Early Symptoms Of Lou Gehrig’s Disease
Published on Mar 19 2010, in the categories: Lou Gehrig's
Basically, amyotrophic lateral sclerosis is a progressive disease that damages motor neurons - specialized cells in the spinal cord and brain stem that control muscle movement. As the disease progresses, the control of muscle degenerates.
The early symptoms of Lou Gehrig's disease are subtle - far less than they can easily be overlooked. Early symptoms of Lou Gehrig’s disease may include muscle jerks, muscle muscles pose obstacles, stiff, or weakness. As the disease advances, a person's speech may be slurred. Finally, a person with Lou Gehrig’s disease has a problem chewing and swallowing. The muscles become weaker as the disease advances, taking the force and finally the ability to walk or use arms and legs. The arms and legs look thinner as muscle tissue atrophies. In the late stages of the disease, respiratory muscles weaken, making it difficult to breathe. Most people with Lou Gehrig’s disease die from respiratory failure.
Most cases of Lou Gehrig's disease - more than ninety percent of cases - occur in people without family history of this disease. The cause of onset in these cases is unknown. Only a small percentage of cases it develops a genetic mutation known - these cases are known as Lou Gehrig’s disease or inherited familial Lou Gehrig’s.
There are eight different types of Lou Gehrig’s disease, distinguished by cause genetic pattern of inheritance, age at onset and disease progression. For example, Lou Gehrig’s type 1 and 8 are the adult-onset Lou Gehrig’s. Type 1 of Lou Gehrig’s progress very rapidly, most people with type 1 Lou Gehrig’s die of respiratory failure five years after onset. Lou Gehrig’s type 2 and 4 are the juvenile or early onset Lou Gehrig’s disease. Types 2, 4, and 8 are relatively rare. Approximately twenty percent of familial cases of Lou Gehrig’s disease and three percent of sporadic cases of Lou Gehrig’s disease are type 1.
Around the world, Lou Gehrig's disease occurs between four and eight people per 100 000. In the United States, approximately five thousand people are diagnosed with Lou Gehrig’s disease each year.
Lou Gehrig's is a disease of motor neurons also called amyotrophic lateral sclerosis or Charcot Mal. This is a progressive disease, failure, caused by degeneration of motor neurons and nerves in the central nervous system that voluntary control of the muscle.
The disorder causes muscle weakness and atrophy in the body as the upper and lower motor neurons degenerate, ceasing to send messages to neurons. By losing muscle function muscles will gradually degrade and eventually lead to atrophy. The patient will ultimately lose the ability to initiate and control voluntary movements, the role of bladder and sphincters as controlling the eye muscles Current usage is preserved, but not always.
Cognitive function is not usually affected except in certain situations where the disease occurs in association with frontotemporal dementia. However, there are reports that changes in frontotemporal type in these patients are very subtle in most patients, when tests are performed more detailed type. The autonomic nervous system will usually remain functional.
The condition is called Lou Gehrig's after the baseball player for the New York Yankess who was diagnosed with the disease in 1939 and died from it in 1941 at the age of 37.
The early symptoms of Lou Gehrig's disease are subtle - far less than they can easily be overlooked. Early symptoms of Lou Gehrig’s disease may include muscle jerks, muscle muscles pose obstacles, stiff, or weakness. As the disease advances, a person's speech may be slurred. Finally, a person with Lou Gehrig’s disease has a problem chewing and swallowing. The muscles become weaker as the disease advances, taking the force and finally the ability to walk or use arms and legs. The arms and legs look thinner as muscle tissue atrophies. In the late stages of the disease, respiratory muscles weaken, making it difficult to breathe. Most people with Lou Gehrig’s disease die from respiratory failure.
Most cases of Lou Gehrig's disease - more than ninety percent of cases - occur in people without family history of this disease. The cause of onset in these cases is unknown. Only a small percentage of cases it develops a genetic mutation known - these cases are known as Lou Gehrig’s disease or inherited familial Lou Gehrig’s.
There are eight different types of Lou Gehrig’s disease, distinguished by cause genetic pattern of inheritance, age at onset and disease progression. For example, Lou Gehrig’s type 1 and 8 are the adult-onset Lou Gehrig’s. Type 1 of Lou Gehrig’s progress very rapidly, most people with type 1 Lou Gehrig’s die of respiratory failure five years after onset. Lou Gehrig’s type 2 and 4 are the juvenile or early onset Lou Gehrig’s disease. Types 2, 4, and 8 are relatively rare. Approximately twenty percent of familial cases of Lou Gehrig’s disease and three percent of sporadic cases of Lou Gehrig’s disease are type 1.
Around the world, Lou Gehrig's disease occurs between four and eight people per 100 000. In the United States, approximately five thousand people are diagnosed with Lou Gehrig’s disease each year.
Lou Gehrig's is a disease of motor neurons also called amyotrophic lateral sclerosis or Charcot Mal. This is a progressive disease, failure, caused by degeneration of motor neurons and nerves in the central nervous system that voluntary control of the muscle.
The disorder causes muscle weakness and atrophy in the body as the upper and lower motor neurons degenerate, ceasing to send messages to neurons. By losing muscle function muscles will gradually degrade and eventually lead to atrophy. The patient will ultimately lose the ability to initiate and control voluntary movements, the role of bladder and sphincters as controlling the eye muscles Current usage is preserved, but not always.
Cognitive function is not usually affected except in certain situations where the disease occurs in association with frontotemporal dementia. However, there are reports that changes in frontotemporal type in these patients are very subtle in most patients, when tests are performed more detailed type. The autonomic nervous system will usually remain functional.
The condition is called Lou Gehrig's after the baseball player for the New York Yankess who was diagnosed with the disease in 1939 and died from it in 1941 at the age of 37.
Alzheimer’s Disease Signs And Symptoms
Published on Mar 18 2010, in the categories: Alzheimer's
Dementia of Alzheimer's usually begins subtle: people begin to forget some things, to get to the point where they can no longer even recognize family members and they need help even for everyday tasks.
Dementia of Alzheimer's now affects about 5% of people over 60 years. And 'the most common form of dementia, one was caused by an alteration of brain function that involves serious difficulties for the patient to conduct normal daily activities. The disease affects memory and cognitive functions, affects the ability to speak and think but can also cause other problems including confusion, disorientation and changes in mood and space.
The disease is named after Alois Alzheimer, a German neurologist who for the first time in 1907 described the Alzheimer’s disease signs and symptoms and neuropathological aspects. At the autopsy examination, the doctor noticed special signs in the brain tissue of a woman who had died as a result of an unusual mental illness. In fact, this indicates the presence of agglomerates, then defined amyloid plaques and tangled bundles of fibers, the neuro-fibrillary tangles. Today, the plaques formed by amyloid proteins and tangles are considered the effects on nerve tissue of a disease which, despite the considerable efforts put into the field, the causes are still unknown.
In patients with dementia of Alzheimer there has been observed a loss of nerve cells in brain areas vital to memory and other cognitive functions. There is also a low level of those chemicals, such as acetylcholine, which work like neurotransmitters and are thus not involved in the communication between nerve cells.
Alzheimer’s disease signs and symptoms
The course of the disease is slow and on average patients can live for up to 8-10 years after diagnosis of the disease.
The Alzheimer's dementia is manifested by mild memory problems, to result in serious damage to brain tissue, but the rapidity with which aggravate the symptoms varies from person to person. In the course of the disease, cognitive deficits are exacerbated and can lead the patient to serious loss of memory, to put the same questions repeatedly, to get lost in familiar places, inability to follow the clear guidance, to have disorientation about time, about people and places, but also to neglect their personal safety, hygiene and nutrition.
The cognitive problems may, however, be present even years before the formulation of a diagnosis of Alzheimer's dementia is made.
Diagnosis
Today the only way to make a definite diagnosis of dementia of Alzheimer's is through the identification of amyloid plaques in brain tissue, possible only with an autopsy after the death of the patient. This means that during the course of the disease can only make a diagnosis of Alzheimer 'possible' or 'probable'. For this reason, doctors use various tests:
-clinical examinations, such as blood, urine or spinal fluid;
-neuropsychological tests to measure memory, problem solving, the degree of attention, the ability to count and dialogue;
-examine the brain to identify any possible sign of abnormality;
These tests allow the doctor to rule out other possible causes that lead to similar symptoms, such as thyroid problems, adverse reactions to drugs, depression, brain tumors, but also diseases of the blood vessels of the brain.
As in other neurodegenerative diseases, early diagnosis is very important because it offers the possibility to treat some symptoms of the disease, because it allows the patient to plan his future, when it is still capable of making decisions.
Dementia of Alzheimer's now affects about 5% of people over 60 years. And 'the most common form of dementia, one was caused by an alteration of brain function that involves serious difficulties for the patient to conduct normal daily activities. The disease affects memory and cognitive functions, affects the ability to speak and think but can also cause other problems including confusion, disorientation and changes in mood and space.
The disease is named after Alois Alzheimer, a German neurologist who for the first time in 1907 described the Alzheimer’s disease signs and symptoms and neuropathological aspects. At the autopsy examination, the doctor noticed special signs in the brain tissue of a woman who had died as a result of an unusual mental illness. In fact, this indicates the presence of agglomerates, then defined amyloid plaques and tangled bundles of fibers, the neuro-fibrillary tangles. Today, the plaques formed by amyloid proteins and tangles are considered the effects on nerve tissue of a disease which, despite the considerable efforts put into the field, the causes are still unknown.
In patients with dementia of Alzheimer there has been observed a loss of nerve cells in brain areas vital to memory and other cognitive functions. There is also a low level of those chemicals, such as acetylcholine, which work like neurotransmitters and are thus not involved in the communication between nerve cells.
Alzheimer’s disease signs and symptoms
The course of the disease is slow and on average patients can live for up to 8-10 years after diagnosis of the disease.
The Alzheimer's dementia is manifested by mild memory problems, to result in serious damage to brain tissue, but the rapidity with which aggravate the symptoms varies from person to person. In the course of the disease, cognitive deficits are exacerbated and can lead the patient to serious loss of memory, to put the same questions repeatedly, to get lost in familiar places, inability to follow the clear guidance, to have disorientation about time, about people and places, but also to neglect their personal safety, hygiene and nutrition.
The cognitive problems may, however, be present even years before the formulation of a diagnosis of Alzheimer's dementia is made.
Diagnosis
Today the only way to make a definite diagnosis of dementia of Alzheimer's is through the identification of amyloid plaques in brain tissue, possible only with an autopsy after the death of the patient. This means that during the course of the disease can only make a diagnosis of Alzheimer 'possible' or 'probable'. For this reason, doctors use various tests:
-clinical examinations, such as blood, urine or spinal fluid;
-neuropsychological tests to measure memory, problem solving, the degree of attention, the ability to count and dialogue;
-examine the brain to identify any possible sign of abnormality;
These tests allow the doctor to rule out other possible causes that lead to similar symptoms, such as thyroid problems, adverse reactions to drugs, depression, brain tumors, but also diseases of the blood vessels of the brain.
As in other neurodegenerative diseases, early diagnosis is very important because it offers the possibility to treat some symptoms of the disease, because it allows the patient to plan his future, when it is still capable of making decisions.
Symptoms Picks Disease
Published on Mar 18 2010, in the categories: Niemann Pick
Niemann Pick disease (NPD "- Niemann Pick Disease) is actually a term that identifies a group of diseases that affect metabolism and are caused by specific genetic mutations. The three most commonly recognized forms of the disease are types A, B and C. In the past, other forms have been recognized.
Niemann Pick Type "A" and "B"
The type "A" and "B" are both caused by the same lack enzymatic activity and there is a growing consensus that the two forms represent opposite ends of a continuum. People with type "A" generally have little or no production of asthma (less than 1% of normal), while those with type "B" have about 10% of normal level of ASM.
While both type "A" that the "B" have an ASM which is significantly lower than normal, the clinical prognosis for these two groups of patients is very different. The type "A" of the NPD is a severe neurological disease that leads to death between 2 and 4 years of age. By contrast, patients with type "B" generally have little or no neurological involvement and may survive into late childhood or adulthood.
Since there is no accurate correlation between ASM activities and neurological involvement is not possible to accurately predict the severity of the disease by examining the enzymes. There are about 1,200 cases worldwide, of which the majority is of type "B" or an intermediate form.
Niemann Pick type "C"
There are considerable variations in either the first symptoms of Pick’s disease type "C", both in the progression of the disease. Symptoms may appear either early as a few months both in adulthood. Vertical gaze paralysis (inability to move the eyes up and down), enlarged liver, enlarged spleen, or jaundice in children are strong indications that the NPC should be taken into account. It is common that only one or two symptoms of Pick’s disease appear early in the disease.
It is believed that the number of people affected is higher, but it is often difficult to be diagnosed correctly. The NPD type "C" was initially diagnosed as a disability 'learning, a slight delay, "a confusion" and delay the development of motor skills. Is not uncommon for a family to spend several years seeking a diagnosis, before the type "C" is identified. The type "C" is always fatal. The majority of children die before the age of 20 years (and many before the age of 10). The delayed onset of symptoms can lead to longer durations, but is extremely rare that anyone reaches the age of 40.
Other forms
In the past, other types of NPD have been identified. The older forms include:
The NPD Type "D" has been described in the French Canadian population of the county of Yarmouth, Nova Scotia. The genealogical evidence indicates that Joseph Muise (c. 1679 to 1729) and Marie Amirault (1684 - c. 1735) are common ancestors to all cases of Nova Scotia. This is now recognized as a variation of the type "C".
The NPD Type "E" has been described for cases initiated in adults. E 'considered a variation of the type "C" in which metabolic processes are only partially compromised by the delay in symptoms and slow progression.
Niemann Pick Type "A" and "B"
The type "A" and "B" are both caused by the same lack enzymatic activity and there is a growing consensus that the two forms represent opposite ends of a continuum. People with type "A" generally have little or no production of asthma (less than 1% of normal), while those with type "B" have about 10% of normal level of ASM.
While both type "A" that the "B" have an ASM which is significantly lower than normal, the clinical prognosis for these two groups of patients is very different. The type "A" of the NPD is a severe neurological disease that leads to death between 2 and 4 years of age. By contrast, patients with type "B" generally have little or no neurological involvement and may survive into late childhood or adulthood.
Since there is no accurate correlation between ASM activities and neurological involvement is not possible to accurately predict the severity of the disease by examining the enzymes. There are about 1,200 cases worldwide, of which the majority is of type "B" or an intermediate form.
Niemann Pick type "C"
There are considerable variations in either the first symptoms of Pick’s disease type "C", both in the progression of the disease. Symptoms may appear either early as a few months both in adulthood. Vertical gaze paralysis (inability to move the eyes up and down), enlarged liver, enlarged spleen, or jaundice in children are strong indications that the NPC should be taken into account. It is common that only one or two symptoms of Pick’s disease appear early in the disease.
It is believed that the number of people affected is higher, but it is often difficult to be diagnosed correctly. The NPD type "C" was initially diagnosed as a disability 'learning, a slight delay, "a confusion" and delay the development of motor skills. Is not uncommon for a family to spend several years seeking a diagnosis, before the type "C" is identified. The type "C" is always fatal. The majority of children die before the age of 20 years (and many before the age of 10). The delayed onset of symptoms can lead to longer durations, but is extremely rare that anyone reaches the age of 40.
Other forms
In the past, other types of NPD have been identified. The older forms include:
The NPD Type "D" has been described in the French Canadian population of the county of Yarmouth, Nova Scotia. The genealogical evidence indicates that Joseph Muise (c. 1679 to 1729) and Marie Amirault (1684 - c. 1735) are common ancestors to all cases of Nova Scotia. This is now recognized as a variation of the type "C".
The NPD Type "E" has been described for cases initiated in adults. E 'considered a variation of the type "C" in which metabolic processes are only partially compromised by the delay in symptoms and slow progression.
Huntington’s Disease Symptoms
Published on Mar 17 2010, in the categories: Huntington
Huntington's disease (MH) is an inherited disorder of degeneration characterized by a movement disorder progressively debilitating behavioral problems, sometimes very serious and affects the intellectual functions leading to dementia. Has a prevalence varying in different parts of the world with values in Europe about 5-10/100.000. In Italy, therefore is estimate that about 6,000 people and 18,000 sick those at risk of inheriting the disease. It was George Huntington in 1872, to describe for the first time the Huntington’s disease symptoms in his article "On Chorea."
Clinical features and genetic
The gene responsible for MH is located on chromosome 4. It contains information for the production of a protein called Huntington whose function is still unknown, although there is evidence that it is a protein essential to life and expressed in all cells. People with MH have alterations in the gene, and therefore their cells produce an abnormal form of this protein, which through an automatic gain functions toxic (gain-of-function) is not yet clarified, induces death of neurons in many brain areas.
In many cases, issues related to behavioral changes occur before Huntington’s disease symptoms occur of motor. The first signs of disease may be irritability, depression, mood changes along with a slight disturbance of motor coordination with mild and sporadic hyperkinesia-like shots. Slow movements (bradykinesia) or muscle contractures (dystonia) may characterize the onset of the disease by contributing to different variations depending on the case.
The age of onset is highly variable because the disease can manifest as a 2 to 90 years although it is generally the first symptoms appear on average between 30 and 50. The MH has a worsening trend that chorea and cognitive problems worsen as the disease progressed. Another common symptom is dysarthria, which is manifested as an alteration of the ability 'to articulate the language, often associated with difficulty swallowing.
Huntington in young people
In approximately 10% of cases, the MH strikes before the age of 20. Fortunately only rarely children or adolescents have this disease. Children most often inherit the disease from their father (MH is inherited with the same frequency from both parents). The symptoms of juvenile form of MH are sometimes different from the adult form, as in the case of the form defined Westphal. Initial symptoms usually involve slow, stiff, awkward gait, difficulty in speech and, sometimes, seizures occurring in 30-50% of cases. The course of the variant of youth may be more severe than that of adults. This group can 'be further divided into those with an outbreak of infantile or before 10 years and those with onset in adolescence 10 to 20 years of age'.
The MH is an autosomal-dominant and is transmitted from one generation to the next through the transmission from parent to child of a gene mutated (altered). Each child of an affected parent has one chance in two (50%) of having inherited the gene that causes MH, and is called "at risk". People who carry the gene develop MH unless they die from other causes before they have the first symptoms. Males and females have the same chance of inheriting the gene from affected parent. Those who have not inherited the gene do not develop the disease, and even their children.
Clinical features and genetic
The gene responsible for MH is located on chromosome 4. It contains information for the production of a protein called Huntington whose function is still unknown, although there is evidence that it is a protein essential to life and expressed in all cells. People with MH have alterations in the gene, and therefore their cells produce an abnormal form of this protein, which through an automatic gain functions toxic (gain-of-function) is not yet clarified, induces death of neurons in many brain areas.
In many cases, issues related to behavioral changes occur before Huntington’s disease symptoms occur of motor. The first signs of disease may be irritability, depression, mood changes along with a slight disturbance of motor coordination with mild and sporadic hyperkinesia-like shots. Slow movements (bradykinesia) or muscle contractures (dystonia) may characterize the onset of the disease by contributing to different variations depending on the case.
The age of onset is highly variable because the disease can manifest as a 2 to 90 years although it is generally the first symptoms appear on average between 30 and 50. The MH has a worsening trend that chorea and cognitive problems worsen as the disease progressed. Another common symptom is dysarthria, which is manifested as an alteration of the ability 'to articulate the language, often associated with difficulty swallowing.
Huntington in young people
In approximately 10% of cases, the MH strikes before the age of 20. Fortunately only rarely children or adolescents have this disease. Children most often inherit the disease from their father (MH is inherited with the same frequency from both parents). The symptoms of juvenile form of MH are sometimes different from the adult form, as in the case of the form defined Westphal. Initial symptoms usually involve slow, stiff, awkward gait, difficulty in speech and, sometimes, seizures occurring in 30-50% of cases. The course of the variant of youth may be more severe than that of adults. This group can 'be further divided into those with an outbreak of infantile or before 10 years and those with onset in adolescence 10 to 20 years of age'.
The MH is an autosomal-dominant and is transmitted from one generation to the next through the transmission from parent to child of a gene mutated (altered). Each child of an affected parent has one chance in two (50%) of having inherited the gene that causes MH, and is called "at risk". People who carry the gene develop MH unless they die from other causes before they have the first symptoms. Males and females have the same chance of inheriting the gene from affected parent. Those who have not inherited the gene do not develop the disease, and even their children.
Signs And Symptoms Of Alzheimer’s Disease
Published on Mar 17 2010, in the categories: Alzheimer's
What is Alzheimer's disease?
Alzheimer's disease is the most common pathologic condition among dementias. Usually presents in the elderly (65 years and over) and causes a progressive deterioration of memory, reasoning that would adversely affect the ability to perform normal daily activities of the patient. It is estimated that one in ten people after 85 years of age is affected by this disease.
Unlike the typical benign forgetfulness of the elderly, Alzheimer's disease is a true disease status, that a doctor can diagnose various tests that explore the area of cognitive and behavioral function, integrating the results of diagnostic imaging examinations of the brain.
This disease is characterized by the death of cells in areas of the brain that control memory, thought and language. With the increase in the number of affected cells, increase the number and severity of symptoms appearing. For this reason the Alzheimer disease is defined as a degenerative disease and progressive.
Who is affected by Alzheimer's disease?
Alzheimer's disease mainly affects people around 65 years of age and older. Since the entire world population is aging, the number of people affected by it is set to increase.
A small percentage of individuals with Alzheimer developed the disease early, i.e. between 35 and 60 years of age. It is believed that this form is inherited early-onset, since the cases tend to occur within a few families.
However, the majority of people with Alzheimer (95 percent) develop the disease later; this form is not strictly hereditary. Alzheimer's disease is widespread in all ethnic groups and social classes, affecting both men and women, although it is somewhat more common among women.
What are the causes of Alzheimer's disease?
The medicine is still investigating to identify the causes of Alzheimer. Current knowledge indicates that the progressive loss of brain cells is associated with abnormal formation of plaques (plaques of beta amyloid) around them. These plaques are accumulations of fragments of a protein insoluble. Another hallmark of the Alzheimer disease and the presence of "tangles" in brain cells made of an abnormal form of tau protein, a protein that has important functions in healthy cells. These structures are the ultimate result of degenerative processes involving different brain systems. It is likely that the Alzheimer disease is not caused by a single cause but several factors that may affect in varying degrees in each individual.
What are the signs and symptoms of Alzheimer's disease?
In general, the signs and symptoms of Alzheimer’s disease affect the ability to store, thinking and reasoning, and behavior and the ability to perform normal daily activities.
Alzheimer begins slowly and gradually and can be difficult to suspect the early stages and is easily confused with depression or with normal signs of aging. Early symptoms include small memory loss, confusion and poor concentration, but can also include disorientation, problems of communication, personality change, lack of motivation.
The person who gets sick of Alzheimer can manifest strange and unusual behavior - a fairly common sign is to wander without a reason and a goal - or imagine seeing things or hearing nonexistent voices (hallucinations). With the worsening of these symptoms, the person becomes obviously more and more dependent on others.
In later stages the physical symptoms become more evident. The person becomes inappropriate behavior, presents problems of understanding, can become aggressive or show signs of depression, because some areas of the brain were damaged.
Alzheimer's disease is the most common pathologic condition among dementias. Usually presents in the elderly (65 years and over) and causes a progressive deterioration of memory, reasoning that would adversely affect the ability to perform normal daily activities of the patient. It is estimated that one in ten people after 85 years of age is affected by this disease.
Unlike the typical benign forgetfulness of the elderly, Alzheimer's disease is a true disease status, that a doctor can diagnose various tests that explore the area of cognitive and behavioral function, integrating the results of diagnostic imaging examinations of the brain.
This disease is characterized by the death of cells in areas of the brain that control memory, thought and language. With the increase in the number of affected cells, increase the number and severity of symptoms appearing. For this reason the Alzheimer disease is defined as a degenerative disease and progressive.
Who is affected by Alzheimer's disease?
Alzheimer's disease mainly affects people around 65 years of age and older. Since the entire world population is aging, the number of people affected by it is set to increase.
A small percentage of individuals with Alzheimer developed the disease early, i.e. between 35 and 60 years of age. It is believed that this form is inherited early-onset, since the cases tend to occur within a few families.
However, the majority of people with Alzheimer (95 percent) develop the disease later; this form is not strictly hereditary. Alzheimer's disease is widespread in all ethnic groups and social classes, affecting both men and women, although it is somewhat more common among women.
What are the causes of Alzheimer's disease?
The medicine is still investigating to identify the causes of Alzheimer. Current knowledge indicates that the progressive loss of brain cells is associated with abnormal formation of plaques (plaques of beta amyloid) around them. These plaques are accumulations of fragments of a protein insoluble. Another hallmark of the Alzheimer disease and the presence of "tangles" in brain cells made of an abnormal form of tau protein, a protein that has important functions in healthy cells. These structures are the ultimate result of degenerative processes involving different brain systems. It is likely that the Alzheimer disease is not caused by a single cause but several factors that may affect in varying degrees in each individual.
What are the signs and symptoms of Alzheimer's disease?
In general, the signs and symptoms of Alzheimer’s disease affect the ability to store, thinking and reasoning, and behavior and the ability to perform normal daily activities.
Alzheimer begins slowly and gradually and can be difficult to suspect the early stages and is easily confused with depression or with normal signs of aging. Early symptoms include small memory loss, confusion and poor concentration, but can also include disorientation, problems of communication, personality change, lack of motivation.
The person who gets sick of Alzheimer can manifest strange and unusual behavior - a fairly common sign is to wander without a reason and a goal - or imagine seeing things or hearing nonexistent voices (hallucinations). With the worsening of these symptoms, the person becomes obviously more and more dependent on others.
In later stages the physical symptoms become more evident. The person becomes inappropriate behavior, presents problems of understanding, can become aggressive or show signs of depression, because some areas of the brain were damaged.
Parkinsons Disease Symptoms In Spanish
Published on Mar 16 2010, in the categories: parkinson, symptoms
Parkinson's disease is a neurodegenerative disease that primarily affects structures of the black substance and the striatum. This disease also compromises the cerebral cortex, the limbic system and hypothalamus, has an unknown origin, recognizing multiple factors in its appearance with a strong genetic component whose importance may vary in different situations.
The EP is chronic, progressive and slow, and affects part of brain responsible for movement control and coordination, muscle tone and posture. In this area, called the black substance, there is a chemical, called dopamine, an essential compound for the regulation of movements, i.e. movements that are undertaken in an effective and harmonious.
Thus, in PD there is a "degeneration" of the black substance (cause unknown) whose consequence is the decline of dopamine. That is why the main manifestations of the disease expressed poor control of movements: tremor, generalized slowness (bradykinesia), rigidity and abnormal posture and gait.
Parkinson described the disease that bears his name as "shaking palsy", indicating the most relevant symptoms: decreased movement (paralysis) and "agitation" (tremor) occurs between 40 and 70 years of age with a higher incidence the decade of the 60s. There is a "Tremor, Benign Familial" of evolution very slow and often present in members of one family. It is not strictly a resting tremor, but in attitude.
Some authors believe it is a benign form of Parkinson's disease, but treatment is radically different. If it is very annoying, it is best to leave it untreated. A known feature of this tremor is its disappearance with small doses of alcohol (which is dangerous). The adrenaline is blocking drugs, which are also used to treat hypertension and angina pectoris, are the best alternative.
What are the symptoms of Parkinson's disease? • Tremor in the arms and legs, initially on one side of the body when walking or resting. • Slowness of movement, especially in the beginning and / or terminate a quick movement ; Repetitive movement, which are known as bradykinesia • Stiffness in the arms, legs and muscles
• Problems with balance and coordination • Tiredness • Emotional changes such as depression • Deterioration of mental function (dementia) • Difficulty sleeping • Difficulty in swallowing, speaking, and urinary control, and constipation • Seborrhea eczema • Small and compressed writing (microfobia) • Deterioration or loss of smell • Visual hallucinations.
How is Parkinson's disease diagnosed?- Parkinson's disease is diagnosed by a doctor who observes symptoms. They take a complete physical examination and medical history. Diagnosis depends on the presence of slow movements (bradykinesia) and at least one of the other main symptoms: tremor, rigidity and balance problems.
Although the tremor and bradykinesia on one side of the body are typical of the gradual development of the disease, 25% of people with Parkinson's do not experience tremor. The best way to verify the diagnosis is watching the reaction of the person on medicines to treat Parkinson's disease. Making the correct diagnosis can take some time. There are a lot of people in U.S. who need to read Parkinson’s disease symptoms in Spanish. You can find Parkinson’s disease symptoms in Spanish on hispanichealth.org.
The EP is chronic, progressive and slow, and affects part of brain responsible for movement control and coordination, muscle tone and posture. In this area, called the black substance, there is a chemical, called dopamine, an essential compound for the regulation of movements, i.e. movements that are undertaken in an effective and harmonious.
Thus, in PD there is a "degeneration" of the black substance (cause unknown) whose consequence is the decline of dopamine. That is why the main manifestations of the disease expressed poor control of movements: tremor, generalized slowness (bradykinesia), rigidity and abnormal posture and gait.
Parkinson described the disease that bears his name as "shaking palsy", indicating the most relevant symptoms: decreased movement (paralysis) and "agitation" (tremor) occurs between 40 and 70 years of age with a higher incidence the decade of the 60s. There is a "Tremor, Benign Familial" of evolution very slow and often present in members of one family. It is not strictly a resting tremor, but in attitude.
Some authors believe it is a benign form of Parkinson's disease, but treatment is radically different. If it is very annoying, it is best to leave it untreated. A known feature of this tremor is its disappearance with small doses of alcohol (which is dangerous). The adrenaline is blocking drugs, which are also used to treat hypertension and angina pectoris, are the best alternative.
What are the symptoms of Parkinson's disease? • Tremor in the arms and legs, initially on one side of the body when walking or resting. • Slowness of movement, especially in the beginning and / or terminate a quick movement ; Repetitive movement, which are known as bradykinesia • Stiffness in the arms, legs and muscles
• Problems with balance and coordination • Tiredness • Emotional changes such as depression • Deterioration of mental function (dementia) • Difficulty sleeping • Difficulty in swallowing, speaking, and urinary control, and constipation • Seborrhea eczema • Small and compressed writing (microfobia) • Deterioration or loss of smell • Visual hallucinations.
How is Parkinson's disease diagnosed?- Parkinson's disease is diagnosed by a doctor who observes symptoms. They take a complete physical examination and medical history. Diagnosis depends on the presence of slow movements (bradykinesia) and at least one of the other main symptoms: tremor, rigidity and balance problems.
Although the tremor and bradykinesia on one side of the body are typical of the gradual development of the disease, 25% of people with Parkinson's do not experience tremor. The best way to verify the diagnosis is watching the reaction of the person on medicines to treat Parkinson's disease. Making the correct diagnosis can take some time. There are a lot of people in U.S. who need to read Parkinson’s disease symptoms in Spanish. You can find Parkinson’s disease symptoms in Spanish on hispanichealth.org.
Poultry Disease And Symptoms
Published on Mar 15 2010, in the categories: Poultry disease, symptoms
EPIDEMIOLOGY - Many species of both domestic and wild birds; The mortality and morbidity rates vary according to species and depending on the viral strain; The chickens are more susceptible to poultry, ducks and geese are the least susceptible; There may be a carrier state in psittacine and some other wild birds
Transmission - Direct contact with secretions from infected birds, particularly feces; Food, water, tools, premises, human clothing, etc.
Sources of virus - Respiratory secretions, feces; All parts of dead birds; The virus is transmitted during the incubation period and for a limited period during convalescence. It has been shown that some parrots pass for more than a year the virus of Newcastle disease intermittently
Geographical Distribution - Newcastle disease is endemic in many countries. For years, some European countries have not had this disease. For more details on geographical distribution, see recent issues of World Animal Health and the OIE Bulletin
DIAGNOSIS - The incubation period of 4-6 days; Clinical diagnosis. Poultry disease and symptoms: Wheezing and coughing; Drooping wings, dragging legs, head and neck twisted, traveling in circles, depression, inapetence, complete paralysis.
Complete or partial interruption of egg production. Deformed eggs, rugged and thin-shelled and contain watery albumen; Green watery diarrhea; Swollen tissues around the eyes and neck. Morbidity and mortality depend on the virulence of the virus strain, degree of immunity to vaccination, environmental conditions and the status of birds on the farm.
Injuries - The poultry disease and symptoms of this disease produce no pathognomonic gross lesions; Several birds should be examined to make a tentative diagnosis. For the final diagnosis must await the virus isolation and identification
The lesions can be found are: Interstitial tissue edema or peritracheal the neck, especially near the thoracic inlet; Congestion and sometimes bleeding from the tracheal mucosa; Petechiae and small ecchymoses on the mucosa of the proventriculus, concentrated around the orifices of the mucous glands; Edema, hemorrhage, necrosis or ulceration of the mucosal lymphoid tissue in the intestinal wall; Edema, hemorrhage, or degeneration of the ovaries
Differential Diagnosis - Fowl cholera; Avian Influenza; Laryngotracheitis; Avian pox (diphtheritic form); Psittacosis (chlamydiosis) (psittacine birds); Mycoplasmoses; Infectious Bronchitis; Pacheco's parrot disease (psittacine birds); Also driving errors, such as lack of water, air, food
Laboratory Diagnosis - Procedure: Identification of agent; Inoculation of chicken eggs embryonated 9-11 days, then: Review of the hemagglutination activity; Hemagglutination inhibition using a specific antiserum to Newcastle disease.
Assessment of pathogenity - Test plaques in cultures of embryonic fibroblasts; Average time of death through embryonated chicken eggs; Intracerebral pathogenity index in 1-day-old chicks; Intravenous pathogenity index in chickens for 6 weeks. Serological tests - Proof of hemagglutination inhibition
ELISA - Hits; Identification of agent; Tracheal and swabs (or stool samples) of live birds or groups of bodies and feces from dead birds. Serological tests - Samples of clotted blood or serum
PREVENTION AND CONTROL - No treatment; Sanitary prophylaxis; Strict isolation of outbreaks; Destruction of all infected and exposed birds to infection; Clean and disinfect the premises thoroughly; Adequate destruction of dead birds; Pest control on farms; A deadline of 21 days before restocking; Avoid contact with birds whose health status is unknown; Control of human movement; It is recommended breeding age group per farm; Medical prophylaxis
Transmission - Direct contact with secretions from infected birds, particularly feces; Food, water, tools, premises, human clothing, etc.
Sources of virus - Respiratory secretions, feces; All parts of dead birds; The virus is transmitted during the incubation period and for a limited period during convalescence. It has been shown that some parrots pass for more than a year the virus of Newcastle disease intermittently
Geographical Distribution - Newcastle disease is endemic in many countries. For years, some European countries have not had this disease. For more details on geographical distribution, see recent issues of World Animal Health and the OIE Bulletin
DIAGNOSIS - The incubation period of 4-6 days; Clinical diagnosis. Poultry disease and symptoms: Wheezing and coughing; Drooping wings, dragging legs, head and neck twisted, traveling in circles, depression, inapetence, complete paralysis.
Complete or partial interruption of egg production. Deformed eggs, rugged and thin-shelled and contain watery albumen; Green watery diarrhea; Swollen tissues around the eyes and neck. Morbidity and mortality depend on the virulence of the virus strain, degree of immunity to vaccination, environmental conditions and the status of birds on the farm.
Injuries - The poultry disease and symptoms of this disease produce no pathognomonic gross lesions; Several birds should be examined to make a tentative diagnosis. For the final diagnosis must await the virus isolation and identification
The lesions can be found are: Interstitial tissue edema or peritracheal the neck, especially near the thoracic inlet; Congestion and sometimes bleeding from the tracheal mucosa; Petechiae and small ecchymoses on the mucosa of the proventriculus, concentrated around the orifices of the mucous glands; Edema, hemorrhage, necrosis or ulceration of the mucosal lymphoid tissue in the intestinal wall; Edema, hemorrhage, or degeneration of the ovaries
Differential Diagnosis - Fowl cholera; Avian Influenza; Laryngotracheitis; Avian pox (diphtheritic form); Psittacosis (chlamydiosis) (psittacine birds); Mycoplasmoses; Infectious Bronchitis; Pacheco's parrot disease (psittacine birds); Also driving errors, such as lack of water, air, food
Laboratory Diagnosis - Procedure: Identification of agent; Inoculation of chicken eggs embryonated 9-11 days, then: Review of the hemagglutination activity; Hemagglutination inhibition using a specific antiserum to Newcastle disease.
Assessment of pathogenity - Test plaques in cultures of embryonic fibroblasts; Average time of death through embryonated chicken eggs; Intracerebral pathogenity index in 1-day-old chicks; Intravenous pathogenity index in chickens for 6 weeks. Serological tests - Proof of hemagglutination inhibition
ELISA - Hits; Identification of agent; Tracheal and swabs (or stool samples) of live birds or groups of bodies and feces from dead birds. Serological tests - Samples of clotted blood or serum
PREVENTION AND CONTROL - No treatment; Sanitary prophylaxis; Strict isolation of outbreaks; Destruction of all infected and exposed birds to infection; Clean and disinfect the premises thoroughly; Adequate destruction of dead birds; Pest control on farms; A deadline of 21 days before restocking; Avoid contact with birds whose health status is unknown; Control of human movement; It is recommended breeding age group per farm; Medical prophylaxis
Celiac Disease Symptoms In Teenagers
Published on Mar 15 2010, in the categories: At teenage period, celiac disease, General info, symptoms
Birthday cake. Pizza. A big cookie and gooey with chocolate pieces. For people who suffer from celiac disease, a digestive system disorder, these foods are not common delights. Why? Because they contain a type of protein called gluten, which causes problems for people with celiac disease.
This article is about celiac disease symptoms in teenagers, because I have been asked by a friend to write it. What is celiac disease and what causes it? The digestive system is the set of organs that digests food and absorbs important nutrients the body needs to grow and stay healthy. An important part of the digestive system is the small intestine, which is lined with millions of microscopic projections called villi finger-shaped. The villi are the vehicles through which the body absorbs nutrients.
People with celiac disease have a disorder that causes a reaction to gluten, a type of protein found in many foods. When these people eat gluten, the immune system's reaction to the protein gradually erodes and destroys the villi of the small intestine. When the villi are damaged, the body can not process the vitamins, minerals and other nutrients it needs to stay healthy. Therefore people with celiac disease are at risk of malnutrition and may develop anemia (decreased red blood cells due to lack of iron) or osteoporosis (brittle bones due to lack of calcium).
The body's inability to absorb nutrients can also mean that teenagers with celiac disease may not grow to their full potential height. In addition, people with celiac disease may be more prone to developing other diseases such as thyroid disease, diabetes, lupus and certain cancers.
No one knows exactly why a person develops celiac disease, also known as celiac sprue, non tropical sprue or gluten enteropathy. However, the disease appears to be genetic, which means that it is common in a family. Same as eye color or hair, people inherit from their parents and grandparents the genes that make them more susceptible to developing celiac disease. If a relative has celiac disease, the probability that you also suffer from it is 10%.
Although celiac disease affects people of all origins, it seems to be more common among people whose ancestors came from northern Europe.
In the past, experts believed that celiac disease was rare in the United States. However, the study results published in early 2003 by the University Of Maryland Center for Celiac Research (Research Center for Celiac Disease at the University of Maryland) in Baltimore indicate that the disease is more widespread than previously thought.
Celiac disease symptoms in teenagers - The symptoms of Celiac disease are the same in children, teenagers and adults. It is important to diagnose celiac disease early before it causes too much damage to the intestine. But as it is easy to confuse the symptoms with other intestinal disorders such as irritable bowel syndrome or lactose intolerance, for those adolescents with celiac disease do not know they have it.
Some common symptoms of celiac disease are diarrhea, abdominal pain, bloating and weight loss. People with the disease may feel tired, irritable or depressed. Some people suffering from the disease have skin rashes and mouth sores. The malnutrition that accompanies celiac disease can cause anemia and other problems associated with nutrition problems. The onset of puberty in adolescents with celiac disease could be delayed.
This article is about celiac disease symptoms in teenagers, because I have been asked by a friend to write it. What is celiac disease and what causes it? The digestive system is the set of organs that digests food and absorbs important nutrients the body needs to grow and stay healthy. An important part of the digestive system is the small intestine, which is lined with millions of microscopic projections called villi finger-shaped. The villi are the vehicles through which the body absorbs nutrients.
People with celiac disease have a disorder that causes a reaction to gluten, a type of protein found in many foods. When these people eat gluten, the immune system's reaction to the protein gradually erodes and destroys the villi of the small intestine. When the villi are damaged, the body can not process the vitamins, minerals and other nutrients it needs to stay healthy. Therefore people with celiac disease are at risk of malnutrition and may develop anemia (decreased red blood cells due to lack of iron) or osteoporosis (brittle bones due to lack of calcium).
The body's inability to absorb nutrients can also mean that teenagers with celiac disease may not grow to their full potential height. In addition, people with celiac disease may be more prone to developing other diseases such as thyroid disease, diabetes, lupus and certain cancers.
No one knows exactly why a person develops celiac disease, also known as celiac sprue, non tropical sprue or gluten enteropathy. However, the disease appears to be genetic, which means that it is common in a family. Same as eye color or hair, people inherit from their parents and grandparents the genes that make them more susceptible to developing celiac disease. If a relative has celiac disease, the probability that you also suffer from it is 10%.
Although celiac disease affects people of all origins, it seems to be more common among people whose ancestors came from northern Europe.
In the past, experts believed that celiac disease was rare in the United States. However, the study results published in early 2003 by the University Of Maryland Center for Celiac Research (Research Center for Celiac Disease at the University of Maryland) in Baltimore indicate that the disease is more widespread than previously thought.
Celiac disease symptoms in teenagers - The symptoms of Celiac disease are the same in children, teenagers and adults. It is important to diagnose celiac disease early before it causes too much damage to the intestine. But as it is easy to confuse the symptoms with other intestinal disorders such as irritable bowel syndrome or lactose intolerance, for those adolescents with celiac disease do not know they have it.
Some common symptoms of celiac disease are diarrhea, abdominal pain, bloating and weight loss. People with the disease may feel tired, irritable or depressed. Some people suffering from the disease have skin rashes and mouth sores. The malnutrition that accompanies celiac disease can cause anemia and other problems associated with nutrition problems. The onset of puberty in adolescents with celiac disease could be delayed.
Symptoms Of MS Disease
Published on Mar 13 2010, in the categories: MS disease
What is Multiple Sclerosis?
Multiple Sclerosis (MS) is a disease of the central nervous system (CNS). The CNS consists of two parts: the brain and spinal cord. Nervous stimuli are transmitted through nerve cells called neurons. Wrapping these CNS neurons is a material composed of proteins, fats called myelin that facilitates driving into electrical impulses between these nerve fibers. Where myelin is destroyed, the plates become hardened tissue (sclerosis). As a result, nerve impulses are interrupted periodically, or in severe cases, permanently.
Multiple sclerosis is a disease related to the loss of the myelin of the brain and spinal nerves. Where myelin is destroyed, the plates become hardened tissue (sclerosis). This teething transmission of nerve stimulation and makes it more expensive or, in severe cases, are interrupted periodically.
Luckily the injury of myelin is often reversible.
People with increased risk of MS are people between 20 and 45 years, and fatigue is a very common symptom. MS is neither contagious, inherited, nor fatal.
Causes of MS disease
Currently, no one knows the exact cause of multiple sclerosis, but it is believed that the destruction of myelin is the result of an abnormal immune response to the organism itself. Usually, the immune system defends the body from viruses and bacteria. In autoimmune diseases, in which the body destroys its own foreign bodies, the body attacks its own cells. In multiple sclerosis, myelin is an attacked substance. Scientists do not know what prompts the immune system to attack myelin. Most agree that several factors are involved (genetic and environmental factors).
Symptoms of MS disease
Symptoms of MS disease vary greatly depending on the person affected by the CNS areas that are affected. The most prominent symptoms are:
- Weakness.
- Tingling.
- Lack of coordination.
- Fatigue.
- Balance problems.
- Visual disturbances.
- Trembling.
- Muscle stiffness.
- Speech disorders.
- Bowel or urinary problems.
- Ataxia (unsteady gait).
- Problems with sexual function.
- Sensitivity to heat.
- Problems with memory and cognitive disorders among others.
Diagnosis
To diagnose this disease is carried primarily by the patient's medical history and neurological examination. The most important test is magnetic resonance imaging (MRI) and cerebrospinal fluid study. The number and location of lesions on MRI may vary over time, but the appearance of lesions on MRI is difficult to diagnose because, sometimes it is difficult to distinguish with certainty demyelinating lesions (which are those that give certainty of disease) from other lesions of different origin.
Forecast
Today it is difficult to predict the onset of symptoms attributable to multiple sclerosis. There are benign forms of multiple sclerosis, in which the disease causes very few disruptions throughout life. Furthermore, after a worsening or relapse often improvement occurs. The complete remission of symptoms usually is important to follow the evolution of the disease through regular visits to the neurologist who is best placed to suggest and warn of the treatments applied at each stage of the pattern of symptoms or complications, if there are any.
Multiple Sclerosis (MS) is a disease of the central nervous system (CNS). The CNS consists of two parts: the brain and spinal cord. Nervous stimuli are transmitted through nerve cells called neurons. Wrapping these CNS neurons is a material composed of proteins, fats called myelin that facilitates driving into electrical impulses between these nerve fibers. Where myelin is destroyed, the plates become hardened tissue (sclerosis). As a result, nerve impulses are interrupted periodically, or in severe cases, permanently.
Multiple sclerosis is a disease related to the loss of the myelin of the brain and spinal nerves. Where myelin is destroyed, the plates become hardened tissue (sclerosis). This teething transmission of nerve stimulation and makes it more expensive or, in severe cases, are interrupted periodically.
Luckily the injury of myelin is often reversible.
People with increased risk of MS are people between 20 and 45 years, and fatigue is a very common symptom. MS is neither contagious, inherited, nor fatal.
Causes of MS disease
Currently, no one knows the exact cause of multiple sclerosis, but it is believed that the destruction of myelin is the result of an abnormal immune response to the organism itself. Usually, the immune system defends the body from viruses and bacteria. In autoimmune diseases, in which the body destroys its own foreign bodies, the body attacks its own cells. In multiple sclerosis, myelin is an attacked substance. Scientists do not know what prompts the immune system to attack myelin. Most agree that several factors are involved (genetic and environmental factors).
Symptoms of MS disease
Symptoms of MS disease vary greatly depending on the person affected by the CNS areas that are affected. The most prominent symptoms are:
- Weakness.
- Tingling.
- Lack of coordination.
- Fatigue.
- Balance problems.
- Visual disturbances.
- Trembling.
- Muscle stiffness.
- Speech disorders.
- Bowel or urinary problems.
- Ataxia (unsteady gait).
- Problems with sexual function.
- Sensitivity to heat.
- Problems with memory and cognitive disorders among others.
Diagnosis
To diagnose this disease is carried primarily by the patient's medical history and neurological examination. The most important test is magnetic resonance imaging (MRI) and cerebrospinal fluid study. The number and location of lesions on MRI may vary over time, but the appearance of lesions on MRI is difficult to diagnose because, sometimes it is difficult to distinguish with certainty demyelinating lesions (which are those that give certainty of disease) from other lesions of different origin.
Forecast
Today it is difficult to predict the onset of symptoms attributable to multiple sclerosis. There are benign forms of multiple sclerosis, in which the disease causes very few disruptions throughout life. Furthermore, after a worsening or relapse often improvement occurs. The complete remission of symptoms usually is important to follow the evolution of the disease through regular visits to the neurologist who is best placed to suggest and warn of the treatments applied at each stage of the pattern of symptoms or complications, if there are any.
ALS Disease Symptoms
Published on Mar 13 2010, in the categories: ALS, Lou Gehrig's, symptoms
What is ALS? - This is the short term for Amyotrophic lateral sclerosis , rarely called also the Lou Gehrig's disease, is a progressive neurological disease, invariably fatal, which attacks nerve cells (neurons) responsible for controlling voluntary muscles. This disease is included into a group of diseases called motor neuron diseases, which are characterized by the gradual degeneration and death of motor neurons.
Motor neurons are nerve cells located in the brain, brainstem, and spinal cord that serve as controlling units and vital communication links between the nervous system and voluntary muscles of the body. Messages from motor neurons brain (called upper motor neurons) are transmitted to motor neurons in the spinal cord (called lower motor neurons) and from there to each particular muscle. In ALS, motor neurons both upper and lower degenerate or die and stop sending messages to muscles. Unable to function, the muscles gradually weaken and become waste (atrophy) and contract. Eventually, the brain loses the ability to initiate and control voluntary movement.
ALS is the cause of weakness having a wide array of disabilities. Are affected eventually all muscles under voluntary control and patients lose their strength and ability to move his arms, legs and body. When muscles of the diaphragm and chest wall fail, patients can't breathe any more without a ventilator or breathing machine. Most people with ALS die from respiratory failure, usually between 3 to 5 years from the onset of ALS disease symptoms. However, about 10 percent of ALS patients survive 10 years or more.
Because ALS affects only motor neurons, the disease does not impair the mind, personality, intelligence or memory of the person. Nor does it affect the senses of sight, smell, taste, hearing or touch. Patients usually maintain control of eye muscles and functions of the bladder and intestines.
What are the ALS disease symptoms? - The onset of ALS may be so subtle that often are overlooked symptoms. The first symptoms may include twitching, cramps or muscle stiffness, muscle weakness affecting an arm or leg, speech impaired or nose, or difficulty chewing or swallowing. These widespread complaints then become more obvious weakness or atrophy, which can lead to the doctor suspecting ALS.
The parts of the body affected by early symptoms of ALS depend on which muscles in the body are damaged first. In some cases, symptoms initially affect one of the legs and patients have difficulty walking or running or realize that they face or stumble more often. At first, some patients see the effects of the disease in a hand or arm when they are hard to do simple tasks requiring manual dexterity such as buttoning a shirt, write or turn the key into a lock. Other patients notice trouble in speaking.
For patients to be diagnosed with ALS, they must have signs and symptoms of damage to the upper and lower motor neurons that can not be attributed to other causes. Although the sequence of emerging symptoms and the rate of disease progression vary from person to person, eventually patients will not stand or walk, lie down or get out of bed alone, or use his hands and arms.
Difficulty swallowing and chewing hurts the ability of patients to eat normally and increase the risk of choking. Maintaining weight becomes a problem. Because the disease usually does not affect cognitive abilities, patients realize their gradual loss of function, and can be anxiety or depression. Health professionals should explain the course of the disease and describe available treatments so that patients can make informed decisions in advance.
Motor neurons are nerve cells located in the brain, brainstem, and spinal cord that serve as controlling units and vital communication links between the nervous system and voluntary muscles of the body. Messages from motor neurons brain (called upper motor neurons) are transmitted to motor neurons in the spinal cord (called lower motor neurons) and from there to each particular muscle. In ALS, motor neurons both upper and lower degenerate or die and stop sending messages to muscles. Unable to function, the muscles gradually weaken and become waste (atrophy) and contract. Eventually, the brain loses the ability to initiate and control voluntary movement.
ALS is the cause of weakness having a wide array of disabilities. Are affected eventually all muscles under voluntary control and patients lose their strength and ability to move his arms, legs and body. When muscles of the diaphragm and chest wall fail, patients can't breathe any more without a ventilator or breathing machine. Most people with ALS die from respiratory failure, usually between 3 to 5 years from the onset of ALS disease symptoms. However, about 10 percent of ALS patients survive 10 years or more.
Because ALS affects only motor neurons, the disease does not impair the mind, personality, intelligence or memory of the person. Nor does it affect the senses of sight, smell, taste, hearing or touch. Patients usually maintain control of eye muscles and functions of the bladder and intestines.
What are the ALS disease symptoms? - The onset of ALS may be so subtle that often are overlooked symptoms. The first symptoms may include twitching, cramps or muscle stiffness, muscle weakness affecting an arm or leg, speech impaired or nose, or difficulty chewing or swallowing. These widespread complaints then become more obvious weakness or atrophy, which can lead to the doctor suspecting ALS.
The parts of the body affected by early symptoms of ALS depend on which muscles in the body are damaged first. In some cases, symptoms initially affect one of the legs and patients have difficulty walking or running or realize that they face or stumble more often. At first, some patients see the effects of the disease in a hand or arm when they are hard to do simple tasks requiring manual dexterity such as buttoning a shirt, write or turn the key into a lock. Other patients notice trouble in speaking.
For patients to be diagnosed with ALS, they must have signs and symptoms of damage to the upper and lower motor neurons that can not be attributed to other causes. Although the sequence of emerging symptoms and the rate of disease progression vary from person to person, eventually patients will not stand or walk, lie down or get out of bed alone, or use his hands and arms.
Difficulty swallowing and chewing hurts the ability of patients to eat normally and increase the risk of choking. Maintaining weight becomes a problem. Because the disease usually does not affect cognitive abilities, patients realize their gradual loss of function, and can be anxiety or depression. Health professionals should explain the course of the disease and describe available treatments so that patients can make informed decisions in advance.
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