Olfactory dysfunction in degenerative ataxias

Connelly, Timothy

doi:10.1136/jnnp.74.10.1435

Cited by 56 publications

(46 citation statements)

References 21 publications

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“…Such a functional role can be deduced only by combining multiple sources of information. In this respect, the current results dovetail nicely with previous results implicating the cerebellum in olfactory identification (Abele et al, 2003;Connelly et al, 2003) and further highlight the genuine olfactory origin of this impairment. Finally, the lateralization pattern of these results provides an initial set of constraints toward mapping the functional path from nose to cerebellum and allows us to conclude that this primarily contralateral path plays a functional role in olfaction.…”

Section: Resultssupporting

confidence: 77%

“…Two recent reports suggested that patients with bilateral cerebellar degeneration exhibit a significant decrement in olfactory identification (Abele et al, 2003;Connelly et al, 2003) that was persistent despite normal olfactory detection thresholds (Abele et al, 2003). This profile of impaired identification despite intact thresholds raises the possibility that cerebellar lesions may impair cognitive mechanisms related to object identification in general, rather than olfactory identification per se.…”

Section: Introductionmentioning

confidence: 99%

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Olfactory Impairments in Patients with Unilateral Cerebellar Lesions Are Selective to Inputs from the Contralesional Nostril

Mainland¹,

Johnson²,

Khan³

et al. 2005

J. Neurosci.

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Functional imaging studies of olfaction have consistently reported odorant-induced activation of the cerebellum. However, the cerebellar role in olfaction remains unknown. We examined the olfactory and olfactomotor abilities of patients with unilateral cerebellar lesions, comparing performance within subjects across nostrils, as well as between subjects with age-matched and young controls. Regarding olfactory performance, initial testing revealed that patients had a contralesional impairment in olfactory identification but not olfactory detection threshold. However, when tested under conditions that prevented compensatory sniffing strategies, the patients also exhibited a contralesional olfactory detection impairment. Regarding olfactomotor function, a healthy olfactomotor system generates sniffs that are (1) sufficiently vigorous and (2) inversely proportional to odorant concentration in sniff mean airflow velocity, maximum airflow velocity, volume, and duration. Patients' sniffs were lower in overall airflow velocity and volume in comparison with control participants. Furthermore, reduced sniff velocity predicted poorer detection thresholds in patients. Finally, whereas young controls used concentration-dependent sniffs, there was a trend in that direction only for age-matched controls. Patients used sniffs that were concentration invariant. In conclusion, cerebellar lesions impacted olfactory and olfactomotor performance. These findings strongly implicate an olfactocerebellar pathway prominent in odor identification and detection that functionally connects each nostril primarily to the contralateral cerebellum.

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Section: Resultssupporting

confidence: 77%

Section: Introductionmentioning

confidence: 99%

Olfactory Impairments in Patients with Unilateral Cerebellar Lesions Are Selective to Inputs from the Contralesional Nostril

Mainland¹,

Johnson²,

Khan³

et al. 2005

J. Neurosci.

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show abstract

“…Following this line of reasoning, the odor threshold deficit should disappear with this test. The odor identification impairment in the group of patients with a cerebellar lesion is consistent with reports of olfactory deficits in patients with cerebellar disease [14][15][16]. This impairment may be related to a disturbance of cerebellar projections to cortical areas involved in processing of cognitive functioning.…”

Section: Discussionsupporting

confidence: 81%

“…Yet, involvement of the cerebellum in olfaction is suggested by cerebellar activation described in functional imaging studies of olfaction [10][11][12][13] and olfactory impairment in patients with cerebellar disease [14][15][16]. The VL thalamus is functionally closely connected to the contralateral cerebellum, and is therefore also referred to as the ''cerebellar thalamus'' [17][18][19].…”

Section: Introductionmentioning

confidence: 97%

Involvement of the human ventrolateral thalamus in olfaction

Zobel

Hummel²,

Ilgner

et al. 2010

J Neurol

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It is widely assumed that the thalamus is not involved in olfaction. The ventrolateral thalamus is, however, closely connected to the contralateral cerebellum, which is involved in the sense of smell based on findings from functional imaging studies and findings of olfactory deficits in patients with cerebellar disease. We hypothesized that olfactory deficits following lesions of the ventrolateral thalamus may be similar to olfactory deficits following cerebellar lesions. Fifteen patients with a focal thalamic lesion involving the ventrolateral thalamus were examined and compared to 15 patients with a focal cerebellar lesion and 15 healthy controls. A detailed olfactory test ("Sniffin' Sticks") was used to assess different olfactory functions separately for each nostril. In the group of patients with a lesion of the ventrolateral thalamus, an impairment of the odor threshold was found at the ipsilateral nostril, consistent with the unilateral orientation of the olfactory system in the telencephalon. In the group of patients with a cerebellar lesion, an olfactory deficit at the contralesional nostril emerged. In controls, no significant side difference was found. The involvement of the ventrolateral thalamus in olfaction is comparable to that of the cerebellum in respect to odor threshold. Further study is needed to assess if these findings are related to an impairment of an olfactomotor loop. Present evidence for this hypothesis is indirect. Effects were subclinical as none of the patients reported olfactory disturbance. The results suggest that the cerebello-thalamic axis plays an adjuvant role in olfaction.

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“…One of these studies reported that eight patients with multiple system atrophy of cerebellar type (MSA-C) and 11 patients with sporadic cerebellar ataxia of unknown etiology had impairments in odor discrimination and identification [1]. The second study tested two patient populations, one Friedreich ataxia group (FRDA) and a combined CNS ataxic group (two SCA2, five SCA3, one SCA7 and five with unidentified cerebral degeneration) [4]. Both groups had olfactory deficits measured with UPSIT.…”

Section: Discussionmentioning

confidence: 97%

Spinocerebellar ataxia type 2 olfactory impairment shows a pattern similar to other major neurodegenerative diseases

et al. 2006

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Olfactory function is affected in different neurodegenerative diseases. Recently, it has been found that some hereditary ataxias are also associated with significant olfactory impairment. However, the initial findings did not examine the nature of the olfactory impairment associated with these ataxias. In the present article the effect of spinocerebellar ataxia type 2 (SCA2) on olfactory function was studied in 53 SCA2 patients and 53 healthy control subjects from Holguín, Cuba. Several tests were applied to evaluate olfactory threshold, description, identification and discrimination. The results show significant impairment in SCA2 patients on all olfactory measurements, and the pattern of olfactory deficits found suggests that they have much in common with those reported for other neurodegenerative diseases such as Parkinson's and Alzheimer's diseases.

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Olfactory dysfunction in degenerative ataxias

Cited by 56 publications

References 21 publications

Olfactory Impairments in Patients with Unilateral Cerebellar Lesions Are Selective to Inputs from the Contralesional Nostril

Olfactory Impairments in Patients with Unilateral Cerebellar Lesions Are Selective to Inputs from the Contralesional Nostril

Involvement of the human ventrolateral thalamus in olfaction

Spinocerebellar ataxia type 2 olfactory impairment shows a pattern similar to other major neurodegenerative diseases

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