Microvascular and large vein abnormalities in young patients after mild head trauma and associated fatigue: A brain SPECT evaluation and posture dependence modeling.

OBJECTIVE: MRI and CT scans are usually normal in mild traumatic brain injury (mTBI) although 15-20% of such patients suffer for months from fatigue, headache, anxiety, sleep and other disorders. mTBI is suspected to be a cerebrovascular injury, similar to moderate and severe TBI. Brain SPECT is more sensitive and shows perfusion abnormalities immediately after mTBI. This work explores the perfusion abnormalities for young patients suffering from fatigue several months after mTBI. PATIENTS AND METHODS: Twelve mTBI patients (age:8-36 yr, 4 male) with no history of fatigue prior to trauma were prospectively studied following onset of fatigue 6-12 months after mTBI utilizing 99 m-Tc ECD brain SPECT with early and delayed radiotracer imaging. RESULTS: The perfusion pattern in the mTBI + fatigue group included left hemispheric deficits in frontal lobes (early phase: 15.2 ±â€¯4.2%, delayed phase: 9.9 ±â€¯2.2%) and medial temporal lobes (early phase 11.2 ±â€¯3.7%, delayed phase: 9.0 ±â€¯2.3%). Seven patients additionally showed excess tracer accumulation in the parenchyma surrounding internal jugular bulb inferior to temporal lobe. This was modeled as due to increased cellular permeability from TBI induced oxidative stress affecting endothelial tight junctions and consequent tracer leakage across jugular bulbs. Prolonged posture changes from erect to supine position during imaging increase jugular cross-sectional area and venous wall pressure as has been observed in other disease processes and seem to be responsible for tracer leakage from jugular bulbs in our study. CONCLUSION: This work supports an oxidative stress and BBB disruption model for mTBI. The frontal and temporal lobe perfusion deficits are attributed to anatomical vulnerabilities of these lobes. During a mild TBI both of these lobes are susceptible to grazing impacts with underlying bony ridges. We propose a relation between mTBI and fatigue arising from oxidative stress in mTBI affecting ATP generation and altering endothelial homeostasis for both micro-and-large vasculatures. The tracer leakage observed around jugular veins is due to posture induced changes in venous cross-sections and wall pressure as well as from compromised endothelium post TBI induced oxidative stress.

Does exercise make migraines worse and tension type headaches better?

Many non-pharmacological treatments have been implicated in the treatment of primary headache, with exercise being a common recommendation. In this review we first provide an overview of the relationship between exercise and primary headaches. We then review the physiology of pain modulation, with focus on the endogenous opioids, endocannabinoids, and neuropeptides calcitonin gene-related peptide (CGRP) and brain-derived neurotrophic factor (BDNF), and their associations with primary headache and exercise. Finally, we summarize current literature evaluating effects of exercise on primary headache in an effort to understand the benefits and disadvantages of exercise in primary headaches.

Parsimonious collection of pain descriptors: classification and calibration by pain patients.

UNLABELLED: Single-word descriptors are commonly used to label and communicate pain in lay as well as clinical settings. Research has shown that the pool of 84 pain descriptors from the McGill Pain Questionnaire (MPQ) can be refined into a parsimonious subset of 36 descriptors that fit into 12 categories. However, the past 3 studies on this issue have been confined to college student samples. The present study investigated the classification structure and calibration of this new system of pain descriptors in 43 chronic pain patients. Employing a 3-point decision rule, a relatively unambiguous classification structure emerged with 3 descriptors for each of the 12 categories. Within and across categories, the intensities implied by these words could be meaningfully rank ordered. The intensities correlated positively and significantly with those previously derived from student samples as well as those of matching MPQ words previously rated by pain patients. This confirms the stability of the intensity ratings of pain words. Information theoretic analysis revealed transmission of 83% of the maximum (3.6 bits) potentially transmissible in a system of such configuration. This lends support to the idea that the 36 pain descriptors are parsimonious and can be used with efficiency to describe chronic pain. PERSPECTIVE: This study found that in the English language, 36 words (classified into 12 subcategories) can be efficiently used to describe pain. These words can also be reliably ordered in terms of implied pain intensity. This has implications for the qualitative and quantitative assessment of pain patients.

Intravenous treatment of chronic daily headaches in the outpatient headache clinic.

The most likely future of aggressive headache treatment will reside in the sphere of the specialist's clinic. This is a far more cost- and time-effective mode of treating intractable chronic daily headaches (CDH), including chronic migraines. We have used this technique successfully in our clinic for many years. Our experience with intravenous treatment of headaches and migraines was summarized recently and a 97.5% success rate for this type of treatment was found in the clinic. Compared with the treatments commonly available in the emergency department, the specialist's clinic can offer more effective headache-altering definitive treatments. Patients can be offered a maximum degree of success for control of their intractable headaches. In this article, approaches to aggressive treatment of ongoing CDH using intravenous methods of therapy are discussed. All of these can be performed in the clinic setting, avoiding some of the costly aspects of treatment that are present in an emergency room setting.

Tension-type headaches: what they are and how to treat them.

Most clinicians and patients traditionally think of the tension-type headache (TTH) as the "unmigraine" or "nonmigraine." This view may be changing as distinctions between migraines and nonmigrainesdissolve. For many years, clinical diagnosis of TTH was based on nonthrobbing, bilateral pain. The mechanisms underlying the cause of TTH are still poorly understood. Some clinicians keep TTH and migraine in two separate clinical environments, while others see the two as a spectrum disorder with a common pathophysiology;however, there is not enough evidence to make anyone theory the clear-cut victor. Treatment strategies for TTH have evolved in favor of the patient. Newer categories of pharmacologic agents, often stabilizing to neuronal networks, are the modern mainstay of therapy for migraines and mixed headache disorders such as TTH.

Treatment of chronic pain with zonisamide.

Mechanistic similarities underlying neuropathic pain and epilepsy suggest that anticonvulsants can be used for treating neuropathic pain. This open-label prospective study assesses the use of zonisamide in patients with chronic neuropathic pain. Fifty-five patients were initiated on zonisamide, given 100 mg every fourth night and titrated to a stable maintenance dosage (mean=285 mg/d, range=100 to 700 mg/d). Patients rated their pain on a 0 to 10 scale in pain diaries. After > or =3 months on a stable maintenance zonisamide dosage, pain ratings were compared with baseline. Adverse events (AEs) were monitored. Forty-two patients had efficacy data available. Fifteen patients (35.7%) had a >50% improvement in daily pain scores; 10 patients (23.8%) had a 25% to 50% improvement. Zonisamide was well tolerated; only 5 patients discontinued for AEs (drowsiness, nausea, and itching). These results suggest that zonisamide may be useful for treating neuropathic pain. Further investigation in double-blind, placebo-controlled trials is warranted.

Prophylaxis for chronic daily headache and chronic migraine with neuronal stabilizing agents.

Approaches to acute and prophylactic migraine and headache treatment are evolving as our understanding of some of the underlying pathophysiology improves. This article focuses on the emerging use of medications originally introduced for the treatment of seizures (anticonvulsants) as primary therapy for eradicating or reducing migraine and chronic daily headaches. A more accurate term for their pharmacologic mechanisms, if they are used to treat headaches and pain disorders, is neuromodulating or neuronal stabilizing agents. This term refers to their many cellular actions to reduce pain transmission supraspinally, in the spinal cord, and in the brainstem.