
Abstract
GUILLAIN-BARRE SYNDROME Guillain-Barré syndrome (GBS) is an acute, frequently severe, and fulminant polyradiculoneuropathy that is autoimmune in nature. It occurs year-round at a rate of about one case per million per month, or approximately 3500 cases per year in the United States and Canada. Males and females are equally at risk, and in western countries adults are more frequently affected than children.
GBS is the most important cause of sudden weakness affecting all four limbs in a previously healthy individual.
Features which make the diagnosis most likely are
- Symmetric disease involving proximal and distal muscles; proximal muscles may be more affected.
- Motor affection more than sensory. Areflexia even when power is not fully lost.
- Cranial nerve affection (in 25% of cases). The commonest involvement is bilateral facial and then bulbar muscles. The patient has difficulty in swallowing, speech, etc.
- Autonomic involvement characterized by postural hypotension, episodes of hypotension, or hypertension, and tachycardia. These are seen frequently.
- CSF shows albuminocytologic dissociation, i.e., increased proteins with normal cells. Very early in the disease CSF may be normal. The albuminocytologic dissociation is more frequently seen if CSF examination is repeated. CSF pleocytosis with cells above 50/ cmm is against the diagnosis of GBS.
- Other causes such as porphyria, post exanthematous, post anti-rabies vaccine, etc. have to be excluded.
- Nerve conduction studies in GBS show demyelination characterized by slow nerve conduction, slowing of distal latency and conduction block. These findings may be seen in only proximal parts of nerves and may require special tests.
Pathophysiology
GBS is considered to be an autoimmune disease triggered by a preceding bacterial or I viral infection. It has been recognized that glycolipids, par} ticularly gangliosides, are immune targets in the subtypes of GBS. Different gangliosides predominate in different locations in peripheral nerves and in different nerve fiber types. Presents the pathology and pathogenesis of the four axonal subtypes of GBS.!° The muscle innervated by the damaged peripheral nerves undergoes denervation and atrophy. If the cell body survives, regeneration of the peripheral nerve takes place and recovery of function is likely.If the cell body dies from intense root involvement in the inflammatory degenerative process, no regeneration is pos. sible. Collateral reinnervation from surviving axons and regenerating axons may take place. In this case, motor recovery is less complete and residual deficits persist.

CLINICAL MANIFESTATIONS
Clinical manifestations may vary depending on subtype. Typical first manifestations are numbness, pain, paraesthesias, or weakness in the limbs. Motor signs manifest as an acute or subacute progressive paralysis. Proximal muscles may be involved earlier and more significantly than distal muscles. The paresis/ paralysis may be present in an ascending pattern involving limbs, respiratory muscles, and bulbar muscles. Only bulbar muscles may be involved, resulting in dysphagia and dysarthria. Weakness usually plateaus or improves by the fourth week in 90% of cases. After weakness plateaus, strength improves over a period of days to months, with the majority of individuals reaching activity levels similar to their predisease state. If sensory symptoms are present in the subtype they may include paresthesias/dysthesias (tingling, burning, shocklike sensations, particularly in the limbs), pain (throbbing, aching, particularly in the lower back, buttocks and legs), and numbness. Position and vibratory sensations are more affected than superficial sensation. Respiratory muscle weakness leads to the need for ventilatory support in 10% to 30% of individuals, Cranial nerve weakness manifests as facial weakness and bulbar weakness involving chewing, swallowing, and cough,
Autonomic dysfunction may manifest as tachycardia or, less frequently, bradycardia; hypotension or hypertension; and loss of or significant increase in sweating in those more severely affected. Persons may undergo respiratory arrest or cardiovascular collapse. Hyponatremia caused by the syndrome of inappropriate antiduretic hormone (SIADH) is common, especially in ventilated individuals.
Treatment
The cornerstone of therapy is nursing care of the paralysed patient, looking after the skin, preventing contractures, stretching and keeping up nutrition. Steroids do not reduce the duration but can increase the risk of infection and worsen the problem. Steroids should be considered contraindicated in the treatment of GBS. The treatments known to reduce the duration of illness are plasmapheresis and IV immunoglobulins. Plasmapheresis not only reduces the duration of the illness but even on follow up after 1 year plasmapheresis treated patients are better than non-treated cases. So, whereas originally it was felt that plasmapheresis should be used only in seriously ill cases it is now believed that any patient, as soon as he loses the ability to walk unaided or shows early bulbar affection, should receive plasmapheresis. About 2000 ml plasma is removed at a time and replaced with albumin (or plasma). Up to 5-6 sittings on alternate days (total 200-250 ml/kg) are advocated. Plasmapheresis should be started within the first 2 weeks. . IV immunoglobulin at 0.4 g/kg daily for 5 days appears to be as effective as plasmapheresis in the short and long term. However IV 1 g in India would cost Rs 60,000-80,000 in an adult while plasmapharesis requires a filter of Rs 10,000 and perhaps Rs 10,000-15,000 for the plasmapheresis. The other major part of treatment in GBS is ventilatory support. It is very important to use the ventilator at an apropropriate time. Indications for the ventilator support are.
- Unexplained tachycardia
- Unexplained sweating
- Fall in single breath count below 10 and
- Paradoxical respiration.
The blood gases alone should not be relied upon as the indicator for ventilatory support. Ventilatory support may be required for 2-6 weeks or longer. Plasmapheresis and IV immunoglobulin have been shown to reduce the duration of ventilator therapy.
SOME LESSER KNOWN HOMEOPATHIC MEDICINES IN THE MANAGEMENT OF GBS
VIPERA BERUS
Viper poisoning causes a temporary increase in reflexes, paresis supervenes, a paraplegia of the lower extremities extending upwards. Resembles acute ascending paralysis of Landry (Wells). Has special action on kidneys and induces hćmaturia. Cardiac dropsy.Indicated in inflammation of veins with great swelling; bursting sensation. Enlargement of liver. Ailments of menopause. Śdema of glottis. Poly-neuritis, polio-myelitis.
Extremities.–Patient is obliged to keep the extremities elevated. When they are allowed to hang down, it seems as if they would burst, and the pain is unbearable (Diad). Varicose veins and acute phlebitis. Veins swollen, sensitive; bursting pain. Severe cramps in lower extremities.
SULFONALUM
Vertigo of cerebral origin, cerebellar disease, ataxic symptoms and chorea, present a field for the homeopathic employment of this drug. Profound weakness, gone, faint feeling, and despondency. Loss of control of sphincter. Muscular inco-ordination
Mind.–Mental confusion, incoherency, illusions; apathetic. Alternation of happy, hopeful states with depression and weakness. Extreme irritability.Head.–Dropsy, stupid; pain on attempting to raise head. Double vision; heavy look about eyes; tinnitus, aphasia; tongue as if paralyzed. Eyes bloodshot and restless. Vertigo, unable to rise. Double vision; ptosis; tinnitus; dysphagia, difficult speech.
Extremities.–Ataxic movements, staggering gait; cold, weak, trembling; legs seem too heavy. Extreme restlessness; muscular twitchings. Knee-jerks disappear. Stiffness and paralysis of both legs. Anaesthesia of legs.
Sleep.–Fidgety, wakeful, drowsy. Insomnia.
THALLIUM METALLICUM
Most horrible neuralgic, spasmodic, shooting pains. Muscular atrophy. Tremors. Relieves the violent pains in locomotor ataxia. Paralysis of lower limbs.Paraplegia
Extremities.–Trembling. Paralytic feeling. Lancinating pains, like electric shocks. Very tired. Chronic myelitis. Numbness in fingers and toes, with extension up lower extremities, involving lower abdomen and perineum. Paralysis of lower limbs. Cyanosis of extremities. Formication, beginning in fingers and extending through pelvis, perineum and inner thighs to feet
LATHYRUS SATIVUS
Affects the lateral and anterior columns of the cord. Does not produce pain. Reflexes always increased. Paralytic affections of lower extremities; spastic paralysis; lateral sclerosis; Beri-beri. Athetosis. Infantile paralysis. After influenza and wasting, exhaustive diseases where there is much weakness and heaviness, slow recovery of nerve power. Sleepy, constant yawning.
Extremities.–Tips of fingers numb. Tremulous, tottering gait. Excessive rigidity of legs; spastic gait. Knees knock against each other when walking. Cramps in legs worse cold, and cold feet. Cannot extend or cross legs when sitting. Myelitis, with marked spastic symptoms. Rheumatic paralysis. Gluteal muscles and lower limbs emaciated. Legs blue; swollen, if hanging down.
Stiffness and lameness of ankles and knees, toe do not leave the floor, heels do not touch floor, Muscles of calves very tense. Patient sits bent forward, straightens with difficulty.
SARCOLACTICUM ACIDUM
Is apparently formed in muscle tissue during the stage of muscle exhaustion. Differs from ordinary Lactic acid in its relation to polarized light. It represents a much broader and more profoundly acting drug and its pathogenesis is quite dissimilar from the normal acid. Proved by Wm. B. Griggs, M. D, who found it of great value in the most violent form of Epidemic influenza, especially with violent and retching and greatest prostration, when Arsenic had failed. Spinal neurasthenia, muscular weakness, dyspnśa with myocardial weakness.
General Symptoms.–Tired feeling with muscular prostration, worse any exertion. Sore feeling all over, worse in afternoon. Restless at night. Difficulty in getting to sleep. Tired feeling in morning on getting up.
Back and Extremities.–Tired feeling in back and neck and shoulders. Paralytic weakness. Wrist tires easily from writing. Extreme weakness from climbing stairs. Stiffness of thigh and calves. Arms feel as if no strength in them. Cramp in the calves.
Some Other Medicines for GBS
- MEPHITIS PUTORIUS
- ARANEA IXABOLA
- MANGANUM ACETICUM
- PILOCYBE CERULEACENS
- ARSENIC
- ALUMINA
- CIMICIFUGA RACEMOSA
- PLUMBUM MET
- LYSSINUM
- MANDRAGORA OFFICINARUM
References
- Textbook of API.
- Golwala Medicine for students.
- Harrison’s principles of internal medicine.
- Http://www.wikipedia.org
Dr Sweety Vyas1, Dr Komal Sharma2
- Asso. Professor, Dept. of Practice of Medicine, Shree Shamalaji Homoeopathic Medical College, Godhra.
- Asst. Prof. Dept. of PSM, Shree Shamalaji Homoeopathic Medical College, Godhra.