INTRODUCTIONComplex regional pain syndrome (CRPS) patients show impaired visuospatial perception in the dark, as compared to normal patients with acute nociceptive pain. The purpose of this study is 2-fold: (i) to ascertain whether this distorted visuospatial perception is related to the chronicity of pain, and (ii) to analyse visuospatial perception of CRPS in comparison with another neuropathic pain condition.

MATERIALS AND METHODSWe evaluated visual subjective body-midline (vSM) representation in 27 patients with post-herpetic neuralgia (PHN) and 22 with CRPS under light and dark conditions. A red laser dot was projected onto a screen and moved horizontally towards the sagittal plane of the objective body-midline (OM). Each participant was asked to direct the dot to a position where it crossed their vSM. The distance between the vSM and OM was analysed to determine how and in which direction the vSM deviated.

RESULTSUnder light condition, all vSM judgments approximately matched the OM. However, in the dark, CRPS patients, but not PHN patients, showed a shifted vSM towards the affected side.

CONCLUSIONWe demonstrated that chronic pain does not always impair visuospatial perception. The aetiology of PHN is limited to the peripheral nervous system, whereas the distorted visuospatial perception suggests a supraspinal aetiology of CRPS.

Adult ; Aged ; Complex Regional Pain Syndromes ; complications ; etiology ; Darkness ; Female ; Functional Laterality ; physiology ; Humans ; Male ; Middle Aged ; Neuralgia, Postherpetic ; complications ; Perceptual Disorders ; etiology ; physiopathology ; Peripheral Nervous System ; physiopathology ; Task Performance and Analysis

OBJECTIVE: To investigate the dynamic experiences of pathological changes in brain and the injured role of brainstem auditory evoked potential (BAEP) after closed Mild Traumatic Brain Injury (MTBI) in rat. METHODS: A closed diffuse brain injury model was successfully produced in rat by hit the parietal bone with a spring-droved steel stick. The auditory brainstem response evoked by click at 50Hz stimulating frequency were recorded at pre-trauma, 15 min and 1, 3, 6, 12 h and 1, 2, 4, 7, 10, 14, 21 d after brain injury. The pathological changes of brain were observed under light microscope and the brain edema was detected by wet weight/dry weight rations. RESULTS: The I-V, III-V of BAEP wave inter peak latency (IPL) in MTBI group increased immediately in 15 minutes after injury. The III, V wave peak latency (PL) and I-V, III-V wave IPL became longer than the pre-trauma level in 6, 12 h post-injury (P<0.05). The III, V wave PL and I - III, I - V, III - V wave IPL became longer than the pre-trauma level in 1, 2 d after injury (P < 0.001), the BAEP retuned to normal level in 14 d after brain injury. At 15 minutes after injury, the water content in brain increased and met its peak in 1 d, decreased gradually in 4 d, then decreased slowly and returned to normal level in 10 d after injury. CONCLUSION The regular changes of BAEP could be an objective tool for evaluating hearing dysfunction after closed mild diffuse traumatic brain injury.
Animals ; Auditory Perceptual Disorders/etiology* ; Brain/pathology* ; Brain Edema/pathology* ; Brain Injuries/physiopathology* ; Brain Stem/physiopathology* ; Disease Models, Animal ; Evoked Potentials, Auditory, Brain Stem/physiology* ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley

OBJECTIVE: To investigate the toxicokinetics profiles of ketamine and its main metabolite norketamine in rabbits. METHODS: The rabbits were administered orally the hydrochloride of ketamine with a dose of 0.15 g/kg. The serum and urine samples were collected before administration and at different time points after drug administration. The concentrations of ketamine and norketamine were determined by GC-NPD and GC-MS. Compartment model and toxicokinetics parameters were simulated and calculated by WinNorLin program. Changes of important vital signs of rabbits were recorded during the experiment. RESULTS: The mean serum concentration-time profile of ketamine and norketamine were fitted to a two-compartment open model with first order kinetics. The kinetic equation of ketamine and norketamine were p(t) = 121.760 e(-0.0025t) +0.980 e(-0.002t) +4.579 e(-0.021 t) and p(t) = 640.919 e(-0.03 t) +1.023 e(-0.001 t) +9.784 e (-0.031 t), respectively. The peak time and the peak concentration of ketamine in serum were (40.950 +/- 12.098) min and (9.015 +/- 1.344) microg/mL, respectively. The elimination half-time of ketamine in rabbits was (430.370 +/- 28.436) min. The serum and urine showed a middle relation in concentrations of ketamine during 30-240 min after drug administration. After oral administration ketamine to rabbits, the toxic symptom on the rabbits occurred at 30 min and disappeared after 120 min. CONCLUSION The toxicokinetics parameters and kinetic equation of ketamine and norketamine in rabbits may provide the theoretical basis for forensic identification of reasonable specimen collection and inferring the time of oral administration ketamine from the ketamine concentration in serum.
Administration, Oral ; Anesthetics, Dissociative/toxicity* ; Animals ; Blood Pressure/drug effects* ; Gas Chromatography-Mass Spectrometry/methods* ; Heart Rate/drug effects* ; Ketamine/urine* ; Male ; Perceptual Disorders/etiology* ; Rabbits ; Random Allocation ; Time Factors