The infant presents with acute GEA without signs of alarm or severe dehydration. The first step would be to try oral tolerance with oral rehydration saline and continue with normal feeding if well tolerated. Answer 1 may give rise to doubts, due to the fact that the statement says that the patient "does not tolerate the oral route". In this case, intravenous rehydration could be started... but it would not be advisable to leave the patient on an absolute diet for 8 hours, nor a subsequent astringent diet, so I prefer answer 2. The rest of the treatments do not provide any benefit.

The infant presents with acute GEA without signs of alarm or severe dehydration. The first step would be to try oral tolerance with oral rehydration saline and continue with normal feeding if well tolerated. Answer 1 may give rise to doubts, due to the fact that the statement says that the patient "does not tolerate the oral route". In this case, intravenous rehydration could be started... but it would not be advisable to leave the patient on an absolute diet for 8 hours, nor a subsequent astringent diet, so I prefer [HIDDEN]. The rest of the treatments do not provide any benefit.

Previously healthy 10-month-old infant with acute gastroenteritis of one day's evolution and signs of mild dehydration, without blood or mucus in the stool and without oral tolerance. What is the initial treatment of choice in our environment?

Intravenous rehydration, absolute diet 8 hours and start feeding with astringent diet.

Rehydration with low osmolality oral rehydration solution (sodium 60-75 mEq/L) and continue with his usual diet.

Rehydration with low osmolality oral rehydration solution (sodium 60-75 mEq/L) maintain usual feeding and oral amoxicillin 10 days.

Rehydration with low osmolality oral rehydration solution (sodium 60-75 mEq/L) and start feeding with lactose-free formulas.

Rehydration with low osmolality oral rehydration solution (sodium 60-75 mEq/L) maintain usual feeding and loperamide 7 days.

[Comparative study of 2 oral rehydration solutions containing 60 or 90 mmol/L of sodium and with different osmolalities].

A total of 186 infants, suffering from acute diarrhea were studied and divided into two groups: 84 children were placed in group A and given the ORS recommended by the World Health Organization which contains sodium and glucose at concentrations of 60 and 90 mmol/L respectively and an osmolality of 311 mOsm/kg (mmol/kg) (ORS-90). Group B included 82 children who received an ORS containing sodium and glucose at concentrations of 60 and 90 mmol/L respectively and with an osmolality of 240 mOsm/kg (mmol/kg) (ORS-60). Seven belonging to group A (8.3%) required intravenous rehydration due to the severity of the diarrhea (three cases), persistent vomiting (three cases) and paralytic ileus (one case), while only two cases belonging to group B (2.5%) required intravenous rehydration due to severe losses through feces (one case) and another due to paralytic ileus (one case). No differences were observed due to the variations in sodium concentrations among either of the groups of patients, whether that be in the natremias when admitted or once rehydrated, with a general tendency towards the correction of the hypernatremia or hyponatremia seen during admittance with both types of ORS. A similar situation was observed with the variations in serum potassium. The results obtained from this study show the different advantages of using an ORS with lesser sodium and glucose concentrations as well as minor osmolality with those from using the solution recommended by the World Health Organization, when a lesser index of failures is observed in the treatment of children with acute diarrhea with oral rehydration therapy. Yet before widely recommending its' use, it should be demonstrated that the new ORS induces lesser losses through feces during the rehydrating period in children dehydrated due to acute diarrhea.

Comparison of two oral rehydration solutions in children with gastroenteritis in Australia.

An open-label inpatient study is in progress to compare the efficacy and safety of two oral rehydration solutions in children and infants with acute diarrhea and mild to moderate dehydration. One solution (ORS-60) contains 60 mmol/L of sodium and 1.8% glucose, with a total osmolality of 240 mosm/kg; the other (ORS-26) contains 26 mmol/L of sodium, 2.7% glucose, and 3.6% sucrose, with a total osmolality of 340 mosm/kg. An outcome analysis of 28 children with gastroenteritis indicated that ORS-60 (n = 13) reduced stool volume during the first eight hours after admission to a significantly greater (P less than 0.05) extent than did ORS-26 (n = 15). Diarrhea had ceased by 24 hours in 64% of ORS-60 patients but in only 31% of ORS-26 patients, and the patients' clinical condition was improved at eight hours in 84% of ORS-60 patients versus 60% of ORS-26 patients. Differences between treatments in degree of dehydration at each follow-up point, total duration of diarrhea, and duration of hospital stay were not detected. No adverse drug reactions occurred. Four patients received intravenous rehydration therapy, but none was considered a treatment failure. We conclude that the lower osmolar solution, ORS-60, conferred earlier recovery and reduced continuing fluid losses in the management of gastroenteritis.

[Oral hydratation with a low osmolality solution in dehydrated children with diarrheic diseases: controlled clinical trial].

A clinical trial was conducted to compare the efficacy of a low-osmolarity solution (245 mOsm/L), and a standard oral rehydration solution (ORS) recommended by WHO for children dehydrated by diarrhea. Group 1 (69 children) received WHO/ORS (311 mOsml/L) and group 2 (71 children) received a low-osmolarity solution (245 mOsm/L). Rehydration was successful in 88.4% in group 1 and 92.9% in group 2 (p = 0.35). Rehydration was completed in 5.2 h (SD +/- 1.8) in group 1 and 5.5 (SD +/- 1.7) in group 2 (p = 0.31). Stool output was 6.3 g/kg/h (SD +/- 5.0) in group 1 and 5.6 g/kg/h (SD +/- 5.1) in group 2 (p = 0.94). Sodium at rehydration-completion was 139.3 mEq/L (SD +/- 7.1) in group 1 and 136.7 mEq/L (SD +/- 4.3) in group 2 (p = 0.014). Group 1 was under observation for 21 hours (SD +/- 5.7) and group 2, for 22 hours (SD +/- 5.6). Stool output in group 1 was 5.2 g/kg/h (SD 4.1) and 4.2 gr./kg/h (SD +/- 4.1) in group 2 (p = 0.16). In group 1, 23.1% required intravenous solutions and 9.8% in group 2 (p = 0.03). In treating dehydrated children, the low-osmolarity solution diminished the need for intravenous solutions, corrected most plasmatic sodium disorders, and produced no-risk of developing hyponatremia.

Oral rehydration therapy

An exception is if the severely malnourished child also has severe diarrhea (in which case ReSoMal may not provide enough sodium), in which case standard reduced-osmolarity ORS (75 mmol sodium/L) is recommended. Malnourished children should be rehydrated slowly. The WHO recommends 10 milliliters of ReSoMal per kilogram body weight for each of the first two hours (for example, a 9-kilogram child should be given 90 ml of ReSoMal over the course of the first hour, and another 90 ml for the second hour) and then continuing at this same rate or slower based on the child's thirst and ongoing stool losses, keeping in mind that a severely dehydrated child may be lethargic. If the child drinks poorly, a nasogastric tube should be used. The IV route should not be used for rehydration except in cases of shock and then only with care, infusing slowly to avoid flooding the circulation and overloading the heart.

[Oral rehydration solutions with 60 or 90 nmol/L of sodium for infants with acute diarrhea in accord with their nutritional status].

A total of 186 infants suffering from dehydration due to acute diarrhea were studied and divided into two groups: 84 children were placed in group A and received the oral rehydration solution (ORS) recommended by the World Health Organization (WHO), know as ORS-90 and those placed in group B were given an ORS with 60 and 90 mmol/L of sodium and glucose, respectively, with an osmolality of 240 mOsm/kg (ORS-60). Seven patients from group A (8.3%) and two from group B (2.5%) could not be orally rehydrated and required intravenous rehydration. The children were divided according to their weight for their age into eutrophics, grade I malnutrition (10 to 25% deficit), grade II (26 to 40% deficit) and grade III (more than 40% deficit). In those patients who evolved favorably, the average rehydration time was 4.5 to 5.3 hours, independently from their nutritional state. In the same way, no important variations were seen in the average sodium and potassium serum levels once the dehydration was corrected, in either of the groups. Yet, both groups showed a persistence in hypokalemia and hyperkalemia seen when admitted, once the dehydration was corrected, demonstrating that the short time needed for the correction of the dehydration was insufficient to completely corrected the changes in serum potassium. Closer studies must be conducted on the hydric balance to adequately demonstrate if the new ORS-60 induces lesser losses through vomiting and feces when compared to the ORS-90 recommended by the WHO.

A double-blind clinical trial comparing World Health Organization oral rehydration solution with a reduced osmolarity solution containing equal amounts of sodium and glucose.

To compare the safety and efficacy of an oral rehydration solution (ORS) containing 75 mmol/L of sodium and glucose each with the standard World Health Organization (WHO) ORS among Egyptian children with acute diarrhea. One hundred ninety boys, aged 1 to 24 months, who were admitted to the hospital with acute diarrhea and signs of dehydration were randomly assigned to receive either standard ORS (311 mmol/L) or a reduced osmolarity ORS (245 mmol/L). Intake and output were measured every 3 hours. In the group treated with reduced osmolarity ORS, the mean stool output during the rehydration phase was 36% lower (95% confidence interval, 1%, 100%) than in those treated with WHO ORS. The relative risk of vomiting during the rehydration phase was significantly lower in children treated with reduced osmolarity ORS (relative risk, 2.4; 95% confidence interval, 1.2, 4.8). During the maintenance phase, stool output, mean intake of food and ORS, duration of diarrhea, and weight gain were similar in the treatment groups. The relative risk of treatment failure (need for unscheduled administration of intravenous fluids) was significantly increased in children receiving standard WHO ORS (relative risk, 7.9; 95% confidence interval, 1.1, 60.9). The mean serum sodium concentration at 24 hours was significantly lower in children receiving the reduced osmolarity ORS solution (134 +/- 6 mEq/L) than in children receiving the standard WHO ORS (138 +/- 7 mEq/L) (p < 0.001). The relative risk of the development or worsening of hyponatremia was not increased in children given the reduced osmolarity ORS, and urine output was similar in the treatment groups. The reduced osmolarity ORS has beneficial effects on the clinical course of acute diarrhea in children by reducing stool output, and the proportion of children with vomiting during the rehydration phase, and by reducing the need for supplemental intravenous therapy. These results provide support for the use of a reduced osmolarity ORS in children with acute noncholera diarrhea.

Oral rehydration therapy

Oral therapy was developed in the 1940s using electrolyte solutions with or without glucose on an empirical basis chiefly for mild or convalescent patients, but did not come into common use for rehydration and maintenance therapy until after the discovery that glucose promoted sodium and water absorption during cholera in the 1960s. It is on the World Health Organization's List of Essential Medicines. Globally, , oral rehydration therapy is used by 41% of children with diarrhea. This use has played an important role in reducing the number of deaths in children under the age of five. Medical uses ORT is less invasive than the other strategies for fluid replacement, specifically intravenous (IV) fluid replacement. Mild to moderate dehydration in children seen in an emergency department is best treated with ORT. Persons taking ORT should eat within six hours and return to their full diet within 24–48 hours.

Clinical experience in Mexico with a new oral rehydration solution with lower osmolality.

A clinical trial was conducted to compare the safety and efficacy of a new oral rehydration solution (ORS) with that of the ORS recommended by the World Health Organization (WHO). One hundred thirty infants with dehydration due to acute diarrhea were randomized into two groups: 68 infants received the WHO ORS containing sodium and glucose in a concentration of 90 and 111 mmol/L, respectively, and an osmolality of 311 mosm/kg (ORS-90); 62 infants received an ORS containing sodium and glucose in a concentration of 60 and 90 mmol/L, respectively, with an osmolality of 240 mosm/kg (ORS-60). Treatment failure was noted in seven infants (10.3%) in the ORS-90 group; the causes of failure were high stool output (three cases), persistent vomiting (three cases), and ileus (one case). Only one patient in the ORS-60 group (1.6%) was considered a failure because of high stool output. No significant differences were noted in the serum sodium levels in either group of patients, both in relation to the natremia seen on admittance or that seen after rehydration. A trend was observed toward correction of hypernatremia or hyponatremia with both types of ORS. A similar situation was observed with respect to the variations seen in serum potassium levels. The results from this study suggest that there may be clinical advantages of using an ORS with concentrations of sodium and glucose and a total osmolality lower than that of ORS-90, because of the lower incidence of treatment failures.

Use of a single solution for oral rehydration and maintenance therapy of infants with diarrhea and mild to moderate dehydration.

To compare the efficacy of two commonly used solutions in the rehydration of infants with mild to moderate dehydration caused by acute diarrhea in the United States. Double-blind, parallel-group, randomized study performed at Children's Hospital Medical Center. Sixty infant boys (< or = 2 years old), with mild (< or = 5%) or moderate (6 to 9%) dehydration caused by acute diarrhea of less than 1 week's duration were included in the study. Infants were randomly assigned to receive treatment with either a glucose-based oral rehydration solution (ORS) (Pedialyte, Ross Laboratories, Columbus, OH) or a rice syrup solids-based ORS (Infalyte, Mead Johnson Nutritional Group, Evansville, IN). After rehydration was achieved, patients entered a maintenance phase during which, in addition to a maintenance ORS, breast milk or a soy-based formula was offered; infants older than 1 year were also given a lactose-free diet. Rehydration was judged clinically. Infants remained on a metabolic bed during the study in to separate and quantitate urine and stool output. Therefore, in addition to clinical outcome, we compared intake, output and apparent absorption and retention of fluid, sodium, and potassium between groups. All patients were successfully rehydrated using an ORS without the use of intravenous fluids. No differences were detected between treatment groups in time to rehydration, percentage of weight gain after rehydration, consumption of ORS to achieve rehydration, or stool output. However, the apparent sodium absorption (net intake less fecal output) was greater in the Infalyte group than the Pedialyte group during the first 24 hours. The two maintenance oral electrolyte solutions (Pedialyte and Infalyte) most commonly used in the United States are effective as rehydration solutions for infants with mild to moderate dehydration. We speculate that a strategy for oral rehydration therapy in the United States, based on the use of a single solution during the rehydration and maintenance phase, might gain additional acceptance by practicing pediatricians and family physicians.

Evaluation of an oral rehydration solution with Na+ 60 mmol/l in infants hospitalized for acute diarrhoea or treated as outpatients.

An oral rehydration solution (ORS) containing 60 mmol/l of Na+ (ORS60) was compared in a randomized trial with the ORS of WHO formula (Na+ 90 mmol/l = ORS90) for the treatment of diarrhoeal dehydration in 66 hospitalized infants aged 3 to 34 months. The infants had a 5 +/- 3% dehydration, and received within 6-10 hours 76 +/- 32 ml/kg of ORS60 or 74 +/- 41 ml/kg of ORS90 corresponding to a sodium input of 4.6 +/- 1.9 mmol/kg and 6.6 +/- 3.7 mmol/kg, respectively. Both treatments were found adequate and equally effective for the correction of dehydration and sodium deficit. The same ORS60 was also compared to a commercial low sodium glucose-electrolyte solution (sodium 35 mmol/l, glucose 3.5 milligrams) for ambulatory treatment of acute diarrhoea in infants. Satisfactory rehydration was achieved within 6 hours in 19 of 23 infants receiving ORS60 as opposed to 6 of 18 infants receiving the commercial solution (p less than 0.001); the poor result with the latter was in most cases attributed to a refusal by the infant to consume the sweetish solution. It is concluded that ORS60 is suitable for the treatment of isotonic diarrhoeal dehydration in hospitalized children as well as outpatients.

Oral rehydration, rapid feeding, and cholestyramine for treatment of acute diarrhea.

Different combinations of fluid therapy, feeding regimen, and cholestyramine were compared in search for optimal treatment of infants hospitalized for acute diarrhea. The infants (n = 81) received either rapid oral rehydration using the oral rehydration solution-World Health Organization formula (sodium 90 mmol/L, ORS-WHO) or traditional oral fluid replacement using a commercial glucose-electrolyte solution (sodium 35 mmol/L). One-half of the infants in both groups received full feedings at 24 h of hospitalization; in the remaining infants, feedings were gradually introduced over a period of 5 days. In addition, all the children were randomized to receive either cholestyramine 2 g four times daily or an equivalent amount of placebo. Rehydration with ORS-WHO, but not traditional fluid replacement therapy, led to correction of initial metabolic acidosis after 6-10 h; no cases of hypernatremia were observed with the use of ORS-WHO. Rapid return to full feedings appropriate for age, including milk products, was associated with better weight gain and significantly shorter duration of diarrhea compared with gradual introduction of feedings. Cholestyramine treatment further shortened the duration of diarrhea without adverse effects in those children who had received ORS-WHO and thus were properly rehydrated. In contrast, in children with poor initial hydration, cholestyramine treatment was associated with prolonged metabolic acidosis. We conclude that treatment of acute diarrhea by rehydration with ORS-WHO and rapid introduction of full feedings is effective and safe, and this combination forms a therapy of choice for typical hospitalized cases of acute infantile diarrhea in Finland. Cholestyramine may be of value as an adjunct therapy after adequate rehydration.

Comparison of three oral rehydration strategies in the treatment of acute diarrhea in a tropical country.

The administration of hydrating solutions and early refeeding improve recovery for infants and children with diarrhea. The aim of this study was to assess the efficacy of a low-osmolarity (30 mEq/L Na(+)) solution administered after the standard, high-osmolarity (90 mEq/L Na(+)) solution via a nasogastric tube (NGT) and followed by early refeeding to achieve more rapid body weight recovery in infants and children with acute diarrhea. Infants and children aged <5 years with acute diarrhea and dehydration (body weight loss of ≥10%) observed from January to August 2001 at Saint Camille Medical Center, Ouagadougou, Burkina Faso, were enrolled. Patients were randomized to 1 of 3 treatment protocols. Patients in group A received, via NGT, rehydration with a high-osmolarity solution for 3 hours, followed by a low-osmolarity solution for at least 3 additional hours. Patients in group B were given only a low-osmolarity solution via NGT. In group C, rehydration was carried out using a high-osmolarity solution via NGT. Four thousand consecutively treated infants and children (2010 boys, 1990 girls; mean [SD] age, 3.5 [2.7] years) were enrolled. After the first 6 hours of infusion, 90% of the patients who had received the combined rehydration (group A) showed significant body weight recovery, versus 80% and 79% of the patients in groups B and C, respectively. Stool output significantly decreased for group A compared with groups B and C (114 vs 125 and 120 g/kg, respectively). Only 7% of the patients in group A required prolonged rehydration (>6 hours) with the low-osmolarity solution, versus 10% and 12% in groups B and C, respectively. A total of 3% of patients treated with combined rehydration required hospitalization, compared with 10% and 9% in groups B and C, respectively. At the end of infusion, 25% of the patients rehydrated only with a low-osmolarity solution showed poor body weight recovery and appeared lethargic, versus 10% in group A and 15% in group C. Patients who were rehydrated with a high-osmolarity solution showed symptoms of hypernatremia (serum Na(+) concentration >140 mEq/L). At the end of rehydration (≥6 hours), all patients recovered their previous body weight, partially or totally, and refeeding was begun. Rehydration and diet were continued at home, or in neighboring areas for those living far away. In this study population, the administration of a high-osmolarity solution followed by a low-osmolarity solution and early refeeding was effective in the treatment of acute diarrhea and was well tolerated.

Simplified treatment strategies to fluid therapy in diarrhea.

Dehydration resulting from diarrhea remains an important cause of morbidity and mortality among infants and children worldwide. Although it is well established that rapid and generous intravenous restoration of extracellular fluid, followed by oral rehydration therapy (ORT) should be used in children with severe dehydration, physicians continue to be reluctant to use such therapy. Applying the principle of body fluid physiology to the current treatment of dehydration, we developed a simple and yet effective treatment strategy to fluid therapy for children with diarrheal dehydration using commercially manufactured solutions. Children with mild-to-moderate dehydration are best treated with ORT using commercially available oral solutions containing 45-75 mEq/l of Na(+). Children who have clinical evidence of severe dehydration should receive intravenous fluids, 60-100 ml/kg of 0.9% saline in the first 2-4 h to restore circulation. Oliguric patients with severe acidosis should receive a physiological dose of bicarbonate to correct blood pH level to 7.25. Once circulation is restored, the ORT should be given in small quantities to replace losses of water and Na(+) over 6-8 h. Age-appropriate diet should be started as soon as tolerated. Those who cannot tolerate ORT should receive intravenous rehydration for the remainder of the deficit and maintenance. Addition of 20 mEq/l K(+) to rehydration solutions permits repair of cellular K(+ )deficits without risk of hyperkalemia. The amount of Na(+) given to replace maintenance and deficit fluids varies with the forms of dehydration. Isonatremic dehydration is best treated with 5% dextrose in 0.45% saline containing 20 mEq/l KCl over 24 h. Hyponatremic dehydration is best treated with 0.9% saline and 0.45% saline alternately in a 1:1 ratio in 5% dextrose containing 20 mEq/l KCl over 24 h. Hypernatremic dehydration is best treated with 5% dextrose in 0.2% saline containing 20 mEq/l KCl over 2-3 days to avoid cerebral edema. Maintenance hydration is best treated with 5% dextrose in 0.2% saline containing 20 mEq/l KCl. Ideal commercial intravenous maintenance and deficit solutions have yet to appear.

Oral rehydration therapy in infectious diarrhoea. Comparison of rehydration solutions with 60 and 90 mmol sodium per litre.

The clinical response and changes in water and salt homeostasis as judged from serum sodium levels, salt and water retention and renal handling of sodium was studied during 36 hours following the start of oral rehydration therapy (ORT) with a solution containing 60 mmol Na/l (ORS60) in 17 well-nourished, moderately dehydrated Turkish infants aged 3 to 15 months who had acute infectious diarrhoea (7 with rotavirus, 3 with enteropathogenic E. coli 0 111: B 84, and one with enteropathogenic E. coli 0 125: B 15, one with salmonella and 5 of unknown etiology. In the successfully treated patients sodium and water balance was normalized within 36 hours. In the cases with hypernatremic dehydration the serum sodium concentration rapidly became normal. The results were compared with those obtained in a previous study of the same type of patients who were rehydrated with a solution containing 90 mmol Na/l (ORS90). Although retention was considered to be satisfactory after ORS60 it was less than after ORS90. The changes in the fractionary urinary sodium excretion and the potassium sodium quotient in the urine indicated a less rapid normalization after ORS60 than after ORS90.

[Fast intravenous rehydration with 90 mmol/L of sodium in dehydrated children with diarrhea].

Twenty-two infants with moderate dehydration due to diarrhea in whom oral rehydration therapy (ORT) was contraindicated or who failed to respond to this method of therapy were treated with rapid intravenous rehydration (RIR). Clinical signs of dehydration without shock allowed us to estimate 5% to 10% of weight loss. Patients were 11 days to 19 months old, and 9 of them were undernourished. A standard solution containing 90 mmol/L sodium, 80 mmol/L chloride, 30 mmol/L bicarbonate, 20 mmol/L potassium and 111 mmol/L glucose was used for all patients. The IV infusion was maintained until the rehydration was completed at a rate of 15 to 20 mL/kg/hour. Complete rehydration was successfully achieved in all patients. A total of 89.5 +/- 25.0 mL/kg (mean +/- SD) was needed and the duration of the IV infusion was 5.1 +/- 1.6 hours. Weight gain achieved was 6.5 +/- 1.6%. None of the patients developed hypernatremia following treatment. The initial base deficit, -9.5 +/- 6.6, was reduced to -3.5 +/- 2.9. All of the patients tolerated refeeding immediately after completion of the IV infusion. Our study suggests that this modality of rehydration is well tolerated, safe and effective and enhances the possibility of an early hospital discharge.

Salt and water homeostasis during oral rehydration therapy in neonates and young infants with acute diarrhoea. II. Rehydration with a solution containing 90 mmol sodium per litre (ORS90).

The clinical response and changes in water and salt homeostasis were studied during oral rehydration therapy (ORT) with a solution containing 90 mmol sodium per 1 (ORS90) in 9 infants less than 2 months old (range 2-60 days). Two infants were still dehydrated 36 hours after starting ORT and were excluded from the study. Fluid was retained more rapidly and also to a larger extent than in infants of the same age treated with a solution with a sodium concentration of 60 mmol/l (ORS60). The stool sodium output was higher than that found previously in infants of the same age treated with ORS60. We conclude that during ORT the gut plays an active role in the regulation of salt homeostasis. When the sodium intake is high the percentage of sodium remaining unabsorbed is higher than when the intake is low. This mechanism reduces the risk of hypernatremia in young infants treated with ORS90. The study thus demonstrates that ORS90 is effective and also seems to be safe in the treatment of neonates and young infants with dehydration secondary to diarrhoea if fluid intake is kept around 200 ml/kg/day during the rehydration period.

Oral rehydration therapy

Feeding should usually resume within 2–3 hours after starting rehydration and should continue every 2–3 hours, day and night. For an initial cereal diet before a child regains his or her full appetite, the WHO recommends combining 25 grams skimmed milk powder, 20 grams vegetable oil, 60 grams sugar, and 60 grams rice powder or other cereal into 1,000 milliliters water and boiling gently for five minutes. Give 130 ml per kilogram of body weight during per 24 hours. A child who cannot or will not eat this minimum amount should be given the diet by nasogastric tube divided into six equal feedings. Later on, the child should be given cereal made with a greater amount of skimmed milk product and vegetable oil and slightly less sugar. As appetite fully returns, the child should be eating 200 ml per kilogram of body weight per day. Zinc, potassium, vitamin A, and other vitamins and minerals should be added to both recommended cereal products, or to the oral rehydration solution itself.

Safety and efficacy of a premixed, rice-based oral rehydration solution.

The authors compared the safety and efficacy of a ready-to-use, premixed, rice-based oral rehydration solution (R-ORS) with a glucose-based oral rehydration solution (G-ORS), each containing 75 mmol/L sodium, in Mexican children with acute diarrhea for less than 5 days. One hundred eighty-nine boys 3 to 24 months old admitted to the hospital with acute diarrhea and signs of dehydration were randomly assigned to receive either G-ORS or R-ORS. Intake and output were measured every 3 hours. In the group treated with R-ORS, significantly fewer patients required supplemental intravenous fluids during the rehydration phase compared to the G-ORS group (1% v 8.7%; P < 0.01). Mean stool output, percent weight gain, ORS intake, urine output, and number of patients who vomited during rehydration were similar in the two groups. The mean total stool output after the first 24 hours of maintenance phase was significantly lower in the R-ORS group than in the G-ORS group. The authors found rice-based ORS to be safe, and its use reduced the rate of intravenous fluid therapy in comparison with the use of a glucose-based ORS.

Chronic diarrhea of infancy

While treatments for chronic diarrhea of infancy aren't clear cut, it is crucial to address the complications of dehydration that may arise from chronic diarrhea with the American Academy of Pediatrics (AAP) guidelines recommendation of oral rehydration therapy (ORT). Oral rehydration solution (ORS), recommended by both AAP and the World Health Organization (WHO), must be composed of 50-90mEq/L sodium and 2% glucose or other complex carbohydrates. ORS is easily found in the US because it is available without a prescription. The typical amount of ORS administered is 50mL/kg over a 4-hour time period for mild dehydration and 100mL/kg over a 4-hour time period for moderate dehydration with an extra 10mL/kg for every loose stool. Repeat this administration regimen for as long as the signs and symptoms of dehydration continue. It is important to take measures early on to maintain hydration. Along with ORT, WHO recommends a 10-14 day course of 20 mg zinc tablet supplementation, stating it

Efficacy comparison of oral rehydration solutions containing either 90 or 75 millimoles of sodium per liter.

In a randomized trial, 62 infants 2 to 35 months of age with dehydration due to acute watery diarrhea were allocated to one of two groups: group A received solution A (World Health Organization-recommended oral rehydration solution), which contained (mmol/L): Na+ 90, K+ 20, Cl- 80, citrate3- 10, and glucose 110; group B received solution B (Pedialyte RS; Abbott Laboratories, North Chicago), which contained (in mmol/L): Na+ 75, K+ 20, Cl- 65, citrate3- 10, and glucose 139. Oral therapy was given until clinical signs of hydration status were normal. During the 48-hour trial, the following laboratory data were collected: blood gases, serum electrolytes, glucose, urea, and creatinine values and sodium and potassium concentrations in stool and urine; serial weights and clinical signs were also reported. Six of the 62 infants, three in each group, required intravenous fluids because of high stool output. Results of clinical outcome and normalization of altered serum electrolyte values were similar in both groups. During the 48-hour trial, eight patients in group A and four in group B had mild, asymptomatic hypernatremia. Pedialyte RS was found to be a safe glucose/electrolyte solution for oral rehydration therapy.

Oral rehydration therapy

The original ORS (90 mmol sodium/L) and the current standard reduced-osmolarity ORS (75 mmol sodium/L) both contain too much sodium and too little potassium for severely malnourished children with dehydration due to diarrhea. ReSoMal (Rehydration Solution for Malnutrition) is recommended for such children. It contains less sodium (45 mmol/l) and more potassium (40 mmol/l) than reduced osmolarity ORS. It can be obtained in packets produced by UNICEF or other manufacturers.

Oral rehydration therapy

Reduced-osmolarity In 2003, WHO and UNICEF recommended that the osmolarity of oral rehydration solution be reduced from 311 to 245 mOsm/L . These guidelines were also updated in 2006. This recommendation was based on multiple clinical trials showing that the reduced osmolarity solution reduces stool volume in children with diarrhea by about twenty-five percent and the need for IV therapy by about thirty percent when compared to standard oral rehydration solution. The incidence of vomiting is also reduced. The reduced osmolarity oral rehydration solution has lower concentrations of glucose and sodium chloride than the original solution, but the concentrations of potassium and citrate are unchanged.

Standard WHO-ORS versus reduced-osmolarity ORS in the management of cholera patients.

The study compared the safety and efficacy of an oral rehydration salts (ORS) solution, containing 75 mmol/L of sodium and glucose each, with the standard World Health Organization (WHO)-ORS solution in the management of ongoing fluid losses, after initial intravenous rehydration to correct dehydration. The study was conducted among patients aged 12-60 years hospitalized with diarrhoea due to cholera. One hundred seventy-six patients who were hospitalized with acute diarrhoea and signs of severe dehydration were rehydrated intravenously and then randomly assigned to receive either standard ORS solution (311 mmol/L) or reduced-osmolarity ORS solution (245 mmol/L). Intakes and outputs were measured every six hours until the cessation of diarrhoea. During maintenance therapy, stool output, intake of ORS solution, duration of diarrhoea, and the need for unscheduled administration of intravenous fluids were similar in the two treatment groups. The type of ORS solution that the patients received did not affect the mean serum sodium concentration at 24 hours after randomization and the relative risk of development of hyponatraemia. However, patients treated with reduced-osmolarity ORS solution had a significantly lower volume of vomiting and significantly higher urine output than those treated with standard WHO-ORS solution. Reduced-osmolarity ORS solution was as efficacious as standard WHO-ORS solution in the management of cholera patients. The results indicate that reduced-osmolarity ORS solution is also as safe as standard WHO-ORS solution. However, because of the limited sample size in the study, the results will have to be confirmed in trials, involving a larger number of patients.

Randomised double blind study of hypotonic oral rehydration solution in diarrhoea.

A hypotonic (osmolality 224 mmol/l, sodium 60 mmol/l) oral rehydration solution (ORS) was compared with an isotonic high glucose ORS (osmolality 304 mmol/l, sodium 60 mmol/l) in children with acute diarrhoea in a randomised double blind study. The stool output and hence the mean consumption of ORS for maintenance hydration was less (p = 0.036) in patients receiving hypotonic (69 ml/kg) than isotonic (97 ml/kg) ORS. Hypotonic ORS was more effective in patients with rotavirus positive than with rotavirus negative diarrhoea.

Oral rehydration therapy

Physiological basis Fluid from the body enters the intestinal lumen during digestion. This fluid is isosmotic with the blood and contains a high quantity, about 142 mEq/L, of sodium. A healthy individual secretes 2000–3000 milligrams of sodium per day into the intestinal lumen. Nearly all of this is reabsorbed so that sodium levels in the body remain constant. In a diarrheal illness, sodium-rich intestinal secretions are lost before they can be reabsorbed. This can lead to life-threatening dehydration or electrolyte imbalances within hours when fluid loss is severe. The objective of therapy is the replenishment of sodium and water losses by ORT or intravenous infusion.

A comparison of rice-based oral rehydration solution and "early feeding" for the treatment of acute diarrhea in infants.

To compare the use of rice-based oral rehydration solution (R-ORS), with the introduction of food immediately after rehydration ("early feeding"), using standard glucose-based oral rehydration solution (G-ORS) in the management of acute diarrhea, we conducted a four-cell randomized, controlled trial among 200 hospitalized Egyptian infants between 3 and 18 months of age. During the rehydration phase (first 4 hours), three groups were given G-ORS and a fourth group was given R-ORS. During the subsequent maintenance phase, the control group was given a soy-based, lactose-free formula (G-ORS + SF), a second group (G-ORS + RF) was given a rice-based formula, and a third group (G-ORS + rice) was given boiled rice. The fourth group (R-ORS + SF) continued to receive R-ORS for the first 24 hours of the maintenance period, followed by a soy-based lactose-free formula. During the first and second 24 hours of the maintenance period, infants in the three treatment groups had a lower mean stool output in comparison with the control group (p = 0.006 and 0.03, respectively). The mean total stool output in the R-ORS + SF group was significantly lower than in the control group (p = 0.02). There were no statistically significant differences among the four groups in the mean duration of diarrhea. We conclude that (1) infants who were given R-ORS had reduced total stool output (by 35%) compared with the control group and (2) feeding of boiled rice or a rice-based formula immediately after rehydration therapy was as efficacious as treatment with R-ORS alone for 24 hours, followed by feeding with a soy-based, lactose-free formula.

Comparative efficacy of rice-based and glucose-based oral rehydration salts plus early reintroduction of food.

The use of oral rehydration salts (ORS) to restore fluid balance in children with diarrhoea is universally accepted. However, there is uncertainty about whether glucose-based ORS or ORS based on precooked rice powder is more effective. In a randomised trial we compared the two types of ORS in children who were given food immediately after completion of rehydration. 460 boys aged 3-18 months, admitted to hospital with acute diarrhoea and signs of dehydration, were randomly assigned to groups receiving rice-based and glucose-based ORS solution (230 to each group). After full rehydration (4-12 h), a weaning food consisting of rice and mixed vegetables was given until the diarrhoea stopped. Continuing losses of liquid stool and vomitus were replaced with the assigned ORS solution. There were no differences between the groups during the rehydration phase in stool volume, volume of ORS solution taken, duration of rehydration phase, or weight gain. However, after initiation of feeding, the glucose-based ORS group had significantly lower stool volumes than the rice-based ORS group (142 [95% CI 117-173] vs 96 [77-120] g/kg); they also took a smaller amount of ORS solution (153 [127-185] vs 111 [90-136] mL/kg) and had a shorter duration of diarrhoea (55 [SD 35] vs 44 [35] h). Glucose-based ORS solution was more effective than rice-based ORS solution for the treatment of diarrhoea in children when feeding with a rice-based diet was started soon after correction of dehydration. These results support the continued recommendation of glucose-based ORS solution as standard therapy for treatment of children with acute diarrhoea and emphasize the importance of resuming feeding as soon as dehydration has been corrected.

Alanine-based oral rehydration therapy for infants with acute diarrhea.

Twenty male infants less than 1 year of age with acute diarrhea and dehydration were randomly assigned to a study group and studied in blind fashion in a metabolic unit to assess the efficacy of the addition of 30 mmol/L alanine to the standard World Health Organization (WHO) oral rehydration solution (ORS). Patients were exclusively rehydrated with one of two types of ORS during the first 24 hours of treatment. On the second day, oral feedings were started with a lactose-free formula, and ORS was given to replace stool losses. Body weight, ORS, food intake, vomitus, stool, and urine output were recorded at 6-hour intervals. Blood was drawn at the time of admission, after rehydration, and at 24 and 48 hours of hospitalization to monitor blood gases and electrolytes. Rehydration was satisfactory in both groups of patients. ORS that contained alanine did not reduce the purging rates of the infants compared with those who received standard ORS. Clinically no adverse effect of the alanine-based ORS was observed during hospitalization. None of the patients had significant hypernatremia or hyponatremia, and serum amino acid levels were not altered. These data show that the addition of 30 mmol/L alanine to the standard WHO-ORS produces no further improvement in the outcome of the infants with acute diarrhea compared with those fed the standard WHO-ORS.

InternalMed_Harrison

Moderatec,d <4 months (<5 kg) 200–400 mL of ORS 4–11 months (5–<8 kg) 400–600 mL of ORS 12–23 months (8–<11 kg) 600–800 mL of ORS 2–4 years (11–<16 kg) 800–1200 mL of ORS 5–14 years (16–<30 kg) 1200–2200 mL of ORS ≥15 years (≥30 kg) 2200–4000 mL of ORS All ages and weights Undertake IV fluid replacement with Ringer’s lactate (or, if not available, normal saline). Give 100 mL/kg in the first 3-h period (or the first 6-h period for children <12 months old); start rapidly, then slow down. Give a total of 200 mL/ kg in the first 24 h. Continue until the patient is awake, can ingest ORS, and no longer has a weak pulse. aAdapted from World Health Organization: First steps for managing an outbreak of acute diarrhoea. Global Task Force on Cholera Control, 2009 (www.who.int/topics/cholera). bContinue normal feeding during treatment. cReassess regularly; monitor stool and vomit output. dVolumes of ORS listed should be given within the first 4 h. Abbreviation: ORS, oral rehydration solution.

Oral rehydration therapy

The reduced osmolarity solution has been criticized by some for not providing enough sodium for adults with cholera. Clinical trials have, however, shown reduced osmolarity solution to be effective for adults and children with cholera. They seem to be safe but some caution is warranted according to the Cochrane review. Administration ORT is based on evidence that water continues to be absorbed from the gastrointestinal tract even while fluid is lost through diarrhea or vomiting. The World Health Organization specify indications, preparations and procedures for ORT.

Rice starch low sodium oral rehydration solution (ORS) in infantile diarrhoea.

The relative efficacy and incidence of hypernatremia of a rice starch based low sodium (sodium of 60 mmol/L) oral electrolyte solution was compared to the standard WHO oral rehydration solution (ORS; sodium 90 mmol/L) in 60 infants with non choleragenic acute diarrhoea. Both solutions were found to be equally effective in correcting dehydration as determined by the respective post hydration weight gain which was 150 +/- 175 gms in the rice starch low sodium ORS group and 164 +/- 125 gms in the standard WHO ORS group. However, the mean frequency of stools was greater and the duration of stay longer in the WHO ORS group compared to the rice starch low sodium group. There were 5 cases of hypernatremia in the WHO ORS group as opposed to only one in the rice starch low sodium ORS group. The present study shows that a rice starch low sodium ORS was as effective as the standard WHO ORS and had a lower incidence of hypernatremia in the fluid and electrolyte management of infants with non choleragenic diarrhoea.

Pediatric Gastroenteritis -- Treatment / Management

The treatment of choice is a low-osmolarity fluid, with 75 mEq of Na, 64 mEq of Cl, 20 mEq of K, and 75 mmol of glucose per liter; the total osmolarity should be 245 mOsm/L. In mild to moderate emesis, give ondansetron (4 mg for children 4 to 11 years, and double the doses for older children) is often considered for better oral rehydration. IV rehydration is done with a lactated Ringer's solution or normal saline at 20 mL/Kg body weight.


This case describes an Alzheimer's disease with insidious onset of short-term memory problems. Clinically it can be distinguished from other options by the absence of behavioral problems (typical of frontotemporal dementia) and hallucinations (early in Lewy body disease). Vascular dementia is diagnosed by criteria that include deficits in memory and two other cognitive areas with consequent functional impairment, but cerebral vascular disease based on history, examination and/or neuroimaging tests, which are not indicated in the case. Creutzfeldt-Jacob disease is mostly rapidly progressive and usually presents with other clinical, abnormal neurological examination and MRI alterations.

A 77-year-old man with a history of type 2 Diabetes Mellitus was diagnosed 2 years ago with mild cognitive impairment. At that time a Minimental (Folstein) 28/30, abbreviated Yesavage Test 14/15, a CBC with normal TSH and maturation factors along with negative LUES and HIV serologies and a magnetic resonance imaging (MRI) showing diffuse cortical atrophy predominantly in the posterior area. The patient was accompanied by his wife, who reported a slow progressive evolution of memory impairment (e.g., sometimes confused with insulin doses). There are no hallucinations or behavioral disorder. Current Minimental is 24/30 and Yesavage test 14/15, there is no neurological focality, tremor or tone or gait disorders on physical examination. Two months ago he came to the emergency department after a mild traumatic brain injury due to an accidental fall (the only one in 2 years) and a CT scan was performed which did not provide new information compared to the previous MRI. What is the most likely diagnosis in this patient?

Dementia

Imaging A CT scan or MRI scan is commonly performed to possibly find either normal pressure hydrocephalus, a potentially reversible cause of dementia, or connected tumor. The scans can also yield information relevant to other types of dementia, such as infarction (stroke) that would point at a vascular type of dementia. These tests do not pick up diffuse metabolic changes associated with dementia in a person who shows no gross neurological problems (such as paralysis or weakness) on a neurological exam. The functional neuroimaging modalities of SPECT and PET are more useful in assessing long-standing cognitive dysfunction, since they have shown similar ability to diagnose dementia as a clinical exam and cognitive testing. The ability of SPECT to differentiate vascular dementia from Alzheimer's disease, appears superior to differentiation by clinical exam.

Alzheimer's disease

Alzheimer's disease is usually diagnosed based on the person's medical history, history from relatives, and behavioral observations. The presence of characteristic neurological and neuropsychological features and the absence of alternative conditions supports the diagnosis. Advanced medical imaging with computed tomography (CT) or magnetic resonance imaging (MRI), and with single-photon emission computed tomography (SPECT) or positron emission tomography (PET), can be used to help exclude other cerebral pathology or subtypes of dementia. Moreover, it may predict conversion from prodromal stages (mild cognitive impairment) to Alzheimer's disease. FDA-approved radiopharmaceutical diagnostic agents used in PET for patients with Alzheimer's disease are florbetapir (2012), flutemetamol (2013), florbetaben (2014), and flortaucipir (2020). Because many insurance companies in the United States do not cover this procedure, its use in clinical practice is largely limited to clinical trials as

InternalMed_Harrison

Abbreviations: CT, computed tomography; EEG, electroencephalogram; MRI, magnetic resonance imaging; PET, positron emission tomography; RBC, red blood cell; RPR, rapid plasma reagin (test); SPECT, single-photon emission computed tomography; TSH, thyroid-stimulating hormone; VDRL, Venereal Disease Research Laboratory (test for syphilis). Abbreviations: AD, Alzheimer’s disease; CBD, cortical basal degeneration; CJD, Creutzfeldt-Jakob disease; DLB, dementia with Lewy bodies; FLAIR, fluid-attenuated inversion recovery; FTD, frontotemporal dementia; MND, motor neuron disease; MRI, magnetic resonance imaging; PSP, progressive supranuclear palsy; REM, rapid eye movement.

Major Neurocognitive Disorder (Dementia) -- Etiology

Several conditions can cause major neurocognitive disorder with Alzheimer dementia (AD) being the most common cause accounting for about 70% of cases. [6] The DSM-5 criteria for major neurocognitive disorder further delineate 13 etiological subtypes that indicate the possible etiology of the disorder. These subtypes include Alzheimer disease, vascular disease, frontotemporal lobar degeneration, Lewy body disease, Parkinson disease, HIV infection, Huntington disease, prion disease, substance and or medication use, traumatic brain injury, another medical condition, multiple etiologies, and unspecified. A patient may have more than one etiology contributing to MND. For example, there may be a mixed picture of Alzheimer disease with vascular disease in the same patient. Other medical conditions that can lead to dementia include progressive supranuclear palsy, corticobasal syndrome, and, less commonly, multiple system atrophy. The etiology is further characterized by "possibly" vs. "probably," assigning the degree of certainty as to the cause of the major neurocognitive disorder. It often takes time to distinguish the etiology and can be aided by many factors, including the results of imaging studies, lab studies, genetic markers, patient comorbidities, medical and family history, and clinical findings. [1]

Psichiatry_DSM-5

Specify if: Acute, Persistent Specify if: Hyperactive, Hypoactive, Mixed level of activity 780.09 (R410) Other Specified Delirium (602) 780.09 (R41.0) Unspecified Delirium (602) Specify whether due to: Alzheimer’s disease, Frontotemporal lobar degeneration, Lewy body disease, Vascular disease, Traumatic brain injury, Substance/medication use, HIV infection, Prion disease, Parkinson’s disease, Huntington’s disease, Another medical condition, Multi- ple etiologies, Unspecified aSpecify Without behavioral disturbance, With behavioral disturbance. For possible major neuro- cognitive disorder and for mild neurocognitive disorder, behavioral disturbance cannot be coded but should still be indicated in writing. bSpecify current severity: Mild, Moderate, Severe. This specifier applies only to major neurocogni— tive disorders (including probable and possible).

Psychoorganic syndrome

Diagnosis Along with occupational and environmental evaluation, a neurological exam, ECHO, EEG, CT-San, and X-ray of the brain may be conducted to determine disorder. Neuroimaging that detects cerebral atrophy or cardiovascular subcortical alterations can help point to psychoorganic syndrome. Strong CNS lesions are detected in POS patients. However, this is found to be difficult as many psychiatric disorders, like dementia, have common diagnosis. Diagnosing POS is an ongoing and developing in the medical and psychiatric industry. Exact diagnosis is difficult due to many symptoms mirroring other psychological disorders in the older aged patients. Various symptom diagnosis CT scan or MRI can confirm dementia via observation of ventricular dilation and cortical substance degeneration. Pick's disease can be confirmed via CT scan or MRI with atrophy of frontal and temporal lobe roots.

Neurology_Adams

Studies with CT and MRI are useful, but not definitive ancillary tests (Fig. 38-3). In patients with advanced Alzheimer disease, the lateral and third ventricles are enlarged to about twice the normal size and the cerebral sulci are proportionately widened, both as a result of cerebral atrophy. Coronal MRI of the medial temporal lobes shows a disproportionate atrophy of the hippocampi and a corresponding enlargement of the temporal horns of the lateral ventricles. Early in the disease, however, the changes do not exceed those found in many mentally intact old persons. For this reason, one cannot rely solely on imaging procedures for diagnosis and CT and MRI are most valuable in excluding alternative causes of dementia such as brain tumor, subdural hematoma, cerebral infarction, and hydrocephalus. The EEG undergoes mild diffuse slowing, but only late in the course of the illness; it is useful again, in the exclusion of alternative causes of mental decline that manifest themselves in

Psichiatry_DSM-5

F0280 Major neurocognitive disorder probably due to Parkinson’s disease, Without F0280 Major neurocognitive disorder due to prion disease, Without behavioral F0280 Major neurocognitive disorder due to traumatic brain injury, Without behavioral disturbance (codefirst SO6.2X9S diffuse traumatic brain injury with loss of consciousness of unspecified duration, sequela) F0280 Probable major frontotemporal neurocognitive disorder, Without behavioral disturbance (codefirst 631.09 frontotemporal disease) F0280 Probable major neurocognitive disorder due to Alzheimer’s disease, Without behavioral disturbance (codefirst 630.9 Alzheimer’s disease) F0280 Probable major neurocognitive disorder with Lewy bodies, Without behavioral disturbance (codefirst 631.83 Lewy body disease) F02.81 Major neurocognitive disorder due to another medical condition, With F02.81 Major neurocognitive disorder due to HIV infection, With behavioral

Pseudodementia

A significant overlap in cognitive and neuropsychological dysfunction in Dementia and pseudodementia patients increases the difficulty in diagnosis. Differences in the severity of impairment and quality of patients' responses can be observed, and a test of antisaccadic movements may be used to differentiate the two, as pseudodementia patients have poorer performance on this test. Individuals with pseudodementia present considerable cognitive deficits, including disorders in learning, memory and psychomotor performance. Substantial evidences from brain imaging such as CT scanning and positron emission tomography (PET) have also revealed abnormalities in brain structure and function. A comparison between dementia and pseudodementia is shown below.

Vascular dementia

The disease is described as both a mental disorder and behavioural disorder within the International Classification of Diseases. Signs and symptoms are cognitive, motor, behavioral, and for a significant proportion of patients, also affective. These changes typically occur over a period of 5–10 years. Signs are typically the same as in other dementias, but mainly include cognitive decline and memory impairment of sufficient severity as to interfere with activities of daily living, sometimes with presence of focal neurologic signs, and evidence of features consistent with cerebrovascular disease on brain imaging (CT or MRI). The neurologic signs localizing to certain areas of the brain that can be observed are hemiparesis, bradykinesia, hyperreflexia, extensor plantar reflexes, ataxia, pseudobulbar palsy, as well as gait problems and swallowing difficulties. People have patchy deficits in terms of cognitive testing. They tend to have better free recall and fewer recall intrusions when

Psichiatry_DSM-5

Probable (code first 332.0 [620] Parkinson’s disease) Major neurocognitive disorder due to prion disease (code first 046.79 [A819] prion disease) Major neurocognitive disorder due to traumatic brain injury (code first 907.0 late effect of intracranial injury without skull fracture [506.2X9S diffuse traumatic brain injury with loss of conscious- ness of unspecified duration, sequela]) Major vascular neurocognitive disorder, Possible Major vascular neurocognitive disorder, Probable Medication-induced delirium (for ICD-IO-CM codes, see specific Mild neurocognitive disorder due to Alzheimer’s disease Mild neurocognitive disorder due to another medical condition Mild neurocognitive disorder due to HIV infection Mild neurocognitive disorder due to Huntington’s disease Mild neurocognitive disorder due to multiple etiologies Mild neurocognitive disorder due to Parkinson’s disease Mild neurocognitive disorder due to prion disease

Frontotemporal dementia

Structural MRI scans often reveal frontal lobe and/or anterior temporal lobe atrophy but in early cases the scan may seem normal. Atrophy can be either bilateral or asymmetric. Registration of images at different points of time (e.g., one year apart) can show evidence of atrophy that otherwise (at individual time points) may be reported as normal. Many research groups have begun using techniques such as magnetic resonance spectroscopy, functional imaging and cortical thickness measurements in an attempt to offer an earlier diagnosis to the FTD patient. Fluorine-18-fluorodeoxyglucose positron emission tomography (FDG-PET) scans classically show frontal and/or anterior temporal hypometabolism, which helps differentiate the disease from Alzheimer's disease. The PET scan in Alzheimer's disease classically shows biparietal hypometabolism. Meta-analyses based on imaging methods have shown that frontotemporal dementia mainly affects a frontomedial network discussed in the context of social

[A 64-year-old woman with progressive gait disturbance and dementia for one year].

We report a 64-year-old Japanese woman who died one year after the onset of progressive gait disturbance and dementia. She noted a difficulty in holding a glass and hand tremor in June of 1996 when she was 63 years old. In July of 1996, she tended to lean toward left when she walked. She also noted truncal titubation. In November of 1996, she started to have visual hallucination and delusion in which she said "I see something is flying on the wall.", "Somebody has come into my room", and things like that. She was admitted to our service on November 22, 1996. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed disturbance in recent memory. Hasegawa's dementia rating scale was 22/30. She showed vivid visual hallucination with colors in which she saw faces of dwarfs and angels, a space ship, and others. Higher cerebral functions were normal. She showed left oculomotor palsy which was a sequel of an aneurysm and subarachnoid hemorrhage nine years before. Otherwise cranial nerves were unremarkable. She showed ataxic gait, limb ataxia, truncal titubation, and postural hand tremor. She had no weakness and no muscle atrophy. Deep tendon reflexes were within normal limits. Plantar response was flexor. Sensation was intact. Laboratory examination was also unremarkable. Complete survey for occult malignancy was negative. CSF was under a normal pressure and cell count was 1/microliter, total protein 27 mg/dl, and sugar 68 mg/dl. Cranial CT scan was unremarkable. MRI was not obtained because of the presence of an aneurysm clip in the left internal carotid-posterior communication artery junction. She showed progressive deterioration in her mental function. By January 1997, she became unable to stand or walk with marked dementia. Repeated CSF exams and cranial CT scans were unremarkable. She suffered from several episodes of aspiration pneumonia. A trial of three days methylprednisolone pulse therapy was given starting on March 7, 1997, which was of no effect on her neurologic status. On March 28, 1997, she was intubated because of acute respiratory distress syndrome. In April 2, her body temperature rose to 38 degrees C. On April 9, 1997, her blood pressure dropped and resuscitation was unsuccessful. She was pronounced dead on the same day. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had primary leptomeningeal lymphoma. Other possibilities entertained among the audience included brain stem encephalitis of unknown type, carcinomatous cerebellar degeneration plus limbic encephalitis, Creutzfeldt-Jakob disease, thalamic degeneration, and progressive multifocal leukoencephalopathy. Post-mortem examination revealed thickening and clouding of the leptomeninges; Gram-positive diplococci were found in the leptomeninges. This meningitis appeared to have been an complication in the terminal stage of her illness. Microscopic examination revealed astrocytosis in the midbrain tegmentum. Cerebral cortices showed only mild astrtocytosis. No cerebellar atrophy was seen and Purkinje cells were retained which excluded paraneoplastic cerebellar degeneration. Neuropathologic diagnosis was bacterial meningitis, however, the presence of brain stem encephalitis prior to the onset of bacterial meningitis could not be excluded. It is interesting to note that the diagnosis of the primary neurologic disease of this patient was not easy even after autopsy. As autopsy permission was obtained only for the brain, it was not clear whether or not this patient had an occult malignancy somewhere in her body, however, there was no evidence to indicate paraneoplastic degeneration of the central nervous system. As the patient did not have meningeal signs until one month before her death, it is difficult to ascribe her entire neurologic problems to her meningitis. Finally, her visual hallucination was vivid and colorful; we thought this might have been

Psichiatry_DSM-5

When a cerebrovascular etiology is contributing to the neurocognitive disorder, the diagno- sis of vascular neurocognitive disorder should be listed in addition to major neurocognitive disorder due to multiple etiologies. For example, for a presentation of major neurocognitive disorder due to both Alzheimer's disease and vascular disease, with behavioral disturbance, code the following: 331.0 (630.9) Alzheimer’s disease; 294.11 (F02.81) major neurocogni- tive disorder due to multiple etiologies, with behavioral disturbance; 290.40 (F01.51) major vascular neurocognitive disorder, with behavioral disturbance. For mild neurocognitive disorder due to multiple etiologies, code 331.83 (631.84). (Note: Do not use the additional codes for the etiologies. Behavioral disturbance cannot be coded but should still be indicated in writing.)

Alzheimer Society of Ireland

The Alzheimer Society of Ireland also operates the Alzheimer National Helpline, offering information and support to anyone affected by dementia on 1800 341 341. Activities The Alzheimer Society of Ireland provides services such as the Alzheimer National Helpline, Social Clubs, Support Groups, Day Care Services, Home Care, Dementia Advisor Service and the Mobile Information Bus. The charity does not exclusively help people with Alzheimer's disease. There are many types of dementia, which is an umbrella term. Dementia types include vascular dementia, dementia with Lewy bodies, frontotemporal dementia, Korsakoff's syndrome, Creutzfeldt–Jakob disease, HIV related cognitive impairment, mild cognitive impairment, and other rarer causes of dementia.

[A 51-year-old man with early onset parkinsonism].

We report of 51-year-old man with early onset parkinsonism. The patient was well until 38 years of age, when he noted a difficulty in the use of his right leg; this difficulty improved after he received a medicine from his physician. He did not take medicine regularly, and he noted difficulty in standing up from a chair and in rolling over at age 40. Tremor was not a feature, but he noted slowness in his movements at age 42; at age 49, he noted diurnal fluctuation in his symptoms and at times he experienced hallucination. He was admitted to our hospital in September of 1992 for the first time when he was 50-year-old. At that time, neurologic examination revealed an alert and somewhat bradyphrenic man; Hasegawa dementia rating scale was 20/30. Cranial nerves were intact except for masked face and small voice. He showed stooped posture and small step gait cogwheel rigidity was noted in the four limbs more on the left; tremor was absent. Deep reflexes were within normal range and the sensation was intact. As he showed diurnal fluctuation in his symptoms, his medication was switched to levodopa 3,000 mg/day without a peripheral decarboxylase inhibitor. He was discharged for out patient follow up. But he did not take drugs regularly, and his neurologic condition deteriorated; he was admitted to another hospital. Neurologic examination at that time was essentially similar to that of his first admission to our hospital, except that he showed more severe rigidity and akinesia; again tremor was not detected. His cranial CT scan showed a mild ventricular dilatation without cortical or brain stem atrophy. During his hospital stay, he developed episodes of oculogyric crisis during peak dose of levodopa, and orthostatic hypotension. He developed pneumonia and expired on October 28, 1993. He was discussed in a neurological CPC, and the chief discussion arrived at the conclusion that the patient had early onset Parkinson's disease of Lewy body type. As differential diagnoses, early onset parkinsonism without Lewy body, pure form of diffuse Lewy body disease, pallidoluysian atrophy, and other conditions were considered; however, all of those possibilities were excluded. Early onset parkinsonism without Lewy body would have much earlier onset than this patient, and diffuse Lewy body disease would show more profound dementia 13 years after the onset. Pallidoluysian atrophy would be complicated with some dystonic features. Post-mortem examination showed marked discoloration and degeneration of the substantia nigra. The degeneration was most prominent in the ventrolateral tier of the substantia nigra.(ABSTRACT TRUNCATED AT 400 WORDS)

Florbetaben (18F)

Single dose pharmacokinetics of 300 MBq florbetaben of low or high mass dose (<=5 and 50–55 μg) showed no relevant differences between Japanese and Caucasian populations. When compared to healthy subjects, cortical uptake of florbetaben was demonstrated to be generally higher in a large proportion of patients with a clinical diagnosis of AD or mild cognitive impairment. Longitudinal data of 45 patients with MCI indicated that florbetaben PET imaging may be useful to identify patients who will progress to AD. A substantial proportion of patients with a positive florbetaben PET scan progressed to AD-dementia over a 2-year and 4-year time frame. At 4-year follow-up, 88% (21/24) of individuals with MCI and positive florbetaben uptake converted to clinical dementia due to AD, whereas none of 21 florbetaben-negative individuals with MCI experienced a conversion. The pivotal phase III study investigated the relationship of florbetaben imaging and amyloid deposition in the brain in patients

Psichiatry_DSM-5

D. The cognitive deficits are not better explained by another mental disorder (e.g., major depressive disorder, schizophrenia). Specify whether due to: Alzheimer’s disease (pp. 611—614) Frontotemporal lobar degeneration (pp. 614—618) Lewy body disease (pp. 618—621) Vascular disease (pp. 621—624) Traumatic brain injury (pp. 624—627) Substance/medication use (pp. 627-632) HIV infection (pp. 632—634) Prion disease (pp. 634—636) Parkinson’s disease (pp. 636—638) Huntington's disease (pp. 638—641) Another medical condition (pp. 641—642) Multiple etiologies (pp. 642—643) Unspecified (p. 643) Coding note: Code based on medical or substance etiology. In some cases, there is need for an additional code for the etiological medical condition, which must immediately pre- cede the diagnostic code for major neurocognitive disorder, as follows: Probable: 331.0 (G309) Probable: 294.1x 331.83 (G31.84)

[An autopsy case of encephalopathy associated with small cell carcinoma of the stomach with nonconvulsive status epilepticus resembling Creutzfeldt-Jakob disease].

A 64-year-old man developed progressive dementia and altered consciousness with myoclonus over 2 months. Neurological examination revealed mild dysphagia and negative myoclonus of both hands. Electroencephalography (EEG) showed continuous periodic synchronous discharge (PSD) of 1 Hz, although his EEG abnormality was not similar to that usually observed in Creutzfeldt-Jakob disease (CJD). Magnetic resonance imaging (MRI) of the brain revealed only few lacunes. Laboratory data were also normal. Since his consciousness level fluctuated and the PSD were spiky, we came to a diagnosis of nonconvulsive status epilepticus (NCSE). After administering the valproic acid, his symptoms and EEG finding improved. Nine months after the onset, despite his continued valproic acid, the patient had recurrent NCSE and PSD of 1 Hz. Diffusion-weighted MRI showed a T2-hyperintense lesion in the right parietal lobe, where SPECT scans showed hyperperfusion. After adding zonisamide, he improved slowly. The follow-up MRI and SPECT showed a disappearance of the previous lesion. Now CT scans of the abdomen showed enlarged periaortic lymph node and endoscopic ultrasonography disclosed a submucosal tumor of the stomach. Biopsy of the periaortic lymph node by laparotomy revealed undifferentiated adenocarcinoma with its origin being unclear. Chemotherapy didn't work well for the tumor and the patient underwent a downhill course, although his mental and neurological manifestation were mostly unremarkable. Two years and four months after the onset, he died in emaciation. Autopsy confirmed small cell carcinoma originating in the stomach and metastases in the liver and lungs. Neuropathological examination revealed only mild scattered gliosis. This case was unique in the prolonged CJD-like manifestations, which turned out to be due to NCSE. Despite anti-neuronal antibodies were not detected, we suspect yet another paraneoplastic brain syndrome in this patient.

[The basics of imaging dementia].

Dementia is becoming more common as the population ages. We review the prevalence of different causes of dementia. Alzheimer's disease heads the list, followed by vascular dementia, Lewy body dementia, and frontotemporal lobar degeneration. Although these are distinct entities, their symptoms overlap and they have many comorbid conditions in common. We review the importance of recognizing the early symptoms and signs of dementia and point out the key differences between different types of dementia. We illustrate the fundamental importance of differentiating between reversible and irreversible disease on imaging and of establishing the follow-up of patients with irreversible conditions.

[Is it Alzheimer disease? Recognizing the first signs of dementia syndrome].

Today, early diagnosis of different forms of dementia is possible with a relatively easy-to-apply set of diagnostic tools. The quality of the medical history, including the information supplied by relatives and friends, together with the psychological and physical findings, determine the diagnostic hit rate. Laboratory investigations and imaging techniques are indispensable for detecting the underlying cause of existing dementia. Standardized rapid screening procedures for the identification of mild cognitive deficits have speeded up the reliable selection of suspicious cases needing referral to a specialist. Identification of individual day-to-day problems and non-cognitive disorders round off the diagnosis of dementia, and establish the conditions for planning a suitable treatment strategy.

Creutzfeldt-Jakob disease presenting with bilateral hearing loss: A case report.

Sporadic Creutzfeldt-Jakob disease (sCJD) is a prion disease characterized as a fatal transmissible neurodegenerative disorder. Dizziness is often the first presenting symptom of sCJD, but hearing loss as an early manifestation is very rare. A 76-year-old man presented with bilateral sudden hearing impairment and dizziness for 10 d. He was taking medications for hypertension and diabetes. He denied any difficulty with activities of daily living or hearing impairment before the onset of symptoms. Pure tone audiometry showed bilateral severe hearing impairment. Brain magnetic resonance imaging (MRI) and laboratory tests were within normal limits. Given his diagnosis of sudden sensory hearing loss, the patient received corticosteroid treatment but it was ineffective. Two weeks later, he complained of aggravated gait impairment, disorientation, and cognitive impairment. Repeat brain MRI showed diffuse cortical high signal intensities on diffusion-weighted imaging. In cerebrospinal fluid analysis, the real-time quaking-induced conversion assay was positive, and 14-3-3 protein was detected in the by western blotting. Considering all the data, we diagnosed probable sCJD, and the patient's symptoms rapidly progressed into akinetic mutism. For patients with abrupt bilateral hearing impairment, especially in the elderly, various differential diagnoses, including sCJD, should be considered.

[Structural neuroimaging in dementia for outpatient clinic visit].

Dementia is a common illness to find in a psychiatric consultation and its incidence is rising as the aged population increases. Traditionally the imagines in dementia were used to rule out etiologies that had pharmacological o surgery treatments. However, in the last years neuroimaging has played a very important role in the field of dementia. Structural imaging (particularly MRI) has become an important tool in the diagnosis of degenerative dementias because of findings that help us to support the diagnosis of different etiologies. Different patterns of atrophy can be identified on visual inspection of MRI in various neurodegenerative conditions. However, it's sometimes difficult to recognize or acknowledge these patterns during a regular outpatient clinic visit. In this review we describe the most important findings in structural neuroimaging in the most common causes of dementia and we analyze the most useful visual scales that can help us in the differential diagnosis of dementia during a regular outpatient clinic visit.

[Frontal dementia or dementia praecox? A case report of a psychotic disorder with a severe decline].

Many authors have described these last years the difficulty to establish a differential diagnosis between schizophrenia and frontotemporal dementia. However treatment and prognosis of these two separate diseases are not the same. Schizophrenia is a chronic syndrome with an early onset during teenage or young adulthood period and the major features consist of delirious ideas, hallucinations and psychic dissociation. However a large variety of different symptoms describes the disease and creates a heterogeneous entity. The diagnosis, exclusively defined by clinical signs, is then difficult and has led to the research of specific symptoms. These involve multiple psychological processes, such as perception (hallucinations), reality testing (delusions), thought processes (loose associations), feeling (flatness, inappropriate affect), behaviour (catatonia, disorganization), attention, concentration, motivation (avolition), and judgement. The characteristic symptoms of schizophrenia have often been conceptualised as falling into three broad categories including positive (hallucination, delision), negative (affective flattening, alogia, avolition) and disorganised (poor attention, disorganised speech and behaviour) symptoms. No single symptom is pathogonomonic of schizophrenia. These psychological and behavioural characteristics are associated with a variety of impairments in occupational or social functioning. Cognition impairments are also associated with schizophrenia. Since the original clinical description by Kraepelin and Bleuler, abnormalities in attentional, associative and volitional cognitive processes have been considered central features of schizophrenia. Long term memory deficits, attentional and executive dysfunctions are described in the neurocognitive profile of schizophrenic patients, with a large degree of severity. The pathophysiology of schizophrenia is not well known but may be better understood by neuronal dysfunctions rather than by a specific anatomical abnormality. Frontotemporal lobar degeneration (FTLD) is one of the most common causes of cortical dementia. FTLD is associated with an anatomical atrophy that can be generalised, with a frontotemporal or focal lobar predominance. Histologically there is severe neuronal loss, gliosis and a state of spongiosis. In a minority of case Pick cells and Pick bodies are also found. The usual clinical features of FTLD are divided in three prototypic syndromes: frontotemporal dementia (FTD), progressive non-fluent aphasia (PA) and semantic dementia (SD). FTD is the most common clinical manifestation of FTLD. FTD is first characterised by profound alteration in personality and social conduct, characterised by inertia and loss of volition or social disinhibition and distractibility. There is emotional blunting and loss of insight. Speech output is typically economical, leading ultimately to mutism, although a press of speech may be present in some overactive, disinhibited patients. Memory is relatively preserved in the early stage of the disease. Cognitive deficits occur in the domains of attention, planning and problems solving, whereas primary tools of language, perception and spatial functions are well preserved. PA is an initial disorder of expressive language, characterised by effortful speech production, phonologic and grammatical errors. Difficulties in reading and writing also occur but understanding of word meaning is relatively well preserved. In SD a severe naming and word comprehension impairment occur on the beginning in the context of fluent, effortless, and grammatical speech output. There is also an inability to recognise the meaning of visual percepts. The clinical syndromes of FTLD are associated with the brain topography of the degeneration. So considerable clinical overlap can exist between schizophrenia and FTLD and the object of the following case report is to remind the difficulty to make a differential diagnosis between these two pathologies. A 34 year old non-married man is admitted in mental health district of a general hospital for behavioural disturbances that include repeated aggressions towards his family. At initial interview visual and auditives hallucinations are described. The patient doesn't care about these abnormalities and a poverty of speech is observed. The affects, globally blunted, show some degree of sadness however. The patient's birth and early development were unremarkable. At the age of 26, the patient dismissed from his job because of poor performance and absenteeism. He spent a lot of time watching TV, showed poverty of speech and become sometimes angry and violent without an explanation. He was hospitalised for several months and a schizophrenia including predominant negative features, hallucinations and delusion was diagnosed. He was treated with bromperidol, could go back to home and was followed by a general practitioner for 8 years. The patient had a stereotyped way of life during these years with a poor communication and little activity. During the months preceding the current hospitalisation, these characteristics and avolition emphasised, urinary incontinence appeared. The patient receives risperidone 8 mg/day associated with citalopram 40 mg/day during several months of hospitalisation. No significant evolution is observed regarding apathic and stereotyped way of live. The capacity of communication remains very poor. Neurocognitive assessments reveal multiple and severe dysfunctions. Memory, executive and attentional tasks are extremely disturbed. Physical and neurological examinations reveal an isolated bilateral Babinski sign. Cerebral scanner and magnetic resonance show bifrontal atrophy and PET scan is normal. There are no significant abnormalities found on blood and urine samples and on lumbar puncture. The patient is sent to a chronic neuropsychiatric hospital and the treatment is stopped. One year later, a comparative evaluation is realised. The general clinical state shows no evolution. Neurocognitive assessments are repeated and severe dysfunctions are observed with more perseverations. A diagnosis of FTLD for this patient can be discussed regarding clinical features, neurocognitive testings and neuroradiological findings. Schizophrenia is a major differential diagnosis. Psychotic symptoms like hallucinations and age of onset are essential observations for the diagnosis of schizophrenia but can not exclude FTLD. Memory, intellectual functions, executive and attentional abilities may all be disturbed in schizophrenia and FTLD. Cerebral abnormalities well established in schizophrenia are lateral ventricles enlargements. Frontal lobar atrophy is a major argument for FTLD and is only a sporadic finding in schizophrenic populations. Schizophrenia and FTLD could be comorbid diseases by several ways. A differential diagnosis between schizophrenia and FTLD is difficult to establish. Schizophrenia is a heterogeneous disease with a large variety of cognitive dysfunctions. Neurocognitive tools may improve our knowledge of schizophrenia.

The diagnosis of Alzheimer's disease.

The diagnosis of Alzheimer's disease is a diagnosis of exclusion. First, dementia must be properly diagnosed using the four-part definition mentioned above and considering the caveat regarding educational levels. Next, the differential diagnosis of dementia must be examined, disease by disease, with clinical and laboratory criteria used to accept or reject each diagnosis. If all other causes of dementia are rejected this way (usually after a thorough history and physical, B-12 and thyroid levels, CT scan, and removal of possibly offending medications), then a diagnosis of probable Alzheimer's disease is made. If at that time the pattern of disease progression, mental status abnormalities, and personality changes is consistent with one of the presentations of Alzheimer's, the diagnosis is made with confidence. If these patterns are not consistent, re-examining the differential diagnosis is indicated.

Computed tomography of the head

Comparison with MRI Magnetic resonance imaging (MRI) of the head provides superior information as compared to CT scans when seeking information about headache to confirm a diagnosis of neoplasm, vascular disease, posterior cranial fossa lesions, cervicomedullary lesions, or intracranial pressure disorders. It also does not carry the risks of exposing the person to ionizing radiation. CT scans may be used to diagnose headaches when neuroimaging is indicated and MRI is not available, or in emergency settings when hemorrhage, stroke, or traumatic brain injury is suspected. MRI (magnetic resonance imaging) provides more sensitivity in the evaluation of the cavernous sinus and the orbital apex. One advantage over a brain MRI is in the evaluation of intracerebral calcifications.

Clinical variables related to the diagnostic stability of demential syndromes.

Assigning a diagnosis to a patient with dementia is important for the present treatment of the patient and caregivers, and scientific research. Nowadays, the dementia diagnostic criteria are based on clinical information regarding medical, history, physical examination, neuropsychological tests, and supplementary exams and, therefore, subject to variability through time. A retrospective observational study to evaluate variables related to clinical diagnostic stability in dementia syndromes in at least one year follow up. From a sample of 432 patients, from a single university center, data were collected regarding sociodemographic aspects, Clinical Dementia Rating, physical examination, neuropsychological tests, and supplementary exams including a depression triage scale. From this sample, 113 (26.6%) patients have their diagnosis changed, most of them adding a vascular component to initial diagnosis or depression as comorbidity or main disease. Our findings show that many factors influence the diagnostic stability including the presence of symmetric Parkinsonism, initial diagnosis of vascular dementia, presence of diabetes and hypertension, the presence of long term memory deficit in the neuropsychological evaluation, and normal neuroimaging. We discuss our findings with previous findings in the literature. Every step of the clinical diagnosis including history, vascular comorbidities and depression, physical examination, neuropsychological battery, and neuroimaging were relevant to diagnosis accuracy.

Dementia with Lewy bodies

PET or SPECT imaging can be used to detect reduced dopamine transporter uptake and distinguish AD from DLB. Severe atrophy of the hippocampus is more typical of AD than DLB. Before dementia develops (during the mild cognitive impairment phase), MRI scans show normal hippocampal volume. After dementia develops, MRI shows more atrophy among individuals with AD, and a slower reduction in volume over time among people with DLB than those with AD. Compared to people with AD, FDG-PET brain scans in people with DLB often show a cingulate island sign. In East Asia, particularly Japan, is used in the differential diagnosis of DLB and AD, because reduced labeling of cardiac nerves is seen only in Lewy body disorders. Other indicative and supportive biomarkers are useful in distinguishing DLB and AD (preservation of medial temporal lobe structures, reduced occipital activity, and slow-wave EEG activity).

Psichiatry_DSM-5

Note: Code first 331.19 (G31.09) frontotemporal disease. 294.1 1 (F02.81) With behavioral disturbance 294.10 (F02.80) Without behavioral disturbance 331 .9 (631.9) Possible Major Neurocognitive Disorder Due to Frontotemporal 331.83 (631.84) Mild Neurocognitive Disorder Due to Frontotemporal Lobar _._ (7.7) Probable Major Neurocognitive Disorder With Lewy Bodiesb Note: Code first 331.82 (631.83) Lewy body disease. 294.1 1 (F02.81) With behavioral disturbance 294.10 (F02.80) Without behavioral disturbance 331.9 (631.9) Possible Major Neurocognitive Disorder With Lewy Bodiesa' b 331.83 (631.84) Mild Neurocognitive Disorder With Lewy Bodiesa 7.7 (7.7 Probable Major Vascular Neurocognitive Disorderb Note: No additional medical code for vascular disease. 290.40 (F01.51) With behavioral disturbance 290.40 (F01.50) Without behavioral disturbance 331.9 (631.9) Possible Major Vascular Neurocognitive Disordera' b 331.83 (631.84) Mild Vascular Neurocognitive Disordera

Homonymous Hemianopsia Associated with Probable Alzheimer's Disease.

Posterior cortical atrophy (PCA) is a rare neurodegenerative disorder that has cerebral atrophy in the parietal, occipital, or occipitotemporal cortices and is characterized by visuospatial and visuoperceptual impairments. The most cases are pathologically compatible with Alzheimer's disease (AD). We describe a case of PCA in which a combination of imaging methods, in conjunction with symptoms and neurological and neuropsychological examinations, led to its being diagnosed and to AD being identified as its probable cause. Treatment with donepezil for 6 months mildly improved alexia symptoms, but other symptoms remained unchanged. A 59-year-old Japanese woman with progressive alexia, visual deficit, and mild memory loss was referred to our neurologic clinic for the evaluation of right homonymous hemianopsia. Our neurological examination showed alexia, constructional apraxia, mild disorientation, short-term memory loss, and right homonymous hemianopsia. These findings resulted in a score of 23 (of 30) points on the Mini-Mental State Examination. Occipital atrophy was identified, with magnetic resonance imaging (MRI) showing left-side dominance. The MRI data were quantified with voxel-based morphometry, and PCA was diagnosed on the basis of these findings. Single photon emission computed tomography with (123)I-N-isopropyl-p-iodoamphetamine showed hypoperfusion in the corresponding voxel-based morphometry occipital lobes. Additionally, the finding of hypoperfusion in the posterior associate cortex, posterior cingulate gyrus, and precuneus was consistent with AD. Therefore, the PCA was considered to be a result of AD. We considered Lewy body dementia as a differential diagnosis because of the presence of hypoperfusion in the occipital lobes. However, the patient did not meet the criteria for Lewy body dementia during the course of the disease. We therefore consider including PCA in the differential diagnoses to be important for patients with visual deficit, cognitive impairment, and cerebral atrophy in the parietal, occipital, or occipitotemporal cortices. A combination of imaging methods, including MRI and single photon emission computed tomography, may help identify probable causes of PCA.

Psichiatry_DSM-5

Specify if: Persistent Major or Mild Neurocognitive Disorder Due to HIV Infection (632) .7) Major Neurocognitive Disorder Due to HIV Infectionb Note: Code first 042 (320) HIV infection. 294.11 (F02.81) With behavioral disturbance 294.10 (F02.80) Without behavioral disturbance 331.83 (631.84) Mild Neurocognitive Disorder Due to HIV Infectiona Major or Mild Neurocognitive Disorder Due to Prion Disease (634) 7.7 ( .7) Major Neurocognitive Disorder Due to Prion Diseaseb Note: Code first 046.79 (A813) prion disease. 294.1 1 (F02.81) With behavioral disturbance 294.10 (F02.80) Without behavioral disturbance 331.83 (631.84) Mild Neurocognitive Disorder Due to Prion Diseasea Major or Mild Neurocognitive Disorder Due to Parkinson’s Disease (636) 7.7 (7.7) Major Neurocognitive Disorder Probably Due to Parkinson’s Note: Code first 332.0 (020) Parkinson’s disease.

Neurology_Adams

Three categories of data are useful for the recognition and differential diagnosis of dementing brain disease: 1. A reliable history of the illness and its impact on daily life 2. Findings on mental examination 3. Ancillary examinations: CT, MRI, functional imaging, sometimes lumbar puncture, EEG, and appropriate laboratory procedures, as described in Chap. 2. The history should be supplemented by information obtained from a person other than the patient, because, through lack of insight, the patient will have limited and variable grasp of his illness or its gravity; indeed, he may be unaware even of his chief complaint. Special inquiry should be made about the patient’s general behavior, capacity for work, personality changes, language, mood, special preoccupations and concerns, delusional ideas, hallucinatory experiences, personal habits and care in hygiene, and such faculties as memory and judgment.