Neurological Emergencies Flashcards

1
Q

What are the types of ischemic strokes?

A

1- embolic: cardioembolic or atheroembolic from carotids

2- atherosclerotic:lacunar small vessel or intracranial large artery

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2
Q

How does an ischemic stroke present?

A

Sudden onset of localizing neurological deficits

do a CT scan immediately to exclude hemorrhagic strokes then give alteplase

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3
Q

What are the contraindications for thrombolytics?

A

1- major head trauma or surgery within the last 3 weeks
2- prior hemorrhagic stroke
3- ischemic stroke within prior 6 months
4- CNS neoplasm
5- GI bleeding within 1 month
6- active bleeding

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4
Q

How are ischemic strokes treated?

A
  • if > 18 years old & <4.5h -> give thrombolytics (alteplase works best for small & medium vessel occlusions)
  • if NIHHS > 6 or there are contraindications -> CT angiogram (look for large vessel occlusion)
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5
Q

What is the cause of a hemorrhagic stroke?

A

rupture of deep penetrating vessels -> rapidly expanding hematoma -> mass effect & tearing off ascending & descending tracts

commonly caused by

  • HYPERTENSION
  • amyloid angiopathy (in elderly)
  • use of anticoagulants (warfarin, enoxaparin, apixaban)
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6
Q

What are the common locations of intracranial hemorrhages?

A

HYPERTENSIVE ICH

  • basal ganglia
  • thalamus
  • brainstem
  • cerebellum

AMYLOID ICH (lobar)

  • frontal
  • parietal
  • occipital
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7
Q

What is the presentation of a hemorrhagic stroke?

A
  • headache
  • focal neurological symptoms
  • depressed level of consciousness
  • coma

DETERIORATES VERY QUICKLY

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8
Q

How is a hemorrhagic stroke managed?

A

1- ABC -> intubation for airway protection
2- treat hypertension
3- reverse anticoagulation -> FFP or PCC
4- rehab

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9
Q

What is the cause of thunderclap headaches?

A

subarachnoid hemorrhage -> rupture of intracranial aneurysm results in spillage of blood contents into subarachnoid space
- Estrella de la muertes -> headahce emergency

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10
Q

What are the complications of subarachnoid hemorrhages?

A
  • death
  • coma
  • rebleeding -> 80% mortality
  • SIADH or cerebral salt wasting
  • Neuromyocardiac stunning -> Takasubo’s cardiomyopathy
  • neurogenic pulmonary edema
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11
Q

How is a subarachnoid hemorrhage treated?

A
1- ABC
2- control blood pressure <120SBP
3- surgical clipping or angiographic coiling or the aneurysm 
4- prevent vasospasm 
5- treat SIADH or CSW
6- supportive care
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12
Q

How does myasthenia gravis manifest?

A

generalized muscle weakness that could lead to respiratory failure

  • any skeletal muscle could be affected
  • antibody production against acetylcholine receptors, MuSK or LPR4
  • could be thymoma or non-thymoma related
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13
Q

What is the presentation of myasthenia gravis?

A

fluctuating muscle weakness that varies in severity precipitated by infections, surgery, immunization, heat, emotional stress, pregnancy, worsening or chronic illnesses

  • worsens with physical activity & improves with rest
  • extra ocular muscles -> diplopia & ptosis
  • bulbar muscle weakness -> difficulty chewing or frequent choking, dysphagia, hoarseness, & dysarthria
  • facial muscles -> expressionless face
  • neck muscles -> dropped-head syndrome
  • limbs -> weakness of the proximal muscles more than distal & upper limb more than lower
  • intercostal muscles & diaphragm -> myasthenic crises
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14
Q

How can myasthenia gravis be diagnosed clinically?

A

patient will fail sustained muscle contraction

  • patient will not be able to abduct their arms > 120s
  • sustained upward gaze >60s results in ptosis
  • sustained lateral gaze results in diplopia
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15
Q

What workups should be ordered to confirm the diagnosis of myasthenia gravis?

A
  • serology -> anti-acetylcholine receptor antibodies, anti-MuSK, & anti-LPR4
  • neurophysiological testing -> DECREMENTAL RESPONSE with repetitive nerve stimulation
  • imaging -> to rule out thymoma
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16
Q

How is myasthenia gravis treated?

A
  • For acute relapses -> IVIG or plasmapheresis

- For maintenance -> steroids & immunosuppressants

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17
Q

Why are steroids contraindicated in acute relapses of myasthenia gravis?

A

could increase myopathy leading to myasthenic crises

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18
Q

What is the presentation of a myasthenic crises?

A

1- progressive generalized weakness & fatigue
2- short sentences, shortness of breath, or respiratory arrest
3- decrease in vital capacity to <1L & negative inspiratory force (NIF) <20
- may have other symptoms of MG -> ptosis, dysphagia, dysphonia, & neck weakness

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19
Q

What is the management of a myasthenic crises?

A

1- ABC -> intubation or BIPAP
2- monitored in ICU & hourly NIF & VC
3- plasmapheresis or IVIG to abort crisis
4- maintenance with immunosuppressants

20
Q

What is the definition of status epilepticus?

A

prolonged generalized seizures > 5 mins OR any back-to-back seizures with no regaining of consciousness in between
- diminished mental status, airway compromise, hypoxia or aspiration -> life-threatening

21
Q

How is status epilepticus managed?

A

1- ABCDEFG (dont ever forget the Glucose)
2- First-line agents (0-5 mins) -> BENZOS (lorazepam or midazolam)
3- Second-line agents (10-15 mins) -> Levetiracetam OR phenytoin OR valproate
4- if refractory (15-20 mins) -> general anesthesia (propofol or ketamine)

22
Q

What are the causes of spinal cord compression?

A
  • TRAUMA is the most common
  • tumors
  • epidural abscess
  • epidural hematoma
  • herniated disc
  • spinal stenosis
23
Q

What is the clinical picture of spinal cord compression?

A
  • symmetric flaccid paralysis below the level of the lesion with sensory loss & bladder dysfunction
  • depending on the location of the compression it may present with -> central cord syndrome, Brown-Sequard syndrome, or Cauda Equina syndrome
24
Q

Compression of the L2-S1 nerve root will result in?

A

Cauda Equina Syndrome

  • sciatica
  • asymmetric weakness of LMNL
  • areflexia
  • sexual & sphincter dysfunction
  • saddle anesthesia
25
Q

What is the most common cause of Cauda Equina syndrome?

A

metastases

26
Q

How is cord compression treated?

A
  • epidural abscess & osteomyelitis -> antibiotics
  • metastatic tumors -> high dose steroids & radiation
  • surgical decompression, drainage, realignment, & fixation
27
Q

What is the pathophysiology of Guillian-Barre Syndrome?

A
  • post-infectious immune-mediated neuropathy
  • autoimmune destruction of nerves in the PNS
  • most common cause of acute, flaccid, neuromuscular paralysis
  • can be demyelination (80% recovery) or axonal (rare recovery)
28
Q

What is the clinical presentation of GBS?

A
  • symmetric ascending paralysis, numbness, & tingling
  • 7 - 10 days after infections (C. jejuni)
  • if respiratory muscles are involved -> respiratory failure & death
  • cranial nerve involvement -> facial weakness, dysphagia, & dysphonia
  • autonomic involvement -> hypotension/hyertension & bradycardia/tachycardia (FATAL)
  • areflexia is the most important sign in the physical exam
29
Q

What are the methods of investigation used to confirm the diagnosis of GBS?

A
  • nerve conduction studies -> conduction block & slow conduction velocities
  • LP -> typical albuminocytological dissociation
  • NIF to assess respiratory muscle function
30
Q

How is GBS treated?

A

IVIG or plasmapheresis

31
Q

What are the causes of meningitis?

A
1- Bacterial 
- Strep. pneumonia 
- N. meningitidis 
- H. influenzae 
- L. monocytogenes (in >65 & <1 years of age & immunosuppressed) 
2- Viral -> herpes simplex 
3- TB
4- Fungal
32
Q

What is the clinical presentation of meningitis?

A
- fever, headache, & altered mental state 
physically 
- fever 
- skin rash (Neisseria & Herpes) 
- neck stiffness 
- Kernig sign 
- Brudzinski sign
33
Q

What are the diagnostics used to confirm diagnosis of meningitis?

A
  • CBC
  • electrolytes -> hyponatremia due to SIADH
  • coagulation profile -> to rule out DIC
  • blood culture
  • LP for CSF
34
Q

How can we differentiate between the causes of meningitis with CSF?

A

Bacterial

  • neutrophils are predominant
  • very low glucose

Viral

  • lymphocytes are predominant
  • normal glucose

Fungal

  • lymphocytes are predominant
  • low glucose

Tubercular

  • lymphocytes are predominant
  • low glucose
35
Q

How is meningitis treated?

A

empirical therapy

  • ceftriaxone & vancomycin
  • ADD ampicillin in extremes of age
  • give steroids incase of Strep. pneumonia -> to prevent deafness
36
Q

What are the causes of encephalitis?

A
  • herpes virus

- enterovirus

37
Q

What is the clinical picture of encephalitis?

A
  • fever
  • headache
  • altered mental status
  • seizures
  • focal features
38
Q

What are the diagnostic tools used to confirm diagnosis of encephalopathy?

A
  • MRI
  • EEG
  • CSF
  • PCR
39
Q

What is the cause of bitemporal encephalitis?

A

herpes

40
Q

How is encephalitis treated?

A

only treatment available is for HSV

  • Acyclovir until PCR is negative
  • supportive care
41
Q

What are the complications of encephalitis?

A
  • cognitive impairment

- seizure disorders (epilepsy)

42
Q

What are the causes of brain abscesses?

A
  • infections -> otitis media, mastoiditis
  • hematogenous seeding -> septic embolus or endocarditis
  • trauma
  • surgery -> craniotomy

can invade brain by direct spread or through hematogenous seeding (caused by multiple multiorganisms)

43
Q

What are the clinical features of a brain abscess?

A
  • headache & fever
  • focal neurological deficits
  • increased intracranial pressure
  • seizure
44
Q

What diagnostic methods should be used to confirm diagnosis of a brain abscess?

A
  • MRI WITH CONTRAST
  • Lumbar puncture
    culture
  • histopathology
45
Q

How are brain abscesses treated?

A
  • broadspectrum antibiotics
  • add toxoplasmosis coverage in HIV patients
  • neurosurgical drainage & send pus for culture
  • maintain intracranial pressure