1. Patients with multiple auras may be good candidates for epilepsy surgery
Auras of multiple types in a single patient do not appear to be very helpful in localizing the seizure focus. Intuitively, such patients appear to be poor candidates for surgery to relieve epilepsy. Not necessarily so, claim Widdess-Walsh et al [4] from Cleveland Clinic epilepsy center. Between 1989 and 2005 they monitored 31 patients who experienced multiple aura types at their unit. Most of the patients who had multiple auras (90% of the total 31 patients, and all 12 patients who had 3 or more aura types) had auras localized to the nondominant hemisphere. Subdural electroencephalogram recordings in 6 patients showed a march of sequential auras. Twenty patients had epilepsy surgery and half of them achieved freedom from seizures. The authors conclude that patients with multiple auras can be good candidates for surgery. It is likely that patients with multiple auras in the nondominant hemisphere can better describe them before losing the ability to speak and thus can be identified.
2. Mini-seizures in a mouse model of Alzheimer's disease
We do not yet know all the ways in which brains deteriorate in Alzheimer's disease (AD). In a recent article in Neuron, Palop et al [2] described an interesting finding in the mouse model of AD. They studied mice that are transgenic for human amyloid precursor protein, which develop AD-like abnormalities in their brains. In their mice, they recorded spontaneous nonconvulsive seizure activity in cortical and hippocampal networks. This activity resulted in enhanced synaptic inhibition and synaptic plasticity deficits in the dentate gyrus, an area important for memory formation. The seizures may work like an excitotoxic challenge. In separate studies in nontransgenic mice, excitotoxic challenges simulated neuronal alterations seen in the transgenic mice. The damage from excitotoxicity could be prevented by blocking overexcitation medically. It would be interesting to see what role aberrant excitation plays in human AD, and whether neuronal damage and symptoms can be delayed by some type of anti-epileptic medication.
3. Facet joint fluid signal on magnetic resonance imaging—what does it mean?
It is not rare to hear an empirical opinion that severe facet degeneration correlates with segmental spinal instability. Two recent articles shed some light on this condition. Last June, an article by Rihn et al [3] was published in the journal Spine. The authors describe a retrospective analysis of imaging data from their institution. Fifty-one consecutive patients who had a lumbar spine magnetic resonance imaging (MRI) were studied. The authors selected those who had L4-L5 degenerative disease and were candidates for lumbar fusion. The goal was to correlate between the amount of facet fluid and degree of spinal instability at the L4-L5 level. The amount of fluid in the facet joints was calculated as a ratio between the length of increased T2 signal and the total length of the facet joints bilaterally. Instability on the flexion radiograph was measured as percent anterior slip at L4-L5. Twenty-eight (55%) of the 51 patients had facet fluid on MRI, and in 23 of the patients with facet fluid instability was noted on flexion-extension imaging. There was a positive linear correlation between the facet fluid ratio and the degree of slip (Pearson coefficient, 0.90; P < .001). Although the study is retrospective in nature, the parameters studied appear to be objective and reproducible. The presence of a linear correlation further supports the notion of the 2 phenomena being physiologically related.
The second article was published 2 months later in the same journal. Chaput et al [1] looked at the correlation of facet degeneration at L4-L5 in 193 patients seen for orthopedic consultation at a single institution. On flexion and extension radiographs, 54 of the patients had degenerative spondylolisthesis at L4-L5. These patients were typically older, female, had synovial cysts, and had larger facet effusion size. Twenty-two percent of the listheses were not detectable on supine MRI. The authors concluded that large facet effusions are highly predictive of degenerative spondylolisthesis at L4-L5, even in the absence of anterolisthesis on supine MRI.
The 2 articles suggest that facet joint effusion is an important marker of facet degeneration and is also associated with spondylolisthesis. The association makes empirical sense, but the clinical implications are not clear. So far most of the treatment attempts have been directed at the disc—discectomy, posterior and anterior interbody fusions have become very common. Has the role of the facet joint been underestimated?
References
[1]. [1]Chaput C, Padon D, Rush J, Lenehan E, Rahm M. The significance of increased fluid signal on magnetic resonance imaging in lumbar facets in relationship to degenerative spondylolisthesis. Spine. 2007;32(17):1883–1887.
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[2]. [2]Palop JJ, Chin J, Roberson ED, Wang J, Thwin MT, Bien-Ly N, et al. Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease. Neuron. 2007;55(5):697–711.
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[3]. [3]Rihn JA, Lee JY, Khan M, Ulibarri JA, Tannoury C, Donaldson WF, et al. Does lumbar facet fluid detected on magnetic resonance imaging correlate with radiographic instability in patients with degenerative lumbar disease?. Spine. 2007;32(14):1555–1560.
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[4]. [4]Widdess-Walsh P, Kotagal P, Jeha L, Wu G, Burgess R. Multiple auras: clinical significance and pathophysiology. Neurology. 2007;69(8):755–761.
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Department of Neurosurgery, University of Illinois at Chicago, Chicago, IL 60612, USA