ABSTRACT
INTRODUCTION: A study of patients with low back pain (LBP) had revealed altered central pain processing. At an equal pain level LBP patients had considerably more neuronal activation in the somatosensory cortices than controls. In a new analysis of this dataset, we further investigated the differences in central pain processing between LBP patients and controls, looking for possible pathogenic mechanisms. METHODS: Central pain processing was studied by functional magnetic resonance imaging (fMRI), using equally painful pressure stimuli in a block paradigm. In this study, we reanalyzed the fMRI data to statistically compare pain-elicited neuronal activation of both groups. RESULTS: Equally painful pressure stimulation resulted in a significantly lower increase of regional cerebral blood flow (rCBF) in the periaqueductal gray (PAG) of the LBP patients. The analysis further revealed a significantly higher increase of rCBF in LBP than in HC in the primary and secondary somatosensory cortex and the lateral orbitofrontal cortex (LOFK), elicited by these same stimuli. CONCLUSIONS: These findings support a dysfunction of the inhibitory systems controlled by the PAG as a possible pathogenic mechanism in chronic low back pain.
Subject(s)
Brain/physiopathology , Fibromyalgia/physiopathology , Low Back Pain/physiopathology , Periaqueductal Gray/physiopathology , Adult , Brain/blood supply , Brain Mapping , Cerebrovascular Circulation , Data Interpretation, Statistical , Depression/diagnosis , Female , Fibromyalgia/diagnosis , Humans , Low Back Pain/diagnosis , Magnetic Resonance Imaging , Male , Middle Aged , Pain Measurement , Patient Selection , Pressure , Surveys and QuestionnairesABSTRACT
We present a case of spontaneous recovery after failed intraoperative cardiopulmonary resuscitation in a patient with a cardiac pacemaker. Of the various mechanisms discussed in the literature, that which seems most relevant in our case of a Lazarus phenomenon, is that of impeded venous return in the course of positive pressure ventilation and hypovolemia.With the disconnection of ventilation, passive cardiac filling combined with electrical stimulation due to the cardiac pacemaker may have caused spontaneous myocardial electrical activity. Corresponding to previous authors,we recommend continued monitoring for 10 min after cessation of cardiopulmonary resuscitation. In addition, we propose a further attempt by disconnecting ventilation and external myocardial stimulation in the case of unresponsiveness to resuscitation efforts.
Subject(s)
Cardiopulmonary Resuscitation , Cardiovascular Physiological Phenomena , Pacemaker, Artificial , Aged , Aged, 80 and over , Blood Gas Analysis , Electrocardiography , Hemodynamics/physiology , Humans , Intraoperative Period , Male , Monitoring, Intraoperative , Positive-Pressure RespirationABSTRACT
We report on a patient intoxicated with ethanol, who was found unconscious with fixed dilated pupils, deviation of eyes, absent cough and corneal reflexes, with her arms in decerebrate posture. Because of an orbital haematoma a traumatic intracranial hemorrhage with elevated intracranial pressure and compression or concussion of the brain stem was suspected. A CT-scan of the head did not reveal an intracranial mass or any radiographic signs of intracranial hypertension. Drug screening, blood gas analysis and other laboratory tests as well anamnestic data were not indicative of other intoxications or a metabolic decompensation. These unusual neurological findings were caused by a life-threatening ethanol intoxication with a blood-alcohol concentration of 700 mg/dl (151.8 mmol/l). The patient was extubated after several hours of mechanical ventilation in the intensive care unit and was discharged to a regular ward on the following day.
