Trivia Flashcards
1
Q
What is a stroke?
A
An injury to the brain from interrupted blood flow or bleeding. Produces abrupt onset of focal neurological deficits and inc. risk of permanent disability/death
2
Q
What is a TIA?
A
- abrupt focal neurologic deficits that resolve within 1 hour
- warning sign of future stroke
3
Q
What is a silent stroke?
A
- abrupt onset of focal neurological deficits that resolve in more than 1 hour
- structural change
4
Q
What does the MCA supply?
A
primary sensory/motor - arm/face
FEF
Broca/Wernicke
Visual Radiation
5
Q
What do the Lenticulostriate branches of the MCA supply?
A
internal capsule
6
Q
What does the ACA supply?
A
mid-sagittal region - lower extremities
parietal lobe
7
Q
What does the PCA supply?
A
mediate occipital lobe (visual radiations)
Deep - thalamus, hippo, corpus callosum
8
Q
“Go to sleep” switch
A
VLPO: inc. in GABA that inhibits the other 6 arousal nuclei. Induces NREM
9
Q
“REM-On” switch
A
PPT and LDT nuclei (ACh)
10
Q
“REM-Off” switch
A
Locus Ceruleus (NE)
11
Q
Somnogens
A
Adenosine
Cytokines (IL-1b, TNFa)
Melatonin
12
Q
Presentation of a supratentorial tumor in kids
A
localized findings - seizures, hemiparesis
13
Q
Presentation of midline tumors in kids
A
endocrinopathies + hydrocephalus (early AM HA, N/V, Lethargy)
** signs of hydrocephalus in kids: sundown eyes, CN6 palsy, bulging fontanelle
14
Q
Dx of brain tumors
A
MRI > CT > Bone Scan (for mets)
MRI is good for distinguishing tumor,
CT is good for seeing calcification
15
Q
MC pediatric tumors (frequency)
A
astrocytoma > PNET > glioma > ependymoma
16
Q
What is the RAS and what composes it?
A
- areas of the reticular formation that produces coma when damaged
- known to receive collaterals from sensory afferents
- intralaminar thalamic nuclei, midbrain, upper 1/3 of pons
- close to the uncus and tentorium cerebelli
17
Q
Lesion to the upper 1/3 of pons
A
causes coma with intact diencephalon
18
Q
Pontine hemorrhage
A
- causes coma if upper 1/3 of pons (intact vertical gaze but not horizontal gaze, flaccid quadriplegia, pinpoint pupils)
- quadriplegia if lower 1/3 of pons
19
Q
Arousal nuclei (ascending arousal system)
A
- Cholinergic: project to thalamus, inh thalamic firing to promote wakefulness. This is why anticholinergics make you sleepy.
- Monaminergic: project to cortex, inc signal from thalamus. Failure results in delirium.
20
Q
VLPO
A
Sleep promoting center.
Uses GABA and galanin to inhibit the ascending arousal system
- where EtOH and Benzos work
- lesion causes insomnia
21
Q
Narcolepsy
A
- selective loss of orexin neurons in the posteriolateral hypothalamus
- sleep attacks and cataplexy
22
Q
Sleeping sickness
A
- lesion to the region between PAG and VLPO
23
Q
Feedback to the ascending arousal system
A
- from thalamus, limbic system, frontal cortex
- emotional memories
- lesion causes apathy/indifference to stimuli (abulia/akinetic mutism)
24
Q
Transtentorial/uncal Herniation
A
- can be caused by epidural hematoma
- Compresses:
1. CN3 - ptosis/paresis
2. Midbrain - lethargy, stupor, coma
3. Descending motor pathways - contralateral/ipsilateral hemiparesis
4. PCA - Contralateral hemianopia
25
Central herniation
- bilateral subdural hematoma, hepatic encephalopathy
- Causes:
1. Lethargy - P on reticular gray in thalamus
2. small reactive pupils - P on hypothalamus dec. SNS
3. loss of pupil tone - P on EW nucleus in midbrain
4. Cheyne Stokes respiration - apneic w. hyperventilation (call a code)
5. decorticate (flexor) --> decerebrate (extensor)
26
Falcine herniation
- unilateral mass effect pushing brain under falx cerebra
| - compresses ACA --> parasagittal ischemic stroke
27
Major difference between structural and metabolic coma
Structural will cause early loss of pupillary reflex. Will happen much later in metabolic coma.
28
Signs/sx of metabolic encephalopathy
- pupils remain reactive to light until end (except atropine, botulism, glutethemide)
- asterix
- multifocal myoclonus
29
What indicates a poor prognosis for coma?
non traumatic coma: absent pupillary light/corneal reflex by day 3
hypoxic coma: absent motor movements by day 3
30
Presentation/Labs of LMN Dz
```
weakness
atrophy (denervation on EMG)
fasciculations
dec. reflexes
normal sensation
normal nerve conduction velocity
atrophic fibers on biopsy
dec. # motor units
```
31
Progressive bulbar palsy
- similar to ALS presentation
- tongue/palate weakness (muscles innervated by medulla neurons)
- swalowing, phonation problems dominate
32
Progressive Lateral Sclerosis
- similar to ALS presentation but more benign
| - but mainly an UMN Dz
33
Spinal Muscular Atrophy
- anterior horn dz
- AR mutation on Chr 5 in the Survival Motor Neuron Gene (inc. copies = less severe)
1. Infantantile: Werdnig Hoffman (AR, frog leg posture)
2. Juvenile: Wohlfart-Kugelberg Welander (AR, pectoralis and thigh atrophy, arm hyperpronation)
3. Adult Onset SMA (sporadic)
34
How can you differentiate a LMN dz from a myopathy? (esp for Wolfart Kugelberg Welander dz)
- normal CPK means it's not a myopathy
| - EMG shows denervation changes in a LMN Dz
35
Etiology of ALS
- most cases are idiopathic (inc. Glutamate activity)
- MCC of genetic form is Chr 9 C90RF72 Expansion
- familial: AD SOD mutation on Chr 21
- juvenile: Ch 9, 2q33, 15q15, 8q21
- with FTD: Chr 17
36
Pathology of ALS
gross: lack of myelin in CST and loss of anterior horn neurons
microscopic: Bunina bodies, eosinophilic inclusion bodies in anterior horn neurons, and inc. in ubiquitin
37
Presentation of ALS
LMN signs: weakness of distal muscles first, tongue atrophy
UMN signs: weakness, inc. reflexes, etc
**Sensation is normal**
38
Differential for ALS
```
Rule out spondylosis via MRI
MSA
Hereditary Cerebellar Dz ( + ataxia)
Craniocervical tumors
Cervical canal dz
Post-Polio syndrome
Polyglucosan body Dz (biopsy)
Tay Sach ( + ataxia)
Kennedy Dz (gynecomastia, bulbar muscular atrophy)
HyperPTH (look for inc. Ca)
```
39
Basic Rules of phototransduction
1. Cells release NT when depolarized
2. Light hyper polarizes photoreceptors
3. Photoreceptors depolarize horizontal cells
4. Horizontal cells hyper polarize photoreceptors
40
Path of transduction via rods
rods --> alpha ganglion cells --> magnocellular of LGN (layers 1/2) --> 4Calpha of cortex via M Pathway
* *space info to cortex**
- - rods are located peripherally
41
Path of transduction of cones
cones --> beta ganglion cells --> parvocellular of LGN (layers 3-6) --> 4Cbeta of cortex via P pathway
* *form info to cortex**
- - cones are located centrally
42
Diabetic retinopathy
- MCC blindness in working age adults
- lose ALL vision (vs. MD)
- high glucose changes vasculature and neurons (dec. photoreceptors and ganglion cells)
- will see light spots (dec. blood flow), inferior optic disc (damaged blood vessels, edema)
- dec. pericytes, BM thickening, inc. permeability
43
Macular degeneration
- MCC blindness in elderly
- Age is the greatest risk factor
- lose central vision from macular damage
- damage to choroidal vasculature, breaks through RPE, gets to macula and distorts vision
- dry form: Drusen, little vision loss often in one eye
- dry can progress to wet: commonly both eyes
44
What is the difference between trophia and phoria?
Trophia is a devision of visual axes that is always present. Phoria is present only when disrupting fusion (covering one eye).
45
What is the difference between paralytic strabismus and non-paralytic strabismus?
Paralytic: adult, has diplopia but no amblyopia
| Non-paralytic (comitant): early childhood type, has amblyopia but no diplopia (b/c brain suppresses one of the images)
46
What eye muscles are intorters?
SR and SO
47
What eye muscles are extorters?
IR and IO
48
Diplopia
- doubling of vision d/t misalignment of visual axes
- CN paresis, dec. muscle response
- deviation is greatest in the direction of action of weak muscle
- relieved by closing one eye; monocular diplopia goes away with affected eye closed; usually cataracts
49
Complete CN 3 palsy
- no PaNS: non reactive pupil
- eye is down and out w. ptosis (no levator palpebri)
- vertical diplopia
- paresis + HA = PCOMM aneurysm unless proven otherwise
50
Microvascular CN 3 palsy
- PaNS function is intact
- motor paresis is the first sign
- DM and HTN
51
CN 6 Palsy
- eye is in eso position from unopposed MR
- horizontal diplopia
- gaze toward weak side
52
CN 4 Palsy
- vertical/oblique diplopia w. spontaneous head tilt to opposite side
53
First thing to do in ocular history
check visual acuity
54
if change in vision is near/far distance
refractive error
55
transient change in vision in 1 eye
papilledema (seconds)
TIA (5-10 min)
Amourosis Fugax
56
transient change in vision in both eyes
basilar artery insufficiency
57
recurrent scintillating scotoma
migraine
58
vision loss + pain
optic neuritis
acute narrow angle glaucoma
uveitis
endopthalmitis
59
vision loss - pain
cataracts
CRA/CRV occlusion
retinal detachment
60
gradual progressive loss of vision
brain tumor
61
sudden loss of vision in 1 eye
adult - vascular
| young - optic neuritis
62
visual loss but normal pupillary reflex
lesion posterior to LGN
63
abnormal RAPD
lesion to optic nerve, optic chiasm, optic tract anterior to LGN
64
lesion posterior to optic chiasm
homonymous hemianiopsia - field defect in contralateral side of both eyes
Congruous HH: occipital cortex lesion
Incongruous HH: more anterior
65
optic neuritis
- optic nerve dz in young/middle aged pts
- presenting sign of MS
- pt can't see object directly but has to look to the side slightly
- normal or swollen optic disk
- abnormal RAPD in that eye
- types: retrobulbar, papillitis (swollen OD)
- improves in 3 weeks. tx steroids
66
optic disk exam
```
color
contour
circumference
cup size
spontaneous venous pulsations (can be physiologic)
retinal vessels
```
67
pale optic disk and altitude hemianopsia
ischemic optic neuropathy (usually one eye)
68
cherry red macula spot
(ischemic infarct in retina)
| = central retinal artery occlusion
69
large optic cups and glaucoma
optic atrophy
70
Rx that can inc. ICP
tetracyclines
| lithium (psych)
71
chronic open ended glaucoma
- inc. intraocular pressure, damage of optic nerve
- enlarged optic cup, atrophy
- early scomata
- subtle visual field defects
72
Where is high frequency sound localized in the inner ear?
on basilar membrane, near the base of the cochlea
73
Where is low frequency sound localized in the inner ear?
on basilar membrane, near apex of cochlea (helicotrema)
74
Meniere's Dz
- dec. resorption of endolymphatic fluid --> builds up and ruptures membrane --> endolymph and perilymph mix --> change in electrical firing
- Sx: vertigo, sensorineural hearing loss, tinnitus
- audiogram: inc. threshold for low frequencies first
- Tx: low salt diet, diuretics
75
Tympanic membrane rupture
- conductive hearing loss commonly caused by infx or trauma
- size of rupture determines hearing loss
- audiogram: inc. threshold for esp 4000Hz
76
Otosclerosis
- inc. in abnormal bond growth around otic capsule can cause stapes fixation
- conductive hearing loss that can b/c sensorineural
- audiogram: inc. threshold for low frequencies
- Tx: hearing aid or stapedectomy can help
77
Vestibular Schwannoma
- cerebellopontine angle compression that caused hearing loss with corrected vertigo
- CN 8 compression is slow and CNS corrects it
- inc. risk of CN 5 and 7 compression, hydrocephalus, damaged pyramidal tract (crus)
78
Sensorineural vs. conductive hearing loss
- conductive is structural blockage: Weber will lateralize to affected ear and Rinne will show BC > AC
- sensorineural is damage to cochlea or auditory N: Weber lateralizes to normal ear and Rinne is normal BC > AC
79
What can tympanometry be useful for?
diagnosis of otitis media and effusion
80
Can sensorineural hearing loss be d/t damage to brain parenchyma?
not likely b/c redundancy (crossover) of afferents
81
Peripheral vertigo
- More common than central vertigo
- Inner ear etiology (semicircular canal debris, vestibular nerve infx, Meniere)
- positional testing: delayed horizontal nystagmus
82
Central vertigo
- Less common than peripheral vertigo
- Brain stem or cerebellar lesion (stroke affecting vestibular nuclei or posterior fossa tumor)
- directional change of nystagmus, skew deviation, diplopia, dysmetria.
- Positional testing: immediate nystagmus in any direction. May change directions. Focal neuro findings
83
Area supplied by ASA
```
medial lemniscus
lateral CST
caudal medulla (hypoglossal n.)
PPRF/MLF
pontine nuclei
```
84
Area supplied by PICA
```
**lateral medulla**
vestibular nuclei
sympathetics
lateral spinothalamic tract
nucleus ambigus
spinal trigeminal
inferior cerebellar peduncle
```
85
Area supplied by AICA
```
**lateral pons**
vestibular nuclei
sympathetics
spinal trigeminal
cranial nerve nuclei
facial nuclei
cochlear nuclei
middle/inferior cerebellar peduncles
```
86
Infantile spasms
- general onset ped seizure
- pyridoxine dependent, PKU, MSUD, Glutx def, tuberous sclerosis
- 3-7mo
- West syndrome: infantile spasm + hypsarrythmia + developmental arrest/regression
- Flexor spasm + stomach crunch + Lightning attack
- EEG: hypsarrythmia, inc amplitude delta waves, multifocal spikes
- Tx: ACTH, Vigabatrin (Tuberous Sclerosis)
87
Lennox Gastaut
- general onset ped seizure
- 1-8yo
- atypical absence seizure + slow spike and wave (1.5-2.5Hz) EEG + developmental delay
- Tx: Rufinamide, difficult to control, lifelong
88
Childhood Absence Epilepsy (CAE)
- general onset ped seizure
- 4-8yo
- Absence seizures with spike and wave 3Hz pattern
- triggered by hyperventilation
- normal neuro status
- Tx: Ethosuximide, Benign outcome
89
Juvenile Myoclonic Epilepsy
- general onset ped seizure
- adolescents
- Ch 6 hereditary
- precipitated by sleep deprivation, EtOH, stress, photic stimuli
- absence (7-13yo), myoclonic (12-18yo, in AM), tonic clonic (13-20yo)
- consciousness intact
90
Benign Rolandic Epilepsy
- MC benign partial epilepsy in kids
- 4-12 yo w/peak 8-9yo
- nocturnal general tonic-clonic seizures
- facial motor ticks
- EEG: central temporal spikes
- Tx: carbamezapine, valproate, lacosamide
91
Febrile Seizure
- MC childhood seizure 18mo
- absence of intracranial infx, metabolic change, or history of afebrile seizures
- usually simple
- 32% recurrence
- first febrile: don't do EEG, blood studies, imaging, or anticonvulsant therapy
- LP doesn't show CSF pleocytosis
92
Work up of first non febrile seizure
determine if true or psychogenic
- EEG recommended (focal slowing inc. recurrence)
- LP, blood studies, imaging optional
- Tx of first unprovoked dec. risk of 2nd seizure BUT NOT long term remission
93
REM sleep
eye movements, muscle paralysis, inc. HR/BP/RR/T/BMR, vivid dreams, erection
inc. brain activity: amygdala, parahippo gyrus, anterior cingulate cortex
dec. brain activity: frontal cortex, posterior cingulate cortex
94
Arousal pathways/nuclei
ACh - PPT + LDT - arousal beta waves (awake and REM)
NE - Locus ceruleus - wake, some in NREM, not in REM
DA - SN - wakefulness
5HT - Raphe Nuclei - wake, some in NREM, not in REM
H - tubulomammary nuc - wake, some in NREM, not in REM
O/H - lateral hypothalamus - inc. wakefulness
95
Activation of VLPO
inc GABA neurons that inhibit the other 6 arousal nuclei, induce NONREM SLEEP
96
Inhibition of VLPO
unbalanced wakefulness = INSOMNIA
97
REM Sleep Behavior Disorder
- loss of paralysis/atonia in REM sleep
- MC men > 50
- primary: alpha synucleopathy (like PD, PSP, MSA)
- secondary to alc withdrawal, or inc. TCA/SSRI
- Tx: clonazepam
