Electrodiagnosis of radiculopathy.

While nerve conduction studies are an important part of the electrodiagnostic examination (EDX), the diagnosis of a radiculopathy rests mainly on the needle electrode examination (NEE) findings. Myotomal spontaneous activity and neurogenic motor unit potential (MUP) changes are the key abnormalities seen. To optimize the rate of identifying a radiculopathy, selection of appropriate muscles for the NEE is paramount. Myotomal charts derived from anatomic, radiographic, and EDX studies may help guide development of the NEE protocol for radiculopathy and increase the diagnostic yield. As recommended by a number of studies, the suggested minimum NEE protocol should consist of at least five proximal and distal limb muscles. NEE of paraspinal muscles should also be included routinely, but several limitations preclude reliance on isolated findings for establishing a diagnosis of radiculopathy. In addition to the NEE, the preservation of sensory nerve action potentials is also important in localizing the lesion to the nerve root. In some cases, they may be absent due to age or technical factors, confounding the diagnosis. Finally, various patterns of EDX findings may be seen in specific nerve root disorders that can help expedite diagnosis and clinical management.

Irreversible optic neuropathy in wernicke encephalopathy and leber hereditary optic neuropathy.

A 52-year-old woman with alcohol abuse presented with recent worsening of vision, imbalance, and confusion. Examination revealed counting fingers acuity in both eyes with central scotomas, color vision loss, horizontal nystagmus, and gait ataxia. Thiamine was initiated as treatment for a presumptive diagnosis of Wernicke encephalopathy (WE). Brain MRI revealed high T2 signal in the dorsal midbrain and thalami characteristic of WE. The lack of optic disc edema, usually present in patients with WE who have severe optic neuropathy, and lack of visual loss reversibility with thiamine treatment, led to the suspicion of coexisting Leber hereditary optic neuropathy (LHON), which was later confirmed when testing revealed the 14484 mitochondrial DNA mutation. Over the ensuing months, vision did not recover despite improvement of other neurologic findings. Irreversible optic neuropathy in WE should prompt consideration of a coexisting mitochondrial disorder such as LHON.

Does seasonal variation affect hallucinations in PD? A longitudinal study.

The objective of this study was to examine the chronobiology of visual hallucinations in Parkinson's disease (PD) patients to test whether hallucinations are more severe during darker months (winter) than summer months. We extracted longitudinal data on the UPDRS Thought Disorder (TD) score, taken as part of regular patient management on sequential visits through a 1-year cycle in hallucinating PD patients. To reduce the confounding effects of medication adjustments, analysis was restricted to patients with a baseline evaluation that did not involve a medication change. The primary outcome was the seasonal change in hallucination severity, defined as a change in TD score or neuroleptic use. Using Wilcoxon rank-sum tests, we compared the exacerbation of hallucination by season, focusing on winter (December through February) versus summer (June through August). A total of 51 hallucinating patients met entry criteria, and their longitudinal data were analyzed. There was no difference in hallucination severity with changing season; the level of wintertime exacerbation was no greater than summertime exacerbation (P = 0.42). Although hallucinations frequently develop in dimmed environments and evening hours, the darkness of wintertime does not exacerbate hallucinations in PD subjects on stable medications. Because we found no evidence of seasonal variations, we cannot recommend phototherapy or other strategies affecting chronobiological systems as research priorities to treat PD hallucinations. (c) 2006 Movement Disorder Society.