Week 2 Flashcards
Explain how sound travels through the periphery…
high versus low frequencies
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
explain how sound thravels through the CNS
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
what is Conductive deafness
etiology
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)
what is sensineuronal deafness
pheripheral versus cenetral damage
- 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
Tinnitus
etiology?
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
what are exams for hearing
screening tools?
- 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
tx of hearing loss
Treatments for hearing loss: cochlear implant (captures sound and stimulates cochlear n.), hearing aid (amplifies sound), masking device (white noise generator)
function and antaomy of vestibula system
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.
explain the vestibular pathway
- 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
what is the Vestibular Ocular Reflex (VOR)
fxn, pathway
- 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
explain VOR testing
- 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
what is…
benign paroxysmal positional vertigo
labyrinthitis
vestibular neuronitis
- 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.
what is…
Acoustic neuroma: (or neurolemmoma)
Ménière’s Disease:
- 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.
Nystagmus
Nystagmus: is a vision condition in which the eyes make repetitive, uncontrolled movements
Types: horizontal and vertical (brainstem issue)
peripheral versus central vertigo
etiology and sx
- 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
hearing loss
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
hypothalamus
function (TANHATS) and causes of dysfunction
- 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)
hypothalamus
where is it located
inputs and outputs
- 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
- Areas that are not protected by blood-barrier (i.e organum vasculosum of the lamina terminalis – OVLT, subfornical organ – SFO)
- Outputs: widespread projections to autonomic areas for cardiovascular regulation
hypothalamus
explian these nuclei
supraoptic, paraventricular, lateral, ventromedial
- 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)
hypothalamus
explian these nuclei
ant, post, suprachiasmatic
- Anterior – cooling (A/C; parasympathetic)
- Posterior – heating (get fired up; sympathetic)
- Suprachiasmatic – circadian rhythm (need sleep to be charismatic)
HPA axis
explain it
- 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
- Anterior (parvocellular pathways) – from oral ectoderm
Hypothalamic Lesions
what is it, what happens
- 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
Pituitary Tumors
- Enlargement may damage regions of hypothalamus
- Dysregulation of pituitary hormones
Role of Hypothalamus in Eating Behavior
- Lateral hypothalamus (hunger center) – lesion causes anorexia
- Ventromedial hypothalamus (satiety center) – lesion causes obesity
Arcuate nucleus of hypothalamus
what is this? what does it do?
- 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
what is thirst
Thirst is a sensation to maintain body fluid homeostasis via ADH release → promote drinking behavior
Osmometric thirst
pathway
- 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
Volumetric thirst
pathway - what does it activate
- 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
- Activation of RAAS → angiotensin II activates neurons in SFO → neurons to hypothalamus →
what is gustation
Sensation via: chemical substances → taste receptors → taste buds (made of taste cells)
types of papillae
- Fungiform papillae (anterior 2/3 of tongue)
- Innervation: chorda tympani n.
- Circumvallate and foliate papillae (posterior 1/3 of tongue)
- Innervation: glossopharyngeal n.
innervation to the tongue
types of taste cells
neuronal pathway
- 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
olfaction
function and pathway
- 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
geniculate vs. extrageniculate pathway
- 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
what happens in each of these lesions
blood supply to visual cortex
Mainly PCA; MCA has supply to some parts of optic radiations
layers of retina
- 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
retinal circuit
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
function of
horizontal and amacrine cells
- 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
rods and cones
function, chracterisitics and types
- 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
- Function: provide color vision via 3 types of opsins and function in bright light (photopic) conditions
- 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
Activation of photoreceptors (Phototransduction)
pathway
- 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
Light and Dark Adaptation
Description: functions to enhance weak signals by increasing neuronal sensitivity, or it decreases neuronal sensitivity of strong signals to prevent saturating and losing information.
explain ON and OFF pathways
- 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
pravocellular and magnocellular streams
- 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
explain color blindness
genetics and types
- 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)
- Anomalous trichromacy (defective three-color vision) – see all three primary colors, but one is weaker
Age-related macular degeneration
wet v dry
- 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)
- Wet (vascular form)
Retinitis pigmentosa (RP)
- 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
open vs closed angle glaucoma
- 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
tx for glaucoma
- 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
erg
- Electroretinogram (ERG)
- Mechanism: recording of electric potential created by activity of neurons in the retina when light is flashed
CN III Palsy
sx, etiology
- Signs/sx: variable dysfunction of levator palpebrae (drooping eyelid), loss of oculomotor functions (“down and out”)
- Etiologies: trauma, infection/inflammation, migraine
CN III palsy
pupil involving vs sparing
- 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
CN IV Palsy
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
CN VI Palsy
Signs/sx: esotropia (eye pointing more inwards) worse on ipsilateral gaze, unable to abduct ipsilateral to lesion
Pathophysiology: microvascular ischemia, elevated ICP, tumor, trauma
Internuclear Lesion/Opthalmoplegia: disruption of MLF
etiology, pathways
- 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
CN VII Palsy
pheripheral vs. central
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
Horner’s Syndrome
etiologies vs. sx
- 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
3 ways to diagnosis horners syndrome
what are MOAs
- 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)
- MOA: weak alpha1 agonist →
- 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)
- In Horner’s syndrome:
- MOA: enhances release of presynaptic norepi from intact 3rdorder neuron → dilation
Relative Pupillary Defect
etiologies, dx
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
Relative Pupillary Defect
afferent vs. efferernt
- 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
Optic Nerve Edema
imaging and causes
papilledema
- 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
- Papilledema: mass effect → increased ICP → optic disc edema
autonomic system
subdivisions, functions, disorders
- Subdivisions
- Sympathetic (thoracolumbar)
- Postganglionic NT: norepinephrine
- Exception: sweat glands are mediated by ACH
- Postganglionic NT: norepinephrine
- Parasympathetic (craniosacral)
- Postganglionic NT: Acetylcholine (ACH)
- Enteric NS
- Sympathetic (thoracolumbar)
- Functions
- Regulates/coordinates: BP, HR, RR, Temp, sweating, lacrimation, nasal secretion, pupil size, GI motility, bladder contraction
- Disorders: Sjogren’s Syndrome, Guillain-Barre Syndrome
Shy-Drager Syndrome (type of Parkinson-plus syndrome)
- 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
Postural Orthostatic Tachycardia Syndrome (POTS)
- 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)
tests available for evaluation of autonomic dysfunction
QSART, TST, HR, BP, vasalva maneuver
- 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
Huntington’s Disease
SPEEDCT
- 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)
- Mutation: due to repeat expansion of CAG in HTT gene (4p16.3)
- 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)
Neurofibromatosis
SPEEDCT
- 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
Alzheimer’s Disease
description, genetics, epidemiology
- 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
- Genetics
Alzheimer’s Disease
pathophys
abnormal vs. normal
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
stroke
definition and risk factors
- 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
Hemorrhagic stroke
3 types
- 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
- Intracranial hemorrhage (ICH)
ischemic stroke
ant. and post. circulation
- 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
- Anterior circulation
- Presentation: no pain, neuro sx (based on location of ischemia)
etiologies of stroke
- 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
acute stroke
imaging and labs
initial and later
- 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
- Initial: non-contrast CT scan (ischemic vs hemorrhagic), echocardiogram
- Labs:
- Initial: blood glucose (stroke presents similarly to hyper/hypoglycemia), pulse ox
- Later: HgbA1C, lipid panel, CBC, coagulation studies
Treatment for ischemic stroke
- 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
stroke
Prevention strategies
- 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
Stroke rehabilitation
lol.
- 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
- Inpatient rehab:
- 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)
- These conditions benefit from rehab: MS, GBS, MG, TBI
