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P3 > NEURO (TBI-Stroke-HA-Neurodegenerative) > Flashcards

NEURO (TBI-Stroke-HA-Neurodegenerative) Flashcards

1
Q

In TBI, approx how many deaths per year occur

A

52,000

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2
Q

Leading cause of death & disability in children/adults from 1-44 y/o

A

Traumatic brain injury

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3
Q

Who are more likely to experience TBI?

A

Males, twice as likely than females

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4
Q

Non-degenerative, non-congenital insult to brain from external mechanical force

A

TBI

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5
Q

Associated diminished or altered state of consciousness

A

TBI

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6
Q

TBI is possibly leading to permanent or temporary impairment of ______, _______, & ________ functions (CPP)

A

Cognitive, physical, & psychosocial

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7
Q

What are the types of TBI

A
  • closed brain injury
  • open brain injury
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8
Q

A type of TBI, without the skull being broken or penetrated & the brain not being exposed

A

Closed brain injury

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9
Q

Type of TBI: When the rapid movement of the head backward and forward (acceleration-deceleration movement) causes the brain to move inside the skull & slam against its hard inner bone.

A

Closed brain injury

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10
Q

What are the two closed head injury

A
  • Coup injury
  • Countercoup injury
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11
Q

Sudden hyperextension of the head & neck forces the brain forward against the front of the skull

A

Coup injury

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12
Q

Hyperflexion of the head & neck forces the brain backward against the skull

A

Countercoup injury

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13
Q

Combination of coup & countercoup injury

A

Whiplash

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14
Q

C1 & C2 damage (use of neckbrace)

A

Paraplegia

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15
Q

N/V
Dizziness
Headache,
V diplopia (severe),
H diplopia (mild)
Transient visual loss (Amaurosis fugax)

A

Concussion

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16
Q

Process where u can obtain bruise/blood clot

A

Contussion

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17
Q

If the contusion hasn’t caused infarction, how can we can stop temporary amnesia from becoming permanent?

A
  • Warm compress: dilate BV to let blood flow
  • Cold compress: ease throbbing/symptom

If there’s external force, don’t let px sleep for 3hrs to prevent infarction even w/o wc

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18
Q

Which part of the brain is affected with temporary/selective amnesia?

A

Any part of the brain

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19
Q

Which part of the brains affected in permanent amnesia?

A

Hippocampus

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20
Q

Open or penetrating head injury

A

Open brain injury

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21
Q

In Open brain injury, TBI can be ______ or _______, damage may be isolated to one specific area of brain in focal injuries or widespread in case of diffuse injuries

A

Focal or diffuse

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22
Q

Etiology of Open brain injury (FVVS)

A
  • Falls
  • Vehicle-related collisions
  • Violence (gunshot wounds, child abuse, shaken baby syndrome)
  • Sports injuries (soccer, boxing, football, extreme sports)
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23
Q

TBI is divided into

A
  • Primary injury / brain damage
  • Secondary injury / brain damage
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24
Q

Induced by mechanical force & occurs at the moment of injury

A

Primary injury

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25
Q

Not mechanically induced, may be delayed from moment of impact & may superimpose injury on a brain already affected by mechanical injury

A

Secondary injury

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26
Q

Cause subdural hemorrhage, drown the brainstem & lead to loss of voluntary response

A

Secondary injury

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27
Q

Secondary injury cause __________, drown the brainstem & lead to loss of voluntary response

A

Subdural hemorrhage

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28
Q

What part of brain is affected if there is a problem in posture/walking

A

Cerebellum (drowning)

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29
Q

What are the two main mechanisms of Primary brain damage

A
  • Contact
  • Acceleration-deceleration
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30
Q

Mechanism of primary brain damage which result in fracture to the skull & surface contusions

A

Contact

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31
Q

Mechanism of primary brain damage which results in unrestricted movement of the head & leads to shear, tensile, & comprehensive strains

A

Acceleration-deceleration

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32
Q

Primary brain damage: These forces can cause _________,__________,________

A

Intracranial hematoma, diffuse vascular injury, & injury to cranial nerves & pituitary stalk

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33
Q

The most common cause of death & clinical deterioration after TBI

A

Intracranial Hematoma

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34
Q

What are the three categories of hematomas (ESS)

A
  • Epidural hematomas
  • Subdural hematomas
  • Subarachnoid hematomas
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35
Q

Hematoma: caused by fracture of temporal bone & rupture of middle meningeal artery

A

Epidural hematoma

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36
Q

Hematoma: such hematomas are usually caused by rupture of the bridging veins in the subdural space

A

Subdural hematomas

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37
Q

Hematoma: these result from damage to blood vessels in the posterior fossa stalk

A

Subarachnoid hematomas

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38
Q

Extracranial hematoma (SIN)

A
  • Scalp lacerations
  • Nasal injuries
  • Injuries to face & neck can lead to significant blood loss
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39
Q

Occurs hours, days after traumatic event.
Injury may result from impairment in cerebral blood flow after TBI

A

Secondary brain damage

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40
Q

Decrease in cerebral blood flow (CBF) are results of _______,________, or __________

A

Local edema, hemorrhage, or increased intracranial pressure (ICP)

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41
Q

As a result of inadequate perfusion, cellular ion pumps may fail, causing a cascade involving intracellular calcium & sodium

A

Secondary brain damage

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42
Q

____________ may contribute to cellular destruction

A

Resultant calcium & sodium overload

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43
Q

Excessive release of excitatory amino acids, such as ________&________ exacerbates failure of ion pumps

A

Glutamate & aspartate

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44
Q

As the cascade continues, cells die causing ______,______&__________

A

Free radical formation, proteolysis, & lipid peroxidation

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45
Q

In secondary brain damage all the factors ultimately cause

A

Neuronal death

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46
Q

Extracranial causes of SBD (FF)

A

-failure of adequate cerebral perfusion from circulatory shock
-failure of cerebral oxygenation from disturbance of pulmonary ventilation from: (aspiration, instability of chest wall (flail chest), neurogenic disturbances of ventilatory drive)

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47
Q

Intracranial causes of SBD (RC)

A

-rise in ICP due to mass lesions & cerebral edema leading to fall in cerebral perfusion pressure & to herniation of brain is a major factor in poor outcome
-cerebral autoregulation impraired

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48
Q

Signs & symptoms of Mild TBI (LMH-DND)

A
  • loss of consciousness for a few seconds
  • memory/concentration problems
  • headache
  • dizziness/loss of balance
  • N/V
  • difficulty sleeping
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49
Q

Signs & symptoms of moderate to severe TBI (LIPS-LW)

A
  • loss of consciousness several mins to hours
  • slurred speech
  • inability to awaken from sleep
  • weakness in fingers & toes
  • loss of coordination
  • persistent headache/ headache that worsens
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50
Q

Children symptoms of TBI (CCCPS)

A
  • change in eating/nursing habits
  • persistent crying & inability to be consoled
  • change in ability to pay attention
  • change in sleeping habits
  • sad/depressed mood
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51
Q

Presentation: Cognitive problems (JAMS-LPD)

A

-Memory
-Learning
-Problem solving
-Speed of mental processing
-Judgement
-Attention or concentration
-Decision making

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52
Q

Presentation: Physical changes (SSCC-PL)

A

-Spasticity
-Physical paralysis
-Chronic pain
-Sensory
-Loss of stamina
-Control of bowel & blader

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53
Q

5th leading cause of death in US, one person dying every 4 mins

A

Stroke

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54
Q

Second leading cause of death in the world

A

Stroke

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55
Q

Approx ________ people have a stroke each year, one every 40 secs

A

800,000

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56
Q

Occur due to problems with blood supply to the brain; either the blood supply is blocked or a blood vessel within the brain ruptures, causing brain tissue to die

A

Stroke

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57
Q

Clinical syndrome of rapid onset of cerebral deficit lasting more than 24hrs or leading to death with no apparent cause other than a vascular one

A

Stroke

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58
Q

Rapid loss of brain function due to disturbance in the blood supply the brain

A

Stroke

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59
Q

A stroke happens when blood flow to a part of the brain stops and is sometimes called

A

Brain attack

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60
Q

Most common cause of severe physical disability

A

Stoke

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61
Q

Prevalence of stroke in India:
Death rate:

A

PrevalenceL 1.54 per 1000
Death rate: 0.6 per 1000

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62
Q

Types of stroke (HIT)

A

-Ischemic stroke
-Hemorrhagic stroke
-Transient Ischemic Attack (TIA)

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63
Q

Most common form of stroke, 85% of strokes

A

Ischemic stroke

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64
Q

Type of stroke caused by blockage or narrowing of arteries that provide blood to the brain resulting in severely reduced blood flow

A

Ischemic stroke

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65
Q

Ischemic stroke: blockages are often caused by _________

A

blood clots

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66
Q

Clots can be caused by fatty deposits within the arteries called

A

Plaque

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67
Q

Type of stroke: Caused by arteries in the brain either leaking or bursting open

A

Hemorrhagic stroke

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68
Q

Hemorrhagic stroke: ruptures can be caused by conditions such as (BATH)

A

-Hypertension
-Trauma
-Blood thinning medications
-Aneurysms (weakness in blood vessel walls)

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69
Q

What are the two types of hemorrhagic stroke

A

-Intracerebral hemorrhage
-Subarachnoid hemorrhage

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70
Q

Most common type of hemorrhagic stroke, occurs when brain tissue is flooded with blood after an artery in the brain bursts

A

Intra cerebral hemorrhage

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71
Q

Second type of hemorrhagic stroek, less common, bleeding occurs in subarachnoid space - area between brain & the thin tissues that cover it

A

Subarachnoid hemorhage

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72
Q

flow of blood to the brain is only briefly interrupted

A

Transient Ischemic Attack (TIA)

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73
Q

How is TIA similar to Ischemic stroke

A

they are often caused by blood clots or other debris

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74
Q

should be regarded as medical emergencies

A

TIA

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75
Q

referred to as “mini strokes”, lasts below 24 hours

A

TIA

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76
Q

serve as warning signs for future strokes & indicate that there is partially blocked artery or clot source in the heart

A

TIA

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77
Q

Between ______% will have major stroke within 3 months of TIA

A

10-15%

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78
Q

due to vasoconstriction induced by stress

A

TIA

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79
Q

Causes of TIA (LUCS)

A
  • Large artery atherosclerosis
  • Cardio-aortic embolism
  • Small artery occlusion
  • Undetermined cases:
    unknown - cryptogenic embolism
    unknown - other cryptogenic
    unknown - incomplete evaluation
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80
Q

Signs of TIA (WTV-HD)

A
  • Weakness (sudden loss of strength/numbness in face, arm, leg)
  • Trouble speaking (sudden difficulty speaking/understanding, confusion)
  • Vision problems (sudden trouble w vision (amaurosis fugax)
  • Headache (sudden severe & unusual headache)
  • Dizziness (sudden loss of balance, w any of the above signs)
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81
Q

Symptoms of TIA (CHNTT)

A
  • Confusion (incl; trouble speaking & understanding)
  • Headache (w altered consciousness or vomiting)
  • Numbness of face, arm/leg on one side of body
  • Trouble seeing in one or both eyes
  • Trouble walking, including dizziness & lack of coordination
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82
Q

Diagnosis of stroke

A

F.A.S.T. - way to remember signs of stroke can help identify onset of stroke quickly

83
Q

What does F.A.S.T. stand for

A

Face drooping: tries to smile & one side of face droop
Arm weakness: tries to raise both arms, one drifts down
Speech difficulty: tries to repeat a phrase & speech is slurred
Time to call 911: if any are observed, contact emergency

84
Q

Diagnostic tests of stroke

A
  • Physical exam
  • Blood test
  • CT scan
  • MRI scan
  • Carotid ultrasound
  • Cerebral angiogram
  • Echocardiogram
85
Q

Treatment for stroke

A

Ischemic: Aspirin (given as injection), Carotid endarterectomy, Angioplasty
Hemorrhagic: Drugs that reduce pressure in the brain, Surgery to repair problems w blood vessel & remove small AVMs if not too big or deep in the brain

86
Q

Rehab for stroke

A
  • Speech therapy
  • Physical therapy
  • Occupational therapy
  • Joining support group
  • Support from friends & family
87
Q

Prevention of stoke

A
  • Eat healthy diet
  • Maintain healthy weight
  • Exercise regularly
  • not smoking
  • avoiding alcohol/moderate consumption
88
Q

What causes vision deficits after stroke?

A
  • damage caused to specific regions of visual cortex or its connecting neural network
  • loss of vision is due to damage done to part of brain that processes visual info transmitted to it using eyes as conduits
89
Q

about ______ nearly 1 of 4 in people had previous stroke

A

185,000

90
Q

about ____% of all strokes are Ischemic strokes

A

87%

91
Q

______% of people hospitalized w stroke are younger than 65

A

34%

92
Q

____% of people suffer from stroke experience changes in their vision. _____% experience permanent visual deficit

A

66%, 20%

93
Q

Types of Post-Stroke Vision Deficits

A
  • Hemianopia
  • Quadrantanopia
  • Scotoma
  • Tunnel vision
94
Q

Type of post-stroke vision deficit: blindness in one half of VF

A

Hemianopia

95
Q

Type of post-stroke vision deficit: loss of vision occur in quarter of VF

A

Quadrantanopia

96
Q

Type of post-stroke vision deficit: spotty vision/small area of blindness than hemi/quadrantanopia

A

Scotoma

97
Q

Type of post-stroke vision deficit: loss of peripheral vision that mimics looking thru a tunnel

A

Tunnel vision

98
Q

3 recovery options of stroke vision deficits

A
  • Vision restoration (Neuroplasticity, Vision restoration therapy)
  • Vision compensation (Neuroeyecoach)
  • Substitution (use of optical aids)
99
Q

study of how nervous system develops, its structure, what it does

A

Neuroscience (Neural Science)

100
Q

specialized cell, transmit commands from the brain to control organs & muscles, thought, feeling & movement

A

Neurons

101
Q

controlling unit of body, comprises billions of cells (neurons) which form communication center (nervous system)

A

Brain

102
Q

progressive loss of nerve structures & function, leads to loss of cognitive abilities

A

Neurodegeneration

103
Q

_______ building blocks of nervous system, doesnt reproduce themselves when damaged

A

Neurons

104
Q

key aspect of large number of diseases that come under umbrella of “neurodegenerative diseases”

A

Neurodegeneration

105
Q

most notable degenerative diseases

A

Alzheimer’s, Parkinson’s, & Huntington disease

106
Q

progressive ND that mostly affects px in later stage of life

A

Alzheimer’s disease

107
Q

typical symptoms are loss of cognitive function, including emotion, learning & memory processing skills leading to dementia

A

Alzheimer’s

108
Q

_____% of the risk is believed to be genetic w many genes involved. And what ND?

A

70%, Alzheimer’s

109
Q

Risk factors of Alzheimer’s (HDH)

A
  • history of head injuries
  • depression
  • hypertension
110
Q

pathological impression of Alzheimer’s is characterized by deposition of _________ in the brain parenchyma & accumulation of ________ within neurons

A

amyloid-beta (AB) protein plaques, tau proteins

111
Q

Typical symptoms of Alzheimer’s

A

Loss of cognitive functions including:
- emotions
- learning
- memory processing leading to dementia

112
Q

These protein plaques interfere with synaptic transmission & neuron-neuron communication leading to _________

A

Neuronal death

113
Q

_____________ within neurons form tangles & block transportation of nutrients or jam other vital cellular factors throughout the cell which becomes the reason for _______ in Alzheimer’s

A

Tau proteins, cell death

114
Q

Symptoms of Alzheimer’s (3P-3D-2M-F)

A
  • Memory loss/changes in memory
  • Difficulty performing familiar tasks/routine chores
  • Drastic changes in personality
  • Misplacing things in inappropriate places
  • Problems w abstract thinking
  • Forgetting words or substituting inappropriate words
  • Problems speaking, writing, reading, understanding
  • Disorientation to time & place
  • Poor/decreased judgement
115
Q

typically considered chronic, progressive neurodegenerative movement disorder

A

Parkinson’s disease

116
Q

causes death of the vital nerve cells in the area of brain called substantia nigra

A

Parkinson’s

117
Q

Parkinson’s causes death of the vital nerve cells in the area of brain called ________

A

substantia nigra

118
Q

as Parkinson’s progresses, amount of dopamine produced from brain ______, leading to person unable to control movement normally

A

decreases

119
Q

in Parkinson’s, dying neurons produce _________ which acts as a messenger & sends messages to part of the brain that controls movement & coordination

A

Dopamine

120
Q

Parkinson’s: proteosomal & lysosomal system dysfunction & reduction in mitochondrial activity due to __________ also cause cell death

A

genetic mutation

121
Q

Parkinson’s: activated neurons over expressing proteins lead to early activation of microglia & release of various inflammatory mediators such as:

A

IL-1, IL-6, TNF-α

122
Q

Parkinson’s: reactive __________ & _______ enhance oxidative stress & trigger cell-death pathways

A

oxygen/nitric oxide species & prostaglandins

123
Q

Symptoms of Parkinson’s

A
  • Depression, sleep disorders, weight loss
  • Forced closure of eyelids (blepharospasm)
  • Orthostatic hypotension
  • Constipation, micturition disorders, sexual problems
  • Difficulty speaking/swallowing, excessive salivation, respiratory problems
  • Increased sweating
  • Bowing of shoulders, swelling of feet
124
Q

chronic neuroinflammatory, progressive, degenerative disorder of CNS characterized by demyelination of nerve fibers of brain & spinal cord affecting people between 20-40

A

Multiple sclerosis

125
Q

initially triggered by a virus genetically susceptible individuals

A

Multiple sclerosis

126
Q

subsequent antigen-antibody reaction leads to demyelination of axons i.e; autoimmunity

A

Multiple sclerosis

127
Q

Symptoms of Multiple Sclerosis

A
  • Fatigue
  • Depression
  • Memory change
  • Pain
  • Spasticity
  • Tremor
  • Double vision/Vision loss
  • Weakness
  • Dizziness/Unsteadiness
  • Numbness/Tingling
  • Ataxia
  • Speech disturbance
  • Bladder/Bowel/Sexual dysfunction
128
Q

rapidly progressive neurodegenerative disease that leads to dementia

A

Huntington’s disease

129
Q

typically presents w alterations in mood & change in character, defects in memory & attention

A

Huntington’s

130
Q

progresses to a movement disorder consisting of involuntary & rapid motions

A

Huntington’s

131
Q

usually not recognized until px is in their early 30’s

A

Huntington’s

132
Q

there is a ______% chance that a child whose parent has Huntington’s will have the disease

A

50%

133
Q

Huntington’s: caused by an autosomal dominant mutation on either of an individual’s two copies of a gene called

A

Huntingtin

134
Q

faulty gene that causes Huntington’s is found on

A

chromosome number four

135
Q

The normal copy of gene produces protein called “Huntingtin” but faulty gene contains abnormal region called

A

CAG repeats

136
Q

Huntington’s: expanded polyglutamine region of pathological form of protein causes impairment of the ubiquitin-proteasome system (True/False)

A

True

137
Q

Huntington’s: dysfunctional protein is removed & destroyed as it should be (True/False)

A

False: dysfunctional proteins is NOT removed & destroyed as it should be

138
Q

Huntington’s: cells in brain, specifically basal ganglia & parts of cortex are NOT sensitive to effects of abnormal huntingtin. This makes them function WELL & NOT DIE (True/False)

A

False: cells in brain, specifically basal ganglia & parts of cortex are VERY sensitive to effects of abnormal huntingtin. This makes them function POORLY & eventually die

139
Q

Symptoms of Huntington’s (Movement)

A

Movement:
- Choreic movements
- Twitching
- Balance problems
- Tracking problems
- Rigidity & dystonia

140
Q

Symptoms of Huntington’s (Cognitive)

A

Cognitive:
- As HD progresses, ability to concentrate becomes more difficult
- Difficulty driving, keeping track of things, making decisions, answering questions, lose ability to recognize familiar objects
- Over time, judgement, memory, & other cognitive functions begin to deteriorate into dementia

141
Q

Symptoms of Huntington’s (Psychiatric)

A
  • Early symptoms: subtle, varied & easily overlooked/misinterpreted
  • Depression - most common symptom & develops early in course of disease
    Signs of depression:
  • Hostility/irritability
  • Inability to take pleasure in life (anhedonia)
  • Lack of energy
  • Hallucinations
142
Q

major hallmark of neurodegenerative disease

A

abnormal deposition of aggregates of misfolded proteins (proteinopathies) that lead to cell dysfunction & eventually cell death

143
Q

pain/discomfort in head, scalp, or neck

A

Headache

144
Q

one of the most common of all human physical complaints

A

Headache

145
Q

HA: a stress response, ________(migraine), _________(tension headache), or combination of factors

A

vasodilation, skeletal muscle tension

146
Q

up to _____% of adults have severe HA each year

A

25%

147
Q

up to ____% have daily/near-daily HA

A

4%

148
Q

Lifetime prevalence of HA

A

90% or more

149
Q

Types/classification of HA

A
  • Primary headache
  • Secondary headache
150
Q

Type of HA: not caused by underlying disease, trauma, or medical condition

A

Primary HA

151
Q

accounts 90% of all headaches

A

Primary HA

152
Q

most px presenting with HA have ___________

A

Primary HA syndromes

153
Q

Primary HA: more common

A

Episodic headache

154
Q

Primary HA: attacks occurring more frequently than 15 days/month for more than 6 months

A

Chronic headache

155
Q

<2% of headaches in primary care offices

A

Secondary headache

156
Q

caused by exogenous disorders

A

Secondary HA

157
Q

What are the exogenous disorders caused by secondary HA: (MISH-VN)

A
  • Head trauma
  • Vascular disease
  • Neoplasms
  • Substance abuse/withdrawal
  • Infection/inflammation (meningitis)
  • Metabolic disorders (hyper/hypogyclemia)
158
Q

What are the Primary Headache Syndromes

A
  • Tension type HA
  • Migraine
  • Trigeminal Neuralgia
  • Cluster HA
159
Q

Primary HA type: most common (69%), episodic or chronic

A

Tension HA

160
Q

Primary HA type: primary disorder if CNS pain modulation

A

Tension HA

161
Q

Precipitating factors of Tension HA (SUICEDS)

A
  • Stress
  • Sleep deprivation
  • Uncomfortable stressful position/bad posture
  • Irregular meal time (hunger)
  • Eyestrain
  • Caffeine withdrawal
  • Dehydration
162
Q

Tension HA signs & symptoms (BLGN)

A
  • Gradual, onset, radiate forward from occiput
  • Bilateral, dull, tight, band-like pain
  • Less in morning, pain increase as day goes on
  • No accompanying NV, throbbing, sensitivity to light, sound, or movement
163
Q

Management of Tension HA

A
  • Paracetamol, Aspirin, NSAIDs
  • Behavioral approach-relaxation
  • Chronic-amitriptyline
164
Q

Primary HA type: 2nd most common (16%)
women (15%), men (6%)

A

Migraine

165
Q

Primary HA type: severe, episodic, unilateral, throbbing pain
-NV, sensitivity to light, sound, movement
-genetic predisposition

A

Migraine

166
Q

What are the three theories of Migraine?

A
  • Vascular theory
  • Second theory
  • Biochemical changes
167
Q

Migraine theory: vasoconstriction followed by vasodilation resulting in changes in blood flow causing throbbing pain

A

Vascular theory

168
Q

Migraine theory: pain results from muscular tension

A

Second theory

169
Q

Migraine theory: changes in serotonin levels

A

Biochemical changes

170
Q

Migraine triggers (3S-2F-CH)

A
  • Flashing lights, loud sounds, strong odors
  • Stress
  • Hunger
  • Fatigue
  • Smoking
  • Menstruation, pregnancy, menopause, oral contraceptives
  • Sleep changes
  • Caffeine, chocolate, tyramine
171
Q

Classical Migraine or Migraine with AURA symptom triad: (PAN)

A
  • Paroxysmal headache
  • Nausea &/ Vomiting
  • Aura of focal neurological events (visual) 20-25%
172
Q

Medical term for aura

A

Scintillating scotoma

173
Q

flashing lights, silvery zigzag lines moving across the VF over a period of 20 mins

A

Aura

174
Q

sometimes leaving trail of temporary VF loss

A

Aura

175
Q

spreading front of tingling & numbness from one body part to another

A

Sensory aura

176
Q

Common migraine or Migraine without AURA

A
  • Paroxysmal headache
  • Vomiting +/-
  • NO AURA
177
Q

Diagnosis of Migraine must at least have 2 of the ff (MUTA)

A
  • Unilateral pain
  • Throbbing pain
  • Aggravation by movement
  • Moderate/severe intensity
178
Q

Diagnosis of Migraine must at least have 2 + at least 1 of the ff:

A

-Nausea/Vomiting
-Photophobia & phonophobia

179
Q

Management of Migraine: Non-drug treatment

A
  • Avoid Ha triggers: foods, drugs, activities
  • Avoid frequent abortive treatment
  • Stop smoking
  • Normalize sleeping & eating
  • Exercise
  • Relaxation & biofeedback
  • Psychotherapy
180
Q

Preventive treatment of Migraine

A
  • Tricyclic antidepressants (first-line) - Amitriptyline
  • Beta-blockers (first-line) - Atenolol, Nadolol
  • Ca++ channel blockers (less effective) - Verapamil- most commonly used
  • Anticonvulsants (2nd line) - Valproate & Topiramate - quite effective
  • Gabapentin
  • Lamotrigine, Levetiracetam
  • Pregabalin
  • Ergots: rarely used, side effects problematic. Methysergide: fibrosis (use 6 months max)
  • MAOIs: can be very effective. Tyramine - free diet a must, Numerous drug interactions
181
Q

Abortive Therapy for Migraine

A
  • Simple & combined analgesics (NSAIDs)
  • Mixed analgesics (Barbiturate + simple analgesics)
  • Ergot derivatives
  • Triptans
  • Opioids
182
Q

Migraine: Triptans

A
  • Serotonin 5-HT1 agonists
  • Reduce neurogenic inflammation
  • Most effective if used at onset of HA or aura, though maybe helpful at other phases
  • Used specifically for Migraines
  • For nonresponders, try ergots (act on NE, DA, other receptors)
183
Q

Migraine: Drugs to avoid

A
  • Butorphanol nasal spray
  • Meperidine
  • Overuse of any short-acting analgesic (opioid, triptans)
184
Q

lancinating pain in 2nd & 3rd divisions of trigeminal nerve, >50 yrs

A

Trigeminal Neuralgia

185
Q

severe, brief, repetitive pain causing px to flinch

A

Trigeminal Neuralgia

186
Q

Trigeminal Neuralgia: touching trigger zones

A

Washing
Shaving
Eating
Cold wind

187
Q

compression of trigeminal N by aberrant loop of cerebellar arteries as nerve enters brainstem

A

Trigeminal Neuralgia

188
Q

occurs due to plaque of demyelination in trigeminal root entry zone

A

Multiple sclerosis

189
Q

caused by other benign compressive lesions

A

Trigeminal Neuralgia

190
Q

Management of Trigeminal Neuralgia

A
  • Carbamazepine
  • Intolerant-Gabapentin/Pregabalin
  • Injection of alcohol into peripheral branch of nerve
  • Posterior craniotomy to relieve vascular compression of trigeminal nerve
191
Q

HA occur during a short time span

A

Cluster headache

192
Q

The cluster then recurs ______

A

periodically

193
Q

A typical cluster HA may last _____ weeks with _____headaches/day during the cluster

A

4-8weeks, 1-2 headaches/day

194
Q

Cluster HA male to female ratio

A

5:1

195
Q

Signs & symptoms of Cluster HA

A
  • abrupt onset of HA originating in eye & spreading over the temporal area
  • pain extremely severe & last 20-60 mins
  • The HA associated w:
    Nasal stuffiness
    Rhinorrhoea
    Redness of the eye
    Flush & edema of the cheek
196
Q

Management of cluster HA (Acute)

A
  • Oxygen inhalation 100%
  • Triptans/ergots
  • Indomethacin
197
Q

Management of cluster HA (Chronic/Preventive)

A
  • Verapamil, lithium
  • Valproate, topiramate
  • Prednisone burst
  • Melatonin
  • Ergots
198
Q

persistent, recurring headache in the setting of regular analgesic use, continues until medication is stopped

A

Medication Overuse Headache

199
Q

often responsible for “transformation” of episodic into chronic HA

A

Medication Overuse Headache

200
Q

band-like pressure

A

Tension-type Headache

201
Q

half head throbbing

A

Migraine

202
Q

periorbital sharp

A

Cluster headache

203
Q

Cluster HA vs Eyestrain

A

Cluster (non-ocular) - relieved by meds, pain scale is >7, associated w sinusitis
Eyestrain (asthenopia) - relieved with rest, pain scale: 5

P3 (11 decks)

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