James R Keane1. 1. University of Southern California Medical School, Los Angeles, California, USA.
Abstract
BACKGROUND: Most studies of third nerve palsy (TNP) antedate computerized imaging and focus primarily on chart review of referral outpatients. METHODS: To compare a large contrasting population, I reviewed 1400 personally-examined municipal hospital inpatients with TNPs seen over 37 years. RESULTS: TNPs were bilateral in 11%, complete in 33%, without other neurological signs (isolated) in 36%, and associated with recurrent cranial neuropathies in 7%. Third nerve damage occurred in the subarachnoid space in 32%, the cavernous sinus in 23%, the brainstem in 14%, as a nonlocalized peripheral neuropathy in 18% and at an uncertain location in 13%. Causes were trauma (26%), tumor (12%), diabetes (11%), aneurysm (10%), surgery (10%), stroke (8%), infection (5%), Guillain-Barre and Fisher syndromes (5%), idiopathic cavernous sinusitis (3%), benign self-limited (2%), miscellaneous (4%), and unknown (3%). Local causes, besides an abundance of trauma, included six cases involving cysticercosis, four with wound botulism, and one with coccidiomycotic meningitis. Of 234 patients with diabetes, microvascular ischemia was the cause of TNP in only two-thirds (five had aneurysms) and 53% of those with diabetic microvascular ischemia had pupillary involvement-often bilateral, suggesting concomitant autonomic neuropathy. Only 2% of aneurysms spared the pupil. Apainful onset occurred with 94% of aneurysm and 69% of diabetic cases. CONCLUSIONS: Bilateral TNPs, multiple cranial neuropathies, and accompanying neurological signs were common among our inpatients, as were causes rare in outpatient settings such as severe trauma, transtentorial herniation, midbrain strokes, and the Guillain-Barre syndrome. Few cases remained undiagnosed and nondiabetic ischemia was rare.
BACKGROUND: Most studies of third nerve palsy (TNP) antedate computerized imaging and focus primarily on chart review of referral outpatients. METHODS: To compare a large contrasting population, I reviewed 1400 personally-examined municipal hospital inpatients with TNPs seen over 37 years. RESULTS: TNPs were bilateral in 11%, complete in 33%, without other neurological signs (isolated) in 36%, and associated with recurrent cranial neuropathies in 7%. Third nerve damage occurred in the subarachnoid space in 32%, the cavernous sinus in 23%, the brainstem in 14%, as a nonlocalized peripheral neuropathy in 18% and at an uncertain location in 13%. Causes were trauma (26%), tumor (12%), diabetes (11%), aneurysm (10%), surgery (10%), stroke (8%), infection (5%), Guillain-Barre and Fisher syndromes (5%), idiopathic cavernous sinusitis (3%), benign self-limited (2%), miscellaneous (4%), and unknown (3%). Local causes, besides an abundance of trauma, included six cases involving cysticercosis, four with wound botulism, and one with coccidiomycotic meningitis. Of 234 patients with diabetes, microvascular ischemia was the cause of TNP in only two-thirds (five had aneurysms) and 53% of those with diabetic microvascular ischemia had pupillary involvement-often bilateral, suggesting concomitant autonomic neuropathy. Only 2% of aneurysms spared the pupil. Apainful onset occurred with 94% of aneurysm and 69% of diabetic cases. CONCLUSIONS: Bilateral TNPs, multiple cranial neuropathies, and accompanying neurological signs were common among our inpatients, as were causes rare in outpatient settings such as severe trauma, transtentorial herniation, midbrain strokes, and the Guillain-Barre syndrome. Few cases remained undiagnosed and nondiabetic ischemia was rare.
Authors: Chengbo Fang; Jacqueline A Leavitt; David O Hodge; Jonathan M Holmes; Brian G Mohney; John J Chen Journal: JAMA Ophthalmol Date: 2017-01-01 Impact factor: 7.389