Causes of anisocoria range from benign (normal) to life-threatening conditions.

Clinically, it is important to establish whether anisocoria is more apparent in dim or bright light to clarify whether the larger pupil or smaller pupil is the abnormal one.

- Anisocoria which is worsened (greater asymmetry between the pupils) in the dark suggests the small pupil (which should dilate in dark conditions) is the abnormal pupil and suggests Horner's syndrome or mechanical anisocoria. In Horner's syndrome sympathetic nerve fibers have a defect, therefore the pupil of the involved eye will not dilate in darkness. If the smaller pupil dilates in response to instillation of apraclonidine eye drops, this suggests Horner's syndrome is present.

- Anisocoria which is greater in bright light suggests the larger pupil (which should constrict in bright conditions) is the abnormal pupil. This may suggest Adie tonic pupil, pharmacologic dilation, oculomotor nerve palsy, or damaged iris.

A relative afferent pupillary defect (RAPD) also known as a Marcus Gunn pupil does not cause anisocoria.

Some of the causes of anisocoria are life-threatening, including Horner's syndrome (which may be due to carotid artery dissection) and oculomotor nerve palsy (due to a brain aneurysm, uncal herniation, or head trauma).

If the examiner is unsure whether the abnormal pupil is the constricted or dilated one, and if a one-sided drooping of the eyelid is present then the abnormally sized pupil can be presumed to be the one on the side of the ptosis. This is because Horner's syndrome and oculomotor nerve lesions both cause ptosis.

Anisocoria is usually a benign finding, unaccompanied by other symptoms (physiological anisocoria). Old face photographs of patients often help to diagnose and establish the type of anisocoria.

It should be considered an emergency if a patient develops acute onset anisocoria. These cases may be due to brain mass lesions which cause oculomotor nerve palsy. Anisocoria in the presence of confusion, decreased mental status, severe headache, or other neurological symptoms can forewarn a neurosurgical emergency. This is because a hemorrhage, tumor or another intracranial mass can enlarge to a size where the third cranial nerve (CN III) is compressed, which results in uninhibited dilatation of the pupil on the same side as the lesion.

Anisocoria is a common condition, defined by a difference of 0.4 mm or more between the sizes of the pupils of the eyes.

Anisocoria has various causes:

- Physiological anisocoria: About 20% of normal people have a slight difference in pupil size which is known as physiological anisocoria. In this condition, the difference between pupils is usually less than 1 mm.

- Horner's syndrome

- Mechanical anisocoria: Occasionally previous trauma, eye surgery, or inflammation (uveitis, angle closure glaucoma) can lead to adhesions between the iris and the lens.

- Adie tonic pupil: Tonic pupil is usually an isolated benign entity, presenting in young women. It may be associated with loss of deep tendon reflex (Adie's syndrome). Tonic pupil is characterized by delayed dilation of iris especially after near stimulus, segmental iris constriction, and sensitivity of pupil to a weak solution of pilocarpine.

- Oculomotor nerve palsy: Ischemia, intracranial aneurysm, demyelinating diseases (e.g., multiple sclerosis), head trauma, and brain tumors are the most common causes of oculomotor nerve palsy in adults. In ischemic lesions of the oculomotor nerve, pupillary function is usually spared whereas in compressive lesions the pupil is involved.

- Pharmacological agents with anticholinergic or sympathomimetic properties will cause anisocoria, particularly if instilled in one eye. Some examples of pharmacological agents which may affect the pupils include pilocarpine, cocaine, tropicamide, MDMA, dextromethorphan, and ergolines. Alkaloids present in plants of the genera "Brugmansia" and "Datura", such as scopolamine, may also induce anisocoria.

- Migraines

Relative afferent pupillary defect (RAPD) or Marcus Gunn pupil is a medical sign observed during the swinging-flashlight test whereupon the patient's pupils constrict less (therefore appearing to dilate) when a bright light is swung from the unaffected eye to the affected eye. The affected eye still senses the light and produces pupillary sphincter constriction to some degree, albeit reduced.

The most common cause of Marcus Gunn pupil is a lesion of the optic nerve (between the retina and the optic chiasm) or severe retinal disease. It is named after Scottish ophthalmologist Robert Marcus Gunn.

A second common cause of Marcus Gunn pupil is a contralateral optic tract lesion, due to the different contributions of the intact nasal and temporal hemifields.

The Marcus Gunn pupil is a relative afferent pupillary defect indicating a decreased pupillary response to light in the affected eye.

In the swinging flashlight test, a light is alternately shone into the left and right eyes. A normal response would be equal constriction of both pupils, regardless of which eye the light is directed at. This indicates an intact direct and consensual pupillary light reflex. When the test is performed in an eye with an afferent pupillary defect, light directed in the affected eye will cause only mild constriction of both pupils (due to decreased response to light from the afferent defect), while light in the unaffected eye will cause a normal constriction of both pupils (due to an intact efferent path, and an intact consensual pupillary reflex). Thus, light shone in the affected eye will produce less pupillary constriction than light shone in the unaffected eye.

A Marcus Gunn pupil is distinguished from a total CN II lesion, in which the affected eye perceives "no" light. In that case, shining the light in the affected eye produces no effect.

Anisocoria is absent. A Marcus Gunn pupil is seen, among other conditions, in optic neuritis. It is also common in retrobulbar optic neuritis due to multiple sclerosis but only for 3–4 weeks, until the visual acuity begins to improve in 1–2 weeks and may return to normal.

When detected during childhood, without any other symptoms and when other disorders are discarded through clinical tests, it should be considered a developmental or genetic phenomenon.

Asymmetric pupil or dyscoria, potential causes of anisocoria, refer to an abnormal shape of the pupil which can happens due to developmental and intrauterine anomalies.

Miosis is excessive constriction of the pupil. The term is from Ancient Greek , "mūein", "to close the eyes.

The opposite condition, mydriasis, is the dilation of the pupil. Anisocoria is the condition of one pupil being more dilated than the other.

The main characteristic that distinguishes physiological anisocoria is an increase of pupil size with lower light or reduced illumination, such that the pupils differ in size between the two eyes. At any given eye examination, up to 41% of healthy patients can show an anisocoria of 0.4 mm or more at one time or another. It can also occur as the difference between both pupils varies from day to day. A normal population survey showed that during poor light or near dark conditions, differences of 1 mm on average between pupils was found.

The presence of physiologic anisocoria has been estimated at 20% of the normal population, so some degree of pupil difference may be expected in at least 1 in 5 clinic patients.

In mechanical anisocoria, this is the result of damage to the iris dilator muscle, which may be caused by trauma, angle-closure glaucoma, surgery such as cataract removal, or uveitis (inflammation of the eye). Slit lamp examination is often used as a diagnostic aid: damage to the dilator muscle is indicated by anisocoria when light intensity is lowered.Anisocoria refers to a common eye condition in which the two pupils differ in size.

Mydriasis () is the dilation of the pupil, usually having a non-physiological cause, or sometimes a physiological pupillary response. Non-physiological causes of mydriasis include disease, trauma, or the use of drugs.

Normally, as part of the pupillary light reflex, the pupil dilates in the dark and constricts in the light to respectively improve vividity at night and to protect the retina from sunlight damage during the day. A "mydriatic" pupil will remain excessively large even in a bright environment. The excitation of the radial fibres of the iris which increases the pupillary aperture is referred to as a mydriasis. More generally, mydriasis also refers to the natural dilation of pupils, for instance in low light conditions or under sympathetic stimulation.

An informal term for mydriasis is blown pupil, and is used by medical providers. It is usually used to refer to a fixed, unilateral mydriasis, which could be a symptom of raised intracranial pressure.

The opposite, constriction of the pupil, is referred to as miosis. Both mydriasis and miosis can be physiological. Anisocoria is the condition of one pupil being more dilated than the other.

A mydriatic is an agent that induces dilation of the pupil. Drugs such as tropicamide are used in medicine to permit examination of the retina and other deep structures of the eye, and also to reduce painful ciliary muscle spasm (see cycloplegia). Phenylephrine (e.g. Cyclomydril) is used if strong mydriasis is needed for a surgical intervention. One effect of administration of a mydriatic is intolerance to bright light (photophobia). Purposefully-induced mydriasis via mydriatics is also used as a diagnostic test for Horner's syndrome.

Light entering the eye strikes three different photoreceptors in the retina: the familiar rods and cones used in image forming and the more newly discovered photosensitive ganglion cells. The ganglion cells give information about ambient light levels, and react sluggishly compared to the rods and cones. Signals from photosensitive ganglion cells have multiple functions including acute suppression of the hormone melatonin, entrainment of the body's circadian rhythms and regulation of the size of the pupil.

The retinal photoceptors convert light stimuli into electric impulses. Nerves involved in the resizing of the pupil connect to the pretectal nucleus of the high midbrain, bypassing the lateral geniculate nucleus and the primary visual cortex. From the pretectal nucleus neurons send axons to neurons of the Edinger-Westphal nucleus whose visceromotor axons run along both the left and right oculomotor nerves. Visceromotor nerve axons (which constitute a portion of cranial nerve III, along with the somatomotor portion derived from the Edinger-Westphal nucleus) synapse on ciliary ganglion neurons, whose parasympathetic axons innervate the iris sphincter muscle, producing miosis. This occurs because sympathetic activity from the ciliary ganglion is "lost" thus parasympathetics are not inhibited.

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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.

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.

Superficial siderosis is characterized by many symptoms resulting from brain damage:

- Sensorineural hearing loss- This is the most common symptom associated with superficial siderosis and its absence is rare. The highest pitches are often lost first, and over a period of one to twelve years hearing loss progresses to total deafness or loss of all hearing but low pitches.

- Ataxia- The impairment of gait, which is the second most common symptom.

- Pyramidal signs- Various signs that indicate a condition of the pyramidal tracts.

- Dementia- Occurs in approximately one-quarter of those affected by superficial siderosis.

- Disturbances of the bladder

- Anosmia- Loss of sense of smell.

- Anisocoria- Unequal size of pupils.

Onset occurs in infancy or early childhood, usually before 3 years of age. Progression is slow until the teenage years at which point it may accelerate, resulting in severe disability.

Symptoms are usually more severe and rapidly progressive than in the other more common Charcot–Marie–Tooth diseases. Some patients may never walk and solely use wheelchairs by the end of their first decade, while others may need only a cane (walking stick) or similar support through life.

Dejerine–Sottas disease is characterized by moderate to severe lower and upper extremity weakness and loss of sensation, which occur mainly in the lower legs, forearms, feet and hands. Loss of muscle mass and reduced muscle tone can occur as the disease progresses. Other symptoms may include pain in the extremities, curvature of the spine, clawed hands, foot deformities, ataxia, peripheral areflexia, and slow acquisition of motor skills in childhood. Symptoms that are less common can include limitation of eye movements, other eye problems such as nystagmus or anisocoria, or mild hearing loss.

Superficial hemosiderosis of the central nervous system is a disease of the brain resulting from chronic iron deposition in neuronal tissues associated with cerebrospinal fluid. This occurs via the deposition of hemosiderin in neuronal tissue, and is associated with neuronal loss, gliosis, and demyelination of neuronal cells. This disease was first discovered in 1908 by R.C. Hamill after performing an autopsy. Detection of this disease was largely post-mortem until the advent of MRI technology, which made diagnosis far easier. Superficial siderosis is largely considered a rare disease, with less than 270 total reported cases in scientific literature as of 2006, and affects people of a wide range of ages with men being approximately three times more frequently affected than women. The number of reported cases of superficial siderosis has increased with advances in MRI technology, but it remains a rare disease.

Dejerine–Sottas disease, also known as Dejerine–Sottas syndrome, Dejerine–Sottas neuropathy, progressive hypertrophic interstitial polyneuropathy of childhood and onion bulb neuropathy (and, "hereditary motor and sensory polyneuropathy type III" and "Charcot–Marie–Tooth disease type 3"), is a hereditary neurological disorder characterised by damage to the peripheral nerves and resulting progressive muscle wasting. The condition is caused by mutations in a various genes and currently has no known cure.

The disorder is named for Joseph Jules Dejerine and Jules Sottas, French neurologists who first described it.

Clinical manifestations of intraparenchymal hemorrhage are determined by the size and location of hemorrhage, but may include the following:

- Hypertension, fever, or cardiac arrhythmias

- Nuchal rigidity

- Subhyaloid retinal hemorrhages

- Altered level of consciousness

- Anisocoria, Nystagmus

- Focal neurological deficits

- Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopsia, aphasia, neglect, or apraxia

- Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion

- Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia

- Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion

- Brain stem - Tetraparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability

- Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousness

Symptoms are dependent on the type of TBI (diffuse or focal) and the part of the brain that is affected. Unconsciousness tends to last longer for people with injuries on the left side of the brain than for those with injuries on the right. Symptoms are also dependent on the injury's severity. With mild TBI, the patient may remain conscious or may lose consciousness for a few seconds or minutes. Other symptoms of mild TBI include headache, vomiting, nausea, lack of motor coordination, dizziness, difficulty balancing, lightheadedness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, and changes in sleep patterns. Cognitive and emotional symptoms include behavioral or mood changes, confusion, and trouble with memory, concentration, attention, or thinking. Mild TBI symptoms may also be present in moderate and severe injuries.

A person with a moderate or severe TBI may have a headache that does not go away, repeated vomiting or nausea, convulsions, an inability to awaken, dilation of one or both pupils, slurred speech, aphasia (word-finding difficulties), dysarthria (muscle weakness that causes disordered speech), weakness or numbness in the limbs, loss of coordination, confusion, restlessness, or agitation. Common long-term symptoms of moderate to severe TBI are changes in appropriate social behavior, deficits in social judgment, and cognitive changes, especially problems with sustained attention, processing speed, and executive functioning. Alexithymia, a deficiency in identifying, understanding, processing, and describing emotions occurs in 60.9% of individuals with TBI. Cognitive and social deficits have long-term consequences for the daily lives of people with moderate to severe TBI, but can be improved with appropriate rehabilitation.

When the pressure within the skull (intracranial pressure, abbreviated ICP) rises too high, it can be deadly. Signs of increased ICP include decreasing level of consciousness, paralysis or weakness on one side of the body, and a blown pupil, one that fails to constrict in response to light or is slow to do so. Cushing's triad, a slow heart rate with high blood pressure and respiratory depression is a classic manifestation of significantly raised ICP. Anisocoria, unequal pupil size, is another sign of serious TBI. Abnormal posturing, a characteristic positioning of the limbs caused by severe diffuse injury or high ICP, is an ominous sign.

Small children with moderate to severe TBI may have some of these symptoms but have difficulty communicating them. Other signs seen in young children include persistent crying, inability to be consoled, listlessness, refusal to nurse or eat, and irritability.

In younger patients, vascular malformations, specifically AVMs and cavernous angiomas are more common causes for hemorrhage. In addition, venous malformations are associated with hemorrhage.

In the elderly population, amyloid angiopathy is associated with cerebral infarcts as well as hemorrhage in superficial locations, rather than deep white matter or basal ganglia. These are usually described as "lobar". These bleedings are not associated with systemic amyloidosis.

Hemorrhagic neoplasms are more complex, heterogeneous bleeds often with associated edema. These hemorrhages are related to tumor necrosis, vascular invasion and neovascularity. Glioblastomas are the most common primary malignancies to hemorrhage while thyroid, renal cell carcinoma, melanoma, and lung cancer are the most common causes of hemorrhage from metastatic disease.

Other causes of intraparenchymal hemorrhage include hemorrhagic transformation of infarction which is usually in a classic vascular distribution and is seen in approximately 24 to 48 hours following the ischemic event. This hemorrhage rarely extends into the ventricular system.

Improvement of neurological function usually occurs for two or more years after the trauma. For many years it was believed that recovery was fastest during the first six months, but there is no evidence to support this. It may be related to services commonly being withdrawn after this period, rather than any physiological limitation to further progress. Children recover better in the immediate time frame and improve for longer periods.

Complications are distinct medical problems that may arise as a result of the TBI. The results of traumatic brain injury vary widely in type and duration; they include physical, cognitive, emotional, and behavioral complications. TBI can cause prolonged or permanent effects on consciousness, such as coma, brain death, persistent vegetative state (in which patients are unable to achieve a state of alertness to interact with their surroundings), and minimally conscious state (in which patients show minimal signs of being aware of self or environment). Lying still for long periods can cause complications including pressure sores, pneumonia or other infections, progressive multiple organ failure, and deep venous thrombosis, which can cause pulmonary embolism. Infections that can follow skull fractures and penetrating injuries include meningitis and abscesses. Complications involving the blood vessels include vasospasm, in which vessels constrict and restrict blood flow, the formation of aneurysms, in which the side of a vessel weakens and balloons out, and stroke.

Movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), myoclonus (shock-like contractions of muscles), and loss of movement range and control (in particular with a loss of movement repertoire). The risk of post-traumatic seizures increases with severity of trauma (image at right) and is particularly elevated with certain types of brain trauma such as cerebral contusions or hematomas. People with early seizures, those occurring within a week of injury, have an increased risk of post-traumatic epilepsy (recurrent seizures occurring more than a week after the initial trauma). People may lose or experience altered vision, hearing, or smell.

Hormonal disturbances may occur secondary to hypopituitarism, occurring immediately or years after injury in 10 to 15% of TBI patients. Development of diabetes insipidus or an electrolyte abnormality acutely after injury indicate need for endocrinologic work up. Signs and symptoms of hypopituitarism may develop and be screened for in adults with moderate TBI and in mild TBI with imaging abnormalities. Children with moderate to severe head injury may also develop hypopituitarism. Screening should take place 3 to 6 months, and 12 months after injury, but problems may occur more remotely.

Cognitive deficits that can follow TBI include impaired attention; disrupted insight, judgement, and thought; reduced processing speed; distractibility; and deficits in executive functions such as abstract reasoning, planning, problem-solving, and multitasking. Memory loss, the most common cognitive impairment among head-injured people, occurs in 20–79% of people with closed head trauma, depending on severity. People who have suffered TBI may also have difficulty with understanding or producing spoken or written language, or with more subtle aspects of communication such as body language. Post-concussion syndrome, a set of lasting symptoms experienced after mild TBI, can include physical, cognitive, emotional and behavioral problems such as headaches, dizziness, difficulty concentrating, and depression. Multiple TBIs may have a cumulative effect. A young person who receives a second concussion before symptoms from another one have healed may be at risk for developing a very rare but deadly condition called second-impact syndrome, in which the brain swells catastrophically after even a mild blow, with debilitating or deadly results. About one in five career boxers is affected by chronic traumatic brain injury (CTBI), which causes cognitive, behavioral, and physical impairments. Dementia pugilistica, the severe form of CTBI, affects primarily career boxers years after a boxing career. It commonly manifests as dementia, memory problems, and parkinsonism (tremors and lack of coordination).

TBI may cause emotional, social, or behavioral problems and changes in personality. These may include emotional instability, depression, anxiety, hypomania, mania, apathy, irritability, problems with social judgment, and impaired conversational skills. TBI appears to predispose survivors to psychiatric disorders including obsessive compulsive disorder, substance abuse, dysthymia, clinical depression, bipolar disorder, and anxiety disorders. In patients who have depression after TBI, suicidal ideation is not uncommon; the suicide rate among these persons is increased 2- to 3-fold. Social and behavioral symptoms that can follow TBI include disinhibition, inability to control anger, impulsiveness, lack of initiative, inappropriate sexual activity, asociality and social withdrawal, and changes in personality.

TBI also has a substantial impact on the functioning of family systems Caregiving family members and TBI survivors often significantly alter their familial roles and responsibilities following injury, creating significant change and strain on a family system. Typical challenges identified by families recovering from TBI include: frustration and impatience with one another, loss of former lives and relationships, difficulty setting reasonable goals, inability to effectively solve problems as a family, increased level of stress and household tension, changes in emotional dynamics, and overwhelming desire to return to pre-injury status. In addition, families may exhibit less effective functioning in areas including coping, problem solving and communication. Psychoeducation and counseling models have been demonstrated to be effective in minimizing family disruption

The early (prodromal) symptoms in adolescents and adults are nausea, loss of appetite, aching muscles, and headache. This is followed by the characteristic rash or oral sores, malaise, and a low-grade fever that signal the presence of the disease. Oral manifestations of the disease (enanthem) not uncommonly may precede the external rash (exanthem). In children the illness is not usually preceded by prodromal symptoms, and the first sign is the rash or the spots in the oral cavity. The rash begins as small red dots on the face, scalp, torso, upper arms and legs; progressing over 10–12 hours to small bumps, blisters and pustules; followed by umbilication and the formation of scabs.

At the blister stage, intense itching is usually present. Blisters may also occur on the palms, soles, and genital area. Commonly, visible evidence of the disease develops in the oral cavity and tonsil areas in the form of small ulcers which can be painful or itchy or both; this enanthem (internal rash) can precede the exanthem (external rash) by 1 to 3 days or can be concurrent. These symptoms of chickenpox appear 10 to 21 days after exposure to a contagious person. Adults may have a more widespread rash and longer fever, and they are more likely to experience complications, such as varicella pneumonia.

Because watery nasal discharge containing live virus usually precedes both exanthem (external rash) and enanthem (oral ulcers) by 1 to 2 days, the infected person actually becomes contagious one to two days before recognition of the disease. Contagiousness persists until all vesicular lesions have become dry crusts (scabs), which usually entails four or five days, by which time nasal shedding of live virus ceases.

The condition usually resolves by itself within a couple of weeks. The rash may, however, last for up to one month. Chickenpox is contagious starting from one to two days before the appearance of the rash and lasts until the lesions have crusted.

Chickenpox is rarely fatal, although it is generally more severe in adult men than in women or children. Non-immune pregnant women and those with a suppressed immune system are at highest risk of serious complications. Arterial ischemic stroke (AIS) associated with chickenpox in the previous year accounts for nearly one third of childhood AIS. The most common late complication of chickenpox is shingles (herpes zoster), caused by reactivation of the "varicella zoster" virus decades after the initial, often childhood, chickenpox infection.

During pregnancy the dangers to the fetus associated with a primary VZV infection are greater in the first six months. In the third trimester, the mother is more likely to have severe symptoms.

For pregnant women, antibodies produced as a result of immunization or previous infection are transferred via the placenta to the fetus.

Varicella infection in pregnant women could lead to spread via the placenta and infection of the fetus. If infection occurs during the first 28 weeks of gestation, this can lead to fetal varicella syndrome (also known as "congenital varicella syndrome"). Effects on the fetus can range in severity from underdeveloped toes and fingers to severe anal and bladder malformation. Possible problems include:

- Damage to brain: encephalitis, microcephaly, hydrocephaly, aplasia of brain

- Damage to the eye: optic stalk, optic cup, and lens vesicles, microphthalmia, cataracts, chorioretinitis, optic atrophy

- Other neurological disorder: damage to cervical and lumbosacral spinal cord, motor/sensory deficits, absent deep tendon reflexes, anisocoria/Horner's syndrome

- Damage to body: hypoplasia of upper/lower extremities, anal and bladder sphincter dysfunction

- Skin disorders: (cicatricial) skin lesions, hypopigmentation

Infection late in gestation or immediately following birth is referred to as ""neonatal varicella"". Maternal infection is associated with premature delivery. The risk of the baby developing the disease is greatest following exposure to infection in the period 7 days before delivery and up to 8 days following the birth. The baby may also be exposed to the virus via infectious siblings or other contacts, but this is of less concern if the mother is immune. Newborns who develop symptoms are at a high risk of pneumonia and other serious complications of the disease.