Spinal Cord, sleep disorders, movement disorders Flashcards

(70 cards)

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
what medication classes are important to look into for movement disorders
anti-psychotics anti-GI like reglan and antiepileptics
26
what are the 4 feautres of parkinsonism?
resting tremor, bradykinesia, rigidity, loss of postural reflexes- need 2 with bradykinesia required
27
dementia with lewy bodies has parkinsonism and dementia, but what else is common
visual hallucinations
28
what is the difference in initial presentation of parkinsons in older vs. younger
younger more tremor, older more rigidity
29
what are the non motor problems with PD?
anosmia, constipation, REM behavior disorder, depression, cognitive or autonomic problems
30
what are the mainstay medications for parkinson's
- levodopa/carbidopa - dopamin agonists- pramipexole, ropinirole, rotigotine - MAOb inhibitors, COMT inhibitors (entacopone) - amantidine - anticholinergics
31
what are other treatments for PD than medicine?
deep brain stim- more in younger healthier patiens
32
when does the intention tremor significantly worsen?
worsens or appears when reaching a target- SUGGESTS CEREBELLAR ORIGIN
33
what metabolic syndrome may suggest/lead to enhanced physiologic tremor?
hyperthyroid
34
what is the big self medication for essential tremor?
alcohol
35
what are the best medications for essential tremor?
propranolol and primidone (then maybe, topirimate, gaba, benzos)
36
what is the last resort for essential tremor?
thalamic DBS
37
what is a is a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both.
dystonia- often twisting
38
The presence of what with dystonia is very unique to it and very helpful from a diagnostic viewpoint?
sensory tricks- touching it helps it go away
39
T-F- the appearance of involuntary movement only with specific activities is unique to dystonia?
true
40
what is the treatment of choice for focal/dystonia?
botulunum toxin
41
generalized dystonia can be treated with what?
anticholinergics
42
all children presenting with idiopathic dystonia should receive a trial of what?
levodopa (due to a genetic condition known as dopa-responsive dystonia
43
what systems are needed for coordination?
cerebellum, proprioception, vestibular
44
how do we tell if it is a cerebellar or sensory gait ataxia....
tuning fork- also sensory is worsen when eyes are closed and cerebellar is bad all the time
45
if we see hemiballism acute onset think what?
cerebro vascular event to contra subthalamic nucleus
46
is asterixis a negative or positive myoclonus?
negative
47
unlike chorea, what is Tics?
sudden abrupt repetitive, PREDICTIVE and COORDINATED gestures
48
are tics involuntary?
no unvoluntray or semivoluntary- patients volitionally do these due to an urge or very uncomfotable feelng
49
TICS IN CHILDRENS MEANS WHAT? TICS IN ADULTS MEANS WHAT?
TOURRETS | ADULT-ONSET TIC DISORDER
50
what brain region primarily generates output for process C circadian rhythm?
suprachiasmatic nuclesu in the anterior hypothalamus- cycles in a period just longer than 24 hours
51
damage to what needs to take place to dissable the circadian rhythm from happening?
optic nerve
52
what is process S and what accumulation starts it?
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
how does caffeine stop sleep
blocks the effect of adenosine on the basal forebrain neurons
54
what is a chosen pattern in which individuals set a schedule in which they are getting an inadequate amount of sleep?
behaviorally induced insufficient sleep syndrome
55
how many OSA patients aren't obese
about 1/3- a lot in children
56
what confirms OSA diagnosis?
polsomnogram showin an apnea-hypopnea index or respiratory disturbance index showin at least 5 events per hour of sleep.
57
patients who remain excessively sleepy despit proper CPAP can use what drugs?
modafinil and armodafinil.
58
what associated symptom is often seen in narcolepsy?
cataplexy (emotional paralysis), hypnogogic hallucinations, and sleep paralysis
59
what is narcolepsy due to?
absence or marked reduction in the number of hypocretin (orexin) neurons in the lateral hypothalamus
60
how can we diagnose narcolepsy?
mean sleep latency on five day naps
61
what are mainstays of narcolepsy treatment?
modafinil and mehtylphenidate TCAs and SSRI suppress ancillary symptoms of REM sleep during wakefulness.
62
what drug helps to control cataplexy?
sodium oxybate
63
40% of people being evaluated for insomnia have what?
Axis I psychiatic diagnosis- most often ancxiety disorder
64
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.
psychophysiologic insomnia
65
what is the mainstay of treatment for anxiety person with insomnia?
CBT- which can be superior to hypnotic medication therapy alone after 6 months
66
what is the most common used z drugs for anxiety sleep insomnia?
zolpidem, zaleplon, aszopiclone-- bind GABA receptors with alpha-1 subunit
67
what is unusual sleep behavior? what are they?
parasomnias | - expression of the reality that elements of sleep and wakefulness can co-exist like sleep walking
68
what sleep level is parasomnias?
N3 deep and REM parasomnias (rem later in the night)
69
when can sleep related epilepsy and enuresisoccur?
any stage
70
what are parasomnias treated with?
clonazepam