Neurology Clerkship

Question 1

Hearing loss
Bilateral
Progressive
Predominantly high-frequency
Sensorineural
Difficulty hearing with competing noise
Subjective bilateral tinnitus

Answer 1

Presbycusis

Question 2

Keratinizing squamous epithelium
Destruction of ossicles and sensorineural structures in the inner ear
Conductive and/or sensorineural hearing loss
Intermittent ear discharge
Tinnitus
Balance problems
Otoscopic exam: White plaque on the tympanic membrane with or w/o perforation or retraction

Answer 2

Cholesteatoma

Question 3

Excessive accumulation of endolymph in the membranous labyrinth
Recurrent episodes of vertigo (lasting 20 minutes to several hours)
Unilateral aural fullness, tinnitus, and sensorineural hearing loss

Answer 3

Meniere disease

Question 4

Sclerotic changes within ossicles of the middle ear
Progressive conductive hearing loss
NORMAL otoscopic exam

Answer 4

Otosclerosis

Question 5

Alzheimer’s disease treatment

a. SSRI
b. Cholinesterase inhibitor
c. Amantadine

Answer 5

Cholinesterase inhibitors.

Donepezil, rivastigmine, and galantamine

Question 6

Fever
Back pain
Neurologic deficits
Focal back pain that progresses over days to nerve root pain (shooting/electric)
Motor weakness, sensory changes, etc

Answer 6

Spinal epidural abscess (most common Staph Aureus)

Question 7

Acute headache
Nausea/vomiting
Blurry vision
Unilateral sluggish/dilated pupil
Conjunctival injection
New medication recently started

Answer 7

Acute angle-closure glaucoma

Sudden rise in intraocular pressure due to impaired drainage of aqueous humor through the pupil into the anterior chamber.
Develops spontaneously or triggered by medications (e.g. decongestants, antiemetics, anticholinergics) in patients with predisposing anatomy.

Question 8

What kind of medications can trigger acute angle-closure glaucoma?

Answer 8

Decongestants, antiemetics, anticholinergics, sympathomimetics. Basically, things that cause MYDRIASIS. Anticholinergic activity causes mydriasis which can cause acute angle-closure glaucoma in patients who have predisposing anatomy.

Question 9

Name 2 sellar masses that can cause bitemporal blindness

Answer 9

1. Craniopharyngioma

2. Prolactinoma

Question 10

Gradual loss of peripheral vision in both eyes
Leads to tunnel vision
No headache or endocrine symptoms

Answer 10

Open-angle glaucoma

Question 11

Ipsilateral hemiparesis
Ipsilateral diminished proprioception, vibratory sensation, and light touch
Contralateral diminished pain and temperature

Answer 11

Brown-Sequard syndrome

Question 12

True or False: A right spinal hemisection at T10 would lead to Brown-Sequard syndrome with left-sided loss of pain and temperature sensation around the T10 level and below.

Answer 12

FALSE.
It would have a loss at T12 and below because the lateral spinothalamic tract tends to decussate 1-2 levels above the entry point for the corresponding sensory neuron.

Question 13

Focal dystonia of the sternocleidomastoid muscle

Answer 13

Torticollis

Question 14

Sustained muscle contraction resulting in twisting, repetitive movements, or abnormal postures

Answer 14

Dystonia

Focal = one muscle, diffuse = many muscles

Question 15

Early executive dysfunction
Stepwise decline
Cerebral infarction and/or deep white matter changes on neuroimaging

Answer 15

Vascular dementia

Question 16

Does Frontotemporal dementia or Alzheimer dementia have early personality changes?

Answer 16

Frontotemporal dementia

Question 17

Early, insidious short-term memory loss
Language deficits & spatial disorientation
Later personality changes

Answer 17

Alzheimer disease

Question 18

Early personality changes

Apathy, disinhibition, compulsive behavior

Answer 18

Frontotemporal dementia (aka Pick disease)

Frontotemporal atrophy seen on neuroimaging

Question 19

Visual hallucinations
Spontaneous parkinsonism
Fluctuating cognition

Answer 19

Lewy body dementia

Question 20

Behavioral changes
Rapid progression
Myoclonus and/or seizures

Answer 20

Creutzfeldt-Jakob Disease (prion disease)

Question 21

Neurologic deficits disseminated in space and time
Women age 15-50
2 or more distinctive episodes of CNS dysfunction with at least some resolution
Cannot be explained by a single lesion

Answer 21

Multiple sclerosis

Question 22

Internuclear opthalmoplegia

Answer 22

Demyelination of the medial longitudinal fasciculus resulting in impaired conjugate horizontal gaze in which the affected eye (ipsilateral to lesion) is unable to adduct and the contralateral eye abducts with nystagmus.

Question 23

Rapidly progressive ascending muscle paralysis generally preceded by infection. Associated symptoms often include reduced/absent reflexes and paresthesias.

Answer 23

Guillain-Barre syndrome

Question 24

Impaired vibration/propioception
Sensory ataxia
Instability during Romberg test
Diminished pain/temperature sensation
Reduced/absent deep tendon reflexes
Miotic eyes. Pupillary constriction with accommodation but not with light

Answer 24

Tabes dorsalis (late neurosyphilis)

Question 25

High-grade astrocytoma CT/MRI: Butterfly appearance with central necrosis Nausea, vomiting, headaches Increased intracranial pressure

Answer 25

Glioblastoma multiforme

Question 26

Which area is most likely affected by stroke if a patient is demonstrating hemi-neglect? ``` A. left frontal cortex B. left temporal cortex C. right parietal cortex D. right occipital cortex E. right frontal cortex ```

Answer 26

Right parietal cortex

Question 27

Does hemi-neglect cause neglect of left or right side of a space?

Answer 27

Hemi-neglect syndrome is characterized by ignoring the LEFT side of a space.

Question 28

What's the difference between peripheral facial palsy (Bell's palsy) and central facial palsy?

Answer 28

Peripheral facial palsy causes loss of forehead and brow movements while central facial palsy has preservation of forehead and brow movements. They both have loss of nasolabial folds and drooping of the lower lip.

Question 29

Name 3 medications/supplements that can cause pseudotumor cerebri.

Answer 29

Glucocorticoids, vitamin A, oral contraceptives

Question 30

What is the pathophysiology of pseudotumor cerebri?

Answer 30

Impaired absorption of CSF by the arachnoid villi causes increased intracranial pressure.

Question 31

How do you treat pseudotumor cerebri?

Answer 31

Weight loss (if obese) and acetazolamide. Shunting or optic nerve sheath fenestration may be performed if needed.

Question 32

What complication occurs if pseudotumor cerebri is left untreated?

Answer 32

Blindness

Question 33

What vessel is injured in anterior cord syndrome?

Answer 33

Anterior spinal artery Injury can be due to disc retropulsion, fragments of bone from vertebral burst fracture

Question 34

Bilateral motor function loss at and below the level of injury with diminished pain and temperature sensation bilaterally that begins 1-2 levels below the cord injury. Proprioception, vibratory sensation, and light touch are unaffected. What's the syndrome?

Answer 34

Anterior cord syndrome 2/2 anterior spinal artery injury

Question 35

``` Usually bilateral, severe radicular pain Saddle hypo/anesthesia Asymmetric motor weakness Hyporeflexia/areflexia Late-onset bowel & bladder dysfunction ``` What's the syndrome?

Answer 35

Cauda equina syndrome

Question 36

``` Sudden-onset severe back pain Perianal hypo/anesthesia Symmetric motor weakness Hyperreflexia Early-onset bowel & bladder dysfunction ```

Answer 36

Conus medullaris syndrome

Question 37

``` Upper or lower motor neuron damage? Spastic paralysis Clasp-knife rigidity Hyperreflexia Babinski sign ```

Answer 37

Upper motor neuron damage

Question 38

``` Upper or lower motor neuron damage? Flaccid paralysis Hypotonia Hyporeflexia Muscle atrophy Fasciculations ```

Answer 38

Lower motor neuron damage

Question 39

How can you tell the difference between caudal equina syndrome and conus medullaris syndrome?

Answer 39

Cauda equina defects are LOWER MOTOR NEURON defects as they are nerve roots of the peripheral nervous system. So, cauda equina syndrome will have hyporeflexia/areflexia while conus medullaris syndrome will have hyperreflexia. Also, cauda equina syndrome typically presents with asymmetric motor weakness while conus medullaris syndrome presents with symmetric motor weakness. This makes sense because it would be unlikely for the impingements/defects of the many nerve roots of the cauda equina to be symmetric in the damage distribution. Another difference is that cauda equina syndrome has late-onset bowel and bladder dysfunction while conus medullaris has early-onset bowel and bladder dysfunction.

Question 40

What's the difference in presentation between ischemic and hemorrhagic stroke?

Answer 40

Ischemic stroke usually has an abrupt onset of focal neurologic deficits but lacks headache and impaired consciousness. Hemorrhagic stroke (e.g. intracranial hemorrhage) classically presents with acute focal neurologic deficits that gradually worsen over minutes to hours (as it bleeds) and can be associated with symptoms of elevated intracranial pressure (e.g. headache, vomiting, altered mental status).

Question 41

Unilateral, intermittent sharp pain of the cheek and lips that lasts several seconds and is triggered by minor stimuli (e.g. brushing teeth, drinking cold water) is likely what?

Answer 41

Trigeminal neuralgia

Question 42

Trigeminal neuralgia more commonly effects which 2 branches of the trigeminal nerve?

Answer 42

V2 and V3 (maxillary and mandibular)

Question 43

What is the pathophysiology of trigeminal neuralgia? (according to UW)

Answer 43

The pathophysiology is thought to be related to demyelination along the trigeminal nerve root (as it enters the pons), likely from localized compression (e.g. vascular structure).

Question 44

What are two medications that can treat trigeminal neuralgia?

Answer 44

Carbamazepine, oxcarbazepine

Question 45

Unilateral foot drop Numbness/tingling over the dorsal foot and lateral shin Impaired ankle dorsiflexion (walking on heels) and great toe extension Preserved plantar flexion (walking on toes) and reflexes Commonly caused by compression from leg immobilization, prolonged leg crossing, or protracted squatting

Answer 45

Common fibular neuropathy is a compressive injury to the common fibular nerve (aka common peroneal nerve) that travels near the fibular head. Manifestations are usually transient (lasting hours) and include foot drop and sensory changes over the dorsal foot and lateral shin. Physical examination shows impaired ankle dorsiflexion and great toe extension with preserved plantar flexion and reflexes. Note that spinal nerve root entrapment of the L5 can also present with foot drop; however, patients with spinal nerve root entrapment typically have back pain radiating to the foot and impaired plantar flexion. With common fibular neuropathy, a peripheral nerve compression, plantar flexion and reflex is spared.

Question 46

``` Unilateral Severe eye pain May see halos around lights Pupil dilated and poorly responsive to light Orbitofrontal headache, nausea, vomiting Eye appears injected ```

Answer 46

Acute angle-closure glaucoma

Question 47

Acute angle-closure glaucoma is more common in what patient population?

Answer 47

Women Asian and inuit populations Individuals with farsightedness

Question 48

Brief episodes of vertigo triggered by head movement (e.g. feeling dizzy when turning over in bed or looking up at objects on a high shelf). Dix-Hallpike maneuver helps to diagnose.

Answer 48

Benign paroxysmal positional vertigo (BPPV)

Question 49

What's the pathophysiology of benign paroxysmal positional vertigo (BPPV)?

Answer 49

BPPV is due to crystalline deposits (canaliths) in the semicircular canals that disrupt the normal flow of fluid in the vestibular system. This leads to contradictory signaling from the corresponding canals on each side, which is interpreted as a spinning/vertigo sensation.

Question 50

What is the Dix-Hallpike maneuver?

Answer 50

This is a maneuver that helps diagnose benign paroxysmal positional vertigo. Vertigo and nystagmus are triggered as the patient quickly lies back into a supine position with the head rotated 45 degrees.

Question 51

How do you treat benign paroxysmal positional vertigo?

Answer 51

BPPV resolves spontaneously in most cases but can recur months or years later. Symptoms can be relieved with the canalith repositioning maneuver. This involves having the patient lie down in a series of positions and holding their head in that position for 30-45 seconds.

Question 52

How do you differentiate dizziness from cardiovascular causes (e.g. arrhythmia, aortic stenosis, hypovolemia) from vertigo (e.g. benign paroxysmal positional vertigo, meniere's disease)?

Answer 52

Cardiovascular related dizziness usually causes global cerebral hypo perfusion and presents as lightheadedness or near-syncope rather than true vertigo. Also, physical exam findings of a crescendo-decrescendo systolic murmur at the aortic position radiating to the carotids with delayed and decreased carotid upstroke may also indicate a cardiac etiology of dizziness.

Question 53

Slow movements Shuffling gait Masked facies Rigidity

Answer 53

Parkinson disease

Question 54

``` Cognitive impairment Low mood Feelings of worthlessness Sleep disturbance Low energy Psychomotor retardation (slowed speech, thinking, and movements) ```

Answer 54

Major depressive disorder

Question 55

Elderly patients who are severely depressed often present with memory loss that is sometimes referred to as _____.

Answer 55

Pseudodementia

Question 56

``` Action tremor (E.g. hands outstretched) Usually bilateral Hands > arms > head >> legs Family history of tremor often present 5% of population affected ```

Answer 56

Essential tremor

Question 57

What is first line therapy for essential tremor? 2nd line?

Answer 57

1st) Beta blockers: propranolol | 2nd) Anticonvulsants: primidone

Question 58

What is central cord syndrome?

Answer 58

Central cord syndrome is a type of traumatic injury that typically occurs in elderly patients with pre-existing degenerative changes in the cervical spine. It typically occurs from hyperextension injuries and is characterized by weakness that is more pronounced in the upper extremities than the lower extremities and may be accompanied by a localized deficit in pain and temperature sensation.

Question 59

Does anterior cord syndrome cause spastic or flaccid motor paresis?

Answer 59

Spastic

Question 60

What is a cerebral contusion and how does it typically present?

Answer 60

Cerebral contusions are bruises of the brain that typically result from blows to the head that result in coup and contra-coup injuries. These injuries typically present with altered level of consciousness due to edema with the risk of seizure. Focal neurologic deficits may or may not be present.

Question 61

Autosomal recessive Younger individuals Liver disease (ranging from asymptomatic elevation of LFTs to fulminant hepatic failure) Neuropsychiatric disease (ranging from tremor and rigidity to depression, paranoia, and catatonia)

Answer 61

Wilson's disease

Question 62

Name 3 lab or physical exam findings unique to Wilson's disease.

Answer 62

1) Decreased serum ceruloplasmin, 2) increased urinary copper, and 3) Kayser-Fleischer rings on slit lamp examination.

Question 63

What biopsy finding can be found in both Wilson's disease and alcoholic liver injury? How can you tell the difference between Wilson's disease and alcoholic liver injury?

Answer 63

Mallory bodies can be found in both Wilson's and alcoholic liver injury. However, Wilson's disease typically presents with neuropsychiatric changes like tremor, rigidity, depression, paranoia, and/or catatonia. Alcoholic liver injury can be identified from a thorough patient history. Occasional drinking isn't enough alcohol to cause alcoholic liver injury.

Question 64

IV drug user Fever/chills Holosystolic murmur at cardiac apex (Red cell casts with proteinuria)

Answer 64

Infective endocarditis

Question 65

23 y/o anorexic hospitalized Acute-onset confusion after IV hydration and parenteral nutrition Horizontal nystagmus Diminished bilateral ankle reflexes Slow walk with short and wide-based steps What is the first step in management?

Answer 65

Give thiamine because this is wernicke encephalopathy 2/2 anorexia. Note that she got confusion after IV hydration and parenteral nutrition. This is because thiamine is a cofactor for many enzymes that have increased activity with high metabolic rate or glucose intake. Giving glucose to a thiamine deficient patient will exacerbate the problem.

Question 66

In anorexic patients and alcoholic patients, what should cross your mind in terms of immediate management? What should you think about giving and what should you avoid giving?

Answer 66

Avoid giving glucose. Consider giving thiamine. Alcoholic and anorexic patients are often thiamine deficient and giving glucose to these patients can cause or worsen wernicke-korsakoff syndrome.

Question 67

More than two-thirds of Guillian-Barre Syndrome patients have an antecedent respiratory or GI infection caused by which bacteria? Aside from this bug, what are 3 other precipitants of Guillian-Barre syndrome?

Answer 67

``` Campylobacter jejuni (2/3 of cases of GBS) Other culprits include herpes viruses, mycoplasma, and hemophilus influenza. ```

Question 68

What is infectious cavernous sinus thrombosis?

Answer 68

Because the facial/ophthalmic venous system is valveless, uncontrolled infection of the skin, sinuses, and orbit can spread to the cavernous sinus. Inflammation of the cavernous sinus subsequently results in life-threatening cavernous sinus thrombosis and intracranial hypertension. Headache is the most common symptom and can become intolerable. A low-grade fever and periorbital edema usually occur several days later secondary to impaired venous flow in the orbital veins. Vomiting is also a result of intracranial hypertension, and funduscopy may reveal papilledema.

Question 69

``` 23 y/o male Worsening headache over past week Lost appetite, vomiting Fever Bilateral eyelid edema and swelling Bilateral extraocular movements restricted Face tender to palpation ```

Answer 69

Cavernous sinus thrombosis secondary to infection. Notice that extraocular movements (CN 3, 4, 6) are effected with cavernous sinus thrombosis.

Question 70

Acute-onset agitation and confusion Disorientation Increased motor activity (e.g. climbing out of bed frequently) Vacillating severity (better in morning, worse at night)

Answer 70

Delirium

Question 71

How do you manage delirium?

Answer 71

Avoid polypharmacy and physical restraints, maintain normal sleep-wake cycle, provide frequent orientation, and treat underlying cause (e.g. infection, electrolyte disturbances, etc)

Question 72

Where in the brain are metastatic brain tumors usually seen?

Answer 72

Grey-white matter junction

Question 73

Brain metastasis is frequently seen in patients with which kind of cancer?

Answer 73

Non-small cell lung carcinoma

Question 74

For metastatic brain cancer, when do you surgically resect and when do you do whole brain radiation therapy?

Answer 74

Surgical resection is recommended for solitary brain metastasis in patients with good performance status and stable extracranial disease. In patients with multiple brain metastases, whole brain radiation therapy is typically used.

Question 75

Mood disturbances (depression, apathy) Dementia Chorea (facial grimacing, ataxia, dystonia, tongue protrusion, writhing movements of extremities) Family history of similar symptoms

Answer 75

Huntington's disease

Question 76

What is the inheritance pattern of Huntington's disease?

Answer 76

Autosomal dominant affecting both sexes equally typically between 30-50 years.

Question 77

Fluctuating and fatiguable ocular/bulbar weakness

Answer 77

Myasthenia gravis

Question 78

Patients with typical features of myasthenia gravis should undergo confirmatory testing by detecting the presence of which antibody?

Answer 78

Acetylcholine receptor antibodies (highly specific)

Question 79

If a patient is found to have typical features of myasthenia gravis and confirmed presence of acetylcholine receptor antibodies in serum, what should be the next step in management?

Answer 79

Chest CT or MRI to evaluate for thymoma. Thymectomy can lead to long-term improvement.

Question 80

``` 56 y/o man Right-handed Right-sided weakness and speech difficulty Speaking in short sentences with considerable effort Fully follows written and verbal commands but has difficulty writing and repeating Lesion location? A. Dominant frontal lobe B. Dominant parietal lobe C. Dominant temporal lobe D. Nondominant frontal lobe E. Nondominant parietal lobe F. Nondominant temporal lobe ```

Answer 80

Dominant frontal lobe | Broca's Aphasia

Question 81

``` Gait disturbance Dementia Urinary incontinence Slow and progressive memory impairment Dilated ventricles ```

Answer 81

Normal pressure hydrocephalus

Question 82

Describe the pathogenesis of subdural hematomas. Also, who is at highest risk for subdural hematomas?(name 4 groups)

Answer 82

Subdural hematomas are caused by shearing forces that tear the bridging veins, causing them to slowly bleed into the subdural space. Elderly (cerebral atrophy and increased fall risk) Alcoholic (cerebral atrophy and increased fall risk) Infants (thin-walled vessels) Patients on anticoagulants

Question 83

Elderly patient History of falls Gradual worsening of headache, nausea, vomiting, impaired consciousness, and confusion (days to weeks) Focal neurologic deficits

Answer 83

Subdural hematoma

Question 84

How does chronic subdural hematoma look on a non-contrast head CT?

Answer 84

Crescent-shaped hypodensity that crosses suture lines

Question 85

Painless, rapid, and transient (<10 minutes) monocular vision loss. Curtain descending over the visual field. Normal funduscopic examination, sometimes plaques and retinal whitening

Answer 85

Amaurosis fugax

Question 86

What is the pathophysiology of amaurosis fugax?

Answer 86

Most commonly caused by retinal ischemia due to atherosclerotic emboli originating from the ipsilateral carotid artery; therefore, patients with vascular risk factors (e.g. HTN, HLD, smoking) should be evaluated with duplex ultrasound of the neck.

Question 87

``` Unilateral headache Jaw claudication Fever Fatigue Proximal muscle weakness/pain ```

Answer 87

Temporal (giant cell) arteritis

Question 88

Altered mental status | Core temperature >105 degrees F

Answer 88

Heat stroke

Question 89

What's the difference between exertional and non-exertional heat stroke?

Answer 89

Exertional heat stroke is most commonly seen in factory workers, military recruits, and athletes who are exposed to hot/humid environments with inadequate access to shade and fluids. Non-exertional heat stroke is most commonly seen in people incapable of obtaining adequate fluids and removing themselves from a hot environment (e.g. babies, disabled, elderly)

Question 90

How many days after stroke until CT scan reaches greater than 95% sensitivity? How about MRI?

Answer 90

CT scan needs 4-5 days to reach greater than 95% sensitivity for stroke while MRI needs only 24 to 48 hours to reach greater than 95% sensitivity.

Question 91

What is the best initial therapy for nonhemorrhagic stroke at less than 3 hours since onset of stroke? at more than 3 hours since onset? What's the best initial therapy for hemorrhagic stroke?

Answer 91

Less than 3 hours since onset of nonhemorrhagic stroke: thrombolytics More than 3 hours since onset of nonhemorrhagic stroke: aspirin. If they are already on aspirin, add dipyridamole or switch to clopidogrel. Hemorrhagic stroke: nothing. Hemorrhagic stroke has no treatment for reversal and surgical drainage will not help outside of the posterior fossa.

Question 92

Every patient with a stroke should be started on a _____.

Answer 92

Statin. Every patient with a stroke should be started on a statin medication regardless of LDL. Although target-based therapy for lipid management is unclear at this time, we want to bring the LDL to 70 or at least under 100.

Question 93

True or False: Carotid angioplasty and stenting is first-line treatment for carotid stenosis of 70% and greater.

Answer 93

False. Carotid angioplasty and stenting is of no proven value for stroke patients and it is ALWAYS a wrong answer.

Question 94

When is carotid endarterectomy indicated?

Answer 94

Carotid endarterectomy has no value for milder stenosis (under 50%) and is unclear if there is benefit with moderate stenosis (50-70%). Definitely do carotid endarterectomy in symptomatic cerebrovascular disease with more than 70% stenosis.

Question 95

Name the 4 risk factor modifications for stroke prevention.

Answer 95

1) Control diabetes to hemoglobin A1C below 7% 2) Control hypertension 3) Reduce LDL to at least below 100 if carotid stenosis is the cause of the stroke 4) Tobacco smoking cessation

Question 96

It is critical to start _____ without waiting for biopsy in giant cell arteritis.

Answer 96

Steroids

Question 97

What is first line abortive therapy for cluster headache?

Answer 97

100% oxygen. If it doesn't work, you can use triptans or ergotamine.

Question 98

Cluster headache prophylaxis?

Answer 98

Verapamil

Question 99

Migraine prophylaxis?

Answer 99

Propranolol is first line. Others include calcium channel blockers, TCAs (amitriptyline), SSRIs, topiramate, and botox injections.

Question 100

Zoster vaccine is indicated in all persons above the age of __ to prevent herpes zoster (shingles)

Answer 100

60

Question 101

True or False: EEGs should be ordered first when working up the cause of a seizure.

Answer 101

FALSE. An EEG would not be the right answer unless all other tests were done and were normal including CT or MRI of the head. There is no point in doing an EEG to identify the cause of a seizure if there is a clear metabolic, toxic, or anatomic defect causing the seizure. Seizures can be caused by hyponatremia, hypernatremia, hypoxia, hypoglycemia, CNS infections, CNS anatomic abnormalities, hypocalcemia, uremia, hepatic failure, alcohol withdrawal, barbiturate withdrawal, benzodiazepine withdrawal, cocaine toxicity, and sometimes hypomagnesemia.

Question 102

What is the best initial therapy for a persistent seizure (status epilepticus)? What if it persists?

Answer 102

Benzodiazepines such as lorazepam or diazepam. If it persists, give phenytoin or fosphenytoin. 1) Benzodiazepines 2) Fosphenytoin 3) Phenobarbital 4) General anesthesia

Question 103

What is a partial seizure? What is a simple partial seizure? Complex partial?

Answer 103

A partial seizure is focal to one part of the body (e.g. limited to just an arm). Simple means that consciousness is intact while complex means there is a loss or alteration of consciousness.

Question 104

What is a tonic-clonic seizure?

Answer 104

This is a generalized seizure with varying phases of muscular rigidity (tonic) followed by jerking of the muscles of the body for several minutes (clonic).

Question 105

What is an absence seizure?

Answer 105

This is a seizure where consciousness is impaired only briefly. The patient remains upright and gives a normal appearance or just seems to be staring into space. Absence seizures occur more often in children.

Question 106

It is typically not necessary to begin antiepileptic drugs for a single seizure episode. What are the 4 exceptions?

Answer 106

If the single seizure episode includes: 1) Presentation in status epilepticus 2) If there are focal neurologic signs 3) If there is an abnormal EEG or lesion on CT 4) If there is a family history of seizures

Question 107

All anti-epileptic drugs have nearly equal efficacy. So, the goal is to choose a medication that has the least side effects for your patient. What anti-epileptic drug typically has the fewest adverse effects?

Answer 107

Levetiracetam (Keppra)

Question 108

What is the best therapy for absence seizures?

Answer 108

Ethosuximide

Question 109

When do you add a second seizure medication and when do you pursue surgical correction of a seizure focus?

Answer 109

If seizures are not controlled with a single agent, an alternate medication should be tried. If seizures are still not controlled, adding a second medication may help. If multiple medications do not control the seizure, surgical correction of a seizure focus may lead to resolution of recurrences.

Question 110

When can you discontinue seizure medication?

Answer 110

The standard of care is to wait until the patient has been seizure free for 2 years.

Question 111

What is the best study to tell if there will be a recurrence of seizure activity?

Answer 111

Sleep deprivation EEG. Sleep deprivation can elicit abnormal activity on an EEG but the test lacks high sensitivity.

Question 112

Aneurysms are more common in patients with? (name 5)

Answer 112

1) Polycystic kidney disease 2) Tobacco smoking 3) Hypertension 4) Hyperlipidemia 5) High alcohol consumption

Question 113

``` Sudden onset Severe headache Stiff neck Photophobia Fever Loss of consciousness ```

Answer 113

Subarachnoid hemorrhage. Note that the presentation of subarachnoid hemorrhage is similar to meningitis. The difference is that subarachnoid hemorrhage has a very sudden onset and can result in loss of consciousness. Subarachnoid often presents with fever due to meningeal irritation.

Question 114

What is the best initial test (most sensitive) for subarachnoid hemorrhage work-up? How about most accurate?

Answer 114

Non-contrast CT head (95% sensitivity). Most accurate test is lumbar puncture demonstrating blood or xanthochromia (yellow discoloration)

Question 115

What electrocardiographic finding can you sometimes observe with intracranial bleeding?

Answer 115

Large or inverted T waves suggestive of myocardial ischemia. This is thought to be from excessive sympathetic activity.

Question 116

True or False: When looking for brain bleeds, use contrast with your CT.

Answer 116

FALSE. Do not use contrast when looking for blood.

Question 117

When treating subarachnoid hemorrhage, what medication can be given to prevent subsequent ischemic stroke?

Answer 117

Nimodipine (calcium channel blocker) Nimodipine has shown good results in preventing a major complication of subarachnoid hemorrhage--vasospasm. This is now the main use of nimodipine.

Question 118

What are the 4 things that should be done for treatment of subarachnoid hemorrhage?

Answer 118

1) Nimodipine to prevent vasospasm causing subsequent ischemic stroke 2) Embolization (coiling). This is when a catheter is used to clog up the site of bleeding to prevent a repeat hemorrhage. IR places platinum wire into the site of hemorrhage. This has been shown to be superior to surgical clipping for survival and complications. 3) Seizure prophylaxis. Usually phenytoin. 4) Ventriculoperitoneal shunt only if hydrocephalus develops.

Question 119

Meningitis and subarachnoid hemorrhage can both present with severe headache, fever, nuchal rigidity, and photophobia. How can you tell the difference between the two?

Answer 119

Meningitis will have a normal CT head while subarachnoid hemorrhage should have bleeding demonstrated on the non-contrast CT. Also, lumbar puncture shows CSF with increased WBCs in meningitis. A normal WBC to RBC ratio for CSF is 1 WBC to 500-1000 RBCs. A elevated WBC/RBC ratio suggests meningitis.

Question 120

What's the best initial therapy for bacterial meningitis?

Answer 120

Ceftriaxone and vancomycin (add acyclovir if viral is on the differential too)

Question 121

True or False: When taking standardized exams, never answer "consultation" for anything.

Answer 121

True. Consultation is only the right answer when you want to do a particular procedure and the procedure is not given as a choice. If the right answer is "embolization" and it is not listed, but "IR consultation" is a choice, then you can choose it.

Question 122

Loss of all function except for the posterior column Flaccid paralysis below the level of infarction Loss of DTRs at the level of infarction Evolves into spastic paraplegia several weeks later Loss of pain and temperature Extensor plantar response

Answer 122

Anterior spinal artery infarction

Question 123

Name 2 things that can cause subacute combined degeneration of the cord. How does this present?

Answer 123

B12 deficiency and neurosyphilis can cause subacute combined degeneration. This presents with loss of position and vibratory sensation.

Question 124

Loss of pain and temperature bilaterally across the upper back and both arms. Loss of reflexes. Muscle atrophy.

Answer 124

Syringomyelia

Question 125

What imaging do you order for syringomyelia? How do you treat it?

Answer 125

Order MRI. Treat with surgical removal of tumor if present and drainage of fluid from cavity.

Question 126

Pathogenesis of brain abscess?

Answer 126

A brain abscess is a collection of infected material within the parenchyma of the brain tissue acting as a space-occupying lesion. A brain abscess can be a result of spread from contiguous infection in the sinuses, mastoid air cells, or otitis media. It can also be from anything that leads to bacteremia (e.g. pneumonia, endocarditis, etc).

Question 127

Symptoms of brain abscess?

Answer 127

Headache, nausea, vomiting, fever, seizures, and focal neurological findings. Presentation is somewhat nonspecific and there is no way to distinguish a brain abscess from a cancer without a biopsy. Note that cancer can cause fever too. Both cancer and infection enhance with contrast. You cannot distinguish them based on CT scan appearance.

Question 128

How do you treat a brain abscess?

Answer 128

You MUST biopsy to distinguish abscess from cancer and to determine the precise organism and sensitivity pattern. Abscesses can be from staph, strep, gram-negative bacilli, and anaerobes. Infections are frequently mixed, so a precise diagnosis is especially important. Duration of treatment is very long (6-8 weeks of IV antibiotics followed by 2-3 months of oral antibiotics).

Question 129

``` Seizures Progressive psychomotor retardation Slowly progressive mental deterioration Reddened facial nodules (adenoma sebaceous) Leathery plaques on trunk (shagreen patches) Hypopigmented patches (ash leaf) Retinal lesions Cardiac rhabdomyomas ```

Answer 129

Tuberous sclerosis

Question 130

Soft, flesh-colored lesions attached to peripheral nerves. 8th cranial nerve tumors Cafe au lait spots Meningiomas and gliomas

Answer 130

Neurofibromatosis

Question 131

``` Port-wine stain of face Seizures Homonymous hemianopsia Hemiparesis Mental subnormality ```

Answer 131

Sturge-Weber syndrome

Question 132

Best medication for essential tremor?

Answer 132

Propranolol

Question 133

Tremor at rest and intention | Improved with alcohol

Answer 133

Essential tremor

Question 134

True or False: There is no test for parkinsonism. The diagnosis is based entirely on clinical presentation.

Answer 134

TRUE

Question 135

``` Tremor Muscular rigidity Bradykinesia Shuffling gait with unsteadiness on turning Cogwheel rigidity Limited facial expression Small handwriting ```

Answer 135

Parkinsonism

Question 136

How do you treat mild parkinsonism? What are some side-effects of this medication? What can you give to patients who are intolerant to these side effects?

Answer 136

Anticholinergic medications like benztropine and trihexyphenidyl. These medications relieve tremor and rigidity. Side effects of anticholinergic medications include dry mouth, worsening prostate hypertrophy, and constipation. Give amantadine in older patients who are intolerant of anticholinergic medications.

Question 137

How do you treat severe parkinsonism? (inability to care for themselves, orthostatic). Name 4 classes and included medications and 1 intervention.

Answer 137

Dopamine agonists like pramipexole and ropinirole are the best initial therapy in severe parkinsonism. Levodopa/carbidopa is the most effective medication. COMT inhibitors (tolcapone and entacapone) are used to extend the duration of levodopa/carbidopa by blocking the metabolism of dopamine. MAO inhibitors (rasagiline, selegiline) can also be used to block the metabolism of dopamine. Deep brain stimulation is electrical stimulation that are highly effective for tremors and rigidity in some patients.

Question 138

What is the on/off phenomena of parkinson's disease treatment?

Answer 138

On/off phenomena results in episodes of insufficient dopamine ("off") characterized by bradykinesia. The "on" effect is too much dopamine resulting in dyskinesia. This phenomena worsens as a patient is on parkinson's treatment.

Question 139

What food should be avoided in patients taking MAO inhibitors?

Answer 139

Tyramine-containing foods (e.g. cheese)

Question 140

What drug class can retard the progression of parkinsonism?

Answer 140

MAO inhibitors. MAO inhibitors are the only drugs associated with the possibility of slowing the progression of parkinsonism.

Question 141

What do you do when a patient with severe parkinsonism presents with psychosis and confusion? The patient is on levodopa/carbidopa, ropinirole, and tolcapone. ``` A. stop levodopa/carbidopa B. start clozapine C. stop ropinirole D. stop tolcapone E. start haloperidol ```

Answer 141

B. start clozapine When a patient with severe parkinsonism presents with psychosis, you shouldn't discontinue the medications as this will cause the patient to become "locked in" with severe bradykinesia. Treat the psychosis and confusion with antipsychotic medications with the fewest extrapyramidal (antidopaminergic) effects (e.g. 2nd gen antipsychotics like clozapine).

Question 142

Parkinsonism with dementia

Answer 142

Lewy body dementia

Question 143

Painful, contracted muscles from damage to the central nervous system.

Answer 143

Spasticity. This is often associated with MS.

Question 144

How do you treat spasticity from central nervous system damage?

Answer 144

Baclofen, dantrolene, and tizanidine (central acting alpha agonist)

Question 145

Uncomfortable sensation in legs at night Discomfort worsened by caffeine Relieved by moving the legs

Answer 145

Restless leg syndrome

Question 146

How do you treat restless leg syndrome?

Answer 146

Dopamine agonists such as pramipexole

Question 147

Choreaform movement disorder (dyskinesia) Dementia Behavior changes (irritability, moodiness, antisocial behavior) Age 30-50 with family history of similar symptoms

Answer 147

Huntington disease

Question 148

How do you diagnose huntington disease?

Answer 148

Genetic testing is 99% sensitive. CAG trinucleotide repeat sequences are found on genetic analysis.

Question 149

How do you treat the dyskinesia in huntington disease? How about the psychosis?

Answer 149

Treat dyskinesia with tetrabenazine and psychosis with haloperidol, quetiapine, or trial of different antipsychotics.

Question 150

Vocal tics, grunts, coprolalia Motor tics (sniffing, blinking, frowning) Obsessive-compulsive behavior

Answer 150

Tourette disorder

Question 151

Coprolalia

Answer 151

The involuntary and repetitive use of obscene language, as a symptom of mental illness or organic brain disease.

Question 152

The involuntary and repetitive use of obscene language, as a symptom of mental illness or organic brain disease.

Answer 152

Coprolalia

Question 153

How do you diagnose tourette disorder?

Answer 153

Clinical symptoms. No diagnostic test is available

Question 154

How do you treat tourette disorder?

Answer 154

Treat with fluphenazine, clonazepam, pimozide, or other neuroleptic medications. Methylphenidate and ADHD treatment are intrinsic to Tourette management.

Question 155

What is the most common initial presentation of multiple sclerosis? Less common presentations?

Answer 155

Focal sensory symptoms with gait and balance problems. Blurry vision or visual disturbance from optic neuritis is also common but not as common as the first presentation. After optic neuritis, the most common abnormalities are motor and sensory. The least common abnormalities are cognitive defects and dementia. Sexual function remains relatively intact. Other findings include fatigue, spasticity, hyperreflexia, and cerebellar deficits.

Question 156

What is internuclear ophthalmoplegia? What disease is it associated with?

Answer 156

Internuclear ophthalmoplegia (INO) is a disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction. When an attempt is made to gaze contralaterally (relative to the affected eye), the affected eye adducts minimally, if at all. The contralateral eye abducts, however with nystagmus. Additionally, the divergence of the eyes leads to horizontal diplopia. That is, if the right eye is affected the patient will "see double" when looking to the left, seeing two images side-by-side. Convergence is generally preserved. This is associated with multiple sclerosis.

Question 157

What is the best initial test for diagnosing MS? What is the most accurate?

Answer 157

MRI is both the best initial test and the most accurate test. Lumbar puncture can show CSF with mild elevation in protein and fewer than 50-100 WBCs. Oligoclonal bands are found in about 85% of patients but are NOT specific to MS. In other words, LP can add to the clinical picture but don't rely on it. They can help in patients with equivocal or nondiagnistic MRI.

Question 158

What is the role of steroids in treating/management of MS?

Answer 158

Steroids shorten the duration of flares but they do not change the course of the disease or lessen the severity of flares and resulting damage.

Question 159

Name 8 drugs that prevent relapse and progression of MS.

Answer 159

``` Glatiramer Beta-interferon Fingolimod Natalizumab Rituximab Mitoxantrone Azathioprine Cyclophosphamide ```

Question 160

Which multiple sclerosis drug has associated risk of progressive multifocal leukoencephalopathy secondary to JC virus infection?

Answer 160

Natalizumab (Tysabri)

Question 161

What two drugs are the best first choice for prevention of relapse?

Answer 161

Glatiramer and beta-interferon

Question 162

Loss of both upper and lower motor neurons

Answer 162

Amyotrophic lateral sclerosis

Question 163

Weakness of unclear etiology starting in the 20s to 40s with a unique combination of upper and lower motor neuron loss. Difficulty in chewing and swallowing and decrease in gag reflex leading to pooling of saliva in the pharynx and frequent episodes of aspiration. Weak cough.

Answer 163

Amyotrophic lateral sclerosis

Question 164

What is spared in amyotrophic lateral sclerosis?

Answer 164

Sensory loss and sphincters are spared in ALS.

Question 165

``` Weakness Spasticity Hyperreflexia Extensor plantar responses Weakness Muscle wasting Fasciculations ```

Answer 165

Amyotrophic lateral sclerosis

Question 166

What are two lab/test findings in amyotrophic lateral sclerosis?

Answer 166

Electromyography revealing loss of neural innervation in multiple muscle groups. Elevated CPK.

Question 167

What drug is thought to prevent progression of amyotrophic lateral sclerosis?

Answer 167

Riluzole reduces glutamate buildup in neurons and may prevent progression of amyotrophic lateral sclerosis.

Question 168

How do you treat the spasticity in amyotrophic lateral sclerosis?

Answer 168

Baclofen

Question 169

How do you treat amyotrophic lateral sclerosis? (4 items)

Answer 169

1. Riluzole to prevent progression of disease. 2. Baclofen to treat spasticity. 3. CPAP or BiPAP to help with respiration difficulties secondary to muscle weakness. 4. Tracheostomy and maintenance on a ventilator with advanced disease.

Question 170

What is the most common cause of death in ALS?

Answer 170

Respiratory failure

Question 171

``` Distal weakness and sensory loss Wasting in the legs Decreased deep tendon reflexes Tremor Foot deformity with high arch ```

Answer 171

Charcot-Marie-Tooth disease (genetic disorder leading to loss of both motor and sensory innervation)

Question 172

How do you diagnose and treat charcot-marie-tooth disease?

Answer 172

You diagnose with electromyography. There is no treatment.

Question 173

What is the most common cause of peripheral neuropathy? What are 3 other causes?

Answer 173

Diabetes mellitus. Other causes include uremia, alcoholism, and paraproteinemias like monoclonal gammopathy of unknown significance.

Question 174

What is the best initial therapy for peripheral neuropathy? What else can be considered for treatment?

Answer 174

Pregabalin or gabapentin are best initial therapy. TCAs and most seizure medications (phenytoin, carbamazepine, lamotrigine) are effective in some people.

Question 175

Wasting of hypobthemar eminence, pain in 4th and 5th fingers. Which nerve neuropathy? Who typically presents with this?

Answer 175

Ulnar nerve. Can be seen in bikers due to pressure on palms while riding or people with trauma to the medial side of the elbow.

Question 176

Wrist drop. Which nerve neuropathy? What causes this?

Answer 176

Radial nerve neuropathy. Can be caused by pressure of inner, upper arm; falling asleep with arm over back of chair, using crutches and pressure in the axilla

Question 177

Pain/numbness of outer aspect of one thigh. Which nerve neuropathy? What causes this?

Answer 177

Lateral cutaneous nerve of thigh. Can be caused by obesity, pregnancy, and sitting with crossed legs.

Question 178

Pain/numbness in ankle and sole of foot. Which nerve neuropathy is this? What worsens it?

Answer 178

Tarsal tunnel (tibial nerve). Worsens with walking.

Question 179

Weak foot with decreased dorsiflexion and eversion. Which nerve is damaged? What can cause this?

Answer 179

Peroneal nerve. Can be caused by high boots putting pressure on back of the knee.

Question 180

Thenar wasting, pain/numbness in first 3 fingers. Which nerve is damaged? What can cause this?

Answer 180

Median nerve. Can be caused by typing on computers or other work with hands (e.g. carpenters).

Question 181

Do you typically worry about stroke if there is paralysis of the entire side of the face or just the lower half?

Answer 181

Only worry about stroke if only the lower half of the face is paralyzed because the upper half of the face receives innervation from both cerebral hemispheres. If the patient can wrinkle their forehead on the affected side, worry about stroke. If not, worry about bell palsy.

Question 182

What are two additional features that can appear with facial nerve or bell palsy?

Answer 182

1) Hyperacusis (sounds are extra loud because the 7th nerve normally innervates the stapedius muscle which acts as a "shock absorber" on the ossicles of the middle ear). 2) Taste disturbance (because the 7th nerve supplies sensation to taste to the anterior 2/3rds of the tongue).

Question 183

How do you diagnose facial nerve palsy?

Answer 183

No test is usually done due to the characteristic presentation of paralysis of half of the face. The most accurate test is electromyography and nerve conduction studies.

Question 184

What is the best initial therapy for facial nerve palsy?

Answer 184

Prednisone. Acyclovir is sometimes added but benefit is not clear.

Question 185

What is the most common complication of 7th cranial nerve palsy? a. corneal ulceration b. aspiration pneumonia c. sinusitis d. otitis media e. deafness f. dental carries

Answer 185

Corneal ulceration. Corneal ulceration occurs because of difficulty closing the eye, especially at night. This leads to dryness of the eye and ulceration. This is prevented by taping the eye shut and using lubricants in the eye. Dental caries don't happen because although there is drooling from difficulty closing the mouth, saliva production is normal. Rather than deafness, sounds are extra loud with 7th cranial nerve palsy. Aspiration does not occur because the gag reflex and cough reflex are normal.

Question 186

Autoimmune damage of multiple peripheral nerves. By definition, there is no CNS involvement. Circulating antibodies attack the myelin sheaths of peripheral nerves. Often associated with campylobacter jejuni infection.

Answer 186

Guillain-Barre Syndrome

Question 187

What is the most specific diagnostic test for guillain-barre syndrome? What do the test results show?

Answer 187

Nerve conduction studies/electromyography demonstrating a decrease in the propagation of electrical impulses along the nerves. It takes about 1-2 weeks for the electrical impulses to demonstrate abnormality on the exam.

Question 188

What testing should you do for guillain-barre syndrome patients to determine respiratory risk?

Answer 188

PFTs. Patients with decreased FVC and peak inspiratory pressure have worse prognosis.

Question 189

How do you treat guillain-barre syndrome?

Answer 189

IVIG or plasmapheresis. They are equal in efficacy.

Question 190

Does administering prednisone or other steroids help in management of guillain-barre syndrome?

Answer 190

No, it may actually make it worse

Question 191

When treating guillain-barre syndrome, can you combine IVIG and plasmapheresis treatments?

Answer 191

No. Combining them wouldn't make any sense as you are putting expensive IVIG into the blood and just taking it back out with plasmapheresis.

Question 192

Woman comes to the ED with bilateral leg weakness developing over the last few days. She has lost her knee jerk and ankle jerk reflexes. The weakness started in her feet and progressed up to her calves and then her thighs. She is otherwise asymptomatic. What is the most urgent step in management?

Answer 192

Pulmonary function testing. The most dangerous thing that can happen with guillain-barre syndrome is dysautonomia or involvement of the respiratory muscles. Peak inspiratory pressure or a decreased in FVC is the earliest way to detect impending respiratory failure. If you wait there until there is CO2 accumulation in ABG, it is too late. Nerve conduction studies are the most accurate test for guillan-barre syndrome but the results of the nerve conduction studies is not as important as determining if the patient is at risk of respiratory failure.

Question 193

Double vision Difficulty chewing Dysphonia (difficulty speaking) Weakness of limb muscles worse at the end of the day

Answer 193

Myasthenia Gravis

Question 194

Weakness with sustained activity Ptosis Normal pupillary response

Answer 194

Myasthenia Gravis

Question 195

What is the best initial test when myasthenia gravis is suspected? What's the most accurate test? What test can be done to test the response of myasthenia gravis to appropriate medication?

Answer 195

Best initial test: acetylcholine receptor antibodies (80-90% sensitive). Most accurate test: electromyography showing decreased strength with repetitive stimulation. Test to determine response to acetylcholinesterase inhibitors: administration of edrophonium (short-acting ACh inhibitor) will demonstrate clear improvement in motor function that lasts for a few minutes.

Question 196

What is the best initial treatment for myasthenia gravis?

Answer 196

Neostigmine or pyridostigmine. These are longer acting acetylcholinesterase inhibitors

Question 197

What is acute myasthenic crisis? How do you treat it?

Answer 197

Acute myasthenic crisis presents with severe, overwhelming disease with profound weakness or respiratory involvement. Treat with IVIG or plasmapheresis.

Question 198

Rapidly progressive dementia Myoclonic jerks Normal head MRI or CT CSF with 14-3-3 protein

Answer 198

Creutzfeldt-Jakob Disease (prion disease)

Question 199

Headache (worse at night) Nausea/vomiting Mental status changes (e.g. decreased level of consciousness, cognitive dysfunction) Focal neurologic symptoms (e.g. vision changes, unsteady gait) Seizure Symptoms worsen by leaning forward, valsalva, or cough.

Answer 199

Intracranial hypertension

Question 200

Hypertension, bradycardia, respiratory depression

Answer 200

Cushing reflex is a worrisome finding suggestive of brainstem compression

Question 201

Signs of meningeal irritation

Answer 201

Headache, photophobia, nuchal rigidity

Question 202

Frontal headache that worsens with leaning forward. Nasal congestion. Purulent nasal discharge. Normal vision.

Answer 202

Sinusitis

Question 203

Most common cause of fatal sporadic encephalitis in the USA, beyond the neonatal period

Answer 203

Herpes encephalitis, typically HSV-1

Question 204

Acute onset (< 1 week duration) Focal neurological findings (altered mentation, focal cranial nerve deficits, ataxia, hyperreflexia, or focal seizures) Fever Behavioral changes (e.g. hypomania, hyperphagia, hyper-sexuality, amnesia) CSF reveals lymphocytic pleocytosis and increased RBC count Elevated CSF protein Normal CSF glucose

Answer 204

Herpes encephalitis

Question 205

Kluver-Bucy syndrome

Answer 205

Hyperphagia, hypersexuality

Question 206

What is the gold-standard for diagnosing herpes encephalitis?

Answer 206

PCR analysis of HSV DNA in CSF (highly sensitive and specific)

Question 207

How do you treat herpes encephalitis?

Answer 207

IV acyclovir

Question 208

What are the characteristic CSF findings in viral meningitis/encephalitis?

Answer 208

Lymphocytic pleocytosis Increased RBCs Elevated protein Normal glucose

Question 209

What type of pain management should be offered for mild to moderate cancer-related pain? How about for severe cancer-related pain?

Answer 209

Non-opioid analgesics (e.g. acetaminophen, NSAIDs) are used for mild to moderate cancer-related pain. Severe cancer-related pain should be treated with short-acting opioids if initial interventions with acetaminophen and NSAIDs are ineffective. Short-acting opioids (e.g. morphine, hydromorphone, oxycodone) are safe and well-tolerated if taken as directed. The dose and schedule can be varied depending on the patient's pain pattern. If the patient has pain requiring frequent dosing or if bedtime dosing does not provide adequate relief throughout the night, long-acting opioids (e.g. sustained-release morphine) may be added.

Question 210

Topical capsaicin is useful for controlling what type of pain?

Answer 210

Mild to moderate neuropathic pain (E.g. postherpetic neuralgia)

Question 211

Does levodopa/carbidopa prevent progression of parkinsonism?

Answer 211

No

Question 212

What is the most effective symptomatic therapy for parkinsonism?

Answer 212

Levodopa/carbidopa

Question 213

What are the most common early side effects of levodopa/carbidopa?

Answer 213

Hallucinations, confusion, agitation, dizziness, somnolence, and nausea.

Question 214

For patients undergoing treatment for parkinsonism, nearly 50% begin to have involuntary movements (e.g. dyskinesia, dystonia) after 5-10 years of which medication?

Answer 214

Levodopa/carbidopa. Because of this reason, it's important to find the lowest therapeutic dose to lessen the chance of patients developing these side effects.

Question 215

Livedo reticularis, a mottled vascular pattern on the lower extremities, is a side effect more commonly seen with which parkinsonism medication?

Answer 215

Amantadine

Question 216

Woman Age 15-50 Neurologic deficits (e.g. ataxia, diplopia, vertigo, pronator drift) Symptoms disseminated in space and time

Answer 216

Multiple sclerosis

Question 217

Acute exacerbations of multiple sclerosis is treated with?

Answer 217

High-dose intravenous glucocorticoids (E.g. methylprednisolone) or plasma exchange for patients who do not respond to glucocorticoids.

Question 218

How do you treat dural sinus thrombosis?

Answer 218

IV heparin

Question 219

When is lumbar puncture indicated for MS workup?

Answer 219

Lumbar puncture is typically performed in patients with suspected MS when the diagnosis is not completely clear. CSF typically shows oligoclonal IgG bands. It is not necessary in patients with classic clinical and radiographic findings.

Question 220

Tremor that tends to worsen at the end of goal-oriented actions (e.g. drinking from a cup)

Answer 220

Essential tremor

Question 221

True or False: Head tremor is often present in parkinsonism

Answer 221

False. Head tremors are commonly involved in essential tremor

Question 222

What is optic neuritis?

Answer 222

It is an inflammatory demyelination of the optic nerve thought to be immune-mediated most commonly seen in women age 20-40. Symptoms develop acutely and usually include monocular vision loss, pain with eye movement, and "washed-out" color vision. Physical exam typically reveals an afferent pupillary defect and central scotoma.

Question 223

How does fundoscopy look in patients with optic neuritis?

Answer 223

Typically normal as the inflammation occurs behind the optic nerve head

Question 224

``` Monocular vision loss Pain with eye movement Washed-out color vision Monocular afferent pupillary defect Central scotoma ```

Answer 224

Optic neuritis

Question 225

46 y/o man being evaluated for gait disorder Frequent falls Symptoms began gradually about a year ago. Progressively worsening. PMH notable for chronic alcoholism. Broad-based, unsteady gait. Tingle tap on patellar tendon elicits persistent, slow, back-and-forth swinging of the leg. Nystagmus and truncal ataxia present. Which of the following additional findings would most likely also been seen in the patient? A. babinski sign B. bradykinesia C. "clasp knife" spasticity D. goiter E. hearing loss F. intention tremor

Answer 225

Intention tremor. The patient has evidence of cerebellar dysfunction likely due to alcoholic cerebellar degeneration.

Question 226

``` Progressive gait dysfunction Truncal ataxia Nystagmus Intention tremor Dysmetria Impaired rapid alternating movements ```

Answer 226

Cerebellar degeneration

Question 227

What is "clasp knife" spasticity?

Answer 227

It is a phenomenon that refers to a velocity-dependent resistance to passive movement of the limb. It is seen in patients with hypertonia due to pyramidal tract disease.

Question 228

For initial management options for acute pain (e.g. trauma etc), do you need to consider substance abuse history (e.g. opioid addiction) in patients?

Answer 228

No. Studies suggests that providers may unnecessarily under treat pain in patients with current or recovering opioid addiction. Initial management options for acute pain is similar for all patients, regardless of substance abuse history. Patients with current or recovering opioid addiction who are given opioid analgesics may need close follow-up care to monitor pain relief and avoid addiction relapse.

Question 229

A C4-C5 disk herniation will impinge which nerve root?

Answer 229

C5. It's most commonly the larger number (lower root).

Question 230

77 y/o man | Healthy. Normal exam except DTR absent in ankles. What to do?

Answer 230

Nothing. It's a normal finding for elderly to have decreased or absent ankle reflexes.

Question 231

72 y/o man Progressive aching in lower extremities on exertion Dorsalis pedis pulses normal bilaterally Claudication-like symptoms

Answer 231

Lumbar spinal stenosis | Presents with claudication but has normal pedal pulses (pseudoclaudication)

Question 232

``` 77 y/o man Unable to urinate Rash 10 days ago now right lower extremity warm and erythematous T2DM Febrile Nuchal rigidity and pain DTRs brisk Babinski sign bilaterally present Sensation to pinprick decreased below C7 ```

Answer 232

Epidural abscess of the spine

Question 233

What is the mechanism of this patient's disease? 57 y/o Progressive weakness of arms and legs Fasciculations in hands and right lower extremity Pseudobulbar palsy Sensation and cranial nerves intact MRI brain normal

Answer 233

Amyotrophic lateral sclerosis. Motor neuron degeneration (of UMN and LMN)

Question 234

Pseudobulbar palsy

Answer 234

Pseudobulbar palsy is a medical condition characterized by the inability to control facial movements (such as chewing and speaking) and caused by a variety of neurological disorders. Patients experience difficulty chewing and swallowing, have increased reflexes and spasticity in tongue and the bulbar region, and demonstrate slurred speech (which is often the initial presentation of the disorder), sometimes also demonstrating uncontrolled emotional outbursts.

Question 235

CNS herniation with CN3 involvement (ptosis and pupillary dilation)

Answer 235

Uncal herniation

Question 236

67 y/o woman Intramuscular haloperidol administered 1 hour later, uncontrolled repetitive hyperextending her neck and repetitive conjugate upward movement of eyes. What is the complication seen here? How do you treat it?

Answer 236

Acute dystonia 2/2 haloperidol. Treat with anticholinergic medication e.g. benztropine

Question 237

``` 47 y/o man 8 month history of progressively worsening bifrontal headache Scant beard Sallow, waxy complexion Bilateral temporal hemianopia ```

Answer 237

Pituitary adenoma (specifically prolactinoma)

Question 238

32 y/o woman Progressive visual dimming of right eye since waking up 8 hours ago. Mild headache over right eye before going to bed last night. Headache was different than her usual migraines which have improved since starting propranolol treatment. Normal funduscopic examination of right eye but patient can't read and can barely count fingers with the right eye. Visual acuity of left eye is normal. Normal CT head.

Answer 238

Optic neuritis

Question 239

10 y/o girl 4-day history of rapid, irregular, involuntary movements of her face, trunk and extremities. Anxious and irritable Headaches No PMH except migratory joint pain that occurred recently

Answer 239

Rheumatic fever. Particularly, Sydenham's chorea. Pathophys: Cross-reactivity! Type 2 hypersensitivity reaction that goes wrong due to molecular mimicry. This cross reactivity can cause reaction against heart (carditis), joints (polyarthritis), basal ganglia (sydenham's chorea), etc.

Question 240

Burning pain or numbness in dermatomal distribution | PMH of T2DM

Answer 240

Diabetic thoracoabdominal neuropathy

Question 241

32 y/o woman w/ metastatic breast cancer to bone 12 hour history of severe pelvic pain and numbness Hasn't urinated for more than 24 hours Decreased rectal sphincter tone Sensation decreased in saddle distribution Placement of urinary catheter yields 800 mL of clear yellow urine MRI of spine shows tumor pushing into L4-S1 intrathecal space. What's the most appropriate immediate next step in management?

Answer 241

IV administration of high-dose dexamethasone

Question 242

25 y/o man 4-month history of increasing low back pain most severe in the morning. Pain relieved by stretching. No history of trauma. Decreased forward flexion of the spine and tenderness over the lumbosacral area and at the insertion site of the Achilles tendon.

Answer 242

Ankylosing spondylitis

Question 243

52 y/o man HIV positive 1-month history of forgetfulness and inappropriate behavior Buying numerous items from the internet Noncompliant with anti-retroviral medication Oral thrush Recalls 0 of 3 objects after 5 minutes Head CT shows prominent atrophy of the cortex and demyelination in the subcortical white matter

Answer 243

Progressive multifocal leukoencephalopathy (2/2 JC virus)

Question 244

32 y/o man Blurred vision in right eye Possible decreased visual acuity Corneal staining defect

Answer 244

Corneal abrasion

Question 245

Damage to which nerve branch causes corneal anesthesia?

Answer 245

V1 (Ophthalmic branch of trigeminal)

Question 246

Severe eye pain Photophobia with reluctance to open the eye Sensation of a foreign body in the eye

Answer 246

Corneal abrasion

Question 247

Action tremor Absence of additional neurologic signs Exacerbated at the end of goal-directed movements

Answer 247

Essential tremor

Question 248

Neurodegenerative disorder caused by accumulation of alpha-synuclein within the neurons of the substantial nigra pars compacta leading to death of these neurons.

Answer 248

Parkinson disease

Question 249

Resting 4 to 6 Hz tremor that frequently first manifests in one hand and may then slowly generalize to involve the other side of the body and the lower extremities. Baseline increased resistance to passive movement. Difficult initiating movement.

Answer 249

Parkinson disease

Question 250

What are the 3 cardinal signs of Parkinson disease?

Answer 250

Resting tremor Rigidity Bradykinesia

Question 251

Contralateral somatosensory and motor deficits predominantly in the lower extremity Abulia (lack of will or initiative) Dyspraxia, emotional disturbances, urinary incontinence

Answer 251

Anterior cerebral artery occlusion

Question 252

Contralateral somatosensory and motor deficits in face, arm, and leg. Conjugate eye deviation toward side of infarct. Homonymous hemianopia. Aphasia or hemineglect.

Answer 252

Middle cerebral artery occlusion. Aphasia if dominant hemisphere. Hemineglect if non-dominant.

Question 253

What is the presentation like for an infarct at the posterior limb of the internal capsule? (lacunar infarct)

Answer 253

Unilateral motor impairment No sensory or cortical deficits No visual field abnormalities

Question 254

What is the presentation like for a middle cerebral artery occlusion?

Answer 254

Contralateral somatosensory and motor deficit in face, arm, and sometimes leg. Conjugate eye deviation toward side of infarct. Homonymous hemianopia. Aphasia (dominant hemisphere). Hemineglect (non-dominant hemisphere).

Question 255

What is the presentation like for an anterior cerebral artery occlusion?

Answer 255

Contralateral somatosensory and motor deficit, predominantly in the lower extremity. Abulia (lack of will or initiative). Dyspraxia, emotional disturbances, urinary incontinence.

Question 256

What is the presentation like for a vertebrobasilar system lesion (supplying the brainstem)?

Answer 256

Alternate syndromes with contralateral hemiplegia and ipsilateral cranial nerve involvement. Possible ataxia.

Question 257

70 y/o right-handed man Sudden onset right-sided weakness and urinary incontinence that began 10 hours ago. PMH: T2DM, HTN 4/5 strength in RUE, 1/5 strength in RLE, babinski sign on right side. Sensation decreased throughout right foot and leg. Visual fields are normal.

Answer 257

Anterior cerebral artery stroke

Question 258

Is normal pressure hydrocephalus caused by decreased CSF absorption or increased CSF production?

Answer 258

Decreased CSF absorption

Question 259

What's the triad of symptoms for normal pressure hydrocephalus?

Answer 259

Abnormal gait, incontinence, and dementia | wet, wild, wacky

Question 260

Is there increased intracranial pressure in normal pressure hydrocephalus?

Answer 260

No. NPH is a clinical syndrome accompanied by increased ventricular size without persistent elevations in intracranial pressure. The prevailing theory for the pathogenesis of NPH is that patients have a transient increase in intracranial pressure that causes ventricular enlargement. After the ventricles enlarge, the pressure returns to normal. The initial increase in ventricular size may be due to either diminished CSF absorption at the arachnoid villi or obstructive hydrocephalus.

Question 261

What symptoms would you expect in spinal cord compression?

Answer 261

Muscle weakness and hyperactive deep tendon reflexes

Question 262

Intermittent foot drop symptoms are most likely caused by?

Answer 262

Common fibular neuropathy due to compression (leg immobilization, cast, bedrest, prolonged leg crossing, or protracted squatting. Foot drop without radiating pain is more likely to be caused by peripheral nerve compression (e.g. lateral aspect of the fibula) while L5 radiculopathy causing foot drop has radiating pain down the leg.

Question 263

86 y/o woman Progressive confusion and lethargy over the past several hours. History of alzheimer dementia, frequent falls, and atrial fibrillation. CT demonstrates hyperdensity in right parietal lobe distribution.

Answer 263

Acute hemorrhage 2/2 amyloid angiopathy Amyloid angiopathy is the most common cause of spontaneous LOBAR hemorrhage, particularly in patients greater than 60 years old. It occurs as a consequence of B-amyloid deposition in the walls of small to medium size cerebral arteries, resulting in vessel wall weakening and predisposition to rupture.

Question 264

Headache | Head CT demonstrates hyper-attenuation of the sulci and basal cisterns

Answer 264

Subarachnoid hemorrhage

Question 265

Footdrop Excessive hip and knee flexion while walking Slapping foot Frequent falls

Answer 265

This is called steppage gait. Typically due to weakness in foot dorsiflexion secondary to common peroneal nerve neuropathy.

Question 266

How does L5 radiculopathy typically present?

Answer 266

Steppage gait (excessive hip and knee flexion while walking, slapping foot, foot drop) Pain radiating to the foot Weakness of foot inversion and plantar flexion. Foot drop without radiating pain is more likely to be caused by peripheral nerve compression (e.g. lateral aspect of the fibula).

Question 267

Both L5 radiculopathy and peripheral neuropathy of the common peroneal nerve can cause foot drop. How can you tell the difference between the two?

Answer 267

L5 radiculopathy presents with radiating pain down while peripheral compression of the common peroneal nerve does not. Also, L5 radiculopathy causes weakness of foot inversion and plantar flexion while compression of the common peroneal nerve does not.

Question 268

A patient presents with an apparent unprovoked first seizure. What should always be done as part of the neurodiagnostic evaluation?

Answer 268

Either CT or MRI should be performed in all patients with an apparent unprovoked seizure as part of neurodiagnostic evaluation. In patients with history of fall or possible head trauma, CT without contrast should be performed as it can be done quickly even in an unstable patient and can screen for life-threatening neurologic problems. If not emergent, MRI is the modality of choice as it is more sensitive than CT for identifying most structural causes of epilepsy.

Question 269

Parkinsonian tremors are more pronounced with? decreased with?

Answer 269

Increased tremor with distractibility (E.g. performing mental tasks) Decreased tremor with movement

Question 270

Lesions that affect the arcuate fasciculus impair the patient's ability to do what?

Answer 270

Repeat phrases (conduction aphasia)

Question 271

``` 35 y/o man Motor vehicle collision Unconscious PERRL Doesn't follow commands. CT demonstrates multiple punctuate hemorrhages with blurring of gray-white matter interface ```

Answer 271

Diffuse axonal injury Frequently due to traumatic deceleration injury and results in vegetative state. Sudden acceleration-deceleration impact produces rotational forces that affect the brain areas where density difference is the maximum, thus most of the diffuse axonal injury occurs at the gray-white matter junction.

Question 272

Painless, rapid, transient (<10 minutes) monocular vision loss. Often described as curtain descending over the visual field.

Answer 272

Amaurosis fugax Retinal ischemia due to atherosclerotic emboli originating from the ipsilateral carotid artery; therefore, patients with vascular risk factors (e.g. HTN, HLD, smoking) should be evaluated with duplex ultrasound of the neck. Funduscopic examination is often normal but may show embolic plaques and retinal whitening (due to ischemia).

Question 273

When stroke is suspected clinically, what test must be performed?

Answer 273

Noncontrast CT scan of the head. This is an essential branch point in management: patients with ischemic stroke may be candidates for thrombolytic therapy whereas patients with intracranial hemorrhage require neurosurgical evaluation and would suffer greatly from thrombolytic administration.

Question 274

65 y/o man Sudden onset of weakness in right arm and leg. In the past month, he had episodes of weakness on his right side that resolved spontaneously. No headache, nausea, vomiting, or loss of consciousness. Vitals: 98/65/14/164-72 Physical exam shows right-sided hemiplegia and right lower facial paresis. Sensory examination is unremarkable. Speech without apraxia. CT head shows no intracranial bleeding.

Answer 274

Lacunar stroke Note that lacunar infarcts typically produce neurologic deficits over minutes to hours and symptoms may follow a STUTTERING COURSE (this explains the episodes of symptoms in this patient) Small penetrating artery occlusion due to hypertensive arteriolar sclerosis. Commonly affecting the basal ganglia, subcortical white matter (e.g. internal capsule, corona radiata), and pons Risk factors include HTN, DM, advanced age, HLD, and smoking Symptoms include absence of cortical signs (e.g. aphasia, agnosia, neglect, apraxia, hemianopia), seizures, or mental status changes. Common syndromes are pure hemiparesis (most frequent), pure sensory stroke, ataxic hemiparesis, or dysarthria-clumsy hand.

Question 275

Unilateral motor weakness without sensory deficits or higher cortical dysfunction

Answer 275

Lacunar stroke affecting the posterior limb of the internal capsule

Question 276

A MMSE/MOCA score of less than what value is suggestive of dementia?

Answer 276

24/30

Question 277

Atrophy pattern of Alzheimer's dementia?

Answer 277

Diffuse cortical and subcortical atrophy. May be disproportionately greater in the temporal and parietal lobes, especially in the hippocampi.

Question 278

Treatment for trigeminal neuralgia?

Answer 278

Carbamazepine

Question 279

27 y/o woman Lost consciousness for 2 minutes while standing in line at the supermarket. Recalls nausea and feeling of warmth spreading over her body right before passing out. ECG normal.

Answer 279

Neurocardiogenic (or vasovagal) syncope This is the most common type of syncope and occurs due to excessive vagal tone. It is benign and self-limited in most cases, lasting about 10 seconds to a few minutes. These episodes can be triggered by prolonged standing, emotional stress, or painful stimuli. Patients frequently experience dizziness, nausea, pallor, diaphoresis, abdominal pain, and/or a generalized sense of warmth prior to these episodes.

Question 280

Triggers: Prolonged standing or emotional distress, painful stimuli. Prodromal symptoms: nausea, warmth, diaphoresis What type of syncope is this?

Answer 280

Vasovagal or neurally mediated syncope

Question 281

What is the most common cause of spontaneous deep intracerebral hemorrhage?

Answer 281

Hypertensive vasculopathy. Chronic hypertension leads to the formation of Charcot-Bouchard aneurysms, which may rupture and bleed within deep brain structures such as the basal ganglia, cerebellar nuclei, thalamus, and pons.

Question 282

Symptoms of meningeal irritation?

Answer 282

Nausea/vomiting, photophobia

Question 283

What is the bedside ice pack test?

Answer 283

This is a test that can be used to help diagnose myasthenia gravis. In this test, an ice pack is applied over the eyelids for several minutes, leading to an improvement in ptosis. The cold temperature improves muscle strength by inhibiting the breakdown of acetylcholine at the neuromuscular junction, thereby increasing acetylcholine availability to the nicotinic receptor. Patients with positive test results should undergo confirmatory testing for myasthenia gravis with acetylcholine receptor antibodies.

Question 284

``` 65 y/o man New-onset ptosis. Had surgery earlier in the day. Developed bilateral ptosis, left greater than right in the postoperative recovery unit. Slurred speech. No prior neurologic history. PERRL Ice pack over the closed eyelids improves ptosis. ```

Answer 284

Myasthenia gravis. Myasthenia gravis may be subclinical and precipitated by various factors, including surgery, infection, and medications (e.g. ahminoglycosides, beta blockers)

Question 285

57 y/o man Right arm and leg weakness, first noticed 2 hours ago. Mild, constant headache the past several days. PMH: HTN, HLD BP 180/100, pulse 80. Mild asymmetry of lower face, decreased muscle strength in right arm, positive babinski sign on right side. Sensory examination is normal. Noncontrast CT reveals no abnormalities

Answer 285

Lacunar infarct AKA small-vessel lipohyalinosis Notice that this patient's symptoms are purely motor. The sensory examination being normal is a significant clue. Lacunar infarcts don't have sensory deficits, mental status changes, seizures, or cortical signs. Due to their small size, lacunes are often not appreciated on non contrast CT scans obtained shortly after the event.

Question 286

Pure motor hemiparesis

Answer 286

Lacunar infarct in the internal capsule

Question 287

Pathophysiology of lacunar infarct?

Answer 287

Lacunar infarcts occurs due to occlusion of deep penetrating arteries in the brain. These vessels are located in highly turbulent regions of the cerebrovascular system and therefore are most susceptible to vascular disease related to HTN, DM, HLD, and smoking. The underlying pathology is a combination of microatheroma formation and lipohyalinosis that ultimately leads to thrombotic small-vessel occlusion. Due to their small size, lacunes are OFTEN NOT APPRECIATED on non contrast CT scans obtained shortly after the event.

Question 288

66 y/o man Low back pain and difficulty walking for past several months. Pain is worse with prolonged standing and relieved by sitting. Pain is also less severe with walking uphill than with walking downhill. PMH: degenerative joint disease in knees No spinal tenderness to palpation. Negative straight leg test and babinski sign. Normal pulse and reflexes.

Answer 288

Lumbar spinal stenosis Results from any condition that narrows the spinal canal and compresses nerve roots, most commonly 2/2 degenerative joint disease. In DJD, disc herniation and facet osteophytes impinge upon the spinal cord. This is most commonly seen in middle-aged and elderly patients. Flexion of the spine causes widening of the spinal canal while extension causes narrowing of the canal. Therefore, symptoms are exacerbated by extension of the spine (e.g. standing and downhill walking) and improved by flexion (e.g. sitting and uphill walking).

Question 289

What test should be done to assess for lumbar spinal stenosis?

Answer 289

Spine MRI

Question 290

Presentation of vascular dementia?

Answer 290

Typically presents as sudden or stepwise decline in executive function after stroke, which interferes with activities of daily living. Patients typically have abnormal neurologic findings on examination (e.g. hemiparesis, pronator drift, romberg sign, etc).

Question 291

2 most common organisms for single brain abscess?

Answer 291

Viridans streptococci, staphylococcus aureus

Question 292

21 y/o man Witnessed generalized tonic-clonic seizure. No past history of seizures. Headaches, fever, nasal congestion, and rhinorrhea over the last 3 weeks. No PMH. Vitals 102/96/130.85 CT reveals 3-cm ring-enhancing lesion in the left frontal lobe. Air-fluid levels and mucosal edema in the paranasal sinuses. HIV - negative

Answer 292

Brain abscess Most common organisms involved are staph aureus, strep viridans, and gram-negative organisms. Caused by direct adjacent infection (E.g. sinusitis, otitis, and dental infections) or hematogenous from distant infection (E.g. endocarditis, osteomyelitis, etc). In this patient, you have nasal congestion and a 3-cm ring-enhanced lesion in the frontal lobe. This should be obvious for brain abscess in an HIV negative patient.

Question 293

What should be suspected when trigeminal neuralgia presents bilaterally?

Answer 293

Multiple sclerosis

Question 294

Sudden-onset severe, stabbing pain along the cheeks and jaws. Episodes last a few seconds to minutes and can be triggered by minor stimuli (e.g. touching, wind, chewing)

Answer 294

Trigeminal neuralgia

Question 295

65 y/o man ED after motor vehicle accident. Marked weakness in both upper extremities but able to move lower extremities. PMH: osteoarthritis and cervical spondylosis secondary to degenerative changes in the cervical spine Plain film x-rays show no abnormalities except mild degenerative arthritis known from PMH.

Answer 295

Central cord syndrome This results from hyperextension injuries, particularly in elderly patients with spondylosis. It is characterized by weakness that is more pronounced in the upper extremities than the lower and may be accompanied by a localized deficit in pain and temperature sensation.

Question 296

22 y/o woman Headaches for past 6 weeks HAs are pulsatile in quality and associated with nausea. They are worse at night and awaken her from sleep. No photophobia, weakness, sensory abnormalities, or history of trauma. Patient doesn't take any medications. BMI is 33. Funduscopy shows papilledema. CT brain shows no abnormalities. LP demonstrates elevated opening pressure with otherwise normal fluid analysis.

Answer 296

Idiopathic intracranial hypertension AKA pseudotumor cerebri

Question 297

What is the first-line treatment for pseudotumor cerebri AKA idiopathic intracranial hypertension?

Answer 297

Acetazolamide. It inhibits choroid plexus carbonic anhydrase, thereby decreasing CSF production.

Question 298

What drug class is trihexyphenidyl and what is it used for?

Answer 298

Trihexyphenidyl is an anti-cholinergic medication used for treatment of parkinson disease.

Question 299

Enlarged blind spot | Intermittent vision loss that can vary with changes in head position

Answer 299

Papilledema due to increased intracranial pressure

Question 300

What is multiple system atrophy (Shy-Drager syndrome)?

Answer 300

This a degenerative disease characterized by parkinsonism, autonomic dysfunction (postural hypotension, abnormal sweating, disturbance of bowel or bladder control, abnormal salivation or lacrimation), and widespread neurological signs (cerebellar, pyramidal, or LMN). Always consider Shy-Drager syndrome when a patient with Parkinsonism experiences orthostatic hypotension, impotence, incontinence, or any other autonomic symptoms. Accompanying bulbar dysfunction and laryngeal stridor may be fatal.

Question 301

Parkinsonism PLUS orthostatic hypotension, impotence, incontinence, or any other autonomic symptoms. What is this syndrome and how is it treated?

Answer 301

Shy-Drager syndrome (aka multiple system atrophy) This is treated by increasing intravascular volume with fludrocortisone, salt supplementation, alpha-adrenergic agonists, and application of constrictive garments to the lower body.

Question 302

What is Riley-Day syndrome AKA familial dysautonomia?

Answer 302

This is an autosomal-recessive disease that is predominantly seen in children of ashkenazi jewish ancestry. It is characterized by gross dysfunction of the autonomic nervous system with severe orthostatic hypotension. This is different from Shy-Drager syndrome because it doesn't have parkinsonism.

Question 303

What's the difference between Riley-Day syndrome (aka familial dysautonomia) and Shy-Drager syndrome (aka multiple system atrophy)? What do they have in common?

Answer 303

They both have autonomic symptoms like orthostatic hypotension, impotence, incontinence but Shy-Drager has parkinsonism as well.

Question 304

32 y/o male progressive ascending paralysis that began 18 hours ago Recent hiking trip in Colorado Vitals stable. Absent DTRs in lower extremities. Normal sensory examination. Weakness in both lower extremities. Normal CBC and CSF studies.

Answer 304

Tick-borne paralysis. Etiology of paralysis is a neurotoxin that is released. The tick needs to feed for 4-7 days for the release of neurotoxin. Unlike Guillain Barre Syndrome, the CSF is normal with tick-borne paralysis. Guillain Barre Syndrome has elevated protein in CSF studies.

Question 305

Patient with myasthenia gravis has deteriorating respiratory status (e.g. declining o2 saturation and vital capacity). What do you do?

Answer 305

First, intubate the patient to protect the airway. Following intubation, acetylcholinesterase inhibitors (e.g. pyridostigmine) used in the daily management of myasthenia gravis are TEMPORARILY HELD to reduce excess airway secretions and the risk of aspiration. Once intubated, treat with either IVIG or plasmapheresis in addition to corticosteroids.

Question 306

A patient with myasthenia gravis has deteriorating respiratory status (e.g. declining o2 saturation and vital capacity). This patient typically takes pyridostigmine at home for management of his condition. What should you do with the pyridostigmine? a. give normal dose b. increase dose c. temporarily hold

Answer 306

In myasthenic crisis, it's important to temporarily hold the pyridostigmine in order to reduce excess airway secretions and the risk of aspiration. With myasthenic crisis, you are going to intubate the patient followed by IVIG or plasmapheresis and corticosteroid treatment.

Question 307

CSF findings for guillain-barre syndrome?

Answer 307

Elevated protein. Everything else is normal.

Question 308

29 y/o man Progressive bilateral lower extremity weakness No history of trauma or back pain Trigeminal neuralgia 3 months ago Self-limited URI 2 weeks ago Physical exam shows increased resistance to passive flexion and extension of the lower limbs. DTRs are 3+ and plantar reflexes are up-going bilaterally. Decreased vibratory and positional sense in his left upper extremity but no other sensory loss. What do you find on LP?

Answer 308

Oligoclonal bands. This is MS. The patient's neurologic deficits are disseminated in space and time. The trigeminal neuralgia came and went. He has spastic bilateral lower limb paralysis and left upper limb sensory loss. When the neurologic symptoms are spread throughout time and cannot be localized to a single lesion, the diagnosis is most likely MS. When the diagnosis of MS is suspected, an MRI is the appropriate study. This question was just seeing if you know what LP may find in an MS patient. Note that this tried to distract with guillain-barre with the URI but guillain-barre is a LMN process. The +3 DTRs and positive babinski signs rule out guillain-barre.

Question 309

Gradually worsening severe local back pain Pain worse in the recumbent position/at night Early signs: symmetric lower-extremity weakness, hypoactive/absent DTRs Late signs: bilateral babinski reflex, decreased rectal sphincter tone, paraparesis/paraplegia with increased DTRs, sensory loss

Answer 309

Spinal cord compression

Question 310

Back pain that is worse when lying down vs better?

Answer 310

With spinal cord compression (e.g. tumor), back pain is usually worse in the recumbent position due to distension of the epidural venous plexus when lying down. In contrast to back pain from degenerative joint disease, which improves with lying down.

Question 311

Treatment for heat stroke?

Answer 311

Rapid cooling preferably with ice water immersion.

Question 312

Rapidly progressive demential 2 out of 4 clinical features: myoclonus, akinetic mutism, cerebellar or visual disturbance, or pyramidal/extrapyramidal dysfunction (e.g. hypokinesia) Periodic sharp wave complexes on EEG Positive 14-3-3 CSF assay

Answer 312

Creutzfeldt-Jakob disease (prion disease) These patients have rapid neuronal loss and most patients die within 1 year. Key features include long incubation period, characteristic spongiform changes, and lack of inflammatory response. This condition should be suspected in older patients (50-70 y/o) who present with RAPIDLY progressing dementia and myoclonus. Other symptoms include insomnia, apathy, behavioral changes, and impaired vision. Patients eventually lose the ability to move and speak and become comatose.

Question 313

What is the typical EEG finding seen in Creutzfeldt-Jakob (prion) disease?

Answer 313

Bi- or tri-phasic sharp wave complexes

Question 314

What CSF finding is characteristic of prion disease Creutzfeldt-Jakob disease (prion disease)?

Answer 314

14-3-3 regulatory proteins. These are characteristic but not required for diagnosis

Question 315

How do you diagnose Creutzfeldt-Jakob disease? How do you treat it?

Answer 315

Diagnosis is typically made postmortem with brain biopsy. Treatment for this disease is merely supportive. Genetic testing for prion protein gene is now used and CSF 14-3-3 regulatory proteins or bi/tri-phasic sharp wave complexes on EEG can also help diagnose this disease pre-mortem.

Question 316

Monocular painless acute vision loss lasting for several hours "like a shade dropping over my eye"

Answer 316

Most likely due to central retinal artery occlusion. Commonly from symbolized plaque from the ipsilateral carotid artery or a cardioembolic source.

Question 317

What is pronator drift?

Answer 317

This is a physical examination finding that is relatively sensitive and specific for upper motor neuron or pyramidal/corticospinal tract disease. The pronator drift test is particularly useful in patients with subtle deficits as it can accentuate pyramidal motor weakness. It is performed by having the patient outstretch arms with the palms up and eyes closed (so that only proprioception is used to maintain arm position). Upper motor neuron lesions cause more weakness in the supinator muscles compared to the pronator muscles of the upper limb. As a result, the affected arm drifts downward and the palm turns (pronates) towards the floor.

Question 318

What's the initial diagnostic evaluation of a first-time seizure in an adult?

Answer 318

First thing is to exclude metabolic and toxic causes. This means looking for hypoglycemia, electrolyte disturbances, and drug levels.

Question 319

How do you treat bacterial endocarditis with acute cardioembolic stroke?

Answer 319

Start IV antibiotics. This significantly reduces the risk of septic cardioembolism within weeks of initiating therapy. Aortic valve surgery can be considered if there is significant valvular dysfunction resulting in heart failure or if the infection is persistent or if septic embolization is recurrent. Use of heparin is not recommended as it is associated with an increased risk of symptomatic intracranial hemorrhage.

Question 320

Myasthenic crisis can be precipitated by many factors. What are they?

Answer 320

``` Infection Surgery Pregnancy Childbirth Tapering immunosuppressive drugs Medications (e.g. aminoglycosides, fluoroquinolones, beta blockers) ```

Question 321

What is brain death?

Answer 321

Brain death is defined as the irreversible cessation of brain activities. Interestingly, the criteria for brain death are not uniform in different countries, but the essential elements in all such criteria include: (1) evaluating cortical and brain stem functions, and (2) proving the irreversibility of brain activity loss (e.g. sufficient observation length, no hypothermia, etc). Brain death is a clinical diagnosis. The characteristic findings are absent cortical and brainstem functions. The spinal cord may still be functioning; therefore, deep tendon reflexes may be present. An isoelectric EEG can be used as a confirmatory test, but it is not absolutely necessary. Other diagnostic tests (e.g. ultrasound, angiography) can demonstrate cerebral blood flow cessation, but these are not commonly employed.

Question 322

What is preserved in a patient with brain death?

Answer 322

Deep tendon reflexes... because the spinal cord may still be functioning. Brain death just means the brain stem and cortical functions are gone.

Question 323

What are two sources of foodborne botulism?

Answer 323

1) improperly canned foods | 2) aged seafood (e.g. cured fish)

Question 324

How does foodborne botulism ingestion present?

Answer 324

Bilateral cranial neuropathies causing blurred vision, diplopia, facial weakness, dysarthria, dysphagia. Symmetric DESCENDING muscle weakness Diaphragmatic weakness with respiratory failure

Question 325

How do you diagnose foodborne botulism? How do you treat it?

Answer 325

Serum analysis for botulism toxin. You treat it by giving horse-derived antitoxin which provides passive immunity.