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Collège Royal 2019 > Neuro > Flashcards

Neuro Flashcards

1
Q

DxD de lésions neurologiques causant de la faiblesse aux différents niveaux neurologiques

A
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2
Q

Causes de neuropathie périphérique

A

Diabète

Alcool

Lésion compressive

Trauma

Démyélinisation

Déficit vitamine

Maladies tissu conjonctif

Paranéo

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3
Q

Dxd coma

A

Métabolique:

hypoglycémie, hyperglycémie, insuffisance surrénalienne, beri-beri, sepsis, hypoNa, hyperCa, urémie, encéphalopathie hépatique, thyrotoxicose, coma myxoedémateux, apoplexie hypophysaire, Wernicke, coup de chaleur, oedème cérébral relié altitude, hyperammoniémie

Toxique:

opioides, sédatifs, alcool, hypoglycémiants, clonidine, beta bloqueurs, médication psychiatrique, anticonvulsivants, salicylates, méthémoglobinémie, CO, SNM, syndrome sérotoninergique, inhalants, asphyxiants simples, cyanure, anticholinergiques

Structurel:

hémorragique, AVC ischémique cortical ou cérébelleux

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4
Q

Décrire le score FOUR

A
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5
Q

Déviation des yeux lors d’une masse a/n cortex, tronc cérébral et convulsion

A

Forced deviation of the eyes, usually in the horizontal plane, may indicate an ipsilateral hemispheric or contralateral pontine lesion. Seizures can also cause horizontal eye deviation, typically away from the cerebral lobe containing the seizure focus.

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6
Q

Prise en charge initiale d’un coma

acronyme

A

ABC

Glycémie

Antidote: glucose, narcan, thiamine

Cause structurelle ou non? Histoire + E/P

TSPINE

toxique: labo, antidote, dialyse?

Seizure: EEG, anticonvulsivant

PRES

Infection: PL, antibio

Nutrition

Endocrino labos, steroides

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7
Q

Indices différentiant confusion d’origine organique vs psychiatrique

A
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8
Q

Décrire l’outil CAM

A
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9
Q

Nommer 20 causes de SE chez l’Adulte

A

Métabo:

hyponatrémie, hypo/hyperglycémie, hypocalcémie, encéphalopathie hépatique, urémie

Sevrage:

Benzo, alcool, barbituriques, antiépileptiques, baclofen

Infectieux

Méningite, encéphalite, abcès cérébral

Lésion SNC: AVC, malformation AV, trauma, hydrocéphalie, tumeur, hémorragie, PRES, éclampsie, insulte hypoxique

Intox: lidocaine, camphor, MDMA, isoniazide, TCA, clozapine, flumazenil, quinolones/imipenem/metronidazole, theophyline, lithium, cannabinoides, bupropion, plomb, cyclosporine

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10
Q

Nommer des indications de TDM cérébral lors d’une convulsion

A

when a serious structural lesion is suspected on clinical grounds, including presence of a new focal deficit, persistent altered mental status, fever, recent trauma, persistent headache, history of cancer, anticoagulant use, suspicion or known history of acquired immunodeficiency syndrome (AIDS), age older than 40 years, and partial complex seizure

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11
Q

Nommer des causes de vertige central et périphérique

A

Peripheral Causes

Benign paroxysmal positional vertigo (BPPV)

Vestibular neuritis (or neuronitis)/labyrinthitis

Ménière’s disease

Foreign body in ear canal

Acute otitis media

Perilymphatic fistula

Trauma (labyrinth concussion)

Motion sickness

Acoustic neuroma

Central Causes

Vertebral basilar artery insufficiency

Cerebellar hemorrhage or infarction

Tumor

Migrainous vertigo

Multiple sclerosis

Post-traumatic injury (temporal bone fracture, postconcussive syndrome)

Infection (encephalitis, meningitis, brain abscess)

Temporal lobe epilepsy

Subclavian steal syndrome

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12
Q

Comment différentier un vertige périphérique de central?

A
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13
Q

Décrire le “hints” test

A

The first part of HINTS is the head impulse test and as described earlier, a corrective saccade indicates a positive test and is more reassuring for vestibular neuritis. The second part (nystagmus) refers to a direction change of nystagmus on eccentric gaze. For example, when the patient looks to the left, the fast component beats to the left; and when the patient looks to the right, the fast component beats to the right. This direction-changing nystagmus may indicate a stroke in a patient with acute vestibular syndrome. The third part (test of skew) refers to vertical ocular misalignment during alternate cover testing and its presence is suggestive of brainstem strokes

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14
Q

Nommer le diagnostic différentiel étourdissement avec exemples pour chacune des catégories

A
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15
Q

DxD de la diplopie

A
  1. Thrombose artère basilaire, méningite basilaire, anévrysme comprimant nerfs crâniens, botulisme
  2. Myasthénie grave, dissection artère vertébrale, Wernicke, thrombose sinus caverneux
  3. Tumeur tronc cérébral/apex de l’orbite, maladie Graves, myosite orbitaire, sclérose en plaques, neuropathie ischémique, migraine, miller-fisher
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16
Q

dxd de la diplopie selon début aigu ou non et condition douloureuse ou non

A
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17
Q

Nommer des syndromes lacunaires entraînant de la diplopie

A
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18
Q

Quels sont les premiers mouvements oculaires atteints lors d’une maladie Graves

A

Élévation et abduction (atteinte du muscle droit inférieur et droit médial)

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19
Q

Décrire la triade de Miller-Fisher

A

Ophtalmoplégie, ataxie, aréflexie

Habituellement pas de faiblesse motrice

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20
Q

algorithme de prise en charge diplopie

A
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21
Q

Prise en charge initiale d’une diplopie

A
  1. ABC - évaluation ventilation
  2. R/O AVC
  3. Méningite/ encéphalite?
  4. Wernicke?

Poursuivre évaluation

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22
Q

Décrire ce que chacune des artères cérébrales perfusent

A
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23
Q

Nommer les catégories de l’échelle NIHSS

A

État conscience

Orientation

Commande motrice

Champs visuels

Suivi regard

Paralysie faciale

Moteur bras- moteur jambe

Sensitifs

Dysarthrie

Langage

Dysmétrie

Extinction et négligence

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24
Q

Traitement de l’hypertension en AVC aigu

A

Systolic >185 mm Hg or diastolic >110 mm Hg

Labetalol 10 to 20 mg IV over 1 to 2 minutes; may repeat 1 time

or

Nicardipine infusion, 5 mg/hr; titrate up by 2.5 mg/hr at 5- to 15-minute intervals, maximum dose 15 mg/hr; when desired BP attained, reduce to 3 mg/hr

Other agents (hydralazine, enalaprilat, and so on) may be considered when appropriate.

If BP does not decline and remains >185/110 mm Hg, do not administer rtPA.

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25
Q

Critères inclusion et exclusion pour thrombolyse 3-4.5hr

A
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26
Q

Que donner en cas HIC post thrombolyse?

A

Cryoprécipités 6-8 unités

Cryoprecipitate, 10 units immediately (infused over 10 to 30 minutes) and more as needed to achieve a serum fibrinogen level of ≥200 mg/dL

●Antifibrinolytic agents: aminocaproic acid 4 to 5 g intravenously (IV) during first hour, followed by 1 g IV until bleeding is controlled, or tranexamic acid 10 to 15 mg/kg IV over 20 minutes

●Prothrombin complex concentrate as adjunctive therapy to cryoprecipitate for patients on warfarin prior to alteplase treatment

●Fresh frozen plasma as adjunctive therapy to cryoprecipitate for patients on warfarin prior to alteplase treatment if prothrombin complex concentrate is not available

●Vitamin K as adjunctive therapy for patients on warfarin prior to alteplase treatment

●Six to eight units of platelets for patients with thrombocytopenia (platelet count <100,000/microL)

●In patients receiving unfractionated heparin (UFH) for any reason, it is reasonable to treat with 1 mg of protamine for every 100 units of UFH given in the preceding 4 hours

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27
Q

Bilan sanguin de base nécessaire lors d’une première convulsion

A

glycémie, Na, et B HCG

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28
Q

Éléments cliniques qui augmentent la probabilité d’avoir un TDM cérébral anormal après une première convulsion

A

Focal abnormality on neurological examination

•

Malignancy

•

Closed head injury

•

Neurocutaneous disorder

•

Focal onset of seizure

•

Absence of a history of alcohol abuse

•

History of cysticercosis

•

Altered mental status

•

Patient older than 65 years old

•

Seizure duration more than 15 minutes

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29
Q

Traitement des convulsions en contexte particulier

A
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30
Q

Élaborer une classification des céphalées

A

Primary Headaches

1.

Migraine

2.

Tension-type headache

3.

Cluster headache and trigeminal autonomic cephalalgias

4.

Other primary headaches

Secondary Headaches

5.

Headache attributed to trauma or injury to the head or neck

6.

Headache attributed to cranial or cervical vascular disorder

7.

Headache attributed to nonvascular intracranial disorder

8.

Headache attributed to a substance or its withdrawal

9.

Headache attributed to infection

10.

Headache attributed to disorder of homeostasis

11.

Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cranial structures

12.

Headache attributed to psychiatric disorder

Painful Cranial Neuropathies, Other Facial Pains, and Other Headaches

13.

Cranial neuralgias and other facial pain

14.

Other headache disorders

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31
Q

Nommer les critères diagnostics de la migraine avec et sans aura

A

At least five attacks fulfilling criteria in B, C, D, and E

B.

Attack lasts 4 to 72 hours (untreated or unsuccessfully treated)

C.

Headache has at least two of the following characteristics:

1.

Unilateral location

2.

Pulsating quality

3.

Moderate to severe pain intensity

4.

Aggravation by or causing avoidance of routine physical activity (eg, walking or climbing stairs)

D.

During headache, at least one of the following:

1.

Nausea or vomiting (or both)

2.

Photophobia and phonophobia

E.

Not attributable to another disorder

A.

At least two attacks that fulfill criterion B

B.

Presence of at least three of the following four characteristics for a diagnosis of classic migraine:

1.

One or more fully reversible aura symptoms indicating focal cerebral cortical or brainstem dysfunction (or both)

2.

At least one aura symptom developing gradually over more than 4 minutes, or two or more symptoms occurring in succession

3.

No single aura symptom lasting longer than 60 minutes

4.

Headache beginning during aura or afterward, with a symptom-free interval of less than 60 minutes (also may begin before aura)

C.

Exclusion of related organic diseases by means of an appropriate history, physical examination, and neurologic examination with appropriate diagnostic tests

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32
Q

Nommer des facteurs de risque de HSA anévrysmale

A

Other risk factors associated with SAH include hypertension, smoking, excessive alcohol consumption, and use of sympathomimetic drugs. A familial association of cerebral aneurysms with several diseases has been described, including autosomal dominant polycystic kidney disease, coarctation of the aorta, Marfan syndrome, and Ehlers-Danlos syndrome type IV

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33
Q

Détailler l’échelle de Hunt and Hess pour les HSA

A

0Unruptured aneurysm

1Asymptomatic or minimal headache and slight nuchal rigidity

2Moderate or severe headache, nuchal rigidity, no neurologic deficit other than cranial nerve palsy

3Drowsiness, confusion, or mild focal deficit

4Stupor, moderate to severe hemiparesis

5Deep coma, decerebrate posturing, moribund appearance

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34
Q

DxD d’une céphalée thunderclap

A

cervical artery dissection (CAD), cerebral venous thrombosis (CVT), reversible cerebral vasoconstriction syndrome, hemorrhagic or ischemic stroke, and primary headache disorders, including migraine and cluster headaches.

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35
Q

Nommer la triade clinique associée à la dissection a. carotide

A

(1) unilateral headache or neck pain, sometimes radiating to the ipsilateral eye; (2) ipsilateral partial Horner’s syndrome; and (3) either blindness, due to retinal ischemia, or contralateral motor deficits, caused by cerebral ischemia.

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36
Q

Nommer des FR de thrombose veineuse cérébrale

A

Coagulopathie: Déficit protéine C/S, antithrombine, mutation V Leiden

Prise contraceptifs oraux, suppléments hormonaux

Néoplasie, maladie inflammatoire/auto-immune

Trauma crânien

Chirurgies, neurochirurgies

Grossesse

Infections para-méningées

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37
Q

Décrire la symptomatologie de la thrombose veineuse cérébrale

A
  1. Sx reliés à HTIC
  2. Sx reliés à atteinte focale 2nd ischémie/hémorragie

Céphalée, convulsions

Dlr occulaire, proptose, chémosis, atteinte mvts extra-oculaires, papilloedème

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38
Q

Critères dx d’hypertension intracrânienne idiopathique

A

Headache that remits with normalization of CSF pressure

Papilledema

Nonfocal neurologic examination

May have CN VI palsy

Increased CSF opening pressure

>250 mm in adults

>280 mm in children

Normal CSF diagnostic studies

Normal neuroimaging studies

No other cause of increased ICP identified

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39
Q

Nommer les critères diagnostiques du délirium

A

Disturbance in attention and awareness.

•

The disturbance develops over a short time period, represents a change from baseline attention and awareness, and tends to fluctuate in severity during the day.

•

There are additional disturbances in cognition, such as memory, disorientation language, visual spatial ability, or perception.

•

The disturbances are not better explained by another preexisting, established, or evolving neurocognitive disorder and do not occur in context of a coma.

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40
Q

Nommer des causes de démence

A

Primary Degenerative Dementias

Alzheimer’s disease

Lewy bodies disease

Frontal lobe disease (Pick’s disease)

Subcortical Dementias

Parkinson’s disease

Huntington’s disease

Vascular Dementia

Multi-infarct dementia

Intracranial Processes

Space occupying lesions (tumor, subdural hematoma)

Hydrocephalus

CNS infections (HIV-1, neurosyphilis, chronic meningitis)

Repetitive head trauma

Endocrinopathies

Addinson’s and Cushing’s diseases

Thyroid and parathyroid disease

Nutritional Deficiencies

Thiamine

Niacin

Folate

Vitamin B12

Toxic Exposures

Heavy metals

Carbon monoxide

Carbon disulfide

Drugs

Psychotropics

Antihypertensives

Anticonvulsants

Anticholinergics

Depression

Pseudo-dementia

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41
Q

Critères de démence

A

A.

Cognitive decline from a previous level of performance in one or more cognitive domains: Complex attention, executive function, learning and memory, language, perceptual motor function, or social cognition.

B.

The disorder has an insidious onset and gradual progression.

C.

The deficits do not occur exclusively during the course of a delirium.

D.

The cognitive deficits are not better explained by another mental disorder, such as major depression or schizophrenia

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42
Q
A
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43
Q

Traitement de choix de la névralgie du trijumeau

A

Carbamazépine

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44
Q

Décrire la fonction du 7e nerf crânien

A
  • Innervation motrice du visage
  • goût + sensibilité 2/3 ant de la langue et palais mou
  • Sensibilité CAE
  • innervation parasympathique glandes sous-mandibulaire, sublinguales, lacrimales, nasale, palatines
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45
Q

Nommer les causes les + fréquentes de paralysie faciale périphérique

A

PAralysie de Bell, maladie Lyme, Ramsey-Hunt, infections de l’oreille moyenne, mastoide et CAE.

Trauma- fracture de l’os temporal, tumeur

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46
Q

Nommer signes/sx associés à la paralysie de Bell

A

PAralysie faciale aigue, s’installant sur 72 heures, devient complète en 1-7 jours

Changements sensitifs a/n visage

Dysgeusie

Hyperacousie

Otalgie

Épiphora (augmentation des larmes coulant sur les joues)

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47
Q

Nommer la triade du syndrome de Ramsey-Hunt

A

Paralysie faciale

Rash vésiculaire herpétiforme a/n oreille externe, CAE, tympan, palais, visage

Dysfonction vestibulocochléaire (audition)

48
Q

Nommer 2 étiologies fréquentes de paralysie faciale bilatérales

A

Maladie de Lyme

Mononucléose infectieuse

49
Q

Traitement de la paralysie de Bell

A

Pred 50mg/jour x 10 jours

Pour sx sévères, considérer ajout valacyclovir 1000mg PO TID x 7jours

50
Q

Traitement Ramsey-Hunt

A

Prednisone 50mg/jour + Valacyclovir 1000mg PO TID x 10jours

51
Q

Discuter du neurinome acoustique (schwanome vestibulaire)

A

Tumeur située à l’angle pontocérébelleux, associé à perte d’audition unilatérale, progressive avec accouphène et déséquilibre,

Ménière cause aussi perte d’audition unilatérale mais avec vertige franc.

Méningiome est la 2e tumeur la + fréquente de l’angle ponto-cérébelleux

52
Q

Quel est le nerf le + affecté dans la mononeuropathie diabétique

A

CN III, puis IV et VI

53
Q

Décrire la présentation d’une thrombose veineuse cérébrale

A

Céphalée, diplopie, atteinte nerfs 3,4,6. Sx d’HTIC

54
Q

Nommer des sx fréquents initiaux d’une sclérose en plaques

A
  • Névrite optique
  • Névralgie du trijumeau
  • Diplopie et nystagmus avec oscillopsie
  • Sx sensitifs diverses: paresthésie, engourdissement, aiguilles, sensation d’oedème
55
Q

DxD de la sclérose en plaques

A

Tumeurs SNC

Encéphalomyélite post-infectieuse/vaccinale

Maladie Lyme

Déficit B12

Vasculites

Behcet

Encéphalopathie VIH

Neuro sarcoidose

Compression moelle épinière

56
Q

Décrire le Uhthoff’s phenomenon

A

Détérioration des sx neurologiques avec une hausse de la température corporelle

57
Q

Traitement de la sclérose en plaque

A
  1. Ralentir la progression de la maladie: interferon ou glatiramer
  2. Tx exacerbation: solumedrol (pas PO)
  3. Tx complications: spasticité avec baclofen, tremblements/ataxie avec propranolol, diazepam, névralgie trijumeau avec carbamazépine
58
Q

Décrire la vascularisation de la moelle épinière

A
  1. Artère spinale antérieure, qui provient des 2 artères vertébrales. Perfuse les 2/3 ant de la moelle
  2. 2 artères spinales postérieures qui irriguent le 1/3 post.
  3. Contribution des artères radiculaires
  4. Artère d’Adamkiewicz, qui origine entre T8 et L4
59
Q

Sydromes de la moelle épinière

A

p.1299

60
Q

Nommer des étiologies de Brown-Sequard syndrome

A

Trauma, tumeur, malformation vasculaire, hématome épidural, manipulation spinale, myélite à herpes zoster, lésion radique, spondylolise cervicale, atteinte discale dégénérative

61
Q

Nommer des causes de syringomyélie

A

Arnold chiari type 1

Post-trauma

Post- méningite

Tumeur compressive

62
Q

Décrire la présentation classique de la syringomyélie

A

The most common features on physical examination are lower limb hyperreflexia, weakness and wasting in the hands and arms, dissociated sensory loss, and gait disorder. The classic pattern of sensory deficit involves a loss of pain and temperature sensation in the upper extremities with preservation of proprioception and light touch

The sensory deficit often is described as being in a “capelike” distribution over the shoulders and arms. The anatomic basis for the neurologic features of a syrinx is the location near the central canal.

63
Q

Schématisez les neuropathies périphériques

A

Atteinte symétrique

  1. distale, mixte (sensitif + moteur): polyneuropathie sym distale
  2. prox/distale, mixte: polyneuropathie aigue démyélinisante (guillain-barré) ou polyneuropathie démyélinisante inflammatoire chronique

Atteinte asymétrique

  1. prox/distale, mixte: plexopathie, radiculopathie
  2. distale, mixte: mononeuropathie ou mononeuropathie multiplex
  3. distale, pure, mononeuropathie motrice ou sensitive
64
Q

Nommer des causes de faiblesse urgente pouvant entraîner détresse respiratoire

A

Autoimmune

Demyelinating

Guillain-Barré syndrome (GBS)

Chronic inflammatory demyelinating polyneuropathy

Myasthenia gravis

Toxic

Botulism

Buckthorn

Seafood

Paralytic shellfish toxin

Tetrodotoxin (puffer fish, newts)

Tick paralysis

Metals

Arsenic

Thallium

Metabolic

Dyskalemic syndromes

Acquired (especially with thyrotoxicosis)

Familial

Hypophosphatemia

Hypermagnesemia

Porphyria

Infectious

Poliomyelitis

Diphtheria

65
Q

Nommer des polyneuropathies démyélinisantes

A

Guillain-Barré syndrome (GBS)

Acute inflammatory demyelinating polyradiculoneuropathy

Acute motor axonal neuropathy

Acute motor and sensory axonal neuropathy

Miller Fisher syndrome

Chronic inflammatory demyelinating polyradiculoplexoneuropathy

Malignant disease

Human immunodeficiency virus (HIV) infection

Hepatitis B

Buckthorn

Diphtheria

66
Q

Nommer 4 pathogènes associés au guillain-barré

A
  1. Campylobacter jejuni

et CMV, EBV, mycoplasme pneumoniae

67
Q

PAramètres respiratoires inquiétant en cas de guillain-barré

A

MIP inférieur à -30 cmH2O

CVF inférieur à 20 mL/kg

68
Q

traitement du Guillain-Barré

A

IVIg ou plasmaphérèse.

IVIg = 400mg/kg / jour x 5 jours

69
Q

Causes de polyneuropathies distales mixtes

A

Diabète

Alcool

VIH

Néo et paranéo

Héréditaires

Toxines: agents industriels

Métaux: mercure, or, arsenic, thallium

Nutritionnel: beriberi (thiamine), anémie pernicieuse B12, pellagre niacine, déficit pyridoxine

Paraprotéines: myélome multiple, waldenstrom, MGUS, amyloidose

Dysfonction d’organes: urémie, maladie pulmonaire, hypoT4, acromégalie

Rx : nitrofurantoine/metronidazole/antirétroviraux/dapsone/ INH, disulfiram, paclitaxel, vinblastine/vincristine, amiodarone, phenytoine, statines, thalidomide

Porphyrie

70
Q

Traitement symptomatique de la polyneuropathie diabétique

A

Gabapentin, lyrica, amitriptyline, duloxetine, carbamazepine, tramadol,

71
Q

Nommer des causes de polyneuropathie distal+ prox asymétrique

A

Plexopathie brachiale / lombosacrée

Brachial Plexopathy

Open

Direct plexus injury (knife or gunshot wound)

Neurovascular (plexus ischemia)

Iatrogenic (central line insertion)

Closed

Traction injuries

“Stingers”

Traction neurapraxia

Partial or complete nerve root avulsion

Radiation

Neoplastic

Idiopathic brachial plexitis

Thoracic outlet

Lumbosacral Plexopathies

Open

Closed

Traction injuries

Pelvic double vertical shearing fracture

Posterior hip dislocation

Retroperitoneal hemorrhage

Vasospastic (deep buttock injection)

Neoplastic

Radiation

Idiopathic lumbosacral plexitis

Infectious

Herpesvirus (sacrococcygeal)

Herpes simplex 2

Herpes zoster

Cytomegalovirus polyradiculopathy (HIV infection)

72
Q

Nommer des mononeuropathies isolées

A

Upper Extremity

Radial nerve

  1. Axilla - rare, implique alors faiblesse triceps + poignet/main
  2. Humerus - saturday night palsy
  3. Elbow (posterior interosseous neuropathy)
  4. Wrist (superficial cutaneous radial neuropathy)

Ulnar nerve

  1. Axilla
  2. Humerus
  3. Elbow
  4. Condylar groove
  5. Cubital tunnel: a/n coude, distal au condyoar groove
  6. Wrist (Guyon’s canal): ne cause pas de sx sensitifs car les branches palmaires et dorsales sortent AVANT le canal de Guyon (sauf branche superficielle terminale)
  7. Hand
    1. Superficial terminal ulnar neuropathy: face palmaire 4e-5e doigts
    2. Deep terminal ulnar neuropathy: innervation des interosseux ad côté radial

Median nerve

  1. Axilla
  2. Humerus (musculocutaneous mononeuropathy)
  3. Forearm
  4. Anterior interosseus
  5. Pronator syndrome
  6. Wrist (carpal tunnel)
  7. Hand (recurrent motor branch)

Suprascapular mononeuropathy

Axillary mononeuropathy

Lower Extremity

Sciatic nerve

Femoral nerve

  1. Iliacus compartment (proximal)
  2. Saphenous mononeuropathy (distal)

Lateral femoral cutaneous (meralgia paresthetica)

Peroneal nerve: inversion possible (via nerf tibial) alors qu’impossible lors d’atteinte du nerf sciatique

  1. Common peroneal mononeuropathy (fibular head, popliteal fossa)
  2. Deep peroneal mononeuropathy (anterior compartment)

Tibial nerve

  1. Popliteal fossa (proximal)
  2. Tarsal tunnel (distal)

Sural nerve

  1. Popliteal fossa, calf (proximal)
  2. Fifth metatarsal base (distal)

Plantar nerve

  1. Distal to tarsal tunnel
  2. Interdigital neuropathies (Morton’s neuroma)

Obturator mononeuropathy

73
Q

Nommer des conditions associées au tunnel carpien

A

Acromegaly

Amyloid

Diabetes mellitus

Hypothyroidism

Obesity

Pregnancy

Renal failure

Rheumatoid arthritis

74
Q
A
75
Q

Nommer des causes de mononeuropathies multiplex

A

Vasculitis

Systemic vasculitis

Polyarteritis nodosa

Rheumatoid arthritis

Systemic lupus erythematosus

Sjögren’s syndrome (keratoconjunctivitis sicca)

Nonsystemic vasculitis

Diabetes mellitus

Neoplastic

Paraneoplastic

Direct infiltration

Infectious

Lyme disease

HIV infection

Sarcoid

Toxic (lead)

Transient (polycythemia vera)

Cryoglobulinemia (hepatitis C)

76
Q

Nommer des causes de neuropathies sensitives

A

Herpes

Herpes simplex 1 and 2

Varicella-zoster (shingles)

Inflammatory sensory polyganglionopathy

Paraneoplastic

Primary biliary cirrhosis

Sjögren’s syndrome (keratoconjunctivitis sicca)

Toxin induced

Pyridoxine (vitamin B6) overdose

Metals

Platinum (cisplatin)

Methyl mercury

Vitamin E deficiency

77
Q

Décrire les caractéristiques des différentes maladies neuromusculaires

A
78
Q

Pourquoi note-on une faiblesse avec stimulation répétée lors d’atteinte de la jonction neuromusculaire?

A

Botulisme: diminution de la libération d’acétylcholine

Myasthénie grave: blocage des récepteurs nicotiniques

Intoxication organophosphates:inactivation de l’acétylcholine par liaison irréversible

Repeated stimulation leads to diminishing motor strength, which is caused by one of three mechanisms: blockage of the receptors, as in myasthenia gravis; decrease in the amount of ACh released, as in botulism; or inactivation of ACh by irreversible binding, as in organophosphate poisoning.

79
Q

Décrire la pathophysiologie du syndrome myasthénique de Lambert-eaton

A

Environ 90% des patients possèdent des anticorps pathogéniques dirigés contre les canaux calciques voltage-dépendants (CCVD) de type P/Q. Le dysfonctionnement et la diminution du nombre de ces canaux inhibe la libération de l’acétylcholine des terminaisons présynaptiques, ce qui conduit à une altération de la transmission neuromusculaire et à une faiblesse musculaire.

In the case of Lambert-Eaton myasthenic syndrome, weakness is more pronounced at the beginning of muscle use and improves with repeated use as more ACh builds up in the synaptic cleft with each stimulation.

80
Q

Décrire la physiopathologie de la myasthénie grave

A
  1. Anticorps contre récepteurs Ach post-synaptique
  2. BLocage transmission Ach
  3. Internalisation et dégradation des récepteurs
  4. Destruction de la membrane par activation du complément
81
Q

Nommer 10 médicaments pouvant exacerber la myasthénie grave

A
82
Q

Traitement crise myasthénique

A

Admission USI

Surveillance respiratoire, MIP/MEP, CVF

Éliminer tous les Rx qui peuvent exacerber sx

Traitement précipitant ex infection

IVIg ou échanges plasmatiques (certains préfèrent plasmaphérèse, mais si pas différence significative démontrée entre les deux

Cortico hautes doses 60mg/jour - ou immunosuppresseurs si cortico CI

* attention cortico pour exacerber faiblesse initialement

pyridostigmine (tx en externe, inhibiteurs de la cholinestérase): non recommandé en crise (éviter augmentation des sécrétions associées)

Intubation: anectine ok mais dose augmentée nécessaire

83
Q

Décrire 2 tests pouvant être réalisés au chevet pour préciser le dx de la myasthénie grave

A

The edrophonium test and ice bag test are performed at the bedside for patients with suspected myasthenia gravis and ptosis. The results based on the effect of the intervention on the ptosis. Edrophonium is a short-acting acetylcholinesterase-blocking agent that produces an increase of ACh in the synaptic cleft and a reduction in ptosis after intravenous (IV) administration. With the ice bag test, cooling decreases symptoms in myasthenia gravis, whereas heat exacerbates symptoms. In both tests, the amount of ptosis is measured before and after administration of edrophonium or application of an ice bag. The distance from the upper to the lower eyelid in the most severely affected eye is measured first. If edrophonium is given, an IV test dose of 1 to 2 mg is given first because some patients have a severe reaction. If no adverse reaction is found and the patient does not dramatically improve in 30 to 90 seconds, a second dose of 3 mg is given. If there is still no response, a final dose of 5 mg is given for a total maximum dose of 10 mg. Atropine should be available at the bedside during the test. Because of the potential for cholinergic-induced increased airway secretions, this test should be used with caution in asthmatics and patients with chronic obstructive pulmonary disease. If the ice bag test is used, an ice pack is applied to the affected eye for approximately 2 minutes. An improvement in the amount of ptosis of at least 2 mm is considered positive. The pooled sensitivity and specificity of the ice bag test for detecting ocular myasthenia The edrophonium test and ice bag test are performed at the bedside for patients with suspected myasthenia gravis and ptosis. The results based on the effect of the intervention on the ptosis. Edrophonium is a short-acting acetylcholinesterase-blocking agent that produces an increase of ACh in the synaptic cleft and a reduction in ptosis after intravenous (IV) administration. With the ice bag test, cooling decreases symptoms in myasthenia gravis, whereas heat exacerbates symptoms. In both tests, the amount of ptosis is measured before and after administration of edrophonium or application of an ice bag. The distance from the upper to the lower eyelid in the most severely affected eye is measured first. If edrophonium is given, an IV test dose of 1 to 2 mg is given first because some patients have a severe reaction. If no adverse reaction is found and the patient does not dramatically improve in 30 to 90 seconds, a second dose of 3 mg is given. If there is still no response, a final dose of 5 mg is given for a total maximum dose of 10 mg. Atropine should be available at the bedside during the test. Because of the potential for cholinergic-induced increased airway secretions, this test should be used with caution in asthmatics and patients with chronic obstructive pulmonary disease. If the ice bag test is used, an ice pack is applied to the affected eye for approximately 2 minutes. An improvement in the amount of ptosis of at least 2 mm is considered positive. The pooled sensitivity and specificity of the ice bag test for detecting ocular myasthenia

84
Q

Décrire la physiopathologie du botulisme et sa présentation clinique

A

LA toxine se lit de facon irréversible à la membrane pré-synaptique et inhibe la libération d’acétylcholine

The botulinum toxin blocks both voluntary motor and autonomic functions. There is no pain or sensory deficit. The onset of symptoms is 6 to 48 hours after the ingestion of tainted food. Symptoms of gastroenteritis may or may not be present. The classic feature of botulism is a descending, symmetrical, flaccid paralysis. Cranial nerves and bulbar muscles are affected first, causing diplopia, dysarthria, and dysphagia, followed later by generalized weakness. Because the toxin decreases cholinergic output, anticholinergic signs may be present: constipation, urinary retention, dry skin and eyes, and increased temperature and dilated, non-reactive pupils. This can help differentiate botulism toxicity from myasthenia gravis. Deep tendon reflexes are normal or diminished.

85
Q
A
86
Q

Pourquoi ne pouvons-nous pas donner de miel à un enfant de moins d’un an?

A

Infantile botulism results from the ingestion of C. botulinum spores that are able to germinate and produce toxin in the high pH of the gastrointestinal tract of infants. Botulism spores can survive in honey, so it is recommended that honey not be fed to infants.

87
Q

Traitement du botulisme

A

Admission USI

Suivi respiratoire

Anti-toxine rapidement

IVIg si disponible

Pas antibio pour botulisme infantile

Antibio si botulisme 2nd plaie: pen G ou flagyl si all. et débridement de la plaie +++

88
Q

Décrire la présentation clinique de la paralysie 2nd tique

A

pathophysiologie identique au botulisme. Paralysie flasque ascendante (similaire à Guillain-Barré), mais parfois atteinte oculaire avec pupilles dilatées et fixes.

Traitement de support et retirer la tique

89
Q

Nommer les 2 grandes catégories de myopathies

A

Inflammatoires et toxico-métaboliques

90
Q

Décrire la présentation classique de la dermato/polymyosite

A

Douleur et faiblesse. Diminution des réflexes proportionnelle à la faiblesse musculaire. Svt post-viral, peut être paranéoplasique. Dermatomyosite avec atteinte cutanée, rash photosensible/ érythème a/n dorsum des mains a/n extenseurs

91
Q

Étiologies métaboliques de myopathies

A

Hypo/hyperkaliémie, hypo/hypercalcémie, hypophosphatémie, hypomagnésémie

Associées aux dysthyroidies, dysparathyroidies, atteintes surrénales

Paralysies périodiques

92
Q
A
93
Q

Discuter de la paralysie périodique

A

3 formes

  1. Hypokaliémique
  2. Hyperkaliémique

Hypo/hyper: maladie héréditaire, forme hypo + fréquente

  1. Thyrotoxique: associé à l’hyperthyroidie, forme acquise de paralysie périodique hypokaliémique. Augmentation de l’activité de la pompe NaKATP ase avec shift intracellulaire de K.

Faiblesse MI > MS, pas d’atteinte bulbaire/ oculaires ou du système respiratoire. Svt après un gros repas (shift de potassium 2nd insuline)

Traitement: autorésolutif, remplacement IV de K prudent car pas de déplétion corporel, max 20 MeQ IV puis PO.

94
Q

Nommer les pathogènes fréquents de la méningite

A

N. meningitidis

S. pneumoniae

L. monocytogenes

H influenzae

Après manipulation chirurgicale, pneumocoque, staph aureus, pseudo, entérobactéries

95
Q

Nommer les facteurs de risque de méningite

A

Age < 5 ans et > 60 ans

Sexe masculin

Africains/américains

Faible statut socio-économique / promiscuité

Alcool/cirrhose / UDIV

Diabète

Immunosuppression / splénectomie

Anémie falciforme / thalassémie majeure

Néoplasie

Atteinte durale (trauma, chirurgie, congénital, shunt)

Infection contigue (sinusite, otite, abcès dentaire)

Endocardite bactérienne

Contact étroit avec méningite

Colonisation antérieure

96
Q

Nommer les complications de la méningite

A

Immédiates: coma, perte protection airway, arrêt respiratoire, mort, convulsions, ép. péricardique, oedème cérébral, choc/CIVD

Retardées: déficit neurologique, surdité, empyème sous-dural, épilepsie, retard intellectuel, hydrocéphalie, thrombose veineuse cérébrale, hémorragie bilatérale surrénales (Waterhouse-Friderichsen associé à la méningococcémie), mort

97
Q

Nommer les causes de méningite aseptique

A

Infectieux: virus / bactérie / fongique/ parasite / rickettsie

Enteroviruses—polio, Coxsackie, echovirus

Herpes group of viruses

Herpes simplex virus (HSV) types 1 and 2

Varicella zoster virus

Cytomegalovirus

Epstein-Barr virus

Human herpes virus 6 (HHV-6)

Respiratory viruses

Adenovirus

Rhino virus

Influenza virus types A and B

Arboviruses

Mumps virus

Lymphocytic choriomeningitis

Human immunodeficiency virus (HIV)

Bacteria

Partially treated meningitis

Parameningeal infection

Endocarditis

Mycoplasma pneumonia

Mycobacterium tuberculosis

Ehrlichiosis

Borrelia burgdorferi

Treponema pallidum

Brucella

Leptospirosis

Fungi

Cryptococcus neoformans

Histoplasma capsulatum

Coccidioides immitis

Blastomyces dermatitides

Candida

Parasites

Toxoplasma gondii

Neurocysticercosis

Trichinosis

Naegleria

Hartmannella

Bartonella henselae

Rickettsiae

Rocky Mountain spotted fever

Typhus

Post-infectieux/ vaccinal

  1. Rubella

Rubella

Varicella

Variola

Rabies vaccine

Pertussis vaccine

Influenza vaccine

Vaccinia

Yellow fever vaccine

Rx:

  1. Nonsteroidal anti-inflammatory drugs (NSAIDs)

Trimethoprim-sulfamethoxazole, amoxicillin

Muromonab CD3 (OKT3)

Azathioprine

Intravenous (IV) immunoglobulin

Isoniazid

Intrathecal methotrexate

Intrathecal cytosine arabinoside

Allopurinol

Carbamazepine

Sulfasalazine

Maladies systémiques

  1. Collagen vascular disorders

Systemic lupus erythematosus

Wegener’s granulomatosis

Central nervous system (CNS) vasculitis

Rheumatoid arthritis

Kawasaki’s disease

Sarcoidosis

Leptomeningeal cancer

Post-transplantation lymphoproliferative disorder

Behçet’s disease

Vogt-Koyanagi syndrome

Néoplasies

  1. Leucémie
  2. Méningite carcinomateuse

Infection contigue

  1. abcès cérébral
  2. abcès épidural

Divers

  1. migraine
  2. Infection urinaire
  3. Arachnoidite
98
Q

Décrire le gram pour les pathogènes fréquents de méningite

A

Seuil maximum normal < 5 GB / mm3

99
Q

Traitement méningite

A
100
Q

Antibioprophylaxie en cas de contact avec méningite

A

Among household contacts, the incidence of transmission of meningococcus is approximately 5%; therefore, we recommend that household contacts of bacteriologically confirmed cases receive rifampin (adults, 600 mg; children older than 1 month, 10 mg/kg; children younger than 1 month, 5 mg/kg) orally every 12 hours for a total of four doses. Ciprofloxacin 500 mg by mouth (adults only) and ceftriaxone 250 mg intramuscularly (125 mg intramuscularly for children younger than 15 years old) provide single-dose alternatives.

PAs de prophylaxie contre pneumocoque

101
Q

Nommer principaux médicaments pouvant précipiter une crise myasthénique

A

Antibios: aminoglycosides, fluoroquinolones, macrolides, vanco

Cardiaque: procainamide, betabloqueurs, quinine

Magnésium

NMB

AC monoclonaux ex pembro

Chloroquine, plaquenil

102
Q

Sx AVC cérébrale antérieure/moyenne/postérieure

A

Antérieure: AEC, jugement altéré, réflexes primitifs, incontinence, apraxie, démarche ébrieuse, paralysie MI opposée à la lésion, dysesthésie MI opposée à la lésion

Moyenne: Paralysie MS/visage opposée à la lésion, sensibilité MS/visage opposé, aphasie broca/wernicke, dysarthrie, négligence, hémianopsie, agnosie, déviation du regard VERS la lésion

Postérieure: Paralysie 3e nerf crânien, hémianopsie, Alexie, syncope, agnosie visuelle, nystagmus, no/vo, vertige

6 signes précoces AVC: artère hyperdense, Diminution sustance grise: perte différenciation/ perte du ruban cortical/disparition des noyaux gris centraux, perte sulcus, effet de masse: effacement des sillons/oedème cérébral, hypodensité aigue

103
Q

Volume hématome intra parenchymateux

A

A x B x C / 2 ( nombre coupes x long x largeur / 2)

104
Q

Inclusion / exclusion thrombolyse

A

Inclusion: age adulte, AVC ischémique avec déficit clinique mesurable, durée des symptômes inférieure 3heures

Exclusion:

Guidelines 2018 - AHA

105
Q

Signes au TDM de thrombose veineuse centrale

A
  • hyperdensité sinus veineux
  • Hyperdensité veine profonde
  • oedème cérébral
  • hémorragie 2nd congestion veineuse
106
Q

Triade dissection carotidienne

A

Horner incomplet (sudation préservée)

Céphalée unilatérale

Perte de vision unilatérale

107
Q

5 dxd névralgie trijumeau

A

lésion ATM

zona

ramsay-hunt

masse

abcès dentaire

108
Q

SEP

A

Diplopie, névrite optique, nystagmus

Dysarthrie, dysmétrie, dysdiadococinésie

Ataxie

Paralysie, parésie 4 membres

Paresthésie

Dysfonction sexuelle, urinaire, fécale

109
Q
A
110
Q

5 signes / sx myélite transverse

A

Paraplégie

Clonus

Hyperréflexie

Babinski

Déficit sensitif transverse

111
Q

Triade botulisme

A

Sx GI

Sx neuro

Sx anticholinergiques

112
Q

4 agents infectieux 2nd Guillain-Barré

A

Campylobacter

CMV

EBV

Mycoplasma

113
Q

Causes de détresse respiratoire aigue

A

Botulisme

Myasthénie grave

Guillain-Barré

Lambert eaton

Tick paralysis

Paralysis periodic

Puffy fish - tetrodotoxine

Shellfish toxine

Diphtérie/poliomyélite

Organophosphates

HyperMg, hypophosphatémie

Buckthorn

114
Q

Mesures de force pour maladies neuromusculaire

A

CVF infé 20 mL/kg

MIP / MEP ( -30 / -40)

PCO2 augmentée

115
Q

Méningite aseptique

A

Carcinomatose méningée

Leucémie

Abcès

Arachnoidite),

Post-vaccinal

INfectieux (viral, bactérien traité, fungique, rickettsie)

Médicament ( AINS, sulfa, carbamazépine, allopurinol)

116
Q
A

Collège Royal 2019 (23 decks)

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