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Preparing for public health emergencies is an ongoing process and involves a variety of approaches and tools. Tabletop exercises are one of the tools designed to simulate the emergence of a public health emergency and address some or all of the phases of emergency management: mitigation, preparedness, response, and recovery.1 They typically are designed to include participation of stakeholders from diverse and complementary backgrounds, including command, operations, logistics, planning, and finance.2 Effective tabletop exercises provide a plausible scenario that require cooperation and communication from these functional areas. Tabletops also require forward thinking and planning in a variety of scenarios. When a public health emergency occurs, decision makers may be overwhelmed with decisions that need their immediate attention. Tabletop exercises can provide a framework to help decision makers anticipate future challenges, which may provide the mental model encompassing knowledge and insights that inform both current and future decisions.

This is a compilation of data on the occurrence of mycotoxins other than aflatoxin in foods and feeds from Africa, Asia and South America with 75 references.

Familial periodic paralysis (FPP), both the hypo- and hyperkalemic variants, is a relatively rare inherited disorder but nevertheless is known to most pediatricians. On the other hand, nonfamilial hypokalemic periodic paralysis associated with thyrotoxicosis (TPP) apparently has not been reported in the pediatric literature. The disorder has been described most frequently in Asian males. A total of 2% of thyrotoxic patients in China and Japan were reported to have this complication, and of these, 23 of the 25 patients were males.1 In the United States, the incidence of TPP in a non-Asian ethnic population is approximately one-tenth that found in Asian countries,2 but it also predominates in males.3 The clinical picture is identical to that of FPP, except that associated hyperthyroidism is an absolute requirement. The typical presenting manifestation is the onset of generalized paralysis, more severe in the lower extremities and in the early morning, often occurring after strenuous exercise and/or a high-carbohydrate meal. Although most attacks resolve spontaneously and leave no residual weakness, cardiac arrhythmias can be life-threatening.4-6Recovery can be hastened by the administration of potassium. Symptoms of hyperthyroidism may be minimal or nonexistent.2Laboratory findings include low potassium and elevated creatine phosphokinase concentrations in serum;7electrocardiographic changes characteristic of hypokalemia may be present,4 and abnormal thyroid function studies are found. A 16-year-old Chinese-American male had an episode of muscle pain in his calves and thighs in July 1995 after 3 days of “sore throat.” The pain had been present for 2 days when he was examined, and was the most severe during the first 2 hours after arising. Physical examination yielded normal findings, with a pulse of 88 and blood pressure of 134/74 mm Hg. No thigh tenderness or swelling of the extremities was present. Reflexes were normal, and …

The case records of 97 patients with proven bacterial meningitis who were referred to a regional neurosurgical unit between 1964 and 1991 were reviewed. Mortality declined from 34% in the first cohort referred between the years 1964–82 to 5% for 1983–91 (X2=11.78;p2=4.43; p2=7.57; p2=17.3; p2=6.73; p

✓ Of 1000 patients with nonmissile depressed skull fractures, 10% had early epilepsy (first week) and 15% developed late epilepsy. The risk of late epilepsy varied widely but could be predicted from clinical data 1 week after injury. In more than one-third of the patients with depressed fractures the risk of late epilepsy is less than 4%, but in some patients it is over 60%. The risk is increased if posttraumatic amnesia exceeds 24 hours, if the dura is torn, if there are focal signs, or if there has been early epilepsy.

Raised intracranial pressure is common in neurosurgical practice, but the clinical effects are variable. The factors which initiate intracranial hypertension are now fairly well established; the extent of the increase of intracranial pressure produced by any combination of these factors is a function of the volume-pressure status of the patient at that particular time and may be expressed in terms of brain clastance. The effects of raised intracranial pressure on the function of the brain are mediated through both changes in cerebral blood flow and brain shift or herniation. Understanding of these principles helps in selection of effective therapy for raised intracranial pressure. Ideal clinical management of raised intracranial pressure should be directed toward the identification of those situations in which intracranial pressure may become increased and should attempt to prevent intracranial hypertension before it actually occurs.

In eight anaesthetized, ventilated adult baboons, the intracranial volume-pressure response was examined at differing levels of raised intracranial pressure during induced changes in systemic arterial pressure and cerebral blood flow. The volume-pressure response is defined as the change in ventricular fluid pressure caused by a volume addition of 0·05 ml to the lateral ventricle. At normal intracranial pressure, the volume-pressure response was unchanged by alterations in systemic arterial pressure and cerebral blood flow. At raised intracranial pressure, however, systemic arterial hypertension rendered the intracranial contents more sensitive to the effects of an addition to the ventricular volume as shown by an increased volume-pressure response. When intracranial pressure was increased, there was a significant linear correlation between the volume-pressure response and both arterial pressure and cerebral blood flow. The clinical implication of this phenomenon is that arterial hypertension in patients with increased intracranial pressure is likely to have a deleterious effect by increasing brain tightness.

Four patients from a larger group of 18 patients receiving dextrose-free isotonic (3%) amino acid solution as nutritional support, form the basis of this report. An additional seven patients received intravenous isotonic (5%) dextrose as their sole support in the postoperative period following major elective surgery (average nitrogen balance = -12.3 +/- 2.7 g). All patients were well-nourished as determined by anthropometric measurements. The nonseptic patients receiving infusions of isotonic amino acids demonstrated an improvement in nitrogen balance (= delta 8.5 +2, P less than 0.001) when compared to the postoperative use of 100 to 150 g of glucose. However, sepsis produced a decreased net utilization of the infused crystalline amino acids such that nitrogen balance was similar to the intravenous glucose group (- 10.6 +/- 2.1). This septic response was associated with decreased plasma free fatty acid concentrations and the absence of starvation ketosis and ketonuria. While the nitrogen balance was not different in the septic and the dextrose control groups, deficiencies in plasma amino acid concentrations were observed in the group receiving intravenous infusion of glucose.

Fourteen well-nourished patients undergoing elective major surgery were maintained on intravenous, dextrose-free isotonic (3%) amino acid solution postoperatively. Seven patients developed fevers greater than 100 F due to a variety of mild infective complica- tions. While all patients developed a negative nitrogen balance postoperatively in this ketonemic state, infection did not appear to increase nitrogen loss. This is in striking contrast to the response observed in the fed state. Adaptation to starvation, particularly the effect of ketones on muscle metabolism, would appear to reduce significantly the nitrogen loss during infection. Am. J.

Intermittent additions of 0·05 ml saline were made into the lateral ventricle of anaesthetized, ventilated baboons at regular intervals during continuous inflation of a supratentorial extradural balloon. Close correlation was observed both between the increase in ventricular fluid pressure (VFP) immediately after the injection and the volume in the balloon (P < 0·001); and between the increase in ventricular pressure and the pressure immediately before the injection (P < 0·001). This change in ventricular fluid pressure, which is termed the volume–pressure response (VPR), helps to delineate the stage reached on the intracranial volume–pressure curve, and is therefore a measure of the capacity of the intracranial contents to compensate for the volume changes produced by an expanding intracranial lesion. The VPR is currently being used in patients and the clinical implications of confirming its validity experimentally are therefore discussed.

The palmomental reflex was elicited, unilaterally or bilaterally, in 28% of a series of 121 patients with neurological disorders. There was no significant variation in the prevalence of the palmomental reflex with the age and the sex of patients, with the cause of the neurological disorder, or with the site of cerebral lesions. However, the reflex was found to be significantly more common among patients with signs of focal or generalized brain dysfunction than among patients with normal cerebral function (P less than 0.001). The side of the body on which the reflex was elicited was no indication of the side on which the cerebral lesion was situated. In three patients, who were examined on several occasions, the reflex disappeared as the psychomotor function of the patients improved. On the basis of the results, the nature of the palmomental reflex and the reasons why its presence is difficult to interpret are discussed.

✓ While corticosteroids in standard neurosurgical dosage do not appear to influence recovery from severe head injury or elevated intracranial pressure (ICP), some reports claim that a much higher dose is effective. A resultant hypothesis is that an abrupt increase in corticosteroid dosage in patients with severe head injury should cause a detectable reduction in ICP and in cerebral elastance within 48 hours. To test this hypothesis, 20 consecutive patients with severe head injury, 12 of whom had had surgical decompression of mass lesions, were studied. All patients were artificially ventilated, and had continuous monitoring of ICP and intermittent testing of elastance by measurement of the volume-pressure response (VPR). For the first 12 hours after admission, patients received methylprednisolone, 40 mg every 6 hours. The dose was then increased abruptly by giving a single dose of 2 gm and 500 mg every 6 hours for the next 24 hours, then tapering rapidly. No significant change in ICP or VPR could be detected after 24 or 48 hours of high-dose steroid therapy. Of the 20 patients, 50% had good recovery or were moderately disabled, 15% were severely disabled or vegetative, and 35% had died. The course of ICP and the outcomes in these patients were not significantly different from those observed in a previous group of 262 patients managed in the same way for the high-dose regimen. There was, however, a high incidence of gastric hemorrhage (50%) and of hyperglycemia with glucosuria (85%) in these 20 patients. These negative results in patients with head injury stand in marked contrast to our experience of the benefit of methylprednisolone in patients with brain tumors.

The future role of the neurosurgeon in the management of head injury is reviewed in terms of the care of patients with minor, moderate and severe head injuries. In minor head injury it is predicted that there will be increasing pressure on the neurosurgeon to undertake the management and follow-up of all patients who have sustained head injury, and this will place a considerable additional load on each neurosurgical unit. This is based on a survey of 1919 head injuries admitted in one calendar year (1981), consisting of 93 severe injuries (GCS less than 8), 210 moderate injuries (GCS 8-12), and 1616 minor injuries (GCS 13/14). In moderate injuries CT will assume a major role in detecting hematoma early and identifying contusions. There may yet be a role for steroids in these cases and there should be a greater use of neurorehabilitation, instead of the current overemphasis on the severely injured. In severe injury future efforts will be to prevent early secondary insults and to find better methods of controlling raised intracranial pressure.

✓ Cerebral blood flow (CBF), intracranial pressure (ICP), brain metabolism (CMRO2), systemic arterial pressure (SAP), and arterial blood gases were measured in comatose patients, most of whom had suffered a head injury. The patients were divided into two groups according to whether a mass lesion was or was not demonstrated by bilateral carotid angiography. In the majority of patients a control run measuring regional cerebral blood flow (rCBF) was followed by a test of cerebral autoregulation; hypertonic mannitol was then administered. During the control period there was marked and unpredictable variability in all of the parameters recorded. There was no correlation between ICP or CBF and neurological status or CMRO2 except at very high levels of ICP. Autoregulation was intact in some patients and defective in others, and there was no correlation between the status of autoregulation on the one hand and CBF or survival on the other. Mannitol increased CBF in nearly all patients, to twice the control value in a few, and CMRO2 increased with CBF in several patients. The change in CBF was independent of the initial ICP or the response of ICP to mannitol. Thus, the relationship of these parameters was unpredictable in acutely brain-damaged patients; the status of autoregulation was also unpredictable.

The lungs of all air-breathing vertebrates contain a form of pulmonary surfactant that lines the alveolar air-water interface where it modifies the interfacial surface tension. These pulmonary surfactants all consist of varying amounts of phospholipids (saturated and unsaturated) and cholesterol. The extent of variation between vertebrate groups and between species within a vertebrate group has been attributed to differences in factors such as phylogeny, body temperature, habitat, and lung structure. The influence of these factors on amphibian surfactant composition and function has been studied, but the reptiles, which comprise a polyphyletic group of vertebrates, have never been critically examined. The surfactant lipid composition from species belonging to the three groups of reptiles, the Archosauria (crocodiles), Lepidosauria (snakes and lizards), and Anapsida (turtles), has been determined. New data is presented in conjunction with already published data to create an evolutionary framework that concentrates particularly on the influence of phylogeny, body temperature, and lung structure on the composition of the surfactant lipids. Large amounts of pulmonary surfactant were found in all species of reptiles. All species lavaged at 23 degrees C (except C. atrox) demonstrated DSP/PL ratios of 23-33%. Animals with multicameral lungs exhibited an elevated CHOL/DSP ratio compared with species with unicameral lungs. In all groups, phosphatidylcholine (PC) was the dominant (60-80%) phospholipid. Phosphatidylserine and phosphatidylinositol (PS/PI) and sphingomyelin (S) represented the other phospholipids, while phosphatidylglycerol (PG), lysophosphatidylcholine (LPC), and phosphatidylethanolamine (PE) were occasionally observed. In two species of lizards (C. nuchalis and P. vitticeps), the saturated fatty acid, palmitic acid (16:0), was the dominant tail group on the phospholipids. Oleic acid (18:1) was the dominant monounsaturated fatty acid, whereas polyunsaturates comprised about a fifth of the total fatty acid profile. Short-term (4 h) changes in temperature did not affect the relative proportions of the fatty acids in either species. Comparison of the current data with previously published literature suggests that phylogeny and habitat do not significantly influence surfactant lipid composition, but body temperature and to a lesser extent lung structure are important determinants of reptilian surfactant lipid composition.