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Week 2 Flashcards

1
Q

Explain how sound travels through the periphery…

high versus low frequencies

A

Peripheral: Sound waves enter external ear canal → TM → ossicles → oval window → vibrations hit perilymph in inner ear → hair cells → cochlear n.

  • High frequencies activate proximal hair cells
  • Low frequencies activate distal hair cells
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2
Q

explain how sound thravels through the CNS

A

Central: Cochlear n. → ipsilateral cochlear nuclei @ ponto-medullary junction → bilateral superior olives @ ponto-medullary junction → ascend to bilateral inferior colliculi @ mid brain → ascend to bilateral medial geniculate nuclei @ thalamus → synapses at primary auditory cortices

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3
Q

what is Conductive deafness

etiology

A

Conductive deafness – loss caused by the conduction system of ear (external auditory canal, TM, middle ear)

Etiology: structural issues (ear wax), infection, ruptured TM, ischemia, Meinere syndrome (obstructed reabsorption of the endolymph)

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4
Q

what is sensineuronal deafness

pheripheral versus cenetral damage

A
  • Peripheral damage: conditions that damage the delicate hair cells of the Organ of Corti or the auditory component of CN VIII due to exposure of loud noises
  • Central damage:
    • Cochlear nuclei damage: unilateral hearing loss
    • Damage beyond cochlear nuclei: bilateral hearing loss
    • Damage to CNS: inability to localize sound
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5
Q

Tinnitus

etiology?

A

Tinnitus – ringing or buzzing in the ears

Etiology: damage to hair cells due to excessive sound exposure, inner ear/CN VIII damage, turbulent blood flow through carotid, aspirin, tumors

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6
Q

what are exams for hearing

screening tools?

A
  • Weber test (tuning fork on head):
    • Sensineuronal deafness: localizes to unaffected ear
    • Conductive deafness: localizes to affected ear
  • Rinne (tuning fork next to ear)
    • Sensineuronal deafness: normal (air > bone)
    • Condcutve deafness: abnormal (bone > air)
  • Screen: watch test or rustling of fingers next ears
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7
Q

tx of hearing loss

A

Treatments for hearing loss: cochlear implant (captures sound and stimulates cochlear n.), hearing aid (amplifies sound), masking device (white noise generator)

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8
Q

function and antaomy of vestibula system

A

Function: vestibular apparatus of the inner ear is specialized to detect movement of the head and, to a lesser extent, position in space; stabilization of eyes.

Anatomy: vestibular system, located in your inner ear consists of the saccule and utricle (otolith – senses gravity and liner acceleration), and three semicircular canals.

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9
Q

explain the vestibular pathway

A
  • Pathway: endolymph flows and pushes on cupula → activates CN VIII (vestibular n.) → vestibular complex @ pontomedullary junction AND vestibulocerebellum @ cerebellum → VP nucleus of thalamus
    • Disruption of this pathway result in vertigo
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10
Q

what is the Vestibular Ocular Reflex (VOR)

fxn, pathway

A
  • Function: stabilizes eyes while moving head
  • Pathway: movement of head to right → information sent to vestibular n. → Scarpa’a ganglion → vestibular nucleus → contralateral abducens nucleus → activation of left lateral rectus and right medial nucleus
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11
Q

explain VOR testing

A
  • Head thrust – testing if VOR is working
  • Caloric testing: test function of inner ear on either side (COWS)
    • Cold Opposite: The cold irrigant provokes a response with fast phases away from the irrigated ear – normal response
    • Warm Same: the warm irrigant provokes a nystagmus response with fast phases towards the irrigated ear – normal response
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12
Q

what is…

benign paroxysmal positional vertigo

labyrinthitis

vestibular neuronitis

A
  • Benign Paroxysmal Positional Vertigo (BPPV) - most common form
    • Sx: short, frequent bouts of vertigo; head movements trigger BPPV.
  • Labyrinthitis
    • Sx: dizziness or a feeling that you are moving when you are not
    • Etiology: inner ear infection such as a cold or flu (bacterial or viral).
  • Vestibular Neuronitis: aka vestibular neuritis.
    • Sx: sudden onset and may cause unsteadiness, earache, nausea, and vomiting.
    • Etiology: viral infection, such as a cold or flu.
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13
Q

what is…

Acoustic neuroma: (or neurolemmoma)

Ménière’s Disease:

A
  • Acoustic neuroma: (or neurolemmoma)
    • Etiology: tumor that grows on the vestibular nerve.
    • Sx: Slow growth rarely causes vertigo due to ample time for compensation of deficits.
  • Ménière’s Disease:
    • Sx: sudden vertigo less than 24 hours, N/V, hearing loss, ringing in the ears, and a feeling of fullness in the ears.
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14
Q

Nystagmus

A

Nystagmus: is a vision condition in which the eyes make repetitive, uncontrolled movements

Types: horizontal and vertical (brainstem issue)

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15
Q

peripheral versus central vertigo

etiology and sx

A
  • Peripheral – dysfunction of vestibular apparatus in inner ear or CN VIII
    • Etiology: described above
    • SX: sudden onset, intermittent severe symptoms, affected by head position, N/V severe, motor fxn, gait and coordination intact
  • Central – dysfunction of connection from vestibular apparatus to vestibular nuclei
    • Etiology: trauma to brainstem/vestibulocerebellum, stroke, isolated hemorrhage in cerebellum, tumors, inflammatory diseases (MS)
    • SX: gradual onset, constant milder symptoms, unaffected by head position, N/V less predictable, motor fxn, gait and coordination deficits
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16
Q

hearing loss

A

If lesion is in the CNS (nucleus), the hearing loss will be bilateral

If lesion is in the PNS (after nucleus), the hearing loss will be unilateral

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17
Q

hypothalamus

function (TANHATS) and causes of dysfunction

A
  • Functions: homeostasis (maintains homeostasis by integrating signals from environment, other brain areas, and peripheral organs)
    • Thirst and water balance, Adenohypohysis, Neurohypohysis,Hunger,Autonomic function,Temperature,Sexual behavior/emotions, memory, circadian rhythm (TANHATS)
  • Causes of hypothalamic damage/dysfunction: tumors, inflammatory conditions, brain injury, genetic (i.e. Prader-Willi)
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18
Q

hypothalamus

where is it located

inputs and outputs

A
  • Location: part of diencephalon, located inferior to thalamus, forms walls and floor of the third ventricle, sits below optic tract
  • Inputs:
    • Areas that are not protected by blood-barrier (i.e organum vasculosum of the lamina terminalis – OVLT, subfornical organ – SFO)
      • Allows for neurons to detect circulating hormones, proteins, etc.
    • Area postrema @ medulla: response to emetics
  • Outputs: widespread projections to autonomic areas for cardiovascular regulation
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19
Q

hypothalamus

explian these nuclei

supraoptic, paraventricular, lateral, ventromedial

A
  • Supraoptic – makes vasopressin
  • Paraventricular – makes oxytocin
  • Lateral area – hunger (if you zap, you shrink laterally)
  • Ventromedial – satiety (if you zap you grown ventrally and medially)
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20
Q

hypothalamus

explian these nuclei

ant, post, suprachiasmatic

A
  • Anterior – cooling (A/C; parasympathetic)
  • Posterior – heating (get fired up; sympathetic)
  • Suprachiasmatic – circadian rhythm (need sleep to be charismatic)
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21
Q

HPA axis

explain it

A
  • Hypothalamus is linked to the pituitary gland via the infundibulum (contains the hypothalamic-hypophyseal tract)
  • Pituitary gland:
    • Anterior (parvocellular pathways) – from oral ectoderm
      • Physiology: hypothalamus synthesizes releasing hormones → sent to median eminence → produces secondary hormones (GH, TSH, PRL, ACTH, FSH/LH) → enters systemic circulation
    • Posterior (magnocellular pathways) – from neural nectoderm
      • Physiology: releases vasopressin and oxytocin synthesized in the hypothalamus
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22
Q

Hypothalamic Lesions

what is it, what happens

A
  • Hypothalamic Lesions (e.g. tumors, trauma)
    • Dysregulation of autonomic and endocrine system, damage to optic tract
    • Example: Hypothalamic hamartoma (benign congenital malformation of ectopic neuronal tissue)
      • Sx: precocious puberty, epilepsy, neurobehavioral sx
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23
Q
A
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24
Q

Pituitary Tumors

A
  • Enlargement may damage regions of hypothalamus
  • Dysregulation of pituitary hormones
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25
Q

Role of Hypothalamus in Eating Behavior

A
  • Lateral hypothalamus (hunger center) – lesion causes anorexia
  • Ventromedial hypothalamus (satiety center) – lesion causes obesity
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26
Q

Arcuate nucleus of hypothalamus

what is this? what does it do?

A
  • Arcuate nucleus of hypothalamus – senses systemic hormones via fenestrated capillary → provides input to lateral and ventromedial hypothalamus
    • Fed: senses leptin (from adipose tissue) and insulin → activates POMC neuron → satiety
    • Fasting: senses ghrelin (from stomach) and fatty acids → activates AgRP/NPY neurons → hunger
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27
Q

what is thirst

A

Thirst is a sensation to maintain body fluid homeostasis via ADH release → promote drinking behavior

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28
Q

Osmometric thirst

pathway

A
  • Pathway: osmolarity change → osmoreceptor neurons and circumventricular organs (SFO and OVLT) activate → neurons to hypothalamus →
    • Activates paraventricular nucleus and supraoptic nucleus → release of ADH
    • Activates median preoptic nucleus → promotes drinking behavior
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29
Q

Volumetric thirst

pathway - what does it activate

A
  • Pathway: hypovolemic state → decreased BP →
    • Activation of RAAS → angiotensin II activates neurons in SFO → neurons to hypothalamus →
      • Activates paraventricular nucleus and supraoptic nucleus → release of ADH
      • Activates median preoptic nucleus → promotes drinking behavior
    • Activation of cardiac and arterial baroreceptors in heart → vagus n. → NTS in medulla → neurons to hypothalamus → median preoptic nucleus → promotes drinking behavior
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30
Q

what is gustation

A

Sensation via: chemical substances → taste receptors → taste buds (made of taste cells)

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31
Q

types of papillae

A
  • Fungiform papillae (anterior 2/3 of tongue)
    • Innervation: chorda tympani n.
  • Circumvallate and foliate papillae (posterior 1/3 of tongue)
    • Innervation: glossopharyngeal n.
32
Q

innervation to the tongue

types of taste cells

neuronal pathway

A
  • Innervation: vagus nerve
  • Types of taste cells: umami, salty, bitter, sour, sweet, fat**
  • Neural pathway: taste cells → NTS @ medulla → VPM nucleus of thalamus → insular cortex – aka primary gustatory cortex → orbitofrontal cortex (OFC) – aka secondary gustatory cortex
33
Q

olfaction

function and pathway

A
  • Functions: enjoying food (flavor), detecting danger (gas leak, spoiled food), recognition (water, alcohol), altering mind/mood (perfume)
    • *Olfactory dysfunction is also one of the earliest clinical features in neurodegenerative diseases (i.e. Parkinsons) and depression
  • Neural pathway: olfactory epithelium → olfactory sensory neuron on olfactory epithelium → olfactory n. → olfactory bulb (ventral brain) → olfactory cortex
    • Only human sense that bypasses the thalamus
34
Q

geniculate vs. extrageniculate pathway

A
  • Geniculate pathway: retinal ganglion cells → optic nerve → optic chiasm → synapse on the lateral geniculate nucleus of thalamus → visual cortex
    • Info: vision
  • Extrageniculate pathway: retinal ganglion cells → optic nerve → optic chiasm → superior colliculus
    • Info: pupillary light reflex, accommodation, sympathetic control of eye
35
Q

what happens in each of these lesions

A
36
Q

blood supply to visual cortex

A

Mainly PCA; MCA has supply to some parts of optic radiations

37
Q

layers of retina

A
  • Outer nuclear layer: contains nuclei of the photoreceptor
  • Inner nuclear layer: contains horizontal cells, bipolar cells, and amacrine cells
  • Ganglion cell layer: contains ganglion cells
38
Q

retinal circuit

A

Retinal circuit: Light –> photoreceptor releases glutamate at a slower rate due to hyperpolarization –> bipolar cell is activated and releases glutamate due to depolarization –> ganglion cell activated –> optic nerve –> optic chiasm –> visual cortex

39
Q

function of

horizontal and amacrine cells

A
  • Horizontal cells: connect postganglionic synapses of photoreceptors to modulate signals based on light (gain control – brightness)
    • Release GABA in order to inhibit activity of photoreceptors and bipolar cells
  • Amacrine cells: connections between neighboring bipolar cells modulating their actions in inhibitor and excitatory pathways
    • Release glycine and GABA in order to modulate bipolar and ganglion cell activity
40
Q

rods and cones

function, chracterisitics and types

A
  • Cones
    • Function: provide color vision via 3 types of opsins and function in bright light (photopic) conditions
      • Red (L – long), Green (M – medium), Blue (S – short)
    • Cones are concentrated in the fovea (center of retina) and have little convergence (one cone activates one bipolar cell) àlow sensitivity, high acuity (detail)
      • Fovea: area of highest detail; only contains red and green cones
  • Rods
    • Function: provide monochromatic vision and function in low light (scotopic) conditions
    • Rods are concentrated in the periphery of the retina and have high convergence (many rods activate one bipolar cell) àhigh sensitivity, low acuity
41
Q

Activation of photoreceptors (Phototransduction)

pathway

A
  • Pathway: opsin containing cis-rhodopsin + light → trans-rhodopsin transformation → transducin (G-protein) activation → Phosphodiesterase production → decrease in cGMP → closure of Na+ channels and K+ efflux → hyperpolarization of cell → decreased release of glutamate → activation of bipolar cells
    • Opposite occurs in off-center rods
42
Q

Light and Dark Adaptation

A

Description: functions to enhance weak signals by increasing neuronal sensitivity, or it decreases neuronal sensitivity of strong signals to prevent saturating and losing information.

43
Q

explain ON and OFF pathways

A
  • Contrast (color, edges, etc) is encoded in these ON and OFF pathways.
    • ON bipolar cells contain mGluR6 receptors and depolarize to light
    • OFF bipolar cell contain ionotropic (Kainate and AMPA) receptors and hyperpolarize to light
  • Rod bipolar cells only synapse with rod photoreceptor, and rods signals are sent to ON and OFF pathways in the inner retina through AII amacrine cells
44
Q

pravocellular and magnocellular streams

A
  • Parvocellular stream (tonic, high contrast and fine grain, small area, color): Cone driven signals.
  • Magnocellular Stream (phasic, respond over larger area): Convergence of rod signals
45
Q

explain color blindness

genetics and types

A
  • Genetics: X-linked recessive
  • Types
    • Anomalous trichromacy (defective three-color vision) – see all three primary colors, but one is weaker
      • Protonomaly (L cone defect – red weak), Deteranomaly (M cone defect – green weak), Tritanomaly (S cone defect – blue weak)
    • Dichromacy (two color vision) – see only two primary color, one is absent
      • Protanopia (L-cone absent – no red), Deutropanopia (M-cone absent – no green), Tritanopia (S-cone absent – no blue)
    • Rod monochromacy (no cones at all – no color)
46
Q

Age-related macular degeneration

wet v dry

A
  • Epidemiology: elderly
  • Pathophysiology: progressive loss/death of photoreceptors in macula → loss of fine visual acuity in macula/fovea
  • Types:
    • Wet (vascular form)
      • Tx: Anti-VEGF therapy (block growth of vessels) – ranibizumab, bevacuzimab, aflibercept
    • Dry (damaged neurons)
      • Tx: implantable miniature telescope (IMT)
47
Q

Retinitis pigmentosa (RP)

A
  • Genetics: AD, AR, X-linked
  • Pathophysiology: loss of rod photoreceptors → loss of night vision → eventual blindness
  • Natural history: presents in childhood, severe disease in adulthood
  • Dx: ERG
48
Q

open vs closed angle glaucoma

A
  • Open-angle glaucoma (angle where the iris meets the cornea is wide – normal): increased production of vitreous humor or blockage of drainage of vitreous humor at trabecular meshwork → increased pressure in the eye → optic nerve is compressed → blindness
  • Closed-angle glaucoma: trauma → decreased angle between iris and cornea → inability to drain vitreous humor effectively → increased pressure → optic nerve is compressed → blindness
49
Q

tx for glaucoma

A
  • Medical:
    • Alpha adrenergic agonists (reduce aqueous humor production and increases outflow)
    • Beta blockers (lowers pressure by reducing production of humor)
    • Carbonic anhydrase inhibitor (eye drops that reduce fluid production in the eye)
    • Miotics (causes the pupil to constrict and increases drainage)
    • Prostaglandin analogs (reduces pressure in the eye by increasing outward flow of fluid
  • Surgery: trabeculoplasty, laser stuff, etc
50
Q

erg

A
  • Electroretinogram (ERG)
    • Mechanism: recording of electric potential created by activity of neurons in the retina when light is flashed
51
Q

CN III Palsy

sx, etiology

A
  • Signs/sx: variable dysfunction of levator palpebrae (drooping eyelid), loss of oculomotor functions (“down and out”)
  • Etiologies: trauma, infection/inflammation, migraine
52
Q

CN III palsy

pupil involving vs sparing

A
  • Pupil-involving:
    • Pathophysiology: aneurysms at PCOM and ICA compress pupillomotor fibers on superficial surface of CNIII
    • Signs/sx: dilated pupil that responds poorly to light (due to loss of PNS)
    • Dx: MRA, CTA, angiography (must be performed)
  • Pupil-sparing:
    • Pathophysiology: microvascular ischemia of CN3 due to diabetes, HTN, hyperlipidemia
    • Signs/sx: pain, may resolve within 3 months
    • Dx: none needed if risk factors align with pathophysiology; pursue if >3 months
53
Q

CN IV Palsy

A

Etiology: congenital, head trauma (CN4 compressed against tentorium cerebelli), microvascular ischemic disease

Signs/sx: hypertropia (HT - one eye is higher than the other) that worsens on contralateral gaze and ipsilateral head tilt, patient will present with head tilt contralateral to side of lesion, diplopia with down-gaze

54
Q

CN VI Palsy

A

Signs/sx: esotropia (eye pointing more inwards) worse on ipsilateral gaze, unable to abduct ipsilateral to lesion

Pathophysiology: microvascular ischemia, elevated ICP, tumor, trauma

55
Q

Internuclear Lesion/Opthalmoplegia: disruption of MLF

etiology, pathways

A
  • Description: lesion named according to the eye with limited adduction; convergence may be spared
  • Medial longitudinal fasciculus (MLF) – connects to abducens nucleus to contralateral oculomotor nucleus → conjugate horizontal movement
    • Description: left lateral eye gaze → contraction of left lateral rectus → firing of left abducens nerve → synapse on right MLF → firing of right CN III nucleus → contraction of right medial rectus → conjugate gaze
  • Etiology: demyelination, stroke
56
Q

CN VII Palsy

pheripheral vs. central

A

Etiology: idiopathic Bell’s palsy, infection, tumor, stroke, demyelination, diabetes, trauma

Signs/sx:

Peripheral: inability to shut affected eye/move forehead; facial droop
Central: forehead and orbicularis m. unaffected due to bilateral innervation of forehead; lower-level facial droop

57
Q

Horner’s Syndrome

etiologies vs. sx

A
  • Etiologies:
    • Adults: compression (tumor, carotid a. dissection, thyroid mass), trauma, stroke/demyelination
    • Children: birth trauma, surgical trauma, neruoblastoma
  • Signs/sx: ptosis (mild), miosis (constriction), anhidrosis (failure of sweat glands)
    • 1storder (medullary): ataxia, nystagmus, hemisensory deficit
    • 2ndorder (superior sulcus): arm pain, cough, hemoptysis, neck swelling
    • 3rdorder: numbness over CN5 distribution and double vision
58
Q

3 ways to diagnosis horners syndrome

what are MOAs

A
  • Topical cocaine drops:
    • MOA: inhibits reuptake of norepi in synaptic cleft → dilation of pupils → pupil that does not dilate is deemed to be affected by Horner’s syndrome
  • Apraclonidine:
    • MOA: weak alpha1 agonist →
      • Normal eyes: no effect
      • Horner’s syndrome eyes: dilation of affected eye more than other eye → reversal of aniscoria (unequal pupils)
  • Hydroxyamphetamine:
    • MOA: enhances release of presynaptic norepi from intact 3rdorder neuron → dilation
      • In Horner’s syndrome:
        • If no effect → lesion of 3rdorder neuron
        • If pupil dilates → lesion is more proximal (1stor 2nd)
59
Q

Relative Pupillary Defect

etiologies, dx

A

Etiologies: traumatic optic neuropathy, ischemic optic neuropathy, glaucoma, retinal detachment (crinkling of retinal tissue), central retinal artery occlusion (cherry red spot)

Dx: Swinging flashlight test

60
Q

Relative Pupillary Defect

afferent vs. efferernt

A
  • Relative Afferent Pupillary Defect:
    • MOA: affected eye does not process light at all and remains dilated → unable to send consensual response to the contralateral eye → contralateral eye also remains dilated
  • Relative Efferent Pupillary Defect:
    • MOA: affected eye processes light, but is unable to constrict itself → sends consensual response to contralateral eye → contralateral eye successfully constricts
61
Q

Optic Nerve Edema

imaging and causes

papilledema

A
  • Imaging: blurred border of optic disc, dilation of capillaries and nerve fibers, hemorrhage
  • Causes: ischemic optic neuropathy, optic neuritis, papilledema
    • Papilledema: mass effect → increased ICP → optic disc edema
      • Etiology: intracranial mass, hydrocephalus, encephalitis, intracranial HTN
62
Q

autonomic system

subdivisions, functions, disorders

A
  • Subdivisions
    • Sympathetic (thoracolumbar)
      • Postganglionic NT: norepinephrine
        • Exception: sweat glands are mediated by ACH
    • Parasympathetic (craniosacral)
      • Postganglionic NT: Acetylcholine (ACH)
    • Enteric NS
  • Functions
    • Regulates/coordinates: BP, HR, RR, Temp, sweating, lacrimation, nasal secretion, pupil size, GI motility, bladder contraction
  • Disorders: Sjogren’s Syndrome, Guillain-Barre Syndrome
63
Q

Shy-Drager Syndrome (type of Parkinson-plus syndrome)

A
  • Description: a form of multi-system atrophy
  • Epidemiology: men in late 50s to early 60s
  • Sx: autonomic dysfunction (ED, bladder dysfunction, abnormal sweating, constipation, sleep disorder), ataxia, parkinsonism
  • Signs: orthostatic hypotension, minimal facial expression
  • Tx: Fludrocortisone (mineralcorticoid àincreases BP), midodrine (stimulant àvasoconstriction), salt tablets, compression stockings
    • L-dopa does not work
64
Q

Postural Orthostatic Tachycardia Syndrome (POTS)

A
  • Description: autonomic failure resulting in orthostatic hypotension and tachycardia when upright
  • Sx: autonomic dysfunction (GI problems), anxiety (increased levels of epi/norepi), hypotension, tachycardia, hypoperfusion (decresed cerebral flow)
  • Complications: vasovagal syncope (fainting due to decreased BP)
    • Rule of B12 deficiency due to similar presentation
  • Tx: lifestyle changes (fluid, no alcohol, salt, caffeine), Fludrocortisone, beta blockers (lowers HR), miodrine, SSRIs/SNRIs, Methylphenidate/Adderall (increase norepi and dopamine)
65
Q

tests available for evaluation of autonomic dysfunction

QSART, TST, HR, BP, vasalva maneuver

A
  • Sudomotor
    • QSART (Quantitative sudomotor axon reflex test): put dye on patient àwatch for color change as they sweat
    • TST (thermoregulatory sweat test): put patient in sauna àmeasure sweat
  • Tests of cardiovagal function
    • Heart rate response to deep breathing (HRDB)
    • Vasalva maneuver (pinching nose shut & forcing exhalation against closed airway)
  • Adrenergic function
    • BP and HR response to head-up tilt
    • Beat to beat BP response to Vasalva and DB
66
Q

Huntington’s Disease

SPEEDCT

A
  • Genetics: autosomal dominant
    • Mutation: due to repeat expansion of CAG in HTT gene (4p16.3)
      • Severity based on number of CAG repeats: >39 (complete penetrance), <36 (normal)
  • Pathophysiology: mutant HTT is unable to be cleaved by capsase 2 àtoxic levels of CAG remain àclump together
  • Testing: PCR (more repeats àbigger fragments àtravel slower)
  • Symptoms:
    • Early: irritable/depressed, subtle loss of intellectual ability, balance issues
    • Late: chorea, seizures, dementia, death (within 18 years of onset)
67
Q

Neurofibromatosis

SPEEDCT

A
  • Description: a group of 3 distinct genetic disorders (NF1, NF2, Schwanomatosis) that cause tumors to grow in the nervous system
  • Genetics: autosomal dominant
    • Mutation: NF1 (tumor suppressor gene – negative regulator of RAS) mutation on 17q11.2
  • Pathophysiology: loss of NF1 àunregulated growth of Schwann cells àneurofibroma or Scwannoma (benign) àmalignant progression
  • Signs: Café au lait spots, neurofibromas, Lisch nodules (in iris of eye), optic nerve tumors, freckling in armpit and groin, epilepsy, bowing of legs
  • Testing: genetic tests, prenatal testing via amniocentesis or chorionic villus sample
68
Q

Alzheimer’s Disease

description, genetics, epidemiology

A
  • Description: neurogenetic disease that results in loss of memory
    • Genetics
      • Amyloid precursor protein (APP) on chromosome 21
      • Presenilin-1, Presenilin-2, ApoLipoprotein E
    • Epidemiology
      • Early onset (age 30-60) is rare: autosomal dominant
      • Late onset (>60) is common: autosomal recessive
69
Q

Alzheimer’s Disease

pathophys

abnormal vs. normal

A

Normal: APP lodges in plasma membrane → secretase-alpha cleaves A-alpha part of cytoplasmic domain → A-alpha becomes important in vital gene transcription

Abnormal: APP lodges in plasma membrane → secretase-beta cleaves A-beta part of cytoplasmic domain → A-beta 42 leaves cells → sticks together

70
Q

stroke

definition and risk factors

A
  • Definition: a sudden onset neurologic deficit from a vascular cause
  • Risk Factors:
    • Non-modifiable: age, gender, race, heredity
    • Modfiable: HTN, atrial fibrillation, dyslipidemia, diabetes, tobacco, carotid stenosis
71
Q

Hemorrhagic stroke

3 types

A
  • Hemorrhagic: vessel rupture leading to intracranial bleeding with progressive onset of deficits accompanies with headaches, nausea, and vomiting
    • Intracranial hemorrhage (ICH)
      • Etiologies: HTN, cerebral amyloid angiopathy, tumors, vascular malformations, traumas
      • Sx: abrupt onset of headache, N/V, neuro sx (based on location)
    • Subarachnoid hemorrhage (SAH)
      • Etiologies: trauma, aneurysm, spontaneous
      • Sx: abrupt onset of worse headache, impaired consciousness, neuro sx (based on location)
    • Subdural hemorrhage is NOT a type of stroke
72
Q

ischemic stroke

ant. and post. circulation

A
  • Ischemic: embolism/thrombosis of a vessel that leads to impaired blood supply of the brain with maximal symptoms at onset
    • Presentation: no pain, neuro sx (based on location of ischemia)
      • Anterior circulation
        • Cortical stroke: aphasia, neglect, gaze preference + subcortical sx (arm >> leg)
        • Subcortical stroke (i.e. internal capsule stroke): weakness, sensory loss, dysarthria, visual loss (face = arm = leg)
      • Posterior circulation:
        • Symptoms: ataxia, vertigo, cranial nerve findings, impaired consciousness, severe dysarthria, visual loss/diplopia
        • Presentation: may be crossed findings due to decussations
          • i.e. Left facial weakness and right arm/leg weakness
73
Q

etiologies of stroke

A
  • Thrombotic: due to atherosclerotic plaques forming on vessel walls
    • Risk factors: HTN, DM, dyslipidemia, smoking
    • Small vessel disease: lacunar arteries near internal capsule
    • Large vessel disease
  • Embolic: due to atrial fibrillation, DVT with associated patent foramen ovale, valvular disease, prosthetic valves
  • Hypoxia: due to hypoperfusion or hypoxia secondary to cardiac surgeries → affects watershed areas (areas most distal to where two major arteries meet)
  • Other/undetermined
    • Other: dissection, hypercoagulable states, vasospasms, vasculitis, paradoxical venous embolism, MoyaMoya, hematological disorders
    • Undetermined: more than two reasons or unknown
74
Q

acute stroke

imaging and labs

initial and later

A
  • Imaging:
    • Initial: non-contrast CT scan (ischemic vs hemorrhagic), echocardiogram
      • CT scan does not show an ischemic stroke early
    • Later: CT/MRI brain, brain/neck angiogram
  • Labs:
    • Initial: blood glucose (stroke presents similarly to hyper/hypoglycemia), pulse ox
    • Later: HgbA1C, lipid panel, CBC, coagulation studies
75
Q

Treatment for ischemic stroke

A
  • Tissue plasminogen activator (tPA) – administer within first 3-4.5 hours to avoid hemorrhagic risk
    • MOA: tPA activates plasminogen → plasminogen cleaved to plasmin → plasmin breaks down fibrin to dissolve clots
    • Contraindications: active bleeding, high risk of bleeding, clotting issues
  • Intra-arterial devices
    • Solitatire stent-retriever, penumbra suction catheter, merci retrieveal device
76
Q

stroke

Prevention strategies

A
  • Prevention strategies (ABCDE): Anti-coagulants (aspirin, warfarin, clopidogrel, -xaban drugs, thrombin inhibitors), BP meds, Cholesterol meds (statins), Diabetes meds, Exercise, Fumar (stop smoking)
    • Also: a-fib meds (heparin) if applicable
77
Q

Stroke rehabilitation

lol.

A
  • Includes: speech therapy (swallowing, language, cognitive function), OT (fine motor and upper extremity coordination), PT (balance and gait, lower extremity coordination)
  • Types
    • Inpatient rehab:
      • Inpatient acute rehab: daily care with services like such as speech therapy, OT, PT (>3 hours)
      • Subacute rehab: nursing facility rehab (<3 hours)
    • Outpatient rehab:
      • Traditional outpatient: a single type of therapy
      • Day program: intense therapy daily until not needed anymore
      • In-home program: must be home-bound to qualify
  • Stroke recovery: everyone recovers to a certain degree, but this is patient-dependent
    • Hyperbolic curve with a plateau
  • Neurological recovery:
    • These conditions benefit from rehab: MS, GBS, MG, TBI
      • Use drugs to complement rehab (i.e. fluoxetine, ACHase inhibitors, dopamine)

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