Neurological Emergencies Flashcards
(122 cards)
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
2
Q
What are five specific types of headaches?
A
Tension Migraine Cluster Sinus Temporal arteritis
3
Q
Describe a tension headache
A
Diffuse, band like pain
Non-pulsating
Treat with Analgesics
4
Q
Describe a migraine headache
A
Throbbing, unilateral pain
Photophobia
Treat with sumatriptan
5
Q
Describe a cluster headache
A
Knifelike, unilateral pain
Associated eye symptoms
6
Q
Describe a sinus headache
A
Pain over sinuses
Associated ear symptoms
Treat with antibiotics
7
Q
Describe temporal arteritis
A
Pain/tenderness to temporal area
Associated visual symptoms
Treat with steroids
8
Q
Components that exert pressure within the cranial vault:
A
Brain = 80% CSF = 10% Blood = 10%
9
Q
4 reasons for increased intracranial-cranial pressure related to the brain
A
Tumor
Abscess
Intracranial bleed
Cerebral edema
10
Q
4 reasons for increased intracranial pressure related to CSF
A
Hydrocephalus
Increased production
Flow obstruction
Impaired absorption
11
Q
1 Reason for increased intercranial pressure related to the blood:
A
Vasodilation
12
Q
What is normal intracranial pressure?
A
0-15 mm Hg
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.
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.
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
16
Q
What is Cushing’s triad?
A
Bradycardia
Hypertension
Bradypnea
17
Q
What is cerebral perfusion pressure?
A
An indirect measurement of cerebral blood flow.
18
Q
What is the equation for cerebral perfusion pressure?
A
CPP = MAP - ICP
19
Q
A Cerebral Perfusion Pressure of ________ is necessary to maintain adequate perfusion?
A
CPP of 60-70 (40 for the pediatric patient)
20
Q
________________ occurs as a protective response with elevated intercranial pressure.
A
Cushing-Kocher Response
21
Q
What is a herniation?
A
When brain tissue protrudes out of normal compartment.
22
Q
What are 3 areas for herniation to occur?
A
Fall Cerebrii
Tentorium Notch
Foramen Magnum
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
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.
25
What is the Babinski reflex?
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.
26
What are the highest and lowest possible Glasgow coma scale?
Best score = 15
| Lowest score = 3
27
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?
Oculomotor nerve compression by:
hematoma
tumor
cerebral edema (in same side of brain as lesion)
28
When checking pupillary responses on a patient, you find bilateral small pupils with a brisk reaction. What could the possible neurological cause be?
```
Bilateral Diencephalon (Thalamus/Hypothalamus)
Consider Metabolic coma (DKA)
```
29
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)
Horner’s Syndrome
Hypothalamus damage
Lesion on lateral medulla or ventrolateral cervical spinal cord
May be an early sign of tentorial herniation
30
When performing pupillary responses on a patient, you find bilateral mid position and non-reactive pupils. What are the possible neurological causes?
```
Midbrain infarction
Tentorial herniation (no sympathetic/parasympathetic innervation)
```
31
When performing pupillary responses on a patient, you find bilateral pinpoint pupils that are non-reactive. What could be the possible neurological cause?
Pontine hemorrhage
| Opiate overdose
32
When performing pupillary responses on a patient, you find bilateral dilated pupils that are non-reactive. What is the possible neurological cause?
Terminal stages of anoxia, ischemia, death.
Also may be caused by atropine-like drugs
Ciliospinal reflex
33
Describe Cheyne-stokes respiratory pattern:
Rhythmic, waxing/waning in both depth and rate with periods of apnea.
34
Damage to what area of the brain causes Cheyne-Stokes respiratory pattern?
Usually bilateral basal ganglia – thalamus/hypothalamus.
35
Describe central neurogenic hyperventilation respiratory pattern:
Increase in the rate and depth.
36
Damage to what area of the brain causes central neurogenic hyperventilation respiratory pattern?
Pons/Midbrain (Respiratory center of brain)
37
Describe apneustic respiratory pattern:
Prolonged inspiration followed by a pause (2–3 seconds).
38
Damage to what area of the brain causes apneustic respiratory pattern?
Lower Pons
39
Describe cluster respiratory pattern:
Clusters of irregular breathing with irregular periods of apnea.
40
Damage to what area of the brain causes cluster respiratory pattern?
Lower pons/upper medulla
41
What is the treatment of increased intercranial pressure? (16)
```
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
```
42
What are four types of hemorrhages in the brain?
Intraparenchymal (Intracerebral)
Subarachnoid
Subdural
Epidural
43
Describe an intraparenchymal hemorrhage:
```
Bleeding within cerebral tissue – can be the result of sharing of small vessels within hemispheres.
Moderate to severe pain.
Confusion.
Vomiting.
Altered gait.
```
44
Describe a subarachnoid hemorrhage:
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.
45
Describe a subdural hemorrhage:
```
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.
```
46
Describe an epidural hemorrhage:
Collection of blood between Dura and the skull.
Associated with temporal skull fractures.
Laceration of middle meningeal artery.
Arterial bleed.
Usually herniates.
47
What are seizures?
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.
48
What are 16 precipitating events that can cause seizures?
```
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
```
49
What are the four types of partial seizures?
Focal motor
Jacksonian
Focal sensory
Complex partial
50
Describe a focal motor seizure
Irritable focus on motor cortex/frontal lobe.
Clonic activity.
Slow repetitive jerking of part involved with increase in intensity.
51
Describe a Jacksonian seizure
Focal motor seizure that spreads in orderly manner.
| Begins in fingers with progression to entire extremity.
52
Describe a focal sensory seizure
Irritable focus within sensory strip of parietal lobe.
Manifestations vary:
Visual/auditory hallucinations
Flashing/zigzag lights
Odd taste/smells
Numbness, tingling, crawling sensations
53
Describe a complex partial seizure:
Temporal lobe origination.
Alteration in consciousness with cognitive, affective, psychosensory, and psychomotor symptoms.
Period of amnesia.
54
What are four types of generalized seizures?
Tonic/clonic
Absence (Petit Mal)
Myoclonic
Atonic (Drop Attack)
55
Describe a Tonic/clonic seizure:
Grand Mal
Loss of consciousness.
May be apneic/incontinent during tonic phase.
Postictal state
56
Describe absence (Petite Mal) seizures:
Cessation of activity and consciousness.
No loss of posture.
Blank stare.
Twitching of eyes or face.
57
Describe myoclonic seizures:
Sudden, brief uncontrollable jerking motions.
Can lose consciousness.
May have postictal state.
58
Describe Atonic (drop attack) seizures:
Sudden, brief loss of muscle tone.
Loss of posture/consciousness.
May be associated with mental retardation.
59
What is the treatment for seizures? (9)
```
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
Name 3 drugs given to stop seizures:
Lorazepam
Diazepam
Ativan
61
Name two drugs given to prevent the recurrence of seizures:
Phenytoin
Fosphenytoin
62
What are some special considerations when giving phenytoin?
Must use cardiac monitor.
Give no faster than 50 mg/ minute
Watch for hypotension.
Mix with normal saline.
63
What are some special considerations when giving fosphenytoin?
Given in PE/kg equivalents.
Cardiac monitoring necessary.
May cause hypotension.
150 mg/min.
64
Describe linear skull fractures associated with head injuries:
Often nondisplaced.
Low velocity blunt or compressive trauma.
Consider epidural.
65
Describe depressed skull fractures associated with head injuries:
Inward displacement of skull fragments.
High velocity or compressive.
High risk of infection.
66
Describe basilar skull fractures associated with head injuries:
Skull films not always reliable.
| Dura frequently torn.
67
Describe symptoms of anterior fossa skull fractures:
```
Rhinorrhea
Epistaxis
Visual problems
Subconjunctival hemorrhage
Anosmia
Raccoon’s eyes
```
68
Describe symptoms of posterior fossa skull fractures:
```
Otorrhea
Hemotympanum
Hearing loss
Facial nerve palsy
Battle’s sign
CSF leak - betatransferrin
```
69
What is a concussion?
Transient loss of consciousness after head injury
| But does not always have to have loss of consciousness.
70
What are signs of post concussion syndrome?
```
Headaches
Dizziness
Tinnitus
Diplopia
Inability to concentrate
Memory disturbances
Personality changes
Decreased energy level
```
71
What is a contusion?
Bruising of the brain
72
What are some manifestations of a brain contusion?
```
Altered LOC
Headache
N/V
Visual disturbances
Seizures
Hemiparesis
```
73
What is a diffuse axonal injury (shearing injury)?
Widespread disruption of neurological function with no focal lesion.
74
What are some causes of diffuse axonal injury?
```
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
Describe second impact syndrome:
Can occur with multiple hits to the head in a short time frame.
Causes brain herniation.
76
What are seven mechanisms of spinal cord injury?
```
Hyperextension
Hyperflexion
Axial loading
Compression
Lateral bend
Over rotation
Distraction
```
77
Describe the hyperextension mechanism of spinal cord injury
Head is forced in backward motion
78
Describe the hyperflexion mechanism of spinal cord injury
Head forced in forward motion
79
Describe the axial loading mechanism of spinal cord injury
Downward force from blow to head
80
Describe compression mechanism of spinal cord injury
Forces from above and below
81
Describe lateral bend mechanism of spinal cord injury
Head bent to left or right
82
Describe over a rotation mechanism of spinal cord injury
Turning of head beyond normal
83
Describe distraction mechanism of spinal cord injury
Pulling force – vertebrae out of alignment
84
Spinal nerve/muscle innervation at the level of C2-C4 is responsible for
Diaphragm
Neck muscles
Ventilation
85
A lesion/injury of the spinal nerve at the level of C2 – C4 results in
Respiratory arrest
Flaccid paralysis
Quadriplegia
86
Spinal nerve/muscle innervation at the level of C5 - C6 is responsible for
Biceps brachii, deltoid, triceps brachii, wrist extensors.
| This allows you to shrug shoulders, flex elbows, and extend wrists
87
A lesion/injury of the spinal nerve at C5 - C6 results in
Decreased respiratory effort
Flaccid paralysis
Quadriplegia
88
Spinal nerve/muscle innervation of C7 is responsible for
Triceps, extensor digitorum, communis, flexor carpi radialis
| This allows you to extend elbow and extend fingers
89
A lesion/injury to the spinal nerve at C7 results in
Reduced respiratory effort
Quadriplegia
Splints may be utilized on forearms for some function
90
Spinal nerve/muscle innervation of T1 - T2 is responsible for
Hand intrinsic muscles, intercostals
| This allows you to spread fingers and vital capacity
91
A lesion/injury to the spinal nerve at T1 - T2 results in
Reduced respiratory effort
Paraplegia
92
Spinal nerve/muscle innervation of T7 is responsible for
Abdominal muscles and abdominal reflexes
93
A lesion/injury of the spinal nerve at C7 will result in
Paraplegia
| walking may be possible with long leg braces
94
Spinal nerve/muscle innervation of L3 - L4 is responsible for
Quadriceps, tibialis anterior
| These are responsible for **me** extension and ankle dorsiflexion
95
A lesion/injury to the spinal nerve at L3 - L4 will result in
Paraplegia
| Walking may be possible with long leg braces
96
Manifestations of spinal cord injury
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
Treatment for spinal cord injuries
```
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
Manifestations of transection injury
No sensation below level of injury.
Neurogenic shock.
Injuries above T6 cause loss of sympathetic stimulation.
99
Manifestations of central cord syndrome
Usually no fracture.
Loss of function of upper extremities.
Lower extremities not affected.
Bowel/bladder not affected.
100
Manifestations of anterior cord syndrome
Loss of motor power.
Loss of pain sensation.
Loss of temperature sensation.
101
Manifestations of posterior cord syndrome
Loss of light touch.
Loss of vibration.
Loss of proprioception.
102
Manifestations of Brown-Sequard syndrome (hemisection in cord)
Ipsilateral paresis and hemiplegia.
| Contralateral loss of pain and temperature sensation.
103
What is autonomic hyperreflexia/dysreflexia?
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
What are the manifestations of autonomic hyperreflexia/dysreflexia?
```
Hypertension
Anxiety
Headache
Blurred vision
Dysrhythmias
Flushing
Profuse diaphoresis (above level of injury)
Nasal congestion
N/V
Coolness below level of injury
```
105
What is the treatment for autonomic hyperreflexia/dysreflexia?
Remove noxious stimuli (e.g. distended bladder, impaction, constipation).
Antihypertensives
Elevate HOB
106
What is Spinal Cord Injury Without Radiographic Abnormality (SCIWORA)?
Occurs in children
No x-ray abnormality
Patient needs MRI
107
What is Cauda Equina Syndrome?
```
Lumbar disc disease.
Manifestations:
Bowel/bladder deficits
Lower extremity deficits
Perineal anesthesia (saddle anesthesia)
```
108
What are the etiologies of spinal cord compression?
```
Tumor
Central disc herniation
Abscess
Hematoma
Displaced fracture fragment
```
109
Describe CVA/TIA:
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
What are some risk factors for CVA/TIA?
```
Hypertension
Atherosclerosis
Atrial fibrillation
Collagen diseases
Smoking
Diabetes
**line valvular diseases**
Subacute bacterial endocarditis
Birth control pills
Recent neck trauma
```
111
What are four types of CVA?
TIA
Reversible ischemia
Stroke in evolution
Completed stroke
112
Describe a TIA:
Temporary
Symptoms <24 hours
No permanent deficit
113
Describe reversible ischemia
Deficits last a few days/weeks
114
Describe a stroke in evolution
Deficits in progressive state.
Deterioration occurs.
Residual deficits.
115
Describe a completed stroke
Patient stable.
Permanent deficits.
116
What is the treatment for a CVA?
```
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
What is anticoagulant therapy for a stroke with the last known well less than four hours?
```
TPA
Total dose is 0.9 mg/kg
Maximum dose = 90 mg
Bolus is 10% of total dose
Reminder given over 60 minutes
```
118
What is Guillain-Barré syndrome?
Acute paralytic disease of the peripheral nervous system that causes decreased myelin at the nerve roots. Nerve transmission is either slowed or blocked.
119
Describe manifestations of Guillian barré syndrome:
Tingling sensation to extremities.
Decreased DTRs
Symmetric ascending paralysis.
Respiratory paralysis.
120
What is the treatment for Guillain-Barré syndrome?
```
ABC’s
Intubation
Ventilatory support
Plasmapheresis
Immunoglobulins
* Do not use succinylcholine – can cause fatal hyperkalemia.
```
121
Describe Alzheimer’s disease
Accounts for 56% of all dementia.
Pathology - disturbed neurotransmitters and beta-amyloid proteins that cause the build up of plaques = brain dysfunction.
122
What are the risk factors for Alzheimer’s disease?
```
Ischemic stroke
Hypertension
Smoking
High cholesterol
Obesity
Diabetes
Familial on chromosomes 14, 19, 21
```
