Diagnostic Criteria for DM according to ISPAD 2018 *Classic symptoms of diabetes with blood glucose > 200mgr/dl or: * Fasting glycemia ≥ 126mgr/dl (fasting at least 8h) or * Glycemia at 2h SOG ≥ 200mgr/dl (on 2 occasions) or * HbA1C ≥ 6.5%.

58-year-old male, obese, asymptomatic, moderate drinker, who presents a first baseline blood glucose of 153 mg/d with negative glycosuria. In the following weeks he has had two other baseline blood glucose readings of 118 and 136 mg/dl. Which of the following is the most appropriate approach to confirm the diagnosis of diabetes mellitus:

Practice a blood glucose curve with 75 g of glucose.

Already meets diagnostic criteria for diabetes mellitus.

Request a determination of basal insulinemia or C-peptide.

Request a determination of glycosylated hemoglobin.

Random glucose test

Reference values The reference values for a "normal" random glucose test in an average adult are 80–140mg/dl (4.4–7.8 mmol/l), between 140-200mg/dl (7.8–11.1 mmol/l) is considered pre-diabetes, and ≥ 200 mg/dl is considered diabetes according to ADA guidelines (you should visit your doctor or a clinic for additional tests however as a random glucose of > 160mg/dl does not necessarily mean you are diabetic). See also Blood glucose Diabetes mellitus Hypoglycemia References External links Glucose Tests @ Lab Tests Online ADA page that hints at random glucose levels Blood tests Diabetes-related tests

Glucose test

Reference ranges Fasting blood sugar A level below 5.6 mmol/l (100 mg/dl) 10–16 hours without eating is normal. 5.6–6 mmol/l (100–109 mg/dl) may indicate prediabetes and oral glucose tolerance test (OGTT) should be done for high-risk individuals (old people, those with high blood pressure etc.). 6.1–6.9 mmol/l (110–125 mg/dl) means OGTT should be done even if other indicators of diabetes are not present. 7 mmol/l (126 mg/dl) and above indicates diabetes and the fasting test should be repeated. Glucose tolerance test Postprandial glucose test Random glucose test See also Hyperglycemia Hypoglycemia References Blood tests

Prediabetes

Diagnosis Prediabetes can be diagnosed with three different types of blood tests: Fasting blood sugar (glucose) level of: 110 to 125 mg/dL (6.1 mmol/L to 6.9 mmol/L) – WHO criteria 100 to 125 mg/dL (5.6 mmol/L to 6.9 mmol/L) – ADA criteria Glucose tolerance test: blood sugar level of 140 to 199 mg/dL (7.8 to 11.0 mM) 2 hours after ingesting a standardized 75 gram glucose solution Glycated hemoglobin (HbA1c) between 5.7 and 6.4 percent, ie 38.9 and 46.4 mmol/mol Levels above these limits would justify a diagnosis for diabetes. Impaired fasting glucose

Diabetes

A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.

Diabetes

Diagnosis Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following: Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight. Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 gram oral glucose load as in a glucose tolerance test (OGTT) Symptoms of high blood sugar and plasma glucose ≥ 11.1 mmol/L (200 mg/dL) either while fasting or not fasting Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol (≥ 6.5 DCCT %).

Review of criteria for diagnosis of diabetes mellitus based on results of follow-up study.

Comparison of the 75-g oral glucose tolerance test (OGTT) method was made with the conventional 50-g method in a fixed population followed for 1--17 yr. The possibility of using the results in establishing the diagnosis of diabetes mellitus was also considered. The following results were obtained: (1) The 75-g method showed significantly higher 2-h and 3-h postchallenge plasma glucose (PG) and immunoreactive insulin values. (2) The two methods showed good correlation in PG values at various time periods, and there was no difference between the two at 1/2 h and 1 h. The 2-h standard value of 200 mg/dl used to diagnose diabetes with the 75-g method was equivalent to 180 mg/dl by the 50-g method. The upper limits of normals were 140 mg/dl and 120 mg/dl, respectively, for the two tests. (3) Those subjects diagnosed as diabetic on the basis of fasting plasma glucose (FPG) values of 140--149 mg/dl only had a high rate of reverting to normal over time. The frequency of "nondiabetic" plasma glucose values after glucose loading steadily decreases as FPG increased, with separation into two asymptotic lines at 150 mg/dl level. Thus, the logical value for diagnosis of diabetes when based only on FPG value is considered to be 150 mg/dl. (4) A smaller number of individuals had 2-h PG values that satisfied criteria for diagnosis of diabetes mellitus, but 1/2-h and 1-h values that were less than 200 mg/dl. Nevertheless, follow-up of these subjects showed a high development rate of diabetes. Thus, the 1/2-h and 1-h values are not considered necessary to establish diagnosis of diabetes mellitus.

Diagnostic criteria for diabetes mellitus in Japan--from a report of the Japan Diabetes Society (JDS) Committee on the Diagnosis of Diabetes Mellitus, 1982.

After the proposal of diagnostic criteria for diabetes mellitus by the National Diabetes Data Group (1979) and by WHO (1980), a committee was set up by the Japan Diabetes Society (JDS) to reconsider the old criteria by the JDS which had been proposed in 1970. Items covered by the report of the committee in 1982 included the concept of diabetes mellitus, describing it's features, and stating that it's diagnosis is a procedure of recognizing the disease 'diabetes' characterized by these features. Cutoff blood glucose values for fasting samples, after a 75 g oral glucose tolerance test, were proposed to define normal and diabetic types. The cutoff values for the diabetic type are identical to those of the WHO defining diabetes, whereas the values for the normal type (fasting < 110 mg/dl and 1-h < 160 and 2-h < 120 mg/dl for venous plasma) are much lower than those for the lower limit of IGT by the WHO. Subjects whose glucose tolerance is neither diabetic nor normal are classified as borderline type, which includes not only IGT but cases with milder glucose intolerance. The cutoff points for the normal type were selected based on the long-term follow-up data for mild glucose intolerance in Japan. The Committee further stated that the clinical diagnosis of diabetes should be made not only on the basis of the glucose tolerance data, but also after clinical consideration of the possibility of any other diseases which might impair glucose tolerance.

Prediabetes

Impaired glucose tolerance Impaired glucose tolerance (IGT) is diagnosed with an oral glucose tolerance test. According to the criteria of the World Health Organization and the American Diabetes Association, impaired glucose tolerance is defined as: two-hour glucose levels of 140 to 199 mg per dL (7.8 to 11.0 mmol/l) on the 75-g oral glucose tolerance test. A patient is said to be under the condition of IGT when he/she has an intermediately raised glucose level after 2 hours, but less than the level that would qualify for type 2 diabetes mellitus. The fasting glucose may be either normal or mildly elevated. From 10 to 15 percent of adults in the United States have impaired glucose tolerance or impaired fasting glucose.

Diabetes

Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to have impaired fasting glucose. People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease. The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL). Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause. Prevention

Glucose tolerance test

Results Fasting plasma glucose (measured before the OGTT begins) should be below 5.6 mmol/L (100 mg/dL). Fasting levels between 5.6 and 6.9 mmol/L (100 and 125 mg/dL) indicate prediabetes ("impaired fasting glucose"), and fasting levels repeatedly at or above 7.0 mmol/L (>126 mg/dL) are diagnostic of diabetes. For a 2 hour GTT with 75 g intake, a glucose level below 7.8 mmol/L (140 mg/dL) is normal, whereas higher levels indicate hyperglycemia. Blood plasma glucose between 7.8 mmol/L (140 mg/dL) and 11.1 mmol/L (200 mg/dL) indicate "impaired glucose tolerance", and levels at or above 11.1 mmol/L at 2 hours confirm a diagnosis of diabetes.

Glucose tolerance test

For gestational diabetes, the American College of Obstetricians and Gynecologists (ACOG) recommends a two-step procedure, wherein the first step is a 50 g glucose dose. If after 1 hour the blood glucose level is more than 7.8 mmol/L (140 mg/dL), it is followed by a 100 g glucose dose. The diagnosis of gestational diabetes is then defined by a blood glucose level meeting or exceeding the cutoff values on at least two intervals, with cutoffs as follows: Before glucose intake (fasting): 5.3 mmol/L (95 mg/dL) 1 hour after drinking the glucose solution: 10.0 mmol/L (180 mg/dL) 2 hours: 8.6 mmol/L (155 mg/dL) 3 hours: 7.8 mmol/L (140 mg/dL)

Type 2 diabetes

fasting plasma glucose ≥ 7.0 mmol/l (126 mg/dl) or with a glucose tolerance test, two hours after the oral dose a plasma glucose ≥ 11.1 mmol/l (200 mg/dl) A random blood sugar of greater than 11.1 mmol/l (200 mg/dl) in association with typical symptoms or a glycated hemoglobin (HbA1c) of ≥ 48 mmol/mol (≥ 6.5 DCCT %) is another method of diagnosing diabetes. In 2009 an International Expert Committee that included representatives of the American Diabetes Association (ADA), the International Diabetes Federation (IDF), and the European Association for the Study of Diabetes (EASD) recommended that a threshold of ≥ 48 mmol/mol (≥ 6.5 DCCT %) should be used to diagnose diabetes. This recommendation was adopted by the American Diabetes Association in 2010. Positive tests should be repeated unless the person presents with typical symptoms and blood sugars >11.1 mmol/l (>200 mg/dl).

Oxyhyperglycemia

Distinction from regular impaired glucose tolerance Most patients (or animals) with prediabetic type impaired glucose tolerance (serum glucose 140–200 mg/dL at 2 hours after OGTT) are generally not oxyhyperglycemic because: Glycosuria is not necessary for mild impaired glucose tolerance (e.g. at approx 140–180 mg/dL range of blood glucose), is necessary for oxyhyperglycemia (i.e. peak >renal threshold). In contrast to the commonly seen shallow OGTT curve, amplitude of the pointy spike in oxyhyperglycemia need not necessarily be restricted to only prediabetic range and in severe oxyhyperglycemia it may cross 250 mg/dL. In oxyhyperglycemia, by two hours, the glucose not only comes back to pre-diabetic range it may even start shooting below the fasting baseline.

Blood glucose monitoring

Healthcare professionals advise patients with diabetes mellitus on the appropriate monitoring regimen for their condition. Most people with type 2 diabetes test at least once per day. The Mayo Clinic generally recommends that diabetics who use insulin (all type 1 diabetics and many type 2 diabetics) test their blood sugar more often (4–8 times per day for type 1 diabetics, 2 or more times per day for type 2 diabetics), both to assess the effectiveness of their prior insulin dose and to help determine their next insulin dose. Purpose Blood glucose monitoring reveals individual patterns of blood glucose changes, and helps in the planning of meals, activities, and at what time of day to take medications. Also, testing allows for a quick response to high blood sugar (hyperglycemia) or low blood sugar (hypoglycemia). This might include diet adjustments, exercise, and insulin (as instructed by the health care provider). Blood glucose meters

[Diagnostic criteria for diabetes mellitus].

In the last three years, new diagnostic criteria for diabetes mellitus have been proposed by the American Diabetes Association (ADA, 1997), the World Health Organization (WHO) consultation (1998), and the Japan Diabetes Society (JDS, 1999). The most important change from the previous WHO criteria (1985) to these criteria is a decrease in fasting plasma glucose level (FPG) from 140 mg/dl to 126 mg/dl, which defines diabetes mellitus. These criteria attach more importance to FPG than to plasma glucose levels 2 hours after 75 g glucose load (2 hPG). According to these criteria, for example, in one instance with FPG > or = 126 mg/dl, the diagnosis of diabetes mellitus is warranted, if the postprandial plasma glucose > or = 200 mg/dl or another FPG > or = 126 mg/dl were reconfirmed on a subsequent day. The ADA criteria did not recommend an oral glucose tolerance test (OGTT) for routine clinical use. These criteria has established a new category of impaired fasting glucose (IFG) (> or = 110 mg/dl and 126 < mg/dl), similar to impaired glucose tolerance (IGT) which is recognized by performing OGTT. We have reported from a cohort study that there was only one risk factor for IGF: worsening of metabolic derangement progressing to overt diabetes. With IGT, however, there are two risks: a risk for progression to diabetes, and a risk for development of cardiovascular disease. Therefore it seems that whether or not OGTT should be performed depends on the purpose: simply diagnosing for overt diabetes, or detecting risk factors for cardiovascular disease. The JDS criteria proposed the use of HbA1C as a supporting diagnostic tool, because JDS has achieved a fruitful standardization in Japan to a considerable extent. According to the JDS criteria, a diagnosis of diabetes mellitus can be made by an FPG > or = 126 mg/dl when HbA1C > or = 6.5% is confirmed. It is expected that these new criteria will promote further efforts against the increasing number of patients with diabetes mellitus.

InternalMed_Harrison

CRiTERiA foR THE DiAgnoSiS of DiAbETES mElliTuS • Symptoms of diabetes plus random blood glucose concentration ≥11.1 mmol/L (200 mg/dL)a or Fasting plasma glucose ≥7.0 mmol/L (126 mg/dL)b or Hemoglobin A1c ≥ 6.5%c or 2-h plasma glucose ≥11.1 mmol/L (200 mg/dL) during an oral glucose aRandom is defined as without regard to time since the last meal. bFasting is defined as no caloric intake for at least 8 h. cHemoglobin A1c test should be performed in a laboratory using a method approved by the National Glycohemoglobin Standardization Program and correlated to the reference assay of the Diabetes Control and Complications Trial. Point-of-care hemoglobin A1c should not be used for diagnostic purposes. dThe test should be performed using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water, not recommended for routine clinical use.

[The reference value of plasma glucose in individuals over 65 years].

The characteristics of plasma glucose in individuals aged over 65 years was investigated by analysis of age dependent changes of fasting and post glucose (75 g) load values in population based studies and some follow-up studies. Institutional differences were surveyed in central laboratory of institutions which joined this study and found that differences were the range of +3.0-3.5% from the mean glucose levels between 100-400 mg/dl. Therefore plasma glucose values around cutoff level should be confirmed by repeated determinations for reaching final diagnosis. The reference interval of plasma glucose does not differ in an age-dependent manner. We may use the reference interval proposed by the Committee of Diagnostic Criteria of Diabetes Mellitus of Japan Diabetes Society for adult individuals. Cases of diabetes diagnosed before 65 years old should be judged by the adult criteria. However, those who were not diabetic before age 65 and were found to be hyperglycemic after that age can be diagnosed classifying as follows: (1) Diabetes should be diagnosed in individuals with a fasting plasma glucose of 140 mg/dl or more and 2 hours after glucose (75 g) of 240 mg/dl or more. Those with some symptoms suggesting diabetes and either 140 mg/dl more or fasting or 240 mg/dl or more 2 hours post 75 g glucose load can also be diagnosed as diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

Glycated hemoglobin

A1c is measured primarily to determine the three-month average blood sugar level and can be used as a diagnostic test for diabetes mellitus and as an assessment test for glycemic control in people with diabetes. The test is limited to a three-month average because the average lifespan of a red blood cell is four months. Since individual red blood cells have varying lifespans, the test is used as a limited measure of three months. Normal levels of glucose produce a normal amount of glycated hemoglobin. As the average amount of plasma glucose increases, the fraction of glycated hemoglobin increases in a predictable way. In diabetes, higher amounts of glycated hemoglobin, indicating poorer control of blood glucose levels, have been associated with cardiovascular disease, nephropathy, neuropathy, and retinopathy.

Diabetes management

"Perfect glycemic control" would mean that glucose levels were always normal (70–130 mg/dl, or 3.9–7.2 mmol/L) and indistinguishable from a person without diabetes. In reality, because of the imperfections of treatment measures, even "good glycemic control" describes blood glucose levels that average somewhat higher than normal much of the time. In addition, one survey of type 2 diabetics found that they rated the harm to their quality of life from intensive interventions to control their blood sugar to be just as severe as the harm resulting from intermediate levels of diabetic complications. In the 1990s the American Diabetes Association conducted a publicity campaign to persuade patients and physicians to strive for average glucose and hemoglobin A1c values below 200 mg/dl (11 mmol/l) and 8%. Currently, many patients and physicians attempt to do better than that.

Gestational diabetes

An alternative test uses a 75 g glucose load and measures the blood glucose levels before and after 1 and 2 hours, using the same reference values. This test will identify fewer women who are at risk, and there is only a weak concordance (agreement rate) between this test and a 3-hour 100 g test. The glucose values used to detect gestational diabetes were first determined by O'Sullivan and Mahan (1964) in a retrospective cohort study (using a 100 grams of glucose OGTT) designed to detect risk of developing type 2 diabetes in the future. The values were set using whole blood and required two values reaching or exceeding the value to be positive. Subsequent information led to alterations in O'Sullivan's criteria. When methods for blood glucose determination changed from the use of whole blood to venous plasma samples, the criteria for GDM were also changed.

Postprandial glucose test

A postprandial glucose (PPG) test is a blood glucose test that determines the amount of glucose, in the plasma after a meal. The diagnosis is typically restricted to postprandial hyperglycemia due to lack of strong evidence of co-relation with a diagnosis of diabetes. American Diabetes Association do not recommend a PPG test for determining diabetes; it though notes that postprandial hyperglycemia does contribute to elevated glycated hemoglobin levels (a primary factor behind diabetes) and recommends testing and management of PPG levels for those patients who maintain optimum pre-prandial blood glucose levels but have high A1C values. Carbohydrate in the form of glucose is one of the main constituents of foods and assimilation starts within about 10 minutes. The subsequent rate of absorption of carbohydrates in conjunction with the resultant rates of secretion of insulin and glucagon secretion affects the time-weighed PPG profile.

Glucose meter

The imprecision is compounded by the relative likelihoods of false positives and negatives in populations with diabetes and those without. People with type 1 diabetes usually have a wider range of glucose levels, and glucose peaks above normal, often ranging from 40 to 500 mg/dl (2.2 to 28 mmol/l), and when a meter reading of 50 or 70 (2.8 or 3.9 mmol/l) is accompanied by their usual hypoglycemic symptoms, there is little uncertainty about the reading representing a "true positive" and little harm done if it is a "false positive." However, the incidence of hypoglycemia unawareness, hypoglycemia-associated autonomic failure (HAAF) and faulty counterregulatory response to hypoglycemia make the need for greater reliability at low levels particularly urgent in patients with type 1 diabetes mellitus, while this is seldom an issue in the more common form of the disease, type 2 diabetes mellitus.

Glycated hemoglobin

Due to glycated hemoglobin's variability (as shown in the table above), additional measures should be checked in patients at or near recommended goals. People with HbA1c values at 64 mmol/mol or less should be provided additional testing to determine whether the HbA1c values are due to averaging out high blood glucose (hyperglycemia) with low blood glucose (hypoglycemia) or the HbA1c is more reflective of an elevated blood glucose that does not vary much throughout the day. Devices such as continuous blood glucose monitoring allow people with diabetes to determine their blood glucose levels on a continuous basis, testing every few minutes. Continuous use of blood glucose monitors is becoming more common, and the devices are covered by many health insurance plans, but not by Medicare in the United States. The supplies tend to be expensive, since the sensors must be changed at least every 2 weeks. Another useful test in determining if HbA1c values are due to wide variations of blood

Gestational diabetes

The test involves drinking a solution containing a certain amount of glucose, usually 75 g or 100 g, and drawing blood to measure glucose levels at the start and on set time intervals thereafter. The diagnostic criteria from the National Diabetes Data Group (NDDG) have been used most often, but some centers rely on the Carpenter and Coustan criteria, which set the cutoff for normal at lower values. Compared with the NDDG criteria, the Carpenter and Coustan criteria lead to a diagnosis of gestational diabetes in 54 percent more pregnant women, with an increased cost and no compelling evidence of improved perinatal outcomes. The following are the values which the American Diabetes Association considers to be abnormal during the 100 g of glucose OGTT: Fasting blood glucose level ≥95 mg/dL (5.33 mmol/L) 1 hour blood glucose level ≥180 mg/dL (10 mmol/L) 2 hour blood glucose level ≥155 mg/dL (8.6 mmol/L) 3 hour blood glucose level ≥140 mg/dL (7.8 mmol/L)

[The validity of basal blood glucose in the control of non-insulin-dependent diabetic patients].

To validate basal glucemia as a control method for non-insulin dependent diabetes mellitus, and to determine the cut-off point that best characterizes good control. A transversal, observational study of 256 patients who participated in a diabetes mellitus follow-up program during 1993. In the study, glucemia validity indicators were evaluated after making 2 X 2 tables and ROC (receiver operating characteristic) curves for the different values. Control values of glycated hemoglobin was used as to define a good (< 6.5%) and moderate (< 8%). The values of glucemia considered to be "good" as regards control (from 80 to 110 mg/dl, 4.4-6.05 mmol/dl) have good sensitivity (from 97.3% to 100%) and negative predictive values (from 85.7% to 100%) but extremely bad specificity (from 3.8% to 22.7%) and only moderate positive predictive values (from 59.5% to 64.1%) in reference to values of glycated hemoglobin of 6.5%. The same occurs for 8% as regards sensitivity (from 98.6% to 100%), negative predictive value (from 96.4% to 100%) and specificity from 2.1% to 14.5%). Positive predictive value worsens (from 27.8% to 30.3%). The most effective and most accurate values of glucemia in the ROC curves are 150 mg/dl (8.25 mmol/l) if the control of glycated hemoglobin is good, and 170 mg/dl (9.35 mmol/l) if it is moderate. The glucemia control figures recommended by consensus produce false positives when they are compared to glycated hemoglobin. In the analysis of effectiveness and ROC curves greater accuracy is obtained with glucemia values that are slightly higher than those recommended.

[The level of diabetic compensation and endogenous secretion of insulin in newly diagnosed diabetics. Prospective study: Part 1].

In a prospective study of newly detected diabetic patients in 1989-1991 the authors focused their attention on the evaluation of blood sugar levels and HbA1c during manifestation of DM and the amount of insulin secretion in relation to diabetes type 1 and 2 in adult patients. Part 1 of the paper reveals great differences in the fasting blood sugar level during manifestation of DM (26% of the group had a blood sugar level lower than 8.5 mmol/l and 14% above 15 mmol/l) even after 1-4 months treatment (3.8-17.2 mmol/l). Similar differences were found in HbA1c values (4.5-12.9%). High C-peptide levels revealed an incorrectly assessed diagnosis of type 1 diabetes in 16.7% diabetics and low C-peptide values on fasting and postporandial values were at variance with the diagnosis of type 2 diabetes in 6% of the group.

[Diagnosis of type 2 diabetes in general practice].

Among 285 patients seen in general practice, all over the age of 40, 11 (4%) new cases of non-insulin-dependent diabetes mellitus was diagnosed. 12 patients (4%) were found to have impaired glucose tolerance. Measurement of glucose levels in unstandardized blood samples is a suitable method of screening for non-insulin-dependent diabetes in general practice. In order to reduce the number of oral glucose tolerance tests we suggest a modification of WHO guidelines.

[Screening methods for diabetes mellitus in aged group].

There are many methods of screening for diabetes mellitus, for example, blood glucose test, urine sugar test, hemoglobin A1c, fructosamine etc. For the purpose of more efficient screening of diabetes mellitus in elderly groups, these data were analyzed to evaluate validity and ability to estimate prognosis. 1) Validity for screening based on diabetic type was analyzed in 27,074 cases. For screening with the standard level of fasting plasma glucose (FPG) > or = 120 mg/dl, sensitivity was 70.5%, specificity, 94.5%, predictive value, 89.0%, hemoglobin A1c > or = 6.5%, 62.7%, 91.2%, 81.5%, respectively, and fructosamine > or = 290 mumol/L, 54.1%, 92.3%, 78.1%, respectively. FPG had the highest validity. Comparison of validity between the > or = 65-yr group and the < or = 55-yr group was mode. There was significant difference in specificity but sensitivity and predictive value were lower in the > or = 65-yr group. 2) Mean blood glucose levels (BG) +/- S.D. by time after meal were studied. Fasting BG was 84.8 +/- 9.8 mg/dl, 0.5-1 hr. BG after meal, 100.8 +/- 24.5 mg/dl, and 4.5 hr or more, 84.1 +/- 12.8 mg/dl. Based on this data, standard levels for screening based on diabetic type using random blood glucose levels for 0.5-1 hr BG after meals were > or = 130 mg/dl, 1.5-2 hr BG > or = 120 mg/dl, and 3.5 hr or more BG and FBG > or = 100 mg/dl.(ABSTRACT TRUNCATED AT 250 WORDS)

[Study of the beta cell function in type I diabetes by the determination of peptide C after glucagon challenge].

In 35 patients (13F/22M; age range 2-15 years), affected by insulin dependent diabetes mellitus (IDDM), basal and glucagon stimulated C peptide was determined and correlated with the daily insulin requirement (U/Kg/die), the glycosylated hemoglobin (HbA1c), the age of onset (months) and the length of the illness (months). The results of C peptide determinations are illustrated in tab. 1: in 20 patients (group I) the basal value of C peptide is higher than 1 ng/ml and increases after glucagon load; in 15 patients (group II) the basal value of C peptide is lower than 1 ng/ml; in 9 ones (group IIA) of these 15 a glucagon load does not elicit a residual insulin secretion; in the other 6 ones (group IIB) a significative C peptide increase is observed after glucagon load. A better metabolic control (p less than 0.01); Student t test) and a shorter length of the illness (p less than 0.05; Mann-Withney U test) was noticed in the group I in comparison with the group IIA, in which no insulin reserve, even after glucagon load, was demonstrated (tab. 2). However, no difference in the metabolic control, insulin requirement, age of onset or length of the illness resulted between group IIA and group IIB (in which an insulin reserve had been demonstrated only after glucagon load). The basal C peptide evaluation and follow up is useful in the assessment of the individual case of IDDM: a glucagon load may demonstrate a residual insulin reserve in some patients with a low basal C peptide.

Blood glucose monitoring

For patients with diabetes mellitus type 2, the importance of monitoring and the optimal frequency of monitoring are not clear. A 2011 study found no evidence that blood glucose monitoring leads to better patient outcomes in actual practice. Randomized controlled trials found that self-monitoring of blood glucose did not improve glycated hemoglobin (HbA1c) among "reasonably well controlled non-insulin treated patients with type 2 diabetes" or lead to significant changes in quality of life. However a recent meta-analysis of 47 randomized controlled trials encompassing 7677 patients showed that self-care management intervention improves glycemic control in diabetics, with an estimated 0.36% (95% CI, 0.21–0.51) reduction in their glycated hemoglobin values. Furthermore, a recent study showed that patients described as being "Uncontrolled Diabetics" (defined in this study by HbA1C levels >8%) showed a statistically significant decrease in the HbA1C levels after a 90-day period of

Glucose tolerance test

Procedure A zero time (baseline) blood sample is drawn. The patient is then given a measured dose (below) of glucose solution to drink within a 5-minute time frame. Blood is drawn at intervals for measurement of glucose (blood sugar), and sometimes insulin levels. The intervals and number of samples vary according to the purpose of the test. For simple diabetes screening, the most important sample is the 2 hour sample and the 0 and 2 hour samples may be the only ones collected. A laboratory may continue to collect blood for up to 6 hours depending on the protocol requested by the physician.

A new look at screening and diagnosing diabetes mellitus.

Diabetes is underdiagnosed. About one third of people with diabetes do not know they have it, and the average lag between onset and diagnosis is 7 yr. This report reconsiders the criteria for diagnosing diabetes and recommends screening criteria to make case finding easier for clinicians and patients. R.M.B. invited experts in the area of diagnosis, monitoring, and management of diabetes to form a panel to review the literature and develop consensus regarding the screening and diagnosis of diabetes with particular reference to the use of hemoglobin A1c (HbA1c). Participants met in open session and by E-mail thereafter. Metrika, Inc. sponsored the meeting. A literature search was performed using standard search engines. The panel heard each member's discussion of the issues, reviewing evidence prior to drafting conclusions. Principal conclusions were agreed on, and then specific cut points were discussed in an iterative consensus process. The main factors in support of using HbA1c as a screening and diagnostic test include: 1) HbA1c does not require patients to be fasting; 2) HbA1c reflects longer-term glycemia than does plasma glucose; 3) HbA1c laboratory methods are now well standardized and reliable; and 4) errors caused by nonglycemic factors affecting HbA1c such as hemoglobinopathies are infrequent and can be minimized by confirming the diagnosis of diabetes with a plasma glucose (PG)-specific test. Specific recommendations include: 1) screening standards should be established that prompt further testing and closer follow-up, including fasting PG of 100 mg/dl or greater, random PG of 130 mg/dl or greater, or HbA1c greater than 6.0%; 2) HbA1c of 6.5-6.9% or greater, confirmed by a PG-specific test (fasting plasma glucose or oral glucose tolerance test), should establish the diagnosis of diabetes; and 3) HbA1c of 7% or greater, confirmed by another HbA1c- or a PG-specific test (fasting plasma glucose or oral glucose tolerance test) should establish the diagnosis of diabetes. The recommendations are offered for consideration of the clinical community and interested associations and societies.


It does not explain pyramidalism.

Answer 1 incorrect: It does not explain pyramidalism. Answer 2 correct: A nonspecific answer, but probably the correct answer. Answer 3 incorrect: We would lack data to think of a Brown Sequard hemimedullary syndrome. It would explain the pyramidalism, but we would be missing data suggestive of this picture such as a contralateral hypoesthesia. Incorrect answer 4: It could explain the difficulty in dorsiflexion and plantar flexion of the foot, but not the pyramidalism. Incorrect answer 5: In a similar way to the previous one, it could explain part of the clinical picture, but not the pyramidalism.

Answer 1 [HIDDEN]: It does not explain pyramidalism. Answer 2 [HIDDEN]: A nonspecific answer, but probably [HIDDEN]. Answer 3 [HIDDEN]: We would lack data to think of a Brown Sequard hemimedullary syndrome. It would explain the pyramidalism, but we would be missing data suggestive of this picture such as a contralateral hypoesthesia. [HIDDEN]: It could explain the difficulty in dorsiflexion and plantar flexion of the foot, but not the pyramidalism. [HIDDEN]: In a similar way to the previous one, it could explain part of the clinical picture, but not the pyramidalism.

A 56-year-old patient with no personal or family history of interest is studied because he has been having difficulty walking with his right leg for six months. He reports no other symptoms. The examination shows a 4/5 weakness for dorsal flexion and eversion of the foot and 4/5 for flexion and inversion of the foot, with increased muscle reflexes and Babinski present, the rest being normal. The syndromic diagnosis would be:

Mononeuropathy of the right common peroneal nerve.

Focal involvement of the first motor neuron and probably of the second.

Right hemimedullary involvement (Brown-Sequard).

Multiple mononeuropathy with involvement of the common peroneal and right posterior tibial nerve.

Clinical neurophysiology in the diagnosis of peroneal nerve palsy.

Peroneal neuropathy is one of the common focal mononeuropathies in the lower extremities occurring in both adults and children. Foot drop due to weakness of ankle dorsiflexion is the most common presentation of a peroneal neuropathy. It may also result from other causes involving the upper or lower motor neurons. Disorders that must be distinguished from peroneal neuropathy include sciatic mononeuropathy, lumbosacral plexopathy, motor neuron disease, polyneuropathy, and an L5 radiculopathy. To establish a diagnosis, electrodiagnostic studies have been used to localize the level of the abnormality and to establish prognosis. The most common site of injury is the fibular head, but focal neuropathies have also been reported at the level of the calf, ankle, and foot. In this article, we overviewed the peroneal nerve palsy, and its diagnosis by neurophysiologic evaluation, conduction study and needle EMG. The neurophysiologic information gives us the underlying pathophysiology and its prognosis. Therefore the neurophysiologic evaluation must be performed not only for the differential diagnosis, but also for planning the treatment strategy.

Peroneal Nerve Palsy Caused by Proximal Fibular Solitary Osteochondroma: Case Report and Literature Review.

Osteochondroma is a relatively common benign tumor of the bone, and compressive neuropathies due to osteochondroma are comparatively rare. Here, we present a rare case of osteochondroma of the fibular head that caused peroneal nerve palsy in an 8-year-old girl. Physical examination revealed 0/5 tibialis anterior, 1/5 extensor hallucis longus, and 1/5 peroneal brevis muscle power-according to the manual muscle testing grading system, as well as numbness on the lateral side of the right leg and the back of the foot. Radiological examination and ultrasound revealed a bone tumor in the head of the right fibula. Magnetic resonance imaging ruled out spinal nerve root compression. It was discovered that the bone tumor in the fibular head had compressed and displaced the common peroneal nerve. The patient underwent surgical decompression of the right peroneal nerve. A bone region measuring 22 × 14 × 8 mm was removed. Three months postoperatively, the preoperative neurological deficits were found to be nearly resolved. The patient presented with a foot drop for 1 year, but symptoms resolved 3 months after surgery. Conventional wisdom states that surgery should be performed within 3 months, but we recommend that surgery be performed as soon as diagnosis is made even in cases with a long history, as it may improve patient symptoms and outcomes.

Neurology_Adams

Just above the popliteal fossa the sciatic nerve divides into the tibial nerve (medial, or internal, popliteal nerve) and the common peroneal nerve (lateral, or external, popliteal nerve). The latter swings around the head of the fibula to the anterior aspect of the leg, giving off the superficial peroneal nerve that provides musculocutaneous branches (to the peroneal muscles) and to the deep peroneal nerve (formerly called anterior tibial nerve). Branches of the latter supply the dorsiflexors of the foot and toes (anterior tibialis, extensor digitorum longus and brevis, and extensor hallucis longus muscles) and carry sensory fibers from the dorsum of the foot and lateral aspect of the lower half of the leg. There was weakness of dorsiflexion of the foot (foot-drop) in all of the 116 cases of common peroneal neuropathy reported by Katirji and Wilbourn, and numbness of the dorsum of the foot was present in most cases. Weakness of eversion of the foot is usually demonstrable; because

A Unique Case of Common Peroneal Nerve Entrapment.

The authors present a case of a previously healthy 36-year-old man with a 3-day history of spontaneous complete right lower extremity foot drop. He noticed the symptoms immediately when he attempted to stand after waking from sleep. The patient had no history of similar symptoms, recent trauma, or peripheral nerve disease. Physical examination showed a slap foot gait, complete numbness of the lateral leg and dorsal foot, and 0/5 strength with ankle and great toe dorsiflexion and ankle eversion. Serum laboratory studies showed normal values. Nerve conduction studies confirmed increased latency and decreased amplitude of the right peroneal nerve at the knee, whereas electromyography showed denervation of the tibialis anterior and extensor digitorum brevis. Anteroposterior and lateral radiographs showed a normal right knee with the exception of a posterior fibular neck exostosis. Physical therapy, an ankle-foot orthosis, and a 5-day course of oral prednisone burst (50 mg) were prescribed. After 1 month of therapy without resolution, the patient underwent surgical release of the common peroneal nerve and excision of the bony prominence. Twelve days postoperatively, the patient had no sensory improvements but had improved findings on motor examination. Three months postoperatively, the patient had near-normal sensation to light touch in the superficial and deep peroneal nerves, with 5/5 strength and a normal gait. The patient returned to all activity without limitations. The authors present this unique case describing a fibro-osseous source of common peroneal compressive neuropathy and review the literature for spontaneous peroneal entrapment, highlighting the importance of prompt diagnosis and treatment.

Repetitive Plantar Flexion (Provocation) Test for the Diagnosis of Intermittent Claudication due to Peroneal Nerve Entrapment Neuropathy: Case Report.

The diagnosis of peroneal nerve (PN) entrapment neuropathy (PNEN) is based on clinical symptoms and nerve conduction studies. However, these studies do not always detect PNEN. Our 64-year-old patient suffered persistent left L5 numbness after two lumbar surgeries. Two years before admission to our institute his left leg pain gradually reappeared. When walking, his numbness in the left lower thigh to the dorsum of the foot increased. Electrophysiological testing revealed no conduction block on the PN. To identify the origin of his intermittent symptoms we performed loading of repetitive ankle plantar flexion in the at-rest posture to avoid the lumbar factor. We used this provocation test to check for PNEN because it occurs at a site where the PN passes the soleus- and the peroneus longus muscle (SM, PLM). The symptoms appeared reproducibly within 10 s of loading. PN neurolysis under local anesthesia showed that the PN was strongly compressed by the SM and PLM. This procedure eased his symptoms and he was able to walk without elicitation of numbness and pain upon repetitive ankle plantar flexion. In our case, repetitive plantar flexion elicited the symptoms and this provocation test may be useful to identify PN dynamic entrapment neuropathy as the origin of intermittent claudication.

Neurology_Adams

Fig. 10-3) and between the fourth and fifth lumbar vertebrae (compressing the L5 root). Lesions of the fifth lumbar root (L5) produce pain in the region of the hip and posterolateral thigh (i.e., sciatica) and, in more than half such cases, lateral calf (to the lateral malleolus), and less often, the dorsal surface of the foot and the first or second and third toes. Pain is elicited by the straight-leg raising test or one of its variants, and protective nocifensive reflexes come into play, limiting further elevation of the leg. Paresthesia may be felt in the entire territory or only in its distal parts. The tenderness is in the lateral gluteal region and near the head of the femur. Weakness, if present, involves the extensors of the big toe and foot and the foot invertors (a distinguishing feature of foot drop originating from peroneal nerve damage, which spares inversion because it is a tibial nerve function). The ankle jerk may be diminished (more often it is normal), but the knee

List of neuromuscular disorders

Lower extremity deep peroneal mononeuropathy at the fibular neck common fibular mononeuropathy at the hip deep fibular mononeuropathy at the ankle superficial fibular mononeuropathy sciatic mononeuroapthy at the hip or thigh piriformis syndrome proximal tibial mononeuropathy tarsal tunnel syndrome interdigital neuropathy (Morton's Neuroma) sural mononeuropathy femoral mononeuropathy saphenous mononeuropathy lateral femoral cutaneous neuropathy ilioinguinal neuropathy iliohypogastric neuropathy genitofemoral neuropathy posterior femoral cutaneous neuropathy obturator neuropathy neuropathy of gluteal nerves

Electrodiagnostic Evaluation of Peroneal Neuropathy -- Introduction

Patients tend to present with either an acute or a gradual foot drop. Patients may give a history of falls and possibly tripping due to the foot drop. They may also complain of paresthesias or numbness in the lower leg's lateral portion and the foot's dorsum. Pain can be absent in many cases presenting with a foot drop. [3] However, pain can be an initial presenting symptom in patients without a foot drop but can show a slight weakness in ankle dorsiflexion only when carefully examined. [4] One-third of these patients can have normal electrodiagnostic tests. [4]

Neurology_Adams

of common peroneal neuropathy reported by Katirji and Wilbourn, and numbness of the dorsum of the foot was present in most cases. Weakness of eversion of the foot is usually demonstrable; because inversion is a function of the L5 root and the tibial nerve, it is spared in peroneal palsy, thereby allowing a distinction between foot-drop at the two sites. (Foot eversion should be tested with the ankle passively dorsiflexed.) Pain is variable.

Foot Drop -- History and Physical

Sciatic neuropathy classically presents with sensory loss of the whole foot and weakness of ankle plantar flexors (gastrocnemius, soleus) and ankle inversion. It can result in a 'flail foot.' Hamstring muscles may also be involved resulting in knee flexion weakness. It is not uncommon for an incomplete sciatic neuropathy to present as a common peroneal neuropathy. Often, the peroneal fascicles in the sciatic nerve are more susceptible to injury than the tibial fascicles.

Neurology_Adams

Mononeuropathy is the most circumscribed form of peripheral nerve disease. It is reflected by weakness and sensory loss in the territory of a single peripheral nerve. Specific features serve to differentiate mononeuropathy from a radiculopathy—for example, weakness in dorsiflexion and eversion of the foot is referable either to the peroneal nerve or to the L5 nerve root; however, if there is weakness of inversion of the foot, innervated by the tibial nerve, the fault must be with the L5 root, not with the peroneal nerve. Conversely, if inversion is spared in a foot drop, the lesion is in the peroneal nerve. The distribution of sensory loss also aids in distinguishing the two processes; for example, in the aforementioned case the region of sensory change corresponding to the L5 root extends almost up to the knee on the anterior surface of the foreleg whereas it ends a limited distance above the ankle in the case of a peroneal nerve lesion (see the sensory maps in Figs. 8-1, 8-2, and

Peroneal Nerve Injury -- Introduction

Sensory Common peroneal nerve: lateral aspect of the leg just distal to the knee Superficial peroneal nerve: the anterolateral distal third of the leg and the majority of the dorsum of the foot (except the first webspace) Deep peroneal nerve: first dorsal webspace Motor Common peroneal nerve: none Superficial peroneal nerve: eversion of the foot Deep peroneal nerve: dorsiflexion of the foot and great toe extension This paper will focus on peroneal nerve injuries, including etiologies, epidemiology, history, and physical exam findings, as well as diagnosis and treatment.

Intraneural Ganglia of the Common Peroneal Nerve in Children: Case Report and Review of the Literature.

Intraneural ganglia are nonneoplastic cystic formations contained within the epineurium of peripheral nerves. The common peroneal nerve at the fibular neck is the most frequently affected site. Intraneural ganglia are not a frequent occurrence in the adult patients and are even rarer in children, with only 10 pediatric cases reported in the English language literature. We report on a new pediatric case of intraneural ganglion of common peroneal nerve and present a review of the English language literature on this topic in children. A 10-year-old girl was admitted to our institution because of pain referred to posterior and anterior aspects of the right leg and right foot drop. The radiologic investigations showed a wide (20 cm long) intraneural ganglion cyst of the right common peroneal nerve. The patient underwent surgical treatment according to the Spinner technique. Postoperative course was uneventful. A gradual improvement of motor and sensory functions was observed, starting from the third postoperative day, with a complete motor function restoration registered 26 months after surgery. Intraneural ganglia of the common peroneal nerve should always be considered in the differential diagnosis of foot drop in pediatric age since because early diagnosis and adequate surgical treatment play a crucial role in the patient's motor and sensory outcomes.

[Peroneal myoatrophy type 4H FGD4 new gene mutation in one case and literature review].

To explore the clinical and gene mutation characteristics of children with peroneal myoatrophy FGD4 mutations. The clinical data of a patient with peroneal myoatrophy with novel FGD4 gene mutations were collected, the related literature was searched from China National Knowledge Infrastructure, Wanfang Data Knowledge Service Platform, National Center for Biotechnology Information and PubMed (up to December 2014) by using search terms"muscular disorders, atrophic""peripheral nervous system diseases""genes". The clinical features and treatment of the patients with FGD4 gene mutations were studied. The patient was a 10-years-old boy, he was presented to our clinic due to lower extremity weakness for 3 years, worsening for one year with normal family history and birth history. When he was 6 years old, his feet turned inward as he walked, at 7 years of age, his toes pointed toward the ground, the heel could not touch the ground, the right foot was more serious. During the recent year his symptoms were worsened, manifested as clubfoot, foot drop, arched feet, crane legs, difficult in squatting, walking with swaying gait, easy to fall. He was brought to a number of domestic general hospitals' neurology clinic, he was clearly diagnosed as peroneal myoatrophy, but failed to make typing. Electromyography (EMG) showed neurogenic damage (peripheral neuropathy - motor and sensory fibers are involved). Target gene sequencing showed that the child had FGD4 genes compound heterozygous mutation: c. 338A> G and c. 1730G> A, where the former was inherited from his father, the latter inherited from his mother, it was a new mutation unreported previously. Literature search retrieved six reports (all in English literature) with FGD4 10 cases with mutations, which were expressed as peroneal myoatrophy, but were homozygous mutation. This study found the FGD4 4th and the 14th exons' c. 338A> G and c. 1730G> A heterozygous mutations, and this mutations may lead to peroneal myoatrophy.

Peroneal Nerve Injury -- History and Physical

The clinician directs the clinical physical examination by the patient’s reported symptoms and requires an understanding of the relevant anatomy and possible underlying etiology. For example, in cases of suspected chronic peroneal nerve palsy with resultant foot drop, the clinician should consider a primary documented part of the examination focusing on gait assessment as it may provide significant clues to the etiology of the symptoms. [8] A patient with weakened or paralyzed dorsiflexors may ambulate with a high steppage gait to prevent dragging their toes on the ground due to nerve injury. Furthermore, numbness or dysesthesia in the upper lateral leg indicates a lesion proximal to the fibular head, which may involve the sciatic nerve or lumbosacral nerve roots. In contrast, if there is a decreased or abnormal sensation in the lower lateral leg and dorsum of the foot, the superficial peroneal nerve may be involved. If there is also altered sensation in the dorsal aspect of the first web space of the foot, the deep peroneal nerve may also be involved. [8]

[A case of tibial nerve palsy due to intraneural ganglion cysts].

A 39-year-old man presented with an 8-month history of pain and paresthesia of the right foot sole and difficulty in the right toe dorsiflexion. A neurological examination revealed weakness in performing both the ankle and right foot toe dorsiflexion, reduced right planta pedis sensation, and absent right Achilles tendon reflex. Tinel's sign was present on the right popliteal fossa and medial part of the right ankle. MRI of the right knee showed multiple cystic lesions in his right tibial nerve. The cystic lesions extended from the popliteal fossa and were thought to be intraneural ganglion cysts. On MRI performed 4 months later, most of the cystic lesions spontaneously vanished. Therefore, intraneural ganglia should be considered when atypical mononeuropathy, such as tibial nerve palsy, is present.

Foot drop

Foot drop is rarely the result of a pathology involving the muscles or bones that make up the lower leg. The anterior tibialis is the muscle that picks up the foot. Although the anterior tibialis plays a major role in dorsiflexion, it is assisted by the fibularis tertius, extensor digitorum longus and the extensor hallucis longus. If the drop foot is caused by neurological disorder all of these muscles could be affected because they are all innervated by the deep fibular (peroneal) nerve, which branches from the sciatic nerve. The sciatic nerve exits the lumbar plexus with its root arising from the fifth lumbar nerve space.

Neurology_Adams

Bicrural palsy presenting as lower leg weakness with inability to walk on the heels and toes, or as paralysis of all leg muscles With the exception of certain distinctive distal types of muscular dystrophies, this pattern, usually due to weakness of peroneal, anterior tibial, and thigh muscles, is usually not a result of myopathy. Symmetrical weakness of the lower legs is more often caused by polyneuropathy. In cases of total leg and thigh weakness, one first considers a spinal cord disease. Motor neuron disease may begin in the legs, asymmetrically and distally as a rule, and affect them disproportionately to other parts of the body. Thus the differential diagnosis of distal or generalized leg weakness involves more diseases than are involved in the restricted paralyses of other parts of the body.

A thorough history and physical exam to assess the status and function of the common peroneal nerve is always required. In patients with a peroneal nerve injury, clinical presentation varies based on the location and severity of the injury and the presence of anatomic variations. The most common presentation of a common peroneal nerve injury is a weakness of ankle dorsiflexion and the classic resultant foot drop or catching the toes while ambulating. [8] Foot drop can develop acutely or over days to weeks, depending on the etiology. It can also be complete or partial in severity. There may also be accompanying numbness or paresthesia present along the lateral leg, dorsal foot, and/or the first toe webspace. Pain may also be present in traumatic cases but is not always present. [8]

Compressive peroneal neuropathy by an intraneural ganglion cyst combined with L5 radiculopathy: A case report.

Most cases of foot drop are known to result from lower motor neuron pathologies, particularly lumbar radiculopathy and peripheral neuropathy, including common peroneal neuropathy. To improve the prognosis of foot drop, it is important to quickly and accurately diagnose the etiology and provide appropriate treatment. A 65-year-old female patient with a history of L4-5 intervertebral disc herniation presented with right foot drop that had developed 1 month previously. Electrodiagnostic examination revealed common peroneal neuropathy combined with L5 radiculopathy, with the former being the main cause of the foot drop. MRI of the right knee was performed to identify the cause of the peroneal nerve lesion, which revealed an intraneural ganglion cyst in the common peroneal nerve. The patient was treated by ultrasound-guided percutaneous cyst aspiration and corticosteroid injection into the decompressed ganglion, followed by strengthening exercise, electrical stimulation therapy, and prescription of an ankle foot orthosis. We confirmed regeneration of the injured peroneal nerve at the follow-up electrodiagnostic examination 12 weeks after the intervention. In addition, the manual motor power test demonstrated an increase in the ankle dorsiflexor function score by one grade. Diagnosing the cause of foot drop can be difficult with multiple co-existing pathologies, and consideration of various possible etiologies is the key for appropriate diagnosis and treatment. In addition to imaging modalities such as MRI, electrodiagnostic examination can help to improve diagnostic accuracy. Intraneural ganglion cyst of the common peroneal nerve is rare, but should be considered as a possible cause of foot drop.

Lower limb axonal mononeuropathies as sequelae of COVID-19: a case report and review of literature.

Neurological symptoms and complications of Coronavirus disease 2019 (COVID-19) were seldom discussed in the literature initially. Neurological symptoms such as headache, dizziness, anosmia, hypogeusia, and neuralgia are, however, now being reported commonly. Mononeuropathies are rare complications of COVID-19, with most cases associated with prolonged intensive care stay. A 61-year-old gentleman with prior history of well-controlled diabetes and hypertension was recently treated for COVID-19 pneumonia with supplemental oxygen and positive pressure ventilation. He now presented with left-sided foot weakness two weeks after recovering from the viral illness. On examination he had normal bulk and tone and a power of 4/5 in proximal and distal muscles of bilateral lower limbs except for ankle dorsiflexion on the left which was 2/5. He also had absent ankle and knee reflexes bilaterally with bilateral flexor plantar reflexes. Since the patient had no back pain and the sensory system was normal, the lesion was localized to the peripheral nerves and a Nerve Conduction Studies and Electromyography (NCS/EMG) was done. NCS/EMG showed findings suggestive of axonal mononeuropathies. Relevant workup done to identify the cause of mononeuropathy was negative including infectious and autoimmune workup. Since diabetes was well-controlled and he had no intensive care stay his findings were presumed to be associated with resolving COVID-19 infection. The patient underwent aggressive daily physical therapy and has started to show improvement in symptoms. Complications such as mononeuropathies should be kept in mind in patients recovering from COVID-19 infection, since timely diagnosis can improve clinical outcomes in patients.

Surgery_Schwartz

being the tibial nerve). It receives contributions from L4, L5, S1, and S2. It emerges as a separate nerve in the popliteal fossa and laterally wraps around the fibular neck, after which it splits to Brunicardi_Ch42_p1827-p1878.indd 184801/03/19 7:16 PM 1849NEUROSURGERYCHAPTER 42form the deep and superficial peroneal nerves. The superficial, fixed location at the fibular neck makes the common peroneal nerve susceptible to compression. The classic cause of traumatic peroneal neuropathy is crush injury from a car bumper striking the lateral aspect of the leg at the knee. Symptoms of common peroneal neuropathy include foot drop (weakness of the tibialis anterior), eversion weakness, and numbness over the anterolat-eral surface of the lower leg and dorsum of the foot. In contrast, a foot drop due to L5 radiculopathy spares eversion because the S1 fibers are intact. Surgical exploration of a common peroneal crush lesion is typically a low yield endeavor. Rare cases may be due to

Peroneal nerve paralysis

Prolonged pressure on nerve may occur because of: Sitting position Blood clots, tumors Casts on lower leg due to tightness Diagnosis For partial nerve palsy, more than 80% of patients will recover completely. For complete nerve palsy, less than 40% of patients will have complete recovery. Peroneal nerve in continuity arises from defined cause will be recovered better than those arise from unknown causes. Examinations are required for following reasons: Considering lumbar radiculopathy during the examination Possibility of foot drop Sensory loss that may be difficult to determine because of variable and small autonomous zone of sensation Tinel's sign over the fibular neck that can help localize the site of nerve compression Checking for direct compression that reproduces nerve symptoms Electromyography

To test for the motor involvement of the superficial peroneal nerve and deep peroneal nerve, one must assess foot eversion (SPN) and foot/toe dorsiflexion (DPN). A finding of weakness of both foot eversion as well as foot/toe dorsiflexion suggests a lesion involving the common peroneal nerve. [8] Proximal lesions, for example, secondary to traumatic knee dislocations, will often present with varying degrees of numbness in both superficial peroneal nerve and deep peroneal nerve distributions. A careful and detailed examination detecting the presence or absence of dorsiflexion of the ankle and/or great toe past neutral is imperative for motor examination testing. The subtle distinction is important in differentiating the ability to actively dorsiflex the great toe from a maximally plantarflexed position to a near-neutral position. Such findings do not rule out deep peroneal nerve injury.

[A case of chronic progressive motor-dominant multiple mononeuritis associated with primary Sjögren's syndrome].

A 45-year-old female with a history of dry eyes presented with chronic progressive disturbance of her right finger extension, bilateral foot drops, and dysesthesia in the left lower leg. On admission, neurological examination revealed decreased tendon reflex in the right upper limb and bilateral lower limbs, and dysesthesia in the distal outer portions of the bilateral lower legs. Her vibration sensation was moderately diminished in both lower legs. Weakness ranging from moderate to severe was predominantly found in the muscles innervated by the radial (r > l), medial (r > l), ulnar (r > l), deep peroneal (r ≒ l), tibial (r < l), and medial planter nerves (r < l). Nerve conduction study showed asymmetrical axonal neuropathy, while chronic neurogenic changes were observed on needle electromyography. Cerebrospinal fluid analysis results were unremarkable, except for an elevated IgG index (1.53) and the presence of oligoclonal IgG bands. Seropositive anti-SS-A antibody and histological findings of the biopsied minor salivary gland, as well as the lack of other connective tissue disorders, indicated primary Sjögren syndrome (SjS). A left sural nerve biopsy showed inhomogeneous reductions in the myelinated fibers within fascicules, mild infiltration of CD8-positive T lymphocytes around small vessels, and no fibrinoid necrosis in the arteries. From these findings, the diagnosis of motor-dominant multiple mononeuritis associated with primary SjS was made. Therapy that comprised a single course of intravenous (IV) methylprednisolone (1 g for 3 days), followed by oral prednisolone (60 mg/day) with gradual tapering, resulted in no amelioration of her symptoms. She then received IV immunoglobulin (0.4 mg/kg/day for 5 days), which resulted in moderate improvement in the strength of several muscles and a reduction of CSF IgG index (0.89). A wide variety of peripheral nerve complications are documented in primary SjS. However, the present case is unique in the symptoms of chronic progressive, motor-dominant, multiple mononeuritic phenotype.

Common peroneal and tibial nerve paralysis secondary to herpes zoster infection: a case report.

The usual presentation of herpes zoster (HZ) is a self-limiting vesicular rash, often accompanied by post-herpetic neuralgia. However, HZ can give rise to other complications, that have unusual presentations and serious sequelae like segmental motor paralysis of the limbs that is a relatively rare complication. A 68-year-old man presented with foot drop on the right side had a history of HZ infection on and around the knee and the popliteal fossa. He was treated with acyclovir by a dermatologist and 10 days after the inital symptoms he developed weakness on the right ankle and on the muscles distal to the knee. In a few days foot drop has developed and he was unable to walk without help. Three months later he was admitted to the neurology out patient clinic. On his electrophysiological examination common peroneal nerve could not be stimulated on the right side. The distal latency of the tibial nerve has prolonged, CMAP amplitude has diminished and the nerve conduction velocity has slowed down. Latency of the sural nerve has prolonged with a small SNAP amplitude and a slow nerve conduction velocity on the right side. Electromyography revealed denervation on the muscles inervated by tibialis anterior and common peroneal nerves distal to the knee. The double mononeuropathy of the tibial and common peroneal nerves secondary to HZ was not found in the published data. HZ should be considered as a possible cause of the paralysis of peripheral nerves and more attention should be paid to it.

Foot Drop -- History and Physical

A lesion of the L5 root, lumbar plexus, sciatic nerve, common peroneal, or the deep peroneal nerve can potentially lead to foot drop due to the weakness of the anterior compartment musculature. The presenting symptom is the inability to ambulate as before. More specifically, weakness of the muscles in the foot that assist in dorsiflexion. There may or may not be a pain. The person will be unable to dorsiflex during the heel strike. The foot remains flat on the ground. Sometimes can also cause toe drag and inability to clear the foot. This can potentially lead to falls.

HIV Neuropathy-Associated Foot Drop, a Presenting Sign of HIV Infection, Resolving After Initiation of Antiretroviral Therapy: A Clinical Vignette.

Peripheral neuropathy is one of the most frequent complaints in patients with HIV. Many complex syndromes exist, with the etiology being secondary to the disease process itself, antiretroviral medication, or immune reconstitution. However, isolated mononeuropathy is rare. In this case, we present a previously healthy man who complained of several months of worsening right foot drop that did not improve with physical therapy or lifestyle interventions. He had begun to use an solid ankle-foot orthotic on this right lower limb to minimize tripping and prevent falls. He had no other neuromuscular involvement or constitutional complaints. Nerve conduction study of the right lower limb showed decreased peak amplitude, prolonged distal latency, and decreased conduction velocity of the deep peroneal nerve. Electromyography revealed abnormal insertional activity and absent motor unit action potentials in both the right tibialis anterior and right extensor digitorum brevis muscles. Magnetic resonance imaging of the right lower limb was suggestive of acute/subacute denervation of the right tibialis anterior muscle. An extensive laboratory workup revealed active HIV infection with a significant viral load. Once the diagnosis was made, the patient was started on antiretroviral treatment. Six months later, his foot drop had entirely resolved, in association with significant improvements in viral load and CD4 count. He has since been ambulating without assistive devices and his HIV/AIDS disease process remains well controlled. This clinical vignette is the first, to our knowledge, to illustrate that an acute focal mononeuropathy causing foot drop and gait dysfunction in an otherwise healthy-appearing individual can be a heralding sign of HIV/AIDS. Furthermore, it also suggests that this functional deficit can be reversed with timely initiation of antiretroviral treatment. Early recognition, diagnosis, and treatment in this patient have not only led to an uncomplicated AIDS disease course but also restored his ability to ambulate with complete independence and improved his quality of life.

Foot Drop -- History and Physical

Radiculopathy affecting the fifth lumbar nerve root typically results in neuropathic pain starting in the lumbar region and radiating down the posterior thigh, anterolateral leg to the foot down to the big toe.  Sensory symptoms include the medial aspect of the foot, including the first webspace. Motor symptoms include weakness of dorsiflexors and evertors of the foot.

InternalMed_Harrison

Symptoms and signs consist of footdrop (ankle dorsiflexion, toe extension, and ankle eversion weakness) and variable sensory loss, which may involve the superficial and deep peroneal pattern. There is usually no pain. Onset may be on awakening in the morning. Peroneal neuropathy needs to be distinguished from L5 radiculopathy. In L5 radiculopathy, ankle invertors and evertors are weak and needle EMG reveals denervation. EDx can help localize the lesion. Peroneal motor conduction velocity shows slowing and amplitude drop across the fibular head. Management consists of rapid weight loss and avoiding leg crossing. Footdrop is treated with an ankle brace. A knee pad can be worn over the lateral knee to avoid further compression. Most cases spontaneously resolve over weeks or months.

Pseudoaneurysm of the popliteal artery complicated by peroneal mononeuropathy in a 4-year-old child: report of a case.

Pseudoaneurysms of the popliteal artery (PPA) rarely occur in children. In fact, we found only 10 cases reported in the medical literature. We report the case of a 4-year-old boy who presented with a painful palpable mass in the right popliteal fossa. He also had mild, painless right foot-drop and difficulty toe-walking on the same side. The diagnosis of a PPA was based on the findings of triplex ultrasound and computed tomographic-angiography. We attributed the cause of the lesion to blunt trauma, which he had suffered 2 years earlier. Thorough preoperative evaluation excluded the possibility of a self-immune process or a bone tumor in the region. Neurological examination demonstrated a mild, isolated, peripheral mononeuropathy of the right peroneal nerve. Thus, we performed surgical repair using an autologous reversed great saphenous vein graft. The patient had an uneventful postoperative course and his peripheral neuropathy and foot-drop resolved completely within 1 month after surgery. Now, after 3 years of follow-up, the patient has a patent graft and a fully functioning limb. PPAs are rare, especially in children, and trauma is the predominating underlying cause. PPAs should be treated immediately after diagnosis because their complications are associated with high rates of functional impairment and even limb loss.

Hereditary neuropathy with liability to pressure palsy: a recurrent and bilateral foot drop case report.

Hereditary neuropathy with liability to pressure palsy is characterized by acute, painless, recurrent mononeuropathies secondary to minor trauma or compression. A 16-year-old boy had the first episode of right foot drop after minor motorcycle accident. Electromyography revealed conduction block and slowing velocity conduction of the right deep peroneal nerve at the fibular head. After motor rehabilitation, he fully recovered. Six months later he had the second episode of foot drop in the opposite site after prolonged squatting position. Electromyography revealed sensorimotor polyneuropathy of left peroneal, sural, posterior tibial, and deep peroneal nerves and also of ulnar, radial, and median nerves of both upper limbs. Histological examination revealed sensory nerve demyelination and focal thickenings of myelin fibers. The diagnosis of hereditary neuropathy with liability to pressure palsy was confirmed by PMP22 deletion of chromosome 17p11.2. He started motor rehabilitation and avoidance of stressing factors with progressive recovery. After one-year followup, he was completely asymptomatic. Recurrent bilateral foot drop history, "sausage-like" swellings of myelin in histological examination, and the results of electromyography led the authors to consider the diagnosis despite negative family history. The authors highlight this rare disease in pediatric population and the importance of high index of clinical suspicion for its diagnosis.