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Citow Review Book > Neurosurgery > Flashcards

Neurosurgery Flashcards

1
Q

<p>What is the adult prevalence of intracranial aneurysms?</p>

A

<p>2%</p>

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2
Q

<p>What is the mortality rate of ruptured aneurysms?</p>

A

<p>30-40%</p>

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3
Q

<p>What percent of ruptured aneurysms develop hydrocephalus?</p>

A

<p>15-20%</p>

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4
Q

<p>What percent of ruptured aneurysms develop cardiac issues?</p>

A

<p>50%</p>

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5
Q

<p>Summarize the rupture risk for aneurysm size based on the International Study of Unruptured Intracranial aneurysms? What kind of study was it?</p>

A

<p>prospective cohort</p>

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6
Q

<p>What percent of bacterial endocarditis patients have mycotic aneurysms?</p>

A

<p>5-15%</p>

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7
Q

<p>What were the conclusions of the Internation Subarachnoid Aneurysm Trial (ISAT)?</p>

A

<p>Initially, large difference in mortality favoring coiling over clipping at 1 year. At 5-year follow-up, no difference in mortality between the two groups, though the incidence of rebleeding and aneurysm recurrence was higher in the coiling group</p>

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8
Q

<p>What were the conclusions of the Barrow Ruptured Aneurysm Trial?</p>

A

<p>initial results at 1 year favoring coiling with regard to poor outcome. At 3-year follow-up, no difference between groups. The rate of recurrence, rebleeding, and aneurysm obliteration were better in the clipping group</p>

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9
Q

<p>What are the general morbidity and mortality for coiling and clipping aneurysms?</p>

A

<p>mortality (1–2% for surgery/<br></br>coiling) and morbidity (4% coiling and 8% surgery)</p>

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10
Q

<p>What is the hemorrhage rate for AVMs?</p>

A

<p>2-4% per year,6–18% in first year following initial hemorrhage if not treated. Lifetime risk of hemorrhage is 17–90%.</p>

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11
Q

<p>What is the mortality of AVM hemorrhage?</p>

A

<p>mortality 10–30%, morbidity 10–30%.</p>

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12
Q

<p>What are dural AVFs?</p>

A

<p>Pathological shunts between meningeal or extracranial arteries and the dural venous sinus, dural veins, or cortical veins</p>

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13
Q

<p>What is the Borden classification for dAVFs?</p>

A

<p>Borden I: Generally benign (conversion rate to higher grade ~ 2%), but occasionally symptoms warrant treatment.</p>

<p><br></br>Borden II: Hemorrhage in 18%, annual hemorrhage rate of 6%.</p>

<p><br></br>Borden III: Present with hemorrhage in 34%, annual hemorrhage rate of 10% which increases to 21% with venous ectasia.</p>

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14
Q

<p>What endovascular treatment is preferred for dAVF?</p>

A

<p>transvenous coiling</p>

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15
Q

<p>Moyamoya in asian adults usually causes \_\_\_\_\_ while in children usually \_\_\_\_\_. In American adults, it usually presents as \_\_\_\_.</p>

A

<p>hemorrhage</p>

<p></p>

<p>ischemia</p>

<p></p>

<p>ischemia</p>

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16
Q

<p>What is the difference between moyamoya disease and syndrome?</p>

A

<p>disease: idiopathic</p>

<p></p>

<p>syndrome: secondary</p>

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17
Q

<p>What is the risk of hemorrhage in cav mals?</p>

A

<p>Risk of symptomatic hemorrhage 0.5–2% per year, may be higher in patients with previous hemorrhages (~5% per year), deep lesions (~10% per year), posterior fossa lesions, familial inheritance, and women (~4% per year)</p>

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18
Q

<p>What does the ICH score predict? What are those values?</p>

A

<p>mortality at 30 days</p>

<p></p>

<p>ICH score</p>

<p>0: 0%</p>

<p>1: 13%<br></br>2: 26%</p>

<p>3: 72%</p>

<p>4: 97%</p>

<p>5: 100%</p>

<p>6: 100%.</p>

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19
Q

<p>What were the conclusions fo the STICH I and II trials?</p>

A

<p>supratentorial ICH surgical evacuation only mild benefit in long term mortality</p>

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20
Q

<p>What were the conclusions of the MISTIE trial?</p>

A

<p>minimally invasive clot aspiration + tPA: 50% reduction in clot burden and at 6 and 12 months increase in number of patients in mRS 0–3 category versus mRS 4 and above</p>

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21
Q

<p>What were the results of the CLEAR trial?</p>

A

<p>clot lysis of IVH with tPA through external ventricular drain (EVD): mortality rate of 18% in treatment group vs 23% in placebo group, similar ventriculitis rates ~8–9%</p>

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22
Q

<p>Malignant cerebral edema presents in what percent of MCA infarcts?</p>

A

<p>10%</p>

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23
Q

<p>What is the prevalence of carotid stenosis in the population?</p>

A

<p>2.5% for age < 65, 35% for age > 75</p>

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24
Q

<p>What percent fo CCFs are from trauma?</p>

A

<p>70%</p>

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25
Q

<p>What are the types of CCFs?</p>

A

<p>direct (carotid artery)</p>

<p></p>

<p>indirect (adjacent branch)</p>

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26
Q

<p>What is the presentation for CCFs?</p>

A

<p>Direct: orbital/retro-orbital pain, chemosis, pulsatile proptosis, ocular/cranial bruit, visual deterioration, diplopia, and ophthalmoplegia.</p>

<p></p>

<p>Indirect: more insidious onset. Conjunctival injection is most prominent feature</p>

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27
Q

<p>What is the management of low flow CCFs?</p>

A

<p>can be watched until they spontaneously thrombose if visual acuity stable and intraocular pressure < 25 mm Hg. Can also perform daily manual compression of cervical ICA</p>

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28
Q

<p>What percent of subdural empyema have an associated cerebral abscess?</p>

A

<p>25%</p>

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29
Q

<p>Where is the pterion?</p>

A

Located at the junction of the frontal, parietal, temporal, and greater wing of sphenoid bones

It is located two fingerbreadths above the zygomatic arch and a thumb’s breadth behind the frontal process of the zygomatic bone

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30
Q

Where is the asterion? What does it signify?

A

located at the junction of the lambdoid, occipitomastoid, and parietomastoid sutures

lies on top of the lower half of the transverse/ sigmoid sinus junction

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31
Q

<p>What is the bregma?</p>

A

<p>located at the junction of the coronal and sagittal sutures</p>

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32
Q

What genetic mutations are characteristic for IDH mutant diffuse astrocytomas?

A

ATRX loss and p53 mutation

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33
Q

Pilocytic astrocytomas on MRI imaging generally are ________ but when in the optic nerve, are generally _____.

A

cystic with mural nodule

solid and enhancing

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34
Q

<p>What disease is associated with pilocytic astrocytoma?</p>

A

<p>NF-1</p>

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35
Q

<p>What is the 5 and 10 yr survival for PXAs?</p>

A

<p>80 and 70%</p>

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36
Q

<p>What is the most common location for oligodendrogliomas?</p>

A

<p>frontal lobe (50%)</p>

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37
Q

<p>Most GBMs that develop from other astrocytomas are \_\_\_\_\_.</p>

A

<p>IDH mutants</p>

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38
Q

<p>What is the Stupp protocol?</p>

A

<p>maximal safe resection followed by adjuvant chemotherapy/radiation</p>

<p></p>

<p>fractionated radiationof 2 Gy 5 days/week for six weeks total 60 Gy, plus daily temozolomide at 75 mg/m^2, 7 days a week for 60 days followed by six cycles of adjuvant temozolomide 150-200 mg/m^2 for 5 of 28 days</p>

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39
Q

<p>In the fourth ventricle, ependymomas usually arise from the \_\_\_\_\_.</p>

A

<p>floor</p>

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40
Q

<p>Spinal ependymomas are associated with a syrinx in what percent of cases?</p>

A

<p>90%</p>

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41
Q

<p>"Tiger stripes" in unilaterally in the cerebellum are pathognomonic for \_\_\_\_\_.</p>

A

<p>Lhermitte Duclos disease</p>

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42
Q

<p>What is the treatment for Lhermitte Duclos disease?</p>

A

<p>surgical resection is curative</p>

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43
Q

<p>What is the chance for seizure freedom after DNET resection?</p>

A

<p>80% at 5 years, 60% at 10 years</p>

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44
Q

<p>What's the difference between a gangliocytoma and ganglioglioma?</p>

A

<p>Gangloicytoma: WHO grade I growth of mature neurons</p>

<p></p>

<p>Ganglioglioma: WHO grade I and II mixed population of ganglion and glial cells</p>

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45
Q

<p>What is the semiology of hypothalamic hamartomas? What other symptoms can they classically present with?</p>

A

<p>gelastic seizures</p>

<p></p>

<p>precocious puberty</p>

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46
Q

<p>What is the overall 5 year survival rate for paragangliomas?</p>

A

<p>90%</p>

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47
Q

<p>What percent of pineoblastomas have CSF seeding?</p>

A

<p>50%</p>

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48
Q

<p>What is the treatment for pineoblastoma?</p>

A

<p>surgical resection + cranial/spinal radiation and chemotherapy</p>

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49
Q

<p>What is the survival rate in pineoblastoma?</p>

A

<p>Fifteen percent 10-year survival in case of residual tumor versus 100% if no residual left</p>

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50
Q

<p>What chromosome abnormality can be seen with medulloblastoma?</p>

A

<p>loss of 17p in 50% of patients</p>

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51
Q

<p>What is the 5 year survival for medulloblastoma in standrard risk patients (no mets, older than 3 years, Gross total resection)?</p>

A

<p>100% if ERBB-2 tumor protein negative, 54% if positive</p>

52
Q

<p>There are many types of meningiomas. What are they and what WHO grade system do they fall under?</p>

A

<p>WHO Grade I: meningothelial, fibrous, transitional, psammomatous, angiomatous, microcystic, secretory, metaplastic, lymphoplasmacyte-rich.</p>

<p><br></br>WHO Grade II: atypical, clear cell (predilection for spinal cord and posterior fossa), chordoid (“chordoma-like”), brain invasive.</p>

<p><br></br>WHO Grade III: anaplastic, rhabdoid, papillary.</p>

53
Q

<p>What is the most common primary CNS sarcome (malignant mesenchymal tumor)?</p>

A

<p>fibrosarcoma</p>

54
Q

<p>Soitary fibrous tumors are distinguished form hemangiopericytomas and meningiomas by \_\_\_\_\_.</p>

A

<p>CD 34 +</p>

55
Q

<p>Leiomyosarcomas are associated with what virus?</p>

A

<p>EBV</p>

56
Q

<p>What is the median survival in primary CNS lymphoma?</p>

A

<p>Median survival 1–4 months without treatment, 1–4 years when treated (2–6 months in AIDS)</p>

57
Q

<p>What is the treatment for germinomas?</p>

A

<p>biopsy followed by chemo/radiation</p>

58
Q

Klinefelter’s syndrome is associated with what CNS tumor?

A

embryonal carcinomas

59
Q

What percent of pituitary adenomas are micro vs macro?

A

<p>50-50 split</p>

60
Q

<p>"Stalk effect" elevated prolactin levels fall into what range?</p>

A

<p>25 - 150 ng/mL</p>

61
Q

<p>For adrenocorticotrophin releasing pituitary adenomas, what medication can be used as a second line treatment?</p>

A

<p>ketoconazole</p>

62
Q

<p>What were the results for the Radiation therapy Oncology Group brain metastases trial?</p>

A

<p>Class 1: KPS > or = 70, < 65 years old, controlled primary with no extra cranial metastases— median survival 7.1 months.</p>

<p><br></br>Class 3: KPS < 70—median survival 2.3 months.</p>

<p><br></br>Class 2: all others—medial survival 4.2 months</p>

63
Q

<p>What is the difference in possible meningitis complications in dermoids vs epidermoids?</p>

A

<p>Epidermoid: aseptic Mollaret recurrent meningitis</p>

<p></p>

<p>Dermoid: septic meningitis</p>

64
Q

<p>What is the most common location for chrodomas?</p>

A

<p>Sacrum (50%) and clival (35%)</p>

65
Q

<p>What type of radiation is most effective for chordoma?</p>

A

<p>proton beam</p>

66
Q

Which intervention for trigeminal neuralgia has the highest incidence of facial numbness?

A

percutaneous rhizotomy via radiofrequency thermocoagulation

67
Q

What are potential severe complications of percutaneous rhizotomy?

A

anesthesia dolorosa, neuroparalytic keratitis

68
Q

What is the success rate of percutaneous rhizotomy? Recurrence rates?

A

90-95%

20% in 6 years, 80% in 12 years

69
Q

What is the success rate of microvascular decompression in TGN? Recurrence rate?

A

85-95%

20% in 6 years, 30% in 10 years

70
Q

What is the success rate of SRS in TGN? Recurrence rate?

A

80-95% after median latency of 3 months

25% at 3 years

71
Q

What is the risk of hearing loss in MVDs for hemifacial spasm?

A

10%

72
Q

What is the success rate of MVD in hemifacial spasm? Recurrence rate?

A

> 80%

10% in 2 years

73
Q

What are the two main targets for DBS in parkinson’s disease? How do they differ in outcomes?

A

GPi: 40% improvement in motor, 65% improvement in dyskinesias

STN: 10% better in both over GPi

74
Q

What is the target in DBS for essential tremor?

A

Vim (also for thalamotomy)

75
Q

What is the target in DBS for dystonia?

A

GPi (also for Pallidotomy)

76
Q

How can disconnection syndrome be reduced in corpus callosotomy?

A

divide only the anterior 2/3 of the corpus callosum

77
Q

Sympathectomy can be used in treatment of what pain disorder?

A

complex regional pain syndrome

78
Q

What are the shunt failure rates?

A

25–40% in first year (most in first few months) then 5% per year, 50% fail at 5 years

79
Q

In NPH, which symptoms respond best to shunting?

A

incontinence and gait

80
Q

How do NPH patients respond to shunting?

A

one-third patients improve, one-third halt decline, and one-third do not respond

81
Q

What percent of weight loss usually causes complete resolution of symptoms in pseudotumor?

A

6%

82
Q

What percent of Chiari I’s associated with other skeletal abnormalities?

A

25%

83
Q

Elevated ICP develops in what percent of severe head injuries?

A

50%

84
Q

In depressed skull fx, greater than ______ mm of depression is highly associated with dural tears.

A

5 mm

85
Q

What are growing skull fractures? How do they present?

A

Fracture with dural laceration and entrapment of arachnoid. Over time, brain will herniate through opening and prevent fracture healing. Presents as enlarging pulsate mass

86
Q

What percent of head injury patients have a traumatic CSF leak? What is the incidence of meningitis?

A

3%

5-10%, highest after 7 days

87
Q

What is the overall mortality of traumatic cerebral contusions?

A

50%

88
Q

What percent of EDH have underlying associated SDH?

A

20%

89
Q

Spinal dural AVMs most commonly present as _____.

A

progressive myelopathy/back pain

90
Q

What is the most common location for epidural abscesses in the spine?

A

thoracic

91
Q

What is the most important predictor of post op function in intramedullary ependymoma surgery?

A

pre-op function

92
Q

Multiple spinal meningiomas is associated with ___.

A

NF-2

93
Q

Giant cell tumor of the spine generally presents where?

A

Sacral

94
Q

What is seen on urine and serum electrophoresis in multiple myeloma?

A

oligoclonal bands and Bence–Jones proteins in myeloma

95
Q

What electrolyte abnormality is common in multiple myeloma?

A

hyeprcalcemia

96
Q

For lumbar herniated discs, what was the difference in outcomes between medical conservative management vs surgical management?

A

surgery superior at 1 year, but little difference at 4 years

97
Q

Where is the most common location for fractures in ankylosing spondylitis?

A

cervical (75%)

98
Q

What are the types of split cord malformations?

A

Type I (diastematomyelia): two hemicords in separate dural tubes separated by osteocartilaginousseptum.

Type II (diplomyelia): two hemicords in same dural tube separated by fibrous septum

99
Q

<p>What is the role of steroid therapy in acute spinal cord injury?</p>

A

<p>considered as an option if can start within 8 hours of SCI (methylprednisolone 30 mg/kg over 1 hour then 5.4 mg/kg/hour for 23 hours)</p>

100
Q

<p>Occipital condyle fractures are due to \_\_\_\_.</p>

A

<p>axial load</p>

101
Q

<p>What are the three types of condyle fractures? What are the treatments?</p>

A

<p>Type I: stable comminuted fracture; treated with collar.</p>

<p></p>

<p>Type II: stable basal skull fracture involving condyle; treated with collar.</p>

<p></p>

<p>Type III: alar ligament avulsion of medial condyle fragment, unstable; treated with halo vest for 6–12 weeks</p>

102
Q

<p>What is the Rule of Spence?</p>

A

<p>on open-mouth view, total overhang of both C1 lateral masses > 7 mm = probable transverse ligament disruption and rigid immobilization is required</p>

103
Q

<p>Odontoid fractures are usually caused by \_\_\_\_\_.</p>

A

<p>flexion injuries</p>

104
Q

<p>What are the types of odontoid fractures? How does the type affect healing and treatment?</p>

A

<p>Type I: through tip of odontoid, rare, usually stable.</p>

<p></p>

<p>Type II: at base of odontoid, least likely to heal with immobilization, 30% nonunion overall with 10% nonunion if < 6 mm displacement, but up to 70% nonunion if ≥ 6 mm displacement. Surgery indicated if age ≥ 50 years, displacement ≥ 6 mm, instability in halo vest, and nonunion</p>

<p></p>

<p>Type III: through body of C2. 90% heal with immobilization (halo vest preferred)</p>

105
Q

<p>Hangman fractures are caused by \_\_\_\_\_\_.</p>

A

<p>hyperextension and axial loading (think head first diving)</p>

106
Q

<p>What are the types of hangman fractures as defined by Effendi? What is the associated treatment for each?</p>

A

<p>Type I: fracture through isthmus with < 3 mm displacement, stable injury, neurologic injury rare, treatment is collar.</p>

<p><br></br>Type II: fracture through isthmus with disruption of C2–C3 disk and posterior longitudinal ligament (PLL) with increased displacement, slight angulation, and anterolisthesis C2 on C3; may be unstable, neurologic deficit is rare, treated with reduction and halo vest for 12 weeks</p>

<p><br></br>Type IIa: fracture has less displacement but more angulation than type II, unstable, treated with reduction and halo vest for 12 weeks.</p>

<p><br></br>Type III: fracture in which C2–C3 facet capsules disrupted followed by isthmus fracture and possibly anterior longitudinal ligament (ALL) disruption and C2–C3 locked facets, unstable and mostly associated with neurologic deficit, treatment typically open surgical reduction of facet dislocation and fusion</p>

107
Q

<p>Facet dislocation fractures occur with \_\_\_\_\_.</p>

A

<p>flexion distraction injuries</p>

108
Q

<p>What are tear drop fractures?</p>

A

<p>Hyperflexion causing injury to disk, facet joints, and all ligaments (highly unstable), associated with small bone chip off anteroinferior vertebral body edge (often mistaken as stable minor avulsion) and posterior displacement of fractured vertebral body into spinal canal. Typically present with severe SCI or anterior cord syndrome. Surgical stabilization required and typically combines anterior decompression and posterior fusion</p>

109
Q

<p>What is the most common type of thoracolumbar fx?</p>

A

<p>burst fx</p>

110
Q

<p>What eprcent of chance fxs have abdominal organ injury?</p>

A

<p>>50%</p>

111
Q

What is the 5 year survival rate for malignant peripheral nerve sheath tumors?

A

30-50% at 5 years

112
Q

What muscles are affected in carpal tunnel syndrome?

A

lumbricals 1 and 2, opponens pollicis, and abductor and flexor pollicis brevis (LOAF) muscles

113
Q

What separates pronator teres syndrome from carpal tunnel syndrome symptomatically?

A

Absence of nocturnal exacerbation and presence of palm numbness in pronator teres syndrome

114
Q

What is the anterior interosseous nerve?

A

Motor branch of median nerve innervating flexor digitorum profundus 1 and 2, flexor pollicis longus, and pronator quadratus

115
Q

What is the symptomatology of AIN syndrome?

A

motor weakness, no sensory loss (manifests with “pinch sign”

116
Q

What are four entrapment locations for the median nerve?

A
  1. Carpel Tunnel
  2. Pronator teres
  3. Struther’s ligament
  4. AIN
117
Q

What are four entrapment locations for the ulnar nerve?

A
  1. Arcade of Struthers (upper arm)
  2. Elbow
  3. Cubital tunnel
  4. Guyon canal (sensation intact)
118
Q

What are four entrapment locations for the radial nerve?

A
  1. Axilla
  2. Spiral groove
  3. PIN (arcade of Frohse)
  4. Radial Tunnel
119
Q

Entrapment of radial nerve at the spiral groove causes _____.

A

wrist drop without triceps involvement

120
Q

PIN syndrome causes _____.

A

finger extension weakness without wrist drop or sensory deficits

121
Q

What is meralgia paresthetica? What are the symptoms? Treatment?

A

lateral femoral cutaneous nerve entrapment

burning dysesthesia in lateral/upper thigh (purely sensory branch—L2, L3)conservative treatment though surgery can be done

122
Q

Seeing both thenar and hypothenar atrophy should be a red flag for what syndrome?

A

neurologic thoracic outlet syndrome

123
Q

For clean sharp nerve injuries, what is the treatment algorithm?

A

directly repaired (end–end) within days

124
Q

For contaminated/blunt nerve injuries, what is the treatment algorithm?

A

acutely debrided, tag nerve ends/suture to surrounding tissue to preserve length, repair ~ 3 weeks later when healthy nerve ends declared/demarcated (often need graft)

125
Q

For closed nerve injuries, what is the treatment algorithm?

A

early intervention only for vascular compression; otherwise establish baseline exam, follow for 3 months to rule out neurapraxic injury; electromyography and nerve conduction studies useful > 3 weeks postinjury; repair in ~ 3 months if no recovery

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