Article Figures & Data
Figures
- Fig 1.
Coronal gadolinium-enhanced T1-weighted images (TR/TE, 600/14) through the cerebral peduncle and cisternal course of cranial nerve III (A) demonstrate marked enhancement and subtle enlargement of cranial nerve III on the left side (white arrows in A). Notice the normal appearance of cranial nerve III on the right (arrowheads in A). There is also subtle enhancement at the cranial nerve III exit zone on the left side (black arrows in A and B), which is better appreciated on the axial gadolinium-enhanced T1-weighted image (B) performed with the same imaging parameters.
- Fig 2.
Axial fluid-attenuated inversion recovery (FLAIR) image (TR/TE, 9500/110) through the midbrain (A) demonstrates a subtle area of increased signal intensity (arrows) along the medial margin of the cerebral peduncle on the left side. No enhancement is seen on the axial gadolinium-enhanced T1-weighted image (600/17) (B) in this region. The coronal gadolinium-enhanced T1-weighted images (600/14) through the cisternal course of cranial nerve III (C) demonstrate subtle enhancement of the cranial nerve III on the left side (arrows in C). Notice the normal appearance of cranial nerve III on the right (arrowheads in C).
- Fig 3.
Coronal FLAIR-weighted image (TR/TE, 10,002/168) obtained at the level of the anterior horns of the lateral ventricles shows a focal area of increased signal intensity (arrows) in the subcortical white matter of the inferior frontal lobe on the left side.
- Fig 4.
Coronal gadolinium-enhanced T1-weighted image (TRTE, 882/14) obtained at the level of the anterior horns of the lateral ventricles shows multiple enhancing white matter lesions (arrows). There is also a nonenhancing lesion in the corpus callosum in midline (arrowhead).
Tables
Third CN palsy and underlying lesions
Anatomic Site 3. CN Dysfunction Features Associated Clinical Findings Etiologies Contrast Enhancement of 3.CN or Its Nuclei Midbrain: Nuclear (+/−) Bilateral pupil involvement Supranuclear ocular motility deficits Infectious: (+/−) Bilateral ptosis Lyme disease Usually present Incomplete paresis (isolated extraocular muscle) Syphilis Variable Inflammatory: Contralateral superior rectus muscle paresis Multiple sclerosis Variable Sarcoidosis Present Autoimmune vasculitis Variable Neoplastic: Primary brain tumor Variable Metastasis Present Lymphoma Present Traumatic Usually none Vascular: Ischemia Variable Cavernous angioma Usually none Arteriovenous malformation (AVM) Enhancement of the AVM only Fascicular Complete or incomplete (divisional) paresis Cerebellar Ataxia: Nothnagel’s Same as above Contralateral dyskinesia: Benedickt’s (+/−) Pupil involvement Contralateral hemiparesis: Weber’s Subarachnoid space Complete or incomplete (divisional) paresis Multiple cranial neuropathies Infectious: Meningeal irritation Bacterial, viral or fungal meningitis Present (+/−) Pupil involvement Mental status changes Syphilis Variable Raised intracranial pressure Lyme disease Usually present HIV Usually present Inflammatory: Multiple sclerosis Variable Sarcoidosis Present Inflammatory demyelinating polyneuropathy Variable Neoplastic: Lymphoma Present Leukemia Present Meningeal carcinomatosis Present Schwannoma Present Traumatic Usually none Vascular: Ischemia Variable Aneurysm Enhancement of the Aneurysm only Other: Ophthalmoplegic migraine Present Cavernous sinus/superior orbital fissure Complete or incomplete (divisional) paresis Multiple cranial neuropathies Infectious: Visual Loss Bacterial, viral or fungal meningitis Present (+/−) Pupil involvement Proptosis Syphilis Variable Lyme disease Usually present HIV Usually present Inflammatory: Tolosa-Hunt syndrome Present Sarcoidosis Present Neoplastic: Lymphoma Present Leukemia Present Metastasis Usually present Schwannoma Present Pituitary macroadenoma Present Cavernous sinus meningioma Present Craniopharyngioma Variable Traumatic Usually none Vascular: Ischemia Variable Aneurysm Enhancement of the aneurysm only Pituitary gland apoplexy Usually none Other: Ophthalmoplegic migraine Present
