[Differences in clinical features of post-traumatic olfactory dysfunction and non-post-traumatic olfactory dysfunction: a follow-up study].

Objective:To analyze the clinical features and recovery rate of post-traumatic olfactory dysfunction (PTOD) in Chinese adults in a case control follow-up study. Method:The clinical data of 202 patients who were diagnosed with olfactory dysfunction between January 2015 and December 2016 and followed up for 14 to 473 days were analyzed in this retrospective study. The patients were divided into those with PTODs (PTOD group) and those without PTODs (non-PTOD group). The two groups were compared with regard to age (years), sex, olfactory function (Sniffin' sticks), gustatory function (triple drop method), chemosensory evoked potentials, and magnetic resonance imaging (MRI) characteristics of olfactory pathways. The recovery rate of PTOD was evaluated by Sniffin' sticks and triple drop method. Result:Patients in the PTOD group (40±11 years) were significantly younger than those in the non-PTOD group (47±15 years), whereas the number of men and women was similar in both groups. The mean TDI score (Sniffin' sticks) was significantly different between the PTOD (12±5) and non-PTOD (19±8) groups (P<0.05). The mean oERP P2 latency was significantly shorter for the non-PTOD group (418±64 ms) than for the PTOD group (483±82 ms, P<0.05). There were no significant differences in the mean oERP N1 latency, N1 amplitude, P2 amplitude, mean tERP P2 latency and MRI between the two groups. After the follow-up period, 8.9% (5/56) and 5.4% (3/56) patients in the PTOD group exhibited an improvement in olfactory function and gustatory function, respectively. Conclusion:PTOD should be considered a type of disability that can lead to serious accidents, and an adequate understanding of its clinical features and etiologies is critical for appropriate diagnosis and treatment and for improving the prognosis of treatment. The rate of recovery of olfactory function is higher than that of gustatory function in patients with PTOD; further investigations are required in this regard.

Patterns of olfactory impairment reflect underlying disease etiology.

OBJECTIVE: We aimed to determine whether the pattern of olfactory impairment seen in psychophysical testing reflects underlying disease etiology. STUDY DESIGN: Retrospective cohort. METHODS: We performed a retrospective analysis of 1,226 patients from our tertiary referral center. Only hyposmic patients with the following conditions were included: postinfectious hyposmia, posttraumatic hyposmia, hyposmia secondary to sinonasal disease, and hyposmia secondary to Parkinson disease. Patients with anosmia were excluded. RESULTS: Using a repeated measures analysis of variance (within subject factor "test": threshold [T], discrimination [D], identification [I]; between subject factor: "etiology") with posthoc Bonferroni corrected t tests, we found significant interaction between the factors "test" and "etiology" (F6,2444 = 8.46, P < 0.001), indicating that different causes of hyposmia produce different patterns of olfactory loss with respect to the individual subtests T, D, and I . Specifically, patients with Parkinson disease performed relatively well in odor threshold testing, but poorly in odor identification and discrimination compared with the other etiology groups. Conversely, patients with sinonasal disease performed well in odor identification and discrimination but poorly in odor threshold. Patients with postinfectious and posttraumatic hyposmia performed relatively well in both thresholds and discrimination but poorly in identification. However, patients with posttraumatic hyposmia had globally reduced scores compared with the other groups. CONCLUSION: This is the first study to comprehensively show that patterns of olfactory impairment reflect underlying disease etiology. We suggest that multicomponent olfactory testing should be performed, especially if there is diagnostic uncertainty. However, to clearly separate different patterns of olfactory loss to the various causes at an individual level, more work is needed. LEVEL OF EVIDENCE: 4. Laryngoscope, 2016 127:291-295, 2017.

Morphological analysis of regenerated bulbar fibers in relation to neonatal olfaction.

It was revealed that regeneration of the lateral olfactory tract (LOT) occurred in developing rats and the regenerated olfactory system was functional 4 weeks after transection. The aim of this study was to determine the earliest onset of functional recovery in LOT-injured rats and to quantify regenerated nerve components with functional correlation. Neonatal rats on postnatal day (P) 2 were subjected to unilateral transection of the left LOT and underwent unilateral removal of the right olfactory bulb on P11. Functional recovery of the tract injury was assessed by the suckling capability, which can be achieved by olfaction. Suckling capability was observed on P12 in most neonatally LOT-transected pups. Rat pups were subjected to unilateral transection of the left LOT on P2, and received injections of biotinylated dextran amine (BDA) into the bilateral olfactory bulb on P5 to quantify normal and regenerated nerve components in the olfactory cortices at the level of the olfactory tubercle. BDA(+) areas and density indices of the olfactory cortices in the neonatally LOT-transected P12 pups were 11.05×105µm2 and 0.35 on the normal right side and 4.34×105µm2 and 0.21 on the transected left side. We concluded that functional recovery of the LOT-transected neonatal rats occurred as early as 10days after tract transection and that areas and densities of regenerated nerve components essential for functional recovery were approximately 40% and 60% of the age-matched normal values in the olfactory cortices at the level of the olfactory tubercle.

A Flight Sensory-Motor to Olfactory Processing Circuit in the Moth Manduca sexta.

Neural circuits projecting information from motor to sensory pathways are common across sensory domains. These circuits typically modify sensory function as a result of motor pattern activation; this is particularly so in cases where the resultant behavior affects the sensory experience or its processing. However, such circuits have not been observed projecting to an olfactory pathway in any species despite well characterized active sampling behaviors that produce reafferent mechanical stimuli, such as sniffing in mammals and wing beating in the moth Manduca sexta. In this study we characterize a circuit that connects a flight sensory-motor center to an olfactory center in Manduca. This circuit consists of a single pair of histamine immunoreactive (HA-ir) neurons that project from the mesothoracic ganglion to innervate a subset of ventral antennal lobe (AL) glomeruli. Furthermore, within the AL we show that the M. sexta histamine B receptor (MsHisClB) is exclusively expressed by a subset of GABAergic and peptidergic LNs, which broadly project to all olfactory glomeruli. Finally, the HA-ir cell pair is present in fifth stage instar larvae; however, the absence of MsHisClB-ir in the larval antennal center indicates that the circuit is incomplete prior to metamorphosis and importantly prior to the expression of flight behavior. Although the functional consequences of this circuit remain unknown, these results provide the first detailed description of a circuit that interconnects an olfactory system with motor centers driving flight behaviors including odor-guided flight.

Olfactory ensheathing cells are the main phagocytic cells that remove axon debris during early development of the olfactory system.

During development of the primary olfactory system, axon targeting is inaccurate and axons inappropriately project within the target layer or overproject into the deeper layers of the olfactory bulb. As a consequence there is considerable apoptosis of primary olfactory neurons during embryonic and postnatal development and axons of the degraded neurons need to be removed. Olfactory ensheathing cells (OECs) are the glia of the primary olfactory nerve and are known to phagocytose axon debris in the adult and postnatal animal. However, it is unclear when phagocytosis by OECs first commences. We investigated the onset of phagocytosis by OECs in the developing mouse olfactory system by utilizing two transgenic reporter lines: OMP-ZsGreen mice which express bright green fluorescent protein in primary olfactory neurons, and S100ß-DsRed mice which express red fluorescent protein in OECs. In crosses of these mice, the fate of the degraded axon debris is easily visualized. We found evidence of axon degradation at embryonic day (E)13.5. Phagocytosis of the primary olfactory axon debris by OECs was first detected at E14.5. Phagocytosis of axon debris continued into the postnatal animal during the period when there was extensive mistargeting of olfactory axons. Macrophages were often present in close proximity to OECs but they contributed only a minor role to clearing the axon debris, even after widespread degeneration of olfactory neurons by unilateral bulbectomy and methimazole treatment. These results demonstrate that from early in embryonic development OECs are the primary phagocytic cells of the primary olfactory nerve.

A cytological and experimental study of the neuropil and primary olfactory afferences to the piriform cortex.

The microscopic organization of the piriform cortex (PC) was studied in normal and experimental material from adult albino rats. In rapid-Golgi specimens a set of collaterals from the lateral olfactory tract (i.e., sublayer Ia) to the neuropil of the Layer II (LII) was identified. Specimens from experimental animals that received electrolytic lesion of the main olfactory bulb three days before sacrificing, were further processed for pre-embedding immunocytochemistry to the enzyme glutamic acid decarboxylase 67 (GAD 67). This novel approach permitted a simultaneous visualization at electron microscopy of both synaptic degeneration and GAD67-immunoreactive (GAD-I) sites. Degenerating and GAD-I synapses were separately found in the neuropil of Layers I and II of the PC. Previously overlooked patches of neuropil were featured in sublayer Ia. These areas consisted of dendritic and axonal processes including four synaptic types. Tridimensional reconstructions from serial thin sections from LI revealed the external appearance of the varicose and tubular dendrites as well as the synaptic terminals therein. The putative source(s) of processes to the neuropil of sublayer Ia is discussed in the context of the internal circuitry of the PC and an alternative model is introduced.

Síndrome olfatorio autorreferencial: revisión sistemática / Olfactory reference syndrome: a systematic review

Introducción. El síndrome olfatorio autorreferencial (SOA) es un cuadro caracterizado por la creencia errónea de emitir un olor desagradable que los demás pueden percibir y les resulta ofensivo. No hay un consenso sobre la validez de este síndrome como entidad clínica independiente. Pacientes y métodos. Se ha realizado una revisión sistemática de la bibliografía (1966-2011) de artículos acerca del SOA que incluyesen algún caso clínico utilizando PsycINFO, PubMed, Medline e ISI Web of Knowledge. Se han analizado los datos obtenidos de 55 casos con la finalidad de evaluar la consistencia clínica y el valor heurístico de este síndrome. Resultados. En las características clínicas la evitación social aparece en el 60% de los casos, humor depresivo en el 42%, ansiedad en un 46% e ideas de referencia en un 44%. En el 36% de los 55 casos se describe un acontecimiento que se identifica como desencadenante. El tratamiento más empleado son los antidepresivos, seguido de los antipsicóticos y la psicoterapia, con una eficacia global del 39%. Conclusiones. El SOA es una entidad clínicamente bien definida, lo que apoyaría la idea de incluirla en el apéndice del DSM-5 como entidad independiente. Clínicamente, destaca la conducta de evitación y el acontecimiento traumático como datos más consistentes. Se propone un modelo etiopatogénico integrador. Se presentan datos de resonancia magnética funcional de un caso que cumple los criterios diagnósticos del SOA. Los resultados de la resonancia magnética funcional apuntan a una leve hiperactivación del sistema límbico (AU)

Introduction. The olfactory reference syndrome (ORS) is a condition characterized by the false belief that one emits a foul or offensive body odor. There is no consensus on the validity of this syndrome as an independent clinical entity. Patients and methods. A systematic review of the literature is done (1966-2011) searching for articles about the ORS that included a case report using PsycINFO, PubMed, Medline and ISI Web of Knowledge. Data obtained from 55 cases were analyzed to evaluate clinical consistency and heuristic value of this syndrome. Results. The clinical picture is: social avoidance 60%, depressed mood 42%, 46% anxiety and ideas of reference 44%. In 36% of the 55 cases described an event that is identified as a trigger. The most common treatment is first antidepressants, second antipsychotics and thirdly psychotherapy, with an overall efficiency of 39%. Conclusions. The ORS is a clinically well defined syndrome, which would support the idea of being included in the appendix of DSM-5, as an independent entity. The avoidance behaviour and the traumatic event are the more consistent data. An integrative model is propose. It also presents the clinical description and results of functional magnetic resonance imaging of a clinical case (AU)

Negative regulation of glial engulfment activity by Draper terminates glial responses to axon injury.

Neuronal injury elicits potent cellular responses from glia, but molecular pathways modulating glial activation, phagocytic function and termination of reactive responses remain poorly defined. Here we show that positive or negative regulation of glial responses to axon injury is molecularly encoded by unique isoforms of the Drosophila melanogaster engulfment receptor Draper. Draper-I promotes engulfment of axonal debris through an immunoreceptor tyrosine-based activation motif (ITAM). In contrast, Draper-II, an alternative splice variant, potently inhibits glial engulfment function. Draper-II suppresses Draper-I signaling through a previously undescribed immunoreceptor tyrosine-based inhibitory motif (ITIM)-like domain and the tyrosine phosphatase Corkscrew (Csw). Intriguingly, loss of Draper-II-Csw signaling prolongs expression of glial engulfment genes after axotomy and reduces the ability of glia to respond to secondary axotomy. Our work highlights a novel role for Draper-II in inhibiting glial responses to neurodegeneration, and indicates that a balance of opposing Draper-I and Draper-II signaling events is essential to maintain glial sensitivity to brain injury.

Odors from proximal species reverse the stress-decreased neurogenesis via main olfactory processing.

Unconditioned foot shock followed by restraint in water was used as a stress regimen to induce decreases in neurogenesis in mouse dentate gyrus (DG). Presence of conspecific odors has been known to reverse the stress-induced decrease in DG neurogenesis. In this study, we found that the conspecific odors did not produce these protective effects in mice whose MOE was impaired by nasal zinc sulfate lavage. Moreover, we observed that the presence of odors from rats, hamsters, and guinea pigs throughout the stress procedure reversed the stress-induced decrease in cell proliferation and neurogenesis in mouse dentate gyrus, while these odors alone did not affect mouse dentate cell proliferation or neurogenesis. In contrast, the presence of rabbit, sugar glider, hedgehog, beetle odors did not affect cell proliferation, neurogenesis, the stress-decreased cell proliferation or neurogenesis in DG. Finally, the presence of fox urine odors decreased mouse dentate cell proliferation and neurogenesis but did not affect the stress-induced decrease in cell proliferation or neurogenesis. Taken together, we conclude that olfactory processing via activation of sensory neurons in MOE is responsible for the conspecific odor-produced protective effect against the stress-decreased cell proliferation and neurogenesis. Phylogenetic distances of the odor-generating species and mice might contribute to the odors' protective effects against the stress-induced decreases in cell proliferation and neurogenesis.

Selective enhancement of main olfactory input to the medial amygdala by GnRH.

In male hamsters mating behavior is dependent on chemosensory input from the main olfactory and vomeronasal systems, whose central pathways contain cell bodies and fibers of gonadotropin-releasing hormone (GnRH) neurons. In sexually naive males, vomeronasal organ removal (VNX), but not main olfactory lesions, impairs mating behavior. Intracerebroventricular (i.c.v.)-GnRH restores mating in sexually naive VNX males and enhances medial amygdala (Me) immediate-early gene activation by chemosensory stimulation. In sexually experienced males, VNX does not impair mating and i.c.v.-GnRH suppresses Me activation. Thus, the main olfactory system is sufficient for mating in experienced-VNX males, but not in naive-VNX males. We investigated the possibility that GnRH enhances main olfactory input to the amygdala in naive-VNX males using i.c.v.-GnRH and pharmacological stimulation (bicuculline/D,L-homocysteic acid mixture) of the main olfactory bulb (MOB). In sexually naive intact males there was a robust increase of Fos protein expression in the anteroventral medial amygdala (MeAv) with MOB stimulation, but no effect of GnRH. There was no effect of stimulation or GnRH in posterodorsal medial amygdala (MePd). In naive-VNX animals, GnRH increased Fos in MeAv and MePv. Only combined MOB stimulation and i.c.v.-GnRH produced a significant increase in Fos in the dorsal (reproduction-related) portion of MeP (MePd). When the animals were sexually experienced before VNX, a condition in which GnRH does not enhance mating, i.c.v.-GnRH combined with MOB stimulation suppressed Fos expression in MePd. This suggests a more selective effect of GnRH on olfactory input in MePd than elsewhere in medial amygdala of VNX males.

Synchronous GABA-receptor-dependent potentials in limbic areas of the in-vitro isolated adult guinea pig brain.

Epileptiform discharges are known to reflect the hypersynchronous glutamatergic activation of cortical neurons. However, experimental evidence has revealed that epileptiform synchronization is also contributed to by population events mediated by GABA(A) receptors. Here, we analysed the spatial distribution of GABA(A)-receptor-dependent interictal events in the hippocampal/parahippocampal region of the adult guinea pig brain isolated in vitro. We found that arterial perfusion of this preparation with 4-aminopyridine caused the appearance of glutamatergic-independent interictal potentials that were reversibly abolished by GABA(A) receptor antagonism. Laminar profiles and current source density analysis performed in different limbic areas demonstrated that these GABA(A)-receptor-mediated events were independently generated in different areas of the hippocampal/parahippocampal formation (most often in the medial entorhinal cortex) and propagated between interconnected limbic structures of both hemispheres. Finally, intracellular recordings from principal neurons of the medial entorhinal cortex demonstrated that the GABAergic field potential correlated to inhibitory postsynaptic potentials (membrane potential reversal, -68.12 +/- 8.01 mV, n = 5) that were interrupted by ectopic spiking. Our findings demonstrate that, in an acute seizure model developed in the adult guinea pig brain, hypersynchronous GABA(A)-receptor-mediated interictal events are generated from independent sources and propagate within limbic cortices in the absence of excitatory synaptic transmission. As spared or enhanced inhibition was reported in models of epilepsy, our data may support a role of GABA-mediated signaling in ictogenesis and epileptogenesis.

Contribution of gustation to the palatability of linoleic acid.

We investigated the palatability of a low concentration of linoleic acid (LA) in short-term two-bottle choice tests and licking tests. To examine the contribution of gustation, mice were rendered anosmic with olfactory nerve transection surgery and test solutions were prepared using mineral oil (saturated long-chain hydrocarbon) to minimize textural effects. In the two-bottle choice tests between various pairs of different concentrations of corn oil and LA, both anosmic and the sham-operated mice constantly preferred a higher concentration of corn oil and LA. In the licking tests, the initial licking rate for 1% LA was higher than that for mineral oil in anosmic mice. In accordance with the results of the two-bottle choice test, the initial licking rate for corn oil and LA increased in a concentration-dependent manner in both anosmic and sham-operated mice in the licking test, and reached its peak at 100% corn oil and 1% LA. A preference comparison between 1% LA and 100% corn oil showed that anosmic mice preferred 1% LA over 100% corn oil. These results suggest that mice could recognize dietary fat and fatty acid solutions in the oral cavity without any olfactory or textural cues and the fatty acid recognition on their tongues might provide a pivotal cue to how dietary fat is recognized in the oral cavity.

Promoting central nervous system regeneration: lessons from cranial nerve I.

The olfactory nerve differs from cranial nerves III-XII in that it contains a specialised type of glial cell, called 'olfactory ensheathing cell' (OEC), rather than Schwann cells. In addition, functional neurogenesis persists postnatally in the olfactory system, i.e. the primary olfactory pathway continuously rebuilds itself throughout adult life. The presence of OECs in the olfactory nerve is thought to be critical to this continuous growth process. Because of this intrinsic capacity for self-repair, the mammalian olfactory system has proved as a useful model in neuroregeneration studies. In addition, OECs have been used in transplantation studies to promote pathway regeneration elsewhere in the nervous system. Here, we have reviewed the parameters that allow for repair within the primary olfactory pathway and the role that OECs are thought to play in this process. We conclude that, in addition to intrinsic growth potential, the presence of an aligned substrate to the target structure is a fundamental prerequisite for appropriate restoration of connectivity with the olfactory bulb. Hence, strategies to promote regrowth of injured nerve pathways should incorporate usage of aligned, oriented substrates of OECs or other cellular conduits with additional intervention to boost neuronal cell body responses to injury and/or neutralisation of putative inhibitors.

Distinct effects of anterior pyriform cortex and the lateral hypothalamus lesions on protein intake in rats.

Several specific locations in brain, including pyriform cortex and hypothalamus, are associated with regulation of food intake. Although lesions of these locations significantly alter food intake, their involvement in the selection of macronutrients is not well characterized. In this study, we examined distinct effects of anterior pyriform cortex (APC) and lateral hypothalamus (LH) lesions on protein intake in rats. The APC or LH of male adult rats were lesioned by treatment with kainic acid, and the rats were then given free access to two kinds of casein diets containing high (60%) and low (5%) protein. Total energy content of these diets was kept constant by changing the carbohydrate content. Following the APC lesions, body weight and food intake decreased, but returned to control levels on day 13 and day 4, respectively. APC lesions did not change the ratio of protein intake. In contrast, LH lesions disturbed body weight gain and the selection of a high protein diet for at least two weeks, although food intake returned to control levels by day 2. Our results suggest that LH, but not APC, may play an important role in the selection of protein intake in rats.

Contribution of olfactory neural stem cells to tissue maintenance and regeneration.

The olfactory neuroepithelium undergoes continual neurogenesis and, after extensive lesions, fully regenerates to maintain sensory function. The stem cell population underlying this regenerative capacity remains elusive. Here we show that mouse horizontal basal cells (HBCs) function as adult olfactory neuroepithelium neural stem cells and examine their distinct dynamics in olfactory neuroepithelium maintenance and regeneration. Fate-mapping analysis after olfactory neuroepithelium lesioning shows that HBCs are competent to regenerate both neuronal and non-neuronal olfactory neuroepithelium lineages. HBCs serve as a reservoir of long-lived progenitors that remain largely quiescent during normal neuronal turnover or even after acute, selective loss of mature neurons. Under these conditions, previously identified progenitors are largely responsible for tissue maintenance. Yet after extensive injuries that deplete resident neuronal precursors, HBCs transiently proliferate and their progeny fully reconstitute the neuroepithelium. Our data support a new model of adult neurogenesis in which distinct cell populations mediate normal neuronal turnover and neuronal replacement upon traumatic injury.

Mechanism of changes induced in plasma glycerol by scent stimulation with grapefruit and lavender essential oils.

In a previous study, we found that stimulation with scent of grapefruit oil (SGFO) elevated plasma glycerol levels in rats. However, stimulation with scent of lavender oil (SLVO) triggered a negative effect. To identify the mechanism of these changes during lipolysis, we examined the role of autonomic blockers and bilateral lesions of the hypothalamic suprachiasmatic nucleus (SCN) in the modification of plasma glycerol in rats exposed to SGFO and SLVO. We found that intraperitoneal injection of propranolol hydrochloride and atropine sulfate eliminated the changes in plasma glycerol levels induced by SGFO and SLVO, respectively. Bilateral lesions of the SCN completely abolished the effects of SGFO and SLVO on lipolysis. In addition, we investigated tyrosine phosphorylation of the transmembrane glycoprotein BIT (a brain immunoglobulin-like molecule with tyrosine-based activation motifs, a member of the signal-regulator protein family), which was found to be involved in the activation of renal sympathetic nerves and increase in body temperature on cold exposure. SGFO was found to enhance the immunoreactivity of BIT to the 4G10 anti-phosphotyrosine antibody in the SCN, whereas SLVO decreased the immunoreactivity. The changes in BIT phosphorylation resulting from the exposure to SGFO and SLVO were eliminated by the corresponding histamine receptor antagonists, which eliminated the changes in plasma glycerol concentration. The results suggest that SGFO and SLVO affect the autonomic neurotransmission and lipolysis. The SCN and histamine neurons are involved in the lipolytic responses to SGFO and SLVO, and tyrosine phosphorylation of BIT is implicated in the relevant signaling pathways.

Quantitative EEG analysis in post-traumatic anosmia.

Many objective and quantitative methods have been developed to create a procedure or a device to prove, describe and quantify olfactory deficit and anosmia, especially after a head trauma. Electrophysiological testing throughout olfactoelectroencephalography (olfactoEEG) is based on brain activity desynchronisation, and on the subsequent disappearance of alpha activity on the posterior regions after an olfactory stimulus. Yet traditional evaluation of EEG can be difficult, because of little or hardly detectable alpha activity on the posterior regions ('alpha rare'). The aim of this study was to evaluate the Olfactory Stop Reaction (OSR) by means of frequency band power calculation and subsequent topographical mapping in patients with post-traumatic anosmia, who presented 'alpha rare' EEG. Twenty-five consecutive patients, affected by anosmia caused by head trauma, were submitted to an EEG recording with olfactory stimulation. After signal processing and analysis, an Olfactory Stop Reaction was detected in 17 out of 25 patients; moreover, in these patients we detected a significant decrease in alpha band power in the occipital regions and an increase in theta band power on midline frontal and central regions after olfactory stimulation. In the remaining eight patients, no significant variation in band power was observed. In conclusion, an objective evaluation of the olfactory function with this method of automatic EEG signal analysis allows the limits given by psychophysical methods and traditional EEG to be overcome and attempts to fulfil the requirements for standardization of olfactory function evalution.

In vivo imaging of functional disruption, recovery and alteration in rat olfactory circuitry after lesion.

Compensatory changes following disruption of neuronal circuitry have been indicated by previous imaging studies of stroke and other brain injury, but evidence of the pathways involved in such dynamic changes has not been shown in vivo. We imaged rats before and after lesion-induced disruption of the lateral olfactory tract to investigate the subsequent recovery and/or reorganization of functional neuronal circuitry. Serial magnetic resonance imaging was performed following intranasal administration of a paramagnetic track tracer Mn(2+). Images were analyzed using statistical mapping techniques in the stereotactic coordinate system. At 1 week post-lesion, Mn(2+) transport caudal to lesion was reduced as expected, and more importantly, increased transport through the anterior commissure was seen. At 4 weeks post-lesion, there was recovery of transport caudal to lesion, and increased transport through the anterior commissure extended to the contralateral olfactory cortex. Correlation analysis of regional Mn(2+) transport indicated that contralateral enhancement was not simply due to septal window spillover. This study demonstrates for the first time in vivo evidence of compensatory changes in functional neuronal activity to a contralateral pathway through the commissure following brain injury.

Functional asymmetry of left and right avian piriform cortex in homing pigeons' navigation.

It has been shown that homing pigeons rely on olfactory cues to navigate over unfamiliar areas and that any kind of olfactory impairment produces a dramatic reduction of navigational performance from unfamiliar sites. The avian piriform cortex is the main projection field of olfactory bulbs and it is supposed to process olfactory information; not surprisingly bilateral lesions to this telencephalic region disrupt homing pigeon navigation. In the present study, we attempted to assess whether the left and right piriform cortex are differentially involved in the use of the olfactory navigational map. Therefore, we released from unfamiliar locations pigeons subjected, when adult, to unilateral ablation of the piriform cortex. After being released, the pigeons lesioned to the right piriform cortex orientated similarly to the intact controls. On the contrary, the left lesioned birds were significantly more scattered than controls, showing a crucial role of the left piriform cortex in processing the olfactory cues needed for determining the direction of displacement. However, both lesioned groups were significantly slower than controls in flying back to the home loft, showing that the integrity of both sides of the piriform cortex is necessary to accomplish the whole homing process.

Microsurgical anatomic features of the olfactory nerve: relevance to olfaction preservation in the pterional approach.

OBJECTIVE: The pterional approach represents the standard approach for most lesions of the anterior and middle cranial fossa. It requires some degree of frontal lobe retraction, which may result in temporary or permanent damage of olfaction because of nerve avulsion or mechanical compression. The purpose of this study, based on microanatomic dissection of human cadaveric specimens, was to review the microsurgical anatomic features of the nerve and suggest operative nuances that may contribute to reducing the rate of postoperative olfactory dysfunction. METHODS: Twenty olfactory nerves and tracts were examined in 10 human cadaveric heads obtained from three fresh and seven formalin-fixed adult cadavers. A standard pterional craniotomy was performed. The olfactory nerve was dissected from its arachnoidal envelopes and then mobilized for an average length of 30 mm (range, 25-35 mm). RESULTS: The possible retraction of the frontal lobe was 10 to 15 mm. More retraction invariably resulted in nerve disruption. CONCLUSION: The standard sylvian and basal cistern opening may be insufficient to guarantee preservation of olfactory function. Early identification and arachnoidal dissection of the nerve may reduce the rate of olfaction compromise. The opening of the subarachnoidal space should be performed in a proximal-to-distal manner to allow early visualization of the olfactory bulb and its dissection. The arachnoidal dissection should be performed with sharp instruments, avoiding any traction on the posterior portion of the olfactory tract. Any direct retractor compression should also be avoided to spare the microvasculature lying on the dorsal surface of the nerve.