Article

Symptoms and disability until 3 months after mild TBI.

Department of Psychiatry, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden.
Brain Injury (Impact Factor: 1.86). 07/2006; 20(8):799-806. DOI: 10.1080/02699050600744327
Source: PubMed

ABSTRACT Examine frequency, character and course of symptoms until 3 months after MTBI and the relation between symptoms and disability.
Prospective cohort study of 122 consecutive patients with MTBI. Symptom assessment after 1, 7 and 14 days and 3 months post-injury by use of Rivermead Post-concussional Questionnaire. Disability assessment by use of Rivermead Head Injury Follow-up Questionnaire.
Patients reporting one or more symptoms declined from 86% on day 1 to 49% 3 months post-injury, when 25% also reported change in one or more domains of everyday activities. Poor memory, sleep disturbance and fatigue were most commonly reported. Symptom and disability scores were correlated (tau = 0.60; p < 0.001). Early symptom load correlated with late symptom load (tau = 0.38; p < 0.01).
Symptoms gradually decline post-injury. Symptoms correlate with disability at 3 months. Patients with early high symptom load are at risk for developing persisting complaints.

0 Followers
 · 
160 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The neurological impairments associated with traumatic brain injury include learning and memory deficits and increased risk of seizures. The hippocampus is critically involved in both of these phenomena and highly susceptible to damage by traumatic brain injury. To examine network activity in the hippocampal CA1 region after lateral fluid percussion injury, we used a combination of voltage-sensitive dye, field potential, and patch clamp recording in mouse hippocampal brain slices. When the stratum radiatum (SR) was stimulated in slices from injured mice, we found decreased depolarization in SR and increased hyperpolarization in stratum oriens (SO), together with a decrease in the percentage of pyramidal neurons firing stimulus-evoked action potentials. Increased hyperpolarization in SO persisted when glutamatergic transmission was blocked. However, we found no changes in SO responses when the alveus was stimulated to directly activate SO. These results suggest that the increased SO hyperpolarization evoked by SR stimulation was mediated by interneurons that have cell bodies and/or axons in SR, and form synapses in stratum pyramidale and SO. A low concentration (100 nM) of the synthetic cannabinoid WIN55,212-2, restored CA1 output in slices from injured animals. These findings support the hypothesis that increased GABAergic signaling by cannabinoid-sensitive interneurons contributes to the reduced CA1 output following traumatic brain injury.
    Frontiers in Cellular Neuroscience 12/2014; 8:435. DOI:10.3389/fncel.2014.00435 · 4.18 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Sleep disturbances are a common symptom following concussions to include athletic concussion. Review: This review applies literature on sleep following traumatic brain injury and concussion to sport concussions and places these considerations in the context of sleep and athletic performance. It also includes a description of sleep abnormalities in sleep duration, quality and timing as well as recommended treatment approaches. Finally, it includes a brief discussion of emerging paradigms of sleep and concussion recovery.
    Brain Injury 01/2015; 29(2). DOI:10.3109/02699052.2014.983978 · 1.86 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Persistent postconcussion syndrome (PCS) occurs in around 5-10% of individuals after mild traumatic brain injury (mTBI), but research into the underlying biology of these ongoing symptoms is limited and inconsistent. One reason for this could be the heterogeneity inherent to mTBI, with individualized injury mechanisms and psychological factors. A multimodal imaging study may be able to characterize the injury better. To look at the relationship between functional (fMRI), structural (diffusion tensor imaging), and metabolic (magnetic resonance spectroscopy) data in the same participants in the long term (>1 year) after injury. It was hypothesized that only those mTBI participants with persistent PCS would show functional changes, and that these changes would be related to reduced structural integrity and altered metabolite concentrations. Functional changes associated with persistent PCS after mTBI (>1 year postinjury) were investigated in participants with and without PCS (both n = 8) and non-head injured participants (n = 9) during performance of working memory and attention/processing speed tasks. Correlation analyses were performed to look at the relationship between the functional data and structural and metabolic alterations in the same participants. There were no behavioral differences between the groups, but participants with greater PCS symptoms exhibited greater activation in attention-related areas (anterior cingulate), along with reduced activation in temporal, default mode network, and working memory areas (left prefrontal) as cognitive load was increased from the easiest to the most difficult task. Functional changes in these areas correlated with reduced structural integrity in corpus callosum and anterior white matter, and reduced creatine concentration in right dorsolateral prefrontal cortex. These data suggest that the top-down attentional regulation and deactivation of task-irrelevant areas may be compensating for the reduction in working memory capacity and variation in white matter transmission caused by the structural and metabolic changes after injury. This may in turn be contributing to secondary PCS symptoms such as fatigue and headache. Further research is required using multimodal data to investigate the mechanisms of injury after mTBI, but also to aid individualized diagnosis and prognosis.
    01/2015; 5(1):45-61. DOI:10.1002/brb3.292

Preview

Download
0 Downloads
Available from