Parkinson's Disease

Introduction - Also called: Paralysis agitans, Shaking palsy

Parkinson's disease (also known as Parkinson disease or PD) is a degenerative disorder of the
central nervous system that often impairs the sufferer's motor skills and speech.

History

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.

Discussion

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. PD is both chronic and progressive.

PD is the most common cause of parkinsonism a group of similar symptoms. PD is also called
"primary parkinsonism" or "idiopathic PD" (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 PD 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 PD. 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 PD 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).
PD 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.

PD 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 PD are:

Tremor. The tremor associated with PD 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 PD. 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 PD,
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 PD. 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 PD 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 PD 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 PD 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 PD, 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 PD.

§ Sleep problems. Sleep problems common in PD include difficulty staying asleep at night,
restless sleep, nightmares and emotional dreams, and drowsiness or sudden sleep onset during
the day. Patients with PD should never take over-the-counter sleep aids without consulting their
physicians.

§ Dementia or other cognitive problems. Some, but not all, people with PD 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 PD, 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 PD
also may contribute to this symptom.

§ Muscle cramps and dystonia. The rigidity and lack of normal movement associated with PD
often causes muscle cramps, especially in the legs and toes. Massage, stretching, and applying
heat may help with these cramps. PD also can be associated with dystonia — sustained muscle
contractions that cause forced or twisted positions. Dystonia in PD 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 PD develop aching muscles and joints because of the rigidity and
abnormal postures often associated with the disease. Certain exercises also may help. People
with PD also may develop pain due to compression of nerve roots or dystonia-related muscle
spasms. In rare cases, people with PD 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 PD 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. PD often causes erectile dysfunction because of its effects on nerve
signals from the brain or because of poor blood circulation. PD-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

What Causes 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
PD 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 PD, including fatigue and abnormalities of
blood pressure regulation.

Scientists have identified several genetic mutations associated with PD, and many more genes
have been tentatively linked to the disorder. Studying the genes responsible for inherited cases
of PD 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 PD 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 PD in genetically susceptible individuals.

Viruses are another possible environmental trigger for PD. 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 PD.
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 PD patients.

Other research suggests that the cell's protein disposal system may fail in people with PD,
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 PD 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 PD, the actual cause
of the dopamine cell death is still undetermined.

How is Parkinson's Disease diagnosed?

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 PD. Indeed, only 75% of
clinical diagnoses of PD are confirmed at autopsy. Early signs and symptoms of PD 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 PD usually appear normal.

The Unified Parkinson's Disease Rating Scale (UPDRS) 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.

PD is not by itself a fatal disease, but it does get worse with time. The average life expectancy of
a PD patient is generally the same as for people who do not have the disease. However, in the
late stages of the disease, PD may cause complications such as choking, pneumonia, and falls
that can lead to death. Fortunately, there are many treatment options available for people with
PD.

The progression of symptoms in PD 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.
Can medicines treat 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 PD

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 PD 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 PD. Selegiline, also called deprenyl, is an
MAO-B inhibitor that is commonly used to treat PD. 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 PD 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 PD 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 PD, 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.

Homeopathic Treatment

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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