Cerebral metabolism during vegetative state and after recovery to consciousness One way to approach the study of consciousness is to explore lesional cases in which impairment of consciousness is the prominent clinical sign. Vegetative state is such a condition wherein awareness is abolished whereas arousal persists. It can be diagnosed clinically soon after a brain injury and may be reversible (as in the following case report) or progress to a persistent vegetative state or death. The distinction between vegetative state and persistent vegetative state is that the second is defined as a vegetative state that has continued or endured for at least 1 month. 1 We present a patient who developed a vegetative state after carbon monoxide poisoning and in whom we had the opportunity to measure brain glucose metabolism distribution during the vegetative state and after recovery to consciousness. Using [18 F]fluorodeoxyglucose (FDG) PET and statistical parametric mapping (SPM) we compared both patient's sets to a normal control population. Our findings oVer an insight into the neural correlates of "awareness", pointing to a critical role for posterior associative cortices in consciousness.A 40 year old right handed woman attempted suicide through CO intoxication and was found unconscious. She was treated with hyperbaric oxygen but evolved to a vegetative state diagnosed according to the following criteria: 1 (1) spontaneous eye opening without evidence of awareness of the environment; (2) no evidence of reproducible voluntary behavioural responses to any stimuli; (3) no evidence of language comprehension or expression; (4) intermittent wakefulness and behaviourally assessed sleepwake cycles; (5) normal cardiorespiratory function and blood pressure control; (6) preserved pupillary, oculocephalic, corneal, and vestibulo-ocular reflexes. Brain MRI performed 14 days after admission was normal. Electroencephalography showed a 6 Hz basal activity with more pronounced slowing on the left parietal regions. Auditory evoked potentials were normal. Somaesthetic evoked potentials of the median nerve showed normal latency and amplitude of P14 and N20 potentials without any late cortical components. After remaining in a vegetative state for 19 days the patient regained consciousness. Her sequelae consisted of a bilateral spastic paresis of upper and lower limbs. Neuropsychological testing 1 month after admission showed an attention deficit with moderate impairment of short term memory. One year after the accident she showed a spastic gait with altered fine motor function, most prominent on the right, a slurred speech, and minor short term memory disturbances. FDG-PET was performed during the vegetative state (day 15 after admission) and after recovery to consciousness (day 37).The control population consisted of 48 drug free, healthy volunteers, aged from 18 to 76 years (mean: 42 (SD 21) years).The study was approved by the ethics committee of the University of Liège. Informed consent was obtained by the husband of the patient and ...

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SummaryIn 32 patients with panic disorder with or without agoraphobia, Bmax measures of 5-HT binding in platelets did not differ from normal controls at baseline. Plasmatic cortisol levels were significantly higher than controls in the morning and in the evening measures as well as in post-dexamethasone assays. Following an 8-week treatment period with alprazolam plus behavioral guidance encouraging exposure, Bmax values did not alter but cortisol measures diminished significantly. Measures of phobic avoidance were negatively correlated with 5-HT Bmax values. Plasmatic cortisol correlated positively with the number of situational panic attacks in the month before treatment. There were no correlations between cortisol and 5-HT Bmax measures. A possible link between serotonin function and phobic avoidance is discussed. Cortisol changes were interpreted as being related to the global severity of the anxious state.