Universal access to education is the ability of all people to have equal opportunity in education, regardless of their social class, race, gender, sexuality, ethnic background or physical and mental disabilities. The term is used both in college admission for the middle and lower classes, and in assistive technology for the disabled. Some critics feel that this practice in higher education, as opposed to a strict meritocracy, causes lower academic standards. In order to facilitate the access of education to all, countries have right to education.
Universal access to education encourages a variety of pedagogical
approaches to accomplish the dissemination of knowledge across the
diversity of social, cultural, economic, national and biological
backgrounds. Initially developed with the theme of equal opportunity
access and inclusion of students with learning or physical and mental disabilities, the themes governing universal access to education have now expanded across all forms of ability and diversity.
However, as the definition of diversity is within itself is a broad
amalgamation, teachers exercising universal access will continually face
challenges and incorporate adjustments in their lesson plan to foster
themes of equal opportunity of education.
As universal access continues to be incorporated into the U.S. education system,
professors and instructors at the college level are required (in some
instances by law) to rethink methods of facilitating universal access in
their classrooms. Universal access to college education may involve the
provision of a variety of different assessment methods of learning and
retention. For example, in order to determine how much of the material
was learned, a professor may enlist multiple methods of assessment.
Methods of assessment may include a comprehensive exam, unit exams,
portfolios, research papers, literature reviews, an oral exam or
homework assignments.
Providing a variety of ways to assess the extent of learning and
retention will not only identify the gaps in universal access but may
also elucidate the ways to improve universal access.
Non-discrimination and equality in education
Examples of marginalized groups
Human rights are universal rights, therefore it applies to everyone equally and without discrimination. However, a significant number of individuals miss out on education due to discrimination preventing access to education.
Discrimination occurs most obviously in terms of accessing education. For example, girls can face gender-based barriers such as child marriage, pregnancy, and gender-basedviolence which often prevent them from going to school or contribute to them dropping-out of school. People with disabilities
often face literal accessibility issues, such as a lack of ramps or
appropriate school transportation, making it difficult to get to school.
Migrants often face administrative barriers that prevent them from
enrolling, effectively barring them from education systems.
However, discrimination also occurs within education systems when
certain groups receiving an inferior quality of education compared with
others, for instance, the quality of education in urban schools tends
to be higher than that found in rural areas.
Discrimination also happens after education where different
groups of people are not able to draw the same benefits from their
schooling. For example, educated boys tend to leave school with higher
wage potential than equally educated girls.
Non-discrimination and equality provisions found in international human rights law
(IHRL) exist to ensure that the principle that human rights are
universal is applied in practice. Non-discrimination and equality are
not abstract concepts under international human rights law (IHRL). They are elaborated human rights
that have been developed over decades to address the discrimination
that people face on a day-to-basis. Particularly education where the
rights to non-discrimination and equality have been applied to the right to education across numerous human rights treaties, including one dedicated to the issue, known as UNESCO CADE.
Despite the strength of non-discrimination and equality law,
eliminating discrimination and inequalities is a challenge that
individual states and the international community face. This was
acknowledged in 2015 when the international community vowed to ‘leave no
one behind’.
International and regional human rights treaties apply the rights to non-discrimination and equality to the right to education of specific marginalised
groups. Marginalised groups are those who have suffered prolonged and
historical discrimination, usually, but not exclusively, on the basis of
identity (gender, for example), characteristics (ethnicity, race), or
circumstance (refugees, migrants, internally displaced persons). Marginalisation are very likely to be subject to multiple, compound, or intersectional forms of discrimination.
In
2009 the House of Indian Parliament and the President of India both
signed and approved a bill that would grant free law mandated education
for children ages six to fourteen.
It was a great step towards universal education for all. Muchkund Dubey
author of the article “The Right of Children to Free and Compulsory
Education Act, 2009 : The Story of Missed Opportunity" discusses and
highlights the issues of access, quality of education, financial
implication, and discrimination.
In the United States, Brown vs. Board of Education was a landmark
decision because it found and declared that, “separate educational
facilities are inherently unequal”. This began the process of desegregation in many schools that had not desegregated yet.
The significance of Brown vs. Board was the universal right of all
students to attend educational institutions equally rather than
separately based on their race. Jonathan Kozol, author of The Shame of
the Nation,
talks about how “physical conditions in these newly integrated schools
were generally more cheerful…state of mind among the teachers and the
children [was] more high-spirited” in the aftermath of desegregation.
Universal access
Universal
Access to education means people have equal opportunities to take part
in any educational system. However, not all individuals, groups, or
ethnic groups are given equal access. The United States is credited with
the current idea of universal access as a concern for handicapped
persons.
Two international agencies (World Health Organization and World Bank)
estimated that around one billion people all over the world various
types of disabilities. Between 93 and 150 million of them are children.
Plan International revealed that these kids will not possibly attend
school and if ever they enroll will be separated from normal pupils.
The Global Partnership for Education said approximately 90 percent of
children afflicted by disabilities from low and middle income nations
are not studying. Historically, these kids are not included in the ordinary education system and referred to special learning schools.
It is unfortunate that education up to this very day is not
accessible to millions of schoolchildren globally. 72 million or more
children of primary education age do not go to school. Some 759 million
adults are uneducated. They do not have the knowledge needed in
improving their families’ living conditions. Poverty leads to lack of education.
In almost all countries (developing and developed), children are denied
education as a result of inequalities that emanate from health, gender,
and cultural identity like religion, language, and ethnic origin.
Factors associated with poverty including unemployment, illiterate
parents, and ailments increase the possibility of non-schooling, and
dropout rates.
Universal primary education has turned out as a major problem for many
nations. Majority of these developing states do not possess sufficient
financial resources to build schools, provide books and other materials,
and recruit, train, and pay teachers. The Sub-Saharan African region is the most affected region as 32 million African children are still uneducated. This is followed by Central and East Asia as well as the Pacific with 27 million or more. However, observers noted that universal access to education remains an attainable goal by 2030.
Bibliography
The Big Test - a history of the twentieth century development in the United States of universal access to colleges.
Beta blockers (beta-blockers, β-blockers, etc.) are a class of medications that are predominantly used to manage abnormal heart rhythms, and to protect the heart from a second heart attack (myocardial infarction) after a first heart attack (secondary prevention). They are also widely used to treat high blood pressure (hypertension), although they are no longer the first choice for initial treatment of most patients.
Beta receptors are found on cells of the heart muscles, smooth muscles, airways, arteries, kidneys, and other tissues that are part of the sympathetic nervous system and lead to stress responses, especially when they are stimulated by epinephrine
(adrenaline). Beta-blockers interfere with the binding to the receptor
of epinephrine and other stress hormones and weaken the effects of
stress hormones.
In 1964, James Black synthesized the first clinically significant beta blockers—propranolol and pronethalol; it revolutionized the medical management of angina pectoris and is considered by many to be one of the most important contributions to clinical medicine and pharmacology of the 20th century.
Controversially,
for reduction of perioperative mortality in non-cardiac surgery, but
the best evidence suggests that they increase mortality when used this
way
Congestive heart failure
Although beta blockers were once contraindicated in congestive heart failure,
as they have the potential to worsen the condition due to their effect
of decreasing cardiac contractility, studies in the late 1990s showed
their efficacy at reducing morbidity and mortality.
Bisoprolol, carvedilol, and sustained-release metoprolol are specifically indicated as adjuncts to standard ACE inhibitor and diuretic
therapy in congestive heart failure, although at doses typically much
lower than those indicated for other conditions. Beta-blockers are only
indicated in cases of compensated, stable congestive heart failure; in
cases of acute decompensated heart failure, beta-blockers will cause a
further decrease in ejection fraction, worsening the patient's current
symptoms.
Beta-blockers are known primarily for their reductive effect on
heart rate, although this is not the only mechanism of action of
importance in congestive heart failure. Beta-blockers, in addition to their sympatholytic β1 activity in the heart, influence the renin–angiotensin system at the kidneys. Beta-blockers cause a decrease in renin
secretion, which in turn reduces the heart oxygen demand by lowering
the extracellular volume and increasing the oxygen-carrying capacity of
the blood. Heart failure characteristically involves increased
catecholamine activity on the heart, which is responsible for several
deleterious effects, including increased oxygen demand, propagation of
inflammatory mediators, and abnormal cardiac tissue remodeling, all of
which decrease the efficiency of cardiac contraction and contribute to
the low ejection fraction.
Beta-blockers counter this inappropriately high sympathetic activity,
eventually leading to an improved ejection fraction, despite an initial
reduction in ejection fraction.
Trials have shown beta blockers reduce the absolute risk of death
by 4.5% over a 13-month period. In addition to reducing the risk of
mortality, the numbers of hospital visits and hospitalizations were also
reduced in the trials.
Therapeutic administration of beta-blockers for congestive heart
failure ought to begin at very low doses (1/8 of target) with a gradual
escalation of the dose. The heart of the patient must adjust to
decreasing stimulation by catecholamines and find a new equilibrium at a
lower adrenergic drive.
Anxiety
Officially, beta blockers are not approved for anxiolytic use by the U.S. Food and Drug Administration. However, many controlled trials in the past 25 years indicate beta blockers are effective in anxiety disorders, though the mechanism of action is not known. The physiological symptoms of the fight-or-flight
response (pounding heart, cold/clammy hands, increased respiration,
sweating, etc.) are significantly reduced, thus enabling anxious
individuals to concentrate on the task at hand.
Musicians, public speakers, actors, and professional dancers have been known to use beta-blockers to avoid performance anxiety, stage fright, and tremor during both auditions and public performances. The application to stage fright was first recognized in The Lancet in 1976, and by 1987, a survey conducted by the International Conference of Symphony Orchestra Musicians,
representing the 51 largest orchestras in the United States, revealed
27% of its musicians had used beta-blockers and 70% obtained them from
friends, not physicians.
Beta-blockers are inexpensive, said to be relatively safe, and on one
hand, seem to improve musicians' performances on a technical level,
while some, such as Barry Green, the author of "The Inner Game of Music"
and Don Greene, a former Olympic diving coach who teaches Juilliard
students to overcome their stage fright naturally, say the performances
may be perceived as "soulless and inauthentic".
Cardiac surgery
The use of beta blockers around the time of cardiac surgery decreases the risk of heart dysrhythmias. Starting them around the time of other types of surgery, however, may worsen outcomes.
Adverse effects associated with β2-adrenergic receptor
antagonist activity (bronchospasm, peripheral vasoconstriction,
alteration of glucose and lipid metabolism) are less common with β1-selective
(often termed "cardioselective") agents, but receptor selectivity
diminishes at higher doses. Beta blockade, especially of the beta-1
receptor at the macula densa, inhibits renin release, thus decreasing the release of aldosterone. This causes hyponatremia and hyperkalemia.
Hypoglycemia can occur with beta blockade because β2-adrenoceptors normally stimulate glycogen breakdown (glycogenolysis) in the liver and pancreatic release of the hormoneglucagon,
which work together to increase plasma glucose. Therefore, blocking
β2-adrenoceptors lowers plasma glucose. β1-blockers have fewer metabolic
side effects in diabetic patients; however, the fast heart rate that
serves as a warning sign for insulin-induced low blood sugar may be
masked, resulting in hypoglycemia unawareness. This is termed beta blocker-induced hypoglycemia unawareness. Therefore, beta blockers are to be used cautiously in diabetics.
A 2007 study revealed diuretics and beta blockers used for hypertension increase a patient's risk of developing diabetes mellitus, while ACE inhibitors and angiotensin II receptor antagonists (angiotensin receptor blockers) actually decrease the risk of diabetes.
Clinical guidelines in Great Britain, but not in the United States,
call for avoiding diuretics and beta blockers as first-line treatment of
hypertension due to the risk of diabetes.
Beta blockers must not be used in the treatment of selective
alpha-adrenergic agonist overdose. The blockade of only beta receptors
increases blood pressure, reduces coronary blood flow, left ventricular function, and cardiac output and tissue perfusion by means of leaving the alpha-adrenergic system stimulation unopposed. Beta blockers with lipophilic properties and CNS penetration such as metoprolol and labetalol may be useful for treating CNS and cardiovascular toxicity from a methamphetamine overdose. The mixed alpha-
and beta blocker labetalol is especially useful for treatment of
concomitant tachycardia and hypertension induced by methamphetamine.
The phenomenon of "unopposed alpha stimulation" has not been reported
with the use of beta blockers for treatment of methamphetamine toxicity. Other appropriate antihypertensive drugs to administer during hypertensive crisis resulting from stimulant overdose are vasodilators such as nitroglycerin, diuretics such as furosemide, and alpha blockers such as phentolamine.
The 2007
National Heart, Lung, and Blood Institute (NHLBI) asthma guidelines
recommend against the use of non-selective beta blockers in asthmatics,
while allowing for the use of cardioselective beta blockers.Cardioselective beta-blocker (β1 blockers), if really required,
can be prescribed at the least possible dose to those with mild to
moderate respiratory symptoms. β2-agonists can somewhat mitigate β-Blocker-induced bronchospasm where it exerts greater efficacy on reversing selective β-blocker-induced bronchospasm than the nonselective β-blocker-induced worsening asthma and/or COPD.
Diabetes mellitus
Epinephrine signals early warning of the upcoming hypoglycemia.
Beta-blockers' inhibition on epinephrine's effect can somewhat exacerbate hypoglycemia by interfering with glycogenesis and mask signs of hypoglycemia such as tachycardia, palpitations, diaphoresis, and tremors. Diligent blood glucose level monitoring is necessary for a patient with diabetes mellitus on beta-blocker.
Hyperthyroidism
Abrupt withdrawal can result in a thyroid storm.
Bradycardia or AV block
Unless
a pacemaker is present, beta-blockers can severely depress conduction
in the AV node, resulting in a reduction of heart rate and cardiac
output. Usage of beta-blockers in tachycardic patients with
Wolff-Parkinson-White Syndrome can result in severe bradycardia,
necessitating treatment with a pacemaker.
Toxicity
Glucagon, used in the treatment of overdose, increases the strength of heart contractions, increases intracellular cAMP, and decreases renal vascular resistance. It is, therefore, useful in patients with beta blocker cardiotoxicity. Cardiac pacing is usually reserved for patients unresponsive to pharmacological therapy.
People experiencing bronchospasm due to the β2 receptor-blocking effects of nonselective beta blockers may be treated with anticholinergic drugs, such as ipratropium, which are safer than beta agonists in patients with cardiovascular disease. Other antidotes for beta blocker poisoning are salbutamol and isoprenaline.
β-receptor antagonism
Stimulation of β1 receptors by epinephrine and norepinephrine induces a positive chronotropic and inotropic effect on the heart and increases cardiac conduction velocity and automaticity. Stimulation of β1 receptors on the kidney causes renin release. Stimulation of β2 receptors induces smooth muscle relaxation, induces tremor in skeletal muscle, and increases glycogenolysis in the liver and skeletal muscle. Stimulation of β3 receptors induces lipolysis.
Beta blockers inhibit these normal epinephrine- and norepinephrine-mediated sympathetic actions, but have minimal effect on resting subjects.
That is, they reduce the effect of excitement or physical exertion on heart rate and force of contraction, and also tremor,
and breakdown of glycogen. Beta blockers can have a constricting effect
on the bronchi of the lungs, possibly worsening or causing asthma
symptoms.
Since β2 adrenergic receptors can cause vascular
smooth muscle dilation, beta blockers may cause some vasoconstriction.
However, this effect tends to be small because the activity of β2 receptors is overshadowed by the more dominant vasoconstricting α1
receptors. By far the greatest effect of beta blockers remains in the
heart. Newer, third-generation beta blockers can cause vasodilation
through blockade of alpha-adrenergic receptors.
Accordingly, nonselective beta blockers are expected to have antihypertensive effects.
The primary antihypertensive mechanism of beta blockers is unclear, but
may involve reduction in cardiac output (due to negative chronotropic
and inotropic effects). It may also be due to reduction in renin release from the kidneys, and a central nervous system effect to reduce sympathetic activity (for those beta blockers that do cross the blood–brain barrier, e.g. propranolol).
Antianginal effects result from negative chronotropic and
inotropic effects, which decrease cardiac workload and oxygen demand.
Negative chronotropic
properties of beta-blockers allow the lifesaving property of heart rate
control. Beta-blockers are readily titrated to optimal rate control in
many pathologic states.
Blockade of the sympathetic nervous system on renin release leads to reduced aldosterone via the renin–angiotensin–aldosterone system, with a resultant decrease in blood pressure due to decreased sodium and water retention.
Intrinsic sympathomimetic activity
Also
referred to as intrinsic sympathomimetic effect, this term is used
particularly with beta-blockers that can show both agonism and
antagonism at a given beta receptor, depending on the concentration of
the agent (beta-blocker) and the concentration of the antagonized agent
(usually an endogenous compound, such as norepinephrine). See partial agonist for a more general description.
Some beta blockers (e.g. oxprenolol, pindolol, penbutolol, labetalol and acebutolol) exhibit intrinsic sympathomimetic activity (ISA). These agents are capable of exerting low-level agonist activity at the β-adrenergic receptor while simultaneously acting as a receptor site antagonist. These agents, therefore, may be useful in individuals exhibiting excessive bradycardia with sustained beta blocker therapy.
Agents with ISA are not used after myocardial infarctions, as
they have not been demonstrated to be beneficial. They may also be less
effective than other beta-blockers in the management of angina and tachyarrhythmia.
Propranolol
is the only agent indicated for the control of tremor, portal
hypertension, and esophageal variceal bleeding, and used in conjunction
with α-blocker therapy in phaeochromocytoma.
Other effects
Beta
blockers, due to their antagonism at beta-1 adrenergic receptors,
inhibit both the synthesis of new melatonin and its secretion by the pineal gland. The neuropsychiatric side effects of some beta blockers (e.g. sleep disruption, insomnia) may be due to this effect.
Some pre-clinical and clinical research suggests that some beta blockers may be beneficial for cancer treatment. However, other studies do not show a correlation between cancer survival and beta blocker usage. Also, a 2017 meta-analysis failed to show any benefit for the use of beta blockers in breast cancer.
Beta blockers have also been used for the treatment of schizoid personality disorder.
However, there is limited evidence supporting the efficacy of
supplemental beta-blocker use in addition to antipsychotic drugs for
treating schizophrenia.
Contrast media are not contraindicated in patients receiving beta blockers.
A tremor is an involuntary, somewhat rhythmic, muscle contraction and relaxation involving oscillations
or twitching movements of one or more body parts. It is the most common
of all involuntary movements and can affect the hands, arms, eyes,
face, head, vocal folds, trunk, and legs. Most tremors occur in the hands. In some people, a tremor is a symptom of another neurological disorder. A very common tremor is the teeth chattering, usually induced by cold temperatures or by fear.
Tremor is
most commonly classified by clinical features and cause or origin. Some
of the better-known forms of tremor, with their symptoms, include the
following:
Cerebellar tremor (also known as intention tremor)
is a slow, broad tremor of the extremities that occurs at the end of a
purposeful movement, such as trying to press a button or touching a
finger to the tip of one's nose. Cerebellar tremor is caused by lesions
in or damage to the cerebellum resulting from stroke, tumor, or disease
such as multiple sclerosis or some inherited degenerative disorder. It
can also result from chronic alcoholism or overuse of some medicines. In
classic cerebellar tremor, a lesion on one side of the brain produces a
tremor in that same side of the body that worsens with directed
movement. Cerebellar damage can also produce a “wing-beating” type of
tremor called rubral or Holmes’ tremor — a combination of rest, action,
and postural tremors. The tremor is often most prominent when the
affected person is active or is maintaining a particular posture.
Cerebellar tremor may be accompanied by other manifestations of ataxia, including dysarthria (speech problems), nystagmus (rapid, involuntary rolling of the eyes), gait problems and postural tremor of the trunk and neck. Titubation is tremor of the head and is of cerebellar origin.
Dystonic tremor occurs in individuals of all ages who are affected by dystonia,
a movement disorder in which sustained involuntary muscle contractions
cause twisting and repetitive motions or painful and abnormal postures
or positions. Dystonic tremor may affect any muscle in the body and is
seen most often when the patient is in a certain position or moves a
certain way. The pattern of dystonic tremor may differ from essential
tremor. Dystonic tremors occur irregularly and can often be relieved by
complete rest. Touching the affected body part or muscle may reduce
tremor severity (a geste antagoniste).
The tremor may be the initial sign of dystonia localized to a
particular part of the body. The dystonic tremor has usually a frequency
of about 7 Hz.[6]
Essential tremor (sometimes inaccurately called benign essential tremor)
is the most common of the more than 20 types of tremor. Although the
tremor may be mild and nonprogressive in some people, in others, the
tremor is slowly progressive, starting on one side of the body but
affecting both sides within 3 years. The hands are most often affected
but the head, voice, tongue, legs, and trunk may also be involved. Head
tremor may be seen as a vertical or horizontal motion. Essential tremor
may be accompanied by mild gait disturbance. Tremor frequency may
decrease as the person ages, but the severity may increase, affecting
the person's ability to perform certain tasks or activities of daily
living. Heightened emotion, stress, fever, physical exhaustion, or low blood sugar
may trigger tremors or increase their severity. Onset is most common
after age 40, although symptoms can appear at any age. It may occur in
more than one family member. Children of a parent who has essential
tremor have a 50 percent chance of inheriting the condition. Essential
tremor is not associated with any known pathology. Its frequency is
between 4 and 8 Hz.
Orthostatic tremor
is characterized by fast (>12 Hz) rhythmic muscle contractions that
occur in the legs and trunk immediately after standing up. Cramps are
felt in the thighs and legs and the patient may shake uncontrollably
when asked to stand in one spot. No other clinical signs or symptoms
are present and the shaking ceases when the patient sits or is lifted
off the ground. The high frequency of the tremor often makes the tremor
look like rippling of leg muscles while standing. Orthostatic tremor may
also occur in patients who have essential tremor, and there might be an
overlap between these categories of tremor.
Parkinsonian tremor
is caused by damage to structures within the brain that control
movement. This resting tremor, which can occur as an isolated symptom or
be seen in other disorders, is often a precursor to Parkinson's disease
(more than 25 percent of patients with Parkinson's disease have an
associated action tremor). The tremor, which is classically seen as a "pill-rolling"
action of the hands that may also affect the chin, lips, legs, and
trunk, can be markedly increased by stress or emotion. Onset is
generally after age 60. Movement starts in one limb or on one side of
the body and usually progresses to include the other side. The tremor's
frequency is between 4 and 6 Hz.
Physiological tremor
occurs in every normal individual and has no clinical significance. It
is rarely visible and may be heightened by strong emotion (such as
anxiety or fear), physical exhaustion, hypoglycemia, hyperthyroidism, heavy metal poisoning, stimulants, alcohol withdrawal or fever.
It can be seen in all voluntary muscle groups and can be detected by
extending the arms and placing a piece of paper on top of the hands.
Enhanced physiological tremor is a strengthening of physiological tremor
to more visible levels. It is generally not caused by a neurological
disease but by reaction to certain drugs, alcohol withdrawal,
or medical conditions including an overactive thyroid and hypoglycemia.
It is usually reversible once the cause is corrected. This tremor
classically has a frequency of about 10 Hz.
Psychogenic tremor (also called hysterical tremor)
can occur at rest or during postural or kinetic movement. The
characteristics of this kind of tremor may vary but generally include
sudden onset and remission, increased incidence with stress, change in
tremor direction or body part affected, and greatly decreased or
disappearing tremor activity when the patient is distracted. Many
patients with psychogenic tremor have a conversion disorder (see Posttraumatic stress disorder) or another psychiatric disease.
Rubral tremor
is characterized by coarse slow tremor which is present at rest, at
posture and with intention. This tremor is associated with conditions
which affect the red nucleus in the midbrain, classically unusual strokes.
Tremor can result from other conditions as well
Alcoholism, excessive alcohol consumption, or alcohol withdrawal can kill certain nerve cells, resulting in a tremor known as asterixis.
Conversely, small amounts of alcohol may help to decrease familial and
essential tremor, but the mechanism behind it is unknown. Alcohol
potentiates GABAergic transmission and might act at the level of the inferior olive.
Tremor in peripheral neuropathy
may occur when the nerves that supply the body's muscles are
traumatized by injury, disease, abnormality in the central nervous
system, or as the result of systemic illnesses. Peripheral neuropathy
can affect the whole body or certain areas, such as the hands, and may
be progressive. Resulting sensory loss may be seen as a tremor or ataxia
(inability to coordinate voluntary muscle movement) of the affected
limbs and problems with gait and balance. Clinical characteristics may
be similar to those seen in patients with essential tremor.
Tobacco withdrawal symptoms include tremor.
Most of the symptoms can also occur randomly when panicked.
Diagnosis
During
a physical exam, a doctor can determine whether the tremor occurs
primarily during action or at rest. The doctor will also check for
tremor symmetry, any sensory loss, weakness or muscle atrophy, or
decreased reflexes. A detailed family history may indicate if the tremor
is inherited. Blood or urine tests can detect thyroid malfunction,
other metabolic causes, and abnormal levels of certain chemicals that
can cause tremor. These tests may also help to identify contributing
causes, such as drug interaction, chronic alcoholism, or another
condition or disease. Diagnostic imaging using CT or MRI imaging may
help determine if the tremor is the result of a structural defect or
degeneration of the brain.
The doctor will perform a neurological examination
to assess nerve function and motor and sensory skills. The tests are
designed to determine any functional limitations, such as difficulty
with handwriting or the ability to hold a utensil or cup. The patient
may be asked to place a finger on the tip of her or his nose, draw a
spiral, or perform other tasks or exercises.
The doctor may order an electromyogram
to diagnose muscle or nerve problems. This test measures involuntary
muscle activity and muscle response to nerve stimulation. The selection
of the sensors used is important. In addition to studies of muscle
activity, tremor can be assessed with accuracy using accelerometers .
Categories
The
degree of tremor should be assessed in four positions. The tremor can
then be classified by which position most accentuates the tremor:
During contraction (e.g. a tight fist while the arm is resting and supported)
Contraction tremors
Tremors that are worse during supported contraction include
essential tremor and also cerebellar and exaggerated physiological
tremors such as a hyperadrenergic state or hyperthyroidism. Drugs such as adrenergics, anticholinergics, and xanthines (such as caffeine) can exaggerate physiological tremor.
During posture (e.g. with the arms elevated against gravity such as in a 'bird-wing' position)
Posture tremors
Tremors that are worse with posture against gravity include essential tremor and exaggerated physiological tremors.
During intention (e.g. finger to nose test)
Intention tremors
Intention tremors
are tremors that are worse during intention, e.g. as the patient's
finger approaches a target, including cerebellar disorders. The
terminology of "intention" is currently less used, to the profit of
"kinetic".
Treatment
There
is no cure for most tremors. The appropriate treatment depends on
accurate diagnosis of the cause. Some tremors respond to treatment of
the underlying condition. For example, in some cases of psychogenic
tremor, treating the patient's underlying psychological problem may
cause the tremor to disappear. A few medications can help relieve
symptoms temporarily.
Medications
Medications remain the basis of therapy in many cases. Symptomatic drug therapy is available for several forms of tremor:
Cerebellar tremor symptoms may decrease with the application
of alcohol (ethanol) or benzodiazepine medications, both of which carry
some risk of dependence or addiction
Rubral tremor patients may receive some relief using L-DOPA or anticholinergic drugs. Surgery may be helpful
Dystonic tremor may respond to diazepam, anticholinergic drugs, and intramuscular injections of botulinum toxin. Botulinum toxin is also prescribed to treat voice and head tremors and several movement disorders
Primary orthostatic tremor sometimes is treated with a combination of diazepam and primidone. Gabapentin provides relief in some cases
Enhanced physiological tremor is usually reversible once the cause is corrected. If symptomatic treatment is needed, beta blockers can be used
Lifestyle
Eliminating tremor “triggers” such as caffeine and other stimulants from the diet is often recommended.
Essential tremor may benefit from slight doses of ethanol, but the potential negative consequences of regular ethanol intake need to be taken into account. Beta blockers have been used as an alternative to alcohol in sports such as competitive dart playing and carry less potential for addiction.
Physical therapy and occupational therapy
may help to reduce tremor and improve coordination and muscle control
for some patients. A physical therapist or occupational therapist will
evaluate the patient for tremor positioning, muscle control, muscle
strength, and functional skills. Teaching the patient to brace the
affected limb during the tremor or to hold an affected arm close to the
body is sometimes useful in gaining motion control. Coordination and
balancing exercises may help some patients. Some occupational therapists
recommend the use of weights, splints, other adaptive equipment, and
special plates and utensils for eating.
Surgery
Surgical
intervention such as thalamotomy and deep brain stimulation may ease
certain tremors. These surgeries are usually performed only when the
tremor is severe and does not respond to drugs. Response can be
excellent.
Thalamotomy,
involving the creation of lesions in the brain region called the
thalamus, is quite effective in treating patients with essential,
cerebellar, or Parkinsonian tremor. This in-hospital procedure is
performed under local anesthesia, with the patient awake. After the
patient's head is secured in a metal frame, the surgeon maps the
patient's brain to locate the thalamus. A small hole is drilled through
the skull and a temperature-controlled electrode is inserted into the
thalamus. A low-frequency current is passed through the electrode to
activate the tremor and to confirm proper placement. Once the site has
been confirmed, the electrode is heated to create a temporary lesion.
Testing is done to examine speech, language, coordination, and tremor
activation, if any. If no problems occur, the probe is again heated to
create a 3-mm permanent lesion. The probe, when cooled to body
temperature, is withdrawn and the skull hole is covered. The lesion
causes the tremor to permanently disappear without disrupting sensory or
motor control.
Deep brain stimulation
(DBS) uses implantable electrodes to send high-frequency electrical
signals to the thalamus. The electrodes are implanted as described
above. The patient uses a hand-held magnet to turn on and turn off a
pulse generator that is surgically implanted under the skin. The
electrical stimulation temporarily disables the tremor and can be
“reversed,” if necessary, by turning off the implanted electrode.
Batteries in the generator last about 5 years and can be replaced
surgically. DBS is currently used to treat parkinsonian tremor and
essential tremor. It is also applied successfully for other rare causes
of tremor.
The most common side effects of tremor surgery include dysarthria
(problems with motor control of speech), temporary or permanent
cognitive impairment (including visual and learning difficulties), and
problems with balance.
Biomechanical loading
As
well as medication, rehabilitation programmes and surgical
interventions, the application of biomechanical loading on tremor
movement has been shown to be a technique that is able to suppress the
effects of tremor on the human body. It has been established in the
literature
that most of the different types of tremor respond to biomechanical
loading. In particular, it has been clinically tested that the increase
of damping or inertia in the upper limb leads to a reduction of the
tremorous motion. Biomechanical loading relies on an external device
that either passively or actively acts mechanically in parallel to the
upper limb to counteract tremor movement. This phenomenon gives rise to
the possibility of an orthotic management of tremor.
Starting from this principle, the development of upper-limb
non-invasive ambulatory robotic exoskeletons is presented as a promising
solution for patients who cannot benefit from medication to suppress
the tremor. In this area robotic exoskeletons have emerged, in the form
of orthoses,
to provide motor assistance and functional compensation to disabled
people. An orthosis is a wearable device that acts in parallel to the
affected limb. In the case of tremor management, the orthosis must apply
a damping or inertial load to a selected set of limb articulations.
Recently, some studies demonstrated that exoskeletons could
achieve a consistent 40% of tremor power reduction for all users, being
able to attain a reduction ratio in the order of 80% tremor power in
specific joints of users with severe tremor.
In addition, the users reported that the exoskeleton did not affect
their voluntary motion. These results indicate the feasibility of tremor
suppression through biomechanical loading.
The main drawbacks of this mechanical management of tremor are
(1) the resulting bulky solutions, (2) the inefficiency in transmitting
loads from the exoskeleton to the human musculo-skeletal system and (3)
technological limitations in terms of actuator technologies. In this
regard, current trends in this field are focused on the evaluation of
the concept of biomechanical loading of tremor through selective
Functional Electrical Stimulation (FES) based on a (Brain-to-Computer
Interaction) BCI-driven detection of involuntary (tremor) motor
activity.
