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What is Horners syndrome and explain in detail?
Horners syndrome, also known as oculosympathetic paresis, 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 (ipsilateral) as it is a lesion of the sympathetic trunk. It is characterized by miosis (a constricted pupil), partial ptosis (a weak, droopy eyelid), apparent anhidrosis (decreased sweating), with apparent 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.

Signs and symptoms
Signs that are found in people with Horners syndrome on the affected side of the face include the following:

ptosis (drooping of the upper eyelid)
anhidrosis (decreased sweating)
miosis (constriction of the pupil)
Enophthalmos (sinking of the eyeball into the face)
inability to completely close or open the eyelid
facial flushing
headaches
loss of ciliospinal reflex
bloodshot conjunctiva, depending on the site of lesion.
unilateral straight hair (in congenital Horners syndrome); the hair on the affected side may be straight in some cases.
heterochromia iridum (in congenital Horners 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 reduces sweat secretion in the face. Patients may have apparent enophthalmos (affected eye looks to be slightly sunken in) but this is not always the case. The ptosis from inactivation of the superior tarsal muscle causes the eye to appear sunken in, but when actually measured, enophthalmos is not present. The phenomenon of enophthalmos is seen in Horners syndrome in cats, rats, and dogs.Sometimes there is flushing on the affected side of the face due to dilation of blood vessels under the skin.  The pupils light reflex is maintained as this is controlled via the parasympathetic nervous system.In children, Horners 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.

Causes
Horners syndrome is usually acquired as a result of disease, but may also be congenital (inborn, associated with heterochromatic iris) or iatrogenic (caused by medical treatment). In rare cases, Horners syndrome may be the result of repeated, minor head trauma, such as being hit with a soccer ball.  Although most causes are relatively benign, Horners syndrome may reflect serious disease in the neck or chest (such as a Pancoast tumor (tumor in the apex of the lung) or thyrocervical venous dilatation).Causes can be divided according to the presence and location of anhidrosis:
Central (anhidrosis of face, arm and trunk)
Syringomyelia
Multiple sclerosis
Encephalitis
Brain tumors
Lateral medullary syndrome
Preganglionic (anhidrosis of face)
Cervical rib traction on stellate ganglion
Thyroid carcinoma
Thyroidectomy
Goiter
Bronchogenic carcinoma of the superior fissure (Pancoast tumor) on apex of lung
Klumpke paralysis
Trauma - base of neck, usually blunt trauma, sometimes surgery.
As a complication of tube thoracostomy
Thoracic aortic aneurysm
Postganglionic (no anhidrosis)
Cluster headache - combination termed Hortons headache
An episode of Horners syndrome may occur during a migraine attack and be relieved afterwards
Carotid artery dissection/carotid artery aneurysm/trauma
Cavernous sinus thrombosis
Middle ear infection
Sympathectomy
Nerve blocks, such as cervical plexus block, stellate ganglion or interscalene block

Pathophysiology
Horner syndrome is due to a deficiency of sympathetic activity.
The site of lesion to the sympathetic outflow is on the ipsilateral side of the symptoms.
The following are examples of conditions that cause the clinical appearance of Horners syndrome:
First-order neuron disorder: Central lesions that involve the hypothalamospinal tract (e.g. transection of the cervical spinal cord).
Second-order neuron disorder: Preganglionic lesions (e.g. compression of the sympathetic chain by a lung tumor) that releases acetylcholine.
Third-order neuron disorder: Postganglionic lesions at the level of the internal carotid artery (e.g. a tumor in the cavernous sinus or a carotid artery dissection) that releases norepinephrine.
Partial Horners syndrome: In case of a third-neuron disorder, anhidrosis is limited to the middle part of the forehead or can be absent, resulting in a partial Horners syndrome.If patients have impaired sweating above the waist affecting only one side of the body, and they  do not have clinically apparent Horners syndrome, then their lesions are just below the stellate ganglion in the sympathetic chain.

Diagnosis
Three tests are useful in confirming the presence and severity of Horner syndrome:

Cocaine drop test: Cocaine eyedrops block the reuptake of post-ganglionic norepinephrine resulting in the dilation of a normal pupil from retention of norepinephrine in the synapse. However, in Horners syndrome the lack of norepinephrine in the synaptic cleft causes mydriatic failure.  A more recently introduced approach that is more dependable and obviates the difficulties in obtaining cocaine is to apply the alpha-agonist apraclonidine to both eyes and observe the increased mydriatic effect (due to hypersensitivity) on the affected side of Horner syndrome (the opposite effect to what the cocaine test would produce in the presence of Horners).
Paredrine test: This test helps to localize the cause of the miosis. If the third order neuron (the last of three neurons in the pathway which ultimately discharges norepinephrine into the synaptic cleft) is intact, then the amphetamine causes neurotransmitter vesicle release, thus releasing norepinephrine into the synaptic cleft and resulting in robust mydriasis of the affected pupil