Category Archives: Neurology

Posts related to neurological diseases and homeopathic treatment for neurological disorders will be posted under this category


Anaemia can be defined as decreased haemoglobin counts or reduced red blood cell counts or reduced oxygen carrying capacity of blood, due to “loss of” or “abnormality of” red blood cells or haemoglobin.

Normal Heamoglobin Counts

  • 6 months to 5 years of age > 11g/dl
  • 5 years to 12 years of age > 11.5g/dl
  • 12years to 16 years of age > 12g/dl
  • Adult Females (non-pregnant) > 12g/dl
  • Adult Females (pregnant) > 11gm/dl
  • Adult Males > 13g/dl


  • Blood losss
  • Excessive Red Blood Cell destruction
  • Heamoglobinopathies
  • Hypovitaminosis B12
  • Hypoferremia
  • Anaemia of Chronic diseases
  • Autoimmune haemolytic anaemia
  • Inflamatory bowel diseases
  • Hypervolemia or water retention due to sodium or other salts.
  • Genetic hereditary conditions like Thalasemia
  • Certain cancers
  • Kidney diseases
  • Reduced erythropoetin production
  • Excessive RBC destruction
  • Impaired RBC production
  • Certain infections like malaria which causes RBC destruction.
  • Certain drugs which causes RBC destruction eg. Quinine causes chinchonism.
  • Bone Marrow lesions and pathologies
  • Etc.


There are many types of anaemias. It can be broadly classified into 7 categories depending upon their causes

Anaemia due to

  1. Blood Loss
  2. Hemolysis
  3. Impaired or abnormal Erythropoesis
  4. Hypervolemia
  5. Chronic Diseases
  6. Nutritional deficiency

Based on RBC morphology it can be classified into 3 groups

  • Microcytic
  • Macrocytic
  • Normocytic


  • Iron Deficiency Anaemia
  • Aplastic Anaemia
  • Megaloblastic Anaemia
  • Pernicious Anaemia
  • Sideroblastic Anaemia
  • Autoimmune Hemolytic Anaemia
  • Myelodysplastic Syndrome
  • Thalasemia
  • Fanconi Anaemia
  • Congenital Dyserythropoetic Anaemia
  • Daimond-Blacfan Anaemia
  • Myelopthisis
  • Anaemia of Prematurity
  • Erythroblastopenia or Pure Red Cell Aplasia
  • Hereditary Spherocytosis
  • Hereditary Elliptocytosis


  • Weakness
  • Lethargy
  • In children it affects growth in general
  • Somnolence, Drowziness in day time
  • Disturbed sleep at night
  • Pallor, general pale appearance of skin, mucous membranes and eyes.
  • Dyspnoea on Exertion.
  • Reduced Immunity, tendency to catch infections and slow recovery and healing.
  • Bodyaches
  • Cyanosis in severe cases
  • Palpitations
  • Tachycardia
  • Low blood pressure
  • Chest pain
  • Depression
  • Craving for indigestible things , PICA
  • Cold clammy extremities
  • Oedematous swelling of extremities, dependent oedema
  • Angina or cardiac failure in severe cases
  • Will impact general growth and repair of all the vital organs and tissue of the body.


Depending upon the cause of anaemia and general constitution of the patient, one of the following medicines may be called for duty by a homeopathic physician.

  • Ferrum Metallicum
  • Ferrum Phosphoricum
  • Cinchonna Officinalis
  • Natrum Muriatic um
  • Arsenicum Album
  • Abrotanum
  • Hamamelis Verginiana
  • Pulsatilla Nigricans
  • Janosia Ashoka
  • Crotalus Horridus
  • Lachesis
  • Acidum Phosphoricum


Epilepsy is condition where in abnormal paroxysmal hyper-synchronous electrical changes within brain causes unpredictable, sudden and repetitive spells of seizures.


  • Neurodegenerative Diseases
  • Brain Injury
  • Infections of Central Nervous System
  • Stroke
  • Brain Tumour
  • Birth defects
  • Etc

It can be due to any structural or physiological abnormality within brain caused due to genetic mutations, injuries, infections, diseases, tumours and other unknown factors. Cause for epilepsy in many cases remains unknown.



Epilepsy is caharacterised by different patterns of seizures.It is a state of sudden onset of varried degree of involuntary muscular stiffness or relaxation or combination of both with varied degree from mildly altered to complete loss in sensations and consciousness due to abnormal electrical changes within brain.

General Signs of Seizure

1)Outwardly seen signs

  • Complete stiffness of body due to contraction of muscles of body Or
  • Complete relaxation of body muscles Or
  • Contraction with relaxation causing twitching and jerking of body.
  • Suddenly losing and regaining of consciousness
  • Eyes turned ind fixed in one direction
  • Fixed, dilated or contracted pupils
  • Locked jaws, causing bitting of tongue between teeth, causing severe injury on tongue and bleeding.
  • Excessive salivation and froth from mouth
  • Excessive Perspiration
  • Involuntary passage of urine
  • Clenched thumbs
  • Etc

2) Signs Within felt only by the patient

  • Strong abnormal smells
  • Strong emotional swings
  • Phobic state
  • Tingling sensation in toes and fingers
  • Rising sensations in abdomen
  • Etc

Epilepsy patient may show varried pattern of symptoms, depending upon type of seizure, which is dependent on which region of brain is involved. Below is the classification of types of seizures

Types of Seizures

I)Focal or Partial Seizures

One Hemisphere or One lobe is involved it can be classified into two types:

  1. Simple Partial – Patient remains conscious, that is aware, realises and understands that something is happening is somewhat responsive, can recollect what had happened(during seizure), comparatively smaller region in brain is involved, patients feels strange sensations, jerking movements.
  2. Complex Partial – Patient loses consciousness completely or loss of awareness and responsiveness, may not be able to recollect episode of seizure or what had happened then.

2)Generalised Seizures

Both the hemisphere are involved, these type of seizures are classified into six sub-types

  1. Atonic – Also called drop seizure or akinetic seizure. Partial or complete loss of muscle tone and control especially of trunk muscles causing patient to fall forwards with head leaning forwards causing injury. Atonic seizures usually doesnt last more than fifteen seconds in some cases followed by paralysis in a muscle group not lasting for more than three minutes. Usually the onset in most cases is during childhood and may persist into aldulthood. All the cases of concurrent Atonic seizures with onset during childhood needs to be carefully evauated for Lenox-Gustaut Syndrome (LGS) characterised by concurrent episodes of either atonic or tonic seizures with cognitive disorders and spikes on electroencephalogram. LGS a rare, complex and fatal condition usually caused due to congenital infections, genetic disorders like Tuberous Sclerosis and West Syndrome, many other genetic mutations, brain lesions. Atonic seizures are also found in Dravets Syndrome.
  2. Tonic – Sudden stiffness due contractions of muscles of limbs and trunk causing patient to fall backwards which may result into injury due to fall, it often occurs in state of sleep as well. These type of seizures usually do not last for more than 20 minutes. Tonic seizures are one of the most commin type of seizures associatex with Lenox -Gustaut syndrome as mentioned above.
  3. Clonic – Sustained uncontrolled violent rythmic jerking of body parts due to rapid contraction and relaxation of muscles, cant be stopped even by exerting force. This type of seizures are also refered as convuslions.
  4. Tonic-Clonic – Tonic and Clonic pattern of seizures follows each other randomly in phases. In Tonic phase the muscles suddenly contracts and body stiffens followed by clonic phase when suddenly patient’s body starts jerking violently in rythm due to rapid contraction and relaxation of muscles.
  5. Myoclonic – Jerking and Twitching of group of muscles. Usually patient is conscious. This type of seizures are seen in many conditions amd syndromes like LGS(mentioned above), juvenile myoclonic epilepsy (usually appears during puberty, morning seizures usually after patient wakes up usually involves neck and upper limb), Progressive Myoclonic Epilepsy(rare syndrome of combination of Tonic-Clonic and Myoclonic)etc.
  6. Abscense – In this type patient suddenly lose conscious and soon regiains consciousness with no other evident external signs except patient suddenly stops and become stand still and visibly , for others, outwardly they seem as if lost out in thought for a while.

Secondary Generalised Seizures

Starts as partial seizure and progresses as generalised seizure. It is termed as secondary generalised seizure, as the primary event was initial partial seizure and then it progressed to generalised seizure.

Status Epilepticus

When seizures fail to stop and keep continuing for more than 5 minutes, usually the seizure pattern is of Tonic-Clonic type. Its a medical emergency and may prove fatal if not treated immediately


  • Confussion lasting for few munuted to couple of hours.
  • Paralysis of limbs one sided, lasting for upto 15 hours and may take upto 2 days for complete recovery, it is called Todd’s Paralysis.


  • MRI
  • CT Scan
  • EEG
  • And may require many other tests to find out underlying cause of epilepsy.


  • NAJA


Dementia is a syndrome of cognitive deficits caused due to certain underlying disease conditions.

It characterised by weak memory, decreased ability to think, calculate, judge, reason, deterioration of language, difficulty in orientation of time and location, lack of initiative, emotional and behavioural problems.


Dementia in most patients is secondary to one or more underlying conditions that affects Central Nervous System like certain –

  • Hereditary or Acquired Genetic Disorders
  • Autoimmune Conditions
  • Metabolic Disorders
  • Vascular Diseases
  • Prions Disorders
  • Infectious Diseases
  • Injuries
  • Surgeries
  • Alcoholism
  • Drug addictions
  • Medications
  • etc.

Below mentioned are the most common diseases that shows symptoms of dementia.

  • Alzheimer’s Disease(60-80% of all cases)
  • Vascular Dementia(20% of all cases)
  • Fronto-Temporal Lobar Degeneration
  • Dementia with Lewy Body
  • Hutington’s Disease
  • Parkinson’s Disease

Of all the causes of dementia, Alzheimer’s Disease is present in almost 60-80% of all the cases as the underlying cause of dementia, making it the most common cause of dementia. In many patients Alzheimer’s Disease co-exists with some other condition as underlying cause of dementia.

Depending upon the underlying cause and its stage of progression it may be either

  • Non-Progressive or Slow-progressive or Fast-progressive
  • Reversible or Irreversible

Presence of number of symptoms, its appearance, sequence and intensity depends upon the underlying causative disease condition.

More or less the overall picture of dementia remains the same in various diseases only weightage to different parameter like (recall, Orientation of Time and Place, Attention and Calculation, Registration, Recall, Repetition, Language, Complex Commands) of cognitive deterioration differs a bit in different diseases and different stages. This helps in rough clinical assessment of underlying condition.


It is characterised by symptoms borne out of cognitive deficits

  • Forgetfulness especially recent events causing patient to misplace things and ask repeated questions, repeats phrases, difficulty in recalling names of objects or persons.
  • Decreased ability to think, making patient seem irrational in judging, reasoning concluding, taking decisions, initiatives
  • Lack of attention and difficulty in calculations makes it difficult for patient to maintain his finances.
  • Reduced vocubulary, causing deterioration in language.
  • Difficulty in orientation of time, directionality and location causing patient of getting lost frequently.
  • Difficulty in recognising and identifying objects due to lack of visuo-spatial articulation.
  • Tremors, difficulty in balancing.
  • Difficulty in eating especially swallowing needs liquid or thickened liquid diet.
  • Difficulty in daily routine, house keeping and self care.

All this above neurocognitive disorders results in emotional problems and low spirits and other neuro-psychiatric symptoms as mentioned below

Common Neuspychiatric symptoms of dementia are termed as “Behavioural and Psychological Symptoms of Dementia -BPSD” listed below

  • Anxiety
  • Depression
  • Agitation
  • Aggression
  • Restlessness
  • Impulsive
  • Elated
  • Sleep disorders
  • Delusions
  • Hallucinations
  • Disturbed Appetite
  • Lack of attention
  • Difficulty in problem solving

Initially symptoms are very difficult to notice and only close relative can judge or evaluate the signs and symptoms.

Over time these symptoms starts becoming more noticable as the patients condition starts deteriorating as the disease progresses.

The progression of disease is divided into four stages, where in, above mentioned symptoms gradually worsen in each progressive stage viz.

1)Mild Cognitive Impairment (MCI)

  • Scores 27-30 on MMSE scale of cognition.
  • No one can notice easily untill patient is evaluated.
  • Impairement is not so severe so as to interfere persons Activities of Daily Living (ADL).
  • At this stage patient is not termed as dementia patient its more of a prodromal phase
  • Not all but most of these patient deteriorate in cognitive deficits and progress in to Early Stage Dementia

2)Early Stage Dementia

  • Scores 20-25 on MMSE scale of cognition.
  • Only close relatives and caretaker can notice the signs and symptoms.
  • Difficulty in complex activity and comands.
  • Signs and symptoms depends much upon the underlying disease, that which symptom will be more pronounced. Eg. In dementia of Alzheimer’s Disease the memory related symptoms will be more pronounced in first stage while in dementia with lewy bodies and frontotemporal difficulty in organisation and planning will be more pronounced.

3)Mid Stage Dementia (or Moderate)

  • Score on MMSE scale 6-17.
  • Now the symptoms are noticable to everyone.
  • Gets confused in unfamiliar place.
  • Can do only simple work much difficulty in Instrumental Activities of Daily Living(IADLS).
  • Needs frequent reminders for everything
  • At these stage they have started becoming dependent and cant be left alone.

4)Late Stage Dementia (or Severe)

  • Sore on MMSE scale below 6.
  • Cannot do even Basic Activities of Daily Living(basicADLS)
  • Requires full-time assistance and become completely dependent cannot be left alone.
  • Patient cant easily recognise even close relative.
  • Tremors and loss of balance, may fall and injure themself.
  • Difficulty in identifying and handling objects in this case they might accidentally injury themself by misshandling objects.
  • Difficulty in eating espescially in swallowing, liquid or thickened liquid diet is prefered.
  • Cannot retain urine or stools and requires assistance in toilet hyegine.
  • Issues with appetite, sleep and behaviour.



There are many patient based/caretaker based/ combination of patient cum caretaker based questionaire tests designed to evaluate cognitive skills of patient.

These tests helps us to evaluate different parameters of cognitive skills like

  • Memory Recall
  • Orientation of Time
  • Orientation of Place
  • Attention
  • Calculation
  • Registration
  • Repetition
  • Language
  • Complex Commands
  • Etc

Based on the score weightage of different parameters and the total score we can not only assess the grading and stage of the condition but also it gives rough differentiation on probable underlying disease that has caused dementia. Accordingly we can determine if any further investigations are required to diagnose the underlying disease.

Every tests has its own pros and cons and specificity and sensitivity. So more than one of the following test may be called in if required.

Patient Specific Tests

  • MMSE – Mini Mental State Examination
  • 3MS – Modified Mini Mental State Examinations
  • AMTS – Abreviated Mental Test Score
  • CASI – Cognitive Abilities Assessment Instrument
  • MoCA – Montreal Cognitive Assessment
  • Trail Making Tests

Questionaires for Caretakers Relatives and other informants

  • IQCODE – Informant Questionnaire on Cognitive Decline in the Elderly

Combination of Patient specific and informant specific questionaires test

  • General Practitioner Assessment of Cognition


  • Blood tests to rule out any other anomalies like and vitamin deficiencies, hormonal imbalances, electrlyte imbalances, infections that may potentially show similar symptoms.
  • MRI, CT, PIB-PET, DTBZ-PET, helps diagnose some of the disease that are know to cause dementia.
  • Brain Biopsy to confirm the doubted underlying disease condition.
  • CSF analysis.




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.




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).




Degenerative changes in vertebral bodies and intervertebral disc at the level of L1 to S1 in vertebral cloumn affecting lumbar region of spine is called Lumbar Spondylosis.

It is characterised by degenerative changes of Lumbar vertebral bodies like osteophyte lippings and spur formation, degeneration of  intervertebral disc, narrowing of intervertebral space, Intervertebral disc bulging, intervertebral disc herniation.

It can also be called Osteoarthritis of Lumbar Spine.


Lumbar Spondylosis may be caused due to many factors that can be broadly classified into Mechanical, Congenital or Acquired Anatomic anomalies, Metabolic, Immunologic, Genetic, Nutritional, Ageing and Septic reasons.

Most common of all are ageing and mechanical reasons like excessive wear and tear due to wrong postural habbits, type of work like driving for long duration regularly, sitting for long hours, lifting weights or working with bent posture etc. that exerts much pressure on lumbar spine on regular basis so as to not giving much time to recover again and resulting into accumulation of wear and tear finally damaging the spine and causing lumbar spondylosis.

Metabolic problems like Hyperuricemia/Gout where high level of uric acid in blood damages lumbar spine also this uric acid may get crystalised to form monosodium urate monohydrate and settle in the intervertebral joints and damage them.

Immunologically mediated chronic inflamation in lumbar spine like in Rheumatoid Arthritis, Chickenguniya, Systemic Lupus Erythematosus etc.

Genetic Complaints like Ankylosing Spondylosis etc

Vitamin D deficiency causes reduced calcium assimilation resulting into reduced bone mineral density causing weak bones easy to damage. Insufficient nutrition compared to requirement, which prevents repair work of regular wear and tear of lumbar spine, due to which damages tend to get accumulated resulting into lumbar spondylosis.

Congenital or acquired Anatomical anomalies in musculoskeletal framework that may cause abnormal posture or abnormal weight distribution which results into pressure on spine in wrong fashion gradually facilitates development of Lumbar spondylosis.

Septic Conditions of spine like Tuberculosis of spine may result into lumbar spondylosis due to tissue lysis as result of infection.


  • Pain and Stiffness  in lower back or Lumbar Region.
  • Sciatica due to compression of nerve roots of sciatic nerve.
  • Pain stinging pain in lumbar spine
  • Pain radiating from lumbar spine to lower limbs
  • Paraesthesia in lower back genitals or lower limbs
  • Cramps calfs, thighs and other muscle and muscle groups of lower limbs
  • Difficulty in walking and maintaining posture and balance.
  • Lack of control on urinary spincter or anal spincter resulting into either retention of urine or bowel or involuntary expulsion of urine and bowel
  • Sexual debility Tabes Dorsalis


Myelopathy – When there is damage to spinal cord it causes Myelopathy.

Raduclopathy – compression of nerve near nerve root where it emerges out of spinal cord.

Vertebrobasilar insufficiency – Vertebral artery insufficiency due to its occulusion while it passes through vertebral foremen sue to degenerative changes for lumbar spine causes vertebrobasilar insufficiency leading to death of condrocytes of intervertebral disc and osteophytes starts accumulating and depositing.


  • Clinical symptoms if indicate towards Lumbar spondylosis it can be then confirmed with X ray.
  • MRI and CT scan gives us better imaging which helps  judge and evaluate the extent of damage and condition
  • Myelograph is dye injected while Xray and CTscan this gives detailed shadow to understand even better
  • Electromyography helps evaluate nerve involvement in spondylosis.