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jK NEURO > daily study > Flashcards

daily study Flashcards

1
Q

csf with elevated proteins and no WBC:

A

GBS, or AIDP

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2
Q

MUSK LRP4 goes with what other antibodies and what disease

A

MG, ACh antibodies

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3
Q

what gene is associated with sma?

A

survival 1

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4
Q

how can you tell botilism from mg or les

A

botolism the eyes are dialted, mg they would constrict

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5
Q

what are the neoparaplastic diseases?

A

LES, Dermatomyositis, polymyositis

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6
Q

what are the AD neuromuscular disorders?

A

charcot marie, myotonic Dystrophy (CTG)

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7
Q

how do you treat acute AIDP?

A

Plasmapharesis or IVIG

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8
Q

if a baby may be “slow” and he has hyporeflexis, you are thinking:

A

lmn damage or muscles: check creatine levels

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9
Q

polymyositis and dermatomyositis have:

A

increased CK levels over 200

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10
Q

In LEMS you can test for:

A

P/Q Voltage-gated calcium channel

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11
Q

Dog given ______ starts walking because it was a ______

A

edrophonium, ACh-ase inhibitor

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12
Q

•Angular atrophy is present in:

A

europathic findings (SMA, ALS)

•We see fiber type grouping. You get groups of Type 1 and Type 2 muscle fibers. It should normally be a checker board pattern, but here you see big blocks of Type 1 and big blocks fo Type 2.

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13
Q

what other inherited diseases are there and what disease is it associated with?

A

muscular dystrophy, X-linked, shows increased levels of Creatine Phosphokinase (CPK)

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14
Q

vasovagal syncope

A

vaSO-hyPO-NO tachycardia reflex

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15
Q

VErTIgo is affiliated with:

A

VEsTIbular: from the vestibular nuclei there are three distinations: occulomotor and abdusens nerve, flocculonodular lobe of the cerebellum helps to coordinate head and eye movement, vestibulospinal white matter: keeps head up straight

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16
Q

bouts of acute, persistant vertigo are related to:

A

acute vestibular syndrome

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17
Q

episodic vertigo that changes with position: if sponstaneous, it’s:

A

bppv, dix hallpike, positive nystagmus; migraine

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18
Q

dysphagia, dysarthia, attaxia and dysmetria are all:

A

cranial nerve symptoms, swallowing (CN 9, 10, 12) speech (cranial nerve 5, 7, 9, 10, 12) cerebellum (you dissin me?) a type of ataxia but attaxia is trunkal (postural)

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19
Q

a persistant vertigo is a sign of, and it can be central or peripheral

A

avs

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20
Q

BPPV is listed under:

A

acute episodic, positional

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21
Q

migraine characteristics

A

5graine, 4-72 hours, 40 avg age, aura develops over 4 minutes, and lasts no longer than 60 (does not always equal

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22
Q

migraine vs tia

A

migraine develops over 4 minutes, tia instant, migraine lasts longer (20), tia less than 15, migraine: positive visual symptoms, tia: loss of vision

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23
Q

what makes a migraine chronic?

A

15 (write ch of chronic backwards)

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24
Q

abc’s of migraine treatment:

A

anti-alpha epileptic drugs, anti-alpha antidepressent, beta blockers, calcium channel inhibitors

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25
Q

sumotryptan is contrindicated for:

A

CAD, prinzmetals, pregnancy

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26
Q

cluster headache lasts:

A

15 min to 3 hours (cluster headache is 15 letters)

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27
Q

familial component is:

A

more common than positive visual aura

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28
Q

woman with intense jaw pain brought on by cold:

A

trigeminal neuralgia: treat with carbemazapine

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29
Q

verapamil is a:

A

prophylactic for cluster headaches and migraines

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30
Q

tensions type headaches may be associated with:

A

slightly reduced neck range of motion and paracervical tenderness

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31
Q

classic migraine:

A

familial, unilateral throbbing, diminishes with age,

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32
Q

stabbing pain on one side just below the eye, lasting 1 second at a time, triggered by drinking cold fluids:

A

trigeminal neuralgia

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33
Q

throbbing npain waking him from sleep while sleeping and persistant in the day. Centered about the left eye and appears nearly daily for several weeks or months

A

cluster headache

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34
Q

dull left side pain with radiation to the right side. No nasuea or vomitting, and has lost 10 pounds over the past 2 months

A

temporal arteritis

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35
Q

obese woman, bilateral papilledema

A

idiopathic intracranial hypertension, headache transient visual obcurations, progressive visual loss, pulsatile tinnitus, diplopia, shoulder and arm pain, papilledema or optic atrophy

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36
Q

sudden severe headache associate with naseua. Maximum intensity after 5 seconds. No prior history of headache, and was engaged in sexual activity just before the onset

A

thunderclap headache

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37
Q

headache upon standing, and it resolves quickly after lying down. Mild nasuea

A

intracranial hypotension, result of recent lumbar puncture,

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38
Q

in vasculitis, you would see ____ in CSF

A

elevated protein levels in the csf

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39
Q

in rcvs, you have to rule out:

A

subarachnoid hemorrage, vasculitis, cerebral venous thrombosis

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40
Q

redish orange eye picture is indicative of:

A

idiopathic intracranial headache

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41
Q

if you see a ct scan with a small tumor in the temporal area, if it most likely:

A

vestibular schwannoma

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42
Q

if you see a ct scan with a small tumor along the falx or meninges of the brain, it is most likely a:

A

meningioma

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43
Q

if you see a tiny tumor in the spinal cord, it is most likely an:

A

epindemoma

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44
Q

if you see a small tumor in the lp area of the bottom of the spine, it is most likely a

A

schwanoma

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45
Q

pancake on back of leg_____ raised up patch of bumps______

A

plexiform neurofibromas 1, shagreen patches tuberous sclerosis

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46
Q

sturge weber gene:

A

GNAQ guanine nucleotide activating gene

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47
Q

whats the story for sturge weber?

A

We took the tram on the calcified track to meso grill in equador. At the restaurant, the specials were sturgin. So, you sporadically chose your sturgin as your entree. In addition to your meal, you ordered 1/2 glasss of port wine. You we’re really upset because your sturgin was so dry, that you had to GNAw on it. Because of that you gave no TIP (GTP). At the end of your meal, they gave you seez candies. They tastes so bad, that you broke your glass and glass went into you eye. You screamed “GLASS-EYE-OW! *GLACOMA” had peed a vast amount

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48
Q

If you see a ct scan with subtle lesions in the top left and bottom left corners, it is:

A

cortical tubers tubero sclerosis

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49
Q

adenoma sebaceum occurs in 90% of patients with:

A

tubero sclerosis

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50
Q

by age 5, more than half of patients with tubero sclerosis will have:

A

subependymal gial nodules that have calcified

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51
Q

parents are concerned that his many areas of hyperpigmented skin (some more than 2.5 in in diameter) may have some significance. This dermatological manifestation is commonly found on patients with:

A

neurofibromatosis

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52
Q

the newborn infant with motor neuron disease is likely to exhibit which of the following:

A

hypotonia (sma)

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53
Q

Bell’s Palsey mnemonic:

A 
Blinking reflex is abnormal
Earache
Lacrimation
Loss of taste for anterior 2/3
Sudden onset in nature
Palsey of CN 7
54
Q

Horner’s syndrome mnemonic:

A

Sensory fibers damaged:
Ptosis
Meiosis
Anhydrosis

55
Q

Cluster headaches: first line treament _____ and they’re associate with _____

A

verapamil and lithium/trigeminal-hypothalamic pathway

56
Q

cluster headache abortive treatment:

A

Sub Q sumotrypsin; 100% oxygen

57
Q

Chronic migraine prophylactic treatment (abcs)

A

Beta-blockers (propranolol, timolol, metoprolol)
Antidepressants (amitriptyline and venlafaxine)
Antiepileptic agents (topiramate and valproate)
Calcium channel blockers (verapamil)

58
Q

sub q sumotryptin and 100% oxygen is ___ treatment for tension headaches

A

abortive

59
Q

horner-like symptoms in a headache indicate:

A

cluster headache

60
Q

treatment for POAG:

A

Open angle glaucoma is treated with topical medications such as:
Beta-blockers (e.g. Timolol)
Alpha agonists
Carbonic anhydrase inhibitors (e.g. acetazolamide)
Prostaglandin analogues (e.g. latanoprost)

61
Q

treatment for closed angle?

A

Closed angle glaucoma requires laser iridotomy immediately. If that fails, then surgical iridectomy is the next step. (this is a medical emergency and must be treated ASAP- open is not)

62
Q

The ABC’s of POAG acts to: while _____ acts to:

A

lower the intraoccular pressure, prostglandins act to increase drainage

63
Q

als exhibits wasting and degeneration of:

A

anterior horn/corticospinal tract

64
Q

17 yr old with initial fever, then progressive weakness, and electromyography says it is a motor neuron disease:

A

Poliomyelitis

65
Q

polyomyelitis is often confused with:

A

guillen berre

66
Q

difference between polio and guillen berre:

A

guillen berre has elevated protein and no elevated wbc, while poliomyelitis has elevated proteins and wbc (during initial stage, poliomyelitis presents with fever)

67
Q

radiculopathies include:

A

c7,L5,S1, and bone spurrs

68
Q

guillain-Berre is a _____ that is prompted by:

A

autoimmune disease, acute illness, gastrointestinal infection (campylobacter) a vaccination, surgery, etc

69
Q

guillain-Berre presents with:

A

diplopia, cn 7 might be affected, eventual dysphagia, as well as loss of bladder control, increased proteins in CSF but no WBC (poliomyelitis)

70
Q

guilain-Berre may need to be treated with:

A

aggressive airway management or ivig

71
Q

Lambert-Eaton:

A

pre-synaptic, Ca2+ inhibition, worse in the morning and gets better as the day progresses, negative tinsilon test, occular sparing, para neoplastic (small cell lung cancer), and autonomic nervous system difficiency

72
Q

a 57 year old woman with a history of smoking , hip and shoulder weakness. No sensory symptoms, or cognitive decline. Proximal muscle weakness, eye movements normal:

A

lambert eaton

73
Q

myotonic dystrophy

A

bald, cataract, ctg repeat, cardiac conduction problems: ecg shows repetitive discharge with minor stimulation,

74
Q

muscular dystrophy

A

increased ck levels, x linked, waddling gate, large calves, gowers, becker is the less harmful

75
Q

pompes:

A

increased creatine kinase, autosomal recessive, deficiency in alpha 1,4, glucosidase

76
Q

mg includes nerve conduction study EMG which shows decrementing response of compound muscle action potential of:

A

3 hz stimulation

77
Q

proximal muscle weakness, pain and rash on her face and about her eyes. Weakness in hip and shoulder girdle:

A

dermatomyositis: purplish discoloration around the eyes

more common in women 40-60

78
Q

carrier of duchenne dystrophy gene might exhibit elevated ____ in serum;

A

creatine phosphokinase (cpk)

79
Q

pseudohypertrophy can be seen in:

A

calves of kids with muscular dystrophy

80
Q

devervation atrophy is the only disease we know that results in:

A

abnormally small muscle fibers interningled with hypertrophied muscle fibers

81
Q

sign of dermatomyositis besides rash?

A

gottran papules on knuckles

82
Q

brain abcess on ct:

A

ring lesion

83
Q

cryptococcosis is usually acquired through:

A

lungs and spreads to cns through blood. Produces meningitis or meningeoencephalitis, occurs in people with defect in immune system (secondary viral infection for aids, etc)

84
Q

82 yr old with recent upper respiratory infection presents with weakness, headache, blurry vision. originally upper respiratory symptoms starting with sore throat nasal congestion and excessive coughing. Didn’t take all antibiotic and then had chills, lightheadedness, vomitting, blurry visual symptos, eye tenderness and photosensitivity, fever, nuchal rigidity, sleepiness. What to do?

A

treat with iv ceftriaxone plus ampicillin

85
Q

recurrent meningitis develops from

A

csf leaks: communication between subarachnoid space and the body surface. Through the nose (rhinorrhea or ear) most common cause of csf leak is head trauma

86
Q

hiv patient with slow responses, difficulty sustaining attention, hemiparesis, increased reflexes on the right:

A

look for infection or malignant mass with a contrast-enhanced CT or MRI

87
Q

woman has 2 days of HA and Fever with worsening confusion, taken to the hospital after generalized seizure. head ct is consistent with left temporal hemorrage and swelling. localization of encephalitis to the medial temporal or orbital frontal regions of the brains is most consistant with:

A

herpes simplex virus

88
Q

21 yr old college student has fever, confusion, neuroimaging of the brain before attempting lp is advisable in cases of acute encephalitis bc:

A

massive edema in the temporal lobe may make herniation imminent

89
Q

man with ha, fever, disorientation and seizures expected to have the most common form of acute encephalitis. CSF will have:

A

type is herpes encephalitis, and the lymphocytes will be increased, normal glucose, usually increased csf pressure

90
Q

woman diagnosed with encephalitis has eeg, the findings will say:

A

bilateral eriodic epileptiform discharges: this is herpes encephalitis, and seizures commonly occur early in the course. The periodic discharges are seen over the temporal regions

91
Q

hiv patient has ha, sluggish mentation, impaired ambulation, ct reveals several ring-enhancing lesions which most likely develop from:

A

hematogenous spread of infection,

92
Q

ring-enhancing lesions are:

A

abscess formation in the brain, most frequently from blood-borne infections from sources in the lung, heart, sinuses and ears

93
Q

a woman presents with lethargy, fever, low blood pressure, and is diagnosed with bacterial endocarditis. A head CT reveals rim-enhancing lesions which are most commonly found in:

A

gray-white matter junction (start

94
Q

umn with no sensory loss and no babinski:

A

lacunar stroke, affects posterior limb of internal capsule

95
Q

lacunar stroke arteries supply:

A

posterior limb of the internal capsule, lenticulostriate arteries

96
Q

focal left-sided seizure. In the emergency room, he is found to have a temperature of 101 degrees orally, but no stiffness of his neck. Neurological examination reveals a mild left-sided weakness and lethargy. A non-contrast CT scan has already been obtained and is normal. Lumbar puncture reveals 80 white blood cells, mostly mononuclear and 12 red blood cells. The protein is 80 and the glucose is 60.

A

viral encephalitis: HSV

97
Q

treating someone with HSV encephalitis?

A

IV acyclovir at herpes encephalitis dosing, anti-epileptic medication

98
Q

HTN, hyperlipidemia, coronary artery disease with prior MI presents with a three month history of weakness

A

statin

99
Q

HTN, hyperlipidemia, coronary artery disease with prior MI presents with a three month history of weakness. She reports that she fatigues easily and has trouble walking up stairs. She says that her muscles ache sometimes. On exam her cranial nerves are all intact. There is no sensory loss. On motor exam her deltoids are 4+/5 bilaterally, biceps are also 4+/5, but triceps and distal arm strength is 5/5. In the lower extremities her hip flexors are barely 3/5. Quads are 4-/5 bilaterally and hamstrings are 4/5. Distally in her legs and feet and strength is 5/5. Reflexes are 1+ throughout and toes go down.

A

a. Where would you localize the lesion? Muscle
b. Are there any tests you would recommend? CK level, EMG, muscle biopsy if EMG confirms myopathic process
c. Could her presentation be due to a drug side effect? Yes, she is most likely on a statin due to her hyperlipidemia and CAD and she could definitely have a statin myopathy
d. Is there any treatment that you would recommend? If testing reveals an inflammatory myopathy, then treatment is steroids. If workup is most consistent with statin myopathy, then treatment is to stop the statin.

100
Q
  1. A 24 year-old male presents to your clinic for evaluation of strange movements. The patient appears restless and while he sits in your office chair cannot seem to stop moving his arms, torso and legs with frequent sudden, involuntary, dance-like quality to his movements. He is accompanied by his mother who reports issues at home relating to gambling, violent behavior, and aggression. His father and grandmother had similar symptoms, both of whom are now deceased. The patient is most likely suffering from which of the following:
A

a. Where would you localize the lesion? Brain, basal ganglia
b. Are there any tests that you might perform? Genetic testing for Huntington
c. Is there any treatment you might recommend? Symptomatic and counseling

101
Q
  1. An 84 year-old man presents for evaluation of falls. The patient’s family states that for the past few years he has developed shuffling of his gait which has recently resulted in falls during which he appears to fall backwards. His wife is most concerned about the fact that he will act out his dreams at night and reports that this has been going on for many years. Examination shows a right upper extremity resting tremor, slowed movements in the right arm, with small but legible handwriting, and problems maintaining posture. He has never been on any medications prior to this but is interested in anything that will help his condition.
A

a. Where would you localize the lesion? Brain, likely substantia nigra!
b. Are there any tests that you would recommend? Needs MRI brain to rule out secondary causes of Parkinsonism.
c. Is there any treatment that you might recommend? If no secondary cause is found, then symptomatic treatment with sinemet (carbidopa/levodopa) or possibly a dopamine agonist

102
Q
  1. A 54 year-old female goes to her physician complaining of difficulty with gait. The patient has a history of gastric bypass performed approximately 3 years ago but was lost to follow up until this appointment. She has chronic diarrhea as a result of her surgery and has to go to the bathroom multiple times per day. She complains of frequent near falls and stumbles when she walks. Examination shows 4+/5 bilateral hip flexors but otherwise near normal strength. Sensory examination reveals decreased light touch, vibration and proprioception in the bilateral lower extremities and slightly reduced vibration in the bilateral hands. Reflexes are 3+ in the lower extremities with clonus at the ankles. Plantar responses are extensor bilaterally. Cranial nerves are normal and the patient is able to complete a basic mental status screen but is only able to report 1/3 items at 5 minute recall and has some difficulty with general fund of knowledge reporting that the president is Clinton and unable to report the first president of the United States.
A

a. Where would you localize the lesion? Multi-focal: brain is involved with cognitive dysfunction, she has either a neuropathic process distally or, since she is hyperreflexic and her sensory abnormalities are all dorsal column dysfunction, must consider a posterior cord syndrome.
b. What kind of pathological process could do this? A multi-focal, systemic process is going on. Time course is chronic. In the setting of gastric bypass and malabsorbtion syndrome, should consider a nutritional deficiency. Sub-acute combined degeneration (brain/spinal cord, mainly dorsal columns) would fit perfectly: B12 deficiency. Whenever B12 is in the differential, then Copper deficiency should also be in the differential since it can present with similar syndrome. From a nutritional standpoint, Vit E deficiency can cause dorsal column degeneration as well.
c. What additional workup would you perform and could you suggest a possible treatment? : Check B12 level, methylmalonic acid level, copper levels, Vit E levels and replace if you uncover a deficiency. She needs MRI brain and cervical cord.

103
Q
  1. An 18 year-old male was violently struck by a car while riding a bicycle and suffered a severe traumatic injury of the spinal cord. The patient suffered traumatic brain injury, multiple rib fractures, and diffuse abrasions. Exam shows relatively full upper extremity strength with withdraw to pain but weakness in the legs bilaterally. Imaging shows a rare traumatic spinal cord injury with jumped facets at T9-10 resulting in significant anterolisthesis of T9 on T10 meaning that the T9 vertebrae is pushed forward over the T10 vertebrae (a somewhat unusual thoracic spine injury). Knowing the nature and location of this injury, you are asked to complete your evaluation and management of the patient.
A

a. Where would you expect his sensory level to be? Belly button line
b. What would you expect his reflex exam to be like? Likely areflexic below the lesion due to spinal shock.

104
Q
  1. 41 y/o administrative assistant complains of tingling and numbness intermittently in her hands. Sometimes her right hand aches. She has noticed that she sometimes drops things. Her neuro exam is normal except for tingling and numbness on the ventral side of her thumbs and first to digits. Her grip is weak on the right hand. When you tap over her wrists bilaterally, this increases the pain and tingling in her hands.
A

a. Where would you localize the lesion? Median nerves bilaterally
b. Is this a stroke or another pathological process? Not a stroke. Compression palsies of nerve – carpal tunnel syndrome
c. Would you recommend any treatment or additional workup? Cock up wrist splint. Carpal tunnel release on side with motor weakness.

105
Q
  1. A 30-year-old engineer fails to report to work on Monday. His friends find him at home acting somewhat confused, but without any other obvious problems. Later in the day, he has a focal left-sided seizure. In the emergency room, he is found to have a temperature of 101 degrees orally, but no stiffness of his neck. Neurological examination reveals a mild left-sided weakness and lethargy. A non-contrast CT scan has already been obtained and is normal. Lumbar puncture reveals 80 white blood cells, mostly mononuclear and 12 red blood cells. The protein is 80 and the glucose is 60.
A

a. Where would you localize the lesion? Brain! Seizure means brain is affected and not just meninges.
b. Is this a stroke or another pathological process? Not a stroke! Infectious process given fevers and LP parameters. LP parameters are consistent with a viral process. With seizures and confusion, worrisome for herpes encephalitis
c. Would you recommend any treatment or additional workup? IV acyclovir at herpes encephalitis dosing, anti-epileptic medication

106
Q
  1. A 32-year-old woman acutely developed nausea, vomiting and transient diarrhea lasting one week. Eleven days following her gastrointestinal disorder she developed numbness and tingling in both feet. With days her sensory symptoms progressed, accompanied by weakness of her hands and unsteadiness of gait.
    On admission to a major university medical center she was found to have sinus tachycardia, distal > than proximal quadriparesis, lower extremity hyporeflexia and marked vibratory and position sense loss in the toes, feet and ankles and to a lesser degree in her fingers. Rapidly over the next 12 hours she developed dyspnea, air hunger and ventilatory failure.
A

a. Where would you localize the lesion? Nerve, possibly cervical cord
b. Is this a stroke or another pathological process? Not a stroke. Likely AIDP but could theoretically be cervical cord
c. Would you recommend any treatment or additional workup? MRI cervical cord to rule out structural cord compression or a cervical cord inflammatory process like MS or idiopathic transvere myelitis, LP, EMG/PNCV. If testing confirms AIDP then treatment with IVIgG or plasmapheresis.

107
Q
  1. A 48-year-old man presents with a history of a left facial weakness that was labeled as a Bell’s palsy about three weeks ago. He has had some slight improvement in the left facial weakness since that time, but now has begun to develop weakness of the right face and double vision. Approximately three months ago he had gone camping on Martha’s Vineyard with his family. He has a history of an expanding rash on his left which he thought was probably ring worm. On the review of systems, he complains of a slight headache.
A

a. Where would you localize the lesion? Multiple cranial nerves on both sides.
b. Is this a stroke or another pathological process? Subacute onset, bilateral cranial nerves without motor or sensory long tract signs is highly unlikely to be brain and time course is not stroke. Preceding rash and location in Lyme endemic area = highly suggestive of Lyme
c. Would you recommend any treatment or additional workup? LP, Lyme titers. IV ceftriaxone.

108
Q
  1. 72 year old man with HTN and hyperlipidemia develops double vision and trouble walking. He sits down on the couch and waits for his son to come home from work. When son comes home, he takes Dad to the hospital where he arrives 8 hours after symptom onset. VS BP 199/115 HR 90. Patient is awake and alert. Speech is normal and language is normal. On cranial nerve testing he has prominent left eye ptosis. The left pupil is 6mm and poorly reactive, the right pupil is 3mm and briskly reactive. When you raise the left lid, the left eye is deviated outward slightly. When testing extraocular movement, he looks to the left without difficulty. When looking right, the left eye stops at midline but the right eye abducts completely but develops prominent nystagmus. When looking up, the left eye tries to go up but only does so slightly, when looking down, again the left eye cannot depress all the way. There are no other cranial nerve problems. There is no motor weakness or sensory loss. There is prominent right-sided dysmetria. Right toe goes up and he has clonus at the right ankle.
A

a. Where would you localize the lesion? Left midbrain
b. Is this a stroke or another pathological process? Sudden onset, stroke syndrome = stroke
c. Would you recommend any treatment or additional workup? Out of window for tPA or thrombectomy probably, and BP too high for tPA as well without treatment. Needs CT and probably CTA and then usual stroke workup.

109
Q
  1. 20 y/o young man brought to the ED by his roommate at Wake Forest. Patient has been sick with sore throat and cough for the last 3 days and this morning felt too bad to go to class. His friend came home for lunch and found him disoriented and confused and complaining of a headache and so brought him to the ED. In the ED VS: BP 111/63, P 105, RR 24, T 102. On exam he is drowsy but answers questions appropriately. He does complain of a bad headache and stiff neck but neuron exam was non-focal
A

a. Where would you localize the lesion? Brain, stiff neck/headache points to meningitic process
b. Is this a stroke or another pathological process? No focality on exam, subacute onset – not stroke. Preceding illness, fever = meningitis until proven otherwise.
c. Would you recommend any treatment or additional workup? Needs head CT then LP. Antibiotics. Most likely organism is S. pneumo, possibly meningococcus. Treat with 3rd or 4th gen cephalosporin +/- Vanc depending on community likelihood of PCN-resistant S. pneumo

110
Q
  1. 80 year old nursing home patient with chronic hypertension and diabetes wake up one morning with slurred speech and is sent to the ED. Patient is awake and alert but severely dysarthric almost to the point of being unintelligible. He is able to follow commands and can write sentences without errors. On cranial nerve testing he has mild left facial weakness that spares the forehead. His tongue deviates to the left, but otherwise cranial nerves are intact. On motor testing he has pronator drift on the left and left grip is 4+/5. Left leg is 5/5. He has decreased RAM in the left hand. There is no dysmetria and no sensory loss. Reflexes are symmetric and toes go down.
A

a. Where would you localize the lesion? Right subcortical. He has clumsy-hand dysarthria syndrome so localization is likely ventral pons or internal capsule
b. Is this a stroke or another pathological process? Lacunar syndrome makes this most likely stroke.
c. Would you recommend any treatment or additional workup? Out of window for tPA – awakened with deficit. Needs aspirin if no blood on head CT and usual stroke workup

111
Q
  1. 53 year old truck driver runs off the side of the road due to sudden onset of weakness and double vision. He is not injured and paramedics take him to the ED where he arrives 90 minutes after onset. VS BP 229/110, HR 155 and irregularly irregular. Patient c/o double vision, he is awake and alert. Speech is dysarthric, language function is intact. On cranial nerve testing he has small but reactive pupils, on right lateral gaze, his eyes will not move past midline, when attempting to look to the left, his eyes have full excursions to the left. He can look up and down, he has a right lower motor neuron facial weakness, his left palate does not elevate well and his tongue deviates to the left when protruding, he has left sided weakness at about 3/5 throughout, he has some sensory loss on the left, left side is hyperreflexic and left toe goes up.
A

a. Where would you localize the lesion? Right pons
b. Is this a stroke or another pathological process? Sudden onset, symptoms fit a vascular distribution = likely ischemic stroke or pontine hemorrhage
c. Would you recommend any treatment or additional workup? Emergent head CT to look for blood. BP is too high for tPA but you can treat to get it within range. Likely cause of stroke is cardioembolic from a-fib given his irregular heart rate in the 150s. With brainstem localization would need emergent CTA to make sure there is not a basilar thrombus which would need thrombectomy.

112
Q
  1. 63 y/o woman with HTN and DM has sudden onset of left sided weakness and her daughter takes her to the ED. She arrives at the ED within 2 hours of symptom onset. VS 166/89 T 99. On exam she is slightly drowsy, states that there is nothing wrong with her; right gaze preference, speech dysarthric, not aphasic, left VF cut, left facial droop, left face sensory loss, poor left palatal elevation, tongue deviates to the left, left hemiplegia, will extensor posture to pain on the left, left toe upgoing. Head CT scan is unremarkable.
A

a. Where would you localize the lesion? Right cortex
b. Is this a stroke or another pathological process? Sudden onset, MCA distribution symptoms point strongly to stroke
c. Would you recommend any treatment or additional workup? She is within tPA time frame and BP parameters. Look for any other exclusions and if none found t then give tPA

113
Q

radiculopathy includes

A

C7, L5, S1, and covers middle finger (C7), big Toe (L5), and Heel (S1) remember heel is 4 letters as is five, and toe and one are both three, so they’re perfect for each other, but only swapped

114
Q

Erb’s Duchenne Palsy occurs from torsion/strain pulling of the upper trunk of the brachial plexus during childbirth, results from damage to:

A

c5/c6 c8/T1

115
Q

______is one of the hereditary motor and sensory neuropathies, a group of varied inherited disorders of the peripheral nervous system characterised by progressive loss of muscle tissue and touch sensation across various parts of the body.

A

Charcot-Marie Tooth

116
Q

Riluzole works by

A

antagonist of NMDA which blocks glutamate and improves muscle activation (fyi, nmda antagonists are anelgeisics and are used for anesthetic)

117
Q

ascending paralysis from demylination that starts 1-3 weeks after an illness of vaccination:

A

Guillan Berre, also presents with decreased deep tendon reflex

118
Q

1-3 weeks after an infection or vaccination, patient presents with diplopia and paralysis of the muscles that control motor movement in the eye

A

Guillan Berre- no pupillary response change!

119
Q

Guillan Berre eventually results in:

A

difficulty speaking dysphagia (diced fajita that you can’t swallow), loss of bladder and bowels, may require aggressive air management

120
Q

LEMS can occur as a result from:

A

lung cancer (paraneoplastic) or Diabetes 1, hypothyroidism

121
Q

LEMS can present with patients who:

A

have trouble climbing stairs or rising from sitting

122
Q

LEMS is a ____ disorder and so you can see:

A

autoimmune disorder, decreased ACh and so you can have all sympathetic problems (i.e. blurred vision, lack of sweating) occular muscles are spared

123
Q

patients with contractures of muscle limbs, lordosis, and pseudohypertrophic calf muscles can present with:

A

waddling gait (weak hip abductors) increased CPK, lack in dystrophen protein

124
Q

myotonic dystrophy will look like:

A

saggy face, weakened facial muscles, ptosis, balding, cataracts, will have decreased cardiac conduction

125
Q

hypotonia can results from:

A

sma type 1 and 4, and pompe (alpha 1,4 glucosidase deficiency)

126
Q

in addition to an alpha 1,4 glucosidase deficiency, patients with pompe’s will present with;

A

increased ck levels and hypotonia

127
Q

Strokes that occur in the posterior cerebral artery (PCA) most commonly present with

A

hemianopia. In addition, infarction of the left PCA may present with:
Alexia without agraphia
Anomic aphasia
Gerstmann syndrome

128
Q

And infarction of the right PCA may present with:

A

Prosopagnosia
Spatial disorientation
Visual neglect

129
Q

only organ to compensate during hypoxia

A

lungs

130
Q

loss of sensation on left body and left face but still full strength, or motor loss

A

not internal capsule
Thalamus
most likely a clot in the VPM and VPL which causes complete sensory loss of face and body

131
Q

MRI of patients with huntingtons will show an abnormally shaped ________

A

lateral ventricle; occurs with degeneration of the caudate nucleus

jK NEURO (35 decks)

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