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Parkinson's Disease. Symptoms of parkinson's disease | Patient

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What is Parkinson's disease?

Parkinson's disease (PD) is a chronic (persistent, or long-term) disorder of part of the brain. It is named after the doctor who first described it. It mainly affects the way the brain co-ordinates the movements of the muscles in various parts of the body.

PD mainly develops in people over the age of 50. It becomes more common with increasing age. About 5 in 1,000 people in their 60s, and about 40 in 1,000 people in their 80s have PD. It affects both men and women but is a little more common in men. Rarely, it develops in people under the age of 50.

PD is not usually inherited, and it can affect anyone. However, genetic (hereditary) factors may be important in the small number of people who develop PD before the age of 50.

A small part of the brain called the substantia nigra is mainly affected. This area of the brain sends messages down nerves in the spinal cord to help control the muscles of the body. Messages are passed between brain cells, nerves and muscles by chemicals called neurotransmitters. Dopamine is the main neurotransmitter that is made by the brain cells in the substantia nigra.

If you have PD, a number of cells in the substantia nigra become damaged and die. The exact cause of this is not known. Over time, more and more cells become damaged and die. As cells are damaged, the amount of dopamine that is produced is reduced. A combination of the reduction of cells and a low level of dopamine in the cells in this part of the brain causes nerve messages to the muscles to become slowed and abnormal.

The brain cells and nerves affected in PD normally help to produce smooth, co-ordinated movements of muscles. Therefore, three common Parkinson's symptoms that gradually develop are:

The symptoms tend slowly to become worse. However, the speed in which symptoms become worse varies from person to person. It may take several years before they become bad enough to have much effect on your life. At first, one side of your body may be more affected than the other.

Some other symptoms may develop due to problems with the way affected brain cells and nerves control the muscles. These include:

Various other symptoms develop in some cases, mainly as the condition becomes worse. These include:

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Multiple Sclerosis. Medical information about MS | Patient

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What is multiple sclerosis (MS)?

MS is a disease where patches of inflammation occur in parts of the brain and/or spinal cord. This can cause damage to parts of the brain and lead to various symptoms (described below).

Many thousands of nerve fibres transmit tiny electrical impulses (messages) between different parts of the brain and spinal cord. Each nerve fibre in the brain and spinal cord is surrounded by a protective sheath made from a substance called myelin. The myelin sheath acts like the insulation around an electrical wire, and is needed for the electrical impulses to travel correctly along the nerve fibre.

Nerves are made up from many nerve fibres. Nerves come out of the brain and spinal cord and take messages to and from muscles, the skin, body organs and tissues.

MS is thought to be an autoimmune disease. This means that cells of the immune system, which normally attack germs (bacteria, viruses, etc), attack part of the body. When the disease is active, parts of the immune system, mainly cells called T cells, attack the myelin sheath which surrounds the nerve fibres in the brain and spinal cord. This leads to small patches of inflammation.

Something may trigger the immune system to act in this way. One theory is that a virus, or another factor in the environment, triggers the immune system in some people with a certain genetic makeup.

The inflammation around the myelin sheath stops the affected nerve fibres from working properly, and symptoms develop. When the inflammation clears, the myelin sheath may heal and repair, and nerve fibres start to work again. However, the inflammation, or repeated bouts of inflammation, can leave a small scar (sclerosis) which can permanently damage nerve fibres. In a typical person with MS, many (multiple) small areas of scarring develop in the brain and spinal cord. These scars may also be called plaques.

Once the disease is triggered, it tends to follow one of the following four patterns.

Nearly 9 in 10 people with MS have the common relapsing-remitting form of the disease. A relapse is when an attack (episode) of symptoms occurs. During a relapse, symptoms develop (described below) and may last for days, but usually last for 2-6 weeks. They sometimes last for several months. Symptoms then ease or go away (remit). You are said to be in remission when symptoms have eased or gone away. Further relapses then occur from time to time.

The type and number of symptoms that occur during a relapse vary from person to person, depending on where myelin damage occurs. The frequency of relapses also varies. One or two relapses every two years is fairly typical. However, relapses can occur more or less often than this. When a relapse occurs, previous symptoms may return, or new ones may appear.

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Multiple Sclerosis. Medical information about MS | Patient

Multiple Sclerosis Information Page: National Institute of …

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An unpredictable disease of the central nervous system, multiple sclerosis (MS) can range from relatively benign to somewhat disabling to devastating, as communication between the brain and other parts of the body is disrupted. Many investigators believe MS to be an autoimmune disease -- one in which the body, through its immune system, launches a defensive attack against its own tissues. In the case of MS, it is the nerve-insulating myelin that comes under assault. Such assaults may be linked to an unknown environmental trigger, perhaps a virus.

Most people experience their first symptoms of MS between the ages of 20 and 40; the initial symptom of MS is often blurred or double vision, red-green color distortion, or even blindness in one eye. Most MS patients experience muscle weakness in their extremities and difficulty with coordination and balance. These symptoms may be severe enough to impair walking or even standing. In the worst cases, MS can produce partial or complete paralysis. Most people with MS also exhibit paresthesias, transitory abnormal sensory feelings such as numbness, prickling, or "pins and needles" sensations. Some may also experience pain. Speech impediments, tremors, and dizziness are other frequent complaints. Occasionally, people with MS have hearing loss. Approximately half of all people with MS experience cognitive impairments such as difficulties with concentration, attention, memory, and poor judgment, but such symptoms are usually mild and are frequently overlooked. Depression is another common feature of MS.

There is as yet no cure for MS. Many patients do well with no therapy at all, especially since many medications have serious side effects and some carry significant risks. However, three forms of beta interferon (Avonex, Betaseron, and Rebif) have now been approved by the Food and Drug Administration for treatment of relapsing-remitting MS. Beta interferon has been shown to reduce the number of exacerbations and may slow the progression of physical disability. When attacks do occur, they tend to be shorter and less severe. The FDA also has approved a synthetic form of myelin basic protein, called copolymer I (Copaxone), for the treatment of relapsing-remitting MS. Copolymer I has few side effects, and studies indicate that the agent can reduce the relapse rate by almost one third. Other FDA approved drugs to treat relapsing forms of MS in adults include teriflunomide and dimethyl fumarate. An immunosuppressant treatment, Novantrone (mitoxantrone), isapproved by the FDA for the treatment of advanced or chronic MS. The FDA has also approved dalfampridine (Ampyra) to improve walking in individuals with MS.

One monoclonal antibody, natalizumab (Tysabri), was shown in clinical trials to significantly reduce the frequency of attacks in people with relapsing forms of MS and was approved for marketing by the U.S. Food and Drug Administration (FDA) in 2004. However, in 2005 the drugs manufacturer voluntarily suspended marketing of the drug after several reports of significant adverse events. In 2006, the FDA again approved sale of the drug for MS but under strict treatment guidelines involving infusion centers where patients can be monitored by specially trained physicians.

While steroids do not affect the course of MS over time, they can reduce the duration and severity of attacks in some patients. Spasticity, which can occur either as a sustained stiffness caused by increased muscle tone or as spasms that come and go, is usually treated with muscle relaxants and tranquilizers such as baclofen, tizanidine, diazepam, clonazepam, and dantrolene. Physical therapy and exercise can help preserve remaining function, and patients may find that various aids -- such as foot braces, canes, and walkers -- can help them remain independent and mobile. Avoiding excessive activity and avoiding heat are probably the most important measures patients can take to counter physiological fatigue. If psychological symptoms of fatigue such as depression or apathy are evident, antidepressant medications may help. Other drugs that may reduce fatigue in some, but not all, patients include amantadine (Symmetrel), pemoline (Cylert), and the still-experimental drug aminopyridine. Although improvement of optic symptoms usually occurs even without treatment, a short course of treatment with intravenous methylprednisolone (Solu-Medrol) followed by treatment with oral steroids is sometimes used.

A physician may diagnose MS in some patients soon after the onset of the illness. In others, however, doctors may not be able to readily identify the cause of the symptoms, leading to years of uncertainty and multiple diagnoses punctuated by baffling symptoms that mysteriously wax and wane. The vast majority of patients are mildly affected, but in the worst cases, MS can render a person unable to write, speak, or walk. MS is a disease with a natural tendency to remit spontaneously, for which there is no universally effective treatment.

The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. Scientists continue their extensive efforts to create new and better therapies for MS. One of the most promising MS research areas involves naturally occurring antiviral proteins known as interferons. Beta interferon has been shown to reduce the number of exacerbations and may slow the progression of physical disability. When attacks do occur, they tend to be shorter and less severe. In addition, there are a number of treatments under investigation that may curtail attacks or improve function. Over a dozen clinical trials testing potential therapies are underway, and additional new treatments are being devised and tested in animal models.

In 2001, the National Academies/Institute of Medicine, a Federal technical and scientific advisory agency, prepared a strategic review of MS research. To read or download the National Academies/Institute of Medicine report, go to: "Multiple Sclerosis: Current Status and Strategies for the Future."

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Multiple Sclerosis Information Page: National Institute of ...

Multiple Sclerosis: Hope Through Research: National …

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Multiple Sclerosis (MS) is the most common disabling neurological disease of young adults. It most often appears when people are between 20 to 40 years old. However, it can also affect children and older people.

The course of MS is unpredictable. A small number of those with MS will have a mild course with little to no disability, while another smaller group will have a steadily worsening disease that leads to increased disability over time. Most people with MS, however, will have short periods of symptoms followed by long stretches of relative relief, with partial or full recovery. There is no way to predict, at the beginning, how an individual persons disease will progress.

Researchers have spent decades trying to understand why some people get MS and others don't, and why some individuals with MS have symptoms that progress rapidly while others do not. How does the disease begin? Why is the course of MS so different from person to person? Is there anything we can do to prevent it? Can it be cured?

This brochure includes information about why MS develops, how it progresses, and what new therapies are being used to treat its symptoms and slow its progression. New treatments can reduce long-term disability for many people with MS. However, there are still no cures and no clear ways to prevent MS from developing.

Multiple sclerosis (MS) is a neuroinflammatory disease that affects myelin , a substance that makes up the membrane (called the myelin sheath) that wraps around nerve fibers (axons). Myelinated axons are commonly called white matter. Researchers have learned that MS also damages the nerve cell bodies, which are found in the brains gray matter, as well as the axons themselves in the brain, spinal cord, and optic nerve (the nerve that transmits visual information from the eye to the brain). As the disease progresses, the brains cortex shrinks (cortical atrophy).

The term multiple sclerosis refers to the distinctive areas of scar tissue (sclerosis or plaques) that are visible in the white matter of people who have MS. Plaques can be as small as a pinhead or as large as the size of a golf ball. Doctors can see these areas by examining the brain and spinal cord using a type of brain scan called magnetic resonance imaging (MRI).

While MS sometimes causes severe disability, it is only rarely fatal and most people with MS have a normal life expectancy.

Plaques, or lesions, are the result of an inflammatory process in the brain that causes immune system cells to attack myelin. The myelin sheath helps to speed nerve impulses traveling within the nervous system. Axons are also damaged in MS, although not as extensively, or as early in the disease, as myelin.

Under normal circumstances, cells of the immune system travel in and out of the brain patrolling for infectious agents (viruses, for example) or unhealthy cells. This is called the "surveillance" function of the immune system.

Surveillance cells usually won't spring into action unless they recognize an infectious agent or unhealthy cells. When they do, they produce substances to stop the infectious agent. If they encounter unhealthy cells, they either kill them directly or clean out the dying area and produce substances that promote healing and repair among the cells that are left.

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Dementia Reconsidered: the Person Comes First …

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"For some years now, Tom Kitwood's work on dementia care has stood out as the most important, innovative and creative development in a field that has for too long been neglected. This book is a landmark in dementia care; it brings together, and elaborates on, Kitwood's theory of dementia and of person-centred care in an accessible fashion, that will make this an essential source for all working and researching in the field of dementia care." Robert Woods, Professor of Clinical Psychology, University of Wales

"Over the last ten years or so Tom Kitwood has made a truly remarkable contribution to our understanding of dementia, and to raising expectations of what can be achieved with empathy and skill. This lucid account of his thinking and work will communicate his approach to a yet wider audience. It is to be warmly welcomed." Mary Marshall, Director of the Dementia Services Development Centre, University of Stirling

* What is the real nature of the dementing process? * What might we reasonably expect when dementia care is of very high quality? * What is required of organizations and individuals involved in dementia care?

Tom Kitwood breaks new ground in this book. Many of the older ideas about dementia are subjected to critical scrutiny and reappraisal, drawing on research evidence, logical analysis and the author's own experience. The unifying theme is the personhood of men and women who have dementia - an issue that was grossly neglected for many years both in psychiatry and care practice.

Each chapter provides a definitive statement on a major topic related to dementia, for example: the nature of 'organic mental impairment', the experience of dementia, the agenda for care practice, and the transformation of the culture of care.

While recognizing the enormous difficulties of the present day, the book clearly demonstrates the possibility of a better life for people who have dementia, and comes to a cautiously optimistic conclusion. It will be of interest to all professionals involved in dementia care or provision, students on courses involving psychogeriatrics or social work with older people, and family carers of people with dementia.

Key features: * One of the few attempts to present the whole picture. * Very readable - many real-life illustrations. * Offers a major alternative to the 'medical model' of dementia. * Tom Kitwood's work on dementia is very well known

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Friedreich's ataxia – Wikipedia, the free encyclopedia

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Friedreich's ataxia is an autosomal recessive inherited disease that causes progressive damage to the nervous system. It manifests in initial symptoms of poor coordination such as gait disturbance; it can also lead to scoliosis, heart disease and diabetes, but does not affect cognitive function. The disease progresses until a wheelchair is required for mobility. Its incidence in the general population is roughly 1 in 50,000.

The particular genetic mutation (expansion of an intronic GAA triplet repeat in the FXN gene) leads to reduced expression of the mitochondrial protein frataxin. Over time this deficiency causes the aforementioned damage, as well as frequent fatigue due to effects on cellular metabolism.

The ataxia of Friedreich's ataxia results from the degeneration of nervous tissue in the spinal cord, in particular sensory neurons essential (through connections with the cerebellum) for directing muscle movement of the arms and legs. The spinal cord becomes thinner and nerve cells lose some of their myelin sheath (the insulating covering on some nerve cells that helps conduct nerve impulses).

The condition is named after the German physician Nikolaus Friedreich, who first described it in the 1860s.[1]

Friedreich, working as a professor of pathology at the University of Heidelberg, reported five patients with the condition in a series of three papers in 1863.[2][3][4] Further observations appeared in a subsequent paper in 1876.[5]

Symptoms typically begin sometime between the ages of 5 to 15 years, but in Late Onset FA may occur in the 20s or 30s. Symptoms include any combination, but not necessarily all, of the following:

It presents before 25 years of age with progressive staggering or stumbling gait and frequent falling. Lower extremities are more severely involved. The symptoms are slow and progressive. Long-term observation shows that many patients reach a plateau in symptoms in the patient's early adulthood. On average, after 1015 years with the disease, patients are usually wheelchair bound and require assistance with all activities of daily living.[7]

The following physical signs may be detected on physical examination:

20% of cases are found in association with diabetes mellitus.[6]

Friedreich's ataxia is an autosomal recessive disorder that occurs when the FXN gene contains amplified intronic GAA repeats. The FXN gene encodes the protein frataxin.[8] GAA repeat expansion causes frataxin levels to be reduced. Frataxin is an iron-binding protein responsible for forming ironsulphur clusters. One result of frataxin deficiency is mitochondrial iron overload which can cause damage to many proteins.[8] The exact role of frataxin in normal physiology remains unclear.[9] The gene is located on chromosome 9.

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Friedreich's ataxia - Wikipedia, the free encyclopedia

Friedreich's Ataxia Fact Sheet: National Institute of …

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Friedreich's ataxia (also called FA or FRDA) is a rare inherited disease that causes nervous system damage and movement problems. It usually begins in childhood and leads to impaired muscle coordination (ataxia) that worsens over time. The disorder is named after Nicholaus Friedreich, a German doctor who first described the condition in the 1860s.

In Friedreichs ataxia the spinal cord and peripheral nerves degenerate, becoming thinner. The cerebellum, part of the brain that coordinates balance and movement, also degenerates to a lesser extent. This damage results in awkward, unsteady movements and impaired sensory functions. The disorder also causes problems in the heart and spine, and some people with the condition develop diabetes. The disorder does not affect thinking and reasoning abilities (cognitive functions).

Friedreichs ataxia is caused by a defect (mutation) in a gene labeled FXN. The disorder is recessive, meaning it occurs only in someone who inherits two defective copies of the gene, one from each parent. Although rare, Friedreichs ataxia is the most common form of hereditary ataxia, affecting about 1 in every 50,000 people in the United States. Both male and female children can inherit the disorder.

Symptoms typically begin between the ages of 5 and 15 years, although they sometimes appear in adulthood and on rare occasions as late as age 75. The first symptom to appear is usually gait ataxia, or difficulty walking. The ataxia gradually worsens and slowly spreads to the arms and the trunk. There is often loss of sensation in the extremities, which may spread to other parts of the body. Other features include loss of tendon reflexes, especially in the knees and ankles. Most people with Friedreich's ataxia develop scoliosis (a curving of the spine to one side), which often requires surgical intervention for treatment.

Dysarthria (slowness and slurring of speech) develops and can get progressively worse. Many individuals with later stages of Friedreichs ataxia develop hearing and vision loss.

Other symptoms that may occur include chest pain, shortness of breath, and heart palpitations. These symptoms are the result of various forms of heart disease that often accompany Friedreich's ataxia, such as hypertrophic cardiomyopathy (enlargement of the heart), myocardial fibrosis (formation of fiber-like material in the muscles of the heart), and cardiac failure. Heart rhythm abnormalities such as tachycardia (fast heart rate) and heart block (impaired conduction of cardiac impulses within the heart) are also common.

About 20 percent of people with Friedreich's ataxia develop carbohydrate intolerance and 10 percent develop diabetes. Most individuals with Friedreichs ataxia tire very easily and find that they require more rest and take a longer time to recover from common illnesses such as colds and flu.

The rate of progression varies from person to person. Generally, within 10 to 20 years after the appearance of the first symptoms, the person is confined to a wheelchair, and in later stages of the disease individuals may become completely incapacitated.

Friedreich's ataxia can shorten life expectancy, and heart disease is the most common cause of death. However, some people with less severe features of Friedreich's ataxia live into their sixties, seventies, or older.

A diagnosis of Friedreich's ataxia requires a careful clinical examination, which includes a medical history and a thorough physical exam, in particular looking for balance difficulty, loss of proprioception (joint sensation), absence of reflexes, and signs of neurological problems. Genetic testing now provides a conclusive diagnosis. Other tests that may aid in the diagnosis or management of the disorder include:

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Ataxia: Recessive – Neuromuscular Home Page

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Home, Search, Index, Links, Pathology, Molecules, Syndromes, Muscle, NMJ, Nerve, Spinal, Ataxia, Antibody & Biopsy, Patient Info

Myelinated nerve fibers in the retina

Types: Usually recessive 1: INPP5E; 9q34 2: TMEM216; 11q12 3: AHI1; 6q23 4: NPHP1; 2q13 5: CEP290; 12q21 6: TMEM67; 8q22 7: RPGRIP1L; 16q12 8: ARL13B; 3q11 9: CC2D2A; 4p15 10: OFD1 (CXORF5); Xp22 11: TTC21B; 2q24; Dominant 12: KIF7; 15q26 13: TCTN1; 12q24 14: TMEM237; 2q33 15: CEP41; 7q32 15A: TCTN2; 12q24 16: TMEM138; 11q12 17: c5orf42; 5p13 18: TCTN3; 10q24 19: ZNF423; 16q12 20: TMEM231; 16q23 21: CSPP1; 8q13 22: PDE6D; 2q37 Joubert: EXOC8; 1q42 COACH syndromes CC2D2A; 4p15 TMEM67; 8q22 Nephronophthisis ATXN10; 22q13.31

Molar Tooth Sign

Metabolic ataxias

References 1. Neurology 2001;56:849-855, Neurology 2003;60:12061208, Neurology 2004;62:818820, Neurology 2007;68:295-297 2. J Med Genet 2000;37:1-8, Pediatr Neurol 2003;28:335-341, J Neurol 2009;256 (Supp 1):3-8 3. Neurology 2000;54:1408-1414, Arch Neurol 2003;60:982-988 4. Am J Med Genet 2000;92:53-56 5. Med Genet 1999;36:759-766 6. Neurology. 2000;55:99-104. 7. Nature Genetics 2000;26:93-96 8. Am J Hum Genet 2000;67:1320-1326, Nature Genetics 2004; March 9. Am J Hum Genet 2001;68:501-508, Arch Neurol 2001;58:173-174, Hum Mol Genet 2004 Online March 10. Neurology 2001;57:1412-1414 11. Neurogenetics 2001;3:127-132 12. Neurology 2001;57:1043-1049 13. Heart 2002;87:346-349 14. Neurology 2001;57:127-130, Brain 2002;125:1760-1771, Am J Hum Genet 2003;72:869878 15. J Clin Endocrinol Metab, April 2002:87:16071612, Pediatr Neurol 2010;42:359-364, N Engl J Med 2013;368:1992-2003 16. Am J Ophthalmol 2002:133:410-413 17. Brain 2003;126 August, J Med Genet 2003;40:441446 18. Neurology 2003;61:274-275 19. Am J Hum Genet 2003; Online August 20. Nature Genet 2003; Online October 21. Brain 2006; On-line May 3, PLoS Biol 2012;10:e1001288 22. Nature Genet 2004; Online August 23. Nature Genet 2004; Online September 24. Nature Genet 2004; Online November 25. Neurology 2005;64:142144 26. Ann Neurol 2005;57:513519 27. Paediatr Anaesth 2005;15:433-434 28. Ann Neurol 2005 Jul 26 29. Hum Mol Genet 2005; Online Aug 30. Nature Genetics 2005; Online Nov 13 31. J Hum Genet 2006; Jul 11 32. Nat Genet 2006 Dec 10 33. Nat Genet 2007;39:534-539 34. Brain 2007; Online April Brain 2013; Online December 35. Neurology 2004;62:818-820 36. Nature Genetics 2007; Online June A; B 37. Am J Human Genet 2007; Online July 38. Am J Med Genet A 2008 Feb 1 39. Am J Human Genet 2008;82:623630, 2008;82:661672 40. Am J Med Genet Part A 143A:22562260 41. Am J Human Genet 2008; Online Aug 42. Nature Genet 2008; Online August 43. Nature Genet 2007;39:454-456 44. Nat Genet 2008 Aug 17 45. Am J Hum Genet 2008 Oct 22 46. American Journal of Human Genetics 2008; November 47. Hum Mutat 2008 Dec 4 48. American Journal of Medical Genetics 2009 Jan 21 49. Proc Natl Acad Sci U S A 2009 Mar 16, NEJM 2009;360:1960-1970 50. PLoS Genet 2009 May;5(5):e1000487 51. Nature Genet 2009; Online August 52. Semin Pediatr Neurol 2009;16:143154 53. American Journal of Human Genetics 2009; October 54. Am J Hum Genet 2009; Online Dec 55. Ann Neurol 2010;68:259-263 56. Neurogenetics 2010; Online July, Am J Human Genet 2011;89-415-423 57. Am J Hum Genet 2010; Online Nov 58. Nature Genetics 2011; On Line January 59. Am J Human Genetics 2011; Online May, Brain 2013 Feb 28 60. Am J Human Genetics 2011;89:320327 61. Cell 2011;145:513-528 62. Human Mutation 2011; Online November 63. Am J Human Genet 2011;89:713-730 64. Nature Genetics 2012: Online Jan 65. European Journal of Human Genetics 2012; On line Jan 66. Am J Human Genet 2012; Online March 67. Arch Neurol 2012; Online Mar 68. J Neurol 2012 May 26 69. Eur J Hum Genet 2012 Aug 15, Plos Genet 2012;8:e1002853 70. Am J Human Genet 2012; Online August 71. Nature Genetics 2012; Online September 72. J Child Neurology 2013; Online April 73. Cerebellum 2013; Online June 74. European Journal of Human Genetics 2013; Online July 75. Cerebellum 2013; Online October 76. Muscle Nerve 2013; Online October 77. PLoS One 2013 Dec 2;8(12):e81884, Hum Mol Genet 2013 Oct 16 78. Brain 2013; Online December 79. Neurology 2014;82: Online February 80. Nature Genetics 2014; Online March 81. Cerebellum 2014;13:79-88, Am J Human Genet 2014; Online August 82. J Neurol 2014;261:21922198 83. Am J Human Genet 2014; Online Nov 84. Am J Human Genet 2015; Online Feb 85. Brain 2015; Online March 86. Brain 2015 Jun 11

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Hormone replacement therapy (male-to-female) – Wikipedia …

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Hormone replacement therapy of the male-to-female type is a type of hormone replacement therapy for transgender and transsexual people. It changes the balance of sex hormones in the body. Some intersex people also receive HRT, either starting in childhood to confirm the assigned sex, or later, if this assignment has proven to be incorrect.

Its purpose is to cause the development of the secondary sex characteristics of the desired sex. It cannot undo many of the changes produced by the first natural occurring puberty, which may necessitate surgery and/or epilation (see below).

The requirements for hormone replacement therapy vary immensely, often psychological counseling is required.

Under WPATH guidelines the Mental Health Provider requires individuals to satisfy two sets of criteria eligibility and readiness to undertake any stage of transition including hormone replacement therapy. Eligibility involves the patient meeting requirements from a major diagnostic tool, such as the ICD-10, DSM-IV-R or the DSM-V. ICD-10 requirements are for either Transsexualism or Gender identity disorder of childhood.[1]

The ICD-10 criteria for Transsexualism include the individual having a transsexual identity of over 2 years, a strong and persistent desire to live as a member of the opposite sex, usually accompanied by the desire to make their body as congruent as possible with the preferred sex through surgery and hormone treatments. These individuals cannot be diagnosed with Transsexualism if it is believed to be a result of another mental disorder, or a genetic, intersex or chromosomal abnormality.

The ICD-10 criteria for Gender identity disorder of childhood in males include the individual being pre-pubescent and having intense and persistent distress about being a boy. The distress must be present for at least six months. The child must either:

The DSM-IV-R criteria for Gender Identity Disorder includes four main criteria. The DSM-IV-R also requests that the individual's sexuality is noted.

In children this may be demonstrated by them meeting four or more of the following criteria:

Adolescents and Adults must display a persistent desire to be the other sex, frequent passing as the other sex, desire to live or be treated as the other sex, or the conviction that they have the typical feelings and reactions of the other sex.

In boys this may manifest as an assertion that their penis or testes are disgusting or will disappear, or asserting that it is better not to have a penis.

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Causes Of Inflammation | Women to Women

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by Marcelle Pick, OB/GYN NP

Systemic or chronic inflammation has a domino effect that can seriously undermine your health. So how does it all begin?

Many experts now see inflammation as arising from an immune system response thats out of control. When you catch a cold or sprain your ankle, your immune system switches into gear. Infection or injury trigger a chain of events called the inflammatory cascade. The familiar signs of normal inflammation heat, pain, redness, and swelling are the first signals that your immune system is being called into action. In a delicate balance of give-and-take, inflammation begins when pro-inflammatory hormones in your body call out for your white blood cells to come and clear out infection and damaged tissue. These agents are matched by equally powerful, closely related anti-inflammatory compounds, which move in once the threat is neutralized to begin the healing process.

Acute inflammation that ebbs and flows as needed signifies a well-balanced immune system. But symptoms of inflammation that dont recede are telling you that the on switch to your immune system is stuck. Its poised on high alert even when you arent in imminent danger. In some cases, what started as a healthy mechanism, like building scar tissue or swelling, just wont shut off.

Are you walking around on simmer? Just yesterday I saw Nancy, a patient who has been with me for years. When she first came to see me, her triglycerides were sky-high (in the 400s!), her cholesterol was elevated, and she was overweight, unhappy and stressed. Her face was flushed and chapped, her lips were dry, and she seemed fluttery and agitated. On the surface she looked like a heart disease candidate, but when I probed deeper I saw a woman on fire from the inside out.

Currently there is no definitive test for inflammation the best that conventional medicine can do is measure blood levels of C-reactive protein (a pro-inflammatory marker) and the irritating amino acid called homocysteine. I use the high-sensitivity CRP test now available at most labs. Anything above 1 mg/dL with this test is too high in my book. With the older tests a reading of between 25 mg/dL was considered normal. (If youve been tested, be sure to ask your doctor for the results). Newer ways to assess risk early on for future inflammatory disease include markers such as the apolipoprotein B to A1 ratio (ApoB/ApoA-1). This and other tests are in experimental use and only available through a few labs.

When I first ran Nancys tests, I was surprised to see that her CRP levels were normal (this was before the high-sensitivity CRP test was widely available as it is today). This was good news for her heart, since elevated CRP and cholesterol increase your risk of heart disease threefold. But her homocysteine levels were high and all of her other symptoms pointed to inflammation. I prescribed an anti-inflammation diet, essential fatty acids, other anti-inflammatory supplements, and a daily exercise regime (for more information, read our article Reducing Inflammation The Natural Approach.) When Nancy next came in, her triglycerides were down by 200 points, her skin was clear, and her mood was much better. Later tests revealed her cholesterol had gone down, too.

A year went by, and as Nancy entered a stressful period in her life, she again began snacking on unhealthy food and going for days without exercise. Her cholesterol crept back up and she started having irritable bowel symptoms. After a brief pep talk, she got back on track and today shes feeling great. When I saw her yesterday she looked like a different person. Her blood tests all looked good and her inflammation was back under control. Nancys fires are well-tended now, and I feel confident she knows what to do if they start to flare up again.

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Causes Of Inflammation | Women to Women

Inflammation – Wikipedia, the free encyclopedia

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Inflammation (Latin, inflammatio) is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants.[1]

Inflammation is a protective response that involves immune cells, blood vessels, and molecular mediators. The purpose of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and to initiate tissue repair.

The classical signs of acute inflammation are pain, heat, redness, swelling, and loss of function. Inflammation is a generic response, and therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, which is specific for each pathogen.[2]

Inflammation is tightly regulated by the body. Too little inflammation could lead to progressive tissue destruction by the harmful stimulus (e.g. bacteria) and compromise the survival of the organism. In contrast, chronic inflammation may lead to a host of diseases, such as hay fever, periodontitis, atherosclerosis, rheumatoid arthritis, and even cancer (e.g., gallbladder carcinoma). Inflammation is therefore normally closely regulated by the body.

Inflammation can be classified as either acute or chronic. Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes (especially granulocytes) from the blood into the injured tissues. A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells present at the site of inflammation and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process.

Inflammation is not a synonym for infection. Infection describes the interaction between the action of microbial invasion and the reaction of the body's inflammatory defensive response the two components are considered together when discussing an infection, and the word is used to imply a microbial invasive cause for the observed inflammatory reaction. Inflammation on the other hand describes purely the body's immunovascular response, whatever the cause may be. But because of how often the two are correlated, words ending in the suffix -itis (which refers to inflammation) are sometimes informally described as referring to infection. For example, the word urethritis strictly means only "urethral inflammation", but clinical health care providers usually discuss urethritis as a urethral infection because urethral microbial invasion is the most common cause of urethritis.

It is useful to differentiate inflammation and infection as there are many pathological situations where inflammation is not driven by microbial invasion - for example, atherosclerosis, type III hypersensitivity, trauma, ischaemia. There are also pathological situations where microbial invasion does not result in classic inflammatory response -- for example, parasitosis, eosinophilia.

Physical:

Biological:

Chemical:

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Parkinson's Disease Information Page: National Institute …

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Parkinson's disease (PD) belongs to a group of conditions called motor system disorders, which are the result of the loss of dopamine-producing brain cells. The four primary symptoms of PD are tremor, or trembling in hands, arms, legs, jaw, and face; rigidity, or stiffness of the limbs and trunk; bradykinesia, or slowness of movement; and postural instability, or impaired balance and coordination. As these symptoms become more pronounced, patients may have difficulty walking, talking, or completing other simple tasks. PD usually affects people over the age of 60. Early symptoms of PD are subtle and occur gradually. In some people the disease progresses more quickly than in others. As the disease progresses, the shaking, or tremor, which affects the majority of people with PD may begin to interfere with daily activities. Other symptoms may include depression and other emotional changes; difficulty in swallowing, chewing, and speaking; urinary problems or constipation; skin problems; and sleep disruptions. There are currently no blood or laboratory tests that have been proven to help in diagnosing sporadic PD. Therefore the diagnosis is based on medical history and a neurological examination. The disease can be difficult to diagnose accurately. Doctors may sometimes request brain scans or laboratory tests in order to rule out other diseases.

At present, there is no cure for PD, but a variety of medications provide dramatic relief from the symptoms. Usually, affected individuals are given levodopa combined with carbidopa. Carbidopa delays the conversion of levodopa into dopamine until it reaches the brain. Nerve cells can use levodopa to make dopamine and replenish the brain's dwindling supply. Although levodopa helps at least three-quarters of parkinsonian cases, not all symptoms respond equally to the drug. Bradykinesia and rigidity respond best, while tremor may be only marginally reduced. Problems with balance and other symptoms may not be alleviated at all. Anticholinergics may help control tremor and rigidity. Other drugs, such as bromocriptine, pramipexole, and ropinirole, mimic the role of dopamine in the brain, causing the neurons to react as they would to dopamine. An antiviral drug, amantadine, also appears to reduce symptoms. In May 2006, the FDA approved rasagiline to be used along with levodopa for patients with advanced PD or as a single-drug treatment for early PD.

In some cases, surgery may be appropriate if the disease doesn't respond to drugs. A therapy called deep brain stimulation (DBS) has now been approved by the U.S. Food and Drug Administration. In DBS, electrodes are implanted into the brain and connected to a small electrical device called a pulse generator that can be externally programmed. DBS can reduce the need for levodopa and related drugs, which in turn decreases the involuntary movements called dyskinesias that are a common side effect of levodopa. It also helps to alleviate fluctuations of symptoms and to reduce tremors, slowness of movements, and gait problems. DBS requires careful programming of the stimulator device in order to work correctly.

PD is both chronic, meaning it persists over a long period of time, and progressive, meaning its symptoms grow worse over time. Although some people become severely disabled, others experience only minor motor disruptions. Tremor is the major symptom for some individuals, while for others tremor is only a minor complaint and other symptoms are more troublesome. It is currently not possible to predict which symptoms will affect an individual, and the intensity of the symptoms also varies from person to person.

The National Institute of Neurological Disorders and Stroke (NINDS) conducts PD research in laboratories at the National Institutes of Health (NIH) and also supports additional research through grants to major medical institutions across the country. Current research programs funded by the NINDS are using animal models to study how the disease progresses and to develop new drug therapies. Scientists looking for the cause of PD continue to search for possible environmental factors, such as toxins, that may trigger the disorder, and study genetic factors to determine how defective genes play a role. Other scientists are working to develop new protective drugs that can delay, prevent, or reverse the disease.

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Menopause – Wikipedia, the free encyclopedia

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Menopause, also known as the climacteric, is the time in most women's lives when menstrual periods stop permanently, and she is no longer able to have children.[1][2] Menopause typically occurs between 45 and 55 years of age.[1] Medical professionals often define menopause as having occurred when a woman has not had any vaginal bleeding for a year.[3] It may also be defined by a decrease in hormone production by the ovaries.[4] In those who have had surgery to remove the uterus but still have ovaries, menopause may be viewed to have occurred at the time of the surgery or when hormone levels fall.[4] Following the removal of the uterus, symptoms typically occurs earlier, at an average of 45 years of age.[5]

Before menopause, a woman's periods typically become irregular, which means that periods may be longer or shorter in duration, or be lighter or heavier in terms of the amount of flow. During this time, women often experience hot flashes; these typically last from 30 seconds to ten minutes, and may be associated with shivering, sweating and reddening of the skin.[6] Hot flashes often stop occurring after a year or two.[2] Other symptoms may include vaginal dryness, trouble sleeping, and mood changes.[6] The severity of symptoms varies between women.[2] While menopause is often thought to be linked to an increase in heart disease, this primarily occurs due to increasing age and does not have a direct relationship with menopause. In some women, problems that were previously present like endometriosis or painful periods will improve after menopause.[2]

Menopause is usually a natural change.[7] It can occur earlier in those who smoke tobacco.[3][8] Other causes include surgery that removes both ovaries or some types of chemotherapy.[3] At the physiological level, menopause happens because of a decrease in the ovaries' production of the hormones estrogen and progesterone.[1] While typically not needed, a diagnosis of menopause can be confirmed by measuring hormone levels in either the blood or urine.[9] Menopause is the opposite of menarche, the time at which a girl's periods start.[10]

Specific treatment is not usually needed. Some symptoms, however, may be improved with treatment. With respect to hot flashes, avoiding smoking, caffeine, and alcohol is often recommended. Sleeping in a cool room and using a fan may also help.[11] The following medications may help: menopausal hormone therapy (MHT), clonidine, gabapentin, or selective serotonin reuptake inhibitors.[11][12] Exercise may help with sleeping problems. While MHT was once routinely prescribed, it is now only recommended in those with significant symptoms, as there are concerns about side effects.[11] High-quality evidence for the effectiveness of alternative medicine has not been found.[2]

During early menopause transition, the menstrual cycles remain regular but the interval between cycles begins to lengthen. Hormone levels begin to fluctuate. Ovulation may not occur with each cycle.[13]

The date of the final menstrual period is usually taken as the point in time when menopause has occurred.[13] During menopausal transition and after menopause, women can experience a wide range of symptoms.

Menstrual patterns can show shorter cycling (by 27 days);[13] longer cycles remain possible;[13]irregular bleeding (lighter, heavier, spotting).[13]

Physical symptoms include: lack of energy, joint soreness, stiffness,[13]back pain,[13] breast enlargement,[13]breast pain,[13]heart palpitations,[13]headache,[13]dizziness,[13]dry, itchy skin,[13] thinning, tingling skin, weight gain,[13]urinary incontinence,[13][14]urinary urgency,[13] interrupted sleeping patterns,[13][15][16][17] heavy night sweats,[13]hot flashes.[13]

Psychological symptoms include: anxiety,[18]poor memory,[13] inability to concentrate,[13] depressive mood,[13][18]irritability,[13]mood swings.[13]

Sexual changes include: painful intercourse,[13] vaginal dryness,[13] less interest in sexual activity.[13]

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Hypopituitarism – Wikipedia, the free encyclopedia

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Hypopituitarism is the decreased (hypo) secretion of one or more of the eight hormones normally produced by the pituitary gland at the base of the brain.[1][2] If there is decreased secretion of most pituitary hormones, the term panhypopituitarism (pan meaning "all") is used.[3]

The signs and symptoms of hypopituitarism vary, depending on which hormones are undersecreted and on the underlying cause of the abnormality. The diagnosis of hypopituitarism is made by blood tests, but often specific scans and other investigations are needed to find the underlying cause, such as tumors of the pituitary, and the ideal treatment. Most hormones controlled by the secretions of the pituitary can be replaced by tablets or injections. Hypopituitarism is a rare disease, but may be significantly underdiagnosed in people with previous traumatic brain injury.[1] The first description of the condition was made in 1914 by the German physician Dr Morris Simmonds.[4]

The hormones of the pituitary have different actions in the body, and the symptoms of hypopituitarism therefore depend on which hormone is deficient. The symptoms may be subtle and are often initially attributed to other causes.[1][5] In most of the cases, three or more hormones are deficient.[6] The most common problem is insufficiency of follicle-stimulating hormone (FSH) and/or luteinizing hormone (LH) leading to sex hormone abnormalities. Growth hormone deficiency is more common in people with an underlying tumor than those with other causes.[1][6]

Sometimes, there are additional symptoms that arise from the underlying cause; for instance, if the hypopituitarism is due to a growth hormone-producing tumor, there may be symptoms of acromegaly (enlargement of the hands and feet, coarse facial features), and if the tumor extends to the optic nerve or optic chiasm, there may be visual field defects. Headaches may also accompany pituitary tumors,[1] as well as pituitary apoplexy (infarction or hemorrhage of a pituitary tumor) and lymphocytic hypophysitis (autoimmune inflammation of the pituitary).[7] Apoplexy, in addition to sudden headaches and rapidly worsening visual loss, may also be associated with double vision that results from compression of the nerves in the adjacent cavernous sinus that control the eye muscles.[8]

Pituitary failure results in many changes in the skin, hair and nails as a result of the absence of pituitary hormone action on these sites.[9]

Deficiency of all anterior pituitary hormones is more common than individual hormone deficiency.

Deficiency of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), together referred to as the gonadotropins, leads to different symptoms in men and women. Women experience oligo- or amenorrhea (infrequent/light or absent menstrual periods respectively) and infertility. Men lose facial, scrotal and trunk hair, as well as suffering decreased muscle mass and anemia. Both sexes may experience a decrease in libido and loss of sexual function, and have an increased risk of osteoporosis (bone fragility). Lack of LH/FSH in children is associated with delayed puberty.[1][5]

Growth hormone (GH) deficiency leads to a decrease in muscle mass, central obesity (increase in body fat around the waist) and impaired attention and memory. Children experience growth retardation and short stature.[1][5]

Adrenocorticotropic hormone (ACTH) deficiency leads to adrenal insufficiency, a lack of production of glucocorticoids such as cortisol by the adrenal gland. If the problem is chronic, symptoms consist of fatigue, weight loss, failure to thrive (in children), delayed puberty (in adolescents), hypoglycemia (low blood sugar levels), anemia and hyponatremia (low sodium levels). If the onset is abrupt, collapse, shock and vomiting may occur.[1][5] ACTH deficiency is highly similar to primary Addison's disease, which is cortisol deficiency as the result of direct damage to the adrenal glands; the latter form, however, often leads to hyperpigmentation of the skin, which does not occur in ACTH deficiency.[10]

Thyroid-stimulating hormone (TSH) deficiency leads to hypothyroidism (lack of production of thyroxine (T4) and triiodothyronine (T3) in the thyroid). Typical symptoms are tiredness, intolerance to cold, constipation, weight gain, hair loss and slowed thinking, as well as a slowed heart rate and low blood pressure. In children, hypothyroidism leads to delayed growth and in extreme inborn forms to a syndrome called cretinism.[1][5]

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What is Hypothyroidism – American Thyroid Association | ATA

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What is the thyroid gland?

The thyroid gland is a butterfly-shaped endocrine gland that is normally located in the lower front of the neck. The thyroids job is to make thyroid hormones, which are secreted into the blood and then carried to every tissue in the body. Thyroid hormone helps the body use energy, stay warm and keep the brain, heart, muscles, and other organs working as they should.

Hypothyroidism is an underactive thyroid gland. Hypothyroidism means that the thyroid gland cant make enough thyroid hormone to keep the body running normally. People are hypothyroid if they have too little thyroid hormone in the blood. Common causes are autoimmune disease, surgical removal of the thyroid, and radiation treatment.

When thyroid hormone levels are too low, the bodys cells cant get enough thyroid hormone and the bodys processes start slowing down. As the body slows, you may notice that you feel colder, you tire more easily, your skin is getting drier, youre becoming forgetful and depressed, and youve started getting constipated. Because the symptoms are so variable and non-specific, the only way to know for sure whether you have hypothyroidism is with a simple blood test for TSH.

KEEPING OTHER PEOPLE INFORMED

Tell your family members. Because thyroid disease runs in families, you should explain your hypothyroidism to your relatives and encourage them to get regular TSH tests. Tell your other doctors and your pharmacist about your hypothyroidism and the drug and dose with which it is being treated. If you start seeing a new doctor, tell the doctor that you have hypothyroidism and you need your TSH tested every year. If you are seeing an endocrinologist, ask that copies of your reports be sent to your primary care doctor.

WHAT CAN YOU EXPECT OVER THE LONG TERM?

There is no cure for hypothyroidism, and most patients have it for life. There are exceptions: many patients with viral thyroiditis have their thyroid function return to normal, as do some patients with thyroiditis after pregnancy.

Hypothyroidism may become more or less severe, and your dose of thyroxine may need to change over time. You have to make a lifetime commitment to treatment. But if you take your pills every day and work with your doctor to get and keep your thyroxine dose right, you should be able to keep your hypothyroidism completely controlled throughout your life. Your symptoms should disappear and the serious effects of low thyroid hormone should stop getting worse and should actually improve. If you keep your hypothyroidism well-controlled, it will not shorten your life span.

There can be many reasons why the cells in the thyroid gland cant make enough thyroid hormone. Here are the major causes, from the most to the least common.

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Hypothyroidism – Wikipedia, the free encyclopedia

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Hypothyroidism (//; from hypo- meaning under or reduced, plus thyroid), often called underactive thyroid or low thyroid and sometimes hypothyreosis, is a common endocrine disorder in which the thyroid gland does not produce enough thyroid hormone. It can cause a number of symptoms, such as tiredness, poor ability to tolerate cold, and weight gain. In children, hypothyroidism leads to delays in growth and intellectual development, which is called cretinism in severe cases. The diagnosis of hypothyroidism, when suspected, can be confirmed with blood tests measuring thyroid-stimulating hormone (TSH) and thyroxine levels.

Worldwide, too little iodine in the diet is the most common cause of hypothyroidism. In countries with enough dietary iodine, the most common cause of hypothyroidism is the autoimmune condition Hashimoto's thyroiditis. Less common causes include the following: previous treatment with radioactive iodine, injury to the hypothalamus or the anterior pituitary gland, certain medications, a lack of a functioning thyroid at birth, or previous thyroid surgery.

Hypothyroidism can be treated with manufactured levothyroxine; the dose is adjusted according to symptoms and normalization of the thyroxine and TSH levels. In Western countries, hypothyroidism occurs in 0.30.4% while subclinical hypothyroidism, a milder form of hypothyroidism characterized by normal thyroxine levels and an elevated TSH level, is thought to occur in 4.38.5%. Dogs are also known to develop hypothyroidism and in rare circumstances cats and horses can also have the disorder.

People with hypothyroidism often have no or only mild symptoms. Numerous symptoms and signs are associated with hypothyroidism, and can be related to the underlying cause, or a direct effect of having not enough thyroid hormones.[1][2] Hashimoto's thyroiditis may present with the mass effect of a goiter (enlarged thyroid gland).[1]

Delayed relaxation after testing the ankle jerk reflex is a characteristic sign in hypothyroidism and is associated with the severity of the hormone deficit.[4]

Man with myxedema or severe hypothyroidism showing an expressionless face, puffiness around the eyes and pallor

Additional finding include swelling of the arms and legs and significant ascites.

Myxedema coma is a rare but life-threatening state of extreme hypothyroidism. It may occur in those who are known to have hypothyroidism when they develop another illness, but it can be the first presentation of hypothyroidism. The illness is characterized by very low body temperature without shivering, confusion, a slow heart rate and reduced breathing effort. There may be physical signs suggestive of hypothyroidism, such as skin changes or enlargement of the tongue.[5]

Even mild or subclinical hypothyroidism has been associated with impaired fertility and an increased risk of miscarriage.[6] Hypothyroidism in early pregnancy, even with limited or no symptoms, may increase the risk of pre-eclampsia, offspring with lower intelligence, and the risk of infant death around the time of birth.[6][7]Women are affected by hypothyroidism in 0.30.5% of pregnancies.[7] Subclinical hypothyroidism during pregnancy has also been associated with gestational diabetes and birth of the baby before 37 weeks of pregnancy.[8]

Newborn children with hypothyroidism may have normal birth weight and height (although the head may be larger than expected and the posterior fontanelle may be open). Some may have drowsiness, decreased muscle tone, a hoarse-sounding cry, feeding difficulties, constipation, an enlarged tongue, umbilical hernia, dry skin, a decreased body temperature and jaundice.[9] A goiter is rare, although it may develop later in children who have a thyroid gland that does not produce functioning thyroid hormone.[9] A goiter may also develop in children growing up in areas with iodine deficiency.[10] Normal growth and development may be delayed, and not treating infants may lead to an intellectual impairment (IQ 615 points lower in severe cases). Other problems include the following: large scale and fine motor skills and coordination, reduced muscle tone, squinting, decreased attention span, and delayed speaking.[9]Tooth eruption may be delayed.[11]

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Hypothyroidism: Symptoms and Treatments of Hypothyroid …

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Hypothyroidism is a condition in which the body lacks sufficient thyroid hormone. Since the main purpose of thyroid hormone is to "run the body's metabolism," it is understandable that people with this condition will have symptoms associated with a slow metabolism. The estimates vary, but approximately 10 million Americans have this common medical condition. In fact, as many as 10% of women may have some degree of thyroid hormone deficiency. Hypothyroidism is more common than you would believe, and millions of people are currently hypothyroid and don't know it. For an overview of how thyroid hormone is produced and how its production is regulated, check out our thyroid hormone production page.

There are two fairly common causes of hypothyroidism. The first is a result of previous (or currently ongoing) inflammation of the thyroid gland, which leaves a large percentage of the cells of the thyroid damaged (or dead) and incapable of producing sufficient hormone. The most common cause of thyroid gland failure is called autoimmune thyroiditis (also called Hashimoto's thyroiditis), a form of thyroid inflammation caused by the patient's own immune system.

The second major cause is the broad category of "medical treatments." The treatment of many thyroid conditions warrants surgical removal of a portion or all of the thyroid gland. If the total mass of thyroid producing cells left within the body are not enough to meet the needs of the body, the patient will develop hypothyroidism. Remember, this is often the goal of the surgery for thyroid cancer.

But at other times, the surgery will be to remove a worrisome nodule, leaving half of the thyroid in the neck undisturbed. Sometimes, this remaining thyroid lobe and isthmus will produce enough hormone to meet the demands of the body. For other patients, however, it may become apparent years later that the remaining thyroid just can't quite keep up with demand.

Similarly, goiters and some other thyroid conditions can be treated with radioactive iodine therapy. The aim of the radioactive iodine therapy (for benign conditions) is to kill a portion of the thyroid to prevent goiters from growing larger or producing too much hormone (hyperthyroidism).

Occasionally, the result of radioactive iodine treatment will be that too many cells are damaged so the patient often becomes hypothyroid within a year or two. However, this is usually greatly preferred over the original problem.

There are several other rare causes of hypothyroidism, one of them being a completely "normal" thyroid gland that is not making enough hormone because of a problem in the pituitary gland. If the pituitary does not produce enough thyroid stimulating hormone (TSH) then the thyroid simply does not have the "signal" to make hormone. So it doesn't.

Each individual patient may have any number of these symptoms, and they will vary with the severity of the thyroid hormone deficiency and the length of time the body has been deprived of the proper amount of hormone.

You may have one of these symptoms as your main complaint, while another will not have that problem at all and will be suffering from an entirely different symptom. Most people will have a combination of these symptoms. Occasionally, some patients with hypothyroidism have no symptoms at all, or they are just so subtle that they go unnoticed.

If you have these symptoms, you need to discuss them with your doctor. Additionally, you may need to seek the skills of an endocrinologist. If you have already been diagnosed and treated for hypothyroidism and continue to have any or all of these symptoms, you need to discuss it with your physician.

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Hypogonadism – Wikipedia, the free encyclopedia

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Hypogonadism is a medical term which describes a diminished functional activity of the gonads the testes and ovaries in males and females, respectively that may result in diminished sex hormone biosynthesis. In layman's terms, it is sometimes called "interrupted stage 1 puberty". Low androgen (e.g., testosterone) levels are referred to as hypoandrogenism and low estrogen (e.g., estradiol) as hypoestrogenism, and may occur as symptoms of hypogonadism in both sexes, but are generally only diagnosed in males and females respectively. Other hormones produced by the gonads which may be decreased by hypogonadism include progesterone, DHEA, anti-Mllerian hormone, activin, and inhibin. Spermatogenesis and ovulation in males and females, respectively, may be impaired by hypogonadism, which, depending on the degree of severity, may result in partial or complete infertility.

Deficiency of sex hormones can result in defective primary or secondary sexual development, or withdrawal effects (e.g., premature menopause) in adults. Defective egg or sperm development results in infertility. The term hypogonadism is usually applied to permanent rather than transient or reversible defects, and usually implies deficiency of reproductive hormones, with or without fertility defects. The term is less commonly used for infertility without hormone deficiency. There are many possible types of hypogonadism and several ways to categorize them. Hypogonadism is also categorized by endocrinologists by the level of the reproductive system that is defective. Physicians measure gonadotropins (LH and FSH) to distinguish primary from secondary hypogonadism. In primary hypogonadism the LH and/or FSH are usually elevated, meaning the problem is in the testicles, whereas in secondary hypogonadism, both are normal or low, suggesting the problem is in the brain.

Hypogonadism can involve just hormone production or just fertility, but most commonly involves both.

Women with hypogonadism will not begin menstruating and it may affect their height and breast development. Onset in women after puberty causes cessation of menstruation, lowered libido, loss of body hair and hot flashes. In boys it causes impaired muscle and beard development and reduced height. In men it can cause reduced body hair and beard, enlarged breasts, loss of muscle, and sexual difficulties. A brain tumor (central hypogonadism) may involve headaches, impaired vision, milky discharge from the breast and symptoms caused by other hormone problems.[2]

The symptoms of hypogonadotrophic hypogonadism, a subtype of hypogonadism, include late, incomplete or lack of development at puberty, and sometimes short stature or the inability to smell; in females, a lack of breasts and menstrual periods, and in males a lack of sexual development, e.g., facial hair, penis and testes enlargement, deepening voice.

Low testosterone can be identified through a simple blood test performed by a laboratory, ordered by a physician. This test is typically ordered in the morning hours, when levels are highest, as levels can drop by as much as 13% during the day.[3]

Normal total testosterone levels range from 3001000ng/dL (nanograms per decilitre)[4]

Treatment is often prescribed for total testosterone levels below 350ng/dL.[5] If the serum total testosterone level is between 230 and 350ng/dL, repeating the measurement of total testosterone with sex hormone-binding globulin (SHBG) to calculate free testosterone or free testosterone by equilibrium dialysis may be helpful.

Treatment may be necessary even if the patient's total testosterone level is within the "normal" range. The standard range given is based off widely varying ages and, given that testosterone levels naturally decrease as humans age, age-group specific averages should be taken into consideration when discussing treatment between doctor and patient.[6] A twenty-seven-year-old male with a testosterone level of 380ng/dL would be in the "normal" range, but would likely have low testosterone to blame if he experiences some or many of the above symptoms. This score would put him in the bottom 5% of his age-group, but would be a more common score for a man who is 80+ years old.[6] Although, this doesn't automatically mean that a young man with 380ng/dL has the same amount of testosterone of an 80+ year old, since there is usually a big difference in SHBG levels in the bloodstream between young and elderly, resulting in a much higher free testosterone level in the young. In fact, some people with low SHBG and low-normal testosterone experience no symptoms of hypogonadism.

A downturn in the circulation of testosterone should cause the hypothalamus and pituitary gland to trigger a release of brain hormones that stimulate the testicles to ramp up production of testosterone. The specific brain hormones include gonadotropin releasing hormone (abbreviated GnRH), which is released by the hypothalamus, and luteinizing hormone (abbreviated LH), released by the pituitary. They act to control the production of testosterone in synchrony. This response system in the body is a negative feedback loop. When this loop is functioning at its best, the body gets enough testosterone to bind to receptors on the various organs that require it. In the bodies of men as they hit their thirties and forties, testosterone falls approximately 1 to 3 percent each year.[7]

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Andropause: Dealing With Male Menopause – HowStuffWorks

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Most people know that women experience menopause, but did you know that some men go through a kind of male menopause? For men who believe they are going through the proverbial midlife crisis, some doctors and researchers say you may actually be experiencing a form of male menopause called "andropause."

Shocking as it may be to some men, male menopause, or andropause, is becoming more widely recognized and accepted by physicians for the changes many middle-aged men experience from energy loss to depression to loss of libido to sexual dysfunction. And some clinicians are recommending that certain men experiencing these symptoms, along with a host of others such as decreased bone density and weight gain, seek hormone replacement therapy and other treatments.

"It's like puberty in reverse," Jed Diamond, a California psychotherapist and author of "Male Menopause" and the forthcoming book, "Surviving Male Menopause", says of andropause. Like puberty, the changes that andropause wreaks in aging men, Diamond says, are "hormonal, psychological, interpersonal, social, sexual and spiritual."

Andropause is characterized by a loss of testosterone the hormone that makes men men. Most men see testosterone levels drop as they age. However, some men are impacted more than others are. Diamond says that as many as 25 million American males between ages 40 and 55 are experiencing some degree of male menopause today.

"Male andropause can be very insidious," explains Dr. Stephen Sinatra, a Manchester, Conn., cardiologist board certified in anti-aging medicine. The loss of testosterone, which can happen to men as young as 35, is gradual, with testosterone levels dropping just 1 percent to 1.5 percent annually. Unlike the precipitous loss of estrogen that women hitting menopause face, the gradual loss of testosterone may take years to exact its mark on men with a host of symptoms not unlike changes menopausal women experience.

Irritability, fatigue, depression, reduced libido and erection problems are hallmark signs of andropause. "I felt like I didn't want to move," says Cecil Dorsey of Vernon, Conn. The 68-year-old retired truck driver, who discovered via a blood test nearly four years ago that his testosterone levels dropped, said, "I just didn't want to be bothered by anything."

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