PubMed Health⌕ Search

Biomedical subjects

B C Shephard

Publications and source records attributed to B C Shephard.

9 recordsLinked to original sources
PubMed1999

Is Parkinson's disease a primary olfactory disorder?

It has been known for over 30 years that olfactory function is disordered in idiopathic Parkinson's disease (IPD). The severity and partial specificity of anosmia was not realized until recently, with the advent of more detailed analysis and sophisticated measurement. The olfactory vector hypothesis suggests that the causative agent for IPD enters the brain via the nasal route, but the reason for olfactory dysfunction may be more subtle. Evidence for olfactory disturbance is reviewed from pathological, psychological, neurophysiological and genetic stand-points. It is proposed that the initial causative event in IPD may start in the rhinencephalon (olfactory brain) prior to damage in the basal ganglia.

Aging↗
PubMed1998

Olfactory evoked responses and identification tests in neurological disease.

UNLABELLED: To assess the value of smell testing we used olfactory evoked potentials (OEP) and an identification test in multiple sclerosis, Parkinson's disease, motor neuron disease and Alzheimer's disease. METHODS: The OEP to H2S (20 ppm) was obtained using an olfactometer designed to stimulate olfactory nerve endings only. Odor recognition was assessed by the University of Pennsylvania Smell Identification Test (UPSIT). In all instances the disease was 'definite' based on standard diagnostic criteria. Controls were derived from 156 healthy people. RESULTS: 1) Multiple Sclerosis: 11/72 patients (15%) were abnormal on UPSIT. For OEP there was significant increase of latency and decrease in amplitude in 6/26 patients (23%). 2) Parkinson's Disease: 126/155 (81%) patients had an abnormal UPSIT score. 12/37 (32%) had prolonged latency with normal amplitude measurement on OEP, but 27 had absent or unclear readings. 4/10 with normal UPSIT displayed abnormality on OEP. 3) Motor Neuron Disease: 9/58 (16%) were abnormal on UPSIT. There was significant delay in 1/10 (10%) patients on OEP. 4) Alzheimer's Disease: UPSIT scores were abnormal in all 8 patients examined. OEP was normal in 4 of these who could be tested. CONCLUSION: Smell dysfunction was found in all 4 conditions but most severely in Parkinson's Disease (over 80%). The UPSIT in general showed abnormality more frequently than OEP. The olfactory defect probably involves peripheral structures in all diseases tested except Alzheimer's. A patient with normal olfaction is unlikely to have idiopathic Parkinson's disease.

Adolescent↗
PubMed1998

Olfactory disorder in motor neuron disease.

In Parkinson's disease and Alzheimer's disease there is profound disorder of olfaction. The extent to which this modality is involved in motor neuron disease (MND) has been studied little. To address this further we assessed olfaction by three methods-a smell identification test ("UPSIT") in 58 patients and 135 controls; olfactory-evoked response (OEP) to H2S in 15 patients, and pathological examination of olfactory bulbs obtained from 8 cadavers. It was found that smell identification compared with the controls was slightly worse overall in the MND group as a whole, but only the bulbar patients scored significantly less on the UPSIT. Patients displayed a subtle defect in cheese odor recognition. OEPs were normal in 9 subjects and delayed in 1 subject. The remaining 5 OEPs were unsuccessful. Histopathological studies of olfactory bulbs showed excess lipofuscin deposition in all 8 cases examined, indicating subclinical neuronal damage. Olfactory neurons with a degree of antioxidant defect may be more susceptible to cellular damage than other neuronal groups because of their direct relationship to environmental agents. Overall we found the degree of olfactory dysfunction in MND to be mild and in contrast with the marked changes described by others.

Adolescent↗
PubMed1997

Olfactory dysfunction in Parkinson's disease.

OBJECTIVE: To evaluate olfactory function in Parkinson's disease. METHODS: A standardised odour identification test was used, together with an evoked potential assessment with hydrogen sulphide. In addition, histological analysis was performed on the olfactory bulbs of cadavers who died from Parkinson's disease. RESULTS: Over 70% of patients studied (71 of 96) were outside the 95% limit of normal on the identification test in an age matched sample and there was an unusual pattern of selective loss to certain odours, not hitherto described. The evoked potentials were significantly delayed but of comparable amplitude to a control matched population. Of the 73 patients studied only 37 had a technically satisfactory record containing a clear response to both gases and of these, 12 were delayed. For H2S there was more delay on stimulating the right nostril than the left. Some patients with normal smell identification test scores had delayed evoked potentials. In the pathological examination of olfactory bulbs from eight brains, changes characteristic of Parkinson's disease (Lewy bodies) were seen in every olfactory bulb, particularly in the anterior olfactory nucleus, and were sufficiently distinct to allow a presumptive diagnosis of Parkinson's disease. CONCLUSIONS: Olfactory damage in Parkinson's disease is consistent and severe and may provide an important clue to the aetiology of the disease.

Adolescent↗
PubMed1997

Assessment of olfaction in multiple sclerosis: evidence of dysfunction by olfactory evoked response and identification tests.

OBJECTIVE: To resolve whether the olfactory pathways are affected in multiple sclerosis. METHODS: Olfaction was assessed by: (1) The University of Pennsylvania smell identification test (UPSIT, which uses microencapsulated odours that are released when scratched with a pencil) in 72 patients with multiple sclerosis and 96 controls, (2) olfactory evoked potentials (OEP) to 20 ppm H2S by volume, and 50% CO2 in air for 45 patients with multiple sclerosis and 47 controls. The abnormality rate in patients with multiple sclerosis for both tests (1) and (2) was compared with that for visual evoked potentials measured using a standard checquerboard technique. RESULTS: By comparison with controls, patients exhibited significantly low scores on the smell identification test with 15% of patients scoring outside the 95% confidence intervals for controls. The UPSIT was occasionally abnormal when the visual evoked potential (VEP) was normal. In general UPSIT scores correlated well with the H2S-evoked response in controls and patients. For H2S, there was a statistically significant increase of latency and decrease of amplitude for patients compared with controls. Increased H2S latency and reduced UPSIT score correlated with greater disability on conventional rating scales. Overall, H2S responses were abnormal in about one quarter of patients with multiple sclerosis. The sensitivity of UPSIT and OEP was similar although disorder on one test did not necessarily indicate abnormality in the other. The visual evoked potential was found to be a more sensitive indicator of disease than OEP or UPSIT. CONCLUSION: These findings confirm the existence of olfactory dysfunction in multiple sclerosis and validate a new evoked potential technique.

Adult↗
PubMed1982

The oral effects of prolonged intermaxillary fixation by interdental eyelet wiring.

The oral effects of prolonged intermaxillary fixation were investigated in 106 severely obese patients who had been jaw wired as an aid to weight loss. The principal complications during fixation were episodes of periodontal pain and tooth mobility (40%). After removal of fixation, the principal sequelae were residual periodontal problems (9%) and mandibular limitation (9%). These findings were confirmed in a subgroup of 11 patients who had detailed measurements made of their periodontal index, oral hygiene index and range of jaw movements. These findings were discussed in relation to other methods of management of obesity.

Adult↗
PubMed1981

The effects of intra-arterial epinephrine and nicotine on gingival circulation.

The purpose of this study was to test the hypothesis that acute necrotizing ulcerative gingivitis (ANUG) was the result of ischemia resulting from three predisposing factors. Vascular stasis, stress, and smoking were said to combine and induce severe vascular constriction at the end arterial locations of the gingivae, resulting in necrosis of the part. The experimental animal used was the rabbit; clinical doses of epinephrine and nicotine were infused intraarterially and the gingival circulation was monitored by the heat-diffusion principle. It was found that the chemicals caused a severe reduction in flow rates in spite of greatly increased pressure within the system. The finding supports the hypothesis that ischemia could play an important role in the initiation of ANUG.

Animals↗