Parkinsonism is the name for a group of neurological disorders with common symptoms like tremor, rigidity, slowness of movement and postural instability.
It is also known as Parkinson’s syndrome, atypical Parkinson’s or secondary Parkinson’s disease. In the initial stages, the symptoms are usually very subtle. Constipation or soft voice may be the prime symptoms. These symptoms usually begin gradually and worsen with time.
Parkinson’s syndromes can be divided into three subtypes according to their origin. Hereditary Parkinsonism, acquired Parkinsonism and Parkinson’s disease.
(Idiopathic Parkinsonism, primary Parkinsonism, paralysis agitans, kamba vata or vira vata.) A large number of cases of Parkinsonism fall in this category. A familial and hereditary factor is present combined with some environmental factors. It was described in an essay on the shaking palsy in 1817 by a British physician, James Parkinson, who published a paper on what he called “the shaking palsy” or paralysis agitans. Jean-Martin Charcot in the 19th century coined the term “Parkinson’s disease”. The term “dementia paralytica” was used to mention similar conditions before 19 the century. Several organizations mark Parkinson’s disease on April 11, the birth anniversary of James Parkinson and a red tulip is used as the symbol of the disease.
Parkinson’s disease is the second most common neuro-degenerative disease after Alzheimer’s disease and affects approximately 1% of individuals older than 60 years. The prevalence in industrialized countries is estimated at 0·3% of the general population. The risk of prevalence is high in those exposed to pesticides, and is low in smokers. The incidence increases with age, with the average age of onset at approximately 60 years. Onset in persons younger than 40 years is due to hereditary causes. It is about 1.5 times more common in men than in women.
Parkinson’s disease is predominantly a disorder of certain nuclei of the basal ganglia situated at the base of the forebrain, and their neural connections. It is a slowly progressive disorder due to degeneration or infarct at the basal ganglia and deeper parts of the cerebral white mater including the ventro-lateral part of the thalamus.
Neurotransmitters like acetylcholine, dopamine and nor epinephrine are responsible for transmitting signals between the corpus striatum, the substantia, its connections in the cerebral cortex, and the thalamus to produce smooth and purposeful movements. The main characteristic features of Parkinson’s disease are insufficient formation and activity of dopamine, due to the death of neurons in certain nuclei of the basal ganglia, especially in the substantia nigra. The other features are microglial proliferation and the accumulation of an insoluble protein -alpha–synuclein, called “Lewy bodies” inside the surviving neurons. Decreased dopaminergic activity in the striatal nuclei and substantia nigra causes increased output through cholinergic and dopaminergic fibers of the caudate nucleus which results in tremor and rigidity (cerebral cortex, caudate nucleus, putman, and globus pallidus internal segment –thalamic pathway direct) in the early stage of Parkinson’s disease.
Further deterioration of dopaminergic fibers in the subatantia nigra, caudate nucleus, putman, sub thalamic nucleus and globus pallidus are responsible for bradykinesia in the later stages of Parkinson’s disease.
|1 Putman||7 Thalamus||13 Amygdaloid|
|2 Caudate nucleus||8 Corpus callosum||14 Hippocampus|
|3 Globus pallidus||9 Vestibular nucleus||15 Hypophysis|
|4 Substantia||10 Lateral geniculate body||16 Cerebral cortex|
|5 Sub thalamic nucleus of Luysi||11 Optic nerve||17 Pineal body (epiphysis)|
|6 Superior colliculus||12 Red nucleus|
The common predisposing factors are cerebral trauma, degenerative lesions and brain tumor (glioma) at the basal ganglia. Iodine deficiency can promote degeneration and deposition of cholesterol in the myelin sheath. Thus it also can result in hypercholesterolemia and fatty liver. Symptoms of Parkinson’s disease occur when 60% of dopamine containing nerve cells in the substantia nigra becomes impaired.
Fatigue, depression, soft voice, cramped or small handwriting, slow movement and infrequent tremor may occur a long time before the more classic and obvious symptoms appear.
SIGNS & SYMPTOMS
The initial motor symptoms typically start insidiously from the distal part of an upper limb and later include other limbs slowly over weeks or months. Initial symptoms in some patients are fatigue and muscular ache in limbs, especially in the latter half of the day. The four cardinal symptoms of Parkinson’s disease are trembling, rigidity, bradykinesia and postural instability.
Tremor is the major symptom for some patients, while for others tremor is very minor. The tremors are most pronounced at rest or when a person is excited or fatigued or under stress; better on voluntary movement and sleep. Tremors are localized in the initial stage. The first affected arm may not swing fully when walking, and the foot on the same side may scrape the floor first. The hand tremor takes the form of a regular back-and-forth motion at a rate of 2-4 cycles per second with a range from 5 mm to 20 mm. It may involve the thumb and forefinger and appear as a “pill rolling” movement. It also appear as rotating, drum tapping, bread crumbling, cigarette rolling, or movement of pronation and supination etc. Tremor may absent and rigidity is well marked, or vice vera. Some patients may exhibit a resting vocal cord tremor.
Normally muscles stretch when they move, and relax when they are at rest. Rigidity is due to increased tone and continuous contraction of muscles. The increased tone may be either continuous (lead pipe- on lower limb) or interrupted (cog wheeling-on neck). Rigidity can cause a general feeling of weakness, regional pain (muscle and joint pain) and cramping. Some patients feel neck stiffness, tension head ache, back ache, or tightness in the calf and shoulder region. Difficulty writing in straight lines occurs due to rigidity in the interosseous muscle. Speech becomes slow and monotonous due to rigidity of muscles of the lip, tongue and larynx. The facial muscles become very rigid in advanced conditions and give the appearance of an expressionless face, something akin to wearing a mask. Failure to express emotional feelings develops. The neck and head rigidity may give a statue like posture. Eyes move before the head when looking at objects on sides. Lips may be held apart allowing saliva to trickle through them. Rigidity and tremor can inhibit shaving, cooking and social visits.
Bradykinesia or slowness of movement is not equal for all movements. Activities once performed quickly and easily such as cooking, washing, sewing or dressing may take several hours. Slowness or difficulty in rising from a chair, turning in bed, or walking, and dragging of one leg also may develop. It is modified by the activity or emotional state of the subject. Some patients have less difficulty when some sort of external cue is provided.
Akinesia (slowness in initiation of voluntary movement) and sudden arrest of volitional movement while carrying purposeful acts can appear. Sudden frozen state in working, eating or during walking may occur. Some patients cannot walk, but can ride a bicycle. Patients may take smaller steps and gait cadence is reduced when walking is affected. Facial weakness is characterized by decreased blink rate and facial expression. Blinking is continuous as long as the tapping is continued on glabellar region. Weakness in right hand causes small and effortful handwriting. Speech may become soft and less distinct.
Some people develop a stooped posture in which the head is bowed and the shoulders are drooped when sitting and standing (Righting reflex-red nucleus). The flexed posture of the patient leads to kyphosis, and causes a reduction in lung capacity. Difficulty in stooping, turning over in bed, rolling over back to front, changing from horizontal to upright posture etc. develop. Elbow semi flexed, elbow pressed on sides, hand carried across the abdomen, fingers pressed together, thumb abducted, metacarpal phalangeal joint being flexed, inter phalangeal joint extended etc., are other features. Gait is slow and shuffling without swinging of arms (Globus pallidus lesion). Steps becomes short in walking. Dragging of feet along the floor, loss of foot grip, tendency to propulsive and retropulsive gait etc. are also seen.
Dystonia is a common initial symptom in young-adult Parkinson’s patients. This sustained, painful, twisting muscle contraction usually affects the foot and ankle. Dorsi flexion of great toe and plantar flexion of the foot occur. It also may affect muscles of upper limbs and cause painful adduction of the arm and elbow.
Non motor symptoms
Several non-motor symptoms are usually accompany Parkinson’s disease. The number of symptoms and their intensity vary with every individual. Mental symptoms are absent until the last stage. Special senses and cranial nerves are not affected. Reflexes are always normal. Rigidity and tremor may lead to depression. Profound asthenia, irritability and hyper sensitiveness to changes of atmosphere may occur.
Dementia is prevalent in 20% of Parkinson’s disease. It occurs after 8 years from the onset of motor features. Executive function, short-term memory and visuo-spacial ability may be impaired. Some people may become irritable, fearful, insecure or uncharacteristically pessimistic. Impulse for heavy eating, hyper sex, over use of medicines, pathological gambling etc. may develop. Sleep disturbances are common. Tendency for daytime sleepiness (excess of dopamine), restless sleep, nightmare, periodic limb movements during sleep etc. appear.
Autonomic dysfunctions are common in patients with Parkinson’s disease. Reflex vomiting, delay in gastric emptying, impaired absorption, constipation, urinary incontinence, urinary retention, erectile dysfunction and orthostatic hypotension can occur. Speech becomes soft and monotonous. Patients speak rapidly or hesitate before speaking. Dysphagia is common. It may lead to excess saliva in the mouth, and ultimately, drooling. Skin on the face may become very oily, particularly on the forehead and at the sides of the nose. Thinning and glossiness of skin of fingers is marked. Other symptoms are seborrhea, dandruff, sweatingand flattened nail.
Other non-motor symptoms include anosmia, dry eyes, watering eyes, decreased eye movement, numbness and emaciation etc.
The progression of symptoms in Parkinson’s disease may take 20 years or more. Most common complications are profound weakness; inter-current respiratory illness and fever. One finds a combination of forward stooped posture, imbalance, and short steps called festination, which mostly occurs in the later stage of the disease and causes frequent falls and fractures. As Parkinson’s disease is a slowly crippling chronic disease, we have to arrest or delay its progression at an early stage.
Parkinson’s disease is mainly diagnosed onclinical history and a neurological examination. Laboratory examinations and brain imaging are helpful in atypical cases. Laboratory tests can include blood tests, such as a complete blood count, biochemistry tests, estimation of ceruloplasmin (25-50mg/100ml); urine analysis, and ECG (Prolonged Q-T interval, high R wave voltage and ventricular tachycardia like pattern).
Neuron imaging like computed tomography (CT), magnetic resonance imaging (MRI), Positron emission tomography (PET) and single-photon emission CT (SPECT) etc. are used to rule out the secondary causes of Parkinsonism, such as basal ganglia tumor, cerebral infarction and hydrocephalus. Other tests include hair analysis for heavy metal poisoning (arsenic), olfactory testing and evaluations of response with levodopa like medications.
Early signs and symptoms of Parkinson’s disease may sometimes be confused with a number of disorders, and each of these disorders have specific features that help to distinguish them from Parkinson’s disease.
These are primary neurodegenerative disorders that have Parkinsonism symptoms with additional features. These include multiple system atrophy, corticobasal degeneration, progressive supranuclear palsy and dementia with diffuse Lewy body disease.Early cognitive dysfunctions, symmetry at onset, faster progression rate, early speech or postural instability with little or no tremor may indicate a Parkinson’s plus disease. These have a worse prognosis than those with Parkinson’s disease. Levodopa related medications are typically less effective at controlling symptoms.
Multiple system atrophy
This slowly progressive disorder affects both the central and autonomic nervous systems. Features of upper motor lesion, cerebellar ataxia, nocturnal stridor, and slurred speech etc. occur with tremor. Tremor is worse on rest. Symptoms of autonomic dysfunctions include hypotension, breathing and swallowing difficulties, impotence, constipation and urinary difficulties also appear.
It results from degeneration and atrophy of multiple areas of cerebral cortex and the basal ganglia. Combined features include cognitive impairments, loss of the ability to make familiar or purposeful movements, difficulty in speech or swallowing, rigidity in arm, impaired balance, poor coordination, tremor worse on rest, myoclonus, and dystonia etc.
Progressive supra nuclear palsy
This progressive disorder is caused by degeneration and atrophy of neurons in the brainstem. Early dementia, depression, apathy, balance complaints, and weakness of eye muscles with involuntary down-gaze are the main features.
Dementia with diffuse Lewy bodies
This degenerative disorder is due to deposit of abnormal protein in certain areas of the brain. Lewy bodies (an insoluble protein called alpha –synuclein) first appear in the olfactory bulb, medulla oblongata, pontine, tegmentum, substantia , area of mid brain, basal fore brain, and last in neo cortex. It also observed in autonomic nerves of the gut and heart (accumulation from below upwards). Dementia, hallucinations, delusions, depression etc are prominent with symptoms of Parkinsonism. Prognosis is good
Often with a history of severe head injury or frequent head trauma that resulted from boxing or other activities.
Sometimes known as pseudo Parkinsonism, Arteriosclerotic Parkinsonism or atherosclerotic Parkinsonism. Dementia is common. Rigidity or tremor is more marked in lower extremities. One sided Parkinsonism may resemble hemiplegia. Age of onset is late. Tremor is less than rigidity. Signs of Pyramidal lesion (increased tone, clasp-knife rigidity, exaggerated knee reflex, absence of abdominal reflex, extensor plantar reflex etc) are present. Hairs may be lost in affected side. Levodopa related medications are less effective at controlling symptoms.
Dementia, progressive mental impairment, symptoms like impaired bladder control with urinary frequency etc are seen with symptoms of Parkinsonism.
Tremor appears more on upper limb and head in aged individuals. It is fine, rapid and non rhythmic; and worse on voluntary movement. Tremors become constant and non progressive. Tone is normal. No weakness.
This non progressive disease begins in adolescence. It is an abortive form of Parkinsonism. Tremor involves both hands and head, but is absent in legs. Tremors are fine and rapid than Parkinson’s disease, worse on emotion, exertion and social functions, and temporarily relieved by drinking alcohol. Family history of tremor is present. Pill-rolling rest tremor, rigidity, akinesia and postural abnormalities etc. are absent.
Amyotrophic lateral sclerosis
It is a rapidly progressive neurodegenerative disorder that appears with combined symptoms of dementia and Parkinsonism. Fibrillatory tremors mostly appear in limb that previously affected with poliomyelitis. Adduction of thumb and sign of lower motor lesion are other features. Neuro fibrillary tangles and Lewy bodies are absent. This disease occurs more in cycad eaters and among the Chamorro populations of Guam and in the Mariana Islands.
Hepatolenticular degeneration (Wilson’s disease)
It occurs due to bilateral degeneration of lenticular nucleus and lobes (parietal and frontal) of cerebrum. It is a genetic disorder in which there is an abnormal metabolism of copper and amino acid. The excess of copper content may be due to either excessive absorption from gut, or less excretion through bile, or lack of copper binding globulin- ceruloplasmin. If it is not deposited in the liver or other organs, it deposits in the brain.
The onset of symptoms is before age 40 years. Males are more affected. History of liver cirrhosis may present. Common features are low ceruloplasmin in blood (ceruloplasmin normal value is 20-50mg/dl); presence of copper in urine (normal value is 100pg/24 hours), glycosuria, amino aciduria, and increased excretion of uric acid and phosphate due to renal lesion by copper deposition; presence of Kayser-Fleischer tinge on cornea, and sunflower cataract in some individual.
Tremor is rhythmical character, and most marked at distal part of limbs. Tremor is worse on excitement, on emotion, voluntary movement, and inversely related to rigidity. It is absent during sleep.
Face loses its expression. There is staring look due to less blinking. Speech is slow and monotonous with slurring of consonants and repetition of syllables. Hand writing may be cramped. Reflexes are normal. No sensory and sphincter changes. Pyramidal signs are absent.
Rapid course of dementia and aphasia are developed. Tremor is less pronounced, no jerky movement. Rigidity may appear. Accumulation of neuron fibrillary tangles and senile plaques in neocortex are the characteristics.
It begins in childhood and is due to glial scarring. It affects proximal group of muscles. Abnormal tone of muscle results in torticollis and tortipelvis or other deformities of pelvis. Spasmodic dorsi flexion of foot causes an abnormal posture. Difficulties in speech are common.
It is due to degeneration of oligo dentroglia of brain and spinal cord due to some allergic reaction. It starts before 35 years of age. Patient feels back pain, numbness, weakness and stiffness especially in leg. Ultimately whole body becomes rigid and tremor tends to spread from limb to limb and he becomes bed ridden. Patient becomes unable to speak or write, but intelligence remains clear. Some patient may feel euphoria. Evidence of upper motor lesion, intention tremor (lesion at red nucleus and cerebellum), nystagmus, diplopia and scanning speech are present. Bladder complaints may occur due to spinal lesion. Other symptoms are due to complications like bronchitis, urinary retention, and gradual failure of mental function. Recurrence and relapse are common.
It is a progressive demyelination disorder of white matter at cerebrum without involvement of spinal cord and brain stem. Blindness, bilateral deafness, bilateral ataxia or bilateral spastic paralysis may occur according to which parts of cerebrum have degenerated. It affects children and the aged.
Anxiety, Thyrotoxicosis, Intoxication (Action tremor)
Tremor is more rapid, low amplitude, irregular (tic, Wilson’s disease) and is worse on movement.
Tremor is better on rest, worse on voluntary movement and sleep.
The word chorea means dance; multiple lesion occur in striatum. Predisposing factors include fear, reflexes, cerebral infections, hyperthyroidism, S L E, carbon monoxide poisoning, rheumatic fever, anemia, low calcium, malnutrition etc).
Sydenham’s chorea (acute form)
It mostly occurs in childhood. Movements are brief, irregular, involuntary, uncoordinated, unpatterned, unpredictable, jerky and explosive. Movements are worse on movement and absent in sleep. Tone is normal. No pain and no wasting. Abnormal gesture on speaking, difficulty in chewing, clumsiness of limbs, hyper extensibility of fingers due to loss of tone. Weakness of abdominal muscles and awkward gait are seen. Wrist is flexed, fingers are hyper extended. Other signs include irritable behavior, emotional instability and poor performance at school.
It is a hereditary, slowly progressive degenerative disorder of cerebral cortex and basal ganglia (especially lesion at caudate nucleus). It begins in adults near age 40 years. Jerky movements begin in shoulder, trunk and lower limbs gives rise to a dancing look. Dementia, high type of irritability and bouts of depression are present. Abnormal gestures of face during speaking may occur. (Rauwolfia can control these movements). Death occurs within 15 years of onset.
Spasms are rapid, brief, sudden, irregular and purposeless. It affects single group of muscles and appears as eye blinking, shrugging of shoulder, or sudden gesture of limbs (Usual cause is stress).
Hemiballism (hemi chorea)
It is a non progressive condition. Movements are irregular, sudden, unilateral, and violent, as throwing movement. The lesion is at the subthalamic nucleus and connections at opposite side due to atherosclerosis or tumor in old age ( 50% of cases).
It is a condition of abnormal fat accumulation in the brain and spinal cord. It occurs more in certain races (Jews). Lecithin is absent. A cherry red spot appears in the retina. Hypochlorohydia, postero-lateral degeneration due to B12 &B1 deficiency and hypoglycemia are the other features. Symptoms of liver cirrhosis also develop due to lecithin deficiency.
Myelitis (Spinal cord lesion -viral origin)
Pain is increased above the level of spinal lesion. Pain is felt at that level, but pain is less below the level of lesion. Other features are flaccid paralysis like lower motor neuron lesion, loss of deep reflexes and lack of sphincter control.
(Lesions are at cerebral cortex, striatum and globus pallidus; pigments or lipids are deposited in myelin sheath. Basal ganglia may become marbled. Common causes include birth injury, lipiodosis, toxins, vascular lesion, or tumor etc). It starts in infancy due to birth trauma. Bilateral, slow, involuntary, irregular, spontaneous, jerky, coarse and worm like movements appear on distal segments of hands, neck and lips. Movements are absent during sleep. Other features include internal rotation of shoulder, flexion of hand, tetany, internal rotation of foot, plantar flexion and dorsi flexion of toe (dystonia).Tone is normal athetosis.
It is a familial cerebral disorder due to lipoidosis or inclusion body encephalitis. The proximal muscle of upper limbs is commonly affected. Unpredictive, irregular shock like movements are better on voluntary control. Speech difficulties may occur.
Kernicterus (lesion is at subthalamic nucleus)
It mostly occurs with haemolytic jaundice (Favism, Rh incompatibility). Movements are brief, irregular, involuntary and hemi chorea type.
Post encephalitis tremor
Lesion is at cortex, sub cortex, central part, substantia or red nucleus.
Convalescent encephalitis appears on 14th day of vaccination against mumps or small pox.The weak virus can activate the other specific viruses dormant in the body. Brain congestion may also be developed due to suppressed eruption, venous thrombosis, or peri-vascular demyelination.
Encephalitis A (naso-oral route) It affects all age groups. Fever, somnolence, diplopia, mid brain syndrome (anorexia and polyuria) are the common symptoms. Encephalitis B infections occur through mosquito bite. Domestic birds, chicken and pigeon are reservoir of infections. Non progressive tremor begins in mid-life with sudden onset. Tremors are less than rigidity. Movements of choriform (brief and explosive), athetoid (slow, coarse and worm-like) or tic (brief, irregular and localized) may appear. It may disappear suddenly. History of fever, narcolepsy, occulogyric crisis, alternation of pupils, changes in temperament. Increased sweating, oily skin and excessive salivation are more prominent than in idiopathic Parkinsonism. Mortality rate is about 20 %.
Causes include vascular lesion, localized tumor, inflammation of interstitial tissue. Spontaneous tremors appear on opposite side. Oversensitivity to touch, pain, heat and cold are seen.
Diseases with pronounced tremor have a better prognosis than diseases with rigidity. Mortality ratios are around twice those of unaffected people. Patients can live 15 years or more after the onset of initial symptoms. Disease affecting the lower limbs have a bad prognosis.
PARKINSONISM AND TREATMENT
Treatment includes medicinal aid and supportive therapy. Early homoeopathic treatment can increase the overall ability of the patient.
The aim of medicinal treatment is to purify neurons, inhibit nerve degeneration, promote formation of new nerve fibrils and control symptoms for as long as possible. The practice of giving one prescription for tremor, rigidity and balance disorder, and another for its side effects is not rational. This disease can be categorized into the early stage with hyperkinetic symptoms and the late stage with hypo kinetic symptoms.
Primary stage (hyperkinesia)
Favorable foods etc. include items with sweet, salt and sour; old ghee, olive oil, cheese, banana, pineapple, almond, and piper nigrim. Massage with camphorated oil, sweating, warmth, heat are beneficial in alleviating tremor (vira vata).
Secondary stage (akinesia)
Favorable foods include those which are pungent, bitter, and astringent; tea, coffea, alcohol, honey, tobacco, extra salt, meat, fish, milk, black gram, Bengal gram, amara beans, fava beans, large beans, heavy food, koval, young mangoes, green vegetables (Mg), fasting, overwork, rain water, cold, sunlight, wind, and high protein diet in night.
HOMOEOPATHIC TINCTURES AND DILUTIONS
Medications for Parkinsonism can be grouped into three categories. The first category of drugs includes medications that help control the mild motor and the non-motor symptoms of the disease.
The second category of drugs includes medications that help eliminate the miasmatic stigma of the patient.
The third category of drugs includes medications that promote the formation of neuron fibrils and neurotransmitters.
General classification of therapeutic items
Central nervous system stimulant
Ephedra, Nux vomica, Piper nigrim, Rauwolfia, Secale cor, Thea chinesis, Spirit of ammonia and cold water.
Cerebral stimulants: Ephedra and Piper nigrim
Midbrain stimulants: Camphor, Cocculus, Coffea arabica, Lobelia and C02
Central nervous system depressants
Acetic acid, High doses of alcohol, Baptisia, Belladonna, China, Colchicum, Gelsemium, Ipecac, Opium, Piper nigrim, Rauwolfia, Salix , Secale cor, Sulphur, Kali bromide, and Magnesium phos; Glucose, protein, and cold sponging.
Brahmi, Grindelia, Hydrocotyle, Ipecac, Phosphoric acid, Physostigma and Trigonella
Belladonna, Hyoscyamus, Stramonium, and Duboisia
Sympathomimetic: Lobelia, Coffea, Ephedra
Sympatholytic: Aristolochia, Asaram, China, Galega, Nux vomica, Rauwolfia, Secale cor, Veratrum album, Viscum album, Yohimbinum,
Peripheral stimulant: Baryta carb, Piper nigrim and Veratrum album
Peripheral relaxant: Calcarea phos
The physical and the mental characteristics of the patient should be taken into consideration when deciding the medicines.