Parkinson Anhang
http://www.zeit.de/2018/09/parkinson-syndrom-erkrankung-zunahme-therapie-neurologie#parkinson-box-1-tab
[Hpathy Ezine, May,
2014]
Information about parkinson’s disease, causes,
symptoms, homeopathy treatment, or homeopathy medicine for the cure of parkinson’s disease.
Also called: Paralysis agitans, Shaking palsy
Parkinson’s disease (a.k.a. Parkinson Disease) is a degenerative
disorder of the central nervous system that often impairs the sufferer’s motor
skills and speech.
History of Parkinson’s Disease
Symptoms of Parkinson’s disease have been known and treated since
ancient times. However, it was not formally recognized and its symptoms were
not documented until 1817, in “An Essay on the Shaking Palsy”. by the British
physician James Parkinson. Parkinson’s disease was then known as paralysis agitans, the term “Parkinson’s disease” being coined later
by Jean Martin Charcot.
The underlying biochemical changes in the brain were identified in the
1950’s, due largely to the work of Swedish scientist Arwid
Carlsson, who later wan a Nobel prize.
Parkinson’s disease affects nerve cells, or neurons, in a part of the
brain that controls muscle movement. In Parkinson’s, neurons that make a
chemical called dopamine die
or do not work properly. Dopamine normally sends signals that help
coordinate your movements. Parkinson’s is a disease that causes a progressive
loss of nerve cell function
in the part of the brain that controls muscle movement. Progressive
means that this disease’s effects get worse over time.
Symptoms of Parkinson’s Disease
Parkinson’s disease belongs to a group of conditions called movement
disorders. The primary symptoms are the results of decreased stimulation of the
motor cortex by the basal ganglia, normally caused by the insufficient
formation and action of dopamine ,which is produced in the dopaminergic
neurons of the brain. Secondary symptoms may include high level cognitive dysfunction
and subtle language problems. Parkinson’s Disease is both chronic and
progressive.
Parkinson’s Disease is the most common cause of parkinsonism a group of
similar symptoms. Parkinson’s Disease is also called “primary parkinsonism” or
“idiopathic Parkinson’s Disease” (having no known cause). While most forms of
parkinsonism are idiopathic, there are some cases where the symptoms may result
from toxicity, drugs, genetic mutation, head trauma, or other medical
disorders.
Early symptoms of Parkinson’s Disease are subtle and occur gradually.
Affected people may feel mild tremors or have difficulty getting out of a
chair. They may notice that they speak too softly or that their handwriting is
slow and looks cramped or small. They may lose track of a word or thought, or
they may feel tired, irritable, or depressed
for no apparent reason. This very early period may last a long time
before the more classic and obvious symptoms appear.
Friends or family members may be the first to notice changes in someone
with early Parkinson’s Disease. They may see that the person’s face lacks
expression and animation (known as “masked face”) or that the person does not
move an arm or leg normally. They also may notice that the person seems stiff,
unsteady, or unusually slow.
As the disease progresses, the shaking or tremor that affects the
majority of Parkinson’s patients may begin to interfere with daily activities.
Patients may not be able to hold utensils steady or they may find that the
shaking makes reading a newspaper difficult. Tremor is usually the symptom that
causes people to seek medical help.
People with Parkinson’s Disease often develop a so-called Parkinsonian gait that includes a tendency to lean forward,
small quick steps as if hurrying forward (called festination),
and reduced swinging of the arms. They also may have trouble initiating
movement (start hesitation), and they may stop suddenly as they walk
(freezing).
Parkinson’s Disease does not affect everyone the same way, and the rate
of progression differs among patients. Tremor is the major symptom for some
patients, while for others; tremor is nonexistent or very minor.
Parkinson’s Disease symptoms often begin on one side of the body.
However, as it progresses, the disease eventually affects both sides. Even
after the disease involves both sides of the body, the symptoms are often less
severe on one side than on the other.
The four primary symptoms of Parkinson’s Disease are:
The tremor associated with Parkinson’s Disease has a characteristic
appearance. Typically, the tremor takes the form of a rhythmic back-and-forth
motion at a rate of 4-6 beats per second. It may involve the thumb and
forefinger and appear as a “pill rolling” tremor. Tremor often begins in a
hand, although sometimes a foot or the jaw is affected first. It is most
obvious when the hand is at rest or when a person is under stress. For example,
the shaking may become more pronounced a few seconds after the hands are rested
on a table. Tremor usually disappears during sleep or improves with intentional
movement.
Rigidity, or a resistance to movement, affects most people with
Parkinson’s Disease. A major principle of body movement is that all muscles
have an opposing muscle. Movement is possible not just because one muscle
becomes more active, but because the opposing muscle relaxes. In Parkinson’s
Disease, rigidity comes about when, in response to signals from the brain, the
delicate balance of opposing muscles is disturbed. The muscles remain
constantly tensed and contracted so that the person aches or feels stiff or
weak. The rigidity becomes obvious when another person tries to move the
patient’s arm, which will move only in ratchet-like or short, jerky movements
known as “cogwheel” rigidity.
Bradykinesia, or the slowing down and loss of spontaneous
and automatic movement, is particularly frustrating because it may make simple
tasks somewhat difficult.
The person cannot rapidly perform routine movements. Activities once performed
quickly and easily -such as washing or dressing- may take several hours.
Postural instability, or impaired balance, causes patients to fall
easily. Affected people also may develop a stooped posture in which the head is
bowed and the shoulders
are drooped.
A number of other symptoms may accompany Parkinson’s Disease. Some are
minor; others are not. Many can be treated with medication or physical therapy.
No one can predict which symptoms will affect an individual patient, and
the intensity of the symptoms varies from person to person.
Depression. This is a common problem and may appear early in the course
of the disease, even before other symptoms are noticed. Fortunately, depression
usually can be successfully treated with antidepressant medications.
Hallucinations, delusions and paranoia may develop.
Emotional changes. Some people with Parkinson’s Disease become fearful
and insecure. Perhaps they fear they cannot cope with new situations. They may
not want to travel, go to parties, or socialize with friends. Some lose their
motivation and become dependent on family members. Others may become irritable
or uncharacteristically pessimistic.
Difficulty with swallowing and chewing. Muscles used in swallowing may
work less efficiently in later stages of the disease. In these cases, food and
saliva may collect in the mouth and back of the throat, which can result in
choking or drooling. These problems also may make it difficult to get adequate
nutrition. Speech-language therapists, occupational therapists, and dieticians
can often help with these problems.
Speech changes. About half of all Parkinson’s Disease patients have
problems with speech. They may speak too softly or in a monotone, hesitate
before speaking, slur or repeat their words, or speak too fast. A speech
therapist may be able to help patients reduce some of these problems.
Urinary problems or constipation. In some patients, bladder and bowel
problems can occur due to the improper functioning of the autonomic nervous
system, which is responsible for regulating smooth muscle activity. Some people
may become incontinent, while others have trouble urinating. In others,
constipation may occur because the intestinal tract operates more slowly.
Constipation can also be caused by inactivity, eating a poor diet, or drinking
too little fluid. The medications used to treat Parkinson’s Disease also can
contribute to constipation. It can be a persistent problem and, in rare cases,
can be serious enough to require hospitalization.
Skin problems. In Parkinson’s Disease, it is common for the skin on the
face to become very oily, particularly on the forehead and at the sides of the
nose. The scalp may become oily too, resulting in dandruff. In other cases, the
skin can become very dry. These problems are also the result of an improperly
functioning autonomic nervous system. Standard treatments for skin problems can
help. Excessive sweating, another common symptom, is usually controllable with
medications used for Parkinson’s Disease.
Sleep problems common in Parkinson’s Disease include difficulty staying
asleep at night, restless sleep, nightmares and emotional dreams, and
drowsiness or sudden sleep onset during the day. Patients with Parkinson’s
Disease should never take over-the-counter sleep aids without consulting their
physicians.
Dementia or other cognitive problems. Some, but not all, people with
Parkinson’s Disease may develop memory problems and slow thinking. In some of
these cases, cognitive problems become more severe, leading to a condition
called Parkinson’s dementia late in the course of the disease. This dementia
may affect memory, social judgment, language, reasoning, or other mental
skills.
Orthostatic hypotension. < Orthostatic hypotension is a sudden drop
in blood pressure when a person stands up from a lying-down position. This may
cause dizziness, lightheadedness, and, in extreme
cases, loss of balance or fainting. Studies have suggested that, in Parkinson’s
Disease, this problem results from a loss of nerve endings in
the sympathetic nervous system that controls heart rate, blood pressure,
and other automatic functions in the body. The medications used to treat
Parkinson’s Disease also
may contribute to this symptom.
Muscle cramps and dystonia. The rigidity and
lack of normal movement associated with Parkinson’s Disease often causes muscle
cramps (legs and toes). Massage, stretching, and applying heat may help with
these cramps. Parkinson’s Disease also can be associated with dystonia - sustained muscle contractions that cause forced
or twisted positions. Dystonia in Parkinson’s Disease
is often caused by fluctuations in the body’s level of dopamine. It can usually
be relieved or reduced by adjusting the person’s medications.
Pain. Many people with Parkinson’s Disease develop aching muscles and
joints because of the rigidity and abnormal postures often associated with the
disease.
Certain exercises also may help. People with Parkinson’s Disease also
may develop pain due to compression of nerve roots or dystonia-related
muscle spasms. In rare cases, people with Parkinson’s Disease may develop
unexplained burning, stabbing sensations. This type of pain, called “central
pain,” originates in the brain. Dopaminergic drugs,
opiates, antidepressants, and other types of drugs may all be used to treat
this type of pain.
Fatigue and loss of energy. The unusual demands of living with
Parkinson’s Disease often lead to problems with fatigue (late in the day). Fatigue
may be associated with depression or sleep disorders, but it also may result
from muscle stress or from overdoing activity when the person feels well.
Fatigue also may result fromakinesia - trouble
initiating or carrying out movement. Exercise, good sleep habits, staying
mentally active, and not forcing too many activities in a short time may help
to alleviate fatigue.
Sexual dysfunction. Parkinson’s Disease often causes erectile
dysfunction because of its effects on nerve signals from the brain or because
of poor blood circulation. Parkinson’s Disease-related depression or use of
antidepressant medication also may cause decreased sex drive and other
problems. These problems are often treatable.
Sensation disturbances
Impaired visual contrast sensitivity, spatial reasoning, colour
discrimination, convergence insufficiency (characterized by double vision) and occulomotor disturbances.
Dizziness and fainting; usually attributable to orthostatic hypotension,
a failure of the autonomous nervous system to adjust blood pressure in response
to changes in
body position
Impaired propriception (the awareness of
bodily position in three-dimensional space)
Reduction or loss of sense of smell (microsmia
or anosmia) - can occur years prior to diagnosis,
Pain: neuropathic, muscle, joints and tendons, attributable to tension, dystonia, rigidity, joint stiffness, and injuries
associated with attempts at accommodation
Cause of Parkinson’s Disease
The main causes could be graded under four headings:
Genetic
Toxins
Head injury
Drug induced
Parkinson’s disease occurs when nerve cells, or neurons, in an area of
the brain known as the substantia nigra
die or become impaired. Normally, these neurons produce an important brain
chemical known as dopamine. Dopamine is a chemical messenger responsible for
transmitting signals between the substantia nigra and the next “relay station” of the brain, the corpus
striatum, to produce smooth, purposeful movement. Loss of dopamine results in
abnormal nerve firing patterns within the brain that cause impaired movement.
Studies shown that most Parkinson’s patients have lost 60 to 80% or more of the
dopamine-producing cells in the substantia nigra by the time symptoms appear. Recent studies have
shown that people with Parkinson’s Disease also have loss of the nerve endings
that produce the neurotransmitter nor epinephrine. Nor epinephrine, which is
closely related to dopamine, is the main chemical messenger of the sympathetic
nervous system, the part of the nervous system that controls many automatic
functions of
the body, such as pulse and blood pressure. The loss of nor epinephrine
might help explain several of the non-motor features seen in Parkinson’s
Disease, including fatigue and abnormalities of blood pressure regulation.
Scientists have identified several genetic mutations associated with
Parkinson’s Disease, and many more genes have been tentatively linked to the
disorder.
Studying the genes responsible for inherited cases of Parkinson’s
Disease can help researchers understand both inherited and sporadic cases. The
same genes and proteins that are altered in inherited cases may also be altered
in sporadic cases by environmental toxins or other factors.
Although the importance of genetics in Parkinson’s Disease is
increasingly recognized, most researchers believe environmental exposures
increase a person’s risk of developing the disease. Even in familial cases,
exposure to toxins or other environmental factors may influence when symptoms
of the disease appear or how the disease progresses. There are a number of
toxins, such as 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine, or MPTP (found
in some kinds of synthetic heroin), that can cause Parkinson Ian symptoms in
humans. Other, still-unidentified environmental factors also may cause
Parkinson’s
Disease in genetically susceptible individuals.
Viruses are another possible environmental trigger for Parkinson’s
Disease. People who developed encephalopathy after a 1918 influenza epidemic
were later stricken with severe, progressive Parkinson’s-like symptoms. A group
of Taiwanese women developed similar symptoms after contracting herpes virus
infections. In these women, the symptoms, which later disappeared, were linked
to a temporary inflammation of the substantia nigra.
Several lines of research suggest that mitochondria may play a role in
the development of Parkinson’s Disease. Mitochondria are the energy-producing
components of the cell and are major sources of free radicals - molecules that
damage membranes, proteins, DNA, and other parts of the cell. This damage is
often referred to as oxidative stress. Oxidative stress-related changes,
including free radical damage to DNA, proteins, and fats, have been detected in
brains of Parkinson’s Disease patients.
Other research suggests that the cell’s protein disposal system may fail
in people with Parkinson’s Disease, causing proteins to build up to harmful
levels and trigger cell death. Additional studies have found evidence that
clumps of protein that develop inside brain cells of people with Parkinson’s
Disease may contribute to the death of neurons, and that inflammation or over
stimulation of cells (because of toxins or other factors) may play a role in
the disease. However, the precise role of the protein deposits remains unknown.
Some researchers even speculate that the protein build up is part of an
unsuccessful attempt to protect the cell. While mitochondrial dysfunction,
oxidative stress, inflammation, and many other cellular processes may
contribute to Parkinson’s Disease, the actual cause of the dopamine cell death
is still undetermined.
Parkinson’s Disease Diagnosis
A doctor may diagnose a person with Parkinson’s disease based on the
patient’s symptoms, neurological examinations and medical history. No blood tests
or x-rays can show whether a person has Parkinson’s disease. Some kinds of
x-rays can help the doctor make sure nothing else is causing symptoms. If
symptoms go away or get better when the person takes a medicine called levodopa, it’s fairly certain that he or she has
Parkinson’s disease.
The disease can be difficult to diagnose accurately. The Unified disease
rating scale is the primary clinical tool used to assist in diagnosis and
determine severity of Parkinson’s Disease. Indeed, only 75% of clinical
diagnoses of Parkinson’s Disease are confirmed at autopsy. Early signs and
symptoms of Parkinson’s Disease may sometimes be dismissed as the effects of
normal aging. The physician may need to observe the person for some time until
it is apparent that the symptoms are consistently present. Usually doctors look
for shuffling of feet and lack of swing in the arms. Doctors may sometimes
request brain scans or laboratory tests in order to rule out other diseases.
However, CT and MRI brain scans of people with Parkinson’s Disease usually
appear normal.
The Unified Parkinson’s Disease Rating Scale (UParkinson’s
DiseaseRS) is a rating scale used to follow the
longitudinal course of Parkinson’s disease. It is made up of the following
sections:
Mentation,
behavior, and mood;
Activities of daily living;
Motor;
Complications of therapy;
Hoehn and Yahr Stage of
Parkinson’s Disease
Stage 1. Symptoms on one side of the body only.
Stage 2. Symptoms on both sides of the body. No
impairment of balance.
Stage 3. Balance impairment. Mild to moderate
disease. Physically independent.
Stage 4. Severe disability, but still able to
walk or stand unassisted.
Stage 5. Wheelchair-bound or bedridden unless
assisted.
Prognosis of Parkinson’s disease.
Parkinson’s Disease is not by itself a fatal disease, but it does get
worse with time. The average life expectancy of a Parkinson’s Disease patient
is generally the same as for people who do not have the disease. However, in
the late stages of the disease, Parkinson’s Disease may cause complications
such as choking, pneumonia, and falls that can lead to death. Fortunately,
there are many treatment options available for people with Parkinson’s Disease.
The progression of symptoms in Parkinson’s Disease may take 20 years or more.
In some people, however, the disease progresses more quickly. There is no way
to predict what course the disease will take for an individual person.
Treatment of Parkinson’s Disease
Allopathic treatment:
There is no cure for Parkinson’s disease. But medicines can help control
the symptoms of the disease. Some of the medicines used to treat Parkinson’s
disease include carbidopa-levodopa (one brand name: Sinemet), bromocriptine (brand
name: Parlodel), selegiline
(one brand name: Eldepryl), pramipexole
(brand name: Mirapex), ropinirole
(brand name: Requip), and tolcapone
(brand name: Tasmar).
Medications to Treat the Motor Symptoms of Parkinson’s disease
Drugs that increase brain levels of dopamine
Levodopa Drugs that mimic dopamine (dopamine
agonists)
Apomorphine
Bromocriptine
Pramipexole
RopiniroleDrugs that inhibit dopamine breakdown
(MAO-B inhibitors)
Selegiline (deprenyl) Drugs that inhibit dopamine
breakdown (COMT inhibitors)
Entacapone
Tolcapone Drugs that decrease the action of acetylcholine
anticholinergics)<
Trihexyphenidyl
Benztropine
Ethopropazine Drugs with an unknown mechanism of
action for Parkinson’s Disease
Amantadine
Side effects of drugs used for Parkinson’s disease:
The most common drugs used in the treatment are:
L-dopa – It is the most widely used drug but
also causes many side effects because only 1-5% of L-dopa enters dopaminergic neurons rest is metabolized to dopamine
elsewhere.
Initially it causes complaints like:
Nausea
Vomiting
Reduced blood pressure
Restlessness
Drowsiness and sudden sleep
Later it can complicate the condition even
further and can cause:
Hallucinations
Psychosis
Younger patients of Parkinson’s suffer more from its side effects as:
Dyskinesis
Painful ‘off’ dystonias
Tremors intensified
Dyskinesias, or involuntary movements such as
twitching, twisting, and writhing, commonly develop in people who take large
doses of levodopa over an extended period. These
movements may be either mild or severe and either very rapid or very slow. The
dose of is often reduced in order to
lessen these drug-induced movements.
The Parkinson’s Disease symptoms often reappear even with lower doses of
medication. Doctors and patients must work together closely to find a tolerable
balance between the drug’s benefits and side effects.
The period of effectiveness after each dose may begin to shorten, called
the wearing-off effect. Another potential problem is referred to as the on-off
effect - sudden, unpredictable changes in movement, from normal to Parkinson
Ian movement and back again. These effects probably indicate that the patient’s
response to the drug is changing or that the disease is progressing.
Dopamine agonists:
Somnolence
Hallucinations
Insomnia
Oedema
Less motor fluctuations
Dyskinesis (twisting / turning) movements
In rare cases, they can cause compulsive behavior,
such as an uncontrollable desire to gamble, hyper sexuality, or compulsive
shopping. Bromocriptine can also cause fibrosis,
or a buildup of fibrous tissue, in the heart
valves or the chest cavity. Fibrosis usually goes away once the drugs are
stopped.
MAO-B inhibitors.
These drugs inhibit the enzyme monoamine oxidase
B, or MAO-B, which breaks down dopamine in the brain. MAO-B inhibitors cause
dopamine to accumulate in surviving nerve cells and reduce the symptoms of
Parkinson’s Disease. Selegiline, also called deprenyl, is an MAO-B inhibitor that is commonly used to
treat Parkinson’s Disease. Studies supported by the NINDS have shown that selegiline can delay the need for levodopa
therapy by up to a year or more. When selegiline is
given with levodopa, it appears to enhance and
prolong the response to levodopa and thus may reduce
wearing-off fluctuations. Selegiline is usually
well-tolerated, although side effects may include nausea, orthostatic
hypotension, stomatitis or insomnia. It should not be
taken with the antidepressant fluoxetine or the
sedative mepiridine, because combining seligiline with these drugs can be harmful.
COMT inhibitors.
COMT stands for catechol-O-methyltransferase,
another enzyme that helps to break down dopamine. Two COMT inhibitors are
approved to treat Parkinson’s Disease in the U.S.: entacapone
and tolcapone. These drugs prolong the effects of levodopa by preventing the breakdown of dopamine. COMT
inhibitors can decrease the duration of “off” periods, and they usually make it
possible to reduce the person’s dose of levodopa. The
most common side effect is diarrhea. The drugs may
also cause nausea, sleep disturbances, dizziness, urine discoloration, abdominal
pain, low blood pressure, or hallucinations. In a few rare cases, tolcapone has caused severe liver disease. Because of this,
patients taking tolcapone need regular monitoring of
their liver function.
Amantadine.
An antiviral drug, amantadine, can help reduce
symptoms of Parkinson’s Disease and levodopa-induced dyskinesia. It is often used alone in the early stages of
the disease.
It also may be used with an anticholinergic
drug or levodopa. After several months, amantadine’s effectiveness wears off in up to half of the
patients taking it.
Amantadine’s side effects may include insomnia,
mottled skin, edema, agitation, or hallucinations.
Researchers are not certain how amantadine works in
Parkinson’s Disease, but it may increase the effects of dopamine.
Anticholinergics.
These drugs, which include trihexyphenidyl, benztropine, and ethopropazine,
decrease the activity of the neurotransmitter acetylcholine and help to reduce
tremors and muscle rigidity. Only about half the patients who receive anticholinergics are helped by it, usually for a brief
period and with only a 30 percent improvement. Side effects may include dry
mouth, constipation, urinary retention, hallucinations, memory loss, blurred
vision, and confusion.
Homeopathy Treatment & Homeopathic Remedies for Parkinson’s Disease
Homeopathy treats the person as a whole. It means that homeopathic
treatment focuses on the patient as a person, as well as his pathological
condition. The homeopathic medicines are selected after a full individualizing
examination and case-analysis, which includes the medical history of the
patient, physical and mental constitution etc.
A miasmatic tendency (predisposition/susceptability) is also often taken into account for the
treatment of chronic conditions. The medicines given below indicate the
therapeutic affinity but this is not a complete and definite guide to the
treatment of this condition. The symptoms listed against each medicine may not
be directly related
to this disease because in homeopathy general symptoms and
constitutional indications are also taken into account for selecting a remedy.
To study any of the following remedies in more detail, please visit our Materia Medica section. None of
these medicines should be taken without professional advice.
Reportorial rubrics:
Murphy: Diseases: Paralysis-agitans.
Clarke: Paralysis agitans.
Boericke: Nervous system: Paralysis-Type - agitans
Levodopa + Carbidopa
+ Entacapon Quelle: Remedia.at
Eigen Erfahrung:
Mir wird kalt nach Einnahme 1 Globuli.
[ABC-homeopathy]
Clarke > Lolium, Delirium tremens.
Paralysis. Paralysis agitans. Tremor. Writer's cramp.
Clarke > Lathyrus
athetosis. Beri-beri. Impotence. Locomotor
ataxy. Lumbago. Paralysis, spinal (spinal sclerosis);
rheumatic. Paralysis agitans. Paraplegia. Rheuma.
Rheumatic Paralysis. Roaring (in horses). Urine, incontinence of.
Clarke > Zincum Picricum
Bright's disease; headaches of. Exhaustion. Facial
Paralysis. Headaches. Nymphomania. Paralysis agitans.
Priapism. Satyriasis. Seminal
emissions. Spinal weakness.
Hering > Mercurius
vivus
Clarke > Heloderma horridus
Of the bite of the reptile Belden says "This animal does not bite
frequently, but when it does it is understood that the result is a benumbing
Paralysis, like that of
Paralysis agitans or locomotor
ataxy.
T.F. Allen > Plumb-met. She
was anaemic, and in a condition analogous to that of a person suffering from
Paralysis agitans,
Boericke > Cocainum
hydrochloricum Chorea; Paralysis agitans;
alcoholic tremors and senile trembling
Enuresis . Goitre. Head, nodding of. Impotence. Jaundice. Mammae, affections of. Nightmare. Nose, swelling of.
Paralysis agitans. Pruritus
vulvae. Staggering.
Boericke > Aur-s.
Paralysis agitans; constant nodding of the head;
affections of mammae; swelling pain, cracked nipples
with lancinating pains.
Clarke > Luesinum Spasmodic twitching of
many muscles, esp. in face (Paralysis agitans), with
great melancholy and depression of spirits.
H.C. Allen > Syph. Spasmodic twitching of
many muscles, esp. in face (Paralysis agitans), with
great melancholy and depression of spiritsfont
As a remedy for meningitis and cerebrospinal meningitis, Paralysis agitans, chores, and hysteria, it has received some
attention
Kent Lectures > Merc-vivus Paralysis agitans. Trembling of the hands with great weakness.
Paralysis of the lower limbs, and twitching,
Materia medica
Agros?.
Weakness of limbs, trembling of extremities (hands). Paralytic agitans. Lacerating pain in joints. Cold and clammy sweat
on limbs. Oily perspiration.Tremors everywhere in
body. Weakness with trembling from least exertion. All symptoms <: at
night/warmth of bed (itching)/damp, cold, rainy weather/during perspiration;
Complaints increase during sweating and rest. All symptoms always associated
with weariness, prostration and trembling.
Slow in answering questions. Memory weakened and loss of will power.
Skin always moist and freely perspiring. Itching < warmth of bed.
Zinc-met.x
Violent trembling (twitching) of the whole body (after emotions).
Twitching in children. Chorea. Paralysis of hands and feet. Trembling of hands while
writing. Lameness, weakness, trembling and twitching of various muscles. Feet
in continued motion, cannot keep still. <: 17 – 19 h./touch/after dinner;
>: eating/discharges;
Rhus-tox.x
When the tremors start with pain > motion. Stiffness affected parts.
Numbness and formication, after overwork and
exposure. Paralysis; trembling after exertion. Limbs stiff and paralysed. All
joints hot and painful. Crawling and tingling sensation in the tips of fingers.
<: at night/sleeping/cold, wet rainy weather/after rain/during
rest/drenching/lying on back
or right side; >: warm, dry weather/motion/walking/change of
position/rubbing/stretching out limbs;
Gels.x
Centers its action on nervous system,
causing various degrees of motor paralysis…Dizziness, drowsiness, dullness and
trembling are the hallmark of this remedy. Trembling ranks the highest in this
remedy, weakness and paralysis (muscles of the head). Paralysis of various groups
of muscles like eyes, throat, chest, sphincters and extremities.
Head remedy for tremors. Mind sluggish and muscular system relaxed.
Staggering gait. Loss of power of muscular control. Cramps in muscles of
forearm. Excessive trembling and weakness of all limbs. <:
dampness/excitement/bad news; >: bending forwards/profuse
urination/continued motion/open air;
Arg-n.x
Complimentary to Gelsemium. Memory impaired;
easily excited and angered; flatulence and greenish diarrhea.
Incoordination, loss of control and imbalance with
trembling and general debility.
Paralysis with mental and abdominal symptoms. Rigidity of calves. Walks
and stands unsteadily. Numbness of body. Specially arms.
Agar.x.
Trembling, itching and jerking, stiffness of muscles; itching of skin
over the affected parts and extreme sensitiveness of the spine. Cannot bear
touch. Jerking and trembling are strong indications.
Chorea and twitching ceases during sleep. Paralysis of lower limbs with
spasmodic conditions of arms. Numbness of legs on crossing them. Paralytic pain
in left arm followed by palpitation.
Stiffness all over with pain over hips.
Cocculus.x
Head trembles while eating and when it is raised higher. Knees sink down
from weakness. Totters while walking with tendency to fall on one side.
Cracking of the knee when moving.
Lameness < bending. Trembling and pain in limbs. One-sided paralysis
worse after sleep. Intensely painful, paralytic drawing. Limbs straightened out
and painful when flexed.
It shows special affinity for light haired females especially during
pregnancy.
Lath-s.x
Tremors of the upper extremities with paralytic weakness of the lower
limbs. “As if limbs are hard and contracted”; limbs feel heavy. Feels as if
floor is irregular and is obliged to keep his eyes on the ground to guide his
feet. Affects the lateral and anterior columns of cord. Does not produce pain.
Reflexes always increased. Lateral sclerosis and Infantile paralysis. Finger
tips numb. Tremulous,
tottering gait. Excessive rigidity of legs with spastic gait. Knees
knock against each other while walking. Cannot extend or cross legs when
sitting. Stiff and lame ankles.
Marked fibrillary tremors and spasms of the
muscles, worse from motion or application of cold water. Palpitation and
fluttering of the heart felt throughout the body. Depresses the motor and
reflex activity of the cord and causes the loss of sensibility to pain, muscle
weakness and paralysis. Paralysis and tremors, chorea. Meningeal
irritation with rigidity of muscles. Pain in right popliteal
space. Burning and tingling in spine. Hands and feet numb with sudden jerking
of limbs on going to sleep. Crampy pain in limbs.
Ambra.x
Tremors with numbness, limbs go to sleep on the slightest movement,
coldness and stiffness of limbs. The finger nails become brittle and are
shrivelled. Cramps in hands and fingers. < grasping. Cramps in legs. Extreme
nervous hypersensitiveness. Dread of people and desire to be alone. Music
causes weeping. One sided complains.
Trembling along nerves in limbs. Tired feeling, very weak and nervous,
fainting, numb sensation. It causes locomotor ataxia.
The eyes become more prominent and corneal opacities visible. Very depressed
and “As if would fall on right side”. “As if walking on sponge”. “As if the
feet were swollen”. When walking, lifts feet higher than usual and puts down
heel hard. Stretching > pains in muscles and limbs.
Mag-p.x
Trembling; shaking of hands, involuntary. Paralysis agitans.
Cramps in calves, feet very tender. Twitching, Chorea, cramps. Numbness of
finger tips. Worse right side, cold, touch, night. >:
warmth, bending double,
pressure and friction;
Bufo.x
Special action on nervous system. Painful paralysis. Pain in loins,
numbness and cramps. Staggering gait. “As if a peg is driven into joints².
<: Warm room; >: bathing or cold air/putting feet in cold water.
Tarent-h.x
Remarkable nervous phenomena. Chorea, extreme restlessness and Paralysis
agitans. Must keep in constant motion and <
walking. Numbness of legs with twitching and jerkings.
Extraordinary contractions and movements.
Plb-met.x
Paralytic agitans. Paralysis of single
muscles. Cannot raise or lift anything. Extension is difficult. Paralysis from
over-exertion of extensor muscles in piano players. Wrist drop. Loss of
patellar reflex. Pain in right big toe at night. Hands and feet cold. Infantile
paralysis and neuritis.
Con.x
Heavy, weary and paralyzed limbs. Trembling and unsteady hands. Muscular
weakness (lower extremities). Perspiration of hands. Putting feet on chair relieves.
Ascending paralysis ending in death by failure of respiration. <
lying down/turning/rising in bed/cold/exertion; >: darkness/limbs hanging
down/motion/pressure;