| Also called: Paralysis agitans, Shaking palsy
Parkinson's disease (also known as Parkinson disease
or Parkinson's 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 went on to win a Nobel prize.
Parkinson's disease is a disorder that 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:
Tremor. 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-. 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. - 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.- 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. 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, especially in the 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, especially 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 from akinesia – 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 oculomotor 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 have shown
that most Parkinson's patients have lost 60 to 80 percent 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 buildup 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. However, 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;
Hoehn and Yahr Staging of Parkinson's Disease
| Stage one
Symptoms on one side of the body only.
Stage two
Symptoms on both sides of the body. No impairment of
balance.
Stage three
Balance impairment. Mild to moderate disease.
Physically independent.
Stage four
Severe disability, but still able to walk or stand unassisted.
Stage five
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
Ropinirole
Drugs 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 levodopa is often reduced in order to
lessen these drug-induced movements. However, 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 United States:
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 rubric:
Murphy: Diseases: Paralysis-agitans.
Clarke: Paralysis agitans.
Boericke: Nervous system: Paralysis-Type - agitans
Homeopathic Remedies
Agar., Am Gr., Arg-n., Aur., Bufo.,Cocc.,
Con., Gels., Helo., Hyos.
,Lathyr., Mag-p., MERC., Nux-v., Phos.,
Plb., Puls., RHUS-T., Stam.,
Tarent., Thuj., ZINC.,.
Materia medica
Mercurius
Weakness of limbs, trembling of extremities, especially 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
are aggravated at night, warmth of bed, Damp, cold, rainy weather
and 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 worse
warmth of bed.
Zincum-Metallicum
Violent trembling (twitching) of the whole body especially
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. Worse touch, between 5-7 pm., after
dinner, better eating, discharges.
Rhus-tox
When the tremors start with pain which is relieved by motion.
There is stiffness of the parts affected. 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. Worse during sleep, cold,
wet rainy weather and after rain, night, during rest, drenching
and when lying on back or right side. Better warm, dry weather,
motion, walking, change of position, rubbing, stretching out limbs.
Gelsemium
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, especially of the 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. Worse by dampness, excitement,
bad news. Better by bending forwards, profuse urination, continued
motion and open air.
Argentum Nitricum
It is complimentary to Gelsemium. Memory impaired; easily excited
and angered; flatulence and greenish diarrhea.Inco-ordination, 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.
Agaricus Muscarius
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
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
worse by 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.
Lathyrus
Tremors of the upper extremities with paralytic weakness of the
lower limbs. Feels 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 siting.Stiff and lame ankles.
Physostigma
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 Grisea
Tremors with numbness, limbs go to sleep on the slightest
movement, coldness and stiffness of limbs. The finger nails
become brittle and are shriveled. Cramps in hands and fingers.
Worse grasping anything. Cramps in legs. Extreme nervous hypersensitiveness.
Dread of people and desire to be alone. Music causes weeping.
One sided complains call for it.
Heloderma
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 sensation as if would fall on right side. Sensation
as if walking on sponge. As if the feet were swollen. When
walking, lifts feet higher than usual and puts down heel hard. Stretching
relieves pains in muscles and limbs.
Mag-phos
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. Better warmth,
bending double, pressure and friction.
Bufo Rana
Special action on nervous system. Painful paralysis. Pain in loins,
numbness and cramps. Staggering gait. Feels as if a peg is driven
into joints. Worse—Warm room. Better bathing or cold air. Putting
feet in cold water.
Tarentula
Remarkable nervous phenomena. Chorea, extreme restlessness and
Paralysis agitans. Must keep in constant motion even though walking
aggravates. Numbness of legs with twitching and jerkings.Extraordinary
contractions and movements.
Plumbum Metalicum
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.
Conium
Heavy, weary and paralyzed limbs. Trembling
and unsteady hands. Muscular weakness especially of lower extremities.
Perspiration of hands. Putting feet on chair relieves. Ascending
paralysis ending in death by failure of respiration. Worse by
lying down, turning or rising in bed, cold, exertion. Better by
darkness, limbs hanging down, motion, pressure.
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