Neuroimaging in the Diagnosis of Chronic Traumatic Encephalopathy: A Systematic Review.

OBJECTIVE: Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy associated with repeated subconcussive and concussive head injury. Clinical features include cognitive, behavioral, mood, and motor impairments. Definitive diagnosis is only possible at postmortem. Here, the utility of neuroimaging in the diagnosis of CTE is evaluated by systematically reviewing recent evidence for changes in neuroimaging biomarkers in suspected cases of CTE compared with controls. DATA SOURCES: Providing an update on a previous systematic review of articles published until December 2014, we searched for articles published between December 2014 and July 2016. We searched PubMed for studies assessing neuroimaging changes in symptomatic suspected cases of CTE with a history of repeated subconcussive or concussive head injury or participation in contact sports involving direct impact to the head. Exclusion criteria were case studies, review articles, and articles focusing on repetitive head trauma from military service, head banging, epilepsy, physical abuse, or animal models. MAIN RESULTS: Seven articles met the review criteria, almost all of which studied professional athletes. The range of modalities were categorized into structural magnetic resonance imaging (MRI), diffusion MRI, and radionuclide studies. Biomarkers which differed significantly between suspected CTE and controls were Evans index (P = 0.05), cavum septum pellucidum (CSP) rate (P < 0.0006), length (P < 0.03) and ratio of CSP length to septum length (P < 0.03), regional differences in axial diffusivity (P < 0.05) and free/intracellular water fractions (P < 0.005), single-photon emission computed tomography perfusion abnormalities (P < 0.01), positron emission tomography (PET) signals from tau-binding, glucose-binding, and GABA receptor-binding radionuclides (P < 0.0001, P < 0.005, and P < 0.005, respectively). Important limitations include low specificity in identification of suspected cases of CTE across studies, the need for postmortem validation, and a lack of generalizability to nonprofessional athletes. CONCLUSIONS: The most promising biomarker is tau-binding radionuclide PET signal because it is most specific to the underlying neuropathology and differentiated CTE from both controls and patients with Alzheimer disease (P < 0.0001). Multimodal imaging will improve specificity further. Future research should minimize variability in identification of suspected cases of CTE using published clinical criteria.

Migraine-tic syndrome: Two further case reports.

Background Migraine-tic syndrome was first reported in 2004 in a 44-year-old woman who had concomitant symptoms of both typical trigeminal neuralgia and migraine. We report here two further cases of migraine-tic syndrome and speculate on the relevance of this condition to the pathophysiology of headache. Case reports A 43-year-old woman presented with typical trigeminal neuralgia symptoms that preceded the onset of migraine headache; both headache types responded to treatment with sumatriptan. A 35-year-old woman presented with trigeminal neuralgia that consistently followed the onset of migraine headache. The former aspect responded to baclofen, but the migraine headache required treatment with amitriptyline. Discussion These two patients provide further support for the presence of an overlap syndrome of migraine-tic. We suggest that there is a common pathway for trigeminal neuralgia and migraine.

The cost of action miscues: hemispheric asymmetries.

Adaptive behaviors require preparation and when necessary inhibition or alteration of actions. The right hemisphere has been posited to be dominant for preparatory motor activation. This experiment was designed to learn if there are hemispheric asymmetries in the control of altered plans of actions. Cues, both valid and invalid, which indicate the hand most likely to be called onto respond, as well as the imperative stimuli that indicate the actual response hand, were presented to either the right or left visual fields of 14 normal right handed participants. The delay after a miscue is dependent on the time taken to inhibit the premotor and motor systems of the incorrectly activated hemisphere, as well as to activate the motor systems of the opposite hemisphere, which might have been interhemispherically inhibited by this miscue. Analyses of reaction times revealed that miscues presented in left hemispace (right hemisphere) cost more time than those miscues presented in right hemispace (left hemisphere), suggesting that activation of the preparatory systems controlled by the right hemisphere may take longer to reverse than those controlled by the left hemisphere. This asymmetry may be related to asymmetries in the strength of hemispheric activation with contralateral inhibition.