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USMLE Step 2 > Neurology/Neurosurgery > Flashcards

Neurology/Neurosurgery Flashcards

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USMLE® Step 1 flashcards
1
Q

Where are post-dural puncture headaches?

A

Bifrontal or Occipital

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2
Q

What positioning tends to make post-dural puncture headaches feel better? Worse?

A

Better when lying down (reduces gravity forces, allowing better access of CSF to brain)
Worse when upright (gravity reduces CSF available in brain area)

This is opposite compared to IIH (pseudotumor cerebri)

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3
Q

What are the treatment options for post-dural puncture headaches?

A

Acute - IV fluids

Persistent/Severe - Epidural blood patch

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4
Q

How often do migraines present with auras? What is the classic aura?

A

15%

Bilateral homonymous scotoma (darkening) with bright, flashing, crescent-shaped images with jagged edges for 10-20 min

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5
Q

What are some common causes for migraines?

A

Inherited - AD incomplete penetrance
Menstrual - estrogen withdrawal
Serotonin - depletion

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6
Q

What are the symptoms of a migraine?

A

Prodromal - excitation/inhibition of CNS
Severe unilateral, throbbing headache that may last 4-72 hours with nausea and vomiting, photophobia, and increased sense of smell

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7
Q

How can migraines be treated?

A

Prophylaxis - Propranolol (beta-blocker) > Amytriptyline (TCAs) > Verapamil (Ca2+ channel blocker) > valproic acid (anticonvulsant), methylsergide

Acute - Sumatriptan or Dihydroergotamine (DHE) (5-HT agonist)

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8
Q

Where are tension headaches?

A

Diffuse across scalp, concentrated in temples, or concentrated in occipital region

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9
Q

What are the most common associations with tension headaches?

A

Depression, anxiety, or stress

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10
Q

How are tension headaches treated?

A

Prophylaxis - Stress reduction

Acute - Acetaminophen/NSAIDs

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11
Q

What are the symptoms associated with temporal arteritis?

A

Headache, visual impairment (25-50%), jaw pain when chewing, tenderness, over temporal artery, absent temporal pulse, polymyalgia rheumatic (40%)

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12
Q

How often does temporal arteritis include the ophthalmic artery? What is seen?

A

25-50%
Optic neuritis
Amaurosis fugax (monocular blindness from lack of blood flow to retina from blood clot from carotid artery traveling to retinal artery)
Blindness

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13
Q

What is amaurosis fugax?

A

Monocular blindness from lack of blood flow to retina from blood clot from carotid artery traveling to retinal artery

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14
Q

How is temporal arteritis treated?

A

High-dose prednisone with IV steroids if visual loss
-Do not wait for biopsy results from temporal artery if suspected
Treat for 4 weeks, and maintain with steroids for 2-3 years

ESR for effectiveness

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15
Q

Where are cluster headaches?

A

Unilateral periorbital pain

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16
Q

What has been found to make cluster headaches worse?

A

Alcohol

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17
Q

When do cluster headaches tend to occur?

A

A few hours after the patient falls asleep, awakening the patient, and lasting for 30-90 minutes

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18
Q

What symptoms are associated with cluster headaches?

A

Nausea without vomiting, ipsilateral conjunctival infection, lacrimation, nasal congestion, rhinorrhea, forehead/facial sweating, miosis, ptosis, and eyelid edema

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19
Q

How are cluster headaches treated?

A

Prophylaxis - Verapamil or Steroids

Acute - O2 or Sumatriptan

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20
Q

What are the most common patients for cluster headaches?

A

Males (80%)

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21
Q

What are the most common patients for migraines?

A

Women

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22
Q

What are the most common patients for temporal arteritis?

A

> 50 year old women

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23
Q

What causes pseudotumor cerebri?

A

Increased resistance to CSF reabsorption at arachnoid villi

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24
Q

What are the most common patients for pseudotumor cerebri?

A

Young obese women

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25
Q

What symptoms are associated with pseudotumor cerebri?

A 
Bilateral papilledeman without mass
Headache
Elevated CSH pressure
Deteriorating vision
Slit-like ventricles
Normal scan
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26
Q

What positioning tends to make pseudotumor cerebri headaches feel better? Worse?

A 
Sitting up (gravity helps pull some CSF away from the brain)
Laying down (the loss of gravitational force redistributes the liquid back onto the brain and eyes)
Leaning forward can also make vision loss greater
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27
Q

What is the most common cause of subarachnoid hemorrhage?

A

Congenital berry/saccular aneurysm rupture

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28
Q

How are subarachnoid hemorrhages diagnosed?

A

Noncontrast CT

  • If no papilledema and CT is negative, but the clinical suspicion is still high, do a lumbar puncture
  • Xanthrochromia (yellow color) is gold standard of lysis from RBC in CSF for subarachnoid hemorrhage
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29
Q

What is the first step after subarachnoid hemorrhage is diagnosed?

A

Cerebral angiography

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30
Q

How are subarachnoid hemorrhages treated?

A

Surgical - clipping

Medical - bed rest, stool softeners, analgesia, IV fluids, HTN - Ca2+ channel blocker

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31
Q

How effective is lowering hypertension in cerebral infarction from post-subarachnoid hemorrhage? Why?

A

Lowers incidence by 1/3rd

Decreases vasospasms

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32
Q

What is a major complication from subarachnoid hemorrhage?

A

Cerebral salt wasting/SIADH -> Hyponatremia

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33
Q

What is the most common cause of viral encephalitis?

A

Herpes simplex

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34
Q

What symptoms are associated with viral encephalitis?

A 
Fever
Headache
Depressed consciousness
Neurological signs
Focal seizures
Slow wave activity on EEG
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35
Q

What symptoms are associated with viral meningitis?

A

Fever
Headache
Meningial signs (nuchal rigidity)
No impaired consciousness

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36
Q

What CSF findings are associated with viral meningitis?

A

Increased lymphocytes
Increased proteins
Normal glucose
Normal opening pressure

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37
Q

What symptoms are associated with bacterial meningitis?

A

Fever
Nuchal rigidity
Change in mental status

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38
Q

What CSF finds are associated with bacterial meningitis?

A

Increased PMN
Increased protein
Decreased glucose
Increased opening pressure

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39
Q

How are neonates with meningitis treated? What do they probably have?

A

Cefotaxime + Ampicillin + Vancomycin

GBS

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40
Q

How are children >3 months with meningitis treated? What do they probably have?

A

Cefotaxime + Vancomycin

Neisseria meningitides

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41
Q

How are adults with meningitis treated? What do they probably have?

A

Cefotaxime + Vancomycin

Streptococcus pneumoniae

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42
Q

How are elderly with meningitis treated? What do they probably have?

A

Cefotaxime + Ampicillin + Vancomycin

Streptococcus pneumoniae

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43
Q

How are immunocompromised with meningitis treated? What do they probably have?

A

Unknown

Listeria monocytogenes

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44
Q

What is done clinically if meningococcus is diagnosed in a community?

A

Prophylactically treat all close contacts with rifampin or ceftriaxone

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45
Q

If bacterial meningitis is suspected, what are the steps done?

A

1st) Draw blood cultures
2nd) CT
3rd) LP if CT allows
4th) Empiric antibiotics, + steroids if cerebral edema

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46
Q

What are the steps for stroke therapy?

A

1st) Non-contrast CT
2nd) ECG
3rd) CXR
4th) CBC/PT/PTT/CMP
5th) Carotid endarterectomy if eligible
6th) tPA if eligible
7th) Supportive with airway, O2, and IV fluids

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47
Q

What are the criteria for tPA?

A

> 18 years old
Clinical diagnosis of stroke with stroke score < 22 (NIH)
Onset of stroke was known to be < 3-4.5 hours

BP < 185/110
Not a minor stroke
No seizure at onset of stroke
Not taking warfarin
PT < 15 or INR < 1.7
Not taking heparin within 48 hours with elevated PTT
Platelets > 100,000
Blood glucose > 50 and < 400
No acute MI
No prior intracranial hemorrhage, neoplasm, AVM, or aneurysm
No major surgical procedures within 14 days
No stroke or head injury within 3 months
No GI or GU bleeding within 21 days
No lactation or pregnancy within 30 days
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48
Q

What is an indicator for a carotid endarterectomy?

A

> 70% stenosis in symptomatic patients

-if no symptoms, reduce atherosclerotic risks and use aspirin

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49
Q

What can cause a Wallenberg syndrome? What are the symptoms?

A

Vertebral artery dissection or PICA occlusion

Lateral medullary ischemia

  • ipsilateral ataxia, vertigo, sensation to pain and temperature of the face, and cranial nerve weakness (dysarthria, dysphagia, dysphonia, facial muscles, and tongue)
  • contralateral motor weakness and sensation to pain and temperature of extremities
  • Horner’s with miosis, ptosis, and anhydrosis
  • palatal myoclonus
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50
Q

What is the most common ischemic stroke?

A

MCA occlusion

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51
Q

What symptoms are seen in a MCA occlusion?

A

Contralateral hemiplegia and hemisensory loss

Aphasia (if dominant hemisphere) or Apraxia, contralateral body neglect, and confusion (if non dominant hemisphere)

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52
Q

How does a thrombotic stroke and embolic stroke presentation differ? How do these differ from an intracranial hemorrhage? Finally, TIA?

A

Thrombotic usually take a little more time to experience neurological deficits, often waking up and experiencing deficits that get worse as time continues
Embolic are rapid onset with maximum deficits initially

Hemorrhage has abrupt pain and neurologic deficits, that will also worsen steadily over 30-90 minutes; has stupor, vomiting, increased intracranial pressure, and eventually coma

Transient ischemic attack is a focal deficit that lasts minutes to hours (1-24 hours) that resolves spontaneously; usually always has ipsilateral amaurosis fugax and/or unilateral hemiplegia/clumsiness

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53
Q

What is a TIA?

A

Transient ischemic attack is a focal deficit that lasts minutes to hours (1-24 hours) that resolves spontaneously

Usually always has ipsilateral amaurosis fugax and/or unilateral hemiplegia, hemiparesis, weakness, or clumsiness < 5 minutes

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54
Q

How can you tell a TIA apart from a vertebrobasilar system problem?

A

TIAs have vision and motor deficits that affect one side

Vertebrobasilar affect both eyes, vertigo, ataxia, diplopia, loss of consciousness/temporary amnesia

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55
Q

Why are TIAs clinically important?

A

They are often precursors to strokes

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56
Q

How can TIAs be diagnosed?

A

Carotid duplex sonography

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57
Q

How can TIAs be treated?

A

Prophylaxis - aspirin or antiplatelet medications

Acute - heparin

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58
Q

How does Broca’s aphasia present?

A

Non-fluent (broken sentences)
Abnormal repetition (can’t mirror your words)
Good comprehension (follows commands)
Abnormal naming

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59
Q

How does Transcortical motor aphasia present?

A

Non-fluent (broken sentences)
Good repetition (mirrors words)
Good comprehension (follows commands)
Abnormal naming

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60
Q

How does Wernicke’s aphasia present?

A

Fluent (word salad)
Abnormal repetition (can’t mirror your words)
Abnormal comprehension (can’t follow commands)
Abnormal naming

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61
Q

How does Transcortical sensory aphasia present?

A

Fluent (word salad)
Good repetition (mirrors words)
Abnormal comprehension (can’t follow commands)
Abnormal naming

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62
Q

How does Conduction aphasia present?

A

Fluent (word salad)
Good repetition (mirrors words)
Good comprehension (follows commands)
Abnormal naming

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63
Q

What are the most common patients for multiple sclerosis?

A

20-40 year old white women with acute exacerbations and remissions

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64
Q

What symptoms are found with multiple sclerosis?

A

Optic neuritis - monocular vision loss, pain on eye movement, central scotoma (darkening), decreased pupillary light reflex
Internuclear ophthalmoplegia (MLF lesion) - ipsilateral palsy of medial adduction, horizontal nystagmus of contralateral abduction
Scanning speech
Lhermitte phenomenon - neck flexion produces electric fatigue in spine, legs, or arms

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65
Q

What is Lhermitte phenomenon?

A

Finding in multiple sclerosis

Flexion of neck produces electric fatigue in spine, legs, or arms

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66
Q

What are the criteria for multiple sclerosis diagnosis?

A

Clinical - Two episodes and two white matter lesions

Lab - Two episodes, one white matter lesion on MRI, and abnormal CSF (oligoclonal bands of IgG)

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67
Q

What electrophysiologic phenomenon may occur with multiple sclerotic patients?

A

Visual impulses are delayed by 30-40ms

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68
Q

How can white matter lesions be seen in multiple sclerosis?

A

T2 MRI

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69
Q

How is multiple sclerosis treated?

A

Maintenance - glatiramer acetate (4 AA-myelin basic protein decoy)
Spasticity - baclofen, IFN-beta, natalizumab (PML-risk), cyclophosphamide
Pain - carbamazepine or gabapentin

Acute - high dose IV steroids

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70
Q

What cranial nerve can be involved with GBS?

A

CN VII

71
Q

What clinical findings are seen with GBS?

A

Ascending paralysis and weakness with intact sensation
Symmetric
Respiratory arrest
Loss of deep tendon reflex

72
Q

How can GBS be diagnosed?

A

CSF - elevated protein, normal cell count

Decreased motor nerve conduction velocity

73
Q

How can GBS be treated?

A

Plasma exchange and IV Ig

Do not give steroids

74
Q

What infections can lead to GBS?

A

Viral
Mycoplasma
Campylobacter jejuni

75
Q

Where does demyelination occur in vitamin B12 deficiency?

A

Posterior columns, lateral corticospinal tracts, and spinocerebellar tracts

  • loss of position/vibratory sense in LE
  • ataxia
  • UMN signs (increased DTR, spasticity, Babinski+, weakness)
  • -GU/GI incontinence
  • -Impotence
  • -Dementia

Can look like Lou Gherigs (subacute combined degeneration)

76
Q

What is the most classical symptom of lead toxicity?

A

Foot drop

77
Q

What damaged muscles would caused foot drop?

A

Tibialis anterior tendon and peroneal nerve palsy (or sciatic)

78
Q

What is the most common cause of carpal tunnel syndrome?

A

Peripheral neuropathy

79
Q

What is the earliest sign of carpal tunnel syndrome? The late sign?

A

Weakness in the thumb (also nocturnal pain, numbness, or tingling in the hand or forearm)

Wasting of thenar eminence

80
Q

How can carpal tunnel syndrome be diagnosed?

A

Tinel’s sign - percussing over nerve sends shock down length of the nerve

Phalen’s sign - pushing dorsal surfaces of both hands against each other for 30-60 seconds; if patient cannot hold that long due to pain, it is positive

Electromyography - reduced nerve conduction velocity

81
Q

What can lead to some peripheral neuropathies?

A

Genetics
Endocrine (DM, hypothyroidism, uremia)
Nutritional deficiencies (B1, B6, B12, E)
Toxic (lead, heavy metals, organophosphates, hexane)
Infectious (leprosy, Lyme, diphtheria, HIV)
Drug (cisplatin, vincristine, amiodarone, isoniazid, metronidazole, perhexeline, and thalidomide)
Autoimmune (RA, PAN, Churg-Strauss, Lupus)
Malignancy
Trauma
Idiopathic

82
Q

What are the most commonly involved cervical radiculopathy?

A

C6 and C7

-herniated disk, spinal stenosis, degenerative disk disease

83
Q

Between C5 and C6, what nerve is coming out? L4 and L5?

If the disc bulges between C5 and C6, what nerve is affected? If the disc bulges between L4 and S1, what nerve is affected?

A

C6
L4

C6
L5 (which is coming out of L5 and S1; this is because the nerve travels up one before exiting)

84
Q

What are the most commonly involved lumbar radiculopathy?

A

L5 and S1 herniated disc

Sciatica is the most common problem, which is a sharp or burning pain that shoots down the leg

85
Q

What can be used to treat Alzheimer’s?

A

Cholinesterase inhibitors

  • donepezil (aricept)
  • tacrine (cognex)
  • rivastigmine (exelon)
  • galantamine (reminyl)

NMDA receptor antagonist
-memantine

86
Q

What are the normal symptoms found in normal pressure hydrocephalus?

A

Abnormal gait
Urinary incontinence
Dementia

“Wobbly, wet, and wacky”

87
Q

What is clinically seen in normal pressure hydrocephalus?

A

No papilledema
Normal CSF opening pressure - but may improve patient’s symptoms
CT or MRI may show enlarged ventricles

88
Q

How is normal pressure hydrocephalus treated?

A

Surgical CSF shunting

89
Q

What is Wernicke encephalopathy?

A

Ophthalmoplegia
Ataxia
Global confusion
Nystagmus

90
Q

How do you approach treating alcoholic patients? Why?

A

Always give thiamine, then glucose

-Giving glucose only may miss Wernicke encephalopathy in an alcoholic that is thiamine deficient

91
Q

What is Korsakoff psychosis?

A

Mental status changes
Confabulation
Anterograde amnesia
Retrograde amnesia

92
Q

Where are peripheral vertigo lesions found?

A

Cochlear or retrocochlear

93
Q

What symptoms are seen in peripheral vertigo? Central vertigo?

A 
Sudden onset
Tinnitus
Hearing loss
Severe intensity
Nausea and vomiting
Nystagmus unilateral
Falls to ipsilateral side

Brainstem symptoms (weakness, hemiplegia, diplopia, dysphagia, facial numbness)
Gradual onset
Mild intensity
Mild nausea and vomiting
Mild nystagmus
Nystagmus is multidirectional and vertical

94
Q

What are the most common patients with benign paroxysmal positional vertigo?

A

> 60 year old patients

95
Q

What is the most common finding of BPPV?

A

Geotropic nystagmus with ear down

96
Q

How is BPPV diagnosed?

A

Dix-Hallpike maneuver - laying down of patient and rotating head with ear down causes nystagmus

97
Q

How is BPPV treated?

A 
Waiting
Vestibulosuppressant
Vestibular rehabilitation
Canalith repositioning
Surgery
98
Q

What is Meniere’s?

A

An increase of fluid in the labyrinth, causing symptoms

  • vertigo
  • nystagmus
  • hearing loss
  • 10% genetic

Last minutes to hours (20 minutes medium)

99
Q

What causes acute labryrinthitis?

A

Viral

100
Q

What is an ototoxic drug?

A

Aminoglycosides

101
Q

What is bilateral acoustic neuroma indicative of?

A

Neurofibroma Type 2

102
Q

What are three common central vertigo-causing diseases?

A

Multiple sclerosis
Cerebrovascular (TIA, Vertebrobasiliar insufficiency, PICA obstruction)
Migraine

103
Q

What are the most common drugs to give for absence epilepsy?

A

1st) Ethosuximide

2nd) Valproic acid

104
Q

What are the most common drugs to give for status epilepticus?

A

1st) Lorazeoam
2nd) Fosphenytoin
3rd) Phenobarbital
4th) Midazolam/Propofol

105
Q

What is the most common patient for juvenile myoclonic epilepsy?

A

Puberty

106
Q

What can make juvenile myoclonic epilepsy worse?

A

Sleep deprivation

Alcohol

107
Q

What is the EEG for juvenile myoclonic epilepsy?

A

1-3 4/6Hz spikes preceding a slow wave that lasts 1-20 seconds
Absence seizures may be present
Myoclonic jerks often have 5-20 10/16Hz spikes before the slow wave

Epileptic discharges may persist briefly after clinical activity has ceased

108
Q

How long do you treat juvenile myoclonic epilepsy? What is the most common medication?

A

For life

Valproic acid

109
Q

What is the most common focus of an intractable seizure?

A

Temporal lobe

110
Q

What can be seen in an MRI of a long-standing epilepsy?

A

Cortical dysplastic lesions

Unilateral atrophy of amygdala and hippocampus

111
Q

What are the first and second most common reasons for seizures in the elderly?

A

1st) Acute stroke (cerebrovascular)

2nd) Alzheimer’s (degenerative)

112
Q

How often are the temporal or frontal lobes included in resection for epilepsy control? How often does temporal lobe resection achieve cure?

A

80%

66%

113
Q

What is mesial temporal lobe epilepsy?

A

Hippocampal sclerosis associated seizures

114
Q

How often can mesial temporal lobe epilepsy be treated with surgery, and what is the procedure?

A

70%

Mesial lobe resection

115
Q

What has corpus callosum transection been used in children to treat?

A

Atonic and tonic-clonic seizures

116
Q

What is seen in complex partial epilepsy?

A

Impaired consciousness
Postictal confusion
Automatisms
Olfactory and gustatory hallucinations

117
Q

What are automatisms?

A

Purposeless, involuntary, repetitive motions; seen in complex partial epilepsy

118
Q

What are some early signs of uncal herniation?

A

Dilation of pupil of ipsilateral eye
Contralateral hemiplegia
*Can be ipsilateral hemiplegia instead due to Kernohan’s notch - this causes a false impression of the side of the lesion

119
Q

What is Kernohan’s notch?

A

The compression of the contralateral cerebral peduncle against the tentorium from an uncal herniation; this causes the crossing motor fibers going from the cortex to be ipsilateral to the lesion to be weak, which is paradoxical to normal uncal herniations

120
Q

What are some late signs of uncal herniation?

A

Loss or reflex movements in contralateral eye
Bilateral decerebrate posturing
Central neurogenic hyperventilation

121
Q

What is the definition of coma?

A

GCS of 8 or less for more than 4 weeks

122
Q

When is intubation necessary when dealing with GCS?

A

With a GCS less than 8

123
Q

What is common in a persistent vegetative state?

A

Unawareness of self
Breathes spontaneously
Has cycles of eye opening and closing

124
Q

What are the timelines of vegetative states?

A

When a coma lasts pasts 4 weeks - vegetative

Lasts 12 months after head injury or 6 months after any other insult - irreversible, permanent vegetative

125
Q

What are the seven criteria for brainstem death?

A 
No pupillary response
No corneal response
No vestibuloocular response
No motor response in CN distribution
No gag response
No respiratory reaction to hypercapnia
Two exams by two different doctors
126
Q

What is the vestibuloocular response?

A

Cold water in ear will cause head and eyes to tilt away

Warm water in ear will cause head and eyes to tilt towards

COWS = cold - opposite, warm - same

127
Q

What are some things that must be done for accurate brainstem death testing?

A

Metabolites and drugs must be ruled out
Retest after 24 hours
Temperature must be >35degC
Identify the coma etiology

128
Q

What are some common features of narcolepsy?

A

Cataplexy
Sleep paralysis
Hypnagogic hallucinations
Sleep onset REM

129
Q

How fast is REM achieved in narcolepsy?

A

10 minutes

130
Q

What are some treatments for narcolepsy?

A

Methylphenidate or dexamphetamine

Modafinil (Provigil)

131
Q

If there is high clinical suspicion for myasthenia gravis, but negative for AChR Ab, what is possible?

A

Anti-MuscarinicSK Ab

132
Q

What are used to diagnose myasthenia gravis?

A

Edrophonium (Tensilon) - give atropine beforehand and have crash cart nearby for bradycardia
Electrophysiology
CT for thymomas

133
Q

How is myasthenia graves treated?

A 
Anticholinesterases (pyridostigmine, neostigmine)
Corticosteroids
Immunosuppressants (azathioprine)
Plasmapheresis
IV Ig
Thymectomy
134
Q

What are the symptoms for Parkinson’s?

A 
Bradykinesia
Resting tremor (fine)
Cogwheel rigidity
Impairment of postural reflexes
Micrographia
Hypophonia
Festinating gait
Masked facies
135
Q

What are the treatments for Parkinson’s?

A

Selegiline (MAO-B inhibitor) and Entocapone (COMT inhibitor)
Benztropine (anticholinergics)
Amantadine (releases dopamine) - can cause livedo reticularis
Bromocriptine, ropinirole, pramipexole (dopamine agonist)
Levodopa, carbidopa (Sinemet) (dopamine) - can cause hallucinations early and dyskinesia later

136
Q

What is livedo reticularis?

A

Side effect of amantadine

Lace-like purplish rash of the skin

137
Q

What treatments for Parkinson’s can cause serious side effects?

A

Amantadine and levodopa/carbidopa (Sinemet)

138
Q

How does a resting tremor present?

A

Present when limb fully supported against gravity

Parkinson’s

139
Q

How does an action tremor present?

A

During any voluntary muscle contraction

140
Q

How does a postural tremor present?

A

During maintenance of a particular posture

Benign essential tremor or physiologic tremor

141
Q

How does kinetic tremor present?

A

During any type of movement

142
Q

How does intention tremor present?

A

Exacerbation of kinetic tremors when a planned movement nears its completion

Cerebellar

143
Q

How does a task-specific present?

A

During a particular skilled action

144
Q

What is benign essential tremor?

A

Postural tremor syndrome that predominates in the upper limbs that 50% gets better with alcohol

145
Q

How can benign essential tremor be treated?

A

50% respond to alcohol…

Primidone, propranolol, or topiramate
-primidone can cause acute intermittent porphyria (colicky abdominal pain)

146
Q

How does herpes encephalitis present?

A

With hemorrhagic lesions in the basal frontal and temporal lobes

147
Q

How often is herpes encephalitis fatal?

A

30%, with significant morbidity in a proportion of survivors

148
Q

How can herpes encephalitis be diagnosed?

A

CSF examination for HSV DNA with PCR

MRI

149
Q

How can herpes encephalitis be treated?

A

Acyclovir

Dexamethasone

150
Q

What is seen in CSF for pseudotumor cerebri?

A

Normal cells, normal glucose, normal protein, but >200 pressure

151
Q

What is the first, second, and third most common causes of death in the US?

A

1) Cardio/Cerebral vascular disease
2) Cancer
3) Trauma

152
Q

In Australia, what percentage of deaths are neurotrauma? Neurotrauma from road traffic?

A

3.5%

65%

153
Q

Why are the terms primary and secondary brain injury becoming blurred and obsolete?

A

Primary brain injury was defined as the initial damage that was irreversible, while secondary was preventable damage with treatment; now, treatment of the primary damage is being treated and being reversible - therefore the terms are not as concrete anymore

154
Q

Is direct trauma more impressive in penetrating or blunt trauma?

A

Penetrating; blunt is widespread and lessened

155
Q

What is cerebral contusion?

A

Bleeding that occurs under the frontal and temporal lobes from sliding across the floor and striking the sphenoid ridge and frontal bones OR bleeding from contrecoup from the opposite pole of the trauma; this results in a lacerated hemorrhagic brain or a burst temporal lobe

156
Q

In addition to contusion damage, what may rotational damage cause from blunt trauma?

A

Shearing of axons and myelin sheathes, as well as resulting in petechial hemorrhages is the upper brainstem, cerebrum, and corpus callosum; retraction balls or microglial scars will be seen

157
Q

If a patient lives for a number a months after a blunt trauma, what can be seen in postmortem?

A

Degeneration of myelin

158
Q

What is a subfalcine hernia?

A

When the medial surface of the hemisphere may be pushed under the falx

159
Q

What herniations can cause 3rd nerve palsy?

A

Uncal and hippocampal

160
Q

What are the three ways in which a trauma may cause hydrocephalus?

A

1) Blood blocking the 4th ventricle
2) Swelling in posterior fossa
3) Subarachnoid hemorrhage obstructing absorption of CSF

161
Q

How is concussion defined?

A

Instantaneous loss of consciousness

Retrograde amnesia, that may last less than one day

162
Q

What are the most commonly affected cranial nerves from blunt trauma? How is this possible?

A

Olfactory nerves

Fracture of the anterior cranial fossa or brain movement (blow back of the head) that tears the delicate nerve rootlets of cribriform

163
Q

What may cause deafness in head trauma? Vertigo and nystagmus?

A

Fracture of petrous temporal bone

  • hemotympanum (conductive)
  • inner ear or nerve damage (sensorineural)
  • vestibular nerve damage
  • cochlear damage
  • both often resolve in a few months
164
Q

What are the main injuries that could happen from a petrous temporal bone fracture?

A

Deafness
Vertigo
Nystagmus
Facial paralysis (delayed or immediate)

165
Q

Why is CN VI easily interrupted?

A

It has a long course into the Dorello canal

166
Q

What nerve is infrequently injured by direct trauma?

A

CN II

167
Q

What may be a false external visual indicator of head trauma?

A

Extent of scalp lacerations

168
Q

What three portions of the neurological examination should have special emphasis in head trauma?

A

1) Conscious state
2) Pupillary size and reaction
3) Focal neurological signs in extremities

169
Q

Why is it difficult to decipher trauma to the eye? How can it be told apart from the other pathology?

A

It results in a dilated pupil, just like a CN III palsy

As time progresses, the CN III palsy pathology pupil will become unresponsive to light, as well as the contralateral eye dilating and becoming unresponsive; this is absent in trauma to the eye

170
Q

Describe gaze center lesions

A

Lesions cause the contralateral gaze center to overact

Frontal cause ipsilateral eye deviation
Pontine cause contralateral eye deviation

171
Q

How are gaze center lesions diagnosed? What is a contraindication?

A

Oculocephalic response - eyes should stay in place, moving opposite to the rotation of the head
COWS as well

Cervical spine fracture

172
Q

What is skew deviation of the eyes indicative of?

A

Brainstem lesion

173
Q

What is ocular bobbing indicative of?

A

Very severe head injury with pontine damage

USMLE Step 2 (1 decks)

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