Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Question Bank > Neuro > Flashcards

Neuro Flashcards

1
Q

Side effects of haloperidol 4 days after therapy

A

acute dystonia (muscle spasm, stiffness, oculogyric crisis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Contracted infection from Central America and died, bx found elongated eosinophilic intracytoplasmic inclusion in pyramidal neurons of hippocampus and Purkinje neurons of cerebellum. What infection?

A

Rabies encephalitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What hypothalamic nucleus controls circadian rhythm?

A

Suprachiasmatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Urinary incontinence following delivery. What nerve roots?

A

S3-4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What passes thru foramen ovale?

A

V3 -> so interferes with mandible stuff (incl motor - muscles of mastication)
Lesser petrosal nerve
Accessory meningeal artery
Emissary veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What passes thru foramen rotundum?

A

V2 -> so interferes with zygomatic stuff

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What passes thru superior orbital fissure?

A

V1 (along with ophthalmic vein, sympa fibers, and all the eye movement nerves - 3,4,6)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What passes thru optic canal?

A

II, ophthalmic artery, central retinal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What passes thru foramen spinosum?

A

Middle meningeal artery and vein

Recurrent (meningeal) branch of V3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What passes thru internal auditory meatus?

A

7 and 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What passes thru jugular foramen?

A

Jugular vein and CNs going to tongue, neck and below (9,10,11)
Inf. petrosal and sigmoid sinuses
Post. meningeal artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What passes thru foramen magnum?

A

Veterbral arteries, brain stem, spinal roots of 11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pt w/ lung mass presented w/ cerebellar sx and bx shows Purkinje cell degeneration. What process mediates the neurologic condition?

A

Autoimmune
Subacute cerebellar degeneration is a paraneoplastic syndrome of small cell lung cancer, it’s mediated by Anti-Yo, Anti-P/Q, Anti-Hu antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What’s the concerning side effect of bupropion?

A

Seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Dx of presenting one day after starting tx for severe agitation&aggressive behaviors w/ fever, confusion, and muscle rigidity

A

NMS associated w/ haloperidol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does pramipexole do for Parkinson?

A

Stimulates dopamine receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Used fluorinated inhaled anesthetic (isoflurane). What parameters are increased during anesthesia? What parameters are decreased?

A

Increase: cerebral blood flow (almost all volatile anesthetics decrease vascular resistance in brain -> undesirable because it leads to increased intracranial pressure), renal vascular resistance, atrial and ventricular pressure
Decrease: CO (so causes hypotension), hepatic blood flow, tidal volume and minute ventilation (so causes hypercapnia), GFR, renal plasma flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe thalamic syndrome

A

Total sensory loss on contralateral body and face (VPL and VPM damaged)
No motor deficits but might get unsteady gaits/falls bc of loss of proprioception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What would you find on autopsy of a lacunar infarct? What are risk factors?

A

Arteriolar sclerosis (risk factors are uncontrolled HTN and DM), 2 forms

1) lipohyalinosis 2ndary to uncontrolled HTN -> might see mural foam cells, fibrinoid wall necrosis, loss of normal vessel architecture
2) microatheromas see lipid-laden macrophages in intimal layer of vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Common cause of cerebral infarction secondary to embolism?

A

Mitral valve disease and carotid atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What would you see in a CNS lesion of MS? What would you see in CSF?

A

Periventricular, pink plaque-like lesions in the white matter tracts (oligodendrocyte apoptosis); astrocyte proliferation (response to injury)
CSF sees increased IgG (found as an oligoclonal band on protein electrophoresis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

AIDs-related meningitis w/ positive latex agglutination test. What’s the characteristic of offending org?

A

Budding yeast (cryptococcus neoformans)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Pure motor stroke (hemiparesis). Damage to what structure?

A

Pos limb of internal capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Pure sensory stroke. Damage to what structure?

A

VPL and VPM of thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Stroke causing ataxia-hemiplegia syndrome. Damage to what structure?

A

Base of pons (ant. pons)

Sx are contralateral (ataxia too, b/c it affects pontocerebellar fibers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Stroke causing dysarthria-clumsy hand syndrome. Damage to what structure?

A

Base of pons or genu of internal capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

See caudate atrophy in what disease?

A

Huntington

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What tract is in genu of internal capsule?

A

Corticobulbar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What tract is in anterior limb of internal capsule? What structures does it separate?

A

Thalamocortical

This limb separates caudate nucleus from globus pallidus&putamen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What tracts are in posterior limb of internal capsule?

A

Corticospinal motor
Somatic sensory fibers
Visual fibers
Auditory fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What 2 things does insula cortex do?

A 
Limbic system (emotion)
Coordination of autonomic fx, esp in cardiac system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What structure do beta blockers affect in the tx of glaucoma?

A

Ciliary epithelium -> decrease aq humor synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What structure does acetazolamide affect in the tx of glaucoma?

A

Ciliary epithelium -> decrease aq humor synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What structure do direct cholinomimetics (pilocarpine and carbachol) affect in the tx of glaucoma?

A

Contract IRIS SPHINCTER and thus open trabecular meshwork

DIRECT cholinomimetics affect structures that are more in front

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What structures do indirect cholinomimetics (AChEi) affect in the tx of glaucoma?

A

Contract CILIARY MUSCLE and thus make the lens more convex

INDIRECT cholinomimetics affect structures that are farther in the back

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Treatment (acute and prophylaxis) of status epilepticus & their mechanisms

A

Acute: lorazepam (increases frequency of Cl- opening -> facilitates GABA-A actions)
Prophylaxis: phenytoin (decreases Na+ currents in cortical neurons)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What ion channels do fish toxins (like puffer fish) affect?

A

Na+ channels (preventing AP or keeping it open to cause persistent depol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Pt returned from Mexico where she underwent cholecystectomy w/ no complications a week back. Now presenting w/ fever, fatigue, nausea, anorexia, rash; died 2 days later. Autopsy shows shrunken liver. What happened? What labs abnormalities would be expected?

A

Probably acute hepatitis from inhaled anesthetics, specifically halothane. Hypersensitivity rxn.
Microscopically will look like viral hepatitis (widespread centrilobular necrosis and inflamed portal tracts & parenchyma)
Labs will show elevated PT (b/c factor VII has the shortest HL of coagulant factors), elevated serum aminotransferase levels, leukocytosis, eosinophilia
WONT see any sign of chronic liver damage like palmar erythema, ascites, decreased albumin, splenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What kind of corpuscle is Meissner and what does it sense?

A

Cyclone-looking
“Meissner” sounds like the name of a smooth guy -> he’s muscular and sharp (large and adapts quickly) and his skin is smooth (found on hairless areas). He travels places (for dynamic touch).
Large myelinated fibers that adapt quickly. In dermal papillae (dermis) of hairless (glabrous) skin
Senses dynamic fine/light touch and position sense

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What kind of corpuscle is Pacinian and what does it sense?

A

“Pacinian” for pressure which is deep down under skin
Large myelinated fibers that adapt quickly. In hypodermis, ligaments, joints
Senses pressure and vibration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What kind of corpuscle is Merkel disc and what does it sense?

A

“Merkel” is harsh sounding (compared to Meissner) -> so think of a guy who’s large and dumb (adapts slowly) w/ lots of hair (found in hairy areas) who stays at the same rural area he was born in (static touch)
Large myelinated fibers that adapt slowly. In basal epidermis and hair follicles.
Senses deep static touch (shapes & edges), pressure, position sense -> kind of a combo of Meissner and Pacinian

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Name and give characteristics of 2 types of free nerve endings

A

1) C - slow, unmyelinated fibers
2) A-delta - fast, myelinated fibers
Both sense pain and temp and are found in skin, epidermis, some viscera

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Where is locus ceruleus and what neurotransmitter does it make? What are the 2 disease associations?

A

Pons
NE
Increased in anxiety
Decreased in depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Where are ventral tegmentum & substantia nigra compacta. And what neurotransmitter do they make? What are the 3 disease associations?

A

Midbrain
Dopamine
Increased in Huntington
Decreased in Parkinson (characteristic) and depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Where is raphe nucleus and what neurotransmitter does it make? What are the 3 disease associations?

A

Pons, medulla, midbrain
5-HT
Decreased in Parkinson, anxiety and depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Where is basal nucleus of Meynert and what neurotransmitter does it make? What are the 3 disease associations?

A

Basal forebrain
ACh
Increased in Parkinson
Decreased in Alzheimer (characteristics) and Huntington

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Where is nucleus accumbens and what neurotransmitter does it make? What are the 2 disease associations?

A

Basal forebrain
GABA
Decreased in anxiety and Huntington

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What waveforms are assc. w/ awake (eyes open and eyes closed)?

A

Eyes open: beta (same wave as REM) - highest freq and lowest amp
Eyes close: alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is N1 sleep and what waveform is assc. w/ it?

A

Light sleep

Theta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is N2 sleep and what waveforms are assc. w/ it?

A

Deeper sleep, longest of NREM; gets bruxism

Sleep spindles and K complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is N3 sleep and what waveform is assc. w/ it?

A

Deepest NREM; gets sleep walking, night terrors, bed wetting

Delta - lowest freq and highest amp -> alcohol, benzo and barbiturates shortens this phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What waveform is assc w/ REM sleep?

A

Beta (same wave as awake w/ eyes open) - highest freq and lowest amp
NE, alcohol, benzo and barbiturates shortens REM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What cerebellar peduncle mediates contralateral input from cortex?

A

MCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What cerebellar peduncle mediates ipsilateral input from spinal cord?

A

ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What cerebellar peduncle mediates output from contralateral cortex?

A

SCP

But crosses again before UMN, so output ends up being IPSILATERAL to the commanding CORTEX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What movement disorder are beta blockers used for?

A

Essential tremor - most common movement disorder, AD (so familial) -> sx improved w/ alcohol consumption, worsened w/ particular posture like when holding objects, as opposed to at rest like Parkinson

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Spatial neglect. Where’s the lesion?

A

Right parietal-temporal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Agraphia, acalculia, finger agnosia, left-right disorientation. Where’s the lesion?

A

Left parietal-temporal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Truncal ataxia + dysarthria (define). Where’s the lesion?

A

Cerebellar vermis

Dysarthria = motor inability to speak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

PPRF lesion. What happen to eyes?

A

Look away from lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

FEF lesion. What happen to eyes?

A

Look toward side of lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Lesion above rostral midbrain. What’s the posture?

A

Decorticate - elbows flexed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Lesion below rostral midbrain. What’s the posture?

A

Decerebrate - elbows extended

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Lesion to arcuate fasciculus (left sup temporal lobe and/or left supramarginal gyrus). What happens to fluency, comprehension, repetition?

A

This is conduction aphasia
Fluent speech
Good comprehension
Poor repetition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Transcortical motor aphasia. What happens to fluency, comprehension, repetition?

A

Non fluent speech
Good comprehension
Good repetition (signature of transcortical aphasia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Transcortical sensory aphasia. What happens to fluency, comprehension, repetition?

A

Fluent speech
Poor comprehension
Good repetition (signature of transcortical aphasia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Mixed transcortical aphasia. What happens to fluency, comprehension, repetition?

A

Non fluent speech
Poor comprehension
Good repetition (signature of transcortical aphasia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What’s the difference between hemiparesis and hemiplegia?

A

Hemiparesis - weakness
Hemiplegia - complete paralysis
A spectrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are the defects in medial medullary syndrome and what vessel is responsible?

A

Defects: most distinctive is tongue deviation to affected side
Also have contralat hemiparesis&proprioception of all limbs
Paramedian branches of ASA (ant spinal artery, comes off of vertebral arteries) and vertebral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the defects in lateral medullary syndrome and what vessel is responsible?

A

Defects: most distinctive is dysphagia & hoarseness (from nucleus ambiguus)
Also have decreased pain&temp from contralat body but ipsilat face, ipsilat Horner, ataxia, dysmetria (ICP)
PICA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the defects in lateral pontine syndrome and what vessel is responsible?

A

Defects: most distinctive is face PARALYSIS
Also have other face defects and decreased hearing, ipsilat Horner, ataxia, dysmetria (MCP and ICP)
AICA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are 3 ways to get locked-in syndrome?

A

CPM (rapid correction of hyponatremia)
Basillar artery stroke
Pontine hemorrhage or tumor
Can still blink and have preserved consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Aneurysm rupture in PCom. What’s the most distinctive defect?

A

CN III pasy (eye down and out, ptosis, pupil dilation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Hx of stroke, now have numbness and tingling followed b allodynia and dysaesthesia. Where’s the lesion

A

Thalamus

“Central post-stroke syndrome”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Cerebral stroke resulting in one of the sx being urinary incontinence. What’s the area involved and what artery is responsible?

A

Mesial frontal lobe and cigulate gyrus -> micturition center

ACA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What brain structure does Wilson’s disease like?

A

Putamen (cystic degeneration)

Other basal ganglia structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Give 3 types of common focal dystonias (sustained contractions)

A

Spasmodic torticollis
Blepharospasm (eyelids)
Writer’s camp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Give 4 examples of myoclonus (brief contractions)

A

Common: hiccups, hypnic jerk (when falling asleep)
Pathologic: epilepsy and Creutzfeldt-Jakob

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Paralysis of upward gaze & convergence. What’s the syndrome and where’s the lesion?

A 
Parinaud syndrome (dorsal midbrain syndrome)
Compression of the tectal area of midbrain (such as by pineal germinoma) -> upward gaze paralysis is from compression on CN III and IV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Give 3 main findings of pineal germinoma

A 
Parinaud syndrome (from compressing tectal area of midbrain -> paralysis of upward gaze & convergence)
Precocious puberty (from b-HCG secretion)
Obstructive hydrocephalus (aqueductal compression)

Germinoma is the most common tumor of pineal gland, similar histologically to testicular seminoma. It’s a tumor “above diaphragma sellae.”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Where’s CTZ (chemoreceptor trigger zone)?

A

Area postrema, which lies in the dorsal surface of the medulla at the caudal end of 4th ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

5 steps in the timeline of neuronal ischemic injury?

A

12-48 hrs: red neurons (eosinophilic cyto, pyknotic nuclei, loss of Nissl)
1-3 days: necrosis + neutrophils
3-5 days: microglia (cells that stain + for lipids -> eat myelin breakdown products)
1-2 wks: reactive gliosis (periphery) & vascular proliferation (liquefactive necrosis 1 wk-1 mo)
> 2 wks: glial scar (cystic area surrounded by gliosis by > 1 mo)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Name 4 sx of narcolepsy besides excessive daytime sleepiness

A

Sleep attack
Hallucinations (hypnagogic, hypnopompic)
Cataplexy
Sleep paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Most common cause of blindness in ppl over 50 yo

A

Macular degeneration -> leading to central scotoma (discrete area of impairment surrounded by normal vision)
2 types: dry (deposition of fatty tissue “drusen” behind retina) and wet (neovascularization of the retina)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Why is visual acuity in macula (esp fovea) greater than any other areas in the retina?

A

Because one macular cone only synapses to one bipolar cell, which only synapses to one ganglion cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What’s one way you can get binasal hemianopsia?

A

Calcified carotid arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Differences between complications of congenital hydrocephalus and acquired hydrocephalus?

A

Congenital: UMN signs (hyperreflexia, muscle hypertonicity), irritability, poor feeding, macrocephaly
Acquired: infection, tumor, SAH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What 3 other things do you get with CN VII palsy besides facial paralysis?

A

Loss of taste in anterior 2/3 of tongue
Hyperacusis (over-sensitivity to certain frequencies and volume ranges) -> from stapedius paralysis
Decreased tearing/lacrimation (VII innervates lacrimal, submandibular, and sublingual glands)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Where is meningioma commonly found? What’s the cell of origin and what do you see under microscope?

A

Attached to dura on lateral hemispheric fissure or parasagittal aspect of brain convexity (so incl sphenoid wing and olfactory groove -> suspect if present w/ headache and anosmia)
Arise from arachnoid villi
See whorled pattern and psammoma bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

6 sx of ammonia intoxication and mechanism?

A

Tremor (asterixis), speech slurring, somnolence, vomiting, cerebral edema, vision blurring
From excess NH4+ depleting alpha ketoglutarate -> inhibition of TCA cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What do you find on autopsy in people w/ Wernicke encephalopathy?

A

Foci of hemorrhage and necrosis in mamillary bodies and periaqueductal gray matter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

4 common sx that MS pts usually present w/? What makes these sx worse?

A

Optic neuritis & pain w/ eye movement, INTERNUCLEAR OPHTHALMOPLEGIA (MLF lesion), sensory deficits (incl bladder and bowel dysfx), cerebellar dysfx
Worsened w/ heat (like getting out of hot shower or after intense exercise) bc of decreased axonal transmission assc w/ heat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What’s amaurosis fugax and what context do you get it?

A

Transient monocular blindness

See this in TIA (< 24 hrs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

3 dopaminergic pathways and assc. disease?

A
  1. mesolimbic-mesocortical -> regulates behavior -> assc. w/ schizophrenia (overactive)
  2. nigrostriatal -> coordination of voluntary movement -> assc. w/ Parkinson
  3. Tuberoinfundibular -> control of prolactin secretion -> hyperprolactinemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

“spongiform transformation of cerebral cortex”?

A

Creutzfeldt-Jakob

vacuoles in gray matter w/ no inflammatory changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

3 progression of neurologic measles

A

W/in days: encephalitis
W/in weeks: acute disseminated encephalomyelitis
W/in years: subacute sclerosing panencephalitis (oligoclonal bands of measles Ab found in CSF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

“brain bx w/ focal demyelinated plaques w/ relative axonal sparing”?

A

MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Dx of gait dysfx + executive fx loss + vertical gaze palsy

A

Progressive supranuclear palsy -> a form of parkinsonism from degeneration of midbrain and subcortical white matter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Ear innervations?

A

Posterior auditory canal: vagal n (small auricular branch) -> so pressing too hard can result in vasovagal syncope
Remainder of external auditory canal: V3 (auriculotemporal branch)
Inner surface of tympanic membrane & ET: glossopharyngeal n (tympanic branch)
Middle ear: facial n. -> innervates stapedius m. (so bell’s palsy will include hyperacusis and ear pain); V3 -> innervates tensor tympani m. (dampening sound transmission)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Stabbing (lancinating) pain + paresthesias + ataxia esp in the dark + areflexia + positive Romberg + loss of bladder fx. Where’s the damage?

A

Damage to dorsal columns of spinal cord (precipitated by damage to nerves in dorsal roots -> 2ndary demyelination & loss of axon w/in dorsal columns) -> suspect tabes dorsalis
Ataxia prevails in the dark b/c loss of proprioception is usually compensated for by visual cues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

3 synapses in the pupilary light reflex pathway?

A

CNII -> 1st synapse in pretectal nucleus (level of sup. colliculus) -> 2nd synapse bilaterally in Edinger-Westphal nucleus (same level) -> CN III (same level) -> 3rd synapse in ciliary ganglion -> miosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Developmental milestones in 12-mo (gross motor, fine motor, language, social/cognitive)

A

Gross motor: stands, walks first steps, throws ball
Fine motor: PINCER GRASP
Language: 1st word
Social/cognitive: separation anxiety, follows 1-step command w/ gesture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Developmental milestones in 18-mo (gross motor, fine motor, language, social/cognitive)

A

Gross motor: runs, kicks ball
Fine motor: remove clothing
Language: 10-25 words
Social/cognitive: pretend play, understands “mine”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Developmental milestones in 2-yo (gross motor, fine motor, language, social/cognitive)

A

Gross motor: jump
Fine motor: copies a LINE, turn pages
Language: 2-word phrases
Social/cognitive: PARALLEL PLAY, toilet-training begins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Developmental milestones in 3-yo (gross motor, fine motor, language, social/cognitive)

A

Gross motor: tricycle
Fine motor: copies a CIRCLE, uses UTELSILS
Language: 3-word phrases
Social/cognitive: IMAGINATIVE PLAY, knows age/gender

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Developmental milestones in 4-yo (gross motor, fine motor, language, social/cognitive)

A

Gross motor: balances/hops on 1 foot
Fine motor: copies a SQUARE
Language: 100% intelligible speech
Social/cognitive: COOPERATIVE PLAY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Developmental milestones in 5-yo (gross motor, fine motor, language, social/cognitive)

A

Gross motor: skips, walks backward
Fine motor: copies a TRIANGLE, dressing/bathing, prints letters
Language: 5-word sentences, counts to 10
Social/cognitive: friends, completes toilet-training

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Cause of rapid plasma decay of barbiturates?

A

Tissue redistribution

NOT metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Cell composition of choroid plexus?

A

Outgrowths of pia mater capillaries (fenestrated) covered by ependymal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What’s pseudomotor cerebri and what’s the pt population?

A

Elevated ICP -> unknown etiology but thought to be related to cerebral venous outflow abnormalities
Classically occurs in young overweight women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

DD for childhood tumor in cerebellum?

A

Most common benign (and overall): pilocytic astrocytomas -> cystic w/ tumor nodule protruding from wall -> see Rosenthal fibers too
Most common malignant (and 2nd most common overall): medulloblastoma -> solid and most commonly in vermis -> sheets of small blue cells w/ scant cyto

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Rosettes in childhood tumor?

A

Ependymomas
Rosettes: gland-like structures
Present w/ hydrocephalus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Location of glioblastoma multiforme? Histological features?

A

W/in hemispheres (frontal, temporal, or near basal ganglia) -> ring-enhancing lesion, might cross midline
Histology: pseudopalisading necrosis w/ vascular proliferation (hemorrhage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What does oligodendroma look like? Pt population?

A

Well-circumscribed gray masses in white matter of frontal lobe, might have calcifications (NO necrosis or hemorrhage typically)
40-50 yo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What is atrophy of hippocampus and temporoparietal lobes suggestive of?

A

Alzheimer’s (also diffuse brain atrophy too)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

3 most common cause of SICH (spontaneous intracranial hemorrhage) in young adults?

A
  1. AVM (might lead to SAH)
  2. ruptured cerebral aneurysms
  3. abuse of sympathomimetic drugs (ie cocaine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What heart condition is assc. w/ ruptured cerebral aneuryms?

A

Coarctation of the aorta -> assc. w/ berry aneurysms of the circle of willis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What are pts w/ adult-type coarctation of the aorta commonly die of?

A

HTN-assc. complications -> LV failure, ruptured dissecting aortic aneuryms, intracranial hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Resulting defect from lesion in optic nerve? Optic tract? Lateral geniculate body? Meyer’s loop? Parietal lobe? Visual cortex?

A

Optic nerve: ipsi loss of vision + abnormal pupillary light reflex (afferent limb defect)
Optic tract (meaning after chiasm): contralat homonymous hemianopia + abnormal pupillary light reflex (afferent limb defect)
Lateral geniculate body & optic radiation: contralat homonymous hemianopia w/out reflex abnormality
Meyer’s loop: contralat UPPER homonymous quadrantic anopia (pie in the sky)
Dorsal optic radiation (parietal lobe): contralat LOWER homonymous quadrantic anopia
Visual cortex: contralat homonymous hemianopia w/ macular sparing w/out reflex abnormality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What 4 structures does optic tract project to?

A

Lateral geniculate nucleus: for seeing
Pretectal nucleus: for light reflex
Sup. colliculus: for reflex gaze
Suprachiasmatic nucleus: for circadian rhythms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Defect from lesion in the frontal eye field?

A

Eye deviate toward the lesion (b/c the other FEF predominates)
(right FEF generates conjugate gaze to the left, left FEF generates conjugate gaze to the right)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Infant born to mother who lives on the street and has little prenatal care. Presenting w/ shrill crying, tremor, mydriasis, rhinorrhea, sneezing, diarrhea, and maybe seizure. What should you suspect? How long after birth does it present? What’s the tx?

A

Neonatal opioid withdrawal
24-48 hrs after birth
Fix w/ tincture of opium or paregoric (not preferred due to potentially toxic ingredients)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What is lower level of hypocretin-1 in CSF + shortened REM latency diagnostic of?

A

Narcolepsy -> they enter REM almost immediately (why get hypnagogic/hypnapompic hallucinations)
Hypocretin-1 is secreted from neurons in lateral hypothalamus and is involved in maintaining wakefulness

124
Q

What does axonal rxn look like? And how long after injury does it occur? What happens at day 12 of injury?

A

Cell body swollen and rounded, nucleus displaced to periphery, Nissl substance dispersed throughout cyto (central chromatolysis) -> NOT a sign of irreversible neuronal injury (which is shrinkage and red neuron)
Happens 24-48 hrs after injury
Day 12: increased protein synthesis to regenerate severed axon

125
Q

What neuronal changes do you expect to see in degenerative diseases?

A

Reactive glial changes

126
Q

What’s an on-off phenomenon?

A

Parkinson pts develop unpredictable response to levodopa w/ long-term use -> this is b/c of niagrostriatal degeneration -> decreased therapeutic window for levodopa -> small changes in level results in motor fluctuations (dyskinesia w/ elevation, rigidity w/ decrease) -> might be to the point where fluctuations develop independently

127
Q

Likely dx of calcified cystic brain mass w/ thick brownish fluid composed of cholesterol? What will you see histologically?

A

Craniopharyngioma

Lined by stratified squamous epi, might see keratin pearls

128
Q

Which spinal cord level can you find lateral horns? And what do they contain?

A

Thoracic & early lumbar level (T1-L2)

They are made up of sympathetic preganglionic neurons (intermediolateral nucleus)

129
Q

4 assc. of Friedreich ataxia?

A 
Predominantly spinal ataxia (dorsal column degeneration also means loss of position and vibration sense)
Hypertrophic cardiomyopathy
Kyphoscoliosis
DM
Foot abnormalities
130
Q

What sx is the central side effect of levodopa and thus cannot be solved w/ carbidopa?

A

Anxiety, agitation -> if get this, reduce dose or use clozapine/atypical antipsychotics to help

131
Q

What’s prescribed for insomnia that also has anxiolytic, anticonvulsant, and muscle relaxant effects on top of sedative/hypnotic effects?

A

Benzodiazepine
NOT barbiturates, which are similar but not commonly prescribed for insomnia + have hangover effects following hypnotic doses

132
Q

2 ways to get CN III palsy?

A

Compression by aneurysm in PComm, PCA, superior cerebellar artery, or uncal herniation
Nerve ischemia assc. w/ DM

133
Q

Cyst formation and rare mitosis on brain bx. What is this called? What’s the usual location and complication?

A

Colloid cyst
Usually 3rd ventricle
Can cause obstructive hydrocephalus

134
Q

Reticulin deposits + chronic inflammatory infiltrates on brain bx. What is this called? What’s the pt population?

A

Pleomorphic xanthoastrocytoma

Children

135
Q

Which intrinsic tongue muscle is innervated by vagus instead of hypoglossal?

A

Palatoglossus m.

136
Q

Most common cause of aseptic meningitis?

A

Enterovirus -> coxsackie, echo, polio -> they’re called enterovirus b/c of their fecal-oral transmission, NOT b/c they cause gastroenteritis (they don’t)

137
Q

Sx of poliomyelitis aseptic meningitis?

A

Classic sx of meningitis in general: fever, headache, photophobia, painful ocular movements
Additional sx characteristics of polio: asymmetric paralysis from damage to ant. horn LMN cell bodies

138
Q

What drug do you use for SAH?

A

Dihydropyridine CCB! (Rupture of aneurysm assc. w/ vasospasm is the problem -> clue is someone w/ polycystic kidney disease & focal neurological deficits)
NOT mannitol -> this is for ICP not SAH

139
Q

Afferent limb of cough reflex and how is it commonly injured?

A

Internal laryngeal n. (branch of sup. laryngeal n. from CN X) -> sensory only
Injured when food gets lodged in PIRIFORM recess (separated from nerve only by mucosa covering)

140
Q

Afferent and efferent limb of gag reflex?

A

Afferent limb: CN IX

Efferent limb: CN X

141
Q

Nerve pathway for salivation?

A

Parasympa fiber from CN IX -> synapses at otic ganglion -> postgang fiber travels in auriculotemporal n. -> parotid gland (remember that the other salivatory glands are actually innervated by CN VII)

142
Q

What’s the role of glycine in nervous system?

A

Inhibitory neurotransmitter in CNS, esp in spinal cord

Causing chloride to enter post-synaptic neuron via inotropic receptors -> hyperpolarization

143
Q

2-yo presenting w/ non-rhythmic conjugate eye movement + myoclonus. What’s the dx of his abd mass?

A

Neuroblastoma - most common extracranial neoplasm in children -> small blue round cells, neurophil pathognomonic, retroperitoneal mass displacing kidney, may be dumbbell tumor (invading epidural space and compressing spinal cord)
Presentation is called opsoclonus-myoclonus and is a paraneoplastic syndrome

144
Q

Dx of loss of neurons in ant. horn, some CNs, and degeneration of corticospinal tract? What’s the most common cause of death?

A

ALS -> b/c you’ve got both LMN (ant. horn and CNs) and UMN (corticospinal) lesion
Amyotrophy will happen to muscles (denervation atrophy)
Resp complication (aspiration pneumonia) -> most common cause of death

145
Q

Tx of ALS?

A

Riluzole, MOA

146
Q

What happens to spinal cord in B12?

A

Subacute combined degeneration -> “combined” b/c it affects asc. (dorsal column) and desc. (lateral corticospinal tracts) pathways -> don’t confuse w/ ALS which is combined UMN and LMN

147
Q

Dx of MULTIPLE ring enhancing lesions in pt w/ oral thrush and cervical lymphadenopathy?

A

AIDs-assc. toxoplasmosis

Seizure is complication

148
Q

Other structures supplied by PCA besides occipital lobe?

A

CN III, IV
Thalamus (why get contralat paresthesia and numbness w/ PCA occlusion)
Medial temporal lobe
Splenium of corpus callosum
Parahippocampal gyrus
Fusiform gyrus
Also get sx of dyslexia visual agnosia, prosopagnosia (can’t recognize face) w/ PCA occlusion

149
Q

Other structures supplied by ACA besides the obvious medial distribution?

A 
Basal ganglia (ant. portion)
Internal capsule
150
Q

Structures supplied by ant. choroidal ar?

A 
Pos. limb of internal capsule
Optic tract
Lateral geniculate body
Choroid plexus
Uncus
Hippocampus
Amygdala
151
Q

Histology of PML?

A

Cytoplasmic inclusions in oligodendrocytes

152
Q

Histology of HIV-assc. viral encephalopathy?

A

Microgial nodules and multinucleated giant cells

153
Q

What is neurophysin and where does it come from?

A

It’s a protein secreted from pos. pitu along w/ ADH and oxytocin (into hypophysial vein)
Plays a role in posttranslational hormone processing w/in secretory vesicles as they travel down axon

154
Q

Where is vestigial intermediate lobe of pituitary derived from?

A

From pos. wall of Rathke’s pouch

Can be source of Rathke’s cysts

155
Q

Difference between pseudobulbar palsy and bulbar palsy?

A

Pseudobulbar: NUCLEI of CN remain intact -> ie MS pt having dysarthria, dysphagia, dysphonia, impaired movement of facial muscles and tongue muscles
Bulbar: nuclei affected

156
Q

Delirium vs. dementia?

A

Delirium: reversible, acute, fluctuating level of consciousness
Dementia: irreversible, gradual, no fluctuating level of consciousness

157
Q

Origin of tumor positive for synaptophysin?

A

Neurons

158
Q

4 examples of tumors positive for GFAP?

A

GBM, oligodendrogliomas, ependymomas, peripheral neural sheath tumors

159
Q

What passes thru inferior orbital fissure?

A

V2, infraorbital vessels, branches from sphenopalatine ganglion
These DON’T enter the orbit

160
Q

CN affected w/ vertical diplopia? Horizontal diplopia?

A 
Vertical diplopia (difficulty reading newspaper or walking downstairs) -> CN IV
Horizontal diplopia -> CN III or CN VI
161
Q

How does internuclear ophthalmoplegia present? And what structure is affected?

A

Impaired horizontal eye movement + weak ADduction of affected eye + simultaneous ABduction nystagmus of the contralat eye
From lesion in MLF (connects IPSILAT abducens w/ CONTRALAT oculomotor)

162
Q

Dx of infant w/ hydrocephalus + intracranial calcifications + chorioretinitis?

A

Congenital toxoplasmosis -> in-utero aka transplacental transmission if mother is infected during first 6 mo of pregnancy -> so dont let pregnant women handle cat litter
Chorioretinitis is cotton-like white/yellow scars on retina seen on funduscopy

163
Q

Common orgs producing ophthalmia neonatorum as intrapartum infection?

A

Intrapartum means acquire during delivery

Chlamydia, Neisseria, viruses

164
Q

Sx of restless leg syndrome? Susceptible pt population?

A

Vague leg discomfort, relief w/ movement

More common in middle age/older pts, those w/ iron deficiency, chronic kidney disease, diabetes

165
Q

Drugs that make RLS worse? Tx of RLS?

A

Drugs that make it worse: glucocorticoids, SSRIs, lithium

Tx of RLS: dopamine agonists (ropinirole, pramipexole)

166
Q

What is cataplexy? What’s the tx?

A

Sudden loss of muscle tone often triggered by strong emotions
Tx: muscarinic antagonists

167
Q

What does cutaneous neurofibroma consist of?

A

Schwann cells and neural fibroblasts -> BENIGN tumor

Neural crest derivative!

168
Q

What’s a button hole sign?

A

Applying pressure to some neurofibromas cause them to retract into subQ tissue

169
Q

2 diseases characterized by slow virus infection?

A

Slow virus infection -> think progressive disorders of CNS
SSPE (subacute sclerosing panencephalitis)
PML

170
Q

Diff bet. base and apex of cochlear?

A

Base: wide&thin&rigid basilar membrane, near oval and round windows -> high frequency sound
Apex: narrow&large&flexible basilar membrane, near helicotrema -> low frequency sound

171
Q

Where are the 3 scalae of the cochlea and what are the differences bet. them?

A

From top to bottom
Scala vestibuli: perilymph (high Na+)
Scala media: endolymph (high K+), separated from scala tympani by basilar membrane, houses tectorial membrane and organ of Corti
Scala tympani: perilymph (high Na+)
Vestibuli and tympani meet at helicotrema

172
Q

Steps of sound propagation

A

Reaches middle ear by vibrating tympanic membrane -> ossicles transfer vibration to oval window -> movement of perilymph in scalavestibuli -> movement transmitted to scala tympani -> scala tympani causes basilar membrane to vibrate -> bending of cilia of hair cells -> nerve impulses

173
Q

Oval window vs. round window?

A

Oval window is the one in communication w/ stapes
Round window moves outward when oval window moves inward
Sound propagation: oval window -> scala vestibuli -> helicotrema -> scala tympani -> round window

174
Q

Diff in tx of drug-induced Parkinsonism and idiopathic Parkinson disease?

A

Drug-induced Parkinson (so tx side effects of antipsychotics): use trihexyphenidyl, benztropine, amantidine -> DONT use levodopa/carbidopa or dopamine agonists because they can precipitate psychosis (pretty much go against the antipsychotics being used)
Avoid benztropine and trihexyphenidyl in elderly esp w/ BPH and angle-closure glaucoma tho
Idiopathic Parkinson: levodopa/carbidopa or dopamine agonists

175
Q

What do you use to treat akathisia?

A

Propanolol

Akathisia is a type of extrapyramidal sx

176
Q

Main diff bet. Charcot-Bouchard pseudoaneurysms and berry/saccular aneurysms?

A

Charcot-Bouchard: assc. w/ HTN, rupture results in intracerebral hemorrhage in pons and deep structures (basal ganglia, internal capsule, thalamus)
Berry/saccular: assc. w/ connective tissue diseases (ADPKD, Marfan, Ehlers-Danlos), rupture results in SAH

177
Q

What are potential causes of stroke if CT picks up hemorrhage vs. doesn’t pick up hemorrhage?

A

If CT picks up hemorrhage: rupture of aneurysms (Charcot, saccular, etc)
If CT doesn’t pick up hemorrhage: think ischemic stroke (carotid artery atherosclerosis, cardiac embolism, etc)

178
Q

Potential cause of lobar parenchymal hemorrhage vs. deep structure hemorrhage?

A

Lobar parenchymal hemorrhage: cerebral amyloid angiopathy is the most common cause (lower mortality and more benign clinical course)
Deep structure: HTN hemorrhage most common cause

179
Q

What does hypertensive encephalopathy refer to?

A

GLOBAL sx caused by cerebral edema in pts w/ severe acute HTN

180
Q

Diff bet. train-of-four stimulation of depolarizing NMJ blockade (succinylcholine) and nondepolarizing NMJ blockade (pancuronium, tubocurarine)?

A

Depolarizing (succinylcholine): phase I sees equal reduction of all 4 twitches -> phase II (if continue to dose or if slow metabolizers) sees fading pattern (progressive reduction in each of 4 responses)
Nondepolarizing (pancuronium, tubocurarine): always displays fading pattern
Neostigmine will reverse nondepol and only phase II of depol NMJ blockade

181
Q

What is kinesin involved in?

A

It’s a microtubule assc. motor protein -> involved in anterograde transport away from cell body towards nerve terminal

182
Q

At what level does conus medullaris end?

A

L2 (“conus medullaris syndrome” if lesion at this level)

183
Q

Saddle anesthesia and loss of anocutaneous reflex. What nerve roots are affected?

A

S2-S4 (cauda equina syndrome)

184
Q

What roots mediate Achilles reflex?

A

S1 and S2

185
Q

2 most common causes of death in Friedreich ataxia?

A

Cardiomyopathy and bulbar dysfx (unable to protect airway)

186
Q

What visual field is transmitted to cuneus gyrus? Lingual gyrus?

A 
Cuneus gyrus (upper portion of occipital): receives from lower visual field (so upper retina)
Lingual gyrus (lower portion of occipital): receives from upper visual field (so lower retina)
187
Q

Why do you have macular sparing w/ PCA infarct?

A

B/c occipital pole is supplied by collateral blood of MCA

188
Q

What visual defect do you get w/ MCA stroke?

A

Homonymous hemianopia WITH MACULAR INVOLVEMENT (supplies occipital pole)

189
Q

What is a role of serotonin outside of CNS?

A

Produced by platelets: vasodilates and increases vascular permeability
Produced by gut enterochromaffin (Kulchitsky) cells: peristalsis and nausea

190
Q

What do you use in long-term tx of pts w/ a combination of tonic-clonic seizures and absence seizures?

A

Valproate

191
Q

What should you be thinking when non-contrast CT shows hyperdensity w/in cisterns/sulci & no focal neurological deficits?

A

SAH (probably from ruptured saccular aneurysm)

192
Q

Alexia w/out agraphia. Where’s the lesion?

A

Splenium of corpus callosum

Alexia = can’t read; agraphia = can’t write

193
Q

Which portion of CN III is more susceptible to compression injury? Ischemic injury?

A 
Compression injury (aneurysm or tumor): parasympa fibers (outer portion)
Ischemic injury (small vessel disease from DM): somatic efferent fibers (inner portion)
194
Q

2 types of accumulation in Alzheimer’s?

A

INTRAcellular neurofibrillary tangles (tau protein = component of microtubules) -> specific to Alzheimer’s
EXTRAcellular A-beta-amyloid plaques -> nonspecific

195
Q

What kind of inclusion is Lewy bodies and what conditions do you find this in?

A

Intracytoplasmic, composed of alpha-synuclein

Seen in Parkinson and Lewy body dementia

196
Q

What does NO do as a brain neurotransmitter? And what’s unique about its mechanism of action?

A

It participates in formation of new memories (so found in cortex, hippocampus, hypothalamus, cerebellum, olfactory system)
It freely diffuse across membrane and does not need to interact w/ other neurons via a synapse

197
Q

What parameter measures potency of inhaled anesthetics? And what does this parameter depend on?

A

MAC
It’s an intrinsic property of anesthetics but also depends on body temp and pt age (MAC decreases meaning more potent w/ increasing pt age) -> does NOT depend on type of surery, duration, sex, height, weight

198
Q

What does a steeper curve of arterial tension vs. inhaled anesthetics conc graph tell you?

A

Steeper = anesthetics is less soluble in blood

199
Q

What does arteriovenous conc gradient of inhaled anesthetics indirectly measure? And what does that mean in terms of onset of action?

A

Indirectly measures solubility in blood
Greater gradient -> more anesthetic is extracted from blood by body tissue -> takes more time for blood to become saturated -> SLOWER onset of action

200
Q

What does blood/gas partition coefficient of inhaled anesthetics correspond to? And what does that mean in terms of onset of action?

A

Corresponds to solubility in blood
High blood/gas partition coefficient -> anesthetics dissolve easily in blod (so larger amount must be absorbed before blood becomes saturated) -> partial pressure in blood rises more slowly -> delays saturation of CNS -> SLOWER onset of action

201
Q

Most likely cause of pt presenting w/ acute & painless monocular vision loss + fundoscopic exam sees pale retina & cherry-red macula?

A

Central retinal artery occlusion (from a-fib,carotid artery stenosis, etc)
Cherry red macula b/c macula has separate blood supply from choroid artery (rest of retina is supplied by central retinal artery)

202
Q

What’s amaurosis fugax?

A

Painless, transient, monocular vision loss caused by small embolus to ophthalmic artery
Doesn’t last more than a few sec

203
Q

What are the unique features of HSV-1 encephalitis?

A

Loves temporal lobe -> so get sx like aphasia, olfactory hallucination, personality changes
Also see edema and hemorrhagic necrosis

204
Q

What 2 groups of drugs cause malignant hyperthermia? And what mutation does the inherited malignant hyperthermia involve?

A

Caused by inhaled anesthetics and succinylcholine

AD susceptibility involves defect in ryanodine receptors on SR

205
Q

Dx of “fever and muscle rigidity soon after surgery under general anesthesia”?

A

Malignant hyperthermia

206
Q

Differences bet. what happens to ACh in nondepolarizing NMJ blockade and depolarizing NMJ blockade?

A

Nondepolarizing NMJ blockade: prevents ACh binding to receptors
Depolarizing NMJ blockade: causes constant stimulation of the receptor

207
Q

What happens to Rinne and Weber test results in conductive hearing loss?

A

Rinne: bone > air in affected ear (negative)
Weber: hear better in affected ear (b/c conduction deficit masks ambient noise in the room)

208
Q

What happens to Rinne and Weber test results in sensorineural hearing loss?

A

Rine: air > bone (normal, positive test)
Weber: hear better in unaffected ear

209
Q

Where do you bleed from in intraventricular hemorrhage? And what is a risk factor?

A

Bleeds from germinal matrix -> highly cellular and vascularized layer in subventricular zone (where neurons and glial cells migrate out during brain development) -> worry esp if bulging ant. fontanelle
Risk factor is prematurity, b/c bet. 24-32 wks gestation you get decreased in cellularity and vascularity of this structure and decreased risk

210
Q

Dx of “sudden onset of transient numbness and tingling of left arm, which resolves completely w/in 20 mins”? Tx?

A

This is TIA!

Put on low-dose aspirin, if worry about GI bleeding, add PPI too

211
Q

What 2 brain lesions do you see oligodendrocyte depletion?

A

MS and PML

212
Q

Pt survived SAH and is being hospitalized. What are potential complications if pt starts to develop neurologic sx and you see no changes on CT vs. see changes on CT?

A

If see no change on CT: secondary vasospasm causing cerebral ischemia (from impaired brain autoregulation, present as new-onset confusion and/or focal deficits 4-12 days after initial SAH) -> use Doppler to dx
If see changes on CT: probably rebleeding pr hydrocephalus

213
Q

3 centers regulating micturition reflex?

A
  1. sacral (S2-S4): bladder contraction
  2. pontine (RF): relaxation of external urethral sphincter & bladder contraction
  3. cerebral cortex (desc cortical fibers in paraventricular area): inhibiting sacral center -> so if lesion here (ie by enlarged ventricular system) you won’t sense bladder fullness so bladder voids reflexively when full; voluntary relaxation of sphincter remains intact tho!
214
Q

How does cluster headache present?

A

Rapid-onset, severe, nonpulsatile, unilateral periorbital and temporal pain + nasal congestion, lacrimation, ptosis -> lasts 30 min to 2 hrs, commonly happens at night, pain-free interval of about a year bet. series of attacks

215
Q

How does tension headache present?

A

Band-like sensation of head and/or neck tightness, lasting hrs to days

216
Q

How does trigeminal neuralgia present?

A

ELECTRIC pain in V2/V3 distribution lasting seconds

217
Q

What’s iridocyclitis?

A

Uveitis

218
Q

Most common cause of night blindness?

A

Hereditary retinitis pigmentosa

219
Q

Tx for ACUTE migraine? Prophylaxis?

A

Acute: triptans
Prophylaxis: B-blockers, antidepressants (amitriptyline and venlafaxine), anticonvulsants (valproate and topiramate)

220
Q

What receptors are depleted in the striatum of Huntington pts?

A

NMDA receptors (NMDA receptors blind glutamate and cause neuronal death)

221
Q

What do you see on EEG w/ absence seizures (petit mal)?

A

Generalized 3-Hz spike-wave complexes superimposed on normal background activity

222
Q

Urine level of what molecules is elevated in neuroblastoma?

A

HVA (homovanillic acid - dopamine metabolite) and VMA (vanillylmandelic acid - NE&epi metabolite)

223
Q

What immunohistochemical stains is neuroblastoma positive for?

A

Neuroendocrine markers: NSE (neuron-specific enolase), chromogranin, synaptophysin, S-100 (neural crest)

224
Q

What nerve roots are blocked by pudendal nerve block?

A

S2-S4 -> anesthesia to majority of perineum
Can also block genitofemoral (L1-L2) and ilioinguinal (L1) nerves if wanna provide complete perineal and genital anesthesia

225
Q

What nerve runs on ant. surface of psoas m.?

A

Genitofemoral nerve (L1-L2)

226
Q

What neurotransmitter mediates morphine tolerance?

A

Glutamate -> binds to activates NMDA receptors -> increased phosphorylation of opioid receptors and increased NO levels -> morphine tolerance
So using things like ketamine (blocks glutamate) or dextromethorphan (blocks NMDA) can block morphine tolerance
(glycine doesn’t play a role even tho it’s a co-agonist for glutamate at NMDA receptor)

227
Q

Which GABA receptors are ion channels (stimulation leads to Cl- influx) and which are G-protein linked?

A

Ion channel: GABA-A (brain) and GABA-C (retina)

Gi: GABA-B (brain) -> sitmulation leads to inhibition of adenylyl cyclase; also get K+ efflux w/ decreased Ca2+ influx

228
Q

3 causes of mononeuropathy?

A

Obvious stuff like compression & trauma
DM
Vasculitis (ie Churg-Strauss)

229
Q

Diff bet. Guillain Barre demyelination and Beriberi demyelination?

A

Guillain Barre: demyelination + endoneural inflammatory infiltrate (bac contains ganglioside-like substance in LPS that Ab is formed against -> cross-reacts w/ ganglioside components of myelin)
Beriberi: demyelination w/out inflammation

230
Q

What’s Werdnig-Hoffman syndrome?

A

Ant. horn cell damage -> LMN stuff -> floppy child syndrome

231
Q

Wernicke syndrome and reversability of each sx?

A

Resolves w/ thiamine administration: oculomotor dysfx, mental status change
Resolves but takes longer: ataxia
Doesn’t resolve (permanent): memory and learning abnormalities (Korsakoff syndrome from damage to anterior and dorsomedial thalamic nuclei -> anterograde amnesia and confabulation -> irreversible)

232
Q

What muscle is involved in accommodation? Focusing at a distant? What is presbyopia?

A

Accommodation: ciliary muscle CONTRACTS -> zonula fibers relax -> lens rounder
Focusing at a distance: ciliary muscle RELAXES -> zonula fibers contract -> lens flatter
Presbyopia: inability to focus at near object -> can cause myopic ppl to believe their vision is initially improving as they age

233
Q

What is low CSF 5-hydroxyindole-acetic acid conc assc. w/?

A

Aggression, suicide violence

234
Q

What is elevated CSF 14-3-3 protein assc. w/?

A

Creutzfeldt-Jakob

235
Q

What is low CSF melatonin assc. w/?

A

Alzheimer progression

236
Q

What is Meniere disease?

A

Defective resorption of endolymph -> increased endolymph volume -> damage to both vestibular and cochlear -> tiad of tinnitus, vertigo, sensorineural hearing loss -> EPISODIC w/ exacerbations and remissions (unlike mass lesions at cerebellopontine angle which will produce the same sx but progressive and constant)

237
Q

What is labyrinthitis and how does it present?

A

Inflammation of vestibular labyrinth

Acute-onset vertigo, n/v

238
Q

What is otosclerosis and how does it present?

A

Inherited condition -> body overgrowth of footplate of stapes
Present middle age w/ conductive hearing loss (NO vertigo)

239
Q

What are 4 characters of acute MS plaques?

A

Demyelination w/ relative axon preservation -> so just impaired saltatory conduction
Accumulation of lipid-laden macrophages (containing myelin breakdown product)
Astrocytosis
Lymphocytes & mononuclear cells

240
Q

Frature where frontal, parietal, temporal, and sphenoid bones meet. What is this called and what artery is at risk?

A

This is called pterion

Damages middle meningeal artery (branch of maxillary artery) -> epidural hematoma

241
Q

Decreased level of consciousness + asymmetric pupils + irregular bleeding after getting tx for MI. What should you worry about?

A

Intracerebral hemorrhage from streptokinase use

242
Q

When does neural tube close?

A

4th wk gestation

243
Q

What do you injure in transtentorial herniation?

A

Medial temporal lobe (uncus) herniates thru gap bet. crus cerebri and tentorium -> so get
CNIII damage -> first sign is fixed & dilated pupil on side of lesion!!!
PCA damage -> contralat homonymous hemianopia w/ macular sparing
Cerebral peduncle -> contralat and/or ipsi hemiparesis
Stretching basilar artery -> brainstem hemorrhage

244
Q

What do you injure in subfalcine herniation?

A

Cingulate gyrus herniates under falx cerebri -> compressing ACA

245
Q

3 seizure meds that work on decreasing Na+ current in cortical neurons?

A

Phenytoin, carbamazepine, and valproic acid (which also works on NMDA and GABA)

246
Q

What sx does retinoblastoma usually present w/?

A

White pupillary reflex (leukocoria)

247
Q

Level where you find CN V? What’s the landmark?

A

Mid-pons -> see MCP

248
Q

Level where you find CN III? What’s the landmark?

A

Midbrain at the level of superior colliculus & red nucleus

249
Q

Level where you find CN IV? What’s the landmark?

A

Midbrain at the level of inferior colliculus (this level is below red nucleus)

250
Q

Level where you find CN VI, VII, VIII?

A

Caudal pons

251
Q

Main diff bet. acute neuronal injury (irreversible) vs. axonal rxn?

A

Acute neuronal injury: LOSS of Nissl substance and nuclear pyknosis
Axonal rxn: DISPERSION of Nissl substance and eccentric nucleus

252
Q

What does schwannomas look like under the microscope?

A

Biphasic: Antoni A intermixed w/ Antoni B
Antoni A: highly cellular areas w/ spindle cells (elongated cells w/ oval nuclei) that form palisading patterns w/ interspersing Verocay bodies (nuclear-free zones)
Antoni B: myxoid regions

253
Q

Schwannomas can arise from any CN except?

A

CN II -> covered by oligodendrocytes instead of Schwann cells

254
Q

What’s the disease assc. w/ optic glioma? What does it look like under the microscope?

A

Assc. w/ NF 1
See immature astrocytes w/ microcystic degeneration and Rosenthal fibers (elongated or corkscrew intracytoplasmic eosinophilic bundles)

255
Q

What does external branch of sup. laryngeal n. innervate? Internal branch? What about recurrent laryngeal n.?

A

External branch of sup. laryngeal n.: cricothyroid m. -> n. gets injured when messing w/ sup. thyroid artery during thyroidectomy)
Internal branch of sup. laryngeal n.: no muscle innervation, just sensory to mucosa above vocal folds
Recurrent laryngeal n.: rest of laryngeal muscles + sensory below vocal folds

256
Q

Location of migraine headaches?

A

Initially unilateral and localized in frontotemporal and ocular area -> progress posteriorly and becomes diffuse

257
Q

What vitamin deficiency mimics Friederich ataxia?

A

Vit E -> b/c get degeneration of spinocerebellar tracts, dorsal column of spinal cord, and peripheral nerves -> ataxia, dysarthria, loss of position and vibration sense

258
Q

What would damage to external globus pallidus vs. internal globus pallidus generate?

A

External globus pallidus damage: decreased movement

Internal globus pallidus damage: excessive movement

259
Q

What parameters does demyelination decrease and increase?

A

Decrease length constant (length constant aka space constant = how far along an axon an electrical impulse can propagate -> so reduced from increased charge dissipation along axon)
Increase time constant (lower time constant means quicker changes in membrane potential and increased axonal conduction speed -> so demyelination would do the opposite)

260
Q

What exactly determines a threshold for AP?

A

Intrinsic properties of voltage-gated Na+ channels present in the membrane

261
Q

What exactly are temporal summation and sequential summation w/ regards to synaptic potentials? Where can they occur?

A

Temporal summation: additive effects of multiple postsynaptic potentials from the same neuron over time
Sequential summation: from several different neurons
Summation can occur on dendrites, body, axon hillock but NOT in the axon

262
Q

How would dry age-related macular degeneration (AMD) be described? Wet? How do you tx severe one?

A

Dry: subretinal drusen deposits or pigment changes
Wet: abnormal blood vessels w/ subretinal fluid/hemorrhage, gray subretinal membrane, or neovascularization
Dry can progress to wet and get acute vision loss w/in days-weeks
Tx severe cases w/ anti-VFGF (ranibizumab and pegaptanib)

263
Q

Dx of rapidly progressive dementia and myoclonic jerks?

A

Creutzfeldt-Jakob -> most commonly iatrogenic

264
Q

What org causes general paresis?

A

Neurosyphilis

Progressive dementia + generalized paralysis

265
Q

What kinds of things constitute sleep hygiene tx of insomnia? What about stimulus control tx?

A

Sleep hygiene: regular schedule, avoid caffeine and alcohol, excercise, etc
Stimulus control: dissociate bedroom from any stimulating activities that don’t involve sleeping (fear of not sleeping included) -> instruction to leave bedroom if can’t fall asleep or only go to bed when sleepy would fall on this one as well

266
Q

CSF shows increased protein w/ normal or slightly elevated cell count (albumino-cytologic dissociation). What do you suspect?

A

Guillain Barre

267
Q

What is myoclonic seizures and what’s the DOC?

A

Brief symmetric contractions w/ loss of body tone (fall forward), no loss of consciousness, usually occur in the morning and precipitated by stress and sleep deprivation -> not preceded by urge to make movement (vs. Tourette, which is managed by haloperidol)
Valproic acid first line

268
Q

Where does complex partial seizure almost always originate from?

A

Temporal lobe -> why usually assc. w/ hallucinations

269
Q

Both normal pressure hydrocephalus and Alzheimer/other dementing diseases present w/ memory loss. How do you distinguish them?

A

NPH: get ataxic gait & urinary incontinence BEFORE dementia and there’s no permanent damage so dementia are sometimes reversed by lowering CSF volume

270
Q

What’s apraxia?

A

Difficulty in carrying out acitivities

271
Q

What’s agnosia?

A

Difficulty recognizing objects

272
Q

Diff in sx from destruction of inf. parietal lobe of dominant hemisphere vs. nondominant?

A

Dominant hemi: Gerstmann syndrome -> R/L confusion, dysgraphia, dyscalculia, finger agnosia
Non-dominant: apraxia, contralat hemi-neglect

273
Q

How does Pick disease manifest?

A

Pick for Personality changes
It’s frontotemporal dementia -> so start w/ changes in personality, social bx, and language (paucity of speech, repeated phrases)

274
Q

What hypothalamic nucleus controls cooling? Heat production?

A

Ant. hypothalamic: cooling, parasympa (just like A/C cools you down)
Pos. hypothalamic: heat production, sympa -> becomes poikilotherm if this is damaged

275
Q

What does damage to nucleus ambiguus classically produce?

A

Myoclonus

276
Q

Dx of “bilateral wedge-shaped bands of necrosis over cerebral convexity, lateral to interhemispheric fissure”?

A

Watershed infarcts! -> severe ischemia (ischemia usually affects pyramidal cells and Purkinje cells first before watershed infarcts happen)

277
Q

What’s a shock-like sensation that radiates to feet upon neck flexion a sign of?

A

Anything involving pos. columns or caudal medulla

So see this w/ MS, B12 deficiency, Behcet’s (along w/ aphthous ulcers), spinal cord compression, trauma and radiation

278
Q

What’s spina bifida cystica?

A

Myelomeningocele -> all herniate (CSF, spinal cord, nerve roots)

279
Q

What’s syringobulbia?

A

Fluid-filled cavities w/in medulla

280
Q

What do greater, lesser, and least thoracic splanchnic nerves transmit?

A

Preganglionic sympathetic nerves -> synapse to postgang in abdomen (except for adrenal glands)

281
Q

What kinds of glands do postganglionic sympathetic nerves mediate?

A

Apocrine glands
Eccrine glands -> what’s responsible for hyperhydrosis -> if on axilla, solve by targeting T2 thoracic sympathetic ganglion (cervical sympa is for face)
NOT sebaceous sweat glands

282
Q

Neurofibroma vs. dermatofibroma?

A

Dermatofibroma: from dermis hyperplasia; firm, hyperpigmented, and tethered to epidermis
Neurofibroma: from Schwann cell hyperplasia; soft, flesh-colored papules

283
Q

What nerves are NOT myelinated?

A

Sensory (afferent fibers) that transmit slow pain, heat sensation, olfaction
Efferent fibers are all myelinated except POSTGANG autonomic nerves

284
Q

Healthy child w/ excessive daytime sleepiness during school days and can’t go to bed til after 3AM, but functions normally during the weekend. Dx?

A

Circadian rhythm disorder -> presumes that he wakes up later on weekends
NOT school phobia (this is unrelated to not being able to go to bed until 3)

285
Q

What’s anisocoria and in what condition do you see this in?

A

Eye pupils are not equal

Horner syndrome

286
Q

Where exactly is pineal gland?

A

Dorsal (behind) sup. colliculus and between thalamic nuclei

287
Q

What does alcoholic cerebellar degeneration involve?

A

Loss of Purkinje neurons in anterior lobe and vermis of cerebellum -> most likely from thiamine deficiency
Present w/ Parkinson-like tremor + wide-base gait ataxia

288
Q

Where is insula and in what context do you see increased activity?

A

On brain cross section, you see it at the end of Sylvian fissure and just lateral to putamen
Control emotional experience, pain, body representation, conscious cravings -> increased activity when drug abusers are exposed to cues that trigger cravings

289
Q

What’s the mechanism behind tardive dyskinesia?

A

HyPERsensitivity to dopamine from upregulation of dopaminergic receptors
Also concomitant decrease in cholinergic tone

290
Q

First sign of cavernous sinus thrombosis?

A

Lateral gaze palsy from CN VI involvement

291
Q

Diff parts of eye that’s affected in disease state?

A

Cornea: Wilson (KF ring)
Iris: NF1 (Lisch nodules)
Sclera: osteogenesis imperfecta
Retina: lots of things -> DM, tay sachs, etc.

292
Q

What does prosencephalon give rise to?

A

Telencephalon: hemispheres & lat. ventricles
Diencephalon: thalamus & 3rd ventricle

293
Q

What does meSencephalon give rise to?

A

Midbrain & aqueduct

Remember that S comes before T, so meSencephalon comes before meTencephalon (pons and cerebellum)

294
Q

What does rhombencephalon give rise to?

A

4th ventricle
MeTencephalon: pons and cerebellum
Remember that T comes after S, so meTencephalon comes after meSencephalon (midbrain)
Myelencephalon: medulla (mye b/c closest to spinal cord)

295
Q

Besides contralat sensory loss, what else would intracerebral hemorrhage to thalamus do?

A

Aphasia and transient homonymous hemianopia

Unilat. abducens palsy, pupil asymmetry and nonreactivity, downward gaze

296
Q

Difference bet. what happens to pupils in hemorrhage of putamen vs. pons?

A

Putamen hemorrhage: dilated pupils

Pons hemorrhage: pinpoint pupils

297
Q

2 ways brain tumor can cause sx of increased ICP?

A

Obstruction of CSF flow

Disrupts BBB -> increased permeability so stuff leaks in -> vasogenic edema

298
Q

Most common cause of intracerebral hemorrhage?

A

Systemic HTN

299
Q

What process failed in anencephaly?

A

Closure of rostral pore

300
Q

In pts w/ chronic peripheral neuropathy, enzyme staining of muscle bx shows fiber grouping. What’s the most likely cause of this finding?

A

Reinnervation of muscle fibers by regenerating axons

301
Q

Deep nuclei of cerebellum from lateral to medial?

A

“Don’t Eat Greasy Food”

Dentate, Emboliform, Globose, Fastigial

302
Q

D1 vs. D2 pathway?

A

Dopamine stimulates both w/ the total outcome of allowing wanted movements and inhibiting unwanted movements
D1 (direct pathway, stimulates movement, doesn’t involve GPe or STN): SNc sends dopamine-> stimulates putamen -> putamen inhibits globus pallidus INTERNUS -> GPi inhibits thalamus -> thalamus stimulates cortex -> contralat UMN
D2 (indirect pathway, inhibits movement, involve GPe and STN): SNc sends dopamine -> inhibits putamen -> putamen inhibits globus pallidus EXTERNUS -> GPe inhibits STN (subthalamic nucleus) -> STN stimulates GPi -> GPi inhibits thalamus (then same steps as D1)

303
Q

Where do vertebral arteries merge to become basilar artery?

A

Where AICA comes off

304
Q

What artery/arteries do/es pontine arteries come off of?

A

Basilar artery

305
Q

What does decreased blood solubility of inhaled anesthetics mean? How about increased lipid solubility?

A

Decreased BLOOD solubility -> rapid induction & recovery times
Increased LIPID solubility -> high potency (1/MAC)
Examples: NO is low on both blood and lipid solubility -> rapid induction but low potency. Halothane is high on both blood and lipid solubility -> slow induction but high potency.

Question Bank (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions