ABSTRACT
Proximal fourth metatarsal injuries are rarely reported. We present five case histories in which athletic patients sustained injuries at the shaft-base junction of the fourth metatarsal. Similar to proximal fifth metatarsal injuries, adduction of the forefoot appears to be associated. Our patients returned to their activities in two to eight months. These patients injuries tended to take longer to heal than other lesser metatarsal fractures and stress fractures (which are typically more distal). Some patients were continually symptomatic, even after three months of rest and immobilization. This coincides with proximal fifth metatarsal injuries and stress fractures. For treatment of proximal fourth metatarsal injuries to be successful, ideal treatment appears to involve nonweightbearing below-knee cast/boot immobilization for three weeks. This is followed by an additional three or more weeks of weightbearing immobilization. Healing may still be prolonged.
Subject(s)
Athletic Injuries/therapy , Fractures, Stress/therapy , Metatarsal Bones/injuries , Adolescent , Adult , Athletic Injuries/diagnostic imaging , Athletic Injuries/physiopathology , Female , Football/injuries , Fracture Healing , Fractures, Stress/diagnostic imaging , Fractures, Stress/physiopathology , Humans , Immobilization , Male , Metatarsal Bones/diagnostic imaging , Middle Aged , Radiography , Running/injuries , Skiing/injuries , Soccer/injuriesABSTRACT
It is generally believed that patients with primary generalized epilepsy have normal cognition and neuroimaging studies. We have previously shown that patients with juvenile myoclonic epilepsy (JME) have impaired visual working memory. In this study we examined relative regional changes in 18FDG uptake during a visual working memory paradigm in patients with JME. At rest, there were regional decreases in relative glucose uptake compared to controls. Unlike control subjects, increased activity in the dorsolateral prefrontal cortex was not found during the working memory task. Other regions with increased uptake in controls, such as premotor cortex and basal frontal cortex, also showed no increases, whereas medical temporal structures appeared to play a role in JME but not in control subjects' task performance. The data suggest that JME, a type of primary generalized epilepsy, may suffer from cortical disorganization that affects both the epileptogenic potential and frontal lobe cognitive functioning.
Subject(s)
Deoxyglucose/analogs & derivatives , Epilepsy, Generalized/diagnostic imaging , Memory/physiology , Visual Cortex/diagnostic imaging , Adult , Epilepsy, Generalized/physiopathology , Female , Fluorodeoxyglucose F18 , Humans , Male , Middle Aged , Tomography, Emission-Computed , Visual Cortex/physiopathologyABSTRACT
INTRODUCTION: We previously demonstrated that patients with frontal lobe epilepsy show deficits on a visual working memory paradigm and that this paradigm produces increased 18FDG uptake in the dorsolateral prefrontal cortex (DPFC), premotor cortex, angular and supramarginal gyri, basal forebrain, and ventral frontal poles of normal subjects when compared with a control task. We hypothesized that subjects with frontal lobe epilepsy would have impaired frontal activation during this task. METHODS: One resting and two activated images were obtained with 18FDG-PET in 15 subjects and 14 controls. One was a delayed (DMS) and one an immediate (IMS) match to sample paradigm. Discriminant and factor analyses were used to analyze the data, supplemented by selected t tests. RESULTS: No differences in glucose uptake were found between the DMS and IMS in the epilepsy subjects, in distinct contrast to controls. A comparison between controls and epilepsy subjects showed differences both ipsilateral and contralateral to the epileptic focus in the frontal regions involved in the task, with small changes in nonfrontal, task-related regions as well. The task itself brought out or highly exaggerated differences seen at rest. There was weak evidence that other frontal and temporal regions were attempting to compensate for the DPFC deficit. CONCLUSION: A unilateral epileptic focus is capable of suppressing function along a large task-related circuit ipsilateral and contralateral to the focus. Peripheral cortical regions compensate poorly for the area of dysfunction.
Subject(s)
Epilepsy, Frontal Lobe/diagnostic imaging , Epilepsy, Frontal Lobe/physiopathology , Fluorine Radioisotopes , Frontal Lobe/diagnostic imaging , Memory/physiology , Tomography, Emission-Computed , Adult , Deoxyglucose/analogs & derivatives , Discriminant Analysis , Factor Analysis, Statistical , Female , Fluorodeoxyglucose F18 , Frontal Lobe/metabolism , Glucose/metabolism , Humans , Male , Middle Aged , Neuropsychological TestsABSTRACT
We evaluated three techniques of analyzing 18FDG-positron emission tomography-(PET) scans in 23 cases of presumed frontal lobe epilepsy (FLE): routine visual or "qualitative linear," "qualitative normalized," and quantitative normalized approaches. Patients were then classified as having pure frontal, probable frontal, frontoparietal and frontotemporal epilepsy based on prolonged surface EEG monitoring with video, magnetic resonance imaging (MRI), chronic intracranial recording (CIR), and results of surgical excision. Overall sensitivity and accuracy of the scans was 52 and 48%for qualitative linear analysis, which was equivalent to that of MRI, and 69 and 43% for qualitative normalized analysis. Quantitative normalized analysis had 96% sensitivity and 74 - 78% accuracy and also detected 9 of 11 (81%) abnormalities in nonlesional cases, improving routine sensitivity from 1 of 11 (9%). We conclude that qualitative linear (routine) analysis is inadequate for diagnosis of FLE lobe or "frontal-plus" epilepsies and does not add to the MRI scan. Because qualitative normalized images improve on routine analysis only slightly, quantitative techniques should be applied for preoperaive evaluations.
