalamus (“Hot Pot”).
  • If you zap your posterior hypothalamus, you become a poikilotherm (cold-blooded, like a snake).
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39
Q

Hypothalamus:

circadian rhythm

A

Suprachiasmatic Nucleus

You need sleep to be charismatic (chiasmatic).

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40
Q

Hypothalamus:

  • synthesize ADH and Oxytocin
  • ADH and Oxytocin are carried by Neurophysins down axons to posterior pituitary, where these hormones are stored and released
A

Supraoptic and Paraventricular Nuclei

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41
Q

Hypothalamus:

  • thermoregulation, sexual behavior
  • releases GnRH
  • failure of GnRH-producing neurons to migrate from olfactory pit → Kallmann Syndrome
A

Preoptic Nucleus

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42
Q

Vomiting Center

A
  • Coordinated by Nucleus Tractus Solitarius (NTS) in the medulla, which receives information from the Chemoreceptor Trigger Zone (CTZ, located within area postrema in 4th ventricle), GI tract (via vagus nerve), vestibular system, and CNS.
  • CTZ and adjacent vomiting center nuclei receive input from 5 major receptors:
    • Muscarinic (M1)
    • Dopamine (D2)
    • Histamine (H1)
    • Serotonin (5-HT3)
    • Neurokinin (NK-1)
  • 5-HT3, D2, and NK-1 antagonists used to treat chemotherapy-induced vomiting.
  • M1 and H1 antagonists used to treat motion sickness and hyperemesis gravidarum.
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43
Q

Sleep Physiology

A
  • Sleep cycle is regulated by the circadian rhythm, which is driven by Suprachiasmatic Nucleus (SCN) of hypothalamus.
  • Circadian rhythm controls nocturnal release of ACTH, Prolactin, Melatonin, Norepinephrine: SCN → Norepinephrine release → Pineal Gland → Melatonin
  • SCN is regulated by environment (eg. light).
  • Two Stages:
    • Rapid-Eye Movement (REM)
    • Non-REM
  • Alcohol, benzodiazepines, and barbiturates are associated with ↓ REM sleep and delta wave sleep.
  • Norepinephrine also ↓ REM sleep.
  • Benzodiazepines are useful for night terrors and sleepwalking by ↓ N3 and REM sleep.
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44
Q

Sleep Physiology

A
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45
Q

Neuroanatomy:

major relay for all ascending sensory information except olfaction

A

Thalamus

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46
Q

Thalamus:

  • Input:
    • spinothalamic and dorsal columns/medial lemniscus
  • Senses:
    • vibration
    • pain
    • pressure
    • proprioception
    • light touch
    • temperature
  • Destination:
    • 1° Somatosensory Cortex
A

Ventral PosteroLateral Nucleus

  • Senses:
    • Vibration
    • Pain
    • Pressure
    • Proprioception
    • Light Touch
    • Temperature
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47
Q

Thalamus:

  • Input:
    • trigeminal and gustatory pathway
  • Senses:
    • face sensation
    • taste
  • Destination:
    • 1° Somatosensory Cortex
A

Ventral PosteroMedial Nucleus

Makeup goes on the face.

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48
Q

Thalamus:

  • Input:
    • CN II
    • optic chiasm
    • optic tract
  • Senses:
    • vision
  • Destination:
    • Calcarine Sulcus
A

​Lateral Geniculate Nucleus

Lateral = Light

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49
Q

Thalamus:

  • Input:
    • superior olive and inferior colliculus of tectum optic chiasm
  • Senses:
    • hearing
  • Destination:
    • Auditory Cortex of Temporal Lobe
A

Medial Geniculate Nucleus

Medial = Music

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50
Q

Thalamus:

  • Input:
    • basal ganglia
    • cerebellum
  • Senses:
    • motor
  • Destination:
    • Motor Cortex
A

Ventral Lateral Nucleus

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51
Q

Neuroanatomy:

  • collection of neural structures involved in emotion, long-term memory, olfaction, behavior modulation, and ANS function
  • Consists of:
    • Hippocampus
    • Amygdalae
    • Mammillary Bodies
    • Anterior Thalamic Nuclei
    • Cingulate Gyrus
    • Entorhinal Cortex
  • Responsible for:
    • feeding
    • fleeing
    • fighting
    • feeling
    • sex
A

Limbic System

5 F’s:

  • Feeding
  • Fleeing
  • Fighting
  • Feeling
  • Fucking
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52
Q

Dopaminergic Pathways:

  • ↓ activity → “negative” symptoms (eg. anergia, apathy, lack of spontaneity)
  • antipsychotic drugs have limited effect
A

Mesocortical

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53
Q

Dopaminergic Pathways:

  • ↑ activity → “positive” symptoms (eg. delusions, hallucinations)
  • 1° therapeutic target of antipsychotic drugs → ↓ positive symptoms (eg. in schizophrenia)
A

Mesolimbic

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54
Q

Dopaminergic Pathways:

  • ↓ activity → extrapyramidal symptoms (eg. dystonia, akathisia, parkinsonism, tardive dyskinesia)
  • major dopaminergic pathway in brain
  • significantly affected by movement disorders and antipsychotic drugs
A

Nigrostriatal

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55
Q

Dopaminergic Pathways:

↓ activity → ↑ prolactin → ↓ libido, sexual
dysfunction, galactorrhea, gynecomastia (in
men).

A

Tuberoinfundibular

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56
Q

Cerebellum Input

A
  • Contralateral Cortex via Middle Cerebellar Peduncle
  • ipsilateral proprioceptive information via Inferior Cerebellar Peduncle from spinal cord
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57
Q

Cerebellum Output:

A
  • Purkinje Cells (always inhibitory) → Deep Nuclei of Cerebellum → Contralateral Cortex via Superior Cerebellar Peduncle
  • Deep Nuclei (lateral → medial)
    • Dentate
    • Emboliform
    • Globose
    • Fastigial

Don’t Eat Greasy Foods.

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58
Q

Neuroanatomy:

  • important in voluntary movements and making postural adjustments
  • receives cortical input, provides negative feedback to cortex to modulate movement
A

Basal Ganglia

  • *D1-R**eceptor = D1Rect Pathway
  • *I**ndirect (D2) = Inhibitory
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59
Q

Basal Ganglia:

Putamen (motor) + Caudate (cognitive)

A

Striatum

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60
Q

Basal Ganglia:

Putamen + Globus Pallidus

A

Lentiform

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61
Q

Cerebral Cortex Regions

A
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62
Q

Homunculus

A
  • Topographic representation of motor (shown) and sensory areas in the cerebral cortex.
  • Distorted appearance is due to certain body regions being more richly innervated and thus having ↑ cortical representation.
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63
Q

Cerebral Perfusion

A
  • Brain perfusion relies on tight autoregulation.
  • Cerebral perfusion is primarily driven by
  • Pco2 (Po2 also modulates perfusion in severe
  • hypoxia).
  • Cerebral perfusion relies on a pressure gradient between mean arterial pressure (MAP) and ICP.
  • ↓ blood pressure or ↑ ICP → ↓ cerebral perfusion pressure (CPP)
  • therapeutic hyperventilation → ↓ Pco2 → vasoconstriction → ↓ cerebral blood flow → ↓ intracranial pressure (ICP)
  • May be used to treat acute cerebral edema (eg. 2° to stroke) unresponsive to other interventions.
  • CPP = MAP – ICP
  • If CPP = 0, there is no cerebral perfusion → brain death.
  • Hypoxemia increases CPP only if Po2 < 50 mm Hg.
  • CPP is directly proportional to Pco2 until Pco2 > 90 mm Hg.
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64
Q

Cerebral Arteries—Cortical Distribution

A
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65
Q

Watershed Zones

A
  • Between anterior cerebral/middle cerebral, posterior cerebral/middle cerebral arteries (cortical border zones); or may also occur between the superficial and deep vascular territories of the middle cerebral artery (internal border zones).
  • Damage by severe hypotension → proximal upper and lower extremity weakness (if internal border zone stroke), higher order visual dysfunction (if posterior cerebral/middle cerebral cortical border zone stroke).
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66
Q

Circle of Willis

A

System of anastomoses between anterior and posterior blood supplies to brain.

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67
Q

Neuropathology:

  • presents with signs/symptoms of ↑ ICP (eg. headache, seizures, focal neurologic deficits)
  • may lead to venous hemorrhage
  • associated with hypercoagulable states (eg. pregnancy, OCP use, factor V Leiden)
A

Venous Sinus Thrombosis

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68
Q

Ventricular System

A
  • Lateral Ventricles → 3rd Ventricle via right and left Interventricular Foramina of Monro
  • 3rd ventricle → 4th ventricle via Cerebral Aqueduct of Sylvius
  • 4th ventricle → subarachnoid space via:
    • Foramina of Luschka = Lateral
    • Foramen of Magendie = Medial
  • CSF made by ependymal cells of choroid plexus.
  • Travels to subarachnoid space via foramina of Luschka and Magendie, is reabsorbed by arachnoid granulations, and then drains into dural venous sinuses.
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69
Q

Brain Stem—Ventral View

A
  • 4 CN are above pons (I, II, III, IV)
  • 4 CN exit the pons (V, VI, VII, VIII)
  • 4 CN are in medulla (IX, X, XI, XII)
  • 4 CN nuclei are medial (III, IV, VI, XII)
    • “Factors of 12, except 1 and 2.”
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70
Q

Brain Stem—Dorsal View

(cerebellum removed)

A
  • Pineal Gland
    • melatonin secretion, circadian rhythms
  • Superior Colliculi
    • direct eye movements to stimuli (noise/movements) or objects of interest
  • Inferior Colliculi
    • auditory
  • Your eyes are above your ears, and the superior colliculus (visual) is above the inferior colliculus (auditory).
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71
Q

Cranial Nerve Nuclei

A
  • Located in tegmentum portion of brain stem (between dorsal and ventral portions):
    • Midbrain—nuclei of CN III, IV
    • Pons—nuclei of CN V, VI, VII, VIII
    • Medulla—nuclei of CN IX, X, XII
    • Spinal cord—nucleus of CN XI
  • Lateral Nuclei = sensory (aLar plate)
  • Medial Nuclei = Motor (basal plate)
  • Sulcus Limitans—separates the cranial nerve motor nuclei from the sensory nuclei
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72
Q

Cranial Nerve and Vessel Pathways

A
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73
Q

Cranial Nerves:

  • eye movement (SO)
  • motor
A

Trochlear IV

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74
Q

Cranial Nerves:

  • mastication
  • facial sensation (ophthalmic, maxillary, mandibular divisions)
  • somatosensation from anterior 2/3 of tongue
  • both sensory and motor
A

Trigeminal V

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75
Q

Cranial Nerves:

  • facial movement
  • taste from anterior 2/3 of tongue (chorda tympani)
  • lacrimation
  • salivation (submandibular and sublingual glands)
  • eyelid closing (orbicularis oculi)
  • auditory volume modulation (stapedius)
  • both sensory and motor
A

Facial VII

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76
Q

Cranial Nerves:

  • taste and sensation from posterior 1/3 of tongue
  • swallowing
  • salivation (parotid gland)
  • monitoring carotid body and sinus chemo- and baroreceptors
  • elevation of pharynx/larynx (stylopharyngeus)
  • both sensory and motor
A

Glossopharyngeal IX

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77
Q

Cranial Nerves:

  • taste from supraglottic region
  • swallowing
  • soft palate elevation
  • midline uvula
  • talking
  • cough reflex
  • parasympathetics to thoracoabdominal viscera
  • monitoring aortic arch chemo- and baroreceptors
  • both sensory and motor
A

Vagus X

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78
Q

Vagal Nuclei:

  • visceral sensory information (eg. taste, baroreceptors, gut distention)
  • CN VII, IX, X
A

Nucleus Solitarius

Solitarius = Sensory

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79
Q

Vagal Nuclei:

  • motor innervation of pharynx, larynx, and upper esophagus (eg, swallowing, palate elevation)
  • CN IX, X, XI (cranial portion)
A

Nucleus Ambiguus

AMbiguus = Motor

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80
Q

Vagal Nuclei:

  • sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI
  • CN X
A

Dorsal Motor Nucleus

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81
Q

Cranial Nerve Reflexes:

  • Afferent:
    • V1 ophthalmic (nasociliary branch)
  • Efferent:
    • bilateral VII (temporal branch: orbicularis oculi)
A

Corneal

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82
Q

Cranial Nerve Reflexes:

  • Afferent:
    • V1 (loss of reflex does not preclude emotional tears)
  • Efferent:
    • VII
A

Lacrimation

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83
Q

Cranial Nerve Reflexes:

  • Afferent:
    • V3 (sensory—muscle spindle from masseter)
  • Efferent:
    • V3 (motor—masseter)
A

Jaw Jerk

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84
Q

Cranial Nerve Reflexes:

  • Afferent:
    • II
  • Efferent:
    • III
A

Pupillary

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85
Q

Cranial Nerve Reflexes:

  • Afferent:
    • IX
  • Efferent:
    • X
A

Gag

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86
Q

Mastication Muscles

A
  • 3 muscles close the jaw:
    • Masseter
    • TeMporalis
    • Medial Pterygoid

M’s Munch

  • 1 muscle opens the jaw:
    • Lateral Pterygoid

Lateral Lowers (when speaking of pterygoids with respect to jaw motion)

  • All are innervated by trigeminal nerve (V3).
  • “It takes more muscle to keep your mouth shut.”
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87
Q

Spinal Nerves

A
  • There are 31 pairs of spinal nerves in total:
    • 8 cervical
    • 12 thoracic
    • 5 lumbar
    • 5 sacral
    • 1 coccygeal
  • Nerves C1–C7 exit above the corresponding vertebra. C8 spinal nerve exits below C7 and above T1.
  • All other nerves exit below (eg. C3 exits above the 3rd cervical vertebra; L2 exits below the 2nd lumbar vertebra).
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88
Q

Neuropathology:

  • nucleus pulposus (soft central disc) herniates through annulus fibrosus (outer ring)
  • usually occurs posterolaterally at L4–L5 or L5–S1
  • nerve usually affected is below the level of herniation (eg. L3–L4 disc spares L3 nerve and involves L4 nerve)
  • compression of S1 nerve root → absent ankle reflex
A

Vertebral Disc Herniation

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89
Q

Spinal Cord—Lower Extent

A
  • In adults, spinal cord ends at lower border of L1–L2 vertebrae.
  • Subarachnoid Space (which contains the CSF) extends to lower border of S2 vertebra.
  • Lumbar puncture is usually performed between L3–L4 or L4–L5 (level of cauda equina).
  • “To keep the cord alive, keep the spinal needle between L3 and L5.”
  • Goal of lumbar puncture is to obtain sample of CSF without damaging spinal cord.
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90
Q

Spinal Cord and Associated Tracts

A
  • Legs (Lumbosacral) are Lateral in Lateral corticospinal, spinothalamic tracts.
  • Dorsal columns are organized as you are, with hands at sides.
  • “Arms outside, legs inside.”
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91
Q

_____ tracts synapse and then cross.

A

Ascending

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92
Q

Clinical Reflexes

A

Reflexes count up in order (main nerve root in bold):

  • Achilles reflex = S1, S2 (“buckle my shoe”)
  • Patellar reflex = L3, L4 (“kick the door”)
  • Biceps and Brachioradialis reflexes = C5, C6 (“pick up sticks”)
  • Triceps reflex = C7, C8 (“lay them straight”)

Additional reflexes:

  • Cremasteric reflex = L1, L2 (“testicles move”)
  • Anal Wink reflex = S3, S4 (“winks galore”)
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93
Q

Primitive Reflexes

A
  • CNS reflexes that are present in a healthy infant, but are absent in a neurologically intact adult.
  • Normally disappear within 1st year of life.
  • These “primitive” reflexes are inhibited by a mature/developing frontal lobe.
  • They may reemerge in adults following frontal lobe lesions → loss of inhibition of these reflexes.
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94
Q

Primitive Reflexes:

  • “hang on for life”
  • abduct/extend arms when startled, and then draw together
A

Moro Reflex

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95
Q

Primitive Reflexes:

  • dorsiflexion of large toe and fanning of other toes with plantar stimulation
  • Babinski Sign—presence of this reflex in an adult, which may signify a UMN lesion
A

Plantar Reflex

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96
Q

Primitive Reflexes:

stroking along one side of the spine while newborn is in ventral suspension (face down) causes lateral flexion of lower body toward stimulated side

A

Galant Reflex

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97
Q

Landmark Dermatomes:

posterior half of skull

A

C2

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98
Q

Landmark Dermatomes:

  • high turtleneck shirt
  • diaphragm and gallbladder pain referred to the right shoulder via phrenic nerve
A

C3

C3, 4, 5 keeps the diaphragm alive.

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99
Q

Landmark Dermatomes:

low-collar shirt

A

C4

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100
Q

Landmark Dermatomes:

includes thumbs

A

C6

Thumbs up sign on left hand looks like a 6.

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101
Q

Landmark Dermatomes:

at the nipple

A

T4

T4 at the teat pore.

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102
Q

Landmark Dermatomes:

at the xiphoid process

A

T7

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103
Q

Landmark Dermatomes:

  • at the umbilicus
  • important point of referred pain in early appendicitis
A

T10

belly butten

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104
Q

Landmark Dermatomes:

at the inguinal ligament

A

L1

Inguinal Ligament

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105
Q

Landmark Dermatomes:

includes the kneecaps

A

L4

down on ALL 4’s

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106
Q

Landmark Dermatomes:

sensation of penile and anal zones

A

S2, S3, S4

S2, 3, 4 keep the penis off the floor

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107
Q

Common Brain Lesions:

  • disinhibition and deficits in concentration, orientation, and judgment
  • may have reemergence of primitive reflexes
A

Frontal Lobe

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108
Q

Common Brain Lesions:

  • eyes look toward (destructive) side of lesion
  • in seizures (irritative), eyes look away from side of the lesion
A

Frontal Eye Fields

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109
Q

Common Brain Lesions:

  • eyes look away from side of lesion
  • ipsilateral gaze palsy (inability to look toward side of lesion)
A

Paramedian Pontine Reticular Formation

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110
Q

Common Brain Lesions:

  • internuclear ophthalmoplegia (impaired adduction of ipsilateral eye; nystagmus of contralateral eye with abduction)
  • Multiple Sclerosis
A

Medial Longitudinal Fasciculus

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111
Q

Common Brain Lesions:

  • agraphia, acalculia, finger agnosia, left-right disorientation
  • Gerstmann Syndrome
A

Dominant Parietal Cortex

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112
Q

Common Brain Lesions:

  • agnosia of the contralateral side of the world
  • Hemispatial Neglect Syndrome
A

Nondominant Parietal Cortex

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113
Q

Common Brain Lesions:

Anterograde Amnesia—inability to make new memories

A

Hippocampus (bilateral)

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114
Q

Common Brain Lesions:

  • may result in tremor at rest, chorea, and athetosis
  • Parkinson Disease
  • Huntington Disease
A

Basal Ganglia

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115
Q

Common Brain Lesions:

contralateral hemiballismus

A

Subthalamic Nucleus

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116
Q

Common Brain Lesions:

Wernicke-Korsakoff Syndrome

  • confusion
  • ataxia
  • nystagmus
  • ophthalmoplegia
  • memory loss (anterograde and retrograde amnesia)
  • confabulation
  • personality changes
A

Mammillary Bodies (bilateral)

Wernicke problems come in a CAN O’ beer.

  • Confusion
  • Ataxia
  • Nystagmus
  • Ophthalmoplegia
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117
Q

Common Brain Lesions:

  • Klüver-Bucy Syndrome
    • disinhibited behavior
      • hyperphagia
      • hypersexuality
      • hyperorality
  • HSV-1 Encephalitis
A

Amygdala (bilateral)

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118
Q

Common Brain Lesions:

  • Parinaud Syndrome
    • vertical gaze palsy
    • pupillary light-near dissociation
    • lid retraction
    • convergence-retraction nystagmus
  • stroke, hydrocephalus, pinealoma
A

Dorsal Midbrain

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119
Q

Common Brain Lesions:

reduced levels of arousal and wakefulness (eg. coma)

A

Reticular Activating System (midbrain)

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120
Q

Common Brain Lesions:

  • intention tremor, limb ataxia, loss of balance
  • ipsilateral deficits
  • fall toward side of lesion
A

Cerebellar Hemisphere

Cerebellar hemispheres are laterally located—affect lateral limbs.

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121
Q

Common Brain Lesions:

  • Decorticate (flexor) Posturing
    • lesion above
    • presents with flexion of upper extremities and extension of lower extremities
  • Decerebrate (extensor) Posturing
    • lesion at or below
    • presents with extension of upper and lower extremities
    • worse prognosis
A

Red Nucleus

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122
Q

Common Brain Lesions:

  • truncal ataxia (wide-based, “drunken sailor” gait), dysarthria
  • degeneration associated with chronic alcohol use
A

Cerebellar Vermis

Vermis is centrally located—affects central body.

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123
Q

Ischemic Brain Disease/Stroke

A
  • Irreversible damage begins after 5 minutes of hypoxia.
  • Most vulnerable: hippocampus, neocortex, cerebellum (Purkinje cells), watershed areas. Irreversible neuronal injury.
  • Hippocampus is most vulnerable to ischemic hypoxia (“vulnerable hippos”).
  • Stroke Imaging:
    • CT Scan
      • Noncontrast CT to exclude hemorrhage (before tPA can be given)
      • CT detects ischemic changes in 6–24 hr
    • MRI
      • Diffusion-Weighted MRI can detect ischemia within 3–30 min
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124
Q

Histologic Features of Stroke:

12-24 hours

A

eosinophilic cytoplasm + pyknotic nuclei (red neurons)

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125
Q

Histologic Features of Stroke:

24-72 hours

A

necrosis + neutrophils

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126
Q

Histologic Features of Stroke:

3-5 days

A

macrophages (microglia)

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127
Q

Histologic Features of Stroke:

1-2 weeks

A

reactive gliosis (astrocytes + vascular proliferation

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128
Q

Histologic Features of Stroke:

> 2 weeks

A

glial scar

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129
Q

Neuropathology:

acute blockage of vessels → disruption of blood flow and subsequent ischemia → liquefactive necrosis

A

Ischemic Stroke

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130
Q

Ischemic Stroke:

  • due to hypoperfusion or hypoxemia
  • common during cardiovascular surgeries
  • tends to affect watershed areas
A

Hypoxic

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131
Q

Ischemic Stroke:

Treatment

A
  • tPA (if within 3–4.5 hr of onset and no hemorrhage/risk of hemorrhage).
  • Reduce risk with medical therapy (eg. Aspirin, Clopidogrel); optimum control of blood pressure, blood sugars, lipids; and treat conditions that ↑ risk (eg. atrial fibrillation, carotid artery stenosis).
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132
Q

Neuropathology:

  • brief, reversible episode of focal neurologic dysfunction without acute infarction (⊝ MRI), with the majority resolving in < 15 minutes
  • deficits due to focal ischemia
A

Transient Ischemic Attack

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133
Q

Neuropathology:

  • bleeding into ventricles
  • increased risk in premature and low-birth-weight infants
  • originates in germinal matrix, a highly vascularized layer within the subventricular zone
  • due to reduced glial fiber support and impaired autoregulation of BP in premature infants
  • can present with altered level of consciousness, bulging fontanelle, hypotension, seizures, and coma
A

Neonatal Intraventricular Hemorrhage

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134
Q

Intracranial Hemorrhage:

  • rupture of middle meningeal artery (branch of maxillary artery), often 2° to skull fracture (circle in A) involving the pterion (thinnest area of the lateral skull)
  • lucid interval
  • scalp hematoma (arrows in A) and rapid intracranial expansion (arrows in B) under systemic arterial pressure → transtentorial herniation, CN III palsy
  • CT shows biconvex (lentiform), hyperdense blood collection (B) not crossing suture lines
A

Epidural Hematoma

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135
Q

Intracranial Hemorrhage:

  • rupture of bridging veins
  • can be acute (traumatic, high-energy impact → hyperdense on CT) or chronic (associated with mild trauma, cerebral atrophy, elderly, alcoholism → hypodense on CT)
  • also seen in shaken babies
  • Predisposing Factors:
    • brain atrophy
    • trauma
  • crescent-shaped hemorrhage (red arrows in C and D) that crosses suture lines
  • can cause midline shift (yellow arrow in C)
  • findings of “acute on chronic” hemorrhage (blue arrows in D)
A

Subdural Hematoma

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136
Q

Intracranial Hemorrhage:

  • bleeding (E, F) due to trauma, or rupture of an aneurysm (such as a saccular aneurysm E) or arteriovenous malformation
  • rapid time course
  • patients complain of “worst headache of my life”
  • bloody or yellow (xanthochromic) spinal tap
  • vasospasm can occur due to blood breakdown or rebleed 3–10 days after hemorrhage → ischemic infarct
  • Nimodipine is used to prevent/reduce vasospasm
  • ↑ risk of developing communicating and/or obstructive hydrocephalus
A

Subarachnoid Hemorrhage

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137
Q

Intracranial Hemorrhage:

  • most commonly caused by systemic hypertension
  • also seen with amyloid angiopathy (recurrent lobar hemorrhagic stroke in elderly), vasculitis, and neoplasm
  • may be 2º to reperfusion injury in ischemic stroke
  • hypertensive hemorrhages (Charcot-Bouchard microaneurysm) most often occur in the putamen of the basal ganglia (lenticulostriate vessels G), followed by thalamus, pons, and cerebellum (H)
A

Intraparenchymal Hemorrhage

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138
Q

Effects of Strokes:

Anterior Circulation

A
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139
Q

Effects of Strokes:

Posterior Circulation

A
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140
Q

Neuropathology:

  • neuropathic pain due to thalamic lesions
  • initial paresthesias followed in weeks to months by allodynia (ordinarily painless stimuli cause pain) and dysesthesia on the contralateral side
  • occurs in 10% of stroke patients
A

Central Post-Stroke Pain Syndrome

141
Q

Neuropathology:

  • caused by traumatic shearing forces during rapid acceleration and/or deceleration of the brain (eg. motor vehicle accident)
  • usually results in devastating neurologic injury, often causing coma or persistent vegetative state
A

Diffuse Axonal Injury

142
Q

Aphasia:

  • repetition impaired
  • nonfluent speech
  • intact comprehension
  • patient appears frustrated
  • insight intact
A

Broca (Expressive)

  • Broca Area in inferior frontal gyrus of frontal lobe

Broca = Broken

143
Q

Aphasia:

  • repetition impaired
  • fluent speech
  • impaired comprehension
  • patients do not have insight
A

Wernicke (Receptive)

  • Wernicke Area in superior temporal gyrus of tempora lobe

Wernicke = Wordy

144
Q

Aphasia:

  • repetition impaired
  • fluent speech
  • intact comprehension
  • can be caused by damage to arcuate fasciculus
A

Conduction (Associative)

arCuate fasciculus

145
Q

Aphasia:

  • repetition impaired
  • nonfluent speech
  • impaired comprehension
  • Arcuate Fasciculus, Broca and Wernicke areas affected
A

Global

146
Q

Aphasia:

  • repetition intact
  • nonfluent speech
  • intact comprehension
  • affects frontal lobe around Broca area, but Broca area is spared
A

Transcortical Motor

147
Q

Aphasia:

  • repetition intact
  • fluent speech
  • impaired comprehension
  • affects temporal lobe around Wernicke area, but Wernicke area is spared
A

Transcortical Sensory

148
Q

Aphasia:

  • repetition intact
  • nonfluent speech
  • impaired comprehension
  • Broca and Wernicke areas and arcuate fasciculus remain intact
  • surrounding watershed areas affected
A

Transcortical, Mixed

149
Q

Aneurysms:

  • also known as berry aneurysm
  • occurs at bifurcations in the Circle of Willis
  • most common site is the junction of ACom and ACA
  • associated with ADPKD and Ehlers-Danlos syndrome
  • Risk Factors:
    • advanced age
    • hypertension
    • smoking
    • race (↑ risk in African-Americans)
  • usually clinically silent until rupture (most common complication) → subarachnoid hemorrhage
  • (“worst headache of my life” or “thunderclap headache”) → focal neurologic deficits. Can also
  • cause symptoms via direct compression of surrounding structures by growing aneurysm.
A

Saccular Aneurysm

150
Q

Saccular Aneurysms:

  • compression → bitemporal hemianopia (compression of optic chiasm)
  • visual acuity deficits
  • rupture → ischemia in ACA distribution → contralateral lower extremity hemiparesis, sensory deficits
A

ACom

151
Q

Saccular Aneurysms:

rupture → ischemia in MCA distribution → contralateral upper extremity and lower facial hemiparesis, sensory deficits

A

MCA

152
Q

Saccular Aneurysms:

  • compression → ipsilateral CN III palsy → mydriasis (“blown pupil”)
  • may also see ptosis, “down and out” eye
A

PCom

153
Q

Aneurysms:

  • common
  • associated with chronic hypertension
  • affects small vessels (eg. lenticulostriate arteries in basal ganglia, thalamus) and can cause lacunar strokes
  • not visible on angiography
A

Charcot-Bouchard Microaneurysm

154
Q

Seizures:

  • affect single area of the brain
  • most commonly originate in medial temporal lobe
A

Partial (Focal) Seizures

155
Q

Seizures:

  • partial
  • consciousness intact
  • motor, sensory, autonomic, psychic
A

Simple Partial

156
Q

Seizures:

  • partial
  • impaired consciousness
  • automatisms
A

Complex Partial

157
Q

Seizures:

diffuse

A

Generalized Seizures

158
Q

Seizures:

  • diffuse
  • 3 Hz spike-and-wave discharges
  • no postictal confusion
  • blank stare
A

Absence (petit mal)

159
Q

Seizures:

  • diffuse
  • quick, repetitive jerks
A

Myoclonic

160
Q

Seizures:

  • diffuse
  • stiffening
A

Tonic

161
Q

Seizures:

  • diffuse
  • “drop” seizures (falls to floor)
  • commonly mistaken for fainting
A

Atonic

162
Q

Seizures:

continuous (≥ 5 min) or recurring seizures that may result in brain injury

A

Status epEilepticus

163
Q

Neuropathology:

  • pain due to irritation of structures such as the dura, cranial nerves, or extracranial structures
  • more common in females, except cluster
A

Headaches

164
Q

Headaches:

  • unilateral
  • 15 min–3 hr
  • repetitive
  • excruciating periorbital pain (“suicide headache”) with lacrimation and rhinorrhea
  • may present with Horner syndrome
  • more common in males
A

Cluster

165
Q

Headaches:

  • bilateral
  • > 30 min (typically 4–6 hr)
  • constant
  • steady, “band-like” pain
  • no photophobia or phonophobia
  • no aura
A

Tension

166
Q

Headaches:

  • unilateral
  • 4–72 hr
  • pulsating pain with nausea, photophobia, or phonophobia
  • may have “aura”
  • due to irritation of CN V, meninges, or blood vessels (release of substance P, calcitonin gene-related peptide, vasoactive peptides)
A

Migraine

POUND:

  • Pulsatile
  • One-day duration
  • Unilateral
  • Nausea
  • Disabling
167
Q

Headache Treatment:

Cluster

A
  • Acute:
    • Sumatriptan
    • 100% O2
  • Prophylaxis:
    • Verapamil
168
Q

Headache Treatment:

Tension

A
  • Analgesics
  • NSAIDs
  • Acetaminophen
  • Amitriptyline for chronic pain
169
Q

Headache Treatment:

Migraine

A
  • Acute:
    • NSAIDs
    • Triptans
    • Dihydroergotamine
  • Prophylaxis:
    • lifestyle changes (eg. sleep, exercise, diet)
    • β-Blockers
    • Amitriptyline
    • Topiramate
    • Valproate
170
Q

Causes of Headache

A
  • Subarachnoid Hemorrhage
    • “worst headache of my life”
  • Meningitis
  • Hydrocephalus
  • Neoplasia
  • Giant Cell (Temporal) Arteritis
171
Q

Neuropathology:

  • produces repetitive, unilateral, shooting pain in the distribution of CN V
  • triggered by chewing, talking, touching certain parts of the face
  • lasts (typically) for seconds to minutes, but episodes often increase in intensity and frequency over time
  • Treatment: Carbamazepine
A

Trigeminal Neuralgia

172
Q

Movement Disorders:

  • restlessness and intense urge to move
  • can be seen with neuroleptic use or as a side-effect of Parkinson treatment
A

Akathisia

173
Q

Movement Disorders:

  • slow, snake-like, writhing movements
  • especially seen in the fingers
  • basal ganglia lesion
A

Athetosis

174
Q

Movement Disorders:

  • sudden, jerky, purposeless movements
  • basal ganglia lesion
  • seen in Huntington disease and in acute rheumatic fever
A

Chorea

175
Q

Movement Disorders:

  • high-frequency tremor with sustained posture (eg. outstretched arms)
  • worsened with movement or when anxious
  • often familial
  • patients often self-medicate with alcohol, which ↓ tremor amplitude.
  • Treatment:
    • Nonselective β-Blockers (eg. Propranolol)
    • Primidone
A

Essential Tremor

176
Q

Movement Disorders:

  • sudden, wild flailing of 1 arm +/− ipsilateral leg
  • contralateral subthalamic nucleus lesion (eg. lacunar stroke)
  • contralateral lesion
A

Hemiballismus

177
Q

Movement Disorders:

  • slow, zigzag motion when pointing/extending toward a target
  • cerebellar dysfunction
A

Intention Tremor

178
Q

Movement Disorders:

  • uncontrolled movement of distal appendages (most noticeable in hands)
  • tremor alleviated by intentional movement
  • substantia nigra lesion (Parkinson disease)
  • occurs at rest
  • “pill-rolling tremor” of Parkinson disease
A

Resting Tremor

179
Q

Movement Disorders:

  • worse at rest/nighttime
  • relieved by movement
  • associated with iron deficiency and CKD
  • Treatment:
    • Dopamine Agonists
      • Pramipexole
      • Ropinirole
A

Restless Legs Syndrome

180
Q

Neuropathology:

  • ↓ in cognitive ability, memory, or function with intact consciousness
  • must rule out depression as cause of dementia (known as pseudodementia)
A

Neurodegenerative Disorders

181
Q

Neurodegenerative Disorders:

  • pill-rolling tremor at rest
  • cogwheel rigidity
  • akinesia or bradykinesia
  • postural instability
  • shuffling gait
  • MPTP, a contaminant in illegal drugs, is metabolized to MPP+, which is toxic to substantia nigra
  • loss of dopaminergic neurons (ie. depigmentation) of substantia nigra pars compacta
  • Lewy Bodies:
    • composed of α-synuclein (intracellular eosinophilic inclusions)
A

Parkinson Disease

Parkinson TRAPS your body:

  • Tremor (pill-rolling tremor at rest)
  • Rigidity (cogwheel)
  • Akinesia (or bradykinesia)
  • Postural instability
  • Shuffling gait
182
Q

Neurodegenerative Disorders:

  • autosomal dominant trinucleotide (CAG)n repeat expansion in the huntingtin (HTT) gene on chromosome 4
  • symptoms manifest between ages 20 and 50:
    • chorea
    • athetosis
    • aggression
    • depression
    • dementia
  • sometimes initially mistaken for substance abuse)
  • anticipation results from expansion of CAG repeats
  • caudate loses ACh and GABA
  • atrophy of caudate and putamen with ex vacuo ventriculomegaly
  • ↑ dopamine, ↓ GABA, ↓ ACh in brain
  • neuronal death via NMDA-R binding and glutamate excitotoxicity
A

Huntington Disease

huntingtin = chromosome 4 (4 letters)

CAG repeats = Caudate loses ACh and GABA

183
Q

Neurodegenerative Disorders:

  • most common cause of dementia in elderly
  • Down syndrome patients have ↑ risk
  • APP is located on chromosome 21
  • ↓ ACh
  • associated with the following altered proteins:
    • ApoE-2: ↓ risk of sporadic form
    • ApoE-4: ↑ risk of sporadic form
    • APP, presenilin-1, presenilin-2: familial forms (10%) with earlier onset
  • widespread cortical atrophy, especially hippocampus
  • narrowing of gyri and widening of sulci
  • senile plaques in gray matter:
    • extracellular β-amyloid core
    • may cause amyloid angiopathy → intracranial hemorrhage
    • Aβ (amyloid-β) synthesized by cleaving amyloid precursor protein (APP)
  • Neurofibrillary Tangles
    • intracellular, hyperphosphorylated tau protein = insoluble cytoskeletal elements
    • number of tangles correlates with degree of dementia
A

Alzheimer Disease

184
Q

Neurodegenerative Disorders:

  • also known as Pick disease
  • early changes in personality and behavior (behavioral variant), or aphasia (primary progressive aphasia)
  • may have associated movement disorders (eg. parkinsonism)
  • frontotemporal lobe degeneration
  • inclusions of hyperphosphorylated tau (round Pick bodies) or ubiquitinated TDP-43
A

Frontotemporal Dementia

185
Q

Neurodegenerative Disorders:

  • visual hallucinations
  • dementia with fluctuating cognition/alertness, REM sleep behavior disorder, and parkinsonism
  • cognitive and motor symptom onset < 1 year apart, otherwise considered dementia 2° to Parkinson disease
  • intracellular Lewy bodies primarily in cortex
A

Lewy Body Dementia

“haLewycinations”

186
Q

Neurodegenerative Disorders:

  • result of multiple arterial infarcts and/or chronic ischemia
  • step-wise decline in cognitive ability with late-onset memory impairment
  • 2nd most common cause of dementia in elderly
  • MRI or CT shows multiple cortical and/or subcortical infarcts
A

Vascular Dementia

187
Q

Neurodegenerative Disorders:

  • rapidly progressive (weeks to months) dementia with myoclonus (“startle myoclonus”) and ataxia
  • commonly see periodic sharp waves on EEG and ↑ 14-3-3 protein in CSF
  • spongiform cortex
  • prions (PrPc → PrPsc sheet [β-pleated sheet resistant to proteases])
A

Creutzfeldt-Jakob Disease

188
Q

Neuropathology:

  • also known as pseudotumor cerebri
  • ↑ ICP with no apparent cause on imaging (eg. hydrocephalus, obstruction of CSF outflow)
  • risk factors include female gender, tetracyclines, besity, vitamin A excess, and Danazol
  • headache, tinnitus, diplopia (usually from CN VI palsy), no change in mental status
  • impaired optic nerve axoplasmic flow → papilledema
  • visual field testing shows enlarged blind spot and peripheral constriction
  • lumbar puncture reveals ↑ opening pressure and provides temporary headache relief
  • Treatment:
    • weight loss
    • Acetazolamide
    • invasive procedures for refractory cases (eg. CSF shunt placement, optic nerve sheath fenestration surgery for visual loss)
A

Idiopathic Intracranial Hypertension

Female TOAD:

  • Female
  • Tetracyclines
  • Obesity
  • Vitamin A excess
  • Danazol
189
Q

Hydrocephalus:

↓ CSF absorption by arachnoid granulations (eg. arachnoid scarring post-meningitis) → ↑ ICP, papilledema, herniation

A

Communicating Hydrocephalus

190
Q

Hydrocephalus:

  • communicating
  • affects the elderly
  • idiopathic
  • CSF pressure elevated only episodically
  • does not result in increased subarachnoid space volume
  • expansion of ventricles distorts the fibers of the corona radiata → triad of urinary incontinence, gait apraxia (magnetic gait), and cognitive dysfunction (sometimes reversible)
  • symptoms potentially reversible with CSF shunt placement
A

Normal Pressure Hydrocephalus

“Wet, wobbly, and wacky.”

  • urinary incontinence
  • gait apraxia (magnetic gait)
  • cognitive dysfunction
191
Q

Hydrocephalus:

caused by structural blockage of CSF circulation within ventricular system (eg. stenosis of aqueduct of Sylvius; colloid cyst blocking foramen of Monro; tumor)

A

Noncommunicating Hydrocephalus

192
Q

Hydrocephalus:

  • appearance of ↑ CSF on imaging, but is actually due to ↓ brain tissue and neuronal atrophy (eg. Alzheimer disease, advanced HIV, Pick disease, Huntington disease)
  • normal pressure hydrocephalus triad is not seen
A

Ex Vacuo Ventriculomegaly

193
Q

Neuropathology:

  • autoimmune inflammation and demyelination of CNS (brain and spinal cord) with subsequent axonal damage
  • Findings:
    • acute optic neuritis (painful unilateral visual loss associated with Marcus Gunn pupil)
    • brain stem/cerebellar syndromes (eg. diplopia, ataxia, scanning speech, intention tremor, nystagmus/INO (bilateral > unilateral)
    • pyramidal tract weakness
    • spinal cord syndromes (eg. electric shock-like sensation along spine on neck flexion [Lhermitte phenomenon], neurogenic bladder, paraparesis, sensory manifestations affecting the trunk or one or more extremity)
  • symptoms may exacerbate with increased body temperature (eg. hot bath, exercise)
  • relapsing and remitting is most common clinical course
  • most often affects women in their 20s and 30s
  • more common in Caucasians living farther from equator
A

Multiple Sclerosis

194
Q

Neuropathology:

  • ↑ IgG level and myelin basic protein in CSF
  • oligoclonal bands are diagnostic
  • MRI is the gold standard
  • periventricular plaques (areas of oligodendrocyte loss and reactive gliosis)
  • multiple white matter lesions disseminated in space and time
A

Multiple Sclerosis

195
Q

Multiple Sclerosis:

Treatment

A
  • Stop relapses and halt/slow progression with disease-modifying therapies (eg. β-interferon, glatiramer, natalizumab).
  • Treat acute flares with IV steroids.
  • Symptomatic treatment for neurogenic bladder (catheterization, muscarinic antagonists), spasticity (baclofen, GABAB receptor agonists), and pain (TCAs, anticonvulsants).
196
Q

Demyelinating and Dysmyelinating Disorders:

  • also known as Central Pontine Myelinolysis
  • massive axonal demyelination in pontine white matter 2° to rapid osmotic changes, most commonly iatrogenic correction of hyponatremia but also rapid shifts of other osmolytes (eg. glucose)
  • acute paralysis, dysarthria, dysphagia, diplopia, and loss of consciousness
  • can cause “locked-in syndrome”
A

Osmotic Demyelination Syndrome

Fast Serum Na+ Correction:

  • “from low to high, your pons will die” (Osmotic Demyelination Syndrome)
  • “From high to low, your brains will blow” (Cerebral Edema/Herniation)
197
Q

Demyelinating and Dysmyelinating Disorders:

  • most common subtype of Guillain-Barré syndrome
  • autoimmune condition associated with infections (eg. Campylobacter jejuni, viruses [eg. Zika]) that destroys Schwann cells by inflammation and demyelination of peripheral nerves (including cranial nerves III-XII) and motor fibers likely due to molecular mimicry, inoculations, and stress, but no definitive link to pathogens
  • results in symmetric ascending muscle weakness/paralysis and depressed/absent DTRs beginning in lower extremities
  • facial paralysis (usually bilateral) and respiratory failure are common
  • may see autonomic dysregulation (eg. cardiac irregularities, hypertension, hypotension) or sensory abnormalities
  • almost all patients survive
  • majority recover completely after weeks to months
  • ↑ CSF protein with normal cell count (albuminocytologic dissociation)
  • respiratory support is critical until recovery
  • Disease-Modifying Treatment:
    • plasmapheresis
    • IV immunoglobulins
    • no role for steroids
A

Acute Inflammatory Demyelinating Polyradiculopathy

198
Q

Demyelinating and Dysmyelinating Disorders:

  • multifocal inflammation and demyelination after infection or vaccination
  • presents with rapidly progressive multifocal neurologic symptoms and altered mental status
A

Acute Disseminated (Postinfectious) Encephalomyelitis

199
Q

Demyelinating and Dysmyelinating Disorders:

  • also known as Hereditary Motor and Sensory Neuropathy
  • group of progressive hereditary nerve disorders related to the defective production of proteins involved in the structure and function of peripheral nerves or the myelin sheath
  • typically autosomal dominant inheritance pattern and associated with foot deformities (eg. pes cavus, hammer toe), lower extremity weakness (eg. foot drop), and sensory deficits
  • most common type, CMT1A, is caused by PMP22 gene duplication
A

Charcot-Marie-Tooth Disease

200
Q

Demyelinating and Dysmyelinating Disorders:

  • demyelination of CNS due to destruction of oligodendrocytes (2° to reactivation of latent JC virus infection)
  • seen in 2–4% of patients with AIDS
  • rapidly progressive, usually fatal
  • predominantly involves parietal and occipital areas
  • visual symptoms are common
  • ↑ risk associated with Natalizumab and Rituximab
A

Progressive Multifocal Leukoencephalopathy

201
Q

Neurocutaneous Disorders:

  • also known as Encephalotrigeminal Angiomatosis
  • congenital, noninherited (sporadic), developmental anomaly of neural crest derivatives due to somatic mosaicism for an activating mutation in one copy of the GNAQ gene
  • affects small (capillary-sized) blood vessels → port-wine stain of the face (nevus flammeus, a non-neoplastic “birthmark” in CN V1/V2 distribution)
  • ipsilateral leptomeningeal angioma → seizures/epilepsy
  • intellectual disability
  • episcleral hemangioma → ↑ IOP → early-onset glaucoma
A

Sturge-Weber Syndrome

STURGE-Weber:

  • Sporadic
  • port-wine Stain
  • Tram track calcifications (opposing gyri)
  • Unilateral
  • Retardation (intellectual disability)
  • Glaucoma
  • GNAQ gene
  • Epilepsy
202
Q

Neurocutaneous Disorders:

  • TSC1 mutation on chromosome 9 or TSC2 mutation on chromosome 16
  • tumor suppressor genes
  • autosomal dominant, variable expression
  • hamartomas in CNS and skin
  • angiofibromas
  • mitral regurgitation
  • ash-leaf spots
  • cardiac rhabdomyoma
  • autosomal dominant
  • mental retardation (intellectual disability)
  • renal angiomyolipoma
  • seizures
  • Shagreen patches
  • ↑ incidence of subependymal giant cell astrocytomas and ungual fibromas
A

Tuberous Sclerosis

HAMARTOMAS:

  • Hamartomas in CNS and skin
  • Angiofibromas
  • Mitral regurgitation
  • Ash-leaf spots
  • cardiac Rhabdomyoma
  • Tuberous sclerosis
  • autosomal dOminant
  • Mental retardation
  • renal Angiomyolipoma
  • Seizures
  • Shagreen patches
203
Q

Neurocutaneous Disorders:

  • also known as von Recklinghausen disease
  • mutation in NF1 tumor suppressor gene on chromosome 17, which normally codes for neurofibromin, a negative regulator of RAS
  • autosomal dominant, 100% penetrance
  • café-au-lait spots ,cutaneous neurofibromas, optic gliomas, pheochromocytomas, Lisch nodules (pigmented iris hamartomas)
A

Neurofibromatosis Type I

Chromosome 17 = 17 letters in “von Recklinghausen”

204
Q

Neurocutaneous Disorders:

  • mutation in NF2 tumor suppressor gene on chromosome 22
  • autosomal dominant
  • Findings:
    • bilateral acoustic schwannomas
    • juvenile cataracts
    • meningiomas
    • ependymomas
A

Neurofibromatosis Type II

NF2 affects 2 ears, 2 eyes, and 2 parts of the brain.

205
Q

Neurocutaneous Disorders:

  • deletion of VHL gene on chromosome 3p
  • autosomal dominant
  • pVHL ubiquitinates hypoxia-inducible factor 1a
  • characterized by development of numerous tumors, both benign and malignant
  • hemangioblastomas (high vascularity with hyperchromatic nuclei) in retina, brain stem, cerebellum, and spine
  • angiomatosis (eg. cavernous hemangiomas in skin, mucosa, organs)
  • bilateral renal cell carcinomas
  • pheochromocytomas
A

von Hippel-Lindau Disease

Chromosome 3p = VHL has 3 letters

HARP:

  • Hemangioblastomas
  • Angiomatosis
  • bilateral Renal cell carcinomas
  • Pheochromocytomas
206
Q

Adult Primary Brain Tumors:

  • grade IV astrocytoma
  • common, highly malignant 1° brain tumor with ~ 1-year median survival
  • found in cerebral hemispheres
  • can cross corpus callosum (“butterfly glioma”)
  • astrocyte origin
  • GFAP ⊕
  • “pseudopalisading” pleomorphic tumor cells border central areas of necrosis, hemorrhage, and/or microvascular proliferation
A

Glioblastoma Multiforme

207
Q

Adult Primary Brain Tumors:

  • relatively rare
  • slow growing
  • most often in frontal lobes
  • “chicken-wire” capillary pattern
  • oligodendrocyte origin
  • “Fried Egg” Cells
    • round nuclei with clear cytoplasm
    • often calcified
A

Oligodendroglioma

208
Q

Adult Primary Brain Tumors:

  • common, typically benign
  • females > males
  • most often occurs near surfaces of brain and in parasagittal region
  • extra-axial (external to brain parenchyma) and may have a dural attachment (“tail”)
  • often asymptomatic
  • may present with seizures or focal neurologic signs
  • treated with resection and/or radiosurgery
  • arachnoid cell origin
  • spindle cells concentrically arranged in a whorled pattern
  • psammoma bodies (laminated calcifications)
A

Meningioma

209
Q

Adult Primary Brain Tumors:

  • most often cerebellar
  • associated with von Hippel-Lindau syndrome when found with retinal angiomas
  • can produce erythropoietin → 2° polycythemia
  • blood vessel origin
  • closely arranged, thin-walled capillaries with minimal intervening parenchyma
A

Hemangioblastoma

210
Q

Adult Primary Brain Tumors:

  • may be nonfunctioning (silent) or hyperfunctioning (hormone producing)
  • most commonly from lactotrophs (prolactinoma) → hyperprolactinemia
  • less commonly adenoma of somatotrophs (GH) → acromegaly/gigantism
  • corticotrophs (ACTH) → Cushing disease
  • rarely, adenoma of thyrotrophs (TSH) and gonadotroph (FSH, LH)
  • nonfunctional tumors present with mass effect (bitemporal hemianopia, hypopituitarism, headache)
  • bitemporal hemianopia due to pressure on optic chiasm
  • sequelae include hyper- or hypopituitarism, which may be caused by pituitary apoplexy
  • hyperplasia of only one type of endocrine cells found in pituitary (ie. lactotroph, gonadotroph, somatotroph, corticotroph)
  • prolactinoma in women classically presents as galactorrhea, amenorrhea, and ↓ bone density due to suppression of estrogen
  • prolactinoma in men classically presents as low libido and infertility
  • Treatment:
    • Dopamine Agonists (eg. Bromocriptine, Cabergoline)
    • transsphenoidal resection
A

Pituitary Adenoma

211
Q

Adult Primary Brain Tumors:

  • classically at the cerebellopontine angle involving both CNs VII and VIII, but can be along any peripheral nerve
  • often localized to CN VIII in internal acoustic meatus → vestibular _____
  • bilateral vestibular _____ found in NF-2
  • treated with resection or stereotactic radiosurgery
  • Schwann cell origin, S-100 ⊕
  • biphasic
  • dense, hypercellular areas containing spindle cells alternating with hypocellular, myxoid areas
A

Schwannoma

212
Q

Childhood Primary Brain Tumors:

  • low-grade astrocytoma
  • most common 1° brain tumor in childhood
  • usually well circumscribed
  • in children, most often found in posterior fossa (eg. cerebellum)
  • may be supratentorial
  • benign, good prognosis.
  • glial cell origin, GFAP ⊕
  • Rosenthal fibers—eosinophilic, corkscrew fibers
  • cystic + solid (gross)
A

Pilocytic Astrocytoma

213
Q

Childhood Primary Brain Tumors:

  • most common malignant brain tumor in childhood
  • commonly involves cerebellum
  • can compress 4th ventricle, causing noncommunicating hydrocephalus → headaches, papilledema
  • can send “drop metastases” to the spinal cord
  • form of primitive neuroectodermal tumor (PNET)
  • Homer-Wright rosettes, small blue cells
A

Medulloblastoma

214
Q

Childhood Primary Brain Tumors:

  • most commonly found in 4th ventricle
  • can cause hydrocephalus
  • poor prognosis
  • ependymal cell origin
  • characteristic perivascular pseudorosettes
  • rod-shaped blepharoplasts (basal ciliary bodies) found near the nucleus
A

Ependymoma

215
Q

Childhood Primary Brain Tumors:

  • most common childhood supratentorial tumor
  • may be confused with pituitary adenoma (both cause bitemporal hemianopia)
  • derived from remnants of Rathke pouch (ectoderm)
  • calcification is common
  • cholesterol crystals found in “motor oil”-like fluid within tumor
A

Craniopharyngioma

216
Q

Childhood Primary Brain Tumors:

  • tumor of the pineal gland
  • can cause Parinaud syndrome (compression of tectum → vertical gaze palsy)
  • obstructive hydrocephalus (compression of cerebral aqueduct)
  • precocious puberty in males (β-hCG production)
  • similar to germ cell tumors (eg. testicular seminoma)
A

Pinealoma

217
Q

Herniation Syndromes

A

① Cingulate (subfalcine)

  • herniation under falx cerebri
  • can compress anterior cerebral artery

② Transtentorial (central/downward)

  • caudal displacement of brain stem → rupture of paramedian basilar artery branches → Duret hemorrhages
  • usually fatal

③ Uncal

  • uncus = medial temporal lobe
  • compresses ipsilateral CN III and contralateral crus cerebri against Kernohan notch (causes contralateral CN III palsy and/or ipsilateral hemiparesis, ie. a false localizing sign)

④ Cerebellar Tonsillar

  • herniation into the foramen magnum
  • coma and death result when these herniations compress the brain stem
218
Q

Motor Neuron Signs:

  • Weakness +
  • Reflexes ↑
  • Tone ↑
  • Babinski +
  • Spastic Paresis +
  • Clasp Knife Spasticity +
A

Upper Motor Neuron

  • everything up (tone, DTRs, toes)
219
Q

Motor Neuron Signs:

  • Weakness +
  • Atrophy +
  • Fasciculations +
  • Reflexes ↓
  • Tone ↓
  • Flaccid Paralysis +
A

Lower Motor Neuron

  • everything lowered (less muscle mass, ↓ muscle tone, ↓ reflexes, downgoing toes)
220
Q

Spinal Cord Lesions:

  • congenital degeneration of anterior horns of spinal cord
  • LMN lesions only, symmetric weakness
  • “floppy baby” with marked hypotonia (flaccid paralysis) and tongue fasciculations
  • autosomal recessive inheritance of mutation in SMN1
  • type 1 is called Werdnig-Hoffmann disease
A

Spinal Muscular Atrophy

3 F’s:

  • “Floppy baby”
  • Flaccid paralysis
  • tongue Fasciculations
221
Q

Spinal Cord Lesions:

  • combined UMN (corticobulbar/corticospinal) and LMN (medullary and spinal cord) degeneration
  • no sensory or bowel/bladder deficits
  • can be caused by defect in Superoxide Dismutase 1
  • LMN deficits due to anterior horn cell involvement (eg. dysarthria, dysphagia, asymmetric limb weakness, fasciculations, atrophy) and UMN deficits (pseudobulbar palsy, eg. dysarthria, dysphagia, emotional lability, spastic gait, clonus)
  • fatal
  • commonly known as Lou Gehrig disease
  • Treatment: Riluzole
A

Amyotrophic Lateral Sclerosis

222
Q

Spinal Cord Lesions:

  • spares dorsal columns and Lissauer tract
  • midthoracic ASA territory is watershed area, as artery of Adamkiewicz supplies ASA below T8
  • can be caused by aortic aneurysm repair
  • presents with UMN deficit below the lesion (corticospinal tract), LMN deficit at the level of the lesion (anterior horn), and loss of pain and temperature sensation below the lesion (spinothalamic tract
A

Complete Occlusion of Anterior Spinal Artery

223
Q

Spinal Cord Lesions:

  • caused by 3° syphilis
  • results from degeneration (demyelination) of dorsal columns and roots → progressive sensory ataxia (impaired proprioception → poor coordination)
  • ⊕ Romberg sign and absent DTRs
  • associated with Charcot joints, shooting pain, and Argyll Robertson pupils
A

Tabes Dorsalis

224
Q

Spinal Cord Lesions:

  • syrinx expands and damages anterior white commissure of spinothalamic tract (2nd-order neurons) → bilateral symmetrical loss of pain and temperature sensation in cape-like distribution
  • seen with Chiari I malformation
  • can affect other tracts
A

Syringomyelia

225
Q

Spinal Cord Lesions:

  • Subacute Combined Degeneration (SCD)
  • demyelination of spinocerebellar tracts, lateral corticospinal tracts, and dorsal columns
  • ataxic gait, paresthesia, and impaired position/vibration sense
A

Vitamin B12 Deficiency

Subacute Combined Degeneration:

  • Spinocerebellar tracts
  • lateral Corticospinal tracts
  • Dorsal columns
226
Q

Spinal Cord Lesions:

  • compression of spinal roots L2 and below, often due to intervertebral disc herniation or tumor
  • unilateral radicular pain, absent knee and ankle reflex, loss of bladder and anal sphincter control, saddle anesthesia
  • Treatment:
    • emergent surgery
    • steroids
A

Cauda Equina Syndrome

227
Q

Neuropathology:

  • caused by poliovirus (fecal-oral transmission)
  • replicates in oropharynx and small intestine before spreading via bloodstream to CNS
  • infection causes destruction of cells in anterior horn of spinal cord (LMN death)
  • Signs of LMN Lesion:
    • asymmetric weakness
    • hypotonia
    • flaccid paralysis
    • fasciculations
    • hyporeflexia
    • muscle atrophy
  • respiratory muscle involvement leads to respiratory failure
  • Signs of Infection:
    • malaise, headache, fever, nausea, etc.
  • CSF shows ↑ WBCs (lymphocytic pleocytosis) and slight ↑ of protein (with no change in CSF glucose)
  • virus recovered from stool or throat
A

Poliomyelitis

228
Q

Brown-Séquard Syndrome

A

Hemisection of spinal cord.:

① ipsilateral loss of all sensation at level of lesion
② ipsilateral LMN signs (eg, flaccid paralysis) at level of lesion
③ ipsilateral UMN signs below level of lesion (due to corticospinal tract damage)
④ ipsilateral loss of proprioception, vibration, light (2-point discrimination) touch, and tactile sense below level of lesion (due to dorsal column damage)
⑤ contralateral loss of pain, temperature, and crude (nonadiscriminative) touch below level of lesion (due to spinothalamic tract damage)

If lesion occurs above T1, patient may present
with ipsilateral Horner syndrome due to
damage of oculosympathetic pathway.

229
Q

Neuropathology:

  • autosomal recessive trinucleotide repeat disorder (GAA)n on chromosome 9 in gene that encodes frataxin (iron binding protein)
  • leads to impairment in mitochondrial functioning
  • degeneration of lateral corticospinal tract (spastic paralysis), spinocerebellar tract (ataxia), dorsal columns (↓ vibratory sense, proprioception), and dorsal root ganglia (loss of DTRs)
  • staggering gait, frequent falling, nystagmus, dysarthria, pes cavus, hammer toes, diabetes mellitus, hypertrophic cardiomyopathy (cause of death)
  • presents in childhood with kyphoscoliosis
A

Friedreich Ataxia

Friedreich is Fratastic (frataxin): he’s your
favorite frat brother, always staggering and
falling but has a sweet, big heart.

Ataxic GAAit

230
Q

Common Cranial Nerve Lesions:

jaw deviates toward side of lesion due to unopposed force from the opposite pterygoid muscle

A

CN V Motor

231
Q

Common Cranial Nerve Lesions:

  • uvula deviates away from side of lesion
  • weak side collapses and uvula points away
A

CN X

232
Q

Common Cranial Nerve Lesions:

  • weakness turning head to contralateral side of lesion (SCM)
  • shoulder droop on side of lesion (trapezius)
  • the left SCM contracts to help turn the head to the right
A

CN XI

233
Q

Common Cranial Nerve Lesions:

  • LMN lesion
  • tongue deviates toward side of lesion (“lick your wounds”) due to weakened tongue muscles on affected side
A

CN XII

234
Q

Neuropathology:

  • most common cause of peripheral facial palsy
  • usually develops after HSV reactivation
  • Treatment: Corticosteroids ± Acyclovir
  • most patients gradually recover function, but aberrant regeneration can occur
  • other causes of peripheral facial palsy:
    • include Lyme disease
    • herpes zoster (Ramsay Hunt syndrome)
    • sarcoidosis
    • tumors (eg. parotid gland)
    • diabetes mellitus
A

Bell Palsy

235
Q

Facial Nerve Lesions:

  • Location:
    • motor cortex
    • connection from motor cortex to facial nucleus in pons
  • Affected Side:
    • contralateral
  • Muscles Involved:
    • lower muscles of facial expression
  • Forehead:
    • spared, due to bilateral UMN innervation
A

Upper Motor Neuron Lesion

236
Q

Facial Nerve Lesions:

  • Location:
    • facial nucleus
    • anywhere along CN VII
  • Affected Side:
    • ipsilateral
  • Muscles Involved:
    • upper and lower muscles of facial expression
  • Forehead:
    • affected
  • Other Symptoms:
    • incomplete eye closure (dry eyes, corneal ulceration)
    • hyperacusis
    • loss of taste sensation to anterior tongue
A

Lower Motor Neuron Lesion

237
Q

Auditory Physiology:

  • visible portion of ear (pinna)
  • includes auditory canal and tympanic membrane
  • transfers sound waves via vibration of tympanic membrane
A

Outer Ear

238
Q

Auditory Physiology:

  • air-filled space with three bones called the ossicles (malleus, incus, stapes)
  • ossicles conduct and amplify sound from tympanic membrane to inner ear
A

Middle Ear

239
Q

Auditory Physiology:

  • snail-shaped, fluid-filled cochlea
  • contains basilar membrane that vibrates 2° to sound waves
  • vibration transduced via specialized hair cells → auditory nerve signaling → brain stem
  • each frequency leads to vibration at specific location on basilar membrane (tonotopy):
    • low frequency heard at apex near helicotrema (wide and flexible)
    • high frequency heard best at base of cochlea (thin and rigid)
A

Inner Ear

240
Q

Hearing Loss:

  • Weber Test: localizes to affected ear
  • Rinne Test: abnormal (bone > air)
A

Conductive Hearing Loss

241
Q

Hearing Loss:

  • Weber Test: localizes to unaffected ear
  • Rinne Test: normal (air > bone)
A

Sensorineural Hearing Loss

242
Q

Hearing Loss:

  • damage to stereociliated cells in organ of Corti
  • loss of high-frequency hearing first
  • sudden extremely loud noises can produce hearing loss due to tympanic membrane rupture
A

Noise-Induced Hearing Loss

243
Q

Hearing Loss:

  • aging-related progressive bilateral/symmetric sensorineural hearing loss (often of higher frequencies)
  • due to destruction of hair cells at the cochlear base (preserved low-frequency hearing at apex)
A

Presbycusis

244
Q

ORL Pathology:

  • overgrowth of desquamated keratin debris within the middle ear space
  • may erode ossicles and mastoid air cells → conductive hearing loss
  • often presents with painless otorrhea
A

Cholesteatoma

245
Q

ORL Pathology:

  • sensation of spinning while actually stationary
  • subtype of “dizziness,” but distinct from “lightheadedness”
A

Vertigo

246
Q

Vertigo:

  • more common
  • inner ear etiology (eg. semicircular canal debris, vestibular nerve infection, Ménière disease [triad: sensorineural hearing loss, vertigo, tinnitus], benign paroxysmal positional vertigo [BPPV])
  • Treatment:
    • antihistamines
    • anticholinergics
    • antiemetics (symptomatic relief)
    • low-salt diet ± diuretics (Ménière disease)
    • Epley maneuver (BPPV)
A

Peripheral Vertigo

247
Q

Vertigo:

  • brain stem or cerebellar lesion (eg. stroke affecting vestibular nuclei or posterior fossa tumor)
  • Findings:
    • directional or purely vertical nystagmus
    • skew deviation
    • diplopia
    • dysmetria
    • focal neurologic findings
A

Central Vertigo

248
Q

Eye Anatomy

A
249
Q

Ophthalmic Pathology:

  • inflammation of the conjunctiva → red eye
  • Allergic
    • itchy eyes
    • bilateral
  • Bacterial
    • pus
    • treat with antibiotics
  • Viral
    • most common
    • often adenovirus
    • sparse mucous discharge
    • swollen preauricular node
    • self-resolving
A

Conjunctivitis

250
Q

Ophthalmic Pathology:

  • common cause of impaired vision
  • correctable with glasses
A

Refractive Errors

251
Q

Refractive Errors:

  • also known as “farsightedness”
  • eye too short for refractive power of cornea and lens → light focused behind retina
  • correct with convex (converging) lenses
A

Hyperopia

252
Q

Refractive Errors:

  • also known as “nearsightedness”
  • eye too long for refractive power of cornea and lens → light focused in front of retina
  • correct with concave (diverging) lens
A

Myopia

253
Q

Refractive Errors:

  • abnormal curvature of cornea → different refractive power at different axes
  • correct with cylindrical lens
A

Astigmatism

254
Q

Refractive Errors:

  • aging-related impaired accommodation (focusing on near objects), primarily due to ↓ lens elasticity, changes in lens curvature, ↓ strength of the ciliary muscle
  • patients often need “reading glasses” (magnifiers)
A

Presbyopia

255
Q

Ophthalmic Pathology:

  • painless, often bilateral, opacification of lens , often resulting in glare and ↓ vision, especially at night
  • Acquired Risk Factors:
    • ↑ age
    • smoking
    • excessive alcohol use
    • excessive sunlight
    • prolonged corticosteroid use
    • diabetes mellitus
    • trauma
    • infection
  • Congenital Risk Factors:
    • Classic Galactosemia
    • Galactokinase Deficiency
    • Trisomies (13, 18, 21)
    • ToRCHeS Infections (eg. rubella)
    • Marfan Syndrome
    • Alport Syndrome
    • Myotonic Dystrophy
    • Neurofibromatosis 2
A

Cataract

256
Q

Aqueous Humor Pathway

A
257
Q

Ophthalmic Pathology:

  • optic disc atrophy with characteristic cupping (thinning of outer rim of optic nerve head versus normal), usually with elevated intraocular pressure (IOP) and progressive peripheral visual field loss if untreated
  • treatment is through pharmacologic or surgical lowering of IOP
A

Glaucoma

258
Q

Glaucoma:

  • associated with ↑ age, African-American race, and family history
  • painless
  • more common in US
  • Primary—cause unclear
  • Secondary—blocked trabecular meshwork from WBCs (eg. uveitis), RBCs (eg. vitreous hemorrhage), retinal elements (eg. retinal detachment)
A

Open-Angle Glaucoma

259
Q

Glaucoma:

  • Primary
    • enlargement or anterior movement of lens against central iris (pupil margin) → obstruction of normal aqueous flow through pupil → fluid builds up behind iris, pushing peripheral iris against cornea and impeding flow through trabecular meshwork
  • Secondary
    • hypoxia from retinal disease (eg. diabetes mellitus, vein occlusion) induces vasoproliferation in iris that contracts angle
A

Closed- or Narrow-Angle Glaucoma

260
Q

Closed- or Narrow-Angle Glaucoma:

often asymptomatic with damage to optic nerve and peripheral vision

A

Chronic Closure

261
Q

Closed- or Narrow-Angle Glaucoma:

  • true ophthalmic emergency
  • ↑ IOP pushes iris forward → angle closes abruptly
  • very painful, red eye, sudden vision loss, halos around lights, frontal headache, fixed and mid‑dilated pupil
  • mydriatic agents contraindicated
A

Acute Closure

262
Q

Ophthalmic Pathology:

  • inflammation of uvea
  • specific name based on location within affected eye
  • anterior = Iritis
  • posterior = Choroiditis and/or Retinitis
  • may have hypopyon (accumulation of pus in anterior chamber) or conjunctival redness
  • associated with systemic inflammatory disorders (eg. sarcoidosis, rheumatoid arthritis, juvenile idiopathic arthritis, HLA-B27–associated conditions)
A

Uveitis

263
Q

Ophthalmic Pathology:

  • degeneration of macula (central area of retina)
  • causes distortion (metamorphopsia) and eventual loss of central vision (scotomas)
A

Age-Related Macular Degeneration

264
Q

Age-Related Macular Degeneration:

  • > 80%
  • deposition of yellowish extracellular material in between Bruch membrane and retinal pigment epithelium (“Drusen”) with gradual ↓ in vision
  • prevent progression with multivitamin and antioxidant supplements
A

Dry (Nonexudative)

265
Q

Age-Related Macular Degeneration:

  • 10–15%
  • rapid loss of vision due to bleeding 2° to choroidal neovascularization
  • treat with anti-VEGF (vascular endothelial growth factor) injections (eg. Bevacizumab, Ranibizumab)
A

Wet (Exudative)

266
Q

Ophthalmic Pathology:

retinal damage due to chronic hyperglycemia

A

Diabetic Retinopathy

267
Q

Diabetic Retinopathy:

  • damaged capillaries leak blood → lipids and fluid seep into retina → hemorrhages and macular edema
  • Treatment: blood sugar control
A

Nonproliferative

268
Q

Diabetic Retinopathy:

  • chronic hypoxia results in new blood vessel formation with resultant traction on retina
  • Treatment:
    • peripheral retinal photocoagulation
    • surgery
    • anti-VEGF
A

Proliferative

269
Q

Ophthalmic Pathology:

  • retinal damage due to chronic uncontrolled HTN
  • flame-shaped retinal hemorrhages, arteriovenous nicking, microaneurysms, macular star (exudate), cotton-wool spots
  • presence of papilledema requires immediate lowering of BP
  • associated with ↑ risk of stroke, CAD, and kidney disease
A

Hypertensive Retinopathy

270
Q

Ophthalmic Pathology:

  • blockage of central or branch retinal vein due to compression from nearby arterial atherosclerosis
  • retinal hemorrhage and venous engorgement (“blood and thunder appearance”)
  • edema in affected area
A

Retinal Vein Occlusion

271
Q

Ophthalmic Pathology:

  • separation of neurosensory layer of retina (photoreceptor layer with rods and cones) from outermost pigmented epithelium (normally shields excess light, supports retina) → degeneration of photoreceptors → vision loss
  • may be 2° to retinal breaks, diabetic traction, inflammatory effusions
  • visualized on fundoscopy as crinkling of retinal tissue and changes in vessel direction
  • breaks more common in patients with high myopia and/or history of head trauma
  • often preceded by posterior vitreous detachment (“flashes” and “floaters”) and eventual monocular loss of vision like a “curtain drawn down”
  • surgical emergency
A

Retinal Detachment

272
Q

Ophthalmic Pathology:

  • acute, painless monocular vision loss
  • retina cloudy with attenuated vessels and “cherry-red” spot at fovea (center of macula)
  • evaluate for embolic source (eg. carotid artery atherosclerosis, cardiac vegetations, patent foramen ovale)
A

Central Retinal Artery Occlusion

273
Q

Ophthalmic Pathology:

  • inherited retinal degeneration
  • painless, progressive vision loss beginning with night blindness (rods affected first)
  • bone spicule-shaped deposits around macula
A

Retinitis Pigmentosa

274
Q

Ophthalmic Pathology:

  • retinal edema and necrosis leading to scar
  • often viral (CMV, HSV, VZV), but can be bacterial or parasitic
  • may be associated with immunosuppression
A

Retinitis

275
Q

Ophthalmic Pathology:

  • optic disc swelling (usually bilateral) due to ↑ ICP (eg. 2° to mass effect)
  • enlarged blind spot and elevated optic disc with blurred margins
A

Papilledema

276
Q

Pupillary Control:

Miosis

A
  • constriction
  • Parasympathetic:
    • 1st neuron: Edinger-Westphal nucleus to ciliary ganglion via CN III
    • 2nd neuron: short ciliary nerves to sphincter pupillae muscles
  • Short ciliary nerves shorten the pupil diameter.
277
Q

Pupillary Control:

Pupillary Light Reflex

A
  • Light in either retina sends a signal via CN II to pretectal nuclei (dashed lines in image) in midbrain that activates bilateral Edinger-Westphal nuclei.
  • Pupils constrict bilaterally (direct and consensual reflex).
  • Result: illumination of 1 eye results in bilateral pupillary constriction.
278
Q

Pupillary Control:

Mydriasis

A
  • dilation
  • Sympathetic:
    • 1st neuron: hypothalamus to ciliospinal center of Budge (C8–T2)
    • 2nd neuron: exit at T1 to superior cervical ganglion (travels along cervical sympathetic chain near lung apex, subclavian vessels)
    • 3rd neuron: plexus along internal carotid, through cavernous sinus; enters orbit as long ciliary nerve to pupillary dilator muscles. Sympathetic fibers also innervate smooth muscle of eyelids (minor retractors) and sweat glands of forehead and face.
  • Long ciliary nerves make the pupil diameter longer.
279
Q

Ophthalmic Pathology:

  • When the light shines into a normal eye, constriction of the ipsilateral (direct reflex) and contralateral eye (consensual reflex) is observed.
  • When the light is then swung to the affected eye, both pupils dilate instead of constrict due to impaired conduction of light signal along the injured optic nerve.
A

Marcus Gunn Pupil

280
Q

Horner Syndrome

A
  • Sympathetic denervation of face (PAM is horny.):
    • Ptosis (slight drooping of eyelid: superior tarsal muscle)
    • Anhidrosis (absence of sweating) and flushing of affected side of face
    • Miosis (pupil constriction)
  • Associated with lesions along the sympathetic chain:
    • 1st neuron: pontine hemorrhage, lateral medullary syndrome, spinal cord lesion above T1 (eg. Brown-Séquard syndrome, late-stage syringomyelia)
    • 2nd neuron (stellate ganglion): Pancoast tumor
    • 3rd neuron: carotid dissection (painful)
281
Q

Ocular Motility

A
  • The “chemical formula” LR6SO4R3.
    • CN VI innervates the Lateral Rectus
    • CN IV innervates the Superior Oblique
    • CN III innervates the Rest
  • The strongest action of the superior oblique is depression when the eye is adducted. The further the eye is abducted, the more the superior oblique acts to intort the eye toward the nose.
  • Obliques go Opposite (left SO and IO tested with patient looking right).
  • IOU: IO tested looking Up
282
Q

CN III, IV, VI Palsies:

  • has both motor (central) and parasympathetic (peripheral) components.
  • Common Causes:
    • ischemia → pupil sparing
    • uncal herniation → coma
    • PCA aneurysm → sudden-onset headache
    • cavernous sinus thrombosis → proptosis, involvement of CNs IV, V1/V2, VI
    • midbrain stroke → contralateral hemiplegia
A

CN III damage

283
Q

CN III, IV, VI Palsies:

eye moves upward, particularly with contralateral gaze (→ going down stairs, head may tilt in the opposite direction to compensate)

A

CN IV damage

Can’t see the floor with CN IV damage.

284
Q

CN III, IV, VI Palsies:

affected eye unable to abduct and is displaced medially in primary position of gaze

A

CN VI damage

285
Q

Visual Field Defects

A
  1. Right Anopia
  2. Bitemporal Hemianopia (pituitary lesion, chiasm)
  3. Left Homonymous Hemianopia
  4. Left Upper Quadrantanopia (right temporal lesion, MCA)
  5. Left Lower Quadrantanopia (right parietal lesion, MCA)
  6. Left Hemianopia with Macular Sparing (PCA infarct)
  7. Central Scotoma (eg. macular degeneration)
  • Meyer Loop
    • Lower retina
    • Loops around inferior horn of Lateral ventricle
  • Dorsal Optic Radiation
    • superior retina
    • takes shortest path via internal capsule
286
Q

Cavernous Sinus

A
  • collection of venous sinuses on either side of the pituitary
  • blood from eye and superficial cortex → cavernous sinus → internal jugular vein
  • CNs III, IV, V1, VI, and V2 plus postganglionic sympathetic pupillary fibers en route to orbit all pass through cavernous sinus
  • cavernous portion of internal carotid artery is also here
287
Q

Ophthalmic Pathology:

  • presents with variable ophthalmoplegia, ↓ corneal sensation, Horner syndrome and occasional decreased maxillary sensation
  • 2° to pituitary tumor mass effect, carotid-cavernous fistula, or cavernous sinus thrombosis related to infection
  • CN VI is most susceptible to injury
A

Cavernous Sinus Syndrome

288
Q

Internuclear Ophthalmoplegia

A

Medial Longitudinal Fasciculus (MLF):

  • pair of tracts that allows for crosstalk between CN VI and CN III nuclei
  • coordinates both eyes to move in same horizontal direction
  • highly myelinated (must communicate quickly so eyes move at same time)
  • lesions may be unilateral or bilateral (latter classically seen in multiple sclerosis)

Internuclear Ophthalmoplegia (INO)

  • lesion in MLF
  • a conjugate horizontal gaze palsy
  • lack of communication such that when CN VI nucleus activates ipsilateral lateral rectus, contralateral CN III nucleus does not stimulate medial rectus to contract
  • abducting eye gets nystagmus (CN VI overfires to stimulate CN III)
  • convergence normal
  • 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
  • directional term (eg. right INO, left INO) refers to which eye is paralyzed
  • INO = Ipsilateral adduction failure, Nystagmus Opposite
289
Q

Epilepsy Drugs:

  • used for Status Epilepticus
  • 1st line for recurrent seizure prophylaxis
  • ↑ GABAA action
  • causes sedation, tolerance, dependence, respiratory depression
  • also for eclampsia seizures (1st line is MgSO4)
A

Benzodiazepines

290
Q

Epilepsy Drugs:

  • commonly used for partial (focal) seizures
  • used for GTC
  • blocks Na+ channels
  • causes diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis (cleft lip/palate, spina bifida), induction of cytochrome P-450, SIADH, Stevens- Johnson syndrome
  • 1st line for trigeminal neuralgia
A

Carbamazepine

291
Q

Epilepsy Drugs:

  • commonly used for absence seizures
  • blocks thalamic T-type Ca2+ channels
  • causes fatigue, GI distress, headache, itching (and urticaria), and Stevens-Johnson syndrome
A

Ethosuximide

EFGHIJ:

Ethosuximide causes Fatigue, GI distress, Headache, Itching (and urticaria), and Stevens-Johnson syndrome.

292
Q

Epilepsy Drugs:

  • used for partial (focal) seizures
  • primarily inhibits high-voltage-activated Ca2+ channels
  • designed as GABA analog
  • causes sedation and ataxia
  • also used for peripheral neuropathy and postherpetic neuralgia
A

Gabapentin

293
Q

Epilepsy Drugs:

  • used for partial (focal), absence and GTC seizures
  • blocks voltage-gated Na+ channels
  • inhibits the release of glutamate
  • causes Stevens-Johnson syndrome (must be titrated slowly)
A

Lamotrigine

294
Q

Epilepsy Drugs:

  • used for partial (focal) and GTC seizures
  • unknown MOA
  • may modulate GABA and glutamate release
  • causes neuropsychiatric symptoms (eg. personality change), fatigue, drowsiness, and headache
A

Levetiracetam

295
Q

Epilepsy Drugs:

  • used for partial (focal) seizures, GTC seizures and status epilepticus
  • ↑ GABAA action
  • causes sedation, tolerance, dependence, induction of cytochrome P-450, and cardiorespiratory depression
  • 1st line in neonates
A

Phenobarbital

296
Q

Epilepsy Drugs:

  • commonly used for GTC
  • used for partial (focal) seizures and status epilepticus
  • 1st line for recurrent seizure prophylaxis
  • blocks Na+ channels
  • zero-order kinetics
  • causes P450 induction, hirsutism, enlarged gums, nystagmus, yellow-brown skin, teratogenicity (fetal hydantoin syndrome), osteopenia, inhibited folate absorption, neuropathy
  • rare adverse reactions include Stevens-Johnson syndrome, DRESS syndrome, and SLE-like syndrome
  • toxicity leads to diplopia, ataxia, and sedation
A
  • Phenytoin
  • Fosphenytoin

PHENYTOIN:

  • P450 induction
  • Hirsutism
  • Enlarged gums
  • Nystagmus
  • Yellow-brown skin
  • Teratogenicity
  • Osteopenia
  • Inhibited folate absorption
  • Neuropathy
297
Q

Epilepsy Drugs:

  • used for partial (focal) seizures
  • ↑ GABA by inhibiting reuptake
A

Tiagabine

298
Q

Epilepsy Drugs:

  • used for partial (focal and GTC seizures)
  • blocks Na+ channels
  • ↑ GABA action
  • causes sedation, mental dulling, word-finding difficulty, kidney stones, weight loss, and glaucoma
  • also used for migraine prevention
A

Topiramate

299
Q

Epilepsy Drugs:

  • commonly used for GTC seizures
  • used for partial (focal) and absence seizures
  • ↑ Na+ channel inactivation
  • ↑ GABA concentration by inhibiting GABA transaminase
  • causes GI distress, rare but fatal hepatotoxicity (measure LFTs), pancreatitis, neural tube defects, tremor, and weight gain
  • contraindicated in pregnancy
  • also used for myoclonic seizures, bipolar disorder, and migraine prophylaxis
A

Valproic Acid

300
Q

Epilepsy Drugs:

  • used for partial (focal) seizures
  • ↑ GABA
  • irreversible GABA transaminase inhibitor
  • causes permanent visual loss (black box warning)
A

Vigabatrin

301
Q

Neurologic Drugs:

Barbiturates

A
  • Phenobarbital
  • Pentobarbital
  • Thiopental
  • Secobarbital
302
Q

Neurologic Drugs:

  • facilitate GABAA action by ↑ duration of Cl− channel opening, thus ↑ neuron firing
  • used for sedation for anxiety, seizures, insomnia, and induction of anesthesia (thiopental)
  • causes respiratory and cardiovascular depression (can be fatal), CNS depression (can be exacerbated by alcohol use), dependence, and drug interactions (induces cytochrome P-450)
  • overdose treatment is supportive (assist respiration and maintain BP)
  • contraindicated in porphyria
A

Barbiturates

Barbidurates = ↑ duration

303
Q

Neurologic Drugs:

Benzodiazepines

A
  • Diazepam
  • Lorazepam
  • Triazolam
  • Temazepam
  • Oxazepam
  • Midazolam
  • Chlordiazepoxide
  • Alprazolam
304
Q

Neurologic Drugs:

  • facilitate GABAA action by ↑ frequency of Cl− channel opening. ↓ REM sleep
  • most have long half-lives and active metabolites (exceptions [ATOM]: Alprazolam, Triazolam, Oxazepam, and Midazolam are short acting → higher addictive potential).
  • used for anxiety, spasticity, status epilepticus (Lorazepam, Diazepam, Midazolam), eclampsia, detoxification (especially alcohol withdrawal–DTs), night terrors, sleepwalking, and general anesthesia (amnesia, muscle relaxation), hypnotic (insomnia)
  • causes ependence and additive CNS depression effects with alcohol
  • less risk of respiratory depression and coma than with barbiturates
  • treat overdose with Flumazenil (competitive antagonist at GABA benzodiazepine receptor)
  • can precipitate seizures by causing acute withdrawal
A

Benzodiazepines

  • Frenzodiazepines = ↑ frequency
  • Benzos, barbs, and alcohol all bind the GABAA receptor, which is a ligand-gated Cl− channel.
  • Oxazepam, Temazepam, and Lorazepam are OK for Terrible Livers: they can be used to treat alcohol withdrawal in patients with liver disease due to minimal first-pass metabolism.
305
Q

Neurologic Drugs:

Nonbenzodiazepine Hypnotics

A

These ZZZs put you to sleep.

  • Zolpidem
  • Zaleplon
  • EsZopiclone
306
Q

Neurologic Drugs:

  • act via the BZ1 subtype of the GABA receptor
  • effects reversed by Flumazenil
  • sleep cycle less affected as compared with benzodiazepine hypnotics
  • used for insomnia
  • causes ataxia, headaches, and confusion
  • short duration because of rapid metabolism by liver enzymes
  • unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects
  • ↓ dependence risk than benzodiazepines
A

Nonbenzodiazepine Hypnotics

307
Q

Neurologic Drugs:

  • orexin (hypocretin) receptor antagonist.
  • used for insomnia
  • causes CNS depression, headache, dizziness, abnormal dreams, and upper respiratory tract infection
  • contraindicated in patients with narcolepsy
  • not recommended in patients with liver disease
  • no or low physical dependence
  • contraindicated with strong CYP3A4 inhibitors
A

Suvorexant

308
Q

Neurologic Drugs:

  • melatonin receptor agonist
  • binds MT1 and MT2 in suprachiasmatic nucleus
  • used for insomnia
  • causes dizziness, nausea, fatigue, and headache
  • no dependence (not a controlled substance)
A

Ramelteon

309
Q

Neurologic Drugs:

  • 5-HT1B/1D agonists
  • inhibit trigeminal nerve activation
  • prevent vasoactive peptide release
  • induce vasoconstriction
  • used for acute migraine and cluster headache attacks
  • causes coronary vasospasm (contraindicated in patients with CAD or Prinzmetal angina), mild paresthesia, serotonin syndrome (in combination with other 5-HT agonists)
A

Triptans (Sumatriptan)

A sumo wrestler trips and falls on your head.

310
Q

Parkinson Disease Drugs

A

Parkinsonism is due to loss of dopaminergic neurons and excess cholinergic activity.

BALSA:

  • Bromocriptine
  • Amantadine
  • Levodopa (with Carbidopa)
  • Selegiline (and COMT Inhibitors)
  • Antimuscarinics
311
Q

Parkinson Disease Drugs:

Dopamine Agonists

A
  • Ergot
    • Bromocriptine
  • Non-Ergot (preferred)
    • Pramipexole and Ropinirole
    • toxicity includes impulse control disorder (eg. gambling), postural hypotension, and hallucinations/confusion
312
Q

Parkinson Disease Drugs:

↑ dopamine availability

A

Amantadine

  • ↑ dopamine release and ↓ dopamine reuptake
  • toxicity = ataxia, livedo reticularis
313
Q

Parkinson Disease Drugs:

↑ L-DOPA availability

A

Agents prevent peripheral (pre-BBB) l-DOPA degradation → ↑ L-DOPA entering CNS → ↑ central L-DOPA available for conversion to dopamine

  • Levodopa (L-DOPA)/Carbidopa
    • Carbidopa blocks peripheral conversion of L-DOPA to dopamine by inhibiting DOPA decarboxylase.
    • Also reduces side effects of peripheral L-DOPA conversion into dopamine (eg. nausea, vomiting).
  • Entacapone
    • Prevents peripheral L-DOPA degradation to 3-O-methyldopa (3‑OMD) by inhibiting COMT.
    • Used in conjunction with Levodopa.
314
Q

Parkinson Disease Drugs:

prevent dopamine breakdown

A

Agents act centrally (post-BBB) to inhibit breakdown of dopamine.

  • Selegiline and Rasagiline
    • Block conversion of dopamine into DOPAC by selectively inhibiting MAO-B.
  • Entacapone
    • Blocks conversion of dopamine to 3-methoxytyramine (3-MT) by inhibiting central COMT.
315
Q

Parkinson Disease Drugs:

curb excess cholinergic activity

A

Benztropine and Trihexyphenidyl

  • antimuscarinic
  • improves tremor and rigidity but has little effect on bradykinesia in Parkinson disease

Park your Mercedes-Benz.

316
Q

Neurologic Drugs:

  • ↑ 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
  • used for Parkinson disease
  • causes nausea, hallucinations, and postural hypotension from ↑ peripheral formation of catecholamines
  • long-term use can lead to dyskinesia following administration (“on-off” phenomenon) and akinesia between doses
A

Levodopa/Carbidopa

  • Carbidopa, a peripheral DOPA decarboxylase inhibitor, is given with L-DOPA to ↑ the bioavailability of L-DOPA in the brain and to limit peripheral side effects.
317
Q

Neurologic Drugs:

  • selectively inhibit MAO-B (metabolize dopamine) → ↑ dopamine availability
  • adjunctive agent to L-DOPA in treatment of Parkinson disease
  • may enhance adverse effects of L-DOPA
A
  • Selegiline
  • Rasagiline
318
Q

Neurologic Drugs:

  • inhibit vesicular monoamine transporter (VMAT) dopamine → ↓ vesicle packaging and release
  • used for Huntington chorea and tardive dyskinesia
A
  • Tetrabenazine
  • Reserpine
319
Q

Neurologic Drugs:

  • ↓ neuron glutamate excitotoxicity
  • used for ALS
  • ↑ survival
A

Riluzole

For Lou Gehrig disease, give Rilouzole.

320
Q

Alzheimer Disease Drugs:

  • NMDA receptor antagonist
  • helps prevent excitotoxicity (mediated by Ca2+)
  • causes dizziness, confusion, hallucinations
A

Memantine

321
Q

Alzheimer Disease Drugs:

  • AChE inhibitors
  • causes nausea, dizziness, and insomnia
A

Dona Riva dances at the gala.

  • Donepezil
  • Rivastigmine
  • Galantamine
322
Q

Anesthetics—General Principles

A
  • CNS drugs must be lipid soluble (cross the blood-brain barrier) or be actively transported.
  • drugs with ↓ solubility in blood = rapid induction and recovery times
  • drugs with ↑ solubility in lipids = ↑ potency = 1/MAC
  • MAC = Minimal Alveolar Concentration
    • inhaled anesthetic required to prevent 50% of subjects from moving in response to noxious stimulus (eg. skin incision)
  • Nitrous oxide (N2O) has ↓ blood and lipid solubility, and thus fast induction and low potency.
  • Halothane, Propofol, and Thiopental, in contrast, have ↑ lipid and blood solubility, and thus high potency and slow induction.
323
Q

Inhaled Anesthetics

A
  • Desflurane
  • Halothane
  • Enflurane
  • Isoflurane
  • Sevoflurane
  • Methoxyflurane
  • N2O
324
Q

Anesthetics:

  • mechanism unknown
  • causes myocardial depression, respiratory depression, nausea/emesis, ↑ cerebral blood flow (↓ cerebral metabolic demand)
  • causes hepatotoxicity (Halothane), nephrotoxicity (Methoxyflurane), proconvulsant (Enflurane, epileptogenic), expansion of trapped gas in a body cavity (N2O)
A

Inhaled Anesthetics

325
Q

Neuropathology:

  • rare, life-threatening condition in which inhaled anesthetics or Succinylcholine induce fever and severe muscle contractions
  • susceptibility is often inherited as autosomal dominant with variable penetrance
  • mutations in voltage-sensitive ryanodine receptor (RYR1 gene) cause ↑ Ca2+ release from sarcoplasmic reticulum
  • Treatment:
    • Dantrolene—ryanodine receptor antagonist
A

Malignant Hyperthermia

326
Q

Intravenous Anesthetics:

  • facilitate GABAA (barbiturate)
  • induction of anesthesia
  • short surgical procedures
  • ↓ cerebral blood flow
  • high lipid solubility
  • effect terminated by rapid redistribution into tissue and fat
A

Thiopental

327
Q

Intravenous Anesthetics:

  • facilitate GABAA (benzodiazepine)
  • procedural sedation (eg. endoscopy)
  • anesthesia induction
  • may cause severe postoperative respiratory depression, ↓ BP, and anterograde amnesia
A

Midazolam

328
Q

Intravenous Anesthetics:

  • potentiates GABAA
  • rapid anesthesia induction
  • short procedures
  • ICU sedation
A

Propofol

329
Q

Intravenous Anesthetics:

  • NMDA receptor antagonist
  • causes dissociative anesthesia
  • sympathomimetic
  • ↑ cerebral blood flow
  • emergence reaction possible with disorientation, hallucination, and vivid dreams
A

Ketamine

330
Q

Local Anesthetics

A
  • Esters
    • Procaine
    • Tetracaine
    • Benzocaine
    • Chloroprocaine
  • Amides (2 I’s in name)
    • LIdocaIne
    • MepIvacaIne
    • BupIvacaIne
    • RopIvacaIne
331
Q

Anesthetics:

  • block Na+ channels by binding to specific receptors on inner portion of channel
  • most effective in rapidly firing neurons
  • 3° amine anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form
  • can be given with vasoconstrictors (usually epinephrine) to enhance local action—↓ bleeding, ↑ anesthesia by ↓ systemic concentration
  • in infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively → need more anesthetic
  • Order of Nerve Blockade:
    • small-diameter fibers > large diameter
    • myelinated fibers > unmyelinated fibers
  • overall, size factor predominates over myelination such that small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers
  • Order of Loss:
  1. pain
  2. temperature
  3. touch
  4. pressure
  • used for minor surgical procedures and spinal anesthesia
  • if allergic to esters, give amides
  • causes CNS excitation, severe cardiovascular toxicity (Bupivacaine), hypertension, hypotension, arrhythmias (Cocaine), methemoglobinemia (Benzocaine)
A

Local Anesthetics

332
Q

Neurologic Drugs:

  • used for muscle paralysis in surgery or mechanical ventilation
  • selective for Nm nicotinic receptors at neuromuscular junction but not autonomic Nn receptors
A

Neuromuscular Blocking Drugs

333
Q

Neuromuscular Blocking Drugs:

  • strong ACh receptor agonist
  • produces sustained depolarization and prevents muscle contraction
  • Reversal of Blockade:
    • Phase I
      • prolonged depolarization
      • no antidote
      • block potentiated by cholinesterase inhibitors
    • Phase II
      • repolarized but blocked
      • ACh receptors are available, but desensitized
      • may be reversed with cholinesterase inhibitors
  • complications include hypercalcemia, hyperkalemia, and malignant hyperthermia
A

Depolarizing Neuromuscular Blocking Drugs

  • Succinylcholine
334
Q

Neuromuscular Blocking Drugs:

  • competitive with ACh for receptors
  • Reversal of Blockade:
    • Neostigmine
      • must be given with atropine or glycopyrrolate to prevent muscarinic effects such as bradycardia
    • Edrophonium
A

Nondepolarizing Neuromuscular Blocking Drugs

  • Atracurium
  • Cisatracurium
  • Pancuronium
  • Rocuronium
  • Tubocurarine
  • Vecuronium
335
Q

Neurologic Drugs:

  • prevents release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle by binding to the ryanodine receptor
  • used for malignant hyperthermia (a toxicity of inhaled anesthetics and succinylcholine) and neuroleptic malignant syndrome (a toxicity of antipsychotic drugs)
A

Dantrolene

336
Q

Neurologic Drugs:

  • skeletal muscle relaxant
  • GABAB receptor agonist in spinal cord
  • used for muscle spasticity, dystonia, and multiple sclerosis
A

Baclofen

337
Q

Neurologic Drugs:

  • skeletal muscle relaxant
  • acts within CNS
  • used for muscle spasms
  • anticholinergic side effects
  • causes sedation
A

Cyclobenzaprine

338
Q

Analgesics:

  • act as agonists at opioid receptors (μ = β-endorphin, δ = enkephalin, κ = dynorphin) to modulate synaptic transmission—close presynaptic Ca2+ channel, open postsynaptic K+ channels → ↓ synaptic transmission
  • inhibit release of ACh, norepinephrine, 5-HT, glutamate, and substance P
  • used for moderate to severe or refractory pain, cough suppression (Dextromethorphan), diarrhea (Loperamide, Diphenoxylate), acute pulmonary edema, maintenance programs for heroin addicts (Methadone, Buprenorphine + Naloxone)
  • causes nausea, vomiting, pruritus, addiction, respiratory depression, constipation, sphincter of Oddi spasm, miosis (except Meperidine → mydriasis), and additive CNS depression with other drugs
  • tolerance does not develop to miosis and constipation
  • toxicity is treated with Naloxone (_____ receptor antagonist) and relapse prevention with Naltrexone once detoxified
A

Opioid Analgesics

  • Full Agonists:
    • Morphine
    • Heroin
    • Meperidine
    • Methadone
    • Codeine
  • Partial Agonist:
    • Buprenorphine
  • Mixed Agonist/Antagonist:
    • Nalbuphine
    • Pentazocine
  • Antagonist:
    • Naloxone
    • Naltrexone
    • Methylnaltrexone
339
Q

Neurologic Drugs:

  • κ-opioid receptor agonist and μ-opioid receptor weak antagonist or partial agonist
  • analgesia for moderate to severe pain.
  • can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (due to competition for opioid receptors)
A

Pentazocine

340
Q

Neurologic Drugs:

  • κ-opioid receptor agonist and μ-opioid receptor partial agonist
  • used for evere pain (eg. migraine, labor)
  • causes less respiratory depression than full opioid agonists
  • use with full opioid agonist can precipitate withdrawal
  • not easily reversed with Naloxone
A

Butorphanol

341
Q

Neurologic Drugs:

  • very weak opioid agonist
  • also inhibits 5-HT receptors
  • used for chronic pain
  • adverse effects are similar to opioids
  • decreases seizure threshold
  • causes serotonin syndrome
A

Tramadol

342
Q

Ophthalmic Pathology:

↓ IOP via ↓ amount of aqueous humor (inhibit synthesis/secretion or ↑ drainage)

A

Glaucoma Drugs

343
Q

Glaucoma Drugs

A

BAD humor may not be Politically Correct.

  • β-Blockers
  • α-Agonists
  • Diuretics
  • Prostaglandins
  • Cholinomimetics (M3)
344
Q

Glaucoma Drugs:

  • ↓ aqueous humor synthesis
  • no pupillary or vision changes
A

β-Blockers

  • Timolol
  • Betaxolol
  • Carteolol
345
Q

Glaucoma Drugs:

  • ↓ aqueous humor synthesis via vasoconstriction (Epinephrine)
  • ↓ aqueous humor synthesis (Apraclonidine, Brimonidine)
  • causes mydriasis (α1)
  • do not use in closed-angle glaucoma
  • causes blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, and ocular pruritus
A

α-Agonists

  • Epinephrine (α1)
  • Apraclonidine
  • Brimonidine (α2)
346
Q

Glaucoma Drugs:

  • ↓ aqueous humor synthesis via inhibition of carbonic anhydrase
  • no pupillary or vision changes
A

Diuretics

  • Acetazolamide
347
Q

Glaucoma Drugs:

  • ↑ outflow of aqueous humor via ↓ resistance of flow through uveoscleral pathway
  • darkens color of iris (browning)
  • causes eyelash growth
A

Prostaglandins (PGF2α)

  • Bimatoprost
  • Latanoprost
348
Q

Glaucoma Drugs:

  • ↑ outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
  • use Pilocarpine in acute angle closure glaucoma—very effective at opening meshwork into canal of Schlemm
  • causes miosis (contraction of pupillary sphincter muscles) and cyclospasm (contraction of ciliary muscle)
A

Cholinomimetics (M3)

  • Direct:
    • Pilocarpine
    • Carbachol
  • Indirect:
    • Physostigmine
    • Echothiophate

Day 4 (3 decks)

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