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Headaches |
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How do they differ?
Tension Type Headaches:
Tension type headaches are the most common effecting
about 75% of all headache sufferers. Tension type headaches typically are a
steady ache rather than a throbbing one, effecting one or both sides of the
head. Some people will get tension type headaches (migraine headaches) in response
to stressful situations or active day. Tension type headaches may also be chronic,
occuring frequently or even everyday. Rebound headaches need to be excluded
as a cause of this. This is created by patients who take frequent over-the-counter
medications particularly Excedrin and will convert a migraine into chronic
daily headaches.
Migraine Headaches:
Migraine headaches are less common than tension headaches. Nevertheless they
afflict 25-30 million people in the US alone. Up to 80% of women experience
a migraine headache at some time. Roughly 2 out of 3 migraine sufferers are
female. The most distinguished feature is a potential disability accompanying
the headaches, prior headache pain of the migraine. Migraines are usually
felt on one side of the head in about 60% of migraine sufferers, the pain
is typically throbbing in nature. Nausea with and without vomiting, as well
as sensitivity to light and sound, may accompany migraines. An aura, a group
of telltale neurological symptoms, sometimes occur before the headache pain
begins. Typically an aura involves a disturbance in vision and may consist
of bright lights or flickering lights in the pattern that moves across the
field of vision. About 1 in 5 migraine suffers experience an aura usually.
The migraine attacks are occasional and sometimes as often as once or twice
a week but not usually daily.
Cluster Headaches:
Cluster headaches are relatively rare, effecting 1% of the population. They
are distinct from migraine headaches and tension type headaches. Most cluster
headache sufferers are male (85%). Cluster headaches come in groups or clusters
lasting for weeks or months. The pain is extremely severe but the attack
is brief lasting no more than an hour or two. The pain centers around one
eye and this eye may be inflamed or watery. There may also be nasal congestion
on the effected side of the face. These alarm clock headaches may strike
in the middle of the night and often occur about the same time each day during
the course of a cluster. A history of heavy smoking and drinking is common.
Alcohol often triggers the attacks.
Rebound Headaches:
Rebound headaches may occur among people with tension type headaches as well
as those with migraine headaches. It appears to be the result of taking prescription
or nonprescription relievers daily or almost every day contrary to directions
on the package label. If the prescription or nonprescription relievers are
overused, the headache may rebound as the last dose wears off leading one
to take more and more pills. This is a good reason to call your doctor.
Treatment of Headaches:
Headache medication is available in several different
kinds of delivery and formulations. Sometimes patients can pick the type
of derivative they prefer for themselves. Medications are available in oral
tablets or disintegrating tablets, nasal sprays, injections under the skin,
or rectal suppositories.
Acute or Preventive:
Medications discussed referred to as acute (or abortive) treatments for headaches
are used to stop or abort the headache attack in progress. If you have frequent
disabling headaches, you may be a candidate for preventive medications which
can reduce both the frequency of headaches and can make any breakthrough
headaches less severe and easier to treat.
Assessing Headache Treatment Needs:
If you are using medications more than one or two times a week on an average.
Do you have three or more severe hard to treat attacks per month? Do you
like the acute therapies you have tried? Do you have infrequent but severe
disabling attacks? Do you have headaches that are predictable, such as headaches
that increase in frequency during stressful times, travel, holidays, or tax
season? Do you miss work, social events, or family activities because of
headaches? If you answer yes to these questions, you would benefit from preventive
medicine for your migraines.
Preventive Medications:
Preventive headache therapies proven in clinical trials:
Class of medications:
Anti-epileptics (anti-convulsants): Depakote or Topamax
Anti-depressants: Amitriptyline, Nortriptyline, Desapramine
Beta Blockers: Inderal, Atenolol
Serontonergics: Sansert
Anti-inflammatories: Naprosyn, Ibuprofen
Triptans such as Imitrex, Relpax, Amerge, Maxalt, Zomig, Axert
Combination medications such as Midrin, Fioricet
Narcotics: Tylenol with Codeine, Vicodin, Percocet
Injections such as Tordol, IV Depakote, steroids, or narcotics
Cluster headaches may also respond to high dose nasal oxygen.
Sometimes the patient’s headaches do not respond to prescription medications
and require the patient to even come into the Emergency Room or to be hospitalized
and be given IV medications which include possibly DHE with a medication for
nausea, IV steroids, IV Depakote, or a narcotic.
References
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Alzheimer's Disease |
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Dementia: Alzheimer’s Disease (AD) is a progressive neurodegenerative
disease characterized in the brain by clumps (amyloidal plaques) and tangled
bundles of fibrous neurofibrili composed of misplaced proteins. Age is the
most important risk factor for AD. The number of people with the disease doubles
every 5 years beyond age 65. Three genes have been discovered that cause early
onset (familial AD). Other genetic mutations that cause excessive accumulation
of amyloidal protein are associated with advanced age (sporadic AD). Symptoms
of AD include memory loss, language deterioration, and impaired ability to
mentally manipulate visual information, poor judgment, confusion, restlessness
and mood swings. Eventually AD destroys cognition, personality, and ability
to function. The early symptoms of AD, which include forgetfulness and loss
of concentration, are often missed because they resemble natural signs of aging.
Is there any treatment?
There is no cure for AD and no way to slow the progression of the disease.
For some people in the earlier and middle stages of AD, medication such as
Aricept, Exelon, and Reminyl may keep some symptoms from becoming worse for
a limited time. A new medication, Namenda, was recently approved. Combining
Namenda with the other AD drugs may be more effective than a single therapy.
Other medications may help control behavior symptoms such as sleepiness,
agitation, wandering, anxiety, and depression.
What is the prognosis?
AD is a progressive disease. Its course can vary from 5-20 years. The most
common cause of death in AD is infection. Patients with Alzheimer’s
live an average of 8 years after diagnosis although some people have lived
as many as 20 years after being diagnosed.
To help understand the changes,
AD is broken into stages: early, middle and late. It is important to understand
that the development of the symptoms differ from one person to another. During
each stage the symptoms will gradually progress over a period of years. It
is not unusual for people with AD to have good and bad days. For example,
a patient with early stage AD may not show any symptoms one day and the next
day the patient may have trouble remembering your name or finding the milk
in the refrigerator.
Early Stage Alzheimer’s
Symptoms include:
Trouble remembering recent events and conversations
Difficulty remembering the month or the day of the week
Loss of ability to manage finances
Withdrawal from social situations and general apathy
Cooking and shopping become more difficult
Poor judgment
Tendency to lose things
Middle Stage Alzheimer’s
Symptoms include:
Difficult behaviors emerge: Anger, suspiciousness, overacting, and paranoia
Wandering
Sundowning with agitation in the evenings
Fever of bathing
Hallucinations
Eating problems
Incontinence
Inappropriate sexual behavior
Will go from needing help in choosing clothes, remembering to change clothes,
to needing help getting dressed
Will progress from needing reminders regarding personal care to needing help
bathing, taking medications, brushing teeth, and toileting
Increased difficulty with verbal expression and comprehension
Loss of reading, writing, and arithmetic abilities
Loss of coordination
Will need 24 hour care 7 days a week
May not recognize family and friends
Late Stage Alzheimer’s:
Symptoms include:
Inability to communicate
Inability to recognize people, places and objects
Cannot participate in any personal care activities
Loses ability to walk
Muscles may become contracted and may lose ability to swallow
Seizures may occur
Majority of the time spent sleeping
Incontinence
Diagnosing Alzheimer’s Disease
Diagnosing Alzheimer’s Disease is reached through a combination of tests.
It must be differentiated from the occasional forgetfulness that occurs during
normal aging, and from depression, malnutrition, or the side effects from medications;
all of which can cause symptoms similar to those of early stage AD. The physician
often begins an evaluation by taking a history and performing a physical examination
as well as evaluating the patient’s cognitive abilities. This approach
can help the doctor determine whether testing is needed. An examination may
likely include a thorough medical evaluation and history followed by an extensive
neurological and neuropsychological testing. The testing may include imaging
of the brain with MRI, EEG testing, lab work-up, and recently approved for
difficult to diagnose cases – PET CT scanning.
Alzheimer’s Caregiver
AD is often a family disease because the chronic stress of watching your loved
one slowly decline affects everyone. Comprehensive treatment must therefore
address the needs for the entire family. This includes emotional support,
counseling, and more educational programs about Alzheimer’s Disease
for the individual’s family members as they strive to provide a safe
and comfortable environment at home. Through training, caregivers can learn
how to control unwanted behaviors, improve communication, and keep the person
with Alzheimer’s safe. Research has shown that caregiver’s benefit
from training and support groups and putting this patient in groups allows
caregivers to care for their loved ones at home longer. For valuable information
regarding caregivers, visit www.caregiver.org and search for Alzheimer’s
Disease.
References
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Multiple Sclerosis |
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What is multiple sclerosis?
Multiple Sclerosis is a chronic progressive neurological disorder. The name
literally means “many scars” referring to the lesions in the
brain and spinal cord that accumulate during the course of the disease. MS
affects approximately 400,000 people in the US and approximately 2 million
people worldwide. The majority of patients with newly diagnosed MS are between
the ages of 20-40, making MS the most common neurological disorder to affect
young adults. MS is more prevalent in women and the disease appears to be
more prevalent in individuals living in the northern temperature zones of
North America and Europe. MS is felt to be an autoimmune disease that affects
the central nervous system (CNS). The CNS consists of the brain, spinal cord,
and optic nerves. Surrounding and protecting the nerves of the CNS is a fatty
coating called myelin, which helps nerve cells conduct electrical impulses.
In MS, myelin is lost in multiple areas leaving scar tissue called sclerosis.
These damaged areas are also known as plaques or lesions. Sometimes the nerve
fiber itself is damaged or broken. Myelin not only protects the nerve cells,
it also makes their job possible. When myelin is destroyed or damaged, the
ability for the nerves to conduct electrical impulses to and from the brain
is disrupted. This results in the various symptoms of MS.
Although a family history of MS plays an important role, MS is not believed
to be a hereditary disease. Genetic factors are thought to play an important
role in predisposing individuals to MS but the precipitating event that results
in the development of the disease is unclear.
What are the symptoms of MS and how is the diagnosis of MS made?
No single diagnostic test confirms or rules out the presence of MS. A positive
diagnosis based on a combination of medical history, clinical symptoms compatible
with MS, abnormal findings on neurological examination, and positive results
of diagnostic tests are markers of the disease. This includes MRI scan, spinal
tap, or special evoked potentials. A differential diagnosis should be performed
to limit any other conditions that may cause similar symptoms, abnormal findings
on examination, or diagnostic test results. The diagnosis of MS also requires
evidence that the disease process is ongoing; therefore a diagnosis may require
some time.
What are the different types of MS?
There are many different ways to classify MS, however the simplest and most
meaningful classification is four courses.
Relapsing-Remitting: Characteristics – People
with this type of MS experience clearly defined flare-ups called relapses
(or attacks). These are evidence of acute or worsening of neurological function
followed by partial complete periods of recovery (remissions). This is the
most common form of MS at initial diagnosis (85%).
Primary progressive. Characteristics – Patients
with this type of MS experience a slow but nearly continuous worsening of
the disease from the onset with no distinct relapses or remissions. However,
there are variations in rates of progression over time, occasionally plateaus
are temporary minor improvements. Frequency is relatively less at approximately
10%.
Secondary progressive. Characteristic – Patients
with this type of MS experience an initial period of relapsing-remitting
followed by a steady worsening course with or without occasional flare-ups
or minor recovers or plateaus. Frequency, 50% of patients relapsing-remitting
develop this form of disease within 10 years of initial diagnosis before
destruction of the disease modifying (drugs). Long-term studies are not yet
available to demonstrate if this is significantly improved by treatment.
Progressive relapsing. Characteristics – Patients
with this type of MS experience a steady worsening of the disease from the
onset but also have clear acute relapses (attacks or exacerbations) with
and without recover in contrast relapsing-remitting appears to have relapses
with continuous progression. Frequency is relatively rare, less than 5%.
What therapies are available to treat MS?
In most patients with MS, information of the brain and destruction of the myelin
are ongoing even when they are not experiencing symptoms. Disease modifying
agents (Copaxone, Rebif, Avonex, Betaserone, and Novantrone) are capable
of suppressing information of the brain and can limit the amount of tissue
related neurological damage caused by MS. Treatment that is initiated early
in the course of MS is more effective in sparing the brain and spinal cord
tissue and expected to be associated with better outcomes including less
long-term disability and improved quality of life. MS is not contagious and
is not directly inherited. It is not considered a fatal disease. The majority
of the patients with MS do not become severely disabled. Although there is
no cure for MS, early treatment helps greatly decrease relapses and slow
the progression of the disease on to the secondary progressive phase. Multiple
web sites are available to further assist in your research regarding MS including
the treatment options outlined below.
What are the symptoms of MS?
The symptoms of MS are unpredictable and vary from person to person and from
time to time in the same person. For example, one person may experience abnormal
fatigue or another may have severe vision problems. Persons with MS could
have loss of balance and muscle coordination making walking difficult. Another
person with MS could have slurred speech, tremors, stiffness, and bladder
problems. Your symptoms depend on where the MS plaque has occurred; whether
it is in the brain, brain stem, spinal cord, or optic nerves.
What are the treatments available for the acute relapses?
During acute relapses, the significant motor features, including weakness and
vision changes, your physician may treat an increased exacerbation with steroids.
This could be administered either orally such as Prednisone or high dose
intravenous Solumedrol since steroids are known to result in a more rapid
recovery from an exacerbation. They do not decrease the progression of the
disease or delay the development of the secondary progressive disease. Therefore,
it is very important to start immune modulating therapies as discussed previously.
What are the treatments available for the symptoms of MS?
For fatigue, which in some is the most disabling symptom, medication often
used is an antiviral drug called Amantadine. Another medication being used
for narcolepsy that has been effective is Provigil. If these fail, sometimes
stimulants such as Ritalin or Adderall may be used. Patients with MS may
have significant muscle stiffness and spasms. This can often be treated with
medications such as Baclofen or Zanaflex. In rare cases, Benzodiapines can
be used. If these fail and with the severe spasticity of individual muscle
groups, sometimes Botox can be used and very rarely if there is spasticity
of the lower extremities which is severe, a Baclofen pump can be considered.
The patient should be treated for depression and may need treatment for bladder
dysfunction with various medications and bowel dysfunction especially constipation.
There are treatments available if there is significant heat intolerance with
a cooling jacket which sometimes insurance does cover.
Websites
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Peripheral Neuropathy |
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What is Peripheral Neuropathy?
Peripheral neuropathy describes damage to the peripheral nerves, the vast communications
network that transmits information from the brain and spinal cord to every
other part of the body. It may be caused by diseases of the nerves or as
the result of systemic illnesses. Many neuropathies have well-defined causes
such as diabetes, uremia, AIDs, or nutritional deficiencies. In fact, diabetes
is one of the most common causes of peripheral neuropathy. Other causes include
mechanical pressure such as compression or entrapment, direct trauma, penetrating
injuries, contusions, fracture or dislocated bones; pressure involving the
superficial nerves (ulna, radial, or peroneal) which can result from prolonged
use of crutches or staying in one position for too long, or from a tumor;
intraneural hemorrhage; exposure to cold or radiation or, rarely, certain
medicines or toxic substances; and vascular or collagen disorders such as
atherosclerosis, systemic lupus erythematosus, scleroderma, sarcoidosis,
rheumatoid arthritis, and polyarteritis nodosa. A common example of entrapment
neuropathy is carpal tunnel syndrome, which has become more common because
of the increasing use of computers. Although the causes of peripheral neuropathy
are diverse, they produce common symptoms including weakness, numbness, paresthesia
(abnormal sensations such as burning, tickling, pricking or tingling) and
pain in the arms, hands, legs and/or feet. A large number of cases are of
unknown cause.
Is there any treatment?
Therapy for peripheral neuropathy differs depending on the cause. For example,
therapy for peripheral neuropathy caused by diabetes involves control of
the diabetes. In cases where a tumor or ruptured disc is the cause, therapy
may involve surgery to remove the tumor or to repair the ruptured disc.
In entrapment or compression neuropathy treatment may consist of splinting
or surgical decompression of the ulnar or median nerves. Peroneal and radial
compression neuropathies may require avoidance of pressure. Physical therapy
and/or splints may be useful in preventing contractures (a condition in
which shortened muscles around joints cause abnormal and sometimes painful
positioning of the joints).
What is the prognosis?
Recovery from peripheral neuropathy is usually slow. Depending on the type
of peripheral neuropathy, the patient may fully recover without residual
effects or may partially recover and have sensory, motor, and vasomotor (blood
vessel) deficits. If severely affected, the patient may develop chronic muscular
atrophy.
What research is being done?
The NINDS supports a broad program of research on disorders of the peripheral
nervous system, including peripheral neuropathy. Much of this research is
aimed at increasing the understanding of peripheral neuropathy and finding
ways to prevent and cure the disorder.
References:
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Stroke |
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Stroke is the second leading cause of death worldwide. It is the third leading
cause of death in the US, and a major cause of neurological disability. An
estimated 750,000 strokes occur every year in the United States while roughly
4 million who survive strokes live with neurological sequali widely ranging
in severity. The financial burden on the nation for the annual health care
expenditure for strokes including direct and indirect is greater than $4 billion.
Although stroke can be prevented, its incidence has been increasing as is the
prevalence of cardiovascular risk factors. Prevention of stroke requires identification
of effect management of the associated major risk factors.
What is a stroke?
A stroke happens when blood flow to the brain stops. There are two different
types of stroke. The most common is ischemic stroke caused by a blood clot
that blocks a blood vessel or artery in the brain. The other less common
is a hemorrhagic stroke caused when a blood vessel in the brain ruptures
and spills blood into the surrounding tissue. Brain cells in the area begin
to die either because they stop getting the oxygen or the nutrients needed
to function or are killed by the ruptured vessel and suddenly spill off blood.
The symptoms of stroke happen immediately. They include:
Loss of ambulation
Numbness or weakness of the arms, face, or legs especially on one side of the
body
Confusion, difficulty speaking or understanding speech
Vision disturbance in one or both eyes
Dizziness, trouble walking, loss of balance or coordination
Severe headache with unknown cause
If you or someone else has these symptoms, seek immediate medical attention.
The longer blood flow is cut off to the brain the greater the potential for
permanent damage.
The prevention of the first stroke
The stroke is well suited for preventive interventions and the recommendations
for treatment of risk factors associated with stroke include:
Hypertension which is the most prevalent and notable modifier risk factor for stroke.
Treatment of hypertension substantially decreases the risk of stroke. A
decrease of 5-6 mm of HG in diastolic blood pressure reduces the stroke by
42%. Treatment of isolated systolic hypertension reduces the stroke by 36%.
Myocardial Infarction
The incidence of stroke after MI is approximately 1-2% per year. It is the
greatest during the first month after MI (31%).
Stroke strategies
Stroke treatment strategies include anti-platelet agents, anticoagulation’s,
and lipid lowering agents.
Atrial Fibrillation (AF)
Nonvalvular atrial fibrillation, which affects 2 million in the US, increases
the incidence of stroke and risk of stroke by 6 times. Preventive treatments
include anticoagulation and antiplatelet agents.
Diabetes Type I and II
Well-established risk factors for stroke. Increased blood sugar at the time
of presentation of a stroke increases with more stroke morbidity and death.
Blood lipids
Patients with high lipids and risk for coronary artery disease are recommended
to maintain lipid lower agents and cholesterol lowering diet.
Asymptomatic carotid artery disease
If there is a hardening of the carotid artery with a narrowing of 60% or
more carotid surgery may be warranted. This depends on the individual’s
risk factors and surgical expertise available.
Lifestyle changes
Cigarette smoking increases the risk of stroke by a factor of 1.5. Alcohol
can increase the risk for hemorrhagic strokes. Regular exercise may decrease
the risk of stroke as well as heart disease.
Stroke prevention after TIA or stroke
Stroke recurrence is the highest during the first 30 days after the initial
event. Patients with a TIA tend to return to the ER with a stroke within
90 days and reoccurring within 2 days. If a patient has symptoms of a stroke
and seeks immediate attention the patient might be a candidate for a clot
buster called TPA. This dissolves a clot or clots and keeps the blood flowing
to the brain. But this has to be administered within 3 hours of the onset
of the symptoms. The patient needs to come for immediate medical attention
and has to have a work-up including a CT scan to make sure there is no hemorrhage
before this clot buster can be administered. Once the stroke has occurred
and there is damage to the brain, treatment can be initiated to prevent another
stroke happening with starting either antiplatelet agents (aspirin, Plavix,
Aggrenox, or Ticlid) or anti-coagulation (Warfarin or Heparin) as well as
treating the underlying risk factors such as hypertension, diabetes, atrial
fibrillation, elevated cholesterol, or carotid stenosis. There should also
be life-style changes such as stopping smoking, decreasing alcohol intake,
and increased exercise. If the patient has paralysis resulting in gait difficulty,
intensive physical therapy or if there is paralysis or difficulty with upper
extremity use then occupational therapy. If there is speech difficulty, then
with speech therapy. Sometimes this can be performed in an inpatient setting,
such as inpatient rehab, in order for the patient to recover sufficiently
for the patient to go home.
Risk factors shortly after a stroke
Risk factors include recurrent stroke, developing clots in the legs such as
DVTs and then can cause clots into the lungs. This could be prevented by
early mobilization using stockings as well as anticoagulation such Heparin
or Lovenox. There is increased risk of pneumonia initially after a stroke
especially if there is difficulty with swallowing. If the patient is mobilized
early, there is risk of skin breakthrough if there is significant paralysis
with the stroke. This is very common after a stroke and this needs to be
treated. If there is significant spasticity on one side, this could be treated
with medications, range of motion, and intensive therapy. If these fail,
potentionally isolated muscles can be treated with Botox.
Web sites to go to include:
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Parkinson's Disease |
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Parkinson’s Disease was first described in 1817 by Dr. James Parkinson,
a British physician after whom the disease is named.
The disease is characterized by a “TRAP”
“T” for
tremor, usually a slow resting tremor of the limb.
“R” for rigidity which is stiffness of the extremity and difficulty
with passive movement.
“A” Achyesthesia or bradykinesia which is slowness of movement.
“P” for poor balance or postural instability.
Parkinson’s Disease is diagnosed clinically. They have to have at least
two of these symptoms present. There has to be an evidence of progression and
exclusion of other potential diseases that can present with Parkinson’s
features. Often, patients present with tremors although they can be a form
of Parkinson’s which presents primarily with slowness and stiffness without
a tremor. The individual may have difficulty with day-to-day activities such
as dressing, walking, and may experience balance problems, difficulty getting
out chairs, and turning in bed. There may be decreased facial expression, difficulty
with writing, usually in the description as very small letters with their writing.
It affects about 1 in 100 people over the age of 60 with an average age of
onset of about 60 years of age. It can affect younger people. More often, they
have a family history. Parkinson’s Disease is a neural degenerative disease
that progresses over time. There is degeneration of the area of the brain called
Substantia Nigra. These cells produce a chemical called dopamine, which is
an important chemical. When these cells are damaged and depleted, symptoms
of Parkinson’s appear. About 8-% of the cells are damaged before symptoms
are clinically evident. At present we have treatments primarily to decrease
the symptoms of Parkinson’s Disease. There are some potential treatments
to slow down the progression.
Is Parkinson’s Disease Inherited?
There is a family history of Parkinson’s Disease in 5-10% of patients.
It may affect people in the same generation like brother or sister or in separate
generations. There are clearly some environmental toxins which are a cause
of Parkinson’s Disease including manganese, carbon monoxide, and rarely
certain pesticides. There is also a “street drug” (MPTP) which
causes Parkinson’s in young patients. Neurogene mutations have been associated
with Parkinson’s Disease in familio forms of Parkinson’s. Most
cases of Parkinson’s Disease are not familio. It appears there is a combination
of a genetic risk with an irritability to environmental toxin and advancing
age which puts these individuals at risk.
Diagnosis of Parkinson’s Disease
The diagnosis of Parkinson’s Disease is made by a physician. This is
primarily made on a clinical examination looking at further features of tremors,
rigidity, bradykinesia, loss of postural reflexes, and exclusion of other factors.
Testing may be done to exclude other diseases such as imaging of the brain
to rule out a stroke or tumor, certain blood tests to rule out viral dysfunction
which can present like Parkinson’s features. There are other forms of
conditions which can look like Parkinson’s Disease and these are called
Parkinson’s Syndromes. These include effects of certain medications that
can look like Parkinson’s particularly psychotropic medications (antipsychotics,
Reglan, Recerpine, and some occasional calcium channel blockers). Other conditions
include progressive super nuclear palsy (PSP). These present usually with initial
balance and frequent falls. These are in the trunk and eventually loss of eye
movements. They usually begin after age 50 and progress more rapidly than Parkinson’s
Disease. Dementia develops later in the disease. There is no treatment available
since usual Parkinson’s medications are not effective. Another form is
corticobasal degeneration (CBD). This is the least common of the atypical forms
of Parkinsonisms. Patients present asymmetrically and progress very rapidly.
They usually develop after age 40 and include asymmetrical bradykinesia, rigidity,
with abnormal dystonia limbs, loss of posture, and language difficulty. There
is no specific treatment available for this. Multi-system atrophy (MSA) is
a neurogenerative disease of unknown cause. This may be difficult to distinguish
initially from Parkinson’s Disease but this file is common and progresses
rapidly. Mean age of onset is 50. They present again with bradykinesia, poor
reflexes, but they can also have associated difficulty with blood pressure
control, difficulty with coordination, impotence, decreased sweating, and constipation.
They may have an initial response to mild Parkinson’s medication but
at later stage they develop an intolerance to this. They do not benefit from
deep brain stimulation. Vascular Parkinson’s is small strokes which cause
the patient to look like a Parkinson’s patient and can be picked up on
imaging of the brain. There is more of a step-wise deterioration as recurrent
strokes.
Treatment for Parkinson’s Disease
Parkinson’s Disease responds very well to medications. The most common
medication is (L-dopa). This treatment has been available for almost 30 years
and has revolutionized the treatment of Parkinson’s Disease. L-dopa is
a precursor for dopamine. It is transported through the gut, to the brain or
at least by the brain cells. It is available in an immediate release or a long
acting version. Also, this is called Sinemet and it is combined with a medication
called Carbidopa which decreases the conversion of dopamine in the gut and
therefore decreases nausea. There is a new medication called Stalevo which
is a combination of carbadopa/levadopa with Comtan which allows even more of
the L-dopa to get into the brain by decreasing the conversion of L-dopa in
the peripheral system. Other treatments that can be started early include Amantadine
which is an antiviral drug which helps decrease some of the tremors and fatigue
seen with Parkinson’s Disease. Anticholerginics such as Artane also can
decrease rigidity and tremors in Parkinson’s Disease if started early.
Agents such as dopamine agonists act directly as a dopamine receptor and the
most common ones were recently released, such as Mirapex or Requip. Older agents
still can be used but have more side effects particularly with nausea, lightheadedness,
and hypertension. These include Polydial, Permax. Side effects of these medications
include hallucinations, orthostatic drop in blood pressure, and drowsiness
in the daytime. There are some protective agents which can help slow down the
disease including Selegeline which may also mask the symptomatic effect, Coenzyme
Q10 which in larger dosages has suggested that it may slow down the progression
of the disease.
Treatment options in the younger patients: A dopamine agonist may be started
early on and then later an L-dopa started. In an elderly patient, they may
start treatment with L-dopa then add in a dopamine agonist later. The disease
is progressive and the patient may develop motor fluctuations in the disease.
These are problems where the medication stops working before the next dose
and this is called an “off period”. There may also be times when
the medication is taken and there are uncontrollable movements of the head
and limbs called dyskinesias. These can sometimes be treated by adjustments
of medications. If the patient is below age 70 and has no underlying dementia
and is a good surgical candidate and if they are having significant motor fluctuations
they may be a candidate for surgery. Previous treatments included resective
surgery. Now the standard care is usually deep brain stimulation most commonly
thalamic which releases tremors, rigidity, bradykinesia and gait disorders.
Other locations for the simulators include thalamic which are more important
for tremors but not for other features of Parkinson’s Disease, globis
palatis which helps reduce tremor, rigidity, and bradykinesia and gait disorders.
This should be done in a specialized center since there needs to be close follow-up
on adjustments of the stimulator.
Web sites
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EMG/NCV |
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 “EMG” is an abbreviation for electromyogram.
“Electro” means electric, “myo” means muscles, and “gram” means
recording of.
“NCV” is an abbreviation for nerve conduction velocity.
N for nerve C for conduction, and V for velocity.
The diagnosis of neuromuscular disease hinges on the doctor’s ability
to identify specific deficit of defects of neuromuscular function. Sometimes
a doctor can infer this functional deficit and the disease associated by a
physical examination, doing a blood test and looking at the anatomy of the
nerves and muscles. At other times, the doctor may have to directly evaluate
the functions of the muscles and nerves and the connections between them by
performing the EMG/NCV test.
How do I prepare for the test?
No special preparation is needed. You may eat a regular meal or snack prior
to the test. If you are on medications, take them as prescribed. If you are
on blood thinners, inform the physician performing the testing since he may
have to modify the needle examination. Please inform the physician if you
are pregnant or have a defibrillator pacemaker.
How is the test done?
Your EMG/NCV study is a two-part test. The first part involves testing the
nerves. Small metal electrodes are taped to your skin. Then an electrical
stimulus will be administered to a nerve. The stimulus is just enough to
make the extremity (arm or leg) twitch depending on your symptoms. Two to
six nerves will be tested and it will take anywhere from 20-45 minutes.
The second portion of the test is to examine the muscles. Muscle activity
is tested by inserting a fine tipped needle into the muscle. You will be asked
to contract and relax the muscle.
Will this test hurt?
There will be some discomfort during the EMG/NCV study. The discomfort will
last for a short period of time.
What happens after the test?
When the test is completed, you may return to your normal activities. If you
still feel some discomfort in the area where the needle was inserted, a warm
bath or hot compress and Tylenol should relieve it.
The doctor performing the test will interpret the test results and report
them to your referring physician. Your doctor or his staff will notify you
of the test results taking into consideration other testing that was performed
on you. The abnormalities in the test may indicate the following: Neuropath
(nerve damage for diabetes, etc), Muscle disorders (myopathy, muscular dystrophy),
entrapment of nerves (Carpal, Cubital Tunnel, etc), or pinched nerves in the
neck or lower back (radiculopathy). |
EEG |
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EEG is an abbreviation for electrocephalogram. An EEG is a test to detect any
abnormalities in the electroactivity of the brain.
“Electro” means electrical activity, “cephalo” means
brain, and “gram” means the study of.
How is the test performed?
The brain cells communicate by producing tiny electrical impulses. In an EEG,
electrodes are placed on the scalp over multiple areas of the brain to detect
and record patterns of electrical activity and check for abnormalities. The
test is performed by an EEG technician in a specially designed room and you
will be asked to lie on your back on a table or reclining chair. The technician
will apply between 16-25 flat metal discs (electrodes) in different positions
on your scalp. The discs are held in place with a sticky paste. The electrodes
are connected by a wire and to an amplifier and then a recording machine.
The recording machine converts electrical signals in a series of waving lines
that are seen on a computer monitor and recorded onto the computer hard disc.
You may be asked to lay still with your eyes closed because any movement
can alter the results. You may be asked to do some things during the recording
such as breathe deeply for several minutes or look at bright flickering light.
How to prepare for the test?
You need to wash you hair the night before the test. Do not use oils, sprays,
or conditioner on your hair before the test. Your healthcare provider may
want you to discontinue some medication before the test. Do not change or
stop medication without first consulting your healthcare provider. You should
avoid all foods containing caffeine 8 hours before the test. Sometimes it
is necessary to sleep during the test so you may be asked to reduce your
sleep the night before. Infants and children, sometimes they will fall asleep
during the test if they are sleep deprived or come in during their usual
naptime. Otherwise, sometimes they are given sedation.
Why is the test performed?
An EEG is used to diagnose the presence of types of seizure disorders, to look
for causes of confusion, and to evaluate head injuries, tumors, infections,
degenerative diseases, and metabolic disturbances that affect the brain.
It may also be used to evaluate sleep disorders and investigate periods of
unconsciousness. The EEG may be done to confirm brain death in a comatose
patient. The EEG cannot be used to read the mind, measure intelligence, or
diagnose mental illness.
What are the risks?
The procedure is considered very safe. If you have a seizure disorder, a seizure
may be triggered by flashing lights or hyperventilation (heavy breathing).
The healthcare provider performing the EEG is trained to take care of you
if this happens.
What happens after the test?
After the test is completed, the electrodes will be carefully removed. You
may have some paste in your hair which will come out easily once you shampoo
or clean your hair later that day.
The test is read by a Neurologist trained in EEG. The results will be sent
to your referring physician. The abnormalities in the test may indicate the
following: seizure disorder such as epilepsy, structural abnormalities such
as brain tumors or abscess, head injury or inflammation of the brain such as
encephalitis, Sleep Disorders, abnormal EEG findings in those with medical
disorders such as kidney or liver failure, or abnormalities from medications. |
Sleep Studies |
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Sleep Apnea. What is it?
Sleep apnea occurs when breathing stops during sleep for at least 10 seconds
at least five times an hour. Mild sleep apnea causes few symptoms, but the
condition may lead to low oxygen levels, which can be life threatening.
Sleep apnea is more common in people who smoke, drink alcohol or are overweight.
It may also occur in people at high altitudes.
There are two types of sleep apnea: "obstructive sleep apnea" and "central
sleep apnea." Obstructive sleep apnea is due to a blockage in the airways.
Central sleep apnea is caused by a problem with the nerves that control breathing.
In some cases a mixture of both types of sleep apnea may occur.
The two types of sleep apnea
Obstructive sleep apnea (OSA) affects primarily men between the ages of 30
and 50. It occurs when air passage in the upper respiratory tract becomes
obstructed during sleep (obstruction is caused by soft tissue of the pharynx
relaxing and blocking the flow of air). It prevents breathing until low levels
of oxygen in the blood cause a person to respond by waking up and taking
a deep, snorting breath. Being overweight or having a small tongue or mouth
can contribute to the obstruction. In children enlarged tonsils or adenoids
are the most common cause of obstruction.
Central sleep apnea is a rare type of sleep apnea where the region of the brain
and nerves that regulate breathing do not function normally and cause breathing
to be impaired. It can be caused by head injury or stroke.
What are the symptoms?
The symptoms of OSA develop gradually whereas the symptoms of central sleep
apnea may develop suddenly. You may not be the first one to notice you
have sleep apnea — it may be a partner or family member who informs
you.
Symptoms of both types include:
- Restless sleep
- Daytime sleepiness
- Poor memory and concentration
- Headache in the morning
- Loud snoring
- Change in personality
- Frequent urination during the night
Who Suffers?
- About 4 - 9 % of middle-aged
men
- About 2 - 4 % of middle-aged women
- About 80 - 90 % of persons
with sleep apnea go undiagnosed
How is it diagnosed?
Your doctor can examine your nose and throat to look for an obstruction in
your breathing. You could also have an endoscopy of the nose and throat done
and X-rays or a CT scan of the head and neck. You may also have to undergo
sleep studies to confirm a diagnosis as variables such as breathing, oxygen
levels in the blood and heart rate need to be measured while you are asleep.
What are its consequences?
Sleep apnea increases the risk of:
- Cardiovascular disease (leading to heart
failure, heart attack and stroke)
- Hypertension (high blood pressure), especially
below age 60*
- Auto accidents: Sufferers of severe sleep apnea are two to
three times more likely to be involved in auto accidents than the general
population, mainly due to falling asleep while driving
How is it treated?
- With lifestyle changes and/or
appliances
- Overweight patients should lose weight (even 5 percent can help)
- Evening
alcohol avoidance
- A Continuous Positive Airway Pressure (CPAP) appliance
- a nose mask worn during sleep to prevent airway collapse - is generally
effective, but many patients dislike it
|
Vagal Nerve Stimulators |
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 One
of the most exciting developments in the field of epilepsy treatment is the
Vagal Nerve Stimulator (VNS). The VNS is a device about the size of a hockey
puck, which is placed in the chest in a manner similar to a pacemaker for the
heart. Once implanted, the neurologist will program the VNS to deliver a series
of stimulations. The VNS does not work by sensing a seizure. Instead it works
by repetitively stimulating the vagus nerve for a period of time and then by
pausing for a period time.
The VNS is also programmed with a special sequence
that is activated when a magnet is swept over the device. For patients who
can sense a seizure is about to start (the aura of a seizure), it can be
useful in aborting the seizure. For patients who cannot sense the impending
seizure, it can be useful for family and caretakers to shorten the seizure
and allow for faster recovery of the patient.
 VNS
has not been shown to be a more effective treatment than any other anti-epileptic
medications. Its advantage lies in its different side effects like neck pain
and voice change (usually transient), not shared by drugs. When effective,
it allows the decrease of other drugs, which improves the quality of life
for the patient and caregivers. It also seems to shorten the duration of
seizures and the recovery time after a seizure occurs. Unfortunately, VNS
does not benefit everyone and there is no way to predict in advance who will
benefit from its implantation.
VNS is also felt to have great potential in
the area of treating depression that often accompanies Epilepsy, however
this is currently under investigation by the FDA and approved only as part
of ongoing research. |
Botox |
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What is botulinum toxin?
Botulinum toxin is a protein. It can stop some of the chemical messages that
are sent from nerves. These messages tell the muscles to contract in spasms
(to tighten up). Botulinum toxin is used to stop muscle spasms because it blocks
these messages.
Are botulinum toxin injections safe?
Botulinum toxin is made by the same bacterium that causes food poisoning. A
high dose of botulinum toxin could be fatal, just as food poisoning can be
fatal. However, the dose given in injections is so small that it's unlikely
you'll have any harmful effects from the toxin.
Botulinum toxin has been used safely in thousands of people. It has been used
for more than 10 years.
Why do I need botulinum toxin injections?
Your doctor may be considering botulinum toxin injections to treat certain
muscle spasms on your face or eyelids. The injections can also be used for
some eye movement disorders, such as a lazy eye. Botulinum toxin is a standard
treatment for spasmodic torticollis, a muscle spasm that causes the head
and neck to pull in one direction. Your doctor may use the botulinum toxin
injections to treat other problems as well. Botulinum toxin has proven
to be useful in the treatment of many forms of dystonia, including the
following:
- blepharospasm — forceful involuntary closure of the eyelids
- strabismus — misalignment
of the eyes
- hemifacial spasm — sudden contraction of the muscles on
one side of the face
- spasmodic torticollis, or cervical dystonia — muscle
spasm in the neck that
causes the head to turn to one side, and sometimes forward or backward
- oromandibular
dystonia — continuous spasms of the face, jaw, neck,
tongue,
larynx, and in severe cases, the respiratory system
- urinary retention — severe
inability to urinate that requires catheterization
- spasmodic dysphonica — spasm
of the vocal cords that causes sudden disruption
of speech
- stuttering — repetitions of parts of words and whole words,
long pauses, elongated sounds
- voice tremor — quavering vocalization
Neurons generate new nerve endings
that reactivate the dystonia, so improvement is not long lasting, and treatment
is usually repeated every 3 to 4 months. Physical or occupational therapy
usually is undertaken to stretch and restore normal muscle function. Some
patients develop antibodies to the toxin over time, rendering the treatment
ineffective.
How are botulinum toxin injections given?
Botulinum toxin is mixed with saline (salt water) and injected into the
muscle with a tiny needle. You may receive 5 to 10 injections.
You might have some soreness at the injection sites. If your injection
sites get sore, you can take acetaminophen (one brand name: Tylenol)
or ibuprofen (one brand name: Motrin). You can also put an ice pack on the
painful area.
Will I have any side effects?
You might have weakness in the muscles that were injected, muscle soreness
that may affect your whole body, difficulty swallowing or a red rash that
lasts several days after the injections. Some people have severe weakness
in the muscles that were injected. All side effects go away quickly. The
most frequently reported adverse reactions in patients with cervical dystonia
are dysphagia (19%), upper respiratory infection (12%), neck pain (11%),
and headache (11%). The most frequently reported adverse reactions in patients
with blepharospasm are drooping of the eyelid (21%), superficial punctate
keratitis (6%), and eye dryness (6%). Patients with neuromuscular disorders
may be at increased risk of clinically significant systemic effects including
severe dysphagia and respiratory compromise from typical doses of Botulinum. |
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