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First Aid Chs Part 2 > Neuro > Flashcards

Neuro Flashcards

1
Q

Multiple Sclerosis HLA association

A

HLA - DR2

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2
Q

Metachromatic Leukodystrophy missing enzyme

A

Arylsulfatase A - buildup of sulfatides leads to impaired degradation of myelin

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3
Q

Adrenoleukodystrophy pathophysiology

A

Impaired addition of CoA to LCFA. LCFA accumulate and destroy the adrenal glands and myelin.

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4
Q

Krabbe’s Disease missing enzyme

A

Galactocerebrosidase. Buildup of galactocerebroside destroys myelin

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5
Q

Oligoclonal IgG bands on LP are seen with…

A

MS

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6
Q

Cause of SSPE

A

Slowly progressing, persistent measles infection

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7
Q

Cause of Progressive Multifocal Leukoencephalopathy

A

Immunosuppressed patient - JC virus reactivation - infection of oligodendrocytes (it’s a bunch of bullshit)

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8
Q

<p>Central Pontine Myelinolysis presents as...</p>

A

<p>Locked In Syndrome - patient can only move eyes and blink

| They have acute paralysis, dysarthria, dysphagia, diplopia and loss of consciousness</p>

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9
Q

Cause of Central Pontine Myelinolysis

A

Rapid IV correction of hyponatremia (usually in alcoholics/malnourished)

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10
Q

<p>Epsilon 4 allele of Apolipoprotein E</p>

A

<p>Increased risk for sporadic Alzheimer disease - late onset
ApoE4 is found on chromosome 19</p>

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11
Q

<p>Epsilon 2 allele of Apolipoprotein E</p>

A

<p>Decreased risk for sporadic Alzheimer disease
protective!
found on chromosome 14</p>

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12
Q

<p>Presenilin - 1 and Presenilin-2</p>

A

<p>Mutation results in early onset (familial) Alzheimer disease
note that presenilin-1 is found on chromosome 14</p>

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13
Q

Why does Down Syndrome increase Alzheimer Disease risk?

A

The amyloid precursor protein, which eventually results in production of A-beta-amyloid, is located on chromosome 21, which patients with DS have 3 of.

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14
Q

Components of neuritic (senile) plaque in AD

A

A-beta-amyloid, Entrapped neuritic processes

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15
Q

Cause of cerebral amyloid angiopathy

A

A-beta-amyloid depositing on blood vessels in the brain, weakening wall of vessel, increasing risk for hemorrhage. Seen with AD

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16
Q

Component of neurofibrillary tangles

A

Hyperphosphorylated tau protein (microtubule associated protein)

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17
Q

Second most common cause of dementia

A

Vascular/Multi-infarct dementia (behind AD)

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18
Q

Component of Pick bodies

A

ROUND aggregates of tau protein (microtubule associated protein that helps the microtubules arrange properly) in neurons of cortex.

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19
Q

Diffuse atrophy of the frontal/temporal lobes

A

Pick disease (frontotemporal dementia)

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20
Q

MPTP leads to

A

Parkinson disease

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21
Q

Composition of Lewy bodies

A

alpha-synuclein. Seen with Parkinson disease and Lewy-Body dementia.

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22
Q

When (chronologically) is dementia seen with Lewy body dementia vs. Parkinson disease?

A

EARLY onset (onset before or concomitant with tremor) with LBD; LATE onset (long after tremor onset) with PD

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23
Q

CORTICAL Lewy bodies are seen in…

A

Diffuse Lewy body dementia

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24
Q

Efferent neurons leaving the striatum use which NT?

A

GABA (inhibitory effect on cortex)

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25
Q

Expansion of the lateral ventricles due to brain atrophy

A

Hydrocephalus ex vacuo

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26
Q

What is the trinucleotide repeat in Huntington disease?

A

CAG (HUNT animals in a CAGe).

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27
Q

Why does anticipation happen in trinucleotide repeat diseases?

A

Expansion of the repeat during SPERMATOGENESIS.

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28
Q

Cause of symptoms in normal pressure hydrocephalus

A

Stretching of corona radiata

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29
Q

What will a LP do for NPH?

A

Improve symptoms because the disease is caused by increased CSF

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30
Q

Pathophysiology of NPH

A

Ineffective resorption of CSF into the arachnoid granulations

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31
Q

What is the conformation of abnormally folded proteins in spongiform encephalopathies?

A

Beta-pleated sheets

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32
Q

Spike wave complexes on EEG is indicative of…

A

CJD

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33
Q

Where do adult/child CNS tumors usually occur with respect to the tentorium cerebelli?

A

Kids - below and Adults - above

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34
Q

Adult CNS tumor that crosses the corpus callosum

A

GBM

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35
Q

Butterfly glioma

A

GBM

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36
Q

Adult CNS tumor with central necrosis surrounded by living cells

A

GBM

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37
Q

GBM histology

A

Pseudopalisading appearance (central necrosis with living cells surrounding it) with endothelial proliferation

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38
Q

Cells which make up a GBM

A

Astrocytes

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39
Q

Stain for GBM

A

GFAP (made of astrocytes)

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40
Q

Why are meningiomas seen more in females?

A

Estrogen most likely plays a role in tumor formation

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41
Q

Whorled appearance of cells on CNS tumor biopsy

A

Meningioma

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42
Q

CNS tumor showing psammoma bodies

A

Meningioma

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43
Q

S100 Positive CNS tumor

A

Schwannoma

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44
Q

CNS neoplasm associated with NF2

A

Bilateral acoustic schwannomas

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45
Q

Meiningioma histology

A

Whorled pattern with psammoma bodies

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46
Q

Calcified tumor in frontal lobe white matter in adults that presents with seizures

A

Oligodendroglioma (note: calcified, but NOT psammoma bodies)

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47
Q

Fried egg appearance on CNS neoplasm biopsy

A

Oligodendroglioma

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48
Q

Chicken wire capillary pattern on CNS neoplasm biopsy

A

Oligodendroglioma

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49
Q

Histology of oligodendroglioma

A

Fried egg appearance, may be calcified (NOT psammoma bodies), with “chicken wire” capillary pattern

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50
Q

1 CNS tumor in kids

A

Pilocytic astrocytoma

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51
Q

Classic gross description of a pilocytic astrocytoma seen on imaging

A

Cystic lesion (piloCYSTic astrocytoma) with a mural nodule connected to it. Usually seen in cerebellum in kids.

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52
Q

Rosenthal fibers

A

Thick, eosinophilic corkscrew fibers seen in pilocytic astrocytoma

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53
Q

Staining for pilocytic astrocytoma

A

GFAP

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54
Q

Medulloblastoma is derived from (embryologically)

A

Neuroectoderm

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55
Q

Histology of medulloblastoma

A

Small, round blue cells with Homer-Wright rosettes.

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56
Q

Homer-Wright Rosettes

A

Medulloblastoma. Small round blue cells wrapping around neuritic processes.

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57
Q

CNS tumor showing small round blue cells wrapping around neuritic processes

A

Medulloblastoma

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58
Q

Childhood CNS tumor which can invade the spinal cord (“drop mets”)

A

Medulloblastoma

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59
Q

Cheesy mnemonic for medulloblastoma

A

David Wright blasts a Homer (medulloBLASToma w/ Homer-Wright rosettes) and drops the Mets (Drop Mets). Mets Suck, go Phils

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60
Q

Childhood CNS tumors that can compress the 4th ventricle and cause hydrocephalus

A

Medulloblastoma (spreads via CSF), ependymoma

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61
Q

Primary location of ependymoma

A

4th Ventricle in children

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62
Q

Perivascular pseudorosette

A

Seen in ependymoma - tumor cells line up around blood vessels

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63
Q

Childhood CNS tumor in which tumor cells line up around blood vessels

A

Ependymoma. This is a description of perivascular pseudorosettes.

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64
Q

Origin of craniopharyngioma (embryo)

A

Oral epithelium - Rathke’s pouch

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65
Q

Classic presentation of craniopharyngioma (visual)

A

Bitemporal hemianopsia

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66
Q

Two types of craniopharyngioma

A

Adamintomatous - seen in kids, calcifices. “Wet keratin” appearance (Dr. Stevens described it as wetting sidewalk chalk and spreading it around with your hands). When drained, fluid has a “machine oil” like consistency. Papillary -seen in adults (>65), no calcifications.

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67
Q

A drained intracranial mass shows “machine oil” consistency…dx?

A

Adamantinomatous craniopharyngioma

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68
Q

A group of progressive hereditary nerve disorders related to defective production of proteins involved in structure and function of peripheral nerves or myelin sheath

A

Charcot-Marie-Tooth disease

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69
Q

3 Hz spikes on EEG is indicative of…

A

Absence seizures

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70
Q

Brief (15 min-3 hr) headaches with excruciating periorbital pain with lacrimation and rhinorrhea.

A

Cluster headaches

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71
Q

Treatment for cluster headaches (abortive and prophylactic)

A

Abortive: Inhaled O2, sumitriptan Prophylactic: verapamil, lithium, prednisone

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72
Q

Pulsating headache with nausea, photophobia, phonophobia. Lasts 4-72 hours, usually unilateral

A

Migraine

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73
Q

Migraine treatments

A

Triptans (5HT-1 agonists) - abortive for an acute migraine; Propanolol/Topiramate - prophylactic

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74
Q

<p>Triad seen with Meniere disease</p>

A

<p>Vertigo, tinnitus and sensorineural deafness

| this is endolymphatic hydrops</p>

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75
Q

Cerebellar hemangioblastoma is associated with which genetic disorder?

A

Von-Hippel-Lindau syndrome.

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76
Q

Foamy cells seen on CNS tumor biopsy

A

Hemangioblastoma

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77
Q

CNS tumor producing EPO and causing secondary polycythemia

A

Hemangioblastoma (associated with VHL disease)

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78
Q

CNS tumor in a child with histology showing sheets of cells with many mitotic figures

A

Medulloblastoma

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79
Q

What effect does demyelination (e.g. in MS or GBS) have on the length and time constants of a nerve?

A

Decreases the length constant (impulses travel shorter distances) and increases time constant

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80
Q

What is the first area damaged as a result of global cerebral ischemia?

A

Hippocampus

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81
Q

Which sequelae of Wernicke-Korsakoff syndrome is permanent?

A

Memory loss

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82
Q

Toxicity of ethylene glycol

A

Nephrotoxicity due to formation of envelope shaped oxalic acid crystals

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83
Q

Toxicity of Methanol

A

Ocular toxicity due to formation of formaldehyde (+ high anion gap acidosis)

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84
Q

Inhibitor of alcohol dehydrogenase used in methanol and ethylene glycol toxicities

A

Fomepizole, (can also use hemodialysis or EtOH)

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85
Q

Antidote for methanol and ethylene glycol toxicities

A

Ethanol (and fomepizole, which inhibits alcohol dehydrogenase)

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86
Q

MOA of disulfiram

A

Inhibits aldehyde dehydrogenase, causing acetaldehyde to build up, resulting in hangover-like effect (METRONIDAZOLE, cefoperazone, cefotetan, chlorpropamide, griseofulvin)

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87
Q

Cause of hypoglycemia in chronic alcoholics

A

Lack of eating + excess NADH due to high EtOH levels inhibiting gluconeogenesis

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88
Q

<p>Why are alcoholics commonly thiamine (vitamin B1) deficient?</p>

A

<p>Chronic high levels of acetaldehyde are broken down by acetaldehyde dehydrogenase, which uses thiamine (and folate) to do its job</p>

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89
Q

Use of Fomepizole

A

Inhibits alcohol dehydrogenase, used in acute methanol and ethylene glycol toxicity

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90
Q

What do you need to give alcoholic patients who are hypoglycemic?

A

Glucose WITH THIAMINE

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91
Q

What can happen if you give a hypoglycemic alcoholic glucose without thiamine?

A

Wernicke encephalopathy

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92
Q

How does alcoholism cause hyperuricemia?

A

Creates a lactic acidosis. Lactic acid competes with uric acid for excretion.

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93
Q

Cancers which alcoholics are at an increased risk for include…

A

Squamous cell CA of the esophagus, Signet ring cell CA of the stomach, Hepatocellular CA

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94
Q

MOA of carbamazepine/phenytoin

A

Decrease axonal conduction by preventing sodium influx through fast Na+ channels

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95
Q

1st Line drug for Tic Douloureux (Trigeminal neuralgia)

A

Carbamazepine

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96
Q

MOA of anti-convulsants lamotrigine/topirimate/felbamate

A

Block excitatory effects of glutamic acid

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97
Q

MOA of ethosuxamide and (maybe) valproic acid

A

Decrease presynaptic calcium influx through T type calcium channels in thalamus (note: this is just one of multiple proposed mechanisms for valproic acid)

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98
Q

DOC for absence seizures

A

Ethosuxamide (can also use valproate)

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99
Q

1st line for acute status epilepticus

A

Benzos (lorazepam/diazepam)

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100
Q

How does fosphenytoin differ from phenytoin?

A

Can be used parenterally because it is more water soluble (for use in status epilepticus)

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101
Q

1st line for prophlaxis against status epilepticus

A

Phenytoin/Fosphenytoin

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102
Q

What is unique about the metabolism of phenytoin (as far as anti-SZ meds are concerned)?

A

It is eliminated by zero order kinetics (constant amount of drug removed per unit time - also EtOH and aspirin)

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103
Q

Which anti-seizure drugs induce P450s?

A

Phenytoin/Carbamazepine

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104
Q

Which anti-seizure drug inhibits P450s?

A

Valproate

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105
Q

Major SFX of phenytoin

A

Gingival hyperplasia, lymphadenopathy, hirsuitism, megaloblastic anemia (decrease folate), sedation, aplastic anemia, nystagmus/diplopia/ataxia

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106
Q

Teratogenicity of phenytoin

A

Cleft lip/palate

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107
Q

DOC (3) for tonic/clonic seizures

A

Phenytoin/Carbamazepine/Valproate

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108
Q

Anti-seizure drugs used for bipolar disorder

A

Carbamazepine.Valproate (manic phase)

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109
Q

What does carbamazepine do to P450s?

A

INDUCES (just like phenytoin)

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110
Q

SFX of carbamazepine

A

Increase ADH secretion, SJS, CNS depression

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111
Q

Teratogenicity of Carbamazepine

A

Cleft lip/palate (like phenytoin) AND NTD’s (like valproate)

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112
Q

Patient with history of seizures presents with symptoms consistent with SIADH. What is causing this?

A

Use of carbamazepine. It increases the release of ADH.

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113
Q

MOA of valproate

A

Inhibits GABA transaminase, which breaks down GABA. Increase GABA = CNS depression. Valproate also blocks T-type calcium channels in the thalamus. This is why it is used for absence seizures.

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114
Q

What does valproate do to P450s?

A

INHIBITS

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115
Q

Toxicity of valproate

A

Hepatotoxicity (measure LFTs); Pancreatitis; Alopecia (opposite of Phenytoin!)

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116
Q

Valproate Teratogenicity

A

Spina Bifida. CI in pregnancy!

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117
Q

Teratoginicities of anti-seizure meds

A

Phenytoin (cleft lip/palate); Valproate (spina bifida); Carbamazepine (cleft lip palate and spina bifida - BOTH)

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118
Q

MOA of ethosuxamide and its use

A

blocks T-type calcium channels in thalamus. DOC for absence seizures

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119
Q

What anticonvulsant is considered safest in pregnancy for treatment of pre-existing seizures?

A

Phenobarbital

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120
Q

Toxicity of Felbamate

A

Hepatotoxicity and aplastic anemia

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121
Q

Toxicity of lamotrigine

A

Stevens Johnson Syndrome (black box warning)

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122
Q

First line drug in febrile seizures (kids)

A

Phenobarbital

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123
Q

MOA, Uses, Toxicity of Vigabatrin

A

MOA: GABA analogue; Uses: infantile spasms, refractory epilepsy; Toxicity: diffuse atrophy of peripheral retinal nerve fiber layer. Patients should have annual visual field testing.

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124
Q

Minimal Alveolar Concentration (MAC) definition

A

Concentration of inhaled anesthetic as a percent of inspired air, at which 50% of patients don’t respond to a surgical stimulus (a measure of potency).

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125
Q

What does an increase in lipid solubility do to the potency of an inhaled anesthetic?

A

Increases it - allows it to cross BBB

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126
Q

What effect does decreased blood solubility have on the onset time of an inhaled anesthetic?

A

Decreases it - decreased solubility in blood = rapid onset (gets to the BBB quickly)

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127
Q

Lipid/blood characteristics of nitrous oxide

A

Low solubility in both. Low blood solubility = fast onset. Low lipid solubility = low potency.

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128
Q

SFX and antidote for halothane

A

Malignant hyperthermia. Antidote = dantrolene. Also causes arrhythmias and hepatitis.

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129
Q

Barbiturate used for anesthesia induction

A

Thiopental - rapid onset, short acting

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130
Q

BZ used for preoparative sedation with anterograde amnesia

A

Midazolam (antidote = flumazenil)

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131
Q

Important characteristics of propfol

A

Anti-emetic, rapid induction

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132
Q

Ketamine MOA

A

NMDA-receptor blocker, used for anesthesia induction

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133
Q

Propofol MOA

A

Potentiates GABA at GABA-A receptors

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134
Q

SFX of Ketamine

A

Hallucination, vivid nighmares, CV stimulation, increased ICP

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135
Q

What terminates the effect of barbiturates such as thiopental?

A

Redistribution into tissues such as skeletal muscle and fat.

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136
Q

What effects do barbiturates have on cerebral blood flow?

A

Decrease

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137
Q

MOA of local anesthetics

A

Bind to and block activated sodium channels (most effective in rapidly firing neurons)

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138
Q

How many molecules of curare-like molecule (nondepolarizing neuromuscular blocking drugs) does it take to block one NMJ?

A

Only ONE. Even though there are two binding sites for acetylcholine, post-synaptic activation of the nicotinic receptor requires BOTH alpha subunits to be simultaneously stimulated by Ach.

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139
Q

MOA of curare drugs (non-depolarizing NMJ blockers)?

A

Competitive antagonist at nicotinic receptors (at the NMJ).

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140
Q

Antidote for curare drugs (non-depolarizing NMJ blockers)?

A

Since they are competitive inhibitors, they can be overcome with acetylcholinesterase inhibitors. Choose neostigmine because it doesn’t cross BBB like physostigmine.

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141
Q

Nondepolarizing NMJ blocker safe in renal/hepatic failure

A

Atracurium, but it is spontaneously broken down to laudanosine, which can cause seizures

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142
Q

MOA of succinylcholine (depolarizing NMJ blocker)

A

Ach receptor agonist, producing sustained depolarization (phase I) and eventual desensitization (phase II)

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143
Q

Two phases of succinylcholine use

A

Phase I: prolonged depolarization due to succinylcholine’s agonist activity. Flaccid paralysis. Potentiated by Ach-esterase inhibitors; Phase II: desensitization of nicotinic receptors. Antidote = Ach-esterase inhibitors.

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144
Q

Enzymes that metabolize succinylcholine

A

Pseudocholinesterase (rapid)

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145
Q

Succinylcholine SFX

A

Hyperkalemia, malignant hyperthermia, hypercalcemia

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146
Q

What receptor does baclofen bind?

A

GABA-B

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147
Q

Adult CNS tumor that crosses the midline

A

GBM

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148
Q

What (embryo) forms the nucleus pulposus?

A

Notochord

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149
Q

Frog-like appearance of aborted fetus

A

Anencephaly

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150
Q

Anencephaly results in maternal poly- or oligo- hydramnios, and why?

A

Polyhyramnios. Fetus has no brain, thus no swallowing centers, and can’t swallow amniotic fluid, so it builds up.

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151
Q

Congenital failure of development of the cerebellar vermis

A

Dandy-Walker formation

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152
Q

Presentation of Dandy-Walker formation

A

Massively dilated 4th ventricle with absent cerebellum w/ hydrocephalus (know the image! http://goo.gl/unfcYT)

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153
Q

Massively dilated 4th ventricle with absent cerebellum w/ hydrocephalus

A

Dandy Walker formation (know the image!!)

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154
Q

Congenital herniation of cerebellar tonsils through the foramen magnum

A

Arnold-Chiari Malformation

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155
Q

<p>Common presentations of Arnold-Chiari malformation (3)</p>

A

<p>Hydrocephalus (due to herniated cerebellar tonsils obstructing CSF flow)
Syringomyelia
thoraco-lumbar Meningomyelocele with paralysis below the defect</p>

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156
Q

Loss of pain and touch position sense in the upper extremity

A

Syringomyelia (SPARES position sense and fine touch - DCML)

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157
Q

Big congenital malformation to associate with syringomyelia

A

Arnold Chiari malformation

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158
Q

Triad of Horner syndrome

A

Ptosis, anhidrosis, miosis

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159
Q

Expansion of a syringomyelia can result in…

A

Compression of the anterior horns (LMN paralysis); Compression of the lateral horn, which includes the hypothalamospinal tracts (Horner syndrome)

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160
Q

Inherited degeneration of anterior motor horn

A

Werdnig-Hoffman disease (autosomal recessive) - “floppy baby”

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161
Q

CNS lesion with random upper and lower motor neuron signs

A

ALS

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162
Q

What distinguishes ALS from syringomyelia?

A

NO sensory impairment with ALS

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163
Q

Mutation in familial ALS

A

Zinc copper superoxide dismutase (removes free radicals)

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164
Q

GAA trinucleotide repeat

A

Friedrich Ataxia - in frataxin gene

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165
Q

SSX of Friedrich ataxia

A

Ataxia with loss of vibratory sense and proprioception + muscle weakness. Due to cerebellar damage + damage to multiple spinal cord tracts.

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166
Q

Frataxin gene function

A

Mitochondrial iron regulation.

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167
Q

Gene Mutated in Friedrich Ataxia

A

Frataxin (GAA trinucleotide repeat)

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168
Q

1 cause of death in Friedrich Ataxia

A

Hypertrophic Cardiomyopathy

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169
Q

Most common causes (3) of meningitis in neonates

A

Group B strep; E.coli; Listeria

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170
Q

Most common cause of meningitis in children/teens

A

Neisseria Meningitidis

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171
Q

Most common cause of meningitis in adults/elderly

A

Strep pneumo

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172
Q

Most common cause of meningitis in unvaccinated kids

A

H. flu

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173
Q

Most common cause of meningitis in immunocompromised

A

Cryptococcus neoformans

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174
Q

How does N. meningitis get from the environment to the meninges?

A

Inhaled -> nasopharynx -> blood -> choroid plexus -> meninges

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175
Q

Most common viral cause of meningitis

A

Coxsackievirus

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176
Q

Where should you stick the needle on an LP and why?

A

L4-L5 vertebral levels. Cord ends at L2, subarachnoid space with CSF ends at S2.

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177
Q

Which meningeal layer is not pierced during an LP?

A

Pia

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178
Q

What are the general CSF characteristics with bacterial meningitis?

A

High neutrophils with low glucose (bacteria consume glucose) + positive gram stain/culture

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179
Q

What are the general CSF characteristics with viral meningitis?

A

High lymphocytes with normal CSF glucose (viruses don’t consume glucose)

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180
Q

What are the general CSF characteristics with fungal meningitis?

A

High lymphoctes with low CSF glucose (fungi consume glucose)

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181
Q

Which infectious cause of meningitis shows the highest rate of complications?

A

Bacterial (pus, exudate increases ICP)

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182
Q

What neuroendocrine tumor can cause global cerebral ischemia?

A

Insulinoma due to repeated episodes of hypoglycemia

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183
Q

Where do infarcts most commonly occur with moderate global ischemia?

A

Watershed regions

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184
Q

What happens in cortical laminar necrosis?

A

Global cerebral ischemia necroses certain layers of more vulnerable cerebral cells but not others (which contains 6 layers). This creates bands of necrosis with non-necrosed cells in-between.

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185
Q

Cerebral lines of necrosis with non-necrosed cells in-between describes…

A

Cortical laminar necrosis - caused by moderate global ischemia.

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186
Q

Why does a thrombotic stroke form a pale infarct?

A

Thrombotic strokes are due to atherosclerosis, which ruptures and forms a thrombus. The body lyses the thrombus, but it keeps forming over and over again because of the exposed subendothelium, so blood never returns to the area.

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187
Q

Why does an embolic stroke form a hemorrhagic (“pink”) infarct?

A

Embolic strokes are due to emboli coming from other areas of the body. They lodge in cerebral arteries for long enough to cause neuronal death, then the body lyses them. Since they don’t recur like thrombotic strokes (because there is no exposed subendothelium), blood rushes back to the area of necrosis, causing hemorrhage.

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188
Q

Where do lacunar strokes most commonly occur?

A

Lenticulostriate arteries in the deep structures of the brain

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189
Q

What underlying vascular pathology leads to lacunar strokes?

A

Hyaline arteriolosclerosis (secondary to HTN/DM)

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190
Q

What is the earliest change seen following CNS ischemia?

A

Red neurons (12-24 hours)

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191
Q

Describe the microscopic changes seen following an ischemic CNS stroke.

A

Red neurons (12-24 hours); Neutrophils (3-5 days); Microglia (5-7 days); Granulation-like tissue; Gliosis (>1 week, final change)

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192
Q

What is the final histologic stage seen with CNS ischemia?

A

Gliosis

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193
Q

What is the main risk factor for Charcot-Bouchard aneurysms?

A

HTN

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194
Q

What does the LP show with a subarachnoid hemorrhage?

A

Blood or Xanthochromia (yellow tinge to CSF due to bilirubin breakdown)

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195
Q

What is the main cause of subarachnoid hemorrhage?

A

Rupture of berry aneurysms

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196
Q

What is the #1 site for berry aneurysms?

A

The branch point of the ACOM in the anterior circle of Willis

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197
Q

Why (histologically) are berry aneurysms weak?

A

VASCULAR MEDIA LAYER FAILS TO DEVELOP AT BRANCH POINT of aneurysm, causing a sacular outpouching of the blood vessel, increasing rupture risk.

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198
Q

List two syndromes that increase risk for development of berry aneurysms.

A

Marfan syndrome and ADPKD

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199
Q

Treatment for wet macular degeneration

A

VEGF inhibitors (bevacizumab)

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200
Q

Presentation of wet macular degeneration

A

Acute vision loss over a period of months to weeks

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201
Q

Physical findings of wet macular degeneration

A

Subretinal fluid/hemorrhage, gray subretinal membrane, or neovascularization

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202
Q

Vessel that ruptures in an epidural hematoma

A

Middle meningeal a.

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203
Q

<p>Lens (biconcave) shaped lesion on head CT</p>

A

<p>Epidural hematoma</p>

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204
Q

Head trauma with lucid interval that precedes neurologic signs

A

Epidural hematoma

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205
Q

Vessels that rupture in a subdural hematoma

A

Bridging cerebral veins

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206
Q

Crescent shaped lesion on head CT

A

Subdural hematoma

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207
Q

Structures (3) compressed with an uncal herniation and sequelae

A

CN III (eye down and out); brainstem (coma); Paramedian artery on brainstem (brainstem hemorrhages)

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208
Q

Which cells are destroyed in MS?

A

Oligodendrocytes

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209
Q

What geographical association is seen with MS?

A

More commonly seen in regions away from the equator.

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210
Q

What is significant about the speech of a person with MS?

A

They commonly exhibit “scanning speech”, which is similar to drunken speech.

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211
Q

Explain INO seen with MS

A

Damage of the MLF is commonly seen with MS. When patient is asked to look laterally, the eye that is adducting (via CN III) receives a signal from the abducting eye (via CN VI) to adduct. If the MLF is damaged, this signal doesn’t make it, and the eye fails to adduct.

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212
Q

25 year old female is asked to look left. Her left eye abducts, but the right eye does’t adduct. What’s the problem?

A

MS - intranuclear ophthalmoplegia secondary to damage to the RIGHT MLF. Note: The MLF is named for eye it GOES TO, (i.e. the adducting eye - CN III nucleus) not where it originates (the abducting eye -CN VI nucleus). See First Aid p 442 for a picture.

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213
Q

Treatment for MS acute attack

A

High dose steroids

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214
Q

Long term MS treatment, shown to slow progression of disease

A

IFN - Beta

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215
Q

Mu, Kappa, and Delta receptors use which type of signaling?

A

Gi (lowers cAMP) - found on interneurons, serves to dampen neurotransmission

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216
Q

What receptor does morphine bind to?

A

Mu opioid receptors

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217
Q

Why should you not give pure oxygen to a patient in opioid-induced respiratory depression (unless they are mechanically ventilated)?

A

CO2 respiratory centers causing increase in breathing via HIGH CO2 are shut down by opioids because they have mu receptors. Thus, the only drive for respiration the patient has at this point is peripheral oxygen sensors, which stimulate breathing with LOW O2. If you shut these receptors off with high O2, there is no drive for the patient to breathe on their own.

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218
Q

Antidotes (IV and oral) for opioid OD

A

IV - naloxone; Oral - naltrexone (has a T in its name, passes by your Teeth)

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219
Q

SFX of opioids

A

Constipation, miosis, respiratory depression, urinary retention, addiction

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220
Q

What is significant about the metabolism of morphine?

A

It is metabolized by glucuronidation, and its metabolite is MORE POTENT than the parent compound - can cause nephrotoxicity

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221
Q

Long-t1/2 opioid agonist used opioid addiction tapering

A

Methadone

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222
Q

MOA & use of pentazocine, and a situation where it should not be given.

A

MOA : weak opioid (mu) agonist; Use: analgesia with limited addiction potential; Should not be used in opioid addiction because it can precipitate an acute withdrawal crisis (because it is only a weak agonist, and acts like an antagonist in the presence of a complete agonist like morphine)

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223
Q

Which opioid antagonist can be used to reduce alcohol craving?

A

PO Naltrexone

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224
Q

What effect do opioid analgesics have on synaptic ion channels?

A

Open K+ channels, increase potassium influx; Close Ca2+ channels, decrease calcium influx; Overall: decreases synaptic transmission

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225
Q

Which side effects aren’t reduced by opioid tolerance? (2)

A

Miosis, constipation

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226
Q

Explain the pharmacodynamic tolerance of opioids.

A

Opioids act through Gi, decreasing cAMP. Unlike most tolerance mechanisms, tolerance to opioids is not because of down-regulation of receptors. Opioid tolerance happens because other GPCR pathways in cells increase cAMP, requiring a bigger stimulus to produce significant inhibition.

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227
Q

Explain why clonidine is used to manage opioid withdrawal.

A

Long term opioid use inhibits norepinephrine release, causing upregulation of alpha-1 and beta-1 receptors. When opioids are withdrawn, NE levels go back to normal, causing the excess sympathetic symptoms secondary to higher number of receptors (agitation, tachycardia, sweating, HTN). Clonidine is given because it is an alpha-2 agonist that decreases the release of NE, thus calming the sympathetic effects.

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228
Q

Opioid agonist used for diarrhea

A

Loperamide

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229
Q

Opioid agonist used for cough suppression

A

Dextromethorphan (abuse potential - makes you trip balls)

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230
Q

Treatment for a neonate born to a heroin-addicted mother showing signs of opioid withdrawal?

A

Tincture of opium

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231
Q

Neurotransmitter changes seen in Parkinson disease (2)

A

Loss of dopaminergic neurons in nigrostriatal pathway; Excess cholinergic activity (leads to muscle rigidity and resting tremor)

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232
Q

<p>MOA of carbidopa</p>

A

<p>Noncompetitive PERIPHERAL (NOT CENTRAL) inhibitor of aromatic amino acid decarboxylase (AAAD). Prevents peripheral conversion of L-dopa to dopamine, so L-dopa can cross BBB. It increases the T1/2 of Levidopa and decreases the plasma dopamine levels</p>

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233
Q

Why is carbidopa given with L-dopa?

A

It blocks PERIPHERAL conversion of L-dopa to dopamine (NOT CENTRAL - AAAD is needed for conversion of L-dopa to dopamine!). Dopamine can’t cross BBB, but L-dopa can. Thus, carbidopa increases the amount of L-dopa available to cross the BBB and decreases peripheral side effects of dopamine.

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234
Q

SFX of levodopa

A

Dyskinesia (on-off effects), psychosis, hypotension, vomiting

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235
Q

Drug which inhibits aromatic amino acid decarboxylase (AAAD)

A

Carbidopa

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236
Q

Explain the on-off effects of levodopa

A

Dyskinesia when on the medicine, bradykinesia when off the medicine

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237
Q

COMT inhibitors used in PD

A

Entacapone, tolcapone

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238
Q

MOA of entacapone/tolcapone

A

Inhibit COMT, decreasing metabolism of L-dopa in the periphery, enhancing L-dopa uptake across BBB

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239
Q

MOA of selegiline

A

MAO-B inhibitor used in PD. Decrease metabolism of dopamine.

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240
Q

MAO-B inhibitor used in PD

A

Selegiline

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241
Q

Selegiline is a selective MAO-B inhibitor, what is significant about this with respect to side effects?

A

There is no interaction with tyramines (compounds found in wine and cheese). MAO-A inhibitors (phenelzine) block GI metabolism of tyramines, allowing them to enter the circulation and precipitate a hypertensive crisis. MAO-B inhibitors do not! Note: according to UWorld, this is the most commonly tested side effect on the USMLE.

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242
Q

Benztropine MOA and use

A

MOA: muscarinic receptor blocker; Use : calms down excess Ach activity in PD (decreases tremor/rigidity, but not bradykinesia)

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243
Q

What is the significance of aromatic amino acid decarboxylase in PD?

A

Metabolizes L-dopa to dopamine

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244
Q

DA agonists (4) used in Parkinson disease.

A

Bromocriptine, pergolide, Pramiprexole, Ropinerole. (the latter 2 are preferred)

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245
Q

Trihexyphenidyl MOA and use

A

MOA: muscarinic receptor blocker; Use : calms down excess Ach activity in PD (decreases tremor/rigidity, but not bradykinesia)

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246
Q

Antimuscarinic drugs (2) used in PD

A

Benztropine, Trihexyphenidyl

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247
Q

MOA of pramiprexole

A

Dopamine agonist used in PD

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248
Q

Antiviral drug used in PD

A

Amantadine (increases dopamine release)

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249
Q

Why is amantadine used in PD?

A

Increases dopamine release

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250
Q

SFX of amantadine

A

Antimuscarinic ; Livedo reticularis (UNIQUE!) - skin looks pale and blood vessels dilate to form a purple mesh

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251
Q

Cocaine MOA

A

Blocks dopamine, NE, and 5HT reuptake

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252
Q

Only drug approved for ALS

A

Riluzole (decreases glutamate release)

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253
Q

MOA of amphetamine

A

Block reuptake of NE/DA, also causes the NE/DA reuptake transporters to work in reverse, releasing more NT into the cleft.

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254
Q

Memantine MOA and use

A

MOA: NMDA receptor antagonist; Use: Alzheimer Disease

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255
Q

Donepezil MOA and use

A

MOA: Acetylcholinesterase inhibitor; Use: Alzheimer Disease

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256
Q

Acetylcholinesterase inhibitors used in Alzheimer disease

A

Donepezil, galantamine, rivastigmine

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257
Q

Antioxidant that may confer some protection to excitotoxicity in Alzheimer disease

A

Vitamin E

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258
Q

Components of the BBB (3)

A

Endothelial cells (non-fenestrated); Basement membrane; Astrocytic end feet

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259
Q

Proximal symmetric weakness with no sensory loss

A

Myopathies

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260
Q

Distal asymmetric weakness with atrophy, fasciculations, sensory loss and pain

A

Peripheral neuropathy

261
Q

Most common causes of peripheral neuropathy (2)

A

DM and EtOHism

262
Q

Signs of a polyneuropathy?

A

Stocking/glove sensory loss.

263
Q

1 motor neuropathy

A

GBS

264
Q

<p>SSX of Guillan-Barre syndrome</p>

A

<p>Ascending symmetric muscle weakness, areflexia, and paresthesias in hands/feet usually following a viral or GI illness or flu shot (don't forget campylobacter!)
NO SENSORY LOSS!</p>

265
Q

CSF findings in GBS

A

Elevated protein without elevated WBC

266
Q

Most common motor neuron disease

A

ALS

267
Q

SSX of MS

A

Weakness, spasticity, sensory loss, incontinence, vision loss that resolve and RETURN PROGRESSIVELY WORSE.

268
Q

Classic MRI finding with MS

A

White matter lesions (plaques)

269
Q

Signs seen with UMN lesions

A

spastic paralysis, hyperreflexia, Babinski sign, Hoffman sign, clonus

270
Q

Signs seen with LMN lesions

A

flaccid paralysis, hyporeflexia, negative babinski sign, fasciculations, atrophy

271
Q

Congenital damage to corticospinal tracts and/or basal nuclei resulting in spasticity, flaccid paralysis, dystonia

A

Cerebral palsy

272
Q

Reflexes seen (immediately) with sudden spinal cord trauma

A

Temporary flaccid paralysis and hyporeflexia (spinal shock) - eventually progresses to UMN characteristics

273
Q

Pt presents with acute onset of weakness and sensory loss in LE, radicular pain, saddle anesthesia, and urinary/bowel incontinence

A

Cauda equina syndrome - surgical emergency

274
Q

Treatment for cauda equina syndrome

A

Immediate surgical repair

275
Q

SSX of anterior spinal artery syndrome

A

BL loss of pain/temperature (spinothalamic tracts); BL weakness with hyperreflexia (corticospinal tract); Only thing spared is DCML

276
Q

Artery occluded in anterior spinal artery syndrome

A

The artery of Adamkiewicz

277
Q

Scrape tip of 3rd digit, thumb and 2nd digit flex in UM neuron lesion

A

Hoffman sign

278
Q

<p>SSX of Sequard syndrome (3 major)</p>

A

<p>CL loss of pain/temp below the lesion (spinothalamic tract); IL loss of position/vibratory below lesion (DCML); IL flaccid paralysis at the level of the lesion (anterior horn)</p>

279
Q

SSX/cause of tabes dorsalis

A

Loss of discriminative touch/proprioception due to loss of DCML. Cause: tertiary syphilis

280
Q

SSX/cause of subacute combined degeneration

A

Peripheral neuropathy, loss of proprioception/balance (loss of DCML), loss of pain/temp (loss of spinothalamic tracts), ataxic gait. Cause: chronic B12 deficiency.

281
Q

Weber/Rinne results with sensorineuronal hearing loss

A

Sound localizes to good ear (Weber); Air conduction > bone conduction (Rinne)

282
Q

Weber/Rinne results with conductive hearing loss

A

Sound localizes to bad ear (Weber); Bone conduction > air conduction (Rinne)

283
Q

What is the term for unequal pupils?

A

Anisocoria

284
Q

Vessel affected in lateral medullary syndrome

A

PICA

285
Q

Lesions to what two nerves can cause anisocoria?

A

CN III or sympathetics

286
Q

Temporal lobe tumor/lesion causes what visual defect?

A

Pie in the sky

287
Q

What is a Marcus-Gunn pupil and what causes it?

A

Pupil appears to dilate with direct stimulation to light. Indicates CN II lesion.

288
Q

What is an Argyll-Robertson pupil and what causes it?

A

Eyes that accommodate, but don’t react to light. Indicates tertiary syphilis.

289
Q

Describe the position of the limbs in decorticate posturing.

A

UL: flexed (held to core); LL: extended

290
Q

What causes flexion of UL in decorticate posturing?

A

Rubrospinal tract

291
Q

Describe the position of the limbs in decerebrate posturing.

A

All 4 limbs are extended.

292
Q

How is nystagmus named?

A

For the fast phase (quick jerk back to midline).

293
Q

Explain the results of caloric testing

A

Cold: nystagmus opposite to the stimulated side; Warm: nystagmus to the same side as is stimulated; COWS

294
Q

Structure(s) degenerated in Huntington disease.

A

Caudate (mainly) and putamen

295
Q

Lesion to sub thalamic nucleus produces

A

Contralateral hemiballismus.

296
Q

Wild unilateral flinging of an arm/leg

A

hemiballismus

297
Q

Slow, writhing movements

A

Athetosis

298
Q

Sudden, brief, uncontrolled muscle contraction

A

Myoclonus (hiccups!)

299
Q

Sustained, involuntary muscle contractions

A

Dystonia

300
Q

Slow, zigzag motion when pointing or extending toward an object

A

Intention tremor. Indicative of cerebellar disease

301
Q

Action tremor exacerbated by holding limb position

A

Essential tremor

302
Q

With what do patients typically self-medicate to reduce essential tremor?

A

EtOH.

303
Q

<p>Function of VPL thalamus</p>

A

<p>Receives input for body pain/temperature, touch, vibration, proprioception
VPL = very painful legs</p>

304
Q

<p>Function of VPM thalamus</p>

A 
<p>Receives pain/temperature from face
also taste (trigeminal and gustatory pathways)
VPM = very painful mouth</p>
305
Q

Function of LGB of thalamus

A

Vision

306
Q

<p>Function of MGB of thalamus</p>

A

<p>Hearing (from the superior olive and inferior colliculus of tectum)
Medial = Musical</p>

307
Q

<p>Function of VL lobe of thalamus</p>

A

<p>Receives input from basal nuclei - fine tunes motor output from cortex before sending it back</p>

308
Q

Function of lateral area of hypothalamus

A

hunger

309
Q

Function of ventromedial area of hypothalamus

A

satiety

310
Q

Function of anterior hypothalamus

A

Cooling

311
Q

Function of posterior hypothalamus

A

heating

312
Q

Function of suprachiasmatic nucleus of hypothalamus

A

Circadian rhythm

313
Q

Romberg test shows that a patient sways with eyes open…dx?

A

Cerebellar ataxia

314
Q

Romberg test shows that a patient sways with eyes closed…dx?

A

Sensory ataxia (DCML)

315
Q

SSX of blockage of anterior choroidal artery

A

CL hemiparesis (CST); CL homonymous hemianopsia (optic tract)

316
Q

SSX of blockage of lenticulostriate arteries

A

CL hemiparesis (posterior limb of internal capsule - pure motor stroke)

317
Q

SSX of MCA blockage

A

Motor/sensory symptoms involving the CL face/upper limb/trunk. May produce Broca aphasia.

318
Q

SSX of ACA blockage

A

Motor/sensory symptoms involving the CL lower limb.

319
Q

Blockage of this artery can cause Broca aphasia

A

Superior division of MCA

320
Q

Blockage of this artery can cause Wernicke aphasia

A

Inferior division of MCA

321
Q

SSX of PCA blockage

A

Visual symptoms - CL hemianopsia - can have macular sparing!

322
Q

Impaired comprehension, repetition, naming and speech output

A

Broca Aphasia

323
Q

Fluent speech full of nonsense words and phrases

A

Wernicke Aphasia

324
Q

Aphasia characterized by poor repetition

A

Conductive aphasia

325
Q

What structure is damaged in conduction aphasia?

A

Arcuate fasciculus

326
Q

SSX of anterior watershed strokes?

A

Broca aphasia and lower limb effects.

327
Q

SSX of posterior watershed stroke?

A

Wernicke aphasia and visual loss.

328
Q

Define apraxia.

A

Loss of ability to perform a learned/familiar task

329
Q

Define agnosia

A

Inability to recognize a familiar object regardless of intact sense

330
Q

SSX of Gerstmann syndrome

A

Acalculia (can’t do math), agraphia (can’t write), finger agnosia (can’t distinguish one finger from another) and left-right confusion

331
Q

Cause of Gerstmann syndrome

A

Damage to the angular gyrus in the dominant hemisphere

332
Q

<p>SSX of Kluver-Bucy syndrome</p>

A

<p>Docility, placidity, hypersexuality, hyperorality and hypermetamorphosis.
"hyperorality, hypersexualty and disinhibited behavior"</p>

333
Q

Cause of Kluver-Bucy syndrome

A

BL amygdala lesions

334
Q

<p>Signs and Symptoms of diffuse Lewy Body Dementia</p>

A

<p>Memory Loss; Parkinsonian-Like Movement disorder (onset at the SAME time as memory loss); Visual hallucinations (pretty specific for DLBD as far as degenerative diseases are concerned); Autonomic dysfunction (urinary incontinence); Sleep disturbances</p>

335
Q

What is the first sign of magnesium toxicity?

A

decreased deep tendon reflexes

336
Q

Patient has a CN III palsy. Where is the most likely aneurysm?

A

Ipsilateral posterior communicating artery (PCOM)

337
Q

SSX of a CN III palsy?

A

Down and out eye; Blown pupil; droopy eyelid (loss of levator palpebrae)

338
Q

What forms from the metencephalon (2) ?

A

Cerebellum and pons

339
Q

What forms from the myelencephalon?

A

Medulla

340
Q

What forms from the mesencephalon?

A

Midbrain

341
Q

What forms from the diencephalon?

A

Anything that has “thalamus” in it: thalamus, hypothalamus, subthalamus, epithalamus

342
Q

What forms from the telencephalon (2) ?

A

Cerebrum and basal nuclei

343
Q

Which nerve gives general sensation to the anterior tongue?

A

CN V3 (lingual branch)

344
Q

CGG triplet repeat

A

Fragile X syndrome

345
Q

CTG triplet repeat

A

Myotonic dystrophy

346
Q

CN (2) providing input to the nucleus ambiguus

A

CN IX and CN X

347
Q

Function of the nucleus ambiguus

A

Provides motor innervation to muscles of the pharynx and larynx via CN IX and X.

348
Q

Functions of the principal (chief) trigeminal nucleus

A

Transmits discriminative touch/pressure to the face, mucous membranes, and other head structures via CN V (all branches).

349
Q

Function of the spinal trigeminal nucleus

A

Transmits pain, temperature, and crude touch to the face via CN V.

350
Q

Function of the spinal mesencephalic nucleus

A

Proprioception for muscles of mastication

351
Q

Things seen with fetal dilantin (hydantoin/phenytoin) syndrome

A

Skull/face abnormalities; Hypoplasia of fingernails/toenails

352
Q

The longest stage of sleep (spend the most time in)

A

2

353
Q

Stage of sleep with sleep spindles and K complexes on EEG

A

2

354
Q

Stage of sleep with delta waves on EEG

A

3

355
Q

Stage of sleep with beta waves on EEG

A

REM (also awake with eyes open)

356
Q

Stage of sleep with theta waves on EEG

A

1

357
Q

Meds (2) for seizure prophylaxis in preeclampsia

A

Magnesium sulfate (more commonly used), Labetalol

358
Q

Meds to lower BP in pregnancy

A

Labetalol; Hydralazine

359
Q

Most important test to perform when assessing toxicity for magnesium sulfate

A

Deep tendon reflexes

360
Q

Magnesium sulfate is primarily used for

A

Seizure prophylaxis in pre-eclampsia

361
Q

What is rameleton?

A

Melatonin agonist used for insomnia

362
Q

Sleepwalking occurs in what stage of sleep?

A

3

363
Q

Night terrors occur in what stage of sleep?

A

3

364
Q

What is the primary neutotransmitter during REM sleep?

A

Ach

365
Q

What neurotransmitter is essential for initiating sleep?

A

5-HT

366
Q

What do EtOH/Benzos/Barbiturates do to sleep?

A

Decrease REM

367
Q

In what stage of sleep do nightmares occur?

A

REM

368
Q

At what age does the Babinski sign disappear?

A

12-15 months

369
Q

At what age should a child be able to sit alone, crawl, transfer toys from hand to hand?

A

7-9 months

370
Q

<p>What makes up APGAR score?</p>

A

<p>Appearance, pulse, grimace, activity, respirators; Taken at 1 and 5 minutes</p>

371
Q

In the embryo, what induces the overlying ectoderm to differentiate into the neuroectoderm and form the neural plate?

A

Notochord (within mesoderm)

372
Q

What does the neural plate give rise to?

A

Neural tube and neural crest cells

373
Q

What does the notochord become?

A

Nucleus pulposus of the intervertebral disc in adults

374
Q

What does the alar and basal plates become?

A 
Alar = dorsal = sensory
Basal = ventral = motor
375
Q

Describe the three primary vesicles

A

Forebrain (prosencephalon)
Midbrain (mesencephalon)
Hind brain (rhombencephalon)

376
Q

What does the forebrain (prosencephalon) develop into?

A

Telencephalon –> cerebral hemispheres, basal ganglia, hippocampus, amygdala, and lateral ventricles

Diencephalon –> thalamus and hypothalamus and optic tract and nerve, third ventricle

377
Q

What does the midbrain (mesencephalon) develop into?

A

Mesencephalon –> Midbrain, Aqueduct

378
Q

What does the hindbrain (rhombencephalon) develop ?into

A

Metencephalon –> Pons and cerebellum and upper part of the 4th ventricle

Myelencephalon –> medulla and lower part of 4th ventricle

379
Q

how do neural tube defects occur?

A

Neuropores fail to fuse during week 4 leading to persistent connection between the amniotic cavity and the spinal canal

380
Q

What can act as a confirmatory test for neural tube defects?

A

Increased acetylcholinesterase in amniotic fluid is helpful confirmatory test (fetal AChE in CSF transudates across defect into the amniotic fluid)

This is after you find an elevated alpha fetoprotein

381
Q

Is anencephaly due to failure of the brain to develop?

A

NO! There is a malformation of the anterior neural tube resulting in no forebrain and an open calvarium. The brain is exposed to the acidic amniotic fluid which eats away at the brain.

382
Q

What is anencephaly associated with?

A

Maternal diabetes type I

maternal folate supplementation also decreases risk

383
Q

What is Holoprosencephaly?

A

Failure of the left and right hemispheres to separate, usually occurs during weeks 5-6
moderate form has cleft palate/lip, and most severe form results in cyclopia

384
Q

What is the mutation in Holoprosencephaly?

A

Sonic hedgehog signaling pathway mutation

Can also be seen in fetal alcohol syndrome and Patau syndrome (trisomy 13)

385
Q

Describe Chiari II malformation

A

Significant cerebellar tonsillar and vermian herniation through the foramen magnum with aqueductal stenosis and hydrocephalus
Often presents with throaco-lumbar myelomenigocele and paralysis below the defect

386
Q

Describe Dandy Walker

A

Agenesis of cerebellar vermis with cystic enlargement of the 4th ventricle that fills the posterior fossa.
Associated with hydrocephalus and spina bifida

387
Q

What will Dandy walker lead to?

A

Truncal ataxia, head tremor and truncal instability

388
Q

Cystic enlargement of the central canal of the spinal cord

A

Syringomyelia

389
Q

Which tracts are typically damaged first with a syringomyelia?

A

Crossing fibers of spinothalamic tract - results in a “cape like” bilateral loss of pain and temp in upper extremities
Fine touch sensation is PRESERVERD!

390
Q

What is the most common level of a syringomyelia?

A

C8-T1

391
Q

What controls the taste of the tongue?

A

anterior 2/3 CN 7

posterior 1/3 CN 9 and 10 (way back)

392
Q

What controls the sensation on the tongue?

A

CNV3 controls the anterior 2/3

CN IX controls the posterior 1/3

393
Q

What controls the motor innervation of the tongue?

A

CNXII

394
Q

What are the muscles of the tongue derived from?

A

Occipital myotomes

395
Q

Describe the tongue development in terms of branchial arches

A

1st branchial arch forms the anterior 2/3 - this is why sensation is via CN V3 and taste from CN 7

3rd and 4th branchial arches form the posterior 1/3 - this is why sensation and taste mainly come from CN9 and the extreme back is CN10

396
Q

What comes from Neuroectoderm?

A

CNS neurons, ependymal cells (inner lining of ventricles, make CSF), oligodendroglia, astrocytes

397
Q

What comes from the neural crest?

A

PNS neurons, Schwann cells

398
Q

What comes from mesoderm?

A

Microglia (macrophages of CNS)

399
Q

What does Nissl substance stain?

A

rough endoplasmic reticulum of neurons - note that rER is not found in axons

400
Q

What do astrocytes to?

A

Physical support, repair, potassium metabolism, removal of XS neurotransmitter, maintenance of BBB
Reactive gliosis occurs in response to injury

401
Q

What is the astrocyte marker?

A

GFAP

402
Q

What are microglia?

A

CNS phagocytes - have small irregular nuclei and relatively little cytoplasm. Respond to tissue damage by differentiating into large phagocytic cells

can be seen with silver stain

403
Q

What happens to microglia cells in HIV infected pts?

A

Fuse to form multinucleated giant cells in the CNS

404
Q

What makes myelin in the CNS? PNS?

A

CNS - oligodendrocytes

PNS - Schwann cells

405
Q

Describe oligodendrocytes

A

White matter, myelinate many axons in the CNS; have a fried egg appearance
note that oligodendrocytes are destroyed in MS

406
Q

Describe Schwann cells

A

Schwann cells myelinate ONE axon in the PNS, they promote axonal regeneration

note that schwann cells are damaged in Guillain Barre

407
Q

What is the predominant glial cell in white matter?

A

Oligodendrocyte

408
Q

What is an acoustic neuroma?

A

Type of schwannoma - typically located in the internal acoustic meatus (CN VIII), bilateral in neurofibromatosis type 2

409
Q

What receptor type is responsible for pain and temperature?

A

Free nerve endings

410
Q

What is the location of free nerve endings?

A

All skin, epidermis and some viscera

411
Q

Describe free nerve endings

A

C fibers - slow, unmyelinated fibers - burning dull pain, itch

Adelta - fast myelinated fibers - pricking pain

412
Q

What receptor type is responsible for dynamic, fine/light touch and position sense?

A

Meissner’s corpuscles

413
Q

Where are meissner’s corpuscles located?

A

Glabrous (hairless) skin like the fingertips eyelids and lips or palsm soles and digits

414
Q

Describe meissern’s corpuscles

A

Large myelinated fibers that adapt quickly

415
Q

Describe Pacinian corpuscles?

A

Large myelinated fibers

resembles an onion

416
Q

Where are pacinian corpuscles located?

A

Deep skin layers, ligaments and joints

417
Q

Which receptor type is responsible for vibration and pressure and increased tension?

A

Pacinican corpuscles

418
Q

Describe Merkel’s discs

A

Large, myelinated fibers that adapt slowly

look like melanocytes

419
Q

Where are merkel’s discs located?

A

Hair follicles, fingertips and oral and anal mucosa

420
Q

Which receptors are responsible for pressure, deep static touch like with shapes and edges and position sense?

A

Merkel’s discs

421
Q

List the layers of a peripheral nerve

A

Endoneurium - inner, single nerve fibers , inflammatory infiltrate in guillain barre
Perineurium - around
Epineurium - outer

422
Q

What must be rejoined in microsurgery for limb reattachment?

A

Perineurium

423
Q

Describe the Epineurium

A

Dense connective tissue that surrounds entire nerve including the fascicles and blood vessels

424
Q

Describe Norepinephrine in disease states

A

Increased in anxiety

decreased in depression

425
Q

Where is norepinephrine synthesized?

A

Locus ceruleus (pons)

426
Q

Describe Dopamine in disease states

A

Increased in schizophrenia

Decreased in Parkinson’s and depression

427
Q

Describe serotonin and disease states

A

Decreased in anxiety and depression

428
Q

Describe Ach in disease states

A

Decreased in Alzheimer’s and Huntington’s and increased in REM sleep, also increased in Parkinson’s disease

429
Q

Describe GABA in disease states

A

Decreased in anxiety and Huntington’s

430
Q

Where is Dopamine synthesized?

A

Ventral tegmentum and SNc (midbrain)

431
Q

Where is serotonin synthesized?

A

Raphe nucleus in the pons

432
Q

Where is ACh synthesized?

A

Basal nucleus of meynert

433
Q

Where is GABA synthesized?

A

Nucleus accumbens

434
Q

What is the Locus ceruleus associated with?

A

Stress and panic

435
Q

What is the nucleus accumbens and septal nucleus associated with?

A

reward center, pleasure, addiction, fear

436
Q

What can cross rapidly across the BBB?

A

Nonpolar/lipid-soluble substances cross rapidly via diffusion

437
Q

What can occur if infarction or neoplasm destroys the endothelial cell tight junctions of the BBB?

A

Vasogenic edema

438
Q

What are the two inhibitory neurotransmitters?

A

GABA and glycine

439
Q

Is glutamate inhibitory or excitatory neurotransmitter?

A

Excitatory

440
Q

What happens to serotonin in the pineal gland?

A

Converted to melatonin

441
Q

What disease is associated with degeneration of the basal nucleus of Meynert and less CNS ACh?

A

Alzheimer’s disease

442
Q

What is GABA?

A

Main inhibitory neurotransmitter of the CNS - made from glutamate
When you block GABA you get an excitatory response

note that Benzodiazepines and barbiturates increased the effect of GABA function (anti-anxiety)

443
Q

What is Glycine?

A

Inhibitory neurotransmitted of the spinal cord

444
Q

What is the main excitatory neurotransmitter of the CNS?

A

Glutamate

445
Q

What happens when you block the Mesocortical dopaminergic pathway?

A

Increased negative symptoms of schizophrenia like social withdrawal and depression

446
Q

What happens when you block the mesolimbic dopaminergic pathway?

A

Relieves the positive symptoms of schizophrenia

447
Q

What happens when you block the nigrostriatal dopaminergic pathway? What if you stimulate it?

A

Block = Parkinson’s disease

Stimulate = extrapyramidal side effects

448
Q

What happens if you block the tuberoinfundibular dopaminergic pathway?

A

Increased release of prolactin from the anterior pituitary

449
Q

Describe the lateral area of the hypothalamus

A

Hunger
Destruction leads to anorexia, failure to thrive
inhibited by leptin
“if you zap your lateral nucleus you shrink laterally”

450
Q

Describe the ventromedial area of the hypothalamus

A

Satiety
Destruction (craniopharyngioma) leads to hyperphagia
stimulated by leptin

451
Q

What does the anterior hypothalamus do?

A

Cooling (AC)
Parasympathetics

damage leads to hyperthermia

452
Q

What does the posterior hypothalamus do?

A

Heating, sympathetic

damage leads to hypothermia

453
Q

What does the suprachiasmatic nucleus do?

A

Circadian rhythm

receives input from retina

454
Q

what is the posterior pituitary derived from?

A

neuroectoderm

455
Q

Which hypothalamic nuclei make ADH and oxytocin?

A

ADH - supraoptic (water balance)

Oxytocin - paraventricular

456
Q

Which hypothalamic nucleus secretes GnRH?

A

Preoptic nucleus

457
Q

What does the Arcuate nucleus of the hypothalamus secrete?

A

Dopamine and GHRH

458
Q

What does the Mamillary body do?

A

Receives input from the hippocampus

hemorrhagic lesion leads to Wernicke’s encephalopathy

459
Q

What is the limbic system?

A

Responsible for the 5 F’s: Feeding, Fleeing, Fighting, Feeling and F-ing
collection of neural structures involved in emotion, long term memory, olfaction, behavior modulation and autonomic nervous system function

460
Q

How do we not let the limbic system rule our lives?

A

The perfrontal cortex can inhibit the limbic system so that we don’t act on instinct alone - prefrontal cortex is for decision making and allows for delayed gratification to exist

461
Q

List the 5 structures that make of the limbic system

A

Hippocampus, amygdala, fornix, mammillary bodies, cingulate gyrus

462
Q

What is the most common cause of damage to the flocculonodualr lobe of the cerebellum?

A

Medulloblastoma in childhood

463
Q

What are the deep nuclei of the cerebellum?

A

From lateral to medial: Don’t Eat Greasy Foods
Dentate, Emboliform, Globose, Fastigial
Interposed nuclei = Emboliform + Globose

464
Q

What is the difference between a medial or lateral injury to the cerebellum?

A

Medial - Balance and truncal coordination
Lateral - voluntary movement of extremities, so when injured you have propensity to fall toward the injured side (ipsilateral side - due to a double CL)

465
Q

What is the major output of the cerebellum?

A

Brachium conjunctivum (Superior cerebellar peduncle) –> CL ventrolateral nucleus of the thalamus) –> motor cortex

466
Q

What is the importance of the basal ganglia?

A

Important in voluntary movements and making postural adjustments

467
Q

What makes up the striatum of the basal ganglia? The Lentiform of the basal ganglia?

A 
Striatum = caudate (cognitive) + putamen (motor)
Lentiform  = putamen + globus pallidus
468
Q

What occurs with lesion to the subthalamic nucleus?

A

Hemiballismus (increased movement)

note that the Hemiballismus matches the CL subthalamic nucleus

469
Q

What is Pramipexole?

A

Dopamine agonist

470
Q

Degenerative disorder of CNS associated with Lewy bodies and loss of dopaminergic neurons

A

Parkinson’s disease

471
Q

What are Lewy bodies composed of?

A

Intracellular inclusions of alpha synuclein

472
Q

What are the symptoms of Parkinson’s disease?

A 
Your body becomes a TRAP
Tremor at rest (pill rolling)
Rigidity
Akinesia (or bradykinesia)
Postural instabilidy
473
Q

What are the symptoms seen in Huntington’s disease?

A

Chorea, aggression, depression and dementia

474
Q

What happens in Huntinton’s disease?

A

AD trinucleotide repeat
neuronal death via NMDA-R binding and glutamate toxicity
Atrophy of striatal nuclei

475
Q

Mutation on Chromosome 4, CAF repeat and Caudate loses ACh and GABA describes…

A

Huntington’s disease

476
Q

what are the side effects of olanzapine?

A

Increased prolactin, orthostatic hypertension, anticholinergic effects, weight gain and somnolence

477
Q

What are some drugs you can use to treat the chorea seen in Huntington’s disease?

A

Tetrabenazine - 1st line treatment

Olanzapine

478
Q

What can cause hemballismus?

A

CL subthalamic destruction due to lacunar stroke

479
Q

What is athetosis and when is it seen?

A

Slow writhing movements especially in the fingers

Seen in Huntington’s disease due to Basal ganglia lesion

480
Q

What is myoclonus?

A

Sudden, brief uncontrolled muscle contraction like jerks, or hiccups
Common in metabolic abnormalities such as renal and liver failure

481
Q

What is dystonia?

A

Sustained involuntary muscle contractions

Blepharospasm (sustained eyelid twitch) or writer’s cramp

482
Q

What is an essential tremor?

A

Postural tremor, Action tremor, exacerbated by holding posture/limb position - seen at rest and with movement
Genetic predisposition

483
Q

How can you teat an essential tremor?

A

Beta blockers of primidone

Patients often self-medicate with EtOH which decrease tremor amplitude

484
Q

What is a resting tremor and when is it seen?

A

Uncontrolled movement of distal appendages - most noticeable in the hands
tremor is alleviated by intentional movement
seen in Parkinson’s disease - pill rolling tremor (at rest)

485
Q

What is an intention tremor?

A

Appears with voluntary movement
Slow, zigzag motion when pointing/extending toward a target
Occurs with Cerebellar dysfunction

486
Q

What is the Arcuate fasciculus?

A

Connects Broca’s and Wernicke’s areas

487
Q

What artery can injure the principal visual cortex?

A

PCA

488
Q

What deficits are seen with injury to the principal visual cortex?

A

deficits are seen in the CL visual field as homonymous hemianopsia with macular sparing

489
Q

What is the precentral gyrus?

A

Primary motor cortex

490
Q

Artery of the lateral aspect of the brain

A

MCA

491
Q

Artery of the medial aspect of the brain

A

ACA

492
Q

Artery involved with lower extremity deficit in sensation or movement?

A

ACA

493
Q

Artery involved with face deficit in sensation or movement?

A

MCA

494
Q

What is Kluver Bucy syndrome associated with?

A

HSV-1 infection

495
Q

A patient can no longer complete complex tasks like balancing a check book

A

Frontal lobe lesion

496
Q

What are the consequences of lesion to the frontal lobe?

A

Disinhibition and deficits in concentration, orientation and judgment, may have reemergence of primitive reflexes

497
Q

What are the consequences of a right parietal lobe lesion?

A

This is the non-dominant lobe

Spatial neglect syndrome (agnosia of the CL side of the world)

498
Q

What are the consequences of a dominant parietal lobe lesion?

A

Gerstmann Syndrome
Agraphia, Acalculia, Finger agnosia, L and R disorientation
- at angular gyrus

499
Q

What 3 things make up the reticular activating system?

A

Reticular formation, locus ceruleus, Raphe nuclei

500
Q

What are the consequences of a lesion at the reticular activating system in the midbrain?

A

Reduced levels of arousal and wakefulness - COMA

501
Q

What are the consequences of a lesion at the cerebellar hemispheres?

A

Intention tremor, limb ataxia, loss of balance

Damage to the cerebellum results in Ipsi deficits - fall toward the side of the lesion

502
Q

What are the consequences of a lesion at the cerebellar vermis?

A

truncal ataxia and dysarthria

503
Q

What are the consequences of a lesion at the hippocampus?

A

Anterograde amnesia - inability to make new memories

504
Q

What are the consequences of a lesion at the paramedian pontine reticular formation?

A

Eyes look away from the side of lesion

505
Q

What are the consequences of a lesion at the frontal eye fields?

A

Eyes look toward the lesion

506
Q

Nonfluent aphasia with intact comprehension

A

Broca’s aphasia - Broken Boca

understands what you’re saying but can’t form words

507
Q

What makes up Broca’s area?

A

Inferior frontal gyrus of the frontal lobe

508
Q

Fluent aphasia with impaired comprehension

A

Wernicke’s aphasia - Wordy but makes no sense

impaired content

509
Q

What makes of Wernicke’s area?

A

Superior temporal gyrus of the temporal lobe

510
Q

Nonfluent aphasia with impaired comprehension

A

Global aphasia

511
Q

Poor repetition but fluent speech and intact comprehension

A

Conduction aphasia
can’t say no ifs ands or buts
damage and arcuate fasciculus

512
Q

when do watershed zones get damaged?

A

severe hypotension

513
Q

What drives cerebral perfusion?

A

PCO2 levels

PO2 can modulate perfusion in severe hypoxia

514
Q

Why would you use therapeutic hyperventilation?

A

Therapeutic hyperventilation (decreased PCO2) helps to decreased intracranial pressure in cases of acute cerebral edema (stroke, trauma) via decreasing cerebral perfusion

515
Q

What is damaged in Weber syndrome?

A

Posterior communicating artery

516
Q

What is damaged in medial inferior pontine syndrome?

A

Basilar artery

517
Q

What is injured in medial medullary syndrome?

A

Anterior spinal artery

518
Q

What is injured in Wallenberg syndrome (lateral medullary syndrome)?

A

Posterior inferior cerebellar artery

519
Q

What is injured in lateral inferior pontine syndrome?

A

Anterior inferior cerebellar artery

520
Q

What is injured in lateral superior pontine syndrome?

A

Anterior inferior cerebellar artery

521
Q

What occurs in Medial medullary syndrome?

A

Injured : Paramedian branch of Anterior spinal artery.

  • CL spastic hemiparesis
  • CL tactile and kinesthetic sensory loss
  • Tongue deviates toward the side of the lesion (hypoglossal nucleus)
522
Q

What occurs in Wallenberg syndrome (AKA Lateral medullary)?

A

Injured: PICA

  • CL loss of pain and temp on body
  • Ipsi loss of pain and temp on face
  • hoarseness, difficulty swallowing and loss of gag reflex
  • ipsi horner syndrome
  • vertigo nystagmus N/V
  • Ipsi cerebellar deficits (inferior cerebellar peduncle injury)
    NO loss of vibratory or position sense
523
Q

What occurs in Weber syndrome?

A

Injured - Paramedian branch of PCA)

  • CL hemiparesis (cerebral peduncle lesion)
  • Ipsi ptosis, pupil dilation and eye down and out (CNIII damage)
524
Q

What occurs in Medial inferior pontine syndrome?

A

Injured: Paramedian branch of Basilar A

  • CL spastic hemiparesis
  • CL loss of light touch vibratory sense
  • Paralysis of gaze tot he side of the lesion
  • Ipsi loss of lateral rectus m.
525
Q

What occurs in Lateral inferior pontine syndrome?

A

Injured: AICA

  • Ipsi facial n paralysis
  • Ipsi loss of tase from ant 2/3 of tongue
  • Ipsi deafness and tinnitus
  • nystagmus, vertigo, N/V
  • Ipsi limb and gait ataxia
  • Ipsi loss of pain and temp on face
  • CL loss of pain and temp on body
  • Ipsi Horner syndrome
526
Q

What occurs in lateral superior pontine syndrome?

A

Injured: AICA

  • Ipsi loss of taste in Ant 2/3 tongue
  • ipsi limb and gait ataxia
  • ipsi loss of pain and temp on face
  • ipsi loss of light touch and vibration on face
  • ipsi jaw weakness and deviation of jaw toward the lesion
  • CL loss of pain and temp on body
  • ipsi horner syndrome
527
Q

What occurs if you have an MCA problem on the left hemisphere? right hemisphere?

A

Left is usually dominant = aphasia

right = hemineglect (nondominant side)

528
Q

What is the injury for someone with hemiparesis and hemiplegia?

A

CL lateral striate artery problem

affects striatum and internal capsule

529
Q

what effects are specific to PICA lesions?

A

Nucleus ambiguous injury like that seen in lateral medullary (Wallenberg) syndrome
“Don’t pick a (PICA) horse (hoarseness) that can’t eat (dysphagia)”

530
Q

What is specific to facial nucleus effects?

A

AICA lesions like seen in lateral pontine syndrome

“Facial droop means AICA’s pooped”

531
Q

What is commonly seen with a saccular aneurysm of the posterior communicating artery?

A

CN III palsy - eye down and out with ptosis and blown pupil

532
Q

What is commonly seen with a saccular aneurysm of the Anterior communicating artery?

A

visual field defects

533
Q

A patient is denying the Left half of their world what is the lesions?

A

MCA Right parietal lobe

534
Q

What is associated with berry aneruysms?

A

ADPKD, Ehlers Danlos syndrome, Marfan’s syndrome

535
Q

What is the most common site of a berry aneurysm?

A

Bifurcation of the anterior communicating artery

536
Q

What is the most common complication of berry aneurysm? second complication?

A

Most common - rupture leading to subarachnoid hemorrhage or hemorrhagic stroke

can also lead to bitemporal hemianopsia if it compresses the optic chiasm

537
Q

What are Charcot - Bouchard microaneurysms?

A

Asociated with chronic hypertension
affects the small vessels like in basal ganglia or hypothalamus
due to lenticulostriate arteries
causes hematomas in the brain parenchyma

538
Q

What is the middle meningeal artery a branch of?

A

Maxillary artery

539
Q

What can an epidural hematoma lead to?

A

transtentorial herniation, CN III palsy

540
Q

Hyperdense blood collection that doesn’t cross suture lines

A

Epidural hematoma

Can cross the falx and tentorium

541
Q

Crescent shaped hemorrhage that can cross suture lines

A

Subdural hematoma

can lead to midline shift
cannot cross the falx or tentorium

542
Q

Where does the bleeding occur in a subdural hematoma?

A

Between the arachnoid and dura

543
Q

Where does bleeding occur in a subarachnoid hemorrhage?

A

Between the arachnoid and pia

544
Q

What are two risks seen with subarachnoid hemorrhage?

A

Risk of vasopasm due to blood breakdown (not visible on CT) - TX with nimodipine (dihydropyridine CCB - dilates blood vessels)
Risk of rebleed - visible on CT

545
Q

List the layers for lumbar puncture

A 
Skin
Superficial fascia
Ligaments - supraspinatus - interspinous - ligamentum flacum
Epidural space (anesthetics)
Dura mater
Subdural space
arachnoid membrane
subaracnoid space - CSF - more potent if you put anesthetics here
546
Q

When does damage start with hypoxia in the brain?

A

Irreversible damage begins after 5 minutes of hypoxia

547
Q

What ares of the brain are most vulnerable to ischemic damage?

A

Hippocampus, neocortex, cerebellum and watershed areas

548
Q

What is seen on MRI and CT with different types of strokes?

A

Bright areas on noncontrast CT indicate hemorrhage
Brign on diffusion weighted MRI in 3-30 mins and remains bright for 10 days = ischemic stroke
dark on noncontrast in 24 hrs = ischemic stroke

549
Q

How does tPA work?

A

degradation of fibrin through conversion of plasminogen to plasmin

550
Q

When can you give tPA?

A

Ischemic stroke
Within 4.5 hrs of the stroke as long as the patient presents within 3 hrs of onset and there is no major risk of hemorrhage

551
Q

Describe a RIA?

A

Brief, irreversible episode of focal neurologic dysfunction typically lasting <24 hrs without acute infarction

552
Q

What causes a communicating hydrocephalus?

A

Decreased CSF absorption

553
Q

What causes a normal pressure hydrocephalus?

A

increased subarachnoid space volume but no increased in CSF pressure - expansion of ventricles distorts the fibers of the corona radiate and leads to the wet, wobbly and wacky
(form of communicating hydrocephalus)

554
Q

What is a non-communicating hydrocephalus?

A

Caused by a structural blockage of CSF circulation within the ventricular system

555
Q

How many spinal nerves are there?

A

31 total

8 cervical, 12 thoracic, 5 lumbar, 5 sacral and 1 coccygeal

556
Q

what is a vertebral disc herniation

A

Nucleus pulposus herniates through the annulus fibrosus

557
Q

Saddle anesthesia

A

Cauda equine syndrome

558
Q

A patient presents with urinary incontinence, paresthesias of medial thigh and she reports shes unable to feel toilet paper on her perineum when wiping after urination. The patient reports mild back pain with the initial onset of her symptoms.

A

Cauda Equina Syndrome

559
Q

What is the Romberg test for?

A 
The Romberg does NOT test the cerebellum@ This was developed to check for Tabes DOrsalis (dorsal columns) in tertiary syphilis
Need 2/3 to work 
1. Proprioception in legs
2. vision
3. vestibular apparatus
560
Q

Describe the findings in Poliomyelitis and Werdnig Hoffman disease?

A

LMN lesions only, due to destruction of anterior horns - flaccid paralysis
Werdnig Hoffman is AR

561
Q

Describe the findings in multiple sclerosis

A

mostly white matter of cervical region, random and asymmetric lesions due to demyelination
Charcot’s triad: scanning speech, intention tremor and nystagmus

562
Q

Describe the findings in Amyotrophic lateral sclerosis

A

Combined UMN and LMN deficits with NO sensory, cognitive or oculomotor deficits. (demyelination of motor neurons of anterior horn and lateral corticospinal tract)

563
Q

What can cause ALS?

A

Defect in superoide dismutase I

564
Q

What drug can be used in ALS?

A

Riluzole treatment modestly increases survival by decreasing presynaptic glutamate release

565
Q

What is seen with complete occlusion of anterior spinal artery?

A

Bilateral loss of paint and temp, motor command and UMN and LMN signs
slow below the lesion you have complete motor loss and loss of pain and temp and areflexia - will have intact pinpoint and vibratory discrimination

566
Q

What is sparred in an injury to the anterior spinal artery?

A

Dorsal columns and Lissauer’s tract

567
Q

What is a water shed area when thinking of an anterior spinal artery lesion?

A

Upper thoracic ASA territory is a watershed area, as artery of Adamkiewicz supplies ASA below T8

568
Q

What are the findings in a patient with Tabes dorsalis?

A

Degeneration of dorsal columns and roots leading to impaired sensation and proprioception and progressive sensory ataxia (inability to sense or feel the legs)

will have absence of DTRs and positive Romberg

569
Q

What can be seen in a Vitamin B12 or vitamin E deficiency?

A

Subacute combined degeneration leading to demyelination of the dorsal columns, lateral corticospinal tracts and spinocerebellar tracts
patients will have ataxia gait, paresthesia, impaired position and vibration sense

570
Q

What are the lab findings in a patient with Poliomyelitis?

A

CSF with increased WBCs with slight elevation of protein with no change in CSF glucose.
Virus can be recovered from stool or throat

571
Q

What is the defect in Friedrich’s ataxia?

A

Impairment in mitochondrial functioning

572
Q

How does Friedrich’s ataxia present?

A

In childhood with kyphoscoliosis

573
Q

In a patient with Horner’s syndrome, what causes the Ptosis?

A

Loss of the superior tarsal muscle

574
Q

What is the dermatome at the inguinal ligament?

A

L1

575
Q

what is the dermatome at the knee caps?

A

L4

576
Q

What is the function of the superior colliculi?

A

Conjugate vertical gaze center

577
Q

WHat is the function of the inferior colliculi?

A

Auditory

578
Q

What is Parinaud syndrome?

A

Paralysis of conjugate vertical gaze due to lesion in the superior colliculi

579
Q

where are the cranial nerve nuclei located?

A 
In tegmentum portion of brain stem
Midbrain - 3 and 4
pons - 5-8
medulla - 9, 10, 12
Spinal cord - 11
580
Q

What is the nucleus solitaries?

A

Visceral sensory info for CN 7, 9, 10

taste, baroreceptors, gut distension

581
Q

What is the nucleus ambiguous?

A

Motor innervation of pharynx, larynx, and upper esophagus
CN 9 and 10
(swallowing, palate elevation)

582
Q

What is the Doral motor nucleus?

A

Sends autonomic (PS) fibers to the heart lungs and upper GI for CN 10

583
Q

what are the branches of the Facial nerve?

A 
Ten Zebras Bit My Chin
Temporalis
Zygomatic
Buccal
Marginal mandibular
Cervical
584
Q

What nerves run through the cavernous sinus?

A

3, 4, V1 and V2, and 6

585
Q

Cavernous sinus syndrome

A

Ophthalmoplegia and decreased corneal and maxillary sensation with normal vision

586
Q

CNV motor lesion

A

Jaw deviates toward the side of lesion due to unopposed force from the opposite pterygoid muscle

587
Q

CN V lesion

A

Uvula deviates away from the side of lesion. Weak side collapses and uvula points away

588
Q

CN XI lesion

A

Weakness turning head to CL side of lesions (SCM) Shoulder droop on side of lesion (trapezius)

589
Q

CN XII lesion

A

Tongue deviates toward the side of lesion due to weakened tongue muscles on the affected side

590
Q

How do aminoglycosides cause hearing loss?

A

By damaging the outer hair cells

591
Q

What can cause Facial nerve palsy?

A

Complication in AIDS, Lyme disease, Herpes simplex and (less common) herpes zoster, sarcoidosis, tumors and diabetes

592
Q

Which mastication muscle opens the jaw? what opens the jaw?

A

Closes: Lateral pterygoid
Opens: Masseter temporalis, medial pterygoid
all by cnV3

593
Q

What can cause retinitis?

A

Commonly viral - CMV, HSV, HZV, or immunosuppresion

594
Q

Acute painless monocular vision loss with retina whitening with cherry-red spot on macula

A

Central retinal artery occlusion

595
Q

Painless acute onset of blurred vision in one eye with Blood and thunder fundus - dilated and tortuous retinal veins

A

Retinal vein occlusion

596
Q

Acute painless onset of monocular vision loss in background of atherosclerosis leading to retinal ischemia that comes and goes, commonly from ischemic originating from atherosclerotic carotid A disease

A

Amaurosis fugax

597
Q

Remembering what nerve innervate the eye muscles…

A

LR6SO4R3
Lateral rectus - CN 6
Superior oblique - CN 4
The rest - CN 3

598
Q

what should you not give a patient with acute closure closed angle glaucoma?

A

Epinephrine - has mydriatic effect (dilation of pupil)

599
Q

Painless often bilateral opacification of the lens leading to decreased vision

A

Cataracts

600
Q

Enlarged blind spot and elevated optic disc with blurred margins seen on fundoscopic exam

A

Papilledema due to increased intracranial pressure causing optic disc swelling

601
Q

What is seen with CNIV damage?

A

Eye moves upward, particularly with CL gaze and ipsilateral head tilt

602
Q

What is a Marcus Gunn pupil?

A

Afferent pupillary defect due to optic nerve damage or retinal detachment
have decreased bilateral pupillary constriction when light is shone in the affected eye relative to the unaffected eye

603
Q

A patient has a posterior communicating artery aneurysm - what effect is seen with CN III?

A

PS output is affected first (periphery of the nerve) signs include a diminished or absent pupillary light reflex and a “blown pupil”

also seen with an uncal herniation

604
Q

A patient has diabetes - what effect is seen with CNIII?

A

effects the inner portion of the CN III leading to los of motor components - ptosis and down and out eye

605
Q

a patient complains of floaters and flashes in their vision followed by monocular loss of vision like a curtain drawn down

A

Retinal detachment

fundoscopy will show a wrinkled retina

606
Q

What exactly is retinal detachment

A

Separation of the neurosensory layer of the retina (photoreceptor layer with rods and cones) from the outermost pigmented epithelium

607
Q

What can cause multi infarct dementia?

A

Syphilis, HIV, Vitamins B1, B3, or B12 deficiency, Wilson’s disease and Normal pressure hydrocephalus

608
Q

What is the gold standard for looking at MS?

A

MRI

609
Q

List 3 treatments for MS?

A

Interferon beta, immunosuppression and natalizumab

610
Q

what is another name for Guillain-Barre?

A

Acute inflammatory demyelinating polyradiculopathy

611
Q

What is Guillain Barre syndrome?

A

Autoimmune condition that destroys Schwann cels leading to inflammation and demyelination of peripheral nerves and motor fibers

612
Q

Results in symmetric ascending muscle weakness/paralysis beginning in lower extremities

A

Guillain Barre

613
Q

What can cause Guillain barre?

A

Campylobacter jejuni or CMV infection leading to molecular mimicry causing autoimmune attack of peripheral myelin

614
Q

What are the lab findings on someone with Guillain Barre?

A

Increased CSF protein with normal cell count (albuminocytologic dissociation).
Increased protein leads to papilledema

615
Q

Progressive multifocal leukoenceophalopathy

A

Demyelination of CNS due to destruction of oligodendrocytes
Seen in 2-4% of AIDS patients due to reactivation of latent viral infection (JC)
rapidly progressive and usually fatal
- virally infected oligodendrocytes

616
Q

Multifocal perivenular inflammation and demyelination after infection (commonly measles or VSV) or certain vaccines (rabies or smallpox)

A

Acute disseminated (postinfectious) encephalomyelitis

617
Q

AR lysosomal storage disease most commonly due to arylsulfatase A deficiency. Causes build up of sulfatides leading to impaired production of myelin sheath

A

Metachromatic leukodystrophy

618
Q

How much of the brain to partial seizures involve?

A

Affect I focal area of the brain - most commonly originates in medial temporal lobe

619
Q

What are causes of seizures in children? adults? elderly?

A

Children - genetics, infection (febrile), trauma, congenital, metabolic
adults - tumors, trauma, stroke, infection
Elderly - stroke, tumor, trauma, metabolic and infection

620
Q

Name 5 types of Diffuse generalized seizures

A 
Absence (petit mal) - 3 Hz no postictal confusion, will have blank stare
Myoclonic
Tonic-clonic (grand mal)
Tonic
Atonic - can be mistaken for fainting
621
Q

Name two types of Partial (focal) seizures?

A

Simple partial - consciousness intact, can be motor, sensory, autonomic, psychic
Complex partial - impaired consciousness

622
Q

what can be triggers for cluster headaches?

A

Alcohol or vasodilators

623
Q

what are migraine patients at increased risk for?

A

Stroke

624
Q

Congenital disorder with port wine stains (nevus flammeus), typically in V1 distribution, ipsilatereal leptomeningeal angiomas, pheochromocytomas.

A

Sturge Weber syndrome

can cause glaucoma, seizures, hemiparesis, and mental retardation
Occurs sporadically

625
Q

Describe Tuberous Sclerosis

A 
AS
HAMARTOMAS: 
Hamartomas in cns and skin
Adenomya sebaceum (cutaneous angiofibromas)
Mitral regurgitation
Ash leaf spots
cardiac Rhabdomyoma
Tuberous sclerosis
autosomal dOminant
Mental retardation
renal Angiomyolipomas
Seizures
626
Q

Café au lait spots, Lisch nodules (pigmented iris hamartomas) neurofibromas in skin, optic gliomas, pheochromocytomas,

A

Neurofibromatosis type I (von Recklinghausen disease)
AS
mutated NF1 gene on Chrom 17 (tumor suppressor)

627
Q

Describe von hippel-landau disease

A

Cavernous hemangiomas in skin, mucosa, organs; bilateral renal cell carcinoma
hemangioblastoma in retina, brain stem, cerebellum, pheochromocytomas
AD
mutated tumor suppressor VHL gene on chrom 3

628
Q

What is the mnemonic for the 4 most common adult tumors?

A 
MGM Studios
Metastasis
Glioblastoma
Meningioma
Schwannoma
629
Q

Brain tumor that arises from arachnoid cells, are external to brain parenchyma and may have a dural attachment (“tail”)

A

Meningioma

often asymptomatic may present with seizures or focal signs

630
Q

Which brain tumor has spindle cells concentrically arranged in a whorled pattern and can often have psammoma bodies?

A

Meningioma

631
Q

how do you treat a schwannoma?

A

Resectable or treated with stereotactic radiosurgery

632
Q

Brain tumor commonly found at the cerebellopontine angle

A

Schwannoma

S-100 positive

633
Q

Where is Oligodendroglioma brain tumor most commonly found?

A

Frontal lobes

634
Q

Brain tumor with a chicken-wire capillary pattern with fried egg cells

A

Oligodendroglioma

635
Q

What are the three most common childhood brain tumors?

A

Animal kingdom, Magic kingdom, Epcot

Astrocytoma
Medulloblastoma
Ependymoma

636
Q

Where is a pilocytic astrocytoma most commonly found?

A

Posterior fossa (cerebellum)

637
Q

Which brain tumor shows Rosenthal fibers?

A

Pilocytic astrocytoma

638
Q

Where is medulloblastoma most commonly found?

A

Cerebellar vermis, highly malignant

639
Q

Which brain tumor shows Homer Wright rosettes and is radiosensitive?

A

Medulloblastoma

640
Q

What can occur with a Medulloblastoma?

A

Can send drop metastasis to spinal cord

641
Q

Which brain tumor has rod shaped belpharoplasts (basal ciliary bodies) found near nuclei?

A

Ependymoma

642
Q

What can Hemagnioblastomas produce?

A

EPO leading to secondary polycythemia

643
Q

Which brain tumor has foamy cells ad high vascularity?

A

Hemangioblastoma

644
Q

What is the most common childhood supratentorial brain tumor?

A

Craniopharyngioma

645
Q

Brain tumor that’s epithelial lined mass with cystic degeneration and calcifications

A

Craniopharyngioma

646
Q

Which hernia can result in compression of the anterior cerebral artery?

A

Cingulate (subfalcine) herniation under the falx cerebri

  • can lead to lower leg weakness with out sensory loss, paralysis of CL foot, re occurrence of primitive reflexes (frontal lobe)
647
Q

List 4 things that can occur with an uncal (transtentorial) herniation

A
  • can compress CN III leading to a blown pupil with down and out eye
  • can have CL homonymous hemianopsia
  • Ipsilateral paresis
  • Compression in paramedian A
648
Q

What is a transtentorial herniation?

A

When medial part of temporal lobe herniates over the free edge of tentorium - can compress ipsilateral posterior cerebral artery, occulomotor nerve and cerebral peduncle

First Aid Chs Part 2 (6 decks)

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