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Neuro > Spinal diseases, demyelinating myelophatyes, neuropathies > Flashcards

Spinal diseases, demyelinating myelophatyes, neuropathies Flashcards

1
Q

C segments injury

A

tetraparesis/tetraplegia

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2
Q

Th to L segments injury

A

Paraparesis/paraplegia

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3
Q

Arnorld-Chiari syndrome

A

Meningomyelocele
Severe tonsilar herniation
Hydrocephalus

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4
Q

Neuromyelitis optica type of disease

A

Autoimmune disease

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5
Q

B12 deficiency leads to

A

Symmetrical sensory disturbances of lower limbs
Ataxia
Spasticity
Loss of reflexes
Loss of vibration and proprioception sense
Problem in posterior column

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6
Q

Spondylosis type of disease

A

Degenerative spine disease.

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7
Q

Spondylosis process

A

Dehydratation and disintegration of the nucleus pulpous–> decreased disc height–> spinal canal stenosis–> compression of the spinal cord

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7
Q

Spondylosis parts more often involved

A

Cervical and lumbar

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8
Q

Spondylosis. Clinical

A

Sciatica
Brachialgia

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9
Q

Cauda equina syndrome type of disease

A

degenerative disease

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10
Q

Cauda equina syndrome what happens

A

lumbar canal stenosis leads to compression of the cauda equina

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11
Q

Cauda equina syndrome. Clinical

A

Pain in back, legs
Weakness or paralisis
Urinary retention and urinary incontinence
Urinary retention, incontinence
Sexual disfunction
Anestesia in buttocks, anus, genitalis

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12
Q

Cauda equina treatment

A

Decompression surgery in 24h

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13
Q

Neuromyelitis optica treatment

A

inmunosupresors, corticoesteroids, anti-B therapy

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14
Q

Neuropathies. Clinical

A

Patient complains about weakness, sensory disturbance (numbness, pain), autonomic disturbance (diarrea, bladder dysfunction)
Exploration:
Pes cavas, ulceration, fasciculation
Nerve thickness, reduce muscle consistency

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15
Q

Axonopathy. Symptoms and signs

A

Burning, tingling and numb feet. Start distally and goes to proximally. Walking difficulties
Atrophy of small feet muscle
Weakness of toe and ankle dorsiflexion
Distal loss of touch and pinprick sensation
diminished/non-elicotable Achilles reflexes

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16
Q

Neuropathy with translation blocks

A

Asymmetric motor nerve impairment, usually starting in the hands
Positive anti-GM-1 antibodies
Good response to treatment with human immunoglobulins

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17
Q

Patient with a current sharp Knife.like” pain in her lower right jaw is likely to have

A

Trigeminal neuralgia

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18
Q

Polyneuropathy that affects nails

A

arsenic poisoning

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19
Q

Antibodies in Miller-Fisher syndrome

A

anti-ganglioside

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20
Q

Charcot-Marie tooth. Clinical

A

Feet deformation
Foot drop because of distal weakness
Atrophies
Sensory symptoms

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21
Q

Type of Charcot-Marie tooth that is demyelinating

A

type 1

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22
Q

Type of Charcot-Marie tooth that is axonal

A

type 2

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23
Q

Fibers that are more affected in Sjogren’s neuropathy

A

Sensory fiber

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24
Q

Gunyon’s canal syndrome

A

Pinched ulnar nerve in the wrist

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25
Q

Nerve that is biopsies in polyneuropathy

A

Suralis

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26
Q

Best treatment for trigéminas neuralgia

A

Carbamazepine

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27
Q

Hallmark of the meralgia of paresthetics is

A

Hypesthesia lateral to the thigh

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28
Q

Nerve affected in meralgia paresthetica

A

cutaneous femurs lateralis

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29
Q

The contraction of the biceps when the doctor elicited the styloradial reflex is due to

A

myelopathy

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30
Q

Diabetic neuropathy. Clinical

A

Painful CN III defect
Numbness of the toes
Inability to flex at the hip and extend at the knee
Unilateral flank pain along the rib arch
Painful paresis
Glove and stocking sensory loss

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31
Q

Subacute combined degeneration of the spinal cord. Clinical

A

Spastic weakness in the legs
Paresthesia in extremities
Loss of vibration and position sense
Cognitive impairment
Optic atrophy
Extensor plantar responses and absent ankle jerks

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32
Q

Subacute combined degeneration of the spinal cord is

A

Progressive degeneration of the spinal cord due to B12 deficiency

33
Q

Neuromyelitis optica type of disease

A

Chronic autoimmune disease which affects atrocities. Antibodies against acquaporines. Necrotic lesion

34
Q

Neuromyelitis optica. Clinica

A

Bilateral paraparesis o tetraparesis
Relapses
Long cervical cord lesion
Nausea and vomiting
Brain lesions
Blindness

35
Q

Neuromyelitis optica treatment

A

Anti-B theraphy, inmunosupresor, corticoesteroids

35
Q

Acute disseminated encephalomyelitis age

A

children and young adults

36
Q

Acute disseminated encephalomyelitis

A

Infection or vaccination precedes the disease. Brain is infiltrated by LT
Fever
Headache
Nausea
Epileptic seizures
Encephalopathy: disartria, dysphonia, foggy vision, ataxia, tetraparesis
Coma

37
Q

Acute disseminated encephalomyelitis treatment

A

Corticosteroids or plasmaforesis

38
Q

Charcot-marie-tooth type of illness

A

Hereditary motor and sensory polyneuropathy

39
Q

Charcot-marie-tooth. Clinical

A

Feet deformation (pes cause)
Foot drop because of distal weakness
Atrophies
Sensory symptoms

40
Q

Guillain-Barré syndrome. Type of disease

A

Acute inflammatory demyelinating polyneuropathy

41
Q

Guillain-Barré syndrome. Antibodies

A

Antibodies antigangliosides

42
Q

Guillain-Barré syndrome. Clinical

A

Parestesia in the lower limbs that ascendents to the upper limbs
Reflexes attenuate or disappear in few days of onset
Nistagmus
Pain
Respiratory failure
Postural hypotension, arritmias, urinary retention, constipation, diarrea
Facial disparesis
Pupillary paralysis
Propioception is more affected than pain and temperature sensation
EMG: prolonge wave F
Antigangliosides antibodies
Lumbar puncture: more proteins with normal cell count

43
Q

Guillain-Barré syndrome. Treatment

A

Immunotherapy. If there is no response, plasmapheresis

44
Q

Progressive multifocal encephalopathy. Clinical

A

Subacute cortical disfunction: aphasia, mental changes, visual problems

45
Q

Types of Multiple sclerosis

A

Relapsing remitting: most common, stable between relapses characterized by attacks of neurological dysfunction
Secondary progressive: evolve from relapsing remitting type. Disability progression independent of relapses. Consequence of secondary degeneration
Primary progressive: Slowly progressive symptoms or infrequent relapses. Disease onset after 40 years. Worse prognosis
Benign: Retrospecting diagnosis. Non accumulation of disability along time

46
Q

Multiple Sclerosis. Clinical

A
  • Visual problems: optic neuritis (pain, central scotoma, color vision disturbance). Vertical gaze palsy
  • Paresis, paraplegia
  • Parestesia Iof the trunk or legs. Lhermitt’s sign: electrical sensation that runs through the back and limbs, elicited by bending the head forward.
    In advanced stages:
  • Cerebellar: incoordination, unbalance
  • Picturing and sexual disfunction
  • Fatigue
  • Cognitive disorders, mood disorders
  • Pain
  • Brainstem signs and symptoms: nystagmus, internuclear ophthalmoplegia
  • Paroximal symptoms: tonic spasms, trigeminal neuralgia, paroxymal dysarthria, ataxia, paroxysmal sensory and pain symptoms, double vision, akinesia, proximal paresis
47
Q

What do you see in MRI of Multiple Sclerosis

A

Lesions in brain, in spinal cord.
Brain atrophy, bigger ventricles

48
Q

Multiple sclerosis treatment

A

Symptomatic
Treatment of relapses: corticosteroids, metilprednisolone
Modifying therapies: INF beta (not for symptoms), glatiramer acetat, Dimetil fumaram, teriflunomid, Natalizumab

49
Q

% of ALS familiar

A

5%

50
Q

Patient with muscle atrophy, fasciculation and plantar response extension is likely to have

A

ALS

51
Q

Riluzole works by

A

Glutamate receptors

52
Q

Amiotrofic lateral sclerosis (ALS) what neurones involves

A

Upper and lower motor neuron

53
Q

ALS clinical features

A

Hypo/hypereflexia
Disartria, disfagia
Spasticity
Amiotrofic
Babinski

54
Q

Mutation of SOD1

A

ALS

55
Q

Primary lateral sclerosis

A

A form of ALS in which only the corticospinal tract is affected

56
Q

Reflex in a patient with ALS that is a sign of pseudobulbar impairments

A

Clonic masseter reflex

57
Q

Incidence of ALS

A

2/100000 per year

58
Q

Motor neuron damage that involves only the upper motor neuron

A

Primary lateral sclerosis
Pseudobulbar palsy
Monomelic amyotrophy
Spastic familiar paraparesis

59
Q

Motor neuron damage that involves only the lower motor neuron

A

Progressive muscular atrophy

60
Q

Lumbar puncture in multiple sclerosis

A

Oligoclonal bands, positive in CSF, negative in serum

61
Q

Multiple sclerosis antopato

A

plaques of demyelination in the withe matter
Perivascular mononuclear infiltrate in the CNS
Axon collapse in the CNS

62
Q

Treatment progressive multiple sclerosis

A

cystostatics

63
Q

70 years old ataxia, forget things, hyperreflexia of the upper and lower limbs, positional sensitivity disturbed

A

Subacute combined degeneration of the spinal cord

64
Q

Drug hyperexcitable bladder in MS

A

Anticholinergics (oxybutynin, imipramine, toterodine)

65
Q

What do black holes on MRI in MS mean

A

Axonal collapse

66
Q

Treatment for fatigue in MS

A

Amantadine

67
Q

Treatment to reduce incidence of seizures in MS

A

Natalizumab

68
Q

Azathioprine is used for

A

Liver damage

69
Q

ADM-specific test

A

Extensive symmetrical changes on the head MRI in both hemispheres
Meningitic fluid
Negative oligoclonal bands in the lymphocyte after remission of the disease

70
Q

Best test for multiple sclerosis

A

MRI

71
Q

Form of MS that shouldn’t be treated with interferon beta

A

Primary progressive

72
Q

Patient with Ms no responding to IFN beta what to give

A

Natalizumab

73
Q

Optic neuritic a year ago now has spasticity is likely to have

A

MS

74
Q

Patient with primmary progressive multiple sclerosis can be treated with interferons)

A

No

75
Q

How do demyelinating lesions look in MRI sequences

A

flair-weighted

76
Q

How do demyelinating lesions look in CT T2

A

increased signal T2

77
Q

Treatment for spasticity in MS

A

Baclofen
Benzodiazepine
Tizanidine
Botulinum

78
Q

Antibodies in a patient that lost her sight months ago and is paretic

A

anti-NMO

79
Q

Vitamin deficiency associated with multiple sclerosis

A

Vitamin D

Neuro (30 decks)

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