Multiple Myeloma of Thoracic Spine

Multiple Myeloma of Thoracic Spine

Multiple myeloma is a malignancy of the plasma cells. Plasma cells are a type of white blood cell present in the bone marrow.
In multiple myeloma, a collection of abnormal plasma cells (myeloma cells) increase, elevating the amount of plasma cells to a more than normal level. The outcome can be erosion of the bones. The disease also obstructs the function of the bone marrow and immune system, which can lead to anemia and infection. Multiple myeloma may also cause kidney problems.
The disease is called multiple myeloma because myeloma cells can occur in numerous bone marrow locations in the body.

Signs and symptoms
Even though multiple myeloma may not cause symptoms early in the disease, it's probable that signs and symptoms will appear as the disease develops.
Signs and symptoms of the disease can differ from person to person. Common multiple myeloma symptoms include:
Bone pain.
Presence of abnormal proteins — which can be created by myeloma, cells — in the blood or urine. These proteins — which are antibodies or parts of antibodies — are called monoclonal, or M, proteins. Frequently revealed through a routine exam, monoclonal proteins may indicate multiple myeloma, but also can indicate other conditions.
High level of calcium in the blood. This can occur when calcium from affected bones dissolves into the blood.
If there is high calcium level in the blood, the signs and symptoms are:
Excessive thirst and urination
Constipation
Nausea
Loss of appetite
Mental confusion
Anemia can occur as myeloma cells restore oxygen-carrying red blood cells in the bone marrow, which may lead to an additional frequent symptom — fatigue.
Other signs and symptoms of multiple myeloma may include:
Bone pain, mainly in the back or ribs
Unexplained bone fractures
Recurring infections — such as pneumonia, bladder or kidney infection, or sinusitis
Weight loss
Weakness or numbness in the legs

Causes
Though the exact cause isn't identified, physicians do know that multiple myeloma begins with one abnormal plasma cell in the bone marrow — the spongy, blood-producing tissue that fills in the middle of most of the bones. This abnormal cell then begins to increase.
Because abnormal cells don't mature and then die as normal cells do, they accumulate, finally overpowering the production of healthy cells. Healthy bone marrow consists of a minute amount of plasma cells, fewer than 5 percent. However in people with multiple myeloma, the number of plasma cells often increases to more than 10 percent.
Because myeloma cells may flow in low numbers in the blood, they can inhabit other bone marrow locations in the body, even distant from where they began. Uncontrolled plasma cell development can harm bones and surrounding tissue. It can also hinder with the immune system's capability to fight infections by reducing the body's production of normal antibodies.

Risk factors
Multiple myeloma isn't contagious. Most people who develop multiple myeloma have no obvious identifiable risk factors for the disease.
Some factors that may increase the risk of multiple myeloma include:
Age. The majority of people who acquire multiple myeloma are older than 50, with most diagnosed around age 70. Few cases occur in people younger than 40.
Sex. Men are more likely to develop the disease than are women.
Race. Blacks are about twice as likely to develop multiple myeloma, as are whites.
History of a monoclonal gammopathy of uncertain importance. Every year 1 percent of the people with MGUS in the United States acquire multiple myeloma. MGUS is more frequent in adults over age 50. This condition, like multiple myeloma, is marked by the presence of M proteins — created by abnormal plasma cells — in the blood. However, in MGUS, the quantity of the abnormal proteins isn't high enough to cause damage, and no injury to the bones occurs.
Obesity. The risk of multiple myeloma is increased if you're overweight or obese.
Other factors that may increase your risk of developing multiple myeloma include exposure to radiation and working in petroleum-related industries.

Screening and diagnosis
The doctor may initially discover signs of multiple myeloma before there are symptoms — through blood and urine examinations conducted through a routine physical exam. If there are no symptoms, these lab tests may be repeated every few months so that the physician can follow whether the disease is progressing and establish the best time to begin treatment.
Blood and urine tests A blood test called serum protein electrophoresis separates the blood proteins and can detect the presence of M proteins, called an "M spike," in the blood. Parts of M proteins may also be detected in a test of the urine — when found in urine; they're referred to as Bence Jones proteins.
If the doctor discovers M proteins, there is a need for additional blood tests to determine blood cell counts and levels of calcium, uric acid, and creatinine. The physician may also order other blood tests to check for beta2-microglobulin — another protein produced by myeloma cells — or to assess the percent of plasma cells in your bone marrow.
Other tests needed They may include:
Imaging. X-rays of the skeleton can demonstrate whether the bones have any thinned-out regions, common in multiple myeloma. If a closer view of your bones is needed, the doctor may use magnetic resonance imaging (MRI) or computerized tomography (CT) scanning.
Bone marrow examination. The doctor may also order a bone marrow examination by using a needle to remove a tiny sample of bone marrow tissue. The sample is then examined below a microscope to test for myeloma cells.
Staging and classification These tests can help verify whether this is multiple myeloma or another condition. If tests indicate this is multiple myeloma, the outcome from these tests permit the doctor to categorize the disease as stage 1, stage 2, or stage 3. People with stage 3 myeloma are more likely to have one or more signs of progressive disease, including larger numbers of myeloma cells and kidney failure.

Complications
Multiple myeloma can result in several complications:
Impaired immunity. Myeloma cells hinder the manufacture of antibodies required for normal immunity. Having multiple myeloma may cause more infections, such as pneumonia, sinusitis, bladder, or kidney infection, skin infections and shingles.
Bone problems. Multiple myeloma also can affect the bones, leading to erosion of bone mass and fractures. The condition may cause compression of your spinal cord. Signs of this medical emergency include weakness, or even paralysis, in the legs.
Impaired kidney function. Multiple myeloma may cause problems with kidney function, including kidney failure. Higher calcium levels in the blood associated to eroding bones can obstruct the kidneys' capability to filter the blood's waste. The proteins created by the myeloma cells can cause related problems, particularly if dehydrated.
Anemia. As cancerous cells crowd out normal blood cells, multiple myeloma can also cause anemia and other blood problems.

Treatment
Normally, for multiple myeloma if there are no symptoms, there is no need for treatment. Though, the doctors will probably monitor the condition at variable periods, checking for signs — such as rising levels of M protein in the blood or urine — that indicate the disease is progressing. If it is, treatment may be needed to help avoid symptoms. In people diagnosed with asymptomatic multiple myeloma, the risk of developing symptoms is about 10 percent a year for the first five years after knowledge of the disease.
For the symptoms, treatment can help ease pain, manage complications of the disease, stabilize the condition, and slow down the development of the disease.

Standard treatments for myeloma

Although there's no cure for multiple myeloma, with good treatment consequences most patients typically return to near-normal activity. The appropriate multiple myeloma treatment depends on the needs, medical status, and general health of the patient. They also may desire to consider accepted clinical trials as an alternative.
Standard treatment options include:
Chemotherapy. Chemotherapy involves using medicines — taken orally as a pill or given through an intravenous (IV) injection — to destroy myeloma cells. Chemotherapy is frequently given in cycles over a period of months, followed by a rest period. Regularly chemotherapy is terminated through what is called a plateau phase or remission, through which the M protein level remains steady. There may be a need for chemotherapy again if the M protein level starts to increase. Common chemotherapy drugs used to treat myeloma are melphalan (Alkeran), cyclophosphamide (Cytoxan), vincristine (Oncovin), doxorubicin (Adriamycin) and liposomal doxorubicin (Doxil).
Corticosteroids. Corticosteroids such as prednisone and dexamethasone (Decadron) have been used for decades to treat multiple myeloma. They are normally given as pills. Some research recommends that high doses of steroids may not be required, and that lower doses may be safer and more effective.

Stem cell transplantation. This treatment involves using high-dose chemotherapy — typically high doses of melphalan — along with transfusion of previously collected undeveloped blood cells (stem cells) to substitute diseased or damaged marrow. The stem cells can come from you or from a donor, and they may be from either blood or bone marrow. Factors such as the risk of your disease progressing, the patient’s age and their general health play a part in determining whether stem cell transplantation may be right for them.
Thalidomide (Thalomid). Thalidomide, a drug originally used as a sedative and to treat morning sickness in the 1950s, was removed from the market after it was established to cause severe birth defects. Nevertheless, the drug received approval from the Food and Drug Administration (FDA) again in 1998, first as a treatment for skin lesions caused by leprosy. Thalidomide is currently FDA-approved in combination with the corticosteroid called dexamethasone for the treatment of recently diagnosed cases of multiple myeloma. This drug is given orally. This is used for candidates for stem cell transplantation for their initial therapy.

Bortezomib (Velcade). Velcade was the first accepted drug in the latest class of medications called proteasome inhibitors. It is given intravenously. It works by blocking the action of proteasomes, which causes cancer cells to die. One study demonstrates that bortezomib had more than twice the response rate of a frequently used drug, dexamethasone. The FDA for use in a treatment approves Bortezomib for people with multiple myeloma who have received at least one previous treatment.
Lenalidomide (Revlimid). Lenalidomide is chemically comparable to thalidomide, but appears to be more powerful and cause fewer side effects. It is given orally. Lenalidomide is FDA-approved for use in combination with dexamethasone as a treatment for people who have received at least one earlier treatment for multiple myeloma. This is commonly used on patients initially considered for stem cell transplantation.
Radiation therapy. This treatment uses high-energy penetrating waves to damage myeloma cells and prevent their development. Radiation therapy may be used to target myeloma cells in a particular area — for example, to more rapidly minimize a tumor that's causing pain or destroying a bone.

Treating complications

Because multiple myeloma can cause a number of complications, you may also need treatment for those particular conditions. For example:
Back pain. Taking pain medication or wearing a back brace can help ease the back pain with multiple myeloma.
Kidney complications. People with severe kidney damage may need dialysis.
Infections. Antibiotics may be needed to help treat infections or to help decrease the risk of them.
Bone loss. Medications called bisphosphonates, such as pamidronate (Aredia) or zoledronic acid (Zometa), which attach to the surface of the bones and help stop bone loss. Treatment with these drugs is related to the risk of damage to the jawbone. If taking these medications, don't have dental procedures done without conferring with the doctor first.
Anemia. If there is constant anemia, the physician may prescribe erythropoietin injections. Erythropoietin is a naturally occurring hormone made in the kidneys that stimulates the manufacture of red blood cells. Research suggests that the use of erythropoietin may increase the risk of blood clots in some people with myeloma.

Information from mayoclinic.com

Cervical Spine Tumors

Cervical Spine Tumors
Neoplasms of the spine can be classified as primary tumors or metastatic tumors. Metastatic is a common term used to describe the spread of a cancer from some other site in the body. The spinal column is one of the most common locations for cancer to metastasize to. Metastatic tumors of the spine are the most common tumors of the spine, and are normally treated without surgery unless there is consequential spinal instability or neurologic concession. The majority of metastatic lesions are treated with chemotherapy and/or radiation therapy that is defined for the primary cancer type. Primary tumors of the spine can be benign or malignant (cancer), and can be additionally subdivided into intradural and extradural neoplasms. Intradural means that the tumor is beginning from or within the dural sac (sac containing the spinal cord and nerves). Extradural tumors are often neoplasms infiltrating the bony structure of the vertebrae, but can also occur within the epidural space. Intradural tumors are further classified as intramedullary or extramedullary, and specify whether or not a tumor is appearing from within the spinal cord itself (intradural-intramedullary), or from the covering of the spinal cord (intradural-extramedullary). Generally, primary spine tumors are uncommon and include almost .04% of all tumors and 10% of all bone tumors.
Extradural Tumors
Benign
· Osteochondroma, Osteoid Osteoma, Osteobalstoma, Osteobalstoma, Aneurysmal Bone Cyst, Hemangioma, Giant Cell Tumor, Eosinophilic Granuloma and Angiolipoma
Malignant
· Multiple Myeloma, Solitary Plasmacytoma, Osteosarcoma, Chondrosarcoma, Ewing’s Sarcoma, Chordoma and Lymphoma
Intradural-Extramedullary Tumors
· Meningioma, Lymphoma, Schwannoma and Ependymomas
Intradural-Intramedullary Tumors
· Astrocytoma, Ependymoma, Hemangioblastoma, Lipoma, Dermoid, Epidermoid, Neuroblastoma, Oligodendrolioma, Cholesteatoma, Subependymoma and PNET
Causes
Neoplasms and cancer are defined as an atypical cellular response that causes cells to develop at an uninhibited rate, or in an unusual site, or both. The original cause of cancer and tumors is frequently unidentified. At times, patients with acknowledged exposure to a cancer-causing agent may be recognized (asbestos, radiation, etc). Cancer is known to spread to the spinal column often, and occurs through the bloodstream or the lymphatic system.
Symptoms
Neck pain is the most common presenting indicator of patients with a cervical spine tumor. Patients frequently have unrelenting pain, as well as night pain, that are not relieved by rest or usual actions. Patients may have neck stiffness and reduced range-of-motion. Patients may have weakness or numbness if the tumor is progressive and causing neurologic compression or irritation. In addition, patients may have constitutional symptoms such as low-grade fever, night sweats, fatigue, malaise, and/or loss of appetite, amid others.
Physical Findings
The physical findings for patients with a spine tumor are restricted. Patients may exhibit tenderness and spasm with lessened cervical range-of motion, but not normally. The neurologic examination will usually be normal unless the spinal tumor is complex and causing neurologic compression or irritation.
Imaging Studies
Plain x-rays of the cervical spine permit the physician to measure the general spinal alignment and bony integrity, and may show a bone-forming or bone-destroying neoplasm if the lesion is great enough. A magnetic resonance imaging test (MRI) with gadolinium is frequently suggested and necessary to correctly identify the size and degree of the neoplasm, and whether it has extended into the spinal canal. Spine tumors can be distinguished from pyogenic spine infections because neoplasms influence the vertebral body primarily and typically do not affect the disc, whereas pyogenic vertebral osteomyelitis preferentially damages the endplate and intervertebral disc. A computed tomography (CT) scan may also be ordered as it permits doctors to better visualize details of the bony anatomy better than an MRI test. A CT-myelogram (dye is injected within the thecal sac) may offer further diagnostic information, particularly when assessing intradural neoplasms. A bone scan is a test often requested when cancer is suspected, and can conclude if there are other lesions in the bones throughout the entire body.
Laboratory Tests
Laboratory tests are frequently ordered when a neoplastic work-up is needed. A complete blood count (CBC) with differential, metabolic panel, serum protein electrophoresis (SPEP), urine protein electrophoresis (UPEP), C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) tests is normally ordered when evaluating a tumor. Laboratory tests may verify the diagnosis of lymphoma, leukemia, multiple myeloma, or infection. A PPD skin test should also be placed to test for tuberculosis, which can mimic a spinal tumor.
Diagnosis
The diagnosis of a spine tumor may be postponed, primarily because the initial signs and symptoms are slight and physicians do not originally suspect it. Patients with "red flags" (symptoms suggesting infection or tumor, such as unrelenting pain, night pain, fevers, chills, night sweats, weight loss, etc) must be properly assessed with imaging and laboratory tests to prove the diagnosis.
Treatment Options
The treatment of a neoplasm of the cervical spine depends on a number of aspects: the patient's age and related medical conditions, the type, grade, and stage of the neoplasm, the severity of a patient's symptoms, and the severity of neurologic compression and bony damage. In contrast to the thoracolumbar spine, metastatic tumors of the cervical spine are more liable to cause instability and/or neurologic compromise and are more frequently treated surgically. Benign primary bone tumors are often treated by surgical tumor resection; however, some benign tumors may be treated conservatively and observed if there is nominal pain and there is no indication of spinal instability or neurologic compression. Malignant primary spine tumors are frequently treated by surgical resection and adjuvant chemotherapy and/or radiation. Surgical treatment often consists of neurologic decompression, fusion, and instrumentation in addition to tumor resection. An anterior or posterior surgical method, or at times a combined approach, may be used depending on where the tumor is positioned and where the neurologic compression is most prominent.

Information from Etna Interactive

Carotid Stenosis

Carotid Stenosis

Carotid stenosis is the narrowing of the carotid artery, located in the neck, and is caused by the buildup of plaque (fatty deposits). The process of atherosclerosis in the carotid artery causes a hardening of the walls of the arteries and, results in a carotid stenosis that decreases the flow of blood and nutrients to the brain.
The carotid arteries are located on the sides of the neck. They are crucial arteries, and are a means of blood to the anterior part of the brain and, through branches, to the eyes, forehead, and nose. The deposition of plaque along the inner wall of an artery narrows its diameter. This makes the blocked artery less efficient in carrying blood. Plaque formation can develop so severe that an artery is effectively blocked.
Carotid stenosis creates another danger when bits of the plaque dislodge. These portions, which are referred to as blood clots or emboli, can travel upward with the flow of blood towards the brain, and can become stuck, blocking blood flow. This obstruction disrupts the supply of nutrients and oxygen to the brain, and is one of the causes of cerebral vascular accidents, known as stroke. Carotid stenosis is a form of cerebral vascular disease and atherosclerosis.
Stroke is the third leading cause of death in the United States after coronary artery disease and cancer, with approximately 750,000 strokes and more than 150,000 deaths occurring each year in the United States. Approximately 50% of these strokes are considered to be the consequence of carotid stenosis.
Causes and symptoms
The cause of carotid stenosis is the buildup of plaque on the inner wall of the carotid artery. The decreased blood flow to the brain and the obstruction of other arteries following the release of emboli can cause a stroke. Increased risk of carotid stenosis is related to smoking, hypertension, elevated levels of cholesterol, obesity, and a sedentary lifestyle. Some of these factors such as hypertension and cholesterol level may also be related to a person's physiology. Another risk factor is diabetes. Older, less active people are more prone to carotid stenosis.
Occasionally, preceding a major stroke, a person can be temporarily affected by the arterial blockage or discharge of a small embolus. The interrupted flow of blood to the brain, which can be very brief or last a few hours, does not continue longer than 24 hours. Symptoms of this transient event, called a transient ischemic attack (TIA), include weakness, as well as visual and speech difficulties. The exact symptoms of carotid stenosis depend on the region of the brain that is affected. Symptoms can also be absent, with the stenosis discovered only incidentally during a clinical examination.
In the event of a stroke, if the blocked blood flow is not restored, brain cells can die, causing permanent brain damage.
Diagnosis
Though not as accurate as other techniques, a physician can listen to the pulsation of blood through the carotid artery by means of a stethoscope. A weaker pulse, which is a result of stenosis, will be evident in the form of altered sounds (bruits) as the blood flows past the region of disruption.
Sometimes, carotid stenosis is suspected if a person has a transient malfunction of blood flow to the brain, or a TIA. A TIA can last anywhere from a few seconds to several hours. The brief blockage of the artery can cause a temporary loss of vision in one eye, a weak or numb sensation on one side of the body, slurred speech, or inability to speak. A TIA can be a warning to a physician of the potential presence of carotid stenosis.
Three main diagnostic tests assist in the diagnosis of carotid stenosis. The first is known as a duplex sonogram, or a carotid duplex. The procedure involves the use of high frequency sound waves (ultrasound). The ultrasonic waves echo off of the carotid artery to create a two-dimensional image on a screen. If narrowing or obstruction of the carotid artery is present, it is often evident on the image.
Another dominant imaging technique is magnetic resonance imaging (MRI) or magnetic resonance angiography (MRA). Both rely on the use of magnetism. Pulses of magnetic energy can be utilized to image the targeted area of the body, based on the disruption of the flow of the electrons in the magnetic field. This information is then converted to a visual image.
The third technique is known as an angiogram or arteriogram. An angiogram is an examination that utilizes x rays after a small tube (catheter) is placed into the base of the carotid artery. An x-ray dye is then injected. The dye reveals the regions of the arteries that are narrowed or blocked.
Treatment
Carotid stenosis is treated surgically or medically. One of two surgical treatments is normally used. The first approach is known as microsurgical carotid endarterectomy. The second approach is known as endovascular angioplasty and stenting.
Carotid endarterectomy is the surgical exposure of the carotid artery and the removal of the plaque. This re-establishes the continuous flow of blood to the brain. This approach is the technique of choice for most patients. Though, the technique does carry a risk of stroke (stroke can be caused in up to 3% of surgeries).
For patients who are unable to undergo surgery, the angioplasty and stenting approach is used. In this approach a catheter that contains an expandable area at one end is inserted into the carotid artery. The end of the catheter is then expanded. This "balloon" squeezes the plaque against the arterial wall, increasing the useful diameter of the artery. Then, a stent is placed inside the artery. A stent is a tubular array of fibers somewhat similar visually to wire fencing rolled up into a tube. The stent strengthens the carotid artery to prevent its collapse and to keep the plaque firmly against the arterial wall.
Surgery and the related risks may not be acceptable in patients whose arterial blockage is less than 50%. Anticoagulant medications such as aspirin can be used instead to decrease the tendency of blood clots to form. Treatment can also consist of lifestyle changes such as stopping smoking, limiting cholesterol intake, or use of cholesterol-lowering medications.
Prognosis
With prompt medical treatment, including surgery, recovery from carotid stenosis can be complete with no residual effects. However, if treatment is delayed or if a stroke occurs, damage can be permanent.
If carotid stenosis is dealt with quickly by surgery, medicine, or lifestyle changes, prognosis is good. For example, at the Johns Hopkins Medical School, carotid stenosis corrective surgery has a mortality rate of 0.8% (80 in 1,000 people) and a morbidity rate (the person survives, but with some complication) of 1.8% (18 in 1,000 people).
However, undiagnosed stenosis can result in stroke. Depending on the severity of the stroke, prognosis is unpredictable. An estimated 325,000 strokes and 75,000 deaths occur each year in the United States due to carotid stenosis.
Special concerns
However if there are no symptoms related with the presence of carotid stenosis, the difficulty is often a warning sign of possible blockage of the arteries of the heart, or coronary artery disease. Therefore, people diagnosed with carotid stenosis should be carefully monitored for coronary artery disease.
Information from mayoclinic.org

Tongue Carcinoma

PET, CT & FUSED PET CT

Tongue Carcinoma

About Tongue Base Cancer
Since these cancers are often diagnosed relatively late, physicians consider cancer of the tongue base to be a serious oropharyngeal cancer. Professionals identify the oropharynx as the region in the oral cavity behind the last molar. Studies demonstrate that individuals with a history of nicotine and alcohol usehave an increased occurrence of tongue base cancer. The condition usually develops from squamous cells on the exterior layer of tongue tissue. Once identified early, the condition is highly curable.
Diagnosis
To diagnose and stage tongue base cancer, physicians will acquire a thorough history and perform a complete head and neck examination and may remove a small sample of the cancer to send to the laboratory for analysis. Pathologists qualified in identifying oral conditions will examine the tissue under a microscope.
Patients may also need to have imaging studies performed to see how far the cancer has spread. These may include:
X-rays produce a one-dimensional view of the head and neck to assist the physician in locating abnormalities in the tongue and additional structures of the mouth.
CT scans create two-dimensional and three-dimensional images of the head and neck that may reveal whether cancer has invaded nearby lymph nodes or other organs.
MRI technology utilizes magnetic fields and radio waves to distinguish small abnormalities in the head and neck (three-dimensional views) and to conclude if cancer has spread to other organs.
PET scans use radioactive materials to recognize metabolically active tissues, such as cancer in the tongue, in lymph nodes and other organs of the body such as the lungs, liver or bones.
Symptoms
The following symptoms commonly occur with tongue base cancer:
A persistent (lasting six weeks or more) sore or ulcer on the back of the tongue
Ongoing pain in the mouth
Difficulty breathing
Difficulty swallowing
Foul breath
Pain with swallowing
Sore throat
Severe pain in one ear
Lumps in the neck
Difficulty speaking
Difficulty chewing and swallowing
Weakness of the tongue
Treatment
Treatment for tongue base cancer depends on the patient's general physical condition and the extent of the disease. Most commonly the cancer develops from squamous cells on the surface of the tongue. Rarely, pathologists conclude the condition to occur from the insignificant salivary glands or lymph tissue.
For many stages of squamous cell carcinoma, or other forms of tongue base cancer that originate deeper in the tongue, the risks of surgery may outweigh the benefits. In these cases radiation therapy or chemoradiation therapy may be considered. The exception is if the cancer can be treated with transoral laser microsurgery.
Surgery
Early cancers of the tongue base can often be removed using a laser or cautery instrument working directly through the mouth. The hospitalization is brief and function of the tongue is exceptional. For most larger tongue base cancers, new surgical methods to the tongue base allow removal of any involved lymph nodes and the tongue cancer through a single neck incision. For extremely large tumors for which surgical removal would considerably compromise speech and swallowing, radiation and chemotherapy are used. In most cases of apparent spread to the neck lymph nodes after chemoradiation, surgical removal of the involved lymph nodes is still needed. This procedure is called a neck dissection and physicians use the newest surgical techniques to protect the appearance and function of the neck and shoulder.
Radiation Therapy
Radiation therapy utilizes high-energy X-rays, electron beams, or radioactive isotopes to destroy cancer cells. Radiation oncologists modify each treatment to protect nearby normal tissue.
IMRT uses digital diagnostic imaging, computers, and specialized software to conform many small radiation beams to the shape of the tumor. This produces exact dosage distributions that protect nearby normal tissue. IMRT helps to reduce the loss of function of the tongue and normal adjacent structures such as the salivary glands.
Patients with tongue base cancer can also receive brachytherapy. Brachytherapy is a form of radiotherapy in which specialists position the source of irradiation near the tumor. In the case of tongue base cancer, radioactive material may be located directly into body tissue by hollow needles (interstitial). Brachytherapy may be used in addition to external beam radiation therapy.
Chemotherapy
In the case of tongue base cancer, oncologists administer chemotherapy for large cancers and/or once the cancer has spread to many lymph nodes or other organs in the body. Chemotherapy uses drugs to destroy cancer cells. Medical oncologists administer chemotherapy orally or through the patient's veins. For tongue base cancer, physicians normally use chemotherapy in combination with radiation therapy. If the cancer has metastasized (spread) to distant parts of the body, chemotherapy alone might be considered to help manage the cancer.
Rehabilitation
Care providers specializing in speech therapy, swallowing therapy, dietetics, physical therapy, and occupational therapy help patients with any rehabilitation needed after radiation therapy. The Nicotine Dependence Center can help patients who want to terminate tobacco use.

Information from mayoclinic.com and medscape radiology

Cerebral Aneurysm

Cerebral Aneurysm
A cerebral aneurysm (also known as an intracranial or intracerebral aneurysm) is a weak spot on a blood vessel in the brain that bulges out and fills with blood that can put pressure on a nerve or the surrounding brain tissue. It may also leak or rupture, spilling blood into the nearby tissue (called a hemorrhage). Some cerebral aneurysms, mostly those that are very small, do not bleed or cause other problems. Cerebral aneurysms can occur anywhere in the brain, but most are located along a loop of arteries that run between the base of the brain and the base of the skull.
Diagnosis
Diagnosis of Ruptured Cerebral Aneurysm
A ruptured cerebral aneurysm leads to bleeding within the brain, causing sudden onset of very severe headaches, loss of consciousness, stiff neck or seizures, serious complications and death. These tests are the main tools used to diagnose a ruptured cerebral aneurysm:
Computed tomography (CT) An X-ray procedure that produces detailed images of the brain in cross-sectional slices. CT scans are very sensitive in detecting blood in the subarachnoid space from a ruptured aneurysm. The scan shows the distribution of blood in the brain, providing significant evidence regarding the aneurysm's location.
Magnetic resonance imaging (MRI) uses computer-generated radio waves and a powerful magnetic field to create detailed images of the brain and other body structures. Magnetic resonance angiography (MRA) produces more detailed images of blood vessels. These painless, noninvasive procedures can demonstrate the size and shape of an unruptured aneurysm and can identify bleeding in the brain.
A cerebrospinal fluid examination (CSF) In some cases, the physician may consider a subarachnoid hemorrhage, but the hemorrhage is not discovered on a CT scan. The CSF can help verify a ruptured aneurysm by identifying blood in the cerebrospinal fluid. A needle is introduced into the lower back to remove a small amount of spinal fluid.
Diagnosis of Unruptured Aneurysm
Unruptured aneurysm patients experience headaches or localized abnormalities in brain function. Physicians use magnetic resonance imaging (MRI), magnetic resonance angiography (MRA) and computed tomography angiography (CTA) to diagnosis this condition.
If an aneurysm or subarachnoid hemorrhage is found, the physician may perform a diagnostic test known as a cerebral angiogram to localize the aneurysm. A catheter (thin tube) is placed into an artery in the leg and guided through the bloodstream to the arteries in the neck that lead to the brain. Dye is injected into the arteries as X-rays are taken. These images provide a map of the arteries. MRI, MRA, and CTA scanning also can be used to find an aneurysm, but a cerebral angiogram usually provides more definitive information.
Screening for cerebral aneurysms using MRI, MRA or CTA is recommended for people at high risk, including those with a considerable family history of cerebral aneurysms and those with a disease called autosomal dominant polycystic kidney disease.
Causes
Usually, no definite cause of the aneurysm is established. Though, factors that increase the risk of cerebral saccular aneurysms include:
Genetics or an inherited condition
High blood pressure or hardening of the arteries in the brain
Cigarette smoking
A blood clot that goes to the brain
Some types of infection
Injury or trauma to the head
Habitual cocaine use
Treatment
The goal of treatment is to prevent future hemorrhage. There are two major ways this can be accomplished.
Surgery
The most common treatment for cerebral aneurysms is open surgery under general anesthesia. The neurosurgeon makes an incision in the scalp, makes a window in the skull, locates the aneurysm, and places a metal clip across the neck of the aneurysm to inhibit rupture. Advanced microsurgical techniques have significantly reduced the risks of surgery; yet, the outcome is related with the aneurysm's size, location, and shape.
Endovascular Therapy
In endovascular therapy, a neuroradiologist passes a catheter through an artery and places detachable platinum coils in the aneurysm. These devices prevent bleeding and protect against subarachnoid hemorrhage. Gaining recognition in the treatment of both ruptured and unruptured aneurysms, endovascular therapy offers a less invasive option to surgery for some patients with difficult-to-reach aneurysms.
The procedure is typically done under general anesthesia to keep the head still during placement of the coils.
Monitoring
Some aneurysms have such a low risk of rupture that periodic monitoring offers a preferable method to treatment.
According to a recent study at Mayo Clinic, patients with rather small aneurysms — under ¼ inch in diameter — located in the front portion of the brain had the lowest risk of subarachnoid hemorrhage. Patients with aneurysms ½ inch or more in diameter in the back part of the brain had the highest risk. Patients with a history of subarachnoid hemorrhage from a previous aneurysm also had a higher risk of subarachnoid hemorrhage. Rupture risk also increased significantly in patient’s age 50 and older, with the highest risk in patients age 60 and above. A history of rupture due to another aneurysm increased the risk of rupture as well.
As a result of this study, many neurologists and neurosurgeons now recommend a more conservative method instead of surgery for patients without a history of subarachnoid hemorrhage who have small aneurysms located in the front portion of the brain.

Information from: mayoclinic.org & HealthLink.com

Angiofibroma

Juvenile Angiofibroma

Juvenile angiofibroma is a benign nasal tumor of the back of the nose or upper throat
Juvenile angiofibroma is somewhat unusual. It characteristically is found in teenage boys. The tumor includes numerous blood vessels, is locally invasive, and can cause bone damage.
Symptoms:
Frequent nosebleeds
Stuffy nose
Difficulty breathing through the nose
Nasal discharge, usually bloody
Hearing loss
Prolonged bleeding
Easy bruising

Exams and Tests:
The doctor may see the angiofibroma when examining the upper throat.
Tests that may be done include:
X-ray or a CT scan of the head
Nasal mucosal biopsy

Treatment :
Treatment is necessary if the angiofibroma is growing larger, blocking the airway, or causing recurring nosebleeds. In some cases, no treatment is necessary.
Surgery may be needed to remove the tumor. Removal is frequently complicated because the tumor is not enclosed and may have spread to other areas.
A procedure called embolization may be done to prevent the tumor from bleeding. The procedure may correct the nosebleeds by itself, or it may be followed by surgery to remove the tumor.

Prognosis:
Although not cancerous, angiofibromas may continue to develop, even after surgery. Several may vanish by themselves.

Possible Complications:
Spread of the tumor to the nose, the sinuses, and other structures
Anemia
Pressure on the brain (rare)

Prevention:
There is no known way to avoid this condition.

References provided by VeriMed Healthcare Network.

Optic Nerve Glioma

Optic Nerve Glioma

Optic nerve glioma is the most common primary neoplasm of the optic nerve causing decreased visual sharpness in the affected eye. Benign optic glioma occurs most often in children, more females with an average age of five years. Another form, aggressive glioma, which is unusual is most common in adults, more males with a median age of fifty-two years; it is often terminal, even with treatment. .
From 10-38% of children with optic nerve glioma is also known to have neurofibromatosis type 1 (NF-1) or, in some cases, the more recently described hybrid phakomatosis. In 66% of NF-1 patients with optic nerve glioma, the growth involves the intraorbital optic nerve. In 10-20%, the tumor is confined to the orbit, with the remainder of these patients showing involvement of the intracranial compartment.
Optic nerve gliomas represent 4% of orbital tumors, 4% of intracranial gliomas, and 2% of intracranial tumors. They also include two thirds of all primary optic nerve tumors.
Benign optic glioma develops gradually, if at all. Yet, some lesions can grow, causing visual impairment, so follow-up is recommended.
Twenty percent of optic gliomas that extend to the optic chiasm or outside, into the optic radiations, exhibit a more aggressive path.
In the absence of NF-1, the optic chiasm is most usually involved, as is, less often, the intraorbital optic nerve. Optic nerve glioma may involve different sections of the retrobulbar visual pathway, including the optic nerve, chiasm, tracts, and radiations. Malignant lesions can occupy the hypothalamus, basal ganglia, and internal capsule directly, or they may extend to the leptomeninges or subpial surfaces.
In most young patients with optic glioma, the symptom is painless proptosis. Optic atrophy is common, as is reduced visual sharpness, (which may be a late symptom). A large lesion may compress the optic chiasm, causing nystagmus. Hypothalamic symptoms, such as changes in appetite or sleep, also may occur. Massive lesions may compress the third ventricle, resulting in obstructive hydrocephalus accompanied by headache, nausea, and vomiting.
In adult patients, bilateral vision loss is a common early finding because most lesions involve the optic chiasm.
Contrasted computed tomography (CT) scanning can be used to differentiate confined involvement of optic nerve glioma within the orbit and the presence of an intraconal mass. CT scanning can distinguish a faint attrition or growth of the optic canal. In addition, fine calcification, which may help to identify a lesion as a meningioma rather than a glioma, is visualized best through CT scanning.
Findings:
In children, unenhanced CT scans normally reveal an evident, diffuse growth of the optic nerve, with typical twisting. The enlargement may be tubular, fusiform, or excrescent.
Areas of lucency may result from mucinous or cystic changes.
Approximately 50% of the lesions reveal enhancement; this characteristic is more common with intracranial (especially retrochiasmatic) extension.
Calcifications are unusual.
Improper examination techniques, including failure to administer contrast or obtain thin sections, can lead to a false-negative diagnosis.
Magnetic Resonance Imaging (MRI), however, is the preferred method for definitive evaluation of optic nerve glioma. Both the intraorbital lesion and its intracranial degree can be effectively differentiated through MRI. When evaluating the orbit, gadolinium-enhanced T1-weighted images with fat saturation can define the degree of aggressive glioma. Intracranially, MRI allows better evaluation of the optic nerve, chiasm, tracts, geniculate body, and optic radiations and shows even slight lesions of the optic nerve than does CT.
Findings:
On T1-weighted images, optic nerve gliomas are usually isointense to the cortex and hypointense to white matter.
Invariably, the lesions are hypointense to orbital fat.
On T2-weighted images, lesions show a varied appearance that is isointense to hyperintense relative to white matter and the cortex.
Following contrast administration, intense enhancement is common.
A diagnosis of NF-1 may be supported by several findings including the following:
Bilateral optic nerve gliomas.
Spongiform changes (hyperintensity on T2-weighted images) in the cerebellum, brain stem, basal ganglia, thalamus, periventricular white matter, and corpus callosum
Adult lesions may involve the orbital, intracanalicular, or prechiasmal portions of the optic nerve, resulting in enlargement; they may exhibit retrochiasmatic extension as well).
Usually, the lesions are hypointense to isointense relative to the optic nerve on T1-weighted images and are hyperintense to it on T2-weighted images. Enhancement is homogeneous and intense.
Patients without NF-1 show cystic components more commonly at T2 -weighted imaging.
The diagnosis may be made with a high level of confidence when the lesion involves the optic chiasm and retrochiasmatic optic pathway.
When limited entirely to the orbit, the lesion may imitate optic neuritis, pseudotumor, lymphoma, or optic nerve meningioma. Characteristically, meningioma, the main differential diagnostic consideration, is distinguished by the "tram-track" sign, with enhancement of the periphery of the nerve–optic sheath unit. Conversely, enhancement in optic nerve glioma is more uniform. Isolated growth of the optic nerve sheath also may present diagnostic complexity; however, this enlargement can generally be distinguished by its signal characteristics, which follow fluid signal on all MRI pulse sequences.
In most occasions, the diagnosis can be made with greater assurance using MRI than it can with CT scanning.
A false-positive diagnosis can occur as an effect of unilateral optic nerve enhancement or other unilateral disorders, such as optic meningioma, vascular lesions, neuritis, pseudotumor, lymphoma, and sarcoidosis. In addition, subtle nerve enhancement occasionally may develop in normal individuals.
Improper examination procedures, including failure to administer contrast, use fat saturation, or obtain thin sections, can result in a false-negative diagnosis.
Local surgical therapy for large lesions may cause significant morbidity, including hypothalamic dysfunction. Stereotactic radiation or gamma-knife therapy also can produce complications, including decreased visual perception, radiation-induced optic neuritis, and ophthalmic artery vasculopathy.
Despite aggressive radiation, chemotherapeutic, or surgical treatment, aggressive glioma is an almost uniformly fatal disease.
Information By: Emory University School of Medicine.org