Look after your brain

Breaking the cycle of medication overuse headache

2011-12-26T04:49:00.001-08:00

When patients who have frequent, disabling migraines take medications to relieve their symptoms, they run the risk that the attacks will increase in frequency to daily or near-daily as a rebound effect comes into play. This pattern, called medication overuse headache, is more likely to happen with butalbital and opioids than with migraine-specific drugs, as partial responses lead to recurrence, repeat dosing, and, eventually, overuse. Breaking the cycle involves weaning the patient from the overused medications, setting up a preventive regimen, and setting strict limits on the use of medications to relieve acute symptoms.
Key pointsMedication overuse headache can occur with as few as 5 days per month of treatment with butalbital or 8 days per month with opioids.The features vary, but the most important is headache on 15 or more days per month, lasting at least 4 hours if untreated, for at least 3 consecutive months. Other common symptoms are morning headaches, neck pain, nonrestorative sleep, and vasomotor instability, all of which tend to improve with weaning from the overused medications.Daily preventive treatment is indicated when patients have 10 or more headaches per month or severe disability from their attacks.With treatment, the prognosis for medication overuse headache is good. However, patients need close followup to prevent recidivism.
Some migraine patients fall into a trap by overusing the medications they take when they get their headaches, ending in a downward spiral of daily or near-daily headaches for which their medications become less and less effective.This condition, called medication overuse headache, makes for a poor quality of life. It is often associated with nonrestorative sleep, neck pain, and vasomotor instability. Comorbid depression and anxiety are common and may complicate treatment. (Depression and anxiety, however, do not cause daily headaches.) Patients can also suffer from the physiologic and psychological consequences of the overused medications.Fortunately, we can break the cycle.1,2 Treatment involves completely weaning the patient from the overused medications and educating her or him to follow a new regimen of prophylaxis and acute treatment with clear limits on frequency of use. Nondrug treatments such as relaxation therapy, biofeedback, and cognitive behavioral therapy can be useful adjuncts.
CROSSING THE LINE: 15 HEADACHE DAYS A MONTHChronic daily headacheWe define chronic daily headache as occurring on at least 15 days per month for at least 3 months in a row and lasting at least 4 hours if untreated.Most patients start with episodic migraine, and many of them remember the period of transformation. Crossing the 15-day-per-month threshold changes the clinical presentation, prognosis, and treatment, all for the worse.In a large population-based study,3 2.5% of patients who began with episodic migraine (headaches on fewer than 15 days per month) had “transformed migraine” (headaches on 15 or more days per month) 1 year later. The prevalence of chronic daily headache is almost 5% of the general population and may account for up to 70% of the initial diagnoses seen in headache centers.The closer a patient is to having 15 headaches per month, the more likely she or he will cross the line.4,5 Katsarava and colleagues5 followed patients for 1 year in a neurology clinic in Germany and found that those starting the year with 6 to 9 headache days per month were 6.2 times more likely to develop chronic daily headache in the next year than those who began the year with 0 to 4 per month—and those starting with 10 to 14 headaches per month were 20 times more likely.Medication overuse headacheMedication overuse headache is a subset of chronic daily headache, also occurring on 15 or more days per month but with the added criterion of medication overuse, ie, regular overuse for more than 3 months of at least one acute treatment drug:Ergotamine, triptans, opioids, or combination analgesic medications on 10 or more days per month on a regular basis for more than 3 months, orSimple analgesics or any combination of ergotamine, triptans, analgesics, or opioids on 15 or more days per month on a regular basis for more than 3 months without overuse of any single class alone.Another criterion is that the patient’s headaches must worsen in some way (usually frequency) as the use of acute medications becomes more frequent.6,7Medication overuse headache is the most common form of secondary chronic daily headache seen in headache practice,8–10 and probably accounts for about half of cases of chronic daily headache.11–13Different terminology confuses the issueMany terms have been used to describe medication overuse headache in the past, such as analgesic-rebound headache (or just rebound headache), transformed migraine with medication overuse, and even chronic migraine. The lack of uniformity in terminology makes for confusion in the literature and difficulty in communicating with patients and colleagues. Some authors mean medication overuse headache when they say chronic daily headache.Complicating this diagnostic confusion is a debate as to whether chronic daily headache in general should be treated as a primary or secondary headache disorder. Some European headache specialists insist on a strict division between primary and secondary daily headaches, and medication overuse headache is one of the latter. Many American specialists believe that chronic daily headache is a collective description or phenotype rather than a diagnostic category, and that it is usually associated with and exacerbated by medication overuse.14,15 The International Classification of Headache Disorders uses the term “chronic migraine” for primary daily headache, and “medication overuse headache” for secondary daily headache or rebound.Many American specialists approach the disorder clinically, treating chronic daily headache in the same way regardless of whether there is medication overuse. They cite randomized controlled trials of topiramate (Topamax) and onabotulinum toxin type A (Botox) that reported comparable benefit with these medications in patients with chronic daily headache with or without medication overuse.16–18
MORE IS LESS: THE PARADOX OF TREATING ACUTE HEADACHEThe clinical paradox and dilemma of treating acute episodic migraine is that more is less: the more days of acute treatment, the less well the migraines are controlled. And thus, the patient is likely to veer out of control.3The compassion that motivates us to prescribe medications for acute episodic migraine must be tempered by the realization that too much of a good thing will result in its malignant transformation to medication overuse headache. Once this develops, preventive and migrainespecific acute medications are less effective, and patients need far more complex interventions.Complicating the dilemma, acute migraine-specific medications such as triptans and dihydroergotamine (Migranal) work better when taken early in migraine attacks, before central sensitization and allodynia develop with attendant photophonophobia and sensitivity to other stimuli. On the other hand, overuse will lead to medication overuse headache.
SYMPTOMS VARYThe symptoms of medication overuse headache vary in frequency, severity, location, quality, and associated features, both among patients and in the same patient. This is because the disease itself varies and also because of differences in the type and frequency of medication intake. Still, some features help to define this problem, and failing to recognize them may account for a widely held clinical feeling that these patients are “difficult.”History of episodic migraine. Generally, medication overuse headache does not occur in nonmigraineurs.Headache on most days of the month. Whenever a migraineur starts having headaches on more days than not, the diagnosis of medication overuse should be considered.Overuse of acute medications. The criteria (see above) allow for combining days of acute medication use. For example, if a patient takes a combination analgesic on 5 days and a triptan on 5 different days, that would still be enough days of acute treatment to trigger medication overuse headache.Variable pain location is a particular characteristic of medication overuse headache. Although the location may differ from day to day (front or back, rostral or caudal, unilateral or bilateral), it is the quantity not the quality or location of the headaches that suggests the diagnosis.A drug-dependent rhythm. Predictably, the headaches come on in the early morning or awaken the patient from sleep. This may be due to variable drug withdrawal.Neck pain. Medication overuse headache frequently involves the neck, and patients often seek and receive treatments such as muscle relaxants or injections to the neck. When patients are weaned from their acute migraine medications, neck pain generally dissipates. The neck pain, however, can recur episodically with their remaining, now-episodic acute migraines. Neck pain associated with medication overuse headache is not usually a sign of a primary neck disorder; rather, it is a symptom of medication overuse headache itself.Concomitant depression and anxiety are comorbid with episodic migraine, but appear to be more common with medication overuse headache. Treating the depression or anxiety does not restore an episodic pattern of migraine; weaning from the overused medications remains the most important intervention. A frequent clinical error is to diagnose and treat the psychiatric issues without recognizing medication overuse as the primary problem.Nonrestorative sleep is almost always reported by patients with medication overuse headache. This is often due to the caffeine contained in combination analgesics or to excessive dietary caffeine intake, but it may also be part of the daily acute drug withdrawal syndrome. The sleep problems are also associated with the concomitant depression. Sleep often improves after weaning from the offending substance or substances. As with neck pain, patients do not have a primary sleep disorder—the sleep disturbance is a symptom of medication overuse headache.Vasomotor instability. Autonomic features are commonly associated with medication overuse headache. Rhinorrhea, nasal stuffiness, and lacrimation are features of medication withdrawal, especially from opioids, and are frequently attributed to sinus disease or “sinus headaches.” Many patients undergo unnecessary sinus procedures or are given antibiotics, decongestants, and other wrong medications for incorrect diagnoses. Decongestants can cause and exacerbate medication overuse headache, so they need to be withdrawn. The sinus features generally remit when the overused migraine medications are eliminated.Preventive medications are less effective or ineffective until the acute medications are withdrawn. Thus, prescribing prevention without weaning is usually futile, and the patients are often dismissed as having a refractory problem. At the same time, migraine-specific acute treatments, ie, triptans and ergots, are usually also less effective. When patients complain that “nothing works,” either preventively or acutely, medication overuse headache should spring to mind.Weaning from overused medications can restore the efficacy of previously ineffective treatments at the same time that a patient is restored to an episodic headache pattern. Thus, complete weaning is the pivotal clinical intervention. Clinically, there is no spontaneous remission from rebound without absolute detoxification, maintained for months.9,19–22
Other diagnoses entertained. The more diagnoses suggested for daily headache, and the more treatments tried unsuccessfully, the more likely the diagnosis is actually medication overuse headache. Because this condition is protean, patients and caregivers alike make more and more fanciful diagnoses such as allergies, cervicogenic headache, temperomandibular disorder, occipital neuralgia, chronic Lyme disease, and systemic candidiasis. A useful strategy is to assume that daily headache is likely due to medication overuse. And since medication overuse headache is generally treatable, patients labeled as having refractory headaches often are dramatically improved by appropriate intervention.
WHY ARE MIGRAINEURS SO SUSCEPTIBLE?Medication overuse headache occurs primarily in people with a history of episodic migraine, but the unique susceptibility of migraineurs is not fully understood.Structural changes in the brain?Episodic migraine attacks appear to be generated in the upper brainstem. This region in turn activates a set of peripheral pain mechanisms, ie, meningeal inflammation and vasodilation. The peripheral pain processes turn on afferent circuits that carry the pain signals to the lower brainstem, where these signals are integrated. Finally, the central signals ascend the brainstem, stimulating autonomic nuclei that account for nausea and other vasomotor changes, proceed through the thalamus, and terminate in the cortex where pain is perceived. Thus, migraine without aura consists of three steps—a central generator, a set of peripheral pain mechanisms, and a series of steps culminating in central integration. (Aura involves other steps, not outlined here.)A possible explanation of why migraine becomes chronic is that a yo-yo effect of repeated migrainous pain processes, followed by repeated medication, results in structural changes. These propagate central sensitization with a lowered threshold for activation of all of the central processing of head pain.This set of disturbances may occur due to undertreatment of migraine pain. With inadequate pain control, headaches recur, and the process repeats until damage occurs. Evidence for this is seen in up-regulation of excitatory serotonin receptors when analgesics are repetitively given to laboratory animals.23A pure withdrawal phenomenon?Also possible is that medication overuse headache is just a complex dependence-and-withdrawal phenomenon. Thus, the cyclical use of various medications results in withdrawal headaches and a set of symptoms, including disturbed sleep, morning headache, and vasomotor signs of withdrawal. Arguing against its being a pure withdrawal phenomenon is that daily use of analgesics or opioids generally does not cause daily headache in nonmigraineurs.24
HOW MUCH MEDICATION USE IS TOO MUCH?For an episodic migraine condition to transform into a chronic one, medications need to be taken on only a modest number of days per month: 5 to 10, depending on the type of medication.A pivotal study3 found that butalbital combinations were most likely to cause medication overuse headache, needing to be taken on merely 5 or more days per month to cause it in migraineurs. Opioids caused it if taken 8 or more days per month, and triptans if taken 10 or more days per month. Nonsteroidal anti-inflammatory drugs (NSAIDs) actually protected against transformation to daily headache if used 5 or fewer days per month, but caused medication overuse headache if used 10 or more days per month.Thus, there was a hierarchy of risk, with butalbital being the worst, opioids in the middle, and NSAIDs and triptans the least risky. None of the agents had to be taken daily to trigger medication overuse headache.
PREVENTION IS THE BEST TREATMENTThe best approach to medication overuse headache is to prevent it while the patient still has episodic migraine.Outcomes are better with triptans or ergotsUndertreatment of migraine leads quickly to overuse of symptomatic medications, and from there to medication overuse headache.Outcomes of episodic migraine are better when triptans or ergots (which are migrainespecific) are used first-line in patients with disabling migraine and no vascular contraindications. Patients who start with nonspecific treatment and step up to a more specific treatment when lower-level medications fail have less favorable outcomes in terms of migraine relief and disability time than those treated with triptans from the beginning.25To put this in perspective, if a patient takes an acute medication, gets only partial relief (not a pain-free response) at 2 hours and then takes another pill, or gets a recurrence and takes another pill, the likelihood of prolonging an attack and using more medications goes up. If a patient takes a triptan and gets a sustained pain-free response, the attack is truncated and the medication usage reduced. Therefore, migraine-specific acute treatments are more likely to not be overused.Daily preventive medication, if necessaryAs noted above, if the number of headache days exceeds 10 per month, the likelihood of developing daily headache escalates steeply. Thus, patients with 10 or more days of headache per month should be prescribed preventive medications to be taken daily to reduce the frequency, severity, and duration of attacks. Preventive treatment may also increase the efficacy of the acute treatments.The drugs used for preventive treatment are different than those used for acute treatment and are not likely to cause medication rebound headache. However, they are not very effective. Those that have the best evidence of efficacy are beta-blockers, tricyclic antidepressants, and anticonvulsants; calcium channel blockers and NSAIDs are also popular. This topic has been reviewed in detail elsewhere.26,27
REVERSING MEDICATION OVERUSE HEADACHEIf a patient already has medication overuse headache, the clinician is faced with the problem of weaning her or him from the overused medication while establishing a reasonable regimen of prophylaxis and acute medications with limits.For the most part, these tasks can be accomplished in a series of clinic visits. However, some patients have such severe comorbid medical and psychiatric illnesses that outpatient treatment is impossible. For them, a day hospital or inpatient program with infusion capabilities is often useful.Outpatient treatment of medication overuse headacheOutpatient treatment of medication overuse headache involves:Educating patients about the genesis of the problem and reassuring them that you are not accusing them of being an addict. Most patients who develop medication overuse headache are habituated inadvertently, and this needs to be made clear, along with the overall plan and the likely prognosis.Weaning from the overused medications can be done gradually, tapering the drugs over 4 to 6 weeks, during which preventive medications are introduced. Alternatively, the discontinuation of rebound medications can be done abruptly, with transitional medications (eg, corticosteroids, NSAIDs, dihydroergotamine, or triptans) used as a bridge to blunt withdrawal, during which the prophylaxis is established.Establishing daily preventive medications. The prophylactic regimen can be established either before or during the weaning.Providing acute medications, with limits. At a certain point in the weaning, advise the patient not to treat low-level headaches, and provide a triptan or dihydroergotamine to use for severe attacks, no more than twice weekly and less than 10 days per month. If the patient is in triptan rebound, dihydroergotamine would be the choice.Instructing the patient to keep a headache diary to follow adherence and outcomes.Psychology consultation can be very helpful to teach patients behavioral techniques to deal with anticipatory anxiety during the weaning.Multidisciplinary programs with infusion capabilitySome patients need a more intensive approach to restore an episodic migraine pattern. Examples: those on very high doses of narcotics or barbiturates, those with comorbid medical illnesses that limit both acute and preventive treatments, and those with severe and complicating comorbid psychiatric illnesses.Multidisciplinary programs are available, with specialists in neurology, primary care, psychology, and physical and occupational therapy providing treatment. Patients check into the hospital or a “day hospital,” where they can also receive intravenous infusions to get through the weaning. The goal is to shift the locus of control back to patients as they revert from daily headache to episodic migraine. Patient education is crucial.
OUTCOMES ARE GOODThere is much good news about medication overuse headache.It can be prevented with careful monitoring of acute medication outcomes and number of headache days. Prophylaxis should be used when treating high-frequency or very disabling migraine.Most patients improve when weaned and treated with preventive medications. “Recovery” means at least 3 months off the overused medications. In studies, more than half of patients who underwent treatment for medication overuse headache remained better and had an episodic pattern of headache 5 years later.26Unfortunately, the initial improvement often seen with patients after weaning and being given preventive medication (72%–85% of patients improve) in the first year is often followed by preventable relapse, so it is very important to follow up with patients regularly. 28–32

Managing patients with Alzheimer’s disease

2011-11-08T10:36:00.000-08:00

• Although there is no treatment that either cures or permanently arreststhe disease, there are presently available two types of Alzheimer specifictherapies: symptomatic approaches to improve memory based onenhancement of neurotransmitter systems, and neuroprotective strategiesusing antioxidants.
• Acetylcholinesterase inhibitors reduce the metabolism of theneurotransmitter acetylcholine, and although they probably do not alterthe progression of neurodegeneration, possible long term benefits mayinclude delayed institutionalisation, perhaps decreased mortality, andsavings in the cost of patient care.
• Optimal management of all medications and any comorbid medicalillnesses, including depression, is crucial and may result in significantimprovement in cognitive and functional status.
• There is insufficient evidence of efficacy of vitamin E in the treatment ofpeople with Alzheimer’s disease.
• Oestrogens do not benefit cognitive function after the onset ofAlzheimer’s, or reduce the risk of its development.
• Alzheimer’s disease results in behavioural problems that can be especiallychallenging to carers but effectively managed if properly identified.
• In addition to medical therapy, the physician should not overlook thenon-pharmacological management interventions that can aid in the careof patients with dementia.
• Patients with more than mild dementia usually have at least one carerand it is important that the clinician recognises his or her vital role inmanagement.

Functional and dissociative neurological symptoms

2010-02-22T00:17:00.000-08:00

Most people with functional or dissociative neurological symptoms have a combination of symptoms like "weakness, numbness and fatigue" or "blackouts and sleep problems".
Patients with functional/dissociative symptoms are often concerned that their diagnosis may be wrong. Especially since there is no 'scan' or blood test that can make the diagnosis.

There are many neurological problems. The commonest ones are

• Stroke

• Epilepsy

• Migraine / Headache

• Functional / Dissociative Symptoms

• Multiple Sclerosis

• Brain Tumour

• Parkinsons Disease

• Myasthenia Gravis

• Motor Neuron Disease (also called Amyotrophic Lateral Sclerosis)

• Peripheral Neuropathy

• Nerve Root or Spinal Cord entrapment

• Many hundreds of others.....

On the other hand there are also only a limited number of neurological symptoms.

The commonest ones are:

• Headache

• Weakness

• Sensory Symptoms

• Blackouts

• Memory / Cognitive symptoms

• Speech / Swallowing Symptoms

• Dizziness

• Visual Symptoms – reduced vision, double vision

• Neck, Back and Limb pain

• Tremors, jerks, spasms and contractures

• Bladder symptoms

In fact there are such a limited number of neurological symptoms you can see that its quite understandable for someone with more than one neurological symptom to start to wonder if they have one of the common (or uncommon) neurological diseases.

This website provides a guide to help with this disorders.

Tourette Syndrome

2008-12-31T08:32:00.000-08:00

The more alcohol consumed, the smaller the total brain volume: the Framingham Study

2008-11-17T11:36:00.000-08:00

Background While adults who drink low to moderate amounts of alcohol have lower rates of cardiovascular disease than other adults, the effect of alcohol on the brain is less clear. There is evidence that drinking large amounts of alcohol is related to brain atrophy. It is uncertain what the effects of low to moderate consumption might be.
Objective To determine whether consumption of smaller amounts of alcohol negatively affects brain volume or is protective in reducing the well-documented age-related decline in brain volume.
Design Total cerebral brain volume (TCBV) was computed, correcting for head size. Multivariate linear regression models were used to evaluate the association between 5 categories of alcohol consumption (abstainers, former drinkers, low, moderate, high) and TCBV, adjusting for age, sex, education, height, body mass index (calculated as weight in kilograms divided by height in meters squared), and the Framingham Stroke Risk Profile. Pairwise comparisons were also conducted between the alcohol consumption groups.
Participants A total of 1839 subjects from the Framingham Offspring Study who had magnetic resonance imaging of the brain between 1999 and 2001.
Results Most participants reported low alcohol consumption, and men were more likely than women to be moderate or heavy drinkers. There was a significant negative linear relationship between alcohol consumption and TCBV (r = –0.25; P < .001). This relationship was modified by sex, with alcohol consumption having a stronger association with TCBV in women than in men (r = –0.29 vs –0.20). Conclusions In contrast to studies on cardiovascular disease, this study found that moderate alcohol consumption was not protective against normal age-related differences in total brain volume. Rather, the more alcohol consumed, the smaller the total brain volume.

Reference:
Carol Ann Paul, MS; Rhoda Au, PhD; Lisa Fredman, PhD; Joseph M. Massaro, PhD; Sudha Seshadri, MD; Charles DeCarli, MD; Philip A. Wolf, MD Association of Alcohol Consumption With Brain Volume in the Framingham Study. Arch Neurol. 2008;65(10):1363-1367 (view)

Alzheimer's disease

2008-10-04T13:27:00.000-07:00

The disease course is divided into four stages, with a progressive pattern of cognitive and functional impairment.

Phases

The first symptoms are often mistaken as related to ageing or stress. Detailed neuropsychological testing can reveal mild cognitive difficulties up to eight years before a person fulfills the clinical criteria for diagnosis of AD. These early symptoms can affect the most complex daily living activities. The most noticeable deficit is memory loss, which shows up as difficulty in remembering recently learned facts and inability to acquire new information. Subtle problems with the executive functions of attentiveness, planning, flexibility, and abstract thinking, or impairments in semantic memory (memory of meanings, and concept relationships), can also be symptomatic of the early stages of AD. Apathy can be observed at this stage, and remains the most persistent neuropsychiatric symptom throughout the course of the disease. The preclinical stage of the disease has also been termed mild cognitive impairment, but there is still debate on whether this term corresponds to a different diagnostic entity by itself or just a first step of the disease.

Early dementia

In people with AD, the increasing impairment of learning and memory eventually leads to a definitive diagnosis. In a small proportion of them, difficulties with language, executive functions, perception (agnosia), or execution of movements (apraxia) are more prominent than memory problems. AD does not affect all memory capacities equally. Older memories of the person's life (episodic memory), facts learned (semantic memory), and implicit memory (the memory of the body on how to do things, such as using a fork to eat) are affected to a lesser degree than new facts or memories. Language problems are mainly characterised by a shrinking vocabulary and decreased word fluency, which lead to a general impoverishment of oral and written language. In this stage, the person with Alzheimer's is usually capable of adequately communicating basic ideas. While performing fine motor tasks such as writing, drawing or dressing, certain movement coordination and planning difficulties (apraxia) may be present, making sufferers appear clumsy. As the disease progresses, people with AD can often continue to perform many tasks independently, but may need assistance or supervision with the most cognitively demanding activities.Moderate dementiaProgressive deterioration eventually hinders independence. Speech difficulties become evident due to an inability to recall vocabulary, which leads to frequent incorrect word substitutions (paraphasias). Reading and writing skills are also progressively lost. Complex motor sequences become less coordinated as time passes, reducing the ability to perform most normal daily living activities. During this phase, memory problems worsen, and the person may fail to recognise close relatives. Long-term memory, which was previously intact, becomes impaired, and behavioural changes become more prevalent. Common neuropsychiatric manifestations are wandering, sundowning, irritability and labile affect, leading to crying, outbursts of unpremeditated aggression, or resistance to caregiving. Approximately % of patients also develop illusionary misidentifications and other delusional symptoms. Urinary incontinence can develop. These symptoms create stress for relatives and caretakers, which can be reduced by moving the person from home care to other long-term care facilities.Advanced dementiaDuring this last stage of AD, the patient is completely dependent upon caregivers. Language is reduced to simple phrases or even single words, eventually leading to complete loss of speech. Despite the loss of verbal language abilities, patients can often understand and return emotional signals. Although aggressiveness can still be present, extreme apathy and exhaustion are much more common results. Patients will ultimately not be able to perform even the most simple tasks without assistance. Muscle mass and mobility deteriorate to the point where they are bedridden, and they lose the ability to feed themselves. Finally comes death, usually caused directly by some external factor such as pressure ulcers or pneumonia, not by the disease itself.

Both amyloid plaques and neurofibrillary tangles are clearly visible by microscopy in brains of those afflicted by AD. Plaques are dense, mostly insoluble deposits of amyloid-beta protein and cellular material outside and around neurons. They continue to grow into insoluble twisted fibres within the nerve cell, often called tangles. Although many older individuals develop some plaques and tangles as a consequence of ageing, the brains of AD patients have a greater number of them in specific brain regions such as the temporal lobe.BiochemistryEnzymes act on the APP (amyloid precursor protein) and cut it into fragments. The beta-amyloid fragment is crucial in the formation of senile plaques in AD.Alzheimer's disease has been identified as a protein misfolding disease (proteopathy), caused by accumulation of abnormally folded A-beta and tau proteins in the brain. Plaques are made up of small peptides, – amino acids in length, called beta-amyloid (also written as A-beta or Aβ). Beta-amyloid is a fragment from a larger protein called amyloid precursor protein (APP), a transmembrane protein that penetrates through the neuron's membrane. APP is critical to neuron growth, survival and post-injury repair. In Alzheimer's disease, an unknown process causes APP to be divided into smaller fragments by enzymes through proteolysis. One of these fragments gives rise to fibrils of beta-amyloid, which form clumps that deposit outside neurons in dense formations known as senile plaques. In Alzheimer's disease, changes in tau protein lead to the disintegration of microtubules in brain cells.AD is also considered a tauopathy due to abnormal aggregation of the tau protein. Every neuron has a cytoskeleton, an internal support structure partly made up of structures called microtubules. These microtubules act like tracks, guiding nutrients and molecules from the body of the cell to the ends of the axon and back. A protein called tau stabilises the microtubules when phosphorylated, and is therefore called a microtubule-associated protein. In AD, tau undergoes chemical changes, becoming hyperphosphorylated; it then begins to pair with other threads, creating neurofibrillary tangles and disintegrating the neuron's transport system.Disease mechanismExactly how disturbances of production and aggregation of the beta amyloid peptide gives rise to the pathology of AD has not been elucidated. The amyloid hypothesis traditionally points to the accumulation of beta amyloid peptides as the central event triggering neuron degeneration. Accumulation of aggregated amyloid fibrils, which are believed to be the toxic form of the protein responsible for disrupting the cell's calcium ion homeostasis, induces programmed cell death (apoptosis). It is also known that Aβ selectively builds up in the mitochondria in the cells of Alzheimer's-affected brains, and it also inhibits certain enzyme functions and the utilisation of glucose by neurons.Various inflammatory processes and cytokines may also have a role in the pathology of Alzheimer's disease. Inflammation is a general marker of tissue damage in any disease, and may be either secondary to tissue damage in AD or a marker of an immunological response.GeneticsWhile the rare, early-onset form of Alzheimer's disease is mainly explained by mutations in three genes, the most common form has yet to be explained by a purely genetic model. The APOE gene is the strongest genetic risk factor for Alzheimer's discovered so far, but its presence is far from explaining all occurrences of the disease.Less than % of AD cases occurring before years of age are due to autosomal dominant (familial) mutations, which therefore represent less than .% of all cases. These mutations have been discovered in three different genes: amyloid precursor protein (APP) and presenilins and . Most mutations in the APP and presenilin genes increase the production of a small protein called Abeta, which is the main component of senile plaques.Most cases of Alzheimer's disease do not exhibit familial inheritance, but genes may act as risk factors. The best known genetic risk factor is the inheritance of the ε allele of the apolipoprotein E (APOE). This gene is implicated in up to % of late-onset sporadic Alzheimer's cases. Geneticists agree that numerous other genes also act as risk factors or have protective effects that influence the development of late onset Alzheimer's disease. Over genes have been tested for association with late-onset sporadic AD. One example is a variant of the reelin gene that may contribute to Alzheimer's risk in women.

Causes

Microscopy image of a neurofibrillary tangle, conformed by hyperphosphorylated tau proteinThree major competing hypotheses exist to explain the cause of the disease. The oldest, on which most currently available drug therapies are based, is the cholinergic hypothesis, which proposes that AD is caused by reduced synthesis of the neurotransmitter acetylcholine. The cholinergic hypothesis has not maintained widespread support, largely because medications intended to treat acetylcholine deficiency have not been very effective. Other cholinergic effects have also been proposed, for example, initiation of large-scale aggregation of amyloid, leading to generalised neuroinflammation.The amyloid hypothesis, currently the most popular, was proposed in . Here amyloid beta (Aβ) deposits are postulated to be the fundamental cause of the disease. It is a compelling theory because the gene for the amyloid beta precursor (APP) is located on chromosome , and people with trisomy (Down Syndrome) who thus have an extra gene copy almost universally exhibit AD by years of age. Also APOE, the major genetic risk factor for AD, leads to excess amyloid buildup in the brain before AD symptoms arise. Thus, Aβ deposition precedes clinical AD. Further evidence comes from the finding that transgenic mice that express a mutant form of the human APP gene develop fibrillar amyloid plaques and Alzheimer's-like brain pathology. An experimental vaccine was found to clear the amyloid plaques in early human trials, but it did not have any significant effect on dementia.Deposition of amyloid plaques does not correlate well with neuron loss. This observation supports the tau hypothesis, the idea that tau protein abnormalities initiate the disease cascade. In this model, hyperphosphorylated tau begins to pair with other threads of tau. Eventually, they form neurofibrillary tangles inside nerve cell bodies. When this occurs, the microtubules disintegrate, collapsing the neuron's transport system. This may result first in malfunctions in biochemical communication between neurons and later in the death of the cells.

Diagnosis

PET scan of the brain of a person with AD showing a loss of function in the temporal lobeAlzheimer's disease is usually diagnosed clinically from the patient history, collateral history from relatives, and clinical observations, based on the presence of characteristic neurological and neuropsychological features and the absence of alternative conditions. Advanced medical imaging with computed tomography (CT) or magnetic resonance imaging (MRI), and with single photon emission computed tomography (SPECT) or positron emission tomography (PET) can be used to help exclude other cerebral pathology or subtypes of dementia. Assessment of intellectual functioning including memory testing can further characterise the state of the disease. Medical organisations have created diagnostic criteria to ease and standardise the diagnostic process for practicing physicians. Sometimes the diagnosis can be confirmed or made at post-mortem when brain material is available and can be examined histologically.Diagnostic criteriaThe National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association (now known as the Alzheimer's Association) established the most commonly used diagnostic criteria for Alzheimer's disease. These criteria require that the presence of cognitive impairment, and a suspected dementia syndrome, be confirmed by neuropsychological testing for a clinical diagnosis of possible or probable AD. A histopathologic confirmation including a microscopic examination of brain tissue is required for a definitive diagnosis. Good statistical reliability and validity have been shown between the diagnostic criteria and definitive histopathological confirmation. Eight cognitive domains are most commonly impaired in AD—memory, language, perceptual skills, attention, constructive abilities, orientation, problem solving and functional abilities. These domains are equivalent to the NINCDS-ADRDA Alzheimer's Criteria as listed in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) published by the American Psychiatric Association.Diagnostic toolsNeuropsychological screening tests can help in the diagnosis of AD. In them patients have to copy drawings similar to the one shown in the picture, remember words, read or sum.Neuropsychological screening tests, such as the mini-mental state examination (MMSE), are widely used to evaluate the cognitive impairments needed for diagnosis. More comprehensive test arrays are necessary for high reliability of results, particularly in the earliest stages of the disease. Neurological examination in early AD will usually provide normal results, except for obvious cognitive impairment, which may not differ from standard dementia. Further neurological examinations are crucial in the differential diagnosis of AD and other diseases. Interviews with family members are also utilised in the assessment of the disease. Caregivers can supply important information on the daily living abilities, as well as on the decrease, over time, of the person's mental function. A caregiver's viewpoint is particularly important, since a person with AD is commonly unaware of his own deficits. Many times, families also have difficulties in the detection of initial dementia symptoms and may not communicate accurate information to a physician. Supplemental testing provides extra information on some features of the disease or is used to rule out other diagnoses. Blood tests can identify other causes for dementia than AD—causes which may, in rare cases, be reversible. Psychological tests for depression are employed, since depression can either be concurrent with AD or be the cause of cognitive impairment.When available as a diagnostic tool, SPECT and PET neuroimaging are used to confirm a diagnosis of Alzheimer's in conjunction with evaluations involving mental status examination. The ability of SPECT to differentiate Alzheimer's disease from other possible causes in somebody already known to be suffering from dementia, appears to be superior to attempts to diagnose by mental testing and history. A new technique known as PiB PET has been developed for directly and clearly imaging beta-amyloid deposits in vivo using a tracer that binds selectively to the Abeta deposits. Another recent objective marker of the disease is the analysis of cerebrospinal fluid for amyloid beta or tau proteins. Both advances have led to the proposal of new diagnostic criteria.PreventionIntellectual activities such as playing chess or regular social interaction have been linked to a reduced risk of AD in epidemiological studies, although no causal relationship has been found.Global studies of measures to prevent or delay the onset of AD have often produced inconsistent results. At present, there appears to be no definitive evidence to support the belief that any particular measure is effective in preventing AD. However, epidemiological studies have proposed relationships between certain modifiable factors, such as diet, cardiovascular risk, pharmaceutical products, or intellectual activities among others, and a population's likelihood of developing AD. Only further research, including clinical trials, will reveal whether, in fact, these factors can help to prevent AD.The components of a Mediterranean diet, which include fruit and vegetables, bread, wheat and other cereals, olive oil, fish, and red wine, may all individually or together reduce the risk and course of Alzheimer's disease. Several vitamins such as B, B, C or folic acid have been found in some studies to be related to a reduced risk of AD but other studies indicate that they do not have any significant effect on the onset or course of the disease and may have important secondary effects. Curcumin from the curry spice turmeric has shown some effectiveness in preventing brain damage in mouse models. The prevalence of AD among the elderly in India has been reported to be about one quarter of that in the U.S., and curry intake has been reported to correlate positively with cognitive function in elderly Asians.Although cardiovascular risk factors, such as hypercholesterolemia, hypertension, diabetes, and smoking, are associated with a higher risk of onset and course of AD, statins, which are cholesterol lowering drugs, have not been effective in preventing or improving the course of the disease. However long-term usage of non-steroidal anti-inflammatory drug (NSAIDs), is associated with a reduced likelihood of developing AD in some individuals. Other pharmaceutical therapies such as female hormone replacement therapy are no longer thought to prevent dementia, and a systematic review concluded that there was inconsistent and unconvincing evidence that ginkgo has any positive effect on cognitive impairment.Intellectual activities such as reading, playing board games, completing crossword puzzles, playing musical instruments, or regular social interaction may also delay the onset or reduce the severity of Alzheimer's disease. Bilingualism is also related to a later onset of Alzheimer's.Some studies have shown an increased risk of developing AD with occupational exposure to magnetic fields, intake of metals, particularly aluminium, or exposure to solvents. The quality of some of these studies has been criticised, and other studies have concluded that there is no relationship between these environmental factors and the development of AD.

Management

There is no cure for Alzheimer's disease; available treatments offer relatively small symptomatic benefit but remain palliative in nature. Current treatments can be divided into pharmaceutical, psychosocial and caregiving.PharmaceuticalThree-dimensional molecular model of donepezil, an acetylcholinesterase inhibitor used in the treatment of AD symptomsMolecular structure of memantine, a medication approved for advanced AD symptomsFour medications are currently approved by regulatory agencies such as the U.S. Food and Drug Administration (FDA) and the European Medicines Agency (EMEA) to treat the cognitive manifestations of AD: three are acetylcholinesterase inhibitors and the other is memantine, an NMDA receptor antagonist. No drug has an indication for delaying or halting the progression of the disease.Reduction in the activity of the cholinergic neurons is a well-known feature of Alzheimer's disease. Acetylcholinesterase inhibitors are employed to reduce the rate at which acetylcholine (ACh) is broken down, thereby increasing the concentration of ACh in the brain and combating the loss of ACh caused by the death of cholinergic neurons. As of , the cholinesterase inhibitors approved for the management of AD symptoms are donepezil (brand name Aricept), galantamine (Razadyne), and rivastigmine (branded as Exelon and Exelon Patch). There is evidence for the efficacy of these medications in mild to moderate Alzheimer’s disease, and some evidence for their use in the advanced stage. Only donepezil is approved for treatment of advanced AD dementia. The use of these drugs in mild cognitive impairment has not shown any effect in a delay of the onset of AD. The most common side effects are nausea and vomiting, both of which are linked to cholinergic excess. These side effects arise in approximately ten to twenty percent of users and are mild to moderate in severity. Less common secondary effects include muscle cramps, decreased heart rate (bradycardia), decreased appetite and weight, and increased gastric acid production. Glutamate is a useful excitatory neurotransmitter of the nervous system, although excessive amounts in the brain can lead to cell death through a process called excitotoxicity which consists of the overstimulation of glutamate receptors. Excitotoxicity occurs not only in Alzheimer's disease, but also in other neurological diseases such as Parkinson's disease and multiple sclerosis. Memantine (brand names Akatinol, Axura, Ebixa/Abixa, Memox and Namenda), is a noncompetitive NMDA receptor antagonist first used as an anti-influenza agent. It acts on the glutamatergic system by blocking NMDA receptors and inhibiting their overstimulation by glutamate. Memantine has been shown to be moderately efficacious in the treatment of moderate to severe Alzheimer’s disease. Its effects in the initial stages of AD are unknown. Reported adverse events with memantine are infrequent and mild, including hallucinations, confusion, dizziness, headache and fatigue. The combination of memantine and donepezil has been shown to be "of statistically significant but clinically marginal effectiveness".Antipsychotic drugs are modestly useful in reducing aggression and psychosis in Alzheimer's patients with behavioural problems, but are associated with serious adverse effects, such as cerebrovascular events, movement difficulties or cognitive decline, that do not permit their routine use.Psychosocial interventionA specifically designed room for sensory integration therapy, also called snoezelen; an emotion-oriented psychosocial intervention for people with dementiaPsychosocial interventions are used as an adjunct to pharmaceutical treatment and can be classified within behaviour-, emotion-, cognition- or stimulation-oriented approaches. Research on efficacy is unavailable and rarely specific to AD, focusing instead on dementia in general.Behavioural interventions attempt to identify and reduce the antecedents and consequences of problem behaviours. This approach has not shown success in improving overall functioning, but can help to reduce some specific problem behaviours, such as incontinence. There is a lack of high quality data on the effectiveness of these techniques in other behaviour problems such as wandering.Emotion-oriented interventions include reminiscence therapy, validation therapy, supportive psychotherapy, sensory integration, also called snoezelen, and simulated presence therapy. Supportive psychotherapy has received little or no formal scientific study, but some clinicians find it useful in helping mildly impaired patients adjust to their illness. Reminiscence therapy (RT) involves the discussion of past experiences individually or in group, many times with the aid of photographs, household items, music and sound recordings, or other familiar items from the past. Although there are few quality studies on the effectiveness of RT, it may be beneficial for cognition and mood. Simulated presence therapy (SPT) is based on attachment theories and involves playing a recording with voices of the closest relatives of the person with Alzheimer's disease. There is preliminary evidence indicating that SPT may reduce anxiety and challenging behaviours. Finally, validation therapy is based on acceptance of the reality and personal truth of another's experience, while sensory integration is based on exercises aimed to stimulate senses. There is little evidence to support the usefulness of these therapies.The aim of cognition-oriented treatments, which include reality orientation and cognitive retraining, is the reduction of cognitive deficits. Reality orientation consists in the presentation of information about time, place or person in order to ease the understanding of the person about its surroundings and his or her place in them. On the other hand cognitive retraining tries to improve impaired capacities by exercitation of mental abilities. Both have shown some efficacy improving cognitive capacities, although in some studies these effects were transient and negative effects, such as frustration, have also been reported.Stimulation-oriented treatments include art, music and pet therapies, exercise, and any other kind of recreational activities. Stimulation has modest support for improving behaviour, mood, and, to a lesser extent, function. Nevertheless, as important as these effects are, the main support for the use of stimulation therapies is the improvement in the person's daily life routines.CaregivingFurther information: Caregiving and dementiaSince Alzheimer's has no cure and it gradually renders people incapable of tending for their own needs, caregiving essentially is the treatment and must be carefully managed over the course of the disease.During the early and moderate stages, modifications to the living environment and lifestyle can increase patient safety and reduce caretaker burden. Examples of such modifications are the adherence to simplified routines, the placing of safety locks, the labelling of household items to cue the person with the disease or the use of modified daily life objects. The patient may also become incapable of feeding themselves, so they require food in smaller pieces or pureed. When swallowing difficulties arise, the use of feeding tubes may be required. In such cases, the medical efficacy and ethics of continuing feeding is an important consideration of the caregivers and family members. The use of physical restraints is rarely indicated in any stage of the disease, although there are situations when they are necessary to prevent harm to the person with AD or their caregivers.As the disease progresses, different medical issues can appear, such as oral and dental disease, pressure ulcers, malnutrition, hygiene problems, or respiratory, skin, or eye infections. Careful management can prevent them, while professional treatment is needed when they do arise. During the final stages of the disease, treatment is centred on relieving discomfort until death.PrognosisThe early stages of Alzheimer's disease are difficult to diagnose. A definitive diagnosis is usually made once cognitive impairment compromises daily living activities, although the person may still be living independently. He will progress from mild cognitive problems, such as memory loss through increasing stages of cognitive and non-cognitive disturbances, eliminating any possibility of independent living.Life expectancy of the population with the disease is reduced. The mean life expectancy following diagnosis is approximately seven years. Fewer than % of patients live more than fourteen years. Disease features significantly associated with reduced survival are an increased severity of cognitive impairment, decreased functional level, history of falls, and disturbances in the neurological examination. Other coincident diseases such as heart problems, diabetes or history of alcohol abuse are also related with shortened survival. While the earlier the age at onset the higher the total survival years, life expectancy is particularly reduced when compared to the healthy population among those who are younger. Men have a less favourable survival prognosis than women.The disease is the underlying cause of death in % of all cases. Pneumonia and dehydration are the most frequent immediate causes of death, while cancer is a less frequent cause of death than in the general population.

Epidemiology

Two main measures are used in epidemiological studies: incidence and prevalence. Incidence is the number of new cases per unit of person–time at risk (usually number of new cases per thousand person–years); while prevalence is the total number of cases of the disease in the population at a given time.Regarding incidence, cohort longitudinal studies (studies where a disease-free population is followed over the years) provide rates between – per thousand person–years for all dementias and – for AD, which means that half of new dementia cases each year are AD. Advancing age is a primary risk factor for the disease and incidence rates are not equal for all ages: every five years after the age of , the risk of acquiring the disease approximately doubles, increasing from to as much as per thousand person years. There are also sex differences in the incidence rates, women having a higher risk of developing AD particularly in the population older than .Prevalence of AD in populations is dependent upon different factors including incidence and survival. Since the incidence of AD increases with age, it is particularly important to include the mean age of the population of interest. In the United States, Alzheimer prevalence was estimated to be .% in the year both overall and in the – age group, with the rate increasing to % in the – group and to % in the greater than group. Prevalence rates in less developed regions are lower. The World Health Organization estimated that in , .% of people worldwide had dementia, and that the prevalence would increase to .% in and to .% in . Other studies have reached similar conclusions. Another study estimated that in , .% of the world population (range .–.%; absolute number . million, range .–. million) were afflicted by AD, and that the prevalence rate would triple and the absolute number would quadruple by the year .HistoryAuguste D, first described patient with AD by Alois Alzheimer in The ancient Greek and Roman philosophers and physicians associated old age with increasing dementia. It was not until that German psychiatrist Alois Alzheimer identified the first case of what became known as Alzheimer's disease in a fifty-year-old woman he called Auguste D. Alzheimer followed her until she died in , when he first reported the case publicly. During the next five years, eleven similar cases were reported in the medical literature, some of them already using the term Alzheimer's disease. The disease was first described as a distinctive disease by Emil Kraepelin, who included Alzheimer’s disease, also named presenile dementia by Kraepelin, as a subtype of senile dementia in the eighth edition of his Textbook of Psychiatry, published in .For most of the twentieth century, the diagnosis of Alzheimer's disease was reserved for individuals between the ages of and who developed symptoms of dementia. The terminology changed after when a conference on AD concluded that the clinical and pathological manifestations of presenile and senile dementia were almost identical, although the authors also added that this did not rule out the possibility of different aetiologies. This eventually led to the diagnosis of Alzheimer's disease independently of age. The term senile dementia of the Alzheimer type (SDAT) was used for a time to describe the condition in those over , with classical Alzheimer's disease being used for those younger. Eventually, the term Alzheimer's disease was formally adopted in medical nomenclature to describe individuals of all ages with a characteristic common symptom pattern, disease course, and neuropathology.

Social costs

Dementia, and specifically Alzheimer's disease, may be among the most costly diseases for society in the developed countries, while their cost in developing countries such as Argentina, or Korea, is also high and rising. These costs will probably increase with the ageing of society, becoming an important social problem. AD associated costs include direct medical costs such as nursing home care, direct nonmedical costs such as in-home day care, and indirect costs such as lost productivity of both patient and caregiver. Numbers vary between studies but dementia costs worldwide have been calculated around $ billion, while costs of Alzheimer in the United States may be $ billion each year.The greatest origin of costs for society is the long-term care by health care professionals and particularly institutionalisation, which corresponds to / of the total costs for society. The cost of living at home is also very high, specially when informal costs for the family, such as caregiving time and caregiver's lost earnings, are taken into account.Costs increase with dementia severity and the presence of behavioural disturbances, and are related to the increased caregiving time required for the provision of physical care. Therefore any treatment that slows cognitive decline, delays institutionalisation or reduces caregivers' hours will have economic benefits. Economic evaluations of current treatments have shown positive results.The role of the main caregiver is often taken by the spouse or a close relative. Alzheimer's disease is known for placing a great burden on caregivers which includes social, psychological, physical or economic aspects. Home care is usually preferred by patients and families. This option also delays or eliminates the need for more professional and costly levels of care. Nevertheless two-thirds of nursing home residents have dementias.Dementia caregivers are subject to high rates of physical and mental disorders. Factors associated with greater psychosocial problems of the primary caregivers include having an affected person at home, the carer being a spouse, demanding behaviours of the cared person such as depression, behavioural disturbances, hallucinations, sleep problems or walking disruptions and social isolation. Regarding economic problems, family caregivers often give up time from work to spend hours per week on average with the person with AD, while the costs of caring for them are high. Direct and indirect costs of caring for an Alzheimer's patient average between $, and $, per year in the United States, depending on the study.Cognitive behavioural therapy and the teaching of coping strategies either individually or in group have demonstrated their efficacy in improving caregivers' psychological health.Research directionsAs of , the safety and efficacy of more than pharmaceutical treatments are being investigated in clinical trials worldwide, and approximately one-fourth of these compounds are in Phase III trials, which is the last step prior to review by regulatory agencies.One area of clinical research is focused on treating the underlying disease pathology. Reduction of amyloid beta levels is a common target of compounds under investigation. Immunotherapy or vaccination for the amyloid protein is one treatment modality under study. Unlike preventative vaccination, the putative therapy would be used to treat people already diagnosed. It is based upon the concept of training the immune system to recognise, attack, and reverse deposition of amyloid, thereby altering the course of the disease. An example of such a vaccine under investigation was ACC-, although the trials were suspended in . Similar agents are bapineuzumab, an antibody designed as identical to the naturally-induced anti-amyloid antibody, and MPC-, a selective amyloid beta- lowering agent. Other approaches are neuroprotective agents, such as AL-, and metal-protein interaction attenuation agents, such as PBT. A TNFα receptor fusion protein, etanercept has showed encouraging results.In , two separate clinical trials showed positive results in modifying the course of disease in mild to moderate AD with methylthioninium chloride (trade name rember), a drug that inhibits tau aggregation, and dimebon, an antihistamine.

Video on epilepsy

2008-09-18T02:43:00.000-07:00

Epilepsy is a seizure disorder in which there is a sudden, temporary change in how the brain functions (video).

Publications from The Alzheimer's Society

2008-08-26T12:01:00.000-07:00

The following publications can be downloaded free of charge from Alzheimer's Society website.

About dementia
Worried about your memory
Worried about your memory? BookletThis booklet is designed to help you understand more about memory loss, so that if you are worried - either about your own or someone else's memory - you can seek advice and, if necessary, get treatment and support.
Worried about your memory? leaflet Worried about your memory? poster
Worried about your memory booklet available in other languages
Please take a look at WAYM? booklets in other languages including Welsh, Arabic, Chinese, Gujurati, Somali, Urdu, Punjabi, Tamil, Benagli, French and Polish
Understanding vascular dementiaThis booklet has been written to help anyone affected by vascular dementia - people with dementia, carers, family members and professionals - to understand the condition.
Be head strongA guide to help you reduce your risk of developing dementia.
Non-pharmacological therapies for the treatment of behavioural symptoms in people with dementiaA 2005 report on non-pharmacological therapies.
Journal of Quality Research in DementiaBack issues of the The Journal of Quality Research in Dementia.
Quality Research in Dementia Annual Round-UpThe Annual Round-Up of Quality Research in Dementia, Alzheimer's Society research grants programme.

Caring for a person with dementia
Love is forever (download only)Couples speak from the heart on facing dementia together - a reminder of how love endures.
Inclusion pack for Gay and Lesbian carersA toolkit for gay and lesbian carers, including a newsletter and a number of useful documents.

Long-term care
When does the NHS pay for care?This booklet has been produced by Alzheimer's Society and is also supported by Age Concern, Help the Aged and the Royal College of Nursing. It contains guidance on eligibility for continuing NHS health care funding in England and how to appeal if it is not awarded.
Have you been paying for care?As part of our campaign for an end to the unfair system of charging for care, we are encouraging people to examine whether they have been wrongly charged for care and, if so, to seek redress. This leaflet explains how to do so.
Putting care rightTaking the decision to move to a care home will always be a difficult one, for the person with dementia and their family. But it can be easier if you are armed with the right information. This booklet can help people facing that kind of decision by setting out what issues to consider and questions to ask.

"Know Stroke" Video

2008-08-26T11:02:00.000-07:00

This eight-minute video features experts in the field of stroke discussing the symptoms of stroke and what to do, as well as stories from people who have successfully recovered from a stroke. View video

Videos on different types of headache

2008-08-21T00:13:00.000-07:00

Clasic migraine:

Tension Type Headache

Combination Migraine & Tension Type Headache

Migraine & Sinusitis

Epilepsy surgery

2008-08-20T14:49:00.000-07:00

Definition
Epilepsy surgery is a procedure that either removes or isolates the area of your brain where your seizures originate. If the section of your brain where your seizures begin is too vital to remove, your surgeon will make a series of incisions that prevent your seizures from spreading to the rest of your brain.
Epilepsy surgery works best for people who have seizures that always originate in the same place in their brains. To be considered for epilepsy surgery, you must have tried at least two anti-seizure drugs without success. If two drugs have failed, it is highly unlikely that any other anti-epileptic drug will help you.

Why it's done
In most cases, epilepsy surgery can reduce — and sometimes even eliminate — your seizure activity. Repeated epileptic seizures can cause:
Broken bones or other injuries from falling during a seizure
Drowning, if the seizure occurs during a bath or swimming
Brain damage from prolonged seizures
Sudden death, a rare complication of epilepsy
Because some childhood seizures stop at puberty, doctors often hesitate to recommend surgery for children. But children may have the most to gain from epilepsy surgery because they risk the greatest harm from epileptic seizures. Because their brains are still developing, children are more vulnerable to permanent brain damage. Seizures also interfere with children's social development.
The type of epilepsy surgery you may have depends on the types of seizures you experience, and where they begin in your brain. They include:
Removing a portion of the brain. The most common type of epilepsy surgery is the removal of the portion of the brain — usually about the size of a golf ball — that's causing the seizures. This type of surgery is highly successful for seizures that start in the temporal lobe, the part of your brain that lies along the sides of your head. Up to 90 percent of those who have this surgery, called temporal lobe resection, either become seizure-free or have a significant reduction in the number of seizures they experience.
Making incisions to seal off part of the brain. If the portion of the brain that's causing seizures is too vital to remove, surgeons may make a series of cuts to help isolate that section of the brain. This prevents seizures from moving into other parts of the brain. About 70 percent of the people who have this type of epilepsy surgery, called multiple subpial transection, report improvement in seizure control.
Severing connection between hemispheres. Another type of epilepsy surgery, called a corpus callosotomy, severs the network of neural connections between the right and left halves (hemispheres) of the brain. This surgery is used primarily in children who have severe seizures that start in one hemisphere and spread to the other side. This can help reduce the severity of seizures.
Removing half the brain. The most radical type of epilepsy surgery removes the outer layer of half the brain. Hemispherectomy is used in children who have seizures because of damage to just one half (hemisphere) of the brain — which occurs in a few rare conditions that are present at birth or that appear in early infancy. The chance of a full recovery is best in younger children.
Risks
Your risks may vary, depending on which variety of epilepsy surgery is used and the portion of your brain involved:
Temporal lobe surgery. This procedure can result in problems with memory or language, two functions handled by the temporal lobe. Double vision also is common after temporal lobe surgery. These problems are typically temporary.
Corpus callosotomy. Severing the network of neural connections between the right and left hemispheres of the brain stops seizure activity from spreading throughout the brain, but it doesn't stop the seizures. In fact, it can sometimes increase the number of seizures you experience, but the seizures should be less severe.
Hemispherectomy. Removing the outer layer of half the brain usually results in a reduced visual field and some paralysis on one side of the body. Intense rehabilitation often brings back nearly normal abilities.

Pinpointing seizure location
If you're a candidate for epilepsy surgery, your pre-surgical evaluation may include:
Baseline electroencephalogram (EEG). In this test, electrodes are placed on the scalp to measure electrical activity produced by the brain.
Video EEG. A continuous EEG with video monitoring records your seizures as they occur. Because your seizure medications have to be reduced or temporarily stopped so that seizures will occur, you'll have to be admitted to the hospital for this test. Correlating the changes in your EEG with your body's movements during a seizure helps "pinpoint" the area of your brain in which your seizures are starting.
MRI or CT of the head. MRI and CT scans can identify structural problems — such as lesions or scar tissue in the brain — that could be causing seizures.
Positron emission tomography (PET) and functional MRI. PET and functional MRI scans can monitor the brain's activity and detect abnormalities.
Single-photon emission computerized tomography (SPECT). The scan image varies in color depending on the amount of blood flow in different areas of the brain. Typically, blood flow is higher in the part of the brain where seizures originate. In some cases, doctors combine several types of imaging techniques to help locate the troublesome area of the brain.

What you can expect
During the procedureTo avoid infection, your hair will need to be clipped short over the section of your skull that will be removed during the operation. Many times the neurosurgical team will be able to shave that area in such a way that other parts of your hair will cover up the bald patch after the surgery. Some people want their entire head shaved.
You will have an intravenous line in place, and your heart rate, blood pressure and oxygen levels will be monitored throughout the surgery. An EEG monitor also may be recording your brain waves during the operation to better localize the part of your brain where your seizures start.
Epilepsy surgery is usually performed under general anesthesia. That means you'll be asleep during the procedure, which involves making a small opening in your skull to access the brain. In rare circumstances, your surgeon may wake you up during part of the operation to help the team determine which parts of your brain control language and movement. After surgery the window of bone is replaced and fastened to the remaining skull for healing. Most epilepsy surgeries take at least four hours.
After the procedureYou'll be in a special recovery area to be monitored carefully as you awaken from the anesthesia. You may need to spend the first night after surgery in an intensive care unit. The total hospital stay for most epilepsy surgeries is usually about three or four days.
When you wake up, your head is going to be swollen and painful. Most people need narcotics for the pain for at least the first few days. An ice pack on your head also may help. Most postoperative swelling and pain resolves within several weeks.
You'll probably not be able to return to work or school for approximately three months. You should rest and relax the first few weeks after epilepsy surgery, and then gradually escalate your activity.
It's unlikely that you would need any rehabilitation as long as the surgery was completed without complications. Complications — such as stroke, paralysis or loss of speech — occur in about 1 percent of the most common variety of epilepsy surgery, where a section of the temporal lobe is removed.

Results
Most people who have epilepsy surgery see a significant reduction in the number of seizures they experience. Many people actually stop having seizures entirely.
Seizures that begin in the temporal lobe are the most likely to be resistant to medication, but they are also the most likely to be helped by epilepsy surgery. Nearly 90 percent of people who experience temporal lobe seizures see a significant reduction or even a cessation of seizures after epilepsy surgery.
You must continue to take anti-seizure medications after epilepsy surgery, to help improve your chances of remaining seizure-free. Your doctor may be able to wean you off anti-seizure drugs after a year or two.

Stroke rehabilitation: What to expect as you recover from stroke

2008-08-20T14:45:00.000-07:00

Stroke rehabilitation (stroke rehab) is an important part of recovery after stroke. Find out what's involved in stroke rehabilitation.
Getting back on your feet is likely one of your top concerns after a stroke. Whether it's returning to work, walking your dog or regaining enough dexterity to tie your shoes, or dress or feed yourself without assistance — all of these are goals of stroke rehabilitation.
Stroke rehabilitation, also called stroke rehab, is a key part of your post-stroke care plan. Each year, more than 700,000 people in the United States have a stroke, and about two-thirds of them will need some type of stroke rehabilitation.
The severity of stroke complications and each person's ability to recover lost abilities varies widely. However, stroke rehabilitation can usually help you achieve the best long-term results.

What is stroke rehabilitation?
The goal of any stroke rehabilitation program is to help you relearn skills lost when stroke damaged part of your brain. Participating in stroke rehabilitation helps you regain as much independence as possible and achieve the best quality of life.
Stroke rehabilitation can include physical and occupational therapy or exercises that help you control your movements. These therapies or exercises also might help you learn new ways to perform tasks or compensate for any weakness in your limbs or other areas of your body. For example, your stroke rehabilitation therapy might include learning to bathe, dress or eat with only one hand. Speech therapy may be needed to learn ways to communicate if your speech has been affected.
It takes time to relearn skills. The most important key to success for any stroke rehabilitation program is well-focused and repetitive practice. The saying "Practice makes perfect" applies to stroke rehabilitation just as it does to learning any new skill.

What's involved in stroke rehab?
Stroke rehabilitation can involve physical therapy or exercise, as well as relearning language and communication skills with speech therapy. Stroke rehabilitation may include some or all of the following therapies:
Therapy for communication disorders. After a stroke, you may have problems speaking, listening, writing or comprehending speech or other forms of communication — a disorder known as aphasia. Aphasia is a common stroke complication, affecting about 40 percent of stroke survivors. Speech therapy can help you regain some or most of your lost ability. The process can be slow and is often frustrating, but with practice you'll likely improve. You may practice basic skills, such as naming objects or explaining the purpose of an object.
Strengthening motor skills. Muscle weakness after a stroke is common. Your therapist may work with you on exercises that improve your strength. Weakened muscles in the throat may also cause problems swallowing (dysphagia). Exercises, new swallowing techniques, and changes in food consistency may help correct this.
Mobility training. More than half of stroke survivors have difficulty walking. Therapy options include the use of walking aids such as braces, walkers or canes to support part of your body's weight while you relearn how to walk.
Range of motion therapy. You may have cramped or contracted muscles after stroke — a disorder known as spasticity. Physical and occupational therapy use exercises and other treatments to help lessen muscle tension and regain range of motion.
Psychological therapy. After stroke, you may feel depressed and have difficulty managing your emotions. Antidepressant medications, counseling with a mental health professional and participation in support groups may help.
Constraint-induced therapy. This therapy involves restricting the use of an unaffected limb while you practice moving the affected limb. Forcing you to use the affected limb more can help improve your limb function. This therapy is also known as "forced-use" therapy because it forces you to use the affected limb.
Electrical stimulation. This involves the use of electricity to stimulate weakened muscles, causing them to contract. This may help with muscle re-education in some individuals.

When should stroke rehabilitation begin?
Stroke rehabilitation should begin as soon as possible after a stroke. The first priority is to stabilize your medical condition and get life-threatening conditions under control. Doctors will also take measures to prevent another stroke and limit any stroke-related complications. However, once these steps have been taken, it's common for stroke rehabilitation to start during your hospital stay. The sooner you begin stroke rehabilitation, the more likely you are to regain lost abilities and skills.

How long does stroke rehabilitation last?
The length of your stroke rehabilitation depends on the severity of your stroke-related complications. While some stroke survivors recover quickly, most stroke survivors need some form of stroke rehabilitation long term, possibly months after their stroke. Your stroke rehabilitation plan will change during your recovery as you relearn skills and your needs change.
The length of time you spend doing stroke rehabilitation during each therapy session will also vary depending on your recovery and severity of your symptoms. You may spend as little as one hour a day three days a week, or up to three to five hours a day, seven days a week.

Where will stroke rehabilitation take place?
You'll probably begin stroke rehabilitation while you're still in the hospital. Before you leave the hospital, you and your family will work with hospital social workers and your care team to determine the best rehabilitation setting for you depending on your needs, what insurance will cover, and what is most convenient for you and your family. These options include:
Inpatient rehabilitation units. These are facilities that are either free-standing or part of a larger hospital or clinic. You may stay here for two to three weeks as part of an intensive rehabilitation program. Expect to receive at least three hours of therapy on most days.
Outpatient units. These facilities are often part of a hospital or clinic. You may spend several hours a day, three days a week, at such units relearning skills.
Nursing facilities. The type of care available at a nursing facility — sometimes referred to as a nursing home — varies widely. Some facilities specialize in rehabilitation, while others offer less intense therapy options. Talk with your doctor and family about the best option for you.
Home-based programs. This type of program — having therapy done in your home — allows greater flexibility than other options. One drawback is you likely won't have access to specialized rehabilitation equipment in your home. In addition, insurance strictly controls who qualifies for home-based therapy.

Who participates in your stroke rehabilitation team?
Stroke rehabilitation involves a variety of specialists. Some of those who will likely help with your recovery include:
Physicians. Ranging from your primary care doctor to specialists in physical medicine and rehabilitation (physiatrists) to neurologists, physicians help guide your care and prevent complications.
Rehabilitation nurses. These nurses specialize in caring for those with disabilities. They help carry forward skills learned in physical, occupational and speech therapy into your daily routines.
Physical therapists. These therapists help you relearn physical tasks, such as walking and keeping your balance.
Occupational therapists. These therapists work with you to relearn daily skills, such as bathing, tying your shoes or buttoning your shirt. They can also address safety issues in your home by suggesting changes or proper home equipment.
Speech and language pathologists. These specialists help you improve your language skills and ability to swallow.
Social workers. Social workers work with you on financial decisions, as well as help you arrange new living arrangements if necessary.
Psychologists. These specialists work to ensure your mental and emotional health concerns are addressed.
Therapeutic recreation specialists. These specialists can help you relearn skills needed to do hobbies or other activities you enjoyed before your stroke.

What factors affect the outcome of stroke rehabilitation?
Because stroke recovery varies so widely from person to person, it's hard to predict how many abilities you might recover and how soon. However, in general, successful stroke rehabilitation depends on:
The amount of damage to your brain
How skilled your stroke rehabilitation team is
Cooperation of your friends and family — having a good support network has a big impact on your recovery
Timing of your rehabilitation — the sooner you start, the better you'll do
Stroke rehabilitation takes time
Recovering from a stroke can be a long and — at times — frustrating experience. The difficulties you face are normal. Dedication and willingness to work toward improvement will help you gain the most benefit.

Cerebral arteriography

2008-08-20T14:40:00.000-07:00

In cerebral arteriography, a catheter is threaded through the major arteries of the trunk and into the carotid or vertebral artery. Dye (or contrast medium) is injected to outline arteries not normally seen in X-ray imaging. This helps reveal abnormalities or obstructions.
See video.

MRI

2008-08-20T14:38:00.000-07:00

Magnetic resonance imaging (MRI) uses a magnetic field and radio waves to create clear and detailed cross-sectional images of your head and body.
You don't need to prepare for an MRI. Unless otherwise instructed, eat normally (before the procedure) and if you take medications, continue to do so. Once checked in, you'll likely change into a gown and robe.
Remove all accessories, such as your watch, jewelry and hairpins. Also remove things like wigs, dentures and hearing aids. Tell your MRI technologist if you have metal or electronic devices in your body, because their presence may be a safety hazard. The magnet may disable your electronic device or affect the MR image quality.
Before your exam, the MRI technologist may confirm your health issues and answer any last-minute questions.
Most MRI machines look like a big doughnut. A large magnet is housed within a circular structure. You'll lie down on a table that slides into the opening of the magnet. Depending on where you need magnetic resonance imaging, a small device called a coil may be placed around the body part being examined. The coil receives the magnetic resonance signal.
Your technologist will monitor you from another room, but you can talk with him or her by microphone. In some cases, a friend or family member may stay with you. If you are especially anxious or have claustrophobia, you may be offered a mild sedative.
Magnetic resonance imaging is safe for children, and an adult may stay in the scanning room for reassurance. Young children, toddlers and infants may need sedation since they must remain still throughout the imaging process.
The exam itself is painless, but noisy. You don't feel the magnetic field or radio waves, and there are no moving parts to see. However, the magnet produces repetitive tapping and thumping sounds, so you'll likely be offered earplugs or special metal-free headphones to help block the noise. MRIs that require your head to be in the machine often include a mirror for you to see out.
Animation: Here's how an MRI is created. Most machines use tube-shaped magnets. The strong magnetic field is produced by passing an electric current through wire loops inside of the magnet's protective housing. Other coils in the magnet send and receive radio waves.
Once you're positioned inside the magnet, some protons within your body will align with the magnetic field. This is harmless and you won't feel it happening.
Once aligned, these protons respond to low-power radio waves that stimulate signals from your body. The radio waves are generated by specialized radio frequency coils (RF coils), which are antennas designed for medical imaging.
The signal that your body returns is detected by the coils surrounding the specific body part targeted for imaging. A computer processes all the signals and reconstructs a highly detailed image.
The final picture is a composite, three-dimensional representation of your body. Any two-dimensional plane — or slice — can be electronically created and displayed on a computer for interpretation. These images can also be converted from the screen into photographic film for further study.
Narrator: An MRI exam lasts between 30 and 90 minutes. Because movement can blur the resulting images, remain still and breathe quietly without moving your head or body.
Although not shown in this video, contrast agents are sometimes injected into your veins to enhance the appearance of certain tissues or blood vessels.
Once your MRI is complete, you may be asked to wait until the images are reviewed to make sure that no additional imaging is necessary. If no further studies are required, you'll be released and can resume your regular activities.

See video.

Lumbar Puncture

2008-03-19T03:08:00.001-07:00

Lumbar puncture, also called a spinal tap, is the procedure doctors use to obtain a sample of cerebrospinal fluid (the liquid that surrounds the brain and spinal cord) for tests. Cerebrospinal fluid (CSF) is formed in special areas of the brain called ventricles. It flows down from the ventricles into the area around the spinal cord. CSF is usually clear and contains small amounts of proteins and glucose (sugar).

REASONS FOR HAVING A LUMBAR PUNCTURE
Suspected meningitis (infection of the covering of the brain and spinal cord)
Leukemia or lymphoma
Evaluation for neurological diseases, such as multiple sclerosis, neuropathy, or recurrent seizures Fever of unknown origin
Lumbar puncture is also done by anesthesiologists to administer spinal anesthesia (also known as subarachnoid block) for some types of surgery.
For cancer treatment, chemotherapy medications are sometimes injected directly through the lumbar puncture needle into the CSF. The medicine flows freely in the CSF and can go to the brain or spinal cord where it is needed.
WHAT TO EXPECT DURING A LUMBAR PUNCTURE
During a lumbar puncture, you either lie on your side or sit upright. Your back is scrubbed with an antiseptic solution. Local anesthetic medicine is injected into the skin. When the skin is numb from the local anesthetic, a small needle is inserted into your back at the level of the hip bones below the bottom of the spinal cord. The needle is pushed forward gently until the CSF is found. For testing, 1 to 2 teaspoonfuls of fluid are removed and put into special sterile tubes. If you are receiving spinal anesthesia for surgery, no spinal fluid is drained out. The anesthetic medicine is injected directly into the CSF, and your legs and buttocks will begin to feel numb.
Sometimes lumbar puncture can be difficult to perform. Persons who have had back surgery, who have an abnormal back shape such as scoliosis (curvature of the spine), are pregnant, or are very obese are at risk for difficulty in the lumbar puncture. Lumbar puncture is easier to perform if the patient follows positioning instructions completely.

FOR MORE INFORMATION
American Academy of Pediatrics http://www.aap.org/
American Society of Anesthesiologists http://www.asahq.org/patienteducation.htm
Video

Herniated Lumbar Disks

2008-03-19T03:05:00.000-07:00

The vertebrae (bones of the spine) are cushioned by blocks or pads of tissue called disks. These disks are round and flat and made up of 2 parts: the annulus (a tough outer capsule or ring) and the nucleus (an inner, spongy core of jellylike material). When these disks are healthy, they act as shock absorbers for the spine and are essential in keeping the spine flexible. The normal, everyday pressures on the spine force the outer surface to bulge slightly. When these disks are damaged from an injury, normal wear and tear, or disease, they may bulge abnormally or rupture (break open). When a damaged disk bulges abnormally or ruptures, it is called a herniated (slipped) disk. Herniated disks can occur in any part of the spine but most often affect the lumbar spine (lower back). The abnormal disk material can place pressure on the adjacent spinal cord or nerve roots, resulting in pain, numbness, or weakness in areas of the lower back, buttocks, and legs. The November 22/29, 2006, issue of JAMA includes 2 articles about surgery for herniated disks.

RISK FACTORS FOR A HERNIATED DISK
Natural aging process—ongoing loss of water and proteins from the disk
Genetic (inherited) predisposition—an accelerated degeneration of disk materials
Obesity—excessive body weight places added stress on the spine
Lack of exercise—results in a loss of trunk muscle strength and diminished spine support
Work activities—long periods of sitting, lifting or pulling heavy objects, frequent bending or twisting, heavy physical exertion, repetitive motions, or exposure to constant vibration
Smoking—deprives blood flow and nutrients needed for disk repairs
History of back injury, previous herniated disk, or prior back surgery
CONSULT YOUR DOCTOR IF
A moderate injury causes immediate numbness or weakness in one or both legs
You have shooting leg pains with coughing, sneezing, or straining
Leg pain is accompanied by persistent weakness, tingling, or numbness
Back pain persists or builds in intensity over a few weeks' duration
Back pain is accompanied by pain during urination
You experience severe deep back muscle pain and muscle spasms
You have loss of bowel or bladder control
DIAGNOSIS AND TREATMENT OPTIONS
Diagnosis is based on a complete medical history accompanied by a thorough physical examination performed by your doctor. Tests involving imaging of the spine are sometimes done. Treatments can include oral medications, drug injections, and physical therapy. Most back and leg pain will resolve with these simple measures. For persons who have chronic pain and disability, surgical options may be considered.
FOR MORE INFORMATION
American Academy of Family Physicians http://familydoctor.org/341.xml
American Association of Orthopaedic Surgeons http://www.aaos.org/
American Association of Neurological Surgeons http://www.neurosurgerytoday.org/what/patient_e/herniated.asp

Multiple Sclerosis

2008-03-19T03:03:00.000-07:00

Multiple sclerosis (MS) is a chronic neurological disorder that affects the central nervous system (brain and spinal cord). The disease process results in inflammation and damage to myelin (insulation of the nerve fibers) and other cells within the nervous system. Because myelin aids the conduction of nerve signals, damage to myelin results in impaired nerve signaling and may impair normal sensation, movement, and thinking. This damage occurs in patches that appear as distinct lesions on magnetic resonance imaging (MRI)—the use of magnetic fields to create detailed images of the body. The patches cause different symptoms depending on their location within the nervous system.
Multiple sclerosis primarily affects adults, with an age of onset typically between 20 and 50 years, and is more common in women than in men. The cause of this disorder is not known, but environmental, viral, and genetic factors are thought to play a role. The December 20, 2006, issue of JAMA includes an article about multiple sclerosis and vitamin D levels. This Patient Page is based on one previously published in the January 26, 2005, issue of JAMA.

SYMPTOMS
Visual disturbances, which may include eye pain, distortion or loss of vision in one eye, or impairment of color perception
Difficulty walking or performing tasks that require coordination
Loss of sensation
Fatigue and/or weakness
Loss of bowel or bladder control
DIAGNOSIS
In addition to a complete medical history and physical examination including a detailed neurological examination, your doctor may order blood tests and refer you to a neurologist (a doctor with specialized training in diseases of the nervous system). Your doctor may also order an MRI scan of your brain and/or spinal cord to look for the characteristic patches of MS and may perform a lumbar puncture ("spinal tap")—sampling of the cerebrospinal fluid (the fluid that surrounds the brain and spinal cord)—to analyze for proteins associated with the disease.
TREATMENTS
Currently there is no cure for MS. However, there are treatments available that may slow its progression and alleviate associated symptoms.
Drug therapies—Medications that target the body's immune system may decrease the frequency and duration of attacks. These medications can be used on a long-term basis and also to treat specific attacks. Additional medications may be prescribed for other symptoms, such as pain or depression.
Additional therapies—Because MS may affect the patient's ability to perform self-care and other activities of daily living, treatment may also include referral to specialists for physical and occupational therapy.
FOR MORE INFORMATION
National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov/
American Neurological Association http://www.aneuroa.org/
National Multiple Sclerosis Society http://www.nationalmssociety.org/

Meningitis

2008-03-19T02:59:00.000-07:00

Meningitis (infection of the coverings of the brain and spinal cord) is a serious illness. Meningitis can occur in adults and children, even in infants, and can be caused by viruses, bacteria, fungi, or parasites. Bacterial meningitis can be fatal or cause severe impairment, particularly if the diagnosis of bacterial meningitis is delayed, but can be treated, especially when diagnosed early in the disease. The common types of bacteria that can cause meningitis are Neisseria meningitidis (also known as meningococcus) and Streptococcus pneumoniae (pneumococcus). These bacteria are highly contagious, spread rapidly, and can be deadly. Nursing homes, college dormitories, day care centers, and schools are often sites of outbreaks of meningitis. Vaccines are available for some bacteria and can be helpful to stop spread of contagious meningitis. The January 3, 2007, issue of JAMA includes an article about meningitis in children.

SIGNS AND SYMPTOMS OF MENINGITIS
Stiff neck
Fever
Headache
Nausea and vomiting
Red or purple rash that does not change color if pressed on
Fatigue or extreme sleepiness
Seizures
Irritability or lethargy—in infants, along with poor feeding, may be the only symptoms of meningitis
Recent flu-like illness or an ear or sinus infection may precede the development of meningitis
DIAGNOSIS AND TESTING
Questions about the history of the illness and a physical examination help determine the likelihood of meningitis.
Lumbar puncture (sampling of the cerebrospinal fluid [CSF]) is the primary test for meningitis and is important for the critical distinction between a bacterial or viral cause. A small needle is inserted into the lower back under sterile conditions and CSF is withdrawn. The CSF may show the presence of bacteria, indicating bacterial infection. White blood cells in the CSF may be related to bacterial meningitis, viral meningitis (no bacteria would be seen in this case), or fungal meningitis. The CSF also is cultured to look for growth of organisms in order to identify them.
Blood tests may show an increased white blood cell count, indicating infection. Other tests may be suggested by your doctor depending on the individual situation.
TREATMENT
If bacterial meningitis is suspected based on the lumbar puncture results, immediate antibiotic therapy is necessary. Intravenous (through a vein into the bloodstream) antibiotics are given to penetrate into the CSF that bathes the spinal cord and brain. Supportive therapy, including medications to reduce fever, can help with other types of meningitis. In serious cases of meningitis, intensive care (including life support medications and ventilators) may be necessary.
FOR MORE INFORMATION
National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov/
American Academy of Pediatrics http://www.aap.org/
Centers for Disease Control and Prevention http://www.cdc.gov/

Dementia

2008-03-19T02:57:00.001-07:00

Dementia is the loss of intellectual ability, which is also known as cognitive (thinking) function. Persons with dementia may be confused, not able to remember things, or lose skills they once had, including performing normal daily activities. Eventually, they may not recognize family members or friends and may display agitated behavior. Although dementia is more common in older adults, it is not a normal consequence of aging. The June 6, 2007, issue of JAMA includes an article about screening tests for dementia. This Patient Page is based on one previously published in the September 22/29, 2004, issue of JAMA.

SIGNS AND SYMPTOMS OF DEMENTIA
Gradually increasing memory loss
Confusion
Unclear thinking, including losing problem-solving skills
Agitated behavior or delusions
Becoming lost in formerly familiar circumstances
Loss of interest in daily or usual activities
ALZHEIMER DISEASE
Alzheimer disease is the most common cause of dementia. Persons with Alzheimer disease lose functioning neurons (nerve cells) in areas of the brain dealing with cognitive function and memory. They also experience buildup of abnormal proteins in some brain cells. Alzheimer disease affects mostly older adults but can sometimes begin in younger individuals. The cause of Alzheimer disease is not known, but risk factors for Alzheimer disease include family history, a specific gene, and advanced age.
OTHER CAUSES OF DEMENTIA
Vascular dementia is usually caused by strokes over a period of time that affect blood flow to areas of the brain related to memory and thinking. Some neurological diseases, such as Parkinson disease (a brain disease that causes tremors and muscle stiffness) and Huntington disease (an inherited disease that causes abnormal movements and dementia), can cause dementia because of their effects on brain tissue. Symptoms like those of dementia may be caused by many other factors, including medications and some illnesses. A careful evaluation by your doctor is important to look for treatable causes.
TREATMENT
Diagnosing dementia can help the person and his or her family members seek help from many available resources. There is no cure for Alzheimer disease or vascular dementia. Some prescription medications may help slow the progression of dementia during treatment. Your doctor can help you decide if medication may be worthwhile. Medical research on Alzheimer disease and the other dementias may someday help in prevention, early recognition, and more effective treatments.
FOR MORE INFORMATION
National Institute on Aging http://www.nia.nih.gov/
Alzheimer's Association http://www.alz.org/
National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov/

Amyotrophic Lateral Sclerosis

2008-03-19T02:55:00.001-07:00

Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig disease, involves progressive loss of motor neurons (a type of nerve cell controlling muscle movements) in the brain and spinal cord. ALS is a progressive, disabling, and ultimately fatal disease of unknown cause. Walking, speaking, swallowing, breathing, and other basic functions become impaired with time. About 30 000 Americans currently have ALS. The yearly incidence rate is 1 to 2 new cases per 100 000 individuals. The disease is commonly discovered during middle age and affects more men than women. The July 11, 2007, issue of JAMA includes an article discussing the diagnosis of ALS and recommendations for palliative (supportive) care.
SYMPTOMS
It is estimated that more than 50% of motor neurons are lost before symptoms such as muscle weakness become apparent.
Gradual muscle weakness and wasting in arms and legs
Muscle fasciculations (twitches visible in muscles)
Difficulty with swallowing, speaking, and breathing
Muscle stiffness, bodily pains, and cramps, especially at night
Respiratory failure is the usual cause of death in ALS. Other causes include pneumonia. In most cases, death occurs within 3 to 6 years after symptoms begin, although some individuals with ALS live for many years, even decades.

DIAGNOSIS
Diagnosis is based on a careful medical history, physical examination, and laboratory tests. Electromyograms (EMGs)—nerve conduction studies that evaluate nerve and muscle function—are the key tests. Other tests may include blood tests and neuroimaging studies such as CT or MRI scans of the brain and spinal cord. Molecular testing, cerebrospinal fluid tests, or muscle biopsy may be necessary.
TREATMENT
Physical, occupational, and speech therapies can assist in daily functioning.
Riluzole is the only medication approved for the treatment of ALS. It may prolong survival by a few months.
Other medications may relieve symptoms such as muscle pain, cramping, drooling, spasms, and fatigue.
SUPPORTIVE CARE
Appropriate exercises to help maintain mobility, strength, and energy
Changes in diet to minimize episodes of choking and ensure adequate nutrition
Effective use of assistive devices and braces such as neck collar, foot brace, cane, walker, or wheelchair
Ramps, handrails, raised toilet seat, shower seat
Erasable writing tablets or voice amplifiers and computers to help communication
A noninvasive ventilator (breathing machine) may be important to support breathing
The progressive, disabling nature of ALS and the fact that there is no cure make it a difficult disease to manage. In addition to medical care, patients need emotional support from family, friends, doctors, and caregivers.
FOR MORE INFORMATION
Muscular Dystrophy Association ALS Division (MDA) http://www.als.mdausa.org/
Amyotrophic Lateral Sclerosis Association (ALSA) http://www.alsa.org/

Transient Neurological Attacks

2008-03-19T02:51:00.000-07:00

With symptoms lasting for up to 24 hours, transient neurological attacks are a warning sign that cerebrovascular disease (disease of the brain's blood vessels) may exist. Also known as a mini-stroke, a transient ischemic attack (TIA) is a focal (affecting one body part or system) type of transient neurological attack. Individuals who experience a TIA are at increased risk of having a stroke. Because TIAs can be caused by several factors, it is important to have an accurate diagnosis for proper treatment and prevention plans. The December 26, 2007, issue of JAMA includes an article about transient neurological attacks.
SIGNS AND SYMPTOMS
Sudden loss of vision
Double vision
Slurred or garbled speech
Trouble finding the right words in conversation
Weakness, paralysis, numbness, or tingling in an extremity (hand, arm, foot, leg) or in the face
Loss of consciousness
Sudden loss of balance or difficulty walking
SEE YOUR DOCTOR, CALL THE EMERGENCY RESPONSE SYSTEM, OR GO TO THE EMERGENCY DEPARTMENT IMMEDIATELY IF YOU EXPERIENCE THESE SYMPTOMS.

DIAGNOSIS
Medical history and a physical examination are important parts of diagnosing transient neurological attacks. Further testing may include blood counts and chemistries, x-rays, computed tomography (CT scan), or magnetic resonance imaging (MRI). Angiography (x-ray pictures taken after injection of dye) may be required to look at the brain's blood vessels. You may see a neurologist (a doctor with specialized education in the diagnosis and treatment of neurological diseases) as part of your evaluation for a transient neurological attack.
PREVENTION AND TREATMENT
Do not smoke.
Exercise daily.
Eat a diet rich in fruits, vegetables, and whole grains.
Take high blood pressure medications as prescribed.
Keep your cholesterol and other blood lipid levels in the healthy range.
Manage diabetes and keep blood sugar under good control.
Medications, including those that make blood platelets less likely to form clots, may be prescribed for stroke prevention.
Aspirin may be recommended for preventing strokes and heart attacks.
Surgical procedures, such as carotid endarterectomy (surgical removal of a blockage in the carotid artery in the neck), may be recommended for some individuals to prevent strokes.
FOR MORE INFORMATION
National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov/
National Stroke Association 800/STROKES (787-6537) http://www.stroke.org/
American Heart Association 800/242-8721 http://www.americanheart.org/

Spinal Stenosis

2008-03-19T02:46:00.000-07:00

Spinal stenosis is a term used to describe a narrowing of the spinal canal, which contains the spinal cord and emerging nerve roots. It can occur in any portion of the spine. Because of limited space, changes in the bone (vertebral bodies) or soft tissues (spinal ligaments) can result in compression of the affected spinal cord and blood vessels. This narrowing can be congenital (genetic) or acquired (arthritis, trauma, bone disease, tumor) or a combination of both. Stenosis can be classified by location: central (involving the spinal cord) or lateral (affecting the nerve roots). Cord compression can also occur in patients with advanced cancer. The February 27, 2008, issue of JAMA includes an article about treatment options for cord compression due to metastatic cancer.

CONDITIONS THAT RESULT IN SPINAL STENOSIS
Osteophytes—formation of bony spurs associated with osteoarthritis
Herniated disk—protrusion of a cartilage disk between vertebrae
Malignancy—cancer
Scarring and inflammation of supporting spinal ligaments
Abscess—localized infection
Spondylolisthesis—a shift or abnormal stacking of 2 vertebral bodies
Congenital—genetic predisposition, which results in a developmentally small spinal canal
Systemic bone diseases (such as Paget disease of bone)

SYMPTOMS OF SPINAL STENOSIS
Pseudoclaudication—difficulty in walking
Paresthesia—abnormal skin sensations such as numbness and tingling
Muscle weakness
Localized or radiating pain
Loss of bladder or bowel control

DIAGNOSIS AND TREATMENT
Spinal stenosis can be diagnosed based on the history of symptoms, a physical examination, and imaging tests. Once the diagnosis is confirmed, treatment may be conservative (rest, steroid injections, medications, and exercise) or surgical. As symptoms become debilitating, surgery may be considered a treatment option. The main goal of any surgical procedure is to remove pressure from the spinal cord or nerve roots. This means that the tube of the spinal canal must be made larger by removing excess bone, ligaments, and abnormal tissues that are compressing the nerve roots. This type of surgical procedure is termed a decompressive laminectomy (removing a portion of the vertebral body and surrounding soft tissue). If individuals have both spinal stenosis and instability of the spine, the surgical procedure should include a decompression coupled with a spinal fusion (use of instrumentation supplemented with bone graft to maintain the structural support of the spinal column).

FOR MORE INFORMATION
American Association of Neurological Surgeons (AANS) http://www.neurosurgery.org/
American Association of Orthopaedic Surgeons (AAOS) http://www.aaos.org/
North American Spine Society (NASS) http://www.spine.org/

Peripheral Neuropathy

2008-03-19T02:41:00.000-07:00

Peripheral nerves carry messages from the brain and spinal cord to muscles, organs, and other body tissues. Damage or disease of these nerves are called peripheral neuropathy. Sometimes one nerve or a group of related nerves is involved in neuropathy; in polyneuropathy, multiple nerves are affected in different areas of the body. Because nerves are made up of several different types of nerve fibers affecting sensation, movement, pain transmission, or balance, symptoms and signs are based on the involved type of nerve fiber. The March 5, 2008, issue of JAMA includes an article about neuropathy related to alcohol consumption.

TYPES AND CAUSES OF NEUROPATHY

Diabetic neuropathy

Trigeminal neuralgia involves a nerve that brings sensation to the face, jaw, and eye area

Inherited neuropathy (present from birth)

Autonomic neuropathy (involving involuntary body functions, such as breathing, intestinal function, and regulation of blood pressure)

Vitamin deficiency

Medication effects

Traumatic injury

Excessive alcohol use

Infections, including human immunodeficiency virus (HIV)

Immune system diseases

Diabetic neuropathy is the most common type of neuropathy and affects up to two-thirds of patients with type 1 and type 2 diabetes. Diabetic neuropathy often involves the feet and legs and is responsible for lack of sensation, ease of injury, and infections.

SIGNS AND SYMPTOMS

Pain
Numbness
Burning sensation
Tingling
Lancinating (shooting) pain
Hypersensitive areas of the skin
Hair loss on the affected part
Shiny skin
Weakness
Muscle atrophy (loss of muscle tissue)

DIAGNOSIS AND TESTING

A detailed medical history and physical examination can identify causes of neuropathy. Blood testing, measurement of glucose levels, an electromyogram (EMG, an electrical test of muscle function), nerve conduction studies, and lumbar puncture may all be part of the evaluation of neuropathy.

TREATMENT

Most neuropathies are not curable but can be improved with treatment. Vitamin deficiencies, often present in patients with alcoholism, can be corrected with a healthy diet and vitamin supplementation. Treatment for alcohol-related neuropathy also includes stopping alcohol consumption. Control of blood glucose levels can slow progression of diabetic neuropathy, in addition to other benefits for individuals with diabetes. Medications may be prescribed, including some medications originally developed for treating seizures or depression, that may improve pain and other sensory symptoms in persons with neuropathies.

FOR MORE INFORMATION

National Institute of Neurological Disorders and Stroke
http://www.ninds.nih.gov

Neuropathy Association
http://www.neuropathy.org

American Diabetes Association
http://www.diabetes.org

Oliver Sacks' experience

2008-03-14T07:20:00.000-07:00

Oliver Sacks discusses decades of work with patients suffering from debilitating brain disorders.

Limbic System: Hallucinations

2008-02-15T13:53:00.000-08:00

Center of Emotion and Memory

2008-02-15T13:52:00.000-08:00

The limbic system, which is concerned with memory and learning, is also believed to be primarily involved in emotional responses. Emotions are the conscious result of the interaction between the activities of the cerebral cortex, the limbic system and the visceral organs of the body which produce specific physical changes. A number of theories have been postulated to explain this relationship between the body and mind. The emotional responses of any individual are, however, also a product of his knowledge and experience.

The anatomy of the limbic system includes:

The amygdaloid bodies, which contain both incoming and outgoing nerve fibers, and may help to regulate emotions, particularly agression.

The fornix, a thick bundle of nerve fibers which forms the outgoing pathway from the hippocampus.

The afferent fibers bring impulses into the dentate gyrus and the area of Ammon's horn.

The dentate gyrus which lies within the hippocampal sulcus and although its function is not fully understood may relay impulses in the hippocampus.

The subiculum is a region of cortex composed of up to six different cell layers and a multitude of nerve pathways.

Ammon's horn, which merges with the subiculum and contains ovoid and pyramidal cells, the function of which are thought to be associated with memory.

The efferent fibers, which carry information out from Ammon's horn to other regions of the brain.

The hippocampus, which is composed of folded layers of cells and fibers and is associated with emotions, learning and short-term memory.

The parahippocampal gyrus, a highly specialized area of nerve cells concerned with memory pathways.

The mammillary bodies, which have incoming and outgoing nerve fibers and acts as a relay station between the limbic system and the brain.

...and the septum pelucidum, which links the amygdala with the hypothalamus and is believed to be concerned with pleasure reactions.

Brain Functions

2008-01-12T12:49:00.000-08:00

Conditions of use

2008-01-11T00:20:00.000-08:00

Privacy Policy
We use your information to help us provide the most comprehensive services to our patients and to include you in our communication efforts. Your personal information will not be sold or used for any purposes outside of our organization. Your trust is important to us.
Disclaimers
We support the efforts of other programs and organizations and sometimes list their information on our site when we believe patients will benefit. We, however, are unable to monitor their activities and as such, are not liable for their effectiveness or appropriateness. We encourage patients to be active participants in their individual care and make reasonable, informed decisions as they proceed with their treatment.
We encourage patients visiting our site to ask questions of our medical staff because we are dedicated to providing the most accurate and useful information, however, e-mail with a healthcare professional or another patient is not a substitute for proper medical care. We encourage patients to use the information offered on our site and others as a basis for moving forward toward the best treatment options for each individual.

Parkinson's disease

2008-01-07T09:55:00.001-08:00

Classic Migraine

2008-01-07T09:52:00.001-08:00

Neurology

2008-01-07T09:47:00.001-08:00

Stroke Evaluation Simulation

2008-01-07T09:42:00.000-08:00

Tremor Action Network-Shaking the World

2008-01-07T09:38:00.001-08:00

Medical Consultation Form

2006-01-07T10:51:00.000-08:00

Medical Consultation Service

2006-01-07T10:44:00.000-08:00

Neurosciences Foundation offeres an on-line Medical Consultation Service for medical questions.
All questions will be attendend by proffesional specialists. Registered neurologists, psychiatrists, geriatrics and psychologists will reply your consults.
The name of the doctor will be displayed with the response.

Go to consultation form

Payment

2006-01-07T10:20:00.000-08:00