Evaluation of Driving Ability in Older Drivers

OBJECTIVE: To assess the driving ability of older drivers, their visual function, cognitive-perceptual function, motor function and driving performance were evaluated. METHOD: Subjects were 55 drivers aged 65 years or older. Visual function test included visual acuity, visual field, color vision and contrast sensitivity. Cognitive perceptual function was evaluated with the cognitive perceptual assessment for driving (CPAD) and clock drawing test. For motor function, muscle strength and range of motion were evaluated. Driving performance was evaluated by virtual reality based driving simulator. For comparision, 48 younger drivers aged between late twenties and early forties underwent the same evaluation. RESULTS: Among older drivers, 21 (38.2%) had visual acuity less than 20/40, 3 (5.5%) had visual field narrower than 140degrees bilaterally. Contrast sensitivity was significantly decreased in both day and night with glare light conditions. In cognitive-perceptual function assessment, 20 subjects (36.4%) passed CPAD test, 3 subjects (5.5%) failed, and 32 subjects (58.1%) fell into borderline group. Mean CPAD score was 50.65+/-5.62, which was significantly lower than that of younger drivers. 18 subjects (32.7%) were incorrect in clock drawing test. In motor function assessment, 4 subjects (7.3%) in older drivers showed hemiparesis secondary to stroke. In driving simulator, 21 subjects (38.2%) failed whereas only 4 subjects (8.3%) did in younger drivers. Average demerit score was 24.09+/-15.53 and was significantly higher than that of younger drivers. CONCLUSION: Older drivers showed significantly higher incidence of visual and cognitive-perceptual dysfunction, and poorer driving performance compared to younger drivers group.

Driving Status, Habits and Safety of Older Drivers

OBJECTIVE: To investigate the actual driving status and driving related safety issues of older drivers aged 65 years or older. METHOD: We conducted a survey on 56 elderly drivers about driving status, driving habits, safe driver self check list, and medical conditions that may affect safe driving. For comparison, 50 younger drivers aged between third and fifth decades were also surveyed. RESULTS: The mean age of total 56 elderly drivers was 69.96 years old. Their mean driving time in life was 23.6 years and the purposes of driving were shopping (23.2%), religion activity (21.4%) and leisure (16.1%). Most vehicles were equipped with automatic transmission (83.9%) and power steering (91.1%) and the most common type of vehicle was a sedan (82.1%). The incidence of their motor vehicle accidents in recent 2 years was 21.4%, which was higher than that of control group (18.0%) without statistical significance. The driving habits questionnaire revealed elderly drivers tend to avoid rush-hour traffic, driving at night, and high-traffic roads in 75.0%, 69.6%, 51.8% of subjects respectively. The result of safe driver self check list showed that mean demerit score of elderly drivers was 4.3, which was higher than that of younger drivers (3.2). Elderly drivers had hypertension (33.9%), diabetes mellitus (17.9%), eye disorders (8.9%), heart disease (8.9%), arthritis (8.9%), stroke (7.1%), and respiratory disease (5.4%). CONCLUSION: Compared to younger drivers, elderly drivers tend to avoid unsafe driving situations and reported more safety problems in the safe driver self check list. Elderly drivers also had more medical conditions that may affect safe driving, such as eye disorders, cardiovascular, and metabolic diseases.

Effects of Repeated Nicotine Treatment on the Changes in Glutamate Receptor Subunits Levels in Mesocorticolimbic Dopamine Areas

Recent studies suggest that alterations in glutamate receptor subunit levels in mesocorticolimbic dopamine areas could account for neural adaptations in response to psychostimulant drugs. Although many drugs of abuse induce changes in ionotropic glutamate receptor subunits in mesocorticolimbic dopamine areas, the changes of ionotropic glutamate receptor subunits by repeated nicotine treatment in these areas are not known. To answer this question, we injected male Sprague-Dawley rats twice daily with nicotine (0.4 mg/kg) or saline (1 ml/kg) for 10 days. The immunoreactivity of NR1, GluR1, and GluR2 glutamate receptor subunits was examined 16~18 h after the last injection of saline or nicotine. Repeated nicotine treatment significantly increased NR1 levels in the ventral tegmental area (VTA). In addition, repeated nicotine treatment showed a tendency towards an increase in GluR1 levels in the VTA as well as in striatum. However, there was no significant change in glutamate receptor subunits in other areas including nucleus accumbens (NAc). These results demonstrate that repeated nicotine treatment increases NR1 levels in VTA similarly to other drugs of abuse, suggesting that elevated glutamate receptor subunits in the VTA, but not NAc may be involved in the excitation of mesocorticolimbic dopamine neurons by nicotine.

Chronic mild stress decreases survival, but not proliferation, of new-born cells in adult rat hippocampus

New-born cells continue to proliferate and survive to become mature granule cells in adult rat hippocampus. Although this process, known as neurogenesis, is inhibited by acute stress, it is not clear whether chronic stress affects neurogenesis. To determine whether chronic mild stress (CMS) influences neurogenesis in the adult rat hippocampus, male Sprague-Dawley rats were exposed to CMS and administered bromodeoxyuridine (BrdU) before or after CMS to observe the survival/differentiation or proliferation of new-born cells, respectively. In addition, we measured brain-derived neurotrophic factor (BDNF) mRNA in the granule cell layer (GCL) of the hippocampus, because BDNF is known to play an important role in the survival of new-born cells. CMS significantly decreased the survival of newborn cells in the GCL, but did not influence the proliferation or differentiation of new-born cells. CMS did not affect the proliferation and survival of new-born cells in the hilus. In addition, CMS did not change BDNF mRNA levels in the GCL. These results demonstrate that CMS reduces the survival of new-born cells but not of their proliferation, suggesting that repeated mild stress could influence a part of neurogenesis, but not the whole part of neurogenesis. These results raise the possibility that the survival of new-born cells may be suppressed in the presence of normal BDNF mRNA levels in GCL.

Changes of Corticotropin-Releasing Factor(CRF) and Neuropeptide Y(NPY) of Rats in Response to Footshock or Reexposure to Conditions Previously Paired with Footshock

Corticotropin-releasing factor(CRF) and neuropeptide Y(NPY) are known to play important roles in mediating stress responses and stress-related behavior. To elucidate the role of neuropeptides in response to the condition that had paired with traumatic event, we observed the changes of CRF and NPY by immunohistochemistry using a conditioned footshock paradigm. Male Sprague-Dawley rats were placed in a shuttle box and exposed to 20 pairings of a tone(< 70dB, 5sec) followed by a footshock(FS, 0.8mA, 1sec) over 60min. A second group was exposed to the tone-footshock pairings, returned to the homecage for 2days, and then reexposed to the test chamber and 20tones alone for 60min, prior to sacrifice. Control groups were : a) sacrificed without exposure to FS ; b) exposed to the tone-footshock pairings and then sacrificed two days later ; or c) exposed to the chamber and tones alone, returned to the homecage for 2days and then reexposed to the chamber and 20tones over 60min prior to sacrifice. CRF was increased in animals exposed to FS or the aversive condition(context and tone) that had paired to FS in bed nucleus of the stria terminalis (BNST) compared to the control. NPY was increased by FS in amygdala and PVN, but the condition previously associated with FS results in slight increase only in amygdala area. These results suggest that the BNST appears to be the mostly involved neural circuit in response to explicit cues previously paired with footshock. Moreover, this study raise the possibility that increased CRF peptide in the BNST in response to re-exposure to the aversive condition may underlie, in part, the experience of conditioned fear-related anxiety behavior.