1. 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

2. 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.
Symptoms of Parkinson’s disease have been known and treated since ancient times.
However, it was not formally recognized and its symptoms were not documenteduntil
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. Dopaminenormally sends signals that
help coordinate your movements. Parkinson’s is a disease that causes aprogressive 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.
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

3. 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.
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.

4. 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

5. 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
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

6. 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.
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
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
messengerresponsible 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

7. 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

8. 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.
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 oneSymptoms on one side of the body only. Stage two
Symptoms on both sides of the body. No impairment of balance.
Stage three

9. 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.
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
LevodopaDrugs 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
TolcaponeDrugs that decrease the action
of acetylcholine anticholinergics)<
Trihexyphenidyl
Benztropine
EthopropazineDrugs with an unknown
mechanism of action for Parkinson’s
Disease
Amantadine
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

10. 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
togamble, hyper sexuality, or compulsive shopping. Bromocriptine can also
causefibrosis, or a buildup of fibrous tissue, in the heart valves or the chest

11. 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 treats the person as a whole. It means that homeopathic treatment focuses

12. 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
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.,.
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
alwaysmoist 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

13. 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.

14. 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.
Sensationas 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

15. 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.