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Muscular dystrophy – Diagnosis and treatment – Mayo Clinic

Posted: December 16, 2017 at 7:43 pm


Your doctor is likely to start with a medical history and physical examination.

After that, your doctor may recommend:

There’s no cure for any form of muscular dystrophy. But treatment can help prevent or reduce problems in the joints and spine to allow people with muscular dystrophy to remain mobile as long as possible. Treatment options include medications, physical therapy, and surgical and other procedures.

Your doctor may recommend:

Several types of therapy and assistive devices can improve quality and sometimes length of life in people who have muscular dystrophy. Examples include:

Surgery may be needed to correct a spinal curvature that could eventually make breathing more difficult.

Explore Mayo Clinic studies testing new treatments, interventions and tests as a means to prevent, detect, treat or manage this disease.

Respiratory infections may become a problem in later stages of muscular dystrophy. It’s important to be vaccinated for pneumonia and to keep up to date with influenza shots.

Dietary changes haven’t been shown to slow the progression of muscular dystrophy. But proper nutrition is essential because limited mobility can contribute to obesity, dehydration and constipation. A high-fiber, high-protein, low-calorie diet may help.

A diagnosis of muscular dystrophy can be extremely challenging. To help you cope:

You may be referred to a doctor who specializes in the diagnosis and treatment of muscular dystrophy.

Don’t hesitate to ask other questions during your appointment.

Your doctor is likely to ask you a number of questions. Being ready to answer them may make time to go over points you want to spend more time on. You may be asked:

Nov. 27, 2014

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Muscular dystrophy – Diagnosis and treatment – Mayo Clinic

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Duchenne & Becker muscular dystrophy – causes, symptoms …

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What are Duchenne and Becker muscular dystrophy? Muscular dystrophy is where the muscles weaken and lose muscle mass; in this case, both Duchenne and Becker muscular dystrophy are caused by a genetic mutation in the dystrophin gene. Subscribe – More videos – Support us on Patreon –

This video covers the pathophysiology of both, as well as clinical signs and symptoms, and diagnosis, and management.

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Sources:Sarkozy A, Bushby K, Mercuri E. Muscular Dystrophies. In: Emery and Rimoin’s Principles and Practice of Medical Genetics (Sixth Edition); 2013.Darras BT, Miller DT, Urion DK. Dystrophinopathies. GeneReviews.…Robbins and Cotran Pathologic Basis of Disease. 1336-1338.

Credits:Audio/visuals: Tanner Marshall, MSScript: Philip M. Boone, MD, PhDReviewer: Rishi Desai, MD, MPH

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Hypothalamus – Wikipedia

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The hypothalamus (from Greek , “under” and , thalamus) is a portion of the brain that contains a number of small nuclei with a variety of functions. One of the most important functions of the hypothalamus is to link the nervous system to the endocrine system via the pituitary gland (hypophysis).

The hypothalamus is located below the thalamus and is part of the limbic system.[1] In the terminology of neuroanatomy, it forms the ventral part of the diencephalon. All vertebrate brains contain a hypothalamus. In humans, it is the size of an almond.

The hypothalamus is responsible for the regulation of certain metabolic processes and other activities of the autonomic nervous system. It synthesizes and secretes certain neurohormones, called releasing hormones or hypothalamic hormones, and these in turn stimulate or inhibit the secretion of pituitary hormones. The hypothalamus controls body temperature, hunger, important aspects of parenting and attachment behaviours, thirst,[2]fatigue, sleep, and circadian rhythms.

The hypothalamus is a brain structure made up of distinct nuclei as well as less anatomically distinct areas. It is found in all vertebrate nervous systems. In mammals, magnocellular neurosecretory cells in the paraventricular nucleus and the supraoptic nucleus of the hypothalamus produce neurohypophysial hormones, oxytocin and vasopressin. These hormones are released into the blood in the posterior pituitary.[3] Much smaller parvocellular neurosecretory cells, neurons of the paraventricular nucleus, release corticotropin-releasing hormone and other hormones into the hypophyseal portal system, where these hormones diffuse to the anterior pituitary.

The hypothalamic nuclei include the following:[4][5][6]

See also: ventrolateral preoptic nucleus, periventricular nucleus.

A cross section of the monkey hypothalamus displays 2 of the major hypothalamic nuclei on either side of the fluid-filled 3rd ventricle.

Hypothalamic nuclei on one side of the hypothalamus, shown in a 3-D computer reconstruction[10]

The hypothalamus is highly interconnected with other parts of the central nervous system, in particular the brainstem and its reticular formation. As part of the limbic system, it has connections to other limbic structures including the amygdala and septum, and is also connected with areas of the autonomous nervous system.

The hypothalamus receives many inputs from the brainstem, the most notable from the nucleus of the solitary tract, the locus coeruleus, and the ventrolateral medulla.

Most nerve fibres within the hypothalamus run in two ways (bidirectional).

Several hypothalamic nuclei are sexually dimorphic; i.e., there are clear differences in both structure and function between males and females.[citation needed]

Some differences are apparent even in gross neuroanatomy: most notable is the sexually dimorphic nucleus within the preoptic area. However most of the differences are subtle changes in the connectivity and chemical sensitivity of particular sets of neurons.[citation needed]

The importance of these changes can be recognized by functional differences between males and females. For instance, males of most species prefer the odor and appearance of females over males, which is instrumental in stimulating male sexual behavior. If the sexually dimorphic nucleus is lesioned, this preference for females by males diminishes. Also, the pattern of secretion of growth hormone is sexually dimorphic, and this is one reason why in many species, adult males are much larger than females.[citation needed]

Other striking functional dimorphisms are in the behavioral responses to ovarian steroids of the adult. Males and females respond to ovarian steroids in different ways, partly because the expression of estrogen-sensitive neurons in the hypothalamus is sexually dimorphic; i.e., estrogen receptors are expressed in different sets of neurons.[citation needed]

Estrogen and progesterone can influence gene expression in particular neurons or induce changes in cell membrane potential and kinase activation, leading to diverse non-genomic cellular functions. Estrogen and progesterone bind to their cognate nuclear hormone receptors, which translocate to the cell nucleus and interact with regions of DNA known as hormone response elements (HREs) or get tethered to another transcription factor’s binding site. Estrogen receptor (ER) has been shown to transactivate other transcription factors in this manner, despite the absence of an estrogen response element (ERE) in the proximal promoter region of the gene. In general, ERs and progesterone receptors (PRs) are gene activators, with increased mRNA and subsequent protein synthesis following hormone exposure.[citation needed]

Male and female brains differ in the distribution of estrogen receptors, and this difference is an irreversible consequence of neonatal steroid exposure. Estrogen receptors (and progesterone receptors) are found mainly in neurons in the anterior and mediobasal hypothalamus, notably:[citation needed]

In neonatal life, gonadal steroids influence the development of the neuroendocrine hypothalamus. For instance, they determine the ability of females to exhibit a normal reproductive cycle, and of males and females to display appropriate reproductive behaviors in adult life.[citation needed]

In primates, the developmental influence of androgens is less clear, and the consequences are less understood. Within the brain, testosterone is aromatized to (estradiol), which is the principal active hormone for developmental influences. The human testis secretes high levels of testosterone from about week 8 of fetal life until 56 months after birth (a similar perinatal surge in testosterone is observed in many species), a process that appears to underlie the male phenotype. Estrogen from the maternal circulation is relatively ineffective, partly because of the high circulating levels of steroid-binding proteins in pregnancy.[citation needed]

Sex steroids are not the only important influences upon hypothalamic development; in particular, pre-pubertal stress in early life (of rats) determines the capacity of the adult hypothalamus to respond to an acute stressor.[11] Unlike gonadal steroid receptors, glucocorticoid receptors are very widespread throughout the brain; in the paraventricular nucleus, they mediate negative feedback control of CRF synthesis and secretion, but elsewhere their role is not well understood.

The hypothalamus has a central neuroendocrine function, most notably by its control of the anterior pituitary, which in turn regulates various endocrine glands and organs. Releasing hormones (also called releasing factors) are produced in hypothalamic nuclei then transported along axons to either the median eminence or the posterior pituitary, where they are stored and released as needed.[12]

In the hypothalamicadenohypophyseal axis, releasing hormones, also known as hypophysiotropic or hypothalamic hormones, are released from the median eminence, a prolongation of the hypothalamus, into the hypophyseal portal system, which carries them to the anterior pituitary where they exert their regulatory functions on the secretion of adenohypophyseal hormones.[13] These hypophysiotropic hormones are stimulated by parvocellular neurosecretory cells located in the periventricular area of the hypothalamus. After their release into the capillaries of the third ventricle, the hypophysiotropic hormones travel through what is known as the hypothalamo-pituitary portal circulation. Once they reach their destination in the anterior pituitary, these hormones bind to specific receptors located on the surface of pituitary cells. Depending on which cells are activated through this binding, the pituitary will either begin secreting or stop secreting hormones into the rest of the bloodstream. (Bear, Mark F. “Hypothalamic Control of the Anterior Pituitary.” Neuroscience: Exploring the Brain. 4th ed. Philadelphia: Wolters Kluwer, 2016. 528. Print.)

Other hormones secreted from the median eminence include vasopressin, oxytocin, and neurotensin.[15][16][17][18]

In the hypothalamic-neurohypophyseal axis, neurohypophysial hormones are released from the posterior pituitary, which is actually a prolongation of the hypothalamus, into the circulation.

It is also known that hypothalamic-pituitary-adrenal axis (HPA) hormones are related to certain skin diseases and skin homeostasis. There is evidence linking hyperactivity of HPA hormones to stress-related skin diseases and skin tumors.[19]

The hypothalamus coordinates many hormonal and behavioural circadian rhythms, complex patterns of neuroendocrine outputs, complex homeostatic mechanisms, and important behaviours. The hypothalamus must, therefore, respond to many different signals, some of which generated externally and some internally. Delta wave signalling arising either in the thalamus or in the cortex influences the secretion of releasing hormones; GHRH and prolactin are stimulated whilst TRH is inhibited.

The hypothalamus is responsive to:

Olfactory stimuli are important for sexual reproduction and neuroendocrine function in many species. For instance if a pregnant mouse is exposed to the urine of a ‘strange’ male during a critical period after coitus then the pregnancy fails (the Bruce effect). Thus, during coitus, a female mouse forms a precise ‘olfactory memory’ of her partner that persists for several days. Pheromonal cues aid synchronization of oestrus in many species; in women, synchronized menstruation may also arise from pheromonal cues, although the role of pheromones in humans is disputed.

Peptide hormones have important influences upon the hypothalamus, and to do so they must pass through the bloodbrain barrier. The hypothalamus is bounded in part by specialized brain regions that lack an effective bloodbrain barrier; the capillary endothelium at these sites is fenestrated to allow free passage of even large proteins and other molecules. Some of these sites are the sites of neurosecretion – the neurohypophysis and the median eminence. However, others are sites at which the brain samples the composition of the blood. Two of these sites, the SFO (subfornical organ) and the OVLT (organum vasculosum of the lamina terminalis) are so-called circumventricular organs, where neurons are in intimate contact with both blood and CSF. These structures are densely vascularized, and contain osmoreceptive and sodium-receptive neurons that control drinking, vasopressin release, sodium excretion, and sodium appetite. They also contain neurons with receptors for angiotensin, atrial natriuretic factor, endothelin and relaxin, each of which important in the regulation of fluid and electrolyte balance. Neurons in the OVLT and SFO project to the supraoptic nucleus and paraventricular nucleus, and also to preoptic hypothalamic areas. The circumventricular organs may also be the site of action of interleukins to elicit both fever and ACTH secretion, via effects on paraventricular neurons.[citation needed]

It is not clear how all peptides that influence hypothalamic activity gain the necessary access. In the case of prolactin and leptin, there is evidence of active uptake at the choroid plexus from the blood into the cerebrospinal fluid (CSF). Some pituitary hormones have a negative feedback influence upon hypothalamic secretion; for example, growth hormone feeds back on the hypothalamus, but how it enters the brain is not clear. There is also evidence for central actions of prolactin.[citation needed]

Findings have suggested that thyroid hormone (T4) is taken up by the hypothalamic glial cells in the infundibular nucleus/ median eminence, and that it is here converted into T3 by the type 2 deiodinase (D2). Subsequent to this, T3 is transported into the thyrotropin-releasing hormone (TRH)-producing neurons in the paraventricular nucleus. Thyroid hormone receptors have been found in these neurons, indicating that they are indeed sensitive to T3 stimuli. In addition, these neurons expressed MCT8, a thyroid hormone transporter, supporting the theory that T3 is transported into them. T3 could then bind to the thyroid hormone receptor in these neurons and affect the production of thyrotropin-releasing hormone, thereby regulating thyroid hormone production.[20]

The hypothalamus functions as a type of thermostat for the body.[21] It sets a desired body temperature, and stimulates either heat production and retention to raise the blood temperature to a higher setting or sweating and vasodilation to cool the blood to a lower temperature. All fevers result from a raised setting in the hypothalamus; elevated body temperatures due to any other cause are classified as hyperthermia.[21] Rarely, direct damage to the hypothalamus, such as from a stroke, will cause a fever; this is sometimes called a hypothalamic fever. However, it is more common for such damage to cause abnormally low body temperatures.[21]

The hypothalamus contains neurons that react strongly to steroids and glucocorticoids (the steroid hormones of the adrenal gland, released in response to ACTH). It also contains specialized glucose-sensitive neurons (in the arcuate nucleus and ventromedial hypothalamus), which are important for appetite. The preoptic area contains thermosensitive neurons; these are important for TRH secretion.

Oxytocin secretion in response to suckling or vagino-cervical stimulation is mediated by some of these pathways; vasopressin secretion in response to cardiovascular stimuli arising from chemoreceptors in the carotid body and aortic arch, and from low-pressure atrial volume receptors, is mediated by others. In the rat, stimulation of the vagina also causes prolactin secretion, and this results in pseudo-pregnancy following an infertile mating. In the rabbit, coitus elicits reflex ovulation. In the sheep, cervical stimulation in the presence of high levels of estrogen can induce maternal behavior in a virgin ewe. These effects are all mediated by the hypothalamus, and the information is carried mainly by spinal pathways that relay in the brainstem. Stimulation of the nipples stimulates release of oxytocin and prolactin and suppresses the release of LH and FSH.

Cardiovascular stimuli are carried by the vagus nerve. The vagus also conveys a variety of visceral information, including for instance signals arising from gastric distension or emptying, to suppress or promote feeding, by signalling the release of leptin or gastrin, respectively. Again this information reaches the hypothalamus via relays in the brainstem.

In addition hypothalamic function is responsive toand regulated bylevels of all three classical monoamine neurotransmitters, noradrenaline, dopamine, and serotonin (5-hydroxytryptamine), in those tracts from which it receives innervation. For example, noradrenergic inputs arising from the locus coeruleus have important regulatory effects upon corticotropin-releasing hormone (CRH) levels.

The extreme lateral part of the ventromedial nucleus of the hypothalamus is responsible for the control of food intake. Stimulation of this area causes increased food intake. Bilateral lesion of this area causes complete cessation of food intake. Medial parts of the nucleus have a controlling effect on the lateral part. Bilateral lesion of the medial part of the ventromedial nucleus causes hyperphagia and obesity of the animal. Further lesion of the lateral part of the ventromedial nucleus in the same animal produces complete cessation of food intake.

There are different hypotheses related to this regulation:[23]

The medial zone of hypothalamus is part of a circuitry that controls motivated behaviors, like defensive behaviors.[24] Analyses of Fos-labeling showed that a series of nuclei in the “behavioral control column” is important in regulating the expression of innate and conditioned defensive behaviors.[25]

Exposure to a predator (such as a cat) elicits defensive behaviors in laboratory rodents, even when the animal has never been exposed to a cat.[26] In the hypothalamus, this exposure causes an increase in Fos-labeled cells in the anterior hypothalamic nucleus, the dorsomedial part of the ventromedial nucleus, and in the ventrolateral part of the premammillary nucleus (PMDvl).[27] The premammillary nucleus has an important role in expression of defensive behaviors towards a predator, since lesions in this nucleus abolish defensive behaviors, like freezing and flight.[27][28] The PMD does not modulate defensive behavior in other situations, as lesions of this nucleus had minimal effects on post-shock freezing scores.[28] The PMD has important connections to the dorsal periaqueductal gray, an important structure in fear expression.[29][30] In addition, animals display risk assessment behaviors to the environment previously associated with the cat. Fos-labeled cell analysis showed that the PMDvl is the most activated structure in the hypothalamus, and inactivation with muscimol prior to exposure to the context abolishes the defensive behavior.[27] Therefore, the hypothalamus, mainly the PMDvl, has an important role in expression of innate and conditioned defensive behaviors to a predator.

Likewise, the hypothalamus has a role in social defeat: Nuclei in medial zone are also mobilized during an encounter with an aggressive conspecific. The defeated animal has an increase in Fos levels in sexually dimorphic structures, such as the medial pre-optic nucleus, the ventrolateral part of ventromedial nucleus, and the ventral premammilary nucleus.[31] Such structures are important in other social behaviors, such as sexual and aggressive behaviors. Moreover, the premammillary nucleus also is mobilized, the dorsomedial part but not the ventrolateral part.[31] Lesions in this nucleus abolish passive defensive behavior, like freezing and the “on-the-back” posture.[31]

According to D. F. Swaab, writing in a July 2008 paper, “Neurobiological research related to sexual orientation in humans is only just gathering momentum, but the evidence already shows that humans have a vast array of brain differences, not only in relation to gender, but also in relation to sexual orientation.”[32]

Swaab first reported on the relationship between sexual orientation in males and the hypothalamus’s “clock”, the suprachiasmatic nucleus (SCN). In 1990, Swaab and Hofman[33] reported that the suprachiasmatic nucleus in homosexual men was significantly larger than in heterosexual men. Then in 1995, Swaab et al.[34] linked brain development to sexual orientation by treating male rats both pre- and postnatally with ATD, an aromatase blocker in the brain. This produced an enlarged SCN and bisexual behavior in the adult male rats. In 1991, LeVay showed that part of the sexually dimorphic nucleus (SDN) known as the 3rd interstitial nucleus of the anterior hypothalamus (INAH 3), is nearly twice as large (in terms of volume) in heterosexual men than in homosexual men and heterosexual women. However, a study in 1992 has shown that the sexually dimorph nucleus of the preoptic area, which include the INAH3, are of similar size in homosexual males who died of AIDS to heterosexual males, and therefore larger than female. This clearly contradicts the hypothesis that homosexual males have a female hypothalamus. Furthermore, the SCN of homosexual males is extremely large (both the volume and the number of neurons are twice as many as in heterosexual males). These areas of the hypothalamus have not yet been explored in homosexual females nor bisexual males nor females. Although the functional implications of such findings still haven’t been examined in detail, they cast serious doubt over the widely accepted Drner hypothesis that homosexual males have a “female hypothalamus” and that the key mechanism of differentiating the “male brain from originally female brain” is the epigenetic influence of testosterone during prenatal development.[35][36]

In 2004 and 2006, two studies by Berglund, Lindstrm, and Savic[37][38] used positron emission tomography (PET) to observe how the hypothalamus responds to smelling common odors, the scent of testosterone found in male sweat, and the scent of estrogen found in female urine. These studies showed that the hypothalamus of heterosexual men and homosexual women both respond to estrogen. Also, the hypothalamus of homosexual men and heterosexual women both respond to testosterone. The hypothalamus of all four groups did not respond to the common odors, which produced a normal olfactory response in the brain.

Human brain left dissected midsagittal view

Location of the hypothalamus

Bear, Mark F. “Hypothalamic Control of the Anterior Pituitary.” Neuroscience: Exploring the Brain. 4th ed. Philadelphia: Wolters Kluwer, 2016. 528. Print.

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Hypothalamus – Wikipedia

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Hypothalamus | You and Your Hormones from the Society for …

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Where is my hypothalamus?

Computer artwork of a person’s head showing the left side of the brain with the hypothalamus highlighted.

The hypothalamus is located on the undersurface of the brain. It lies just below the thalamus and above the pituitary gland, to which it is attached by a stalk. It is an extremely complex part of the brain containing many regions with highly specialised functions. In humans, the hypothalamus is approximately the size of a pea and accounts for less than 1% of the weight of the brain.

One of the major functions of the hypothalamus is to maintain homeostasis, i.e. to keep the human body in a stable, constant condition.

The hypothalamus responds to a variety of signals from the internal and external environment including body temperature, hunger, feelings of being full up after eating, blood pressure and levels of hormones in the circulation. It also responds to stress and controls our daily bodily rhythms such as the night-time secretion of melatonin from the pineal gland and the changes in cortisol (the stress hormone) and body temperature over a 24-hour period.The hypothalamus collects and combines this information and puts changes in place to correct any imbalances.

There are two sets of nerve cells in the hypothalamus that produce hormones.One set sends the hormones they produce down through the pituitary stalk to the posterior lobe of the pituitary gland where these hormones are released directly into the bloodstream.These hormones are anti-diuretic hormone and oxytocin. Anti-diuretic hormonecauses water reabsorption at the kidneys and oxytocin stimulates contraction of the uterus in childbirth and is important in breastfeeding.

The other set of nerve cells produces stimulating and inhibiting hormones that reach the anterior lobe of the pituitary gland via a network of blood vessels that run down through the pituitary stalk.These regulate the production of hormonesthat control the gonads, thyroid gland and adrenal cortex, as well as the production of growth hormone, which regulates growth, and prolactin, which is essential for milk production. The hormones produced in the hypothalamus are corticotrophin-releasing hormone, dopamine, growth hormone-releasing hormone, somatostatin, gonadotrophin-releasing hormone and Thyrotrophin-releasing hormone.

Hypothalamic function can be affected by head trauma, brain tumours, infection, surgery, radiation and malnutrition.It can lead to disorders of energy balance and thermoregulation, disorganised body rhythms, (insomnia) and symptoms of pituitary deficiency due to loss of hypothalamic control.Pituitary deficiency (hypopituitarism)ultimately causes a deficiency of hormones produced by the gonads, adrenal cortex and thyroid gland, as well as loss of growth hormone.

Lack of anti-diuretic hormone production by the hypothalamus causes diabetes insipidus. In this condition the kidneys are unable to reabsorb water, which leads to excessive production of dilute urine and very large amounts of drinking.

Last reviewed: Jan 2015

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Multiple Sclerosis (MS) Symptoms and Treatment

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What Is MS?

Multiple sclerosis (MS) is an autoimmune disease in which the body’s immune system attacks its own central nervous system (the brain and spinal cord). In MS, the immune system attacks and damages or destroys the myelin, a substance that surrounds and insulates the nerves. The myelin destruction causes a distortion or interruption in nerve impulses traveling to and from the brain. This results in a wide variety of symptoms.

Multiple sclerosis is estimated to affect 2.3 million people worldwide. Most people are diagnosed between the ages of 20 to 50, though it can also occur in young children and the elderly.

Multiple sclerosis is three times more common in women than in men. In addition, nearly all women afflicted with MS get the condition before menopause. This could mean that hormones play an important role in the disease’s development.

Usually, MS in men is more severe than it is in women. They typically get MS in their 30s and 40s, just as their testosterone levels begin to decline.

Although MS is more common in women than men overall, one form of the disease contradicts this pattern. People with primary progressive (PP) MS are about as likely to be male as female. (The four main types of MS are described later).

People who smoke are more likely to develop MS, and to develop it more severely and with a faster progression.

MS is more prevalent among Caucasians than other ethnicities. MS is believed to have a genetic component as people with a first-degree relative with the disease have a higher incidence than the general population.

The exact cause of multiple sclerosis is unknown, but it is believed to be some combination of immunologic, environmental, infectious, or genetic factors. Researchers are examining the possible role of viruses in the cause of MS, but this is still unproven.

A range of scientific disciplines are being employed to find the cause of MS. Immunologists, epidemiologists and geneticists are all working to narrow in on the cause of multiple sclerosis.

One unusual finding that has emerged is that MS occurs more frequently the farther people live from the equator. This suggests a possible connection between the condition and vitamin D deficiency.

Multiple sclerosis (MS) is an autoimmune disorder where the immune system mistakenly perceives its own myelin (the sheath around the nerves) as an intruder and attacks it, as it would a virus or other foreign infectious agent. To understand how this harms the body, it helps to understand how nerves work.

A nerve can be seen by the naked eye, but it is made up of hundreds or even thousands of microscopic nerve fibers wrapped by connective tissue. Nerves conduct messages to and from the brain by way of electrical impulses.

Often the nerve fibers that make up a nerve are all individually wrapped in myelin, a protective sheath that causes electric impulses to conduct down the nerve much faster than fibers that lack myelin. (The same principle is used to improve electric wires by covering them with a plastic outer layer.)

In multiple sclerosis, the immune system’s T cells attack the myelin sheath. By attacking myelin, the immune system in a person with MS causes inflammation and degeneration of the myelin that can lead to demyelination, or stripping of the myelin covering of the nerves. It can also cause scarring (the sclerosis in the name multiple sclerosis). This causes electrical impulses to travel more slowly along the nerves resulting in deterioration of function in body processes such as vision, speech, walking, writing, and memory.

While multiple sclerosis is not hereditary, genetics are believed to play a role. In the U.S., the chances of developing MS are one in 750. Having a first-degree relative (parent, sibling) increases the risk to up to 5%. An identical twin of someone with MS has a 25% chance of being diagnosed with the disorder. It is thought there is an outside trigger and genetics only makes certain people susceptible to getting MS. which is why the disease is not considered hereditary. Genes may make a person more likely to develop the disease, but it is believed that there still is an additional outside trigger that makes it happen.

There are four different types of multiple sclerosis that have been identified and each type can have symptoms ranging from mild to severe. The different types of MS can help predict the course of the disease and the patient’s response to treatment. The four types of MS are discussed on the next four slides.

Relapsing-remitting multiple sclerosis (RR-MS) is the most common type of MS, affecting about 85% of MS sufferers. RR-MS is defined by inflammatory attacks on the myelin and nerve fibers causing a worsening of neurologic function. Symptoms vary from patient to patient, and symptoms can flare up (called relapses or exacerbations) unexpectedly, and then disappear (remission).

Primary-progressive multiple sclerosis (PP-MS) is characterized by steady worsening of neurologic functioning, without any relapses or remissions. There may be occasional plateaus, but overall the progression of the disability is continuous. This form of MS occurs equally in men and women, and the age of onset is about 10 years later than in relapsing-remitting MS.

Secondary-progressive multiple sclerosis (SP-MS) is a form of MS that follows relapsing-remitting MS. The majority of people diagnosed with RR-MS will eventually transition to having SP-MS. After a period of relapses (also called attacks, or exacerbations) and remissions the disease will start to progress steadily. People with SP-MS may or may not experience remissions.

Progressive-relapsing multiple sclerosis (PR-MS) is the least common form of MS, occurring in about 5% of MS patients. People with PR-MS experience steady disease progression and worsening neurological function as seen in primary-progressive multiple sclerosis (PP-MS), along with occasional relapses like people with relapsing-remitting multiple sclerosis (RR-MS).

Symptoms of multiple sclerosis may be single or multiple and may range from mild to severe in intensity and from short to long in duration.

Multiple sclerosis is often difficult to diagnose as symptoms are so varied and can resemble other diseases. It is often diagnosed by a process of exclusion that is, by ruling out other neurological diseases so the diagnosis of MS may take months to years. A physician will do a complete history and neurological exam, along with tests to evaluate mental, emotional and language functions, strength, coordination, balance, reflexes, gait, and vision.

One of the main ways to diagnose multiple sclerosis is an MRI (magnetic resonance imaging) scan. Characteristic areas of demyelination will show up as lesions on an MRI scan. On the left is a brain MRI scan of a 35-year-old man with relapsing remitting multiple sclerosis that reveals multiple lesions with high T2 signal intensity and one large white matter lesion. The right image shows the cervical spinal cord of a 27-year-old woman representing a multiple sclerosis demyelination and plaque (see arrow).

There are several aspects to treating multiple sclerosis.

Treatment for multiple sclerosis may include drugs to manage attacks, symptoms, or both. Many medications carry the risk of some side effects so patients need to manage their treatment with their doctors.

Corticosteroids are drugs that reduce inflammation in the body and affect the function of the immune system. They are often used to manage MS attacks, but can have numerous side effects.

There are currently 10 medications approved for disease modification

Many medications are used to treat and manage symptoms associated with multiple sclerosis. Here are some common multiple sclerosis symptoms, followed by the medical treatments often used to treat them.

Continued from the last slide, here are some common multiple sclerosis symptoms, followed by the medical treatments often used to treat them.

There has been a lot of progress over the years in managing multiple sclerosis, and research is ongoing into new therapies. There are several new avenues of research including techniques to allow brain cells to generate new myelin or prevent the death of nerves. Other research involves use of stem cells that might be implanted into the brain or spinal cord to regrow the cells that have been destroyed by the disease. Some therapies being investigated include methods that would improve the nerve impulse signals. In addition the effects of diet and the environment on multiple sclerosis are being investigated.

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Pill for Relapsing MS | RRMS Treatment | GILENYA (fingolimod)

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GILENYA has a pregnancy registryclick here to learn more.

*GILENYA can result in a slow heart rate when first taken. You will be observed by a health care professional for at least 6 hours after you take your first dose. You may need to repeat this monitoring if you miss a dose.

In 2016, most eligible patients paid a $0 co-pay. Call 1-800-GILENYA for details. People for whom GILENYA has been prescribed are required to report any benefits they receive through the GILENYA Prescription Co-Pay Support Program to their commercial insurance company. Limitations apply. Valid only for those with commercial insurance. Offer not valid under Medicare, Medicaid or any other federal or state program. Not valid for cash-paying patients, where product is not covered by patient’s commercial insurance, or where plan reimburses you for entire cost of your prescription drug. Offer is not valid where prohibited by law. Valid only in the US and Puerto Rico. This program is not health insurance. Offer may not be combined with any other rebate, coupon, or offer. This program is subject to termination or modification at any time.

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Pill for Relapsing MS | RRMS Treatment | GILENYA (fingolimod)

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Parkinson Disease Treatment & Management: Approach …

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Hauser RA, Grosset DG. [(123) I]FP-CIT (DaTscan) SPECT Brain Imaging in Patients with Suspected Parkinsonian Syndromes. J Neuroimaging. 2011 Mar 16. [Medline].

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It is our belief that knowledge is power. The easier information is to obtain and understand, the more your child benefits. Information is the vital tool that equips us all with an ability to make clear, informed decisions on health, education, wellness, and more. Its almost always true that the more information, the better the potential outcome.

MyChild provides information on topics from A to Z, all made available here, for your convenience. After decades representing families of special needs children, and protecting their rights in the courts and in state legislative hearings, attorney Ken Stern recognized the need for an informative resource where all parents could quickly access needed information to learn, understand and to protect their child. My ChildTM, including the website, its Facebook page, and the MyChildTM Call Center are owned by Ken Stern and serve to make information and compassionate understanding readily available to those who need it most parents just like you.

Beyond an informational resource, our website features stories of success and inspiration regarding children and adults living with Cerebral Palsy, embracing their challenges and achieving amazing things we hope inspire you as much as they do us. Contact us today for free information on anything related to Cerebral Palsy were here to help your child achieve their full potential in any way that we can. For the information you need, and that your child deserves, were here for you!

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Cerebral Palsy | What Are the Symptoms, Causes, & Treatment …

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The mission of Cerebral Palsy Group is simple: to educate and support those who live with a CP diagnosis. To do so, we have created a resource where anyone can learn more about the symptoms and causes of muscular disorders and find resources and support for assessment and comparison of treatment options and technologies. We strive to cover everything from traditional approaches to cutting-edge research.

Any type of disability diagnosis raises difficult questions about long-term plans for those affected. Uncertainty and fear of the unknown can cause a ripple effect of stress throughout a family. Our goal is to break through the confusion and make it easier for parents to seek appropriate care.

For those who play an active role in a childs development, nothing is more critical than defining and identifying the symptoms of CP as quickly as possible. The sooner that families are educated on cerebral palsy, the sooner both health professionals and loved ones can start working toward a better life for the affected child.

The Cerebral Palsy Group helps you understand what to look for and explains the underlying causes behind possible symptoms and behaviors. When you need answers, weve created ways for you to get information (and hope) at any hour of the day.

Though it may look a little bit different, the future is bright for those with Cerebral Palsy. Our focus is on bringing to light the mechanisms of the disability in hopes that education can help affected families plan for this future.

Children may develop muscle disorders for any number of reasons, including birth injury or trauma. Experts are still struggling to understand the full scope of these disorders. Our goal is to continue to bring you the most up-to-date information from trusted sources as it becomes available.

This resource goes beyond the physical aspects of the condition. Emotional well-being is also key to treatment. Those living with cerebral palsy may face social stigmas, bullying or other related pressures. Coping skills and behavioral techniques can be taught as lifelong tools to handle these concerns. We give you the means to learn more about the different options available, so you can make smart decisions from the start.

Nothing compares to having a safety net, which is what our group is always striving to be for you. We offer a space for families to read about any and all concerns. We strive to provide the network that will point the way toward a more positive life for the child with CP and his or her family. For instance, physical therapy is a proven way for those with CP to gain more muscle strength and control, so children can feel more empowered in daily life. Behavioral therapy is also an excellent option for children with emotional roadblocks when confronting limitations. There is always something that can be done to aid a child living with cerebral palsy, and our work here is geared toward helping you find it.

Whether you want to know about the different muscle groups in the body or you want to engage in more therapeutic daily routines, we work to offer the expertise you need with the compassion you deserve.

It can often be difficult to know when and if you are making the right decisions for your child or loved one. It is our mission to help you be confident every step of the way.

By advocating for those with cerebral palsy, we seek to give them their best chance to be productive members of the community. It is important to us that public perception of those with disabilities shifts. It is key to show that individuality is still first and foremost, and this disability is not all-consuming.

Support is important. It is our hope that finding a resource on the future you may be facing can help ease your anxieties and help you to feel just a little bit less overwhelmed.

Nothing in the medical world stays the same for long. We are here to update our resources and respond to the immediate concerns of those who seek our help. We stay informed on cutting edge research developments and treatment options, so you can continue to assess what to do next in the life of the child or the individual with the condition.

While Cerebral Palsy can add challenges to your and your child or loved ones life, it does not have to be isolating, or overwhelming. We seek to give you small, manageable goals that are practical for the whole family. We take sincere pride in bringing people together to create the best path to physical, mental and emotional wellness.

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Cerebral Palsy | What Are the Symptoms, Causes, & Treatment …

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Cerebral palsy – Diagnosis and treatment – Mayo Clinic

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If your family doctor or pediatrician suspects your child has cerebral palsy, he or she will evaluate your child’s signs and symptoms, review your child’s medical history, and conduct a physical evaluation. Your doctor may refer you to a specialist trained in treating children with brain and nervous system conditions (pediatric neurologist).

Your doctor will also order a series of tests to make a diagnosis and rule out other possible causes.

Brain-imaging technologies can reveal areas of damage or abnormal development in the brain. These tests may include the following:

Magnetic resonance imaging (MRI). An MRI uses radio waves and a magnetic field to produce detailed 3-D or cross-sectional images of your child’s brain. An MRI can often identify any lesions or abnormalities in your child’s brain.

This test is painless, but it’s noisy and can take up to an hour to complete. Your child will likely receive a mild sedative beforehand. An MRI is usually the preferred imaging test.

If your child has had seizures, your doctor may order an electroencephalogram (EEG) to determine if he or she has epilepsy, which often occurs in people with cerebral palsy. In an EEG test, a series of electrodes are affixed to your child’s scalp.

The EEG records the electrical activity of your child’s brain. If he or she has epilepsy, it’s common for there to be changes in normal brain wave patterns.

Laboratory tests may also screen for genetic or metabolic problems.

If your child is diagnosed with cerebral palsy, you’ll likely be referred to specialists for assessments of other conditions often associated with the disorder. These tests may identify:

Children and adults with cerebral palsy require long-term care with a medical care team. This team may include:

Medications that can lessen the tightness of muscles may be used to improve functional abilities, treat pain and manage complications related to spasticity or other cerebral palsy symptoms.

It’s important to talk about drug treatment risks with your doctor and discuss whether medical treatment is appropriate for your child’s needs. Medication selection depends on whether the problem affects only certain muscles (isolated) or the whole body (generalized). Drug treatments may include the following:

Isolated spasticity. When spasticity is isolated to one muscle group, your doctor may recommend onabotulinumtoxinA (Botox) injections directly into the muscle, nerve or both. Botox injections may help to improve drooling. Your child will need injections about every three months.

Side effects may include pain, mild flu-like symptoms, bruising or severe weakness. Other more-serious side effects include difficulty breathing and swallowing.

Generalized spasticity. If the whole body is affected, oral muscle relaxants may relax stiff, contracted muscles. These drugs include diazepam (Valium), dantrolene (Dantrium) and baclofen (Gablofen).

Diazepam carries some dependency risk, so it’s not recommended for long-term use. Its side effects include drowsiness, weakness and drooling.

Dantrolene side effects include sleepiness, weakness, nausea and diarrhea.

Baclofen side effects include sleepiness, confusion and nausea. Note that baclofen may also be pumped directly into the spinal cord with a tube. The pump is surgically implanted under the skin of the abdomen.

Your child also may be prescribed medications to reduce drooling. Medications such as trihexyphenidyl, scopolamine or glycopyrrolate (Robinul, Robinul Forte) may be helpful, as can Botox injection into the salivary glands.

A variety of nondrug therapies can help a person with cerebral palsy enhance functional abilities:

Physical therapy. Muscle training and exercises may help your child’s strength, flexibility, balance, motor development and mobility. You’ll also learn how to safely care for your child’s everyday needs at home, such as bathing and feeding your child.

For the first 1 to 2 years after birth, both physical and occupational therapists provide support with issues such as head and trunk control, rolling, and grasping. Later, both types of therapists are involved in wheelchair assessments.

Braces or splints may be recommended for your child. Some of these supports help with function, such as improved walking. Others may stretch stiff muscles to help prevent rigid muscles (contractures).

Occupational therapy. Using alternative strategies and adaptive equipment, occupational therapists work to promote your child’s independent participation in daily activities and routines in the home, the school and the community.

Adaptive equipment may include walkers, quadrupedal canes, seating systems or electric wheelchairs.

Speech and language therapy. Speech-language pathologists can help improve your child’s ability to speak clearly or to communicate using sign language.

Speech-language pathologists can also teach your child to use communication devices, such as a computer and voice synthesizer, if communication is difficult.

Another communication device may be a board covered with pictures of items and activities your child may see in daily life. Sentences can be constructed by pointing to the pictures.

Speech therapists may also address difficulties with muscles used in eating and swallowing.

Surgery may be needed to lessen muscle tightness or correct bone abnormalities caused by spasticity. These treatments include:

Orthopedic surgery. Children with severe contractures or deformities may need surgery on bones or joints to place their arms, hips or legs in their correct positions.

Surgical procedures can also lengthen muscles and tendons that are proportionally too short because of severe contractures. These corrections can lessen pain and improve mobility. The procedures may also make it easier to use a walker, braces or crutches.

Explore Mayo Clinic studies testing new treatments, interventions and tests as a means to prevent, detect, treat or manage this disease.

Some children and adolescents with cerebral palsy use some form of complementary or alternative medicine.

For example, hyperbaric oxygen therapy is widely promoted for cerebral palsy treatment despite limited evidence of efficacy. This and other unproven therapies for cerebral palsy should be viewed with skepticism. Controlled clinical trials involving therapies such as hyperbaric oxygen therapy, resistance exercise training using special clothing, assisted motion completion for children and certain forms of electrical stimulation have been inconclusive or showed no benefit to date, and the therapies are not accepted mainstream clinical practice.

Stem cell therapy is being explored as a treatment approach for cerebral palsy, but research is still assessing whether such approaches are safe and effective. Studies in the U.S. and elsewhere are examining the safety and tolerability of umbilical cord blood stem cell infusion in children with cerebral palsy.

When a child is diagnosed with a disabling condition, the whole family faces new challenges. Here are a few tips for caring for your child and yourself:

Find support. A circle of support can make a big difference in helping you cope with cerebral palsy and its effects. As a parent, you may feel grief and guilt over your child’s disability.

Your doctor can help you locate support groups, organizations and counseling services in your community. Your child may also benefit from family support programs, school programs and counseling.

If your child has cerebral palsy, how you learn about your child’s condition may depend on the severity of the disabilities, when problems first appeared, and whether there were any risk factors during pregnancy or delivery.

Your doctor may ask you several questions during appointments, including:

If your family doctor or pediatrician believes that your child exhibits signs of cerebral palsy, you may want to discuss the following questions:

It’s important to take your child to all regularly scheduled well-baby visits and annual appointments during childhood. These visits are an opportunity for your child’s doctor to monitor your child’s development in key areas, including:

Aug. 25, 2016

Cerebral palsy – Diagnosis and treatment – Mayo Clinic

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