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The in-step plantar fasciotomy has remained a viable option for treatment of plantar fasciitis. The level of the in-step procedure has previously been described as 1.5 cm distal to the anterior heel fat pad. The authors are unaware of any study defining mean width and thickness of the plantar fascia at specific distances from its insertion. The authors performed a standardized cadaveric dissection of 25 fresh frozen cadaveric specimens from a local region in Pennsylvania. Each fascial band width and thickness of the plantar fascia was measured at the fascial insertion, 2 cm distal from insertion, and 3 cm distal from insertion. The mean (± standard deviation) width of the medial, central, and lateral band of the plantar fascia 3 cm from its insertion was 25.3 ± 5.3, 25 ± 3.41, and 23.3 ± 4.49 mm, respectively. At the same anatomic distance, the band thicknesses were 1.5 ± 0.82, 3.3 ± 0.85, and 1.9 ± 0.33 mm, respectively. The literature describes 2 techniques. The first is transecting between one-third to two-thirds of the plantar fascia during a fasciotomy from medial to lateral. The second is identifying, isolating, and releasing the central band. Our study allows to further quantify this, equating to 24.5 to 49 mm in total medial to lateral transection at 3 cm distal from insertion and an isolated central band equating to 25 ± 3.41 mm. With quantitative measurements of transection length, the surgeon will avoid having to estimate and potentially overtransect. This may help in preventing postoperative sequela related to overcorrection., (Copyright © 2020 the American College of Foot and Ankle Surgeons. Published by Elsevier Inc. All rights reserved.)

Objective: To evaluate the analgesic efficacy and safety of a novel intravenous (IV) formulation of meloxicam (30 mg) in patients with moderate-to-severe pain following a standardized, unilateral bunionectomy with first metatarsal osteotomy and internal fixation., Materials and Methods: Patients who met the criteria for moderate-to-severe postoperative pain were randomized to receive bolus injections of meloxicam IV 30 mg (n=100) or placebo (n=101) administered once daily. The primary efficacy endpoint was the Summed Pain Intensity Difference over 48 hours (SPID48). Secondary efficacy endpoints included sum of time-weighted pain intensity differences (SPID) values at other timepoints/intervals, time to first use of rescue analgesia, and number of rescue doses taken. Safety assessments included the incidence of adverse events (AEs), physical examinations, laboratory tests, 12-lead electrocardiography, and wound healing., Results: Patients randomized to meloxicam IV 30 mg exhibited a statistically significant difference in SPID48 versus the placebo group (P=0.0034). Statistically significant differences favoring meloxicam IV over placebo were also observed for secondary efficacy endpoints, including SPID at other times/intervals (SPID6: P=0.0153; SPID12: P=0.0053; SPID24: P=0.0084; and SPID24-48: P=0.0050) and first use of rescue medication (P=0.0076). Safety findings indicated that meloxicam IV 30 mg was generally well tolerated; no serious AEs or bleeding events were observed. Most AEs were assessed by the investigator to be mild in intensity, and no patients discontinued due to AEs. There were no meaningful differences between the study groups in vital signs, electrocardiographic findings, or laboratory assessments. In most cases, investigators found that wound healing followed a normal course and mean wound-healing satisfaction scores were similar for meloxicam IV 30 mg and placebo., Discussion: Meloxicam IV doses of 30 mg provided effective pain relief when administered once daily by bolus injection to patients with moderate-to-severe pain following bunionectomy, and had an acceptable safety profile.

Background: Pseudotumor cerebri, or idiopathic intracranial hypertension, is a condition most commonly affecting women of childbearing age who are obese or who have experienced recent weight gain. Frequently the patient complains of headache accompanied by dizziness, nausea, or visual defects, and it is characterized by elevated intracranial pressure in the absence of a space-occupying lesion or infection, Methods: A patient had been prescribed minocycline and subsequently developed symptoms 6 weeks after an increase in the original dosage. She was initially examined by an ophthalmologist, then was sent to the Emergency Department, and finally admitted under the family practice service. Articles were searched through MEDLINE, MD Consult, and Google. Key words included "pseudotumor cerebri," benign intracranial hypertension," idiopathic intracranial hypertension," and "minocycline.", Results and Conclusion: Although the pathogenesis of pseudotumor cerebri is not completely understood, an association has been observed with minocycline use. This report describes a 16-year-old girl who developed idiopathic intracranial hypertension while taking minocycline for acne. Symptoms of blurred vision and severe headache unrelated to position or activity; an absence of fever, bilateral disk edema, and focalizing neurologic signs; negative neuroradiographic findings; increased cerebrospinal fluid pressure with a normal cell count; and exclusion of systemic or structural cause of increased intracranial pressure satisfy the criteria for the diagnosis of idiopathic intracranial hypertension. Minocycline is often used by family physicians for the treatment of acne, and this complication requires vigilance to protect against potential vision loss.

During nonentrained sleep--wake conditions in man, healthy adult subjects spontaneously develop "long" biological days (greater than 35 hr) in addition to the normal, approximately 25 hr day. The ratio of sleep to total time remains constant (approximately 0.30), with long sleep episodes occurring approximately 180 degrees out of phase with the short sleep episodes. The timing and amount of REM sleep advance to an earlier time within the sleep episode during free-running, whereas stage 3 + 4 sleep is related to the initiation and course of the sleep process itself. The REM--NREM cycle length does not change, comparing entrained and nonentrained conditions. The study of the chronophysiology of humans under nonentrained conditions may serve as a model of the chronopathology of sleep--wake changes which occur in sleep disorders associated with depression, narcolepsy--cataplexy, sleep--wake dyssomnias, delayed sleep phase insomnia, and aging.

Two- to threefold variations in sleep length were observed in 12 subjects living on self-selected schedules in an environment free of time cues. The duration of polygraphically recorded sleep episodes was highly correlated with the circadian phase of the body temperature rhythm at bedtime and not with the length of prior wakefulness. Furthermore, the rate of REM (rapid eye movement) sleep accumulation , REM latency, bedtime selection, and self-rated alertness assessments were also correlated with the body temperature rhythm.

In order to test the hypothesis that cortisol secretion is inhibited during sleep, six healthy young men (ages 18-24) were studied in a 4-day protocol. A baseline nocturnal sleep period was followed by one night's total sleep deprivation, then sleep at 180 degrees phase shift, and then return to a normal nocturnal sleep episode (SP-3). Plasma cortisol concentrations were measured every 20 min (obtained by an indwelling venous catheter), rectal temperature was measured every minute, and sleep was polygraphically defined. During the first 4 h of sustained sleep, cortisol secretion was decreased even when sleep occurred during a time when the subject was usually awake; conversely, it was elevated if awake at the usual daily time of sleeping. This was not the case for the last 4 h of sleep. Body temperature was also decreased but during each entire 7- to 8-h sleep period. Meals produced only a small brief rise of cortisol and produced no change in body temperature. Stage 4 sleep was increased during the 180 degrees inverted sleep episode and decreased during SP-3, REM sleep however was increased during SP-3. A reciprocal relationship was found between REM and stages 3 and 4 for the second, third, and fourth, and sixth h of sleep for SP-3. These results demonstrate the inhibitory effect of the behavioral complex of sleeping on cortisol secretion superimposed on its endogenous circadian and ultradian rhythm. These neurophysiological events may be used to entrain and time the period and phase of biological rhythms in relation to shift work, sleep deprivation, and transmeridian jet travel.

We describe a new syndrome called "delayed sleep phase insomnia." Thirty of 450 patients seen for a primary insomniac complaint had the following characteristics: (1) chronic inability to fall asleep at a desired clock time; (2) when not on a strict schedule, the patients have a normal sleep pattern and after a sleep of normal length awaken spontaneously and feel refreshed; and (3) a long history of unsuccessful attempts to treat the problem. These patients were younger than the general insomniac population and as a group did not have a specific psychiatric disorder. Six patients' histories are described in detail, including the successful nonpharmacological chronotherapy regimen (resetting the patients' biological clock by progressive phase delay). Delayed sleep phase insomnia is proposed to be a disorder of the circadian sleep-wake rhythm in which the "advance" portion of the phase response curve is small.

We report here the development of a brief drug-free rescheduling treatment ("chronotherapy") for Delayed Sleep Phase (DSP) insomnia, a syndrome characterized by sleep-onset insomnia with difficulty in morning awakening. We postulated that patients with DSP insomnia had an inadequate capacity to achieve phase advance shifts of the circadian pacemaker which times the sleep-wake cycle. Chronotherapy was therefore designed to reset these patients' biological clocks by the phase delay route. This single 5-6 day treatment was tested in 5 patients with a 4-15 year history of DSP insomnia. All 5 patients reported a lasting resolution of their symptoms substantiated by systematic long-term self-reports and objective polygraphic recording before and after treatment (average follow-up of 260 days; range, 42-910 days). The average sleep onset advanced from 4:50 a.m. before treatment to 12:20 a.m. afterwards, and wake times advanced from 1:00 p.m. to 755 a.m. (for both, p less than 0.001), with no reduction in sleep efficiency. As a result, all 5 patients were able to end their chronic dependence on hypnotic medications.

Studies were carried out on a group of six young (ages 23-30) and six older (ages 53-70) normal men who lived under conditions of temporal, but not social isolation, from three to eight weeks. During entrained and non-entrained (free-running) conditions, comparative measurements were made of sleep-wake cycles, sleep stages and rectal temperature rhythms for these two age groups. Results demonstrated a reduction in the period and amplitude of the body temperature rhythms during free-running in the older group. Sleep efficiency, total sleep time, REM sleep latency, REM episode length, percent REM in the last 2 hours of sleep, the length and frequency of arousals during sleep, and the terminal wake latency were all age related and dependent on entrainment. The period of the sleep-wake cycle, terminal awakenings from REM and percent REM in the first 3 hours of sleep were not age related but were dependent on entrainment. Sleep stages as percents of total sleep time were found to be age related but independent of entrainment, while sleep latency, mid-REM to mid-REM cycle length and the ratio of sleep to total time were neither age related nor dependent on entrainment. In addition, individual chronobiological differences were prominent in the older group. Changes of period and of the phase relationship of sleep-wake and temperature rhythms occurred in several subjects during the non-entrained condition.

Ten male subjects were studied for a total of 306 days on self-selected schedules. Four of them developed bedrest-activity cycle period lengths very different from 24 hr (mean = 36.8 hr) despite the persistence of near-24-hr oscillations in other physiologic functions, including that of body temperature (mean = 24.6 hr). The percentage of sleep time spent in REM sleep varied significantly with the phase of that near-24-hr body temperature cycle. The peak in REM sleep propensity (RSP) occurred on the rising slope of the average body temperature curve, coincident with the phase of peak sleep tendency. This was associated with a significantly increased REM episode duration and shortened REM latency (including sleep-onset REM episodes), but without a significant change in the REM-NREM cycle length. We conclude that there is an endogenous circadian rhythm of REM sleep propensity which is closely coupled to the body temperature rhythm and is capable of free-running with a period different from both 24 hr and the average period of the sleep-wake cycle.