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Neurology > Week 1 > Flashcards

Week 1 Flashcards

1
Q

What are the four key features of narcolepsy?

A
  • excessive daytime sleepiness
  • hypnagogic hallucinations
  • sleep paralysis
  • cataplexy
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2
Q

What is the first line therapy for narcolepsy?

A

sleep hygiene, scheduled naps, and modafinil

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3
Q

Describe the presentation, diagnosis, and treatment of Guillain-Barre syndrome.

A
  • the illness is preceded by a GI or respiratory infection
  • symptoms include neuropathic pain, a symmetric and ascending weakness with diminished DTRs, and autonomic dysfunction; there are no UMN signs
  • it is a clinical diagnosis supported by an LP finding elevated protein and normal leukocytes or EMG/NCS
  • management includes serial spirometry for FVC and negative inspiratory force with intubation for respiratory distress or autonomic instability
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4
Q

Diabetics are at increased risk for what sort of spinal cord lesion?

A

a spinal abscess

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5
Q

What is neuralgia paresthetica?

A

it is a mononeuropathy caused by compression of the lateral femoral cutaneous nerve (L2-3) at the inguinal ligament, typically due to tight belts or clothing and presenting with paresthesias or numbness in the lateral thigh

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6
Q

What are the symptoms of common peroneal nerve dysfunction?

A

foot drop, impaired foot eversion, and numbness of the posterolateral leg and dorsolateral foot

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7
Q

How can superficial peroneal and deep peroneal nerve injuries be distinguished from one another?

A
  • the superficial nerve carries sensory fibers from the dorsum of the foot and supplies the muscles for foot eversion
  • the deep nerve carries sensory fibers from the first web space of the toes and supplies the muscles for foot dorsiflexion and toe extension
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8
Q

What often leads to obturator nerve injury and what are the symptoms?

A
  • often the result of anterior hip dislocation or damaged during pelvic surgery
  • presents with weakness of the adductors and sensory loss over the medial thigh
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9
Q

A long history of alcohol abuse and slowly progressive postural gait dysfunction is suggestive of what disease process?

A

alcohol neurotoxicity affecting the Purkinje cells of the vermis, contributing to cerebellar degeneration

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10
Q

What are the developmental milestones expected of a two year old?

A
  • walk up and down stairs with both feet on each step
  • build a tower of 6 cubes and copy a line
  • vocabulary of more than 50 words and using 2 word pharses
  • follows 2 step commands, engages in parallel play, and begins toilet training
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11
Q

What is Todd paralysis?

A

a self-limited, focal weakness or paralysis that occurs in the postictal period following a focal or generalized seizure

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12
Q

What is athetosis?

A

a slow, writhing movement characteristic of Huntington’s disease

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13
Q

What causes hemiballismus?

A

a lesion to the contralateral sub thalamic nucleus

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14
Q

What are the symptoms of uncal herniation and what lesions explain them?

A

dilation of the ipsilateral pupil due to oculomotor nerve compression and ipsilateral hemiparesis due to compression of the contralateral crus cerebri

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15
Q

What is amaurosis fugax?

A

a transient, monocular blindness lasting only a few seconds, most often due to atherosclerotic emboli originating from the ipsilateral carotid

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16
Q

What are the features of optic neuritis? With what condition is it classically associated?

A
  • associated with MS

- presents with unilateral eye pain, loss of vision, and an afferent pupillary defect

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17
Q

Describe the vision loss associated with papilledema.

A

it is transient, lasting only a few seconds, and corresponds to changes in head position

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18
Q

How can glucocorticoid-induced myopathy be differentiated from polymyalgia rheumatica?

A
  • glucocorticoid-induced presents with weakness and atrophy but no pain and a normal ESR and CK
  • PR presents with pain, stiffness, and diminished ROM as well as an elevated ESR and normal CK
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19
Q

Where are Broca’s and Wernicke’s areas?

A

Broca’s is in the posterior inferior frontal gyrus and Wernicke’s is in the superior temporal lobe

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20
Q

How can Marfan syndrome be differentiated from homocystinuria?

A
  • Marfan is more likely to have normal intellect, aortic root dilation, and upward lens dislocation
  • homocystinuria is more likely to have intellectual disability, thrombosis, downward lens dislocation, megaloblastic anemia, and a fair complexion
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21
Q

Describe the presentation, diagnosis, and treatment of homocystinuria.

A
  • presents with marfanoid habitus, intellectual disability, thrombosis, downward lens dislocation, megaloblastic anemia, and a fair complexion
  • the diagnosis is supported by finding elevated levels of homocysteine and methionine levels
  • treat with vitamin B6, B12, and folate
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22
Q

What is the Cushing reflex?

A

a syndrome of hypertension, bradycardia, and respiratory depression produced by increases in ICP that contribute to brainstem compression

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23
Q

What is the most important risk factor for intracerebral hemorrhage?

A

hypertension

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24
Q

How is orthostatic hypotension diagnosed?

A

based on a drop in SBP greater than 20 mmHg or DBP greater than 10 mmHg

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25
Q

What is the Dix-Hallpike test?

A

a test used to diagnosed benign paroxysmal positional vertigo

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26
Q

What two ocular manifestations are common in those with MS?

A
  • optic neuritis

- internuclear ophthalmoplegia

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27
Q

What are five risk factors for MS?

A
  • HLA-DRB1 genotype
  • low vitamin D levels
  • living at higher longitude
  • living in colder climate
  • smoking
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28
Q

What are the three things used to diagnose MS?

A
  • a history of episodic/progressive symptoms disseminated over time and space
  • MRI finding demyelinating in the periventricular white mater
  • finding oligoclonal IgG bands on CSF analysis
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29
Q

What are the acute and maintenance therapies for MS?

A
  • acute: glucocorticoids; plasmapheresis if refractory

- maintenance: interferon beta and glatiramer acetate

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30
Q

What is the likely cause and etiology of a pure motor stroke?

A

it is likely the result of a lacunar stroke in the posterior limb of the internal capsule secondary to hypertension and the lipohyalinosis and arteriolar sclerosis that follows

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31
Q

What is the pathogenesis for lacunar strokes?

A

these are the result of chronic hypertension which leads to arteriolar sclerosis and lipohyalinosis and subsequently occlusion of small vessels

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32
Q

Which parkinson’s treatment has the highest risk for causing hallucinations?

A

direct dopamine agonists like pramipexole more so than levodopa or COMT and MAO inhibitors which have an indirect effect on dopamine levels

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33
Q

What are the criteria for diagnosing dementia with levy bodies?

A

dementia and two of the following four:

  • visual hallucinations
  • parkinsonism
  • REM sleep behavior disorder
  • fluctuating cognitive function
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34
Q

What are the criteria for diagnosing dementia with levy bodies?

A

dementia and two of the following four:

  • visual hallucinations
  • parkinsonism
  • REM sleep behavior disorder
  • fluctuating cognitive function
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35
Q

Describe the organization of CN III fibers within the fiber bundle.

A

parasympathetic fibers for pupillary constriction run on the outside of the bundle and are thus more affected by extrinsic compression while motor fibers for extra ocular movements run more interior and are more affected by ischemia

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36
Q

How does the management of pupil-sparing CN III palsies differ from that of pupil-involving CN III palsies?

A
  • pupil-involving are more often due to compression secondary to intracranial aneurysm, thus the first step is MRA or CTA
  • pupil-sparing are more often due to microvascular ischemia secondary to diabetes, hypertension, HLD, or age, thus observation, supportive care, and metabolic workup are indicated
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37
Q

What are the criteria for a simple febrile seizure and what is the management?

A
  • they are defined as generalized seizures lasting less than 15 minutes and no recurring within 24 hours
  • they can be managed with reassurance and do not require workup or treatment
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38
Q

Describe the risk factors, presentation, diagnosis, and treatment of orbital cellulitis.

A
  • the most common risk factor is sinusitis but orbital trauma or local infection are also risk factors
  • presents with ophthalmoplegia, vision change, eye pain, and proptosis
  • diagnosis is clinical but CT is performed to identify any drainable fluid collections
  • treat with IV antibiotics; drainage if there is an abscess
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39
Q

What is the difference between orbital cellulitis and preseptal cellulitis?

A
  • orbital cellulitis is a deeper infection, one that extends behind the orbital septum
  • because of this preseptal cellulitis does not involve vision change, proptosis, and ophthalmoplegia
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40
Q

Huntington’s disease is associated with what gross anatomical change?

A

atrophy of the putamen and caudate nucleus

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41
Q

What are the three key features of Huntington’s disease?

A
  • motor disturbance, particularly chorea
  • cognitive disturbance
  • psychiatric symptoms (e.g. depression, psychosis, OCD)
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42
Q

Decreased dopamine has what effect in the following pathways:

  • mesolimbic
  • nigrostriatal
  • tuberoinfundibular
A
  • mesolimbic: antipsychotic effect
  • nigrostriatal: EPS
  • tuberoinfundibular: hyperprolactinemia
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43
Q

What is the most common cause of SAH and what syndrome suggests SAH over other kinds of stroke?

A
  • usually due to Berry aneurysms

- have a syndrome of thunderclap headache and meningismus, typically without focal deficits

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44
Q

What is the most common cause of intraparenchymal hemorrhage and what syndrome suggests IPH over other kinds of stroke?

A
  • usually secondary to uncontrolled hypertension

- focal deficits tend to present early followed by symptoms of increased ICP

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45
Q

What features suggest thrombotic stroke and what features are more suggestive of an embolic stroke?

A
  • patients with thrombosis tend to have more atherosclerotic risk factors and a stuttering progression of symptoms
  • patients with emboli tend to have more cardiac disease, multiple infarcts in different vascular territories, and symptoms that are maximal at the start
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46
Q

What features suggest thrombotic stroke and what features are more suggestive of an embolic stroke?

A
  • patients with thrombosis tend to have more atherosclerotic risk factors and a stuttering progression of symptoms
  • patients with emboli tend to have more cardiac disease, multiple infarcts in different vascular territories, and symptoms that are maximal at the start
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47
Q

What is the mechanism of action for tetanus toxin?

A

it undergoes retrograde transport within the lower motor neuron and is taken up by the presynaptic cell where it blocks the release of inhibitory neurotransmitters GABA and glycine

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48
Q

What is autonomic dysreflexia?

A
  • a potential complication of spinal cord injury above T6 whereby noxious stimuli in the form of constipation, urinary retention, or pressure ulcers can precipitate an unregulated sympathetic response due to the loss of descending input
  • the resulting vasoconstriction and hypertension is met by a compensatory parasympathetic response above the level of the lesion with flushing, diaphoresis, and bradycardia
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49
Q

Pronator drift can be localized to a lesion where in the nervous system?

A

to the pyramidal/corticospinal tract

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50
Q

The Romberg test is an evaluation of what?

A

proprioceptive functioning

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51
Q

What is transverse myelitis?

A

a combination of motor and sensory loss below the level of the lesion along with incontinence, often a symptom of MS

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52
Q

What is believed to be the pathogenesis for NPH?

A

decreased CSF reabsorption through the arachnoid granulations

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53
Q

What is the best test to run for someone with amaurosis fugax?

A

a duplex ultrasound of the neck since most cases are caused by atherosclerotic emboli from the ipsilateral carotid

54
Q

What is the key clinical feature that distinguishes Parkinson disease from dementia with Lewy bodies?

A

by definition, Parkinson disease is diagnosed when parkinsonism predates cognitive impairment by more than 1 year

55
Q

How does GBM look on imaging?

A

it classically has a butterfly appearance with central necrosis and surrounding serpiginous contrast enhancement

56
Q

How can peripheral and central vertigo be differentiated?

A
  • peripheral: horizontal nystagmus that lasts less than one minute with 2-30 seconds of latency, no postural instability, auditory symptoms like tinnitus or hearing loss, and no other neurologic signs
  • central: purely vertical or torsional nystagmus lasting more than one minute with no latency period, severe instability, no auditory symptoms, and other neurologic signs
57
Q

What are possible etiologies for peripheral and central vertigo?

A
  • peripheral: BPPV, Meniere disease, vestibular neuritis, or acoustic neuroma
  • central: stroke, MS, migraine, CNS tumor, or cerebellar infarction
58
Q

Which patients with vertigo require CT? MRI?

A
  • CT if patients have new onset vertigo with vascular risk factors, neurologic signs/symptoms, or accompanying headache in order to rule out stroke
  • MRI if the CT is negative to evaluate for brainstem or cerebellar infarction
59
Q

What is albuminocytologic dissociation?

A

the finding of elevated CSF protein with a normal cell count, most characteristic of Guillain-Barre syndrome

60
Q

What is the best next step for a child with increasing head circumference and signs of increased ICP?

A

a CT of the brain

61
Q

What are four features of absence seizures that can help differentiate them from inattentive staring spells?

A
  • occurrence during all activities, not just “boring” ones
  • length less than 20 seconds
  • lack of a response to vocal or tactile stimulation
  • presence of automatisms
62
Q

Describe the pathogenesis, presentation, diagnosis, and treatment of cervical myelopathy.

A
  • it is the process whereby cervical spine degeneration, usually in the form of spondylosis, leads to canal stenosis and cord compression
  • it presents with slowly progressive gait dysfunction, LMN signs at the level of the lesion, UMN signs below the level of the lesion, and diminished proprioception, vibration, and pain sensation
  • it is diagnosed with MRI or CT myelogram
  • treatment is surgical decompression
63
Q

What is the presentation for the three following conditions:

  • galactokinase deficiency
  • galactose-1-phosphate uridyl transferase deficiency
  • uridyl diphosphate galactose-4-epiderase deficiency
A
  • galactokinase deficiency: cataracts alone
  • galactose-1-phosphate uridyl transferase deficiency: cataracts, failure to thrive, jaundice, and hypoglycemia
  • uridyl diphosphate galactose-4-epiderase deficiency: cataracts, failure to thrive, jaundice, hypoglycemia, hypotonia, and nerve deafness
64
Q

What are the unique features of herpes encephalitis that can help make the diagnosis?

A
  • CSF with lymphocytic pleocytosis, elevated protein, normal glucose, and erythrocytes
  • temporal lobe lesions on brain imaging
  • positive PCR for HSV DNA is the gold standard for diagnosis
65
Q

REM sleep behavior disorder is predictive of the development of what diseases?

A

alpha-synuclein neurodegenerative disorders such as Parkinson disease or dementia with Lewy bodies

66
Q

What sort of gross anatomical change is most characteristic of Alzheimer’s disease?

A

temporal lobe atrophy most prominent in the hippocampi

67
Q

Bell palsy is thought to be due to what?

A

reactivation of a neurotrophic virus, particularly herpes simplex

68
Q

What is the treatment for Bell palsy?

A

glucocorticoids are the mainstay of treatment; however, some add valacyclovir

69
Q

What is the predominate symptom of macular degeneration?

A

painless, bilateral, progressive blurring of central vision

70
Q

What is the most significant risk factor and the presentation of vitreous hemorrhage?

A
  • most cases are secondary to proliferative retinopathy of diabetes
  • presents with a sudden loss of vision, floaters, difficulty visualizing the fundus, and a dark red glow on fundoscopy
71
Q

Which dementias are highly sensitive to the effects of antipsychotics?

A

those with parkinsonism, including Parkinson disease and DLB

72
Q

What is the motor and sensory function of the femoral nerve?

A

it is responsible for knee extension and hip flexion and provides sensation to the anterior thigh and medial leg

73
Q

What is the motor and sensory function of the tibial nerve?

A

it is responsible for plantar flexion and inversion of the foot and provides sensation to the plantar surface of the foot

74
Q

What is a psychogenic nonepileptic seizure and what helps distinguish it from a seizure?

A
  • it is a form of conversion disorder
  • it is suggested by forceful eye closure, side-to-side head or body movements, rapid alerting/no postictal period, a lack of incontinence, and the absence of self-injury
75
Q

What is paroxysmal dyskinesia?

A

a type of movement disorder in which attacks of involuntary motor dysfunction such as dystonia or choreoathetosis occur

76
Q

What is synringomyelia and what are possible etiologies?

A
  • it is a disruption of CSF drainage from the central canal which leads to the formation of a fluid-filled cavity that compresses surrounding tissue
  • it is most commonly associated with a type I Chiari but can also be secondary to meningitis, tumors, and trauma
77
Q

Compare and contrast Niemann-Pick and Tay-Sachs diseases.

A
  • both present with loss of motor milestones, hypotonia, feeding difficulties, and a cherry-red macula
  • NP, which is due to a sphingomyelinase deficiency, also presents with hepatosplenomegaly and areflexia
  • whereas TS, due to B-hexosaminidase A deficiency, presents with hyperreflexia and no hepatosplenomegaly
78
Q

What are the features of neurofibromatosis I?

A
  • cutaneous manifestations include cafe-au-lait macule, axillary/inguinal freckles, iris hamartomas (Lisch nodules), and neurofibromas
  • they are also at risk for developing intracranial neoplasms, particularly optic gliomas
79
Q

Anterior dislocation of the humeral head threatens what nerve?

A

the axillary nerve

80
Q

What is the best abortive and prophylactic medication for cluster headaches?

A
  • abortive: 100% oxygen

- prophylaxis: verapamil or lithium after the first attack

81
Q

What is the management for first time seizures in an adult?

A
  • always begin with basic laboratory tests to exclude metabolic and toxic causes
  • this can be followed by neuroimaging to search for structural abnormalities and a routine EEG to look for epileptiform activity
82
Q

What features suggest a subarachnoid hemorrhage and what are five possible complications?

A
  • will typically present with severe headache, focal deficits, and meningismus
  • complications include rebreeding within the first day, vasospasm after 3 days, hydrocephalus, seizures, or SIADH
83
Q

What features suggest a subarachnoid hemorrhage and what are five possible complications?

A
  • will typically present with severe headache, focal deficits, and meningismus
  • complications include rebreeding within the first day, vasospasm after 3 days, hydrocephalus, seizures, or SIADH
84
Q

What is Shy-Drager syndrome/MSA and how is it treated?

A
  • it is the syndrome of parkinsonism, autonomic dysfunction, and widespread neurologic signs (cerebellar degeneration, LMN signs, etc.)
  • it is refractory to dopaminergic agents, so treatment is aimed at volume expansion and BP maintenance
85
Q

What is Riley-Day syndrome?

A

an autosomal recessive dysautonomia which presents as severe orthostatic hypotension and autonomic dysfunction in children

86
Q

What group of medications must be avoided in those with acute angle closure glaucoma?

A

those that cause dilation of the eye (anticholinergics or sympathomimetics)

87
Q

What complication of meningitis is most common following S. pneumo infection?

A

sensorineural hearing loss secondary to inflammation of the vestibulocochlear nerve

88
Q

What are the typical features of Lambert-Eaton myasthenia syndrome?

A
  • progressive, symmetric, proximal limb muscle weakness and diminished reflexes, which both improve with use
  • autonomic dysfunction
89
Q

What is subclavian steal syndrome?

A
  • a stenosis of the subclavian due to atherosclerosis proximal to the origin of the vertebral artery, which leads to reversal of flow in the ipsilateral vertebral artery
  • may present with pain, fatigue, or paresthesias in the ipsilateral upper extremity, vertebrobasilar ischemia in the form of dizziness and ataxia, and a lower brachial systolic blood pressure in the affected arm
90
Q

Describe the symptoms, diagnosis, and treatment of pseudotumor cerebri.

A
  • it is also known as idiopathic intracranial hypertension
  • associated with overweight women, tetracycline use, and hypervitaminosis A
  • presents with headache, transient vision loss, pulsatile tinnitus, and diplopia; exam finds papilledema, visual field deficits, and CN VI palsy
  • diagnosis is made based on MRI (often showing an empty sella) and a lumbar puncture with elevated opening pressure but normal analysis
  • treat with weight loss and acetazolamide
91
Q

What are the symptoms of hypokalemia?

A
  • weakness, fatigue, muscle cramps, flaccid paralysis, hyporeflexia, tetany, rhabdo, and arrhythmias
  • ECG will show broad, flat T waves, U waves, ST depression, and PVCs
92
Q

Describe the appearance of a meningioma on CT?

A

it is extra-axial, dural-based, well-circumscribed, and homogeneously enhancing; it may also undergo calcification

93
Q

Which three groups of chemotherapeutic agents are known for causing peripheral neuropathy? What is the typical description for this sort of neuropathy?

A
  • vincristine, cisplatin and other platinum-based agents, and paclitaxel and other taxanes
  • presents about 1 week after initiation with a stocking-glove distribution of paresthesia, spinothalamic involvement, and earlier motor involvement than diabetic peripheral neuropathy
94
Q

What is the classic triad of symptoms seen in those with a spinal epidural abscess?

A

fever, back pain, and progressive neurologic findings

95
Q

Describe the presentation, diagnosis, and treatment of a spinal epidural abscess.

A
  • typically due to S. aureus and thus present in patients with distant infections, recent spinal procedures, or a history of IV drug use
  • present with a classic triad of fever, back pain, and progressive neurologic findings
  • diagnosis is based on an MRI of the spine
  • treat with vancomycin and ceftriaxone with or without decompression
96
Q

What is the pathologic basis for Huntington disease and what gross change is evident on neuroimaging?

A
  • due to a CAG repeat that leads to the loss of GABAergic neurons
  • imaging reveals atrophy of the caudate nucleus and putamen
97
Q

What are the three key features of Friedrich ataxia?

A
  • neurologic impairment, predominately ataxia
  • insulin resistance
  • cardiomyopathy
98
Q

What are the two key features of spinocerebellar ataxia?

A

cerebellar ataxia and cranial nerve dysfunction

99
Q

What is the preferred treatment for trigeminal neuralgia?

A

carbamazepine

100
Q

What is the mechanism of action for botulinum toxin?

A

it inhibits acetylcholine release at the NMJ

101
Q

What is the best first step in the management of botulinum toxin?

A

when suspected, begin botulism immune globulin as soon as possible, even before diagnostic confirmation is obtained

102
Q

What are the features of Wernicke encephalopathy?

A

confusion, oculomotor dysfunction, and gait ataxia

103
Q

Describe the presentation of tick-borne paralysis.

A
  • it manifests as a rapidly progressive, ascending paralysis without fever, sensory abnormalities, or autonomic abnormalities
  • CSF is typically normal and diagnosis is made by finding the tick
104
Q

Describe Brown-Sequard syndrome.

A
  • ipsilateral hemiparesis at the level of the injury and below
  • ipsilateral loss of proprioception, vibratory sensation, and light touch at the level of the injury and below
  • contralateral loss of pain and temperature sensation 2 levels below the injury and below
105
Q

Describe the presentation and diagnosis of a carotid artery dissection.

A
  • most commonly follows a penetrating trauma, neck manipulation, or fall with an object in one’s mouth
  • presents with gradual-onset hemiplegia, aphasia/neglect, neck pain, and thunderclap headache
  • diagnose with a CTA or MRA
106
Q

Review the neurocutaneous disorders.

A

NF1, NF2, Sturge-Weber, Tuberous Sclerosis

107
Q

What is myotonic muscular dystrophy?

A
  • an autosomal dominant, adolescent/adult-onset muscular dystrophy caused by a CTG trinucleotide repeat
  • it presents with myotonia (delayed muscle relaxation often manifesting as an inability to release a handshake), skeletal muscle weakness particularly in the face and ankle dorsiflexors, and cardiac conduction problems
  • complications include cataracts, testicular atrophy and infertility, and baldness
108
Q

Describe the presentation and treatment for malignant hyperthermia.

A
  • presents as generalized rigidity, dyspnea, tachycardia, and dark urine secondary to rhabdo and myoglobinuria soon after anesthesia
  • treatment involves respiratory support and dantrolene
109
Q

If an infant presents with a history suggesting non accidental trauma, what are the three best next steps?

A
  • funduscopic examination looking for retinal hemorrhages
  • CT of the head
  • skeletal survey
110
Q

What is the mechanism for death in those who suffer from shaken baby syndrome?

A

subdural venous shearing and hemorrhage

111
Q

What are the classic features of Creutzfeldt-Jakob disease?

A
  • rapidly progressive dementia
  • myoclonus
  • and an EEG showing sharp, triphasic, synchronous discharges
112
Q

Parkinson’s disease patients with tremor as their predominate symptom should be started on what medication?

A

trihexyphenidyl

113
Q

What are the imaging guidelines for children who suffer TBI?

A
  • those with minor head trauma meaning GCS of 15 with a non-severe mechanism, and no vomiting, headache, LOC, etc. are not imaged
  • mild TBI is defined as GCS of 15 with a severe mechanism of injury, vomiting, headache, or brief LOC and these patients can get a CT or be observed for 4-6 hours
  • severe TBI involves a fracture or results in a seizure, GCS less than 13, prolonged LOC, or focal neurologic signs and these patients should all get a CT
114
Q

What are the presenting features for those with fetal alcohol syndrome?

A
  • characteristic facies include smooth philtrum, thin vermillion border, small palpebral fissures, and microcephaly
  • patients have diminished growth, intellectual disability, ADHD, social withdrawal, and delays in motor and language development
115
Q

What are three ways to describe the gait of someone with Parkinson’s disease?

A
  • shuffling
  • festinating
  • hypokinetic
116
Q

Describe sensory ataxia.

A
  • this results from lesions of the peripheral nerves, dorsal roots, or posterior columns
  • it manifests as a wide-based, high-stepping gait, often with a positive Romberg’s sign
117
Q

Describe sensory ataxia.

A
  • this results from lesions of the peripheral nerves, dorsal roots, or posterior columns
  • it manifests as a wide-based, high-stepping gait, often with a positive Romberg’s sign
118
Q

What is the ice pack test?

A

resting an ice pack on the eye of someone with MG will lead to an improvement in their ptosis by inhibiting the breakdown of acetylcholine at the NMJ

119
Q

The ulnar nerve most commonly becomes entrapped where?

A

at the elbow where the ulnar nerve lies at the medial epicondylar groove

120
Q

The ulnar nerve most commonly becomes entrapped where?

A

at the elbow where the ulnar nerve lies at the medial epicondylar groove

121
Q

Describe the presentation of neurogenic shock in a patient who suffers a spinal cord injury.

A
  • there is an initial period of massive sympathetic stimulation leading to hypertension and tachycardia
  • this is followed by unopposed parasympathetic stimulation manifesting as hypotension, hypothermia, and bradycardia
122
Q

What is the typical presentation of polymyositis?

A

insidious onset of symmetric, proximal limb muscle weakness and myalgia associated with elevated muscle enzymes

123
Q

Describe a breath-holding spell.

A

these occur in children 6 months to 6 years old and present with cyanosis or pallor following an upsetting event or minor injury

124
Q

What are thalamogeniculate arteries and how do thalamogeniculate strokes present?

A
  • they are the deep, penetrating arteries of the PCA, which supply the posterolateral thalamus
  • strokes of these vessels result in a pure contralateral sensory stroke and may later lead to thalamic pain syndrome with allodynia
125
Q

What is the classic triad for Wernicke encephalopathy?

A

ataxia, ophthalmoplegia, and encephalopathy

126
Q

What is the primary contraindication to triptans? What would you then use for abortive migraine therapy?

A
  • significant coronary artery disease due to the risk of triggering coronary vasospasm
  • use an IV antiemetic like prochlorperazine
127
Q

How is herpetic neuralgia treated?

A
  • in the acute and subacute phases (less than 4 months after rash onset) use NSAIDs and analgesics
  • for postherpetic neuralgia (that which persists more than four months after rash onset), use TCAs, gabapentin, and pregabalin
128
Q

What role does antiviral therapy play in the treatment of shingles and herpetic neuralgia?

A

it can help shorten the course of shingles; however, post-herpetic neuralgia isn’t associated with viral replication so antivirals don’t play a part in treatment

129
Q

What are the absolute contraindications for tPA?

A
  • stroke or head trauma in the past 3 months
  • history of intracranial hemorrhage or vascular malformation
  • recent intracranial or spinal surgery
  • active bleeding in the past 7 days
  • blood pressure greater than 185/110
  • platelets less than 100K
  • INR greater than 1.7
130
Q

What is the presentation and treatment for heat stroke?

A
  • presents with core temperature greater than 104 F, CNS dysfunction, and additional organ or tissue damage
  • treat with ice water immersion, fluid resuscitation, and electrolyte correction
131
Q

What is fragile X syndrome?

A
  • an inherited intellectual disability caused by a trinucleotide CGG repeat in the FMR1 gene, which leads to methylation and silencing of the gene
  • presents with a long face, prominent forehead, protruding ears, macroorchidism, speech and motor delays

Neurology (2 decks)

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