Medscape is available in 5 Language Editions – Choose your Edition here.


Oculomotor Nerve Palsy Clinical Presentation

  • Author: James Goodwin, MD; Chief Editor: Andrew G Lee, MD  more...
Updated: Mar 18, 2016


The following symptoms are encountered with lesions producing third cranial nerve dysfunction:

  • The most common lesions to affect the third cranial nerve involve the fascicular portions of the nerve at some level. The symptoms reflect reduced function in the muscles innervated by the nerve, usually in combination; isolated involvement of one or another muscle from fascicular third cranial nerve lesions is very rare. The prime symptom is mixed horizontal and vertical binocular diplopia from deviation of the 2 visual axes.
  • Ptosis may be sufficient to cover the pupil in which case the patients complain that they cannot see from the eye on the involved side. In fact, this component may mask the symptom of diplopia if the ptosis is prominent before the visual axes diverge.
  • Pupil enlargement and lack of light reaction produces little in the way of symptoms, although there may be some glare sensation and photoaversion in bright light.

Neurologic symptoms

Neurologic symptoms associated with lesions involving various portions of the third cranial nerve include those discussed below.

Nuclear portion

Most of the lesions causing nuclear, third cranial nerve palsy are from dorsal midbrain infarction. These tend to be small lesions with few associated neurologic symptoms or signs.

Fascicular midbrain portion

Benedikt syndrome of the upper mid brain includes third cranial nerve palsy on the side of the lesion, ipsilateral flapping hand tremor (rubral tremor from red nucleus involvement), and ataxia.

Weber syndrome results from a slightly more ventral lesion at the level of the third cranial nerve fascicles in the mid brain, with involvement of the cerebral peduncle giving rise to contralateral hemiplegia or hemiparesis along with ipsilateral third cranial nerve palsy.

Subarachnoid portion

The fascicles of the third cranial nerve exit the mid brain through the medial aspect of the cerebral peduncles and are not near any of the other cranial nerves at this point.

The findings of third cranial nerve palsy tend to occur in isolation from lesions in this location.

Since the most common lesion to affect the third cranial nerve in the subarachnoid space is aneurysm, the signs and symptoms of subarachnoid hemorrhage, including sudden severe headache, stiff neck, and loss of consciousness, may be present.

Infundibulum refers to widening of the proximal segment of the posterior communicating and other arteries, and, unlike aneurysm in this location, it is usually asymptomatic. A case of posterior communicating artery infundibulum has been documented causing recurrent ipsilateral third cranial nerve palsy and headache that masqueraded as ophthalmoplegic migraine.[2]

Basal meningeal infection, neoplastic infiltration, and miscellaneous inflammatory lesions may involve the third and all the other cranial nerves. The primary symptoms of meningitis are often present, including headache, stiff neck, fever, and alteration of consciousness. Eventually, these diseases tend to involve other cranial nerves, which is not the case with a very localized lesion, such as berry aneurysm.

Ophthalmoplegic migraine presents in childhood with recurring bouts of unilateral headache and ipsilateral third cranial nerve palsy that can last several weeks at a time. The link to migraine in general has come under question because many or most of these patients demonstrate thickening and enhancement of the cisternal portion of the third cranial nerve on MRI with gadolinium.[3]

Cavernous sinus portion

The third cranial nerve is more susceptible to compression against the interclinoid ligaments above and the petroclinoid ligament below than are the other cranial nerves in the cavernous sinus. For this reason, isolated third cranial nerve palsy may result from lateral extension of pituitary adenoma or other primary intrasellar mass.

More diffuse lesions within the cavernous sinus, often inflammatory in nature, typically give rise to simultaneous involvement of the third, fourth, sixth, and first 2 divisions of the fifth cranial nerves in various combinations, which serve to define a cavernous sinus syndrome. Nonspecific or granulomatous inflammation within the cavernous sinus is referred to as Tolosa-Hunt syndrome.

Carotid artery dural branch to cavernous sinus fistulas typically present with third cranial nerve palsy plus other cranial nerve involvement in the cavernous sinus and proptosis with arterialized conjunctival veins due to a large volume shunt of arterial blood into the anterior draining veins of the cavernous sinus. Isolated third cranial nerve involvement without the orbital congestion can occur when the primary drainage is posterior from the cavernous sinus, the so-called white eye fistulas.[4]

Involvement of the fourth cranial nerve does not add any symptoms to patients with Tolosa-Hunt syndrome since the eye on the side of the third cranial nerve palsy already has a deficit of depression from involvement of the inferior rectus muscle.

Involvement of the sixth cranial nerve in patients with Tolosa-Hunt syndrome leads to an associated deficit of ocular abduction, but this does not change the symptom complex when there is associated third cranial nerve palsy.

Often, the involvement of the first 2 divisions of the fifth cranial nerve (trigeminal) presents with severe pain and numbness in the face, including the forehead back to the interaural line and the cheek down to the angle of the mouth. The pain may be constant and burning with unpleasant paresthesia, or it may include a lancinating component that can be confused with trigeminal neuralgia.

Orbital portion

Lesions in the orbit tend to produce associated proptosis, lid swelling, conjunctival injection, and chemosis.

There also may be involvement of the other cranial nerves that innervate extraocular muscles (fourth and sixth) or involvement of the muscles themselves.

Nonspecific or granulomatous inflammation in the orbit is referred to as orbital inflammatory pseudotumor.



Initially, physical findings attributable to involvement of the fascicles of one or the other third cranial nerve are described. Subsequently, additional physical findings that are associated with lesions of particular portions or segments of the third cranial nerve are described.

Unilateral third cranial nerve palsy

Horizontal deviation is divergent or temporal (exotropia) because of weakness of the medial rectus muscle of the involved side. Vertical deviation results from weakness of the superior rectus, inferior oblique (both elevators), and inferior rectus (depressor) muscles.

Residual function of the superior oblique muscle (depressor, intact fourth cranial nerve function) tends to produce downward deviation of the involved eye. A way to remember this combination is to think of a losing boxer, "down and out".

Diagnosing partial third cranial nerve palsy is facilitated by an alert patient. The deficit of adduction, supraduction, and infraduction should be apparent even if partially paralyzed.

In very mild cases, one might have to resort to eliciting latent deviation or phoria with Maddox rod or alternate cover testing (to dissociate the 2 eyes and interrupt fusion).

Ptosis results from weakness of the levator palpebrae, and this often is complete or nearly so, in which case the pupil is covered and the patient cannot see from the involved eye.

Milder degrees of ptosis are examined best using measurements of the palpebral fissure width; more information can be gained from measuring the margin reflex distances (MRD), as follows:

  • The examiner sits in front of the patient and directs a point source of light (eg, handlight, Finnoff head, penlight) into both the eyes of the patient.
  • The examiner can observe the pinpoint light reflex in the center of the cornea. The position of this reflex is not affected by deviation of the eye, which makes it a useful reference point for measuring the distance to the upper and lower lids, respectively.
  • The MRD1 usually refers to the distance from the light reflex to the upper lid margin, and the MRD2 is the distance to the lower lid margin.
  • Levator palpebrae weakness reduces the MRD1 but will not affect the MRD2. On the other hand, ptosis from ocular sympathetic palsy (Horner or Claude Bernard syndrome) causes weakness of Mueller muscle in both the upper and lower lids, with consequent reduction of both the MRD1 and the MRD2.
  • Pseudoptosis from widening of the contralateral palpebral fissure may result from mild or old contralateral seventh cranial nerve lesion and orbicularis oculi weakness. In both these cases, MRD1 and MRD2 are increased on the side opposite to the apparent ptosis.
  • Careful examination of facial muscle strength and symmetry usually confirms the cause of the apparent ptosis in these cases.

Pupillary dilatation and sluggish or absent reaction to light results from involvement of parasympathetic fibers that originate in the Edinger-Westphal subnucleus of the third cranial nerve complex, as follows:

  • Fascicular involvement from compressive lesions often affects these autonomic fibers because they are situated very superficially within the nerve trunk.
  • This contingent of fibers are medially placed as the nerve exits the brainstem and gradually migrate to a more inferior and lateral position as they proceed anteriorly along the nerve.

If there is partial preservation of parasympathetic pupillary innervation with third cranial nerve disorders, the pupil on the involved side may react to light nearly as briskly as the pupil of the other eye, as follows:

  • Distinguishing pupillary involvement caused by third cranial nerve lesions from ocular sympathetic palsy (Horner or Claude Bernard syndrome) or physiological anisocoria requires detailed examination of pupil size in dim and in bright, ambient light.
  • With sphincter weakness due to parasympathetic involvement in third cranial nerve lesions, the involved pupil is larger than the fellow pupil.
  • The size difference between the 2 pupils (anisocoria) is greater in bright light (when the sphincter is called upon to act most strongly) and less in dim light (when the sympathetically innervated dilator fibers are the dominant contributors to pupil size). The reverse is true for ocular sympathetic lesions, the pathological pupil is the smaller one and the difference (anisocoria) is greater in dim light than in bright light. The anisocoria remains the same in dim and bright light in simple central anisocoria, also called physiological anisocoria.

Nuclear portion

Nuclear third cranial nerve palsy demonstrates in addition to the ipsilateral findings, contralateral partial ptosis and elevation palsy.

The contralateral partial ptosis stems from the bilateral distribution of innervation to the levator from the caudal central subnucleus.

Ptosis is more complete ipsilateral to the lesion because function is lost in both the ipsilateral neural cell bodies and their fibers on the lesioned side, plus the crossed fibers coursing through the lesion from the other side.

There is partial ptosis contralateral to the lesion because of the residual integrity of the uncrossed neural cell bodies and fibers from the caudal central subnucleus contralateral to the lesion.

Superior rectus nucleus output is totally contralateral with fascicles from the nucleus on one side coursing through the opposite superior rectus subnucleus. A lesion of the superior rectus subnucleus on one side causes bilateral elevation palsy. The deficit ipsilateral to the lesioned nucleus reflects involvement of fascicles coming from cell bodies on the opposite side, and the deficit contralateral to the lesion reflects loss of the cell bodies in the lesioned nucleus.

Fascicular midbrain portion

Ask the patient to hold both arms outstretched in front of them.

Patients with Benedikt syndrome have a gross "flapping" tremor that has been attributed to red nucleus involvement, usually from midbrain infarction. The tremor and ataxia is ipsilateral to the lesion and to the third cranial nerve palsy.

In Weber syndrome, the patient usually has a dense hemiplegia contralateral to the third cranial nerve palsy resulting from a lesion that also involves the pyramidal tract motor pathways in the cerebral peduncle. This should be obvious on simple inspection of the patient, since it is usually a fairly prominent hemiplegia.

Subtle hemiparesis may be observed by asking the patient to hold both arms outstretched forward with palms rotated upward. Slight pronation of the turned-up hand and downward drift of the outstretched arm are sensitive indicators of even very mild hemiparesis.

The hemiparetic gait is also characteristic with foot drop causing circumduction as the involved leg is swung out and forward before the next step. The arm on the involved side typically is held semiflexed at the elbow and wrist as the patient walks.

Another subtle sign in very mild hemiparesis is loss of the associated arm swing on the involved side as the patient walks.

Fascicular subarachnoid portion

Many patients who have had subarachnoid hemorrhage from rupture of a berry aneurysm have alteration of consciousness and may be difficult to examine. Even if they cannot co-operate with ocular motility assessment, the findings of a dense third cranial nerve palsy should be obvious. The eye on the involved side is deviated "down and out" from residual tone in the fourth cranial nerve (superior oblique muscle) and the sixth cranial nerve (lateral rectus muscle).

Usually, there is prominent ptosis also, but this may be difficult to observe if the patient is unconscious with eyes closed. Efforts should be made to arouse the patient at least to the point that there is some effort at eye opening, when the ptosis should be apparent.

The dilated, light-fixed pupil should be apparent on inspection without requiring any co-operation from the patient.

Pupillary involvement is the rule in third cranial nerve palsy resulting from posterior communicating artery aneurysm, with or without overt subarachnoid hemorrhage. This is probably because the pathophysiology of the third cranial nerve lesion involves leakage of blood from the aneurysm dome into the nerve across its outer margin. The pupil fibers are located very superficially and are nearly always involved in this process. On the other hand, pupil-sparing third cranial nerve palsy is a hallmark of ischemic lesions that tend to involve the central core of the nerve. This is the type of nonsurgical or medical third cranial nerve palsy that often results from microvascular disease and tends to resolve uneventfully within a few weeks.[5, 6]

Fascicular cavernous sinus portion

Fourth cranial nerve palsy

Fourth cranial nerve palsy is difficult to diagnose in the presence of third cranial nerve palsy because the small increment of depressor deficit (superior oblique muscle) cannot be discerned readily from the depressor palsy that results from weakness of the third nerve innervated depressor (inferior rectus muscle).

The superior oblique muscle depresses the globe most efficiently with the eye in adduction, a position that may not be achievable with medial rectus palsy from third cranial nerve involvement.

The best marker for fourth cranial nerve function in the presence of dense third cranial nerve palsy is intorsion of the globe on attempted down gaze. If no intorsion is present, one should suspect concomitant fourth cranial nerve palsy as part of a cavernous sinus syndrome. Torsion of the globe can be discerned by simultaneously watching landmarks, such as conjunctival vessels lateral and medial to the iris. With intorsion, the lateral vessels rise and the nasal vessels drop.

Trigeminal nerve sensory function

Trigeminal nerve sensory function can be tested with the aid of a cotton-tipped applicator. Tease a few fibers of the cotton into a pointed bundle by twirling it between the thumb and the forefinger after a small tuft of cotton is pulled free of the tip.

This little wisp of cotton can be touched to the cornea near the limbus to test the corneal reflex. It should elicit a blink response that is symmetric between the sides.

Failure to blink may indicate reduced sensory function in the first division of the trigeminal nerve on the side of decreased response. The cotton wisp can be dragged lightly across the skin in various locations. With the eyes closed, the patient is asked to indicate when it is felt.

Asymmetry of light touch between sides should be sought. The wooden stick, when broken, can serve as a "pinprick" tester. Usually, the break is jagged and there is a pointed end that can be used like a pin to test for pain sensation. Lightly tap the point on the skin at various points. The patient should compare the "sharpness" of the feeling at homologous points on the right and left sides of the face.

Fascicular orbital portion

Orbital signs are usually matters for direct inspection, including conjunctival injection and chemosis; proptosis; and lid swelling.

Obtain exophthalmometry measurements with a Hertel instrument or similar equipment since it provides a more sensitive measure of relative proptosis.



Any focally destructive lesion along the course of the third cranial nerve can cause oculomotor nerve palsy or dysfunction. A painful pupil-involved oculomotor nerve palsy may result from a life-threatening intracranial aneurysm.

Some of the most frequent causes include the following:

  • Nuclear portion
    • Infarction
    • Hemorrhage
    • Neoplasm
    • Abscess
  • Fascicular midbrain portion
    • Infarction
    • Hemorrhage
    • Neoplasm
    • Abscess
  • Fascicular subarachnoid portion
    • Aneurysm
    • Infectious meningitis - Bacterial, fungal/parasitic, viral
    • Meningeal infiltrative
    • Carcinomatous/lymphomatous/leukemic infiltration, granulomatous inflammation (sarcoidosis, lymphomatoid granulomatosis, Wegener granulomatosis)
    • Ophthalmoplegic migraine
  • Fascicular cavernous sinus portion
    • Tumor - Pituitary adenoma, meningioma, craniopharyngioma, metastatic carcinoma
    • Pituitary apoplexy (infarction within existing pituitary adenoma)[7]
    • Vascular
    • Giant intracavernous aneurysm
    • Carotid artery-cavernous sinus fistula
    • Carotid dural branch-cavernous sinus fistula
    • Cavernous sinus thrombosis
    • Ischemia from microvascular disease in vasa nervosa
    • Inflammatory - Tolosa-Hunt syndrome (idiopathic or granulomatous inflammation)
  • Fascicular orbital portion
    • Inflammatory - Orbital inflammatory pseudotumor, orbital myositis
    • Endocrine (thyroid orbitopathy)
    • Tumor (eg, hemangioma, lymphangioma, meningioma)
Contributor Information and Disclosures

James Goodwin, MD Associate Professor, Departments of Neurology and Ophthalmology, University of Illinois College of Medicine; Director, Neuro-Ophthalmology Service, University of Illinois Eye and Ear Infirmary

James Goodwin, MD is a member of the following medical societies: American Academy of Neurology, Illinois State Medical Society, North American Neuro-Ophthalmology Society, Royal Society of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Andrew G Lee, MD Chair, Department of Ophthalmology, Houston Methodist Hospital; Clinical Professor, Associate Program Director, Department of Ophthalmology and Visual Sciences, The University of Texas Medical Branch; Clinical Professor, Department of Surgery, Division of Head and Neck Surgery, University of Texas MD Anderson Cancer Center; Professor of Ophthalmology, Neurology, and Neurological Surgery, Weill Medical College of Cornell University; Clinical Associate Professor, University of Buffalo, State University of New York School of Medicine

Andrew G Lee, MD is a member of the following medical societies: American Academy of Ophthalmology, Association of University Professors of Ophthalmology, American Geriatrics Society, Houston Neurological Society, Houston Ophthalmological Society, International Council of Ophthalmology, North American Neuro-Ophthalmology Society, Pan-American Association of Ophthalmology, Texas Ophthalmological Association

Disclosure: Received ownership interest from Credential Protection for other.

Additional Contributors

Edsel Ing, MD, FRCSC Associate Professor, Department of Ophthalmology and Vision Sciences, University of Toronto Faculty of Medicine; Consulting Staff, Hospital for Sick Children and Sunnybrook Hospital

Edsel Ing, MD, FRCSC is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Ophthalmic Plastic and Reconstructive Surgery, Royal College of Physicians and Surgeons of Canada, Canadian Ophthalmological Society, North American Neuro-Ophthalmology Society, Canadian Society of Oculoplastic Surgery, European Society of Ophthalmic Plastic and Reconstructive Surgery, Canadian Medical Association, Ontario Medical Association, Statistical Society of Canada, Chinese Canadian Medical Society

Disclosure: Nothing to disclose.


Brian R Younge, MD Professor of Ophthalmology, Mayo Clinic School of Medicine

Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

  1. Warwick R. Representation of the extraocular muscles in the oculomotor nuclei of the monkey. J Comp Neurol. 1953 Jun. 98(3):449-503. [Medline].

  2. Vieira JP, Castro J, Gomes LB, et al. Ophthalmoplegic migraine and infundibular dilatation of a cerebral artery. Headache. 2008 Oct. 48(9):1372-4. [Medline].

  3. Bharucha DX, Campbell TB, Valencia I, et al. MRI findings in pediatric ophthalmoplegic migraine: a case report and literature review. Pediatr Neurol. 2007 Jul. 37(1):59-63. [Medline].

  4. Acierno MD, Trobe JD, Cornblath WT, et al. Painful oculomotor palsy caused by posterior-draining dural carotid cavernous fistulas. Arch Ophthalmol. 1995 Aug. 113(8):1045-9. [Medline].

  5. Ko JH, Kim YJ. Oculomotor nerve palsy caused by posterior communicating artery aneurysm: evaluation of symptoms after endovascular treatment. Interv Neuroradiol. 2011 Dec. 17(4):415-9. [Medline].

  6. Santillan A, Zink WE, Knopman J, Riina HA, Gobin YP. Early endovascular management of oculomotor nerve palsy associated with posterior communicating artery aneurysms. Interv Neuroradiol. 2010 Mar. 16(1):17-21. [Medline].

  7. Bahmani Kashkouli M, Khalatbari MR, Yahyavi ST, et al. Pituitary apoplexy presenting as acute painful isolated unilateral third cranial nerve palsy. Arch Iran Med. 2008 Jul. 11(4):466-8. [Medline].

  8. Quisling SV, Shah VA, Lee HK, et al. Magnetic resonance imaging of third cranial nerve palsy and trigeminal sensory loss caused by herpes zoster. J Neuroophthalmol. 2006 Mar. 26(1):47-8. [Medline].

  9. Yamada K, Shiga K, Kizu O. Oculomotor nerve palsy evaluated by diffusion-tensor tractography. Neuroradiology. 2006 Mar 15. [Medline].

  10. Chen W, Yang Y, Xing W, et al. Sixteen-row multislice computed tomography angiography in the diagnosis and characterization of intracranial aneurysms: comparison with conventional angiography and intraoperative findings. J Neurosurg. 2008 Jun. 108(6):1184-91. [Medline].

  11. Uysal E, Oztora F, Ozel A, et al. Detection and evaluation of intracranial aneurysms with 16-row multislice CT angiography: comparison with conventional angiography. Emerg Radiol. 2008 Sep. 15(5):311-6. [Medline].

  12. Asbury AK, Aldredge H, Hershberg R, et al. Oculomotor palsy in diabetes mellitus: a clinico-pathological study. Brain. 1970. 93(3):555-66. [Medline].

  13. Trobe JD. Isolated pupil-sparing third nerve palsy. Ophthalmology. 1985 Jan. 92(1):58-61. [Medline].

  14. Jacobson DM, McCanna TD, Layde PM. Risk factors for ischemic ocular motor nerve palsies. Arch Ophthalmol. 1994 Jul. 112(7):961-6. [Medline].

  15. Trobe JD. Third nerve palsy and the pupil. Footnotes to the rule. Arch Ophthalmol. 1988 May. 106(5):601-2. [Medline].

  16. Jacobson DM. Pupil involvement in patients with diabetes-associated oculomotor nerve palsy. Arch Ophthalmol. 1998 Jun. 116(6):723-7. [Medline].

  17. Yerramneni VK, Chandra PS, Kasliwal MK, Sinha S, Suri A, Gupta A, et al. Recovery of oculomotor nerve palsy following surgical clipping of posterior communicating artery aneurysms. Neurol India. 2010 Jan-Feb. 58(1):103-5. [Medline].

  18. Daniell MD, Gregson RM, Lee JP. Management of fixed divergent squint in third nerve palsy using traction sutures. Aust N Z J Ophthalmol. 1996 Aug. 24(3):261-5. [Medline].

  19. Chen PR, Amin-Hanjani S, Albuquerque FC, et al. Outcome of oculomotor nerve palsy from posterior communicating artery aneurysms: comparison of clipping and coiling. Neurosurgery. 2006 Jun. 58(6):1040-6; discussion 1040-6. [Medline].

  20. Leivo S, Hernesniemi J, Luukkonen M, et al. Early surgery improves the cure of aneurysm-induced oculomotor palsy. Surg Neurol. 1996 May. 45(5):430-4. [Medline].

  21. Burgess AW, Scheraga HA. A hypothesis for the pathway of the thermally-induced unfolding of bovine pancreatic ribonuclease. J Theor Biol. 1975 Sep. 53(2):403-20. [Medline].

  22. Jacobson DM, Broste SK. Early progression of ophthalmoplegia in patients with ischemic oculomotor nerve palsies. Arch Ophthalmol. 1995 Dec. 113(12):1535-7. [Medline].

  23. Keane JR. Aneurysms and third nerve palsies. Ann Neurol. 1983 Dec. 14(6):696-7. [Medline].

  24. Keane JR, Ahmadi J. Third-nerve palsies and angiography. Arch Neurol. 1991 May. 48(5):470. [Medline].

  25. Miller NR. The ocular motor nerves. Curr Opin Neurol. 1996 Feb. 9(1):21-5. [Medline].

  26. Park YH, Huh YE, Kim JS. Oculomotor nerve palsy as an initial manifestation of polycythemia vera. J Clin Neurosci. 2012 Feb. 19(2):328-30. [Medline].

  27. Trobe JD. Isolated third nerve palsies. Semin Neurol. 1986 Jun. 6(2):135-41. [Medline].

  28. Turner SJ, Dexter MA, Smith JE, Ouvrier R. Primary nerve repair following resection of a neurenteric cyst of the oculomotor nerve. J Neurosurg Pediatr. 2012 Jan. 9(1):45-8. [Medline].

Angiography anteroposterior and lateral views, left posterior communicating artery aneurysm, indicated by red arrow. Courtesy of James Goodwin, MD.
Patient with left posterior communicating artery aneurysm and third cranial nerve palsy. Courtesy of James Goodwin, MD.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.