Olfactory Function and Olfactory Bulb Volume in Patients with Postinfectious Olfactory Loss

Rombaux, Philippe; Mouraux, André; Bertrand, Bernard; Nicolas, Georges; Duprez, Thierry; Hummel, Thomas

doi:10.1097/01.mlg.0000195291.36641.1e

Cited by 156 publications

(139 citation statements)

References 13 publications

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“…There is evidence from numerous studies that magnetic resonance imaging (MRI) offers an ideal means to reliably evaluate the volume of the OB which appears to be of interest in olfactory loss. OB size has already been studied in patients with post-traumatic [ and post-infectious olfactory deficits [31,34], congenital anosmia [1,43], schizophrenia [39], and in subjects with a normal sense of smell [8,45].…”

Section: Olfactory Bulb Volumes In Patients With Parkinson's Diseasementioning

confidence: 99%

Immunohistochemical, volumetric, and functional neuroimaging studies in patients with idiopathic Parkinson's disease

Hummel¹,

Witt

Reichmann³

et al. 2010

Journal of the Neurological Sciences

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Section: Olfactory Bulb Volumes In Patients With Parkinson's Diseasementioning

confidence: 99%

Immunohistochemical, volumetric, and functional neuroimaging studies in patients with idiopathic Parkinson's disease

Hummel¹,

Witt

Reichmann³

et al. 2010

Journal of the Neurological Sciences

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“…Axotomy or ZnSO 4 irrigation of the olfactory neuroepithelium does lead to a 33 to 75% decrease of bulb weight in rats after a month, [73][74][75] largely reflecting degenerative changes within the glomerular and external plexiform layers of the bulb. In humans, decreased olfactory bulb volumes determined using magnetic resonance imaging have been reported secondary to age, 76 head trauma, 77 upper respiratory infections that induce epithelial damage, 78 and schizophrenia. 79 Volume decrements of approximately 23% were reported for both older persons and those with schizophrenia.…”

Section: Centrifugal Afferent Innervation Comes From the Horizontal Lmentioning

confidence: 99%

The olfactory vector hypothesis of neurodegenerative disease: Is it viable?

Doty

2008

Annals of Neurology

348

279

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Environmental agents, including viruses, prions, and toxins, have been implicated in the cause of a number of neurodegenerative diseases, most notably Alzheimer's and Parkinson's diseases. The presence of smell loss and the pathological involvement of the olfactory pathways in the formative stages of Alzheimer's and Parkinson's diseases, together with evidence that xenobiotics, some epidemiologically linked to these diseases, can readily enter the brain via the olfactory mucosa, have led to the hypothesis that Alzheimer's and Parkinson's diseases may be caused or catalyzed by agents that enter the brain via this route. Evidence for and against this concept, the “olfactory vector hypothesis,” is addressed in this review. Ann Neurol 2008;63:7–15

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“…The figures shown in (12) and (13) do not even show fluid accentuation in the vitreous humor. Therefore it remains unclear to us how these investigators could be expected to detect fluid (12)(13)(14). As a positive control, we have also been able to detect fluid in the central canal of the spinal cord using this technique.…”

mentioning

confidence: 60%

Response to Comment on "Human Neuroblasts Migrate to the Olfactory Bulb via a Lateral Ventricular Extension"

Curtis

Kam

Nannmark

et al. 2007

Science

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In contrast to a previous study of Sanai et al., our study had the advantage of using serial sagittal sections of the human basal forebrain, combined with 5-bromo-2′-deoxyuridine labeling, rigorous magnetic resonance imaging, and polymerase chain reaction analysis. We believe these methods convincingly demonstrate the presence of a rostral migratory stream in the human brain that resembles that in other mammals. W e recently identified a previously partly undefined structure in the human forebrain, which we named the ventriculo-olfactory neurogenic system (VONS) (1). We proposed the VONS to be defined as the subventricular zone (SVZ), the rostral migratory stream (RMS), and the olfactory tract and bulb. Sanai et al. (2) previously reported that an RMS did not exist in the human brain, but they missed vital clues in their study that pointed to the possibility of an RMS. We expand on this idea and on their questions and critiques (3) regarding our study below.Concerning the questions of Sanai et al.(3) about the number of proliferating cell nuclear antigen (PCNA)-positive cells in the RMS, we have the following responses. First, not all of the RMS cells are dividing. Second, the images in figure 1 in our original study (1) were captured from 50-mm-thick sections, so a tightly packed PCNA appearance exists. In thick sections from human hippocampus, another neurogenic region (Fig. 1A), PCNA-positive cells are also tightly packed, but clearly not all are PCNA-stained (evidenced by calbindin staining). Third, we have previously published results of the control experiments that show that PCNA detects proliferating cells (4) and have carefully evaluated PCNA and K i -67 as markers for proliferation, with similar results (5). Sanai and colleagues appear not to have used PCNA in their studies or to have experimental proof of what their cell cycle markers detected. Perhaps this is why their study did not reveal an RMS. In our RMS mapping studies, we used human brain cases that were neurologically normal (all our cases died from heart or lung pathology), whereas Sanai et al. studied many cases that had brain tumors or vascular malformations that normally would have been treated with radiotherapy. It may therefore be possible that such treatment reduced the abundance of dividing cells and migrating neuroblasts in the specimens they used.Cells positive for 5-bromo-2′-deoxyuridine (BrdU) and neuronal nuclei (NeuN) in the olfactory bulb were seen in the periglomerular layer of all examined BrdU cases. As stated in the supporting online material for (1), the cause of death in these cases was squamous cell carcinoma at the base of the tongue, and patients were not treated by radiotherapy. The ages of the patients were (B1) 57, (B2) 64, and (B3) 70 years of age, and the time between injection and mortem date was 274, 128, and 578 days, respectively. NeuN labeling was found in two forms: (i) with strong cytoplasmic labeling and (ii) with weaker nucleus-specific labeling (Fig. 1, B to D). Similar cytoplasmic labeling has previously...

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Olfactory Function and Olfactory Bulb Volume in Patients with Postinfectious Olfactory Loss

Abstract: The study emphasizes that OB volume is a gauge of olfactory function.

Cited by 156 publications

References 13 publications

Immunohistochemical, volumetric, and functional neuroimaging studies in patients with idiopathic Parkinson's disease

Immunohistochemical, volumetric, and functional neuroimaging studies in patients with idiopathic Parkinson's disease

The olfactory vector hypothesis of neurodegenerative disease: Is it viable?

Response to Comment on "Human Neuroblasts Migrate to the Olfactory Bulb via a Lateral Ventricular Extension"

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