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Clinical Med > post midterm 6: neurology and HA > Flashcards

post midterm 6: neurology and HA Flashcards

1
Q

what kind of HA s do you get in pseudotumor cerebri?

A

Headache (94%) is daily, severe, pulsatile, lasting hours

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2
Q

what are some miscellanous possible causes of pseudotumor cerebri?

A

Anabolic steroid abuse
Systemic lupus erythematosis
Drugs: isotretinoin (Acutane)

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3
Q

what are some endocrine/metabolic issues with pseudotumor?

A

Adrenal insufficiency or glucocorticoid withdrawal
Hypoparathyroidism
Vitamin A intoxication

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4
Q

T/F: can get transient vis obscurations with pseudotumor?

A

true

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5
Q

cerebral vein thrombosis affects what pop?

A

Disease of children and young adults primarily
Rare: 3 - 4 cases per million population
75% of cases in young adults are women
Attributable to oral contraceptives and childbirth

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6
Q

what kind of findings do you see in those with cerebral vein thrombosis?

A
  • Headache
  • Neurological signs in 50% of patients
  • Seizures in 40% of patients
  • Papilledema if accompanied by ↑ intracranial pressure
  • Ocular symptoms in cavernous vein thrombosis
  • Periorbiral edema
  • Proptosis
  • EOM paralysis
  • Fevers if infectious
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7
Q

what causes migraines?

A

Triggering event(s) uncertain
-Involves brainstem, trigeminal nerve (ophthalmic branch), thalamus
Exact causes of pain remain to be elucidated
? vascular; ?dura

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8
Q

what are the 3 types of migraines?

A

Migraine without aura
Migraine with aura
Retinal migraine

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9
Q

T/F: can actually get migraine from de-stressing

A

true

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10
Q

how are triptans used for migraines?

why should they be used cautiously?

A

Effects: cranial vasoconstriction, neuronal inhibition

**Precautions in patients at risk for CAD/CVA due to vasoconstrictive effects (eg older age, smoker, HTN)

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11
Q

what is the main concern with tx of migraines?

A

can get rebound with overuse

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12
Q

who gets tension type HAs?

A

-Most common primary headache disorder
-Prevalence in population is significant
Women > Men
Onset 2nd decade

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13
Q

describe the pain associated with tension HAs

A 
Pain usually bilateral
Pressing or tightening in quality
“Band around my head”
Mild or moderate intensity
Not increased with physical activity
Photo- and/or phonophobia may be present
Headache duration 30 minutes to 7 days
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14
Q

what are classified as secondary HAs?

A

Headaches attributed to disorders of the eyes:

  • Acute glaucoma
  • Ocular inflammatory disorders
  • Refractive errors
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15
Q

If HAs are caused by ref error, how long should they last after corrected?

A

Headache and eye pain resolve within 7 days after correction of refractive error

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16
Q

Myasthenia is assoc with what other clinical disorders/problems?

A
  • Associated with thymoma or thymic hyperplasia
  • Associated with other autoimmune disorders
  • Exacerbated by hyperthyroidism, infection, other illness, some drugs (eg aminoglycoside antibiotics)
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17
Q

what is myasthenia gravis and what pops does it occur in?

A

*Anti-acetylcholine receptor antibodies blocking neuromuscular transmission

Peak incidence: women in the 3rd and 4th decade men in the 6th and 7th decade
Female to male ratio 3:2

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18
Q

what is the Edrophnium test (short-acting anticholinesterase)
for MG?

A

Increases acelcholine in neuromuscular junction

IV edrophonium given – positive test if improvement

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19
Q

how can you dx MG clinically?

A

1) Repetitive stimulation – decreasing amplitude of muscle action potentials (EMG)
2) Laboratory: Anti receptor antibodies 80% patients, 50% if eye symptoms only
3) Thyroid function tests
4) Pulmonary function tests
5) Chest CT or MRI (assess thymus gland)

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20
Q

Bell’s is typically found in what pop?

A

Female : Male = 1:1
Onset at any age
Median age 40
Incidence is higher in older people

21
Q

what is Bell’s palsy?

A

Unilateral facial nerve paralysis
Peripheral nerve
Acute onset
Idiopathic

22
Q

how will a peripheral vs central lesion affect the facial nerve?

A

Peripheral lesion: Upper AND lower facial nerve paralysis

Central lesion: Upper facial function preserved; lower facial weakness

23
Q

when should you get an MRI for Bell’s?

what is the prognosis?

A

Further evaluation (MRI imaging) if no response within 3 to 6 weeks
Recovery: 71%
Near-normal recovery: 84%

24
Q

how can you tx Bell’s palsy?

A
  • Oral glucocorticoid + HSV antiviral (valacyclovir/famciclovir)
  • Lyme antibodies – many initiate empiric treatment (can stop if Abs neg)
  • Taping of eyelid +/- artificial tears
25
Q

how long does recovery take for optic neuritis?

A

~4weeks

26
Q

what signs are assoc with optic neuritis?

A
  • Decreased visual acuity
  • Impaired color vision
  • Visual field defects
  • -Central or paracentral scotomata
  • -Constriction of fields
  • -Quadrantic or altitudinal defects
  • -Bitemporal hemianopia (with chiasmal involvement)

-RAPD

27
Q

what is MS?

A

A disease limited to the central nervous system and characterized by multiple demyelinating lesions distributed in both space and time
-by def, it is recurrent with multiple plaques

28
Q

MS is common in what pop?

A

females, 20-40, higher socioeconomic group, in temperate climate

29
Q

what are some presenting signs in MS:

A
  • Optic neuritis (unilateral)
  • Diplopia (internuclear ophthalmoplegia)
  • nystag and dizziness
  • Sensory / motor abnormalities
  • Lhermitte’s sign
  • Ataxia
  • Vertigo
  • Bowel / bladder symptoms
  • Sexual dysfunction
30
Q

what is Lhermittes sign?

A

(Paresthesias in limb w/ neck flexion)

Can be seen in other causes of cervical cord compression

31
Q

what is the prognosis for vision? does it recur?

A
  • 90% with previously normal vision improve to 20/40 or better at 1 year
  • ONTT: 64% of patients with light perception improved to 20/40 or better
  • Residual deficits in color vision are common
  • Residual optic atrophy (despite 20/20 vision)
  • Recurrence: ONTT 35% at 10 years
32
Q

what is Uhtoff’s symptom?

A

Worsening symptoms seen at elevated body temperature

33
Q

how can you diagnose clinically MS?

A

1) Appropriate history of exacerbations/remissions of symptoms and signs that cannot be explained by a single CNS lesion.
2) CSF abnormalities (oligoclonal bands, increased IgG) - not specific
3) Abnormal visual evoked responses
4) Cranial MRI can demonstrate lesions silent clinically or on CT

34
Q

what is prognosis in MS?

A
  • *Prognosis is highly variable
  • 20-35% exhibit a relatively benign overall course
  • 5% have isolated acute attack without recurrence
  • 3-12% exhibit an aggressive, downhill course with significant disability within 1 year
  • unfortunately damage is cumulative each time it recurs
35
Q

how can you treat MS?

A

*High-dose glucocorticoids (methylprednsolone IV)
Hasten recovery from acute attacks
May reduce frequency of recurrent optic neuritis
Recurrence may be INCREASED with initial Rx of oral prednisone
No effect on natural history of underlying disease
-immunotherapy

36
Q

what is transverse myelitis?

A

Sudden onset of motor and sensory deficits attributable to involvement of the entire area of the spinal cord at a particular level

  • Spastic paraplegia below lesion
  • Sensory deficits
37
Q

what is Neuromyelitis optica (Devic’s disease)?

A

Bilateral (80%) optic neuritis
Transverse myelitis
May resolve or relapse (and progress)
Probably some overlap of cases with MS

38
Q

what can trigger transverse myelitis?

A

May occur after neurosurgery or viral illness

Similar in presentation to multiple sclerosis

39
Q

what is Adrenoleukodystrophy (ALD)?

A

A spectrum of disorders of lipid metabolism

Most common form of peroxisomal fatty acid oxidation

40
Q

what clinical features are associated with Adrenoleukodystrophy (ALD)?

A

CNS demyelination
Adrenal insufficiency
Hypogonadism

41
Q

what is Acute Disseminated Encephalomyelitis?

A

A rare complication in childhood of certain viral infections / vaccinations

*Presents as acute illness up to 2 weeks after initial viral illness

Symptoms: fever, vomiting, headache, stiff neck, neurologic deterioration
**Cranial neuropathies including optic neuritis may occur

Most children recover
Neurological deficits may persist in a minority

42
Q

Progressive Multifocal Leukoencephalopathy occurs in what kind of people? causes what?

A

immunocompromised

  • Progressive, multiple neurologic deficits
  • Caused by JC virus infection
43
Q

what happens in measles virus? stages?

A

1) Prodromal phase
-Fever, dry cough, *conjunctivitis, *photophobia
2) Koplik spots=hallmark
Gray/white spots oral mucosa
3) High fever / rash
Temp 104
Erythematous rash begins on neck, face; spreads to feet
Duration 2 days – resolves in the order of appearance

44
Q

what are the clinical findings in rubella?

A

Clinical findings:
Neck lymphadenopathy
Rash; begins on face, spreads, gone after 3 days

Human only natural host

45
Q

when are you at risk for congenital rubella? what triad is assoc with it?

A 
First trimester primary risk
Triad:
Ocular abnormalities
Cataract
Salt and pepper pigmentation of fundus 
Hearing loss
Cardiac abnormalities
46
Q

what is Subacute Sclerosing Panencephalitis (SSPE)? how do you dx it?

A

Progressive, degenerative disease of CNS
Reactivation of latent measles virus infection

Diagnose:
Brain imaging reveals atrophy
Cerebrospinal fluid - high IgG levels, antibodies to measles

47
Q

list 3 nutritional and metabolic conditions that can cause Optic Neuropathy

A

Diabetes mellitus

Pernicious anemia

Thyroid ophthalmopathy

48
Q

list some vascular disorders that can cause Optic Neuropathy

A

Giant-cell arteritis
Atherosclerosis
Systemic lupus erythematosis
Polyarteritis nodosa

(*sarcoid can also be granulomatous cause)

49
Q

what are some infectious causes of optic neuropathy

A

syph and lyme disease

Clinical Med (10 decks)

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