Cranial Nerve I Makes a Comeback

Plus Other AAN 2013 Highlights

Andrew N. Wilner, MD


April 02, 2013

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Cranial Nerve I Makes a Comeback

Welcome. This is Dr. Andrew Wilner reporting for Medscape with highlights from the 65th Annual Meeting of the American Academy of Neurology in San Diego, California. Today I will be summarizing 4 interesting posters. The topics are traumatic brain injury in olfaction, Parkinson disease progression, treatment of mild cognitive impairment with intravenous immunoglobulin (IVIG), and telemedicine and stroke mimics.

The first poster is "A Quantitative Test for Olfaction in the Most Sensitive Physical Examination Biomarker for Residual Neurological Dysfunction Due to Mild Traumatic Brain Injury That Can Be Performed in the Setting of a Clinical Examination Room," by Ruff and colleagues.[1] These investigators looked at 6 groups of patients, with and without traumatic brain injury (TBI) and loss of consciousness (LOC), and a civilian reference group (Table 1).

Table 1. Neurologic Deficits in 6 Groups

Group n Neurologic Deficits
Combat TBI with LOC 126 52%
Combat TBI without LOC 21 9.5%
Combat without TBI 52 0%
Civilian TBI with LOC 21 9.5%
Civilian TBI without LOC 21 0%
Civilian without TBI 21 0%

Overall, 69 of 262 (26%) had neurologic deficits. The patients with the most neurologic deficits, as might be expected, were those in the combat group who had both TBI and LOC. Of the 126 patients in this category, 52% had neurologic deficits, of which olfactory dysfunction was the most common (51%). The other deficits were impaired balance (11%), abnormal eye movements (10%), motor asymmetry (1.6%), and sensory changes (1.6%).

The only neurologic deficit experienced by 54% of patients with neurologic sequelae was impaired olfaction, which also correlated with the presence of cognitive impairment following TBI. The olfactory deficit could not be explained by a history of smoking, sinus disease, or inhalation of irritants. This finding is interesting because the first cranial nerve is often neglected in the routine neurologic examination. These findings may resurrect the first cranial nerve, because its assessment is a way to objectively document the presence of TBI in patients who might otherwise be considered to be neurologically normal.

Parkinson Disease: Not Just Dopamine Loss

The next poster is "Progression to Advanced Scores on the Hoehn and Yahr Scale in Parkinson Disease Is Not Explained by Degree of Dopaminergic Denervation," by Kotagal and colleagues.[2] They studied 20 patients with Parkinson disease whose Hoehn and Yahr scores were below stage 2.5. The patients had a clinical examination and a PET scan with dihydrotetrabenazine at baseline and 4 years later. Over the intervening 4 years, 9 patients converted to Hoehn and Yahr stage 3, and 11 patients remained below stage 2.5. The converters tended to be older than the nonconverters. The duration of disease was the same between patients who became clinically worse and those who did not. It was interesting that the rate of change in nigrostriatal dopaminergic denervation as assessed by the PET scan was the same in both groups.

The conclusion of this study is that the increased disability evidenced by progression is a consequence of extranigral pathology, not just increased loss of dopaminergic nerve terminals. This conclusion is consistent with the relative lack of response to dopamine in advanced disease. This study emphasizes that Parkinson disease is much more than just the loss of dopamine and should inspire more wide-ranging approaches to treatment.