Health information on the non neurological aspects of essential tremors and tremors in Parkinson's disease

1. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3070808/
http://catalog.ninds.nih.gov/ninds/facet/Health-Topics/term/Parkinson-s-Disease
Terri
Misdiagnosis
See above Study on Essential Tremor and Parkinson Disease Link: Lack of a link (keyword
alpha-synuclein and lewy bodies)
It appears that the above abstract offers insight into the lewy bodies associatedwith
Parkinson’s that essential tremors mimic the involuntary muscle movements that are
generally normal but may be a precursor to more intensive tremors if not prevented. I
needed to operationally define Essential Tremor (ET) as a pervasive symptom. However is
reversiable according to the literature.
Perhaps a natural antidote can be also have application that addresses the hypothesis that
alpha synuclein is based on this study
Parkinson's disease (PD) is characterized as a neurodegenerative movement disorder presenting with
rigidity, resting tremor, disturbances in balance and slowness in movement.
An important pathologic feature of PD is the presence of Lewy bodies.
The primary structural component of Lewy bodies are fibrils composed primarily of alpha-synuclein, a
highly conserved 140 amino acid protein that is predominantly expressed in neurons and which may play
a role in synaptic plasticity and neurotransmission.
Numerous studies suggest the aggregation and modification of alpha-synuclein as a key step leading to
Lewy body formation and neuronal cell loss associated with PD.
CNS Neurol Disord Drug Targets. 2012 Mar;11(2):174-9.
Targetingalpha-synuclein for the treatmentof Parkinson'sdisease.
Their recommendation phamacologically is
…Because of the central role of alpha-synuclein in PD, it represents a novel drug target for the possible
treatment of this disease. In this review, an overview of the role of alpha-synuclein in PD will be discussed
with an emphasis on recent studies utilizing an immunization approach against alpha-synuclein as a
possible treatment option for this debilitating disease.
There is of course a natural process that can be considered 140 amino acids replacement therapy. Amino
Acid Therapy exists at
http://www.blog.parkinsonsrecovery.com/category/amino-acid-therapy/

2. Operational Definition for Tremor
A tremor is an involuntary,[1]
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 chattering of teeth, usually induced by cold
temperatures or by fear.
Causes
Tremor can be a symptom associated with disorders in those parts of the brain that control
muscles throughout the body or in particular areas, such as the hands. Neurological disorders or
conditions that can produce tremor including multiple sclerosis, stroke, traumatic brain injury,
chronic kidney disease and a number of neurodegenerative diseases that damage or destroy parts
of the brainstem or the cerebellum, Parkinson's disease being the one most often associated with
tremor.
Other causes include the use of drugs (such as amphetamines, cocaine, caffeine, corticosteroids,
SSRI), alcohol, mercury poisoning; or the withdrawal of drugs such as alcohol or
benzodiazepine.
Tremors can also be seen in infants with phenylketonuria (PKU), overactive thyroid or liver
failure. Tremors can be an indication of hypoglycemia, along with palpitations, sweating and
anxiety. Tremor can also be caused from lack of sleep, lack of vitamins, or increased stress.[citation
needed]
Deficiencies of magnesium and thiamine have also been known to cause tremor or shaking,
which resolves when the deficiency is corrected. See magnesium in biology. Some forms of
tremor are inherited and run in families, while others have no known cause. Tremors can also be
caused by some spider bites, e.g. the redback spider of Australia.
Characteristics may include a rhythmic shaking in the hands, arms, head, legs, or trunk; shaky
voice; and problems holding things such as a fork or pen. Some tremors may be triggered by or
become exacerbated during times of stress or strong emotion, when the individual is physically
exhausted, or during certain postures or movements.
Tremor may occur at any age but is most common in middle-age and older persons. It may be
occasional, temporary, or occur intermittently. Tremor affects men and women equally.
Types
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:

3.  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 and/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 often can 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.
 Essential tremor (sometimes 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
“yes-yes” or “no-no” 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 and/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.
 Orthostatic tremor is characterized by fast (>12 Hz) rhythmic muscle contractions that
occur in the legs and trunk immediately after standing. 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

4. 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.
 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[2]
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 [3]
 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 and/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 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.

5. 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 .[4]
Categories[edit]
The degree of tremor should be assessed in four positions. The tremor can then be classified by
which position most accentuates the tremor:[5]
Position Name Description
At rest
Resting
tremors
Tremors that are worse at rest include Parkinsonian
syndromes and essential tremor if severe. This includes
drug-induced tremors from blockers of dopamine
receptors such as haloperidol and other antipsychotic
drugs.
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.[5]
Drugs such as
adrenergics, anticholinergics, and xanthines 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.[5]
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,

6. 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:
 Parkinsonian tremor drug treatment involves L-DOPA and/or dopamine-like drugs
such as pergolide, bromocriptine and ropinirole; They can be dangerous, however, as
they may cause symptoms such as tardive dyskinesia, akathisia, clonus, and in rare
instances tardive (late developing) psychosis. Other drugs used to lessen parkinsonian
tremor include amantadine and anticholinergic drugs like benzatropine
 Essential tremor may be treated with beta blockers (such as propranolol and nadolol) or
primidone, an anticonvulsant
 Cerebellar tremor symptoms may decrease with the application of alcohol (ethanol) or
benzodiazepine medications, both of which carry some risk of dependence and/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 (is there a natural beta
blocker?)
Lifestyle[edit]
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.

7. Physical therapy may help to reduce tremor and improve coordination and muscle control for
some patients. A physical 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 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 and/or inertia in the upper limb leads to a reduction

8. 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.[6]
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.[7]
See also
 Chronic solvent-induced encephalopathy
 Fasciculation These twitches of "at rest" skeletal muscle are too weak to cause any joint
movements, and fall short of the definition of a tremor. Usually benign, but also a
symptom of some very serious neurological disorders such as ALS.
 Neurology
 Shivering
References
1. Jump up ^ "tremor" at Dorland's Medical Dictionary
2. Jump up ^ Allan H. Goroll; Albert G. Mulley (1 January 2009). Primary care medicine: office
evaluation and management of the adult patient. Lippincott Williams & Wilkins. p. 1178.
ISBN 978-0-7817-7513-7. Retrieved 30 May 2011.
3. Jump up ^ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC497216/pdf/jnnpsyc00292-0020.pdf
4. Jump up ^ Grimaldi G, Manto M. "Neurological tremor: sensors,signal processing and
emerging applications." Sensors. 2010;10:1399–1422
5. ^ Jump up to: a b c
Jankovic J, Fahn S. Physiologic and pathologic tremors. Diags, mechanism, and
management. Ann Intern Med. 1980;93:460–465. PMID 7001967

9. 6. Jump up ^ Rocon E, Belda-Lois JM, Ruiz AF, Manto M, Moreno JC, Pons JL. "Design and
Validation of a Rehabilitation Robotic Exoskeleton for Tremor Assessment and Suppression."
IEEE Transactions on Neural Systems and Rehabilitation Engineering. 2007;15(3):367–378
7. Jump up ^ Tremor project – ICT-2007-224051[dead link]
External links
Wikimedia Commons has media related to Tremor.
 "NINDS Tremor Information Page". National Institute of Neurological Disorders and
Stroke. July 20, 2007. Retrieved 2007-10-08. Some text copied with permission and
thanks.
 "Leonid L. Rubchinsky et al. (2007) Tremor. Scholarpedia 2(10):1379".
 orthostatictremor.org
[show]
 v
 t
 e
Pathology of the nervous system, primarily CNS (G04–G47, 323–349)
Brain
 Encephalitis
o Viral encephalitis
o Herpesviral encephalitis
o Limbic encephalitis
o Encephalitis lethargica
 Cavernous sinus thrombosis
 Brain abscess
o Amoebic
o
Spinal cord
 Myelitis: Poliomyelitis
 Demyelinating disease

10. o Transverse myelitis
 Tropical spastic paraparesis
 Epidural abscess

Both/either
 Encephalomyelitis
o Acute disseminated
o Myalgic
 Meningoencephalitis
Degenerative
Extrapyramidal and
movement disorders
 Basal ganglia disease
o Parkinsonism
 PD
 Postencephaliti
c
 NMS
o PKAN
o Tauopathy
 PSP
o Striatonigral
degeneration
o Hemiballismus
o HD
o OA
 Dyskinesia
o Dystonia
 Status
dystonicus
 Spasmodic
torticollis

11.  Meige's
 Blepharospasm
o Athetosis
o Chorea
 Choreoathetosi
s
o Myoclonus
 Myoclonic
epilepsy
o Akathisia
 Tremor
o Essential tremor
o Intention tremor
 Restless legs
 Stiff person

Dementia
 Tauopathy
o Alzheimer's
 Early-onset
o Primary progressive
aphasia
 Frontotemporal
dementia/Frontotemporal
lobar degeneration
o Pick's
o Dementia with Lewy
bodies
 Posterior cortical atrophy
 Vascular dementia

12. 
Mitochondrial
disease
 Leigh's disease
Demyelinatin
g
 autoimmune
o Multiple sclerosis
o Neuromyelitis optica
o Schilder's disease
 hereditary
o Adrenoleukodystrophy
o Alexander
o Canavan
o Krabbe
o ML
o PMD
o VWM
o MFC
o CAMFAK syndrome
 Central pontine myelinolysis
 Marchiafava-Bignami disease
 Alpers' disease

Episodic/
paroxysmal
Seizure/epilepsy
 Focal
 Generalised
 Status epilepticus
 Myoclonic epilepsy


13. Headache
 Migraine
o Familial hemiplegic
 Cluster
 Tension

Cerebrovascular
 TIA
o Amaurosis fugax
o Transient global amnesia
o Acute aphasia
 Stroke
o MCA
o ACA
o PCA
o Foville's
o Millard-Gubler
o Lateral medullary
o Weber's
o Lacunar stroke
o
Sleepdisorders
 Insomnia
 Hypersomnia
 Sleep apnea
o Obstructive
o Ondine's curse
 Narcolepsy
 Cataplexy
 Kleine-Levin
 Circadian rhythm sleep disorder

14. o Advanced sleep phase
disorder
o Delayed sleep phase
disorder
o Non-24-hour sleep–wake
disorder
o Jet lag
CSF
 Intracranial hypertension
o Hydrocephalus/NPH
o Choroid plexus papilloma
o Idiopathic intracranial hypertension
 Cerebral edema
 Intracranial hypotension

Other
 Brain herniation
 Reye's
 Hepatic encephalopathy
 Toxic encephalopathy
 Hashimoto's encephalopathy

Degenerative
SA
 Friedreich's ataxia
 Ataxia telangiectasia


15. MND
 UMN only:
o Primary lateral sclerosis
o Pseudobulbar palsy
o Hereditary spastic paraplegia
 LMN only:
o Distal hereditary motor neuropathies
o Spinal muscular atrophies
 SMA
 SMAX1
 SMAX2
 DSMA1
 Congenital DSMA
 SMA-PCH
 SMA-LED
 SMA-PME
o Progressive muscular atrophy
o Progressive bulbar palsy
 Fazio–Londe
 Infantile progressive bulbar palsy
 both:
o Amyotrophic lateral sclerosis
 v
 t
 e
Index of the central nervous system
Description
 Anatomy
o meninges

16. o cortex
 association fibers
 commissural fibers
o lateral ventricles
o basal ganglia
o diencephalon
o mesencephalon
o pons
o cerebellum
o medulla
o spinal cord
 tracts
 Physiology
o neutrotransmission
 enzymes
 intermediates
 Development

Disease
 Cerebral palsy
 Meningitis
 Demyelinating diseases
 Seizures and epilepsy
 Headache
 Stroke
 Sleep
 Congenital
 Injury
 Neoplasms and cancer
 Other
o paralytic syndromes
o ALS
 Symptoms and signs

17. o head and neck
o eponymous
o lesions
 Tests
o CSF
o
Treatment
 Procedures
 Drugs
o general anesthetics
o analgesics
o addiction
o epilepsy
o cholinergics
o migraine
o Parkinson's
o vertigo
o other
[show]
 v
 t
 e
Symptoms and signs: nervous and musculoskeletal systems (R25–R29,
781.0, 781.2–9)
Primarily CNS Movement disorders
 Dyskinesia: Athetosis
 Tremor
 Dyskinesia

18. 
Gait abnormality
 Scissor gait
 Cerebellar ataxia
 Festinating gait
 Marche a petit pas
 Propulsive gait
 Stomping gait
 Spastic gait
 Magnetic gait

Lack of coordination
 Dyskinesia: Ataxia
o Cerebellar
ataxia/Dysmetria
o Sensory ataxia
o Dyssynergia
 Dysdiadochokinesia
 Asterixis

Other
 Abnormal posturing:
Opisthotonus
 Sensory processing disorder:
Hemispatial neglect
 Facial weakness
 Hyperreflexia
 Pronator drift
Primarily PNS Gait abnormality  Steppage gait

19.  Antalgic gait
Movement disorders
 Spasm
o Trismus
 Fasciculation
 Fibrillation
 Myokymia
 Cramp

Gait abnormality
 Myopathic gait
 Trendelenburg gait
 Pigeon gait

Other
 Tetany
 Meningism


[show]
Further indexes
 v
 t

20.  e
Index of the central nervous system
Description
 Anatomy
o meninges
o cortex
 association fibers
 commissural fibers
o lateral ventricles
o basal ganglia
o diencephalon
o mesencephalon
o pons
o cerebellum
o medulla
o spinal cord
 tracts
 Physiology
o neutrotransmission
 enzymes
 intermediates
 Development

Disease
 Cerebral palsy
 Meningitis
 Demyelinating diseases
 Seizures and epilepsy
 Headache
 Stroke
 Sleep
 Congenital

21.  Injury
 Neoplasms and cancer
 Other
o paralytic syndromes
o ALS
 Symptoms and signs
o head and neck
o eponymous
o lesions
 Tests
o CSF
o
Treatment
 Procedures
 Drugs
o general anesthetics
o analgesics
o addiction
o epilepsy
o cholinergics
o migraine
o Parkinson's
o vertigo
o other
 v
 t
 e
Index of the peripheral nervous system
Description
 Anatomy
 Nerves

22. o cranial
o trigeminal
o cervical
o brachial
o lumbosacral plexus
o somatosensory
o spinal
o autonomic
 Physiology
o reflexes
o proteins
o neurotransmitters
o transporters
 Development
o neurotrophins
o
Disease
 Autonomic
 Congenital
 Injury
 Neoplasms and cancer
 Other
 Symptoms and signs
o eponymous
o
Treatment
 Procedures
 Local anesthetics
 v
 t

23.  e
Index of muscle
Description
 Anatomy
o head
o neck
o arms
o chest and back
o diaphragm
o abdomen
o genital area
o legs
 Muscle tissue
 Physiology
o connective tissue
o
Disease
 Myopathy
 Soft tissue
 Connective tissue
 Congenital
o abdomen
o muscular dystrophy
 Neoplasms and cancer
 Injury
 Symptoms and signs
o eponymous
o
Treatment
 Procedures
 Drugs

24. o anti-inflammatory
o muscle relaxants
 v
 t
 e
Index of bones and cartilage
Description
 Anatomy
o bones
o skull
 face
 neurocranium
 compound structures
 foramina
o upper extremity
o torso
o pelvis
o lower extremity
 Physiology
 Development
 Cells

Disease
 Congenital
 Neoplasms and cancer
 Trauma
o fracture
 Other
 Symptoms and signs
o eponymous

25. o
Treatment
 Procedures
 Drugs
 Surgery
o approaches
 v
 t
 e
Index of joint
Description
 Anatomy
o head and neck
o cranial
o arms
o torso and pelvis
o legs
o bursae and sheathes
 Physiology

Disease
 Arthritis
o acquired
o back
o childhood
o soft tissue
 Congenital
 Injury
 Symptoms and signs
o eponymous
o orthopaedic

26.  Examination

Treatment
 Procedures
 Drugs
o rheumatoid arthritis
o gout
o topical analgesics
<img src="//en.wikipedia.org/wiki/Special:CentralAutoLogin/start?type=1x1" alt="" title=""
width="1" height="1" style="border: none; position: absolute;" />
Retrieved from "https://en.wikipedia.org/w/index.php?title=Tremor&oldid=670022408"
Categories:
 Symptoms and signs: Nervous system
Essential tremor disorder affects about 14 percent of individuals 65 and over. Although half of
these cases occur because of a genetic mutation (familial tremor), it is unknown what contributes
to the disorder in people without this mutation. Currently, there is no cure for essential tremor
disorder, but therapies may include physical therapy, beta-blockers, or anti-convulsant drugs. In
other cases, it may be helpful to eliminate stimulants from the diet, i.e., caffeine.
What may be more concerning is that your friend is smoking weed (aka marijuana, pot)
everyday. Individuals who smoke weed may become addicted, which means that they need more
and more of the drug to get the same "high." The American Academy of Family Physicians
mentions that marijuana use may actually cause tremors (shaking) and decreased coordination,
along with the following common side effects:
 Trouble remembering things
 Slowed reaction time
 Difficulty concentrating
 Sleepiness
 Anxiety
 Paranoia (feeling that people are "out to get you")
 Altered time perception
 Red, bloodshot eyes
Moreover, marijuana may also have long-term health effects on the lungs — emerging research
shows that smoking pot may even be associated with cancer. You may want to consider having a
talk with your friend about why she smokes and whether she believes she is gaining anything
from her marijuana use. While you can't force her to quit, you can express your concern and

27. point out that the marijuana may be contributing to her tremors. If your friend is a student at
Columbia and would like to speak with a health care provider about her tremors or her smoking,
she can make an appointment by calling x4-2284 or visiting Open Communicator. She can also
see any provider from Counseling and Psychological Services by calling x4-2878 to make an
appointment.
For more resources, check out Wants to stop smoking pot in the Go Ask Alice! alcohol and other
drugs archives. What your friend is dealing with is no small matter, but she is certainly fortunate
to have a concerned and supportive friend like yourself.
Good luck,
Beta blockers (β-blockers, beta-adrenergic blocking agents, beta antagonists, beta-adrenergic
antagonists, beta-adrenoreceptor antagonists, or beta adrenergic receptor antagonists) are a class
of drugs that are particularly used for the management of cardiac arrhythmias, protecting the
heart from a second heart attack (myocardial infarction) after a first heart attack (secondary
prevention),[1]
and, in certain cases, hypertension.[2][3]
Beta blockers block the action of endogenous catecholamines epinephrine (adrenaline) and
norepinephrine (noradrenaline) -in particular on adrenergic beta receptors, of the sympathetic
nervous system, which mediates the fight-or-flight response.[4][5]
Some block all activation of β-
adrenergic receptors and others are selective.
Three types of beta receptors are known, designated β1, β2 and β3 receptors.[6]
β1-adrenergic
receptors are located mainly in the heart and in the kidneys.[5]
β2-adrenergic receptors are located
mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal
muscle.[5]
β3-adrenergic receptors are located in fat cells.[7]
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, Sir James W. Black [8]
found the first clinically significant beta blockers—propranolol
and pronethalol; it revolutionized the medical management of angina pectoris[9]
and is considered
by many to be one of the most important contributions to clinical medicine and pharmacology of
the 20th century.[10]
In comparison with other antihypertensive drugs, beta blockers are less than optimal for the
treatment of primary hypertension, with a raised risk of stroke.[11]
Contents
[hide]

28.  1 Medical uses
o 1.1 Congestive heart failure
o 1.2 Anxiety
o 1.3 Surgery
 2 Adverse effects
o 2.1 Contraindications
o 2.2 Toxicity
 3 β-Receptor antagonism
 4 Intrinsic sympathomimetic activity
 5 α1-Receptor antagonism
 6 Other effects
 7 Examples
o 7.1 Nonselective agents
o 7.2 β1-selective agents
o 7.3 β2-selective agents
o 7.4 β3-selective agents
 8 Comparative information
o 8.1 Pharmacological differences
o 8.2 Indication differences
 9 See also
 10 References
 11 External links
Medical uses[edit]
Large differences exist in the pharmacology of agents within the class, thus not all beta blockers
are used for all indications listed below.
Indications for beta blockers include:
 Angina pectoris[12][13]
 Atrial fibrillation[14]
 Cardiac arrhythmia
 Congestive heart failure
 Essential tremor
 Glaucoma
 Hypertension
 Migraine prophylaxis
 Mitral valve prolapse
 Myocardial infarction
 Phaeochromocytoma, in conjunction with α-blocker
 Postural orthostatic tachycardia syndrome
 Symptomatic control (tachycardia, tremor) in anxiety and hyperthyroidism
 Theophylline overdose
Beta blockers have also been used for:

29.  Acute aortic dissection
 Hypertrophic obstructive cardiomyopathy
 Marfan syndrome (treatment with propranolol slows progression of aortic dilation and its
complications)
 Prevention of variceal bleeding in portal hypertension
 Possible mitigation of hyperhidrosis
 Social and other anxiety disorders
 Controversially, for reduction of perioperative mortality
Congestive heart failure[edit]
Although beta blockers were once contraindicated in congestive heart failure, as they have the
potential to worsen the condition, studies in the late 1990s showed their efficacy at reducing
morbidity and mortality.[15][16][17]
Bisoprolol, carvedilol, and sustained-release metoprolol are
specifically indicated as adjuncts to standard ACE inhibitor and diuretic therapy in congestive
heart failure.
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.[citation needed]
Beta blockers, in
addition to their sympatholytic B1 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 extracellular volume and increasing the oxygen-carrying capacity of
blood. Beta blockers' sympatholytic activities reduce heart rate, thereby increasing the ejection
fraction of the heart 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.[18]
Anxiety[edit]
Officially, beta blockers are not approved for anxiolytic use by the U.S. Food and Drug
Administration.[19]
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.[20]
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.[21]
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

30. 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".[21]
Since they promote lower heart rates and reduce tremors, beta blockers have been used in
professional sports where high accuracy is required, including archery, shooting, golf[22]
and
snooker.[22]
Beta blockers are banned by the International Olympic Committee.[23]
A recent, high-
profile transgression took place in the 2008 Summer Olympics, where 50- metre pistol silver
medallist and 10-metre air pistol bronze medallist Kim Jong-su tested positive for propranolol
and was stripped of his medals.
For similar reasons, beta blockers have also been used by stutterers[citation needed]
and surgeons.[24]
Surgery[edit]
The use of beta blockers around the time of cardiac surgery decreases the risk of heart
dysrhythmias.[25]
Starting them around the time of other types of surgery, however, worsens
outcomes.[25]
Adverse effects[edit]
Adverse drug reactions associated with the use of beta blockers include: nausea, diarrhea,
bronchospasm, dyspnea, cold extremities, exacerbation of Raynaud's syndrome, bradycardia,
hypotension, heart failure, heart block, fatigue, dizziness, alopecia (hair loss), abnormal vision,
hallucinations, insomnia, nightmares, sexual dysfunction, erectile dysfunction and/or alteration
of glucose and lipid metabolism. Mixed α1/β-antagonist therapy is also commonly associated
with orthostatic hypotension. Carvedilol therapy is commonly associated with edema.[26]
Due to
the high penetration across the blood–brain barrier, lipophilic beta blockers, such as propranolol
and metoprolol, are more likely than other, less lipophilic, beta blockers to cause sleep
disturbances, such as insomnia, vivid dreams and nightmares.[27]
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
hepatic glycogen breakdown (glycogenolysis) and pancreatic release of glucagon, 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
tachycardia that serves as a warning sign for insulin-induced hypoglycemia may be masked.
Therefore, beta blockers are to be used cautiously in diabetics.[28]
A 2007 study revealed diuretics and beta blockers used for hypertension increase a patient's risk
of developing diabetes, while ACE inhibitors and angiotensin II receptor antagonists

31. (angiotensin receptor blockers) actually decrease the risk of diabetes.[29]
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.[30]
Beta blockers must not be used in the treatment of cocaine, amphetamine, or other alpha-
adrenergic stimulant overdose. The blockade of only beta receptors increases hypertension,
reduces coronary blood flow, left ventricular function, and cardiac output and tissue perfusion by
means of leaving the alpha-adrenergic system stimulation unopposed.[citation needed]
The appropriate
antihypertensive drugs to administer during hypertensive crisis resulting from stimulant abuse
are vasodilators such as nitroglycerin, diuretics such as furosemide, and alpha blockers such as
phentolamine.[31]
Contraindications[edit]
Beta blockers are contraindicated in patients with asthma as stated in the British National
Formulary 2011.[citation needed]
They should also be avoided in patients with a history of cocaine use
or in cocaine-induced tachycardia.[citation needed]
Beta blockers should not be used as a first-line treatment in the acute setting for cocaine-induced
acute coronary syndrome (CIACS). No recent studies have been identified that show the benefit
of beta blockers in reducing coronary vasospasm, or coronary vascular resistance, in patients
with CIACS. In the multiple case studies identified, the use of beta blockers in CIACS resulted
in detrimental outcomes, and the discontinuation of beta blockers used in the acute setting led to
improvement in clinical course.[citation needed]
The guidelines by the American College of
Cardiology/American Heart Association also support this idea, and recommend against the use
of beta blockers in cocaine-induced ST-segment elevation myocardial infarction (MI) because of
the risk of coronary vasospasm.[citation needed]
Though, in general, beta blockers improve mortality in
patients who have suffered MI, it is unclear whether patients with CIACS will benefit from this
mortality reduction because no studies assess the use of beta blockers in the long term, and
because cocaine users may be prone to continue to abuse the substance, thus complicating the
effect of drug therapy.[32]
Toxicity[edit]
Glucagon, used in the treatment of overdose,[33][34]
increases the strength of heart contractions,
increases intracellular cAMP, and decreases renal vascular resistance. It is, therefore, useful in
patients with beta-blocker cardiotoxicity.[35][36]
Cardiac pacing is usually reserved for patients
unresponsive to pharmacological therapy.
Patients 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[edit]

32. 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.[37]
Stimulation of β1 receptors on the kidney causes renin release.[38]
Stimulation of β2 receptors
induces smooth muscle relaxation,[39]
induces tremor in skeletal muscle,[40]
and increases
glycogenolysis in the liver and skeletal muscle.[41]
Stimulation of β3 receptors induces lipolysis.[42]
Beta blockers inhibit these normal epinephrine- and norepinephrine-mediated sympathetic
actions,[4]
but have minimal effect on resting subjects.[citation needed]
That is, they reduce
excitement/physical exertion on heart rate and force of contraction,[43]
and also tremor[44]
and
breakdown of glycogen, but increase dilation of blood vessels[45]
and constriction of bronchi.[46]
Therefore, nonselective beta blockers are expected to have antihypertensive effects.[47]
The
primary antihypertensive mechanism of beta blockers is unclear, but may involve reduction in
cardiac output (due to negative chronotropic and inotropic effects).[48]
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.
The antiarrhythmic effects of beta blockers arise from sympathetic nervous system blockade—
resulting in depression of sinus node function and atrioventricular node conduction, and
prolonged atrial refractory periods. Sotalol, in particular, has additional antiarrhythmic properties
and prolongs action potential duration through potassium channel blockade.
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[edit]
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, 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.

33. 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.[26]
α1-Receptor antagonism[edit]
Some beta blockers (e.g., labetalol and carvedilol) exhibit mixed antagonism of both β- and α1-
adrenergic receptors, which provides additional arteriolar vasodilating action.
Other effects[edit]
Beta blockers decrease nocturnal melatonin release, perhaps partly accounting for sleep
disturbances caused by some agents.[49]
They can also be used to treat glaucoma because they decrease intraocular pressure by lowering
aqueous humor secretion.[50]
Examples[edit]
Dichloroisoprenaline, the first beta blocker
Nonselective agents[edit]
 Propranolol
 Bucindolol
 Carteolol
 Carvedilol (has additional α-blocking activity)
 Labetalol (has additional α-blocking activity)
 Nadolol
 Oxprenolol (has intrinsic sympathomimetic activity)
 Penbutolol (has intrinsic sympathomimetic activity)
 Pindolol (has intrinsic sympathomimetic activity)
 Sotalol
 Timolol
 Eucommia bark (herb) [51]
β1-selective agents[edit]

34. Also known as cardioselective
 Acebutolol (has intrinsic sympathomimetic activity)
 Atenolol
 Betaxolol
 Bisoprolol
 Celiprolol
 Esmolol[52]
 Metoprolol
 Nebivolol (also increases nitric oxide release for vasodilation)
β2-selective agents[edit]
 Butaxamine (weak α-adrenergic agonist activity): No common clinical applications, but
used in experiments
 ICI-118,551: Highly selective β2-adrenergic receptor antagonist—no known clinical
applications, but used in experiments due to its strong receptor specificity
β3-selective agents[edit]
 SR 59230A (has additional α-blocking activity): Used in experiments
Comparative information[edit]
Pharmacological differences[edit]
 Agents with intrinsic sympathomimetic action (ISA)
o Acebutolol, carteolol, celiprolol, mepindolol, oxprenolol, pindolol
 Agents with greater aqueous solubility (hydrophilic beta blockers)
o Atenolol, celiprolol, nadolol, sotalol
 Agents with membrane stabilizing effect
o Acebutolol, propranolol
Indication differences[edit]
 Agents specifically indicated for cardiac arrhythmia
o Esmolol, sotalol, landiolol
 Agents specifically indicated for congestive heart failure
o carvedilol, sustained-release metoprolol, bisoprolol,
 Agents specifically indicated for glaucoma
o Betaxolol, carteolol, levobunolol, metipranolol, timolol
 Agents specifically indicated for myocardial infarction
o Atenolol, metoprolol, propranolol
 Agents specifically indicated for migraine prophylaxis
o Timolol, propranolol

35. Propranolol is the only agent indicated for control of tremor, portal hypertension, and esophageal
variceal bleeding, and used in conjunction with α-blocker therapy in phaeochromocytoma.[26]
See also[edit]
 Alpha blockers
References[edit]
1. Jump up ^ Freemantle N, Cleland J, Young P, Mason J, Harrison J (June 1999). "beta Blockade after
myocardial infarction: systematic review and meta regression analysis".BMJ 318 (7200): 1730–7.
doi:10.1136/bmj.318.7200.1730. PMC 31101. PMID 10381708.
2. Jump up ^ Cruickshank JM (August 2010). "Beta blockers in hypertension". Lancet 376 (9739): 415;
authorreply 415–6. doi:10.1016/S0140-6736(10)61217-2. PMID 20692524.
3. Jump up ^ Kaplan, Norman M. (October 2010). "Choice of therapy in primary (essential) hypertension:
Clinical trials". UpToDate.
4. ^ Jump up to: a b
Frishman W.H.; Cheng-Lai A; Nawarskas J (2005). Current Cardiovascular Drugs.
Current Science Group. p. 152. ISBN 978-1-57340-221-7. Retrieved 2010-09-07.
5. ^ Jump up to: a b c
Arcangelo V.P.; Peterson A.M. (2006). Pharmacotherapeutics for advanced practice:a
practical approach.Lippincott Williams & Wilkins. p. 205. ISBN 978-0-7817-5784-3. Retrieved 2010-09-
07.
6. Jump up ^ Frishman W.H.; Cheng-Lai A; Nawarskas J (2005). Current Cardiovascular Drugs. Current
Science Group. p. 153. ISBN 978-1-57340-221-7. Retrieved 2010-09-07.
7. Jump up ^ Clément K, Vaisse C, Manning BS, Basdevant A, Guy-Grand B, Ruiz J, Silver KD, Shuldiner
AR, Froguel P, Strosberg AD (August 1995). "Genetic variation in the beta 3-adrenergic receptor and an
increased capacity to gain weight in patients with morbid obesity".The New England Journal of Medicine
333 (6): 352–4. doi:10.1056/NEJM199508103330605. PMID 7609752.
8. Jump up ^ "Sir James Black inventor of beta-blockers passes away".Retrieved 2010-09-06.
9. Jump up ^ van der Vring JA, Daniëls MC, Holwerda NJ, Withagen PJ, Schelling A, Cleophas TJ,
Hendriks MG (June 1999). "Combination of calcium channelblockers and beta blockers for patients with
exercise-induced angina pectoris: a double-blind parallel-group comparison of different classes of calcium
channel blockers. The Netherlands Working Group on Cardiovascular Research (WCN)". Angiology 50 (6):
447–54. doi:10.1177/000331979905000602. PMID 10378820.
10. Jump up ^ Stapleton MP (1997). "Sir James Black and propranolol. The role of the basic sciences in the
history of cardiovascular pharmacology". Texas Heart Institute Journal 24 (4): 336–42. PMC 325477.
PMID 9456487.
11. Jump up ^ Lindholm LH, Carlberg B, Samuelsson O (2005). "Should beta blockers remain first choice in
the treatment of primary hypertension? A meta-analysis". Lancet 366 (9496): 1545–1553.
doi:10.1016/s0140-6736(05)67573-3. PMID 16257341.
12. Jump up ^ Cleophas, Ton (1995). Beta-blockers in hypertension and angina pectoris:different
compounds,different strategies. Kluwer Academic Publishers. ISBN 0-7923-3516-3.
13. Jump up ^ Khan, M.I. Gabriel (2007). Cardia Drug Therapy. Humana Press. ISBN 1-59745-238-6.
14. Jump up ^ Meinertz T, Willems S (December 2008). "Die Behandlung von Vorhofflimmern im Alltag"
[Treatment of atrial fibrillation in every day practice]. Der Internist 49 (12): 1437–42. doi:10.1007/s00108-
008-2152-6. PMID 19020848.
15. Jump up ^ Hjalmarson A, Goldstein S, Fagerberg B, Wedel H, Waagstein F, Kjekshus J, Wikstrand J, El
Allaf D, Vítovec J, Aldershvile J, Halinen M, Dietz R, Neuhaus KL, Jánosi A, Thorgeirsson G, Dunselman
PH, Gullestad L, Kuch J, Herlitz J, Rickenbacher P, Ball S, Gottlieb S, Deedwania P (2000). "Effects of
controlled-release metoprolol on total mortality, hospitalizations, and well-being in patients with heart
failure: the Metoprolol CR/XL Randomized Intervention Trial in congestive heart failure (MERIT-HF).
MERIT-HF Study Group". JAMA 283 (10): 1295–302. doi:10.1001/jama.283.10.1295. PMID 10714728.
16. Jump up ^ Leizorovicz A, Lechat P, Cucherat M, Bugnard F (2002). "Bisoprolol for the treatment of
chronic heart failure: a meta-analysis on individual data of two placebo-controlled studies--CIBIS and

36. CIBIS II. Cardiac Insufficiency Bisoprolol Study". Am. Heart J. 143 (2): 301–7.
doi:10.1067/mhj.2002.120768. PMID 11835035.
17. Jump up ^ Packer M, Fowler MB, Roecker EB, Coats AJ, Katus HA, Krum H, MohacsiP, Rouleau JL,
Tendera M, Staiger C, Holcslaw TL, Amann-Zalan I, DeMets DL (2002). "Effect of carvedilol on the
morbidity of patients with severe chronic heart failure: results of the carvedilol prospective randomized
cumulative survival (COPERNICUS) study". Circulation 106 (17): 2194–9.
doi:10.1161/01.CIR.0000035653.72855.BF. PMID 12390947.
18. Jump up ^ Pritchett AM, Redfield MM (2002). "Beta-blockers: new standard therapy for heart failure"
(PDF). Mayo Clin.Proc. 77 (8): 839–46. doi:10.4065/77.8.839. PMID 12173717.
19. Jump up ^ Schneier FR (2006). "Clinical practice. Social anxiety disorder". N. Engl. J. Med. 355 (10):
1029–36. doi:10.1056/NEJMcp060145. PMID 16957148.
20. Jump up ^ Tyrer P (1992). "Anxiolytics not acting at the benzodiazepine receptor: Beta blockers".
Progress in Neuro-Psychopharmacology and Biological Psychiatry 16 (1): 17–26. doi:10.1016/0278-
5846(92)90004-X. PMID 1348368.
21. ^ Jump up to: a b
Blair Tindall. "Better Playing Through Chemistry", The New York Times, 17 October
2004. Retrieved 3 July 2011.
22. ^ Jump up to: a b
http://www.independent.co.uk/sport/golf-ogrady-says-players-use-betablockers-drugs-
helped-win-majors-1368307.html
23. Jump up ^ World Anti-Doping Agency (2005-09-19). "The Worl Anti-Doping Code: The 2006 Prohibited
List International Standard" (PDF). World Anti-Doping Agency.Retrieved 2006-12-13.
24. Jump up ^ Elman MJ, Sugar J, Fiscella R, Deutsch TA, Noth J, Nyberg M, Packo K, Anderson RJ (1998).
"The effect of propranolol versus placebo on resident surgical performance". Transactions of the American
Ophthalmological Society 96:283–91; discussion 291–4. PMC 1298399. PMID 10360293.
25. ^ Jump up to: a b
Blessberger H, Kammler J, Domanovits H, Schlager O, Wildner B, Azar D, Schillinger M,
WiesbauerF, Steinwender C (Sep 18, 2014). "Perioperative beta-blockers for preventing surgery-related
mortality and morbidity". The Cochrane database of systematic reviews 9: CD004476.
doi:10.1002/14651858.CD004476.pub2. PMID 25233038.
26. ^ Jump up to: a b c
Editor Rossi S, ed. (2006). Australian Medicines Handbook.Adelaide: Australian
Medicines Handbook.
27. Jump up ^ Cruickshank JM (2010). "Beta-blockers and heart failure". Indian Heart J 62 (2): 101–10.
PMID 21180298.
28. Jump up ^ Beta-Adrenoceptor Antagonists (Beta-Blockers);
http://www.cvpharmacology.com/cardioinhibitory/beta-blockers.htm
29. Jump up ^ Elliott WJ, Meyer PM (2007). "Incident diabetes in clinical trials of antihypertensive drugs:a
network meta-analysis". Lancet 369 (9557): 201–7. doi:10.1016/S0140-6736(07)60108-1.
PMID 17240286.
30. Jump up ^ Mayor S (2006). "NICE removes beta blockers as first line treatment for hypertension".BMJ
333 (7557): 8. doi:10.1136/bmj.333.7557.8-a. PMC 1488775. PMID 16809680.
31. Jump up ^ eMedicine - Toxicity, Amphetamine : Article by Neal Handly
32. Jump up ^ Page RL, Utz KJ, Wolfel EE (December 2007). "Should beta-blockers be used in the treatment
of cocaine-associated acute coronary syndrome?". The Annals of Pharmacotherapy 41 (12): 2008–13.
doi:10.1345/aph.1H643. PMID 17956961.
33. Jump up ^ Weinstein RS, Cole S, Knaster HB, Dahlbert T (February 1985). "Beta blocker overdose with
propranolol and with atenolol". Ann Emerg Med 14 (2): 161–3. doi:10.1016/S0196-0644(85)81081-7.
PMID 2857542.
34. Jump up ^ "Toxicity, Beta-blocker: Treatment & Medication - eMedicine Emergency Medicine".
Retrieved 2009-03-06.
35. Jump up ^ Beta-Adrenergic Blocker Poisoning;
http://www.courses.ahc.umn.edu/pharmacy/6124/handouts/Beta%20blockers.pdf
36. Jump up ^ USMLE WORLD 2009 Step1, Pharmacology, Q85
37. Jump up ^ Perez, Dianne M. (2006). The Adrenergic Receptors In the 21st Century. Humana Press.
p. 135. ISBN 1-58829-423-4. Retrieved 2010-09-08.
38. Jump up ^ Jameson, J. Larry; Loscalzo, Joseph (2010). Harrison's Nephrology and Acid-Base Disorders.
McGraw-Hill Companies. p. 215. ISBN 0-07-166339-8. Retrieved 2010-09-08.
39. Jump up ^ O'Donnell, John M.; Nácul, Flávio E. (2009). Surgical Intensive Care Medicine.Springer.
p. 47. ISBN 0-387-77892-6. Retrieved 2010-09-08.

37. 40. Jump up ^ Ahrens RC (1990). "Skeletal muscle tremor and the influence of adrenergic drugs". The
Journal of Asthma 27 (1): 11–20. doi:10.3109/02770909009073289. PMID 1968452.
41. Jump up ^ Reents, Stan (2000). Sport and exercise pharmacology.Human Kinetics. p. 19. ISBN 0-87322-
937-1. Retrieved 2010-09-10.
42. Jump up ^ Martini, Frederic H. (2005). Anatomy and Physiology.Pearson Education. p. 394. ISBN 0-
8053-5947-8. Retrieved 2010-09-10.
43. Jump up ^ Khan, M. I. Gabriel (2006). Encyclopedia of Heart Diseases. Elsevier. p. 160. ISBN 978-0-12-
406061-6. Retrieved 2010-09-10.
44. Jump up ^ Lamster, Ira B.; Northridge, Mary E., eds.(2008). Improving Oral Health for the Elderly: An
Interdisciplinary Approach.New York: Springer. p. 87. ISBN 978-0-387-74337-0. Retrieved 2010-10-23.
45. Jump up ^ Manger, William Muir; Gifford, Ray Wallace (2001). 100 Questions and Answers about
Hypertension. Blackwell Science. p. 106. ISBN 0-632-04481-0. Retrieved 2010-09-10.
46. Jump up ^ Rothfeld, Glenn S.; Romaine, Deborah S. (2005). The Encyclopedia of Men's Health.
Amaranth. p. 48. ISBN 0-8160-5177-1. Retrieved 2010-10-23.
47. Jump up ^ Hurst, J.W. (1997). Schlant, Robert C., ed. Hurst's the Heart 2. Blackwell Science. p. 1564.
ISBN 0-07-912951-X. Retrieved 2010-10-07.
48. Jump up ^ Reid, J.L. (2001). Lecture notes on clinical pharmacology 6.Blackwell Science. p. 76. ISBN 0-
632-05077-2. Retrieved 2011-03-11.
49. Jump up ^ Stoschitzky K, Sakotnik A, Lercher P, Zweiker R, Maier R, Liebmann P, Lindner W (1999).
"Influence of beta-blockers on melatonin release". Eur. J. Clin.Pharmacol. 55 (2): 111–5.
doi:10.1007/s002280050604. PMID 10335905.
50. Jump up ^ Shen, Howard (2008). Illustrated Pharmacology Memory Cards: PharMnemonics.
Minireview. p. 15. ISBN 1-59541-101-1.
51. Jump up ^ Greenway F, Liu Z, Yu Y, Gupta A (2011). "A clinical trial testing the safety and efficacy of a
standardized Eucommia ulmoides Oliver bark extract to treat hypertension" (PDF).Alternative medicine
review 16 (4): 338–47. PMID 22214253.
52. Jump up ^ Umehara S, Goyagi T, Nishikawa T, Tobe Y, Masaki Y (2010). "Esmolol and landiolol,
selective beta1-adrenoreceptor antagonists,provide neuroprotection against spinal cord ischemia and
reperfusion in rats". Anesthesia and Analgesia 21 (3): 1133–7. doi:10.1213/ANE.0b013e3181cdb06b.
PMID 20103544.
External links[edit]
 Musicians and beta-blockers by Gerald Klickstein, March 11, 2010 (A blog post that
considers "whether beta-blockers are safe, effective, and appropriate for performers to
use.")
 Better Playing Through Chemistry by Blair Tindall, New York Times, October 17, 2004.
(Discusses the use of beta blockers among professional musicians)
 Musicians using beta blockers by Blair Tindall. Condensed version of above article.
 In Defense of the Beta Blocker by Carl Elliott, The Atlantic, August 20, 2008. (Discusses
the use of propranolol by a North Korean pistol shooter in the 2008 Olympics)
 beta-Adrenergic Blockers at the US National Library of Medicine Medical Subject
Headings (MeSH)
[show]
 v
 t

38.  e
Beta blockers (C07)




o
 v
 t
 e
Index of the circulatory system
Description
 Anatomy
 Arteries
o head and neck
o arms
o chest
o abdomen
o legs
 Veins
o head and neck
o arms
o chest
o abdomen and pelvis
o legs

39.  Development
 Cells
 Physiology
o proteins
o
Disease
 Congenital
 Neoplasms and cancer
 Lymphatic vessels
 Injury
 Vasculitis
 Other
 Symptoms and signs
o eponymous
o
Treatment
 Procedures
 Drugs
o beta blockers
o channel blockers
o diuretics
o nonsympatholytic vasodilatory antihypertensives
o peripheral vasodilators
o renin–angiotensin system
o sympatholytic antihypertensives
o vasoprotectives
[show]
 v
 t

40.  e
Pharmacology: major drug groups

o
o




o
o






41. [show]
 v
 t
 e
Sympatholytic (and closely related) antihypertensives (C02)
Central
α2 agonist
 Clonidine
 Guanabenz
 Guanfacine
 Methyldopa#

Adrenergic release inhibitors
 Bethanidine
 Bretylium
 Debrisoquine
 Guanadrel
 Guanazodine
 Guanethidine
 Guanoclor
 Guanazodine
 Guanoxabenz
 Guanoxan

Imidazoline receptor agonist
 Moxonidine
 Rilmenidine


42. Ganglion-blocking/nicotinic antagonist
 Mecamylamine
 Pentolinium
 Trimethaphan
Peripher
al
Indirec
t
MAOI
 Pargyline‡

Adrenergic uptake inhibitor
 Bietaserpine
 Deserpidine
 Methoserpidi
ne
 Rescinnamin
e
 Reserpine

Tyrosine hydroxylase
inhibitor
 Metirosine
Direct
α1 blockers
 Prazosin
 Indoramin
 Trimazosin
 Doxazosin
 Urapidil


43. Non-selective α blocker
 Phentolamine
Serotonin antagonist
 Ketanserin
 Lidanserin

Endothelin antagonist (for PH)
 dual (Bosentan, Macitentan)
 selective (Ambrisentan, Sitaxentan)
 #
WHO-EM
 ‡
Withdrawn from market
 Clinical trials:
o †
Phase III
o §
Never to phase III
 v
 t
 e
Index of the circulatory system
Description
 Anatomy
 Arteries
o head and neck
o arms
o chest
o abdomen
o legs
 Veins

44. o head and neck
o arms
o chest
o abdomen and pelvis
o legs
 Development
 Cells
 Physiology
o proteins
o
Disease
 Congenital
 Neoplasms and cancer
 Lymphatic vessels
 Injury
 Vasculitis
 Other
 Symptoms and signs
o eponymous
o
Treatment
 Procedures
 Drugs
o beta blockers
o channel blockers
o diuretics
o nonsympatholytic vasodilatory antihypertensives
o peripheral vasodilators
o renin–angiotensin system
o sympatholytic antihypertensives
o vasoprotectives

45. [show]
 v
 t
 e
Drugs used for glaucoma preparations and miosis (S01E)

muscarinic
 Aceclidine
 Pilocarpine

muscarinic/nicotinic
 Acetylcholine
 Carbachol

Acetylcholinesterase inhibitors
 Demecarium
 Ecothiopate
 Stigmine (Fluostigmine
 Neostigmine
 Physostigmine)
 Paraoxon



46. 

 v
 t
 e
Index of the eye
Description
 Anatomy
o orbit
o neural pathways
 Physiology
o Phenomena
 appearance
 visual
 optical illusions
o proteins
 Development

Disease
 Congenital
 Corneal dystrophy
 Neoplasms and cancer
 Other
 Symptoms and signs

Treatment
 Procedures
 Drugs

47. o infection
o glaucoma and miosis
o mydriatics
o vascular
[show]
 v
 t
 e
Adrenergics
[show]
Receptor ligands
α1
Agonists
6-FNE
Amidephrine
Anisodamine
Anisodine
Buspirone
Cirazoline
Corbadrine
Dipivefrine
Dopamine
Ephedrine
Epinephrine
Etilefrine
Ethylnorepinephrine
Indanidine
Metaraminol
Methoxamine

48. Methyldopa
Midodrine
Naphazoline
Norepinephrine
Octopamine
Oxymetazoline
Phenylephrine
Phenylpropanolamine
Pseudoephedrine
Synephrine
Tetrahydrozoline
Antagonists
Abanoquil
Adimolol
Ajmalicine
Alfuzosin
Amosulalol
Arotinolol
Atiprosin
Atypical antipsychotics (e.g., clozapine, olanzapine, quetiapine, risperidone)
Benoxathian
Buflomedil
Bunazosin
Carvedilol
Corynanthine
Dapiprazole
Domesticine
Doxazosin
Ergolines (e.g., ergotamine, dihydroergotamine, lisuride, terguride)
Etoperidone
Eugenodilol
Fenspiride
Hydroxyzine

49. Indoramin
Ketanserin
L-765,314
Labetalol
mCPP
Mepiprazole
Metazosin
Monatepil
Moxisylyte
Naftopidil
Nantenine
Nefazodone
Neldazosin
Niaprazine
Nicergoline
Niguldipine
Pardoprunox
Pelanserin
Phendioxan
Phenoxybenzamine
Phentolamine
Piperoxan
Prazosin
Quinazosin
Ritanserin
Silodosin
Spiperone
Talipexole
Tamsulosin
Terazosin
Tiodazosin
Tolazoline
Trazodone
Tetracyclic antidepressants (e.g., amoxapine, maprotiline, mianserin)

50. Tricyclic antidepressants (e.g., amitriptyline, clomipramine, doxepin,
imipramine, trimipramine)
Trimazosin
Typical antipsychotics (e.g., chlorpromazine, fluphenazine, loxapine,
thioridazine)
Urapidil
WB-4101
Zolertine
α2
Agonists
(R)-3-Nitrobiphenyline
4-NEMD
6-FNE
Amitraz
Apraclonidine
Brimonidine
Cannabivarin
Clonidine
Corbadrine
Detomidine
Dexmedetomidine
Dihydroergotamine
Dipivefrine
Dopamine
Ephedrine
Ergotamine
Epinephrine
Etilefrine
Ethylnorepinephrine
Guanabenz
Guanfacine
Guanoxabenz
Lofexidine
Medetomidine

51. Methamphetamine
Methyldopa
Mivazerol
Naphazoline
Norepinephrine
Oxymetazoline
Phenylpropanolamine
Piperoxan
Pseudoephedrine
Rilmenidine
Romifidine
Talipexole
Tetrahydrozoline
Tizanidine
Tolonidine
Urapidil
Xylazine
Xylometazoline
Antagonists
1-PP
Adimolol
Aptazapine
Atipamezole
Atypical antipsychotics (e.g., asenapine, clozapine, lurasidone, paliperidone,
quetiapine, risperidone, zotepine)
Azapirones (e.g., buspirone, tandospirone)
BRL-44408
Buflomedil
Cirazoline
Efaroxan
Esmirtazapine
Fenmetozole
Fluparoxan

52. Idazoxan
mCPP
Mianserin
Mirtazapine
NAN-190
Olanzapine
Pardoprunox
Phentolamine
Phenoxybenzamine
Piperoxan
Piribedil
Rauwolscine
Rotigotine
SB-269970
Setiptiline
Spiroxatrine
Sunepitron
Tolazoline
Typical antipsychotics (e.g., chlorpromazine, fluphenazine, loxapine,
thioridazine)
Yohimbine
β
Agonists
Amibegron
Arbutamine
Arformoterol
Arotinolol
BAAM
Bambuterol
Befunolol
Bitolterol
Broxaterol
Buphenine
Carbuterol

53. Cimaterol
Clenbuterol
Corbadrine
Denopamine
Dipivefrine
Dobutamine
Dopamine
Dopexamine
Ephedrine
Epinephrine
Etafedrine
Etilefrine
Ethylnorepinephrine
Fenoterol
Formoterol
Hexoprenaline
Higenamine
Indacaterol
Isoetarine
Isoprenaline
Isoxsuprine
Levosalbutamol
Mabuterol
Methoxyphenamine
Methyldopa
Mirabegron
Norepinephrine
Orciprenaline
Oxyfedrine
Phenylpropanolamine
Pirbuterol
Prenalterol
Ractopamine
Procaterol

54. Pseudoephedrine
Reproterol
Rimiterol
Ritodrine
Salbutamol
Salmeterol
Solabegron
Terbutaline
Tretoquinol
Tulobuterol
Vilanterol
Xamoterol
Zilpaterol
Zinterol
Antagonists
Acebutolol
Adaprolol
Adimolol
Afurolol
Alprenolol
Alprenoxime
Amosulalol
Ancarolol
Arnolol
Arotinolol
Atenolol
Befunolol
Betaxolol
Bevantolol
Bisoprolol
Bopindolol
Bornaprolol
Brefonalol

55. Bucindolol
Bucumolol
Bufetolol
Bufuralol
Bunitrolol
Bunolol
Bupranolol
Butaxamine
Butidrine
Butofilolol
Capsinolol
Carazolol
Carpindolol
Carteolol
Carvedilol
Celiprolol
Cetamolol
Cicloprolol
Cinamolol
Cloranolol
Cyanopindolol
Dalbraminol
Dexpropranolol
Diacetolol
Dichloroisoprenaline
Dihydroalprenolol
Dilevalol
Diprafenone
Draquinolol
Ecastolol
Epanolol
Ericolol
Ersentilide
Esatenolol

56. Esprolol
Eugenodilol
Exaprolol
Falintolol
Flestolol
Flusoxolol
Hydroxycarteolol
Hydroxytertatolol
ICI-118,551
Idropranolol
Indenolol
Indopanolol
Iodocyanopindolol
Iprocrolol
Isoxaprolol
Isamoltane
Labetalol
Landiolol
Levobetaxolol
Levobunolol
Levomoprolol
Medroxalol
Mepindolol
Metipranolol
Metoprolol
Moprolol
Nadolol
Nadoxolol
Nebivolol
Nifenalol
Nipradilol
Oxprenolol
Pacrinolol
Pafenolol

57. Pamatolol
Pargolol
Penbutolol
Pindolol
Practolol
Primidolol
Procinolol
Pronethalol
Propafenone
Propranolol
Ridazolol
Ronactolol
Soquinolol
Sotalol
Spirendolol
SR 59230A
Sulfinalol
Talinolol
Tazolol
Tertatolol
Tienoxolol
Tilisolol
Timolol
Tiprenolol
Tolamolol
Toliprolol
Xibenolol
Xipranolol
[show]
Reuptake inhibitors
NET Selective norepinephrine reuptake inhibitors

58. Amedalin
Atomoxetine (tomoxetine)
Ciclazindol
Daledalin
Edivoxetine
Esreboxetine
Lortalamine
Mazindol
Nisoxetine
Reboxetine
Talopram
Talsupram
Tandamine
Viloxazine
Norepinephrine-dopamine reuptake inhibitors
Amineptine
Bupropion
Fencamine
Fencamfamine
Hydroxybupropion
Lefetamine
Levophacetoperane
LR-5182
Manifaxine
Methylphenidate
Nomifensine
O-2172
Radafaxine
Serotonin-norepinephrine reuptake inhibitors
Bicifadine
Desvenlafaxine
Duloxetine

59. Eclanamine
Levomilnacipran
Milnacipran
N-Methyl-PPPA
PPPA
Sibutramine
Venlafaxine
Serotonin-norepinephrine-dopamine reuptake inhibitors
Brasofensine
Dasotraline
Desmethylsertraline
Diclofensine
DOV-102,677
DOV-21,947
DOV-216,303
HDMP-28
JNJ-7925476
JZ-IV-10
Liafensine
Naphyrone
NS-2359
Perafensine
PRC200
Tesofensine
Tricyclic antidepressants
Amitriptyline
Butriptyline
Cianopramine
Clomipramine
Desipramine
Dosulepin
Doxepin

60. Imipramine
Lofepramine
Melitracen
Nortriptyline
Protriptyline
Trimipramine
Tetracyclic antidepressants
Amoxapine
Maprotiline
Mianserin
Oxaprotiline
Setiptiline
Others
Antihistamines (e.g., brompheniramine, chlorphenamine, pheniramine,
tripelennamine)
Arylcyclohexylamines (e.g., ketamine, phencyclidine)
CP-39,332
Ethanol
EXP-561
Fezolamine
Ginkgo biloba
Indeloxazine
Loxapine
Nefazodone
Nefopam
Opioids (e.g., methadone, pethidine (meperidine), tapentadol,
tramadol)
Pridefine
Tedatioxetine
Teniloxazine
Tofenacin
Tropanes (e.g., cocaine)

61. Ziprasidone
VMATs
 Amiodarone
 Amphetamines (e.g., amphetamine, methamphetamine, MDMA)
 Bietaserpine
 Deserpidine
 Efavirenz
 GBR-12935
 Ibogaine
 Ketanserin
 Lobeline
 Reserpine
 Rose bengal
 Tetrabenazine
 Vanoxerine (GBR-12909)
[show]
Releasing agents
Morpholines
Fenbutrazate
Fenmetramide
Morazone
Morforex
Phendimetrazine
Phenmetrazine
Pseudophenmetrazine
Oxazolines
4-MAR
Aminorex

62. Clominorex
Cyclazodone
Fenozolone
Fluminorex
Pemoline
Thozalinone
Phenethylamines (also amphetamines, cathinones, etc)
2-OH-PEA
4-CAB
4-FA
4-FMA
4-MA
4-MMA
Alfetamine
Amfecloral
Amfepentorex
Amfepramone
Amphetamine
Dextroamphetamine
Levoamphetamine
Amphetaminil
β-Me-PEA
BDB
Benzphetamine
BOH
Buphedrone
Bupropion
Butylone
Cathine
Cathinone
Clobenzorex
Clortermine
Dimethylamphetamine

63. DMA
DMMA
EBDB
Ephedrine
Ethcathinone
Ethylone
Etilamfetamine
Famprofazone
Fenethylline
Fenproporex
Flephedrone
Fludorex
Furfenorex
Hordenine
4-Hydroxyamphetamine
5-APDI (IAP)
5-MAPDI (IMP)
Iofetamine (123I)
Lisdexamfetamine
Lophophine
MBDB
MDA
MDEA
MDMA
Metamfepramone
MDMPEA
MDOH
MDPEA
Mefenorex
Mephedrone
Mephentermine
Methamphetamine
Dextromethamphetamine
Levomethamphetamine
Methcathinone

64. Methedrone
Methylone
Morforex
Naphthylaminopropane
Ortetamine
pBA
pCA
Pentorex
Phenethylamine
Pholedrine
Phenpromethamine
Phentermine
Phenylpropanolamine
pIA
Prenylamine
Propylamphetamine
Pseudoephedrine
Selegiline (also D-Deprenyl)
Tiflorex
Tyramine
Xylopropamine
Zylofuramine
Piperazines
2C-B-BZP
BZP
MBZP
mCPP
MDBZP
MeOPP
pFPP
Others
2-ADN

65. 2-AI
2-AT
2-BP
4-BP
5-IAI
Clofenciclan
Cyclopentamine
Cypenamine
Cyprodenate
Feprosidnine
Gilutensin
Heptaminol
Hexacyclonate
Indanorex
Isometheptene
Methylhexanamine
Octodrine
Phthalimidopropiophenone
Propylhexedrine (Levopropylhexedrine)
Tuaminoheptane
[show]
Enzyme inhibitors
PAH
 3,4-Dihydroxystyrene

TH
 3-Iodotyrosine
 Aquayamycin
 Bulbocapnine
 Metirosine

66.  Oudenone

AAAD
 Benserazide
 Carbidopa
 DFMD
 Genistein
 Methyldopa

DBH
 Bupicomide
 Disulfiram
 Dopastin
 Fusaric acid
 Nepicastat
 Phenopicolinic acid
 Tropolone

PNMT
 CGS-19281A
 SKF-64139
 SKF-7698

MAO
Nonselective
Benmoxin
Caroxazone
Echinopsidine
Furazolidone
Hydralazine

67. Indantadol
Iproclozide
Iproniazid
Isocarboxazid
Isoniazid
Linezolid
Mebanazine
Metfendrazine
Nialamide
Octamoxin
Paraxazone
Phenelzine
Pheniprazine
Phenoxypropazine
Pivhydrazine
Procarbazine
Safrazine
Tranylcypromine
MAO-A selective
Amiflamine
Bazinaprine
Befloxatone
Brofaromine
Cimoxatone
Clorgiline
CX157 (Tyrima)
Eprobemide
Esuprone
Harmala alkaloids
Harmine
Harmaline
Tetrahydroharmine
Harman

68. Methylene blue
Metralindole
Minaprine
Moclobemide
Pirlindole
Sercloremine
Tetrindole
Toloxatone
MAO-B selective
Ladostigil
Lazabemide
Milacemide
Mofegiline
Pargyline
Rasagiline
Safinamide
Selegiline (also D-Deprenyl)
COMT
Entacapone
Nitecapone
Tolcapone
[show]
Others
Precursors
 L-Phenylalanine → L-Tyrosine → L-DOPA (Levodopa) →
Dopamine
 L-DOPS (Droxidopa)


69. Cofactors
 Ferrous Iron (Fe2+
)
 S-Adenosyl-L-Methionine
 Vitamin B3 (Niacin
 Nicotinamide → NADPH)
 Vitamin B6 (Pyridoxine
 Pyridoxamine
 Pyridoxal → Pyridoxal Phosphate)
 Vitamin B9 (Folic acid → Tetrahydrofolic acid)
 Vitamin C (Ascorbic acid)
 Zinc (Zn2+
)

Neurotoxins
 DSP-4
 Oxidopamine (6-OHDA)

Others
Activity enhancers
BPAP
PPAP
Release blockers
Bethanidine
Bretylium
Guanadrel
Guanazodine
Guanethidine
Guanoxan
<img src="//en.wikipedia.org/wiki/Special:CentralAutoLogin/start?type=1x1" alt="" title=""
width="1" height="1" style="border: none; position: absolute;" />
Retrieved from "https://en.wikipedia.org/w/index.php?title=Beta_blocker&oldid=672097058"

70. Categories:
 Beta blockers
 Scottish inventions
Connectionbetween AlphaSynuclein,essential tremor,andbetablockerinteraction
Tremor
Leonid L. Rubchinsky et al.
(2007), Scholarpedia, 2(10):1379. doi:10.4249/scholarpedia.1379
revision #135551 [link
to/cite this article]
Post-publication activity
Curator: Karen A. Sigvardt
Contributors:
0.50 -
Leonid L. Rubchinsky
0.38 -
Eugene M. Izhikevich
0.38 -
Alexey S. Kuznetsov
0.12 -
Andrey Dovzhenok
0.12 -
Leo Trottier
0.12 -
Benjamin Bronner
0.12 -
Vicki L. Wheelock MD
Tobias Denninger
Nick Orbeck
Marc-Oliver Gewaltig

71.  Prof. Leonid L. Rubchinsky, Indiana University Purdue
University, Indianapolis, IN, and Indiana University School
of Medicine, Indianapolis, IN, USA
 Dr. Alexey S. Kuznetsov, Indiana University Purdue
University, Indianapolis, IN
 Dr. Vicki L. Wheelock MD, University of California
Davis , Sacramento, California
 Dr. Karen A. Sigvardt, Department of Neurology and
Center for Neuroscience, University of California Davis &
VA Northern California HCS
Tremor is an involuntary, rhythmic oscillatory movement of at least one functional body
region.
Contents
[hide]
 1 Introduction
 2 Classifications of tremors
 3 Physiology of some tremors
3.1 Parkinsonian tremor
 3.1.1 Description
 3.1.2 Pathophysiology
 3.1.3 Origin
 3.1.4 Animal models
 3.1.5 Dynamics of tremor-supporting networks
 3.1.6 Treatment
 3.1.6.1 Pharmacological treatment
 3.1.6.2 Surgical treatment
3.2 Essential tremor
 3.2.1 Description
 3.2.2 Pathophysiology
 3.2.3 Origin
 3.2.4 Dynamics of tremor-supporting networks

72.  3.2.5 Treatment
 3.2.5.1 Pharmacological treatment
 3.2.5.2 Surgical treatment
3.3 Physiological tremor and enhanced physiological tremor
 3.3.1 Description
 3.3.2 Properties
 3.3.3 Dynamics of tremor-supporting networks
3.4 Orthostatic tremor
3.5 Other tremors
 4 Summary
 5 References
 6 External Links
Introduction
Tremor is found in every person, typically a barely visible tremor that occurs when the arms are
extended and that is also observed during activities that require great precision. Pathological
tremor occurs in a number of conditions, where it can appear as an isolated phenomenon, or
together with other signs and symptoms. There are several practical methods of tremor
diagnosis (for clinically oriented references, see Elble and Koller, 1990; Findley and Koller,
1995). While tremor amplitude and frequency are important features, they are insufficient for
tremor classification. Even though time-series analysis methods have been suggested to detect,
classify and diagnose tremors, none of the available methods is simple and efficient; therefore,
observation by a neurologist dominates clinical practice.
For patient-oriented information about treatment of tremor and related conditions, one may
look at the NIH web site http://www.ninds.nih.gov/disorders/disorder_index.htm and WE
MOVE web site http://www.wemove.org
Classifications of tremors
Clinical neurological features are traditionally used to differentiate between tremors.

73.  Resting tremor occurs when the affected body part is not
active and is supported against gravity.
 Action tremor occurs during voluntary muscle activation,
and includes numerous tremor types.
 Postural tremor occurs while the affected limbs are
voluntarily maintained against gravity, such as whenthe
patient extends the arms forward in front of the body.
 Kinetic tremor occurs in both goal-directed and non goal-
directed movements, as typically seen during the finger-to-
nose-to-finger test in a neurological exam.
 Intention tremor is characterized by an increase in
tremor amplitude as the target is approached.
 Task-specific tremors occur during isolated tasks such as
writing.
Clinical assessment of tremor should include description of the location of tremor, activation
condition (i.e. resting or action tremor), and tremor frequency. The presence of additional
abnormal neurological signs can be an important indicator of diagnoses such as Parkinson’s
disease or other neurological disorders associated with tremor.
Tremor may be classified in several other ways. Examples of tremor types in each category are
given in parentheses:
 Normal or pathological condition:
physiological tremor
pathological tremors (with essential tremor and
parkinsonian tremor being most common).
 Conditions under which tremor is most often activated:
rest tremor (parkinsonian tremor, Holmes’ tremor,
palatal tremor)
postural tremor (physiological tremor, enhanced
physiological tremor, essential tremor, orthostatic
tremor, dystonic tremor, neuropathic tremor,
psychogenic tremor)
kinetic/intention tremor (cerebellar tremor, task-
specific tremor, dystonic tremor, Holmes’ tremor)

74.  Tremor frequency:
low frequency, less than 4 Hz (cerebellar tremor,
Holmes’ tremor, palatal tremor, drug-induced tremor)
medium frequency, 4-7 Hz (parkinsoniantremor,
physiological tremor, essential tremor, task-specific
tremor, dystonic tremor, neuropathic tremor, palatal
tremor, drug-induced tremor, psychogenic tremor)
high frequency, above 7 Hz (orthostatic tremor, essential
tremor, physiological tremor)
Several basic tremor types and their properties are summarized in the table below.
Properties of several basic tremor types
Tremor type Frequency Activation condition
Resting Postural Kinetic
Parkinsonian 3-7 Hz X x x
Essential 4-12 Hz X x
Orthostatic 13-18 Hz X
Physiological 3-30 Hz X
Enhanced physiological 8-12 Hz X
Cerebellar 3-5 Hz x X
Dystonic 4-7 Hz X X
Holmes' <4.5 Hz X X
Neuropathic 4-7 Hz X
Palatal <7 Hz X
Psychogenic 4-7 Hz X
Task-specific 5-7 Hz X
X - characteristic condition; x - occurs in some
The differentiation between tremor categories above is somewhat blurred; however there have
been attempts to streamline tremor nomenclature for clinical and research purposes (Deuschl et
al., 1998). The amplitude of tremor does not help to distinguish tremor types, as the same
tremor type (and the same pathology) may have markedly different amplitude. Clinical tremor
rating scales include the Fahn-Tolosa-Marin scale (Fahnet al., 1988), which assigns 0 to 4
points for tremor amplitude under a variety of conditions and 0 – 4 points for severity in daily
activities, while the Unified Parkinson’s Disease Rating Scale (Langston et al., 1992) assigns 0 –

75. 4 points for amplitude and severity of resting and postural or kinetic tremor. Rating scale scores
are on average proportional to logarithm of the displacement amplitude (Elble et al., 2006).
Physiology of some tremors
Even though each type of tremor exhibits some type of involuntary oscillatory motion, the
features of the movement and of the neuronal activity in different tremor types can be quite
different. These differences represent the differences in the underlying physiological mechanism
and/or pathological condition. Several different mechanisms for the origin of tremor have been
suggested, though for many types of tremor, the relationship between the type of tremor and
these suggested mechanisms is not yet clearly established. Several types of tremor mechanisms
are possible (reviewed in Deuschl et al., 2001): mechanical mechanism (every limb or limb
segment has a certain resonance frequency, which depends on the load), sensory reflex
mechanisms, or central oscillator mechanisms, i.e. pool of oscillatory neurons localized in a
specific brain structure, or manifested as a network or loop of several different structures. Here
we will consider several types of tremor, some of which are commonand studied in a detail;
others are less studied, but have some interesting features.
Parkinsonian tremor
Description
Tremor associated with Parkinson disease (PD) is one of the most widely studied and the second
most common pathological tremor, with prevalence of 102-190 cases per 100,000 population in
Western countries. Age at disease onset is usually after 60 and incidence increases with
advancing age (Van Den Eden et al., 2003). Resting tremor is present in 80% of patients with
autopsy-proven PD (Gelb et al., 1999). Asymmetrical onset of tremor is commonly observed, and
tremor onset may be coincident with other parkinsonian symptoms of rigidity and slowness of
movement (bradykinesia). As PD progresses the severity of tremor may diminish.
Parkinsonian tremor is episodic tremor with the frequency typically in the range of 3-7 Hz.
Tremor is accentuated by performing mental tasks or contralateral voluntary movements
("reinforcement maneuvers") and during ambulation. In a subset of PD patients, resting tremor
may be inhibited by voluntary movement. Up to 20% of PD patients also exhibit postural or
kinetic tremor (Hughes et al., 1992).
PD is characterized by the severe degeneration of dopaminergic neurons in substantia nigra pars
compacta (SNc; Bernheimer et al., 1971; Pifl et al., 1991) and is associated with widespread

76. alpha-synuclein pathology (reviewed in Golbe, 2003), with the Lewy body as the pathological
hallmark (Bethlem et al., 1960). The severity of tremor is poorly correlated with the degree of
dopaminergic degeneration, but even in cases where parkinsonian-like tremor is not
accompanied by other PD symptoms (monosymptomatic rest tremor) dopaminergic deficit is
usually present (Antonini et al., 1998). PD tremor is probably linked to the specific spatial
pattern of degeneration of SNc (Paulus & Jellinger, 1991; Jellinger, 1999; reviewed in Carr,
2002).
Figure 1:Simultaneous recordings oftremor-related activity in a muscle ofa tremulous limb and basal
ganglia (GPi) of a parkinsonian patient undergoing pallidotomy.GPi spikes and EMG are weakly
correlated.
Pathophysiology
Significant insights into tremor pathophysiology have been provided by analysis of the
oscillatory activity, recorded in different parts of the nervous system. Tremor-related activity in
the CNS is defined as activity in the same frequency range as and coherent with either
electromyograms from tremulous muscles or tremor movements [Note: the term “tremor-
related activity” is often used when two signals have oscillations within the range of tremor
frequencies, without an appropriate statistical analysis of correlation.] Electrophysiological
recordings in parkinsonian patients and primate models of parkinsonism have revealed tremor-
related activity in different parts of the basal ganglia, such as globus pallidus (primarily in the
internal segment, GPi, Hutchison et al., 1997) and subthalamicnucleus (STN, Levy et al., 2000),
motor thalamus (Lenz et al., 1994) and motor cortex (Timmermann et al., 2003). Tremor-
related activity has also been observed in the ipsilateral cerebellar cortex and contralateral
premotor and somatosensory cortical regions (Volkmann et al., 1996).
Synchronized oscillatory activity, as revealed by LFP recordings, may be important for the
function of basal ganglia and may be very widespread in PD (Hutchison et al., 2004; Boraud et

77. al., 2005). However it is not necessarily relevant to parkinsonian tremor (e.g. reviewed in Rivlin-
Etzion et al., 2006). Activity near or within the parkinsonian tremor-frequency range in LFP
may correspond to the presence of involuntary movements induced by dopamine-replacement
therapy – levodopa-induced dyskinesia (Silberstein et al., 2003; Alonso-Frech et al., 2006).
Tremor-related activity may not be reflected in LFP recordings in tremulous patients, as the LFP
is an averaged signal and, thus, depends upon the phase relationship between oscillatory units;
if phase relationships are highly variable, the oscillatory signals will be averaged out (Brown and
Williams, 2005).
Origin
Multiple lines of evidence support the central generation of parkinsonian tremor. Earlier studies
showed that the proprioceptive feedback slightly modifies the frequency of the tremor, but does
not affect its existence (Pollock & Davis, 1930; Hassler, 1970; Rack and Ross, 1986; Burne et al.,
1987). The origin of the central tremor oscillator(s) remains unknown, but several hypotheses
have been put forward (reviewed in Deuschl et al., 2000), including the rebound excitation
thalamic oscillator hypothesis (Llinas, 1984), thalamic filter hypothesis (Pare et al., 1990), the
basal ganglia pacemaker hypothesis (Plenz and Kitai, 1999; Wichmannand DeLong, 1999), and
the basal ganglia – thalamo – cortical loop hypothesis (Lenz et al., 1993). Thalamic hypotheses
are at odds with analysis of spike correlations in thalamic activity during parkinsoniantremor
(Zirh et al., 1998). The loop hypothesis appears to be attractive, not only because anatomical and
electrophysiological data point to the existence of the loop, but also because surgical lesions in
different locations in the loop suppress tremor partially or completely. Cellular properties of
basal ganglia and thalamic cells can support pacemaking (Surmeier et al., 2005; Llinas, 1998)
and thus can contribute to the genesis of PD tremor. Recently, computational evidence has been
obtained that further supports the basal ganglia – thalamo - cortical loop hypothesis and
provides a possible explanation for the loop mechanism of tremor oscillations (Dovzhenok and
Rubchinsky, 2012). A cerebellar origin of parkinsonian tremor has largely been ruled out based
by several lines of evidence (reviewed in Deuschl et al., 2000).
Animal models
Animal models of parkinsonian tremor are available (Burnes et al., 1983; DeLong, 1990;
Bergman et al., 1998). In vervet monkeys, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
(MPTP) induces medium-frequency rest tremor, which resembles human parkinsonian tremor.
In the other monkey species studied, MPTP treatment leads to either no tremor or high-

78. frequency tremor different from PD tremor (Wilms et al., 1999). This is probably due to the
differences in the area of the representation of the distal musculature (where tremor is most
prominent) in the basal ganglia thalamocortical neuronal networks. Nevertheless, the MPTP
primate model of PD is a source of valuable data on parkinsonian tremor.
Dynamics of tremor-supporting networks
Dual recordings in GPi tremor-related cells during stereotactic surgery have shown that
although cells may be correlated to restricted portions of the musculature or to each other,
uncorrelated oscillations within GPi are commonplace as well, even those in the close proximity
to each other (Hurtado et al., 1999). During tremor episodes, limb specific regions of GPi are
oscillatory overall, but the oscillation in the individual tremor-related units within that region is
more sporadic. The same is true for muscular tremor. Furthermore, the synchrony betweenan
oscillatory unit in a particular field and a particular trembling muscle within that field is
intermittent (Hurtado et al., 2004, 2005). Coherence of tremor between muscles differs for
different muscle pairs, with muscles from the same limb having larger coherence and muscles
from different limbs (especially different sides of the body) being largely uncorrelated (Hurtado
et al. 2000; Raethjen et al., 2000). The tremor in such muscles still may engage in short
episodes of statistically significant coherence, but the phase difference in each episode varies
(Hurtado et al., 2005). All of these findings are consistent with the view that there is a general,
though not precise, topographic organization of the individual structures that comprise the
tremor generating network, which exhibits spatiotemporal patterns of intermittent
synchronization (Hurtado et al., 2006).
Besides oscillations and synchronous activity in the tremor frequency range, cells in STN are
also oscillatory and coherent in the higher 15-30 Hz range with a very small phase lag. This
synchronization is observed in tremulous patients, even when tremor is temporarily absent in
limbs, but it is not observed in non-tremulous PD patients (Levy et al., 2000, 2002). 1:2 phase
synchronization in cortex has also been observed in parkinsonian tremor (Tass et al., 1998).
Treatment
Pharmacological treatment
The recognition of the dopaminergic deficit in PD led to the development of highly successful
pharmacologic treatments, first with the dopamine precursor levodopa (L-
dihydroxyphenylalanine), and then with a wide array of dopamine agonists, monoamine oxidase

79. inhibitors and COMT (catechol-O-methyltransferase) inhibitors (Goetz, 2005). Monoamine
oxidase and COMT inhibitors slow the break down of dopamine in the brain and, thus, can
decrease the dose of levodopa needed as well as stabilize fluctuations in motor symptoms. Older
agents such as amantadine and anticholinergics are considered second-line therapy. However,
anticholinergic drugs are sometimes useful for tremor that is refractory to dopaminergic therapy
(Nutt et al., 2005). Despite the possibility of significant improvement in motor behavior with
dopaminergic therapy, the patterns of oscillatory activity in the basal ganglia are not fully
reversed to the normal patterns of activity (Heimer et al., 2006).
Over time, dopaminergic therapy of PD becomes less effective as complications of on/off motor
fluctuations and uncontrolled involuntary movements (dyskinesia) develop (Lang and Lozano,
1998). Medication adjustment may help, but ultimately 10-20% of PD patients with moderate to
advanced disease are candidates for surgical treatment (reviewed in Tarsy et al., 2003; Walter
and Vitek, 2004).
Surgical treatment
Surgical treatment involves placement of surgical lesions, deep brain stimulation (DBS) and
experimental cell transplantation. There are three major targets for lesion placement: motor
thalamus, GPi and STN. Thalamotomy is used to treat tremor-dominant forms of PD (Hua et al.,
2003). Pallidotomy (usually lesions in posteroventral GPi) is less effective against tremor, but is
effective against other PD motor symptoms (Alkhani and Lozano, 2001; Baronet al., 2000).
Finally, subthalamotomy may ameliorate parkinsoniantremor, but is rarely used because of
potential side effects (Alvarez et al., 2005; Gill et al., 2003).
The target for anti-tremor thalamotomy (or thalamic DBS) is the nucleus ventralis intermedius
(Vim) of the thalamus, even though the nucleus ventro-oralis posterior (Vop) receives input
from the basal ganglia (e.g. see discussion in Jones, 2001). In fact, Vim is an effective target for
treatment of most other types of tremor, not only parkinsonian (Ohye et al., 1976; Deuschl and
Bergman, 2002; Gross et al., 2006). However, there remains some debate whether the benefit of
surgery arises from direct effects on the targeted nucleus or from effects on areas adjacent to the
surgical target. For example, DBS in the zona incerta in close proximity to STN may be more
effective than STN stimulation (probably affecting pallido-subthalamic pathways, Plaha et al.,
2006).
The most common neurosurgical procedure for PD is deep brain stimulator implantation
(Benabid, 2003). The same structures are targeted during electrode implantation as in ablative
surgeries: STN (Abosch et al., 2003), pallidum (Volkmann and Sturm, 2003) as well as Vim
thalamus (Speelmanet al., 2002). After implantation, DBS electrodes deliver current pulses

80. from a subcutaneously implanted generator. Because the tissue surrounding the electrode
remains relatively intact and parameters of stimulationcan be adjusted (and the electrode can
be removed surgically if necessary), DBS is favored over ablative procedures.
The frequency of effective anti-parkinsonian DBS usually lies within the 100-200 Hz range and
the values around 100 Hz are considered to be the threshold rate for the beneficiary effects of
stimulation with the optimal frequencies being around 130 Hz (Volkmann and Sturm, 2003;
Moro et al., 2002). During thalamic deep brain stimulation the amplitude of parkinsonian
tremor gradually decreases with the increase of the stimulation voltage; longer duration
stimulation pulses are also slightly more effective, but the frequency of stimulation does not
affect the amplitude of tremor (O’Suilleabhain et al., 2003). The mechanisms of DBS are still
being debated, whether blockade of action potentials or synaptic modulation, and the resultant
changes in the balance of excitation/inhibition within the network or regularization of a
pathological pattern of firing (Lozano et al., 2002; McIntyre et al., 2004). STN DBS reduces
oscillatory activity and enforces more regular tonic spiking, correlated with the stimulation
signal (Meissner et al., 2005; Garcia et al., 2005). Patients who have been treated long-term
with DBS still require dopamine-replacement therapy (reviewed in Perlmutter and Mink, 2006).
Recently, attempts of adaptive, “demand-controlled” DBS were introduced in theoretical studies
(Rosenblum and Pikovsky, 2004; Popovych et al., 2006). The idea is that adaptive DBS will
desynchronize the activity of stimulated neuronal population and thus will suppress tremor and
other symptoms. It remains to be shown experimentally that desynchronization is technically
achievable and can suppress tremor.
Finally, cell implantation (dopaminergic cells or stem cells form various sources) is being
explored for treatment of Parkinson’s disease, but in early trials tremor was the least improved
among motor symptoms. This line of treatment remains controversial and requires further
investigation (reviewed in Kuan and Barker, 2005).
Essential tremor
Description
Essential tremor (ET) is the most commonmovement disorder, with prevalence of 40-390 per
100,000 (Louis, 2005). Clinically, ET presents with action tremor (postural and kinetic) with
tremor frequency in the range of 4-12 Hz primarily affecting arms, but potentially also affecting
neck and head, trunk and legs. ET is a slowly progressive, presumably neurodegenerative,
disorder, which can sometimes become very disabling. ET is inherited as an autosomal
dominant disorder in 60% of cases. The age of onset is primarily after 50 years, but there are