Cerebrovascular333

8/7/2019 Cerebrovascular333

1/10

Vascular Diseases 1

Vascular Diseases of the Central Nervous System

XXXXX

XXXX

XXXXX


2/10

Vascular Diseases 2

Abstract

Vascular disease of the central nervous system, or cerebrovascular disease as it is also know, is a

group of brain dysfunctions that can lead to severe complications for those that are affected. It

can be properly defined as any process that is caused by an abnormality of the blood vessels or

blood supply to the brain. The type of cerebrovascular disease that this report will focus on are

stroke syndrome, transient ischemic attacks, intraparenchymal hemorrhage, and subarachnoid

hemorrhage. The main focus of this paper is to discuss the treatment options, pathology,

radiographic appearance and the preferred modality for accurate diagnosis of these conditions.


3/10

Vascular Diseases 3

Vascular Diseases of the Central Nervous System

Let us consider the human brain. While at first glance it may seem just a simple mass of

gray, organic substance it is in reality one of the most complex aspects of nature. It acts as the

command center of our body, controlling all of our actions, thoughts, and emotions. Even our

senses, the gateways through which we access the world are in its control. The cerebral cortex of

humans contain over 15 billion neurons; each one linked up to around 10,000 synaptic

connections. While the brain is quite sophisticated and almost completely surrounded by the

skull, it is still extremely vulnerable. Numerous injuries and diseases pose constant threat to our

minds. Thankfully, using imaging modalities of CT scans, MRI, and ultra-sound we can probe

the brain to see whether any damage or injury has occurred.

Vascular disease of the central nervous system, or cerebrovascular disease as it is also

known, can take several forms. The first of these diseases is known as a stroke, also know as a

cerebral infarction. According to Stephen Grand (2010) a stroke can be defined as a rapidly

developing clinical signs of focal (or global) disturbance of the cerebral function with symptoms

lasting 24 hours or longer or leading to death, with no apparent cause other than of vascular

origin (p. 39) The appearance of a stroke and its signs and symptoms are further described by

Stephen Gran (2010) as:

Stroke Symptoms can range from mild to dramatic to sudden death. They can also come

on gradually, slowly or rapidly increase, or come on quite suddenly. Symptoms and signs

can include (among others) the following: sudden speech disturbances, gait disturbances,

sudden sleepiness, severe headache, sudden temporary blindness or other visual defects,

sudden numbness or weakness or paralysis of one or more body parts or even an entire


4/10

Vascular Diseases 4

side, difficulty in swallowing, and even coma or convulsions. (p. 39)

The specific neurologic defect depends on the arteries involved;most commonly

involving the circulation of the internal carotid arteries (Eisenberg, R. L. & Johnson, N.M. 2007,

p. 339). David S. Knopman (2006) wrote that both mild cognitive impairment & dementia

maybe caused by cerebrovascular disease.

Noncontrast CT is the examination of choice for the evaluation of a the stroke patient, or

MRI when available (Eisenberg, R. L. & Johnson, N.M. 2007, p. 339). Contrast would not be

used due to the risk of crossing the disrupted blood-brain barrier which could lead to an

increased edema and a slower recovery of the patient. (Eisenberg, R. L. & Johnson, N.M. 2007,

p. 339). A cerebral infarction's initial appearance, within 8 to 24 hours of incident, is triangular

area of hypodensity on a CT and a high signal intensity on the T2-weighted MRI sequences

involving both the cortex and the underlying white matter down to the vascular surface within;

the abnormality is confined to the vascular area of the involved artery (Eisenberg, R. L. &

Johnson, N.M. 2007, p. 340). Little to no mass effect is evident during the first day, though

progressive edema produces a mass effect no later than 7 to 10 days after the event(Eisenberg, R.

L. & Johnson, N.M. 2007, p. 340). Brain tissues atrophies with the adjacent ventricular system

and sulci enlarge as the infarct ages. (Eisenberg, R. L. & Johnson, N.M. 2007, p. 340).

The treatment of most stroke patients involve being placed on bed rest with reduced

external stimuli to lower cerebral oxygen demands, medications to decrease intracranial edema

and intracranial pressure (Eisenberg, R. L. & Johnson, N.M. 2007, p. 341). If the patient suffered

a thombotic stroke they are given anticoagulants and possibly thrombolytic agents (Eisenberg, R.

L. & Johnson, N.M. 2007, p. 341). There is also a small window of effectiveness, about 3 hours


5/10

Vascular Diseases 5

after an acute ischemic stroke, when a tissue plasminogen activator, is considered effective in

dealing with the blood clots (Grand, Stephen 2010, p. 40).

Another form of cerebrovascular disease is a Transient ischemic attack. Transient

ischemic attacks present as focal nerologic deficts that are completely resolved within 24 hours

form the initial attack (Eisenberg, R. L. & Johnson, N.M. 2007, p. 341). TIAs, which precedes

almost two thirds of all arteriosclerotic strokes, can result from emboli originating from the

surface of an arteriosclerotic ulcerated plaque, causing temporary occlusion of cerebral vessels,

or from stenosis of an extracerebral artery, leading to a reduction in critical blood perfusion

(Eisenberg, R. L. & Johnson, N.M. 2007, p. 341).

Surgically treatable arteriosclerotic disease causing TIAs are commonly located in the

region of the carotid bifurcation in the neck (Eisenberg, R. L. & Johnson, N.M. 2007, p. 341).

Carotid duplex color-flow Doppler scanning is often the initial screening study in patients with

an asymptomatic bruit, a rumbling noise heard by a stethoscope, or an unclear history of a TIA

(Eisenberg, R. L. & Johnson, N.M. 2007, p. 341). The technique combines both Doppler

ultrasound with spectral analysis and high-resolution ultrasound imaging into a duplex unit

that avoids many of the problems associated with each of these modalities when used alone

(Eisenberg, R. L. & Johnson, N.M. 2007, p. 341). When carotid duplex scanning is combined

with MRA it can reliably determine, in most cases, whether the extent of the disease is sufficient

enough to warrant a more invasive procedure, like an angiography; patients with a normal or

near-normal carotid duplex scan do no need to dundergo more invasive diagnostic procedures for

assesing the carotid bifurcation. (Eisenberg, R. L. & Johnson, N.M. 2007, p. 341). If a patient has

a clear-cut case of a TIA or a neruologic deficit they are usually subjected to an angdiographic


6/10

Vascular Diseases 6

study, such as intravenous or intraarterial DSA or selective intraarterial carotid arteriography, for

evaluating the carotid arteries (Eisenberg, R. L. & Johnson, N.M. 2007, p. 341).

While TIAs has many scanning options there are just a few methods to treat TIAs.

Prevention of permanent deficits due to TIAs require accurate diagnosis and the appropriate

treatment such as anti-platelet therapy, anticoagulation therapy, or carotid dendarterectomy

though thrombolytic agents can also be used(Eisenberg, R. L. & Johnson, N.M. 2007, p. 342).

According to Eisenberg and Johnson (2007) write that intraparenchymanl hemorrhages,

or a hemorrhagic stroke, is principally cuased by hypertensive vascular disease, when not

accounting for cases resulting form head trama (p. 342). Eisenberg and Johnson (2007) also

write that they can be caused less frequently by a rupture of a congenital berry aneurysm or an

arteriovenous malformation (p. 342-343). Hypertensive hemorrhages which are most frequent

in the basal ganglia, white matter, thalamus, cerebral hemispheres and the pons, results in oval

collections which displace the surrounding brain and can cause a significant mass effect

(Eisenberg, R. L. & Johnson, N.M. 2007, p. 343). Eisenber and Jonson (2007) write that

congenital berry (saccular) aneurysms that result in intraparenchymal hemorrhages are usually

associated with subarachnoid hemorrhages and tend to develop in the sylvian fissure and the

midline subfrontal area (p. 343).

Patients that may be suffering with an intraparenchymal hemorrhage should be evaluated

with MRI, though a noncontrast CT scan will suffice (Eisenberg, R. L. & Johnson, N.M. 2007, p.

343). Eisenberg and Johnson write that a fress hematoma appears on CT as a homogeneous

dense, well-defined lesion with a round to oval configuration (Eisenberg, R. L. & Johnson,

N.M. 2007, p. 343). Eisenberg and Johnson (2007) also write that hematomas produce


7/10

Vascular Diseases 7

ventricular compression and, when large, considerable mid-line shift and brain herniation

(p. 343). When looking at a hematoma on CT, after they pass an isodense stage, the hematoma

becomes hypodense; by 6 months it will appear as a well-defined, low-density region that is

often smaller than the original lesion, with contrast enhancement usually developing 7 to ten

days. (Eisenberg, R. L. & Johnson, N.M. 2007, p. 343). While looking at a hematoma MRI, the

high signal intensity within arises after a few days and will continue for several months

(Eisenberg, R. L. & Johnson, N.M. 2007, p. 343).

Steroid therapy can usually control the edema that produces most of the mass effect,

especially in nontraumatic hematomas (Eisenberg, R. L. & Johnson, N.M. 2007, p. 344).

Eisenberg and Johnson (2007) write that in cases of hemmorrhagic strokes, the first line of

treament consists of stopping the bleeding, and the second is to try to prevent a recurrence of

bleeding, and finally surgery is performed to correct the pathology ( p. 344). Surgical placement

of a clip at the neck of the lesion is required for aneurysms to close the pouch, while

Ateriovenous malformations require surgery or neurointerventional procedures. (Eisenberg, R. L.

& Johnson, N.M. 2007, p. 344).

The last form of cerebrovascular disease that this paper will discuss is a subarachnoid

hemorrhage. Eisenberg and Johnson (2007) state that the major cuase of subarachnoid

hemorrhage is the rupture of a berry aneurysm (p. 344). Patients affected by this condition

usually develop a generalized, excruciating headache followed by unconsciousness (Eisenberg,

R. L. & Johnson, N.M. 2007, p. 345). Berry anneurysms are commonly located at the origins of

the posterior cerebral and anterior communicating arteries and the trifurcation of the internal

Carotid and vertebral arteries bilaterally (Eisenberg, R. L. & Johnson, N.M. 2007, p. 345).


8/10

Vascular Diseases 8

The radiographic procedure of choise for subarachnoid hemorrhage is a noncontrast CT

scan, which will demonstrate high-density blood in the subarachnoid spaces of the basal cisterns

(Eisenberg, R. L. & Johnson, N.M. 2007, p. 345). According to Eisenberg and Johnson (2007)

bleeding may extend into the brain parenchyma adjacent to the aneurysm (p. 345). CT scans

should not be accompanied by the use of contrast because a surgeon will not operate on a patient

with a suspected aneurysm without an angiogram, and the patient would then be exposed to the

risk of an excessive load of contrast media (Eisenberg, R. L. & Johnson, N.M. 2007, p. 345-346).

MRI, according to Eisenberg and Johnson (2007), is relatively insensitive for identifying acute

subarachnoid bleeds, but it does demonstrate chronic blood staining of the meninges (p. 346).

Now high resolution CTA scans can demonstrate aneurysms greater than 3mm and is becoming

more accepted for the use of per-surgical planning (Eisenberg, R. L. & Johnson, N.M. 2007, p.

343). The timing of angiongraphy, as written by Eisenberg and Johnson (2007), depends on the

philosophy of the surgeon (p. 346). Blood in the subarachnoid spaces acts as an irritant, causing

a vasospasm of the vessels of the circle of Willis and the middle cerebral artery; this spasm is

greatest 3 to 14 days after the acute episode, and can lead to frank infarction and cerebral

ischemia (Eisenberg, R. L. & Johnson, N.M. 2007, p. 346).

Emergency selective angiography is indicated if emergency surgery is planned within the

first 72 hours after the hemorrhage(Eisenberg, R. L. & Johnson, N.M. 2007, p. 346). According

to Eisenberg and Johnson (2007) if surgical intervention is to be delayed, ganiography should

be postponed until just before surgery(p. 346).

Vascular disease of the central nervous system, or cerebrovascular disease, can be defined

simply when any abnormality of the blood vessels or blood supply to the brain occurs. This can


9/10

Vascular Diseases 9

happen in several ways, either due to trauma, high blood-pressure, or even lack of a healthy

lifestyle. A improvement in your life style, such as quitting smoking and changing your diet, can

drastically reduce the likely hood of contracting these conditions. Thankfully, even if you do end

up suffering form a cerebrovascular disease, modern medicine has managed to lessen the likely

hood of severe and lasting damages.


10/10

Vascular Diseases 10

References

Eisenberg, R. L., & Johnson, N. M. (2007). Comprehensive Radiographic Pathology.

St. Louis, MO: Mosby Elsevier.

Grand, Stephen (2010). Cerebrovascular Risk Factors and Prevention form a Nutritional

Perspective. Nutrional Perspectives. Journal of the Council on Nutrition of the American

Chiropractic Association, 33(1), 39-42. Retrieved September 20, 2010, form CINAHL

database.

Knopman, David S. (2006) Dementia and Cerebrovascular Disease. Mayo Clinic Proceedings,

81(2), 223-230, Retrieved November 6, 2010, from CINAHL database.

Cerebrovascular333

Documents

Transcript of Cerebrovascular333