NEJM. Volume 358:306-307  January 17, 2008  Number 3
Prednisolone or Acyclovir in Bell's Palsy
Sullivan et al. (Oct. 18 issue) report that early treatment with prednisolone significantly improves the chances of complete recovery in patients with Bell's palsy, whereas no evidence of a benefit of acyclovir could be found. Idiopathic peripheral-facial-nerve paralysis of sudden onset is difficult to diagnose because other causes that are associated with a significantly higher risk of defective healing must be ruled out. Since zoster sine herpete — which can mimic the signs and symptoms of Bell's palsy — caused by varicella–zoster virus has an incidence rate of up to 34% among patients with "Bell's palsy," information about the virologic backgrounds of all participating patients, obtained by means of serologic and polymerase-chain-reaction examinations, is needed. However, the authors have not provided virologic data to ensure the exclusion of patients with zoster sine herpete from this study.

BMJ  2008;336:88-92 (12 January), doi:10.1136/bmj.39412.705868.AD
Clinical Review Tension-type headache
Tension-type headache is a neurological disorder characterised by a predisposition to attacks of mild to moderate headache with few associated symptoms. The diagnosis is based on the history and examination. Over the past few decades research on headache has centred on migraine, and much of the best quality evidence for the treatment of tension-type headache is decades old. Some consensus based treatment guidelines are available (see Additional Educational Resources box towards the end of this article). Treatment has changed little over the past two decades. Many patients self treat acute attacks and seek advice when attacks become frequent or chronic. This review focuses on how to identify and manage patients who require medical advice about acute attacks and preventive treatment to minimise further attacks.

Science 18 January 2008: Vol. 319. no. 5861, p. 269
NEUROSCIENCE: Mirror Neurons May Help Songbirds Stay in Tune
In work published this week, researchers describe mirror neurons in songbirds that fire when a bird sings or hears another bird sing a song similar to its own, a finding that may pave the way to insights into how songbirds learn and maintain their complex songs.

Science 18 January 2008: Vol. 319. no. 5861, pp. 288 - 289
NEUROSCIENCE:Organizing the Source of Memory
Signals from the midline of the embryonic brain direct formation of the hippocampus.

Science 18 January 2008: Vol. 319. no. 5861, pp. 304 - 309
Lhx2 Selector Activity Specifies Cortical Identity and Suppresses Hippocampal Organizer Fate
The earliest step in creating the cerebral cortex is the specification of neuroepithelium to a cortical fate. Using mouse genetic mosaics and timed inactivations, we demonstrated that Lhx2 acts as a classic selector gene and essential intrinsic determinant of cortical identity. Lhx2 selector activity is restricted to an early critical period when stem cells comprise the cortical neuroepithelium, where it acts cell-autonomously to specify cortical identity and suppress alternative fates in a spatially dependent manner. Laterally, Lhx2 null cells adopt antihem identity, whereas medially they become cortical hem cells, which can induce and organize ectopic hippocampal fields. In addition to providing functional evidence for Lhx2 selector activity, these findings show that the cortical hem is a hippocampal organizer.

Nature 451, 249-250 (17 January 2008) | doi:10.1038/451249a; Published online 16 January 2008
Behavioural neuroscience: Neurons of imitation
In songbirds, a class of neurons shows a striking similarity in activity when the bird sings and when it hears a similar song. This mirroring neuronal activity could contribute to imitation.
Songbirds are champion mimics. A nightingale, for example, can imitate at least 60 different songs after a few exposures to each.

Nature 451, 305-310 (17 January 2008) | doi:10.1038/nature06492; Received 10 October 2007;
Precise auditory–vocal mirroring in neurons for learned vocal communication
Brain mechanisms for communication must establish a correspondence between sensory and motor codes used to represent the signal. One idea is that this correspondence is established at the level of single neurons that are active when the individual performs a particular gesture or observes a similar gesture performed by another individual. Although neurons that display a precise auditory–vocal correspondence could facilitate vocal communication, they have yet to be identified. Here we report that a certain class of neurons in the swamp sparrow forebrain displays a precise auditory–vocal correspondence. We show that these neurons respond in a temporally precise fashion to auditory presentation of certain note sequences in this songbird's repertoire and to similar note sequences in other birds' songs. These neurons display nearly identical patterns of activity when the bird sings the same sequence, and disrupting auditory feedback does not alter this singing-related activity, indicating it is motor in nature. Furthermore, these neurons innervate striatal structures important for song learning, raising the possibility that singing-related activity in these cells is compared to auditory feedback to guide vocal learning.

Nature 451, 330-334 (17 January 2008) | doi:10.1038/nature06493; Received 11 October 2007;
Reversal of pathological pain through specific spinal GABA-A receptor subtypes
Inflammatory diseases and neuropathic insults are frequently accompanied by severe and debilitating pain, which can become chronic and often unresponsive to conventional analgesic treatment. A loss of synaptic inhibition in the spinal dorsal horn is considered to contribute significantly to this pain pathology. Facilitation of spinal γ-aminobutyric acid (GABA)ergic neurotransmission through modulation of GABA-A receptors should be able to compensate for this loss8, 9. With the use of GABA-A-receptor point-mutated knock-in mice in which specific GABA-A-receptor subtypes have been selectively rendered insensitive to benzodiazepine-site ligands, we show here that pronounced analgesia can be achieved by specifically targeting spinal GABA-A receptors containing the α2 and/or α3 subunits. We show that their selective activation by the non-sedative ('α1-sparing') benzodiazepine-site ligand L-838,417 is highly effective against inflammatory and neuropathic pain yet devoid of unwanted sedation, motor impairment and tolerance development. L-838,417 not only diminished the nociceptive input to the brain but also reduced the activity of brain areas related to the associative-emotional components of pain, as shown by functional magnetic resonance imaging in rats. These results provide a rational basis for the development of subtype-selective GABAergic drugs for the treatment of chronic pain, which is often refractory to classical analgesics.

Nature 451, 363-367 (17 January 2008) | doi:10.1038/nature06482; Received 23 March 2007;
Structural basis of microtubule severing by the hereditary spastic paraplegia protein spastin
Spastin, the most common locus for mutations in hereditary spastic paraplegias, and katanin are related microtubule-severing AAA ATPases involved in constructing neuronal and non-centrosomal microtubule arrays and in segregating chromosomes. The mechanism by which spastin and katanin break and destabilize microtubules is unknown, in part owing to the lack of structural information on these enzymes. Here we report the X-ray crystal structure of the Drosophila spastin AAA domain and provide a model for the active spastin hexamer generated using small-angle X-ray scattering combined with atomic docking. The spastin hexamer forms a ring with a prominent central pore and six radiating arms that may dock onto the microtubule. Helices unique to the microtubule-severing AAA ATPases surround the entrances to the pore on either side of the ring, and three highly conserved loops line the pore lumen. Mutagenesis reveals essential roles for these structural elements in the severing reaction. Peptide and antibody inhibition experiments further show that spastin may dismantle microtubules by recognizing specific features in the carboxy-terminal tail of tubulin. Collectively, our data support a model in which spastin pulls the C terminus of tubulin through its central pore, generating a mechanical force that destabilizes tubulin–tubulin interactions within the microtubule lattice. Our work also provides insights into the structural defects in spastin that arise from mutations identified in hereditary spastic paraplegia patients