Treatment taken

9/ 7/ 2006        -           Gelsemium      30/ 4 d

12/ 7/ 2006      -           phos                 30/ 1 d

19/ 7/ 2006      -           phos                 200/ 1 d

Patient is relieved and discharged on 5/ 8/ 2006.

GUILLAIN- BARRE SYNDROME (GBS)

[LANDRY- GUILLAIN- BARRE DISEASE, ACUTE IDIOPATHIC POLYNEURITIS, ACUTE INFLAMMATORY DEMYELINATING POLYRADCULONEUROPATHY, ACUTE IMMUNE-MEDIATED POLYNEURITIS (AIMP)]

This is an acute anterior radiculopathy occurring as an allergic manifestation to a preceding viral illness. It is an autoimmune disease due to the production of antibodies against the myelin sheath.

This disease occurs in all parts of the world and in all seasons. It affects children and adults of all ages and both sexes. Its cause is unknown. A mild respiratory or gastrointestinal infection precedes the neuritic symptoms by 1 to 3 weeks in 60- 70% of the patients. Other preceding events include surgical procedures, viral exanthems and other viral illnesses including AIDS, mycoplasma infections, the spirochetal infection of Lyme disease and lymphomatous diseases particularly Hodgkin’s Disease.

The brunt of attack is borne by the anterior roots. About 10- 30 days after a viral illness, the patient complains of paraesthesia in the extremities. This is followed symmetrical ascending paralysis starting in the lower limbs, esp. in the proximal muscles.

The paralysis may ascend up gradually over days or abruptly within hours. Respiratory paralysis may occur. Majority of cases do not affect the cranial nerves and bilateral facial palsy may develop. Cases with rapid progress and those with respiratory paralysis have a poor prognosis.

Clinical examination reveals lower motor neuron signs such as hypotonia, weakness and areflexia. The disease may progress for upto 2 weeks. Usually fever is absent at the onset of paralysis.

Dysautonomic features may be present in the form of Brady or tachycardia and fluctuations in blood pressure. Objective sensory deficit and bladder involvement are uncommon. Respiratory paralysis may develop due to affection of the intercostals nerves.

Diagnosis

Any illness in which rapid or sub acute symmetrical polyneuropathy develops, should be suspected to be infective polyneuritis.

Differential Diagnosis

1. Poliomyelitis: Distinguished by an epidemic occurrence, meningeal symptoms, fever, purely motor and usually asymmetric, areflexic paralysis.

2. Acute Myelopathy: Marked by sensory motor paralysis below a given spinal level. Sphincteric paralysis may occur.

3. Acute Polyneuritis: Acute inflammation of several peripheral nerves simultaneously.

4. Transverse Myelitis: It is an acute inflammatory demyelinating disorder affecting the spinal cord over avariable number of segments. It presents with sub-acute paraparesis (Symmetrical partial paralysis of the lower limbs) with a sensory level.

5. Other demyelinating diseases:

6. Post Vaccinal Neuropathies

Investigations:

Blood count and blood chemistry are non contributory. C.S.F shows albuminocytological dissociation if examined a week after the onset of the disease. This abnormality may persist for a few weeks. The term albuminocytological dissociation refers to the rise in proteins without a corresponding rise in cell count. EMG and nerve conduction studies help to distinguish the condition from myopathies and poliomyelitis.

Nerve conduction velocities are slowed soon after the paralysis develops, sometimes more in proximal parts of the nerves (abnormal H and F responses) than distal.

Nerve Conduction Studies

1. The basic requirements for motor nerve conduction studies are that a suitable muscle nerve is available and that its nerve supply can be stimulated at 2 points along its course. The time taken from the stimulus nearest to the muscle is known as the distal latency and includes not only the time taken by the impulse to travel down the nerve, but also the delay at the end plate and initiation of contraction. If the nerve is then stimulated higher up, a second latency can be obtained; the difference in the time taken being an accurate measurement of the time taken for the impulse to traverse a measured length of nerve. From this the conduction velocity in meters per second is easily calculated. Very carefully documented velocity ranges for all the nerves that can be studied in this way have been reported. These are the median and ulnar nerves in the arm and peroneal and tibial nerves in the leg. Nerves such as the radial and femoral can only be readily stimulated at one point and latency to an appropriate muscle is all that can be measured.

In general if a muscle is denervated and it can be shown that the lesions responsible are above the proximal stimulus, it is probably affecting the nerve root or ventral Lorn cell.

2. Nerve action potentials can be measured in 2 ways, orthodromically or antidromically. Here the main requirement is a nerve near enough to the surface to be picked up by a surface electrode or anatomically constant in position allowing needle electrodes to be inserted near to the nerve. Both the medial and ulnar nerve action potentials can be detected at the wrist by stimulating the inter-digital nerves of the appropriate fingers.

3. In the case of ulnar nerve lesions at the elbow or the peroneal nerve at the fibula neck, due to compression some points do not demonstrate slowed conduction through the damaged area. A very useful ancillary test is the study of quantitative muscle action potentials.

Prognosis

In about 10% of the cases rapid on set and progress, respiratory failure may threaten life. Mortality is around 5%. Vast majority of patients start improving after a week or so of onset and recovery is complete within 6 weeks; in about 25% of cases resolution is slow. In a smaller number, severe paralysis may persist and the patients may become crippled for life. Presence of axonal degeneration and occurrence of the disease at the extremes of age are associated with bad prognosis.
 

Management 

During the period of progression the patient should be kept under close observation and respiratory failure should be managed with ventilator assistance. On recovery graded physiotherapy and rehabilitation should be started

Homoeopathic Management 

1.      Homoeopathic Medical Repertory by Robin Murphy 

Diseases GUILLAIN-barre syndrome- carc, con, lath, thuja

Nerves, CONDUCTION, nerves delayed- alum, cocc

Nerves GUILLAIN- barre syndrome- carc, con, lath, thuja

Legs PARALYSIS, legs- ARG-N, AGAR, ARS, CANN-I, CON, LATH, NUX-V, PLB, RHUST

2.      Repertory of Homoeopathic Materia Medica by J T Kent 

EXTREMITIES, PARALYSIS, ascending: ars, con, kali-c, agar, hydr-ac, mang

EXTREMITIES, PARALYSIS, lower limbs: agar, arg-n, cann-i, nux-v, plb, rhust

EXTREMITIES, WEAKNESS, lower limbs: aesc, Alum, arg-n, Ars, Aur, Calc, Carb-ac, Caust, cocc, con, gel, alon, Nat-C, mur-ac, Nux-v, Phos, pic-ac, plb, Rhust, sil, Zinc

3.    SYNTHESIS by Dr. Frederick Schroyens

EXTREMITIES, PARALYSIS, ascending

EXTREMITIES, PARALYSIS, lower limbs

EXTREMITIES, WEAKNESS, lower limbs

           GENERALS COMPLAINTS, nervous system

§  accompanied by: polyneuropathy-brass-n-o (brassica napus oleifera.)

Indications of some important medicines for ascending paralysis

1.   CONIUM: It is an excellent remedy for ascending paralysis. There may be difficult gait, trembling; sudden loss of strength while walking, painful stiffness of legs etc.There may be weakness of body and mind. Muscular weakness; especially of lower extremities. Putting feet on a chair relieves pain.

2.   LATHYRUS: Affects the lateral and posterior columns of the cord. Does not produce pain. Reflexes are always increased. Paralytic affections of lower extremities. After influenza and wasting, exhaustive diseases where there is much weakness and heaviness, slow recovery of nerve power. Tremulous, tottering gait. Excessive rigidity of legs. Spastic gait. Knees knock each other when walking. Cramps in legs aggravation cold. Cannot extend or cross legs when sitting. Gluteal muscles and lower limbs emaciated.

3.   PHOSPHOROUS: ascending sensory and motor paralysis from ends of fingers and toes. Burning of feet. Weakness and trembling from every exertion. Can scarcely hold anything with his hands. Arms and hands become numb. Can be only on right side. Post diphtheritic paralysis. Joints suddenly give way.

4.   THUJA: When walking, limbs feel as if made of wood or glass and would break easily. Muscular twitching, weakness and trembling. Cracking in the joints. Pain in heels and tendo-Achilles.

5.   CARCINOSIN: When apparently well indicated remedy fails to cure a case or produce a temporary amelioration carcinosin acts as complementary drug. Family history of cancer, Diabetes, syphilis or any other degenerative condition is traced, if symptoms agree carcinosin should be thought of.  Personal history of recurrent attack of bronchitis, pneumonia, wooping cough in childhood, even tendency to suffer repeatedly from measles, chicken pox, diphtheria, mumps, and tonsils in very early life is an indication for carcinosin. 

Craving or aversion to salt, sweet, milk, egg, meat, fat and fruits.

Great desire to lie on the chest or knee-elbow position.

Tendency to insomnia in children occurring in early age.

Mind: There may be a back ground of fright, prolonged fear or unhappiness. Mental troubles may originate from anticipation.

Mentally the patient is very intelligent and artistic or very dull and idiotic. Display of spontaneous sympathy to others (phos) . The child if reprimanded reacts either mentally or physically or through both.

6.    ALUMINA: Pain in arm and fingers, as if hot iron penetrated. Arms feel paralysed. Legs feel asleep, especially when sitting with legs crossed. Staggers on walking. Heels feel numb. Inability to walk, except when eyes are open or day time. Spinal degeneration and paralysis of limbs.

7.    ARS ALB: Trembling, twitching, spasms, weakness, heaviness and uneasiness of extremities. Cramps in calves. Burning pains. Paralysis of lower limbs with atrophy.

8.      CAUSTICUM: Paralysis of single parts. Heaviness and weakness. Unsteadiness of muscles of forearm and hand. Numbness and loss of sensation of hands. Contracted tendons, burning in joints. Slow learning to walk and unsteady walking and easy falling. Restless legs at night.

9.      COCCULUS: Trembling and pain in limbs, one side paralysis, < after sleep. Hands are alternately hot and cold; knees crack on motion, lower limbs very weak.

10.  GELSEMIUM: It causes motor paralysis. General prostration. Dizziness, drowsiness, dullness and trembling. Paralysis of various groups of muscles. Post diphtheritic paralysis. Muscular weakness. Lack of muscular co-ordination, fatigue after slight exercise.

REFERANCES:

1. Synthesis Repertory by Fredericke Schroyens

2. Homoeopathic medical repertory by Robin Murphy

3. Repertory of Homoeopathic Materia Medica by J T Kent.

4. Text book of medicine- K V Krishna Das

5. Harrison’s principles of internal medicine

6. Allen’s Key notes.

7. Boericke’s Materia Medica