Week 4 - Head Injury Flashcards
(89 cards)
1
Q
Syndrome of acute focal neurologic deficit from a _____ that injures brain tissue.
A
vascular disorder
2
Q
“_____”- to raise awareness that time-dependant tissue damage occurs.
A
Brain attack
3
Q
Two main types of stroke:
A
Ischemic
Hemorrhagic
4
Q
Risk Factors for Ischemic Stroke
A
Age Gender Race Family history Hypertension Cigarette smoking Diabetes mellitus Atrial fibrillation Asymptomatic carotid stenosis Sickle cell disease Hyperlipidemia
5
Q
- Caused by cerebrovascular obstruction by thrombosis or emboli.
Account for 87% of all strokes.
A
Ischemic Stroke
6
Q
5 main mechanisms of stroke subtypes (classes):
A
Large artery atherosclerotic disease Small vessel or penetrating artery disease (lacunar) Cardiogenic emboli Cryptogenic stroke Unusual causes
7
Q
Central core of dead or dying cells, surrounded by ischemic cells
- Impaired cell metabolism
- Electrical failure of cells in area
- Structural integrity of cells maintained.
A
Penumbra
8
Q
Cell survival depends on: (4)
A
Return of adequate circulation,
Volume of toxic products released by dying cells
Cerebral edema
Blood flow alterations
9
Q
_____ are the most common cause of ischemic strokes.
- Tend to occur in atherosclerotic blood vessels, commonly at arterial bifurcations
- Leads to occlusion at site with or without emboli
- Blocks perfusion distal to site
A
Thrombi
10
Q
Large Vessel (Thrombotic) Stroke affects cerebral cortex causing: (4)
A
Aphasia
Neglect
Visual defects
Transient monocular blindness
11
Q
“_____” is a temporary disturbance in cerebral blood flow which reverses before infarction occurs.
Most deficits resolve within 1 hour.
- Zone of penumbra without central infarction.
- Causes include atherosclerosis of cerebral vessels & emboli.
- Considered a warning of impending stroke.
A
Ministroke or Transient Ischemic Attacks (TIA)
12
Q
- Most frequently fatal type of stroke
- Rupture of a blood vessel leads to hemorrhage into brain tissue
- Results in a focal hematoma or intraventricular hemorrhage
- Edema, compression of brain contents, or spasm of adjacent vessels may also occur
A
Hemorrhagic Stroke
Also called intracerebral hemorrhage
13
Q
Risk Factors for Hemorrhagic Stroke
A
Most Common:
Advancing age
Hypertension
Other causes: Aneurysm Trauma Erosion of the vessels by tumors Arteriovenous malformations Blood coagulation disorders Vasculitis Drugs
14
Q
Manifestations of Hemorrhagic Stroke
A
- Sudden onset
- Vomiting occurs at onset
- Headache
- Focal symptoms depend on vessel affected
- Hemorrhage into basal ganglia results in contralateral hemiplegia.
- Hematoma & edema compress brain tissue and may lead to coma or death (Monro-Kellie hypothesis)
15
Q
Hemorrhagic Stroke is Diagnosed by
A
CT Scan
16
Q
Hemorrhage into basal ganglia results in __________.
A
contralateral hemiplegia.
17
Q
- the cranial compartment is incompressible, and the volume inside the cranium is a fixed volume.
- The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium
- Any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another.
A
The Monro-Kellie hypothesis states that:
18
Q
Treatment of Hemmorhagic Stroke focuses on: (3)
A
- Management of increased arterial pressure & intracranial pressure (ICP)
- Prevention of recurrent hemorrhage
- Supportive care
19
Q
Symptoms of _____________ always are sudden in onset and focal, and usually one-sided.
A
stroke/TIA
20
Q
Most common manifestation of Acute Stroke
A
Weakness of the face and arm, sometimes leg
21
Q
Other Manifestations of Acute Stroke
A
Unilateral numbness
amaurosis fugax, hemianopia
aphasia, dysarthria
sudden, unexplained ataxia.
22
Q
vision loss in one eye
A
Amaurosis fugax
23
Q
vision loss to one side
A
Hemianopia
24
Q
language disturbance
A
Aphasia
25
slurred speech
Dysarthria
26
imbalance
Ataxia
27
In ____, symptoms rapidly resolve spontaneously, usually within minutes.
Specific stroke signs depend on specific vascular territory compromised.
TIA
28
Post-Stroke Motor Deficits
Profound weakness (hemiparesis) on the contralateral side.
Within 6-8 weeks:
Initial weakness and flaccidity replaced by hyperreflexia and spasticity.
Related deficits:
Foot drop, circumduction of leg with gait, flexion at wrist, elbows, fingers, lower facial paresis, slurred speech, babinski sign, dependant edema.
Tx- Passive ROM important.
29
______ requires:
Motor or mechanical act of articulating language
Written or spoken symbolic formulations of language
Verbal communication
30
is disorder of speech (motor) from stroke affecting muscles of pharynx, palate, tongue, lips or mouth.
Dysarthria
31
is inability to comprehend, integrate & express language
Sub-classified into expressive & receptive ____
SLP is key
Aphasia
32
Cognitive Post-Stroke:
- Hemi-neglect is the inability to attend to and react to stimuli coming from the contralateral side.
- Unaware of deficit (anosognosia).
- Apraxia, agnosia, memory loss, behavioural syndromes & depression.
33
Sensory Post-Stroke:
```
Paresthesias
Distorted sensation (i.e. neuropathic pain)
```
34
Visual disturbances Post-Stroke:
Hemianopia
| Monocular blindness.
35
Diagnosis of Acute Stroke
- Clinical history and physical examination
- CT scans &/or MRIs are essential in differentiating between ischemic & hemorrhagic stroke
- Vascular imaging
36
Vascular imaging accomplished by; (4)
CT angiography (CTA)
Magnetic resonance angiography (MRA)
Catheter based conventional arteriography
Ultrasonography (carotids arteries)
37
Goals in Treating Acute Stroke: (3)
salvage brain tissue
preventing secondary stroke
minimizing long-term disability
38
Reperfusion techniques include: (3)
thrombolytic therapy: tPA
catheter-directed mechanical clot/disruption
augmentation of CPP (cerebral perfusion pressure) during acute stroke
39
Stroke recurrence highest during ____ after stroke or TIA
first week
40
Early implementation of Stroke (Pharmacologic):
- Antiplatelet agents (i.e. Plavix) for most ischemic strokes
- Warfarin (anticoagulant) in cardioembolic stroke.
41
Aggressive risk factor reduction to prevent recurrence in _____ (secondary prevention)
long-term
42
Early hospital care focuses on the prevention of (3).
| Early, aggressive rehabilitation
aspiration, DVTs, and falls
43
- Bulge at site of a localized weakness in the muscular wall of an arterial vessel.
- Most are small, sac-like
- Commonly found at bifurcations and vessel junctions
- Arise from congenital defect in the medial layer of vessels
Aneurysm
44
Rupture of aneurysms causes bleeding into the _____.
subarachnoid space (SAH)
45
Aneurysms higher incidence in people with;
Polycystic kidney disease
Coarctation of the aorta
Arteriovenous malformations (AVM) in the brain
46
Other causes of Aneurysms: (3)
Artherosclerosis, hypertension and bacterial infections
47
Rupture most commonly occurs between ____years of age.
40-60
48
Risk of rupture increases with the ________.
aneurysm size
49
Greatest risk factors to SAH are: (4)
cigarette smoking, hypertension, excessive alcohol intake
50
Rupture may occur at any time but often occurs with acute rises in ______.
intracranial pressure (ICP)
51
- Most small aneurysms are _____.
asymptomatic
52
Large aneurysms cause _______ and_________.
chronic headache and/or neurologic deficits.
53
History of atypical headaches occurring days to weeks before SAH, maybe due to ______.
small leak
54
Headaches characterized by ______ and often cause nausea, vomiting and dizziness.
sudden onset
55
Manifestations After Rupture of Aneurysm
- Sudden and severe headache
- Severe bleeding can cause collapse and loss of consciousness
- Vomiting
56
Other manifestations of rupture of aneurysm:
Nuchal rigidity, photophobia, diplopia and blurred vision, focal motor and sensory deficits, cerebral edema, increased ICP and hypertension.
57
Diagnosis of SAH
Clinical presentation
CT scan
Lumbar puncture
Angiography
58
Treatment of SAH depends on extent of _______.
| Best outcomes achieved when aneurysm can be secured early and complications prevented.
neurologic deficit
59
Treatment of Mild to No neurologic deficit:
```
may undergo cerebral arteriography
early surgery (craniotomy with aneurysm clipping)
```
60
Endovascular techniques:
Surgically inaccessible aneurysms or poor surgical candidates.
Ex. balloon embolization & platinum coil electrothrombosis
61
Complications of Aneurysmal Rupture
```
Rebleeding
Vasospasm with cerebral ischemia
Hydrocephalus
Hypothalamic dysfunction
Seizure activity
Death
```
62
- Difficult to treat
- High incidence of morbidity and mortality.
- Usually occurs within 3-10 days after rupture.
- Involves focal narrowing of the cerebral artery or arteries.
- Deteriorating neurologic status as blood supply decreases to area of ____.
Vasospasm
63
Treatment of Vasospasms
1. Maintain adequate CPP through use of:
- Vasoactive drugs to increase BP
- Large amounts of intravenous fluid to increase intravascular volume and produce hemodilution
But…these can increase the risk for rebleeding
2. Early surgery thought to be protective
3. Endovascular techniques such as balloon dilation may be used
4. Medication:
64
Medication Treatment for Vasospasms
Nimodipine (calcium channel blocker) to blocks calcium channels and acts selectively on cerebral blood vessels to prevent/treat vasospasm.
65
- Complex tangle of abnormal arteries and veins linked by one or more fistulas.
- Lack a capillary bed and small arteries have a deficient muscularis layer.
Arteriovenous Malformations (AVMs)
66
Etiology of AVMs
Congenital
Lack development of the capillary network in the embryonic brain.
- As child’s brain grows, malformation acquires additional arterial contributions that enlarge to form tangled collection of thin-walled vessels that shunt blood directly from the arterial to venous circulation.
67
Typical presentation of AVMs
Before 40 years of age.
Affect men and women equally.
Rupture of AVM causing hemorrhagic stroke (2% of all stroke)
68
Rupture of AVM causing ___________.
hemorrhagic stroke (2% of all stroke)
69
Major manifestations of AVM: (4)
Intracerebral & subarachnoid hemorrhage
Seizures
Headaches
Progressive neurological deficits
70
Other focal deficits depend on location of AVM:
| 4
Visual symptoms( ie. diplopia, hemianopia), Hemiparesis, Mental deterioration & Speech deficits.
71
Diagnosis of AVM
Cerebral angiography
72
Treatment methods for AVM (3):
surgical excision
endovascular occlusion
radiation therapy
73
A process in which aims to maintain adequate and stable cerebral blood flow.
• Cerebral autoregulation
74
A circulatory anastomosis that supplies blood to the brain and surrounding structures
• Circle of Willis
75
relating to or denoting the opposite side of a body, structure
• Contralateral
76
A surgical operation in which a bone flap is temporarily removed from the skull to access the brain
• Craniotomy
77
lacking firmness; soft and limp; flabby
• Flaccid
78
A usually congenital condition in which an abnormal accumulation of fluid in the cerebral ventricles causes enlargement of the skull and compression of the brain, destroying much of the neural tissue.
• Hydrocephalus
79
Overactive or overresponsive reflexes.
• Hyperreflexia
80
Belonging to or occurring on the same side of the body.
• Ipsilateral
81
an unfilled space or interval; a gap
• Lacunae
82
fail to care for properly.
Neglect
83
a blockage of a blood vessel, usually with a clot
Occlusion
84
a sensation of tingling, tickling, prickling, pricking, or burning of a person's skin with no apparent long-term physical effect.
Parasthesia
85
a condition in which bright lights hurt your eyes. Light sensitivity.
Photophobia
86
is a protein involved in the breakdown of blood clots.
tPA - Tissue plasminogen activator
87
impaired neck flexion resulting from muscle spasm (not actual rigidity) of the extensor muscles of the neck; usually attributed to meningeal irritation.
Nucal rigidity
88
Tissue death (necrosis) caused by a local lack of oxygen, due to an obstruction of the tissue's blood supply.
Infarction
89
The pressure inside the skull and thus in the brain tissue and cerebrospinal fluid (CSF)
Intracranial pressure
