Tag Archives: homoeopathic doctor in Borivali


Alzheimer’s Disease (AD) is a chronic progressive neuro-degenerative disorder affecting cognitive functioning and reducing life expectancy.

AD is one of the most common cause of dementia. It accounts almost 60-70% of all dementia cases. In most cases it co-exists with other conditions as a cause for dementia.

Its estimated that there are more than 40million cases of AD world wide. It is assumed to be one of the top 3 leading causes of death in developed countries, to take its place just after heart disease and cancer.


  • BASED ON AGE OF APPEARANCE – EARLY ONSET(before age of 65yrs, most of the cases are of FAD or Familial Alzheimer’s disease) or LATE ONSET(after 65yrs of age, most of them are sporadic cases)
  • BASED ON INHERITANCE – FAMILIAL(Familial Alzheimer’s Disease also called FAD is Autosomal-Dominant Inherent condition which in almost all cases is early onset type)or SPORADIC(not of autosomal dominant inherant type and is usually late onset type)


Alzhermer’s Disease is characterised by gradually progressing loss of cognitive functions, especially memory and other related cognitive skills like thinking and reasoning, leading to difficulty in day to day activity – like language deterioration, forgetting and misplacing thing making it difficult to independently manage house and finances, forgeting recent events, repeatedly asking same question even after getting answer, difficulty in learning and recollecting recently learnt thing, difficulty in articulating image, recognisation of objects things and beings (non-occular visuo-spatial) all this deteriorating patients skill of reasoning and executing judgement and take initiatives resulting in dependence, further triggering mood and personality disorders.

All these basic symptoms are present in general in patient which are slowly progressing and increasing in severity throughout the continuum of the disease advancement so based on symptoms and its severity AD can be divided into four stages.


Based on disease progression, symptoms and its severity Alzheimer’s Disease can be divided into 4 stages which are progressive worsening of symptoms in same continuum.

  • Pro-dromal phase
  • Early/Mild
  • Moderate
  • Severe

Pro-dromal Phase

Its the phase of Mild Cognitive Impairment (MCI) or pre-dementia, not all cases of MCI are of AD as it can be seen in ageing and other conditions as well, so at this stage one cannot confirm AD untill patient shows other definitive signs and symptoms of AD which may take upto 8yrs to develop.

This stage shows following symptoms, which are of very mild degree and needs through neurophysiological evaluation to get detected.

  • Occasional problems in recollecting recent events
  • Occasional difficulty in exactly recollecting recently lernt facts and information
  • Reduced Empathy noticed on some instances
  • Mild changes is sense of humour


As disease progresses further the severity of symptoms of cognitive disorders of memory, thinking, reasoning increases so as to easily becoming evident and establish diagnosis of AD and excluding other condition based on slow and gradually and progressively deteriorating cognition especially in front of memory.

  • Cannot recollect event of forgetfulness, names of family and friends.
  • Reduced fluency in speaking due to difficulty in recollecting words
  • Difficulty grasping, learning and recollecting new facts and information. Causing minor confusions in unfamiliar simple tasks or situations.
  • Unnoticeable problems in execution of complex activities of daily life, like orientation and organisation of cloths on self, and fine motor activity like drawing writting etc.
  • Irrational, inability in making decisions.
  • Melancholy and despondency


Disease progressess to an extent that it starts affecting bodily functioning and day to day life to an extent that patient starts losing self confidence and starts becoming dependent on others and is now evident not only to family and his physician but also to others.

  • Sometimes cannot even recollect name of close family members.
  • Loss of vocabulary resulting in Language deterioration
  • Reduced coordination in complex motor sequence, needs assistance in many cases in certain complex routine tasks like wearing dress. This may even cause frequent injuries and falls.
  • Visuo-spatial disturbances causing difficulty in articulating image, recognisation of objects things and being causing illusionary misidentification and also delusions is seen.
  • Irritability, resistance to caregivers, wandering, insecurity,frequent or constant crying.
  • Difficulty determining their location.
  • Difficulty differentiating relations and designations
  • Lack of ability of reasoning judging and concluding.
  • Sleep disorders


  • General apathy
  • Abusive, Cursing, paranoid, anxious
  • Repeats same conversation again and again.
  • Difficulty in speaking as can find word nor can frame sentence, speaks in few words or phrases
  • General exhaustion and debility with muscular atrophy making person immobile giving rise to other complications like bedsores and secondary infection.
  • Patients usually dies of secondary complications rather than disease itself


Causes of Alzheimer’s Disease are not exactly known. It is believed to have one or more major fundamental reasons behind its pathology and pathogenesis along with multiple other factors contributing to it, in is development. With each case varing and may have the other factor more dominant than that found in the other case. Most of the hypothesis revolve around production of beta amyloid and tau protien as fundamental cause of AD.

Smoking, stress, depression, head injuries, certain CNS infections and high blood pressure are believed to increase risk in susceptible persons. Susceptibility much depends on genetics.

There are certain genes that are found to be associated but only in 5% of all the cases, head injury, depression, hypertension, smoking are also believed to be causative or contributory factors for AD.


Type, mode of onset, symptoms, its severity and specificity is determined by which and how many genes are involved and at which point there is SNP or mutations. More than 30 genes are found with more than 60 locus of SNP which are associated with Alzheimer’s Disease few of them are listed below.

Familial (Autosomal-Inheritant Dominant) – Familial Alzheimer’s Disease.

  • Amyloid Precursor Protein
  • Presenilin 1 & 2
  • ABCA7
  • SORL1

Mutations in above mentioned genes causes increase in a protein called Aβ42, which forms major component of Senile Plaques in Alzheimer’s Disease.

Sporadic (Not of Autosomal-Inherant Dominant type)

  • APOEε4 allele – increases risk by 3 times in heterozygous and by 15 times in homozygous.
  • TREM2 allele have been found to increase risk of Alzheimer’s Disease by upto 3-5times as it reduces or ceases ability of leucocytes to control the amount of βAmyloid.
  • There are 19 Other genes found to be involved in Late Onset Alzheimer’s Disease (LOAD).


Alzheimer’s Disease is considered to be disease of Proteopathy where there is plaque deposits due ti misfolded Beta Amyloid proteins and Tau proteins in Central Nervous System which plays central role in disease pathology resulting in neurodegeneration.

There are many hypothesis trying to explain the cause and pathogenesis of Alzheimer’s Disease.


Oldest hypothesis which believes that reduced acetyle choline synthesis is the fundamental cause for Alzheimer’s Disease, based on which many drugs for AD are prepared and marketed without any significant results so its not been widely accepted.


Hypothesis states that extracellular deposits of β-amyloid is the fundamental cause behind pathogenesis of Alzheimer’s Disease.

There are many evidence to suggest that there is fundamental role of beta amyloid in development of AD.

As many genetic study shows association of amyloid related genes allele and isoforms to be major risk factors in development of AD.

Examples of allele and isoforms of genes that are associated with amyloid and are present in many patients of Alzheimer’s Disease.

  • Presence of Amyloid Precursor Protein gene that’s present on chromosome 21 has extra copy in people with trisomy making its expression pronounced and these people develop some features of Alzheimer’s Disease as early as 40yrs of age.
  • Apolipoprotein APOEε4 breaks down Amyloid but its isoforms are not that potent in breaking down of amyloid.
  • Allele of TREM2 reduces the activity of WBCof controling the amount of amyloid.

Also certain other factors that are related or associated to Beta Amyloid are found to be associated in development of Alzheimer’s Disease.

  • Beta Amyloid oligomers called Amyloid Derived Diffused Ligands (ADDL) attach to neuron surface and disrupt synaptic signals.
  • Presence of receptor of Amyloid oligomer, which is believed to be a misfolded three dimensional proteineceous infectious particle (prion protein).
  • N-AAP is fragment of AAP adjecent to its another fragment beta-amyloid. This N-AAP undergoes self destruction by binding to TNFRSF21 also called Death Receptor6 (DR6), due to ageing genome and brain the N-AAP and TNFRSF21 pathway gets disrupted and βamyliod plays complimentary role in it.

But to contradict above findings there is also the fact that the drugs that help reduce production of beta amyloid or reduce concerntration of beta amyloid have no significant impact on disease so again amyloid hypothesis is not completely accepted.


Tau proteins stabilises microtubules and are present in neurons of central nervous system and non-neuronal cells like astrocytes and oligodendrocytes.

As per tau hypothesis of pathogenesis of Alzheimer’s Disease, series of consequential pathological changes takes place post abnormalities in tau protein which starts with hyperphosphorilation of tau protein causes pairing with other threads giving rise to neurofibrillary tangles within the cell bodies evetually destroying microtubules resulting into destruction of cytoskeletal structure, causing disruption of neuronal transortation of biochemical mechanism and finally cell death.


Most of the other hypothesis revolve around production of beta amyloid and tau protien as fundamental cause of AD and are more of supportive or initiating or maintaining or risk factors that trigger fundamental pathological factor that is amyloid or tau related anomalies.

Blood Brain Barrier Hypothesis – Disturbance in integrity of blood brain barrier .

Spirochete Infection Hypothesis – Spirochete infection induced damages may further progress into AD especially by disrupting blood brain barrier

Disrupted Cellular Homeostasis of Biometals Hypothesis – It is doubted that certain ionic biometals in cells like ionic iron, copper and zinc either affect or are being affected or both by tau protein, Amyloid Precursor Protein, APOE.

Oligodendrocye Dysfunction Hypothesis – Ageing and other factors causes dysfunction of oligodendrocyes and their associated myelin, contributing to axon damage and resultant production of amyloid.

Retrogenesis Hypothesis of Barry Reisberg – This hypothesis states that certain errors in sequence of neucleotides in genome causes initiation of the reverse process of stages of neurogenesis. That is during embryogenesis the process begins with neurulation ending with myelination as final stage, just opposite to that in AD due to disturbed genetic code the reverse process is initiated that is – first demyelination, then axon death that is white matter and finally grey matter death.

Celiac Disease Association Hypothesis – Though earlier study failed to prove any relation of celiac disease with AD but more recent studies have found some link between AD and celiac disease which is under further investigation for any confirmations regarding any role.

Autoimmune Hypothesis – Autoimmune Conditions directly or indirectly affecting oligodendrocytes and myelin sheath and causing inflamatory process may trigger excessive production of amyloid production.




DMD – DUCHENNE MUSCULAR DYSTROPHY also called DUCHENNE SYNDROME is a X linked recessive genetic disorder; classified under progressive neuromuscular disorders; where in there is mutation of gene expressing the cytoplasmic protein “Dystrophin” causing muscle weakness and wasting.


Dystrophin expressing gene is one of the longest human genes known with 2.3 megabases present on short arm of chromosome X present at locus xp21,

Various proteins colocalises with dystrophin to form Dystrophin-Associated Protein Complex or Costamere. Costamere is an integral component in maintaining structural-functional integrity of striated muscle cells. As Costamere are responsible for linking of internal cytoskeletal system of each muscle fibers to extracellular matrix of collagen and laminin through cell membrane. So costamere connects sarcomere through sarcolemma to the extracellular matrix. So mutation in gene responsible for expressing cytoplasmic protein dystrophin causes structural-functional loss of muscle cell resulting into muscular dystrophy.

Dystrophin plays major role in function of binding of following molecules

  • Nitric Oxide Synthase
  • Dystroglycan
  • Vinculin
  • Myocin
  • Actin
  • Other proteins
  • Zinc and other metal ion
  • Other cytoskeletal and muscle constituents


  • Regulates Ryanodine-sensitive calcium-release channel activity, release of sequestered calcium ion into cytosol by sarcoplasmic reticulum, activity of voltage-gated calcium channel. It is required in activity of Sodium ion transmembrane activity.
  • Downregulates peptidyl-cysteine S-nitrosylation and peptidyl-serine phosphorylation, Cellular protein localization, cellular macromolecular complex assembly, peptide biosynthetic process.
  • Upregulates Neuron differentiation, neuron projection development, sodium ion transmembrane transporter activity.
  • Cardiomyocyte action potential, contractibility by regulating release of sequestered calcium ion thus playing major role in regulating the Heart Rate.
  • Myocyte cellular homeostasis. Myofibril development, sliding, response to stretching, Regulates skeletal muscle contraction by regulating release of sequestered calcium ion, required in cytoskeleton organization.
  • It regulates cellular response to Growth Factor stimulus. Thus it is also required in growth and development of muscle organ.


Duchenne’s Muscular Dystrophy one of the most common type of muscular dystrophy affecting 1 in every 5000 male at birth with life expectancy of affected individuals of around 25 years on an average. Many cases show increase in life expectancy of up to additional 10-15 years with proper care and management.


DMD presents itself with progressive muscle wasting, general weakness fatigue, debility, in later stages complete loss of power in muscles. This loss of power is attributed to muscular dystrophy rather than nerve involvement which is evident on EMG.

Initially there are not many noticeable symptoms but some parents may complaint of child having difficulty in milestone of turning over, or they may say not able to walk properly or “never saw him running or climbing stairs”.

Mental signs and symptoms may start presenting itself more evidently, well in advance, even before physical symptoms become evident. They may show cognitive difficulty, parents may complaint about child having difficulty in talking or getting words, short term verbal memory, many show symptoms of Dyslexia or ADHD and mental symptoms tend to improve after occupational and speech therapy during early childhood but again worsens in later stage of disease.

Physical signs and symptoms starts becoming frankly noticeable only after age of 2-3yrs as described below

General muscle wasting with muscle contractures due to fibrosis the muscles becomes short and they have hypertonicity with much of muscle fibre replaced with fibrous tissue or fat accumution all this gives rise to Pseudo-hypertrophy of muscles especially of calf, hips and shoulders, even tongue becomes thick and enlarged.

At first the muscles of calfs, extensor of knees other muscles of thigh and hip joint are involved then other pelvic muscles and shoulder gets involved so the disease progresses from below upwards

Skeletal deformities due to abnormal muscle tension distribution causing abnormal gait and resultant skeletal deformities like scoliosis, lumbar hyperlordosis

Difficulty walking -typically patient walks on forefeet or toes, running, jumping, hopping, climbing upstairs or down stairs.

Difficulty standing up from lying or sitting posture. Positive Gower’s Sign. If patient is sitting on ground he typically first puts his arms on floor and transfer upper body weight to ground through arms and the lifts pelvic region now with both arms and both knees touching ground and middle body lifted up, he then lifts one knee by putting foot on ground then he works his arms to lift other knee and then stand up by supporting thigh.

Due to muscle dystrophy and weakness patient has abnormal gait and they tend to fall to frequently so they frequently complaint about bodyaches which seems more to be due to trauma due to frequent falls rather than due to disease itself.

In later stages there is complete loss of ability to walk at around 12 yrs of age around and later on at around age of 20yrs there is complete inability to move body from below neck.

Patient’s respiratory muscles gets involved in later stage causing respiratory disorders where in they are required to be assisted with artificial ventilation. Food and fluids pass into respiratory passage. Patient may suffer from severe frequent Pneumonia.

Average life span of person is around 25 years and very few with extreme care have reported to reach out 45yrs of age.

Laboratory Investigations Shows

  • Cardiomyopathies (disorders of heart muscles) causing arrythmias (abnormal heart rhythm)
  • High blood Creatine-Kinase level.
  • Defects in Xp21 gene
  • Biopsy of muscles shows absence of dystrophin
  • High blood Creatine-Kinase level.
  • EMG shows changes of muscle dystrophy rather than nerve involvement


  • DNA testing
  • Muscle Biopsy
  • Prenatal Screening


As DMD is a deep seated genetic complaint that passes on generation to generation. So Homeopathic constitutional approach is required and more the disease becomes deep seated and more it passes on from generation to generation the more it starts manifesting it’s symptoms in mental sphere. So mental symptoms are to be carefully evaluated for Homeopathic individualisation at the same time one should not forget that even though the disease has manifested in mental sphere but it’s more pronounced on physical sphere where it shows typical ascending type of muscle wasting. Muscle dystrophy is due to defective production of dystrophin which primarily is functional disturbance and structural loss is secondary to it. So basically Psora has strongly established itself from generations to generations within the constitution of these patients.


  • Abrotanum – ascending muscle wasting – If one medicine for DMD patients is to be opted, which in most cases will act to certain degree, then my bet will be on abrotanum – personally I have got notable results with this medicine in cases of DMD if posology is well taken care of while administering, as in homeopathy it’s potency selection and repetition is the key to break the case!
  • Baryta Carb
  • Calcarea Carb
  • Calcarea Phos
  • Stannum Metallicum
  • Alfalfa
  • Agaricus Muscarious
  • Arsenicum Album
  • Zincum Metallicum
  • Phosphorus
  • Acidum Nitricum


Exercise -mild non-jarring like swimming helps maintain muscle strength without stressing or damaging it much

Physiotherapy helps to maintain muscle tone.

Supportive rehabilitation kits and orthopedic appliances like braces etc

Artificial respirator support in later stages when respiratory muscles starts weaknening

Pacemakers in patients with arrhythmia


Motor Neuron Disease though most commonly used to mention one specific disease ie Amyotropic Lateral Sclerosis(ALS), Motor Neuron Disease is actually a classification category that comprises all the diseases that are of motor-neurodegeneratory in nature. But Amyotropic Lateral Sclerosis being the most common form of Motor Neuron Disease, it has vaguely become synonymous to its parent classification category.

Diseases Classified Under Motor Neuron Diseases

Diseases are very vaguely placed into this category with inconclusive inclusion and exclusion criteria. Following are the basic disease types that fall under this category or one can say they form this category.

  • Amyotropic Lateral Sclerosis(ALS) or Lou Gehrig’s Disease
  • Progressive Bulbar Palsy(PBP)
  • Progressive Muscular Atrophy(PMA)
  • Primary Lateral Sclerosis(PLS)
  • Pseudobulbar Palsy
  • Monomelic Amyotrophy
  • Other Rare Forms

Motor Neuron Diseases are characterised by progressive muscle weakness and degeneration of motor neuron. But as explained earlier that classification is vague, so not all motor neuron degeneratory disorders fall under this category and rather they are placed into a broader category called “Motor Neuron Disease Disorders” example Spinal Muscular Atrophies falls into this broader category.

Motor Neuron Diseases can be further differentiated based on three creterias as follows

  1. Sporadic or Inherited
  2. Type of Neuron Involved
  3. Pattern of Muscle weakness.

1)Sporadic or Inherited

Except Familial Amyotropic Lateral Sclerosis rest all are Sporadi

2) Type of Neuron Involved

There can be Involvement of neuron in three different patterns

  1. Upper Motor Neuron Degeneration – Except Progressive Muscular Atrophy(PMA) all other types have UMN involvement
  2. Lower Motor Neuron Degeneration – Except Primary Lateral Sclerosis, Pseudobulbar Palsy and Monomelic Amyotrophy rest all have LMN involvement.
  3. Both Upper And Lower Motor Neurons Involved – Types under this category are ALS PBP(bulbar)

3)Pattern of Muscle Weakness.

Pattern of muscle weakness can be in combination of following three factors

  1. Symmetric or Asymmetric
  2. Proximal or Distal
  3. With or Without Sensory Loss.

Based on combination of above three criterion the pattern is categorised into three major pattern of combination.

  1. Asymmetric – Distal -Without Sensory Loss : ALS, PLS, PMA, MMA
  2. Symetric – Without Sensory Loss : PLS, PMA
  3. Symmetric Focal Midline – Proximal : ALS, PBP, PLS


MND can present itself in children or in adults. If the onset is during childhood then it’s usually inherited and in most of the cases it is Familial Amyotropic Lateral Sclerosis. In adults usually it’s found to affect after age of 40years.

Most of the cases of MND tend to progress during course of time and worsen and in many cases they are even fatal depending on type of MND, say for instance ALS is a fatal type where as PLS is not.

Motor Neuron Disease presents itself in various patterns of muscular weakness due to motor neuron degeneration which can show combination of patterns of symmetric or asymmetric, proximal or distal, focal midline or lateral, with or without sensory loss. Some of the signs and symptoms of Motor Neuron Disease are listed below.

  • Muscle Wasting, Twitching, Fasciculations.
  • Atropthy of tongue
  • Brisk reflexes
  • Babinski’s reflex
  • Hoffman’s reflex
  • Increased Muscle tone
  • Difficulty in breathing, aggravated while lying down or on exertion. It may also cause respiratory failure.
  • Dysphagia – Difficulty in swallowing
  • Sialorrhoea – Excessive salivation
  • Dysarthria – Difficulty in speaking
  • Cognitive and behavioral changes like decision making, computing, word fluency, memory etc.

Common Homeopathic Medicines for Motor Neuron Disease

Homeopathic Medicine should be selected as per type of Motor Neuron Disease and it’s symptomatology.

  • Plumbum Metallicum
  • Strycininum
  • Alumina
  • Anacardium Orientale
  • Baptisia Tinctoria
  • Kalium Phosphoricum
  • Ruta Graveolens
  • Syphillinum
  • Medhorrinum
  • Gelsemium Sempervirens
  • Thuja Occidentalis
  • Cactus Grandiflorus
  • Causticum


Multiple Sclerosis(MS) is disorder of central nervous system characterised by Demyelination, Inflamation and Sclerosis supposed to be either immune mediated or due to defective myelin production or combination of both.

Myelin sheath is produced by cells called oligodendrocytes. Myelin sheath is necessary to conduct electrical signals through neurons.

Genetics, Lifestyle and Environmental factors are believed to be contributing to the development of the disease and viral infection is believed to be the triggering factor.


Multiple Sclerosis in many patients starts as Clinically Isolated Syndrome (CIS), it is the term used for the very first episode of neurological symptoms in demyelinating diseases. It is currently considered as the best indicator of future probability of development of multiple sclerosis. In multiple it typically develops over days in which

  • 45% of cases presents with signs of motor and sensory deficits
  • 20% of cases presents with optic neuritis
  • 10% of cases presents with brain stem dysfunctions
  • 25% of cases shows more than one of the above

Types Of Multiple Sclerosis

Multiple Sclerosis International Federation Classifies MS into 4 types

  1. Clinically Isolated Syndrome (CIS)
  2. Relapsing Remitting Multiple Sclerosis(RRMS)
  3. Primary Progressive Multiple Sclerosis(PPMS)
  4. Secondary Progressive Multiple Sclerosis(SPMS)

MS may present itself in three basic pattern as mentioned below

  • RELAPSING – 85% of all the cases shows this pattern. In this the symptoms comes and goes away lasting for few days to months.
  • PROGRESSIVE – 10% of all the cases shows this pattern. In this form the symptoms develops and persists and keeps building up over time.
  • COMBINED – In this the symptoms appears stays there and keeps building even further on every subsequent attack. In many cases it starts as relapsing and later turns into progressive form

A patient may show symptoms of neurological deficits in any part or system depending upon the region of Central nervous system involved. The most commonly affected regions are white matter of optic nerve, brain stem, basal ganglia, spinal cord, white matter tract close to lateral ventricles causing following common symptoms.

  • Weakness
  • Fatigue
  • Mood disorders
  • Depression
  • Anxiety
  • Cognitive disorders
  • Hypoaesthesia
  • Paraesthesia
  • Spasms
  • Ataxia
  • Pain
  • Optic neutitis
  • Diplopia
  • Nystagmus
  • Dysarthria
  • Dysphagia
  • Incontinence of stools and/or urine
  • Retention of stools and/or urine

Though present in many other condition but still regarded as classical symptom of Multiple Sclerosis called “Lhermitte’s Phenomenon” is observed in many cases; where in; patient feels electric shock like pain running up and down the spine and through the spine towards the limbs.

Uhthoff’s Phenomenon is seen in patients with demyelinating diseases especially in Multiple Sclerosis, wherein the nerve impulse conduction is blocked whenever the body gets overheated due to hot climate or over exercise or fever etc. and symptoms subsides as soon as body temperature normalises.

Scales to Measure Severity and Quantifying Disability of MS

  • Multiple Sclerosis Composite – It is a scale developed by National Multiple Sclerosis Society to measure severity of MS basically used by reasearchers. It is based on testing timed movement of arm walking and cognitive ability.
  • Expanded Disability Status Scale (EDSS Scale) – Quntifies disability in eight different Functional System each having its own score based on clinical findings


Multiple Sclerosis typically shows lesions with inflamation and cholestrol crystal deposits resulting into destruction of neuronal myelin sheath.

MS is believed to be partly immune mediated disorder, if not fully. Still its exact causative factors are not known but is believed to be combination of genetic and environmental factors.

It is believed that inflamatory process is triggered due to T-cell that crosses Blood-Brain Barrier and enters brain due to increased permeability of capillaries as a result of infection or some other unknown factors. This infiltration and harbouring of T-cell into brain causes inflamatory process which not only directly damages myelin sheath but also damages oligodendrocytes which are responsible for production and regeneration of myelin sheath. Thus resulting into deficient myelin sheath. Also there is seen release of astrocytes due to dying oligodendrocytes and cholestrol crystal deposits which further triggers inflamatory process damaging even further. The inflamatory process finally leaves behind scars or so-called “Plaques of Multiple Sclerosis”.

Multiple usually damages myelin sheath of white matter. Myelin sheath is responsible for electrical signal conduction and White Matter is responsible for conduction of signals between two regions of Grey Matter. A deficient or damaged myelin sheath results into deficient signal conduction.

Its observed that MRI taken during acute episode of MS typically show more scars or so-called Sclerotic Plaques of Multiple Sclerosis compare to MRI taken later on. This indicates that to some extent brain has capablity to recover many of the damages after an acute episode of MS.


There is no definitive test available for confirmation of Multiple Sclerosis. Even risky and invasive technique like Biopsy is not definitive.

Usually non-invasive techniques like Intravenous Injected Gadolinium Contrast MRI are used in suspected cases. Gadolinium doesnot cross normal blood brain barrier, so if found in brain after Intravenous injection it suggests leaky blood brain barrier.


  • NAJA


Parkinson’s Disease is a chronic, slow progressive, degenerative disease of central nervous system affecting the motor neurons.

There is gradually increasing cell death in subsrantia nigra resulting in reduced dopamine secretion with accumulation of abnormal alpha-synuclien (lewy bodies) in remaining neurons due to which its classified under Synucleopathies.

It is characterised with parkinsonism, where in, patient has tremors, bradykinesia, rigidity and postural instability. Patients with parkinson’s disease also presents with neuropsychiatric disorder(mood, cognition, thought, behavioural). Parkinson’s Disease is also called Idiopathic Parkinsonism.


Causes of Parkinson’s Disease are not known but it is believed to be due to environmental and genetic factors and has familial predesposition towards the condition. Those who has history of head injury, psychological stress, frequently exposed to certain toxins, have increased risk of developing Parkinson’s Disease. It is found that those addicted to stimulants like tobacco smoking tea and coffee are less prone to this condition.

There are certain genes identified, mutations in which are believed to increase the risk of developing Parkinson’s Disease viz.

  • SNCA – responsible for production of normal Alpha-Synuclein, an essential protein.
  • PARK7 – Encodes Protein Deglycase DJ-1 also called parkinson disease protein 7, inhibits aggregation of alpha-synuclein and protects neurons from oxidative stress and cell death
  • LRRK2 – responsible for production of Dardarin(Lucine-Rich Repeat Kinase 2) an essential cytoplasmic protein.
  • GBA – responsible for production of Beta – Glucocerebrosidase an essential enzyme localised in lysosome which has essential intermediate role in metabolism glycolipid (abundantly present in cell membrane)
  • PRKN – responsible for production of Parkin a ligase responsible for labelling molecules covallently with ubiquitin (ubiquitination) for degradation in proteosome or lysosome.
  • PINK1 – responsible for production of PTEN Induced Kinase 1 is a mitochondrial serine which is involved in process of quality control check on mitochondria where in damaged mitochondria are identified and recruited for degradation this its believed to protect cells from stress induced mitochondrial damage.
  • VPS35 – Encodes Vacoular Protein Sorting-associated protein 35 is component of retromer complex responsible for retrograde transportation of proteins from endosomes to trans-Golgi network.
  • EIF4G1 – encodes Eukaryotic Translation Initiation Factor 4 Gamma 1 involved in process of mRNAcap recognition, ATP dependent unwinding 5′-terminal secondary structure and recruits mRNA to ribosome
  • DNAJC13 – encodes “DnaJ(Hsp40), homolog, subfamilyC, member13”, involved on endosome organisation.
  • CHCHD2 – Encodes protein called “Coiled coil Helix Coiled coil Helix Domain containing 2”, it acts as negative regulator of mitochondrial apoptosis


Although Parkinson’s Disease is classically recognised by 4 cardinal symptoms of parkinsonism viz tremor, bradykinesia, rigidity, postural instability which belong to sphere of motor neurons, Parkinson’s Disease also presents non motor symptoms of autonomic nerves and neuropsychiatric symptoms(cognitive, behavioural, mood, thoughts) of which neuropsychiatric cognitive deficits tends to appear in very early stage of disease even before classical cardinal motor symptoms are perceptible but its often not properly evaluated or linked to PD by physicians and diagnosis is delayed. Also sleep disorder starts appearing in patients years before motor or other neuropsychiatric symptom appear like somnolence, insomnia, REM sleep behavioural disorder(RBD) where in dreamy sleep patient starts acting and may inflict injury to self or others in bed.



  • Comes during rest and subsides on active voluntary motion and in deeper stages of sleep.
  • Usually tremors ranges 4-6Hz per second
  • Classically many patients presents with a common pill-rolling pattern of tremor, where in, thumb and index finger are set in circular motion as if making pill manually.


  • Slowness of movement throughout its course right from planning the course of movement to execution of movement.
  • Slughishness and difficulty in day to day routine activity
  • Impaired sequential and simultaneous movements.


  • Increased muscle tone causes rigidity in limbs.
  • Initially rigidity may be due to pain in joints and typically starts asymetrically from neck and shoulder and in later stages of disease whole body is involved.
  • Rigidity may be Uniform (Lead-Pipe Rigidity) or Retchety(Cogwheel rigidity)

Postural Instability

  • Appears in later stages of disease
  • Festination
  • Forward flexed posture
  • Freezing of gait as if feet were made of wood and were stucked to ground especially while turning or changing direction.
  • Toneless flat and sluggish voice
  • Mask-Like facial expressions or hang-dog appearance
  • Postural Instability also causes lack of balance and falls causing various injuries.



Cognitive Disorders causing dificulty in Executive Functions due to cognitive difficulty in.

  • Planning Action
  • Flexibility
  • Abstract thinking
  • Rule Acquisition
  • Inhibiting inappropriate action
  • Initiating appropriate action
  • Memory
  • Attention
  • Processing speed
  • Recall – needs cues
  • Perception and estimation of time
  • Visuospatial – face recognition and geometric Orientation

Behaviour, Thoughts and Mood

  • Depression
  • Apathy
  • Anxiety
  • Hallucinations
  • Illusion
  • Delusion
  • Dementia
  • Psychosis with delusion and associated delirium
  • Paranoid ideation


These symptoms in most appears years before the disease is classically diagnosed

  • Orthostatic Hypotension
  • Oily Skin
  • Copious perspiration
  • Incontinence of Urine
  • Sexual Dysfunctions
  • Fatal Gastric Dismolity
  • Fatal Constipation
  • Altered olfaction
  • Visual disturbances
  • Paraesthesia limbs


  • NAJA


Parkinsonism is a disorder characterised by tremors, twitching, trembling, bradykinesia, stiffness and rigidity causing gait and postural imbalances. It is present in many disease conditions especially in Parkinson’s Disease from which it derives its name.


  • Neurodegenerative Diseases Parkinson Plus Syndrome
  • Metabolic disorders
  • Vascular disorders
  • Drugs
  • Toxins
  • Trauma
  • Neoplasms
  • Immune Mediated
  • Infections



  • Parkinson’s Disease
  • Dementia with Lewy Bodies
  • Parkinson’s Disease Dementia
  • Rapid Onset Dystonia Parkinsonism
  • Autosomal Recessive Juvenile Parkinsonism
  • X-linked Dystonia Parkinsonism
  • Parkin Mutation (Hereditary Juvenile Dystonia)
  • Corticobasal Degeneration
  • Fronto-Temporal Dementia
  • Gertsmenn Straussler Scheinker Syndrome
  • Progressive Supra-neuclear Palsy
  • Olivopontocerebellar Atrophy
  • Multiple System Atrophy (Shy Drager Syndrome)
  • Lytico Bodig Disease (ALS complex of Guam)
  • Neuroacanthocytosis
  • Neuronal Ceroid Lipofusinosis
  • Pantothenate-Kinase Associated Neurodegeneration
  • Hutington’s Disease
  • Wilson’s Disease
  • Binswanger’s Disease
  • Hyopthyroidism
  • Vascular Dementia
  • Paraneoplastic Syndrome
  • Orthostatic Tremor
  • Chronic Traumatic Encephalopathy


  • Creutzfeldt Jakob Disease
  • Encephalitis Lethargica


While treating Parkinsonism its of utmost importance to first diagnose the underlying cause and treat the cause first.

Certain Homeopathic medicines that can be administered based on Symptomatic presentation and pathological background examples given are theraputic based, relate patients symptoms to that of medicine before selecting.

  • TERRENTULA HISPANICA – Well indicated in patients with neurodegenerative disorders. Orthostatic Tremors.
  • GELSEMIUM SEMPERVIRENS – due to psychosomatic reasons. Orthostatic tremors.
  • RUTA GRAVEOLENS – due to neoplasms in Central nervous system.
  • LYSINUM/HYDROPHOBINUM/LAC CANNUM – Typically suits in cases with dementia of Lytico-Bodig disease
  • BELLADONNA – Typically suits well in cases due to inflamatory or congestive or infective origin like that in Creutzfeldt-Jacob’s disease and Encephailitis Lethargica.
  • ARNICA MONTANA – Typically Suits well in cases due to Chronic Traumatic Encephalopathy.
  • BAPTISIA TINCTORIA – accompanying delirium typically of infective origin
  • NUX VOMICA – Typically suits well in cases due to bad effects of drugs and toxins.


CARPEL TUNNEL SYNDROME CTS is a condition where in the compression symptoms arise due to bundle compression of structures that pass within carpel tunnel affecting the the Median Nerve.


CARPEL TUNNEL is normal anatomical structure in our body found in every normal individual. It is formed by carpel bones forming a groove as its floor on dorsal side of hand and flexor retinaculum forming the flat roof of carpel tunnel on palmar side of hand.

It provides attachment and passage at the wrist level for the structures to pass through arm to hand. Muscles related to flexing movements of finger pass through this tunnel alomg with median nerve

Structures Passing Through Carpel Tunnel

  • Flexor Digitalis Superficialis – 4 tendons
  • Flexor Digitalis Profundus – 4 tendons
  • Flexor Pollicis Longus – 1 tendon
  • Median Nerve
  • Flexor Carpi Radialis not exactly pass within the carpel tunnel but it traverse through Flexor Retinaculum that is forming the roof of carpel tunnel.


Anything that exerts pressure to median nerve giving rise to nerve compression symptoms cause carpel tunnel syndrome. In most cases the cause remains obscure and are idiopathic. Any inflamatory process or water retention or metabolites deposition within tissue may cause increase in volume of structures and total content within the carpel tunnel and will cause in pressure of whole bundle which may cause Carpel tunnel due to increased bundle pressure, similarly the adjecent structures to carpel tunnel if inflamed or injured or any overgrowth of it, may exert pressure on carpel tunnel and median nerve within giving rise to carpel tunnel syndrome. Mechanical reasons like wear-tear and injuries are mostly regarded as major factors with ageing and certain genetic, structural and physiological anomalies are known to increase the risk of Carpel Tunnel Syndrome.

Age and Gender

  • Age – Ageing plays a major role in development of CTS its more commonly found in age above 40yrs
  • Gender –  Female sex is more prone to this condition compared to male.


  • OCCUPATIONAL – Work related frequent repetitive forceful pressures jerk and vibrations on hand on regular basis where in there is no sufficient time given to repair the wear and tear and the damage tend to accumulate over time.
  • POSTURAL HABBITS such that it exerts unusual strain on hand and wrist on regular basis.
  • INJURIES to wrist distal part of forearm and wrist. Fractures involving radius ulna carpel and metacarpel bones like Colle’s Fracture, Boxer’s Fracture etc.

Genetic and Systemic 

  • Prediabetics and Diabetics
  • Obesity
  • Metabolic Syndrome
  • Hypothyroidism
  • Arcomegaly
  • Amyloidosis
  • Rheumatoid Arthritis
  • Gout
  • Tumours
  • Hereditary Neuropathy with Susceptibility to Pressure Palsy – Carcot Marie Tooth Syndrome casused due to mutation in gene HS3TC2
  • Narrow Carpel Tunnel
  • Certain drugs like Corticosteriods or Oestrogen therapy.


  • Paraesthesia in Index finger, Middle finger, Thumb and the lateral half of  Ring finger
  • Myalgias or neuralgia in forearm upwards to arm, less commonly in wrist and hand
  • Loss of strength of grip and Loss of Manual Dexterity
  • Atrophy of muscles at the base of thumb visible on proximal, thumb-related quadrant of palm (ie proximal lateral quadrant/upper outer quadrant).




TRIGGER FINGER or TRIGGER THUMB is a condition where in joints of one or more of the digits(finger/thumb) gets stucked up/locked up at certain postion which is difficult to move and moving it with force may cause popping or clicking sound with pain.

Though it can present in any sex and at any age, it is more commonly found in females around age of 50-60 yrs.


Its is also termed as digital Stenosing Tenosynovitis, although there is no predominant inflamation to Tendosynovium but inflamation is found in Tendon Sheath. And also its not comfirmed that inflamatory process has any primary role in its development

Though exact cause behind trigger finger/thumb is not known but the risk factors that tend to increase the incidence of this condition are identified

  • Over straining and over use of hand and fingers espescially activities involving prolonged forceful flexion of digits(fingers/thumb) may be occupational or habbitual routine activities.
  • Frequent injuries – occupational, accidental or even injuries of planned surgery of hand especially ofter surgery for carpel tunnel syndrome
  • Systemic connective tissue disorders
  • Autoimmune diseases especially Rheumatoid Arthritis
  • Hypothyroidism
  • Renal Disease
  • DeQuervain’s Diseases
  • Amyloidosis
  • Diabetes Mellitus and Other Metabolic disorders.


  • Though it may involve any digit(thumb/finger) Index finger and Thumb are more frequently involved. One or more digits may be involved.
  • Patient presents with stucked up digit at certain position. It may be at any level from flexed  to extended position usually found at semiflexed position.
  • This locking up may be persistent for a prolonged period of time or may be momentary and recurrent.
  • Aggravations are more commonly experienced at night, especially while holding heavy article with hand or while gripping or applying pressure with fingers or hand.
  • On moving and or forcefully unlocking the stucked finger is bit painful and causes clicking and popping sound
  • In severe cases the finger may be persistently locked for prolonged period of time with constant pain which may also extent to whole hand and wrist.


Diagnosis of trigger finger/thumb is based on clinical symptomatology of the patient where in inflamation or involvement of tendon sheath of flexors is confirmed and excluding probability of other condition like

  • Tumour
  • Sprain of digit
  • Osteoarthritis of metacarpo-phalangeal joint
  • Fracture
  • Tendon Entrapment post-trauma
  • Extensor Apparatus Injury
  • Game Keeper’s Thumb
  • Sesamoid anomaly
  • Dupuytren’s Contracture
  • Focal Dystonia

An injection of lidnocaine in tendon sheath of flexors reduced the pain then it confirms diagnosis Trigger Finger/thumb.


Treatment of trigger finger/thumb is dependent on combination of modalities of physiotherapy, splinting and medication.




Reactive Arthritis was also called Reiter’s Arthritis is RF-negative and HLA-B27 Linked Imflamatory oligoarthritis typical with Enthesitis, accompanied with Inflamatory occular and/or inflamatory genitourinary and other systemic manifestation usually post gastrointestinal or genitourinary infection.

During world war one and two many cases emerged with the Triad of Symptoms viz. Inflamation of Joints, Inflamation of eyes and Inflamation of Uretha. Which drew attention of medical community due to common presentation in many giving it some syndrome like picture. On further investigations it was found out that most of them were exposed to urogenital or Gastro-intestinal infection 1-4 weeks prior to onset of this Triad of Symptoms. This was initially termed as “Fessenger-Leroy-Reiter’s Syndrome” or simply  “Reiter’s Syndrome”. But as the physician Hans Conard Julius Reiter  was involved in attrocities and war crimes with Hitler, so his name was removed and later renamed and termed as “Reactive Arthritis”.


  • AGE – It more frequently affects age group of 20-40 years.
  • SEX – It is more common in Males then in Females.
  • ETHNICITY – Due to its association with HLA-B27 it is frequently found in white race compared to dark race as comparatively HLA-B27 occurs more commonly in white population.
  • RISK FACTOR – Person with HIV positive status are more prone to develop reactive arthritis.


The onset of symptoms of Reactive Arthritis typically starts 4-35 days after an initial infection of gastro-intestinal system or genito-urinary system.


Reactive arthritis in most of the cases presents where patient cant – SEE, PEE, climb the TREE! due to following Classical Triad of Symptoms of reactive arthritis


Oligoarthritis involving less than five joints. It may frequently involve knee and sacroilliac joint as well. May present itself in additive pattern where it starts with one joint and add another joints subsequently or it may be migratory in pattern where the set of inflamed joints keep changing by addition and simultaneous substraction of joints involved.


Inflamation of genitourinary system classically presents itself at the onset of the disease. Not always but in many its typically after initial sexual exposure. It presents as frequent burning micturation, uritheritis, prostatitis, balanitis in men and salpingitis, vulvitis and vaginitis in women.


Occular Inflamation may present itself as mild conjunctivitis or uveitis in 75% of cases with gastrointestinal origin and 50% of cases with urogenital  involvement. patients have intermittent irritation in eyes with blurred vision typically commences at onset of disease.


  • Few patients also presents with peculiar symptom which is specific to reactive arthritis, its Keratoderma Blenorrhagica which are small hard nodule commonly appear on soles occasionally on palms and rarely on other parts of body subcutaneous nodules are not incluced. Even in absence of above mentioned triad of symptom the presence of Keratoderma Blenorrhagica is diagnostic for reactive arthritis.
  • In reactive arthritis; typical to HLA B27 related immunological reactions; involves Entheses that is where skeletal muscles attaches with bones through tendons, where it causes Enthesitis and tendon inflamation especially the tendo-achilles and also fascia in particular Plantar Tendinitis.
  • Occasionally patients also suffer from dactilitis giving finger sausage-like apperance “sausage finger” due to inflamation.
  • Mucocutaneous involvement presents as ulcerative or non ulcerative stomatitis, apthous ulcers and geographic tongue are also seen as presentation of this disease
  • Cardiac involvement causing pericarditis and aortic regurgitation in cases which do no recover soon or if its recurring or progressive.
  • Gastrointestinal manifestation like pain and cramps with frequent semiformed stools with mucous and insome cases blood due to  inflamation and ulcceration in gastrointestinal tract.

Most of the cases of Reactive Arthritis recover within six months, in many cases it keeps comming back time and again and in few it becomes chronic and progressive which may increase risk of severe complications.


In chronic progressive and recurring cases the patient may develop following complications

  • Ankylosing Spondylosis
  • Disabling Arthritis
  • Aortitis
  • Aortic Regugitation
  • Conduction defects of Heart
  • Pericarditis
  • Amyloid deposits
  • Immunoglobulin A Nephropathy


Reactive Arthritis is is HLA B27 linked inflamatory arthritis and enthesitis preceeded by a spell of infection either of genito-urinary system  or gastro-intestinal system by following commonly involved organisms


  • Chlamydia Trachomatis
  • Ureaplasma Urealyticum


  • Salmonella Spp.
  • Shigella Spp.
  • Campylobacter Spp.
  • Yersinia Spp.

4-35 days after the spell of urethritis or food poisoning by above mentioned organisms the symptoms of reactive arthritis sets in, where the synovial fluid has negative culture ans is free from infection and but the HLA B27 linked  inflamation is thought to be triggered due to

  • Autoimmune reaction due to cross reactivity of micro-organism antigen with joint tissue  or
  • Micro-organism antigenic components that may have settled in joint tissue.


Clinically the Reactive Arthritis can be diagnosed with help of Sensitivity and Specificity Guidlines laid down by American College of Rheumatology, for clinical diagnosis with given set of presenting symptom, its as follows

  1. Arthritis > 1 month with Urethritis and/or cervicitis has  sensitivity of 84.3% and specificity of 98.2%.
  2. Arthritis > 1 month with Urethritis or Cervicitis or bilateral Conjunctivitis has Sensitivity of 85.5% Specificity of 96.4%.
  3. Arthritis, Urethritis and Conjunctivitis has Sensitivity of 50.8% and sensitivity of 98.8%.
  4. Arthritis > 1 month, Conjunctivitis and Urethritis has Sensitivity 48.2% and Specificity of 98.2%.

Patients falling in above criteria or those showing just Keratoderma Blenorrhagica without any other symptoms and other suspected cases can be sent for following test for further evaluation.

  • HLA B27 testing
  • Urine routine and culture
  • STOOL Routine and culture
  • Throat swab culture
  • Cervix and Urethral swab culture
  • Erythrocytes Sedimentation Rate
  • C-Reactive Protein Test


Being an immune mediated systemic reaction that too the one that is triggered with different causative agents and even to same agents different individuals will respond differently.

Though they may have same set of general symptoms like the classical triad of reactive arthritis but intensity of each of the symptom of triad will differ in each individual,

Now this is where the homeopathic individualisation process starts. In Homeopathy we believe that though majority of human genome is the same but the minor variations in gene and the epigenome make the whole lot of difference in various characteristerics of each individual, similarly their immune reaction also varies, so every person should have individualised medicine.

Homeopathic Treatment is based on symptom similarity and individualisation of case based on peculiar symptoms based on which the case is individualised and medicine is selected.

Alternatively as per Homeopathic principle of Genus Epidemicus or pathology based symptomatology there can be disease specific homeopathic medicine derived from common symptomatic representation of a disease condition in a group of population.

Now this can not be the most similimum homeopathic prescription but roughly it can hit the disease condition within an indivudual though not accurate but will yeild some results in most of the cases.

To yield best homeopathic results there can be no generalised common approach for all cases.

But still if we have to attempt common standardised pathology based approach then to give some guidelines on homeopathic approach towards cases of reactive arthritis I have attempted following rough guidelines which may help to give some vision in approach towards such cases.

Its seen that in few case it begins after gastro-intestinal infection and in some case post genito-urinary infection. So this will further guide determining “morbid cause” behind the disease directing us in homoeopathic similimum medicine selection.

Now reactive Arthritis shows a triad of symptom in most of the cases. So this triad helps us to reach to group of medicines with such combination of symptoms.

Intensity, occurance of symptoms and its sequence in triad differs in each individuals. For example

  • In some person urogenital symptoms may be more severe compared to occular symptoms or arthritis symptoms, where as in others arthritis and ocular symptoms would be more severe than urogenital symptoms.
  • Some may not have occurence of  conjunctivitis
  • In some all three triad occur at a time where as in some patients it may occur gradually one after another in different sequence.

All this helps us find out the “seat of disease” in an individual and its degree of affinity towards various organs which can be related to homeopathic medicines during selection process.

Further arthritis may show different pattern like

  • progressive
  • migratory
  • additive
  • symetry
  • predominantly involved joint
  • sequence of joint involvement
  • number of joints involved
  • severity
  • intensity
  • type of sensation and other symptoms

Also similarly symptoms of occular involvement and urogenital involvement should be take in to account in absolute detail. This further helps refine and classify the patient and the respective medicines to be repertorised.

Which other systems and organs are involved like mucous membranes, skin, heart, kidney etc and what type of pathology they are showing like tissue destruction or just inflamation and functional disturbance or tissue lysis with regenerated and degenerative changes this will help to decide what “type of miasm” is underlying wether its psoric, syphillitic or psychotic type pathology.

Certain symptom are very “peculiar” for the  disease and occurs in few individuals like Keratoderma Blenorrhagica eruption, now location of this eruption will further help individualise the case.

Enthesitis – Inflamation of tendo-achilles and plantar fascitis is  “very specific” to the disease but does not occur in all individuals, so if plantar fascitis or inflamation of tendo-achilles if occurs in someine with this disease then it helps further in individualisation of during homeopathic medicine selection.

Other than this the general health and family background should be noted to derive  constitutional types and association of HLA B27 in 75% of this individual further helps in individualisation and homeopathic medicine selection.




Frozen Shoulder also called Adhesive Capsulitis of shoulder joint is painful stiffness limiting range of motion of shoulder joint caused due to inflammation related pathophysiology in capsule of shoulder joint.



Exact cause of Frozen Shoulder remains unclear but there are many factors that increases the risk and lead to frozen shoulder



Frozen shoulder is more common in females than in males


Person above 40yrs of age are more prone to this condition


  • Injury to shoulder joint involving any of its companent especially gleno-humeral joint capsule or rotator cuff.
  • Sports persons typically develop calcifications of tendons around shoulder joint and also in joint structures due to repeated injury and result of prolonged inflamation such persons are at high risk of developing frozen shoulder.


  • Injuries to arm and neck may indirectly affect shoulder joint, due lack of motion in general of that region as a whole and changes pattern of gait and movements of that region.
  • Immobility or reduced mobility post surgerr with general debility and delayed recovery.
  • Immobility post stroke.


  • Certain congenital structural anomaly of Musculoskeletal framework which has influence on movement, gait and weight distribution pattern on shoulder joint in abnormal pattern, which may put the person at risk of develooing Frozen Shoulder.
  • Kyphosis or Scoliosis or other congenital or acquired spinal anomaly especially those above thoracic spinal level may increase risk of frozen shoulder.
  • Patients with cervical spondylosis are at risk of developing frozen shoulder.




  • Pain in affected shoulder aggravates on movement
  • Loss of rang in motion of affected shoulder joint

Frozen Shoulder is divided into 3 stages

1) Freezing Stage

In Freezing Stage there is pain in joint which aggravates on motion and he range of motion gradually starts decreasing.

2) Frozen Stage

In Frozen Stage the pain is not much as compared to freezing stage but the range of motion is completely diminished so much so that patient can barely move the joint or cant move at all.

3) Thawing Stage

In Thawing Stage pain subsides and range of motion gradually starts improving and complete recovery is established in few weeks.

If it is acted upon quickly in freezing stage with intervention of physiotherapy and proper medication the progress of the disease is arrested and soon resolves completely.


On clinical presentation of symptoms of the patient frozen shoulder can be diagnosed and radiological tests like X-rays, CT scan and MRI may be suggested inrequired cases to find out extent, severity of pathological condition within and also to rule out any other pathological condition within or around shoulder joint.

If along with shoulder joint if there are other joints involved simultaneously or frequently different joints in past then it becomes necessary to rule out other underlying systemic conditions like Rheumatoid ArthritisGout, Ankylosing Spondylosis, Systemic Lupus Erythematosus etc and for that your doctor may suggest blood tests like RA factor, ESR, CRP, ANA, S.uric acid and HLA B27 (where there is severe spinal involvement along with shoulder). Vitamin D should also be checked wether its in optimal range for better recovery.


Treatment of frozen shoulder is based on combination of both Physiotherapy and Medicines.

Physiotherapy plays a major role in cases of frozen shoulder. Physiotherapist takes support of certain modalities, recomends certain exercises and manual physical intervention where in he may exert mild force or pressure along and within the axis of movement of shoulder joint and try to open up the freezed shoulder and gradually retain its laxity and mobility.

Pain may temporarily increase during and  after physical intenvention but with regular recomended exercise and medicines it finally subsides and joint regains its complete range of axis of movement subsequently.


If the frozen shoulder is without any underlying condition specific medicines will work well but if it is secondary to some underlying condition like autoimmune diseases or metabolic disorders or Infections or some other systemic or acute or chronic complaints then constitutional trearment along with initial acute specific remedy may be required.

List of Common Homeopathic Remedies Used in Frozen shoulder

  • Calcarea Flourica
  • Silicea
  • Calcarea Phosphorica
  • Thiosinaminum
  • Rhus Toxicodendron
  • Bryonia Alba
  • Arnica Montana
  • Plantago Major
  • Belladonna
  • Ledum Palusture