Peptic Ulcer and Homeopathy Management

Dr Lizme Ajith

Peptic Ulcer Disease
Burning epigastric pain exacerbated by fasting and improved with meals is a symptom complex associated with peptic ulcer disease (PUD). An ulcer is defined as disruption of the mucosal integrity of the stomach and/or duodenum leading to a local defect or excavation due to active inflammation. Ulcers occur within the stomach and/or duodenum and are often chronic in nature.

Pathophysiologic Basis of Peptic Ulcer Disease

PUD encompasses both gastric and duodenal ulcers. Ulcers are defined as a break in the mucosal surface >5 mm in size, with depth to the submucosa. Duodenal (DU) and gastric ulcers (GU) share many common features in terms of pathogenesis, diagnosis, and treatment, but several factors distinguish them from one another.

Duodenal Ulcers DUs occur most often in the first portion of duodenum (>95%), with ~90% located within 3 cm of the pylorus. They are usually £1 cm in diameter but can occasionally reach 3 to 6 cm (giant ulcer). Ulcers are sharply demarcated, with depth at times reaching the muscularis propria. The base of the ulcer often consists of a zone of eosinophilic necrosis with surrounding fibrosis. Malignant duodenal ulcers are extremely rare.

Gastric Ulcers In contrast to DUs, GUs can represent a malignancy. Benign GUs are most often found distal to the junction between the antrum and the acid secretory mucosa. This junction is variable, but in general the antral mucosa extends about two thirds of the distance of the lesser curvature and one third the way up the greater curvature. Benign GUs are quite rare in the gastric fundus and are histologically similar to DUs. Benign GUs associated with H. pylori are associated with antral gastritis.

Clinical Features
History Abdominal pain is common to many gastrointestinal disorders, including DU and GU, but has a poor predictive value for the presence of either DU or GU. Up to 10% of patients with NSAID-induced mucosal disease can present with a complication (bleeding, perforation, and obstruction) without antecedent symptoms. Despite this poor correlation, a careful history and physical examination are essential components of the approach to a patient suspected of having peptic ulcers.

Epigastric pain described as a burning or gnawing discomfort can be present in both DU and GU. The discomfort is also described as an ill-defined, aching sensation or as hunger pain. The typical pain pattern in DU occurs 90 min to 3 h after a meal and is frequently relieved by antacids or food. Pain that awakes the patient from sleep (between midnight and 3 A.M.) is the most discriminating symptom, with two-thirds of DU patients describing this complaint. Unfortunately, this symptom is also present in one-third of patients with NUD. The pain pattern in GU patients may be different from that in DU patients, where discomfort may actually be precipitated by food. Nausea and weight loss occur more commonly in GU patients. In the United States, endoscopy detects ulcers in <30% of patients who have dyspepsia. Despite this, 40% of these individuals with typical ulcer symptoms had an ulcer crater, and 40% had gastroduodenitis on endoscopic examination.

The mechanism for development of abdominal pain in ulcer patients is unknown. Several possible explanations include acid-induced activation of chemical receptors in the duodenum, enhanced duodenal sensitivity to bile acids and pepsin, or altered gastroduodenal motility.

Physical Examination Epigastric tenderness is the most frequent finding in patients with GU or DU. Pain may be found to the right of the midline in 20% of patients. Unfortunately, the predictive value of this finding is rather low. Physical examination is critically important for discovering evidence of ulcer complication. Tachycardia and orthostasis suggest dehydration secondary to vomiting or active gastrointestinal blood loss. A severely tender, boardlike abdomen suggests a perforation. Presence of a succussion splash indicates retained fluid in the stomach, suggesting gastric outlet obstruction.

PUD-Related Complications
Gastrointestinal Bleeding Gastrointestinal bleeding is the most common complication observed in PUD. It occurs in ~15% of patients and more often in individuals >60 years old. The higher incidence in the elderly is likely due to the increased use of NSAIDs in this group. As many as 20% of patients with ulcer-related hemorrhage bleed without any preceding warning signs or symptoms.

Perforation The second most common ulcer-related complication is perforation, being reported in as many as 6 to 7% of PUD patients. As in the case of bleeding, the incidence of perforation in the elderly appears to be increasing secondary to increased use of NSAIDs. Penetration is a form of perforation in which the ulcer bed tunnels into an adjacent organ. DUs tend to penetrate posteriorly into the pancreas, leading to pancreatitis, whereas GUs tend to penetrate into the left hepatic lobe. Gastrocolic fistulas associated with GUs have also been described.

Gastric Outlet Obstruction Gastric outlet obstruction is the least common ulcer-related complication, occurring in 1 to 2% of patients. A patient may have relative obstruction secondary to ulcer-related inflammation and edema in the peripyloric region. This process often resolves with ulcer healing. A fixed, mechanical obstruction secondary to scar formation in the peripyloric areas is also possible. The latter requires endoscopic (balloon dilation) or surgical intervention. Signs and symptoms relative to mechanical obstruction may develop insidiously. New onset of early satiety, nausea, vomiting, increase of postprandial abdominal pain, and weight loss should make gastric outlet obstruction a possible diagnosis.

Recurrent Ulceration The risk of ulcer recurrence is directly related to the procedure performed. Ulcers that recur after partial gastric resection tend to develop at the anastomosis (stomal or marginal ulcer). Epigastric abdominal pain is the most frequent presenting complaint. Severity and duration of pain tend to be more progressive than observed with DUs before surgery.

Afferent Loop Syndromes Two types of afferent loop syndrome can occur in patients who have undergone partial gastric resection with Billroth II anastomosis. The most common of the two is bacterial overgrowth in the afferent limb secondary to stasis. Patients may experience postprandial abdominal pain, bloating, and diarrhea with concomitant malabsorption of fats and vitamin B12.

Maldigestion and Malabsorption Weight loss can be observed in up to 60% of patients after partial gastric resection. A significant component of this weight reduction is due to decreased oral intake. However, mild steatorrhea can also develop. Reasons for maldigestion/malabsorption include decreased gastric acid production, rapid gastric emptying, decreased food dispersion in the stomach, reduced luminal bile concentration, reduced pancreatic secretory response to feeding, and rapid intestinal transit.

Gastric Adenocarcinoma The incidence of adenocarcinoma in the gastric stump is increased 15 years after resection. Some have reported a four- to fivefold increase in gastric cancer 20 to 25 years after resection. The pathogenesis is unclear but may involve alkaline reflux, bacterial proliferation, or hypochlorhydria. Endoscopic screening every other year may detect surgically treatable disease.


The term gastritis should be reserved for histologically documented inflammation of the gastric mucosa. Gastritis is not the mucosal erythema seen during endoscopy and is not interchangeable with “dyspepsia.” The etiologic factors leading to gastritis are broad and heterogeneous. Gastritis has been classified based on time course (acute vs. chronic), histologic features, and anatomic distribution or proposed pathogenic mechanism.

Acute Gastritis The most common causes of acute gastritis are infectious. Acute infection with H. pylori induces gastritis. However, H. pylori acute gastritis has not been extensively studied. Reported as presenting with sudden onset of epigastric pain, nausea, and vomiting, limited mucosal histologic studies demonstrate a marked infiltrate of neutrophils with edema and hyperemia. If not treated, this picture will evolve into one of chronic gastritis. Hypochlorhydria lasting for up to 1 year may follow acute H. pylori infection.

The highly acidic gastric environment may be one reason why infectious processes of the stomach are rare. Bacterial infection of the stomach or phlegmonous gastritis is a rare potentially life-threatening disorder, characterized by marked and diffuse acute inflammatory infiltrates of the entire gastric wall, at times accompanied by necrosis. Elderly individuals, alcoholics, and AIDS patients may be affected. Potential iatrogenic causes include polypectomy and mucosal injection with India ink.

Chronic Gastritis Chronic gastritis is identified histologically by an inflammatory cell infiltrate consisting primarily of lymphocytes and plasma cells, with very scant neutrophil involvement. Distribution of the inflammation may be patchy, initially involving superficial and glandular portions of the gastric mucosa. This picture may progress to more severe glandular destruction, with atrophy and metaplasia. Chronic gastritis has been classified according to histologic characteristics. These include superficial atrophic changes and gastric atrophy.

The early phase of chronic gastritis is superficial gastritis. The inflammatory changes are limited to the lamina propria of the surface mucosa, with edema and cellular infiltrates separating intact gastric glands. Additional findings may include decreased mucus in the mucous cells and decreased mitotic figures in the glandular cells. The next stage is atrophic gastritis. The inflammatory infiltrate extends deeper into the mucosa, with progressive distortion and destruction of the glands. The final stage of chronic gastritis is gastric atrophy. Glandular structures are lost; there is a paucity of inflammatory infiltrates. Endoscopically the mucosa may be substantially thin, permitting clear visualization of the underlying blood vessels.

Gastric glands may undergo morphologic transformation in chronic gastritis. Intestinal metaplasia denotes the conversion of gastric glands to a small intestinal phenotype with small-bowel mucosal glands containing goblet cells. The metaplastic changes may vary in distribution from patchy to fairly extensive gastric involvement. Intestinal metaplasia is an important predisposing factor for gastric cancer.

Chronic gastritis is also classified according to the predominant site of involvement. Type A refers to the body-predominant form (autoimmune) and type B is the central-predominant form (H. pylori-related). This classification is artificial in view of the difficulty in distinguishing these two entities. The term AB gastritis has been used to refer to a mixed antral/body picture.

Type A Gastritis The less common of the two forms involves primarily the fundus and body, with antral sparing. Traditionally, this form of gastritis has been associated with pernicious anemia (Chap. 107) in the presence of circulating antibodies against parietal cells and intrinsic factor; thus it is also called autoimmune gastritis. H. pylori infection can lead to a similar distribution of gastritis. The characteristics of an autoimmune picture are not always present.

Antibodies to parietal cells have been detected in >90% of patients with pernicious anemia and in up to 50% of patients with type A gastritis. Anti-parietal cell antibodies are cytotoxic for gastric mucous cells. The parietal cell antibody is directed against H+,K+-ATPase. T cells are also implicated in the injury pattern of this form of gastritis.

Parietal cell antibodies and atrophic gastritis are observed in family members of patients with pernicious anemia. These antibodies are observed in up to 20% of individuals over age 60 and in ~20% of patients with vitiligo and Addison’s disease. About half of patients with pernicious anemia have antibodies to thyroid antigens, and about 30% of patients with thyroid disease have circulating anti-parietal cell antibodies. Anti-intrinsic factor antibodies are more specific than parietal cell antibodies for type A gastritis, being present in ~40% of patients with pernicious anemia. Another parameter consistent with this form of gastritis being autoimmune in origin is the higher incidence of specific familial histocompatibility haplotypes such as HLA-B8 and -DR3.

The parietal cell-containing gastric gland is preferentially targeted in this form of gastritis, and achlorhydria results. Parietal cells are the source of intrinsic factor, lack of which will lead to vitamin B12 deficiency and its sequelae (megaloblastic anemia, neurologic dysfunction).

Gastric acid plays an important role in feedback inhibition of gastrin release from G cells. Achlorhydria, coupled with relative sparing of the antral mucosa (site of G cells), leads to hypergastrinemia. Gastrin levels can be markedly elevated (>500 pg/mL) in patients with pernicious anemia. ECL cell hyperplasia with frank development of gastric carcinoid tumors may result from gastrin trophic effects. The role of gastrin in carcinoid development is confirmed by the observation that antrectomy leads to regression of these lesions. Hypergastrinemia and achlorhydria may also be seen in non-pernicious anemia-associated type A gastritis.

Type B gastritis Type B, or antral-predominant, gastritis is the more common form of chronic gastritis. H. pylori infection is the cause of this entity. Although described as “antral-predominant,” this is likely a misnomer in view of studies documenting the progression of the inflammatory process towards the body and fundus of infected individuals. The conversion to a pan-gastritis is time-dependent¾estimated to require 15 to 20 years. This form of gastritis increases with age, being present in up to 100% of people over age 70. Histology improves after H. pylori eradication. The number of H. pylori organisms decreases dramatically with progression to gastric atrophy, and the degree of inflammation correlates with the level of these organisms. Early on, with antral-predominant findings, the quantity of H. pylori is highest and a dense chronic inflammatory infiltrate of the lamina propria is noted accompanied by epithelial cell infiltration with polymorphonuclear leukocytes.

Multifocal atrophic gastritis, gastric atrophy with subsequent metaplasia, has been observed in chronic H. pylori-induced gastritis. This may ultimately lead to development of gastric adenocarcinoma. H. pylori infection is now considered an independent risk factor for gastric cancer. Worldwide epidemiologic studies have documented a higher incidence of H. pylori infection in patients with adenocarcinoma of the stomach as compared to control subjects. Seropositivity for H. pylori is associated with a three- to sixfold increased risk of gastric cancer. This risk may be as high as ninefold after adjusting for the inaccuracy of serologic testing in the elderly. The mechanism by which H. pylori infection leads to cancer is unknown. However, eradication of H. pylori as a general preventative measure for gastric cancer is not recommended.

Infection with H. pylori is also associated with development of a low grade B cell lymphoma, gastric MALT lymphoma. The chronic T cell stimulation caused by the infection leads to production of cytokines that promote the B cell tumor. Tumor growth remains dependent upon the presence of H. pylori in that its eradication is often associated with complete regression of the tumor. The tumor may take more than a year to regress after treating the infection. Such patients should be followed by EUS every 2 to 3 months. If the tumor is stable or decreasing in size, no other therapy is necessary. If the tumor grows, it may have become a high-grade B cell lymphoma. When the tumor becomes a high-grade aggressive lymphoma histologically, it loses responsiveness to H. pylori eradication.

Homoeopathic Therapeutics
Gnawing, hungry faint feeling at the epigastrium. Burning and distension of stomach with palpitation. Tendency to eat far beyond the capacity for digestion. Great appetite, craving for meat, pickles, radish, turnips, coarse food. Flatulence disturbs the heart’s action. Wants to lie down all the time.

Pain in stomach always comes on after eating. Sensation as if a hard boiled egg had lodged in the cardiac end of stomach. Great craving for food at noon and night. Dyspepsia of the aged, after tea or tobacco. Sour eructations.

Burning pains as of an ulcer. Cancer of stomach. Sour eructations. Vomits every kind of food. Heartburn and water brash. Hyperchlorhydria. Profuse salivation. Intense burning thirst. Haemorrhage from bowels. Great prostration. Pale, lean, emaciated persons.

Duodenal ulcer; All gone sensation when stomach is empty, > by eating, during the process of digestion. Apt to choke while eating and drinking. Swallows food and drink hastily. Ineffectual desire for stool, rectum seems to be plugged up. Sensation of a band or hoop around a part. Sudden loss of memory. Hypochondriac.

Ulceration of stomach with radiating pains. Gnawing, burning splinter like pains. Belching accompanies most gastric ailments. Nausea, retching, vomiting of glairy mucus. Flatulent dyspepsia, stomach distended as if it would burst with wind. Diarrhoea, green mucus like chopped spinach.< eating candy, sugar, sweets, icecreams. Diseases from unusual or long continued mental exertion.

Burning pains in abdomen, burns like fire, as if hot coals were applied to the parts. > by heat, hot drinks. Vomiting of bile, blood, brown black mucus mixed with blood. Gastralgia < at mid day and mid night. Cannot bear the smell or sight of food. Excessive thirst for warm drinks at short intervals. Diarrhoea, stool scanty, dark, offensive < after eating and drinking. Bad effects of decayed food or animal matter. Gastric derangements after fruits, ice creams, beer, strong cheese, alcohol. Fear, anxiety, restlessness. Prostration.

Chronic stomach affections. Paroxysms of gastric pains. Vomiting of all food. Hyperchlorhydrea. Pyrosis. Great dryness of throat, almost impossible to swallow.

Gastralgia, pain from stomach through to spine. Vomiting of water as soon as it reaches the stomach, food retained longer, of enormous quantities at intervals of several days when food has filled the stomach. Purging, offensive stools. Pressure in stomach as from a load in one spot, alternating with burning, pain crampy, spasmodic. Anguish, always desire company.

Acidity of the digestive tract, sour eructations, sour vomiting, sour stool, sour odour of the whole body. Ravenous hunger. Pit of stomach swollen like an inverted saucer, painful to pressure. Aversion to milk and meat, craving for eggs. Habitual constipation, stool has to be removed mechanically. Leucophlegmatic, fair, obese persons.

At every attempt to eat colicky pain in stomach. Heart burn. Much flatulence. Craving for bacon, ham, salted or smoked meat. Flatulence temporarily > by sour eructations. Easy vomiting. Green, hot, spluttering diarrhea. Sunken, flabby abdomen. Feeble digestion. anaemic, thin, spare subjects. Ailments from grief, disappointed love. Feels complaints more when thinking about them.

Burning and cutting pains in stomach. Carcinoma. Persistent vomiting, violent nausea, retching, vomiting of black, coffee ground matter, of blood. Severe prostration. Black offensive clots of blood from bowels. Chilliness and coldness.

Weak digestion, simplest food disagrees, excessive accumulation of gas in stomach and intestines ( upper abdomen), sensation as if abdomen would burst. Eructations give temporary relief. Haematemesis and malena. Bad effects of fatty food, pork, butter, late supper, debauch, salted meat, spoiled fish or meat. Frequent involuntary cadaverous smelling stools. Carcinoma of stomach, late stages of disease. Complaints from loss of vital fluids, broken down constitution.

Hyperacidity, vomiting of undigested food. Hungry with out appetite. Excessive flatulence of stomach and bowels ( lower abdomen ), fermentation, belching gives no relief. Colic at a certain hour, each day, periodical. < night, eating fruits, touch. > hard pressure, bending double. Diarrhoea painless at night, undigested food particles. Haematemesis and malena. Haemorrhage long continued. Ulcers with persistent suppuration. Longing for sour things. Broken down constitution, loss of vital fluids.

Gastric ulcer, carcinoma of stomach. Constant burning pains. Vomiting of food, burning behind sternum, where food seems to stick. Stricture of oesophagus. Chronic gastric catarrh. Painful cracks at corners of mouth.

Gastric ulcer, cancer of stomach. Vomiting of bloody slimy mucus. Black or coffee ground vomiting. Violent vomiting of food. Haematemesis and malena. Chronic alcoholism. Intolerance of clothing around stomach. Diarrhoea, stool black, offensive, like coffee grounds. Black, dark, fluid, non coagulable blood. Tongue fiery red, smooth and polished. Prostration, broken down constitution.

Terrible pains in stomach. Sharp, piercing and pricking pains. Increased appetite followed by loathing of food. Feeling of warmth in stomach

Catarrhal gastritis with profuse secretion, tendency to ulceration and passive haemorrhage. Lessens the vomiting in gastric ulcer. Vomiting of blood. Atonic, foul ulcers. Constant desire to go to stool, with inability to pass anything for sometime.

Duodenal ulcer; Pain in abdomen temporarily relieved after eating, drinking hot milk. Aversion to meat, fish, salt, cooked food and sweets. Chronic constipation, stool hard knotty with lumps united by mucus threads. Women inclined to obesity, delayed menstruation, at climacteric.

Gastric ulcer, gastric pains associated with splenic congestion. Nausea and retching. Hyperchlorhydria. Hyperaemia of gastric mucus membrane. Dullness and pain in left hypochondrium. Paresis of pneumogastric. Gastritis with asthmatic symptoms. Smothering when falling asleep.

Gastroduodenal catarrh. Carcinoma of stomach. Cachetic or malignant dyscrasia. Ulcerations, profuse discharge of thick yellow stringy mucus. Atonic dyspepsia, cannot eat bread or vegetables. Chronic constipation. Enlarged liver, jaundice. Cancer pains. Broken down by excessive use of alcohol. Old debilitated persons.

Duodenal ulcer; Ravenous hunger ,must eat every few hours, feels ameliorated while eating or after eating. Empty eructations, as if every particle of food was turned in to air. Constipation > by drinking cold milk. Emaciation, loosing flesh while eating well. Scrofulous diathesis.

Hyperacidity, burning of the whole alimentary canal. Vomiting sour, bloody, biliary. Nausea, profuse salivation. Deficient appetite. Diarrhoea stools watery with burning of anus.

Gastric ulcer ; punched out or round ulcer of stomach. Pain immediately after eating. Pain in small spots, can be covered with the point of finger; appears and disappears suddenly, rapidly shifting. Neuralgia every day at the same hour. Weight in pit of stomach, flatulence, vomiting of stringy, ropy mucus and blood. Loss of appetite.

Gastric ulcers; Carcinoma of stomach. Vomiting of food several hours after eating, vomiting of sweetish water with ptyalism. Haematemesis and malena. Flow passive, dark, oozing. Diarrhoea offensive, dark brown, bloody stools. Corrossive fetid ichorous discharges from mucus membranes.

Canine hunger, the more he eats, the more he craves, wakes up at night feeling hungry. Excessive accumulation of flatulence, especially in lower abdomen. Good appetite, but a few mouth ful fills up to the throat. Everything tastes sour. Heartburn, sour vomiting. Constipation with ineffectual urging. Prefers warm food and drinks. Very sensitive, cannot endure opposition. Avaricious, irritable, cross.

Excessive acidity, sour eructations, sour vomiting, spits mouth fuls of food. Gastritis. Flatulence. Yellow creamy coating at the back part of tongue and roof of mouth.

Gastric ulcer; Pain in stomach while or immediately after eating. Eating a little too much causes headache. Abdomen enormously distended after every meal. Flatulent dyspepsia. Diarrhoea, stool white, fetid. Great dryness of mouth without thirst. Women, hysterical temperament, drowsiness, sleepiness, inclination to faint.

Gastric ulcer; Pain or pressure in stomach an hour or two after eating as from a stone. Nausea constant, after eating, ineffectual desire to vomit, feels if I could only vomit, I would be much better. Alternate constipation and diarrhea. Frequent ineffectual desire for stool. Sour bitter eructations. Bad effects of coffee, tobacco, alcohol, highly spiced food, over eating, long continued mental exertion, sedentary habits, anxiety, worry. Literary, studious, responsible persons.

Gastric ulcer, carcinoma of stomach and caecum. Haematemesis and malena. Vomiting of coffee ground matter. Pains increased when food passes pyloric outlet. Frequent belching of offensive flatus. Flatus rolls in balls from one side to another. Loss of appetite, phlegmy retchings, loss of flesh.

Duodenal ulcer; Ravenous hunger, must rise at night to eat. Pain abdomen > by constant eating <empty stomach, eating cabbage. Heartburn, nausea. Diarrhoea only in day time. Symptoms appear and disappear suddenly.

Burning pains in stomach > by cold drinks, ice creams, juicy refreshing things. A weak empty all gone sensation in entire abdomen.Vomiting, water is thrown up as soon as it gets warm in stomach. Vomiting of blood. Carcinoma of stomach. Bleeding ulcers, frequent, profuse. Discharge of blood from rectum during stool. Diarrhoea, stool involuntary, watery, sago like particles, coffee ground.

Pain in stomach an hour after eating. Pain with chilliness, rapidly shifting, appear suddenly, goes gradually. Vomiting of food eaten long before. Eructations, taste of food remains a long time. All gone sensation in tea drinkers. Complaints from eating rich food, cake, pork, sausage. Thirstlessness with dry mouth and tongue. Diarrhoea only at night, greenish yellow, very changeable.

Hyperchlorhydria. Nausea, sour eructations. Profuse vomiting of an intensely sour fluid. Great distension of stomach and bowels. Flatulent colic. Sour stools. Nightly burning pains in stomach. Acidity accompanied by frontal headache.

Burning pains in stomach < at night, warm food and drinks. Weak empty all gone sensation at about 11 am > by eating, cannot wait for lunch. Acidity, sour eructations. Desire for sweets. Diarrhoea, driving out of bed early in the morning. Constipation, stools hard, dry as if burnt, painful. Redness of external orifices. Chronic alcoholism. Nervous temperament, scrofulous diathesis.

Hyperacidity, heartburn, sour eructations, sets teeth on edge. Sour vomiting. Haemorrhage of black blood from bowels. Ulcers bleed easily. Water causes coldness of stomach, must be mixed with alcohol. Pains come gradually and goes suddenly. Tremor and weakness.

Gastric and duodenal ulcers. Gastralgia. Stimulates the growth of epithelium on ulcerated surfaces.

Gastric and duodenal ulcers. Ravenous appetite, eating followed by flatulence. Boring pain in pyloric region. Excessive thirst, nausea, vomiting. Burning pains. Abdomen distended. Great emaciation, debility. Diabetes, ascites, nephritis, hypertension, degeneration of liver.

Dr Lizme Ajith MD(Hom)
Dept. Practice of Medicine
Govt. Homeopathic Medical College. Calicut. Kerala


  1. Nux MOschata,nervous hysterical state of mind irritated nervous system affects heart palpitation and cause circulation congestion here there affects digestion as bloated abdomen,has symptoms dry mouth dry eyes sleepy stupor type will find such cases in offices due to such nervous weakness they half sleep with head on table equal to as old man wants sleep in day time,clinical some symptoms match with catalepsy,charges nerves removes drowsy state probably sister concern of cocculus which has added nausea dizziness has to sit down symptoms.

  2. All medicines are very well described for stomach ulcer
    Very good article about stomach
    Homeopathy has wide variety of medicine to treat symptoms.

Leave a Reply

Your email address will not be published.