Nervous tissue
Content:
- Disorders of the nervous tissue
- Guillen barre syndrome
- Multiple sclerosis
- Gliomas
- Stroke
Nervous system disorders
A satisfactory classification of diseases of the nervous system should include not only the type of reaction (congenital malformation, infection, trauma, neoplasm, vascular diseases, and degenerative, metabolic, toxic, or deficiency states) but also the site of involvement (meninges, peripheral nerves or gray or white matter of the spinal cord, brainstem, cerebellum, and cerebrum). To these may be added various other correlates, such as age and sex. The nerve cell may be damaged primarily, as in certain infections, but much more commonly the nerve cell is damaged secondarily as the result of metabolic or vascular diseases affecting other important organs, such as the heart, lungs, liver, and kidneys.
Malformation
The central nervous system develops as a hollow neural tube by the fusion of the crests of the neural groove, beginning in the cervical area and progressing rostrally and caudally, the last points to close being termed the anterior and posterior neuropores. If the anterior neuropore fails to close (about 24 days of fetal age), anencephaly develops. The poorly organized brain is exposed to amniotic fluid and becomes necrotic and hemorrhagic, with death usually within hours after birth. See Congenital anomalies
If the posterior neuropore fails to close (about 26 days of fetal age), the lumbosacral neural groove is exposed to amniotic fluid. The nervous tissue becomes partially necrotic and incorporated in a scar. Such a meningomyelocele is readily infected unless buried surgically within a few hours after birth. In addition, in about 95% of such infants hydrocephalus occurs, which usually can be adequately treated by shunting the ventricular fluid into the venous system or peritoneal cavity.
Other developmental disorders of the nervous system may appear as hypoplasia or hyperplasia (decrease or increase in growth of cells, respectively) or as a destruction of otherwise normally developing tissues. Rapidly growing tissues such as the embryonic nervous system are generally rather easily damaged by many toxic agents. The time of onset and the extent of repair rather than the nature of the agent determine the resulting pattern of abnormal development.
Infection
Infections of the nervous system may occur through a defect in the normal protective coverings caused by certain congenital malformations, as mentioned above, but also through other defects as the result of trauma, especially penetrating wounds or fractures opening into the paranasal sinuses or mastoid air cells. Subsequent infection of the nervous system may be the major complication of such “open head” injuries.
Infections may also spread directly from adjacent structures, as from mastoiditis, sinusitis, osteomyelitis, or subcutaneous abscesses. Such infections usually spread along venous channels producing epidural abscess, subdural empyema, leptomeningitis, and brain abscess. All of these infections are characteristically caused by pyogenic (pus-forming) bacteria. Other pyogenic bacteria may metastasize by way of the bloodstream from more distant infections, such as bacterial endocarditis, pneumonia, and enteritis.
Infections of the nervous system must be treated promptly as medical emergencies. The diagnosis is easily established by spinal puncture; the microorganisms can be visualized with special stains.
Many other microorganisms can infect the nervous system: Mycobacterium tuberculosis (the organism causing tuberculosis), Treponema pallidum (the organism causing syphilis), several fungi and rickettsiae, and many viruses.
Viral infections vary widely geographically, generally related to the necessity for intermediate hosts and vectors (animal reservoirs) by which the virus is spread. Poliomyelitis, now largely prevented by effective vaccination of most children, is primarily an intestinal infection which occasionally spreads to the nervous system, infecting and destroying motor nerve cells, thereby producing weakness of certain muscles. Herpes zoster has a similar preference for infecting sensory nerve cells and producing an acute skin eruption in the distribution of the affected sensory cells. Herpes simplex is closely related to herpes zoster, resides in the trigeminal or sacral sensory nerve cells, and intermittently produces eruptions in the distribution of these cells: “fever blisters” in and around the mouth in type I herpes, or similar blisters in the genital area in type II herpes. The latter is increasingly being recognized as a venereal disease. Rabies virus also affects certain nerve cells in the temporal lobe of the brain, as well as in the cerebellum, and is transmitted through the saliva of animals that bite other animals or humans; rabies is the single exception to the rule that immunization must precede infection to be effective, and the immunization must begin promptly after the bite. See Animal virus, Herpes, Poliomyelitis
Inflammation
Certain viruses frequently produce a meningitis in humans from whose cerebrospinal fluid the virus is relatively easily grown. Other viruses, such as measles and varicella, occasionally produce meningitis or encephalomyelitis, but the cerebrospinal fluid does not contain the virus. See Meningitis
Allergy to one's own tissue elements is an interesting possibility that has evoked many experimental approaches. Two human diseases, multiple sclerosis, a demyelinating disease affecting the central nervous system, and the Landry-Guillain-Barré syndrome, a demyelinating disease affecting the peripheral nervous system, are considered likely candidates to be related to experimental allergic encephalomyelitis and experimental allergic neuritis, respectively. See Autoimmunity
Vascular disease
Vascular diseases of the nervous system are commonly called strokes, a term which emphasizes the suddenness of onset of neurological disability. Such a cataclysmic onset is characteristic of vascular diseases, since the nerve cell can function without nutrients for only a matter of seconds and will die if not renourished within several minutes.
Two main types of hemorrhage occur: hemorrhage into the subarachnoid space from rupture of an aneurysm (a focal weakening and dilatation) of a large artery; and hemorrhage into the brain from rupture of an aneurysm of a small artery or arteriole. Both types of hemorrhage occur more commonly in hypertensive adults.
Nerve cells require oxygen and glucose for functional activity, and can withstand only brief periods of hypoxia or hypoglycemia. Even a few seconds of hypoxia can block the nerve cell's function, and more than 10 min is almost certainly fatal to most nerve cells. Transient ischemic attacks may result, with temporary impairment of blood flow to a part of the brain and consequent focal neurological dysfunction. These attacks may also be successfully treated with drugs or surgery and the disastrous major stroke prevented. Myocardial infarction, postural hypotension, and stenosis or narrowing of the carotid or vertebral arteries greater than 60% are common causes of cerebral ischemia. If the ischemia is not rapidly reversed, the neurons undergo selective necrosis; if the ischemia is more severe or prolonged, the glia and blood vessels in the gray matter also undergo necrosis; and if the ischemia is still more severe or prolonged, all the gray and white matter in the ischemic zone becomes necrotic, a condition known as cerebral infarction or encephalomalacia. One of the common ways the brain reacts to small or large hemorrhages or ischemic episodes is by swelling. Such swelling itself may be fatal within a few days to a week or so by a process known as transtentorial herniation, compressing the brainstem, where there are important neural circuits for vital functions, such as breathing and maintenance of blood pressure.
Degenerative and other diseases
Degenerative, metabolic, toxic, and deficiency states include the largest numbers of both common and rare diseases of the nervous system. Since neurons in the brain may be destroyed after birth and cannot be replaced, mental deterioration, deafness and blindness, incoordination and adventitious movements, and other neurologic signs that are so typical of these disorders are generally not reversible even if the basic metabolic defect can be corrected. Advances have been made in the early diagnosis and treatment of several diseases usually manifest in infancy with mental retardation. Three examples are phenylpyruvic oligophrenia (phenylketonuria or PKU), which is treatable with a phenylalanine-deficient diet; galactosemia, requiring a galactose-free diet also as early as possible to avoid cataracts and mental retardation; and cretinism, which requires treatment with thyroid.
Neoplasm
Neoplasms of the nervous system can be divided into primary and metastatic, the primary into gliomas and others, and the metastatic into bronchogenic and others. These four groups each account for about 25% of all intracranial neoplasms.
A satisfactory classification of diseases of the nervous system should include not only the type of reaction (congenital malformation, infection, trauma, neoplasm, vascular diseases, and degenerative, metabolic, toxic, or deficiency states) but also the site of involvement (meninges, peripheral nerves or gray or white matter of the spinal cord, brainstem, cerebellum, and cerebrum). To these may be added various other correlates, such as age and sex. The nerve cell may be damaged primarily, as in certain infections, but much more commonly the nerve cell is damaged secondarily as the result of metabolic or vascular diseases affecting other important organs, such as the heart, lungs, liver, and kidneys.
Malformation
The central nervous system develops as a hollow neural tube by the fusion of the crests of the neural groove, beginning in the cervical area and progressing rostrally and caudally, the last points to close being termed the anterior and posterior neuropores. If the anterior neuropore fails to close (about 24 days of fetal age), anencephaly develops. The poorly organized brain is exposed to amniotic fluid and becomes necrotic and hemorrhagic, with death usually within hours after birth. See Congenital anomalies
If the posterior neuropore fails to close (about 26 days of fetal age), the lumbosacral neural groove is exposed to amniotic fluid. The nervous tissue becomes partially necrotic and incorporated in a scar. Such a meningomyelocele is readily infected unless buried surgically within a few hours after birth. In addition, in about 95% of such infants hydrocephalus occurs, which usually can be adequately treated by shunting the ventricular fluid into the venous system or peritoneal cavity.
Other developmental disorders of the nervous system may appear as hypoplasia or hyperplasia (decrease or increase in growth of cells, respectively) or as a destruction of otherwise normally developing tissues. Rapidly growing tissues such as the embryonic nervous system are generally rather easily damaged by many toxic agents. The time of onset and the extent of repair rather than the nature of the agent determine the resulting pattern of abnormal development.
Infection
Infections of the nervous system may occur through a defect in the normal protective coverings caused by certain congenital malformations, as mentioned above, but also through other defects as the result of trauma, especially penetrating wounds or fractures opening into the paranasal sinuses or mastoid air cells. Subsequent infection of the nervous system may be the major complication of such “open head” injuries.
Infections may also spread directly from adjacent structures, as from mastoiditis, sinusitis, osteomyelitis, or subcutaneous abscesses. Such infections usually spread along venous channels producing epidural abscess, subdural empyema, leptomeningitis, and brain abscess. All of these infections are characteristically caused by pyogenic (pus-forming) bacteria. Other pyogenic bacteria may metastasize by way of the bloodstream from more distant infections, such as bacterial endocarditis, pneumonia, and enteritis.
Infections of the nervous system must be treated promptly as medical emergencies. The diagnosis is easily established by spinal puncture; the microorganisms can be visualized with special stains.
Many other microorganisms can infect the nervous system: Mycobacterium tuberculosis (the organism causing tuberculosis), Treponema pallidum (the organism causing syphilis), several fungi and rickettsiae, and many viruses.
Viral infections vary widely geographically, generally related to the necessity for intermediate hosts and vectors (animal reservoirs) by which the virus is spread. Poliomyelitis, now largely prevented by effective vaccination of most children, is primarily an intestinal infection which occasionally spreads to the nervous system, infecting and destroying motor nerve cells, thereby producing weakness of certain muscles. Herpes zoster has a similar preference for infecting sensory nerve cells and producing an acute skin eruption in the distribution of the affected sensory cells. Herpes simplex is closely related to herpes zoster, resides in the trigeminal or sacral sensory nerve cells, and intermittently produces eruptions in the distribution of these cells: “fever blisters” in and around the mouth in type I herpes, or similar blisters in the genital area in type II herpes. The latter is increasingly being recognized as a venereal disease. Rabies virus also affects certain nerve cells in the temporal lobe of the brain, as well as in the cerebellum, and is transmitted through the saliva of animals that bite other animals or humans; rabies is the single exception to the rule that immunization must precede infection to be effective, and the immunization must begin promptly after the bite. See Animal virus, Herpes, Poliomyelitis
Inflammation
Certain viruses frequently produce a meningitis in humans from whose cerebrospinal fluid the virus is relatively easily grown. Other viruses, such as measles and varicella, occasionally produce meningitis or encephalomyelitis, but the cerebrospinal fluid does not contain the virus. See Meningitis
Allergy to one's own tissue elements is an interesting possibility that has evoked many experimental approaches. Two human diseases, multiple sclerosis, a demyelinating disease affecting the central nervous system, and the Landry-Guillain-Barré syndrome, a demyelinating disease affecting the peripheral nervous system, are considered likely candidates to be related to experimental allergic encephalomyelitis and experimental allergic neuritis, respectively. See Autoimmunity
Vascular disease
Vascular diseases of the nervous system are commonly called strokes, a term which emphasizes the suddenness of onset of neurological disability. Such a cataclysmic onset is characteristic of vascular diseases, since the nerve cell can function without nutrients for only a matter of seconds and will die if not renourished within several minutes.
Two main types of hemorrhage occur: hemorrhage into the subarachnoid space from rupture of an aneurysm (a focal weakening and dilatation) of a large artery; and hemorrhage into the brain from rupture of an aneurysm of a small artery or arteriole. Both types of hemorrhage occur more commonly in hypertensive adults.
Nerve cells require oxygen and glucose for functional activity, and can withstand only brief periods of hypoxia or hypoglycemia. Even a few seconds of hypoxia can block the nerve cell's function, and more than 10 min is almost certainly fatal to most nerve cells. Transient ischemic attacks may result, with temporary impairment of blood flow to a part of the brain and consequent focal neurological dysfunction. These attacks may also be successfully treated with drugs or surgery and the disastrous major stroke prevented. Myocardial infarction, postural hypotension, and stenosis or narrowing of the carotid or vertebral arteries greater than 60% are common causes of cerebral ischemia. If the ischemia is not rapidly reversed, the neurons undergo selective necrosis; if the ischemia is more severe or prolonged, the glia and blood vessels in the gray matter also undergo necrosis; and if the ischemia is still more severe or prolonged, all the gray and white matter in the ischemic zone becomes necrotic, a condition known as cerebral infarction or encephalomalacia. One of the common ways the brain reacts to small or large hemorrhages or ischemic episodes is by swelling. Such swelling itself may be fatal within a few days to a week or so by a process known as transtentorial herniation, compressing the brainstem, where there are important neural circuits for vital functions, such as breathing and maintenance of blood pressure.
Degenerative and other diseases
Degenerative, metabolic, toxic, and deficiency states include the largest numbers of both common and rare diseases of the nervous system. Since neurons in the brain may be destroyed after birth and cannot be replaced, mental deterioration, deafness and blindness, incoordination and adventitious movements, and other neurologic signs that are so typical of these disorders are generally not reversible even if the basic metabolic defect can be corrected. Advances have been made in the early diagnosis and treatment of several diseases usually manifest in infancy with mental retardation. Three examples are phenylpyruvic oligophrenia (phenylketonuria or PKU), which is treatable with a phenylalanine-deficient diet; galactosemia, requiring a galactose-free diet also as early as possible to avoid cataracts and mental retardation; and cretinism, which requires treatment with thyroid.
Neoplasm
Neoplasms of the nervous system can be divided into primary and metastatic, the primary into gliomas and others, and the metastatic into bronchogenic and others. These four groups each account for about 25% of all intracranial neoplasms.
Guillain-Barré syndrome
Guillain-Barré syndrome is a disorder in which the body's immune system attacks part of the peripheral nervous system. The first symptoms of this disorder include varying degrees of weakness or tingling sensations in the legs. In many instances, the weakness and abnormal sensations spread to the arms and upper body. These symptoms can increase in intensity until the muscles cannot be used at all and the patient is almost totally paralyzed. In these cases, the disorder is life-threatening and is considered a medical emergency. The patient is often put on a ventilator to assist with breathing. Most patients, however, recover from even the most severe cases of Guillain-Barré syndrome GBS), although some continue to have some degree of weakness. Guillain-Barré syndrome is rare. Usually Guillain-Barré occurs a few days or weeks after the patient has had symptoms of a respiratory or gastrointestinal viral infection. Occasionally, surgery will trigger the syndrome. In rare instances, vaccinations may increase the risk of GBS. The disorder can develop over the course of hours or days, or it may take up to 3 to 4 weeks. No one yet knows why Guillain-Barré strikes some people and not others or what sets the disease in motion. What scientists do know is that the body's immune system begins to attack the body itself, causing what is known as an autoimmune disease. Guillain-Barré is called a syndrome rather than a disease because it is not clear that a specific disease-causing agent is involved. Reflexes such as knee jerks are usually lost. Because the signals traveling along the nerve are slower, a nerve conduction velocity (NCV) test can give a doctor clues to aid the diagnosis. The cerebrospinal fluid that bathes the spinal cord and brain contains more protein than usual, so a physician may decide to perform a spinal tap.
Is there any treatment?
There is no known cure for Guillain-Barré syndrome, but therapies can lessen the severity of the illness and accelerate the recovery in most patients. There are also a number of ways to treat the complications of the disease. Currently, plasmapheresis (also known as plasma exchange) and high-dose immunoglobulin therapy are used. Plasmapheresis seems to reduce the severity and duration of the Guillain-Barré episode. In high-dose immunoglobulin therapy, doctors give intravenous injections of the proteins that in small quantities, the immune system uses naturally to attack invading organism. Investigators have found that giving high doses of these immunoglobulins, derived from a pool of thousands of normal donors, to Guillain-Barré patients can lessen the immune attack on the nervous system. The most critical part of the treatment for this syndrome consists of keeping the patient's body functioning during recovery of the nervous system. This can sometimes require placing the patient on a ventilator, a heart monitor, or other machines that assist body function.
What is the prognosis?
Guillain-Barré syndrome can be a devastating disorder because of its sudden and unexpected onset. Most people reach the stage of greatest weakness within the first 2 weeks after symptoms appear, and by the third week of the illness 90 percent of all patients are at their weakest. The recovery period may be as little as a few weeks or as long as a few years. About 30 percent of those with Guillain-Barré still have a residual weakness after 3 years. About 3 percent may suffer a relapse of muscle weakness and tingling sensations many years after the initial attack.
Guillain-Barré syndrome is a disorder in which the body's immune system attacks part of the peripheral nervous system. The first symptoms of this disorder include varying degrees of weakness or tingling sensations in the legs. In many instances, the weakness and abnormal sensations spread to the arms and upper body. These symptoms can increase in intensity until the muscles cannot be used at all and the patient is almost totally paralyzed. In these cases, the disorder is life-threatening and is considered a medical emergency. The patient is often put on a ventilator to assist with breathing. Most patients, however, recover from even the most severe cases of Guillain-Barré syndrome GBS), although some continue to have some degree of weakness. Guillain-Barré syndrome is rare. Usually Guillain-Barré occurs a few days or weeks after the patient has had symptoms of a respiratory or gastrointestinal viral infection. Occasionally, surgery will trigger the syndrome. In rare instances, vaccinations may increase the risk of GBS. The disorder can develop over the course of hours or days, or it may take up to 3 to 4 weeks. No one yet knows why Guillain-Barré strikes some people and not others or what sets the disease in motion. What scientists do know is that the body's immune system begins to attack the body itself, causing what is known as an autoimmune disease. Guillain-Barré is called a syndrome rather than a disease because it is not clear that a specific disease-causing agent is involved. Reflexes such as knee jerks are usually lost. Because the signals traveling along the nerve are slower, a nerve conduction velocity (NCV) test can give a doctor clues to aid the diagnosis. The cerebrospinal fluid that bathes the spinal cord and brain contains more protein than usual, so a physician may decide to perform a spinal tap.
Is there any treatment?
There is no known cure for Guillain-Barré syndrome, but therapies can lessen the severity of the illness and accelerate the recovery in most patients. There are also a number of ways to treat the complications of the disease. Currently, plasmapheresis (also known as plasma exchange) and high-dose immunoglobulin therapy are used. Plasmapheresis seems to reduce the severity and duration of the Guillain-Barré episode. In high-dose immunoglobulin therapy, doctors give intravenous injections of the proteins that in small quantities, the immune system uses naturally to attack invading organism. Investigators have found that giving high doses of these immunoglobulins, derived from a pool of thousands of normal donors, to Guillain-Barré patients can lessen the immune attack on the nervous system. The most critical part of the treatment for this syndrome consists of keeping the patient's body functioning during recovery of the nervous system. This can sometimes require placing the patient on a ventilator, a heart monitor, or other machines that assist body function.
What is the prognosis?
Guillain-Barré syndrome can be a devastating disorder because of its sudden and unexpected onset. Most people reach the stage of greatest weakness within the first 2 weeks after symptoms appear, and by the third week of the illness 90 percent of all patients are at their weakest. The recovery period may be as little as a few weeks or as long as a few years. About 30 percent of those with Guillain-Barré still have a residual weakness after 3 years. About 3 percent may suffer a relapse of muscle weakness and tingling sensations many years after the initial attack.
Multiple sclerosis
Multiple sclerosis (MS) is a potentially debilitating disease in which your body's immune system eats away at the protective sheath that covers your nerves. This interferes with the communication between your brain and the rest of your body. Ultimately, this may result in deterioration of the nerves themselves, a process that's not reversible.
Symptoms vary widely, depending on the amount of damage and which nerves are affected. People with severe cases of multiple sclerosis may lose the ability to walk or speak. Multiple sclerosis can be difficult to diagnose early in the course of the disease because symptoms often come and go — sometimes disappearing for months.
There's no cure for multiple sclerosis. However treatments can help treat attacks, modify the course of the disease and treat symptoms.
Symptoms vary widely, depending on the amount of damage and which nerves are affected. People with severe cases of multiple sclerosis may lose the ability to walk or speak. Multiple sclerosis can be difficult to diagnose early in the course of the disease because symptoms often come and go — sometimes disappearing for months.
There's no cure for multiple sclerosis. However treatments can help treat attacks, modify the course of the disease and treat symptoms.
Signs and symptoms of multiple sclerosis vary widely, depending on the location of affected nerve fibers. Multiple sclerosis signs and symptoms may include:
Numbness or weakness in one or more limbs, which typically occurs on one side of your body at a time or the bottom half of your body
Partial or complete loss of vision, usually in one eye at a time, often with pain during eye movement (optic neuritis)
Double vision or blurring of vision
Tingling or pain in parts of your body
Electric-shock sensations that occur with certain head movements
Tremor, lack of coordination or unsteady gait
Fatigue
Dizziness
Most people with multiple sclerosis, particularly in the beginning stages of the disease, experience relapses of symptoms, which are followed by periods of complete or partial remission. Signs and symptoms of multiple sclerosis often are triggered or worsened by an increase in body temperature.
Numbness or weakness in one or more limbs, which typically occurs on one side of your body at a time or the bottom half of your body
Partial or complete loss of vision, usually in one eye at a time, often with pain during eye movement (optic neuritis)
Double vision or blurring of vision
Tingling or pain in parts of your body
Electric-shock sensations that occur with certain head movements
Tremor, lack of coordination or unsteady gait
Fatigue
Dizziness
Most people with multiple sclerosis, particularly in the beginning stages of the disease, experience relapses of symptoms, which are followed by periods of complete or partial remission. Signs and symptoms of multiple sclerosis often are triggered or worsened by an increase in body temperature.
The cause of multiple sclerosis is unknown. It's believed to be an autoimmune disease, in which the body's immune system attacks its own tissues. In multiple sclerosis, this process destroys myelin — the fatty substance that coats and protects nerve fibers in the brain and spinal cord.
Myelin can be compared to the insulation on electrical wires. When myelin is damaged, the messages that travel along that nerve may be slowed or blocked.
Doctors and researchers don't understand why multiple sclerosis develops in some people and not others. A combination of factors, ranging from genetics to childhood infections, may play a role.
Myelin can be compared to the insulation on electrical wires. When myelin is damaged, the messages that travel along that nerve may be slowed or blocked.
Doctors and researchers don't understand why multiple sclerosis develops in some people and not others. A combination of factors, ranging from genetics to childhood infections, may play a role.
These factors may increase your risk of developing multiple sclerosis:
Being between the ages of 20 and 40. Multiple sclerosis can occur at any age, but most commonly affects people between these ages.
Being female. Women are about twice as likely as men are to develop multiple sclerosis.
Having a family history. If one of your parents or siblings has had multiple sclerosis, you have a 1 to 3 percent chance of developing the disease — as compared with the risk in the general population, which is just a tenth of 1 percent. But the experiences of identical twins show that heredity can't be the only factor involved. If multiple sclerosis was determined solely by genetics, identical twins would have identical risks. However, an identical twin has only a 30 percent chance of developing multiple sclerosis if his or her twin already has the disease.
Having certain infections. A variety of viruses have been linked to multiple sclerosis. Currently the greatest interest is in the association of multiple sclerosis with Epstein-Barr virus, the virus that causes infectious mononucleosis. How Epstein-Barr virus might result in a higher rate of MS remains to be clarified.
Being white. White people, particularly those whose families originated in northern Europe, are at highest risk of developing multiple sclerosis. People of Asian, African or Native American descent have the lowest risk.
Living in countries with temperate climes. Multiple sclerosis is far more common in Europe, southern Canada, northern United States, New Zealand and southeastern Australia. The risk seems to increase with latitude.
A child who moves from a high-risk area to a low-risk area, or vice versa, tends to have the risk level associated with his or her new home area. But if the move occurs after puberty, the young adult usually retains the risk level associated with his or her first home.
Having certain other autoimmune diseases. You're very slightly more likely to develop multiple sclerosis if you have thyroid disease, type 1 diabetes or inflammatory bowel disease.
Being between the ages of 20 and 40. Multiple sclerosis can occur at any age, but most commonly affects people between these ages.
Being female. Women are about twice as likely as men are to develop multiple sclerosis.
Having a family history. If one of your parents or siblings has had multiple sclerosis, you have a 1 to 3 percent chance of developing the disease — as compared with the risk in the general population, which is just a tenth of 1 percent. But the experiences of identical twins show that heredity can't be the only factor involved. If multiple sclerosis was determined solely by genetics, identical twins would have identical risks. However, an identical twin has only a 30 percent chance of developing multiple sclerosis if his or her twin already has the disease.
Having certain infections. A variety of viruses have been linked to multiple sclerosis. Currently the greatest interest is in the association of multiple sclerosis with Epstein-Barr virus, the virus that causes infectious mononucleosis. How Epstein-Barr virus might result in a higher rate of MS remains to be clarified.
Being white. White people, particularly those whose families originated in northern Europe, are at highest risk of developing multiple sclerosis. People of Asian, African or Native American descent have the lowest risk.
Living in countries with temperate climes. Multiple sclerosis is far more common in Europe, southern Canada, northern United States, New Zealand and southeastern Australia. The risk seems to increase with latitude.
A child who moves from a high-risk area to a low-risk area, or vice versa, tends to have the risk level associated with his or her new home area. But if the move occurs after puberty, the young adult usually retains the risk level associated with his or her first home.
Having certain other autoimmune diseases. You're very slightly more likely to develop multiple sclerosis if you have thyroid disease, type 1 diabetes or inflammatory bowel disease.
Glioma
“Glioma” is a general term used to describe any tumor that arises from the supportive (“gluey”) tissue of the brain. This tissue, called “glia,” helps to keep the neurons in place and functioning well.
There are three types of normal glial cells that can produce tumors. An astrocyte will produce astrocytomas (including glioblastomas), an oligodendrocyte will produce oligodendrogliomas, and ependymomas come from ependymal cells. Tumors that display a mixture of these different cells are called mixed gliomas.
Tumors such as “optic nerve glioma” and “brain stem glioma” are named for their locations, not the tissue type from which they originate.
Location
The location of the tumor depends on the type of cells from which it originates.
Description
Three types of normal glial cells can produce tumors—astrocytes, oligodendrocytes, and ependymal cells. Tumors that display a mixture of these cells are called mixed gliomas.
Astrocytoma: Click here to learn more about astrocytomas, including juvenile pilocytic astrocytoma, low grade astrocytoma, anaplastic astrocytoma, or glioblastoma.
Ependymoma: Click here to learn more about ependymoma.
Mixed Glioma (also called Oligoastrocytoma): These tumors usually contain a high proportion of more than one type of cell, most often astrocytes and oligodendrocytes. Occasionally, ependymal cells are also found. The behavior of a mixed glioma appears to depend on the grade of the tumor. It is less clear whether their behavior is based on that of the most abundant cell type.
Oligodendroglioma: Click here to learn more about oligodendroglioma.
Optic Glioma: These tumors may involve any part of the optic pathway, and they have the potential to spread along these pathways. Most of these tumors occur in children under the age of 10. Grade I pilocytic astrocytoma and grade II fibrillary astrocytoma are the most common tumors affecting these structures. Higher-grade tumors may also arise in this location. Twenty percent of children with neurofibromatosis (NF-1) will develop an optic glioma. These gliomas are typically grade I, pilocytic astrocytomas. Children with optic glioma are usually screened for NF-1 for this reason. Adults with NF-1 typically do not develop optic gliomas.
Gliomatosis Cerebri: This is an uncommon brain tumor that features widespread glial tumor cells in the brain. This tumor is different from other gliomas because it is scattered and widespread, typically involving two or more lobes of the brain. It could be considered a “widespread low-grade glioma” because it does not have the malignant features seen in high-grade tumors.
The widespread nature of gliomatosis cerebri causes enlargement of any part of the brain it involves. This may include the cerebral hemispheres, or less often, the cerebellum or brain stem.
Symptoms
Symptoms vary based on tumor type:
Astrocytoma:Click here to learn more about astrocytoma symptoms.
Ependymoma: Click here to learn more about ependymoma symptoms.
Mixed Glioma (also called Oligoastrocytoma): The initial symptoms, including headache and nausea, usually are the result of increased pressure inside the brain. Vision problems, as well as changes in behavior and personality, are also fairly common in mixed glioma patients.
Oligodendroglioma: Click here to learn more about oligodendroglioma symptoms.
Optic Glioma: These tumors may cause few or no symptoms. Their placement along the optic nerve, however, can cause vision loss (depending on the location of the tumor) or strabismus (“crossed eyes”). Hormonal disturbance might also occur, causing developmental delay(s), early puberty, and other symptoms.
Gliomatosis Cerebri: Symptoms are often nonspecific and can include personality and behavioral changes, memory disturbance, increased intracranial pressure with headache and sometimes seizures.
Incidence
The incidence of this tumor varies by type.
Cause
Like many tumor types, the exact cause of glioma is not known.
Treatment
Treatment is based on tumor type:
Astrocytoma: Click here to learn more about treatment for astrocytoma.
Ependymoma: Click here to learn more about treatment for ependymoma.
Mixed Glioma (also called Oligoastrocytoma): Treatment may include surgery followed by radiation therapy, particularly if the tumor is high-grade. Chemotherapy will also generally be used in high-grade tumors.
Oliogdendroglioma: Click here to learn more about treatment for oligodendroglioma.
Optic Glioma: Careful observation may be an option for patients with stable or slow-growing tumors. Surgery might be recommended for a growing tumor which involves only the optic nerve. Radiation might be used for a tumor of the chiasm or other pathways. Local radiation and chemotherapy with radiation therapy are used for recurrent tumors. Patients with primary and/or recurrent tumors may wish to take part in a clinical trial.
Gliomatosis Cerebri: Treatment is less well defined because this tumor is so rare. Surgical removal is generally not attempted, because it is so widespread. Radiation and chemotherapy may be considered.
There are three types of normal glial cells that can produce tumors. An astrocyte will produce astrocytomas (including glioblastomas), an oligodendrocyte will produce oligodendrogliomas, and ependymomas come from ependymal cells. Tumors that display a mixture of these different cells are called mixed gliomas.
Tumors such as “optic nerve glioma” and “brain stem glioma” are named for their locations, not the tissue type from which they originate.
Location
The location of the tumor depends on the type of cells from which it originates.
Description
Three types of normal glial cells can produce tumors—astrocytes, oligodendrocytes, and ependymal cells. Tumors that display a mixture of these cells are called mixed gliomas.
Astrocytoma: Click here to learn more about astrocytomas, including juvenile pilocytic astrocytoma, low grade astrocytoma, anaplastic astrocytoma, or glioblastoma.
Ependymoma: Click here to learn more about ependymoma.
Mixed Glioma (also called Oligoastrocytoma): These tumors usually contain a high proportion of more than one type of cell, most often astrocytes and oligodendrocytes. Occasionally, ependymal cells are also found. The behavior of a mixed glioma appears to depend on the grade of the tumor. It is less clear whether their behavior is based on that of the most abundant cell type.
Oligodendroglioma: Click here to learn more about oligodendroglioma.
Optic Glioma: These tumors may involve any part of the optic pathway, and they have the potential to spread along these pathways. Most of these tumors occur in children under the age of 10. Grade I pilocytic astrocytoma and grade II fibrillary astrocytoma are the most common tumors affecting these structures. Higher-grade tumors may also arise in this location. Twenty percent of children with neurofibromatosis (NF-1) will develop an optic glioma. These gliomas are typically grade I, pilocytic astrocytomas. Children with optic glioma are usually screened for NF-1 for this reason. Adults with NF-1 typically do not develop optic gliomas.
Gliomatosis Cerebri: This is an uncommon brain tumor that features widespread glial tumor cells in the brain. This tumor is different from other gliomas because it is scattered and widespread, typically involving two or more lobes of the brain. It could be considered a “widespread low-grade glioma” because it does not have the malignant features seen in high-grade tumors.
The widespread nature of gliomatosis cerebri causes enlargement of any part of the brain it involves. This may include the cerebral hemispheres, or less often, the cerebellum or brain stem.
Symptoms
Symptoms vary based on tumor type:
Astrocytoma:Click here to learn more about astrocytoma symptoms.
Ependymoma: Click here to learn more about ependymoma symptoms.
Mixed Glioma (also called Oligoastrocytoma): The initial symptoms, including headache and nausea, usually are the result of increased pressure inside the brain. Vision problems, as well as changes in behavior and personality, are also fairly common in mixed glioma patients.
Oligodendroglioma: Click here to learn more about oligodendroglioma symptoms.
Optic Glioma: These tumors may cause few or no symptoms. Their placement along the optic nerve, however, can cause vision loss (depending on the location of the tumor) or strabismus (“crossed eyes”). Hormonal disturbance might also occur, causing developmental delay(s), early puberty, and other symptoms.
Gliomatosis Cerebri: Symptoms are often nonspecific and can include personality and behavioral changes, memory disturbance, increased intracranial pressure with headache and sometimes seizures.
Incidence
The incidence of this tumor varies by type.
Cause
Like many tumor types, the exact cause of glioma is not known.
Treatment
Treatment is based on tumor type:
Astrocytoma: Click here to learn more about treatment for astrocytoma.
Ependymoma: Click here to learn more about treatment for ependymoma.
Mixed Glioma (also called Oligoastrocytoma): Treatment may include surgery followed by radiation therapy, particularly if the tumor is high-grade. Chemotherapy will also generally be used in high-grade tumors.
Oliogdendroglioma: Click here to learn more about treatment for oligodendroglioma.
Optic Glioma: Careful observation may be an option for patients with stable or slow-growing tumors. Surgery might be recommended for a growing tumor which involves only the optic nerve. Radiation might be used for a tumor of the chiasm or other pathways. Local radiation and chemotherapy with radiation therapy are used for recurrent tumors. Patients with primary and/or recurrent tumors may wish to take part in a clinical trial.
Gliomatosis Cerebri: Treatment is less well defined because this tumor is so rare. Surgical removal is generally not attempted, because it is so widespread. Radiation and chemotherapy may be considered.
Stroke
Symptoms of stroke are
Sudden numbness or weakness of the face, arm or leg (especially on one side of the body)
Sudden confusion, trouble speaking or understanding speech
Sudden trouble seeing in one or both eyes
Sudden trouble walking, dizziness, loss of balance or coordination
Sudden severe headache with no known cause
If you have any of these symptoms, you must get to a hospital quickly to begin treatment. Acute stroke therapies try to stop a stroke while it is happening by quickly dissolving the blood clot or by stopping the bleeding. Post-stroke rehabilitation helps individuals overcome disabilities that result from stroke damage. Drug therapy with blood thinners is the most common treatment for stroke.
