Photophobia Associated with Traumatic Brain Injury: A Systematic Review and Meta-analysis.

SIGNIFICANCE: This study reports the prevalence and relative risk of photophobia in patients with traumatic brain injury (TBI). OBJECTIVES: This study aimed to conduct a systematic review and meta-analysis to determine the prevalence and relative risk of photophobia in patients with TBI. DATA SOURCES: Three databases were used for literature search: PubMed, EMBASE, and Cochrane Library. STUDY APPRAISAL AND SYNTHESIS METHODS: Publications reporting the prevalence of photophobia after TBI in patients of any age were included. A series of meta-regression analyses based on a generalized linear mixed model was performed to identify potential sources of heterogeneity in the prevalence estimates. RESULTS: Seventy-five eligible publications were identified. The prevalence of photophobia was 30.46% (95% confidence interval [CI], 20.05 to 40.88%) at 1 week after the injury. Prevalence decreased to 19.34% (95% CI, 10.40 to 28.27%) between 1 week and 1 month after TBI and to 13.51% (95% CI, 5.77 to 21.24%) between 1 and 3 months after the injury. The rapid decrease in the prevalence of photophobia in the first 3 months after a TBI injury was significant (P < .001). Three months post-TBI, the prevalence of photophobia leveled off to a near plateau with nonsignificant variability, increasing between 3 and 6 months (17.68%; 95% CI, 9.05 to 26.32%) and decreasing between 6 and 12 months since TBI (14.85%; 95% CI, 6.80 to 22.90%). Subgroup analysis of 14 publications that contained control data showed that the estimated risk ratio for photophobia was significantly higher in the TBI than in the control group during the entire 12 months after TBI. CONCLUSIONS AND IMPLICATIONS OF KEY FINDINGS: This study demonstrates that photophobia is a frequent complaint after TBI, which largely resolves for many individuals within 3 months after the injury. For some patients, however, photophobia can last up to 12 months and possibly longer. Developing an objective quantitative methodology for measuring photophobia, validating a dedicated photophobia questionnaire, and having a specific photophobia International Classification of Diseases, Tenth Revision code would greatly improve data gathering and analysis.

Speech in Alzheimer's disease: can temporal and acoustic parameters discriminate dementia?

AIMS: The study explores how speech measures may be linked to language profiles in participants with Alzheimer's disease (AD) and how these profiles could distinguish AD from changes associated with normal aging. METHODS: We analysed simple sentences spoken by older adults with and without AD. Spectrographic analysis of temporal and acoustic characteristics was carried out using the Praat software. RESULTS: We found that measures of speech, such as variations in the percentage of voice breaks, number of periods of voice, number of voice breaks, shimmer (amplitude perturbation quotient), and noise-to-harmonics ratio, characterise people with AD with an accuracy of 84.8%. DISCUSSION: These measures offer a sensitive method of assessing spontaneous speech output in AD, and they discriminate well between people with AD and healthy older adults. This method of evaluation is a promising tool for AD diagnosis and prognosis, and it could be used as a dependent measure in clinical trials.

Subchronic use of rivastigmine increases procognitive flexibility across multimodal behavioral tasks in healthy male rats.

Rivastigmine (RVT) is a reversible inhibitor of cholinesterase approved worldwide for the treatment of cognitive dysfunctions, especially in Alzheimer's disease. Most previous pre-clinical studies have examined the effects of RVT treatment in a wide variety of pathological research models. Nonetheless, the effects of this drug on sensorimotor gating, memory, and learning tasks in healthy subjects remains unclear. In this study, we investigate the procognitive effects of RVT treatment in healthy rats through sensorimotor gating evaluations (measured as prepulse inhibition of the acoustic startle reflex), active avoidance learning, and spatial memory learning in a radial maze. There is an increase in the amplitude of the startle reflex in RVT-treated rats compared to the control groups, whereas the latency remained constant. Sensorimotor gating values were also incremented compared to those values from controls. In active avoidance, rats treated with RVT learned faster to successfully perform the task compared to controls, but afterwards all groups exhibited virtually identical results. During the sessions in the radial maze, RVT-treated rats committed fewer errors in both the working and reference memory compared to controls. All in all, our results support the hypothesis that RVT treatment may entail procognitive effects in healthy subjects.

Relations between Sensorimotor Integration and Speech Disorders in Parkinson's Disease.

BACKGROUND: Sensorimotor integration mechanisms can be affected by many factors, among which are those involving neuromuscular disorders. Parkinson's disease (PD) is characterized by well-known motor symptoms, among which lately have been included motor speech deficits. Measurement of the acoustic startle reflex (ASR) and its modulations (prepulse inhibition and prepulse facilitation, PPI and PPF respectively) represent a simple and quantifiable tool to assess sensorimotor function. However, it remains unknown whether measures of the PPI and PPF are associated with motor speech deficits in PD. METHODS: A total of 88 subjects participated in this study, 52 diagnosed with PD and 36 control subjects. After obtaining written informed consent, participants were assessed with PPI at several interstimulus intervals, and PPF at 1000 ms using the SRH-Lab system (San Diego, CA). Percentage of change in the amplitude and latency of the ASR was analyzed between groups. Voice recordings were register of a specific text given to the subjects with a professional recorder and temporal patterns of speech were analyzed. RESULTS: Statistical analysis conducted in this study showed differences in PPI and PPF in subjects with PD compared to controls. In addition, discriminative parameters of voice abnormalities were observed in PD subjects related to control subjects showing a reduction in phonation time, vowel pulses, breaks, breakage and voice speech periods. CONCLUSIONS: PD presents a disruption in sensorimotor filter mechanisms and speech disorders, and there is a relationship between these alterations. The correlation between the PPI and PPF with an alteration of the voice in PD subjects contributes toward understanding mechanism underlying the neurophysiological alterations in both processes. Overall, easy and non-invasive tests such as PPI, PPF together with voice analysis may be useful to identify early stages of PD.

Origin and function of short-latency inputs to the neural substrates underlying the acoustic startle reflex.

The acoustic startle reflex (ASR) is a survival mechanism of alarm, which rapidly alerts the organism to a sudden loud auditory stimulus. In rats, the primary ASR circuit encompasses three serially connected structures: cochlear root neurons (CRNs), neurons in the caudal pontine reticular nucleus (PnC), and motoneurons in the medulla and spinal cord. It is well-established that both CRNs and PnC neurons receive short-latency auditory inputs to mediate the ASR. Here, we investigated the anatomical origin and functional role of these inputs using a multidisciplinary approach that combines morphological, electrophysiological and behavioral techniques. Anterograde tracer injections into the cochlea suggest that CRNs somata and dendrites receive inputs depending, respectively, on their basal or apical cochlear origin. Confocal colocalization experiments demonstrated that these cochlear inputs are immunopositive for the vesicular glutamate transporter 1 (VGLUT1). Using extracellular recordings in vivo followed by subsequent tracer injections, we investigated the response of PnC neurons after contra-, ipsi-, and bilateral acoustic stimulation and identified the source of their auditory afferents. Our results showed that the binaural firing rate of PnC neurons was higher than the monaural, exhibiting higher spike discharges with contralateral than ipsilateral acoustic stimulations. Our histological analysis confirmed the CRNs as the principal source of short-latency acoustic inputs, and indicated that other areas of the cochlear nucleus complex are not likely to innervate PnC. Behaviorally, we observed a strong reduction of ASR amplitude in monaural earplugged rats that corresponds with the binaural summation process shown in our electrophysiological findings. Our study contributes to understand better the role of neuronal mechanisms in auditory alerting behaviors and provides strong evidence that the CRNs-PnC pathway mediates fast neurotransmission and binaural summation of the ASR.