Category Archives: HOMEOPATHIC TREATMENT

Diseases and their homeopathic treatment.

LYMPHOMA

LYMPHOMA – Malignant neoplasm of lymphoid tissue is called Lymphoma.

They are type of blood cancers where in there is abmormal cell-proliferation of Lymphoid Tissue.

Lymphomas and Leukemias both fall under a broader category “Malignant Neoplasms of Lymphoid and Heamatopoetic Tissue” or cancer of Lymphocytes”. Wherein unlike Leukemias, the term Lymphomas is precisely restricted only to the Tumours of Lymphoid tissue.

Types of Lymphoma

  • Hodgkin’s Lymphoma
  • Non Hodgkin Lymphoma
  • Multiple Myeloma
  • Immunoproliferative diseases

RISK FACTORS

Hodgkin’s Lymphoma

  • Hereditary
  • Epstein Barr Virus Infection

Non Hodgkin’s Lymphoma

  1. Autoimmune Conditions
  2. HIV infection/AIDS
  3. Human T-Lymphotropic Virus Infection
  4. Immunosupressive Medication
  5. Exposure to certain Pesticides
  6. Tobacco Smoking

SIGN’s AND SYMPTOM’s

  • Lymphadenopathy
  • Pel-Ebstein Fever – Intermittent Fever of around 38C lasting for 1-2weeks and relapsing again after days to weeks
  • Weight loss of more than 10% within 6 months.
  • Profuse perspiration especially at night.
  • Anorexia – loss of appetite
  • Weakness and fatigue
  • General Pruritus
  • Dyspnoea on slightest exertion

Ann Arbor Staging System

Principle Stages

  • StageI – Single Lymphnode and surrounding area involved
  • StageII – Two areas involved a lymph node and another area and both are on the same side of daiphram either above or below
  • StageIII – Affected areas on both the sides of daiphram with one organ or region near lymphnode or spleen
  • StageIV – Diffused and disseminated with more than one Extra-Lymphatic organ involved incliding Liver, Bone Marrow, nodular involvement of Lungs.

Modifiers

  • A or B – type symptom – When patient has following three constitutional symptoms then patient is categorised into B-type symptoms 1) Pel-Ebstein Fever. 2) Weight loss and 3)Night Sweats. When there are no above mentioned combination of B-type constitutional symptoms present then patient is categorised into A type.
  • S ” – Disease with Slpeen involvement is denoted with S modifier.
  • ” E” – When disease involves extranodal region that is region surrounding the lymphnodes it is denoted with E modifier.
  • “X” – X is denominated when the largest bulky deposit region is more than 10cm or if more 35% area of chest is occupied by mediastenum on X-Ray.

Nature of Stage

  • Clinical Staging “C.S.” – C.S. Mentioned when staging is done based on clinical examination and test.
  • Pathological Staging “P.S.” – When Staging is done based on pathological findings through invasive techniques like surgical excision etc its Mentioned as P.S.

DIAGNOSIS

Biopsy of Lymph node to confirm Lymphoma.

Further to classify Lymphoma:

  • Immunophenotyping
  • Flow Cytometry
  • Fluorescence in-situ Hybridisation.

CT scan and PET scans helps us evaluate extent of spread of the condition and its staging.

HOMEOPATHIC MEDICINES FOR HODGKIN’s LYMPHOMA and NON- HODGKIN’s LYMPHOMA

  • BARYTA CARBONICA
  • CALCAREA CARBONICA
  • CINCHONNA OFFICINALIS
  • CALCAREA FLOURICA
  • CONIUM MACULATUM
  • PHYTOLACCA
  • BARYTA MURIATICUM
  • TUBERCULINUM
  • CALCAREA PHOSPHORICA
  • CALCAREA CARBONICA

LEUKEMIA

Abnormal proliferation of blood cells due to defective medullary heamatopoetic stem cells is called leukemia.

In Layman terms, defective bone marrow causes uncontrolled multiplication and abnormal growth of cells that are components of blood causing blood cancer.

TYPES AND CLASSIFICATION

Based on speed of progression and maturity level of most cells most of the Leukemia can be categorised into

  • Acute – Fast progressing takes weeks to few months, Most of the cells are blast cells (immature cells), Requires immediate treatment, Commonly seen in children.
  • Chronic – Relatively slow progressing takes months to years, has relatively mature cells, patient usually inder observation before commencing any aggressive treatment, Common in elderly people.

There are some leukemia which do not follow fixed pattern also presentation of symptom may vary in different individual and also there are cases where in they change the classical course of and speed of progression.

Based on types of cells involved, most of the Leukemia can be categorised into

  • Lymphoid (Lymphocytic) – Precursors of Lymphocytes are involved. It is further classified as per which lymphocytes are involved wether B-cells or T-cells.
  • Myeloid(Non-Lymphocytic) – Precursors of RBC, Non-Lymphocyte WBC and Platelets are involved.

A Lymphoid or Myeloid leukemia can Either Acute or Chronic as described below

  1. Acute – Lymphoblastic(ALL)
  2. Chronic – Lymphocytic (CLL)
  3. Acute – Myeloid (AML)
  4. Chronic – Myeloid (CML)

ACUTE

Acute Lymphoblastic Leukemia (ALL) –

When there are multiple mutations in the locus, that control cell proliferation, cell maturation and cell death of precursor cells of Lymphocytes called Lymphoblast then this results in ALL. ALL can be of T cell type or B cell type.

Genes associated with ALL –

  • KMT2A – Infant ALL – onset before 10yr of age
  • ARID5B
  • CKDN2A
  • CKDN2B
  • TP53
  • GATA3
  • PIP4K2A
  • IKZF1
  • CEBPE
  • PAX5 – Inherant Autosomal Dominant
  • ETV6 – Inherant Autosomal Dominant

Certain syndromes that increases risk of ALL

  • Down’s Syndrome
  • Bloom Syndrome
  • Fanconi Anaemia
  • X-Linked agamaglobulinaemia
  • Neurofibromatosis Type 1
  • Li-Fraumani Syndrome
  • Paroxysmal Nocturnal Heamoglobinuria
  • Severa Combined Immunodeficiency
  • Costmann Syndrome
  • Ataxia Telangiectasia
  • Schwachmann Daimond Syndrome

SUBTYPES OF ALL

  • Precursor B-cell ALL
  • Precursor T-cell ALL
  • Mature B-cell ALL(also called Burkitts Leukemia due to its similarity with Burkitts Lymphoma)
  • Acute Biphenotypic Leukemia.

Acute Myeloid Leukemia (AML)

It is an acute Non-Lymphocytic type of malignanacy which involves myeloblast cells(precursor of monocytes and granulocytes).

In AML there is mutation of genes that mature and differentiate the myeloblast cell will arrest maturation and differentiation and the cell will freeze in undifferentisted immature state and when this type of mutations combined with mutations in genes controlling proliferation in same cell will result in clonning of immature undifferentiated cells resulting in AML

Genes associated with AML

Subtypes of AML

Subtypes of AML are classified based on staging of maturation i.e. at which stage the msturation of the cell is arrested and how is the general behaviour of cells and which genes are involved.

  • Undifferentiated Acute Myeloblastic Leukemia
  • Acute Myeloblastic Leukemia with Minimal Maturation
  • Acute Myeloblastic Leukemia with Maturation
  • Acute Pro-Myelocytic Leukemia (APL)
  • Acute Myelomonocytic Leukemia
  • Acute Myelomonocytic Leukemia with Eosinophilia
  • Acute Monocytic Leukemia
  • Acute Erythroid Leukemia
  • Acute Megakaryoblastic Leukemia

Adult T-Cell Leukemia

Blast Crisis of CML

CHRONIC

Chronic Lymphocytic Leukemia (CLL)

  • B-cell Pro-Lymphocytic Leukemia(B-PLL)
  • T-Cell Pro-Lymphocytic Leukemia(T-PLL), T-PLL doesnt completely fit into this category.

Hairy-Cell Leukemia(HCL)

Large Granular Lymphocytic Leukemia(LGLL)

Chronic Myeloid Leukemia (CML)

  • Chronic Granulocytic Leukemia
  • Juvenile CML
  • Chronic Neutrophillic Leukemia
  • Chronic Myelo-Monocytic Leukemia(CMML)
  • Atypical CML (aCML)

Chronic Eosinophillic Leukemia

Few other types, preleukemias and syndromes that cannot be classified in above category

  • Clonal Eosinophilia
  • Other Myelodysplastic Syndromes
  • Other Myeloproliferative Syndromes

CAUSES

Leukemia is caused due to mutations in genes that are associated with proliferation, differentiation, growth, maturation and cell death of blood cells. With different types of mutations responsible for different types of leukemia.

These genetic mutations can be inherited or acquired due to multiple reasons of which few known risk factors are

  • Exposure to certain chemicals (e.g. benzene, petrochemicals, hair-dyes, agent orange herbicide, certain insecticides)
  • Radiation – ionising radiations and doubtedly non-ionising radiations too.
  • Smoking and tobacco use.
  • Prior alkylating chemotherapy for some other form of malignancy.
  • Viruses – Human T-cell Lymphotropic Virus – 1 HTLV-1 is associated with Adult T-cell Leukemia and Hepatitis C is associated with CLL
  • Diseases and Syndromes – Down’s Syndrome, Kline Felter syndrome, Fanconi Anaemi, Ataxia-Telangiectasia or Louis-Bar Syndrome, Myelodysplastic syndrom, Myeloproliferation syndrome.

Few of these factor are seen responsible for specific type of cancer (eg HTLV1 causes Adult T-cell Leukemia, Tobacco and Down’s Syndrome increases risk of AML).

SIGNS AND SYMPTOMS

Symptoms may vary in different types of leukemia, different individuals and different stages of disease.

  • Tired feeling
  • Paleness due to anaemia
  • Shortness of breath
  • Headache, lethargy, stiffness of neck
  • Loss of appetite
  • Weight loss
  • Tendency to catch infection too frequently
  • Fever usually due to secondary infections
  • Painful long bones
  • (Heamorrhagic diathesis) easily bleeds and frequent ecchymosis and petechiae (bruises).
  • Painless lymphomegaly (Enlarged lymphnodes)
  • Hepatospleenomegaly – can easily palpate liver and spleen due to its increased size.
  • Fibrosis of bone marrow
  • Chloroma or Leukemia Cutis or myeloid sarcoma or granular sarcoma or extramedullary myeloid tumour
  • Swollen painfull and bleeding gums
  • Sweet’s Syndrome
  • Pitting Oedema
  • Enlarged Testis
  • Mediastinal mass
  • Cranial nerve Paralysis if CNS is involved
  • Increased blood cell count , WBC or RBC or Platelets, depending on type with most if the cells immature and lacking differentiation.

DIAGNOSIS

  • Complete Blood Count
  • Bone Marrow Biopsy
  • Lymph Node Biopsy

HOMEOPATHIC TREATMENT WITH INDICATED HOMEOPATHIC MEDICINES

  • Arsenicum Album
  • Phosphorus
  • Hekla lava
  • Lachesis
  • Benzinum
  • Carica Papaya
  • Cinchonna Officinalis
  • X-ray
  • Thuja Occidentalis
  • Syphillinum
  • Baryta Carbonica
  • Calcarea Phosphorica
  • Ruta Graveolens
  • Calcarea Fluorica
  • Calcarea Carbonica
  • Symphytum Officinalis
  • Hyocyamus Niger
  • Medhorrhinum

UNDER CONSTRUCTION

MYCOSIS FUNGOIDES

Mycosis Fungoides is a type of Non-Hogkin Lymphoma. It is the most common type of Cutaneous T-Cell Lymphoma(CTCL).

Mycosis Fungoides is a misnomer which means “Mushroom-like fungal disease” but by no means it is a fungal condition. It is a type of blood cancer caused due to unusual expression of Skin-associated CD4 T-Cells. This cancer affects skin and produces various lesions on skin and rarely metastatise in other tissues.

It is a fatal condition with 10year survival rate of less than 70% which is even less in elderly.

It usually appears in people above 20years of age and is more common after age of 50yrs , males are affected more than females, the disease tends to be more fatal in black race. Survival rate has been found good in married white women.

CAUSES

Causes of Mycosis Fungoides remains unclear

No hereditary or genetic factors have been found associated to the disease.

It is considered to be non-contagious but some studies suggest that Human T-cell Lymphotropic Virus is associated with this condition.

SYMPTOMS

Initially disease shows symptoms that are not distinguishing and in most of the cases it resembles psoriasis or eczema. Even on biopsy it can not be diagnosed easily in early stages. Even in later stages multiple biopies are required to establish diagnosis.

Disease presentation begins from skin as exfoliating, pruritic, erythodermic eruptions resembling to Eczema or Psoriasis and is almost always mistaken initially in most cases. These eruptions tends to appear first on buttocks in vast majority of cases and then spreads throughout the body. Pruritus is present in only 20% of all the cases. In later stages tumourous and ulcerative lesions may also appear. Disease usually in most cases starts appearing at around age of 45-50 and is a slow prohressing condition with and its usually around age of 60+ that mist patient starts presenting symptoms of later stages like tumours, generalised pruritus and erythrodrema and ulceration. Though in many cases it may start as early as age of 20 and rarely before 20yrs of age. The diseases is classified into three stages

Stages of Mycosis Fungoides

Mycosis fungoides is divided into three stages viz.

  1. Pre-Mycotic
  2. Mycotic
  3. Tumourous

Pre Mycotic Stage

It starts appearing on skin at this stage as erythematous, pruritic, exfoliating skin eruptions.

On biopsy it cannot be diagnosed at this stage as histopsthology shows pattern of non specific dermatosis with epidermal psoriasiform changes.

Mycotic Stage

In Mycotic stage Infiltrative Plaques starts appearing as slightly raises or wrinkled spots.

On histopathology polymorphs and few atypical lymphoid cells are seen inflamatory infiltrates in dermis. When this cells are seen lined up.in epidermal basal layer without spongiosis then its confirmatory finding to establish diagnosis of mycosis fungoides.

Tumorous Stage

Nodular overgrowths are seen on skin ranging from few milimeters to centimeters scattered throughout the body along with plaques and patches. Usually it appears on the same place where the plaques and patches are. Also there is erosion of the tumours and ulcerations is seen in many cases over the tumour and plaques.

On histopathology they show medium sized lymphocytes with cerebroid nuclei expands dermis.

DIAGNOSIS OF MYCOSIS FUNGOIDES

Diagnosis is based primarily on histopathological findings of the skin lesions

Clinically patients showing features suggestive of or doubted mycosis fungoides are closely monitored over the time untill biopsy confirms. Multiple boipsies of various lesions might be required at every progressing stage untill confirmed, as its very difficult to estsblish diagnosis in initial stafe wether clinically or histopathologically as it resembles psoriasis or eczema.

On histopathology following findings are required to establish diagnosis of mycosis fungoides

  • Band-like lymphocyte infiltrate in superficial papillary dermis
  • Epidermotropism
    • Cerebroid T-cells in dermal and epidermal infiltrate
  • Pautriers Microabscesses – though not present in most cases but is characteristic finding of mycosis fungoides where in the epidermal infiltrate shows atypical lymphocytes arranged in aggregates of four or more.

HOMOEOPATHIC MEDICINES FOR MYCOSIS FUNGOIDES

  • Thuja Occidentalis
  • Syphillinum
  • Antimonium Crudum
  • Arsenicum Album
  • Ars Sulph Flavum
  • Phosphorus
  • Argentum Nitricum
  • Hepar Sulphuris
  • Sulphur
  • Silicea

EPILEPSY

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

CAUSES OF EPILEPSY

  • 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.

SIGNS AND SYMPTOMS OF EPILEPSY

ICTAL STAGE OR SEIZURE

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

POST-ICTAL STATE

  • 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.

DIAGNOSIS OF EPILEPSY

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

HOMOEOPATHIC MEDICINES FOR EPILEPSY

  • TARRENTULA HISPANICA
  • STANNUM METALLICUM
  • BELLADONNA
  • GELSEMIUM SEMPERVIRENS
  • AETHUSA CYNAPIUM
  • PLUMBUM METALLICUM
  • ZINCUM METALLICUM
  • LACHESIS
  • NAJA
  • STROMONIUM

SEPTIC ARTHRITIS

Septic Arthritis is invasion of joint by micro-organisms causing inflamation, it is also called infection of joint or Arthrtis due to infection or infective arthritis.

CAUSES

VECTORS

Septic Arthritis can be caused due to infection of any of the following vectors

  • Bacteria
  • Virus
  • Fungus
  • Parasite

Most Common Organisms Known to Cause Septic Arthritis.

  • Staphylococci – Methycillin Resistant Staphylococcus Auris(MRSA)
  • Streptococci
  • Escherichia Coli
  • Pseudomona Aeruginosa
  • Neisseria Gonorrhoeae
  • Neisseria Meningitidis
  • Myocbacterium Tuberculosis
  • Salmonella spp.
  • Brucella spp.
  • Eikenella Corodens
  • Pasteurella Multocida
  • Borrelia Burgdorferi
  • Rubella virus
  • Parvovirus B19
  • Chickungunya virus

RISK FACTORS

Usually its not common to get joint infection unless the immunity of a person is weak or there is history of surgery, prosthesis, deep tissue infections etc.

  • Joint Surgery
  • Prosthetic implants
  • HIV
  • Immuno-suppressive Medication
  • Intravenous drug users
  • Rheumatoid Arthritis
  • Osteoarthritis
  • Arthritis due to Gout
  • Gonorrhoea
  • Infective Endocarditis
  • Deep and /or nonhealing wounds
  • Other deep tissue infections
  • Other causes of septicemia
  • Old age

SIGNS AND SYMPTOMS OF SEPTIC ARTHRITIS

  • Usually single joint infected, less frequently more than one joints are involved.
  • Most commonly involved joint is knee joint and other freqently involved joints are hip, spine, shoulder, wrist, elbow, sacroilliac and sternoclavicular joints.
  • Sudden onset of symptoms, fast progression of disease.
  • Swelling, redness with increased local Heat and pain around joint. Swelling and redness is comparatively much more than other types of arthritis.
  • Fever with or without chills and headache.
  • Cant move joint due to severe pain.
  • Pain aggravated in slightest motion or jarring, pain is ususally aching type with stitching, stinging and pulsating.

DIAGNOSIS OF SEPTIC ARTHRITIS

  • Athrocentesis – microorganisms usually found on culture, WBC count above 50,000-1,00,000/cubic mm, neutrophils more than 90%, lactate count more than 10mmol/l.
  • CBC – increased wbc
  • Blood culture positive for micro-organism
  • ESR – elevated
  • CRP – elevated
  • Procalcitonin – elevated
  • NAAT – to rule out gonorehoea
  • Ultrasound – joint effusion
  • CT scan – Region involved type and extent of damage
  • MRI – Region involved type and extent of damage

HOMOEOPATHIC MEDICINES FOR SEPTIC ARTHRITIS

Septic Arthritis is a medical emergeny case and requires immediate medical intervention any delay in treatment can cause damagr and complete destruction of joint with hours to days.

Acute fast acting Homeopathic Medicines are selected with special affinity to joints and pathogenesis that of sudden, severe, acute inflamation with much swelling redness. Below is the list of indicated homeopathic medicines that I prefer in case of infective arthritis.

  • APIS MELIFICA
  • BELLADONA
  • LEDUM PALUSTURE
  • RHUS TOXICODENDRON
  • BRYONIA ALBA
  • PYROGENUM
  • ACONITUM NEPELLUS
  • MEDHORRINUM
  • TUBERCULINUM
  • SYPHILLINUM

DEMENTIA

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.

CAUSES OF DEMENTIA

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.

SIGNS AND SYMPTOMS

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.

DIAGNOSIS

COGNITION TESTS

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

LABORATORY INVESTIGATIONS

  • 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.

HOMEOPATHIC MEDICINES FOR DEMENTIA

  • LACHESIS
  • HYOCYAMUS NIGER
  • GELSEMIUM SEMPERVIRENS
  • ANACARDIUM ORIENTALE
  • BACOPA MONNEIRI
  • OPIUM
  • CANABIS INDICA
  • BELLADONNA
  • BAPTISIA TINCTORIA
  • TERRENTULA HISPANICA

ALZHEIMER’S DISEASE AD

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.

CLASSIFICATION ALZHEIMER’S DISEASE

  • 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)
  • BASED ON INFLAMATION – INFLAMATORY or NON-INFLAMATORY
  • BASED ON STAGES OF DISEASE PROGRESSION– PRODROMAL, EARLY/MILD, MODERATE and SEVERE

SIGNS AND SYMPTOMS OF ALZHEIMER’s DISEASE

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.

STAGES OF ALZHEIMER’s DISEASE

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

Early/Mild

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

Moderate

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

Severe

  • 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

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.

GENETICS

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).

PATHOGENESIS

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.

CHOLINERGIC HYPOTHESIS

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.

AMYLOID HYPOTHESIS

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 HYPOTHESIS

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.

OTHER HYPOTHESIS

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.

HOMEOPATHIC MEDICINES FOR ALZHEIMER’s DISEASE

  • ANACARDIUM ORIENTALE
  • HYOCYAMUS NIGER
  • BACOPA MONNIERI
  • LYCOPODIUM CLAVATUM
  • BARYTA CARBONICA
  • CONIUM MACULATUM

DMD – DUCHENNE MUSCULAR DYSTROPHY

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

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

THUS DYSTROPHIN PLAYS MAJOR ROLE IN BIOCHEMISTRY OF MANY PHYSIOLOGICAL ACTIVITIES

  • 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.

EPIDEMIOLOGY OF DMD

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.

SIGNS AND SYMPTOMS OF DMD

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

DIAGNOSIS OF DMD

  • DNA testing
  • Muscle Biopsy
  • Prenatal Screening

HOMEOPATHIC TTREATMENT WITH INDICATED MEDICINES FOR DMD

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.

HOMEOPATHIC MEDICINES FOR DMD

  • 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

SUPPORTIVE TREATMENT AND MANAGEMENT

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 (MND)

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

SIGNS AND SYMPTOMS OF MOTOR NEURON DISEASE

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)

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.

SIGNS AND SYMPTOMS OF MULTIPLE SCLEROSIS

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

CAUSES AND PATHOPHYSIOLOGY OF MULTIPLE SCLEROSIS

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.

DIAGNOSIS OF MULTIPLE SCLEROSIS

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.

HOMEOPATHIC MEDICINES FOR MULTIPLE SCLEROSIS

  • GELSEMIUM
  • CIMICIFUGA/ACTEA RACEMOSA
  • TERRENTULLA HISPANICA
  • NUX VOMICA
  • STRYCHININUM
  • NAJA
  • LACHESIS
  • LYSSINUM
  • ACONITUM
  • OPIUM
  • RUTA GRAVEOLENS