-The syndrome may occur at any age, but is most common in people of both sexes between ages 30 and 50.-Exactly what triggers Guillain-Barre syndrome is unknown-According to the National Institute of Neurological Disorders and Stroke, about 30% of patients still have some weakness after 3 years. Mild weakness may persist for some people.
-Although hydrocephalus was once known as "water on the brain," the "water" is actually cerebrospinal fluid (CSF)--a clear fluid that surrounds the brain and spinal cord. The excessive accumulation of CSF results in an abnormal widening of spaces in the brain called ventricles. This widening creates potentially harmful pressure on the tissues of the brain.-Hydrocephalus may be congenital or acquired. Congenital hydrocephalus is present at birth and may be caused by either events or influences that occur during fetal development, or genetic abnormalities. Acquired hydrocephalus develops at the time of birth or at some point afterward. This type of hydrocephalus can affect individuals of all ages and may be caused by injury or disease.-However, experts estimate that hydrocephalus affects approximately 1 in every 500 children.-Hydrocephalus is most often treated by surgically inserting a shunt system. This system diverts the flow of CSF from the CNS to another area of the body where it can be absorbed as part of the normal circulatory process.
-1.6% of population self-reported having oedema in Australia 2001 -approx 1 in 62 or 1.60% or 4.4 million people in USA
-EDH occurs in approximately 2% of patients with head injuries and 5- 15% of patients with fatal head injuries. EDH is considered to be the most serious complication of head injury, requiring immediate diagnosis and surgical intervention. EDH may be acute (58%), subacute (31%), or chronic (11%).Subdural hematomas are usually the result of a serious headc injury.The bleeding fills the brain area very rapidly, compressing brain tissue.This often results in brain injury and may lead to death.- A subdural hematomoa is an emergency condition. Emergency surgery may be needed to reduce pressure within the brain. This may involve drilling a small hole in the skull, which allows blood to drain and relieves pressure on the brain.-Large hematomas or solid blood clots may need to be removed through a procedure called a craniotomy.
-As with other traumatic injuries, this type of bleeding can typically be seen on a CT scan.-After surgery, your doctor may prescribe anticonvulsant drugs to control or prevent post-traumatic seizures. These medications are continued up to a year after the trauma. Long-term anticonvulsant therapy may be needed if seizures continue. Amnesia, attention difficulties, anxiety, sleep problems and headaches may occur and continue for some time.-
-Dechambre first used the term "lacune" in 1838 to describe softenings in subcortical regions of the brain found on autopsy-lacunar infarcts are small subcortical infarcts that result from occlusion of a single perforating artery-In the United States and other Western nations, lacunes account for 15-25% of all ischemic strokes (see Classification of Ischemic Strokes).[5, 6, 7] However, reports of incidence rates of lacunar strokes between US and European studies may be due in part to different definitions used in the studies. In 2 community-based studies in the United States, the annual incidence rates of lacunar strokes were 13.4 and 19.5 cases per 100,000 population. However, 2 European community-based studies found higher annual incidence rates (31.7 and 53 cases per 100,000 population). The incidence of lacunar strokes increases with age (mean age of first lacunar stroke, 65 y), and men may be affected more than women. Some studies have also found higher frequencies of lacunar strokes in black persons, Mexican Americans, and Hong Kong Chinese.
-There are three (3) types of bacteria (germs) that cause the disease: H. Influenzae (Hib), Strep pneumoniae, and Neisseriameningitidis.The Strep pneumoniae germ is the same one that causes most cases of ear infections and pneumonia. This is a very common bacteria and can be found in up to 70% of all adults, most of whom experience no symptoms.-These non-polio enteroviruses are second only to the "common cold" viruses, the rhinoviruses, as the most common viral infectious agents in humans. The enteroviruses infect an estimated 10-15 million or more people a year in the United States. However, fewer than 1 in 1,000 of the people infected with these viruses ever develop viral meningitis.-Bacterial meningitis can be treated with antibiotics. It is very important that the disease be diagnosed early and treated as soon as possible. This disease can cause death in about 15% of all people who are infected, so anyone who has any of these symptoms should see a doctor as soon as possible.-Most people recover completely on their own. The best treatment is supportive treatment, which includes rest, drinking plenty of fluids and over-the-counter medications to reduce the fever and headache.-How do people catch this disease?Bacterial Meningitis:The Strep pneumoniae germ is very common. It is usually spread through close, personal or prolonged contact with respiratory or oral secretions. Unlike a cold or the flu, the bacteria that cause meningitis cannot be spread by casual contact or by breathing the air where a infected person has been.Viral Meningitis: The viruses that cause viral meningitis are very common. They can be spread through close, personal or prolonged contact with respiratory or oral secretions. Some of the viruses can also be spread through the oral-fecal route.-What can be done to prevent this disease?Bacterial Meningitis:There is a very effective vaccine for the Hib bacteria that all children are required to have before attending school.There are two (2) vaccines that can be used to prevent Strep pneumonia, one for children from 2 months to 2 years of age and another for those over age 65 and some other high risk people.There is a vaccine available for N. Meningitis that is an optional vaccine sometimes recommended for college students living in close dormitory rooms. Close contacts of someone who is infected with N. Meningitis are often treated with antibiotics to prevent the disease.Viral Meningitis: The best prevention is frequent, thorough hand washing. Is the public at risk?Bacterial Meningitis:There is no increased risk to the general public. Even close personal contacts (household, personal care workers) are at only minimal increased risk.Viral Meningitis: There is no increased risk to the general public. Even close personal contacts (household, personal care workers) are at only minimal increased risk. Most people infected with these viruses do not become sick.-
Oocysts are not capable of producing infection until approximately 24 hours after being excreted, but they remain infective in water or moist soil for approximately one year. When cattle, sheep, or other livestock forage through areas with contaminated cat feces, these animals become carriers of the disease. Fruits and vegetables can also become contaminated when irrigated with untreated water that has been contaminated with cat feces. In humans and other animals, the organisms produce thick-walled, dormant structures called cysts in the muscle and other tissues of the body.Most humans contract toxoplasmosis by eating cyst-contaminated raw or undercooked meat, vegetables, or milk products. Humans can also become infected when they come into contact with the T. gondii eggs while cleaning a cat's litterbox, gardening, or playing in a sandbox, for instance. Once infected, an individual is immune to reinfection. The incubation period or period between infection and the start of the disease ranges from several days to months.Anyone can be infected by T. gondii, but usually only those individuals with weakened immune systems (immunocompromised) develop symptoms of the disease. For them, toxoplasmosis can be severe, debilitating, and fatal. Immunocompromised individuals at risk include those with AIDS, cancer, or other chronic illnesses.There is no person-to-person transmission, except from an infected mother to her child in the womb. Approximately six out of 1,000 women contract toxoplasmosis during pregnancy. Nearly half of these maternal infections are passed on to the fetus. Known as congenital toxoplasmosis, this form of the disease is acquired at birth by approximately 3,300 infants in the United States every year. The risk of fetal infection is estimated to be between one in 1,000 to one in 10,000. In children born with toxoplasmosis, symptoms may be severe and quickly fatal, or may not appear until several months or even years after birth.Causes and symptomsHealthy individuals do not usually display symptoms. When symptoms do occur, they are usually mild, resembling infectious mononucleosis, and include the following:enlarged lymph nodes muscle pains intermittent fever general sick feeling The distinction is made between acquired toxoplasmosis, in which an individual becomes infected, and neonatal congenital toxoplasmosis, in which a fetus is born with the infection because the mother became infected during pregnancy. If a fetus becomes infected early in pregnancy, the disease can cause the fetus to spontaneously abort, be stillborn. If full-term, the infant may die in infancy or suffer from central nervous system lesions. If the mother becomes infected in the last three months of pregnancy, however, the prognosis is good and the baby may not even display any symptoms.In adults, if the infection continues for an extended period of time, chronic toxoplasmosis can cause an inflammation of the eyes called retinochoroiditis, which can lead to blindness, severe yellowing of the skin and whites of the eyes (jaundice), easy bruising, and convulsions.Adults with weakened immune systems have a high risk of developing cerebral toxoplasmosis, including inflammation of the brain (encephalitis), one-sided weakness or numbness, mood and personality changes, vision disturbances, muscle spasms, and severe headaches. If untreated, cerebral toxoplasmosis can lead to coma and death. This form of encephalitis is the second most common AIDS-related nervous system infection that takes advantage of a person's weakened immune system (opportunistic infection).DiagnosisA diagnosis of toxoplasmosis is made based on clinical signs and supporting laboratory results, including visualization of the protozoa in body tissue or isolation in animals and blood tests. Laboratory tests for toxoplasmosis are designed to detect increased amounts of a protein or antibody produced in response to infection with the toxoplasmosis organism. Antibody levels can be elevated for years, however, without active disease.TreatmentMost individuals who contract toxoplasmosis do not require treatment because their immune systems are able to control the disease. Symptoms are not usually present. Mild symptoms may be relieved by taking over-the-counter medications, such as acetaminophen (Tylenol) and ibuprofen (Motrin, Advil). Sore throat lozenges and rest may also ease the symptoms.Although the treatment of women infected with toxoplasmosis during pregnancy is controversial, most physicians feel that treatment is justified. Transmission of toxoplasmosis from the mother to the fetus may be prevented if the mother takes the antibiotic spiramycin. Later in a pregnancy, if the fetus has contracted the disease, treatment with the antibiotic pyrimethamine (Daraprim, Fansidar) or sulfonamides may be effective. Babies born with toxoplasmosis who show symptoms of the disease may be treated with pyrimethamine, the sulfa drug sulfadiazine (Microsulfon), and folinic acid (an active form of folic acid).AIDS patients who have not been infected may be given a drug called TMP/SMX (Bactrim or Septra) to prevent toxoplasmosis infection. To treat cases of toxoplasmosis in immunocompromised AIDS patients, a combination of pyrimethamine and a sulfa-based drug, either sulfadiazine or clindamycin (Cleocin), have been used together and can be effective in treating this disease. Other antibiotic combinations and dosing schedules are still being investigated. Physicians have reported success in alleviating symptoms by using trimethoprim-sulfamethoxazole (Proloprim or Trimpex) or dapsone (DDS) plus pyrimethamine. These drugs can produce side effects, such as allergic reaction, itching, rashes;, and nausea and patients must be monitored closely.Key termsCyst — The thick-walled dormant form of many organisms.Immunocompromised — A state in which the immune system is suppressed or not functioning properly.Oocyst — The egg form of the toxoplasmosis organism.Protozoan — A single-celled, usually microscopic, organism.PrognosisThe prognosis is poor when congenital toxoplasmosis is acquired during the first three months of pregnancy. Afflicted children die in infancy or suffer damage to their central nervous systems that can result in physical and mental retardation. Infection later in pregnancy usually results in only mild symptoms, if any. The prognosis for acquired toxoplasmosis in adults with strong immune systems is excellent. The disease often disappears by itself after several weeks. However, the prognosis for immuniodeficient patients is not as positive. These patients often relapse when treatment is stopped. The disease can be fatal to all immunocompromised patients, especially AIDS patients, and particularly if not treated. As a result, immunocompromised patients are typically placed on anti-toxoplasmosis drugs for the rest of their lives.PreventionThere are no drugs that can eliminate T. gondii cysts in animal or human tissues. Humans can reduce their risks of developing toxoplasmosis by practicing the following:freezing (to 10.4°F/−12°C) and cooking foods to an internal temperature of 152°F/67°C will kill the cyst practicing sanitary kitchen techniques, such as washing utensils and cutting boards that come into contact with raw meat keeping pregnant women and children away from household cats and cat litter disposing of cat feces daily, because the oocysts do not become infective until after 24 hours helping cats to remain free of infection by feeding them dry, canned, or boiled food and by discouraging hunting and scavenging washing hands after outdoor activities involving soil contact and wearing gloves when gardening
Is there any treatment?Treatment for myotonia may include mexelitine, quinine, phenytoin, and other anticonvulsant drugs. Physical therapy and other rehabilitative measures may help muscle function. What is the prognosis?Myotonia is a chronic disorder. Symptoms may improve later in life.What research is being done?The National Institute of Neurological Disorders and Stroke supports and conducts an extensive research program on neuromuscular disorders. The goals of this research are to learn more about these disorders and to find ways to treat, prevent, and cure them. http://videos.howstuffworks.com/animal-planet/40889-weird-true-and-freaky-fainting-goats-video.htm
The cause of dermatomyositis is unknown. Experts think it may be due to a viral infection of the muscles or a problem with the body's immune system. It can also sometimes occur in patients who have cancer of the abdomen, lung or other body area.Anyone can develop dermatomyositis, but it most commonly occurs in children age 5 - 15 and adults age 40 - 60. Women develop this condition more often than men do.-The muscle weakness may appear suddenly or develop slowly over weeks or months. You may have difficulty raising your arms over your head, rising from a sitting position, and climbing stairs.The rash may appear over the face, knuckles, neck, shoulders, upper chest, and back.-idiopathic inflammatory myopathy with characteristic skin manifestations. -Although the disorder is rare, with a prevalence of one to 10 cases per million in adults and one to 3.2 cases per million in children, early recognition and treatment are important ways to decrease the morbidity of systemic complications.-Dermatomyositis is an idiopathic disorder that includes an inflammatory myopathy and characteristic skin manifestations; polymyositis includes the inflammatory myopathy without the cutaneous findings. The etiology of dermatomyositis remains unknown; some studies have reported an association with histocompatability antigens, environmental agents (e.g., virus, drugs) and autoimmunity.1 The average age at diagnosis is 40, and almost twice as many women are affected as men.2 The average age of onset in juvenile dermatomyositis is between five and 14 years. This subgroup of patients has a better prognosis than adult patients. Modern therapy has reduced mortality from near 50 percent to less than 10 percent.3
http://www.wikidoc.org/images/d/db/CSFposter1p.png-The total volume of CSF in the adult ranges from140 to 270 ml.-CSF is produced at a rate of 0.2 - 0.7 ml per minute or 600-700 ml per day.
-During a lumbar puncture, a needle is carefully inserted into the spinal canal low in the back (lumbar area). Samples of CSF are collected. The samples are studied for color, blood cell counts, protein, glucose, and other substances. Some of the sample may be put into a special culture cup to see if any infection, such as bacteria or fungi, grows. The pressure of the CSF also is measured during the procedure.-Normal results Appearance:CSF is normally clear and colorless.Pressure: Normal CSF pressure in the lower back for an adult ranges from 90-180 millimeters (mm) water. For children younger than 8 years old, the normal opening pressure range is 10-100 mm water.Protein:The normal protein content of CSF in an adult's lower back (lumbar) region is 15-45 milligrams per deciliter (mg/dL) or 150-450 milligrams per liter (mg/L). Older adults and children may have higher values that are still in the normal range.Glucose:The normal range for glucose content in the CSF is about 60% of the blood glucose level. The levels may be slightly increased if the person has just eaten.Cell counts:Normal CSF contains no red blood cells (RBCs). The white blood cell (WBC) count for adults is 0-5 WBCs per cubic millimeter (mm3). Children may normally have a higher WBC count. No neutrophils are present. The number of lymphocytes or monocytes is usually less than 1 per mm3.Other results: No infectious organisms (such as bacteria, fungi, or a virus) are found in the CSF sample. No tumor cells are present.Abnormal results Appearance:Blood in the CSF can result from bleeding (hemorrhage) in or around the spinal cord or brain, but it may also be caused by tiny blood vessel poked during the spinal tap. If a brain hemorrhage has occurred, the color of the CSF may change from red to yellow to brown over several days. Bleeding caused by the lumbar puncture itself will show more red blood cells in the first sample collected than in later samples. Cloudy CSF may mean an infection (such as meningitis or a brain abscess) is present.Pressure: High CSF pressure may occur as a result of swelling (edema) or bleeding (hemorrhage) in the brain, infection (such as meningitis), stroke, or other circulatory problems. Below-normal pressure may mean a blocked spinal canal.Protein:A high level of protein may be caused by bleeding in the CSF, a tumor or spread of a cancer from another area of the body, diabetes, infection, injury, Guillain-Barr� syndrome, severe hypothyroidism, or other nerve diseases. An increase in antibodies (immunoglobulins) may be caused by inflammation in people who have multiple sclerosis, immune system disorders, or other bacterial and viral diseases.Glucose:Low glucose levels in the CSF are abnormal and may be caused by bacterial meningitis. Viral meningitis does not often cause low glucose levels in the CSF. Brain hemorrhage may also cause low glucose levels several days after bleeding begins. Higher-than-normal glucose levels are often caused by diabetes.Cell counts:Red blood cells (RBCs) in the CSF means bleeding. High levels of white blood cells (WBCs) mean meningitis. Tumor cells and abnormal levels of white blood cells mean cancer.Other results: Antibodies, bacteria, or other organisms in the CSF means that an infection (such as syphilis) or disease is present. Bacterial markers (bacterial antigens) that show up mean meningitis. Cultures or stains of the CSF may also help show the cause of meningitis or encephalitis.
The four main types of brain herniation syndromes include an uncinate and central transtentorialherniations, as well as a subfalcine or tonsillarherniations.An uncinate or uncaltranstentorial herniation (1) occurs when the inner part (medial aspect) of the temporal lobe is pushed against the free margin of the tentorium. In severe cases, it can compress the brainstem. Another type, known as a central transtentoral herniation, or just a central herniation (2), occurs when there is downward pressure centrally. It may cause a bilateral uncal herniation, meaning an uncal herniation (1) on both sides.A subfalcine herniation (3) occurs when there is uneven, usually one-sided expansion of the cerebral hemisphere which pushes a portion of the brain tissue known as the cingulategyrus under the falxcerebri. Hence this type of herniation is also known as a cingulate herniation.The fourth main type of brain herniation is known as the tonsillar herniation and involves the cerebellum. Swelling or bleeding within the cerebellum pushes the cerebellar tonsils downwards into the foramen magnum. It is also known as the downward cerebellar herniation and can be life-threatening because it compresses the brainstem. A less commonly seen cerebellar herniation is the upward cerebellar herniation (5) where pressure from the back of the cranial cavity pushes the cerebellar tissue upwards.An extracranial herniation (4) is when the brain tissue pushes through an opening in the cranial cavity formed by trauma or at a surgical site. It is also known as a transcalvarial herniation.-
http://youtu.be/qiC2Efbxa3Q-Researchers were initially puzzled as to why such extensive damage occurred without direct trauma. The mechanism of DAI was subsequently discovered to occur as a result of rotational movement of the brain during acceleration-deceleration events.-Slightly less than 10% of individuals with DAI will regain consciousness.-90% of individuals with DAI remain in a persistent vegetative state indefinitely, and may remain so for decades. Of the 10% who regain consciousness, the majority will sustain permanent and far-reaching functional deficits as reviewed above. Only a small percentage of these individuals will attain near-normal neurological function. What improvement occurs does so within the first 12 months after the injury. Significant improvement occurring more than one year after injury is rare.
United StatesPeripheral injuries account for 80% of all cases of vascular trauma. The lower extremities are involved in two thirds of all patients with vascular injuries. Penetrating trauma accounts for 70-90% of vascular injuries. In the past, iatrogenic injuries related to endovascular procedures accounted for less than 10% of all cases. This percentage is increasing due to the growing use of endovascular procedures for diagnostic and therapeutic purposes. Mortality/MorbidityDeath due solely to peripheral vascular injuries is uncommon, but does occur due to exsanguination or development of a necrotizing myofascial infection. Major venous injuries accompany 13-51% of significant arterial injuries.Compartment syndrome may result from ischemia of a muscle compartment. Limb survival is threatened by delays in diagnosis and treatment, particularly when limb perfusion is compromised for more than 6 hours at body temperature ("warm" ischemia). Extensive concurrent musculoskeletal, nerve, and skin injuries indicate a poor prognosis.Crush injuries associated with open tibial fractures are particularly likely to result in loss of the lower leg and amputation.SexNinety percent of patients with peripheral vascular injuries are male.AgeVascular injuries most often occur in patients aged 20-40 years.
Deep vein thrombosis is the primary cause of embolism. In deep vein thrombosis, blood clots form in the large veins of the legs. Sometimes a blood clot breaks free and is carried through the bloodstream. It may then cause an embolism by blocking an artery in the lungs, brain, or other organs.Treatment of an embolism varies greatly depending on its severity. The underlying cause of the embolism should be identified and treated promptly. Medications are used to control the formation and growth of blood clots and to restore blood flow to the affected area of the body.
These calculations were based on the US 2000 census data, published rates of VTE in various conditions and rates of prophylaxis, and ICD-9 codes for discharge diagnoses from the Healthcare Utilization and Cost Database which includes major discharge diagnoses from all US acute-care hospitals. Event Community (fatal*) Hospt. (fatal*) Total (fatal*) DVT 108,889 (649) 269,734 (1,609) 378,623 (2,258) PE 191,260 (105,902) 339,910 (188,210) 531 (294,112) Combined 300,149 (106,551) 609,644 (189,819) 909,793 (296,370) http://clotcare.com/deepveinthrombosispulmonaryembolismstats.aspx
\\It is now considered by the medical profession and supported by legal and some ethical consensus that if a person's entire brain is dead, the person is dead. The reason is that if the entire brain is destroyed, there is absence of spontaneous breathing and expected cessation of heartbeat soon. It is on the basis of this concept that all life support treatments which the patient may have had in place before brain death has been established can be removed because the patient is now dead. It also provides the opportunity to obtain organs from a brain dead patient, who had previously given consent, while the organs are still in good condition for transplantation. Families of a brain dead patient may have to be educated about the physiology. However, some religious groups and even some healthcare workers are uncomfortable with a brain death definition of death since the patient may still have a heart beat and wish to wait until there is persisting absence of heart beat, the classical criterion.
Ujihiraet al in 1993 conducted a clinico-neuropathological study on 60 cases of brain death (29 patients died of cerebrovascular disease) . The average duration of brain death was 99 hours. Histologically, the cytoplasm of neurons was pale and ghost-like. In the white matter, myelin staining was pale, and nuclei of the glial cells were shrunken and pyknotic. Autolysis of the cerebellar granular layer and the pituitary gland was evident in all cases. No reactive astrocytosis or infiltration of the cells in or around necrotic tissue could be seen. Correlation between the degree of autolysis and duration of brain death was observed, but no relationship between the degree of autolysis and the difference of underlying disease could be found. Autolysis in the cerebral cortex, thalamus, tegmentum of the brain stem, cerebellar granular layer and pituitary gland was most prominent. Purkinje cells of the cerebellum, the pyramidal cells of the CA1 subfield of the hippocampus, and the pyramidal cells in layers 3 and 5 of the cerebral cortex are extremely sensitive to the effect of cerebral anoxia.Ogata et al in 1986 analyzed granular layer autolysis (GLA) of the cerebellar cortex in 45 patients who died of acute cerebrovascular diseases (CVDs) . Twelve patients who died of causes other than intracranial disease served as controls. Tonsillar herniation occurred in all who died of acute CVDs. More advanced GLA was seen in the central folia adjacent to the central white medullary body of the cerebellum as compared with the peripheral folia. According to the author's opinion, widespread granular layer autolysis extending to the peripheral folia could be a pathological finding characteristic of brain death, where intracranial blood flow could be absent or significantly reduced. The authors concluded that brain death for less than 1 day would be necessary for granular layer autolysis to develop. In our study, the first signs of autolytic damages of the neurons were seen at 12 hours after warm cerebral anoxia by electron microscopy, while H&E sections and sections stained with Thionine were fully devoid of autolytic changes up to 24 hours. Our results demonstrated a lack of autolytic damage to the same regions on both H&E and on Nissl staining. These findings suggest a possible correlation between pre-existing vascular disease and the development of autolytic histopathology.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2480568/
A concussion is a minor traumatic brain injury (TBI) that may occur when the head hits an object, or a moving object strikes the head. It can affect how your brain works for a while. A concussion can lead to a bad headache, changes in alertness, or loss of consciousness. Causes, incidence, and risk factorsA concussion can result from a fall, sports activities, and car accidents. A big movement of the brain (called jarring) in any direction can cause you to lose alertness (become unconscious). How long you stay unconscious may be a sign of the severity of the concussion.However, concussions don't always involve a loss of consciousness. Most people who have a concussion never pass out, but they may describe seeing all white, black, or stars. You can have a concussion and not realize it.SymptomsSymptoms of a concussion can range from mild to severe. They can include:Acting confused, feeling spacey, or not thinking straightBeing drowsy, hard to wake up, or similar changesHeadacheLoss of consciousnessMemory loss (amnesia) of events before the injury or right afterNausea and vomitingSeeing flashing lightsFeeling like you have "lost time"The following are emergency symptoms of a concussion. Seek immediate medical care if there are:Changes in alertness and consciousnessConvulsions (seizures)Muscle weakness on one or both sidesPersistent confusionRemaining unconsciousness (coma)Repeated vomitingUnequal pupilsUnusual eye movementsWalking problemsHead injuries that cause a concussion often occur with injury to the neck and spine. Take special care when moving people who have had a head injury.While recovering from a concussion, you may:Be withdrawn, easily upset, or confusedHave a hard time with tasks that require remembering or concentratingHave mild headachesBe less tolerant of noiseSigns and testsThe doctor will perform a physical exam and check your nervous system. There may be changes in your pupil size, thinking ability, coordination, and reflexes.Tests that may be performed include:EEG (brain wave test) may be needed if seizures continueHead CT scanMRI of the headTreatmentA more serious brain injury that involves bleeding or brain damage must be treated in a hospital.Healing or recovering from a concussion takes time. It may take days, weeks, or even months for a child's condition to improve. Parents and caregivers must learn how to treat the child's symptoms, how to monitor for problems, and when to allow the child to return to normal activities.Expectations (prognosis)Healing or recovering from a concussion takes time. It may take days, weeks, or even months. You may be irritable, have trouble concentrating, be unable to remember things, have headaches, dizziness, and blurry vision. These problems will probably go away slowly. You may want to get help from family or friends before making important decisions.ComplicationsLong-term problems are rare but may include:Brain swelling (which can be life threatening), if you have a second concussion while still recovering from the first oneLong-term changes in the brain (if you have future brain injuries)Symptoms of the concussion stay for a long period of time (in a small group of patients)
GLOBALConsequently, absolute cerebral blood flow falls off from 0.8 ml/g/min to zero within seconds. Loss of consciousness follows after approximately 10 seconds. EEG activity ceases after 30 to 40 secs, and a few minutes of global ischemia lead to irreversible cellular damage that evolves over days. The typical histological picture following global ischemic insults is described by delayed neuronal death sparing glial cells (sometimes even associated with astrogliosis). As a general rule, under normothermic conditions, 10 min of global ischemia are lethal in man. In the United States approximately 500,000 people/year die because of circulatory arrest leading to global ischemia.FocalTypically, flow reduction is due to embolic or thrombotic vessel occlusion. In contrast to the situation after global ischemia, focal ischemia is characterized by the formation of a so-called “ischemic penumbra”. The penumbra is defined as the ischemia border-zone which is (still) metabolically active but functionally silent. While absolute regional blood flow in the ischemic core is diminished to levels <0.1 ml/g/min, blood flow in the penumbra typically remains at 0.2-0.4 ml/g/min. The typical histological picture following focal ischemia is a pan-necrosis that includes all cell types in the brain (neurons, astrocytes, oligodendrocytes, endothelial cells).
Segmental Axonal originally described in Clinically, neuropathy causes experimental lead weakness and atrophy ofpoisoning, is characterized by muscle, loss of sensation orbreakdown and loss of myelin altered sensation over a few segments. The (pain, paresthesias), andaxon remains intact and there weak or absent tendon is no change in the neuronal reflexes. Nerve conduction body. The loss of saltatory studies can distinguish conduction that results from demyelinative neuropathy segmental demyelination (slowing of conduction leads to decrease of velocity or conduction block) conduction velocity and from axonal neuropathy (low- conduction block. action potential amplitudes).Demyelination is the root cause of the symptoms that people with MS experience. When it occurs the speed at which messages pass along the nerves is slower than normal. Evenwhen the patches of scarring caused by demyelination have healed and re-myelination has occurred, the response time of the nerve endings tends to remain slower.
Study • 77 heart transplant recipients Restoration of nerve •1-5 years after transplantationfunction to a part from •Partial reinnervation was which it was lost; it observed in 52 patients at various times after may occur transplantation spontaneously or be •Reinnervation extent achieved by nerve correlated with time after grafting. surgery but also inversely with donor age and recipient age
a serious disorder that occurs when the bodys defense immune system mistakenly attacks part of the nervous system. This leads to nerve inflammation that causes muscle weakness and other symptoms.www.gbs-cidp.org – Support Group
The term hydrocephalus is derived from the Greek words "hydro" meaning water and "cephalus" meaning head. As the name implies, it is a condition in which the primary characteristic is excessive accumulation of fluid in the brain.
Vasogenic edema: Cerebral edema occurs due to the is an excess failure of tight accumulation of junctions and water in the astrocyte processesintracellular and/or which normallyextracellular spaces maintain an adequate of the brain. blood-brain barrier.
Subdural Epidural A collection of (EDH) is the blood on the accumulation of surface of the blood in the brain. potential space Accumulation ofbetween brain dura blood between the and bone. the dura and the brain.
Traumatic Intraparenchymal hemorrhage is bleeding into thetissue of the brain caused by trauma to the head. This type of bleeding can cause a hematoma which expands inside thebrain, pushing aside adjacent brain tissue and compressing it.The term intraparenchymal basically means "within the brain tissue".
A small tear within the brain that starts to hemorrhage.
Lacunar infarcts are small (0.2 to 15 mm in diameter) noncortical infarcts caused by occlusion of a single penetrating branch of a large cerebral artery. Thesebranches arise at acute angles from the large arteries of the circle of Willis, stem of the middle cerebral artery (MCA), or the basilar artery. Although this definition implies that pathological confirmation is necessary, diagnosis in vivo may be made in the setting of appropriate clinical syndromes and radiological tests.
Meningitis is an inflammation of the tissue around the spinal cord and brain. Viral meningitis isThere are three (3) types relatively common andof bacteria (germs) that can be caused by cause the disease: H. different viruses. The Influenzae (Hib), Strep most common cause is pneumoniae, and from a group of viruses Neisseria meningitidis. known as enteroviruses.
Cats, the primary Toxoplasmosis is carriers of the organism, an infectious become infected by disease caused by eating rodents and birds infected with the the one-celled organism. Onceprotozoan parasite ingested, the organismToxoplasma gondii. reproduces in the intestines of cats, In the United States, it is producing millions of estimated that eggs known as oocysts, which are excreted in cat approximately 30% of cats feces daily for have been infected by T. approximately two weeks. gondii.
•Relaxation of muscle is impaired •Can affect any muscle group •Repeated effort needed to relax•Trouble releasing grip on objects, rising from a seated position and many other problems •Abnormality in the muscle membrane •Often associated with inherited neurological disorders Tennessee Fainting goats have myotonia as well as humans.
is a muscle disease characterized by inflammation and a skin rash. It is a type of inflammatory myopathy.The disease is treated with anti-inflammatorymedicines called corticosteroids and drugs that suppress the immune system.
Happens when blood AKAflow to a part Cerebrovascular disease of the brain CVA stops. Cerebral infarction Cerebral hemorrhage Ischemic stroke Stroke – ischemic Cerebrovascular accident Stroke - hemorrhagic
The cerebrospinal fluid (CSF) is produced from arterial blood by the choroid plexuses of the lateral and fourth ventricles by a combined process of diffusion, pinocytosis andactive transfer. A small amount is also produced by ependymal cellsCSF from the lumbar region contains 15 to 45 mg/dl protein (lower in childen) and 50-80 mg/dl glucose (two-thirds of blood glucose).
A lumbar puncture (also called a spinal tap) is a procedure to collect and look at the fluid(cerebrospinal fluid, or CSF) surrounding the brain and spinal cord.
is when the brain tissue is pushed from its normal position and protrudes into adjacent compartments or may even push out of the skull if there is an opening present. 1. Uncinate/Uncal rranstentorial herniation 2. Central transtentorial herniation 3. Subfalcine (cingulate) herniation 4. Extracranial(transcalvarial) herniation 5. Upward cerebellar herniation 6. Tonsillar (downward cerebellar) herniation
DAI involves massive loss of neuronal functiontowards the central area of the brain, well away from any areas of direct trauma with the skull.
Peripheral vascular injuriesmay result from penetrating or blunt trauma to theextremities. If not recognizedand treated rapidly, injuries to major arteries, veins, and nerves may have disastrousconsequences resulting in the loss of life and limb.
a blockage in one of thearteries of the body due to a blood clot that has broken off from another location in the body (embolus) and traveled through the bloodstream to lodge in a small blood vessel. The blockage may limit or stop blood flow. An embolism is a clot thattravels from the site where it formed to another location in the body.
A thrombus is a blood clot that forms in a vessel and remainsthere. This can result in damage,destruction (infarction), or evendeath of the tissues (necrosis) in that area. Community Hospital Event Total (fatal) (fatal) DVT (Deep Vein 108,889 (649) 269,734 (1,609) 378,623 (2,258) Thrombosis) According to the US Census data of 2000
It is now considered by the medical profession and supported by legal and some ethical consensus that if a persons entire brain is dead, the person is dead.
A swollen and congested brain with necrotic andautolytic changes seen inpatients who have been on a respirator.
In 1993 conducted a clinico- neuropathological study on 60 cases of brain death. The average duration of brain death was 99 hours. Autolysis of the cerebellar granular layer and the pituitary gland was evident in all cases.Autolysis – is a breakdown of a part or whole cell or tissue by self-produced enzymes
An alteration of consciousawareness after head trauma. Thecollection of symptoms following a concussion is called the postconcussion syndrome (PCS), and includedizziness, nausea, vomiting, headache, disorientation, forgetfulness, i rritability, depression, mood swings, insomnia, and loss of libido. Most cases of PCS resolve after a few months, but approximately 20% of cases can involve longer term problems.
A contrecoup injuryA "coup" injury is the happens at the oppositeinitial site of impact. side as the site of injury, so if you struck your forehead, the brain injury would be at the back of the brain.
Global ischemia in man develops Focal ischemia followsafter transient circulatory arrest transient or permanent flowwith resuscitation or after near- reduction in the territory of a drowning cerebral artery. Due to: Due to: •Hanging •Hemispheral stroke •Circulatory arrest •Transient ischemic • Drowning attack
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