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CEN > Neurological Emergencies > Flashcards

Neurological Emergencies Flashcards

1
Q

What characteristics of headaches are important?

A 
Time of onset
Precipitating event
Type of pain
Rating
Location
Home remedies
Past history
Associated symptoms
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2
Q

What are five specific types of headaches?

A 
Tension
Migraine
Cluster
Sinus
Temporal arteritis
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3
Q

Describe a tension headache

A

Diffuse, band like pain
Non-pulsating
Treat with Analgesics

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4
Q

Describe a migraine headache

A

Throbbing, unilateral pain
Photophobia
Treat with sumatriptan

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5
Q

Describe a cluster headache

A

Knifelike, unilateral pain

Associated eye symptoms

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6
Q

Describe a sinus headache

A

Pain over sinuses
Associated ear symptoms
Treat with antibiotics

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7
Q

Describe temporal arteritis

A

Pain/tenderness to temporal area
Associated visual symptoms
Treat with steroids

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8
Q

Components that exert pressure within the cranial vault:

A 
Brain  = 80%
CSF     = 10%
Blood = 10%
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9
Q

4 reasons for increased intracranial-cranial pressure related to the brain

A

Tumor
Abscess
Intracranial bleed
Cerebral edema

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10
Q

4 reasons for increased intracranial pressure related to CSF

A

Hydrocephalus
Increased production
Flow obstruction
Impaired absorption

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11
Q

1 Reason for increased intercranial pressure related to the blood:

A

Vasodilation

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12
Q

What is normal intracranial pressure?

A

0-15 mm Hg

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13
Q

Why is cerebral edema a problem?

A

There are no lymphatic pathways in the central nervous system to carry the excess fluid away.

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14
Q

How does increased intercranial pressure cause a problem?

A

It causes cerebral ischemia (which causes an interference with delivery of both oxygen and glucose as well as an inability to remove waste products), increases the concentration of carbon dioxide and decreases oxygen concentration in the cerebral vessels. Carbon dioxide dilate blood vessels which further exacerbates the problem. Ischemia can be global as with an adequate blood flow or focal as with a stroke. In the presence of severe global ischemia, unconsciousness occurs within seconds.

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15
Q

What are 12 manifestations of increased ICP?

A 
Pain
N/V
Diplopia
Visual disturbances
Decreased LOC
Pupil changes – usually ipsilateral to lesion
Abnormal respiratory patterns
Hemiparesis – usually contra lateral to lesion
Hemiplegia
Seizures
Possible increase temperature
Loss of reflexes
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16
Q

What is Cushing’s triad?

A

Bradycardia
Hypertension
Bradypnea

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17
Q

What is cerebral perfusion pressure?

A

An indirect measurement of cerebral blood flow.

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18
Q

What is the equation for cerebral perfusion pressure?

A

CPP = MAP - ICP

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19
Q

A Cerebral Perfusion Pressure of ________ is necessary to maintain adequate perfusion?

A

CPP of 60-70 (40 for the pediatric patient)

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20
Q

________________ occurs as a protective response with elevated intercranial pressure.

A

Cushing-Kocher Response

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21
Q

What is a herniation?

A

When brain tissue protrudes out of normal compartment.

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22
Q

What are 3 areas for herniation to occur?

A

Fall Cerebrii
Tentorium Notch
Foramen Magnum

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23
Q

What are normal eye reflexes?

A

Corneal – eye blink
Oculo-cephalic (Dolls eyes) – the eyes should move in opposite direction
Oculo-vestibular - inject ice water into the ear and the eyes should move toward the ice water

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24
Q

What are two types of posturing associated with intracranial pressure and what do they signify?

A

Decerberate - rigid extension that signifies midbrain damage.
Decorticate - rigid flexion that signifies cortex damage.

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25
Q

What is the Babinski reflex?

A

An abnormal reflex in an adult that is illicited by rubbing the solar of the foot. A positive Babinski is where the great toe extends up and the remaining toes fan out.

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26
Q

What are the highest and lowest possible Glasgow coma scale?

A

Best score = 15

Lowest score = 3

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27
Q

When checking pupillary responses on a patient, you find one pupil larger and non-reactive and the smaller pupil reacts normally. What could be the possible neurological cause?

A

Oculomotor nerve compression by:
hematoma
tumor
cerebral edema (in same side of brain as lesion)

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28
Q

When checking pupillary responses on a patient, you find bilateral small pupils with a brisk reaction. What could the possible neurological cause be?

A 
Bilateral Diencephalon (Thalamus/Hypothalamus)
Consider Metabolic coma (DKA)
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29
Q

When checking pupillary response on a patient, you find one pupil smaller but both react (ptosis on smaller side). What are the possible neurological causes? (4)

A

Horner’s Syndrome
Hypothalamus damage
Lesion on lateral medulla or ventrolateral cervical spinal cord
May be an early sign of tentorial herniation

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30
Q

When performing pupillary responses on a patient, you find bilateral mid position and non-reactive pupils. What are the possible neurological causes?

A 
Midbrain infarction
Tentorial herniation (no sympathetic/parasympathetic innervation)
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31
Q

When performing pupillary responses on a patient, you find bilateral pinpoint pupils that are non-reactive. What could be the possible neurological cause?

A

Pontine hemorrhage

Opiate overdose

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32
Q

When performing pupillary responses on a patient, you find bilateral dilated pupils that are non-reactive. What is the possible neurological cause?

A

Terminal stages of anoxia, ischemia, death.
Also may be caused by atropine-like drugs
Ciliospinal reflex

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33
Q

Describe Cheyne-stokes respiratory pattern:

A

Rhythmic, waxing/waning in both depth and rate with periods of apnea.

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34
Q

Damage to what area of the brain causes Cheyne-Stokes respiratory pattern?

A

Usually bilateral basal ganglia – thalamus/hypothalamus.

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35
Q

Describe central neurogenic hyperventilation respiratory pattern:

A

Increase in the rate and depth.

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36
Q

Damage to what area of the brain causes central neurogenic hyperventilation respiratory pattern?

A

Pons/Midbrain (Respiratory center of brain)

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37
Q

Describe apneustic respiratory pattern:

A

Prolonged inspiration followed by a pause (2–3 seconds).

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38
Q

Damage to what area of the brain causes apneustic respiratory pattern?

A

Lower Pons

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39
Q

Describe cluster respiratory pattern:

A

Clusters of irregular breathing with irregular periods of apnea.

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40
Q

Damage to what area of the brain causes cluster respiratory pattern?

A

Lower pons/upper medulla

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41
Q

What is the treatment of increased intercranial pressure? (16)

A 
Maintain neutral head position
Avoid hip/knee flexion
Logroll
No prophylactic hyperventilation
Limited suctioning
Elevate HOB
Decrease stimuli
Medical decompression - diuretics - mannitol - hypertonic saline
Seizure precautions
OG tube preferred over NG tube
Fully
Anti-convulsive
No D5W
Paralytics with sedation
Barbiturate coma
Neuroprotective agents (decrease cerebral ischemia/ secondary injury/ neuronal deterioration, and stabilize cell membrane
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42
Q

What are four types of hemorrhages in the brain?

A

Intraparenchymal (Intracerebral)
Subarachnoid
Subdural
Epidural

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43
Q

Describe an intraparenchymal hemorrhage:

A 
Bleeding within cerebral tissue – can be the result of sharing of small vessels within hemispheres.
Moderate to severe pain.
Confusion.
Vomiting.
Altered gait.
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44
Q

Describe a subarachnoid hemorrhage:

A

Aneurysm.
Arterial bleed.
Described as “worst headache of my life.”
Blood in subarachnoid space causes meningeal signs (nuchal rigidity).
Can also be caused by trauma.
Sentinel headaches.

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45
Q

Describe a subdural hemorrhage:

A 
Acute/subacute/chronic.
Venous bleed.
Collection of blood between arachnoid and Dura Mater.
History is very important.
Progressive personality changes.
Elderly and alcoholics or shaken baby.
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46
Q

Describe an epidural hemorrhage:

A

Collection of blood between Dura and the skull.
Associated with temporal skull fractures.
Laceration of middle meningeal artery.
Arterial bleed.
Usually herniates.

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47
Q

What are seizures?

A

Abnormal electrical activity in brain from cerebral neurons.
May be primary or secondary in nature depending on cause.
Secondary seizures usually caused by an insult to cerebral tissue.
May have precipitating events.

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48
Q

What are 16 precipitating events that can cause seizures?

A 
Sleep deprivation
Emotional stress
Alcohol withdrawal/OD
Fever
Prescription drugs
Diet
Antihistamines
Hypoglycemia
Anti-cholinergics
Head trauma
Amphetamines
Illicit drugs
Anti-depressants
Marijuana
Anti-psychotics
Cocaine
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49
Q

What are the four types of partial seizures?

A

Focal motor
Jacksonian
Focal sensory
Complex partial

50
Q

Describe a focal motor seizure

A

Irritable focus on motor cortex/frontal lobe.
Clonic activity.
Slow repetitive jerking of part involved with increase in intensity.

51
Q

Describe a Jacksonian seizure

A

Focal motor seizure that spreads in orderly manner.

Begins in fingers with progression to entire extremity.

52
Q

Describe a focal sensory seizure

A

Irritable focus within sensory strip of parietal lobe.
Manifestations vary:
Visual/auditory hallucinations
Flashing/zigzag lights
Odd taste/smells
Numbness, tingling, crawling sensations

53
Q

Describe a complex partial seizure:

A

Temporal lobe origination.
Alteration in consciousness with cognitive, affective, psychosensory, and psychomotor symptoms.
Period of amnesia.

54
Q

What are four types of generalized seizures?

A

Tonic/clonic
Absence (Petit Mal)
Myoclonic
Atonic (Drop Attack)

55
Q

Describe a Tonic/clonic seizure:

A

Grand Mal
Loss of consciousness.
May be apneic/incontinent during tonic phase.
Postictal state

56
Q

Describe absence (Petite Mal) seizures:

A

Cessation of activity and consciousness.
No loss of posture.
Blank stare.
Twitching of eyes or face.

57
Q

Describe myoclonic seizures:

A

Sudden, brief uncontrollable jerking motions.
Can lose consciousness.
May have postictal state.

58
Q

Describe Atonic (drop attack) seizures:

A

Sudden, brief loss of muscle tone.
Loss of posture/consciousness.
May be associated with mental retardation.

59
Q

What is the treatment for seizures? (9)

A 
Protect airway.
Protect patient.
May need intubation for status.
Naloxone for drug overdose induced.
D50 for possible hypoglycemia.
Thiamine for alcoholism.
Status epilepticus occurs when a series of seizures follows each other or when a seizure does not respond to therapy.
Drug therapy to stop seizures.
Drug therapy to prevent recurrence.
60
Q

Name 3 drugs given to stop seizures:

A

Lorazepam
Diazepam
Ativan

61
Q

Name two drugs given to prevent the recurrence of seizures:

A

Phenytoin

Fosphenytoin

62
Q

What are some special considerations when giving phenytoin?

A

Must use cardiac monitor.
Give no faster than 50 mg/ minute
Watch for hypotension.
Mix with normal saline.

63
Q

What are some special considerations when giving fosphenytoin?

A

Given in PE/kg equivalents.
Cardiac monitoring necessary.
May cause hypotension.
150 mg/min.

64
Q

Describe linear skull fractures associated with head injuries:

A

Often nondisplaced.
Low velocity blunt or compressive trauma.
Consider epidural.

65
Q

Describe depressed skull fractures associated with head injuries:

A

Inward displacement of skull fragments.
High velocity or compressive.
High risk of infection.

66
Q

Describe basilar skull fractures associated with head injuries:

A

Skull films not always reliable.

Dura frequently torn.

67
Q

Describe symptoms of anterior fossa skull fractures:

A 
Rhinorrhea
Epistaxis
Visual problems
Subconjunctival hemorrhage
Anosmia
Raccoon’s eyes
68
Q

Describe symptoms of posterior fossa skull fractures:

A 
Otorrhea
Hemotympanum
Hearing loss
Facial nerve palsy
Battle’s sign
CSF leak - betatransferrin
69
Q

What is a concussion?

A

Transient loss of consciousness after head injury

But does not always have to have loss of consciousness.

70
Q

What are signs of post concussion syndrome?

A 
Headaches
Dizziness
Tinnitus
Diplopia
Inability to concentrate
Memory disturbances
Personality changes
Decreased energy level
71
Q

What is a contusion?

A

Bruising of the brain

72
Q

What are some manifestations of a brain contusion?

A 
Altered LOC
Headache
N/V
Visual disturbances
Seizures
Hemiparesis
73
Q

What is a diffuse axonal injury (shearing injury)?

A

Widespread disruption of neurological function with no focal lesion.

74
Q

What are some causes of diffuse axonal injury?

A 
Microscopic damage to axons.
Diffuse white matter degeneration.
Global neurological dysfunction.
Diffuse cerebral swelling.
*Most common cause for persistent vegetative state
*high risk for herniation
75
Q

Describe second impact syndrome:

A

Can occur with multiple hits to the head in a short time frame.
Causes brain herniation.

76
Q

What are seven mechanisms of spinal cord injury?

A 
Hyperextension
Hyperflexion
Axial loading
Compression
Lateral bend
Over rotation
Distraction
77
Q

Describe the hyperextension mechanism of spinal cord injury

A

Head is forced in backward motion

78
Q

Describe the hyperflexion mechanism of spinal cord injury

A

Head forced in forward motion

79
Q

Describe the axial loading mechanism of spinal cord injury

A

Downward force from blow to head

80
Q

Describe compression mechanism of spinal cord injury

A

Forces from above and below

81
Q

Describe lateral bend mechanism of spinal cord injury

A

Head bent to left or right

82
Q

Describe over a rotation mechanism of spinal cord injury

A

Turning of head beyond normal

83
Q

Describe distraction mechanism of spinal cord injury

A

Pulling force – vertebrae out of alignment

84
Q

Spinal nerve/muscle innervation at the level of C2-C4 is responsible for

A

Diaphragm
Neck muscles
Ventilation

85
Q

A lesion/injury of the spinal nerve at the level of C2 – C4 results in

A

Respiratory arrest
Flaccid paralysis
Quadriplegia

86
Q

Spinal nerve/muscle innervation at the level of C5 - C6 is responsible for

A

Biceps brachii, deltoid, triceps brachii, wrist extensors.

This allows you to shrug shoulders, flex elbows, and extend wrists

87
Q

A lesion/injury of the spinal nerve at C5 - C6 results in

A

Decreased respiratory effort
Flaccid paralysis
Quadriplegia

88
Q

Spinal nerve/muscle innervation of C7 is responsible for

A

Triceps, extensor digitorum, communis, flexor carpi radialis

This allows you to extend elbow and extend fingers

89
Q

A lesion/injury to the spinal nerve at C7 results in

A

Reduced respiratory effort
Quadriplegia
Splints may be utilized on forearms for some function

90
Q

Spinal nerve/muscle innervation of T1 - T2 is responsible for

A

Hand intrinsic muscles, intercostals

This allows you to spread fingers and vital capacity

91
Q

A lesion/injury to the spinal nerve at T1 - T2 results in

A

Reduced respiratory effort
Paraplegia

92
Q

Spinal nerve/muscle innervation of T7 is responsible for

A

Abdominal muscles and abdominal reflexes

93
Q

A lesion/injury of the spinal nerve at C7 will result in

A

Paraplegia

walking may be possible with long leg braces

94
Q

Spinal nerve/muscle innervation of L3 - L4 is responsible for

A

Quadriceps, tibialis anterior

These are responsible for me extension and ankle dorsiflexion

95
Q

A lesion/injury to the spinal nerve at L3 - L4 will result in

A

Paraplegia

Walking may be possible with long leg braces

96
Q

Manifestations of spinal cord injury

A

Pain/tenderness along spine.
Extremity weakness/numbness/tingling/paralysis.
Altered LOC.
Priapism.
Feeling of “Electric shock.”
Mouth breathing.
Decreased motor activity (below level of injury).
Loss of sensation (below level of injury).
Flaccid paralysis (below level of injury).
Anhidrosis (below level of injury).
Loss of spinal reflexes (below level of injury).
Loss of bowel/bladder control.
Symptoms of neurogenic shock.

97
Q

Treatment for spinal cord injuries

A 
ABC’s
Intubate for lesions above C4.
**Orange for Arby’s performer**
Foley catheter.
NG tube.
Treat neurogenic shock.
Warmth.
Monitor for dysrhythmias.
Application of cervical tongs.
Consider other causes of hypotension.
Methylprednisolone.
Within eight hours of injury a bolus of 30 mg/kg. Wait 45 minutes then give 5.4mg/kg/hr x 23 hours (this treatment is controversial)
98
Q

Manifestations of transection injury

A

No sensation below level of injury.
Neurogenic shock.
Injuries above T6 cause loss of sympathetic stimulation.

99
Q

Manifestations of central cord syndrome

A

Usually no fracture.
Loss of function of upper extremities.
Lower extremities not affected.
Bowel/bladder not affected.

100
Q

Manifestations of anterior cord syndrome

A

Loss of motor power.
Loss of pain sensation.
Loss of temperature sensation.

101
Q

Manifestations of posterior cord syndrome

A

Loss of light touch.
Loss of vibration.
Loss of proprioception.

102
Q

Manifestations of Brown-Sequard syndrome (hemisection in cord)

A

Ipsilateral paresis and hemiplegia.

Contralateral loss of pain and temperature sensation.

103
Q

What is autonomic hyperreflexia/dysreflexia?

A

Hypertensive emergency that occurs after the acute phase of spinal cord injuries with lesions above T6 in which the sympathetic nervous system overreacts below the level of the lesion causing vasoconstriction.
Must occur in the Post acute phase when reflex activity has returned.
Etiology - noxious stimuli.

104
Q

What are the manifestations of autonomic hyperreflexia/dysreflexia?

A 
Hypertension
Anxiety
Headache
Blurred vision
Dysrhythmias
Flushing
Profuse diaphoresis (above level of injury)
Nasal congestion
N/V
Coolness below level of injury
105
Q

What is the treatment for autonomic hyperreflexia/dysreflexia?

A

Remove noxious stimuli (e.g. distended bladder, impaction, constipation).
Antihypertensives
Elevate HOB

106
Q

What is Spinal Cord Injury Without Radiographic Abnormality (SCIWORA)?

A

Occurs in children
No x-ray abnormality
Patient needs MRI

107
Q

What is Cauda Equina Syndrome?

A 
Lumbar disc disease.
Manifestations:
	Bowel/bladder deficits
	Lower extremity deficits
	Perineal anesthesia (saddle anesthesia)
108
Q

What are the etiologies of spinal cord compression?

A 
Tumor 
Central disc herniation
Abscess
Hematoma
Displaced fracture fragment
109
Q

Describe CVA/TIA:

A

Disruption of blood flow to brain occurs by either rupture or occlusion.
Majority of strokes are ischemic in nature (84%) as opposed to hemorrhagic (16%).
150,000 deaths per year.
550,000 new strokes per year.
3 million stroke survivors.
40% – minor neurological deficits – retain independence.

110
Q

What are some risk factors for CVA/TIA?

A 
Hypertension
Atherosclerosis
Atrial fibrillation
Collagen diseases
Smoking
Diabetes 
**line valvular diseases**
Subacute bacterial endocarditis
Birth control pills
Recent neck trauma
111
Q

What are four types of CVA?

A

TIA
Reversible ischemia
Stroke in evolution
Completed stroke

112
Q

Describe a TIA:

A

Temporary
Symptoms <24 hours
No permanent deficit

113
Q

Describe reversible ischemia

A

Deficits last a few days/weeks

114
Q

Describe a stroke in evolution

A

Deficits in progressive state.
Deterioration occurs.
Residual deficits.

115
Q

Describe a completed stroke

A

Patient stable.

Permanent deficits.

116
Q

What is the treatment for a CVA?

A 
ABC’s
Decrease blood pressure (but not sudden drop)
Treat dysrhythmias
Aspirin
Osmotic diuretics
Steroids
Seizure prophylaxis
Antipyretics
* No D5W 
Merci retriever
Anticoagulant therapy
117
Q

What is anticoagulant therapy for a stroke with the last known well less than four hours?

A 
TPA
Total dose is 0.9 mg/kg
Maximum dose = 90 mg
Bolus is 10% of total dose
Reminder given over 60 minutes
118
Q

What is Guillain-Barré syndrome?

A

Acute paralytic disease of the peripheral nervous system that causes decreased myelin at the nerve roots. Nerve transmission is either slowed or blocked.

119
Q

Describe manifestations of Guillian barré syndrome:

A

Tingling sensation to extremities.
Decreased DTRs
Symmetric ascending paralysis.
Respiratory paralysis.

120
Q

What is the treatment for Guillain-Barré syndrome?

A 
ABC’s
Intubation
Ventilatory support
Plasmapheresis
Immunoglobulins
* Do not use succinylcholine – can cause fatal hyperkalemia.
121
Q

Describe Alzheimer’s disease

A

Accounts for 56% of all dementia.
Pathology - disturbed neurotransmitters and beta-amyloid proteins that cause the build up of plaques = brain dysfunction.

122
Q

What are the risk factors for Alzheimer’s disease?

A 
Ischemic stroke
Hypertension
Smoking
High cholesterol
Obesity
Diabetes
Familial on chromosomes 14, 19, 21

CEN (6 decks)

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