Objective: To investigate differences between peripheral idiopathic and central sixth nerve palsies from brainstem damage by comparing peak velocities and durations of horizontal saccades. Methods: Fourteen patients with unilateral incomplete sixth nerve palsies caused by idiopathic, presumed ischemic, peripheral damage, 5 with incomplete central (fascicular) palsy caused by brainstem lesions, and 10 controls were studied. Palsies under 1 month in duration were designated as acute and those of longer duration were chronic. Among peripheral palsies, five were acute, nine were chronic. Among central palsies, two were acute, three were chronic. Subjects made ±10 deg horizontal saccades while wearing search coils. Serial recordings were made in seven patients with acute palsy (five peripheral, two central). Results: Centrifugal abducting saccadic velocities in the paretic eye were subnormal in both central and peripheral acute palsies, as anticipated from lateral rectus weakness. In chronic central palsies, abducting velocities in the paretic eye remained reduced. However, in chronic peripheral palsies, velocities became normal in the tested range of excursion, within 2 months of onset, despite persisting abduction deficit. Conclusions: Saccade peak velocities are reduced and their durations are prolonged in the field of action of acutely palsied peripheral and central nerves. Speeds remain reduced in chronic central (fascicular) palsies, consistent with limited regeneration within the brain. Saccade speeds are repaired in chronic peripheral palsies, probably by remyelination and axonal regeneration, and perhaps also by central monocular adaptation of innervation selectively to the paretic eye, in order to drive both eyes rapidly and simultaneously into the paretic field of motion.
Objective:To investigate differences between peripheral idiopathic and central sixth nerve palsies from brainstem damage by comparing peak velocities and durations of horizontal saccades.Methods:Fourteen patients with unilateral incomplete sixth nerve palsies caused by idiopathic,presumed ischemic,peripheral damage,5 with incomplete central(fascicular)palsy caused by brainstem lesions,and 10 controls were studied.Palsies under 1 month in duration were designated as acute and those of longer duration were chronic.Among peripheral palsies,five were acute,nine were chronic.Among central palsies,two were acute,three were chronic.Subjects made ± 10 deg horizontal saccades while wearing search coils.Serial recordings were made in seven patients with acute palsy(five peripheral,two central).Results:Centrifugal abducting saccadic velocities in the paretic eye were subnormal in both central and peripheral acute palsies,as anticipated from lateral rectus weakness.In chronic central palsies,abducting velocities in the paretic eye remained reduced.However,in chronic peripheral palsies,velocities became normal in the tested range of excursion,within 2 months of onset,despite persisting abduction deficit.Conclusions:Saccade peak velocities are reduced and their durations are prolonged in the field of action of acutely palsied peripheral and central nerves.Speeds remain reduced in chronic central(fascicular)palsies,consistent with limited regeneration within the brain.Saccade speeds are repaired in chronic peripheral palsies,probably by remyelination and axonal regeneration,and perhaps also by central monocular adaptation of innervation selectively to the paretic eye,in order to drive both eyes rapidly and simultaneously into the paretic field of motion.
Purpose: Diabetes mellitus and systemic hypertension are frequently reported as ischemic causes of sixth nerve palsy/-paresis, but there are few rigorous studies to support these associations. We conducted a population-based case-control study to determine the presence and magnitude of any association of preexisting diabetes mellitus and systemic hypertension with isolated sixth nerve palsy. Design: Retrospective population-based case-control study. Participants and Controls: Participants were patients with new onset of neurologically isolated sixth nerve palsy or paresis (n=76) in Olmsted County, Minnesota, from January 1, 1978, to December 31, 1992. Controls (n=76) were selected from the same general population and were matched for age, gender, and length of medical follow-up. Methods: Using the Rochester Epidemiology Project medical records linkage system, which captures virtually all medical care provided to residents of Olmsted County, Minnesota, we identified all incident cases of neurologically isolated sixth nerve palsy/paresis (n=76) among county residents between the given dates. An equal number (n=76) of controls were randomly selected from the general population. We reviewed the entire medical record of each case and control, using stringent predetermined criteria to define the presence of diabetes mellitus and systemic hypertension. We compared the prevalence of diabetes and systemic hypertension between cases and controls by use of chi-square tests, and we calculated odds ratios (OR)with 95%confidence intervals (CI). MainOutcome Measures: Presence or absence of diabetes mellitus and systemic hypertension. Results: Diabetes mellitus occurred more frequently in cases (23.7%) than in controls (5.3%; P=0.001; OR, 5.59; 95%CI, 1.79-17.42). Systemic hypertension occurred with similar frequency in cases (51.3%) and controls (39.5%; P=0.14; OR, 1.62; 95%CI, 0.85-3.08). Coexistent diabetes mellitus and hypertension were more common in cases (18.4%) than in controls (2.6%; P=0.002; OR, 8.36; 95%CI, 1.83-38.18
The authors investigated the evolution of third nerve palsy in patients with posterior communicating artery aneurysms who underwent coiling vs clipping.There was no statistical difference of complete third nerve palsy recovery in both treatments.Both techniques were of clinical benefit.Older age,diabetes,delayed interventions,and complete third nerve palsy at presentation indicated a poor prognosis for recovery.
