Stroke (Cerebrovascular Accident)

1. QXCI Treatment Possibilities

1.1. Circulation related treatment

Systemic Treatment

Click Programs (from menu bar on top of main test screen)

Click Spinal and Sarcodes (from drop down menu)
Show Sarcode System
Click Circulation (middle left of page)
Add an Additional therapy superimposed (by selecting or unselecting above and on left side)
Click Start Treatment

Sarcode Stimulation

Click Programs (from menu bar on top of main test screen)

Click Spinal and Sarcodes (from drop down menu)
Click Timed Therapies (from middle of page)
Select treatment time by moving bar
Optionally select or unselect any additional treatment
Click Circulation Stim (from first column)

 To close click on OK in Therapy Over window and then

click Close

1.2.Rehabilitation related treatment

Sarcode Stimulation

Click Programs (from menu bar on top of main test screen)

Click Spinal and Sarcodes (from drop down menu)
Click Timed Therapies (from middle of page)
Select treatment time by moving bar
Optionally select or unselect any additional treatment
Click Memory Stim (from third column)
To close click on OK in Therapy Over window and then click Close

Biofeedback

Click Programs (from menu bar on top of main test screen)

Click Biofeedback (from drop down menu)
Have patient look at screen and focus mind on area of concern
Click Reduce stress in nerves (from drop down menu)
To stop click STOP PROGRAM (from upper right corner)

Systemic Treatment

Click Programs (from menu bar on top of main test screen)

Click Spinal and Sarcodes (from drop down menu)
Show Sarcode System
Click Nerves (middle left of page)
Add an Additional therapy superimposed (by selecting or unselecting above and on left side)
Click Start Treatment

Organ specific biofeedback

Click Programs (from menu bar on top of main test screen)

Click Biofeedback (from drop down menu)
Click Organ Systems (from menu bar on top of biofeedback screen)
Have patient look at screen and focus mind on area of concern
Click Brain (from drop down menu)
To stop click STOP PROGRAM (from upper right corner)
Click Nerve Conduction (from drop down menu)
To stop click STOP PROGRAM (from upper right corner)
Click Synapse Stabilization (from drop down menu)
To stop click STOP PROGRAM (from upper right corner)

2. General Information
Cerebrovascular Accident

(Stroke)
Impairment of one or more vessels in the cerebral circulation, caused by thrombosis,
embolus, stenosis, or hemorrhage, which interrupts the blood supply and results in
ischemia of brain tissues.
Causes and Incidence A cerebrovascular accident (CVA) is caused by occlusion of a
cerebral vessel. Most cerebrovascular occlusions occur secondary to atherosclerosis or
hypertension, or a combination of the two. Other risk factors are diabetes mellitus,
myocardial infarction, bacterial endocarditis, rheumatic heart disease, aneurysms, head
trauma, sick sinus syndrome, and a history of previous stroke or transient ischemic
attacks (TIAs). CVA is the second most common cause of neurologic disability and the
third most common cause of death in the Western Hemisphere. More than 500,000
people are diagnosed with CVA each year in the United States, and of those 200,000 die.
The incidence increases with age, with adults 65 years of age or older at greatest risk.
Disease Process The general pathophysiology of a CVA involves occlusion of a
cerebral vessel, which leads to ischemia of the brain tissue supplied by that vessel. If the
obstruction is not removed, the affected tissue infarcts and dies, causing permanent
neurologic deficit or death. The severity of the CVA depends on the location and extent
of the obstruction, the degree of collateral circulation, and the promptness of diagnosis
and treatment.
Thrombotic strokes account for approximately 40% of ischemic cerebrovascular
disease. The occlusion develops slowly over time as the atherosclerotic plaque builds up
in the large-vessel walls. A TIA is a common precursor. Symptoms often evolve over
hours or even days and frequently are noticed when the person awakens in the morning.
Damage from a CVA is generally extensive because of the large vessels involved and
the likelihood that collateral circulation is diminished or absent.
Emboli, which cause 30% of strokes, arise when platelets, cholesterol, fibrin, or other
miscellaneous hematogenous material breaks off from the arterial walls or the heart and
travels to and blocks a cerebral vessel. The onset of symptoms generally is sudden and
usually occurs in small distal cortical vessels, affecting cortical functions.
Lacunar strokes, which account for 20% of all CVAs, occur where small perforating
arterioles branch off large cerebral vessels in the basal ganglia, internal capsule, and
brainstem. The small subcortical arterioles are exposed to the constant high-pressure
flow of the large branch arteries. Over the years the smaller vessels become thickened,
thrombosed, and then obstructed. The resulting damage is distinctive, and these strokes
are often labeled ipure motori or ipure sensoryi strokes.
Intracerebral hemorrhage accounts for 10% of all strokes and is the most catastrophic
type. The onset is sudden, often occurs during exertion, and is triggered by bleeding that
obstructs and ruptures the small subcortical arterioles in the deep brain. The pathology
of the bleeding is not well understood, although some research indicates that it may be
precipitated by microaneurysms that cause arteriolar necrosis.
Symptoms The signs and symptoms of a stroke depend on the site and size of the
obstruction. They typically include altered mental status, hemiparesis or hemiplegia,

receptive or expressive aphasia, dysarthria, dysphagia, apraxia, hemianopsia, urinary

incontinence, and emotional lability. Headache, seizures, stupor, and marked
hypertension may also be present.
Potential Complications Coma and death are the most severe consequences of CVA.
Permanent neurologic deficits (e.g., paralysis, impaired intellectual capability, speech
defects, loss of short-term memory, impaired judgment and problem-solving abilities,
reduced impulse control) are common residual complications.
Diagnostic Tests
Clinical evaluation
Any of the above manifestations, particularly in individuals with identifiable risk factors
Computed tomography/ magnetic resonance imaging
To identify area of infarct or bleeding
Ultrasonography
To identify diminished blood flow in vessels
Angiography
To detect occlusion of large vessels
Treatments
Surgery
Evacuation of hematoma or clot; placement of intracranial pressure monitor;
endarterectomy to remove atherosclerotic plaques
Drugs
Anticoagulants during stroke evolution; antihypertensives to control blood pressure;
diuretics to reduce edema in the brain; anticonvulsants to control seizures; long-term
aspirin therapy to prevent future stroke
General
Monitoring and support of vital functions; prevention of decubitus ulcers, thrombosis,
and pneumonia; rehabilitation: occupational therapy for adapting activities of daily
living, physical therapy to increase strength and endurance; gait training to improve
ambulation; cognitive therapy to improve memory and problem solving; speech therapy
to improve communication; counseling for poststroke depression and altered sexual
functioning; vocational retraining