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OMS III > IM Neurology > Flashcards

IM Neurology Flashcards

1
Q

Stroke

definition

A

sudden onset of a neurological deficit fromt eh death of brain tissue. stroke is the third most common cause of death in the united states

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2
Q

Stroke

risk factors

A

same as MI:

htn

diabetes

hyperlipidemia

tobacco smoking

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3
Q

Stroke is caused by

A

caused by a sudden blockage in the flow of blood to the brain in 85% of cases and by bleeding in 15% of cases. a cerebral vessel is blocked either by a trhmbosis occurring in the vessel or by an embolus to the vessl

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4
Q

Stroke

emboli

A

heart: afib, valvular heartd disease, dvt paradoxically getting into the brain trhough a patent foramen ovale

carotid stenosis

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5
Q

Stroke Middle Cerebral Artery

presentation

A

(more than 90%)

weakness of sensory loss on the opposite of the lesion

homonymous hemianopsia

aphasia if the stroke occurs on the same side as the speech center. this is left side in 90% of pts

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6
Q

homonymous hemianopsia

A

loss of visual field on the opposite side of the stroke. a left sided mca stroke results in loss of the right visual fields. the eye cant see the right side so the eyes deviate to the left.

so the eye looks towards the side of the lesion

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7
Q

Stroke Anterior cerebral artery

presentation

A

personality/cognitive defects such as confustion

urinary incontinence

leg more than arm weakness

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8
Q

Stroke Posterior cerebral artery

presentation

A

ipsilateral sensory loss of the face, ninth and 10th cranial nerves

contralatleral sensory loss of the libs

limb ataxia

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9
Q

Stroke

best initial test

A

CT scan of the head without contrast

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10
Q

Stroke

most accurate test

A

MRI

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11
Q

Stroke diagnostic testing

A

do a CT first to exlcued hemorrhage as a cause of the stroke prior to initiating treatment

CT scan needs 4-5 days to reach 95% sensitivity

MRI needs 24-48 hours to reach 95% sensitivity

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12
Q

best initial therapy for nonhemorrhagic stroke

A

less than hourse since onset of stroke: thrombolytics (some places go up to 4.5 hours)

more than 3 hours since onset of stroke: aspirin

hemorrhagic stroke: nothing

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13
Q

how do you treat a pt with a nonhermorrhagic storke who is already on apsirin

A

add dipyerimadole

or

switch to clopidogrel

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14
Q

when can you drain a hemorrhagic stoke

A

posterior fossa

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15
Q

treatment for prevention of a stroke

A

either aspirin or clopidogre, do not combine them you will only make pt bleed. use dipyridamole with aspirin as an equivalent of clopidogrel

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16
Q

thrombolytics

A

can sometimes be used up to 4.5 hours (must get conformed consent)

standard of care is under 3 hours since onset and are fda approved

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17
Q

Statins with stroke

A

every pt with a storke hsould be started on a statin medication regarldess of ldl. although target based therapy for lipid maagement is unclear at this time, we want to bring the ldl to 70 or at least under 100

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18
Q

stroke=

A

statin (put pt on one)

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19
Q

acute blood appears what color on a CT

A

white

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20
Q

Evaluation of causes of stroke and their treatment

echocardiogram

A

surgical replacement or repair of certain damaged valves

Thrombi: heparin followed by warfarin to an INR of 2 to 3. rivaroxaban and dabigatran are aletnative medications

pfo

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21
Q

Evaluation of causes of stroke and their treatment

EKG

A

a fib or flutter is treated with warfarin to an INR of 2 to 3 as long as the arrhythmia persists

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22
Q

Evaluation of causes of stroke and their treatment

holter monitor

A

if the intial ekg is normal a holter monitor should be perormed to detect atrial arrhytthmias with greater sensitivity

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23
Q

Evaluation of causes of stroke and their treatment

carotid duplex us

A

carotid stenosis is a frequent cause of emboli to the brain. if a pt has symptomatic cerebrovascular disease and more than 70% stenosis is detected, surgical correction of the narrowing should be performed. endartectomy is superior to carotid angioplasty.

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24
Q

Evaluation of causes of stroke and their treatment

endarterectomy

A

has not value for milder stenosis (under 50%), it is unclear is endarterectomy will benefit moderate stenosis (50-70%), if the stenosis is 100% however no inteverntion is needed there is no point in opening a passaged that is 100% occluded

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25
Q

stroke pts should be place don telemetry to

A

dtect afib/flutter

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26
Q

carotid angioplasty and stenting is what with storke

A

not proven and is always the wrong answer

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27
Q

control of risk factors for stroke

A

diabetes to a hemoglobin A1C below 7%

hypertension

reduce LDL to at least below 100 if carotid stenosis is the cause of the stroke

tobacco smoking should be stopped

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28
Q

carotid stenosis is considered and equivalent of

A

coronary artery disease, so control the LDL to less than 100mg/dl

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29
Q

Headache, What is the most likely dx

migraine

A

visual disturbance (flasehs, sparks, stars, luminous hallucinations), photophobia, aura, relationshiop to menses, association with food (chocolate, red wine, cheese), precipitated by emotions, associated with nausea and vomiting

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30
Q

Headache, What is the most likely dx

cluster headache

A

frequent, short duration, high intesnity, headaches, with men affected 10 times more than women

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31
Q

Headache, What is the most likely dx

giant cell (temporal) arteritis

A

visual distubance, systemic symptoms such as muscle pain, fatigue, and weakness. jaw claudication

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32
Q

Headache, What is the most likely dx

pseudotumor cerebri

A

associated with obestiy, venous sinus thrombosis, oral contraceptives, and vitamin A toxicity. Mimics a brain tumor with nausea, vomiting, and visual distrubance

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33
Q

Physical Exam

tension headache

A

no physical finding

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34
Q

Physical Exam

migraine

A

no physical findings usually, but reare cases have aphasia, numbness, dysarthria, or weakness

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35
Q

Physical Exam

cluster headach

A

red rearing eye with rhinorrhea, horner syndrome occasionally

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36
Q

Physical Exam

giant cell (temporal) arteritis

A

visual loss, tenderness of the temporal area

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37
Q

Physical Exam

pseudotumor cerebri

A

papilledema with diplopia from sixth crnial nerve (abducens) palsy

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38
Q

evaluate for glaucoma with

A

a headach and a red eye

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39
Q

Diagnostic tests

tension, migraine, and cluster headaches

A

no specific diagnostic tests, do a head CT or MRI to exclude intracranial mass lesions if the diagnosis is unclear or the syndrome has recently started. there is no reason to perform imaging if there is a clear hx of headach of a particular type

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40
Q

Diagnostic tests

pseudotumor cerebri

A

the diagnosis cnnot be made wihtout a CT or MRI to exclude an intracranial mass lesion and a lumbar puncture showing increased pressure, CSF fluid is normal just higher pressure

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41
Q

Diagnostic tests

giant cell arteritis

A

markedly elevated ESR and the most accureate test is a biopsy

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42
Q

Treatment

tension headache

A

nsaids and other analgesics

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43
Q

Treatment

migraine

A

triptans or ergotamine as abortive therapy

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44
Q

Treatment

cluster headach

A

triptans, ergotamine, or 100% oxygen as abortive therapy

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45
Q

Treatment

giant cell temporal arteritis

A

prednisone

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46
Q

Treatment

pseudotumor cerebri

A

weight loss

acetazolamide to decrease production of cerebrospinal fluid

steroids help

repeated lumbar puncture rapidly lowers inracranial pressure

place a ventriculoperitoneal shunt or fenestrate (cut into) the optic nerve if medical therapy does not control it

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47
Q

it is critical to start steroids without waitng for biopsy in

A

giant cell arteritis

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48
Q

abortive therapy for migraine and cluster headache

A

both of these can be rapidly interrupted by either ergotamine or one of the triptans. the main idfference is that 100% oxygen, prednisone, and lithium are effective at interrupting cluster headaches but not migraines.

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49
Q

Provide cluster prophylaxis with

A

verapamil

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50
Q

prophylactic therapy for migraine

A

pts experiencing 3 or more migraine headaches per month should be starte don treatment to prevent them

propranolol is the best

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51
Q

other migraine preventative meds

A

ccb

tca

ssris, topiramate

botulinum toxin injection

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52
Q

Tension headach summary

A

b/l bandlike pressure

lasts 4-6 hours

normal pe

nsaids/tylenol

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53
Q

migraine summary

A

w/ or w/o aura

related to food emotions menses

rare: pahasia, numness, dysarthria

avoid triggers

nsaids

5ht1 agonists (triptans)

if 3 attacks/month
propranolol
sodium valproate

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54
Q

cluster headach summary

A

episodic pain

unilateral periorbital intense pain

lacrimation

eye reddening

nasal stuffiness

lid ptosis

sumatriptan

octreotide

oxygen

verapamil

prednisone

sodium valproate

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55
Q

trigeminal neuralgia unimproved by meds needs

A

gamma knife surgery

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56
Q

peripheral neuropathy treatment

A

there is no clear routinely effective treatment with postherpetic neuralgia

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57
Q

Trigeminal Neuralgia

definition

A

idiopathic disorder of the fifth cranial nerve resulting in severe, overwhelming pain in the face.

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58
Q

Trigeminal Neuralgia

presentation

A

attacks can be precipitated by shewing touching the face or pronouncing certain words in which the tongue strikes the back of the front teeth.

pts describe the pain as feeling as if a knife is being stuck into the face

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59
Q

trigem neuralgia

testing

A

no diagnostic test

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60
Q

trigem neuralgi

treatment

A

oxcarbazepine or carbamazepine

baclofen and lamotrigin have also been effective

gamma knife surgery or surgical decompression if meds dont work

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61
Q

Postherpetic Neuralgia

definition

A

hepres zoster reactivation, or shingles, is associated with a pain syndrome after resolution of the vesicular lesions in about 15% of cases

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62
Q

Postherpetic Neuralgia

treatment

A

antiherpetics like acyclovir famcyclovir, of valganciclovir reduce the incidence

steroids dont work!

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63
Q

Postherpetic Neuralgia

pain management

A

tca

gabapentin

pregabalin

carbamazepine

or phenytoin until an effective one is found

topical capsaicin is helpful

most antiepileptic meds have some beneficial effect in neuro pain but non work in more than 50-70% of pts

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64
Q

Prevention of herpes zoster (shingles)

A

zoster vaccine is indicated in all persons above the age of 60 to prevent shingles. this vaccin is similar to the varicella vaccine routinely administered to children to prevent chicken pox, except the dose is higher

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65
Q

gerneralized tonic-clonic seizures are caused by

A 
hypo or hypernatremia
hypoxia
hypoglycemia
any cns infection (encephalitis, meningitis, abscess)
any cns anatomic abnormality (trauma, stroke, tumor)
hypocalcemia
uremia (elevated creatinine)
hepatic failure
alcohol, barbiturate, and benzo w/drawal
cocaine toxicity
hypmagnesemia (rare)
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66
Q

Seizure diagnostic tests

A

an electoencephaloram would not be the right answer unless all of these tests wer done and were normal including a ct or mri ofth ehead

there is no point in doing an eeg to dientify the cause of a seizure if there is a clear metabolic, toxic, or anatomic defect causing the seizure

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67
Q

seizures of unclear etiology are called

A

epilepsy

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68
Q

confusion is to coma and seizure as angina

A

is to mi

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69
Q

treatment of status epilepticus

best initial therapy

A

benzos for a persistent seizure (lorazepam or diazepam iv)

if the seizure persists then give phenytoin or fosphenytoin

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70
Q

phenytoin and fosphenytoin

A

have the same efficacy but fosphenytoin has fewer side effects

like lidocaine phenytoin is a class 1b antiarrhythmic, and when given iv it is associated with hypotension and AV block

fosphenytoin does not do this and so it can b given rapidly

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71
Q

if benzos and phenytoin and fosphenytoin do not stop the seizure

A

administer phenobarbital

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72
Q

ultimate therapy for unresolving siezure is to use

A

a neuromuscular blocking agent like succinylcholine vecuronium or pancuronium to allow you to intubate the pt and then give genreal ansethesia such as midazolam or propofol. the pt must be placed on a ventilator before propafol

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73
Q

partial seizure

A

like the name implies this is a seizure that is focal to one part of the body. for instance, a ptmay have a seizure that is limited just to an arm or leg. partial seizures can either be simple (intact consciousness) or complex (loss or alteration of consciousness)

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74
Q

tonic-clonic seizure

A

this is a generalized seizure with varying phases of muscular rigidity (tonic) followed by jerking of th emuscles of the body for several minutes (clonic)

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75
Q

absence (petit-mal) seizures

A

consciousness is impaired only briefly. the pt often remains upright and gives a nomral appearance or seems to be staring into space, occur more often in children

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76
Q

treatment of status epilepticus treatment

A
  1. benzos
  2. fosphenytoin
  3. phenobarbital
  4. general anesthesia
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77
Q

indications for treatment of seizuresbe

A

status eplepticus or with focal neurological signs

abnormal eeg or lesion on CT

family hx of seizures

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78
Q

do you start seizure meds after first seizure

A

no

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79
Q

treatment of epilepsy

A

best treatment is not clear

levetiracetam, phenytoin, valproic acid, and carbamazepine are all eqully effective

alternate treatment with gabapentin, topiramate, lamotrigine, oxcarbazepine or levetericatam

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80
Q

what antiseizure med has the least amount of side effects

A

levetericatem

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81
Q

ethosuximid is the best therapy for

A

absence seizures

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82
Q

if seizures are not treated by changing meds or adding a second med

A

surgery

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83
Q

alcohol withdrawal seizure treatment

A

benzos

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84
Q

discontinuing seizure med

A

pt must be seizure free for 2 years

sleep deprivation eeg is best way to tell if there is possibility of recurrence (can elicit abnomral activity but not very specific)

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85
Q

Subarachnoid Hemorrhage

Definition/etiology

A

caused by rupture of an aneurysm tht is usually located in the anterior portion of the circle of willis. aneurysms ware present in 2% of routine autopsis. the vast majority never rupture

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86
Q

Subarachnoid Hemorrhage

is most frequent with

A

polycystic kidney disease

tobacco smoking

htn

hyperlipidemia

high alcohol consumption

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87
Q

Subarachnoid Hemorrhage

what is the most likely diagnosis

A

look for the sudden onset of an extremely severe headachwith menigneal irritation (stiff neck, photophobia) and fever. fever is secondary to blood irritating the meninges. loss of consciousness occurs in 50% from the sudden increase in intracranial pressure. focal neurological complications aoccur in as many as 30%

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88
Q

how sah differs from meningitis

A

very sudden onset

loss of consciousness

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89
Q

Subarachnoid Hemorrhage

best initial test

A

ct w/out contrast (95%) sensitive

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90
Q

Subarachnoid Hemorrhage

most accurate test

A

lumbar puncture showing blood

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91
Q

Subarachnoid Hemorrhage

LP

A

may show xanthochromia, which is a yellow discoloration of CSF fromt he breakdown of red blood cells in the CSF. LP is necesary only for the 5% that have a false negative CT scan. CSF may have an increaed WBC which may mimic meningitis but the ratio of RBC to WBC will be normal

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92
Q

normal WBC to RBC

A

1 WBC to 500-1000 RBC

93
Q

contrast on head CT

A

improves detection of mass lesions like cancer or abscess

dont use contrast when looking for blood

94
Q

Ekg with intracranial bleeding

A

may show large or inverted T waves suggestive of myocardial ischemia (cerebral T waves). this is thought o be from excessive sympathetic activity

95
Q

Angiography with Intracranial bleeding

A

determines the site of the aneurysm in order to guide repair of the lesion

96
Q

Subarachnoid Hemorrhage

treatment

A

no way to reverse the hemorrhage

97
Q

Subarachnoid Hemorrhage

nimodipine

A

(calcium chanel blocker) prevents subsequent ischemic stroke

98
Q

Subarachnoid Hemorrhage

embolization

A

(coiling) uses a catheter to gloc up the site of lbeeding to prevent a repeated hemorrhage. an interventional neuroradiologist places platinum wire into the site of hemorrhage. embolization is superior to urgical clipping in terms of survival and complications

99
Q

Subarachnoid Hemorrhage

ventriculoperitoneal shunt

A

SAH is associated with hydrocephalus. place a shunt only if hydrocephalus develops

100
Q

Subarachnoid Hemorrhage

seizure prophylaxis

A

phenytoin is generally given to prevent seizures. if the question asks “which of the following is indicated?” antiepileptic therapy is the answer, although controversial

101
Q

bacterial meningitis treatment

A

ceftriaxone and vancomycin

102
Q

Amterio spinal artery infarction

A

loss of all function except for the posterior column (poistion and vibratory sensation intact)

flaccid paralysis below the level of the infarction

loss of deep tendon relfexes (DTRs) at the level of the infarction

evolves into spastic paraplegia several weeks later

loss of pain and temp

extensor plantar response

103
Q

Subacute combined degeneration of the cord

A

from b12 deficiency or neurosyphilis

position and vibratory sensation are lost

104
Q

Spinal trauma

A

acute onset of limb weakness and/or sensory disturbance below the level of th einjury with the severity in proportion to the degree of injury.

sphincter function impaired

loss of DTRs at the level of the injury followed by hyperreflexia below the level of the trauma.

105
Q

spinal trauma initial treatment

A

glucocorticoids

106
Q

Brown-Sequard Syndrome

A

after unilateral hemisection of the spinal cord you lose pain and temperature on the contralateral side from teh injury and lose motor function, position and vibratory sense on the ipsilateral side of the injury

107
Q

Syringomyelia

definition/etiology

A

fluid filled dilated cenral canal in the spinal cord. this wiedening buble or cavitation first damages neural fibers passing near the center of the spine.

cause by tumor or sever trauma tot he spine or is congenital

108
Q

Syringomyelia

what is the most likely diagnosis

A

look for the loss of pain and temp bilaterally across teh upper back and both arms.

look for the phrase capelike distribution of deficits

also cause lack of reflexes and muscle atrophy in the same b/l distribution

109
Q

Syringomyelia

diagnostic tests

A

mri is the most accurate test

110
Q

Syringomyelia

treatment

A

surgical removal of tumor if present and drainage of fluid from the cavity

111
Q

Brain Abscess

definition

A

collection of infected material within the parenchyma of the brain tissue acting as a space-occupying lesion

112
Q

Brain Abscess

etiology

A

can spread from contiguous infection in the sinuses, mastoid air cells, or otitis media.

anything that leads to bacteremia can allow infected material to lodge in the brain

pneumonia and endocarditis cause bacteremia which causes brain abscess

113
Q

Brain Abscess

presentation

A

look for headache, nausea, vomiting, fever, seizures, and focal neurological findings

no way to distinguish from cancer w/o biopsy

cancer can give a fever

114
Q

Brain Abscess

best initial test

A

head ct or mri will show a ring or contrast enhancing lesion that will ikely have surrounding edema and mass effect

115
Q

Brain Abscess

most accurate test

A

brain biopsy

116
Q

in the brain, cancer and infection are indistinguishable based on

A

an imaging study alone

117
Q

Brain Abscess

CSF

A

unlikely to be helpful and lp is ci bc of the possibility of herniation

118
Q

Brain Abscess

Microbiology

A

Biopsy is essential to distinguiash abscess from cancer as well as to determine the organism and its sensitivity

can be staph stre gram neg and anaerobs

frequently mixed bugs so a precise dx is important given that duration of treatment is long (6-8 weeks iv, 2-3 months orally)

119
Q

Brain Abscess

Treatment

A

empiric therapy with penicllin plus metro plus ceftraixone (or cefepime) is acceptable while waitin gfor the results of culture.

vanco can be sued instead of penicillin particularly if there has been recent neurosurgery and the risk of staph is greater

120
Q

Tuberous Sclerosis

Neurological abnormalities

A

seizures

progressive psychomotor retardation

slowly progressive mental deterioration

121
Q

Tuberous Sclerosis

skin

A

adenoma sebaceum (reddend facial nodules)

shagreen patches (leathery plaques on the trunk)

ash leaf (hypopigmented patches)

122
Q

Tuberous Sclerosis

other lesions

A

retinal lesions

cardiac rhabdomyomas

123
Q

Tuberous Sclerosis

treatment

A

no specific treatment, control seizures

124
Q

Neurofibromatosis

A

von recklinhausen disease

neurofibromas

eight cranial nerve tumors

cutaneous hyperpigmented lesions (cafe au lait spot)

meningioma and gliomasTuberous Sclerosis

125
Q

Neurofibromatosis

treatment

A

there is no specific treatment

eight crnial nerve lesions may need surgical decompresion to help preserve hearing

126
Q

Sturge-Weber Syndrome

A

port wine stain of the face

seizures

homonymous hemianopsia

hemiparesis

mental subnormality

skull xray shows calcification of angiomas

tbere is no treatment beyond controlling seizures

127
Q

Neurofibromas

A

soft

flesh colored

attached to peripheral nerves

128
Q

Essential Tremor

A

occurs at both rest and with intention (reaching for things) the remor is gretes in the hands, but can affect the head as well, exam is otherwise normal. the tremor may affect some manual skills such as hadnwriting or the use of a computer

129
Q

Essential Tremor

what makes it worse

A

caffeine

130
Q

Essential Tremor

best therapy

A

propranolol

gets better with alcohol

131
Q

Parkinsonism

definition

A

the loss of cells int he substantia nigra resulting in a decrease in dopamine which leads to a significant movement disorder presenting with tremor gait distrubance and rigidity

132
Q

Parkinsonism

etiology

A

head traua

anitpsychoitic (thoazine)

encephalitis

reserpine

metoclopromide

idiopathic

133
Q

Parkinsonism

most common cause

A

idiopathic

134
Q

Parkinsonism

diagnosis

A

no test, clearly on clinical presentation

135
Q

Parkinsonism

presentation

A

50-60

tremor, rigidity, bradykinesia, shuffling gate and a lot of falls

cogwheel rigidity is the slowing of movement on passive lfexion or extension

limited facial expression (hypomimia)

small writing (micrographia)

postural instability is orthostatic hypotension

syncope

136
Q

most frquent Parkinsonism questions

A

treatment

137
Q

Parkinsonism Treatment

antihcholinergics

A

mild disease

benztropine and trihexyphenidyl

relieve tremor and rigidity

unclear why it works

ae are dry mouth, worse bph and consitpation

138
Q

Parkinsonism Treatment

amantadine

A

mild disease

increase release of dopamine from substantia nigra

give to pts older than 60 who dont tolerate anticholinergis

139
Q

Parkinsonism Treatment

dopamine agonists

A

severe disease

pramipexole and ropinirole

best initial treatment for severe disease

140
Q

Parkinsonism Treatment

levodop/carbidopa

A

severe disease

most effective med

associated with on/off phenomena which results in episodes of insufficient dopamine (off) characterized by bradycardia

use if pt has this on/off thing

141
Q

Parkinsonism Treatment

COMT inhibitors

A

severe disease

tolcapone and entacapone

extend the duration of levodopa/carbidopa by blocking hte metabolism of dopamine

use only with carbidopa/levodopa

142
Q

Parkinsonism Treatment

MAO inhibitors

A

severe disease

rasagiline selegiline

on its own or adjunct to lveodopa/carbidopa

block metabolism of dopamine

143
Q

Parkinsonism Treatment

deep brain stimulation

A

severe disease

electrical stimulation is highly effective for tremors and rigidity in some pts

144
Q

avoid what with mao inhibitors

A

tyramine containing foods (chees e)

they precipitate hypertension

145
Q

what slows the prpgression pf parkinsonism

A

mao inhibitors

146
Q

lewy body dementia

A

parkinsonism with dementia

147
Q

shy-drgaer syndrome

A

parkinsonism predominantly with orthostasis

148
Q

pt with sever parkinsonism presenting with psychosis and confusion

A

cant stop parkinson drugs bc pt will get bradykinesia, use antipsychotics with fewest effects (clozapine)

149
Q

spasticity

A

painful contracted muscles form damage to the central nervous system is called spasticity

associated with ms

baclofen, dantrolen and the cnetral acting alpha agonsit tizanadine may all owrk

150
Q

Restless leg syndrome

A

pts rpeort an uncomfortable sensation in the legs that is creepy and crawly at night

worsened by caffeine

releived by moving the legs

can kick while sleeping

151
Q

Restless leg syndrome

treatment

A

treat with dopamine agonists like pramipexole

152
Q

Huntington Disease

definition/etiology

A

hereditary disease characterized by CAG trinucleotide repeat sequences on chromosome 4

153
Q

Huntington Disease

what is the most likely diagnosis

A

choreaform movement disorder (dyskinesia)

dementia

behavior chagnes (irritability, moodiness, antisocial behavior)

onset between the ages of 30 and 50 with a familyx

154
Q

Huntington Disease

movement disorder

A

starts with fidgetiness or restlessness progressing to dystonic posturing rigidity and akinesia

155
Q

Huntington Disease

diagnostic test

A

specific genetic test, 99% sensitive, cag tri repeat

sx triad of movement memory and mood

156
Q

Huntington Disease

treatment

A

no treatment can reverse it

dyskinsease is treted with tetrabenazine

pyschosis is treated with haloperidol quetiapine or a trial of different antipsychotics

157
Q

Huntington Disease

ct or mri of head show

A

caudate nucleus involvement

158
Q

Tourette Disorder

idopathic disorder of:

A

vocal tics, grunts, and coprolalia

motor tics (sniffing, blinking, frowning

obsessive-compulsive behavior

159
Q

Tourette Disorder

dx

A

no specific diagnostic tests

160
Q

Tourette Disorder

treatment

A

fluphenazine, clonazepam, pimozide, or other neuroleptic mediaction

methylphenidate and ADHD treatment are intrinsic to Tourette Disorder management

161
Q

Multiple Sclerosis

definition

A

idiopathic disorder exclusively of CNS white matter

mre common in white women who live in colder climates

162
Q

Multiple Sclerosis

What is the most likely diagnosis

A

multiple neurological deficits

most common presentation is focal sensory sx with gait and balance problems

blurry bision or visual distubrance form optic neuritis is no longer as common as the first presentation

163
Q

Multiple Sclerosis

most common abnormalities

A

optic neuritis then motor and sensory

164
Q

Multiple Sclerosis

least common abnormalities

A

cognitive defects and dementia

sexual function remains rleatively intact

165
Q

Multiple Sclerosis

other findings

A

fatigue

spasticity and hyperreflexia

cerebellar deficits

166
Q

internuclear ophthalmoplegia (INO)

A

is the inability to adduct one eye with nystagmus in the other eye

characteristic of ms

167
Q

Multiple Sclerosis

diagnostic tests

A

mri is best initial and most accurate

lp show csf with amild elevatin in protein and fewer than 50-100 WBCs . oligoclonal bands are found in about 85% of pts but ar enot specific to ms

168
Q

oligoclonal bands are the answer

A

in the 3-5% of pts with equivocal or nondiagnostic MRI

169
Q

Multiple Sclerosis

treatment, best initial for acute disease

A

high dose steroids

170
Q

Multiple Sclerosis

drugs that prevent relapse and progression

A 
glatiramer (copolymer 1)
beta-interferon
fingolimod (oral)
natalizumab
mitoxantrone
azathiprine
cyclophospamid
171
Q

in ms steroids do what

A

shorten the duration of exacerbation

172
Q

natalizumab

A

inhibitor of alpha 4 intergrin

development of progresive mutlifocal leukoencephalopathy (PML) (multiopel white atter hypodense lesions)

173
Q

Multiple Sclerosis

best choice for prevetnion of relapse

A

glatiramer and beta interferon

174
Q

Motor Neuron Disease and Amyotrophic Lateral Sclerosis

Definition/etiology

A

the cause of als is unknow it is a loss exclusively of upper and lower motor neurons

175
Q

Motor Neuron Disease and Amyotrophic Lateral Sclerosis

what is the most likely diagnosis

A

weakness of unclear etiology starting int he 20s to 40s with a unique combination of upper and lower motor neuron loss

176
Q

Motor Neuron Disease and Amyotrophic Lateral Sclerosis

most serious presentation

A

difficulty in chewing and swallowing and a decrease in gag reflex, leads to pooling of saliva in the pharynx and frequent episodes of aspiration

a weak cough and loss of swallowing are also bad

177
Q

Motor Neuron Disease and Amyotrophic Lateral Sclerosis

sensory and sphincters

A

are spared

178
Q

Motor Neuron Disease and Amyotrophic Lateral Sclerosis

umn presentation

A

weakness

spasticity

hyperreflexia

extensor plantar responses

179
Q

Motor Neuron Disease and Amyotrophic Lateral Sclerosis

lmn presentation

A

weakness

wasting

fasciculation

180
Q

in als the most common cause of death is

A

respiratory failure

181
Q

Motor Neuron Disease and Amyotrophic Lateral Sclerosis

diagnostic tests

A

elecromyography reveals loss of neural innervation in multiple muscle groups

cpk levels are elevated

182
Q

Motor Neuron Disease and Amyotrophic Lateral Sclerosis

treatment

A

riluzole reduces glutamate bluidup in neurons and may prevent progression of disease

baclofen treats spasticity

cpap and bipap help with resp diff secondary to muscle weakness

tracheostomy and maintenance on a ventilator is necessary with advanced disease

183
Q

Charcot-Marie tooth disease

definition

A

genetic disorder with loss of both mtor and sensory innervation

184
Q

Charco-Marie tooth disease

presentation

A

distal weakness and sensory loss

wasting in the legs

decreased deep tendon relfexes

tremor

pes cavus (foot deformity with a high arch)

legs look like inverted champagne bottles

185
Q

Charco-Marie tooth disease

most accurate test

A

electromyography

186
Q

Charco-Marie tooth disease

treatment

A

none

187
Q

Peripheral Neuropathy

most common cause

A

diabeetus

188
Q

Peripheral Neuropathy

other causes

A

uremia

alcoholism

paraproteinemias like moncolonal gammopathy of unkown significance

189
Q

Peripheral Neuropathy

best initial therapy

A

pregabalin or gabapentin

tca and most seizure meds are effective in some people

190
Q

ulnar Neuropathy

precipitating event

manifestations

A

biker, pressure on palms of hands, trauma to the medial side of elbow

wasting of hypthenar eminence, pain in fourth and fifth fingers

191
Q

radial Neuropathy

precipitating event

manifestations

A

pressur eof inner, upper arm. falling asleep with arm over back of chair, using crutches and pressure in the axilla

wrist drop

192
Q

lateral cutanesou nerv of thigh Neuropathy

precipitating event

manifestations

A

obesity, pregnancy, sitting with crossed legs

pain/numbness of outer aspect of one thigh

193
Q

tarsal tunner (tibial nerve) Neuropathy

precipitating event

manifestations

A

worsens with wlaking

pain/numbness in ankle and sole of foot

194
Q

peroneal Neuropathy

precipitating event

manifestations

A

hgih boots, pressur eon back of knee

weak foot with decreased dorsiflexion and eversion

195
Q

MEdian Neuropathy

precipitating event

manifestations

A

typists, carpenters, working with hands

thenar wasting, pain/numbness in first 3 fingers

196
Q

Facial (7th cranial) nerver palsy or bell palsy

etiology

A

most are idiopathic can be from lyme sarcoidosis herpes or tumors

197
Q

Facial (7th cranial) nerver palsy or bell palsy

presentation

A

paralysis of the entire side of the face is classic

stroke will paralyze only the lower half of the face bc the upper havlf of the race receives innervation from both cerebral hemispheres

difficulty closing the eye

if pt can wrinkle forhead worry about stroke

198
Q

Facial (7th cranial) nerver palsy or bell palsy

2 additional features

A

hyperacusis: sounds are extra loud bc the 7th cranial nerve nromally supplies the stapedius muscle which acts as a shock absorber on the ossicels of the middle ear

tast disturbances: the sevent cranial nerve supplies the senastion of taste the anterior 2/3rds of the tongue

199
Q

Facial (7th cranial) nerver palsy or bell palsy

what is the most likely dx

A

face feels stiff

pulled to one side

200
Q

Facial (7th cranial) nerver palsy or bell palsy

diagnostic tests

A

no test is usually done

most accurate test is electromyography and nerve conduction studies

201
Q

Facial (7th cranial) nerver palsy or bell palsy

treatment

A

most pts have full recovers w/o treatment

best initianl therapy is prednisone

202
Q

Facial (7th cranial) nerver palsy or bell palsy

most common complication

A

corneal ulceration bc it is hard to close the eye

203
Q

Acute Inflammatory Polyneuropathy (guillan-barre syndrome)

definition

A

autoimmune damage ofmultiople peripheral nerves

no cns involvment

a circulating antibody attacks the myelin sheaths of the peripheral nerves removing theri insulation

204
Q

Acute Inflammatory Polyneuropathy (guillan-barre syndrome)

associated with

A

campylobacter jejuni infection

205
Q

Acute Inflammatory Polyneuropathy (guillan-barre syndrome)

what is the most likely dx

A

look for weakness in the legs that ascends from the feet and moves toward the chest, associated with a loss of DTRs. a few pt have a mild sensory disturbance. the main problem is that hwen GBS hits the diaphragm, it is assocaited with respiratroy muscle weakness. Autonomic dysfunction with hypotension, hypertension, or tachycardia can occur

206
Q

ascending weakness + loss of reflexes =

A

GBS

207
Q

Acute Inflammatory Polyneuropathy (guillan-barre syndrome)

diagnostic tests

A

the most specific diagnostic test is nerve conduction studies/electromyography

these show a decrease in the propagation of electrical impulses along the nerves, but it takes 1-2 weeks to become abnormal

csf shows increased protein with a normal cell count

208
Q

Acute Inflammatory Polyneuropathy (guillan-barre syndrome)

Tests of mrespiratory muscle involvement

A

when the diaphragm is involved there is a decreae in forced vital capacity and peak inspiratyor pressure. inspiration is the active part of breathing and the pt loses the strength to nhale. pfts tell who might die from BGS

209
Q

Acute Inflammatory Polyneuropathy (guillan-barre syndrome)

treatment

A

intravenous immunoglobulin or pasmapheresis are equal in efficacy, dont combine them

210
Q

what does not help GBS

A

prednisone

211
Q

most urgent thing to do in GBS

A

pfts, peak inspiratoyr pressure or decrease in fvc are signs of resp doom

212
Q

Myasthenia Gravis

definition

A

disorder of muscular weakness from the production of antibodies against acetylcholine receptors at the neuromuscular junction

213
Q

Myasthenia Gravis

presentation

A

double vision

difficulty chewing

dysphonia or weakness of limbs worse at the end of the day

214
Q

Myasthenia Gravis

pe

A

psosis

weakness with sustained activity

normal pupillary response

215
Q

severe Myasthenia Gravis affects

A

respiratory muscles

216
Q

Myasthenia Gravis

best initial test

A

acetylcholine receptor antibodies (80-90% sensitive).

this is a better first answer than edrophonium testing

for pts w/o those antibodies get anti-musk antibodies (muscle specific kinase)

217
Q

Myasthenia Gravis

edrophonium

A

short acting inhibitor of acetylcholinesterase. the bump up in acetylcholin levels is associated with aclear improvement in motor function that lasts for a few minutes

218
Q

Myasthenia Gravis

most accurate test

A

electromyogrpahy shows decreases strength with repetitive stimulation

219
Q

Myasthenia Gravis

what imaging should be done

A

chest cray ct or mri are done to look for thymom or thymic hyperplasia

ct with contrast is best

220
Q

Myasthenia Gravis

best initial treatment

A

neostigmine or pyridostigmine these are longer acting versions of edrophonium

221
Q

Myasthenia Gravis

most appropriate next step after neo and pyridostigmine

A

thymectomy if pt isunder age 60

if over age 60 use prednisone

azathiprine tacrolimus cyclophosphamide or mycophenolate are used in order to get the pt off of steroids before serious adverse effects occur

want to suppress t cell function in order to control antibodies made against acetylcholine receptors

222
Q

deat from gbs

A

is rare but is from dysautonomia and respiratory failure

223
Q

Myasthenia Gravis

management of acute crisis

A

presents with severe overwhelming disease with profound weakness or respiratory involvmeent it is treated with ivig or plasmapheresis

224
Q

Dementia

A

alzheimer’s disease is by far the most commonc ause of dementia. since there is no specific test for alzheimers disease your challenge is to know how far to go in testing to diagnose it and what the other dementia syndromes are

225
Q

Dementia

Diagnostic testing

A

mri of brain

vdrl or rpr to exlude syphilis

b12 with possible methylmalonic acid level

thyroid function test

226
Q

Dementia

treatment

A

donepezil, rivastigmine, and galantamine are equal in efficacly all increase acetylcholine levels

memantine

227
Q

Dementia

lewy body dementia

A

assocaited wiht parkinsons disease

treat both parkinsons disease and alzheimer’s disease with levodopa/carbidopa

228
Q

frontotemporal dementia

A

emotional and socail appropriateness are lost first

memory deteriorates later

no special therpy beyond ach medications

229
Q

Creutzfeldt-jakob disease

A

rapidly progressive dementia

myoclonic jerks

normal head mri or ct

csf with 14-3-3 protein

biopsy is most accurate

no specific therapy

OMS III (21 decks)

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