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NEURO CLERKSHIP > Spinal Cord, sleep disorders, movement disorders > Flashcards

Spinal Cord, sleep disorders, movement disorders Flashcards

1
Q

where is artery of adamkiewicz?

A

at T10 major source for lower cord

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2
Q

do polyneuropathies have a truncal sensory level?

A

no that’s what makes spinal lesions different

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3
Q

what is lhermitte sign?

A

electric like sensation extending down back and into arms with neck flexion
(seen with focal cevical lesions most notably demyelinating)

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4
Q

what important dysfunction is very prominent in spinal cord lesions?

A

urinary urgency/incontinence

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5
Q

kernig vs. brudinski?

A

kernig- painful knee extension/resistance with hips and knees flexed
brudinski- involuntary lifting of legs with neck flexion in spine position

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6
Q

what is- initial flaccid paraplegia or quadriplegia depending on location of artery occlusion followed by the flaccidity converting to spasticity with increased reflexes and Babinski signs. Sensory loss is dissociated with loss of pain and temperature and sparing of vibration, position sense, and partially touch. Bladder and bowel function are impaired.

A

anterior spinal artery syndrome

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7
Q

is anterior spinal artery syndrome or posterior spinal artery syndrome more common?

A

anterior spinal artery

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8
Q

Classically, presents with pain and temperature loss in cape distribution, weakness/atrophy in arms, and, ultimately, corticospinal and dorsal column dysfunction below lesion?

A

syringomyelia- cavity within the cord, sometimes with chiari 1

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9
Q

what is progressive involvement of corticospinal tracts and dorsal columns with increased reflexes, Babinski signs, and loss of position and vibration? what are the 3 most common causes?

A

subacute degeneration

  • vitamin B12- anemia post gastric surgery
  • copper deficiency- post gastric surgery or zinc toxicity
  • Vitamin E deficiency- post gastric, CF, abetalipoproteinemia
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10
Q

what is hereditary spacstic paraparesis? autosomal dominant or recessive or x-linked

A

degeneration of distal corticospinal axons and dorsal column degeneration and manifested primarily by slowly progressive spastic paraparesis

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11
Q

what do patients with hereditary spastic paraparesis?

A

spasticity, hyperactive reflexes and babinski signs

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12
Q

What are key points of friedreich ataxia?

A

autosomal recessive, degeneration of the most of the parts of the spinal cord, childhood onset
-ataxia, sensory loss, dysarthria, areflexia, and babinski

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13
Q

what associated clinical findings can be found with ALS?

A

frontotemporal dementia and parkinson disease

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14
Q

what is progressive spastic paraparesis due to the transmission of a type C oncovirus by semen, blood, breast milk and shared needles. It is endemic in the Caribbean and South America?

A

HTLV-1 myelopathy

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15
Q

what occurs late in the course of theAIDS systemic illness. Major symptoms are spastic paraparesis, weakness, painless vibratory and position sense loss and sensory ataxia?

A

AIDS associated vacuolar myelopathy

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16
Q

where does polio attack? what characterizes it?

A

anterior horns

-flaccid weakness,

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17
Q

primary/idiopathic movement disorders may start unilaterally, but?

A

usually become bilateral overtime

acute onset unilateral movements are frequently secondary and should prompt brain imaging

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18
Q

T of F- the tardive syndromes can persist for many years after the offending drug has been discontinued?

A

true

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19
Q

substania nigra inclusion bodies are called what in parkonsins?

A

lewy bodies

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20
Q

sensory ataxia usually comes from what? how do you tel difference?

A

dysfunction of large-fiber sensory nerves and/or posterior columns in the spinal cord

patients will not have position or vibration senses

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21
Q

patients with sensory ataxia should be assessed for what?

A

B12

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22
Q

where does CO poisoning attack

A

globu pallidus .parkinsonism

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23
Q

primary or idiopathic movement disorders have what type of onset?

A

slow and progressive

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24
Q

lack of progression of a syndrome with an acute onset is suspicsious of what?

A

secondary structural lesion

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25
Q

what medication classes are important to look into for movement disorders

A

anti-psychotics
anti-GI like reglan
and antiepileptics

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26
Q

what are the 4 feautres of parkinsonism?

A

resting tremor, bradykinesia, rigidity, loss of postural reflexes- need 2 with bradykinesia required

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27
Q

dementia with lewy bodies has parkinsonism and dementia, but what else is common

A

visual hallucinations

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28
Q

what is the difference in initial presentation of parkinsons in older vs. younger

A

younger more tremor, older more rigidity

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29
Q

what are the non motor problems with PD?

A

anosmia, constipation, REM behavior disorder, depression, cognitive or autonomic problems

30
Q

what are the mainstay medications for parkinson’s

A
  • levodopa/carbidopa
  • dopamin agonists- pramipexole, ropinirole, rotigotine
  • MAOb inhibitors, COMT inhibitors (entacopone)
  • amantidine
  • anticholinergics
31
Q

what are other treatments for PD than medicine?

A

deep brain stim- more in younger healthier patiens

32
Q

when does the intention tremor significantly worsen?

A

worsens or appears when reaching a target- SUGGESTS CEREBELLAR ORIGIN

33
Q

what metabolic syndrome may suggest/lead to enhanced physiologic tremor?

A

hyperthyroid

34
Q

what is the big self medication for essential tremor?

A

alcohol

35
Q

what are the best medications for essential tremor?

A

propranolol and primidone (then maybe, topirimate, gaba, benzos)

36
Q

what is the last resort for essential tremor?

A

thalamic DBS

37
Q

what is a is a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both.

A

dystonia- often twisting

38
Q

The presence of what with dystonia is very unique to it and very helpful from a diagnostic viewpoint?

A

sensory tricks- touching it helps it go away

39
Q

T-F- the appearance of involuntary movement only with specific activities is unique to dystonia?

A

true

40
Q

what is the treatment of choice for focal/dystonia?

A

botulunum toxin

41
Q

generalized dystonia can be treated with what?

A

anticholinergics

42
Q

all children presenting with idiopathic dystonia should receive a trial of what?

A

levodopa (due to a genetic condition known as dopa-responsive dystonia

43
Q

what systems are needed for coordination?

A

cerebellum, proprioception, vestibular

44
Q

how do we tell if it is a cerebellar or sensory gait ataxia….

A

tuning fork- also sensory is worsen when eyes are closed and cerebellar is bad all the time

45
Q

if we see hemiballism acute onset think what?

A

cerebro vascular event to contra subthalamic nucleus

46
Q

is asterixis a negative or positive myoclonus?

A

negative

47
Q

unlike chorea, what is Tics?

A

sudden abrupt repetitive, PREDICTIVE and COORDINATED gestures

48
Q

are tics involuntary?

A

no unvoluntray or semivoluntary- patients volitionally do these due to an urge or very uncomfotable feelng

49
Q

TICS IN CHILDRENS MEANS WHAT? TICS IN ADULTS MEANS WHAT?

A

TOURRETS

ADULT-ONSET TIC DISORDER

50
Q

what brain region primarily generates output for process C circadian rhythm?

A

suprachiasmatic nuclesu in the anterior hypothalamus- cycles in a period just longer than 24 hours

51
Q

damage to what needs to take place to dissable the circadian rhythm from happening?

A

optic nerve

52
Q

what is process S and what accumulation starts it?

A

metabolic activity of itself that promotes sleep, accumulation of adenosine– cholinergic neurons of basal forebrain project to ant. hypothalaums and inhibit sleep, adenosine receptors on them stops their inhibitory effects

53
Q

how does caffeine stop sleep

A

blocks the effect of adenosine on the basal forebrain neurons

54
Q

what is a chosen pattern in which individuals set a schedule in which they are getting an inadequate amount of sleep?

A

behaviorally induced insufficient sleep syndrome

55
Q

how many OSA patients aren’t obese

A

about 1/3- a lot in children

56
Q

what confirms OSA diagnosis?

A

polsomnogram showin an apnea-hypopnea index or respiratory disturbance index showin at least 5 events per hour of sleep.

57
Q

patients who remain excessively sleepy despit proper CPAP can use what drugs?

A

modafinil and armodafinil.

58
Q

what associated symptom is often seen in narcolepsy?

A

cataplexy (emotional paralysis), hypnogogic hallucinations, and sleep paralysis

59
Q

what is narcolepsy due to?

A

absence or marked reduction in the number of hypocretin (orexin) neurons in the lateral hypothalamus

60
Q

how can we diagnose narcolepsy?

A

mean sleep latency on five day naps

61
Q

what are mainstays of narcolepsy treatment?

A

modafinil and mehtylphenidate

TCAs and SSRI suppress ancillary symptoms of REM sleep during wakefulness.

62
Q

what drug helps to control cataplexy?

A

sodium oxybate

63
Q

40% of people being evaluated for insomnia have what?

A

Axis I psychiatic diagnosis- most often ancxiety disorder

64
Q

what is is a manifestation of conditioned behaviors usually seen in an individual with an intense, perfectionistic personality and a long history of being a poor or “light” sleeper, who experiences some kind of precipitating event (e.g., loss of job, divorce) and then develops perpetuating behaviors that continue the sleeplessness.

A

psychophysiologic insomnia

65
Q

what is the mainstay of treatment for anxiety person with insomnia?

A

CBT- which can be superior to hypnotic medication therapy alone after 6 months

66
Q

what is the most common used z drugs for anxiety sleep insomnia?

A

zolpidem, zaleplon, aszopiclone– bind GABA receptors with alpha-1 subunit

67
Q

what is unusual sleep behavior? what are they?

A

parasomnias

- expression of the reality that elements of sleep and wakefulness can co-exist like sleep walking

68
Q

what sleep level is parasomnias?

A

N3 deep and REM parasomnias (rem later in the night)

69
Q

when can sleep related epilepsy and enuresisoccur?

A

any stage

70
Q

what are parasomnias treated with?

A

clonazepam

NEURO CLERKSHIP (7 decks)

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