Symptoms of entropion include:

- Redness and pain around the eye

- Sensitivity to light and wind

- Sagging skin around the eye

- Epiphora

- Decreased vision, especially if the cornea is damaged

Entropion is a medical condition in which the eyelid (usually the lower lid) folds inward. It is very uncomfortable, as the eyelashes continuously rub against the cornea causing irritation. Entropion is usually caused by genetic factors. This is different from when an extra fold of skin on the lower eyelid causes lashes to turn in towards the eye (epiblepharon). In epiblepharons, the eyelid margin itself is in the correct position, but the extra fold of skin causes the lashes to be misdirected. Entropion can also create secondary pain of the eye (leading to self trauma, scarring of the eyelid, or nerve damage). The upper or lower eyelid can be involved, and one or both eyes may be affected. When entropion occurs in both eyes, this is known as "bilateral entropion." Repeated cases of trachoma infection may cause scarring of the inner eyelid, which may cause entropion. In human cases, this condition is most common to people over 60 years of age.

In medicine, enophthalmia describes eyes that are abnormally sunken into their sockets. This condition usually affects elderly persons. Surgery can be done to correct it. Bilateral progressive enophthalmos may be the presenting sign of metastatic breast carcinoma even when local symptoms in the breast are absent.

Enophthalmos is the posterior displacement of the eyeball within the orbit due to changes in the volume of the orbit (bone) relative to its contents (the eyeball and orbital fat), or loss of function of the orbitalis muscle. It should not be confused with its opposite, exophthalmos, which is the anterior displacement of the eye.

It may be a congenital anomaly, or be acquired as a result of trauma (such as in a blowout fracture of the orbit), Horner's syndrome (apparent enophthalmos due to ptosis), Marfan syndrome, Duane's syndrome, silent sinus syndrome or phthisis bulbi.

Signs that are found in patients on the affected side of the face include

- partial ptosis

- upside-down ptosis (slight elevation of the lower lid)

- anhidrosis

- miosis

- pseudoenophthalmos (the impression that the eye is sunken, caused by a narrow palpebral aperture)

- pupillary dilation lag

- loss of ciliospinal reflex

- bloodshot conjunctiva, depending on the site of lesion.

- unilateral straight hair (in congenital Horner's syndrome); the hair on the affected side may be straight in some cases.

- heterochromia iridum (in congenital Horner's syndrome)

Interruption of sympathetic pathways leads to several implications. It inactivates the dilator muscle and thereby produces miosis. It inactivates the superior tarsal muscle which produces ptosis. It inactivates the orbitalis muscle which produces the effect of enophthalmos. It also reduces sweat secretion in the face.

Sometimes there is flushing on the affected side of the face due to dilation of blood vessels under the skin. The pupil's light reflex is maintained as this is controlled via the parasympathetic nervous system.

In children, Horner's syndrome sometimes leads to heterochromia, a difference in eye color between the two eyes. This happens because a lack of sympathetic stimulation in childhood interferes with melanin pigmentation of the melanocytes in the superficial stroma of the iris.

In veterinary medicine, signs can include partial closure of the third eyelid, or nictitating membrane.

Horner's syndrome is a combination of symptoms that arises when a group of nerves known as the sympathetic trunk is damaged. The signs and symptoms occur on the same side as the lesion of the sympathetic trunk. It is characterized by miosis (a constricted pupil), partial ptosis (a weak, droopy eyelid), apparent anhidrosis (decreased sweating), with or without enophthalmos (inset eyeball).

The nerves of the sympathetic trunk arise from the spinal cord in the chest, and from there ascend to the neck and face. The nerves are part of the sympathetic nervous system, a division of the autonomic (or involuntary) nervous system. Once the syndrome has been recognized, medical imaging and response to particular eye drops may be required to identify the location of the problem and the underlying cause.

Enophthalmos (recession of the eyeball within the orbit) is the most common eye abnormality observed in Parry–Romberg syndrome. It is caused by a loss of subcutaneous tissue around the orbit. Other common findings include drooping of the eyelid (ptosis), constriction of the pupil (miosis), redness of the conjunctiva, and decreased sweating (anhidrosis) of the affected side of the face. Collectively, these signs are referred to as Horner's syndrome. Other ocular abnormalities include ophthalmoplegia (paralysis of one or more of the extraocular muscles) and other types of strabismus, uveitis, and heterochromia of the iris.

Some clinically observed signs and symptoms include:

- Orbital pain

- Eyes displaced posteriorly into sockets (enophthalmos)

- Limitation of eye movement

- Loss of sensation (hypoesthesia) along the trigeminal (V2) nerve distribution

- Seeing-double when looking up or down (vertical diplopia)

- Orbital and lid subcutaneous emphysema, especially when blowing the nose or sneezing

- Nausea and bradycardia due to oculocardiac reflex

Neurological abnormalities are common. Roughly 45% of people with Parry–Romberg syndrome are also afflicted with trigeminal neuralgia (severe pain in the tissues supplied by the ipsilateral trigeminal nerve, including the forehead, eye, cheek, nose, mouth and jaw) and/or migraine (severe headaches that may be accompanied by visual abnormalities, nausea and vomiting).

10% of affected individuals develop a seizure disorder as part of the disease. The seizures are typically Jacksonian in nature (characterized by rapid spasms of a muscle group that subsequently spread to adjacent muscles) and occur on the side contralateral to the affected side of the face. Half of these cases are associated with abnormalities in both the gray and white matter of the brain—usually ipsilateral but sometimes contralateral—that are detectable on magnetic resonance imaging (MRI) scan.

Common medical causes of blowout fracture may include:

- Direct orbital blunt injury

- Sports injury (squash ball, tennis ball etc.)

- Motor vehicle accidents

Silent sinus syndrome is a spontaneous, asymptomatic collapse of the maxillary sinus and orbital floor associated with negative sinus pressures. It can cause painless facial asymmetry, diplopia and enophthalmos. Usually the diagnosis is suspected clinically, and it can be confirmed radiologically by characteristic imaging features that include maxillary sinus outlet obstruction, sinus opacification, and sinus volume loss caused by inward retraction of the sinus walls. Treatment is surgical involving making an outlet for mucous drainage from the obstructed sinus.

The ‘Harlequin Sign’ is unilateral flushing and sweating of the face, neck, and upper chest usually after exposure to heat or strenuous exertion. Horner syndrome, another problem associated with the sympathetic nervous system, is often seen in conjunction with harlequin syndrome.

Since Harlequin syndrome is associated with a dysfunction in the autonomic nervous system, main symptoms of this dysfunction are in the following: Absence of sweat(anhidrosis) and flushing on one side of the face, neck, or upper thoracic area. In addition, other symptoms include cluster headaches, tearing of the eyes, nasal discharge, abnormal contraction of the pupils, weakness in neck muscles, and drooping of on side of the upper eyelid.

One possible cause of Harlequin syndrome is a lesion to the preganglionic or postganglionic cervical sympathetic fibers and parasympathetic neurons of the ciliary ganglion. It is also believed that torsion (twisting) of the thoracic spine can cause blockage of the anterior radicular artery leading to Harlequin syndrome. The sympathetic deficit on the denervated side causes the flushing of the opposite side to appear more pronounced. It is unclear whether or not the response of the undamaged side was normal or excessive, but it is believed that it could be a result of the body attempting to compensate for the damaged side and maintain homeostasis.

Since the cause and mechanism of Harlequin syndrome is still unknown, there is no way to prevent this syndrome.

Lefort I - Slight swelling of the upper lip, ecchymosis is present in the buccal sulcus beneath each zygomatic arch, malocclusion, mobility of teeth. Impacted type of fractures may be almost immobile and it is only by grasping the maxillary teeth and applying a little firm pressure that a characteristic grate can be felt which is diagnostic of the fracture. Percussion of upper teeth results in cracked pot sound. Guérin's sign is present characterised by ecchymosis in the region of greater palatine vessels.

Lefort II and Lefort III (common) - Gross edema of soft tissue over the middle third of the face, bilateral circumorbital ecchymosis, bilateral subconjunctival hemorrhage, epistaxis, CSF rhinorrhoea, dish face deformity, diplopia, enophthalmos, cracked pot sound.

Lefort II - Step deformity at infraorbital margin, mobile mid face, anesthesia or paresthesia of cheek.

Lefort III - Tenderness and separation at frontozygomatic suture, lengthening of face, depression of ocular levels (enophthalmos), hooding of eyes, and tilting of occlusal plane, an imaginary curved plane between the edges of the incisors and the tips of the posterior teeth. As a result, there is gagging on the side of injury.

Diagnosis is suspected by physical exam and history, in which, classically, the hard and soft palate of the midface are mobile with respect to the remainder of facial structures. This finding can be inconsistent due to the midfacial bleeding and swelling that typically accompany such injuries, and so confirmation is usually needed by radiograph or CT.

In Marfan syndrome, the health of the eye can be affected in many ways but the principal change is partial lens dislocation, where the lens is shifted out of its normal position. This occurs because of weakness in the ciliary zonules, the connective tissue strands which suspend the lens within the eye. The mutations responsible for Marfan syndrome weaken the zonules and cause them to stretch. The inferior zonules are most frequently stretched resulting in the lens shifting upwards and outwards but it can shift in other directions as well. Nearsightedness and blurred vision are common, but farsightedness can also result particularly if the lens is highly subluxated. Subluxation (partial dislocation) of the lens can be detected clinically in 80% of patients by the use of a slit-lamp biomicroscope. If the lens subluxation is subtle then imaging with high-resolution ultrasound biomicroscopy might be used.

Other signs and symptoms affecting the eye include increased length along an axis of the globe, myopia, corneal flatness, strabismus, exotropia, and esotropia.

Most of the readily visible signs are associated with the skeletal system. Many individuals with Marfan syndrome grow to above-average height, and some have disproportionately long, slender limbs with thin, weak wrists and long fingers and toes. Besides affecting height and limb proportions, people with Marfan syndrome may have abnormal lateral curvature of the spine (scoliosis), thoracic lordosis, abnormal indentation (pectus excavatum) or protrusion (pectus carinatum) of the sternum, abnormal joint flexibility, a high-arched palate with crowded teeth and an overbite, flat feet, hammer toes, stooped shoulders, and unexplained stretch marks on the skin. It can also cause pain in the joints, bones and muscles. Some people with Marfan have speech disorders resulting from symptomatic high palates and small jaws. Early osteoarthritis may occur. Other signs include limited range of motion in the hips due to the femoral head protruding into abnormally deep hip sockets.

Aside from cancer general symptoms such as malaise, fever, weight loss and fatigue, Pancoast tumour can include a complete Horner's syndrome in severe cases: miosis (constriction of the pupils), anhidrosis (lack of sweating), ptosis (drooping of the eyelid) and enophthalmos (sunken eyeball). In progressive cases, the brachial plexus is also affected, causing pain and weakness in the muscles of the arm and hand with a symptomatology typical of thoracic outlet syndrome. The tumour can also compress the recurrent laryngeal nerve and from this a hoarse voice and bovine cough may occur.

In superior vena cava syndrome, obstruction of the superior vena cava by a tumour (mass effect) causes facial swelling cyanosis and dilatation of the veins of the head and neck.

A Pancoast tumor is an apical tumour that is typically found in conjunction with a smoking history. The clinical signs and symptoms can be confused with neurovascular compromise at the level of the superior thoracic aperture. The patient's smoking history, rapid onset of clinical signs and symptoms and pleuritic pain can suggest an apical tumour. A Pancoast tumor can give rise to both Pancoast syndrome and Horner's syndrome. When the brachial plexus roots are involved it will produce Pancoast syndrome; involvement of sympathetic fibres as they exit the cord at T1 and ascend to the superior cervical ganglion will produce Horner's syndrome.

A Pancoast tumor is a tumor of the pulmonary apex. It is a type of lung cancer defined primarily by its location situated at the top end of either the right or left lung. It typically spreads to nearby tissues such as the ribs and vertebrae. Most Pancoast tumors are non-small cell cancers.

The growing tumor can cause compression of a brachiocephalic vein, subclavian artery, phrenic nerve, recurrent laryngeal nerve, vagus nerve, or, characteristically, compression of a sympathetic ganglion (the superior cervical ganglion), resulting in a range of symptoms known as Horner's syndrome.

Pancoast tumors are named for Henry Pancoast, a US radiologist, who described them in 1924 and 1932.