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Neurology > Weakness, paralysis, spinal cord compression > Flashcards

Weakness, paralysis, spinal cord compression Flashcards

spinal cord compression, GBS, demyelination, Todd's palsy and toluene solvent inhalation, myasthenia gravis, ALS,

1
Q

Causes of spinal cord compression

A

spinal injury (MVA), malignancy (lung, breast, prostate, myeloma) infection (epidural abscess)

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2
Q

Symptoms of spinal cord compression

A

gradually worsening, severe local back pain,

back pain worse in the recumbent position/ at night

Early signs: symmetric lower extremity weakness and hypoactive absent deep tendon reflexes

Late signs : bilateral babinski reflex, decreased rectal sphincter tone, paraparesis/paraplegia with increased DTR and sensory loss

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3
Q

Management of spinal cord compression

A

emergency MRI IV steroids vs antibiotics neurosurgery, radiation oncology consult

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4
Q

when to use intrathecal chemotherapy?

A

only for leptomeningeal (dura, arachnoid and pia mater)

metastasis due to certain solid and hematological cancers (breast, lymphoma, leukemia)

But not used to tx acute compression

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5
Q

Guillane barre syndrome presentation is:

A

produces flaccid quadriparesis, no hypokalemia or non anion gap metabolic acidosis. CSF fluid with no WBCs, high protein and normal glucose.

See ascending symmetrical muscle weakness and absent DTR after infectious illness. 10% of pts may have arm or facial weakness instead of leg weakness.

80% complain of paresthesias of hands and feet but sensory exam is NORMAL. May have pain in back or extremities.

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6
Q

Todd’s Palsy

A

focal weakness of hand arm or leg after seizure.

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7
Q

Toluene inhalation presentation

A

cognitive impairment, flaccid weakness and absent DTR see non anion gap metabolic acidosis and RTA type 1 and hypokalemia.

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8
Q

transverse myelitis

A

rare inflammatory disorder causing segmental spinal cord injury.

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9
Q

cause of transverse myelitis

A

idiopathic and likely from underlying autoimmune disorder following viral infection (50% of cases)

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10
Q

pt presents in spinal shock and with a band like squeezing pain. They will have bowel and bladder dysfunction. After one week they have spasticity, hyperreflexia, Babinski signs and clonus

A

transverse myelitis

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11
Q

spinal shock is

A

lower extremity weakness, flaccidity, areflexia, and absent Babinski sign sensory level to all primary sensory modalities a

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12
Q

Diagnosis of transverse myelitis is via

A

MRI with contrast shows enhancing cord segments with surrounding edema

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13
Q

CSF analysis of transverse myelitis is

A

elevated protein moderate lymphocytosis and normal glucose and NO oligoclonal bands

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14
Q

Treatment of transverse myelitis

A

supportive care with PT and IV steroids can help with pts who have an autoimmune component of dx

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15
Q

prognosis of transverse myelitis

A

3 month recovery but 40% may have some residual disability

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16
Q

Cauda equina syndrome is from

A

affects lumbosacral roots as they exit the spinal cord and caused by a herniated disk or tumor

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17
Q

severe unilateral pain in the saddle region that radiates down to the legs with associated asymmetrical lower extremity weakness and proximal or distal

A

cauda equina syndrome

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18
Q

features that distinguish cauda equina syndrome vs GBS vs transverse myelitis

A

Cauda equina syndrome - bowel and bladder sphincter weakness

GBS- no bowel or bladder sphinter weakness

Cauda equina will have severe lancinating or shooting pain in back

transverse myelitis no back pain

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19
Q

Difference between transverse myelitis from GBS

A

both can have spinal shock with reflexes and Babinski sign will be absent

GBS –NO bowel and bladder symptoms or a sensory loss below the spinal segment

transverse myelitis –WILL have bowel and bladder symptoms or a sensory loss below the spinal segment

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20
Q

Spinal cord infarction will have

A

back pain weakness, loss of sensation and reflexes and autonomic dysfunction and this happens abruptly in minutes to hours.

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21
Q

vitamin B12 deficiency will have

A

slow progressive weakness, ataxia and neuropsychiatric disturbances.

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22
Q

anterior horn cell (poliomyelitis) injury rather than transverse leukomyelitis thus will have sparing of ascending (pain and temperature and vibration or proprioception) and descending (pyramidal and extrapyramidal motor system and autonomics)

A

how west nile virus works

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23
Q

pt has asymmetric flaccid paralysis and extrapyramidal symptoms with fever and maculopapular rash on chest and extremities

A

West Nile virus

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24
Q

Treatment of west nile virus

A

supportive and try mosquito prevention programs.

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25
Q

diagnosis of west nile virus

A

IgM serology in pts with only fever. CNS symptoms need LP to rule out other etiologies and confirm diagnosis with IgM antibody titer

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26
Q

Guillain Barre syndrome

A

progressive and symmetrical ascending paralysis and paresthesias and decreased to absent reflexes and possible respiratory distress.

This is a monophasic disease - meaning after it hits its nadir at 4 weeks pts will slowly have weakness improve.

They will be stable and autonomically should improve.

Rates of full recovery can be slow and 80% are able to walk at 6 months

No need to repeat any IVIG after reaching the nadir of weakness. Also avoid steroids - can worsen GBS.

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27
Q

post polio syndrome

A

See progressive weakness, fatigue, muscle aches and joint pain which worsens abruptly >50.

seen in pts who had history of paralytic polio due to age related drop out of existing motor units.

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28
Q

ALS is

A

progressive neurodegenerative dx that happens in men >40 yrs

29
Q

risk factors for ALS

A

age, family hx, cigarette smoking

30
Q

ALS pathophysiology

A

affects upper (affects corticospinal tract of upper motor neuron) and lower motor (anterior horns of lower motor neuron) neurons with relative sparing of sensory neurons

NOTE if you were to get LP and CSF would be normal.

31
Q

ALS presentation

A

see bulbar, cervical and thoracic and lumbosacral neuronal involvement and this is PROGRESSIVE see asymmetrical limb weakness - hand or foot drop.

See bulbar symptoms of dysarthria, dysphagia and respiratory muscle weakness and weight loss and muscle cramps or atrophy

See upper and lower motor neuro signs - spasticity, hyperreflexia, and positive Babinski sign.

32
Q

diagnosis of ALS is

A

clinically

but can get EMG (electromyogram) and nerve conduction studies and neuro imaging to rule out other causes

33
Q

Treatment of ALS

A

riluzole (glutamine antagonist) only drug to improve clinical outcomes

34
Q

median survival for ALS

A

5 years and respiratory failure is the main cause of death

35
Q

What separates ALS from GBS?

A

no upper motor neuron signs are seen with GBS

36
Q

asymmetrical limb weakness, no loss of sensory symptoms and see dysphagia and hand and tongue fasciculations

A

ALS

37
Q

Upper motor neuron signs

A

spastic paralysis,

clasp knife rigidity,

hyperreflexia,

hypertonia

no fasciulations

Babinski sign

38
Q

lower motor neuron signs

A

flaccid paralysis

hypotonia

hyporeflexia

muscle atrophy

fasciculations

39
Q

CSF analysis for GBS and meningitis?

A
40
Q

Diagnosis of GBS syndrome?

A

diagnosis is made via LP and neurophysiology studies (EMG).

CSF for GBS: elevated CSF prtoein with normal WBC (albuinocytological dissociation) and normal glucose. This is seen 1 week after onset of symptoms.

EMG and nerve conduction studies will show evidence of polyneuropathy.

41
Q

Prognosis of GBS

A

generally good.

‘Nearly 25% get mechanically ventilated due to respiratory muscle weakness. 20% of severely affected are unable to walk after symptom onset.

42
Q

Treatment of GBS

A

supportive + plasmapheresis or IVIG which can help accelerate recovery.

43
Q

female with double vision and difficulty swallowing which is worse at end of day. Cannot lift hands above her head and can’t walk up or down stairs. See horizontal binocular diplopia and bilateral ptosis.

increased generalized and oropharyngeal weakness,

respiratory insufficiency and dyspnea which is worse when supine.

A

features of a myasthenia crisis.

44
Q

Treatment of myasthenia crisis initially and why is this 1st choice?

A

Plasma exchange or IVIG = because of rapid onset of action and benefits are transient.

Don’t pick steroids.

These start within a few days and last for 3 weeks

steroids are added for providing longer term benefit.

45
Q

what is also added to treatment of myasthenia crisis and why do we like this?

what if they cannot tolerate 2nd line treatment then what to do next?

A

Plasma exchange (IVIG) followed by glucocorticoids because they add longer term symptom relief and their onset of action starts 2-3 weeks later with peak effect at 5.5 months

Cannot treat acute myasthenia crisis with steroids at first. need to IVIG or plasma exchange.

If people cannot tolerate steroids, they can be started on azathioprine, mycophenolate mofetil, or cyclosporine but have delayed onset of working compared to steroids.

46
Q

do we ever use methotrexate with myasthenia crisis?

A

No. not indicated for myasthenia crisis.

47
Q

how to distinguish between Horner’s syndrome vs Bell’s Palsy vs Myasthenia gravis when a patient presents like this?

A

Myasthenia gravis: will not have an abnormal pupillary response. Will see abnormal response from extraocular muscles (oculomotor, trochlear and abducens nerve and palate and vagus nerves

Horner’s: will have abnormal mydiasis with pupil or fixed pupil. Able to move muscles and smile.

Bell’s palsy (facial nerve 7) - normal pupil response. no extraocular eye muscle abnormalities. But won’t be able to smile. Able to move eye muscles

48
Q

cervical spondylosis is from

A

progressive degenerative process of cervical vertebral bodies and discs in adults>55 yrs

seen disc herniation, osteophyte formation and hypertrophy of posterior longitudinal ligament and ligament flava.

See spinal canal stenosis and medical spinal cord compression in 5 to 10% of individuals and flexion and extension of neck can exacerbate cord compression while extension - when pt bicycles can reduce diameter of spinal canal and cause inward buckling of the ligamentum flavum.

49
Q

Treatment of cervical spondylosis is

A

conservative with cervical immobilization for mild myelopathy

and surgical decompression is needed for those who fail conservative measures, severe myelopathy or progressive deficits or acute deterioration with cord compression

50
Q

diagnosis of cervical spondylosis is with

A

MRI and CT for cervical cord compression

MRI is needed for better intramedullary detail of the spinal cord while giving CT better images of bone and calcified tissues

51
Q

difference between ALS and cervical spondylitis

A

ALS - lower motor neuro deficits and fasciculations and cranial muscles. NO sensory deficits

Cervical cord compression - see subtle or absent sensory deficits and along dermatome.

EMG is needed to distinguish between both disorders

52
Q

pufferfish poisoning

A

tetrodotoxin - stops voltage gated sodium channels and prevents sodium depolization. acts on skeletal muscle through same mechanism and cuases relaxation

seen within minutes and starts with perioral numbness, paralysis with loss of reflexes and severe hypotension. can cuase subsequent respiratory distress

Give charcoal within 1 hour of symptom onset and treatment is supportive.

53
Q

ciguatoxin is from

A

dinoflagellate poisoning is reponsible for ciguatera poisoning via activation of voltage gated sodium channel and causes GI, cardiac, and neuro symptoms. See nausea, vomiting, and diarrhea before cardiac (complete heart block) and neuro symptoms.

see perioral numbness. See temperature dysesthias.

54
Q

saxitoxin is seen with

A

paralytic shell fish poisoning

see saxitonxin in urine.

55
Q

Diagnosis of Myasthenia Gravis is by

If this is negative what is done next?

Do we still diagnose based off edrophonium test?

A

serological testing: 85% of generalized MG will have positive acetylcholine receptor autoantibodies

50% of ocular MG will have positive AChR antibodies

40% of pts who are seronegative for AchR antibodies are positive for muscle-specific tyrosine kinase autoantibodies

If serology is completely negative, EMG and nerve conduction study is done with repetitive stimulation to confirm diagnosis.

We no longer do edrophonium and ice pack test due to high false positive rates.

56
Q

4T’s of anterior mediastinal masses

A

thymoma’s - most common

teratoma - and other germ cells

thyroid gland or goiter

terrible lymphoma - located in middle or posterior medastinum.

57
Q

Thymoma management

A

surgery in clinical setting with thymom and thymic carcinomas

Thymectomy is suggested for people who are <60 yrs and have generalized myasthenia gravis.

58
Q

Lambert Eaten myasthenic syndrome is

A

paraneoplastic syndrome with small cell lung cancer that presents with slowly progressive proximal muscle weakness and decreased DTR, dry mouth, and ED.

See vigorous muscle activation improves with recovery of DTR and muscle strength.

Rarely see ocular symptoms.

59
Q

back pain, paresthesias and symmetrical weakness worse in lower extremities and hyporeflexia

A

Guillain Barre syndrome or acute inflammatory demyelinated polyneuropathy

see ascending progressive symmetric weakness or paralysis after a week of URI or GI (campylobacter)

  • 1/3 won’t have prior symptoms. As weakness ascends see weakness with walking, 3/5 strength of lower extremities compared to 4/5 strength of upper extremities in this pt.

See bulbar symptoms (ophthalmoplegia, facial diplegia, dysarthria, dysphagia) and respiratory compromise.

Back pain is from dx targeting the primary proximal polyneuropathy and pts having mild sensory symptoms such as paresthesias and sensory ataxia.

they can develop dysautonomia = tachycardia, diaphoresis and sluggish pupils and absent reflexes.

60
Q

if suspecting acute inflammatory demyelinated polyneuropathy then need to get

A

LP - in all suspected GBS pts to rule out infectious causes and document elevated CSF protein in normal CSF WBC. See albuminocytologic dissociation.

LP is not diagnostic for GBS because it can see abnormal symptoms a week after symptom onset.

Nerve conduction and study and EMG are needed to confirm GBS.

61
Q

All suspected Guillian Barre Syndrome pts should get this diagnostic test?

A

LP to rule out underlying infection.

62
Q

How to treat acute GBS?

How to treat acute myasthenia gravis crisis?

A

IVIG or plasmapheresis

don’t pick steroids. Steroids is 2nd choice for myasthenia crisis

don’t use steroids in GBS.

63
Q

chronic inflammatory demyelinating polyradiculopathy is CIPD

A

acquiring inflammatory disorder characterized by demyelination of peripheral nerves and nerve root.

progressive, symmetric, proximal and distal muscle weakness along distal sensory loss affecting arms and legs. See diminished or absent deep tendon reflexes.

distal sensory loss is normally vibration and proprioception due to larger involvement of myelin fibers.

symptoms occur >8 weeks (so different from AIDP–GBS)

64
Q

progressive, symmetric, proximal and distal muscle weakness along distal sensory loss affecting arms and legs. See diminished or absent deep tendon reflexes.

distal sensory loss is normally vibration and proprioception due to larger involvement of myelin fibers.

>8 weeks of symptom onset

A

chronic inflammatory demyelinating polyradiculopathy

EMG will show peripheral nerve demyelination and (reduced conduction velocity and prolonged distal motor latencies).

Lumbar puncture will show albuminocytologic disassociations in 90% of pts.

65
Q

ciguatera fish poisoning is from

A

person ingests a reef fish or a grouper, amberjack, moray eel, snapper, barracuda

predatory fish ate dinoflagellates that produce cigatoxin and concentrate it in their ograngs that increases potency of their neurotoxin.

stable and cannot be altered by cooking and so see 3 hrs after eating or delayed by 2 days.

66
Q

ciguatera fish poisoning affects

A

three organ systems

GI - vomiting, diarrhea, abd cramping

Cardiac - bradycardia, compelte heart block and hypotension

CNS - perioral paresthesias, pruritis without urticaria, painful dentition or a feeling that teeth are loose, painful urination, and blurred vision are the most specific finding

see temperature related dysesthesia.

67
Q

organophophate poisoning:

A

salivation, bronchorrhea, bronchospasm and weakness and paralysis

hallmark test is anticholinergic challenge with atropine where lack of response would support diagnosis of organophosphate poisoning.

68
Q

what is scromboid poisoning?

A

this is where fish is left above 40 (104’F) and this allows bacteria on the fish’s skin to convert histidine to histamine

when you eat it it causes vasodilatory symptoms including, nausea, vomiting, and palpitations, headaches, and rash and pruritis. Difficult to distinguish between scromboid poisoning and anaphylaxis until after treatment is given.

distinction is that rapid improvement of symptoms upon treatment with antihistamine agent which is definitive tx.

seen more with self caught fish due to higher chance of improper storage.

Neurology (27 decks)

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