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Step 1 Miscellanous > Nervous System Supplement > Flashcards

Nervous System Supplement Flashcards

1
Q

What does the Nissl stain actually stain?

A

RER

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2
Q

What happens to the glial cells in the CNS during HIV infection?

A

When infected, they fuse to form multinucleated giant cells

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3
Q

What type of skin are Meissner’s corpuscles found in?

A

Thick skin only, as they are a spiralling nerve ending

Thin skin will have Hair-tylotrich receptors instead

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4
Q

Is size or myelination more important in blocking anesthetics?

A

Size - just think “bigger is better” aka bigger will take more to block

Myelinated fibers are easier to block than unmyelinated

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5
Q

What is the function of the Merkel cell neurite complex?

A

Present in fingertips and superficial skin -> used for detecting shapes and edges

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6
Q

What is the purpose of the Ruffini endings as sensory receptors?

A

Detect joint angle changes from the deep dermis

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7
Q

What portion of the peripheral nerve is invaded in Guillaine-Barre syndrome vs rejoined in a microsurgery for limb reattachment?

A

Guillain-Barre - Endoneurium

Rejoined - Perineurium (organizes the nerve bundle, blood-nerve permeability barrier.

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8
Q

How does the activity of the locus ceruleus pathway differ between anxiety and depression?

A

Anxiety - Increased activity (increased NE = overexcitation)

Depression - decreased activity (lack of NE associated with depression -> explains use of SNRIs as antidepressants)

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9
Q

How does the activity of the raphe nucleus pathway differ between anxiety and depression?

A

Serotonin is decreased in both conditions

-> actually they both decrease activity

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10
Q

Does the ventromedial hypothalamus get stimulated or inhibited by leptin?

A

Stimulated, since it is the satiety center, and leptin is made by fat tissue

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11
Q

What does the posterior hypothalamus stimulate?

A

Vasoconstriction / shivering -> sympathetic response, for heat conservation

remember than anterior = cooling = parasympathetic.

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12
Q

How does the inferior colliculus communicate with the diencephalon?

A

Sends auditory fibers to the medial geniculate nucleus via a tract called “brachium of inferior colliculus” which literally means arm.

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13
Q

What does the medial geniculate nucleus do with the auditory fibers of the brachium of the inferior colliculus once they synapse there?

A

Sends fibers to traverse temporal gyri in temporal lobe via “auditory radiation”.

Just remember that superior olivary nucleus receives bilateral information from cochlear nuclei for sound localization and also sends fibers to the MGN within the lateral lemniscus

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14
Q

What areas of the brain control the positive vs negative symptoms of Schizophrenia?

A

Negative - i.e. anergia, apathy, lack of spontaneity
-> controlled by mesocortical pathway (VTA to dorsolateral PFC), due to decreased activity

Positive - i.e. delusions, hallucinations
-> Mesolimbic pathway -> ventral tegmental area to nucleus accumbens (part of caudate nucleus of BG, but part of the limbic system)

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15
Q

What inputs / outputs are generally contained in the inferior, middle, and superior cerebellar peduncles?

A

Inferior - spinocerebellar -> ipsilateral proprioceptive information from GTO and muscle spindles

Middle - contralateral cerebral cortex (via pontocerebllar tract)

Superior - projections from deep cerebellar nuclei (Purkinje cells are always inhibitory to them and control them).

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16
Q

Why do panic attacks cause you to pass out?

A

Hyperventilation -> respiratory alkalosis -> decreased CO2 levels -> decreased cerebral blood flow -> syncope

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17
Q

Do neurons have glycogen?

A

No, they do not store glycogen, but it is stored for them by astrocytes and can be passed by them and broken down for usage

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18
Q

What cranial nerve nuclei tend to be located mediallary or laterally?

A

Medial = Motor (basal plate derivatives)

Lateral = aLar plate derivatives (sensory)

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19
Q

Where do cranial nerves 7 and 8 exit from the head?

A

Internal auditory meatus

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20
Q

Where is the hypoglossal canal located?

A

Anterolateral to foramen magnum -> exit of hypoglossal nerve

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21
Q

What are the main arteries supplying the basal ganglia and thalamus?

A

Basal ganglia - lenticulostriate arteries - arise from M1 segment of MCA

Thalamus - branches of the posterior cerebral artery

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22
Q

Is the superior tarsal muscle or levator palpebrae superioris innervated by the oculomotor nerve?

A

Oculomotor nerve (CN3) = Levator Palpebrae Superioris

Sympathetics = Superior tarsal

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23
Q

Does CN5 innervator levator veli palatini or tensor veli palatini?

A

Tensor veli palatini (along with tensor tympani)

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24
Q

What nucleus processes visceral sensory information (i.e. taste, aortic baroreceptors, and gut distension)?

A

Nucleus solitarius

Taste -> next goes to VPM thalamus

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25
Q

What is the dividing spinal level between fasciculus gracilis and fasciculus cuneatus?

A

Gracilis - Below T6

Cuneatus - Above T6

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26
Q

What is the most likely cause of death due to stroke?

A

Inflammatory edema in 3-5 days with macrophages and neutrophils -> swelling -> lethal brain herniation

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27
Q

How do children often get subdural vs subarachnoid hemorrhages?

A

Subdural - shaken baby syndrome

Subarachnoid - congenital arteriovenous malformation

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28
Q

What visual symptom is Wernicke’s aphasia usually associated with?

A

Pie in the sky - due to involvement of Meyer’s loop

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29
Q

Why is consciousness spared in basilar artery stroke? Why is vertical gaze intact? What syndrome is this?

A

“Locked in syndrome”

Reticular activating system is spared -> preserved consciousness

Basilar artery supplies lateral gaze (PPRF -> abducens nucleus), but not vertical gaze (level of rostral midbrain)

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30
Q

How do transcortical motor / transcortical sensory aphasia differ from other aphasias?

A

Transcortical motor - affects frontal lobe around Broca’s area. Similar symptoms except repetition is intact (Broca’s area not affected)

Transcortical sensory - affects temporal lobe around Wernicke’s area. Similar symptoms except repetition is intact (Wernicke’s area not affected)

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31
Q

What is transcortical mixed aphasia also called and what characterizes it?

A

Also called pure echolalia

  • > patient has intact Wernicke’s, Broca’s, and arcuate fasciculus but frontal and temporal lobes are damaged
  • > can only repeat, nonfluent speech production and comprehension
  • > analogous to transcortical version of global aphasia
32
Q

What is asterixis? When does it often happen?

A

“negative myoclonus” - Intermittent lapses in postural tone -> not truely rhythmic

Flapping of hands when trying to hold extension is an example
-> Happens often in Wilson’s disease (along with dystonia) and hepatic encephalopathy

33
Q

What type of tremor is essential tremor, and what is the frequency? Is it unilateral or bilateral?

A

High-frequency tremor (8-12 Hz), postural tremor (worsens with sustained posture)

Onset is BILATERAL, although it may be asymmetric

34
Q

How is essential tremor inherited? Treated?

A

Familial -> autosomal dominant

Drugs: Nonselective beta blockers + primidone

Self-medication: Transient suppression by alcohol

35
Q

Where do myoclonus jerks originate from and what are they frequently seen in?

A

Originate from any part of CNS (cortex, brainstem, spinal cord)

Frequently seen in metabolic abnormalities -> renal or liver failure

36
Q

How does Parkinsonian tremor differ from essential tremor?

A

Parkinson’s onset is usually unilateral (Rather than bilateral) and remains asymmetric (vs essential is often symmetrical)

Furthermore, PD is a resting tremor (improves with intentional movement) while essential is not

37
Q

What is the treatment of choice for AIDP? Are there circulating antibodies which are pathogenic? Should you use prednisone?

A

Plasmapheresis and IVIg
-> Pathogenic circulating antibodies have never been demonstrated, but disease is thought to be mediated by molecular mimicry

Note: Steroid therapy is NOT helpful

38
Q

What is Charcot-Marie-Tooth disease also known as? Is the myelin or axon defected?

A

Hereditary motor and sensory neuropathy (HMSN)
-> myelin or axon could be affected, depending on the subtype -> need to do nerve conduction studies or biopsy to confirm

-> affects peripheral nerves (vs Pelizaeus-Merzbacher which affects central nerves)

39
Q

What are the symptoms of Charcot-Marie-Tooth disease and how is it usually inherited?

A

Usually autosomal dominant

Associated with foot deformities (i.e. pes cavus, like Friedrich Ataxia), lower extremity weakness / foot drop, and sensory deficits

40
Q

What are the possible ocular consequences of Sturge-Weber?

A

Glaucoma - can develop in early or late childhood due to hemangiomas in V1 distribution increasing intraocular pressure

Buphthalmos (referring to enlargement of eyeballs common in bovines) - marked enlargement of eye which is congenital (due to glaucoma) -> pediatric emergency that could lead to blindness

41
Q

What is the mnemonic for Sturge-Weber?

A

STURGE

Sporadic - noninherited
Tram-track calcifications + leptomeningeal angiomas
Unilateral
Retardation
Glaucoma, GNAQ gene - due to episcleral hemangioma
Epilepsy

42
Q

What brain tumor are you at increased risk for with tuberous sclerosis? How is this condition inherited?

A

Subependymal giant cell astrocytomas

Inherited via autosomal dominant on chromosome 16

43
Q

What are the clinical findings of NF-1?

A

Multiple cafe au lait spots
Axillary / inguinal freckling - Crowe sign most specific (axillary)
Multiple cutaneous neurofibromas or plexiform neurofibroma (tortuous structure)
Iris Lisch nodules
Optic glioma - pilocytic astrocytoma of adults

44
Q

What is the function of the NF-1 gene?

A

Encodes neurofibromin, a tumor suppressor gene that acts as a GTPase, inactivating Ras

45
Q

What chemical can some hemangioblastomas produce? What do they look like on histology?

A

Erythropoietin, especially when associated with von Hippel-Lindau (i.e. cerebellar hemangioblastoma)

-> looks like thin-walled capillaries with minimal intervening parenchyma

46
Q

What bony structure are vestibular schwannomas occurring at?

A

Internal acoustic meatus

-> where CN7/8 exit, this is where the cerebellopontine angle nerves dump into

47
Q

Which tumor has “blepharoplasts” or basal ciliary bodies found near the nucleus?

A

Ependymoma, probably just important to know the association

48
Q

How can pinealoma cause precocious puberty?

A

It is most often a germ cell tumor -> can produce beta-HCG

49
Q

What structure is damaged in cingulate / subfalcine herniation?

A

Anterior cerebral artery

50
Q

Is decorticate or decerebrate posturing associated with flexion?

A

Decorticate -> due to loss of UMN inhibition of red nucleus

Decerebrate -> loss of the entire cerebrum -> red nucleus flexion is also lost

51
Q

What degenerates in Spinal Muscular Atrophy (SMA)? Is it common?

A

Symmetrical degeneration of anterior horn cells leading to muscle weakness and wasting of voluntary muscles

Second most common lethal autosomal recessive disease in Caucasians, after CF. So pretty common

52
Q

How is SMA categorized? Which one is most severe?

A

Based on age of onset and severity

Most severe: infantile form (SMA I) called Werdnig-Hoffmann disease, presents a floppy baby with fasciculations

Least severe form is SMA III: Kugelberg-Welander, adolescent onset

53
Q

How do patients present with ALS? Is bowel / bladder dysfunction common?

A

Any combination of UMN and LMN weakness involving limbs / bulbar innervated muscles -> can cause swallowing / voice problems

It is asymmetrical.

Bowel / bladder dysfunction is relatively rare until late in the disease -> sphincters are spared

NO sensory nerve involvement

54
Q

Will reflexes be intact for those with syphilis?

A

No -> the afferent limb of the reflex is gone -> demyelination of dorsal root (also carries fibers from Golgi tendon organ)

55
Q

What structures are affected in subacute combined degeneration?

A

Spinocerebellar tracts
Corticospinal tracts
Dorsal colums
(SCD)

56
Q

What is the usual cause of death in polio?

A

Involvement of respiratory muscles (LMN) leads to respiratory failure

57
Q

How are DC-ML and ALS pathway affected in Brown-Sequard?

A

Spinal cord hemisection:
Loss of ALL sensation AT the level of the lesion
Contralateral ALS loss
Ipsilateral DC-ML loss (decussates in medulla via internal arcuate fibers)

58
Q

What is the most common hereditary ataxia in the Western world? What causes it?

A

Friedreich’s ataxia

  • Trinucleotide repeat “GAA”
  • Frataxin gene - iron binding protein in mitochondria causing free radical damage - chromosome 9

-> damage to multiple spinal cord tracts, ataxia with hypertrophic cardiomyopathy

Presents in childhood as kyphoscoliosis

59
Q

How will CN11 palsy present?

A

Weakness in turning head to contralateral side, and ipsilateral shoulder droop

60
Q

What is pseudobulbar palsy vs bulbar palsy?

A

Pseudobulbar - Loss of key medullary cranial nerves due to BILATERAL UMN defect

Bulbar - loss of key medullary cranial nerves due to LMN defect

61
Q

What is the helicotrema?

A

Junction between scala vestibuli (1st portion, where oval window conducts sound) and scala tympani (second portion, where round window dampens sound)

62
Q

What type of problem is cholesteatoma likey to cause?

A

Conductive hearing loss -> due to erosion of ossicles of ear via production of lytic enzymes
-> overgrowths of desquamated keratin debris caused by chronic negative pressure in middle ear, inducing formation of cysts

63
Q

What is Meniere disease vs BPPV? Labyrinithitis?

A

Meniere -> increased fluid pressure causes vertigo, hearing loss, and tinnitus

BPPV - otoliths misplaced, will only cause vertigo but NOT tinnitus / hearing loss (otoliths not involved in hearing)

Labyrinthitis - post-URI inflammation of inner ear / nerves
-> also a peripheral vertigo

64
Q

What type of nystagmus is seen in peripheral vs central vertigo?

A

Peripheral - horizontal, delayed, suppressable by fixation

Central - any direction, immediate, not suppressable by fixation
-> due to vestibular nuclei or cerebellar lesions

65
Q

What is the most common cause of viral conjunctivitis?

A

Adenovirus

66
Q

Why does presbyopia occur?

A

Decreased strength of ciliary muscle (lack of ability to make a converging lens -> cannot accommodate as well)

Decreased lens elasticity to make a biconvex converging lens as well

-> overall, light starts being focused more behind retina -> farsightedness

67
Q

What is astigmatism caused by?

A

Abnormal corneal curvature

68
Q

What layer of the ciliary body produces the aqueous humor?

A

Nonpigmented epithelium

69
Q

What is the cause of optic disc cupping in glaucoma?

A

Optic disc atrophy (atrophy of outer rim of optic nerve head)
-> weakening pulls it open

70
Q

How will acute angle closure glaucoma present?

A

Very painful, red eye, sudden vision loss, iwth halos around lights and frontal headache

71
Q

Why is inflammed in uveitis and what is it called if pus accumulates in anterior chamber?

A

Anterior uveitis - iritis

Posterior uveitis - ciliary bodyitis (lmao not really) or choroiditis

Pus in anterior chamber: hypopyon

Associated with sarcoidosis, rheumatoid arthritis, JIA, and HLA-B27 associated conditions

72
Q

What is proliferative vs nonproliferative diabetic retinopathy and what is the treatment for proliferative?

A

Nonproliferative - damaged capillaries leak blood / hemorrhage, and can cause macular edema

Proliferative - Chronic hypoxia -> neovascularization (similar to wet ARMD) -> treate with anti-VEGF and retinal photocoagulation (lazering of new blood vessels)

73
Q

Why does retinal detachment cause visual loss?

A

RPE detaches from outer segments of rods / cones

  • > photoreceptors rely on choroidal vessels (Are on inner 1/3) for oxygen
  • > retinal detachment causes ischemia -> monocular vision loss (“curtain drawn down”)
74
Q

Why is the macula red in Tay-Sach’s disease vs central retinal artery occlusion?

A

Tay-Sach’s -> macula is the area of fewest neurons -> least lipid found in lysosomes

Central retinal artery occlusion - rest of retina will be infarcted (white), but macula still receives blood from choroid arteries
-> makes sense b/c it’s only rods / cones, outer 1/3 of retina is these receptors, rest is displaced to fovea which receives blood from central retinal artery

75
Q

What is the order of neurons in the pupillary constriction (miosis) pathway, and what type of reflex is it?

A

Subcortical reflex controlled at the pretectal level

  1. Axons from ipRGCs project to ipsilateral (or bilateral, if on nasal side of retina) pre-tectal nucleus.
  2. Pretectal nucleus sends axons bilaterally, some through pretectal/posterior commissure and some to ipsilateral Edinger-Westphal nucleus
  3. Edinger-Westphal nucleus is origin of preganglionic PANS cellbodies for pupillary constrictor, axons follow CN3
  4. Synapse in ciliary ganglion, send axons to to pupillary contrictor muscles.

Reflex will be bilateral due to pretectal nucleus sending to both sides, but even if one pretectal nucleus was knocked out, it would still be bilateral since light is sent to both pretectal nuclei from one eye if the whole eye is illuminated

76
Q

Which nerve is most susceptible to injury in cavernous sinus syndrome?

A

CN6 - since it travels in the interior of the cavernous sinus

CN 3, 4, and V1/V2 may also be involved

Step 1 Miscellanous (40 decks)

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